FBN CASE STUDY 2012 Nikolina Docheva & Momina Yazdani

STROKE Focal neurological deficit (e.g. hemiplegia) lasting longer than 24h, which is the result of a vascular lesion.

Types of Stroke 1. Ischaemic 80% Thrombus at the site of an atheromatous plaque in one of the major cerebral vessels. Embolus (atherom. plaques, atrial fibrillation)

2. Haemorrhagic 15% Rupture of an intracranial microaneurysms, in a patient with hypertension 3. Subarachnoid 5% Rupture of a congenital Berry aneurysm

Some Risk Factors Age Male>Female Previous vascular event i.e. MI, stroke High BP Heart disease – AF Diabetes Smoking Alcohol High lipids…………………. Others

Excitotoxicity

Neuronal ischaemia and infarction 1. ↓ blood flow -> ↓ in O 2 and ATP -> ↑H+ via anaerobic metabolism of glucose 2. failure of Na+/K+ ATPase pump -> cytotoxic oedema + membrane depolarization -> Ca 2+ entry + release of glutamate 3.Ca 2+ enters via glutamate-gated channels and activates destructive intracellular enzymes 4.destruction of intracellular organelles and cell membrane, with release of free radicals. Free fatty acid release exacerbate local ischaemia by activation of procoagulant pathway. 5.glial cells take up H+, so cannot take up extracellular glutamate -> glial cell death  result of 1-5 Liquefactive necrosis of the whole arterial territory

Time 18-24h – early neurone damage After 24h – early damage and necrosis of neurons After few days – organization of the infarct, macrophages, oedema goes down After weeks/months – shrinkage of scarred area, ventricles dilate, cyst with yellowish fluid

Blood supply Internal Carotid System: middle cerebral arteries (artery of stroke) anterior cerebral arteries (hypophysial, ophthalmic and posterior communicating arteries also arise from the internal carotid before its terminal bifurcation.) Vertebrobasilar System: vertebral arteries basilar arteries posterior arteries Circle of Willis

Middle cerebral artery 2 branches: Lateral striate arteries – supply anterior limb, genu and posterior limb (note anterior limb and genu also receive branches from the anterior cerebral and communicating arteries (recurrent artery of Hubner) Anterior choroidal artery – supplies inferior and posterior regions of the internal capsule Supplies the lateral external part of each hemisphere Contralateral hemiplegia, hemianaesthsia, sensory loss of face and arms, vision-spatial disturbances Sometimes contralateral homogenous hemianopia. L sided lesion more likely to lead to globus dysphasia R sided lesion more likely to lead to neglect, expressive and receptive dysphasia

Clinical effects of Middle Cerebral artery occlusion Segment Left temporalWernicke aphasia Either stemHemiplegia, hemihypesthesia, hemianopia Left stemSame + global aphasia Right stemSame + sensory neglect Either upper divisionParesis and hypesthesia of face and arm, dysarthria Left upper divisionSame + Broca aphasia Right upper divisionSame + hemineglect or expressive aprosodia Either lower divisionHemianopia ± agitated state Left lower divisionSame ± Wernicke aphasia, alexia, ideomotor apraxia Branches OrbitofrontalPrefrontal syndrome Left precentralBroca aphasia Right precentralMotor aprosodia CentralLoss of motor ± sensory function in face and arm Inferior parietalHemineglect Either angularHemianopia Left angularAlexia Right temporalReceptive aprosodia

Orbital-frontopolarApathy with some memory loss Medial striateParesis of face and arm Callosomarginal Paresis and hypesthesia of face and arm ± abulia ± mutism ± inability to reach across PericallosalIdeomotor apraxia (anterior lesion), tactile anomia (posterior lesion) Clinical Effects of Anterior Cerebral Artery Branch occlusion Stem EitherHomonymous hemianopia LeftAlexia in visible field BothCortical blindness ± amnesia Branch MidbrainIpsilateral third nerve palsy + contralateral hemiplegia Thalamus Contralateral numbness ± hemianopia ± thalamic syndrome Subthalamic nucleusContralateral ballism Corpus callosumAlexia in contralateral visual field Clinical Effects of Posterior Cerebral Artery Branch occlusion

Case Study Right sided hemiparesis –lLeft hemisphere affected-> corticospinal tract Reduced pinprick on right side -> left hemisphere -> spinothalamic tract Reduced right 2 point disctimination – left hemisphere ->PCML (medial lemniscus)

Motor Pathways Pyramidal Pathway – Direct motor innervation Corticospinal & Corticobulbar Tracts Extra Pyramidal Pathways - Modulatory Basal Ganglia – Cordate & Lentiform Nucleus, (putamen/globus pallidus 1&2) Cerebellum

Double vision Stroke can affect the nerve fibers or the cranial nerve nuclei innervating eye muscles, leading to double vision. The nerves fibers can be damaged/stretched due to the infarction/oedema process.

Eye muscle movement controlled by Occulomotor nerve (CN III) – superior + inferior + medial recti, inferior oblique, levator palpebrae superioris Trochlear neve (CN IV) – superior oblique Abducent nerve (CN VI) – lateral rectus

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Upper Motor Neuron Lesion Spastic paralysis Hyperreflexia Babinski sign +ve Increased muscle tone Muscle weakness Atrophy of muscle b/c of disuse Decreased speed of voluntary movements Large area of the body invovled Lower Motor Neuron Lesion Flaccid paralysis Areflexia No Babinski Fasciculations Decreased muscle tone Atrophy of the muscles Loss of voluntary movements Small area of the body affected

References FitzGerald et al: Clinical Neuroanatomy & Neuroscience 5E Colledge et al: Davidson's Principles and Practice of Medicine 21E Dr. Parker lecture on Anatomy of the Motor System (NLE)