Cerebrovascular Accident

(C.V.A)
 It is one of the four leading causes of death in most
countries and the leading cause of severe neurologic
disability in adults.
 It is commoner in black & south Asian populations.
The high incidence in blacks may reflect the prevalence
of hypertension in this ethnic group, as well as inadequate
access to primary prevention services.
 Glossary Definitions:

C.V.A is focal neurological deficit within central nervous system, due to vascular
pathology.

It is of sudden onset except that of anterior spinal artery which being usually of acute
onset.

C.V.A that last, clinically, for at lest 24 hrs or more & confirmed by brain imaging
studies (CT scan & / or MRI) called stroke.

Ischemic C.V.A that clinically resolved completely or almost completely & NOT
associated with brain imaging trace is called transient ischemic attack (T.I.A)
whatever time period it’s clinical features lasted for.

Ischemic C.V.A that clinically resolved completely or almost completely within 10 days
from it’s onset is called reversible ischemic neurological deficit (R.I.N.D) providing it
leaves a trace on brain imaging studies.
 Pathological Classification:
1) Ischemic C.V.A, representing around 80% of all C.V.A cases. There are 4 sub types
within this category, vz:
a. Embolic, up to 30% of ischemic. Most happen in middle cerebral artery because it
receives about 80% of blood supply of brain.
b. Thrombosis (atherosclerosis) of large artery , 14 – 25% of ischemic
c. Thrombosis (atherosclerosis) of small arteries (lacunar infarction), 15 – 30% of
ischemic
d. Cryogenic (nature of ischemic pathology is undetermined), between 20 – 40% of all
ischemic
2) Hemorrhagic C.V.A (Intracranial Hemorrhage), representing about 20% of all C.V.A
cases.
There are 2 sub types within this group, vz:
a. Intraparenchymal hemorrhage (IPH)
b. subarachnoid hemorrhage (SAH)
 Differential diagnosis:

subdural hematoma

epidural hematoma

focal fit (gain of function ± march spreed to half of body over about 30 seconds)

migraine with aura (in case of march it will spreed to half of body over 10 – 25 minutes)

brain tumor (in case of hemorrhage into tumor or when tumor become source for fit, it
will produce sudden presentation)

brain abscess

hypoglycemia & hyperosmolar nonketotic hyperglycemia

meningitis (when associated with focal signs) & encephalitis
 Ischemic Stroke & T.I.A:

there is a substantial risk after TIA, with up to 15% of patients having a
stroke within 90 days, the bulk of which occur in the first 48 hours.

roughly 50% of patients who suffer from ischemic stroke have returned
to work by 6-12 months after stroke. Post ischemic stroke mortality is
~10% at 30 days, ~20% at 1 year, and ~40% at 5 years.

due to the shared pathophysiology and risk of subsequent ischemic
stroke, the approach to TIA and ischemic stroke is similar.
 Risk Factors:

Non-modifiable:
- increased age (highest incidence of stroke occurring in people
older than 80 years)
- male sex (men are at slightly higher risk of stroke compared to
women except after age 80)
- low birth weight
- family history of stroke

Modifiable:
- hypertension (BP >140 mm Hg systolic or >90 mm Hg diastolic)
- cigarette smoking
- asymptomatic carotid stenosis (>60% of diameter)
- peripheral artery disease
- atrial fibrillation (with or without valvular disease)
- congestive heart failure
- coronary artery disease
- diabetes mellitus
- postmenopausal hormone therapy (estrogen ± progesterone)
- oral contraceptive use
- high total cholesterol (top 20%)
- low HDL cholesterol (<40 mg/dL)
- obesity (especially abdominal)
- sickle cell disease
- physical inactivity
- obstructive sleep apnea
 High-risk vs low-risk cardioembolic sources.
High Risk Low Risk
- Atrial fibrillation/flutter - Patent foramen ovale
- Left ventricular thrombus - Reduced ejection fraction
- Mitral stenosis (critical, - Valvular fibroelastoma
rheumatic)
- Mechanical heart valves
- Infective and noninfective
endocarditis
- Atrial myxoma
 Course:
Title
Severity

Time

Stroke in Evolution (Thrombotic) Completed Stroke (Embolic) Thrombo-embolic


A stroke that is actively progressing beyond 8 hrs (up to 72
hrs) from it’s onset, as a direct consequence of the
underlying vascular disorder (but not because of associated
cerebral edema), is termed stroke in evolution or
progressing stroke.

