Clinical

Skills
Additional Notes 2009

CLINICAL SKILLS

Medical History
Taking

CLINICAL COACHING:

TAKING A HISTORY

The most important part if a medical consultation is the gathering of information. A good history is
all a diagnostician needs to formulate a hypothesis. The examination is then used to test the
hypothesis
i)
History taking
ii)
Examination
iii)
Investigations

HISTORY TAKING
Introduce yourself
e.g. Hello Mr Smith, my name is Rachel and I am a first year medical student. I have been asked to
chat with you about why youre in hospital, and your medical history. Is that OK with you?
Could you tell me a little but about yourself? patients age, birth date, address, occupation,
marital and family status etc
PC (Presenting Complaint)
What concern brought you in here today?
HPC (History of the Presenting Complaint)
Nature
Intensity
Location
Duration
Onset
Contributing
Aggravating
Alleviating
Radiating
Features
Impact
Attribute (What do you think is causing this Problem?)
Treatment (Taking anything for it?)
Associated symptoms (e.g. if cough sputum?; Is there anything else you can think to
tell me?
PMH (Past Medical History)
-Medical, Surgical, Trauma, Obstetric (female)
Apart from this illness, please tell me about any other illnesses, accidents or operations you have
had
Have you ever been in hospital for anything?
Have you ever been pregnant? Tell me about your pregnancies.

 Drugs and Allergies

-current medications, dosages, and why taking it, (ask for contraceptive pill and
asthma inhaler!!!)
- over the counter meds
-recently stopped meds and why
-adverse drug reactions
-vaccinations
-herbal, vitamin and nutritional supplements
-recreational drug use
-allergies?
FH (Family History)
Are your parents still alive? How is their health?
-brothers, sisters, children, How are they
Any disease/ conditions that run in the family?

SH (Social History)
- age, race, sex, religion, partner, education
-Occupation (where, what?)
-Lifestyle
- cigarettes # pack years (1 pack year = 20 cig/ day/ year)
- alcohol, caffeine, recreational drugs
-diet, exercise, hobbies
-living conditions
ROS (Review of Systems)
Apart from the presenting complaint, how is your health?

Conclusion:
Is there anything else youd like to take about today?
That has given me a pretty clear history of your presenting problem. Is there anything you would
like to add at all? Any other concerns? Thank you very much for you time Mr Smith.
-a follow up arrangement should be arranges (and the patient should be encouraged to make
contact sooner if symptoms worsen or they have further concerns.

EXAMPLE OF PATIENT HISTORY TEMPLATE (blank template on next page...)

Name: _____________________

INTRODUCTION

Age: _____

Date:________

PP (Patient Particulars)
-name, age, DOB, occupation?

PC (Presenting Complaint)
HPC

What concern brought you in here today?

(History of Presenting Complaint)

*Also-Associated
associated symptoms
andROS
ROScan
canbe
be done
done here
symptoms?
here.

Nature
Intensity
Location
What concern brought you in here today?
Duration
Onset
Contributing
Aggravating
Alleviating
Radiating
Features
Impact
Attribute (What do you think is causing this Problem?) -Anyone around with similar symptoms?
Treatment (Taking anything for it?)
-Psych impact?
*Psych impact?

SUMMARY of PC

PMH (Past Medical History)

Apart from this can you tell me about any other illnesses/
surgeries youve had?

-medical, surgical, trauma, obstetrics

-drugs/ allergies
-asthma meds, OCP, vaccinations, supplements?
-asthma meds, OCP, vaccinations, supplements?

History)
FH
-Home(Family
life?
-stressed? Over-worked?
-How is home life?
-stressed? Overwhelmed?

SH (Social History)

Are your parents still alive? How is there health?

How about brothers or sisters?
Any diseases or conditions that run in the family?

e.g. Smoking

How many packs a day?

What sized packs?
When did you start smoking?
Has the amount you have smoked changed over time?

-age, race, sex, religion, partners, education

-occupation
QUANITIFY
-lifestyle (cigarettes, alcohol, caffeine, recreational drugs, diet, exercise, travel) (QUANTIFY)

ROS (System Review)

SUMMARY of IMPORTANT POINTS Is there anything else you want to tell me?
CONCLUSION Thats given me a pretty clear history of your PC. Is there anything you would like to add
at all? Any other concerns? Thank-you for your time.

INTRODUCTION

Name: ___________________________

Age: _____

Date:__________

PP (Patient Particulars)

-name, age, DOB, occupation?

PC (Presenting Complaint)
HPC

(History of Presenting Complaint)

*Also-Associated
associated symptoms
andROS
ROScan
canbe
be done
done here
symptoms?
here.

Nature
Intensity
Location
Duration
Onset
Contributing
Aggravating
Alleviating
Radiating
Features
Impact
Attribute (What do you think is causing this Problem?) -Anyone around with similar symptoms?
Treatment (Taking anything for it?)
-Psych impact?
*Psych impact?

SUMMARY of PC

PMH (Past Medical History)

-medical, surgical, trauma, obstetrics
-drugs/ allergies
-asthma meds, OCP, vaccinations, supplements?
-asthma meds, OCP, vaccinations, supplements?

History)
FH
-Home(Family
life?
-stressed? Over-worked?
-How is home life?
-stressed? Overwhelmed?

SH (Social History)
-age, race, sex, religion, partners, education
-occupation
QUANITIFY
-lifestyle (cigarettes, alcohol, caffeine, recreational drugs, diet, exercise, travel) (QUANTIFY)

ROS (System Review)

SUMMARY of IMPORTANT POINTS
CONCLUSION

ASSOCIATED SYMPTOMS/ ROS

CARDIO-VASCULAR
Pain, shortness of breath, heart beating irregularly, pain in legs or feet, high blood pressure,
ever had blue hands or feet?
RESPIRATORY
Short of breath, cough- sputum/ phlegm (colour? blood? etc), wheeze, fever, recent chest xray?
GASTRO-INTESTINAL
Indigestion, heart-burn, difficulty swallowing, nausea/ vomiting (blood?), pain, bloating,
bowel habits/ stool (blood?), weight loss, yellow skin or eyes, blood transfusions?
MUSCKULO-SKELETAL
Pain, skin rash, swelling, eyes dry or red, back/ neck pain
ENDOCRINE
Unusually thirsty, sweating, appetite or weight changes, lethargy, hair distribution, polyuria,
menstruation?
REPRODUCTIVE
History of high blood pressure or diabetes with pregnancy, miscarriage?

MEDICAL INTERVIEW: CLINICAL COMMUNICATION SKILLS SHEET

STUDENTS NAME: __________________________________ GROUP No.____
DATE OF ASSESSMENT: _______________TUTORS NAME: _______________
Code: 1=not acceptable, 2=not quite good enough, 3=OK, 4=good, 5=excellent
MICRO SKILLS
INTRODUCTION
introduces self
explains purpose of interview
enquiries if patient is comfortable with the situation
LANGUAGE
avoids ambiguous and technical jargon
avoids repetition.
ACTIVE LISTENING
listens with minimal interruptions unless necessary
paraphrases
facilitates the discussion
gives verbal and non-verbal encouragement
encourages interaction, receptivity
uses transition statements
QUESTIONS
shows good use of open questions
avoids excessive use of leading, loaded or closed questions
avoids double-barrelled and multiple questions
avoids irrelevant questions
EYE CONTACT, BODY POSTURE, MANNERISMS
natural, regular, attentive and direct eye contact (without staring)
relaxed but attentive body posture - not rigid, symmetrical, slouched or
bored
no awkward, excessive or intrusive mannerisms, verbal or non-verbal
behaviour which occurs repetitively
VERBAL FLUENCY, VOICE PROJECTION
average to slightly slower than average speech rate, not too fast,
impatient, slow or hesitant
clearly audible voice volume not too loud or too soft
SELF ASSURANCE
confident, open and relaxed not shy or embarrassed
WARMTH AND EMPATHY
voice tone warm and expressive, smiling where appropriate
positive regard for the patient
caring, attentive and non-judgemental concern
APPROPRIATE NOTE-TAKING
took notes
does not intrude or interfere with the interview
May use paper-and-pen or laptop
CLOSING
gives clear concluding statement summarises main points
enquires if patient has anything to add or ask

CODE

Comments

thanks the patient

(B)HIGHER ORDER SKILLS
CUE IDENTIFICATION AND INTERPRETATION
appropriate response to, and understanding of patients statements
follows up on verbal leads
sensitive to patients non-verbal cues
CONCENTRATES ON PATIENT RATHER THAN THE MECHANICS OF THE
INTERVIEW
not preoccupied with What will I say next.
CONTROL
controls and gives some direction to the interview but does not
dominate the interview
keeps patient relevant without overriding the patients free flow of
information
*HANDLES EXPLICIT QUESTIONS APPROPRIATELY
HANDLES PATIENTS FEELINGS AND CONCERNS
elicits patients feelings, fears, apprehensions, expectations and
acknowledges patients feelings appropriately (e.g. reflects patients
feelings non-judgmentally)
HISTORY TAKING
uses the bio-psychosocial approach
elicits course, duration and current treatment of the problem
encourages patient to be precise about dates of onset of illness, major
events and recent events
establishes patients
past illnesses
operations
family history
medications
establishes lifestyle
diet
exercise
smoking
alcohol
marital status/family responsibilities
occupation
SYSTEMATIC APPROACH
logical sequence and structure to the interview
HYPOTHESIS GENERATION AND TESTING
appears to generate and test hypotheses about the nature of the
patients problem/s.
TIME MANAGEMENT
manages time in the interview appropriately.
*Patient may not always ask questions (score N/A )

CLINICAL SKILLS

Introduction to
Physical
Examination

NOTE:
Leave distressing/ uncomfortable examinations LAST!
It is tradition to examine from the RIGHT SIDE of the patient.
Tell me if you feel uncomfortable of in pain at any time.

These are the lymph nodes that can be palpated when performing a physical examination.

LYMPH NODES:
LYMPHADENOPATHY: swollen, enlarged lymph nodes

CLINICAL SKILLS

Gastro-intestinal
System Exam

GASTRO-INTESTINAL EXAMINATION
The Gastro-intestinal History
Red flags to look for:
-Change in appetite
-Unintentional weight loss/ gain
-Dysphagia (difficulty swallowing)
-Indigestion/ heart-burn
-Nausea or vomiting
-Haematemesis (vomiting blood) (is blood fresh (red), or is it like coffee grounds)
-Abdominal pain
-Jaundice (yellowish tinge to eyes and skin)
-Change in bowel motions
-Blood in stool?- obvious red blood- lower GIT (e.g. haemorrhoids, cancer)
-mixed blood (e.g. inflammatory bowel)
-malaena upper GIT black digested blood (e.g. gastric ulcer)

The Gastro-intestinal Examination

2

BMI (body mass index) = mass (kg)/ height (m)

<18: very underweight
18-20: underweight
NOTE
20-25: acceptable
Waste-to-hip ratio is a better predictor
26-29: overweight
of heart attack than BMI
30-39: obese
>40: morbidly obese
Hepatic Flap (asterixis):
Asterixis describes a motor disturbance characterised by intermittent lapses of an assumed posture. It is commonly
associated with liver failure where it produces the flapping tremor of hepatic encephalopathy characterised by jerky,
irregular flexion-extension movements at the wrist and metacarpophalangeal joints, often accompanied by lateral
movements of the fingers.
The motor disturbance may rarely involve the arms, neck, tongue, jaw and
eyelids. It is usually bilateral, absent at rest, and asynchronous on each side.
The mechanism is attributed to interference with the inflow of joint position
sense to the reticular formation in the brainstem.

Bruising: Petechiae (small red dots), Purpura (bruises), Ecchymoses (very large bruises)
-can be caused by aspirin, steroids, in elderly, malignancy with platelets, problems with clotting factors
(synthesized in LIVER)

Petechiae: red or purple spot caused

by minor haemorrhage (<0.3cm)

Purpura: (0.3-1cm)

Ecchymosis: larger size than

petechia, but more diffuse
border than purpure (>1cm)

Linea nigra:
A dark vertical line that appears on the abdomen during about three quarters of all
pregnancies. The brownish streak is usually about a centimeter in width. The line runs
vertically along the midline of the abdomen from the pubis to the xiphoid process.
It is a type of hyperpigmentation resulting from increased production of the pigment
melanin thought to be caused by increased estrogen, the same process that causes the
areolas to darken

Divarication of the Recti (hernia):

The rectus abdominis muscles should meet in the midline at the linea alba. Superior to the umbilicus, some people
have a congenital defect that results in a wider gap between them. As a result, when a patient flexes the abdominal
muscles as when doing a sit-up, the rectus muscles spread apart (divaricate), and causes a bulge (slight hernia). The
divarication is made more obvious when the patient lifts their head or legs off the bed when supine.
Divarication is common in obese men, and those with poor muscle tone. It can be surgically corrected, although such
an operation would be almost entirely for cosmetic purposes and not of any functional value.

Palpation: check for pain/ tenderness, shape (are borders smooth?), size, texture or organs (firm?), pulsations
is a mass part of or behind abdominal wall? Tense abdomen (lift/ raise head) and if you can still feel the mass
its part of the abdominal wall)

Murphys sign:
Pain -sub-costal, upper-right quadrant semi-lunaris = GALLBLADDER pathology sign

Splenomegaly:
Splenomegaly is usually associated with increased workload (such as in hemolytic anemias), which suggests that it is a
response to hyperfunction. Splenomegaly is associated with any disease process that involves abnormal red blood cells
being destroyed in the spleen. Other common causes include congestion due to portal hypertension and infiltration by
leukaemias and lymphomas. The finding of an enlarged spleen; along with caput medusa; is an important sign of portal
hypertension.
Percussion in last intercostals space on left side, breath in and out, in resonance?- if becomes dull- indication
of splenomegaly

Bruit:
Any of several generally abnormal sounds heard on auscultation <an audible bruit produced by an artery. A hard,
whooshing sound. E.g. turbulence in an artery, sign of atherosclerosis (especially in carotid artery).

Oedema:
An abnormal excess accumulation of serous fluid in connective tissue or in a serous cavity. Can indicate diabetes or
alcoholism. If bed bound- oedema will be sacral and not in the legs.
Five factors can contribute to the formation of edema:
i)
It may be facilitated by increased hydrostatic pressure or,
ii)
reduced oncotic pressure within blood vessels;
iii)
by increased blood vessel wall permeability as in inflammation;
iv)
by obstruction of fluid clearance via the lymphatic; or,
v)
by changes in the water retaining properties of the tissues themselves. Raised hydrostatic
pressure often reflects retention of water and sodium by the kidney.

Ascites: is an accumulation of fluid in the peritoneal cavity. Although most commonly due to cirrhosis and
severe liver disease, its presence can portend other significant medical problems

Finding Direction of Venous Blood Flow

Examiners
fingers

If fills, blood flow

Push blood away

Let go of
finger

Vein
X filling,
blood flow

Hereditary haemochromatosis is associated with bronzing/

hyperpigmentation of the skin (excess iron deposition in the liver,
heart and pancreas leads to fibrosis and organ failure, if untreated)

Leukonychia- white
nail bed, typically of
thumb index finger
Koilonychia: spoon-shaped
nails due to iron deficiency

Palmar erythema: reddening of thenar

(thumb)/ hypothenar (pinky) eminences;
suggestive of liver disease (disturbed
[hormones], or alcohol)

Dupuytrens Contracture: thickeing of

palmar fascia, esp ring finger
(associated with alcoholism, diabetes
mellitus, epilepsy and smoking) -feel for
it as well

Clubbing: ~1/3 cirrhosis patients,

angle between plate and proximal nail
fold >180 (also respiratory disorders
and inflammatory bowel disease)

Xanthelasma: yellowish periorbital plaques, associated with

hyperlipidaemia

Spider naevi: small angiomata on surface

of skin, particularly on face, neck,
shoulders. Thorax, arms, hands
(~[hormones], eg. Oestrogen (males 2-3,
females 5-6)

Bruises (purpura):
-petechiae (1-2mm); small, red dots
-ecchymoses; very large bruises
NB. Can be due to problem with clotting
factors, .: liver problem, & VitK
deficiency)

Jaundice: (scleral icterus) yellowing

of skin and eyes due to bilirubin (sign
of liver disease)

Hepatic Flap (asterixis): bilateral

asynchronous flapping of outstretched
dorsiflexed hands seen in patients with
hepatic encephalopathy (aka flapping
tremor, liver flap)

Iritis: a form of anterior uveitis, and

refers to inflammation of the iris (acute
and chronic), can get with Crohns
Disease

Telangiectasia: small dilated blood vessels

near surface of skin or mucous membranes
Geographic tongue (benign
migratory glossitis) Papillae missing
from some areas and over-crowded in
others

Gingivitis: erythema and oedema of

gingival margins (with blunting and
hypertrophy of the interdental papillae)

Oral candidiasis: creamy, white curdlike patches, caused by Candida

albicans, can be scraped away leaving
bleeding surface

Glossitis: infection/ inflammation of

tongue (smoothened appearance- loss
of papillae) (IF & VitB deficiency~ one
cause)

Leukoplakia: white thickened patched

on mucosa, gums or tongue
Aphthous stomatitis: single or
multiple painful ulcerations of the
buccal mucosa (immune reaction to
oral bacteria?)

Striae: Caused by stretching due to growth

and also hormonal changes

Gynaecomastia: hormone-induces
swelling of male breast
(hyperoestrogenism?)- seen frequently with
cirrhosis

Caput Medusae
with ascites

Ascites:
fluid in
peritoneal
cavity,
abdominal
flanks and wall
appear tense,
shallow or
everted
umbilicus
facing
downwards
(gross ascites
umbilical
hernia?)

Caput Medusae: rare sign of porto-systemic shunting (engorged

para-umbilical veins radiating fro umbilicus to join systemic vein)
severe portal hypertension (flows to legs)
(check direction of venous blood flow)
VS Inferior Vena Cava Obstruction: Abdominal collateral veins
develop to bypass the blocked IVC and flows to head

CLINICAL SKILLS

Respiratory
System Exam

RESPIRATORY EXAMINATION
Bronchiectasis: a chronic inflammatory or degenerative condition of one or more bronchi or bronchioles marked by
dilatation and loss of elasticity of the walls
Bronchitis: acute or chronic inflammation of the bronchial tubes
Displaced Septum: deviation of the nasal septum from its normal position that results from a developmental
abnormality or trauma and may be asymptomatic or cause nasal obstruction and predispose to sinusitis and nosebleed
(nasal obstruction?? Talley and OConnor)
Engorged Turbinates (nasal chonchae): can be caused by various allergic conditions
Flapping Tremor: (asterixis) may occur with severe carbon dioxide retention, usually due to severe chronic obstructive
pulmonary disease, however this is a late and unreliable sign
Haemoptysis: expectoration of blood from some part of the respiratory tract
Horners syndrome: a syndrome marked by sinking in of the eyeball, contraction of the pupil, drooping of the upper
eyelid, and vasodilation and anhidrosis of the face, and caused by paralysis of the cervical sympathetic nerve fibers on
the affected side
PND (postnasal drip): occurs when excessive mucus is produced by the sinuses. The excess mucus accumulates in
the throat or back of the nose. It can be caused by rhinitis (allergic or non-allergic), sinusitis (acute or chronic),
laryngopharyngeal acid reflux (with or without heartburn), or by a disorder of swallowing (such as an esophageal motility
disorder).
Pulsus paradoxus: a pulse that weakens abnormally during inspiration and is symptomatic of various abnormalities (as
in pericarditis)
Rhinitis: inflammation of the mucous membrane of the nose marked especially by rhinorrhea, nasal congestion and
itching, and sneezing
Sinusitis: sinuses are tender on palpation
Stridor: a harsh vibrating sound heard during respiration in cases of obstruction of the air passages <laryngeal stridor>
-high ptch sound from turbulent air flow
Urticaria: (hives) an allergic disorder marked by raised oedematous red patches of skin or mucous membrane and
usually by intense itching and caused by contact with a specific precipitating factor (as a food, drug, or inhalant) either
externally or internally

Dyspnoea: difficult or laboured respiration,

~breathlessness
Class I: disease present but no dyspnoea or
dyspnoea only on heavy exertion
Class II: dyspnoea on moderate exertion
Class III: dyspnoea on minimal exertion
Class IV: dyspnoea at rest

Clubbing: patient with carcinoma of the lung has

clubbing and hypertrophic pulmonary osteroarthopathy.
Clubbing may be caused by platelet-derived growth
factor, which activates fibroblasts and other connective
tissue cells when platelet precursors lodge in the digitis.

