Clinical approach to a case of Hemiplegia

1. Clinical evaluation of hemiplegia Dr. S. Aswini Kumar. MD 1

2. Anatomy of Brain Fore brain receiving sensory information from various sensory inputs of body processing the information received and correlating them with prior ones thinking, perceiving, producing and understanding language controlling motor function and autonomic functions Mid brain: auditory and visual responses Hind brain balancing equilibrium and co-ordination 2

3. Physiology of brain 3 Frontal lobe: Provides executive control over much of the brain's higher functions Consciousness, self-awareness, judgment, initiation, motivation Planning, sequencing, word formation, control over emotional responses Parietal lobe: Perceives, analyzes, and assembles touch information from the body Integrates visual, auditory, and touch information to formulate complete impression of the world Left - letters come together to form words and where words are put together in thoughts Right - recognizing shapes, being aware of one's body in space Temporal lobe: Hearing, memory acquisition, perception, and categorization of objects Comprehension of language, listening, reading; music Occipital lobe: Dedicated entirely to vision In terms of detection, identification, and interpretation of objects.

4. Handedness & Contra-laterality of brain control 90% of general population-right handed 10% left handed Handedness By birth not by training Test by natural skill; not learned skills Throwing stones, kicking football Determination of hemispherical dominance Right handed – 99% left dominant hemisphere Left handed 70% of left handed – left dominant hemisphere 4

5. Blood supply of brain 5

6. The Circle of Willis 6 Named after Thomas Willis (1621–1673) Anterior cerebral artery (left and right) Anterior communicating artery Internal carotid artery (left and right) Posterior cerebral artery (left and right) Posterior communicating artery (left and right) Physiologic significance In event of narrowed or blocked vessel preserve the cerebral perfusion avoid the symptoms of ischemia Considerable anatomic variation exists

7. The internal capsule 7 Anterior limb: lenticulostriate branches of middle cerebral artery (superior half) recurrent artery of Heubner off of the anterior cerebral artery (inferior half) Genu: lenticulostriate branches of middle cerebral artery Posterior limb: lenticulostriate branches of middle cerebral artery (superior half) anterior choroidal artery off of the internal carotid artery (inferior half)

8. Corticospinal tract 8 Originates from pyramidal cells in layer V of the cerebral cortex Axons that travel down through the brain stem and spinal cord - upper motor neurons Long axons to the motor cranial nerve nuclei mainly of the contralateral side of the midbrain (cortico-mesencephalic tract) pons (cortico-pontine tract) medulla oblongata (cortico-bulbar tract) spinal cord (corticospinal tract)

9. Pathophysiology of ischemic stroke 9

10. Ischemic penumbra and clinical significance 10 A central area of irreversible infarction the point of maximum insult called “core” Surrounding area of potentially reversible Called as ischemic penumbra. It has two different segments Inner area of diffusion abnormality Outer area of perfusion abnormality Hypoxia of the cells near the location of the original insult Target for revascularization if given within 60 minutes

11. History taking in Hemiplegia 11 When did the event start? When was he last found to be in a normal state? What is the total duration of the illness? If multiple, of each episode? What according to the patient or relatives were the initial presenting symptoms? What was the exact mode of onset; was it abrupt, sudden, sub-acute or gradual? When was the maximum deficit noted; was it in the beginning or later? What was the progress of the initial symptoms; static, progressing or regressing? What were the associated symptoms; in CNS as well as CVS, RES and GIT? What investigations he has under gone so far and what are the ones planned? What treatment the patient has received so far and what the ones planned?

12. History specific for assessing the CNS function 12 Was there any loss of consciousness in the beginning/later; did he recover from it? Is he able to co-operate in interview and the physical examination? What is the emotional state of the patient; memory and intelligence? Is speech affected and if so in what way? Motor, sensory or conductive aphasia? Which of the cranial nerves are affected and what are the symptoms related? What is the degree of motor weakness, wasting, flaccidity or stiffness of muscles? Are all the modalities of sensations normally appreciated or are they abnormal? Is the patient able to stand with/without support; swaying while standing/walking? Any symptoms of increased intra-cranial tension like headache or vomiting?

