Cns clinical evaluation of hemiplegia slideshare upload

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Clinical approach to a case of Hemiplegia

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Cns clinical evaluation of hemiplegia slideshare upload

  1. 1. Clinical evaluation of hemiplegia<br />Dr. S. Aswini Kumar. MD<br />1<br />
  2. 2. Anatomy of Brain<br />Fore brain<br />receiving sensory information from various sensory inputs of body<br />processing the information received and correlating them with prior ones<br />thinking, perceiving, producing and understanding language<br />controlling motor function and autonomic functions<br />Mid brain: <br />auditory and visual responses<br />Hind brain<br />balancing equilibrium and co-ordination<br />2<br />
  3. 3. Physiology of brain<br />3<br />Frontal lobe: Provides executive control over much of the brain's higher functions<br />Consciousness, self-awareness, judgment, initiation, motivation <br />Planning, sequencing, word formation, control over emotional responses<br />Parietal lobe: Perceives, analyzes, and assembles touch information from the body<br /> Integrates visual, auditory, and touch information to formulate complete impression of the world <br />Left - letters come together to form words and where words are put together in thoughts <br />Right - recognizing shapes, being aware of one's body in space <br />Temporal lobe: Hearing, memory acquisition, perception, and categorization of objects<br />Comprehension of language, listening, reading; music  <br />Occipital lobe: Dedicated entirely to vision <br />In terms of detection, identification, and interpretation of objects. <br />
  4. 4. Handedness & Contra-laterality of brain control<br />90% of general population-right handed<br />10% left handed<br />Handedness<br />By birth not by training<br />Test by natural skill; not learned skills<br />Throwing stones, kicking football<br />Determination of hemispherical dominance<br />Right handed – <br />99% left dominant hemisphere<br />Left handed<br />70% of left handed – left dominant hemisphere<br />4<br />
  5. 5. Blood supply of brain<br />5<br />
  6. 6. The Circle of Willis<br />6<br />Named after Thomas Willis (1621–1673)<br />Anterior cerebral artery (left and right)<br />Anterior communicating artery<br />Internal carotid artery (left and right)<br />Posterior cerebral artery (left and right)<br />Posterior communicating artery (left and right)<br />Physiologic significance<br />In event of narrowed or blocked vessel<br />preserve the cerebral perfusion<br />avoid the symptoms of ischemia<br />Considerable anatomic variation exists<br />
  7. 7. The internal capsule<br />7<br />Anterior limb: <br />lenticulostriate branches of middle cerebral artery (superior half)<br />recurrent artery of Heubner off of the anterior cerebral artery (inferior half)<br />Genu: <br />lenticulostriate branches of middle cerebral artery<br />Posterior limb: <br />lenticulostriate branches of middle cerebral artery (superior half) <br />anterior choroidal artery off of the internal carotid artery (inferior half)<br />
  8. 8. Corticospinal tract<br />8<br />Originates from pyramidal cells in layer V of the cerebral cortex<br />Axons that travel down through the brain stem and spinal cord - upper motor neurons<br />Long axons to the motor cranial nerve nuclei mainly of the contralateral side of the <br />midbrain (cortico-mesencephalic tract) <br />pons (cortico-pontine tract) <br />medulla oblongata (cortico-bulbar tract)<br />spinal cord (corticospinal tract)<br />
  9. 9. Pathophysiology of ischemic stroke<br />9<br />
  10. 10. Ischemic penumbra and clinical significance<br />10<br />A central area of irreversible infarction <br />the point of maximum insult called “core”<br />Surrounding area of potentially reversible<br />Called as ischemic penumbra.<br />It has two different segments<br />Inner area of diffusion abnormality<br />Outer area of perfusion abnormality<br />Hypoxia of the cells near the location of the original insult<br />Target for revascularization if given within 60 minutes<br />
  11. 11. History taking in Hemiplegia<br />11<br />When did the event start? When was he last found to be in a normal state?<br />What is the total duration of the illness? If multiple, of each episode?<br />What according to the patient or relatives were the initial presenting symptoms?<br />What was the exact mode of onset; was it abrupt, sudden, sub-acute or gradual?<br />When was the maximum deficit noted; was it in the beginning or later?<br />What was the progress of the initial symptoms; static, progressing or regressing?<br />What were the associated symptoms; in CNS as well as CVS, RES and GIT?<br />What investigations he has under gone so far and what are the ones planned?<br />What treatment the patient has received so far and what the ones planned?<br />
