Stroke Flashcards

Question

MCA Stroke Syndromes: | (1) Complete MCA syndromes: clinical features -

Answer 1

Complete MCA syndromes (occlusion of entire MCA at its origin, eg. by thrombus): - contralateral hemiplegia - contralateral hemianaesthesia - homonymous hemianopia - temporary gaze preference to ipsilateral side ( a few days) - dysarthria (secondary to facial weakness) DOMINANT hemisphere: global aphasia NON-DOMINANT hemisphere: anosognosia, constructional apraxia, neglect.

Answer 2

Anosognosia ("without disease knowledge"): | A condition in which an ill patient is unaware of her own illness or the deficits resulting from her illness

Answer 3

Most likely occipital (whether superior or inferior quandrant affected). If isolated superior quadrantanopia also need to consider temporal lobe lesion. Parietal lesion can cause INFERIOR quadrantanopia, but usually accompanied by other parietal lobe signs.

Answer 4

Partial MCA syndromes (due to collateral flow / variable arterial configurations, or emboli causing partial MCA occlusion / occlusion of distal branches): - Brachial syndrome = hand +/- arm weakness alone - Frontal opercular syndrome = Facial weakness + Broca aphasia (non-fluent) +/- arm weakness - Superior division occlusion (frontal and parietal infarction): sensory disturbance, motor weakness, non-fluent aphasia. - Inferior division occlusion (temporal cortex): DOMINANT hemisphere: : fluent (Wernicke's / receptive) aphasia, without weakness. +/- homonymous superior quadrantanopia. NON-DOMINANT hemisphere: hemineglect or spatial agnosia (parietal lobe) without weakness

Answer 5

Lacunar stroke syndromes (of MCA): ie. white matter strokes, no 'cortical' signs. 1. Pure motor stroke (contralateral) - occlusion of lenticulostriate vessels --> internal capsular infarct 2. Pure sensory stroke (contralateral) - occlusion of lenticulostriate vessels --> internal capsular infarct 3. Ataxic hemiparesis: ipsilateral weakness and limb ataxia that is out of proportion to the motor deficit. +/- dysarthria, nystagmus, and gait deviation towards the affected side. 4. Sensorimotor stroke: weakness and numbness of face, UL and LL on one side, but without cortical signs. 5. Dysarthria clumsy-hand syndrome (least common): Facial weakness, dysarthria, dysphagia, and slight weakness and clumsiness of one hand. No sensory deficit.

Answer 6

Occlusion of the proximal ACA is usually well tolerated due to collateral flow from through the Anterior Communicating Artery and collaterals from the MCA and PCA. Exception: Contralateral A1 segment atresia - if both A2 segments arise from a single ACA stem --> occlusion affects both hemispheres. Results in profound abulia (delay in verbal and motor response), bilateral pyramidal signs, paraparesis or quadriparesis, urinary incontinence.

Answer 7

- Frontal lobe behaviours - Grasp reflex (may also have sucking reflex and paratonia) - Abulia = akinetic mutism (if complete) - Contralateral hemiplegia and sensory loss (leg affected > arm if partial) - Left limb dyspraxia (corpus callosum involvement) - Urinary incontinence (if complete) DOMINANT ACA: motor +/- sensory aphasia NON-DOMINANT ACA: contralateral hemineglect

Answer 8

Is the ability to execute learned purposeful tasks. Eg. ideomotor praxis: ability to perform learned motor movements. Other forms of praxis: ideational, orofacial, limb-kinetic, dressing, writing, speech, constructional. Apraxia is the inability to execute purposeful tasks despite having the desire and the physical capacity to perform the movements. It is an acquired disorder of motor planning, but is not caused by incoordination, weakness, sensory loss, or failure to comprehend commands. Frank problems with ideomotor praxis may be obvious when patient or family member reports difficulty dressing, feeding, and bathing that is not explained by gross motor deficits. Localisation: Frontal cortex, parietal cortex, basal ganglia, and white matter tracts connecting these areas (ie. corpus callosum). Often thought to be localised to dominant hemisphere (ie. left hemisphere controls praxis for both left and right limbs), although probably more complex than this. Therefore, occurs more often with left-sided lesion. Unilateral left-limb dyspraxia (callosal apraxia) occurs when there is damage to the anterior corpus callosum and adjacent frontal cortex. The lesion presumably disconnects right hemisphere premotor and motor cortex from left hemisphere praxis input. May be seen in stroke (ACA, MCA), and disorders of the basal ganglia: corticobasal degeneration (prominent feature), PD, supranuclear palsy, and Huntington’s disease.