Very important: any ischemic stroke that shows
progress of deficit over time should be treated as stroke
in evolution even still not crossing limit of 8 hrs.
 Clinical features:

Occlusion of superior division of middle cerebral artery:
- contralateral hemiparesis that affects the face, hand, and arm
more then leg
- contralateral hemisensory deficit in the same distribution
- no homonymous hemianopia
- If the dominant hemisphere is involved, there will be Broca
(expressive) aphasia

Occlusion of inferior division of middle cerebral artery:
- contralateral homonymous hemianopia that may be denser inferiorly,
- impaired cortical sensory functions (eg, graphesthesia and
stereognosis) on the contralateral side
- disorders of spatial thought (eg, anosognosia [unawareness of deficit],
neglect of the contralateral limbs and contralateral side of external
space, dressing apraxia, and constructional apraxia).
- if the dominant hemisphere is involved, Wernicke (receptive) aphasia
- with involvement of the nondominant hemisphere, an acute
confusional state may occur.

Occlusion at the bifurcation or trifurcation
of the middle cerebral artery:
- combined the features of superior and inferior
division stroke

Occlusion of anterior cerebral artery:
- contralateral paralysis and sensory loss exclusively primarily affecting
the leg more than upper limb.
- abulia (apathy)
- disconnection syndromes such as the alien hand (involuntary
performance of complex motor activity)
- transcortical expressive aphasia
- urinary incontinence.

Occlusion of posterior cerebral artery:
- homonymous hemianopia affecting the contralateral visual field,
denser superiorly, sparing the macular vision
- vertical gaze palsy, oculomotor (III) nerve palsy, internuclear
ophthalmoplegia, and vertical skew deviation of the eyes can occur if
occlusion is near the origin of artery at level of mid-brain.
- anomic aphasia (difficulty in naming objects), alexia without agraphia
(inability to read without impairment of writing), or visual agnosia can
happen if dominant hemisphere is involved.

Basilar artery occlusion:
- often incompatible with survival.
- It causes bilateral symptoms and signs of brainstem and cerebellar
dysfunction
- unilateral or bilateral abducens (VI) nerve palsy
- horizontal eye movements are impaired
- vertical nystagmus (up beat & down beat) and ocular bobbing may be present
- The pupils are constricted, but may be reactive
 Beware! Temporary occlusion of one or both
vertebral arteries, leading to transient brain-stem
dysfunction, can also result from rotating the head
in patients with cervical spondylosis.
 Unilateral infarction of brain-stem, due to
occlusion of it’s ipsilateral circumferential arteries,
will result in crossed palsy [ipsilateral cranial
nerve palsies & contra-lateral spastic hemiparesis]
if infarction above level of pyramidal decussation

Posterior inferior cerebellar artery occlusion (lateral medullary
“Wallenberg” syndrome):
- ipsilateral cerebellar ataxia, Horner syndrome, and facial sensory deficit
- contralateral impaired pain and temperature sensation
- nystagmus, vertigo, nausea, vomiting
- dysphagia, dysarthria, and hiccup.
- the motor system is characteristically spared because of its ventral
location in the brainstem.
 Lacunar infarction:

many are asymptomatic and are detected only incidentally.

In other cases, however, they produce distinctive clinical syndromes.

variety of deficits can be produced, but there are four classic and distinctive
lacunar syndromes (pure motor hemiparesis, pure sensory stroke, ataxic
hemiparesis & dysarthria-clumsy hand syndrome.

Headache is absent or minor

level of consciousness is unchanged.

hypertension and diabetes are commonly associated, but can be absent.

The prognosis for recovery is good, but

recurrent stroke is common.
Non Traumatic Intraparanchiamal Hemorrhage
(I.P.H)

accounts for 10 – 15% of all strokes.

Incidence worldwide is 10 – 20 cases per 100,000 persons

Increases with age.

It is more common in men, blacks, and people of Asian descent.

38 – 50% mortality rate.

However, if escape from death, there will be usually complete or near
complete recovery of deficit because deficit in this type of stroke is
resulted from compression of neurons by hematoma.
 Risk factors:

hypertension (most common for non-traumatic cases)

smoking

heavy alcohol use

low serum cholesterol (so avoid high-intensity statin therapy)

positive family history (there is familial tendency in about
10% of cases)
 Causes:

hypertension

cerebral amyloid angiopathy

vascular malformations (arteriovenous fistula or malformations, cavernous angiomas)