13. Precise and complete neurological examination 13 Confirms the presence of a stroke syndrome, distinguishes stroke from stroke mimics Evaluation of level of consciousness and mental status, speech and gait Cranial nerves, motor function, sensory function, superficial, deep tendon reflexes Special reference to Optic fundus - papilledema III – sign of uncalherniation VI – sign of increased ICT Signs of meningeal irritation Signs of head injury

14. 1. Is the patient having neurological problem? 14 Yes or No? Or is it only hysterical or malingering? Is it a medical condition simulating hemiplegia? Post ictal Todd’s paralysis, episode of multiple sclerosis? ADEM? If Yes what are the neurological deficits Hemiplegia, UMN Facial weakness, hemianesthesia, homonymous hemianopia Dysphasia in a right hemiplegia and dysarthria in a left hemiplegia Faciobrachialmonoplegia Crossed hemiplegia Cervical cord lesion?

15. 2. Which are the CNS structures involved? 15 Which are the CNS tracts involved? Pyramidal tract Extra-pyramidal tract Cerebellum Brainstem nucleii Cranial nerve II-papilledema, optic atrophy, III palsy, VI palsy VII UMN or LMN It is it an UMN lesion, LMN lesion of neuronal shock state of UMN lesion? Based on weakness, tone, presence of muscle atrophy or fasciculations A prolonged neuronal shock state predicts poor or late recovery

17. Upper half of face spared

18. Lower half affected

19. No Bell’s phenomenon

20. Taste not affected

21. LMN Facial Palsy

22. Entire half of face affected

23. Bell’s phenomenon present

24. Other signs of pontine lesion

26. 5. What is the site of localization of lesion? 18 Cortex Partial deficit, speech involvement, quadrantinopia, cortical sensory, focal seizures Sub-cortical region Denser lesion, Full hemiplegia, Internal capsule Dense hemiplegia, sparing of speech, absence of speech defects and seizures Thalamic Hemiparalysis, hemianopia, hemisensory loss and emerging hyperpathia Brain stem Crossed hemiplegia - Nuclear type of cranial nerve lesions + contralateralhemiplegia

27. 6. What is the possible pathology of the lesion? 19 Is it an ischemic infarct embolic infarct hemorrhagic infarct hemorrhagic transformation of an ischemic infarct hemorrhage Is there evidence of significant or dangerous cerebral edema? Its it a demyelination Acute Disseminated Encephalomyelitis or Episode of MS Is it a space occupying lesion: cerebral abscess cerebral tumor, cerebral secondaries

28. 7. Is it an ischemic stroke? 20 Blood supply to part of the brain is decreased, leading to dysfunction of the brain Cerebral atherosclerosis (producing flow limiting stenosis of a cerebral vessel) Thrombosis (obstruction of a blood vessel by a blood clot forming locally) Embolism (obstruction due to an embolus from elsewhere in the body) Systemic hypoperfusion (general decrease in blood supply, e.g. in shock) Venous thrombosis (infarcts are more likely to undergo hemorrhagic transformation) Clinical features Start suddenly, over seconds to minutes, and in most cases do not progress further Classically detected by the patient in the morning when waking up May or may not be preceded by episodes of transient ischemic attakcs

29. 8. Is it a TIA/evolving stroke/completed stroke? 21 Transient Ischemic Attacks Acute focal non-convulsive neurological dysfunction caused by reversible ischemia recovering in 24h Evolving stroke Deficit occurs in a progressive or step wise fashion culminating in major deficit In carotid territory within 24 hours and in vertebrobasilar territory within 72 hours Completed stroke The deficit is prolonged and permanent causing demonstrable parenchymal damage Most completed strokes reach the maximum neurological deficits within an hour of onset Reversible Ischemic Neurological deficit The neurological deficit lasts beyond 24 hours but resolves within 3 weeks

30. 9. Is it in carotid artery/vertebrobasilar territory? Contralateral weakness Contralateral numbness Dysphasia Dysarthria Ipsilateral mono-ocular Contralateral homonymous Combination of above Bilateral or shifting weakness Bilateral/shifting numbness Diplopia Dysarthria Inco-ordination of upper limbs Ataxia/imbalance/disequilibrium Visual loss in both homonymous ields 22 Carotid Vertebral

31. 10. Is it an Internal carotid artery syndrome Often asymptomatic Reason – collateral circulation Ext. carotid ophthalmic anastamosis Superficial/deep cervical Opposite carotid anterior segment Warning symptoms Episodes of confusion Speech dysfunction Amourosisfugax Fleeting paresthesia Neurological deficits Minimal neurological signs Same as that of MCA territory infarct Contralateralhemiplegia Contralateral sensory symptoms Local examination of carotid Feeble carotid pulsation Feeble temporal artery pulsation Cervical bruit over carotid Carotid doppler angiography 23