Yellow Nail Syndrome: rare

condition caused by hypoplasia
of the lymphatic system. The
nails are thickened and yellow,
and there is separation of the
distal nail plate from the nail bed
(onchyolysis). It may be
associated with pleural effusion
and bronchiectasis, and usually
lymphoedema of the legs.

Clubbing of the fingers of a HIV- positive 11 year old

child due to chronic hypoxia. Pulmonary complications
are common in HIV-infected children in the first decade
of life and may progress to bronchiectasis.

Horners Syndrome: (left) The pupil of the affected eye

is smaller (miotic), due to unbalanced sympathetic action;
there is a partial ptosis of the upper eyelid, since
sympathetic fibres supply the smooth muscle of the
eyelid, and perhaps loss of sweating on the left forehead.
The meiotic pupil responds briskly to light and near effort.
This may be caused by a carcinoma in the apex of the
left lung compressing the brachial plexus. If this is the
case, the patient may also show weakness of finger
abduction, and clubbing. Disruption of the sympathetic
innervations to the eye anywhere along its path from the
brain can result in an ipsilateral Horners syndrome.

Nasal Polyp: a projecting mass of swollen and

hypertrophied or tumorous membrane of the nose
or para-nasal sinuses. They are overgrowths of the
mucosa that frequently accompany allergic rhinitis.
They are freely moveable and non-tender.
Associated with asthma (Talley and OConnor).

Oral/ pharyngeal thrush: due to candida infection

Exudative tonsillitis: caused by the Epstein Barr

virus. It may be mistaken for a bacterial tonsillitis,
although glandular fever may be accompanied by
tender enlargement of the liver and spleen, fevers
and fatigue. If a penicillin, especially amoxicillin,
is prescribed to a patient with glandular fever, the
patient develops a rash.

Ulceration: The oral lesions

of hand, foot and mouth
disease are various-sized
erosions and ulcerations on a
surrounding erythematous
base. Coxsackie virus A16 is
the most common cause.
Hand, foot and mouth
disease most commonly
occurs in children under the
age of ten, and is also
associated with lesions on
the hands, palms and soles.

Pharyngitis (Streptococcal): Typically affects

school-aged children, although adults may also
be susceptible. This slide illustrates pharyngeal
erythema, exudates and lymphoid enlargement.
There is a right peritonsillar abscess, displacing
the tonsil to the midline.

Barrel-Chest: when AP diameter is

increased compared to lateral diameter
beyond 0.9 is abnormal, and is seen in
patients with sever asthma or
emphysema

Pectus excavatum: funnel-chest.

Concurrent respiratory diseases
may occur in association with pectus
excavatum, including bronchiectasis,
asthma and chronic bronchitis.

Pectus carinatum: pigeon chest,

involving anterior displacement of the
sternum and costal cartilage. May be
manifestation of childhood respiratory
illness, in which case it is thought to
result from repeated strong
contraction of diaphragm while thorax
is still pliable. Also occurs in rickets.

Chest X-ray Checklist

Kyphoscoliosis: backward and lateral curvature of the spine.

Kyphoscoliosis may be idiopathic (80%), secondary to
poliomyelitis, or associated with Marfans syndrome. Severe
thoracic kyphoscoliosis may reduce lung capacity and
increase work of breathing.

Normal Chest X-Ray

A- Airway (midline, no obvious deformities, no

paratracheal masses)
B- Bones and soft tissue (no fractures, subcutaneous emphysema)
C- Cardiac size, silhouette and retrocardiac
density normal
D- Diaphragms (right above left by 1cm to 3cm,
costophrenic angles sharp, diaphragmatic
contrast with lung sharp)
E- Equal volume (count ribs, look for mediastinal
shift)
F- Fine detail (pleura and lung parenchyma)
G- gastric bubble (above the air bubble one
shouldnt see an opacity of more than 0.5cm
width)
H- Hilum (left normally above right by up to 3cm,
no larger than a thumb), hardware (in the
intensive care unit: endotracheal tube, central
venous catheters).

Bilateral lower lobe consolidations: (in a HIV patient).

Clinically, we would expect reduced lung expansion,
dullness to percussion, bronchial breath sounds, crackles,
increased vocal resonance, and perhaps pleural rubs. The
blood cultures were positive for Haemophilus influenza.
This illness followed a rapidly fulminating course, and the
patient died.
Consolidations: due to bacterial lobar pneumonia, but a
central bronchostenotic lesion should be considered.

Pneumothorax: (right-side) a condition in which air or

other gas is present in the pleural cavity and which
occurs spontaneously as a result of disease or injury of
lung tissue, rupture of air-filled pulmonary cysts, or
puncture of the chest wall or is induced as a therapeutic
measure to collapse the lung

Chronic Obstructive
Pulmonary Disease: This
chest X-ray of a heavy
smoker shows hyperinflated lungs, a flattened
diaphragm, and a long
narrow cardiac silhouette.
Clinically, there may be the
use of accessory muscles
during inspiration, pursed
lips during expiration, a
barrel-shaped chest with
reduced lung expansion,
hyper-resonant
percussion, decreased
liver dullness, decreased
breath sounds and early
inspiratory crackles.

Pleural Effusion: This chest x-ray

shows moderate-sized right side
pleural effusion. This patient
presented with a fever, cough and
dyspnoea. Clinically, we would expect
reduced lung expansion on the right,
stony dullness to percussion, reduced
or absent breath sounds, and reduced
vocal resonance. Chlamydia
pneumonia was isolated from the
pleural fluid and nasopharyngeal
culture.
NB: the upper margin of the effusion
is curved meniscus sign (Talley).

Right Lower Lobe

Pneumonia: This Xray shows a density in
the right lower lobe.
Clinically you may find
reduced expansion on
the affected side,
dullness (but not stony
dullness) to
percussion, bronchial
breath sounds,
inspiratory crackles,
increased vocal
resonance, and
perhaps a pleural rub.

NOTES FROM CLINICAL COACHING ~ RESPIRATORY EXAMINATION

th

-mitral valve 5 intercostals space inside the mid-clavicular line on the left side
GENERAL OBSERVATIONS
-barrel-chest can be normal body shape (esp if excess weight), or due to asthma or smoking (i.e.
emphysema)
HAND & UPPER LIMB
- look for anaemia- pallor of the palmar creases
-check for peripheral cyanosis (bluish tinge)
NOTE: If RBCs cyanosis occurs later on (as low O2 saturation occurs later on)
Vs RBCs (e.g. due to polycythemia, if hypoxic more RBCs flushed and really pink skin but
becomes cyanosed easily) cyanosis earlier
Peripheral cyanosis:- sludging of blood in the periphery/ vascular shunting (e.g. due to cold); but
oxygenation of blood near heart is normal
Central cyanosis: -deoxygenated arterial blood around heart
~watch out for pulse oximetry- do on hand without BP cuff
-look for muscle wasting (esp of hands and fingers chronic hypoxia)
-look for asterixis (flapping tremor) can be caused by respiratory acidosis
Respiratory Rate: (chronic anaemia can also cause RR)
-average for adult ~18-20 breaths per minute, for accuracy take over 30secs to 1 min (if slower RR
take for 1 min over longer period)
-must be taken when patient is UNAWARE (.: take when checking patients radial pulse)
-patient should not be talking
Look for: chest moving, back moving, hearing (only if laboured breathing) etc
Axillary Lymph Nodes (can be taken at end of examination)
-(i) apex of axilla, lateral chest wall (arm of patient can be resting down on your hand?)
-(ii) turn hand around (palm superior), up against medial/ inner side of arm

Apex

Medial
arm

Lateral
chest wall

HEAD/ FACE

(ii) Hand
(palm towards
(i)
Hand medial arm)
(palm towards lat
chest wall)

To check axillary lymph nodes:

press hand into all 4 walls of
the axilla (anterior, posterior,
medial, lateral) and then up
into apex

NOSE:
-look for object in nose can interfere with breathing sounds (e.g. can sound like stridor)
-check septum especially the antero-inferior part known as Littles Area or Kiesselbacks plexus
major blood vessels where you get nose bleeds

-check turbinates (chonchae)- inflamed??

-check for nasal polyps- red pearls/ grapes in nose, usually covered with mucous

Infection/ allergy
situation

MOUTH:
-check under tongue for bluish tinge indicative of central cyanosis
-tonsils? inflamed, exudative?; scarred, white nothingness = tonsils removed
-adenoids nose itchy? Blocked?
-check for Kopliks spots
Kopliks spots: Little spots inside the mouth that are highly characteristic of the early phase of
measles (rubeola). The spots look like a tiny grains of white sand, each surrounded by a red ring.
They are found especially on the inside of the cheek (the buccal mucosa) opposite the 1st and 2nd
upper molars.
Koplik's spots. Bright erythema of buccal
mucosa with pinpoint white macules in rubeola.

FACE
-inflamed sinuses? = inflamed face
percuss sinuses by tapping with single finger (not onto another finger), and not too hard
-ethmoid and frontal (frontal headaches?) and maxillary sinuses
-NB many children and some adults dont have frontal sinuses
-if painful = sinusitis?
-transillumination? torch into inflammatory cavity and then sinuses light up like lantern

NECK:
-palpation of trachea in sternal notch (warn patient first!!!)
-extend head back slightly
- check windpipe is equal distance from strap muscles
-watch out- may cause coughing fit- dont do too deeply or for too long
Neck

strap muscles
trachea

fingers

-also look for

tracheal tug

IMPORTANT LANDMARKS
Ribs (12 pairs)
-7 true
-5 false (2 floating)

Jugular notch
manubrium
2

nd

rib

Sternal angle

-C6/C7 most prominent spinous process of neck

vertebrae (at back)
-spinous process of T2 ~ spine of scapula

Body of sternum

Xiphoid process
of sternum
NOTE inferior spine of scapula has muscle attachments muffles sound
.: patient hugs chest to move scapula laterally out of the way

CHEST MOVEMENT
- look for symmetry (COMPARE LEFT AND RIGHT SIDES)
- quiet respiration & ask to take deep breath in
- pleural rub/ pneumonia/ broken rib = less movement on affected side
-FRONT? Look for use of accessory muscles (e.g. sternocleido-mastoid muscles strap muscles)
- bracing against object/ hips??

PALPATION look for symmetry (difference between sides??)

Apex of lungs

1
2
3

cm expansion?
around nipples
1
2
3

Costal margin and fingers

on lower ribs (max flare)

Note expansion
-diaphragmatic excursion
should be ~3-5cm
(4) -can also do on lateral side of
chest under arms (lateral to (3))

Compare Left/ Right

(i) expansion
(ii) vocal fremitus (palpable vibration) say 99 (the more inferior, the further from the
voice box, the less strong the vocal fremitis)
(iii) may be able to feel a wheeze (can sometimes transmit through

PERCUSSION
-hit enough areas to cover all lobes and determine dullness/ resonance
-fingers should be positioned parallel to ribs
- L/R comparative percussion at same level
How many levels?? (7)
-in pneumothorax hyper-resonance at apex
Patient: mouth slightly open, and deep breath, but not too deep (just slightly more than normal)

Normal breath sounds:

-heard over near all parts of chest
-ask to breathe through mouth so sounds form
nasopharynx does not interfere
-louder and longer on inspiration vs expiration, and there is
no gap between inspiratory and expiratory sounds

Normal
bronchial
breathing

apex

Bronchial breath sounds:

-hollow, blowing quality
-they are audible throughout expiration and there is often a
gap between inspiration and expiration
-expiratory sound has a higher intensity and pitch than the
inspiratory sound
-heard over areas of consolidation

1
2
3
4

7
6

Added (adventitious) sounds:

(i) continuous wheezing
(ii) interrupted crackles
NOTE when sound occurs,
Beginning of inspiration? Throughout?

If long chest...

can also percuss clavicles

AT EVERY POINT
(1) Percussion (resonance?)
(2) breath sounds
(3) vocal sounds (say 99)

Percussion Notes and Their Meaning

Flat or Dull

Pleural Effusion or Lobar Pneumonia

Normal

Healthy Lung or Bronchitis

Hyperresonant Emphysema or Pneumothorax

Adventitious (Extra) Lung Sounds

Crackles

These are high pitched, discontinuous sounds similar to the sound produced by rubbing your
hair between your fingers. (Also known as Rales)

Wheezes

These are generally high pitched and "musical" in quality. Stridor is an inspiratory wheeze
associated with upper airway obstruction (croup).

Rhonchi

These often have a "snoring" or "gurgling" quality. Any extra sound that is not a crackle or a
wheeze is probably a rhonchi.

CORRELATION OF PHYSICAL SIGNS & DISEASE

CONSOLIDATION (lobar pneumonia)

Pneumonia = inflammation of the lung with exudation into alveoli
Expansion: reduced on affected side
Vocal fremitus: increased on affected side
Percussion: dull, but not stony dull
Breath Sounds: bronchial
Additional Sounds: medium, late or pan-inspirational crackles as pneumonia resolves
Vocal Resonance: increased
Pleural Rub: may be present

COLLAPSE
e.g. bronchus obstructed by tumour mass, foreign body
Trachea: displaced towards collapsed side
Expansion: reduced on affected side with flattening of chest on same side
Percussion: dull over the collapsed area
Breath Sounds: reduced, with or without bronchial breathing above area of collapse
Note: there may be no signs with complete lobar collapse, the early changes after inhalation of a
foreign body may be over-inflation of the affected side.

PLEURAL EFFUSION
Collection of fluid in pleural space (blood = haemothorax, chyle = chylothorax, pus =
empyema)
(cardiac failure, hypothyroidism, pneumonia, neoplasm, TB, pulmonary infarction etc)
Trachea and apex beat: displaced away from a massive effusion
Expansion: reduced on the affected side
Percussion: stony dullness over the fluid
Breath Sounds: reduced or absent, there may be an area of bronchial breathing audible
above the effusion due to compression of overlying lung
Vocal Resonance: reduced

PNEUMOTHORAX
Leakage of air from the lung or a chest wall puncture into the pleural space causes
pneumothorax; spontaneous or traumatic
Expansion: reduced on affected side
Percussion: hyper-resonance if the pneumothorax is large
Breath Sounds: greatly reduced of absent
There may be subcutaneous emphysema. There may be no signs if the pneumothorax is
small (less than 30%).

TENSION PNEUMOTHORAX
This occurs when there is communication between the lung and the pleural space, with a flap
of tissue acting as a valve, allowing air to enter the pleural space during inspiration and
preventing it from leaving during expiration. Air accumulates under increasing pressure in
pleural space, causing considerable displacement of mediastinum with obstruction and
kinking of great vessels.
Trachea and apex beat: displaced away from the affected side

Expansion: reduced or absent on affected side

Percussion: hyper-resonant over affected side
Breath sounds: absent
Vocal resonance: absent
The patient is often tachypnoeic and cyanosed, and may be hypotensive.

BRONCHIECTASIS
Pathological dilation of the bronchi, resulting in impaired clearance of mucus, and chronic
infection. A history of chronic cough and purulent sputum since childhood is virtually
diagnostic.
Systemic signs: fever, cachexia, sinusitis (70%0
Clubbing and cyanosis
Sputum: voluminous, purulent, foul-smelling, sometimes bloodstained
Coarse pan-inspiratory or late inspiratory crackles over the lobe
Signs of severe bronchiecstasis: copious sputum, haemoptysis, clubbing, widespread
crackles, signs of airway obstruction, signs of respiratory failure, signs of secondary
amyloidosis

BRONCHIAL ASTHMA
This may be defined as paroxysmal recurrent attacks of wheezing (or in childhood of cough)
due to airways narrowing which changes in severity over short periods of time.
Wheezing, tachypnoea, dry or productive cough, tachycardia, prolonged expiration, prolonged
forced expiratory time, use of accessory muscles of respiration, hyperinflated chest,
inspiratory and expiratory wheezes
Signs of severe asthma: appearance of exhaustion and fear, breathlessness, drowsiness,
cyanosis, tachycardia, pulsus paradoxus, reduced breath sounds

CHRONIC OBSTRUCTIVE PULMONARY DISEASE- chronic airflow limitation

(From predominantly emphysema)
Diagnosis on basis of three findings
(i) History of heavy smoking (more than 70 pack years)
(ii) Previous diagnosis of emphysema or COPD
(iii) Reduced breath sounds.

EMPHYSEMA
Hyperinflation, patients are usually not cyanosed but are dyspnoeic and are sometimes called
pink puffers, usually caused by smoking
Barrel shaped chest, increased AP diameter
Pursed lip breathing
Use of accessory muscles of respiration
Palpation: reduced expansion and a hyper-inflated chest
Percussion: hyper-resonant with decreased liver dullness
Breath Sounds: decreased, early inspiratory crackles
Wheeze is often absent
Signs of right heart failure may occur, but only in late course of disease

CHRONIC BRONCHITIS
Defined clinically as the daily production of sputum from three months of the year for at least
two consecutive years.
Loose cough and sputum (mucoid or muco-purulent)
Cyanosis: present in latter stages, and associated oedema from right ventricular failure

Palpation: hyper-inflated chest with reduced expansion

Percussion: increased resonance
Breath Sounds: reduced with end-expiratory high or low pitched wheezes and early
inspiratory crackles
Signs of right ventricular failure
(Smoking is major cause, but recurrent bronchial infection may cause progression)

PULMONARY FIBROSIS:
Diffuse fibrosis of lung parenchyma impairs gas transfer and causes ventilation-perfusion
mismatching. Can result from inhalation of mineral dusts (focal fibrosis), replacement of lung
tissue following disease which damages the lungs (e.g. TB), or interstitial disease (fibrosing
alveolitis).
General: dyspnoea, cyanosis and clubbing may be present
Palpation: expansion is slightly reduced
Auscultation: fine (Velcro-like) late inspiratory or pan-inspiratory crackles heard over the
affected lobes
Signs of associated connective tissue disease: rheumatoid arthritis, systemic lupus
erythrematosus, scleroderma, Sjgrens syndrome, polymyositis and dermatomyositis

TUBERCULOSIS:
Primary: Usually no abnormal chest signs, but segmental collapse, due to bronchial
obstruction by the hilar lymph nodes, occasionally occurs.
Post-primary TB: Often no chest signs. The clues to the diagnosis are the classical
symptoms of cough, haemoptysis, weight loss, night sweats and malaise.
Miliary TB: Fever, anaemia and cachexia are the general signs. The patient may also be
dyspnoeic, and pleural effusions, lymphadenopathy, hepatosplenomegaly or signs of
meningitis may be present.

