CVA/ Stroke localization

Arun GeorgeCMC Vellore

• Stroke (or ‘Cerebrovascular accident’) is a syndrome of rapidly developing clinical signs of focal (or global) disturbance of cerebral function, with symptoms lasting 24 hours or longer or leading to death with no apparent cause other than of vascular origin.

• Transient Ischaemic Attack (TIA) or ‘mini stroke’ is where those symptoms resolve in 24 hours (usually under 30 minutes).

• Strokes are divided into those with an ischaemic or haemorrhagic cause.

Risk Factors

What type of stroke is it ?

Etiology

• Evidence of thrombosis: progressive deterioration, atherosclerosis risk factors, a carotid bruit.

• Evidence of embolism: Abrupt onset, history of atrial fibrillation, Recent Myocardial infarction, Prior TIA/ Stroke.

• Evidence of haemorrhage: abrupt onset, headaches, fits, hypertension risk factors, rapid decrease in level of consciousness.

Stroke types / frequency

Ischemic 80%• Thrombotic 60%• Embolic 20%

Hemorrhagic 20%• Intracerebral hemorrhage 12%• Subarachnoid hemorrhage 8%

Following clinical and bedside data are helpful

1. Past , personal and family history2. History of old strokes or TIAs3. Time of onset of the symptoms4. Activity at the time of onset of the symptoms5. Temporal course and progression6. Accompanying symptoms – Headache, vomiting,

decreased level of consciousness

Past, present . Personal and family history 1. Presence of diabetes &coronary heart disease Atherosclerotic2. Prior heart disease Embolic 3. Hypertension *

Hemorrhagic4. Pt on anticoagulant Hemorrhagic

Activity at onset Classical teaching – Thrombotic strokes - during sleep – when the

circulation is least activeHemorrhage and Embolism - during activity –

when circulation is active

Cortical stroke

If the cerebral cortex is involved, the CNS pathways can be but can also produce the following symptoms:• Aphasia (inability to speak or understand

language from involvement of Wernicke’s or Broca’s area)

• Apraxia (altered voluntary movement)• Visual field defect

• Memory Deficits (involvement of Temporal lobe)

• Hemi neglect (involvement of the Parietal lobe)

• Disorganised thinking, confusion, hypersexual gestures (with involvement of the frontal lobe)

• Anosognosia (persistent denial of the existence of a, usually stroke-related deficit).

Frontal lobes• executive function, movement and behavior. • primary motor cortex• Broca’s speech area • micturition center• inferior frontal lobes may be associated with anosmia.• behavioral disturbance.

1. medial frontal lesions- withdrawn, unresponsive and mute (abulic), and this is often associated with urinary incontinence, gait apraxia and the type of increase in tone known as gegenhalten.

2. lateral convexity lesions of the frontal lobes become disinhibited

Parietal

• Nondominant Parietal Lobe (Usually the Right one) does Intellectual Processing of Sensory Information for Visual-Spatial Tasks

• Right Parietal Lobe Lesion - refuses to accept there is a problem, Neglects the left side, has Constructional Apraxia

Temporal

• Cerebral Cortex part that does Emotion, Memory, Language

• Commonly affected by Herpes Virus• Medial Temporal Lobe Lesion causes learning

impairment but spares short and long-term memory• Dominant Temporal Lobe Lesion - Euphoria, Auditory

Hallucinations, Delusions, Thought Disorders• Right Temporal Lobe Lesion - Irritability, Dec Visual

and Music Ability

Internal capsule

• Anterior limb

• Genu

• Posterior limb

CorticobulbarCorticospinalSensory (spinothalamic)

• Retrolenticular and sublenticular parts of internal capsule – visual and auditory fibres

• The corticospinal tract conducts impulses from the brain to the spinal cord.

• It contains mostly axons originated from the motor cortex. • The corticospinal tract is made up of two separate tracts in

the spinal cord: the lateral corticospinal tract and the anterior corticospinal tract.