32. 11. Is it a Middle cerebral artery syndrome? Largest branch and continuation of ICA Most common site of ischemic stroke Clinical picture depends on site of occlusion: Stem, Superior, Inferior or LS Contralateral weakness Face UL LL Contralateralhemisensory loss Brocas, Wernecke, conduction, global aphasia Contralateral homonymous hemianopia or Qopia Paresis of conjugate gaze to opposite Gerstmann’s syndrome (dominant parietal) 24

33. 12. Is it a Anterior cerebral artery syndrome? 25 Areas supplied by the ACA include: Medial surface of the frontal lobe Anterior 4/5th of corpus callosum, parietal lobes Anterior 1/2 internal capsule and basal ganglia 1’ of lateral surface of frontal and parietal lobe If stroke occurs prior to ACoA (A1) well tolerated due to collateral circulation If stroke occurs distal to the ACoA (A2) Paralysis of the contralateral foot and leg Sensory loss in the contralateral foot and leg, Gait apraxia

34. 13. Is it a Anterior choroidal artery syndrome? 26 Supply blood to structures which include internal capsule & cruscerebri lateral geniculate body globuspallidus, tail of caudate nucleus Neurological deficits: ContralateralHemiplegia Contralateral hemihypesthesia Homonymous hemianopia These arise from ischemic damage to the posterior limb of the internal capsule

35. 14. Is it a Posterior cerebral artery syndrome? 27 Thalamic syndrome of Déjerine-Roussy Hemi-sensory loss along with hemiplegia Followed by an agonizing or searing pain Also termed as thalamic hyperpathia Other features: Persistent pain Aggravated by heat and cold Even by emotions of listening to music Responds poorly to analgesics. Up regulation of threshold for pain Once pain threshold is overcome

36. 15. Is it a crossed hemiplegia? 28 Weber Syndrome Ipsilateral III + Contrlateral HP Benedicts Syndrome Ipsilateral III + Contralateralhemiplegia and tremor Millard Gubler Syndrome Ipsilateral VI + VII + ContralateralHemiplegia Raymond Foville Ipsilateral VI + VII Medial Medullary Syndrome Ipsilateral XII +ContralateralHemiplegia Benedict’s Weber Raymond Foville Millard Gubler

37. 16. Is it cerebral embolism? 29 1. Cardiac sources – various sites Aortic root Native aortic valve Prosthetic aortic valve Left ventricular chamber Native mitral valve Prosthetic mitral valve Left atrial chamber Pulmonary veins 2. Non-cardiac source

38. 17. Is it a cardiac source of cerebral embolism? 30 Aortic root aneurysm with thrombus Aortic valve Endocarditis acute/subacute Aortic Prosthetic valve Tissue/mechanical Left ventricular mural thrombus Left ventricular aneurysm with thrombus Mitral valve stenosis-rheumatic in origin Mitral valve endocarditis Mitral valve prolapse Atrial fibrillation

39. 18. Is it a non-cardiac source of embolism? 31 Pulmonary venous thrombosis Suppurative lung – abscess, bronchiectasis Bronchogenic carcinoma – secondaries Air embolism Fat embolism Amniotic fluid embolism Paradoxical embolism – PFO Tetralogy of Fallot, Eisenmenger syndrome Carotid artery – cerebral artery embolism

40. 19. Is it a Hemorrhagic stroke? 32 Severe essential hypertension 55-75 years of age Smooth onset over minutes or hours steady progress in spite of treatment Features of increased ICT Types: Epidural/ Subdural Intra-parenchymal Intra-ventricular Sub-arachnoid Thalamic hemorrhage

42. 21. Is it a stroke mimic? Post ictal Todd’s paralysis Transient and follows aseizure Brain infections Fever, headache and papilledema Brain tumors Progressive headache, papilledema Demyelinating Disease (ADEM, MS) Recurrent episodes, distant lesions Hemi-parkinsonism Rigidity rather than spasticity Hypertensive Encephalopathy Accelerated hypertension, convulsion Subdural hematoma Waxing-waning neurological deficit Conversion disorder Stress situation underlying 34

43. Summary Basic Sciences Applied anatomy Functional components Handedness Hemispherical dominance Blood supply Circle of Willis Internal Capsule Corticospinal tract Pathophysiology Neurological Assessment TIA, RIND, Evolved/completed stroke Carotid/vertebrobasilar territory Localization: Cortical/internal capsule Arterial territory: MCA, ACA, AChA Thalamic/crossed hemiplegia Type: Ischemic, embolic, hemorrhage Cardiac/non-cardiac source Location of hemorrhage Young stroke/cerebral palsy 35

44. 36 Thank You