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Neurology; Self Determined Learning TargetHuizhong He

Clinical Group LSemester 2 2010

On interviewing a patient who had a stroke of unknown aetiology, presenting

atypically

What are the pathophysiology, signs and symptoms for patients

experiencing a transient ischaemic attack?

Transient Ischaemic Attack (1) Focal, ischemic, cerebral neurologic deficits that last for

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Injured endothelium allows intimate contact between the blood and

prothrombotic subendothelial connective tissue, triggering a thrombogenic

cascade

Platelets are activated; monocytes adhere and emigrate into the intima,enhancing lipid accumulation and stimulating inflammatory mediators.

Platelet activation causes release of adenosine diphosphate (ADP) and

thromboxane A2, which fuel platelet aggregation

Coagulation cascade is initiated by the production of cytokines from

dysfunctional endothelium, reinforming the platelet plug with a fibrin

meshwork

Such clotting pathway prepares for ulceration and thromboembolism Resultant plaque can rupture, exposing highly thrombogenic substances,

which may encourage thrombus formation or the release of emboli

Myocardial infarction and cardiomyopathy predispose to thrombus formation

in the left ventricle, as can rheumatic heart disease in the atria

Subsequent arrhythmias such as atrial fibrillation can convert these thrombi to

emboli

Cardiac thrombi give rise to the majority of arterial emboli

Sources of Emboli (1)

Cardiac

Atrial Fibrillation

Rheumatic Heart Disease

Mitral Valve Disease

Infective Endocarditis Atrial Myxoma

Mural Thrombi subsequent to Myocardial Infarct

Venous emboli via Atrial Septal Defect (paradoxical emboli)

Cerebrovascular

Ulcerated plaque on vessel distributing to brain

Haematological

Polycythemia

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Sickle Cell Disease

Hyperviscosity

Subclavian steal syndrome may lead to transient vertebrobasilar ischemia from

stenosis/ occlusion of one subclavian artery proximal to the source of the vertebralartery

Signs/symptoms

Abrupt onset, resolution in few minutes (2)

Related to the artery affected and its territory of distribution

o Blue; Anterior Cerebral Artery

o Red; Middle Cerebral Arteryo Yellow; Posterior Cerebral Artery

Diagram from Grays Anatomy Online

Carotid territory (3)

Distributes to (4)

o Orbit via ophthalmic artery

o Lateral cerebral hemisphere via middle cerebral artery

Wernickes area (superior temporal gyrus)

Temporal lobe

o Anterior cerebral hemisphere via anterior cerebral artery

Frontal gyrusCingulate gyrus

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Prefrontal cortex

Primary (precentral gyrus) and secondary Motor cortex

Primary (postcentral gyrus) and secondary Somatosensory

cortexBrocas area (Inferior frontal gyrus)

Signs/Symptoms (1)

Weakness/heaviness in contralateral arm/leg/face

Numbness/paresthesia or motor deficit

Vision loss in eye contralateral to affected limb

Flaccid weakness (pyramidal distribution), sensory changes, hyperreflexia,

dysphagia, extensor plantar response on affected side Carotid bruit

Table by strokestop (3)

Blocked Vessel or

BranchPatterns of Possible Deficits

Extracranial

Internal

Carotid

Deficits depend on the extent of collateral supply and how quickly

occlusion occurred. 30-40% of carotid occlusions near the bifurcation are

clinically silent.

MCA-main stem

(M1)

Contralateral hemiplegia and hemisensory loss

Contralateral hemianopsia

Global aphasia (L)* or denial, neglect, and disturbed spatial perception

perhaps with emotional 'flatness' (R)*

Eye and head deviation toward lesion in acute stage

MCA-superior

cortical division

Contralateral Hemiparesis and hemisensory loss (face and arm more than

leg; often motor more than sensory)

Expressive (Broca's) aphasia (L)* or neglect and disturbed spatial

perception (R)*

Eye and head deviation toward lesion in acute stage

MCA- inferior

cortical division

Receptive (Wernicke's) aphasia (L) or denial, neglect and disturbed spatial

perception (R)*

Contralateral hemianopsia-usually upper quadrants are most affected

MCA-lenticulostriate

branch

"Pure motor" stroke often, but not necessarily, involving lower face, arm

and leg equally but sparing sensation

*Assuming left hemisphere dominance for language

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Vertebrobasilar territory (3)

Distributes to (4):

o Cerebellum via Superior Cerebellar Artery, Anterior Inferior

Cerebellar Artery, Posterior Inferior Cerebellar Arteryo Occipital Lobe via Posterior Cerebral Artery

o Diencephalon via various

o Mesencephalon via various

Signs/Symptoms (1)

Vertigo

Ataxia

Diplopia Dysarthria

Dimness/ blurring of vision

Perioral numbness/paresthesia, weakness on both or alternating sides of body

Bilateral leg weakness without headache or loss of conscious related to head

movements

Table by Strokestop (3)

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Subclavian Steel Syndrome (1)

o Supraclavicular fossa bruit

o Unequal Radial Pulses

o Unequal systolic pulses (>20mmHg) in different arms

Word Count: 984

Blocked Vessel/ Branch Deficit Pattern

One vertebral artery in the rostral medulla, or

in some cases its Posterior Inferior Cerebellar

Artery branch

Wallenberg's syndrome

Sensory loss on ipsilateral side of face but contralateral

trunk and limbsIpsilateral ataxia

Ipsilateral Horner's syndrome

Ipsilateral vocal cord paralysis

Hoarseness

Impaired swallowing

Vertigo, nausea, vomiting

Penetrating paramedian basilar branches in

pons

Pure motor stroke

Contralateral hemiplegia

Involvement of face depends on infarction location

Basilar occlusion affecting the rostral pons

bilaterally

"locked-in syndrome"

Complete bilateral paralysis rendering patient

motionless and mute yet capable of perceiving sensory

stimuli

Vertical components of 3rd and 4th nerve function

may be spared

Penetrating Posterior Cerebral Arteries

branches supplying thalamus

Pure sensory loss

Involves face, arm, trunk and legInitially hemianesthesia but may eventually develop

into thalamic pain syndrome with painful dysesthesias

in affected parts

Unilateral cortical branches of PCA supplying

occipital lobe

Contralateral homonymous hemianopsia

May have macular sparing (central vision) depending

on location of PCA-MCA border zone

Bilateral occlusion of all Posterior Cerebral

Artery cortical branches distal to thalamicpenetrating branches

Inability to form and/or consolidate new memories

Cortical blindness; in acute stage, possible denial of any vision problem

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References

1. "Transient Ischemic Attack." Quick Answers to Medical Diagnosis and Therapy:http://www.accessmedicine.com/quickam.aspx .

2. Hogan N, Boenau Ioliene. The Emergency Patient; Transient Ischaemic Attack Emerg Med 38(3):41-46, 2006

3. Billings-Gagliardi S et. al. StrokeSTOP University of Massachusetts. [Internet,updated March 2010 accessed 26/10/10] Available from:http://www.umassmed.edu/strokestop/

4. Romanes GJ, et. al. Cunninghams Manual of Practical Anatomy Vol.3 15 th ed.2008. Oxford University Press

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http://www.accessmedicine.com/quickam.aspxhttp://www.umassmed.edu/strokestop/http://www.accessmedicine.com/quickam.aspxhttp://www.umassmed.edu/strokestop/