  12. 12. History specific for assessing the CNS function<br />12<br />Was there any loss of consciousness in the beginning/later; did he recover from it?<br />Is he able to co-operate in interview and the physical examination?<br />What is the emotional state of the patient; memory and intelligence?<br />Is speech affected and if so in what way? Motor, sensory or conductive aphasia?<br />Which of the cranial nerves are affected and what are the symptoms related?<br />What is the degree of motor weakness, wasting, flaccidity or stiffness of muscles?<br />Are all the modalities of sensations normally appreciated or are they abnormal?<br />Is the patient able to stand with/without support; swaying while standing/walking?<br />Any symptoms of increased intra-cranial tension like headache or vomiting?<br />
  13. 13. Precise and complete neurological examination<br />13<br />Confirms the presence of a stroke syndrome, distinguishes stroke from stroke mimics<br />Evaluation of level of consciousness and mental status, speech and gait<br />Cranial nerves, motor function, sensory function, superficial, deep tendon reflexes<br />Special reference to<br />Optic fundus - papilledema<br />III – sign of uncalherniation<br />VI – sign of increased ICT<br />Signs of meningeal irritation<br />Signs of head injury<br />
  14. 14. 1. Is the patient having neurological problem?<br />14<br />Yes or No? <br />Or is it only hysterical or malingering?<br />Is it a medical condition simulating hemiplegia?<br />Post ictal Todd’s paralysis, episode of multiple sclerosis? ADEM?<br />If Yes what are the neurological deficits<br />Hemiplegia, UMN Facial weakness, hemianesthesia, homonymous hemianopia<br />Dysphasia in a right hemiplegia and dysarthria in a left hemiplegia<br />Faciobrachialmonoplegia<br />Crossed hemiplegia<br />Cervical cord lesion?<br />
  15. 15. 2. Which are the CNS structures involved?<br />15<br />Which are the CNS tracts involved?<br />Pyramidal tract<br />Extra-pyramidal tract<br />Cerebellum<br />Brainstem nucleii<br />Cranial nerve II-papilledema, optic atrophy, III palsy, VI palsy VII UMN or LMN<br />It is it an UMN lesion, LMN lesion of neuronal shock state of UMN lesion?<br />Based on weakness, tone, presence of muscle atrophy or fasciculations<br />A prolonged neuronal shock state predicts poor or late recovery<br />
  16. 16. 3. Is there UMN or LMN facial paralysis<br />16<br />Inspect the face at rest for voluntary & mimetic movements<br />Examine symmetry of eye blinking and speech motion<br />Ask to raise eyebrows (frontalis)<br />Close eyes (orbicularisoculi)<br />Bell’s phenomenon (Superior rectus)<br />Show teeth (orbicularisoris)<br />Blow out cheeks (buccinator)<br />Scrunch up nose (nasalis) <br />Retract chin (platysma)<br /><ul><li>UMN Facial palsy
  17. 17. Upper half of face spared
  18. 18. Lower half affected
  19. 19. No Bell’s phenomenon
  20. 20. Taste not affected
  21. 21. LMN Facial Palsy
  22. 22. Entire half of face affected
  23. 23. Bell’s phenomenon present
  24. 24. Other signs of pontine lesion
  25. 25. Taste affected</li></li></ul><li>4. In what way speech is affected?<br />17<br />First test spontaneous speech? – What the patient asks for in the morning – Broca’s aphasia<br />For tea/food/going to toilet<br />Now test the comprehension – Whether he understands the meaning of words - Wernickes<br />Give some simple commands “lift up the unaffected arm” “show the tongue”<br />Test for intactness of conduction pathway – Conductive aphasia<br />Whether the patient is able to repeat what the examiner says. Use a phrase<br />Test for naming – intactness of the arcuate bundle – Anomic aphasia<br />Show an object like a pen and ask to name it; not merely to handle it or even use it<br />Try whether the patient can read aloud? – Pure word blindness<br />Give a news paper and ask the patient to read aloud from it<br />Try whether a patient can understand spoken language? – Pure word deafness<br />inability to comprehend the meaning of speech, but still being able to hear, speak, read, and write. <br />
  26. 26. 5. What is the site of localization of lesion?<br />18<br />Cortex<br />Partial deficit, speech involvement, quadrantinopia, cortical sensory, focal seizures<br />Sub-cortical region<br />Denser lesion, Full hemiplegia, <br />Internal capsule<br />Dense hemiplegia, sparing of speech, absence of speech defects and seizures<br />Thalamic<br />Hemiparalysis, hemianopia, hemisensory loss and emerging hyperpathia<br />Brain stem<br />Crossed hemiplegia - Nuclear type of cranial nerve lesions + contralateralhemiplegia<br />
