Dizziness and disturbance of

consciousness
Getahun Mengistu, MD, MSc, Internist,
Neurologist, specialist of headache
medicine, Associate professor and
consultant of medicine
 Dizziness- definition and classification
• Is common and vexing symptom---lightheadedness,
fainting, spinning, giddiness

• Usually means either faintness (presyncope) or vertigo

( an illusory or hallucinatory sense of movement of the
body or environment, most often a feeling of spinning)

• Classified as:
1. faintness
2. vertigo
3. miscellaneous head sensations
 Faintness
• Prior to an actual faint( syncope) THERE ARE OFTEN
PRODROMAL PRESYNCOPAL SYPTOMS ( FAINTNESS) :

-Lightheadedness
-dizziness without true vertigo
-a feeling of warmth
-diaphoresis
-nausea
-visual blurring occasionally preceding to blindness

• Reflects ischemia insufficient enough to impair consciousness

 Vertigo
• Vestibular system:- is one of three sensory systems subserving :

a, spatial orientation and posture

b, the visual system—retina to occipital cortex

c, the somatosensory system that conveys peripheral information

from skin joint and muscle receptors

• Vertigo may represent either physiologic stimulation or pathologic

dysfunction in any of the three sensory systems
 Physiologic vertigo
• Occurs in normal individuals when:

1. the brain is confronted with an intersensory mismatch among the

three stabilizing sensory systems eg carsickness, height
vertigo

2. the vestibular system is subjected to unfamiliar head movement

eg seasickness

3. unusual head/neck position eg painting of a ceiling

4. following a spin
 Pathologic vertigo
• Results from the lesions of the visual, somatosensory or vestibular
system

• Visual vertigo- is caused by a new or incorrect eyeglass, or by a

sudden onset of extraocular muscle paresis with diplopia

• Somatosensory vertigo- rare in isolation, is usually due to peripheral

neuropathy or myelopathy that reduces sensory input

• The most common cause is vestibular dysfunction involving its end

organ (labyrinth), nerve or central connections. The vertigo is
associated with jerk nystagmus and frequently accompanied by
nausea, postural unsteadiness, and gait ataxia. Vertigo increases
with rapid head movement
 Labyrinthine dysfunction
• Causes severe rotational or linear vertigo

• Rotational:-
-movement is directed away from the side of the lesion
-the fast phases of the nystagmus beat away from the lesion side
- the tendency to fall is towards the lesion (in darkness or eyes closed)

• acute Labyrinthine dysfunction:-

-Is caused by infection, ischemia and trauma
-vertiginous attacks are brief and mild vertigo for several days

• acute bilateral Labyrinthine dysfunction: is due to drugs or alcohol

• recurrent unilateral Labyrinthine dysfunction:- associated with signs and

symptoms of cochlear disease (progressive hearing loss and tinnitus)
=Meniere’s disease
 Positional vertigos
• BPPV=benign paroxysmal positional vertigo- debri in the posterior
semicircular canal
• Central positional vertigo- due to lesion in and around the 4th
ventricle
•
Factors BPPV central

Latency 3-40 s None:immediate

Fatigability yes No

Habituation yes No

Intensity Severe Mild

Reproducibility Variable Good

 Vertigo of vestibular nerve origin

• Occurs in disease of the nerve at the petrous bone or

cerebellopontine angle

• Unilateral hearing loss and tinnitus occur

• Tumors associated are schwannoma (acustic neuroma) or

menigioma
Central vertigo: due to lesions the brain stem or cerebellum
Signs or symptoms Peripheral Central
Direction of nystagmus unidirectional Bi or uni-
Purely horizontal nystgmus uncommon common
Vertical or purely torsional Never present May be present
nystagmus
Visual fixation Inhibits nyst & vertigo No inhibition
Severity of vertigo Marked Often mild
Direction of spin Towards fast phase variable
Direction of fall Towards slow phase variable
Duration of symptoms Finite, minutes, days, May be chronic
weeks, recurrent
Tinnitus/deafness Often present Usually absent
CNS abnormalities None Common eg diplopia,
hiccup, dysarthria
Common causes BPPV, infection, Meniere’s, Vascular, demyelination,
ischemia, trauma, toxins neoplasm
 Psycogenic vertigo= phobic postural vertigo

• Concomitant of panic attacks or agoraphobia

• Incapacitated patients= Because of fear of moving

 Miscellaneous head sensations

• Hyperventilation

• Hypoglycemia

• Depression
 Approach to patients with dizziness and vertigo
• Detailed history –meaning of dizziness to the patient