MEDIASTINAL COMPRESSION
Mediastinal structures may be compressed by a variety of pathological masses, including
carcinoma of the lung (90%), other tumours (lymphoma, thyroma, dermoid cyst), a large
retrosternal goitre or rarely an aortic aneurism.
Superior vena cava obstruction
Tracheal compression: stride, usually accompanied by respiratory distress
Recurrent laryngeal nerve involvement: hoarseness of voice
Horners syndrome
Paralysis of the phrenic nerve

CARCINOMA OF THE LUNG

NOTE many patients have no signs
Haemoptysis
Clubbing
Lobar collapse or volume loss
Pneumonia
Pleural effusion
Fixed inspiratory wheeze
Tender ribs (secondary deposits of tumour in ribs)
Mediastinal compression, including signs of nerve involvement
Supraclavicular or axillary lymphadenopathy
Distant metastases brain, liver and bone most commonly affected organs
Non metastatic extrapulmonary manifestations:

-anorexia, weight loss, cachexia, fever

-endocrine changes
-neurological manifestations
-haematological manifestations
-skin and renal effects

SARCOIDOSIS
Systemic disease characterised by the presence of non-caseating granulomas which
commonly affect the lungs, skin, eyes, lymph nodes, liver and spleen and the nervous
system. The aetiology is unknown.
Pulmonary signs:
Lungs: no signs usually, although 80% of patients have lung involvement. In severe disease
there may be signs of pulmonary fibrosis.
NOTE: there are many other extrapulmonary signs

PULMONARY EMBOLISM
Embolism to the lungs often occurs without symptoms. One should always entertain this
diagnosis if there has been a sudden and unexplained dyspnoea. Pleuritic chest pain and
haemoptysis occur only when there is an infarction. Syncope or the sudden onset of sever
substernal pain can occur with massive embolism. NB a firm diagnosis cannot be made from
signs and symptoms alone.
General signs: tachycardia, tachypnoea, fever (with infarction)
Lungs: pleural friction rub if infarction has occurred
Massive Embolism: elevated jugular venous pressure, right ventricular gallop, right
ventricular heave, tricuspid regurgitation murmur, increased pulmonary component of the
second heart sound
Signs of deep venous thrombosis: fewer than 50% of patients have clinical evidence of a
source

CLINICAL SKILLS

Cardio-vascular
System Exam

Look for evidence for oedema/

ascites
This patient with cor pulmonale
has marked peripheral cyanosis,
increased venous filling pressure
with hepatomegaly, abdominal
distension secondary to ascites,
severe peripheral oedema, and
elevated jugular venous pressure.
Cor pulmonale may be caused by
primary or secondary pulmonary
hypertension with associated right
ventricular failure.
Cor pulmonale is the effect of a
chronic respiratory disease (e.g.
COPD) on the heart. RV failure
JVP, enlarged liver and
peripheral oedema

Cyanosis:
This shows a 17 year old male with an
unrepaired ventricular septal defect, and
secondary pulmonary hypertension. Cold
weather alone can cause peripheral cyanosis of
the fingertips and lips. Central cyanosis, caused
by abnormal amounts of arterial deoxygenated
haemoglobin, is best noted in parts of the body
with good circulation, e.g. the tongue.

Hands and Upper Limbs:

Tendon xanthomata: yellow orange deposits of lipid in the tendons that occur in type II
hyperlipidaemia. These can be seen over the tendons of the hand and arm.

C, Achilles tendon xanthomas. Note the marked thickening of the tendons. D, Tendon xanthomas.

Palmar xanthomata and tuboeruptive xanthomata: over the elbows and knees are
characteristics of type III hyperlipidaemia.

E, Tuberous xanthomas. F, Palmar xanthomas. G, Eruptive xanthomas

Peripheral cyanosis and clubbing in a 36 year old

woman sue to a complete atriovenrticular canal
defect, and advanced pulmonary hypertension.

Raynauds phenomenon: is an abnormal response

of the fingers and toes to cold, due to spasm of the
distal arteries. The fingers turn white, then blue,
and finally red after exposure to cold. It is during
the red phase that the pain is most sever. Females
are more likely to be affected.

Signs of infective endocarditis:

Splinter haemorrhages (of the nail beds): linear haemorrhages
lying parallel to the long axis of the nail. They are most often
due to trauma, particularly in manual workers. However, an
important cause is infective endocarditis, which is bacterial or
other infection of the heart valves or part of the endocardium.
Other rare causes of plinter haemorrhages include vasculitis,
sepsis anywhere else in the body, haematological malignancy
or profound anaemia.

Check every nail bed!!!

Janeway lesions: are non-tender erythematous

maulopapular lesions containing bacteria, which
occur very rarely on the pals or pulps of the
fingers in patients with infective endocarditis.

Oslers nodes: are rare manifestations of

infective endocarditis. These re red, raised
tender nodules on the pulps of fingers (or
toes), or on the thenar or hypothenar
eminences. They are seen in fewer than 5% of
patients.

Mouth
Xanthelasma is characterised by soft yellowish
plaques of the eyelids. Xanthelasma is the most
common form of xanthomatosis. In xanthomatosis,
lipid-laden histioncytes are deposited in the skin,
due to hyperlipidaemia.

Check mouth and teeth as potential source of endocarditis. Although many bacteria can cause endocarditis, one type
that lives in the mouth, called Streptococcus viridans, is responsible for half of all cases, which is why dental procedures
are the most common cause of endocarditis. Therefore children with congenital heart disease should take antibiotics
before undergoing dental procedures.

Neck

Inspect the neck for a visible

jugular venous pulse with the
patient lying at 45o.
Estimate the JVP (measured
vertically from the sternal
angle), and it should be less
than 3cm.

Assessing Pulse Character:

Rate: normal for adults is between 60 and 80 beats per minute. Bradycardia
<60. Tachycardia >100. An athlete may have a resting pulse rate of 40-50.
Rhythm: regular (intervals between beats is constant) or irregular (interval is
not constant)
Pulse force: A full pulse is felt as if a strong wave had passed beneath fingertips.
When a pulse feels weak and thin, the pulse is described as thready. A bounding
pulse is a strong and forceful pulse often associated with high blood pressure or
fluid overload.

Radial Pulse

Carotid pulse: (common carotid artery) beneath the angle of the mandible, medial to sterno-cleido mastoid
muscle. Palpate only one at a time. Check for rate, rhythm and character.

Chest:
Palpation:

(i) find apex beat

(ii) describe location and note if it is displaced
(>2cm lateral to mid-clavicular line) indicates
hypertrophy, cardiomegaly, mediastinal shift

Auscultation:

Apex beat: most distal and lateral

palpable beat of heart, take heart rate

-listen to all areas with diaphragm, then use the bell to auscultate the mitral (M) area. While holding the bell
against M, turn the patient over into the left lateral position. Next, auscultate the A and P areas while the
patient is sitting up and leaning forward, after a full expiration and holding their breath.
*Mechanical murmur (patent ductus arteriosus)listen posteriorly between scapula

Left lateral position

ALSO do auscultation of the back between the two scapulae (while the
patient is holding their breath) and listen for a machinery mumur: he
long continuous rumbling murmur of patent ductus arteriosus

Abdomen
Liver palpation:
(i) is the liver edge palpable?
(ii) is it tender?
(iii) is it pulsatile ( suggesting tricuspid regurgitation)

MEASURING BLOOD PRESSURE:

Take 2 readings for each arm and then
staning. If readings dont correlate,
take until 2 similar readings achieved.

Lower Limbs:
Peripheral arterial disease: Other findings commonly noted in inspection include ulcerations, petechiae, infarcted
areas and various trophic skin changes. Trophic changes include thinning or thickening of the skin in response to
chronically inadequate blood flow, changes in hair growth, callus formation etc.

Pitting oedema: a mark persists on this patients foot after

pressure has been applied by the thumb for at least 15
seconds. The skin indentation only slowly refills. Pitting
oedema occurs in a range of conditions, including cardiac
failure. It is important to assess the upper level of the
oedema (e.g. pitting oedema to mid-thigh).

Neuropathic ulcer: on the right hallux has developed in

a pressure points with diminished sensation due to
diabetes. Surrounding skin is usually calloused. There is
no pain, which sometimes results in the ulcer going
unnoticed. Associated signs include decreased
sensation and absent ankle jerks.

This picture shows an ischaemic toe due to peripheral arterial disease. The
peripheral pulses will be decreased, with foot pallor on elevation, and dusky
rubor on dependency. The patient may experience intermittent claudication
when walking (i.e. painful ischaemia of the lower leg which is relieved by rest).
Gangrene may develop. Ischaemic skin ulceration is most likely to occur on the
heel, the lateral malleoli, or at the base of the toes, since these sites are
subjected to repeated trauma during ambulation. Skin surrounding the ulcer
shows no callous or excess pigment.

Varicose veins: are dilated tortuous and elongated superficial veins in the leg.
The veins are dilated because of incompetence of the valves in the superficial
veins, or in the perforating veins between the deep and superficial systems.
Inspect for varicosities of the long saphenous vein (below the femoral vein in the
groin to the medial side of the lower leg), as shown here, then inspect the back of
the calf dor varicosities of the short saphenous vein (from the popliteal fossa to
the back of the calf and lateral malleolus).

Chronic venous insufficiency. Due

to venous occlusion or
incompetence of the venous
valves, may result in ulceration on
the inner or sometimes outer
ankle. This ulceration is associated
with pigmentation, sub-cutaneous
oedema (induration) and varicose
eczema (or stasis dermatitis).
There may be diffuse aching of the
leg.

Get patient to stand to check for varicose veins

Buerger's test is used to assess the adequacy of the arterial supply to the leg. It is performed in two
stages.
With the patient supine, elevate both legs to an angle of 45 degrees and hold for one to two minutes.
Observe the color of the feet. Pallor indicates ischaemia. It occurs when the peripheral arterial pressure
is inadequate to overcome the effects of gravity. The poorer the arterial supply, the less the angle to
which the legs have to be raised for them to become pale.
Then sit the patient up and ask them to hang their legs down over the side of the bed at an angle of 90
degrees. Gravity aids blood flow and colour returns in the ischaemic leg. The skin at first becomes blue,
as blood is deoxygenated in its passage through the ischaemic tissue, and then red, due to reactive
hyperaemia from post-hypoxic vasodilatation.
Both legs are examined simultaneously as the changes are most
obvious when one leg has a normal circulation.
This test is not very sensitive (~50%), but it is specific

LOWER LIMB PULSES

Femoral Pulse: Locate the superior border of the pubis in the mid line of the body; this is the uppermost part of the pubic
symphysis. Feel the anterior limit of the iliac crest. The femoral pulse can be found midway between these two bony points
(the mid-inguinal point)

Dorsalis Pedis Pulse

The dorsalis pedis artery pulse can be palpated readily
lateral to the extensor hallucis longus tendon (or medially
to the extensor digitorum tendons) on the dorsal surface
of the foot. Place your fingers half way down the dorsum
of the foot on the bony area in the line between the first
and second toes. The bones you can feel are the dorsal
aspect of the navicular and the intermediate cuneiform
bones. It is absent, unilaterally or bilaterally, in 2-3 % of
young healthy individuals.

Posterior Tibial Pulse:

Locate the medial malleolus. 2-3cm below
and behind it you should find the posterior
tibial pulse. when taking the pulse on your
own foot it is easier to use the thumb. In
clinical practice the pulse is palpated using
the pulps of the index and middle fingers.
The artery is slightly deeper placed than the
dorsalis pedis and therefore more
concentration is often required to feel its
pulsations.

Popliteal pulse:
Ask the subject to bend the knee so that it is flexed to about
90 degrees. Sit on the right hand edge of the bed close to
the subject right foot. As before gently clasp the sides of
the knee (of either limb) and press the pulps of your fingers
into the popliteal fossa.

Heart sounds and murmurs:

http://depts.washington.edu/physdx/heart/tech.html

S1: First heart sound (M & T)

Check for loud heart sound (hyperdynamic (fever, exercise), mitral stenosis, atrial myxoma (rare)
soft first sound (low cardiac output, tachycardia, severe mitral reflux)
variable intensity (atrial fibrillation, complete heart block)
S2: second heart sound (A & P)
Check for loud aortic component (systemic hypertension, dilated aortic root)
soft aortic component (calcific aortic stenosis)
loud pulmonary component (pulmonary hypertension)
SPLITTING (see below)
Splitting of S2
Audible expiratory splitting means > 30 msec difference
in the timing of the aortic (A2) and pulmonic (P2)
components of the second heart sound.
-Splitting of S2 is best heard over the 2nd left intercostal
space
-The normal P2 is often softer than A2 and rarely audible
at apex
Differential Diagnosis of P2 audible at apex = Significant
pulmonary hypertension, Atrial septal defect
Findings should be present in both upright and supine
positions: normal subjects may have expiratory splitting
when recumbent that disappears when upright.

Extra Heart Sounds (S3 & S4)

A triple rhythm in diastole is called a gallop and results from the presence of a S3, S4 or both.
Description: Both sounds are low frequency and thus best heard with the bell of the stethoscope.
Location: If originating from LV
-Usually best heard over apex with patient in the left lateral position
-Softer during inspiration
If originating from RV
-Usually best heard over left lower sternal border
-Louder during inspiration
S3: third heart sound
-Low frequency sound in early diastole, 120 to 180 ms after S2
-Lub du bub S1S3S2 cadence similar to "Kentucky"
-Results from increased atrial pressure leading to increased flow rates, as seen in congestive heart failure, which
is the most common cause of a S3. Less commonly, valvular regurgitation and left to right shunts may also result
in a S3 due to increased flow. May be normal physiological finding in patients less than age 40.
S4: fourth heart sound
-Low frequency sound in presystolic portion of diastole,
-Belub dup S1S4S2 cadence similar to "Tennessee"
-Seen in patients with stiffened left ventricles, resulting from conditions such as hypertension, aortic stenosis,
ischemic or hypertrophic cardiomyopathy. In patient with mitral regurgitation, suggestive of acute onset of
regurgitation due to the rupture of the chorda tendinae that anchor the Valvular leaflets.

Clicks and Snaps

Ejection click: Most common early systolic sound; Results from abrupt halting of semilunar valves
Aortic: loud high frequency, does not vary with inspiration, best heard at apex, Causes associated with
aortic valve with decreased but some residual mobility: i.e., aortic stenosis, bicuspid aortic valves and
dilated aortic root; not generally heard with calcific aortic stenosis due to non-mobile valve
Pulmonary: early systolic ejection sound with associated murmur, often diminishes on inspiration, sterna
edge 2 or 3 ICS, Causes associated with pulmonic valve: pulmonic stenosis, pulmonary hypertension and
dilated pulmonary trunk
Opening snap
Description: High-frequency early diastolic sound (occurs 50-100 msec after A2) associated with mitral
stenosis; sound due to abrupt deceleration of mitral leaflets sound with associated murmur. Often
diminishes with inspiration' accentuated in left lateral position.
Location: Between apex and left lower sternal border
Sounds like:RUP bu Dup rrrrrrRup Bu Dup
Correlating to s1, s2, OS, murmur of mitral stenosis,
Clinical significance: The OS plus typical murmur indicates the murmur is due to mitral stenosis and not a
flow rumble across a non-stenotic valve. The timing of the OS has been suggested as a gauge of the severity
of the stenosis but has not been found to be reliable for this.
Mid-systolic click (plus late systolic murmur of mitral valve prolapse)
Others:
Prosthetic valves
Prosthetic mitral valve sounds: (opening sound analogous to opening snap, closing sound coincides with S1 )
Prosthetic aortic valve sounds: (opening sound analogous to ejection click, closing sound coincides with S2)
Murmurs:
Cardiac murmurs can be divided into three categories based on where they occur in the cardiac cycle; systolic,
diastolic and continuous.
Analyse the murmur for
Intensity (Grade)
Where it occurs in systole
Where it is best heard and where it radiates to
What it sounds like
What happens during special maneuvers
Note: Short, quiet systolic murmurs are generally benign.
Long systolic murmurs, diastolic murmurs and continuous
murmurs are generally pathologic. (Two continuous murmurs that are benign are mammary souffl and cervical venous hum.)

Systolic
Causes
-Blood flow through a structure normally closed
during systole (mitral or tricuspid valves or the
interventricular septum).
-Blood flow through a valve normally open in
systole but abnormally narrowed (e.g. aortic or
pulmonary stenosis).
-Increased blood flow through a normal valve
(a flow murmur).

CLINICAL SKILLS

Musculoskeletal
System Exam

MUSCULO-SKELETAL SYSTEM:

CLINICAL EXAMINATION

HISTORY TAKING

- Chronic > 6 weeks (if <6 weeks- still acute phase)

Systems Review
- Does it involve the muscle, bone or joint?
or is there another association? - vasculitis of skin, liver, kidney
- inflammatory bowel ( bowel habits? Loose? Blood?)
-if 1 problem is related to
- neisseria gonorrhoea joint pain (with urinary burning)
joints ask about specific
- iritis (red eyes)- found in types of arthritis
conditions
- smokey urine, kidney pain??

PAIN is a common presenting problem

Stiffness, deformity, functional impairment
-What joints are involved?
-Level of impairment?
-Characteristics? e.g. psoriatic arthritis have you ever had skin rashes?
Where is the pain?
-In the joint? Bone? Or muscles around it? (You cant move because joint is sore or are
the muscles weak?)

When do you get the pain? And how long does the pain last?
-claudication (ischaemic pain) dissipates in minutes vs arthritic pain that takes
30min to hours to dissipate
-can you walk normally afterwards? Yes for claudication, but stiff and sore for
arthritis.
-Do you have pain at rest? Does it get worse or better as you go along?
-arthritis: bad better bad again with movement
-inflammation: exercise = bad for ~30min, then settles down, but pain at rest

BACK PAIN a lot of limb pain can be referred to the pain

-sciatic pain: sciatica is nerve pain arising from the sciatic nerve. It can be produced by pressure on
the nerve, where it passes through the buttock.
-also visceral referred pain to shoulder (e.g. gallbladder), jaw etc...

*Degree of pain? How much pain relief do you need? Paracetamol, NSAIDs, narcotics (opiates)?
*How does it interfere in your daily living? how aggressive does treatment need to be? What are the
patients lifestyle requirements: sitting all day (.: only control) vs athlete (level of commitment?- if you have a
full reconstruction you need to adhere to post op)

DISTIBUTION? one joint vs multiple

One joint: -have you injured this joint before, and did it involve the joint surface
(e.g. tibial plateau fracture).
-suggestive of acute condition (~injury) or infection (septic arthritis)
Multiple: - is it symmetrical?
-suggestive of generalised inflammatory disorders
i) Rheumatoid arthritis: symmetrical, small joints
ii) Psoriatic arthritis: can be a asymmetrical

AGGRAVATING and RELIEVING Factors

-Degenerative rest eases pain
-Inflammation- no change (pain wont go away though it might ease)
STIFFNESS- all diseases of the joints cause stiffness
- Inflammatory- long time to wear off (hour or more)m nay be diurnal, improves with
exercise
- Degenerative- settles quite quickly (<1 hour), mechanical (worse with exercise)
SWELLING: in joint or in surrounding tissue e.g. oedema; (distinguish by palpation)
-boggy? Around joint reactive swelling (infective, inflammatory process)
Bakers cyst (popliteal cyst):
benign swelling of the semimembranous bursa found behind
the knee joint that usually arise
from almost any form of knee
arthritis and cartilage (particularly
the meniscus) tear
calf soreness (need to exclude
DVT)

TENDERNESS: is it the joint, bone or muscle?

-bone tenderness is fairly constant wakes you at night (malignancy related? Acute
osteomyelitis)
FAMILY HISTORY?
-psoriasis, rheumatoid arthritis, Crohns disease
RED FLAGS
1. Multitude of diseases- AIDs, inflammatory joint disorders, haematological malignancies
(multiple myeloma)
2. Weight loss- malignancy or thyroid?
3. Bone scan: multiple myeloma, bone tumour, abscess (e.g. extra dural abscess of spine)
4. <20yo: juvenile onset of destructive joint disease?
>50yo secondary malignancy (does patient have history of breast cancer? bony
metastases)
-osteoporotic crush fracture (impacted fracture?)- post menopausal women and
men >70yo
5. IV drug use- increase risk of infection
6. cauda equina pressure on sacral/ lumbar spinal nerves
IF back pain?- do you have control or urine (urinary incontinence) and bowels
(toneless anus?) = orthopaedic emergency
YELLOW FLAGS
- Will maximise their condition
-Sleep disturbance classic depression: sleep in the afternoon, but wake early in the
morning and cant get back to sleep.

Nature
Intensity
Location
Duration
Onset
Characteristics
Aggravating factors
Relieving factors
Features
Impact
Attribute- what do you think caused it?
Treatment
Inflammatory

Non-Inflammatory

-present at rest, many joints

-long lasting stiffness, >1 hour
-haphazard variance of pain, rest and stiff next day, X related
to meds
-affected by weather (cold/ rain?)
-swelling- intermittent and often not related to pain and can
move between joints
-e.g. Reiters syndrome/ reactive arthritis: autoimmune
condition that develops in response to an infection in
another part of the body. Coming into contact with bacteria
and developing an infection can trigger reactive arthritis
-chlamydia can also cause reactive arthritis

-pain when start moving joint, better with

rest
-stiffness is short lasting
-improves with periods of rest
-busy one day, stiff next day, related to med
use
-swelling- usually localised (no systemic
associated symptoms usually)
-e.g. osteoarthritis

THE CERVICAL SPINE EXAMINATION

Positioning and Exposure: the patient should be sitting down and exposed from the waist up
Look:
1.
2.
3.

You can do spinal

examinations in
isolation, or do all
three at once.

