13. AHA/ACC (2009) defines TIA as:
“a transient episode of neurologic dysfunction caused
by focal brain, spinal cord, or retinal ischemia, without
acute infarction.’’
TIA
16. Cerebral Venous Thrombosis
• Uncommon cause of cerebral infarction
• Thrombosis of one of the venous sinuses
• May present as headache, with or without cranial nerve palsies
• More severely affected patients may present with seizures and/or
coma
• Papilledema is frequently present
17. • Blood supply to thebrain is autoregulated
• Blood flow
• If zero leads to death of brain tissue within 4-10min
• <16-18ml/100g tissue/min infarction within an hour
• Ischemia leads to development of an ischemic
core and an ischemic penumbra
Pathophysiology of IschemicStroke
18. IschemicPenumbra
• Tissue surrounding thecore region of
infarction which is ischemic but
reversibly dysfunctional
• Maintained by collaterals
• Can be salvaged if reperfused intime
• Primary goal of revascuralization
therapies
19. Pathophysiology Of HemorrhagicStroke
• Explosive entry of blood into the brain parenchyma
structurally disrupts neurons
• White matter fibre tracts are split
• Immediate cessation of neuronal function
• Expanding hemorrhage can act as a mass lesion and
cause further progression of neurological deficits
• Large hemorrhages can cause transtentorial coning
and rapid death
20. StrokeSyndromes
Stroke syndromes are divided into:
1. Large-vessel stroke within the anteriorcirculation
2. Large-vessel stroke within the posterior circulation
3. Small-vessel disease of either vascular bed
Basis of stroke syndrome:
• Predictable anatomy of the brain’s vascular supply
• Localization of particular functions to certain areas of the
brain
• Predilection of stroke for certain vascular territories
21. Internal carotid artery syndrome
Clinical features:
ICA occlusions often asymptomatic
( 30–40% of cases)
1. Amaurosis fugax
- “curtain dropping over the
eye and rising again”
2. Watershed infarct (distal MCA)
-partial contralateral
hemiplegia and a sensory
deficit affecting the shoulder
more than the hand and leg
22. Anterior choroidal artery syndrome
• Contralateral hemiplegia (injury to the posterior limb of the internal
capsule)
• Contralateral hemianopsia and reduced pupillary reaction (injury
to the optic tract), also in lesion to the geniculocalcarine tract in the
medial temporal lobe
• Contralateral hemianopsia with median horizontal sparing (lateral
geniculate nucleus is injured): diagnostic of an AChA occlusion
23. Anterior cerebral artery
syndrome
• Constitutes 3% or fewer of all strokes
• complex physical and cognitive deficits
• Unilateral ACA infarcts: contralateral hemiplegia
worse in the leg and shoulder than in the arm, hand,
and face
• If facial weakness is noted, the recurrent artery of
Heubner likely occluded
• Sensory loss minimal, usually impaired two-point
discrimination if present, and in the same distribution
as the motor impairment
24. • Urinary incontinence
• Gait apraxia
• Mutism, delay and lack of
spontaneity of motor acts
• Apraxia of left sided limbs (with
left sided lesion and corpus
callosum involvement)
Anterior cerebral artery syndrome
25. Primitive reflexes:
-the grasp reflex of the affected hand
-frontal release signs -palmomental or snout reflexes
-paratonia (a force-dependent limb rigidity that becomes
more prominent with an increase in effort by the examiner
during muscle stretches)
Anterior cerebral artery syndrome
26. Middle Cerebral Artery Syndromes
Mainstem Middle Cerebral Artery (M1 Segment)
• Those who survive M1 infarcts usually
have significant neurologic impairment
• Complete contralateral hemiplegia
• Contralateral hemisensory loss or
hemianesthesia (injury to subcortical
sensory tracts and the S1 cortex)
• Dominant MCA distribution infarct:
Broca’s aphasia
• Non-dominant MCA distribution: severe visual and perceptual
deficits with disrupted spatial body orientation, dressing apraxia,
constructional apraxia, and a severe left hemineglect syndrome
27. Superior-Division Middle Cerebral Artery
• Results in infarct of the frontal lobe convexity,
sparing the medial frontal lobe and subcortical
tissue
• Symptoms include contralateral hemiplegia
affecting the arm and hand more than the leg, and
loss only of two-point discrimination in the same
distribution as the weakness
• Patients may have transient head and eye
deviation away from the hemiplegia, but visual
fields are usually spared
28. Inferior-Division Middle Cerebral Artery
• Results in primarily cortical infarct of the
lateral convexity of the parietal, occipital,