• Provocative test-orthostatic hypotension or Valslva maneuvers

• Hyperventilation for 1 minute

• Swivel chair –rapid rotation and abrupt cessation-vestibular

dysfunction

• Frenzel eyeglass test-( self illuminated goggles with convex lenses

that blur the patients vision but allow the doctor to see the eyes greatly
magnified) vigorous head shaking for 10 s =nystagmus=vestibular
dysfunction
 Evaluation of pathologic vertigo

• 1. MRI for central pathology

• 2. vestibular function tests-elctronystagmography (caloric) cold or
warm water test
 Treatment of vertigo

• Treatment of acute vertigo

• 1. bed rest for 1-2 days
• 2. drugs:-
a. antihistamines: meclizine 25-50 mg TID, dimenhydrinate 50mg
1-2x /day, promethazine 25-50mg suppository
b. benzodiazepines, diazepam 2,5mg 1-3x/d, clonazepam 0.25mg
1.3x/d
c. phenothiazines – prochlorperazine
d. anticholinergic- scopolamine transdermal patch
e. sympathomimetics – ephedrine 25mg /day
f. combination- ephedrine + promethazine 25mg each
g. exercise repositioning and rehablitation
 Disturbance of consciousness
Definitions
• Coma
Deep sleeplike state
Can not be aroused.

• Stupor
Lesser degrees of unarousability.
Require vigorous stimuli

• Drowsiness
Simulates light sleep
Easy arousal
Persistence of alertness for a brief periods.

• Vegetative state
Out come of severe brain injury
Preserved sleep-wake cycles (normal arousal)
No meaningful interaction with the environment
 Definition cont
Akinetic mutism

• Partially or fully awake

• Able to form impressions & think but remains
immobile & mute, particularly when unstimulated.

Locked–in sate
• An awake patient with no means of producing speech or
volitional movement in order to indicate that he is awake
• Vertical eye movement & lid elevation remains unimpaired,
allowing patient to signal.
e. g - Infarction or hemorrhage of ventral pons, GBS
pharmacologic neuromuscular blockade, critical illness
neuropathy
 Anatomy and physiology of coma

• The anatomic substrate for consciousness involves the cerebral

hemispheres and the RAS

• Cerebral hemispheres- For all complex waking behaviors

• RAS - maintains the cerebral cortex in a state of wakeful

consciousness (arousal)
 Pathophysiology of coma

• Structural - Operate by compressing the

brainstem
• Metabolic - May affect either region
 Pathophysiology cont

structural

Lateral
supratentorial infratentorial
shift

Central uncal
 Central
Diencephalic level Midbrain & upper pons Lower pons & medulla

•Drowsy •Lapses into coma •Ataxic breathing, irregular

pulse & blood pressure
•Pupil-remain mid position &
•Miotic pupil but •Pupils dilate to mid unreactive
reactive position & unreactive
to light •Absent reflex eye
movement
•Intact reflex eye •Reflex eye movement
movement difficult to elicit & may
take the form of an Inter-
•Babinski signs, grasp nuclear ophthalmoplegia
reflexes & decorticate
posturing contra-
laterally to the mass. •Decerebrate posturing •Flaccid tone, No response
to deep pain.
 uncal

Early Mid brain

•Approach normal wakefulness

•Ipsitateral pupil dilatation, • Pupils mid dilated & unreactive

reacts sluggishly to light

•Normal eye movement

•Evolution to coma is rapid & • Subsequent rostro caudal

focal motor signs develop deterioration merges with that
ipsilateral to the mass with of central syndrome.
bilateral decerebrate posturing
 Pathophysiology cont

Subtentorial lesions

Posterior fossa lesions cause coma in three

ways:

• Intrinsic brain stem process may destroy

RAS

• Extrinsic mass by compression or upward herniation

through the tentorium cerebelli

• Down ward herniation via foramen magnum.

 Pathophysiology cont
lateral shift

• Displacement of deep brain structures by a mass,

with or with out herniation, is adequate to
compress the region of the RAS & result in coma.

• Drowsiness & stupor typically occur with moderate

horizontal shift at the level of diencephalon well
before transtentorial or other hernations are evident.

• Acutely appearing masses are more likely to affect level of

consciousness.
 Pathophysiology cont

Metabolic causes

• Many systemic metabolic abnormalities cause coma either;

 By interrupting the delivery of energy substrates
eg- hypoxia, ischemia, hypoglycemia
 By altering neuronal excitabillity
e.g – drug & alcohol intoxication,anesthesia & epilepsy.

• Conditions such as hypoglycemia, hyponatremia, hyperosmolarity,

hypercapnia, hypercalcemia, and hepatic & renal failure are associated with
a variety of alterations in neurons & astrocytes.