Look at the patients posture, and whether they are in any discomfit
Inspect the whole spine and shoulders and assess symmetry
Inspect for: spinal scoliosis, lordosis, flattening of the chin, scars, wasting, spasm, rashes,
deformities of any other joint

Kyphosis: Kyphosis is the extreme curvature of the upper

Lordosis- chin
sticks out

back also known as a hunchback; The upper back bone

(thoracic region), is normally curved forward. If the curve
exceeds 50 it is considered abnormal (kyphotic).

Lordosis: describes an inward curvature of a portion of the

vertebral column. Excessive lordotic curvature is also called
hollow back, saddle back, and swayback. Common causes
of excessive lordosis including tight low back muscles,
excessive visceral fat, and pregnancy. Although lordosis
gives an impression of a stronger back, ironically it can lead
to moderate to severe lower back pain. Loss of lordosis is
sometimes seen with painful spinal conditions.

Scoliosis: side-to-side curvature of the spine. While a small

Scoliosis

degree of lateral curvature does not cause any medical

problems, larger curves can cause postural imbalance and
lead to muscle fatigue and pain. More severe scoliosis can
interfere with breathing and lead to arthritis of the spine
(spondylosis).

*ask patient any tenderness?

Feel:

*any headaches?- feel

occipital insertion of
trapezius (muscle tension
= cause of band-like
headache?)

1. Muscles noting tenderness, spasm, bulk, wasting:

a. Anteriorly: sternocleidomastoid muscles, scalene, levator scapulae, rhomboids
b. Posteriorly: trapezius, semispinalis capitus, splenius capitus, levator scapulae, rhomboids
2. Spinous processes and along the interspinous ligaments for tenderness and stiffness
3. Facet joints for stiffness and pain.

Semispinalis capitis

Splenius capitis
Trapezius
Splenius cervicis
Levator scapulae
Rhomboid minor (cut)

Move: active movement only, passive movement is for the skilled examiner
1.
2.
3.
4.

Flexion
Extension
Left and right lateral flexion
Left and right rotation

NOTE limitation of movement, and any pain

If the neck is very painful, it is useful to lie the patient down and
roll them into supine position to complete the exam.

***TEST: bend forward in flexion to look for scoliosis (one side has hump due to muscle imbalance)

THE THORACIC SPINE EXAMINATION

Positioning and Exposure: standing, sitting, and lying down; preferably undressed except for underwear
Look:
Look at the patient from behind:
1. Height of the shoulders
2. Scoliosis
3. Spasm of intervertabral muscles
4. Wasting: paraspinal muscles, gluteal muscles
You can palpate using
5. Symmetry: inferior angle of scapulae,
the pulp of your thumb
posterior superior iliac crests,
or the hook of your
gluteal folds, popliteal creases
hamate on your thenar
6.
Foot posture
eminence

Paraspinal muscles

Look from the side:

1. Thoracic kyphosis
2. Lumbar lordosis

Feel:
Lie patient face-down and palpate: Tenderness? Spasm?
1. Paraspinal muscles
2. Spinous processes and interspinous ligaments for stiffness and tenderness
3. Costovertebral articulation
Should be firm
Roll the patient over:
1. Feel the costochondral joints for tenderness (between ribs and costal cartilage)

Move:
Sit the patient up, preferably on a stool this position locks the patients pelvis, but if you are worried
that they may fall off, stand them up and hold the pelvis steady during rotation.
1. Rotation left and right (60)
To isolate rotation: hold both sides of
pelvis as Pt cross arms over onto
-rotation
is
the
major
thoracic
spine
movement
Pt touches knee and
shoulders and turns left and right
2. Flex the patient forwards until their fingers touch their knees
tucks chin in- is arch
even???
- look for one side of the thorax higher than the other scoliosis
X much extension of thoracic spine

THE LUMBAR SPINE EXAMINATION

Positioning and Exposure: The patient should be undressed except for underwear. Shoes and socks should
be off.

Look & Feel: as per Thoracic Spine Examination

Move: Ask the patient to actively move in the following directions:
1.
2.
3.
4.

Extension: 20 to 30
Flexion: 75 to 90
Lateral flexion: 30 (left and right)
Rotation minimal at lumbar spine.

*Ask Pt to put hands on side and slide down leg

towards their knee

SPECIAL TESTS: the following are neurodynamic tests. If positive, perform a neurological exam.
1. Femoral nerve stretch
-With the knee prone, place a palm on the hamstrings
of the limb to be examined and flex knee gently
-Pain should be reproduced in distribution of femoral
nerve
-This test is positive is almost all patients with high
lumbar disk lesions
Do with patient PRONE

2. Straight leg raise

-With the patient supine, raise the leg slowly until
pain in the posterior aspect is elicited
-The leg must remain straight and not bent at
knee.
-The test is positive when pain is reproduced in
the range of 30 to 40
Tests for SCIATICA (sciatic nerve impingement)- more
commone that femoral nerve, do SUPINE

THE HIP EXAMINATION

Positioning and Exposure: The patient should be in their underwear. Start the exam with the patient
standing.
GAIT: any hops, jumps, limps,
swaying???

Look:
1.
2.
3.

ASIS
(ant. superior
iliac spine)

Inspect: deformity
Posture: inspect the patients spinal, leg and foot posture
Gait: observe how they walk over 10 paces, get into/out of a chair,
use of aids (walker?)
4. Spine: look for scoliosis, paravertebral spasm
5. Hip: inspect gluteal folds, popliteal creases
6. Leg length: measure for leg length discrepancy (measure supine)
i. True leg length = ASIS to medial malleolus
Top edge of ASIS to distal
ii.
Apparent leg length = umbilicus to medial malleolus
edge of medial malleolus
iii. Note the best measure of leg length is standing X-ray

Look at the bulk of the gluteus maximus. If uneven bulk ~congenital hip dislocation?
- Leg length inequality can cause scoliosis.
-Also assess equality of popliteal creases and muscle bulk.

Medial
malleolus
True Leg Length

Feel: Invite the patient to lie down supine for the remainder of the examination.
The hip joint is difficult to palpate.
-Try at about 2cm distal to the midpoint of the inguinal ligament (this is a sensitive area)
1. Note any swellings
2. Feel the pubic symphysis, adductor muscles, iliopsoas, greater trochanter of the femur
(+) Tighten both rectus femoris muscles and compare bulk of both sides. A torn muscle will bruise 2448 hours post injury. Also note any bruises on the posterior, at the gluteal fold. This can occur with a
torn hamstring, and the bruise can track inferiorly to the popliteal fossa.
NOTE: there is too much muscle bulk to feel for minor swelling or heat of the hip joint. You can feel laterally,
but mostly you are just feeling the greater trochanter of the femur, and bursa.

Move: (you can do both active and passive movement for each move and then go on to the next move)
NOTE: Degree of movement varies with changing body habitus; values are only an average. BUT
compare left and right sides, and at different times (e.g. pre- and post-injury)
1.

2.

Ask the patient to actively make the following movements

a. Flexion 90 (with knee extended) or 135 (with knee flexed)
b. Abduction 50
c. Adduction 45
d. Internal rotation 45 (with knee/hip flexed 90)
e. External rotation 45 (with knee/hip flexed 90)
Repeat passively, noting any crepitus and watching for signs of discomfort.
CREPITUS: a peculiar crackling, crinkly, or grating feeling or sound under the skin, around
the lungs, or in the joints. Crepitus in a joint can represent cartilage wear in the joint space.

3.
4.

Roll the patient onto the unaffected side, stabilise the pelvis and test extension (should be 15).
Roll the patient supine to perform the Thomas test.
*Examiner can fix Pt ASIS to hold pelvis

Flexion (knee extended) 90

Flexion (knee flexed) 135

Extension 15
*Do this one last, as it requires Pt
to be rolled over

Abduction 50

Adduction (cross-over) 45

External rotation 45

Internal rotation 45

Function: assessed at the beginning of the examination when observing gait

Special Tests:

THOMAS TEST- a test for fixed flexion deformity

inflammation (e.g. septic arthritis of hip) or structural deformity of hip
if checking the left hip joint, raise the right leg

*Under hip side, not leg side

The patient lies supine and the examiner flexes one of the hips (one hand can be placed under patients
back to check for lumbar lordosis), bringing the knee to the chest to flatten out the lumbar spine.

If there is NO flexion contracture, the hip being tested

(the straight leg) remains flat on the examination couch.

If there is CONTRACTURE, the leg rises off the couch.

The angle of contracture can be measured.

TRENDELENBERG TEST a test for hip instability due to gluteus medius weakness or tear, short femoral
neck or unstable hip due to dysplasia, (e.g. congenital dislocation of the hip)
Traditionally, this test is performed with the examiner viewing the patient from behind, however, it may be
safer to test facing the patient (aiding with balance).

1. Hold the patients hands with the patient facing

you.

2. Ask the patient to stand on the (R) foot by

lifting the (L) foot off the ground, keeping the
(L) thigh is position and bending the knee so
that the foot is lifted behind the patient.

3. The iliac crest on the side with the foot off the
ground (in this case the left) should rise or stay
level.

4. The test is abnormal if the hemipelvis falls,

refecting gluteal weakness or inhibition from
hip pain on the contralateral side.

gait: sag into step and swing leg around

THE KNEE EXAMINATION

Positioning and Exposure: Begin with the patient in a standing position. Your patient should be in exercise
shorts or underwear.

Look:
1.
2.
3.

Tibial tuberosity (in children- growing fat- stretching growth plate) Osgood Shlatter
-growing pain of knee

Inspect for: swelling, wasting, spasm, scars, erythema, deformities (e.g. the knock-knees of genu
valgum and the bow-legs of genu varum)
Posture: inspect the posture of the foot
NOTE: medial injuries are more common (note whether walking
Gait
with genu varum posture eases pressure on medial side of knee
a. Observe the patient walk 10 steps
b. Watch the patient getting in/out of a chair and taking shoes and socks on/off.

SCARS

Modern arthroscopic surgery of the knee, only leaves slight scars at the
outer corners of the knee joint.

Older scars are larger, are

more easily seen.

Genu valgum: knock knees is a condition in which the lower

legs are positioned at an outward angle. When the knees are
touching, the ankles are separated. Most children develop
slight knock-knees by 2-3yo, that often persists through age 56. Causes of genu valgum include osteomalacia, Marfans
sundrome, Ehlers-Danlos syndrome, osterogenesis imperfecta
and pseudochonroplasia.
Genu varum: bowlegs is a condition in which the knees remain
wide apart when a person stands with the feet and ankles
together. Infants are born bowlegged, with normal appearance
attained ~3yo. Severely bowed legs can be a sign of rickets.
Other causes of bowleggedness include Blount's disease, bone
dysplasias, and lead or fluoride intoxication.

Feel:
1.
2.
3.
4.
5.
6.
7.
8.
9.

Skin: temperature (use back of the hand)

Quadriceps: loss of tone/bulk, spasm, tenderness, signs of tear/rupture
Patella: mobility, thickenings
Patellar ligament: tenderness (esp where ligament inserts to tibia and patella), thickening, gaps
Medial condyle/ epicondyle of femur: attachment of medial ligament
Lateral condyle of femur and head of fibula: attachment of lateral ligaments
Joint line: feel for tenderness (suggests a meniscal tear) and swelling
Bursae: supra- and prepatellar, assess temperature, colour, fluctuance, and tenderness
Effusion: test for effusion using patella tap and bulge test.

Congenital dislocation of the patella?

Patella slips out of

femoral groove and
dislocation occurs.

Can be due to either:

i) flattened femoral groove
OR ii) flattened posterior surface of patella bone

- Check evenness of L and R patella, and compare bulk. Any bulges? Is an effusion obscuring the outline of the
patella bone?
- Feel for heat; check both sides at the same time.
*Place rolled towel under knee to examine knee slightly flexed (to open up joint line)

CHECKING STRUCTURE (when possible you can do L and R sides at the same time)
Note pain at any time (look for toe curl, grimacing), does it feel boggy? bruising?
i)

Feel quadriceps (relaxed and tense; if injury- one side feels floppy and cant sustain tension
properly due to pain)
ii) Feel the medial thigh and then the lateral thigh (if one side is painful, do that side last)
iii) Feel around the knee as follows...

10
3

8
5

12

11
4

7
6

13

Behind the knee

*Also check bursae

1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.

Upper pole of the patella

Medial femoral condyle (superior attachment of the medial collateral ligament)
Medial collateral ligament (MCL)
Tibial condyle (medial), inferior attachment of the MCL
Inferior pole of the patella
Tibial tuberosity (move superiorly and feel patellar ligament for tenderness)
Tibio-fibular articulation (inf. attachment of LCL)
Lateral collateral ligament (LCL), tends to lie more posterior than MCL, dont
confuse with ilio-tibial band
Lateral femoral condyle (superior attachment of LCL)
Patella (feel for tenderness)*
Lateral meniscus: from the lower pole feel laterally along the joint line, where
the cartilage attaches, if there is a meniscal injury = tender
Medial meniscus, medially from lower pole of patella
Popliteal fossa: check for the posterior of the knee for cystic swelling (e.g.
Bakers cysts)

*NOTE when the muscles of the leg are relaxed the patella should move a little, and if it has never had a
dislocation, it should not be painful.

PATELLAR TAP will only occur when there is effusion

Slide one hand down the thigh towards the knee to empty
the suprapatellar pouch. When you reach the upper edge of
the patella, keep your hand in place.
With your other examining hand, push down gently on the
patella.
1
If effusion is present, the
patella will press down on
the effusion before hitting
(tap) the femur.

2
3

Tap??

BULGE TEST test for effusion

*Can be caused by mechanical injury/ inflammation

-If there is no obvious patellar tap, stroke the medial side of

the knee upwards (towards the suprapatellar border) to
empty the medial compartment.
-Then stroke the lateral side downwards (towards feet).
-A mild effusion may refill the medial compartment
producing a bulge.

Move:

Lateral

Medial

1
4

Is there a
bulge???

*Also test KNEE ROTATION (one hand holds thigh, the other holds
the lower leg above the ankle and TWIST

Active and passive movements

1. Flexion: 135
2. Extension: 0 - 10 of hyperextension is acceptable
Observe tracking of patellar and palpate for crepitus during passive movement.

Pathophysiology: Between 0 and 30 of flexion, the patella

Function: (assessed at the beginning of the examination)

Special Tests:

is at its highest point in the trochlea. Pressure from the medial

side will push the patella in a lateral direction, causing it to
dislocate from the trochlear groove. This will cause not only
pain, but apprehension on the part of the patient.

Patellar Apprehension Test: this is a test for patellar dislocation

1. The patient must be supine with the test knee flexed
to 30.
2. The examiner places a thumb along the medial
patellar border and applies a laterally directed force.
3. The test is positive if the patient becomes
apprehensive about the patella dislocating and the
quadriceps contract.

NOTE knee caps tend to dislocate laterally

Medial and Lateral Collateral Ligament Stress Test

Bracing side opposite to
ligament being tested.

Applying lateral force

to distal tibia.

MCL Stress Test

1. With the patient lying supine, flex the knee to 15 30.

2. Alternatively stress medial and collateral
ligaments by bracing the opposite side of the joint
line to the ligament you are testing and applying
varus (medial) or valgus (lateral) force to the distal
tibia.
3. Repeat both movements in full extension.
If ligament is torn? = big movement

Anterior Draw Test:

-this is a test for anterior cruciate ligament integrity. This test is positive if there is evident laxity or pain
1. Place both hands around the upper tibia with thumbs
over the tibial tuberosity and index fingers tucked behind
the hamstrings to grasp the leg.
2. Feel with fingers to detect if hamstring spasm is
present.
3. Stabilise lower tibia by carefully sitting on patients
foot.
4. Gently pull the upper tibia forward.

Lachmans Test
-This is a test of anterior cruciate ligament integrity. The test is positive if there is evident laxity or pain.
1. The patient lies on their back with their knee held
between full extension and 15 flexion.
2. The femur is stabilised with one hand, while pressure
is applies to the posterior aspect of the proximal tibia in
an attempt to move it anteriorly.

The posterior cruciate ligament can also be tested by

pushing down, while supporting the femur.

*Can hold Pts anterior knee along meniscal line (joint line)

McMurrays Test for Medial/ Lateral Meniscal Tear

1. The patient lies on their back, the knee is flexed and the foot is
held by the heel.
2. The ankle held by the examiner is rotated causing relative
internal and external tibial rotation (this tests the posterior
cartilage).
3. Variations of this test include addition of abduction-adduction
forces and gradual extension of the knee.

APLEY TEST: alternative to McMurrays test

If the examiner is not strong enough for the McMurray test, the Apley test can be performed, which is easier
on the examiner.

The test is performed with the patient in the

prone position.
1. The examiner pushes down on the heel
(applying axial pressure), rotating the
tibia on the femur (~grinding test).
2. Anchor the femur and rotate the leg at
the heel, this time holding the tibia up off
the femur. If it is a meniscal injury this
will lessen the pain, but if it is a collateral
ligament injury, the pain will be
uncharged.

Additional Test: The Sag Sign

-Tests the integrity of the posterior cruciate ligament
The sag sign reveals posterior displacement of the
tibial tuberosity as the knee is flexed at 90.
Ask patient to fully extend leg, raising it off the
examination couch. Ask the patient to slowly drop
their foot back into the couch and the relax. The
sign is positive if the proximal tibia drops in relation
to the end of the femur.

THE ANKLE AND FOOT EXAMINATION

Positioning and Exposure: both lower limbs should be completely exposed

Look:
1.
2.
3.

Footwear: abnormal/ asymmetrical wearing, poor fit, special insoles

Gait: observe normal cycle of heel strike, stance and toe-off, toe in/ toe out?
Standing (weight bearing): toe alignment, midfoot arch position, swelling, redness, bruising, scars,
foot posture (pronated/ supinated), wasting of calf, fibular muscles, hamstrings, calcaneal tendon
thickening, varus/ valgus deformity
Check for xanthomata
Sit patient on couch with feet hanging over end (pillow under knees).
th
4. Ankles: anterior joint swelling, medial and lateral malleoli (swelling/ bruising/ deformity), 5
metatarsal bases (swelling/ bruising/ deformity), tibialis posterior, flexor digitorum longus, flexor
hallucis longus
5. Feet: nail changes (psoriasis), skin colour, rashes, ulcers, infection, callus formation, joint swelling,
look at plantar surface
st
6. Toes: alignment (straight, hammer, claw, mallet), swelling/ redness of 1 MTP joint, hallux valgus

ANATOMY OF THE LOWER LEG:

*Can easily miss tarsal
fractures with X-ray .: CT

GAIT: normal gait cycle and common gait abnormalities

-Heel-toe gait?
-skipping gait?

MIDFOOT ARCH POSITION AND FOOT POSTURE

Pes cavus
(high arch)

Normal
arch

Pes planus
(flatfoot)

-Is the foot splayed

outwards?
-Pidgeon toed?
-Look at wear on soles
of Pts shoes

?? What is the line

of the calcaneal
(Achilles) tendon
from the posterior
view?

- Is weight bearing uniform (same time spent on both R and L legs), if not uniform = limp
- Is gait heel toe
-Is there a rolling in (eversion) of the trailing foot when taking a step? ]- gives knee/ ankle problems
-Is there inversion of leading foot when stepping down?

NOTE lateral/ collateral ligament injuries are more common for ankles, as inversion is more common

SKIN & NAIL CHANGES with PSORIATIC ARTHRITIS

Psoriatic arthritis: Psoriatic arthritis is a chronic disease characterized by inflammation of the skin
(psoriasis) and joints (arthritis). Psoriasis is a common skin condition affecting 2% of the Caucasian
population in the United States. It features patchy, raised, red areas of skin inflammation with scaling.
Psoriasis often affects the tips of the elbows and knees, the scalp, the navel, and around the genital
areas or anus. Approximately 10% of patients who have psoriasis also develop an associated
inflammation of their joints. Patients who have inflammatory arthritis and psoriasis are diagnosed as
having psoriatic arthritis

Psoriatic nail: pitting (small depressions in nail),

onycholysis and, less commonly, hyperkeratosis
(thickening of the nail), ridging and
discolouration. The presence of vascular changes
around nailfolds, implies active disease (black to
brown 1-2mm lesions due to skin infarction and
occur typically in Rheumatoid arthritis).