• left hemisphere of the brain controls the right side of the body, while the right hemisphere of the brain controls the left side of the body. The signals cross in the medulla oblongata, this process is also known as decussation.

• The spinothalamic tract is a sensory pathway originating in the spinal cord.

• The pathway decussates at the level of the spinal cord, rather than in the brainstem like the posterior column-medial lemniscus pathway and corticospinal tract.

There are two main parts of the spinothalamic tract (STT):

• The lateral spinothalamic tract transmits pain and temperature.

• The anterior spinothalamic tract (or ventral spinothalamic tract) transmits crude touch and pressure.

posterior column-medial lemniscus pathway, PCML

•sensory pathway responsible for transmitting fine touch, vibration and conscious proprioceptive information from the body to the cerebral cortex; as well as tactile pressure, barognosis, graphesthesia, stereognosis, recognition of texture, kinesthesia and two-point discrimination.

The name comes from the two structures that the sensation travels up: the posterior (or dorsal) columns of the spinal cord, and the medial lemniscus in the brainstem.

Crosses over at medulla.

Cranial nerve nuclei

• 3, 4 – midbrain PCA• 5,6,7,8 - Pons basilar artery• 9,10,11,12 – Medulla vertebral artery

• Reticular formation – important role in arousal – situated in the brainstem

• Connections of the cerebellum with the spinal cord and cortex traverse the brainstem

• Cerebellar signs may be produced by the lesions in the brainstem

• Respi, CVS centres – in medulla

• Cerebellar peduncles – superior, middle and inferior arises from midbrain, pons and medulla respectively

Internal carotid branches and their blood supply

• Anterior cerebral artery Medial surface of the hemisphere and internal capsule

• Middle cerebral Lateral surface of the hemisphere, basal ganglia and internal capsule

• Post communicating artery – internal capsule• Ant choroidal artery – internal capsule• Ophthalmic artery - eye

• Vertebral artery medulla and cerebellum

• Basilar artery pons and cerebellum

• Posterior cerebral midbrain, thalamus, hippocampus, occipital lobe, temporal lobe and cerebellum

Internal capsule – blood supply

Middle cerebral occlusion

• Motor aphasia – frontal lobe• Sensory aphasia – superior temporal gyrus• Cortical sensory loss – parietal lobe• Homonymous hemianopia – visual radiation• Motor paralysis – internal capsule, motor

cortex

DDx of Stroke

• Chronic subdural hematoma – hx of trauma, headache and drowsiness >> hemiparesis

• Glioblastoma multiforme – rapidly growing tumor – no recognisable vascular territories, progression over days; papilloedema

• Metastasis – CXR, CT to rule out

Signs of cortical involvement

• Left hemisphere (dominant) – aphasia • Right hemisphere (non dominant)– dressing/

constructional apraxia

• Apraxia is the inability to perform learned motor acts on command due to a lesion in the cerebral hemisphere

• Ideomotor apraxia – unable to do simple motor acts on command. Eg: use a razordominant hemisphere - parietal

• Constructional apraxia- unable to reproduce simple diagrams/ designsnon dominant parietal

• Dressing apraxia

Signs of cortical involvement

• Neglect – parietal cortex being unaware of the hemiplegia (anosognosis), ignoring the paralyzed half of the body

• Jacksonian seizures• Cortical sensory loss – two point

discrimination, graphaesthesia, stereognosis

• Frontal lobe dysfunction – weakness of one or both legs occur with ACA occlusionfeatures include frontal lobe release signs like sucking, snout, glabellar tap, grasp, palmomental, urinary incontinence, easy distractability, behavioural, personality and memory disturbances

• Anomia/ Alexia –Anomia is inability to name objects which are shown to the patient.Alexia inability to readAgraphia inability to write