Answer 9

Is the ability to execute learned purposeful tasks. Eg. ideomotor praxis: ability to perform learned motor movements. Other forms of praxis: ideational, orofacial, limb-kinetic, dressing, writing, speech, constructional. Apraxia is the inability to execute purposeful tasks despite having the desire and the physical capacity to perform the movements. It is an acquired disorder of motor planning, but is not caused by incoordination, weakness, sensory loss, or failure to comprehend commands. Frank problems with ideomotor praxis may be obvious when patient or family member reports difficulty dressing, feeding, and bathing that is not explained by gross motor deficits.

Answer 10

1. Loss or impairment of the ability to perform voluntary actions or to make decisions. 2. Reduction in speech, movement, thought, and emotional reaction; a common result of bilateral frontal lobe disease. Seen in: - Mental illness - Processes damaging cortical structures, eg. ACA infarct.

Answer 11

Anterior choroidal artery - arises from ICA and supplies posterior limb of internal capsule. Usual mechanism of occlusion: in-situ thrombosis, iatrogenic during clipping of ICA aneurysm. Complete syndrome of occlusion: - contralateral hemiplegia and hemianaesthesia - homonymous hemianopia Complete syndrome uncommon, or may recover substantially. Overlap in supply by: proximal MCA, PCA, posterior choroidal arteries.

Answer 12

Internal carotid artery ischaemia / infarction: Presentation varies depends on mechanism (thrombus, embolism, low flow) and competence of Circle of Willis (can vary from relatively asymptomatic to catastrophic). - MCA territory most commonly affected. - ACA + MCA may be occluded at top of ICA (--> abulia, stupor, hemiplegia, hemianaesthesia, aphasia, anosognosia). - PCA can be affected if arises from ICA ('foetal posterior cerebral artery'). - Ophthalmic artery. Recurrent transient monocular blindness (amaurosis fugax) may warn of symptomatic ICA lesion. Rarely infarcted at time of TIA / CVA. - Listen for carotid bruit. Carotid doppler USS. Common carotid artery: - symptoms / signs of ICA occlusion - jaw claudication due to low flow in ECA branches - Takayasu's arteritis may be implicated (eg. bilateral CCA stenoses at their origin).

Answer 13

Cerebral amyloid angiopathy: - amyloid beta peptide deposits - within small to medium-sized blood vessels - vessels brain and leptomeninges. Usually asymptomatic, but an important cause of primary lobar intracerebral haemorrhage in the elderly. Can occur as: - a sporadic disorder - in association with Alzheimer disease - familial syndrome Incidence increases with age (onset >50 but usually at least 60-65+yo). No overlap with non-CNS amyloidosis.

Answer 14

Usually asymptomatic, but an important cause of primary lobar intracerebral haemorrhage in the elderly. Lobar haemorrhage is the most common clinical manifestation. Other complications: - transient neurological symptoms - inflammatory leukoencephalopathy - contributor to cognitive impairment - incidental microhemorrhages or hemosiderosis on MRI.

Answer 15

The most common clinical manifestation of cerebral amyloid angiopathy is spontaneous LOBAR haemorrhage. LOBAR = in the cortex and subcortical white matter. - as vascular amyloid deposits favour cortical vessels and largely spare white matter, deep gray matter, and the brainstem. - therefore largely spare the ventricles, but may rupture into SAS. (cf. deep locations characteristic of hypertensive hemorrhage such as putamen, thalamus, and pons). More often posterior (temporal & occipital > frontal & parietal) - reason unknown. Probably underlie substantial proportion of anticoagulant-associated ICH.

Answer 16

Should be suspected in anyone ≥60yo with lobar haemorrhage. Definitive diagnosis is pathological. However, a probable diagnosis can be made with MRI: ≥2 haemorrhages or microhaemorrhages - restricted to regions typical of CAA (cortex or "grey-white" junction) - entirely sparing regions typical of hypertensive haemorrhage (basal ganglia, thalamus, or pons)

Answer 17

Symptomatic managment only (eg. in ICH) Lobar haemorrhages tend to recur. Therefore: - avoid anticoagulants and antiplatelet agents - control hypertension (Some rare inflammatory forms may respond to immunosuppression)

Answer 18

Cerebellar haemorrhage: The most common symptoms are of severe nausea and vomiting and ataxia. Headache may be severe. Patients with cerebellar haemorrhage can rapidly become comatose within hours after the onset from herniation, because of its limited space in the posterior fossa. Pontine haemorrhage: There are numerous nuclei located within the pons. Rapidly deteriorating level of consciousness, impaired extraocular movement and extensive sensorimotor deficits are clinical clues to pontine haemorrhage. Basal ganglia haemorrhage: Contralateral hemiparesis, hemisensory loss, or hemi-inattention. Aphasia, especially non-fluency and impaired comprehension, is frequently seen if haemorrhage occurs in the posterior limb of the left internal capsule.

Stroke Flashcards

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