• The reversible effect of these conditions on the brain are not understood,
but may result from impaired energy supply, change in ion fluxes across
neuronal memberanes, & neuro transmitter abnormalities
 Pathophysiology cont

• Coma & seizures are a common accompaniment of any large

shifts in sodium & water balance.
e .g DKA, NHHS, hyponatremia from any
cause ( e. g water intoxication, SIADHS )

• The severity of neurologic changes depends to a

large degree on the rapidity with which the serum changes
occur.

• The pathophysiology of other metabolic encephalopathies

such as hypothtroidism, vitamin B12 deficiency, &
hypothermia are incompletely understood but must also
reflect derangements of CNS biochemistry & memberane
function.
 Approach to the patient

• Acute respiratory & cardiovascular problems

should be attended to prior to neurologic
assessment.

• Vital signs, funduscopy & examination for

nuchal rigidity

• Neurologic assessment

• Complete medical evaluation

 History

• In many cases, the cause is immediately

evident like trauma, cardiac arrest , or
known drug ingestion
• In the remainder, certain points are
especially useful;
 Circumstances & rapidity with which neurologic
symptoms developed
 The antecedent symptoms (confusion, weakness,
headache, fever, seizure, vomiting)
 The use of medications , illicit drugs , or alcohol
 Chronic liver, kidney, lung, heart , or other
medical disease
 General physical examination

• Hyperthermia -Infection, brain lesion disturbing temperature

regulating center, heat stroke, anticholinergic
drug intoxication

• Hypothermia -alcoholic, barbiturate, phenothiazine intoxication,

hypothyroidism
• Hypertension-Hypertensive encephalopathy
Rapid rise in ICP
• Hypotension- Alcohol ,barbiturate intoxication
MI , internal hemorrhage, Addisonian crisis.
• Funduscopy
 Hypertensive encephalopathy (exudates, hemorrhage, AV
nicking, papilledema).
 Increased ICP

 Petechiae
TTP , meningococcemia, or a bleeding diathesis
from which an intracerebral hemorrhage arises.
 Respiration

• Less localizing value

• Cheyne-stokes
Bilateral hemispheral damage or metabolic suppression
Commonly accompanied by light coma

• Kussmaul
Usually metabolic acidosis
Also in pontomesencephalic lesion .

• Agonal gasp
Bilateral lower brain stem damage terminal respiratory

pattern of severe brain damage.

 Pupils
Horner’s syndrome

• Lesion in sympathetic efferents originating in

hypothalamus & descending in the brain stem
to the cervical cord produces miosis with ptosis.

 Seen in thalamic & hypothalamic lesions from cerebral,

thalamic hemorrhage or from herniation.

 Bilateral miosis in pontine stroke

 Light reaction is preserved in all cases of oculosympathetic

paralysis.
 Pupil cont
Unreactive pupils
• Normally reactive & round pupils of mid size
essentially exclude mid brain damage.

• Bilaterally dilated, unreactive suggest

intraxial involvement of third nerve at mid
brain, could be result of stroke, tumor

• Unilaterality implies a peripheral third nerve

palsy :
 uncal herniation at the tentorium
 nerve compression by PCA
 traction at the superior orbital fissure.
 Pupil cont
• Metabolic Vs structural lesion
 Normally reactive pupils in a comatose patient strongly
support a metabolic process

• Structural causes with reactive pupil

 Early phase of central transtentorial herniation
 Pontine hemorrhage

• Metabolic conditions with unreactive pupil

 Doriden ( gluthetimide )
 Anoxia
 Anticholinergic agents – not respond to 1% pilo carpine.
 Hypothermia
 Eye movement
Eyelids
• Remain closed in coma.

• Exception – some case of pontine stroke with persistent ,

tonic eyelid retraction.

• Spontaneous blinking indicates intact pontine reticular

formation

• Blinking to light indicates intact functioning visual afferent

pathway but not occipital cortex.

• Corneal reflex
 both metabolic & structural disease of
brain- stem or cortex depress it.
 Depth of coma may correlate with the degree of
depression.
 Eye movement cont
Roving eyes

• Slow, random, usually horizontal movements that

occur spontaneously in coma.

• Can not be duplicated by hysterical patients.

• Indicate intact oculomotor pathways, one

parameter of brain stem function.

• Appear in many metabolic & bilateral hemispheric

structural processes causing coma,
& their presence excludes brain stem structural
lesions.
 Eye movement cont
Horizontal gaze deviation
Congugate horizontal ocular deviation to one side indicates

 damage to the pons on the opposite side or

 a lesion in the frontal lobe on the same side.

 “the eyes looks toward a hemispheral lesion & away

from a brainstem lesion.”

 epileptic phenomina produce deviation of eyes to the

opposite side of the body.
 “ wrong way eyes”- the eyes may turn paradoxically away
from the side of a deep hemispheral lesion.
 Eye movement cont

• Oculocephalic testing

• Depend on the integrity of the oculomotor nuclei

& their interconnecting tracts that extend from
the mid brain to the pons & the medulla.