Anomia for faces

• Cortical blindness – blindness due to b/l homonymous hemianopia and presence of pupillary response and normal optic disc on fundoscopy; patient unaware of his blindness as he has areas of intact vision

• Korsakoff’s amnesic state – profound loss of recent memory. Usually associated with bilateral or unilateral homonymous hemianopia; due to infarction of hippocampus

• Internal capsule stroke – preservation of consciousness

• Intracranial h’ge anywhere (even in int capsule) causes loss of consciousness secondary to raised ICT

• Broca’s area (in inf frontal gyrus)– superior division of MCA

• Sensory aphasia (sup temporal gyrus) – inferior division of MCA)

• Conduction aphasia (parietal cortex) – sup division of MCA

• Global aphasia – Internal carotid artery occlusion or main trunk occlusion of MCA

• Apraxia, Neglect, Focal seizures, Cortical sensory loss – sup. Division of MCA

• Frontal lobe signs – ACA• Anomia/ Alexia, Anomia for faces – PCA• Cortical blindness – occipital lobe – Basilar

artery• Korsakoff’s amnesic state – hippocampus- PCA

Int capsule stroke - features

• Dense uncrossed hemiplegia – CN involved is same side of the hemiplegiacommonly seen – UMN type of weakness in 7,12, 10 and 5th cranial nervesUMN type of weakness in these cranial nerves due to involvement of corticobulbar fibres in the genu of the internal capsule

• Absence of cortical involvement – no aphasia• Preservation of consciousness • Rapid recovery associated with power

Brainstem strokes

• Crossed hemiplegia• LMN lesion of cranial nerves• Vertigo• Bilateral involvement• Unconscious- reticular system is involved

• Consensual reflex – because of b/l innervation of the edinger westphal nucleus by the fibres carrying the light reflex

• CN 3,4,6 – no UMN lesions (as they have bilateral innervation)

• CN 5 – jaw jerk exaggerated in UMN, diminished in LMN lesion

• CN 7 – LMN both Upper and Lower part of face affected; UMN only lower part affected

• CN 12 – longstanding LMN lesions produce fasciculations and wasting on the affected side

Note

• Absent corneal reflex, absent sensation in affected area of the face LMN lesion of CN 5

• Absent sensations over the palate, pharynx and post. third of the tongue – LMNL of CN 10

• Vertigo = brainstem stroke due to vestibular nuclei (largest nuclei, spread over a great length of the brainstem)

• Bilateral involvement – in brainstem lesion basilar occlusion or brainstem damage

hemorrhage

• SAH – rupture of berry aneurysm/ av malformation H, V, meningeal signs, papilloedema, LOC

• Intracerebral h’ge: a. putamenal/ capsular dense uncrossed hemiplegiab. thalamic hemorrhage hemi anesthesia +/- hemiparesisc. Pontine h’ge deep coma, bilateral fixed pinpoint pupils, hyperpyrexia and decerebrate posturingd. cerebellar h’ge repeated vomiting, occipital headache and meningeal signs

• Thrombosis – a/c onset, stepwise increase, consciousness preserved (except brainstem strokes)

• Embolism – acute, maximal deficit at onset; probably Hx of a cardiac lesion – MS

• Hemorrhage – a/c onset, gradual development of deficit over 10-30 minutes; LOC common can go into coma

• Pure motor hemiplegia – internal capsule or pontine lesion

• Pure sensory stroke – thalamus• Dysarthria, clumsy hand syndrome –

dysarthria, facial palsy, ataxia of the hand lesion in the internal capsule or pons

Pseudobulbar palsy

• capsular/cortical strokes – occur one after the other in both sides bilateral infarct 10th and 12th gone in both sides like in a bulbar palsy. This is characterised by dysphagia, dysphonia, dysarthria, emotional lability. Basically it’s a b/l UMN type of 10th and 12th nerve lesion.

• Features of a medullary lesion are produced by b/l corticospinal tract infarction