CHAPTER 13: Stroke

1. Define stroke and transient ischemic attack (TIA) =Stroke is a syndrome characterized by 4 key features

#1. Sudden onset #2. Focal involvement of CNS --suggest by nature of s/s, delineated more precisely by neurologic exam, confirmed by imaging. #3. Lack of rapid resolution --duration of neuro deficits is documented. 1. Standard definition of stroke required deficits to persist for at least 24 hours. a. This distinguishes stroke from transient ischemic attack. i. Time point is arbitrary, TIA's resolve within 1 hour #4. Vascular cause --may be inferred from the acute onset of Sx and often from the patient's age, presence of risk factors for stroke, and occurrence of Sx and sign referable to the territory of a particular vessel

5. Recall the sensory and motor cerebral representation as it relates to vascular supply.

-look at module or review from neuro-anatomy Kuleza blood supply lecture

6. vertebrobasilar artery strokes clinical features AICA

AICA - infarction of lateral portion of caudal pons. =Produces a syndrome with many of the same features. =IL facial weakness, gaze palsy, deafness, and tinnitus are common findings. =Horner syndrome, dysphagia, dysarthria, and hiccup *do NOT occur*. =Syndrome of lateral rostral pontine infarction from superior cerebellar artery occlusion resembles AICA lesions. --Impaired optokinetic nystagmus or skew deviation of the eyes may occur. --Auditory function is NOT affected. --CL sensory disturbance may involve touch, vibration, position sense as well as P and T.

2. stroke significance of onset

Acute onset: =Strokes begin abruptly --Neuro deficits may be maximal at onset (embolic stroke), or may progress over second to hours (progressive arterial thrombosis or recurrent emboli). --Stroke in evolution or progressing stroke: one that is actively progressing as a direct consequence of the underlying vascular disorder (not because of associated cerebral edema) or has done so in recent minutes. --*Focal cerebral deficits developing slowly (weeks - months) are unlikely to be due to stroke and are more suggestive of another process*, such as tumor or inflammatory degenerative disease

3. signs and symptoms of anterior circulation ischemia

Anterior (carotid) circulation: =Supplies most cerebral cortex and subcortical white matter, basal ganglia, and internal capsule. =Consists of the ICA and its branches: --Anterior choroidal, ACA, MCA. =MCA gives rise to deep penetrating lenticulostriate branches. =*Anterior circulation strokes are commonly associated w. s/s that indicate hemispheric dysfunction (aphasia, apraxia, agnosia)*. =Often produce hemiparesis, hemissensory distrubances, visual field defects, which can also occur w. posterior circulation strokes.

6. anterior cerebral artery strokes clinical features

Anterior cerebral: =Uncommon: --Emboli from extracranial vessels or the heart are more apt to enter larger-caliber MCA which gets the bulk of cerebral blood flow. =*CL paralysis and sensory loss affecting the leg*. =*Voluntary control of micturition may be impaired*. --Failure to inhibit reflex bladder contractions, resulting in precipitate micturition (a sudden emission of urine without any warning and without being able to stop it)

2. stroke duration

Duration of deficits: =Stroke produces *neurologic deficits that persist*. --*When symptoms resolve completely over brief period, then it's a Transient ischemic attack (TIA)*. --Recurrent TIAs with identical clinical features are usually caused by thrombosis or embolisms arising within the cerebral circulation. --TIAs that differ in character from event to event suggest recurrent emboli from a cardiac source. --Although TIAs do not themselves produce lasting neurologic dysfunction, they are important to recognize because *approximately 1/3 of patients with TIAs will go on to have stroke within 5 years. 1. Risk may be reduced with treatment.*

6. basilar artery strokes clinical features Embolism

Embolism: =*Immediate loss or impairment of consciousness* =Unilateral or bilateral *CN III palsies are characteristic* =Hemi- or quadriplegia with decerebrate or decorticate posturing occurs. --Because of involvement of the cerebral peduncles in midbrain. =Top of basilar syndrome may be confused w. midbrain damage caused by transtentorial uncal herniation. =*If conscious: patients display a variety of visual, visuomotor, behavioral abnormalities without prominent motor dysfunction* =Sluggish pupillary response are helpful sign of midbrain involvement.