and temporal lobes
• No motor or somatosensory deficits, but
may have a partial contralateral
hemianopsia
• Dominant hemisphere: Wernicke aphasia
• Non-dominant: hemineglect syndrome
• Sensory aprosodia, or affective agnosia,
individual has difficult time
comprehending the prosody in another’s
speech
29. Posterior Cerebral Artery Syndromes
• Occlusion occurs in the P1 segment,
hypoperfusion occurs in the distal
PCA and the thalamoperforating
arteries supplying the thalamus
• Results in contralateral sensory
syndrome with hypoesthesia, and in
some cases dysesthesia (Déjerine-
Roussy syndrome)
• Contralateral homonymous
hemianopsia from direct injury to
the primary visual cortex
30. PCA infarct in the left occipital
lobe: alexia without agraphia
Posterior Cerebral Artery Syndromes
31. Lacunar Stroke Syndromes
• Infarcts are 1.5 cm or less in the largest diameter
associated with hypertension
• Caused by small-vessel occlusion from lipohyalinosis of
the vascular intima
• 5 commonly seen lacunar syndromes
1. Pure sensory stroke:
• Numbness in the face, arm, and
leg on one side of the body
• No associated motor or cognitive deficits
• The infarct is usually located in the thalamus
• Can develop late or chronic pain syndromes as a result
of disruptions of normal sensory tracts
32. 2. Pure motor hemiparesis:
• Only motor loss in the face,
arm, and leg, with or without spastic dystonia
• Stroke usually occurs in the posterior limb of the
internal capsule, cerebral peduncle, or in the base of
the pons
• Prognosis for functional recovery is good because
patients lack other symptoms, such as language,
visual deficits, or apraxia
• Spastic dystonia may complicate the rehabilitation
process
Lacunar Stroke Syndromes
33. 3. Dysarthria-clumsy hand syndrome
• Lesions in the base of the pons caused by occlusions
of the paramedian pontine perforating vessels from
the basilar artery, infarcts of the genu of the internal
capsule in the somatotopic regions for face and hand,
as well as other areas of subcortical white matter
• Dysarthria and unilateral facial weakness without
language deficits, and a mild hemiparesis of the
upper limb on one side of the body
• Prognosis for recovery is usually very good
Lacunar Stroke Syndromes
34. 4. Ataxic hemiparesis:
• occlusions of the paramedian pontine perforating
vessels from the basilar artery
• Patients with ataxic hemiparesis often have a
considerable challenge regaining independence in
mobility because of problems with dynamic balance
• The prognosis is still very good, because the ataxic
component often recovers more rapidly than the
hemiparesis
Lacunar Stroke Syndromes
35. 5. Sensorimotor strokes
• Occurs at the junction of the ventrolateral thalamus
and the internal capsule, resulting in sensory and
motor loss on the contralateral side of the body
• Because the vascular supplies to thalamus and
internal capsule are distinct, the likely explanation is
that edema from a thalamic stroke compresses
adjacent motor fibers in the internal capsule
Lacunar Stroke Syndromes
36. Syndromes of the Vertebrobasilar System
I. Lateral Medullary (Wallenberg’s)
Syndrome
Occlusion of the following:
1. Vertebral arteries (involved in 8 out of 10 cases)
2. Posterior inferior cerebellar artery (PICA)
3. Superior lateral medullary artery
4. Middle lateral medullary artery
5. Inferior lateral medullary artery
37. Wallenberg’s syndrome
S/S
-Ipsilateral side
• Horner’s syndrome (ptosis, anhydrosis, and miosis)
• Decrease in pain and temperature sensation on the face
• Cerebellar signs such as ataxia on extremities (patient falls to side of
lesion)
-Contralateral side
• Decreased pain and temperature
-Dysphagia, dysarthria, hoarseness, paralysis of vocal cord
-Vertigo; nausea and vomiting
-Hiccups
-Nystagmus, diplopia
Note: No facial or extremity muscle weakness seen in this
syndrome
38. II. Benedikt’s Syndrome (Red
Nucleus/Tegmentum of Midbrain)
• Obstruction of interpeduncular
branches of basilar or posterior
cerebral artery or both
• Ipsilateral III nerve paralysis with
mydriasis
• Contralateral hypesthesia (medial
lemniscus), hyperkinesia (ataxia,
tremor, chorea, athetosis) due to
damage to red nucleus
39. III. Syndromes of the Paramedian Area
(Medial Brainstem):
Paramedian area contains:
• Motor nuclei of CNs
• Cortico-spinal tract
• Medial lemniscus
• Cortico-bulbar tract
Signs/symptoms include:
• contralateral hemiparalysis
• ipsilateral CN paralysis
41. Weber Syndrome
• Obstruction of interpeduncular branches of
posterior cerebral artery or posterior choroidal
artery or both.