  27. 27. 6. What is the possible pathology of the lesion?<br />19<br />Is it an <br />ischemic infarct<br />embolic infarct<br />hemorrhagic infarct<br />hemorrhagic transformation of an ischemic infarct <br />hemorrhage<br />Is there evidence of significant or dangerous cerebral edema?<br />Its it a demyelination<br />Acute Disseminated Encephalomyelitis or Episode of MS<br />Is it a space occupying lesion: cerebral abscess cerebral tumor, cerebral secondaries<br />
  28. 28. 7. Is it an ischemic stroke?<br />20<br />Blood supply to part of the brain is decreased, leading to dysfunction of the brain<br />Cerebral atherosclerosis (producing flow limiting stenosis of a cerebral vessel)<br />Thrombosis (obstruction of a blood vessel by a blood clot forming locally)<br />Embolism (obstruction due to an embolus from elsewhere in the body)<br />Systemic hypoperfusion (general decrease in blood supply, e.g. in shock)<br />Venous thrombosis (infarcts are more likely to undergo hemorrhagic transformation)<br />Clinical features<br />Start suddenly, over seconds to minutes, and in most cases do not progress further<br />Classically detected by the patient in the morning when waking up<br />May or may not be preceded by episodes of transient ischemic attakcs<br />
  29. 29. 8. Is it a TIA/evolving stroke/completed stroke?<br />21<br />Transient Ischemic Attacks<br />Acute focal non-convulsive neurological dysfunction caused by reversible ischemia recovering in 24h<br />Evolving stroke<br />Deficit occurs in a progressive or step wise fashion culminating in major deficit<br />In carotid territory within 24 hours and in vertebrobasilar territory within 72 hours<br />Completed stroke<br />The deficit is prolonged and permanent causing demonstrable parenchymal damage<br />Most completed strokes reach the maximum neurological deficits within an hour of onset<br />Reversible Ischemic Neurological deficit<br />The neurological deficit lasts beyond 24 hours but resolves within 3 weeks<br />
  30. 30. 9. Is it in carotid artery/vertebrobasilar territory?<br />Contralateral weakness<br />Contralateral numbness<br />Dysphasia<br />Dysarthria<br />Ipsilateral mono-ocular<br />Contralateral homonymous <br />Combination of above<br />Bilateral or shifting weakness<br />Bilateral/shifting numbness<br />Diplopia<br />Dysarthria<br />Inco-ordination of upper limbs<br />Ataxia/imbalance/disequilibrium<br />Visual loss in both homonymous ields<br />22<br />Carotid<br />Vertebral<br />
  31. 31. 10. Is it an Internal carotid artery syndrome<br />Often asymptomatic<br />Reason – collateral circulation<br />Ext. carotid ophthalmic anastamosis<br />Superficial/deep cervical<br />Opposite carotid anterior segment<br />Warning symptoms<br />Episodes of confusion<br />Speech dysfunction<br />Amourosisfugax<br />Fleeting paresthesia<br />Neurological deficits<br />Minimal neurological signs<br />Same as that of MCA territory infarct<br />Contralateralhemiplegia<br />Contralateral sensory symptoms<br />Local examination of carotid<br />Feeble carotid pulsation<br />Feeble temporal artery pulsation<br />Cervical bruit over carotid<br />Carotid doppler angiography<br />23<br />
  32. 32. 11. Is it a Middle cerebral artery syndrome?<br />Largest branch and continuation of ICA<br />Most common site of ischemic stroke<br />Clinical picture depends on site of occlusion: Stem, Superior, Inferior or LS<br />Contralateral weakness Face UL LL<br />Contralateralhemisensory loss<br />Brocas, Wernecke, conduction, global aphasia<br />Contralateral homonymous hemianopia or Qopia<br />Paresis of conjugate gaze to opposite<br />Gerstmann’s syndrome (dominant parietal)<br />24<br />
  33. 33. 12. Is it a Anterior cerebral artery syndrome?<br />25<br />Areas supplied by the ACA include:<br />Medial surface of the frontal lobe <br />Anterior 4/5th of corpus callosum, parietal lobes<br />Anterior 1/2 internal capsule and basal ganglia<br />1’ of lateral surface of frontal and parietal lobe<br />If stroke occurs prior to ACoA (A1)<br />well tolerated due to collateral circulation<br />If stroke occurs distal to the ACoA (A2)<br />Paralysis of the contralateral foot and leg<br />Sensory loss in the contralateral foot and leg, Gait apraxia<br />