4. Compare and contrast thrombotic versus *embolic stroke.*

Embolism: =Produce stroke when *cerebral arteries are occluded by distal passage of thrombus from heart, aortic arch, or large cerebral arteries* =In anterior cerebral circulation most often *occlude the MCA or branches*, because approximately 85% of hemispheric blood flow is carried by this vessel. =Emboli in posterior cerebral circulation usually lodge in *apex of basilar artery or in PCA's*. =Embolic strokes characteristically produce *neurologic deficits that are maximal at onset* =When TIAs precede embolic strokes, esp. those arising from a cardiac source: --*Symptoms typically vary* between attack because different vascular territories are affected (different from thrombotic).

2. stroke pattern of signs and symptoms

Focal involvement: =Produces focal s/s that correlate with the area of brain supplied by the vessel. =*Ischemic stroke*: occlusion of blood vessel interrupts flow of blood to specific region, interfering with neurological function of that region. =*Hemorrhage* produces a less predictable pattern of focal involvement because complications (increased ICP, cerebral edema, compression of brain tissue/vessels, dispersion of blood through subarachnod space/ventricle) can impair brain function at remote sites. =*History and neuro exam provide enough info to localize the lesion to one side of the brain (i.e. to side opposite hemiparesis or hemisensory deficit or to the left side if aphasia is present) and to the anterior or posterior cerebral circulation.*

6. middle cerebral artery strokes clinical features =Vessel most commonly involved in large vessel ischemic stroke. =Depending on site of involvement, several clinical syndromes can occur: *Inferior division*

Inferior division: =Less common in isolation, results in: =CL homonymous hemianopia that may be denser inferiorly. =*Impaired cortical sensory functions (graphesthesia, steognosis on CL body)*. =Disorders of spatial thought (lack awareness of deficit existing, neglect of CL limbs, neglect of CL external space, dressing apraxia, constructional apraxia). =If dominant hemisphere is involved: *Wernicke* (*receptive aphasia* occurs and is manifested by impaired comprehension and fluent but often nonsensical) =If nondominant hemisphere involved: acute confusional state.

6. internal carotid artery strokes clinical features

Internal carotid: =Intra- or extracranial ICA occlusion is responsible for about 20% of ischemic strokes. =15% of cases: progressive atherosclerotic occlusion of the ICA is preceded by premonitory TIAs or by transient monocular blindness caused by ipsilateral retinal a. ischemia. =Carotid a. occlusion may be asymptomatic. =Symptomatic occlusion results in a *syndrome similar to that of MCA*: --*CL hemiplegia, hemisensory deficit, homonymous hemianopia, together with aphasia (if dominant hemisphere involved).*

6. middle cerebral artery strokes clinical features =Vessel most commonly involved in large vessel ischemic stroke. =Depending on site of involvement, several clinical syndromes can occur: *bifurcation or trifurcation of MCA*

Occlusion at *bifurcation or trifurcation of MCA*: =Involves a lesion situated at the point where the a. splits into 2 or 3 major division. =Severe stroke syndrome combines the features of superior and inferior division strokes. --CL hemiparesis and hemisensory deficit involving the face and arm far more than the leg. --Homonymous hemianopia. --If the dominant hemisphere - *global aphasia (combined expressive and receptive)*.

6. middle cerebral artery strokes clinical features =Vessel most commonly involved in large vessel ischemic stroke. =Depending on site of involvement, several clinical syndromes can occur: *main stem of MCA*

Occlusion of stem of MCA: =Occurs proximal to origin of lenticulostriate branches. =*Entire territory of a. is affected, most devastating of the MCA strokes.* =Similar clinical presentation to the occlusion at the trifurcation. --Except, infarction of motor fibers in the internal capsule *causes paralysis of the CL leg*. =CL hemiplegia and sensory loss affecting face, hand arm, leg

6. vertebrobasilar artery strokes clinical features PICA

PICA - lateral medullary aka Wallenburg syndrome. =Varies in presentation. =*IL cerebellar ataxia* =*Horner syndrome* =Facial sensory deficit. =CL impaired pain and temperature sensation. =Nystagmus, vertigo, nausea, vomiting, dysphagia, dysarthria, hiccup. =*Motor system is characteristically spared* because of ventral location in brainstem