Psoriasis: is a chronic, non-contagious autoimmune disease

which affects the skin and joints. It commonly causes red
scaly patches to appear on the skin. The scaly patches caused
by psoriasis, called psoriatic plaques, are areas of
inflammation and excessive skin production. Skin rapidly
accumulates at these sites and takes on a silvery-white
appearance. Plaques frequently occur on the skin of the
elbows and knees, but can affect any area including the scalp
and genitals. In contrast to eczema, psoriasis is more likely to
be found on the extensor aspect of the joint.

Corns and calluses form on the skin because

of repeated pressure or friction. A corn is a
small, tender area of thickened skin that occurs
on the top or side of a toe. A callus is a rough,
thickened area of skin that appears because of
repeated irritation or pressure to an area of
skin. Calluses usually develop on the palms of
the hand and soles of the feet.

ALIGNMENT OF THE TOES

Hammer Toe
A hammer toe occurs when the middle of the toe points upwards
abnormally. This most often occurs in the second toe, and is often the
result of a big toe bunion pushing on the second toe. A painful callous
often forms on to on the first joint in the toe.
Claw Toe
Claw toes appear as the name would describe--like a clenched fist.
While most other toe deformities are the result of footwear, claw toes
are the result of muscle imbalance. The cause of the imbalance may be
rheumatoid arthritis, neuromuscular disorders, a stroke, or other
conditions.
Mallet Toe
The mallet toe is the deformity where the most distant joint points
downward. This is most common in the second toe in patients whose
second toe is the longest toe. A painful callous can form at the tip of a
mallet toe.

Hammer toe

Claw toe

Mallet toe

Hallux valgus (bunion):

A bunion or hallux valgus is a prominence on the inner border of the foot
effecting the big toe and at the level of the 1st metatarso-phalangeal (MTP)
joint. The bunion prominence which is seen and felt on the inner border of
the foot is not due to any growth of bone but is due to the 1st metatarsal
bone. With a bunion this has become more prominent than normal because
the 1st metatarsal has moved away from its immediate neighbour the 2nd
metatarsal. This widens the forefoot thus producing the bunion. The
tendons have an off-centre pull with the first metatarsal moving away from
the second.
Hallux varus:
A deformity of the great toe joint where the hallux is deviated medially
(towards the midline of the body) away from the first metatarsal bone.
Hallux varus has variable degrees of severity, symptomatology, and
etiology. Causes range from the most common iatrogenic postoperative
variety to idiopathic, rheumatic, and posttraumatic (tear of the hallux
lateral collateral ligament) forms. Flexible hallux varus is a common
finding in newborn children and usually corrects to valgus in early
childhood when walking begins

Feel:
1.
2.

3.

Temperature over the ankle and forefoot

Ankle
a. Distal 1/3 of fibula (deformity, tenderness, swelling)- especially posterior aspect
b. Media and lateral malleoli
c. Medial and lateral ligaments
d. Fibular tendons
th
e. Base of 5 metatarsal
f. Talus and anterior joint line of the ankle
g. Posterior tibialis pulse
Foot
th
a. Base and shaft of the 5 metatarsal (common fracture)
b. Gently squeeze across metatarsal heads (watch the patients face for discomfort (neuromas, stress
fractures)

c. Feel the MTP and interphalangeal joints

d. Medial tuberosity of the navicular bone
e. Tendons of tibialis anterior, extensor hallucis extensor digitorum
f. Plantar surface- the medial tubercle of the calcaneus (this is tender in plantar fasciitits)
g. Dorsalis pedis pulse
Turn patient supine:
4. Feel the calcaneal tenden for tenderness or deformity and perform the Thompsons test.

Palpation of the ankle and foot:

7
2
5

6
9

*Also feel posteriorly

for CALCANEAL
TENDON integrity.

-common avulsion injury with

Distal 1/3 of the tibia
eversion
Medial malleolus
Talo-navicular joint (and medial ligaments)
bulges, effusions, boggy?
4. Anterior joint line (usually can feel extensor
digitorum longus and extensor hallucis longus)
5. Lateral malleolus (+ fibular tendons)
6. Lateral ligaments (it is usually the anterior talofibular ligament that is damaged with an inversion
injury- check with anterior draw test)
7. Distal 1/3 of the fibula
th
8. Base and shaft of 5 metatarsal
9. Gently squeeze across the metatarsal heads
10. Tendons, plantar surface, dorsal surface

1.
2.
3.

THOMPSONS TEST: test of the integrity of the calcaneal tendon

1.

2.

3.

Anterior drawer test: to assess the

integrity of the anterior talofibular
ligament. If the ligament is torn, the
talus will subluxate anteriorly
compared with the unaffected ankle.

The patient should be prone with the

foot extending over the end of the
examination couch.
The calf muscles are then squeezed in
the middle one-third below the widest
girth
Passive plantar flexion of the foot is
normal, and a positive test is the
absence of passive plantar foot
flexion. This indicates a rupture
of the calcaneal tendon.

Morton's neuroma: is a benign neuroma of an

intermetatarsal plantar nerve, most commonly of the third
and fourth intermetatarsal spaces. This problem is
characterised by numbness and pain, relieved by removing
footwear.
The thickening, or enlargement, of the nerve that defines a
neuroma is the result of compression and irritation of the
nerve. This compression creates swelling of the nerve,
eventually leading to permanent nerve damage.

Move:
Active movement
1. Dorsiflexion: 20
2. Plantar flexion: 30
3. Inversion: 25-30
4. Eversion: 5-10
5. Dorsiflexion of the toes
6. Plantar flexion of the toes
Passive movement
1. Fix heel in one hand, and using the other, passively invert / evert forefoot.

-Plantar surface of
foot is medial

Function: assessed at the beginning of the examination

-Plantar surface of
foot is lateral

THE SHOULDER EXAMINATION

Positioning and Exposure: ideally standing (so that the patient can move their shoulder in all directions
unimpeded). Both shoulders should be fully exposed.
-Bare from waist up (males) or with bra or sports top (females)
-Watch the patient undress to assess functional impairment

Look:
1.
2.
3.
4.

General: skin changes, muscle wasting, muscle spasm, swelling, deformity, asymmetry, posture
Front: muscle wasting (esp. deltoid)
Side: position of shoulders in sagittal plane, posture of spine and limbs
Behind: supraspinatus, infraspinatus, trapezius, rhomboids, scapula winging, scoliosis

Winged scapula (scapula alata) is a condition in which the medial

border (the side nearest the spine) of a person's scapula is
abnormally positioned outward and backward. The resulting
appearance of the upper back is said to be wing-like because the
inferior angle of the shoulder blade protrudes backward rather
than lying mostly flat like in people without the condition.
A winged scapula is associated with damage or a contusion to the
long thoracic nerve of the shoulder and / or weakness in the
serratus anterior muscle. If the long thoracic nerve is damaged or
bruised it can cause paralysis of the serratus anterior muscle and
winging of the scapular or shoulder blade.

Normal Shoulder

Ear, shoulder,
elbow, knee and
ankle should be
approximately
aligned.

Dislocated Shoulder

The deltoid is responsible for the curved outline of the

normal shoulder. However, with dislocation, the angle
of the shoulder is much sharper.

Feel:
1.
2.

3.

Temperature over anterior of shoulders (use back of hand)

Assess bony landmarks for tenderness, swelling and deformity
a. Sternoclavicular joint
b. Clavicle
c. Acromioclavicular joint
d. Coracoid and acromion process
e. Spine and borders of scapula
Deltoid muscle, biceps, triceps (& pectoralis major) assess tone and muscle bulk

Superior border

Medial border

Inferior angle

Anterior

Posterior

Move:
Active movement: ask the patient to mimic you as you perform the following movements:
1. Abduction to 90- abduction through to elevation is 180
2. Flexion to 90- flexion through to elevation is 180
3. Internal rotation to 70
4. External rotation to 90
5. Extension to 60
6. Adduction to 30 (humerus passes in front of trunk)
7. Look from behind for scapulohumeral rhythm (abduct both arms) and painful arc
180
120
Glenohumeral
joint

120

Painful arc is
observed during
abduction form
60 to 120 and is
the result of
pinching of
inflamed or tender
structures under
acromion process.

Painful
arc
60
60
0
scapulothoracic
joint

Scapulohumeral
rhythm is observed
during abductionthere should be 120
of movement
occurring at the
glenohumeral joint and
60 occurring at the
scapulothoracic joint.

Passive movement:
1. Sit or lie the patient down and repeat the movements passively.
2. Note any discrepancy.
Note total range of movement and sequencing. E.g. for abduction, normal movement is straight out to side
keeping the shoulders back and down, vs hitching your shoulders first, throwing the arms forward to start
movement (problem with supraspinatus to originate movement).
Compare PASSIVE to ACTIVE movement. Active movements will stop when motor-unit stops due to pain or
nerve/ muscle problem.
i)
If passive movement in normal (suggesting joint is OK), but active movement is not = neural
or muscle problem
ii)
If passive movement = active movement = less than normal, this suggests a joint problem.

outward rotation
(external)
abduction
flexion

adduction

extension

inward rotation
(internal)

Function:
Ask the patient about washing, grooming and dressing. Observe if possible.

Special Tests:

APLEYs SCRATCH TEST: this is a quick, non-specific assessment of active function

The patient is instructed to reach and scratch at three points on the body:
1. Reach over the opposite shoulder (adduction)
2. Reach behind the neck (adduction, external rotation)
3. Reach behind the back (internal rotation)

HAWKINS-KENNEDY TEST: this is a test of impingement

1.
2.

Flex the patients elbow and shoulder to 90.

The examiner supports the shoulder with one
hand and uses the other to forcibly internally
rotate the shoulder.

The test is positive if pain is reproduced. This

suggests supraspinatus impingement
(supraspinatus tear = most common rotator
cuff injury).

APPREHENSION TEST: this is a test of anterior stability

1.
2.

3.

The patient may be standing or is a supine position.

The examiner passively abducts the arm to 90 and
externally rotates the arm with one hand while also
applying posterior pressure to humerus. Ensure you watch
the patient for signs of distress.
The test is positive if the patient experiences
apprehension about impending subluxation/
dislocation.

Any pain, sliding, patient resistance?

ROTATOR CUFF TEST 1: DROP ARM TEST: this is a test for supraspinatus (rotator cuff) injury
Patient raises arm to 90 out to the side and holds that
position. Patient slowly lowers arm. If the arm drops quickly
and not smoothly = sign of rotator cuff tear.
A gently applied pressure to the abducted arm may force arm
to give way. Examiner can also place hands on forearm and ask
patient to push up against them.

~PASSIVE ABDUCTION (perform passive abduction whilst

supporting the arm.

ROTATOR CUFF TEST 2: EMPTY CAN TEST

Abduct the arm to 90 in neutral position and test
abduction strength.
Then internally rotate the arm and to adduct 30
and test again.
The test is positive if there is pain and suggests a
supraspinatus tear.

*With thumb facing up, Pt pushes arm up against Dr, and with Pts thumb facing down repeat

WINGED SCAPULA
To accentuate winging of a scapula stand the patient about arms length facing a wall. Ask the patient
to push with both hands against the wall. Observe from behind the patient.

THE ELBOW EXAMINATION

Positioning and Exposure: Patient standing with both upper limbs completely exposed. Watch patient
undress to assess functional impairment.

Look:
5.
6.
7.

General: swelling, deformity, erythema, nodules, rashes

Effusion: usually seen on the lateral aspect in the triangle between epicondyle, head of the
radius, and olecranon process
Carrying angle: 5-10 (slightly greater in females than males)
Rheumatoid Nodules: As part of the rheumatoid process, firm, nontender, subcutaneous nodules develop in about 25 percent of
rheumatoid arthritis patients. These are commonly found at pressure
points like the elbow, back of the forearm, and metacarpophalangeal
joint. Nodules usually occur in chronic active cases of rheumatoid
arthritis, and are commonly associated with more joint deformity and
serious extra-articular manifestations including those in the lungs, eyes,
and blood vessels.

NB Should also be
same on both sides.

5-10

*Ulnar nerve around

medial epicondyle

coronoid fossa
capitullem

humerus
trochlear

lateral
epicondyle

medial
epicondyle

head of
radius

coronoid process

olecranon
fossa
olecranon
process

lateral
epicondyle

ulna
radius

radius
bicipital tuberosity

Carrying Angle
If increased carrying angle on one side =
fracture of lateral epicondyle as child???

Ulnar (medial)
collateral ligament

Radial (lateral) collateral

ligament
Annular ligament

ANTERIOR VIEW

POSTERIOR VIEW

Feel:
1.
2.
3.
4.
5.

Olecranon process and bursa if palpable

Tendon of triceps
Lateral and medial epicondyles
Head of radius, biceps tendon
Bulk of the flexor and extensor muscle groups

NOTE: nerve around medial

epicondyle = funny bone fingers
th
tingling especially 5 digit

Move:
Active movement: ask the patient to mimic you as you perform the following movements:
1. Flexion to 140 (depends on muscle bulk)
2. Extension to 0
3. Pronation to ~70
4. Supination to ~85
Passive movement: repeat the same movement passively noting any discrepancy

Flexion

Supination
Extension

Pronation

Function: ask the patient about functional activities such as eating, brushing teeth and dressing (also lifting up
a cup of coffee, eating, cutting up food)
Assess if possible

Special Tests:

GRIP STRENGTH
1. Ask the patient to make a fist and squeeze tightly
This will be painful at the elbow if epicondylitis
-The examiner can place a finger in both fists of the patient and compare grip strength.

VARUS & VALGUS STRESS TEST: this is a test of the integrity of the medial & lateral ligamentous complexes
1.

The patients arm is flexed to 20 at the elbow and supinated.

2.

The examiner supports the humerus with one hand and gently
stresses the medial or lateral side of the elbow joint with the
other hand.

Valgus
Varus

~ Valgus movement tests the medial ligaments, while varus

movement tests the lateral ligaments.

LATERAL EPICONDYLITIS (Tennis Elbow)

With the elbow extended, extending the wrist against resistance will elicit pain.

MEDIAL EPICONDYLITIS (Golfers Elbow)

With the elbow flexed, flexing the wrist against resistance will elicit pain.

ENTRAPMENT
Entrapment of radial, median and ulnar nerves may occur.
Refer to the neurological examination of the upper limb.

THE WRIST & HAND EXAMINATION

Positioning and Exposure: The patient and examiner should be seated, ideally across the corner of a table.
The whole of both upper limbs should be exposed.

Look:
1.
2.

Observe how the wrist / hand is held

Look for: scars, deformities, swelling, wasting, colour (erythema, pallor, cyanosis), skin changes (e.g.
rashes), wounds (especially seemingly minor puncture wounds)

~ulnar deviation

Heberden's nodes: are hard or bony swellings that can develop in

the distal interphalangeal joints. They are a sign of osteoarthritis and
are caused by formation of osteophytes (calcific spurs) of the
articular cartilage in response to repeated trauma at the joint.
Heberden's nodes typically develop in middle age, beginning either
with a chronic swelling of the affected joints or the sudden painful
onset of redness, numbness, and loss of manual dexterity. This initial
inflammation and pain eventually subsides, and the patient is left
with a permanent bony outgrowth that often skews the fingertip
sideways.

Bouchard's nodes may also be present; these are similar bony

growths in the proximal interphalangeal (PIP) joints (middle joints of
the fingers), and are also associated with osteoarthritis.

Typical hand deformities in

rheumatoid arthritis

Heberden's nodes are more common in women than in men, and

there seems to be a genetic component involved in predisposition to
the condition.

Feel:
1.

2.
3.

Palpate the dorsal aspect of the wrist

Distal forearm
Snuff box tenderness
Styloid process
scaphoid bone injury??
Ulna
Radius
Snuff box
Base of metacarpals
Lunate
Any swelling along the extensor tendon sheaths, ganglia, joint swelling, warmth
Palpate the palmar aspect of the wrist
Feel for the pisiform and hook of hamate
Palpate the hand
Assess for swelling, tenderness, warmth, nodules, thickening and contracture of fascia.
Feel the distal carpal, metacarpal and interphalangeal joints these are bedt felt from
the lateral sides, squeezing gently between your fingers

Move the Wrist:

Active movement: ask the patient to actively mimic your movements at the wrist
1. Flexion 80
*You can get Pt to hold pen in fist while
2. Extension 70
pronating and supinating to check range
3. Ulnar deviation 60
of movement
pen
4. Redial Deviation 20
Passive movement: repeat these movements passively, feeling for crepitus
fist

Flexion 80

Radial Deviation 20

Neutral position

Extension 70
Ulnar Deviation 60

Move the Hand:

Active movement followed by passive movement
1. Flexion:
a. Ask the patient to actively make a fist
b. Note any decreased ranger of finger flexion
c. All fingers should point towards scaphoid
d. Metacarpal heads should have normal aligment
e. Feel for creptis
2. Extension:
-Note any decreased range, suggestive of tendon avulsion. It may be useful to resist
finger movements to elicit tendon integrity.
3. Thumb opposition, abduction and adduction
-Test with grip strength, OK sign, key grip, and opposition of thumb to little finger
*Piece of paper between OK grip- try to pull out

5th Metacarpal Fracture

(Boxers Fracture): is the
term for a pinky-side hand
fracture, most often at the
neck of the pinkys metacarpal
bone. As the name indicates,
the condition is generally a
punching injury, occurring in
such sports as boxing,
kickboxing, karate, and mixed
martial arts.

An Avulsion fracture is a bone fracture which occurs when a

fragment of bone tears away from the main mass of bone as a result of
physical trauma. This can occur at the ligament due to the application
forces external to the body (such as a fall or pull) or at the tendon due
to a muscular contraction that is stronger than the forces holding the
bone together. Generally muscular avulsion is prevented due to the
neurological limitations placed on muscle contractions

Adduction

Abduction

Opposition

Function: Assess the patients limitation by asking them to open a jar, and tie their shoelaces.
Special Tests:

PHALENS TEST: this is a test for medial nerve compression/ entrapment

3.

The patient flexes both wrists and pushes the dorsal

aspect of their hands together, in a reverse prayer
sign for 1 minute.

4.

The test is positive if paraesthesia is evident on the

palmar surface of the thumb, index, middle and
lateral half of the ring finger.

Carpal tunnel syndrome (CTS), or median neuropathy

at the wrist, is a medical condition in which the median
nerve is compressed at the wrist,

TINELS SIGN: this is a test for CTS

ANATOMICAL SNUFF BOX:

Position the patients wrists in

supination and tap over the flexor
retinaculum at the proximal part of
the palm.

Pressure in the middle of the

anatomical snuff box can elicit
a fracture of the scaphoid, but
can also be tender in sprain.

This test is positive if this

reproduces the paraesthesia and is
suggestive of carpal tunnel syndrome.

Check with pressure over the

scaphoid tubercle.

Other causes of Hand Disease:

-

Seropositive and seronegative arthritidis are systemic diseases, so think systematically

An apical lung tumour can cause wasting of the hand muscles
Also remember the many hand, nail and finger signs from CVS / RESP / GIT

DIAGNOSTIC IMAGING FOR THE MUSCULO SKELETAL SYSTEM

1. X-ray

2. Ultrasound

3. Computed Tomography

4. Magnetic Resonance Imaging

CLINICAL SKILLS

Neurological
System Exam

NEUROLOGICAL SYSTEM:

CLINICAL EXAMINATION

NEUROLOGICAL SURFACE ANATOMY

Dermatomes: the lateral wall of a somite from which the dermis is produced
NOTE: that the domains of the dermatomes (spinal nerve roots) differs from that of individual nerves. Radicular
pain is pain that radiates along a dermatome, corresponding to a spinal root injury.
Key Sensory Points:

C4: ~ necklace
C5: ~ tip of
shoulder

T4: nipples

T10: umbilicus

S6: thumb
S7: middle digit
L1: ~ underwear

S8: little finger

You sit on S3/S4

S5: anus
L3: knee

You stand on L5 (medial) and

S1 (lateral)

Anterior and posterior views of the dermatomes. Each segment

is named for the principal spinal nerve serving it. V, trigeminal
segments; C, cervical segments; T, thoracic segments; L,
lumbar segments; S, sacral segments.