  34. 34. 13. Is it a Anterior choroidal artery syndrome?<br />26<br />Supply blood to structures which include<br />internal capsule & cruscerebri<br />lateral geniculate body<br />globuspallidus, tail of caudate nucleus<br />Neurological deficits:<br />ContralateralHemiplegia   <br />Contralateral hemihypesthesia<br />Homonymous hemianopia<br />These arise from ischemic damage to the posterior limb of the internal capsule<br />
  35. 35. 14. Is it a Posterior cerebral artery syndrome?<br />27<br />Thalamic syndrome of Déjerine-Roussy<br />Hemi-sensory loss along with hemiplegia<br />Followed by an agonizing or searing pain <br />Also termed as thalamic hyperpathia<br />Other features:<br />Persistent pain<br />Aggravated by heat and cold<br />Even by emotions of listening to music<br />Responds poorly to analgesics. <br />Up regulation of threshold for pain <br />Once pain threshold is overcome<br />
  36. 36. 15. Is it a crossed hemiplegia?<br />28<br />Weber Syndrome<br />Ipsilateral III + Contrlateral HP<br />Benedicts Syndrome<br />Ipsilateral III + <br />Contralateralhemiplegia and tremor<br />Millard Gubler Syndrome<br />Ipsilateral VI + VII + ContralateralHemiplegia<br />Raymond Foville<br />Ipsilateral VI + VII<br />Medial Medullary Syndrome<br />Ipsilateral XII +ContralateralHemiplegia<br />Benedict’s<br />Weber<br />Raymond Foville<br />Millard Gubler<br />
  37. 37. 16. Is it cerebral embolism?<br />29<br />1. Cardiac sources – various sites<br />Aortic root<br />Native aortic valve<br />Prosthetic aortic valve<br />Left ventricular chamber<br />Native mitral valve<br />Prosthetic mitral valve<br />Left atrial chamber<br />Pulmonary veins<br />2. Non-cardiac source<br />
  38. 38. 17. Is it a cardiac source of cerebral embolism?<br />30<br />Aortic root aneurysm with thrombus<br />Aortic valve Endocarditis acute/subacute<br />Aortic Prosthetic valve Tissue/mechanical <br />Left ventricular mural thrombus<br />Left ventricular aneurysm with thrombus<br />Mitral valve stenosis-rheumatic in origin<br />Mitral valve endocarditis<br />Mitral valve prolapse<br />Atrial fibrillation<br />
  39. 39. 18. Is it a non-cardiac source of embolism?<br />31<br />Pulmonary venous thrombosis<br />Suppurative lung – abscess, bronchiectasis<br />Bronchogenic carcinoma – secondaries<br />Air embolism<br />Fat embolism<br />Amniotic fluid embolism<br />Paradoxical embolism – PFO<br />Tetralogy of Fallot, Eisenmenger syndrome<br />Carotid artery – cerebral artery embolism<br />
  40. 40. 19. Is it a Hemorrhagic stroke?<br />32<br />Severe essential hypertension <br />55-75 years of age<br />Smooth onset over minutes or hours <br />steady progress in spite of treatment<br />Features of increased ICT<br />Types:<br />Epidural/ Subdural<br />Intra-parenchymal<br />Intra-ventricular<br />Sub-arachnoid<br />Thalamic hemorrhage<br />
  41. 41. 20. Is it a Young stroke?<br />Embolic stroke<br />Carotid artery dissection<br /><ul><li>Procoagulant states: SLE, TTP, DIC</li></ul>Polycythemia<br />B Thalassemia<br />Sickle Cell disease<br />Protein S deficiency<br />Protein C deficiency<br />Factor V Leiden mutation<br />Hyperhomocystinemia<br />Antiphospholipid antibodies<br />Vasculitis<br />PAN, Waegner’s,Takayasu’s, GCA<br />Primary CNS Vasculitis<br />Secondary to Meningits<br />Subarachnoid Hemorrhage<br />Miscellaneous<br />Oral contraceptives<br />Eclampsia of pregnancy<br />Cocaine and amphetamine<br />Fibromuscular dysplasia<br />33<br />
  42. 42. 21. Is it a stroke mimic?<br />Post ictal Todd’s paralysis<br />Transient and follows aseizure<br />Brain infections<br />Fever, headache and papilledema<br />Brain tumors<br />Progressive headache, papilledema<br />Demyelinating Disease (ADEM, MS)<br />Recurrent episodes, distant lesions<br />Hemi-parkinsonism<br />Rigidity rather than spasticity<br />Hypertensive Encephalopathy<br />Accelerated hypertension, convulsion<br />Subdural hematoma<br />Waxing-waning neurological deficit<br />Conversion disorder<br />Stress situation underlying<br />34<br />
  43. 43. Summary<br />Basic Sciences<br />Applied anatomy<br />Functional components<br />Handedness<br />Hemispherical dominance<br />Blood supply<br />Circle of Willis<br />Internal Capsule<br />Corticospinal tract<br />Pathophysiology<br />Neurological Assessment<br />TIA, RIND, Evolved/completed stroke<br />Carotid/vertebrobasilar territory<br />Localization: Cortical/internal capsule<br />Arterial territory: MCA, ACA, AChA<br />Thalamic/crossed hemiplegia<br />Type: Ischemic, embolic, hemorrhage<br />Cardiac/non-cardiac source<br />Location of hemorrhage<br />Young stroke/cerebral palsy<br />35<br />
  44. 44. 36<br />Thank You<br />

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