• Are normally suppressed in the awake patient by

visual fixation.
• Their presence indicate reduced cortical
influence on the brain stem.
 Eye movement cont
oculovestibular testing
• Assess virtually the same brain stem reflex as
oculocephalic test.

• Tonic deviation of both eyes to the side of cool

water irrigation & nystagmus in the opposite
direction.

• Absent cold water calories usually suggest

structural posterior fossa
lesion or drug intoxication.

 pupillary reactivity preserved in drug induced coma.

 Eye movement cont
ocular bobbing
• A brisk down ward & slow upward movement of the
eyes.

• Associated with loss of horizontal eye movements.

• Diagnostic of bilateral pontine damage usually from

thrombosis of basilary artery
ocular dipping
• A slower , arrhythmic down ward movement followed by
a faster upward movement

• In patients with normal reflex horizontal gaze.

• Indicates diffuse cortical anoxic damage.

 Motor signs

postures
• Primitive non purposeful reflex, which may occur spontaneously
In response to sensory stimuli (pain)

• Lesions producing flexion tend to be more rostral & those producing

extension more caudal.

• Acute destructive lesions tend to induce the extensor posture,

whereas evolution over time results more in a chronic flexor position.

• Distinction of weak flexor posturing from purposeful with drawal can

be made by noting the response to a painful stimulus applied to the
medial upper arm.
 Adduction is a reflex response
 Abduction suggests a high level (with drawal) response.
 posture cont…

• In asymmetric /mismatched posturing, the more

abnormal posture points to the opposite side of
the brain as the more compromised.

• Lack of restless movements on one side or an

out turned leg suggests a hemiplegia.

• Abnormal postural responses do have some

relation to out come , extensor tends to fare
worse, probably as a function of the acuity and
depth of the lesion
 Motor signs cont…
• Multifocal myoclonus almost always indicates a
metabolic disorder (uremia, anoxia, drug
intoxication)

• Frontal release phenomena

 Constitute forced grasping, perioral primitive reflexes
( e.g suck, snout, root ) paratonic rigidity

 Unduly marked in a patient who appears awake but immobile-

akinetic mutism a disturbance principally of motivation.

 Assymetry of a grasp phenomena suggests a hemiparesis

on the side of weaker response.
 Psychogenic unresponsiveness
• May mimic real coma
• In coma, the release of eyelids opened by the examiner produces
gradual, incomplete closure, this can not be voluntarily duplicated
• In psychogenic cases, the lids may voluntarily resist opening , & close
too rapidly or in a fluttering manner
• Presence of roving eye movements strongly mitigates against a
psychogenic state.
• Truly comatose patients can not stop their arm from being dropped
on their face.
• Demonstration of unambiguous full, uninhibited oculocephalic
response or complete paralysis of this response during passive head
movement strongly supports a diagnosis of nonpsyohogenic coma.

• Presence of caloric-evoked nystagmus defines ‘’ coma ‘’ as

psychogenic.
 In clinical practice , the pain of the procedure most often terminates the
‘’unconsciousness.’’
 Brain death
• The criteria endorsed by the American Academy of
neurology include :
 documentation of both cessation of brain function
 and the irreversibility of such cessation.

• Cessation
 Hemispheric function
unreceptivity & unresponsivity.

 Brain stem function

Absence of pupillary light, corneal, oculocephalic,
oculovestibular, oropharyngeal, & respiratory
reflexes.
 Brain death cont
• Irreversiblity

 The absence of reversible causes of coma must be

documented, like hypothermia (<32.3 ºc ), sedative drugs,
neuromuscular blockade , & shock.

• Duration of observation
 The cessation of brain function must persist for ‘’an
appropriate period of observation’’

 6 hours when confirmatory EEG documentation is

available.

 12 hours in the absence of confirmatory test

 For ischemic brain damage , 24 hours is suggested, in the
absence of EEG confirmation.
 INVESTIGATION
• Blood or urine chemical- toxicologic analysis
• Cranial CT or MRI scan
• EEG
• CSF analysis
 Differential diagnosis
• Three broad categories causes of coma
• 1.without focal neurologic signs eg metabolic
• 2. meningitis syndrome
• 3. with prominent focal sighns
 Treatment of coma

1. admission
2. ABC rules
3. prevention of further CNS damage
4. thiamine and glucose
5. treatment of the specific cause
6. electrolyte correction
7. nursing care and feeding
8. physiotherapy and rehabilitations
 References
1. Harrison’s; principles of medicine, 17th
edition
2. Adam’s and Victor principles of neurology
3. De Jong’s. physical examination in Neurolgy
4. Brazis; Localization in Neurology
5. Bradly; principles and practice of Neurology
•Thank you