3. Compare and contrast the signs and symptoms of anterior versus *posterior circulation ischemia*

Posterior (vertebrobasilar) circulation: =Supplies brainstem, cerebellum, thalamus and portions of occipital and temporal lobes. =Consists of paired vertebral arteries, basilar artery, and their branches: PICA, AICA, superior cerebellar, and PCA. =Posterior cerebral also gives off thalamoperforating and thalamogeniculate branches. =Post circulation strokes: *s/s of brainstem dysfunction* --*Coma, drop attack, vertigo, nausea, vomiting, cranial nerve palsies, ataxia, crosses sensorimotor deficits affecting the face on one side of body and limbs on the other side*

6. posterior cerebral artery strokes clinical features

Posterior cerebral: =Occlusion of PCA produces *homonymous hemianopia affecting the CL visual field* --Macular vision may be spared: dual blood supply to the portion of visual cortex. =Vs. visual field defects from infarction of MCA territory, those caused by PCA occlusion may be *denser superiorly*. --With *occlusion near the origin of the PCA* at midbrain, ocular abnormalities can include *vertical gaze palsy, CN III palsy, INO, vertical skey deviation of eyes* =When it affects dominant occipital lobe, patient may exhibit *anomic aphasia (difficulty naming objects), alexia without agraphia (can't read, can write), or visual agnosis* =The last is a failure to ID objects presented in the left side of the visual field, caused by a lesion of the corpus callosum disconnecting right visual cortex from language areas in left hemisphere. =*Bilateral PCA infarct* may lead to *cortical blindness, memory impairment (temporal lobe involvement), or inability to recognize familiar faces (prosopagnosia)*, as well as a variety of exotic visual and behavioral syndromes

6. middle cerebral artery strokes clinical features =Vessel most commonly involved in large vessel ischemic stroke. =Depending on site of involvement, several clinical syndromes can occur: *Superior division*

Superior division: --CL hemiparesis affecting face, hand, and arms but sparing leg. --CL hemisensory deficits in same distribution. --NOT homonymous hemianopia. --If dominant hemisphere involved: these feature are combined with *broca aphasia - expressive aphasia* --Impaired language

4. Compare and contrast *thrombotic stroke* versus embolic stroke.

Thrombosis: =Occlude large cerebral arteries (especially ICA, MCA or basilar), small penetrating arteries (i.e. lacunar stroke), cerebral veins, or venous sinuses. =Symptoms typically *evolve over minutes to hours*. =Thrombotic strokes are *often preceded by TIA's: --*Tend to produce similar Sx because they affect the same territory recurrently*

6. basilar artery strokes clinical features Thrombosis:

Thrombosis: =Often not compatible with survival. =Bilateral neurologic signs referable to involvement of multiple branch arteries. =Occlusion of both vertebrals or of lone unpaired vertebral a. produces similar syndrome. =Major stenosis or occlusion of subclavian a. before it has given rise to vertebral a. can lead to 8subclavian steal syndrome8 (blood passes from vertebral a. into distal subclavian a. with physical activity of the ipsilateral arm). =Manifestation of generalized atherosclerosis and is not predictive of stroke in verbrobasilar system. =*Patients are usually asymptomatic and stroke, when it occurs, is typically due to coexisting carotid lesions* =Usually effects proximal portion of basilar artery, supplies the pons. =Dorsal portion of pons produces unilateral or bilateral abducens (VI) nerve palsy; horizontal eye movements are impaired, but vertical nystagmus and ocular bobbing may be present. =Pupils are constricted as a result of involvement of descending sympathetic pupillodilator fibers in pons, but remain reactive. =*Hemiplegia or quadriplegia is usually present, and coma is common* =*Syndrome of basilar occlusion in unconscious patients may be confused with pontine hemorrhage*. --CT or MRI will differentiate. =8Some patients with basilar occlusion: ventral pons is infarcted and tegmentum is spared. --"Locked in" syndrome: patient remain conscious but quadriplegic.8 --Patient may be able to signify that they are conscious by opening their eyes or moving their eyes vertically on command. --In other cases, conventional EEG with stimulation may be needed to distinguish locked in state from coma.