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Clinical Presentation of Stroke Syndromes
By Ken Hui Yee for PBL group 7 Case 24 Clinical Presentation of Stroke Syndromes
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Ischaemic Stroke Causes: Thrombosis & Embolism (65% of strokes)
Artery-to-artery Cardioembolic Thrombosis in-situ Small vessel (lacunar) strokes (20% of strokes) atherothrombotic or lipohyalinotic occlusion of a small intracranial artery Often symptomless Artery-to-Artery Embolic Stroke Thrombus formation on atherosclerotic plaques may embolize to intracranial arteries producing an artery-to-artery embolic stroke. Alternatively, a diseased vessel may acutely thrombose; the resulting blockage causes stroke by producing ischemia within the region of brain it supplied. Unlike the myocardial vessels, artery-to-artery embolism, rather than local thrombosis, appears to be the dominant vascular mechanism causing ischemia. Any diseased vessel may be a source, including the aortic arch, common carotid, internal carotid, vertebral, and basilar arteries. Carotid bifurcation atherosclerosis is the most common source of artery-to-artery embolus lipohyalinotic - Degenerative changes in small blood vessels, marked by the accumulation of a glassy- or waxy-appearing lipid within the vessel wall. This type of vascular degeneration occurs in hypertension and atherosclerosis, and predisposes patients to small infarcts, esp. in penetrating arteries of the brain.
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Artery-to-Artery Embolic Stroke
Thrombus formation on atherosclerotic plaques embolize to intracranial arteries Carotid bifurcation most common site (10% of ischaemic strokes) Diseased vessel may acutely thrombose Including aortic arch, common carotid, internal carotid, vertebral, and basilar a. Thrombus formation on atherosclerotic plaques may embolize to intracranial arteries producing an artery-to-artery embolic stroke. Alternatively, a diseased vessel may acutely thrombose; the resulting blockage causes stroke by producing ischemia within the region of brain it supplied. Unlike the myocardial vessels, artery-to-artery embolism, rather than local thrombosis, appears to be the dominant vascular mechanism causing ischemia. Any diseased vessel may be a source, including the aortic arch, common carotid, internal carotid, vertebral, and basilar arteries. Carotid bifurcation atherosclerosis is the most common source of artery-to-artery embolus
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Cardioembolic Arrhythmias Mural thrombus DCM Valvular lesions
AF Mural thrombus DCM Valvular lesions Mitral stenosis, Endocarditis, Rheumatic fever Paradoxical embolus Atrial septal defect, Patent foramen ovale, Atrial septal aneurysm mural thrombosisn.Formation of a thrombus in contact with the endocardial lining of a cardiac chamber or, if not occlusive, with a wall of a large blood vessel. Mural Thrombi 2^0 to AMI Dilated cardiomyopathy or DCM is a condition in which the heart becomes weakened and enlarged, and cannot pump blood efficiently.
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Less Common Causes of Ischaemic Stroke
Venous sinus thrombosis Complication of: OCP Pregnancy & the postpartum period Inflammatory bowel disease Intracranial infections (meningitis) Dehydration
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Haemorrhagic Stroke Less common (only 15% of all strokes)
Higher mortality rate than Ischaemic
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Haemorrhagic Stroke Causes: Head trauma Hypertensive haemorrhage
Most common cause of SAH Hypertensive haemorrhage Aneurysm
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Hypertensive Haemorrhage
Spontaneous rupture of small penetrating artery Common sites: Basal ganglia (especially the putamen), thalamus, cerebellum, and pons.
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Aneurysm SAH from berry aneurysm Mycotic aneurysm
AcomA, PcomA, MCA (locations from most common to less common) Mycotic aneurysm Eg. Endocarditis
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Other Causes of Hemorrhage Stroke
Amyloid angiopathy Degen of intracranial vessels Rare in <60 Tumour Drugs (eg. Cocaine) Young pts
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Ischaemic vs. Haemorrhagic Stroke
Can’t be distinguished on basis of the history or clinical examination Ischaemic stroke tends to be painless However h/a may still occur Haemorrhagic stroke causes h/a esp. If ICP is raised Dura is stretched
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Ischaemic vs. Haemorrhagic Stroke
Investigations: Determine between ischaemic and haemorrhagic CT MRI CSF
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Acute Onset vs. Stuttering Onset
Sudden onset Abrupt neurological deficit More likely to be thrombotic and lacunar onset Neurological deficits wax and wane Proceeds towards complete neurological deficits
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Case 1 HOPC: Pt describes a shade or curtain being pulled over the front of the eye (right) Vision in right eye is lost only for a short time (seconds to minutes) On examination patient has carotid bruits Painless
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Amaurosis Fugax Ddx: Amaurosis Fugax Retinal migraine Rise in ICP
Central retinal artery occlusion Retinal migraine Develops more slowly (15 to 20mins) Rise in ICP Can compromise optic disc perfusion
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Case 2 HOPC: IX: Sudden onset of headache with aura
Nausea and vomiting Tingling, numbness and vague weakness on the right side of the body Patient prefers a dark room Patient reports that the aura has persisted for more than a week. IX: CT and MRI show focal ischaemia
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Migrainous Infarction
Rare complication of migraines Definition: Aura and a migraine headache, with the aura symptom persisting > 7/7 + neuroimaging focal ischaemia
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Complete vs Incomplete Strokes
Total area of the brain supplied by an occluded vessel is damaged Further prophylaxis Rx is pointless some cellular damage Additional tissue in the affected vascular distribution is at risk Prophylaxis Rx is useful Not that practical as distinction based on clinical findings can be impossible
