Hemiplegia

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Hemiplegia

  1. 1. Hemiplegia By Dr. Osman Sadig Bukhari
  2. 2. <ul><li>1- lecture at 8:30 </li></ul><ul><li>2- No student is allowed to attend za lecture </li></ul><ul><li>after 8:45 & is considered as absen </li></ul>
  3. 3. <ul><li>- Hemiplegia : </li></ul><ul><li>Complete loss of power or weakness on </li></ul><ul><li>one side of za body </li></ul><ul><li>- Hemiparesis: </li></ul><ul><li>Incomplete loss of power or weakness on </li></ul><ul><li>one side of za body </li></ul><ul><li>Hemiplegia & hemiparesis are most commonly due to stroke i.e. CVA . </li></ul>
  4. 6. <ul><li>Stroke is: </li></ul><ul><li>- is za 3 rd commonest cause of death and </li></ul><ul><li>disability in za developed world </li></ul><ul><li>- mortality from stroke is 20-30% in the </li></ul><ul><li>1 st month & 60% of survivors are dependant. </li></ul><ul><li>- prevalence is2- 5 /1000/year & it is rising because of the aging population. </li></ul><ul><li>- male > females </li></ul>
  5. 7. <ul><li>Risk factors for hemiplegia </li></ul><ul><li>1- Non modifiable factors </li></ul><ul><li>- age - gender </li></ul><ul><li>- race - hereditary </li></ul><ul><li>2- Modifiable factors </li></ul><ul><li>- Arterial HT - Cardiac diseases </li></ul><ul><li>- DM - Cigarette smoking </li></ul><ul><li>- Hyperlipidaemia - Thrombocythemia </li></ul><ul><li>- Polycythemia - Physical inactivity </li></ul><ul><li>- Obesity - OCPs </li></ul><ul><li>- High alcohol intake - Trauma </li></ul><ul><li>- Peripheral vascular disease </li></ul>
  6. 8. <ul><li>Stroke is: </li></ul><ul><li>uncommon before 40years except with: </li></ul><ul><li>- trauma </li></ul><ul><li>- cardiac diseases e.g RHD </li></ul><ul><li>- congenital vascular abn </li></ul><ul><li>- inflammatory arteritis </li></ul><ul><li>- vascular disease </li></ul><ul><li>- SS anaemia </li></ul>
  7. 9. <ul><li>Hemiplegia is either due to: 1- Thromboembolic infarction (ischemic) (80%): thrombosis/embolism </li></ul><ul><li>2- Haemorrhage (15%): </li></ul><ul><li>intracerebral/ subarachnoid </li></ul><ul><li>3- Dissection of carotid & vertebral arteries </li></ul><ul><li>4- Cortical venous or dural venous sinus thromb </li></ul><ul><li>5- Subdural & extradural bleeding </li></ul><ul><li>Site of stroke </li></ul><ul><li>- internal capsule - brainstem </li></ul><ul><li>- cerebral cortex - basal ganglia </li></ul><ul><li>- cerebellum </li></ul>
  8. 10. <ul><li>Mechanism of stroke: </li></ul><ul><li>1- Cerebral infarction (Ischemic) </li></ul><ul><li>- thrombosis at za site of atheroma </li></ul><ul><li>- embolism to a cerebral artery from </li></ul><ul><li>- extracranial vessels </li></ul><ul><li>- heart </li></ul><ul><li>* cerebral oedema may complicate infarction </li></ul><ul><li>and impair blood supply & cause further </li></ul><ul><li>damage </li></ul>
  9. 11. <ul><li>2- Cerebral haemorrhage </li></ul><ul><li>- subarachnoid haemorrhage </li></ul><ul><li>- ruptured beri aneurysm </li></ul><ul><li>- ruptured AVM </li></ul><ul><li>- intracerebral haemorrhage </li></ul><ul><li>- rupture of perforating vessels weakened </li></ul><ul><li>by HT or atheromatous degeneration </li></ul><ul><li>( micro aneurysm= 0.8-1.0 mm) </li></ul><ul><li>- rupture of aneurysms or AVM </li></ul><ul><li>* SAH arterial spasm & cerebral infarction </li></ul><ul><li>* ICH may extend to subarachnoid space. </li></ul>
  10. 12. <ul><li>* Disability from stroke depends on the </li></ul><ul><li>site & extent of damage </li></ul><ul><li>* Cerebellar hage can be fatal if there is </li></ul><ul><li>compression of brain stem. </li></ul>