OVERVIEW OF THE NERVOUS SYSTEM

CENTRAL NERVOUS SYSTEM DISORDERS:

Lesions in the two components of the central nervous system (CNS)the brain and the spinal cordtypically
cause paresis, sensory loss, and visual deficits. In addition, lesions in the cerebral hemispheres (the cerebrum)
cause neuro-psychologic disorders. Symptoms and signs of CNS disorders must be contrasted to those
resulting from peripheral nervous system (PNS) and psychogenic disorders.

Signs of Cerebral Hemisphere Lesions

Of the various signs of cerebral hemisphere injury, the most prominent is usually
Contralateral hemiparesis: weakness of the lower face, trunk, arm, and leg opposite to the side of the lesion.
It results from damage to the corticospinal tract, which is also called the pyramidal tract. During the corticospinal
tract's entire path from the cerebral cortex to the anterior horn cells of the spinal cord, it is considered the upper
motor neuron (UMN). The anterior horn cells, which are part of the PNS, are the beginning of the lower motor neuron
(LMN). The division of the motor system into upper and lower motor neurons is a basic tenet of clinical neurology.

Each corticospinal tract originates in the cerebral cortex, passes through

the internal capsule, and descends into the brainstem. It crosses in the
pyramids, which are long protuberances on the inferior portion of the
medulla, to descend in the spinal cord as the lateral corticospinal tract. It
terminates by forming a synapse with the anterior horn cells of the spinal
cord, which give rise to peripheral nerves. The corticospinal tract is
sometimes called the pyramidal tract because it crosses in the pyramids. A
complementary tract, which originates in the basal ganglia, is called the
extrapyramidal tract.

UPPER MOTOR NEURONE(UMN) vs LOWER MOTOR NEURONE (LMN) DISEASE:

Characteristics of lower motor neurone disease include: weakness and wasting, hypotonicity, decreased reflexes,
fasciculation.
Characteristics of upper motor neurone disease include: weakness, spasticity, increased tendon reflexes with clonus,
extensor plantar response.

Cerebral lesions that damage the corticospinal tract are characterized by signs

of UMN injury

Signs of UMN injury:

- Paresis with muscle spasticity (muscular hypertonicity)
- Hyperactive deep tendon reflexes (DTRs)
- Babinski signs

HEMIPARESIS (UMN)
Severe right hemiparesis typically has
weakness of the right arm, leg, and lower
face. The right-sided facial weakness causes
the widened palpebral fissure and flat
nasolabial fold; however, the forehead
muscles are normal. The right arm is limp,
and the elbow, wrist, and fingers are flexed.
The right hemiparesis also causes the right
leg to be externally rotated and the hip and
knee to be flexed.
When the patient stands up, his weakened
arm retains its flexed posture. His right leg
remains externally rotated, but he can walk
by swinging it in a circular path. This
manoeuvre is effective but results in
circumduction or a hemiparetic gait.

Mild hemiparesis may not be obvious. To exaggerate a

subtle hemiparesis, the physician has asked this patient to
extend both arms with his palms held upright, as though each
outstretched hand were holding a water glass or both hands
were supporting a pizza box (the pizza test). After a minute,
a weakened arm slowly sinks (drifts), and the palm turns
inward (pronates). The imaginary glass in the right hand
would spill the water inward and the imaginary pizza would
slide to the right. This arm's drift and pronation represent a
forme fruste of the posture seen with severe paresis.

In contrast, peripheral nerve lesions, including anterior horn cell or motor neuron diseases, are
associated with signs

of LMN injury:

-Paresis with muscle flaccidity and atrophy

-Hypoactive DTRs
-No Babinski Signs

Deep Tendon Reflex in UMN and LMN Disease:

Normal

UMN Lesion

LMN Lesion

A, Normally, when the quadriceps tendon is struck with the percussion hammer, a deep tendon reflex
(DTR) is elicited. In addition, when the sole of the foot is stroked to elicit a plantar reflex, the big toe bends
downward (flexes).

B, When brain or spinal cord lesions involve the corticospinal tract and cause upper motor neuron (UMN)
damage, the DTR is hyperactive, and the plantar reflex is extensor (i.e., a Babinski sign is present).

C, When peripheral nerve injury causes lower motor neuron (LMN) damage, the DTR is hypoactive and the
plantar reflex is absent.

Cerebral lesions are not the only cause of hemiparesis. Because the corticospinal tract has such a long course,
lesions in the brainstem and spinal cord as well as the cerebrum may produce hemiparesis and other signs of
UMN damage. Signs pointing to injury in various regions of the CNS can help identify the origin of hemiparesis,
that is, localize the lesion.

LOCALISING LESIONS in the CEREBRUM (e.g. APHASIA)

Wernicke Aphasia (Receptive aphasia): Speech is preserved,
but language content is incorrect. This may vary from the
insertion of a few incorrect or nonexistent words to a profuse
outpouring of jargon. Grammar, syntax, rate, intonation and
stress are normal. Substitutions of one word for another
(paraphasias) are common. Comprehension and repetition are
poor.

Brocas Aphasia: Sufferers of this form of aphasia exhibit the

common problem of agrammatism. For them, speech is difficult
to initiate, non-fluent, labored, and halting. Similarly, writing is
difficult as well. Intonation and stress patterns are deficient.
Language is reduced to disjointed words and sentence
construction is poor, omitting function words and inflections
(bound morphemes).

Signs of Basal Ganglia Lesions

The basal ganglia, located subcortically in the cerebrum, are composed of the globus pallidus and the putamen
(the striatum), the substantia nigra, and the subthalamic nucleus (corpus of Luysii). They give rise to the
extrapyramidal tract, which modulates the corticospinal (pyramidal) tract. The extrapyramidal tract controls
muscle tone, regulates motor activity, and generates the postural reflexes through its efferent fibers that play
on the cerebral cortex, thalamus, and other CNS structures. However, the extrapyramidal tract's efferent fibers
are confined to the brain and do not act directly on the spinal cord or LMNs.

Signs of basal ganglia injury include a group of fascinating, often dramatic, involuntary movement
disorders:

Parkinsonism is the combination of resting tremor, rigidity, bradykinesia (slowness of

movement) or akinesia (absence of movement), and postural abnormalities. Minor features
include micrographia and festinating gait. Parkinsonism usually results from substantia nigra
degeneration (Parkinson's disease and related illnesses), dopamine-blocking antipsychotic
medications, or toxins.

Athetosis is the slow, continuous, writhing movement of the fingers, hands, face, and throat.
Kernicterus or other perinatal basal ganglia injury usually causes it.

Chorea is intermittent, randomly located, jerking of limbs and the trunk. The best-known
example occurs in Huntington's disease (previously called Huntington's chorea), in which the
caudate nuclei characteristically atrophy.

Hemiballismus is the intermittent flinging of the arm and leg on one side of the body. It is
classically associated with small infarctions of the contralateral subthalamic nucleus, but
similar lesions in other basal ganglia may be responsible.

Signs of Brainstem Lesions:

IF appropriate, attribute lesion to one of three divisions of the brainstem:

Midbrain, Pons or Medulla.

The brainstem contains the cranial nerve nuclei, the corticospinal tracts and other long tracts that travel
between the cerebral hemispheres and the limbs, cerebellar afferent (inflow) and efferent (outflow) tracts, and
several largely self-contained systems.
Combinations of cranial nerve and long tract signs indicate the presence and location of a brainstem lesion.
The localization should be supported by the absence of signs of cerebral injury, such as visual field cuts and
neuropsychologic deficits. For example, brainstem injuries cause diplopia (double vision) because of cranial
nerve impairment, but visual acuity and visual fields remain normal because the visual pathways, which pass
from the optic chiasm to the cerebral hemispheres, do not travel within the brainstem.

Massive brainstem injuries, such as extensive infarctions or barbiturate overdoses, cause coma, but
otherwise brainstem injuries do not impair consciousness or mentation. With the exception of MS and
metastatic tumors, few illnesses simultaneously damage the brainstem and the cerebrum.
Although these particular brainstem syndromes are distinctive, the most frequently observed sign of
brainstem dysfunction is nystagmus (repetitive jerk-like eye movements, usually simultaneously of both
eyes). Resulting from any type of injury of the brainstem's large vestibular nuclei, nystagmus can be a
manifestation of various disorders, including intoxication with alcohol, phenytoin (Dilantin), or barbiturates;
ischemia of the vertebrobasilar artery system; MS; Wernicke-Korsakoff syndrome; or viral labyrinthitis.

Signs of Cerebellar Lesions:

The cerebellum (Latin, diminutive of cerebrum) is composed of two hemispheres and a central portion, the
vermis. Each hemisphere controls coordination of the ipsilateral limbs, and the vermis controls coordination
of midline structures: the head, neck, and trunk. Because the cerebellum controls coordination of the
limbs on the same side of the body, it is uniquea quality captured by the aphorism, Everything in the
brain, except for the cerebellum, is contralateral. Another unique feature of the cerebellum is that when
one hemisphere is damaged, the other will eventually assume the functions for both. Thus, although loss of
one cerebellar hemisphere will cause incapacitating ipsilateral incoordination, the disability improves as the
remaining hemisphere compensates almost entirely. For example, patients who lose one cerebellar
hemisphere to a stroke or trauma typically regain their ability to walk, although they may never dance or
perform other activities requiring both cerebellar hemispheres. Young children who sustain such an injury
are more resilient and often can learn to ride a bicycle, dance, and perform various athletic activities.
In addition to incoordination, cerebellar lesions cause subtle motor changes, such as muscle hypotonia and
pendular DTRs. However, they do not cause paresis, hyperactive DTRs, or Babinski signs.

GAIT ATAXIA:
Damage to either the entire cerebellum or the vermis alone causes incoordination of the trunk (truncal ataxia).
It forces patients to place their feet widely apart when standing and leads to a lurching, unsteady, and widebased pattern of walking (gait ataxia). A common example is the staggering and reeling of people intoxicated
by alcohol or phenytoin.
SCANNING SPEECH:
Extensive damage of the cerebellum also causes scanning speech, a variety of dysarthria. Scanning speech,
which reflects incoordination of speech production, is characterized by poor modulation, irregular cadence,
and inability to separate adjacent sounds. Dysarthriawhether from cerebellar injury, bulbar or pseudobulbar
palsy, or other neurologic conditionsshould be distinguishable from aphasia, which is a language disorder
that stems from dominant cerebral hemisphere injury.
NOTE: Age related change of the cerebellum.
Before considering the illnesses that damage the cerebellum, physicians must appreciate that the
cerebellum undergoes age-related changes that appear between ages 50 and 65 years in the form of
mildly impaired functional ability and abnormal neurologic test results. For example, as people age
beyond 50 years, they walk less rapidly and less sure-footedly. They begin to lose their ability to ride a
bicycle and to stand on one foot while putting on socks. During a neurologic examination they routinely
tend to topple when walking heel-to-toe, that is, performing the tandem gait test

ILLNESSES THAT AFFECT THE CERBELLUM:

The illnesses that are responsible for most cerebral lesionsstrokes, tumors, trauma,
AIDS, and MSalso cause most cerebellar lesions. The cerebellum is also particularly
vulnerable to toxins, such as alcohol, toluene, and organic mercury; medications, such as
phenytoin; and deficiencies of certain vitamins, such as thiamine and vitamin E. Some
conditions damage the cerebrum as well as the cerebellum and may cause a combination
of cognitive impairment and incoordination

Signs of Spinal Cord Lesions:

SPINAL TRACTS

In this sketch of the spinal cord, the centrally located

gray matter is stippled. The surrounding white matter
contains myelin-coated tracts that ascend and descend
within the spinal cord.

Clinically important ascending tracts are the

-spinocerebellar tracts (SC) (light blue),
-lateral spinothalamic tract (ST) (light blue),
-the posterior column (fasciculus cuneatus [FC], from
the upper limbs, and fasciculus gracilis [FG], from the
lower limbs) (gray).

The major descending pathway is the lateral corticospinal tract.

The major ascending pathways, which are virtually all sensory, include the following:

The most important descending tract is the:

Posterior columns, composed of the fasciculi cuneatus and gracilis, carry position and
vibration sensations to the thalamus.-lateral corticospinal (CS) tract (dark blue).

Lateral spinothalamic tracts carry temperature and pain sensations to the thalamus.

Anterior spinothalamic tracts carry light touch sensation to the thalamus.

Spinocerebellar tracts carry joint position and movement sensations to the cerebellum.

Conditions that affect the spinal cord:

Discrete Injuries:
The site of a spinal cord injurycervical, thoracic, or lumbosacraldetermines the nature
and distribution of the motor and sensory deficits.
In general, all spinal cord injuries disrupt bladder control and sexual function, which rely on
delicate, intricate systems

Neurlogical Diseases:
MS, the most common CNS demyelinating illness, typically causes myelopathy alone or in
combination with cerebellar, optic nerve, or brainstem damage. Tumours of the lung, breast,
and other organs that spread to the vertebral bodies often compress the spinal cord and
cause myelopathy. Similarly, regions of degenerative spine disease, such as cervical
spondylosis, can narrow the spinal canal enough to compress the spinal cord. There are also
several illnesses damage only specific spinal cord tracts (e.g. tabes dorsalis (syphilis),
Friedreichs ataxia etc).

Cerebellum

Cord

Pain- Severe

Sensory Loss

Babinski
upgoing

Brainstem

Hyper-reflexia

Muscle
Fasciculations

Muscle
atrophy

Muscle
weakness

Visual Field
Loss

Bowel/ Bladder
Incontinence

Dysarthria

Dysconjugate
Gaze

Language
(aphasia)

Cortex/
hemisphere

Seizure

Neuraxis
Level

Cognitive
Function

NEURAXIS LOCALISATION:

Anterior
Horn Cell

Root

Plexus

Nerve
NMJ

Muscle

Aphasia: loss or impairment of the power to use or comprehend words usually resulting from brain damage
Dysarthria: difficulty in articulating words due to disease of the central nervous system
Dysconjugate Gaze: failure of the eyes to turn together in the same direction
Fasciculations: muscular twitching involving the simultaneous contraction of contiguous groups of muscle fibers
NMJ: Neuromuscluar junction

WHERE is the lesion?

-cortex/ hemisphere
-brainstem
-cerebellum
-spinal cord
-anterior horn cell
-nerve root
-plexus
-peripheral nerve
-neuromuscular junction
-muscle

WHAT is the lesion?

CITTEN DVM
-Congenital
-Inflammatory (autoImmune,
Infectious)
-Toxic
-Trauma
-Endocrine
-Neoplastic and Nutritional
-Degenerative or Drugs
-Drugs
-Metabolic

What is the TEMPORAL profile?

-Acute
-Subacute
-Chronic
-Progressive
-Paroxysmal/ relapsing

Age-Related Special Sense Impairments (more degeneration of sensory organ than of cranial nerve)
Smell

Some degree of anosmia in 75% of individuals older than 80 years

Vision

Presbyopia: mostly inability to accommodate to see closely held or small objects; cataracts

Taste

Loss of taste sensitivity and discrimination, as well as anosmia for aroma

Hearing Presbycusis: loss of speech discrimination, especially for consonants; poor high-pitched sound detection, tinnitus

Mini-mental state examination

The mini-mental state examination (MMSE) is a brief 30-point questionnaire test that is used to screen for cognitive
impairment. It is commonly used in medicine to screen for dementia. It is also used to estimate the severity of cognitive
impairment at a given point in time and to follow the course of cognitive changes in an individual over time, thus making it
an effective way to document an individuals response to treatment.

Mini-Mental State
Write in the points for each correct response. A total of 30 points is possible.
Score Points
Orientation
1. What is the:

2. Where are we?

Year?
Season?
Date?
Day?
Month?
State?
Country?
Town or city?
Hospital?
Floor?

Registration
3. Name three objects, taking 1 second to say each. Then ask the patient to repeat all three
names after you have said them. (Give one point for each correct answer.) Repeat the answers
until the patient learns all three.
Attention and calculation
Serial sevens. Have the patient count backward from 100 by 7's. (Stop after five answers: 93,
86, 79, 72, 65. Give one point for each correct answer.) Alternatively, have the patient spell
WORLD backwards.
Recall
5. Ask for the names of the three objects learned in question 3. (Give one point for each correct
answer.)
Language
6. Point to a pencil and a watch. Have the patient name them as you point.
7. Have the patient repeat "No ifs, ands or buts."
8. Have the patient follow a three-stage command: "Take a paper in your hand. Fold the paper
in half. Put the paper on the floor."
9. Have the patient read and obey the following: "CLOSE YOUR EYES." (Write the words in
large letters.)
10. Have the patient write a sentence of his or her choice. (The sentence should contain a
subject and an object, and it should make sense. Ignore spelling errors when scoring.)
11. Have the patient copy the following design. (Give one point if all sides and angles are
preserved and if the intersecting sides form a quadrangle.)

Total

_____
_____
_____
_____
_____
_____
_____
_____
_____
_____

1
1
1
1
1
1
1
1
1
1

_____ 3

_____ 5

_____ 3
_____ 2
_____ 1
_____ 3
_____ 1
_____ 1
_____ 1

_____

THE CRANIAL NERVE EXAMINATION

Positioning and Exposure: the patient should be sitting on the edge of the bed
General Inspection:
4.
5.
6.
7.
8.
9.

Craniotomy scars
Neurofibromas
Facial asymmetry
Ptosis
Proptosis
Deviation of the eyes or unequal pupils

Neurofibromatosis (type 1,
affecting peripheral nerves) is
characterised by more than
five face-au-lait spots
(discoloured patched of skin),
and soft, sometimes
pedunculated neurofibromas
(fibrous tumours or nodules
growing from the peripheral
nerve sheath). Associated
abnormalities may include
scoliosis and gigantism of a
limb.

This patient has a right-sided occulomotor nerve

palsy, due to a large pituitary adenoma invading
the cavernous sinus. He has paralysis of the right
levator palpebral superioris muscle (complete

ptosis), and a dilated right pupil (mydriasis).

Proptosis ( or exopthalmos). Proptosis is a forward displacement of

the eyeball from the orbit, associated with eyelid retraction, so that the
sclera is visible above the iris. Unilateral proptosis may be a sign of an
orbital tumour, haemorrhage, or infiltration, and requires prompt
treatment to avoid damage to the optic nerve. This patient has
proptosis due to thyrotoxicosis.
Proptosis may be difficult to detect if the eyeball protrusion is subtle.
If suspicious, view from above the seated patient. Draw the upper
eyelids gently upward, then compare protrusion of the eyeballs.

This congenital right-sided occulomotor nerve palsy is

characterised by potosis, divergent strabismus (eye down and
out) and a dilated pupil, which is unreactive to direct light and
accommodation. Consensual reaction in the opposite normal
eye is intact. Third nerve lesions may also be caused by trauma.

This patients abducens palsy results in an abduction

deficit of the left eye, convergent strabismus (cross
eye) and diplopia (double vision). Sixth nerve lesions
may be caused by vascular lesions, tumour, trauma,
raised intracranial pressure, or diabetes.

THE CRANIAL NERVES

CN
I
II
III

Name
Olfactory
Optic
Oculomotor

Nerve Type *
S
Special Sensory
S
Special Sensory
M Motor

Autonomic
IV
V

Trochlear
Trigeminal

M
B

Motor
Motor
Sensory

VI
VII

Abducens
Facial

M
B

Motor
Motor
Autonomic
Sensory

VIII

Special Sensory
Special Sensory

IX

Vestibulocochlear
(Auditory)
Glossopharyngeal

Vagus

XI

Accessory

Special Sensory
Motor
Autonomic Motor
Sensory
Motor

XII

Hypoglossal

Motor

Motor
Autonomic Motor
Autonomic Sensory
Sensory

Functions
Smell- direct extension from the brain
Vision- direct extension from the brain
Moves muscles of eye and eyelid
(superior, inferior and medial recti; levator
palpebrae superioris)
Parasympathetic (ciliaris and sphincter
papillae)
Moves eye (superior oblique)
Muscles of mastication (masseters,
temporalis)
Face and neck, sinuses, meninges and external
tympanic membrane
Moves eye (lateral rectus)
Muscles of facial expression
Parasympathetic (salivary glands except
parotid and lacrimal)
Sensory around ear and external tympanic
membrane
Taste anterior 2/3 tongue
Hearing
Balance
Moves pharynx upwards (Stylopharageus)
Parasympathetic (parotid gland)
Carotid body
Sensory posterior 1/3 tongue and internal
surface of tympanic membrane
Taste posterior surface of tongue
Muscles of pharynx & larynx swallow & speech
Parasympathetic to neck, thorax, abdomen
Sensory from pharynx, larynx, viscera
Trapezius and sternocleidomastoid (shrugs ans
turns head)
Muscles of tongue movement

* S: sensory / M: motor / B: both

pneumonic for remembering the nerve type for the cranial nerves:
Some Say Money Matters But My Brother Says Big Boobs Matter More

OLFACTORY NERVE (I)

From the olfactory receptors located deep in the nasal cavity, branches of the pair of olfactory nerves pass
upward through the multiple holes in the cribriform plate of the skull to several areas of the brain. Some
terminate on the undersurface of the frontal cortex, home of the olfactory sensory areas. Others terminate
deep in the hypothalamus and amygdalacornerstones of the limbic system. The olfactory nerves' input into
the limbic system, at least in part, accounts for the influence of smell on psychosexual behaviour and memory.