• Ipsilateral CN 3 palsy
• Contralateral hemiplegia, Parkinson’s signs,
dystaxia (mild degree of ataxia)
Millard-Gubler Syndrom
• Obstruction of circumferential branches of basilar
artery
• Ipsilateral facial (CN 7) and abducens (CN 6)
palsy
• Contralateral hemiplegia, analgesia, hypoesthesia.
Extension to medial lemniscus = Raymond-Foville’s
Syndrome (with gaze palsy to side of lesion)
42. Medial Medullary Syndrome:
• Caused by infarction of the medial medulla due to occlusion
(usually atherothrombotic) of penetrating branches of the
vertebral arteries (upper medulla) or anterior spinal artery
(lower medulla and medullo-cervical junction)
• Rare; ratio of medial medullary infarct to lateral medullary
infarct ~ 1–2 : 10
• Typical syndrome:
– Ipsilateral CN 12 palsy (with deviation toward the side
of the lesion)
– Contralateral hemiparesis
– Contralateral lemniscal sensory loss (proprioception and
position sense)
43. IV. Basilar Artery Occlusion Syndrome
Occlusion may arise in several ways:
• atherosclerotic plaque in the basilar artery itself
(usually lower third)
• occlusion of both vertebral arteries
• occlusion of one vertebral artery when it is the only
one of adequate size
44. Basilar artery occlusion
Clinical features
1. Paralysis of all four limbs
2. Bulbar paralysis
3. Eye movements
Abnormalities-Nystagmus
4. Coma
Note: The neurological deficit is variable depending
upon the ischemia –modifying factors
45. Locked-In Syndrome
• Occlusion of the basilar artery causing
infarction of the basis pontis bilaterally
• Corticospinal and corticobulbar tracts are
interrupted, resulting in tetraplegia and
paralysis of all cranial nerve muscles
except for those controlling eye movements
• Vertical eye movements are preserved
• Horizontal eye movements may be affected (paramedian
pontine reticular formation)
• Remain awake and aware
• Means of communication is systematic eye movements or with
augmentative communication devices
Anatomic variations are numerous,
including hypoplastic portions of the circle as well as the
absence of the PComA on one side. In the presence of
atherosclerotic disease of an internal carotid, retrograde
blood flow from the external carotid artery through the
ophthalmic artery may provide collateral flow. Leptomeningeal
arteries may also provide another helpful but limited
source of collateral blood supply to the cerebral cortex.
Variable - based on the
collaterals and mechanism of
stroke (embolism, extension of
thrombus, low flow)
Hemianopsia can also occur, depending on what structures are involved.
and usually require comprehensive neurorehabilitation services
as a result of injury to the medial M1 cortex at the paracentral lobule
Patients with ACA infarcts will often have limb apraxia that is limited to the left side when a verbal command is given. This is because the ACA supplies the anterior corpus callosum, which disconnects the right premotor and M1 cortex from the left language network.
When the eye fields of the dorsomedial frontal cortex are damaged, the head and eyes deviate away from the hemiplegia Associated findings include
Occlusion of the M1 segment can cause injury to most of the lateral convexity of the cerebral hemisphere, as well as subcortical structures—including the internal capsule, visual radiations, and thalamocortical white matter— resulting from hypoperfusion of the lenticulostriate arterial branches.
Because the reticular formation above the caudal pons is spared, that can be used manually to respond to questions