  11. 13. <ul><li>Clinical classification of stroke </li></ul><ul><li>1 - Transient ischemic attack (TIA): sudden </li></ul><ul><li>loss of focal neurological fn lasting < 24hrs. 2- Completed stroke : loss of focal neurological fn with symptoms lasting > 24hrs. </li></ul><ul><li>- Major stroke </li></ul><ul><li>- Minor stroke ( recovery in 1-2Ws), RIND. </li></ul>
  12. 14. <ul><li>3- Evolving stroke (stroke –in-evolution ) </li></ul><ul><li>symptoms worsening gradually or in </li></ul><ul><li>stepwise fashion over hrs or days or Ws involving adjacent motor or sensory sites within za distribution of a major cerebral artery (DD= tumour, SDH). </li></ul>
  13. 15. <ul><li>Disorders causing stroke comprises: </li></ul><ul><li>1- Thromboembolic disease (infarction) </li></ul><ul><li>- atherosclerosis </li></ul><ul><li>- arteriosclerosis (HT, degenerative) </li></ul><ul><li>- embolism (20%) </li></ul><ul><li>- arteritis (syph, TA, PAN, SLE) </li></ul><ul><li>- dissection (spontaneous, traumatic) </li></ul><ul><li>- Vasospasm (migraine, SAH, angiogr) </li></ul><ul><li>- hyper viscosity (PRV) </li></ul><ul><li>- anti phospholipid syndrome </li></ul><ul><li>- SS disease - hypotension - OCPs </li></ul>
  14. 16. <ul><li>2- Haemorrhage( intracerebral in 50% & 50% SAH </li></ul><ul><li>- rupture of a vessel or micro aneurysm in HT </li></ul><ul><li>- AVM </li></ul><ul><li>- Beri aneurysms </li></ul><ul><li>- Degenerative aneurysms </li></ul><ul><li>- HT arteriolar aneurysms </li></ul><ul><li>- Mycotic aneurysms </li></ul><ul><li>- Anticoagulants, thrombolytic therapy </li></ul><ul><li>- Bleeding disorders (ITP, DIC, haemophilia) </li></ul><ul><li>- Alcohol, cocaine, amphetamine. </li></ul><ul><li>- Sub dural or extra dural bleeding </li></ul>
  15. 17. <ul><li>Clinical features of stroke </li></ul><ul><li>Depends on za site & extent & involves a combination of features that may include: </li></ul><ul><li>- hemiparesis - loss of speech </li></ul><ul><li>- hemianaethesia </li></ul>
  16. 18. <ul><li>- The clinical onset is often rapid and reaches max within few hours - Unilateral weakness +/- dysphasia is the commonest presentation. </li></ul><ul><li>- Hypotonia, depressed reflexes and extensor reflex occur initially, followed later by hypertonia, hyper reflexia & extensor planter </li></ul><ul><li>response </li></ul><ul><li>- There may be impaired consciousness because of brain oedema (+/- papilloedema). </li></ul>
  17. 19. <ul><li>- With severe strokes flaccid paralysis is </li></ul><ul><li>accompanied by HA, vomiting, seizures </li></ul><ul><li>gaze paresis, impaired consciousness +/- papilloedema 2ndry to cerebral oedema - - Ataxia & hemisensory loss occur with deeply </li></ul><ul><li>seated lacunar infarcts. </li></ul>
  18. 20. <ul><li>- Monoparesis or dysphasia occur wz cortical lesions - Hemianaethesia & visual fields defects </li></ul><ul><li>- With brain stem lesions C/f depends on the structures involved. The cardinal feature is ipsilateral nuclear signs and contralateral pyramidal and S/T tract lesions signs ( crossed ). Coma may occur due to damage to reticular activating system. </li></ul><ul><li>- Recovery from stroke takes days, weeks or </li></ul><ul><li>months. </li></ul>
  19. 21. <ul><li>** In cerebral hage there is profound hemiplegia </li></ul><ul><li>from the start </li></ul><ul><li>** The onset in cerebral emboli is abrupt with </li></ul><ul><li>clear predisposing factor </li></ul><ul><li>** In cerebral thrombosis there is usually no </li></ul><ul><li>coma </li></ul><ul><li>** In HT encephalopathy the BP is very high </li></ul><ul><li>** Always consider head injury & intra cranial </li></ul><ul><li>bleeding in pts with hemiplegia. </li></ul>