Smell
1.

Ask the patient if they can smell normally

-If they answer YES this is usually sufficient and you may proceed to CNII.

2.

If altered olfaction is suspected

-Inspect nares with light and speculum
-Ask the patient to close his/her eyes
-Test one nostril at a time by offering a variety of materials with common smells
-Either use materials close at hand with an aroma (fruit, soap, coffee, perfume) or specially
prepared materials
-Ask the patient if they can identify the smell
-Ask the patient if the smell is the same on both sides

NB: Volatile and irritative substances, such as ammonia and alcohol, are not suitable because they may trigger intranasal
trigeminal nerve receptors and bypass a possibly damaged olfactory nerve.

anosmia, cannot perceive smells

One-sided anosmia may result from tumors adjacent to the olfactory nerve, such an olfactory groove meningioma. In the
classic Foster-Kennedy syndrome, a meningioma compresses the olfactory nerve and the nearby optic nerve. The damage to
those two nerves causes the combination of unilateral blindness and anosmia. If the tumor grows into the frontal lobe, it
can also produce personality changes, dementia, or seizures.
In most cases of bilateral anosmia, the underlying disturbance is mundane. Anosmia is routine in anyone with nasal
congestion and those who regularly smoke cigarettes. Head trauma, even from minor injuries, can shear off the olfactory
nerves as they pass through the cribriform plate and cause anosmia
Olfactory hallucinations may represent the first phase or aura (Latin, breeze) of partial complex seizures that originate in
the medial-inferior surface of the temporal lobe.

OPTIC NERVE (II)

Visual Acuity
1. Test visual acuity with the patient wearing his/ her
spectacles
2. Each eye is tested separately with a Snellen chart,
while the other is covered with a small card.
(record last full line;
6/3 (good), 6/6 (normal), 6/9 (acuity))
-also COMPARE eyes (and can you improve with pin
hole?- glasses will then help.
Ishihara dot chart for assessing red/ green colour blindness:

Visual Fields
1.

2.

Examine the visual fields by confrontation using a hat pin or pen

a. Ask the patient to remove their spectacles
b. The examiners eyes should be level with the patients eyes, and the patient should be at arms
length
c. Ask the patient to cover one eye and mirror them by covering whichever of your eyes is opposite.
Both you and the patient need to stare straight ahead and not move the eye from its neutral
position
d. With an outstretched arm, position the pin halfway between you and the patient and gradually
bring the pin diagonally into the visual field and towards the centre of vision
e. Ask the patient to report when they first sight the pin in their peripheral vision and if it disappears
while travelling to the centre of their vision
f. Test each eye separately and compare to your own visual fields.
If visual acuity is poor, map the fields with a finger.

Centre of vision
3

Patient closes one eye (or covers with card) and doctor
closes mirroring eye.

When can you see it and does it ever disappear?

4

Visual inattention: test fields by wriggling two

in front
Pt and
in peripherally.
NB:fingers
Make sure
youoftest
fieldcoming
HALFWAY
between examiner
and patient.

Fundi
1.

Use an opthalmoscope to examine the fundi

Check optic disc for papillodema (normal vision vs vision loss with oedema for MS), optic neuritis (X
vision and blurry disc)

This is a normal fundus of the left eye. The field of view

is much wider here than in direct opthalmoscopy. Look for
the pale yellow optic disc (where the optic nerve exits from
the back of the eye), the four retinal vascular arcades
radiating out from the optic disc, the orange light-sensitive
retina, and the dark red of the macula (the most sensitive
area of the retina, located centrally).

Visual defect is dependent on location of lesion.

e.g. pituitary adenoma, push up against optic chiasm,
affecting medial tracts
.: loss of temoral (lateral) visual fields

Papilloedema may be caused by raised intracranial pressure, optic nerve or

vascular disease. This patient has a brain tumour, resulting in raised ICP.
Vascular congestion and axonal swelling within the optic nerve causes fuzziness
and heaping up of the disc margins, loss of pulsation of the retinal veins, and
obliteration of the physiological cup. Initially there are few visual symptoms,
but as the oedema progress, the blind spot enlarges and vision blurs. Finally,
arterial blood flow falls, and infarction of the optic nerve occurs, with sudden,
severe visual loss.

In this diabetic, frond-like

proliferations of new vessels
appear on the (yellow) optic disc.
Such neovascularisation is typical
of early proliferative

diabetic retinopathy, and

places the patient at risk of visual
loss.

This fundus demonstrates retinopathy

due to severe acute hypertension. There
are flame-shaped and blot retinal

haemorrhages, and hard

exudates, caused by leakage of lipids
and proteins in this instance around the
macular.

In optic atrophy, the disc is flat, white and

has sharp margins due to axonal death and
decreased vascularity. Optic atrophy may
result from papilloedema, or from various
other processed including thromboembolism.
A total optic nerve lesion causes unilateral
blindness with loss of direct and consensual
papillary light reflex.

OCULOMOTR, TROCHLEAR & ABDUCENS NERVES (III, IV, VI)

The oculomotor, trochlear, and abducens nerves constitute the extraocular muscle system because, acting in
unison, they move the eyes in parallel to provide normal conjugate gaze. Damage of any of these nerves causes
dysconjugate gaze, which results in diplopia (double vision). Extraocular muscle nerve damage leads to
characteristic patterns of diplopia. In addition, with oculomotor nerve damage, patients also lose their pupillary
constriction to light and strength of the eyelid muscle.

Diplopia is most often attributable to a lesion in the oculomotor nerve on one side or the abducens nerve on
the other. For example, if a patient has diplopia when looking to the left, then either the left abducens nerve or
the right oculomotor nerve is paretic.
Inspect the pupils: shape, relative sizes, associated ptosis
Reaction to light
1.
2.
3.

Use a pocket torch and shine the light from the side to gauge the reaction of the pupils to light
Assess both the direct and consensual responses
Look for an afferent papillary defect by moving the torch in an arc from pupil to pupil
(swinging torch reflex)

The light reflex, which is more complex than a deep tendon reflex, begins with its afferent limb in the optic nerve (cranial nerve II).
1. The optic nerve transmits light impulses from the retinas to two neighboring midbrain structures: (1) In conveying vision, axons
synapse on the lateral geniculate body. Then postsynaptic tracts convey visual information to the occipital lobe's visual cortex. (2) In
conveying the light reflex, optic nerve axons also synapse in the pretectal region.
2. Postsynaptic neurons travel a short distance to both the ipsilateral and contralateral Edinger-Westphal nuclei, which are the
parasympathetic divisions of the oculomotor (third cranial nerve) nuclei. Those nuclei give rise to parasympathetic oculomotor nerve
fibres, which constitute to the reflex's efferent limb. Their fibres synapse in the ciliary ganglia and postsynaptic fibres terminate in the
iris constrictor (sphincter) muscles. Thus, light shone in one eye constricts the pupil of that eye (the direct *ipsilateral+ light reflex)
and the contralateral eye (the consensual *indirect or contralateral+ light reflex).

Conjugate gaze: the normal movement of the two eyes simultaneously in the same direction to bring something into view.
Dysconjugate gaze: failure of the eyes to turn together in the same direction
Binocular vision: vision with a single image, by both eyes simultaneously
Monocular vision: vision with one eye

Accommodation
1.

Test accommodation by asking the patient to look into the distance and then at the hat pin placed about 30cm
from the nose
Normally both pupils will constrict (accommodate) and eyes converge
Focus on point, move close (constrict) and away (dilate)

Eye movements
1.
2.
3.
4.

Ask the patient to keep their head still and to follow the hat pin with their eyes only
Assess both eyes first and as they follow the hat pin in an H pattern (do it slowly)
Look for failure of movement and for nystagmus
Ask the patient to report diplopia (double vision) in any direction
Dr should say: Keep looking... is it double???

*Nystagmus: Rapid rhythmic

repetitious involuntary (unwilled)
eye movements. Nystagmus can
be horizontal, vertical or rotary.

Doctor holds patients head, slowly moves hatpin,

stopping at each point asking can you see double?.
Watch for nystagmus.

Superior rectus

Inferior oblique
UP

NOSE SIDE

G
Lateral
rectus

Medial
rectus

A
Z
DOWN
Inferior rectus

Superior oblique

TRIGEMINAL NERVE (V)

The trigeminal (Latin, threefold) nerves convey sensation from the face and innervate the large, powerful
muscles that protrude and close the jaw. Because these muscles' main function is to chew, they are often called
the muscles of mastication.
NB: tongue (sensory) is also part of CNV-3, but usually not tested

Corneal Reflex
1.
2.
3.

Gently touch the cornea with a piece of cotton wool brought form the side (just inside iris)
Ask the patient if they felt the touch (sensory component via CNV)
The normal response is reflex blinking (motor component via CNVII)
Contact lens: reflex; NB- dont let cotton touch eyelashes

Assessing the corneal reflex is useful, especially in examining patients whose sensory loss does not conform to
neurologic expectations. The corneal reflex is a superficial reflex that is essentially independent of upper motor
neuron (UMN) status. It begins with stimulation of the cornea by a wisp of cotton or a breath of air that triggers the
trigeminal nerve's V1 division, which forms the reflex's afferent limb. A brainstem synapse stimulus innervates both
facial (seventh cranial) nerves, which form the efferent limb. The synapse innervates both sets of orbicularis oculi
muscles.
Normally, because of the synapse, stimulating one cornea will provoke bilateral blinking. However, if the cotton tip is
first applied to the right cornea and neither eye blinks, and then to the left cornea and both eyes blink, the right
trigeminal nerve (afferent limb) is impaired. On the other hand, if cotton stimulation on the right cornea fails to
provide a right eye blink but succeeds in provoking a left eye blink, the right facial nerve (efferent limb) is impaired.

Facial Sensation
1.
2.
3.

Test facial sensation in the ophthalmic, maxillary and mandibular divisions of CNV
Test pain sensation with the pin first and map any areas of sensory loss from dull to sharp (sharp: use point
of paper clip, soft: cotton wool)
Test light touch as well so that sensory dissociation can be detected if present

L
Patient closes their eyes:

Forehead

Testing the three branches of

the trigeminal nerve.

L
R

Cheek

forehead
cheek
chin

sharp
soft

Chin

Hypalgesia : areas of reduced sensation, should conform to anatomic outlines

-The first division (V1) supplies the forehead, the cornea, and the scalp up to the vertex;
-the second (V2) supplies the malar area;
-the third (V3) supplies the lower jaw, except for the angle.
These distributions have more than academic importance. These dermatomes may be mapped by
herpes zoster infections (shingles), trigeminal neuralgia, and facial angioma in the Sturge-Weber syndrome

Herpes zoster
(or shingles)
commonly affects
the ophthalmic
division of the
trigeminal nerve.

Muscles of mastication
1.
2.

Examine the motor division of CNV by asking the patient to clench their teeth while you feel the masseter
muscles
Ask the patient to open the mouth while you attempt to force it closed

Jaw Jerk
1.
2.

Ask the patient to relax their jaw

Place a finger tip on the midline of the jaw and strike this lightly with a tendon hammer
Normal reflex response is slight elevation of the mandible (close the mouth)
-Stretch reflex, an increased jerk is abnormal

Abnormalities are mostly a matter of rapidity and strength.

In a hypoactive reflex, as found in bulbar palsy and other lower
motor neuron (LMN) injuries, there is little or no rebound.
In a hyperactive reflex, as in pseudobulbar palsy and other upper
motor neuron (UMN) (corticobulbar tract) lesions, there is a quick and
forceful rebound.

FACIAL NERVE (VII)

Muscles of Facial Expression (first LOOK- is face symmetrical???- PALSY???)

Palsy: In medicine, palsy is the paralysis of a body part, often accompanied by loss of sensation and by
uncontrolled body movements, such as shaking. Medical conditions involving palsy include cerebral palsy
(caused by certain intracranial lesions), brachial palsy (the paralysis of an arm), and Bell's palsy (the paralysis
of half the face due to inflammation of the facial nerves).
-Test the muscles of facial expression by asking the patient to mimic your facial expressions
1.

Raise your eyebrows and wrinkle your forehead

As the patient mimics your expression, look for loss of wrinkling and feel their muscle
strength by pushing down on each side
2. Ask the patient to shut their eyes as tight as they can, and keep them closed as you try to open them
(compare two sides)
3. Smile- compare the patients nasolabial grooves
4. Puff out your cheeks, as if you are holding a mouthful of water check the patients cheeks for
symmetry
*If muscle wasting- flattening of nasolabial fold and cant keep eyes closed (CNVII- obicularis oris)
To test POWER
i)
ii)
iii)

Dr pokes puffed cheeks

Pt keep eyebrows up while Dr pushed them down
Pt keeps eyes closed by Dr tries to open them

**In the classic portrayal, corticobulbar tracts originating in the ipsilateral, as well as in
the contralateral, cerebral hemisphere supply each facial nerve nucleus. Each facial
nerve supplies the ipsilateral muscles of facial expression. Because the upper half of
the face receives cortical innervation from both hemispheres, cerebral injuries lead to
paresis only of the lower half of the contralateral face. In contrast, facial nerve injuries
lead to paresis of both the upper and lower half of the ipsilateral side of the face. **

If there are herpes zoster vesicles found in the ear or the

palate, unilateral LMN 7th nerve palsy is known as Ramsay
Hunt syndrome (shown here). An UM 7th nerve palsy, most
commonly caused by vascular lesions or tumours, spares the
muscles of the forehead. The muscles of the upper face are
controlled by pathways from both sides of the cerebral
cortex.

VESTIBULOCOCHLEAR NERVE (VIII)

The cochlear nerve, one of the two divisions, transmits auditory impulses from the middle and inner ear mechanisms to
the superior temporal gyri of both cerebral hemispheres The other division of the acoustic nerve, the vestibular nerve,
transmits impulses from the labyrinth governing equilibrium, orientation, and change in position. The most characteristic
symptom of vestibular nerve damage is vertigo, a sensation that one is spinning within the environment or that the
environment itself is spinning.
-Test hearing first and then vestibular.

Auditory Acuity
1.

2.

Softly whisper a number 60cm away from each ear

-Cover the external acoustic meatus of the opposite ear with your finger
(or whisper 3 letters from behind, ask the Pt to block other ear with finger)
Ask the patient to repeat the number back to you.

Webers Test
1.
2.

Strike a 256Hz tuning fork and place the base on the centre of the patients forehead
Ask the patient where they hear the ringing fork
-Ringing should normally be heard in the midline or equally in both ears
-If ringing is reported to be louder in one ear, this may indicate a conductive loss of that ear, or a
sensorineural loss of the opposite ear

Rhinnes Test
1.
2.

3.

Strike a 256Hz tuning fork and place the base of the fork on the patients mastoid process
Ask the patient to report when they can no longer hear the tuning fork ringing
-At this point, position the prongs of the fork in front of the auditory canal
-The test is positive if the patient can hear ringing again
Repeat for other side

Rhinne positive:
Rhinne negative:

Air conduction > Bone conduction

Bone conduction > Air conduction

(Normal or sensorineural deadness)

(Conduction deafness)

Otoscopy
1.

Examine the external auditory canals and the eardrum with an otoscope if this is indicated.
Wax build up or middle ear infection?

Other Questions:
Have you had an ear infection lately?
Any buzzing in ears?
Occupations?
When you fly is it hard to equalize pressure? (Eustachian tube problem?)

This right sided view shows:

(1) the umbo (where the ear-drum meets
the tip of the malleolus)
(2), the light reflex
(3,4,5), the malleolus
(8), and a healthy tympanic
membrane, which is translucent, pearly
grey and with little vascularity.

Acute otitis media may be suspected in the

presence of otalgia (ear ache), an upper
respiratory tract infection, and fever. The
tympanic membrane is dull, opaque, and
bulging, with obscured landmarks and increased
vascularity. The light reflex is absent.

TESTING VESTIBULAR COMPONENT by Dix- Hallpike manoeuvre for testing vertigo

The Dix-Hallpike test: determines whether vertigo is triggered by certain head movements. Your doctor will
carefully observe any involuntary eye movements (nystagmus) that may occur during this test to determine if the
cause of your vertigo is central or peripheral. Central vertigo is caused by a problem inside the brain, and peripheral
vertigo is caused by a problem with the inner ear or the nerve leaving the inner ear. The Dix-Hallpike test also can
help determine which ear is likely affected.
During the test:
1.

2.

3.

You sit with your legs extended on the examination table.

Your doctor turns your head 30 to 45 toward one side
and helps you quickly lie back so your head hangs over the
end of the table.
Your doctor watches your eyes for involuntary eye
movements (called nystagmus). The timing and
appearance of the eye movements will identify the cause
of vertigo as either the inner ear or the brain.
After you sit upright for a few minutes to recover from
the vertigo, the procedure is repeated with your head
turned in the opposite direction.

-Not for those with neck problems

GLOSSOPHARYNGEAL & VAGUS NERVES (IX, X)

Inspect the Soft Palate

1.
2.

Note any uvular displacement

Ask the patient to say Ah and look for symmetrical movement of the soft palate (straight up = normal)
If uvular removed (e.g. sleep apnoea)- also, puff out cheeks and if cant or air goes out through the nose
= problem)

Gag Reflex- this test is unpleasant and is not indicated if the soft palate rises symmetrically (drugs also stop this)
1.

Illicit the gag reflex by gently touching the palate with a tongue depressor (touch around tonsillar pillar)
i)
The sensory component of the reflex is mediated by CN IX
ii)
The motor component is mediated via CN X
X Gag = aspiration pneumonia

Hoarseness and Cough (Vagus closes vocal cords)

-Conversation with the patient may already have alerted you to a hoarse voice
-To assess hoarseness further, ask the patient to cough
-A bovine cough suggests bilateral recurrent laryngeal nerve lesions
Bovine cough" is used to describe the non- explosive cough of someone unable to close their glottis. It is seen vagus nerve lesions, and
may be associated with dysphonia.

Bulbar Palsy (bulbar nerves= CN IX, CN X)

Bulbar cranial nerve injury within the brainstem or along the course of the nerves leads to bulbar palsy. This
commonly occurring disorder is characterized by dysarthria (speech impairment), dysphagia (swallowing
impairment), and hypoactive jaw and gag reflexes.

A, The soft palate normally forms an arch from which the uvula
seems to hang.
B, When the pharynx is stimulated, the gag reflex elicits
pharyngeal muscle contraction; the soft palate rises with the
uvula remaining in the midline. With bulbar nerve injury (bulbar
palsy)lower motor neuron (LMN) injurythe palate has little,
no, or asymmetric movement. With corticobulbar tract injury
(pseudobulbar palsy)upper motor neuron (UMN) injurythe
reaction is brisk and forceful. Unfortunately, it often
precipitates retching, coughing, or crying. (If the purpose of the
examination is to assess the patient's ability to swallow, a more
reliable decision can be reached by simply observing the patient
attempt to swallow a few sips of water.)