ruptured aneurysm

neoplasm

coagulopathy

severe thrombocytopenia

sympathomimetic drug abuse

anticoagulant or antiplatelet therapy

herpes simplex encephalitis

cerebral vasculitis
 Locations:
A: Lobar hemorrhage often due to
cerebral amyloid angiopathy.
B: Hemorrhage of basal ganglia and
internal capsule.
C: Thalamic hemorrhage.
D: Pontine hemorrhage.
E: Cerebellar hemorrhage.
- B to E are often due to hypertension.
- Hemorrhage due to tumor, arteriovenous
malformation, and other etiologies may
occur anywhere.
 Clinical Features:
Site: Features:
Putamen contralateral hemiparesis
contralateral hemisensory loss
hemiballism (uncommon)
aphasia (when in dominant hemisphere)
Caudate headache
nuchal rigidity
nausea and vomiting
hydrocephalus
decreased verbal fluency
Thalamic contralateral hemiparesis
contralateral hemisensory loss
oculomotor abnormalities
aphasia
coma
 Site: Features:
Pontine quadriplegia
coma
extensor posturing
facial diplegia
absence of horizontal eye movements
pinpoint reactive pupils
hyperthermia
headache (uncommon)
Cerebellar headache (common)
nausea and vomiting
nystagmus
dysarthria
ipsilateral limb ataxia
gait instability
 Non Tramatic Subarachnoid Hemorrhage
(S.A.H)

usually the result of a ruptured cerebral arterial aneurysm or an AVM.

saccular (berry) aneurysm accounts for approximately 75% of cases.

annual incidence of berry aneurysm is 6 per 100,000.

most berry aneurysm arise sporadically, but some are familial.

families with two or more affected persons by berry aneurysm should have all
members screened.

both autosomal dominant and recessive patterns of inheritance occur.

rupture of berry aneurysm occurs most often during the fifth and sixth decades.

sex distribution for berry aneurysm is approximately equal.

intracranial AVMs, a less frequent cause of
subarachnoid hemorrhage (10%), occur twice as
often in men as in women, and usually bleed in the
second to fourth decades.

blood in the subarachnoid space can also result
from extension of intracerebral hemorrhage, embolic
stroke, and trauma.
 Clinical Features:

the classic (but not invariable) presentation is with the sudden onset of an
unusually severe generalized headache, classically described as the worst
headache the patient has ever experienced.

the absence of headache essentially excludes the diagnosis.

headache may remain unchanged for several days and may subside slowly
over approximately 2 weeks.

recurrence of the headache usually signifies rebleeding.

loss of consciousness is frequent at onset, as are vomiting and neck stiffness,
but latter may not occur for several hours after the onset of headache.

blood pressure frequently rises

Typically patient is afebrile, but there may be reactionary
hyperthermia & can reach to 39°C during 1st 2 weeks.

confusion, stupor, or coma are common

preretinal globular subhyaloid hemorrhages (found in 20% -
40% of cases) are most suggestive of the diagnosis.

papilledema reflecting raise in intracranial pressure (I.C.P)

with aneurysmal rupture, bleeding occurs mainly in
the subarachnoid space rather than within brain
parenchyma. Therefore, prominent focal neurologic
signs are uncommon.

ruptured AVMs tend to occur within brain tissue and
accordingly produce focal neurologic signs, such as
hemiparesis, aphasia, or visual field defects.
 Complications:
1) recurrence of hemorrhage:
- recurrence of aneurysmal hemorrhage occurs in
approximately 20% of patients over 10 to 14 days. It is
the major acute complication and roughly doubles the
mortality rate.
- recurrence of hemorrhage from AVM is less common.
2) intraparenchymal extension of hemorrhage.
3) arterial Vasospasm: happens in more than one-third of cases &
lead to ischemic neurologic deficits. Typically does not appear
before day 4 after the hemorrhage, peaks at day 7 to 8, and then
resolves spontaneously. It associated with bad prognosis
4) acute or subacute hydrocephalus: develop during the first three
days or after several weeks.
5) seizures: occur in fewer than 10% of cases.
6) inappropriate secretion of antidiuretic hormone and resultant
diabetes insipidus can occur, they are uncommon.
 Cerebral Vinous Infarction & Cerebral Vinous Sinus Thrombosis:

frequently co-existed, but not always.

frequently associated with dehydration & hypercoagulable state(s)

2 types: septic & aseptic
1) Septic (patient is febrile): due to intracranial infection like encephalitis, TB; local
infection on head & neck (via emissary veins) like shaving wounds, tonsillitis, otitis;
or systemic infection like septicemia, endocarditis.
2) Aseptic (patient is afebrile): head trauma, oral contraceptives like estrogen,
pregnancy, puerperium, tumor obstructing vinous drainage, tumor generates
hypercoagulable state, other medical condition associated with hypercoagulable
state, connective tissue diseases like S.L.E, antiphospholipid syndrome, Bechets
disease, autoimmune disorders, & heart failure.

early symptoms may be subtle, with headache due to vessel occlusion or increased
ICP. As condition evolves, however, other symptoms such as seizures will develop,
leading to hemorrhagic conversion of the infarction, herniation, and death.