Stroke localization

Neurology, Stroke, Localization, Medicine, CVA, Cerebrovascular Accident, Diagnosis, MBBS, Clinical Neurology, simplified

1. CVA/ Stroke localization Arun George CMC Vellore

2. 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.

3. Risk Factors

4. What type of stroke is it ?       

5. 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.

6. Stroke types / frequency Ischemic 80% Thrombotic 60% Embolic 20% Hemorrhagic 20% Intracerebral hemorrhage 12% Subarachnoid hemorrhage 8%

7. Following clinical and bedside data are helpful Past , personal and family history History of old strokes or TIAs Time of onset of the symptoms Activity at the time of onset of the symptoms Temporal course and progression Accompanying symptoms – Headache, vomiting, decreased level of consciousness

8. Past, present . Personal and family history   Presence of diabetes &coronary heart disease Atherosclerotic Prior heart disease Embolic Hypertension * Hemorrhagic Pt on anticoagulant Hemorrhagic

9. Activity at onset   Classical teaching – Thrombotic strokes - during sleep – when the circulation is least active Hemorrhage and Embolism - during activity – when circulation is active

10. 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

11. 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).

12. 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

13. 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

14. 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

15. Internal capsule Anterior limb Genu Posterior limb Corticobulbar Corticospinal Sensory ( spinothalamic )

16. Retrolenticular and sublenticular parts of internal capsule – visual and auditory fibres

17. 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 .

18. 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 .

19. 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.

20. 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.

21. Cranial nerve nuclei 3, 4 – midbrain  PCA 5,6,7,8 - Pons  basilar artery 9,10,11,12 – Medulla  vertebral artery

22. Reticular formation – important role in arousal – situated in the brainstem Connections of the cerebellum with the spinal cord and cortex  traverse the brainstem

23. 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

24. 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

25. Vertebral artery  medulla and cerebellum Basilar artery  pons and cerebellum Posterior cerebral  midbrain, thalamus, hippocampus, occipital lobe, temporal lobe and cerebellum

26. Internal capsule – blood supply

27. 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

28. 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

29. Signs of cortical involvement Left hemisphere (dominant) – aphasia Right hemisphere (non dominant)– dressing/ constructional apraxia

30. 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 razor dominant hemisphere - parietal Constructional apraxia - unable to reproduce simple diagrams/ designs non dominant parietal Dressing apraxia Signs of cortical involvement

31. 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

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

33. Anomia / Alexia – Anomia is inability to name objects which are shown to the patient. Alexia inability to read Agraphia 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

34. Internal capsule stroke – preservation of consciousness Intracranial h’ge anywhere (even in int capsule) causes loss of consciousness secondary to raised ICT

35. 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

36. 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

37. Int capsule stroke - features Dense uncrossed hemiplegia – CN involved is same side of the hemiplegia commonly seen – UMN type of weakness in 7,12, 10 and 5 th cranial nerves UMN 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

38. Brainstem strokes Crossed hemiplegia LMN lesion of cranial nerves Vertigo Bilateral involvement Unconscious- reticular system is involved

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

40. 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

41. 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

42. hemorrhage SAH – rupture of berry aneurysm/ av malformation  H, V, meningeal signs, papilloedema , LOC Intracerebral h’ge : a. putamenal / capsular  dense uncrossed hemiplegia b. thalamic hemorrhage  hemi anesthesia +/- hemiparesis c. Pontine h’ge  deep coma, bilateral fixed pinpoint pupils, hyperpyrexia and decerebrate posturing d. cerebellar h’ge  repeated vomiting, occipital headache and meningeal signs

43. 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

44. 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

45. Pseudobulbar palsy capsular/cortical strokes – occur one after the other in both sides  bilateral infarct  10 th and 12 th 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 10 th and 12 th nerve lesion. Features of a medullary lesion are produced by b/l corticospinal tract infarction