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Case 3 HOPC: A 62-year-old woman was admitted to MMC with acute onset of left-sided hemiparesis. On admission, she had left-sided hemiplegia and facial palsy with minor dysarthria
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Case 3 IX: CT right MCA mainstem occlusion but no early ischemic changes Thrombolysis commenced pt improved initially but then developed sudden decline of consciousness
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Case 3 Repeat CT Ruled out ICH MRI New occlusion in Left MCA discovered Underlying cause was due to cardioembolic ischaemic stroke due to AF
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Case 4 HOPC: Pt presents to ED with global aphasia
Pt’s partner reports that pt is right handed
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MCA
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Case 5 HOPC: Pt presents to ED with right leg and foot paralysis
Sensory impairment (pain, temperature) over right lower limb Examination of upper limb = normal Impairment of gait
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ACA
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Case 6 HOPC: Pt presents with homonymous hemianopia
Has a failure to see to-and-fro movements, inability to perceive objects not centrally located
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Case 6 HOPC: Pt presents with homonymous hemianopia
Has a failure to see to-and-fro movements, inability to perceive objects not centrally located Reports peduncular hallucinosis
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PCA
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PCA – Specific Named Syndromes
Midbrain – Subthalamic -Thalamic Weber Syndrome Contralateral hemiplegia Thalamic Dejerine-Roussy Contralateral hemisensory loss Claude’s Syndrome Third nerve palsy Contralateral ataxia
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PCA – Specific Named Syndromes
Anton's syndrome Bilateral infarction in the distal PCAs producing cortical blindness Pt maybe unaware of blindness and may deny it Balint’s syndrome Watershed infarction between PCA and MCA Disorder of the orderly visual scanning of the environment
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Watershed Infarction Hypotension due to eg. AMI low perfusion in borderzones/junctional territories of the cerebral end arteries Ischemia between the territories of the ACA and MCA bilaterally may result in bibrachial cortical sensorimotor impairment (person-in-a-barrel)
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Watershed Infarction Clinical Presentation:
“Man-in-the-barrel” clinical presentation Optic ataxia Cortical blindness Difficulty in judging size, distance, and movement Memory loss Dysgraphia
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Case 7 81 yr old man with HT and AF on anticoagulants, right-handed
HOPC: h/a, diaphoresis, dizziness, diplopia Sudden onset of R arm tingling, numbness and weakness Progressive slurred speech
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Case 7 Signs & Symptoms continued:
Horizontal eye movements/conjugated gaze restricted Jaw deviation to the right Bilateral facial weakness Difficulty wrinkling forehead or close eyes Dysphagia Balance issues Cheyne-Stokes breathing Dry oral pharynx Sign Implicated Neural Structure Vertical movements and adduction CN III, IV, oculomotor and of the eyes trochlear Deviation of the jaw CN V, trigeminal motor Conjugated gaze and horizontal adduction of the eyes CN VI, abducent Facial weakness and difficulties closing the eyes CN VII, facial Balance/equilibrium CN VIII, vestibular components Audition CN VIII, cochlear components Salivatory function CN IX, glossopharyngeal Cheyne-Stokes breathing CN X, vagus Trapezius and levator scapulae muscle function CN XI, spinal accessory Tongue movement and gag reflex CN XII, hypoglossal Contralateral cerebellar signs Central tegmental tract Arousal Nucleus raphe magnus and pontis Discriminative touch/proprioception Medial lemniscus Pain and temperature sensation Anterolateral tract
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Case 7 IX: CT - progressive hemorrhagic stroke intrinsic to the pontine tegmentum of the brain stem, with rupture into the fourth ventricle
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Basilar Artery – Midbrain
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Basilar Artery Mid pons
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Basilar Artery Inferior Pons
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Vertebral and Posterior Inferior Cerebellar Arteries Medulla
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Presentation of Brainstem Infarction
Clinical Feature Structure Involved Hemiparesis Sensory loss Diplopia Facial numbness Facial weakness Nystagmus & vertigo Dysphagia & dysarthria
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Presentation of Brainstem Infarction
Clinical Feature Structure Involved Hemiparesis Corticospinal tracts Medial midpontine syndrome, Medial inferior pontine syndrome Sensory loss Medial lemniscus and spinothalamic tracts Lateral midpontine syndrome Diplopia Oculomotor/Adducens Facial numbness Trigeminal Lateral midpontine syndrome, Lateral inferior pontine syndrome Facial weakness Facial Nystagmus & vertigo Vestibular Dysphagia & dysarthria Glossopharyngeal & vagus Medullary Syndrome
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Summary Occluded Blood Vessel Clinical Manifestations ICA
Ipsilateral blindness (variable) MCA syndrome MCA Contralateral hemiparesis, sensory loss (arm, face worst) Expressive aphasia (dominant) or anosognosia and spatial disorientation (nondominant) Contralateral inferior quadrantanopsia ACA Contralateral hemiparesis, sensory loss (worst in leg) PCA Contralateral homonymous hemianopia or superior quadrantanopia Memory impairment Basilar apex Bilateral blindness Amnesia Basilar artery Contralateral hemiparesis, sensory loss Ipsilateral bulbar or cerebellar signs Vertebral artery or PICA Ipsilateral loss of facial sensation, ataxia, contralateral hemiparesis, sensory loss Superior cerebellar artery Gait ataxia, nausea, dizziness, headache progressing to ipsilateral hemiataxia, dysarthria, gaze paresis, contralateral hemiparesis, somnolence
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