Unilateral vagus nerve paralysis may cause difficulty in

initiating swallowing of solids and liquids and hoarseness. This
picture demonstrates the clinical findings on examination.
The tenth nerve received sensory fibres from the pharynx and
larynx, and innervates muscles of the pharynx, larynx and palate.
Uvular movement towards unaffected side

HYPOGLOSSAL NERVE (XII)

The hypoglossal nerves originate from paired nuclei near the midline of the medulla and descend through the base
of the medulla (see Fig. 2-9). They pass through the base of the skull and travel through the neck to innervate the
tongue muscles. Each nerve innervates the ipsilateral tongue muscles. These muscles move the tongue within the
mouth, protrude it when people eat and speak, and push it to the contralateral side. Because of the muscle
contractions, each side is balanced, and the tongue protrudes in the midline.

Tongue
1.
2.

Inspect the tongue for wasting and fasciculation while examining the mouth
Ask the patient to protrude the tongue
a. If the tongue deviates to one side, this is suggestive of a CN XII lesion (to test strength ask
Pt to push tongue against inside of cheek)
b. The tongue will deviate towards the side of the lesion

Fasciculation: A fasciculation is a small, local, involuntary muscle contraction (twitching) visible under the skin arising from the
spontaneous discharge of a bundle of skeletal muscle fibres

If one hypoglossal nerve is injured, that side of the tongue will

become weak and, with time, atrophic. When protruded, the partly
weakened tongue deviates toward the weakened side which
illustrates the adage, the tongue points toward the side of

the lesion.
If both nerves are injured, as in bulbar palsy, the tongue will
become immobile. Patients with hypoglossal LMN dysfunction from
ALS have tongue fasciculations, as well as atrophy.

When a patient with a

right hypoglossal nerve

palsy is asked to poke out
the tongue, it deviates
towards her weaker,
affected right side,
demonstrating unilateral
lower motor neuron lesion
of CN XII. The tongue has a
bilateral UMN innervations,
so a unilateral UMN lesion
causes no deviation.

The hypoglossal nerve is

the motor nerve for the
tongue. Wasting and
fasciculations (fine
irregular non-rhythmical
muscle fibre
contractions) of the
tongue are signs of CN
XII LMN lesion. This
patient had motor
neurone disease.

ACCESSORY NERVE (XI)

1.
2.
3.

Inspect for torticollis

Ask the patient to shrug their shoulders
a. Assess the strength of the tapezius as you push the shoulders down
Ask the patient to turn their head against resistance
a. Assess the bulk and strength of the sternocleidomastoid mucle

Torticollis, or wry neck, is a condition in which the head is tilted toward one side (cervical rotation), and the chin is
elevated and turned toward the opposite side (cervical extension).

EXAMINATION OF THE PERIPHERAL NERVOUS SYSTEM

The peripheral nervous system (PNS) resides or extends outside the central nervous system (CNS), which consists of
the brain and spinal cord. The main function of the PNS is to connect the CNS to the limbs and organs. Unlike the central
nervous system, the PNS is not protected by bone or by the blood-brain barrier, leaving it exposed to toxins and
mechanical injuries. The peripheral nervous system is divided into the somatic nervous system, the autonomic nervous
system, and the sensory system.
The somatic nervous system is responsible for coordinating the body movements, and also for receiving external stimuli. It
is the system that regulates activities that are under conscious control.
The autonomic nervous system is then split into the sympathetic division, parasympathetic division, and enteric division.
The sympathetic nervous system responds to impending danger or stress, and is responsible for the increase of one's
heartbeat and blood pressure, among other physiological changes, along with the sense of excitement one feels due to the
increase of adrenaline in the system. The parasympathetic nervous system, on the other hand, is evident when a person is
resting and feels relaxed, and is responsible for such things as the constriction of the pupil, the slowing of the heart, the
dilation of the blood vessels, and the stimulation of the digestive and genitourinary systems.
The role of the enteric nervous system is to manage every aspect of digestion, from the esophagus to the stomach, small
intestine and colon.

NEUROLOGICAL EXAMINATION OF THE UPPER LIMB

Upper limb peripheral nerve innervation with the arm supinated on an arm board

Ant
Post
Dermatomes
Test each dermatome
*Pain testing: sharp (tip of
paperclip) & dull (end of pen/
curve of paperclip)
*Light touch (cotton wool)

Upper limb peripheral nerve innervation with the arm pronated on an arm board

Mononeuropathies:
Disorders of single peripheral nerves, mononeuropathies, are characterized by flaccid paresis, deep tendon reflex loss
(areflexia), and reduced sensation, particularly for pain (hypalgesia or analgesia). Paradoxically, mononeuropathies and
other peripheral nerve injuries sometimes lead to spontaneously occurring sensations, paresthesias that may be painful,
dysesthesias. They also convert stimuli that ordinarily do not cause pain, such as a light touch or cool air, into painful
sensations, allodynia; exaggerate painful responses to mildly noxious stimuli, such as the point of a pin, hyperalgesia; or
delay but then exaggerate and prolong pain from noxious stimuli, hyperpathia.
Major Mononeuropathies
Nerve

Motor Paresis

DTR Lost

Pain or Sensory Loss

Examples

Median

Thumb abduction with thenar atrophy

None

Thumb, 2nd and 3rd fingers, and

lateral of 4th

Carpal tunnel syndrome

Ulnar

Finger and thumb adduction (claw

hand)

None

5th and medial of 4th fingers

Radial

Wrist, thumb, and finger extensors

(wrist drop)

Brachioradialis*

Dorsum of hand

Femoral

Knee extensors

Quadriceps
(knee)

Anterior thigh, medial calf

Sciatic

Ankle dorsi flexors and plantar flexors

(flail ankle)

Achilles (ankle)

Buttock, lateral calf, and most of

foot

Sciatica from a herniated

disk

Peroneal

Ankle dorsiflexors and evertors (foot

drop)

None

Dorsum of foot and lateral calf

Foot drop from lower

knee injury

Saturday night palsy

DTR, deep tendon reflex.

* When radial nerve is damaged by compression in the spiral groove of the humerus, the triceps DTR is spared.

CARPAL TUNNEL SYNDROME: The median nerve passes through the carpal tunnel,
which is a relatively tight compartment. The usual sensory distribution of the
median nerve is the palm, thenar eminence (thumb base), thumb, and adjacent two
fingers. In carpal tunnel syndrome, pain that spontaneously shoots distally from the
wrist is superimposed on this area. The Tinel's sign, a reliable indication of carpal
tunnel syndrome, can be elicited by a physician's tapping the palmar wrist surface
and producing pain or paresthesias in the median nerve distribution.

ULNAR NERVE INJURIES: With ulnar nerve injuries, the palmar view shows that
intrinsic muscles of the hand, particularly those of the hypothenar eminence (fifth
finger base), undergo atrophy. The fourth and fifth fingers are flexed and abducted.
When raised, the hand and fingers assume the benediction sign. In addition, the
medial two fingers and palm are anesthetic. Right, Ulnar nerve injuries also produce
a claw hand because of atrophy of the muscles between the thumb and adjacent
finger (first dorsal interosseous and adductor pollicis), as well as of those of the
hypothenar eminence.
WRIST DROP (RADIAL INJURY): As the
radial nerve winds around the
humerus, it is vulnerable to
compression and other forms of
trauma. Radial nerve damage leads to
the readily recognizable wrist drop
that results from paresis of the
extensor muscles of the wrist, finger,
and thumb. Saturday night palsyalcohol induced stupor who lean
against upper arm.

POLYNEUROPATHIES
The most frequently occurring PNS disorder, polyneuropathy
or, for short, neuropathy, is generalized, symmetric
involvementto either a greater or lesser extentof all
peripheral nerves. In polyneuropathy, pain and other
sensations are typically lost symmetrically, more severely in the
distal than proximal portions of the limbs, and more severely in
the legs than the arms. This pattern of sensory loss is termed
stocking-glove hypalgesia.

LOOK for:
- movement of limb (any abnormal movement?)
-Parkinsonian movement?
-Huntingtons chorea
-fasciculations (involuntary muscle tremors)
-skin changes, herpes virus changes
-autonomic nervous system signs (rare; e.g. diabetes) sweating in certain areas, too dry (cracking?)

Positional Drift (with eyes closed): especially with cerebellar disease (toxins- most common = alcohol)

Tone: (ask patient to go limp)

Spasticity: tone and resistance of muscle lengthening in one group of muscles is greater than another
Cogwheel Rigidity (Parkinsonian): basal ganglia disease will cause a cog or interruption of tone in the examined
extremity
Leadpipe Rigidity: if it is equally difficult to extend and flex the arm against resistance
Clasp Knife: the patient may have an increased tone on extension of the arm that suddenly because of 1b fibre
inhibition from tendons that project to inhibitory interneurons or the anterior horn cells themselves and the tone
suddenly lessens
-Shaking the hands gently as if you are drying them often demonstrates hypotonicity

Loss of tone: occurs by breaking the reflex arc (no input to anterior horn cells) of the firing from anterior horn
cells is decreased which occurs with cerebellar disease, spinal or cerebral shock (decrease of facilitation of
anterior horn cells which decrease the drive of the gamma loop). The gamma loop controls the muscle spindle.
When activated, the intrafusal muscle fibres of the spindle contract which in turn brings the anterior horn cells
closer to depolarisation and discharges some with consequent muscle contraction. Not enough muscle fibres to
move the joint, but muscle tone is increased.

CLONUS:
Sudden stretching of a disinhibited muscle induces repetitive reflex contractions which are
often caused by a supranuclear lesion of the pyramidal tract. It may be evident in any
muscle but is most easily seen in the legs. The ankle is suddenly or rhythmically extended,
which induces the repetitive contractures. It may be easily seen in the quadriceps muscle
by displacing the patella sharply downward. Extremely nervous patients may demonstrate
the sign. It is associated with weakness, poor fractionated movement and hyperactive
reflexes. Spasticity and Babinskis or Hoffmans signs are often associated.

Method for eliciting

ankle clonus

Reflexes:
(Absence of reflexes can occur in normal patients (or with LMN lesion). It is really only important if the reflex is strong
(indicates an UMN lesion). NOTE reflex alone does not rule in/out a disease, need other signs.

Diagram illustrating the pathways responsible for

the stretch reflex and the inverse stretch reflex.
Stretch reflex: Stretch stimulates the muscle
spindle, which activates Ia fibers that excite the
motor neuron.
Inverse stretch reflex ( golgi apparatus): Stretch
also stimulates the Golgi tendon organ, which
activates Ib fibers that excite an interneuron that
releases the inhibitory mediator glycine.
With strong stretch, the resulting hyperpolarization
of the motor neuron is so great that it stops
discharging.

Block diagram of peripheral motor control

system. The dashed line indicates the nonneural
feedback from muscle that limits length and
velocity via the inherent mechanical properties
of muscle. d, dynamic -motor neurons; s,
static -motor neurons.

BICEPS JERK
TRICEPS JERK
(three methods)

SUPINATOR JERK
FINGER JERK

3/5

5/5
5/5

5/5
4/5

POWER MAP
(compare symmetry)

5/5

COODINATION:
FINGER-TO-NOSE MOVEMENTS: This patient, who has a multiple sclerosis (MS) plaque
in the right cerebellar hemisphere, has a right-sided intention tremor. During repetitive
finger-to-nose movements, as his right index finger approaches his own nose and then
the examiner's finger, it develops a coarse and irregular path. This irregular rhythm is
called dysmetria.
Another sign of a cerebellar lesion that reflects incoordination of the limbs is
impaired ability to perform rapid alternating movements,
dysdiadochokinesia. When asked to slap the palm and then the back of the
hand rapidly and alternately on his or her own knee, for example, a patient
with dysdiadochokinesia will use uneven force, move irregularly, and lose the
alternating pattern.

Pain testing:
Patient closes eyes and says whether they are feeling sharp or dull and point with other hand to where they are feeling it.
Areas of dullness (where sharp feels dull)- map out and tell me when it feels sharp (dermatome distribution or peripheral
nerve distribution.

Area of dullness
Map out!
Sensory testing (upper limb):
(Light touch and pain sites routine)

1
2
3
4
5
6
7
8

Location
Supraclavicular fossa
Shoulder AC joint
Lateral elbow
Thumb
Middle finger
Little finger
Medial elbow
Axilla

Dermatome
C3
C4
C5
C6
C7
C8
T1
T2

E.g. L6, R2, L3, R8, R7, L1, L8, R6, L2, L5, R4, L3, R5, R1, L4, R3

Vibration and Proprioception (Joint) Sense

Clinical examination of joint position sense and vibration sense can provide important information concerning specific
cutaneous sensory receptors, peripheral nerves, dorsal roots, and central nervous system pathways and should be included
as a regular component of the neurological examination. Although these sensory modalities share a spinal cord and
brainstem pathway (dorsal column-medial lemniscus pathway), they arise in different receptors and terminate in separate
distributions within the thalamus and cerebral cortex. Consequently, both modalities should be tested as part of the
neurological examination. Clinical testing of these modalities requires simultaneous stimulation of tactile receptors; hence
this review will include information about the receptors and pathways responsible for tactile sensation.
Note: test vibration sense most distally first. If sensation is present, there is no need to test the more proximal sites.

Motor Testing
Segmental innervations of muscles simplified:
UPPER LIMB

Reflexes
UPPER LIMB

C5 Elbow flexors (biceps, brachialis) and shoulder abductionsupraspinatus and deltoid)

C6 Wrist extensors (ext carpi radialis longus brevis)
C7 Elbow extensors (triceps)
C8 Finger flexors (flex digitorum profundus- middle finger)
T1 Small finger abductors (abductor digiti minimi)
Brachioradialis (wrist flick) Radial nerve C5/6
Biceps Musculoskeletal nerve C5/6
Triceps Radial nerve C7/8

NEUROLOGICAL EXAMINATION OF THE LOWER LIMB

Sensory testing (lower limb):

(Light touch and pain sites routine)

1
2
3
4
5
6
7
8
9
10
11

Location
Umbilicus
Mid-inguinal ligament
Upper 1/3 thigh
Mid front thigh
Medial knee
Medial malleolus
Base dorsum middle toe
Lateral heel
Popliteal fossa
Ischial tuberosity
Perianal skin

Dermatome
T10
T12
L1
L2
L3
L4
L5
S1
S2
S3
S4/5

Ant
Post
Dermatomes

Peripheral Subcutaneous Nerves

KNEE JERK

ANKLE JERK

COODINATION: In the heel-to-shin test, the patient with

the right-sided cerebellar lesion in Figure 2-11 displays
limb ataxia as his right heel wobbles when he pushes it
along the crest of his left shin.

Gait Abnormalities Associated with CNS Disorders

Gait

Associated Illness

Apraxic

Normal pressure hydrocephalus

Astasia-Abasia

Psychogenic disorders

Ataxic

Cerebellar damage

Festinating (marche petits pas) Parkinson's disease

Hemiparetic
Circumduction

Cerebrovascular accidents

Spastic hemiparesis
Tabes dorsalis (CNS syphilis)

Steppage*

Peripheral neuropathies

Waddling

Duchenne's dystrophy and other myopathies

CNS, central nervous system.

*The steppage gait consists of each knee being excessively raised when walking. This maneuver compensates for a loss of
position sense by elevating the feet to ensure that they will clear the ground, stairs, and other obstacles. It is a classic sign
of posterior column spinal cord damage from tabes dorsalis. However, peripheral neuropathies more commonly impair
position sense and lead to this gait abnormality.

Motor Testing
Segmental innervations of muscles simplified:
LOWER LIMB

Reflexes
LOWER LIMB

L2
L3
L4
L5
S2

Hip flexors (iliopsoas)

Knee extensors (quadriceps)
Ankle dorsiflexion (tib ant)
Long toe extensors (ext hallucis longus)
Ankle plantar flexors (gastrocnemius, soleus)

Patellar Femoral nerve L2, L4

Ankle Tibial nerve S1

Differences between CNS & PNS

Differences Between Central (CNS) and Peripheral Nervous System (PNS) Signs
CNS

PNS

Motor system Upper motor neuron Lower motor neuron

Paresis

Patterns*

Distal

Tone

Spastic

Flaccid

Bulk

Normal

Atrophic

Fasciculations No

Sometimes

Reflexes
[+]

DTRs

Hyperactive

Hypoactive

Plantar

Babinski sign(s)

Absent

Sensory loss

Patterns*

Hands and feet

Examples: motor and sensory loss of one side or lower half of the body (e.g., hemiparesis or paraparesis), and
hemisensory loss.

May be flaccid initially.

May be absent initially.

Another contrast arises from the difference between demyelinating diseases of the CNS and PNS. Despite performing a
similar insulating function, CNS and PNS myelin differ in chemical composition, antigenicity, and cells of origin.
-Oligodendrocytes produce CNS myelin, and Schwann cells produce PNS myelin. Also, each oligodendrocyte produces
myelin that covers many nearby CNS axons, but each Schwann cell produces myelin than covers only one portion of a
single PNS axon. From a clinical viewpoint, Schwann cells regenerate damaged PNS myelin and Guillain-Barr patients
usually recover. In contrast, because oligodendrocytes do not regenerate damaged CNS myelin, impairments are
permanent in patients who have lost CNS myelin to toxins and infections. For example, the CNS demyelination that results
from toluene use represents a permanent loss.
-Multiple sclerosis (MS) appears to be an exception. In this illness, episodes of demyelination of several CNS areas,
including the optic nerves, partially or even completely resolve. However, the improvement results from resolution of
myelin inflammation rather than regeneration. When MS finally encompasses large areas of cerebral CNS myelin, it often
results in dementia and other mental status changes.

SOME NEUROLOGICAL DISORDERS

Diabetic neuropathies are a family of nerve disorders caused by diabetes. People with diabetes can, over time, develop
nerve damage throughout the body. Some people with nerve damage have no symptoms. Others may have symptoms
such as pain, tingling, or numbnessloss of feelingin the hands, arms, feet, and legs. Nerve problems can occur in every
organ system, including the digestive tract, heart, and sex organs. There are four factors thought to be involved in the
development of diabetic neuropathy. i) microvascular disease, ii) advanced glycated end products, iii) protein kinase C and
iv) polyol pathway.

Parkinson's disease (also known as Parkinson disease or PD) is a degenerative disorder of the central nervous system
that often impairs the sufferer's motor skills, speech, and other functions. It is characterized by muscle rigidity, tremor, a
slowing of physical movement (bradykinesia) and, in extreme cases, a loss of physical movement (akinesia). The primary
symptoms are the results of decreased stimulation of the motor cortex by the basal ganglia, normally caused by the
insufficient formation and action of dopamine, which is produced in the dopaminergic neurons of the brain. Secondary
symptoms may include high level cognitive dysfunction and subtle language problems. PD is both chronic and progressive.

Huntington's disease or chorea (HD) is an incurable neurodegenerative genetic disorder that affects muscle coordination
and some cognitive functions, typically becoming noticeable in middle age. It is the most common genetic cause of
abnormal involuntary writhing movements called chorea. It is much more common in people of Western Europe descent
than in people from Asia or Africa. The disease is caused by a dominant mutation on either of the two copies of a specific

gene, located on an autosomal chromosome. Physical symptoms of Huntington's disease can begin at any age from infancy
to old age, but usually begin between 35 and 44 years of age. The exact way HD affects an individual varies, and can differ
even between members of the same family, but the symptoms progress predictably for most individuals. The earliest
symptoms are a general lack of coordination and an unsteady gait. As the disease advances, uncoordinated, jerky body
movements become more apparent, along with a decline in mental abilities and behavioural and psychiatric problems.
Physical abilities are gradually impeded until coordinated movement becomes very difficult, and mental abilities generally
decline into dementia.

Multiple sclerosis is an autoimmune disease in which the body's immune response attacks a person's central nervous
system (brain and spinal cord), leading to demyelination. Almost any neurological symptom can appear with the disease,
and often progresses to physical and cognitive disability and neuropsychiatric disorder. MS takes several forms, with new
symptoms occurring either in discrete attacks (relapsing forms) or slowly accumulating over time (progressive forms).
Between attacks, symptoms may go away completely, but permanent neurological problems often occur, especially as the
disease advances.

Vertigo is a specific type of dizziness, a major symptom of a balance disorder. It is the sensation of spinning or swaying
while the body is actually stationary with respect to the surroundings. The effects of vertigo may be slight. It can cause
nausea and vomiting and, in severe cases, it may give rise to difficulties with standing and walking.
Vertigo is typically classified into one of two categories depending on the location of the damaged vestibular pathway.
These are peripheral (arising from inner ears vestibular system) or central vertigo (affected cerebellum).