  20. 22. <ul><li>Differential diag of acute stroke </li></ul><ul><li>1- cerebral tumours </li></ul><ul><li>2- subdural haematoma </li></ul><ul><li>3- cerebral abscess, cysts </li></ul><ul><li>4- Todd's paralysis </li></ul><ul><li>5- demyelinating disorders </li></ul><ul><li>6- hypoglycemia </li></ul><ul><li>7- encephalitis </li></ul><ul><li>8- hysterical conversion </li></ul><ul><li>- eye lids firmly shut, pt resisting opening </li></ul><ul><li>- normal corneal reflex </li></ul><ul><li>- normal caloric response is diagnostic. </li></ul>
  21. 23. <ul><li>Investigation of stroke </li></ul><ul><li>1- Investigations to confirm the diagnosis </li></ul><ul><li>Is it ischemic or haemorrhagicgic?? - CT brain - MRI </li></ul><ul><li>- MRA - L puncture. </li></ul><ul><li>* Exclusion of hage is important if any form of </li></ul><ul><li>anti thrombotic therapy is contemplated. </li></ul>
  22. 24. Rt cerebral haemorrhage
  23. 25. Rt cerebral infarction
  24. 26. Subdural haematoma
  25. 27. <ul><li>2- Investigations to establish za underlying </li></ul><ul><li>disease and the possibility of a treatable </li></ul><ul><li>cause : </li></ul><ul><li>a/ embolism from the heart b/ embolism from large arteries c/ temporal arteritis d/surgical treatable hage. - ECG - CXR - Echo Doppler US - Carotid angiography </li></ul>
  26. 28. <ul><li>3- Investigations to identify risk factors : </li></ul><ul><li>CBC, blood sugar, lipid profile, serology </li></ul><ul><li>for syphilis, clotting studies, serology for </li></ul><ul><li>collagen diseases, blood cultures for </li></ul><ul><li>SBE is suspected, sickling test, tests for </li></ul><ul><li>thrombophilia (protein C & S, anti thrombin 3) </li></ul>
  27. 29. <ul><li>Management of Hemiplegia </li></ul><ul><li>The aim is :- </li></ul><ul><li>1- To minimize brain damage </li></ul><ul><li>2- To reduce disability through rehabilitation </li></ul><ul><li>3- To prevent complications </li></ul><ul><li>4- To treat za underlying cause . </li></ul><ul><li>5-To prevent za recurrence of stroke </li></ul><ul><li>6- To refer pts wz SAH to neurosurgery . </li></ul><ul><li>** To admit or not depends on za clinical </li></ul><ul><li>state & facilities at home ( TIAs & min </li></ul><ul><li>stroke at home) </li></ul>
  28. 30. <ul><li>No specific treatment is available for most pts with stroke, so their immediate management is supportive with General measures : </li></ul><ul><li>- ABC </li></ul><ul><li>- nursing care </li></ul><ul><li>- fluid balance & nutrition= NG feeding and </li></ul><ul><li>hydration. TR of infections. </li></ul><ul><li>- urinary cath if not continent </li></ul><ul><li>- physiotherapy, occupational, speech </li></ul><ul><li>and psychotherapy. </li></ul>
  29. 31. <ul><li>Med treatment: </li></ul><ul><li>1- Anti hypertensives not given at the </li></ul><ul><li>start unless very high (> 180/110) </li></ul><ul><li>as some pts show reactive increase in BP. </li></ul><ul><li>It is gradually lowered after za 1 st week </li></ul>
  30. 32. <ul><li>2- Anti platelets reduce za incidence of </li></ul><ul><li>stroke by 25% e.g. aspirin 75-300mg </li></ul><ul><li>dipyridamol 75 tds, clopidogrel </li></ul><ul><li>3 - Anti coagulants only if there is a </li></ul><ul><li>source of emboli & avoided in za 1 st </li></ul><ul><li>2Ws following infarction. It may be </li></ul><ul><li>used in evolving stroke, but C/I in </li></ul><ul><li>intra cranial hage & cerebral tumours </li></ul><ul><li>which should be rouled out by CT </li></ul>
  31. 33. <ul><li>4- Thrombolysis (tpA) in USA given within </li></ul><ul><li>3 hours of cerebral infarction. </li></ul><ul><li>5- Manitol 200ml 20% & dexamethazone </li></ul><ul><li>reduce mortality in pts with brain oedema </li></ul><ul><li>2ndry to severe stroke (dilating pupils, </li></ul><ul><li>increasing BP & reduced PR= Cushing’s </li></ul><ul><li>sign). </li></ul><ul><li>6- Baclofe n (GABA antagonist) for spasticity </li></ul>
  32. 34. <ul><li>Surgical treatment: </li></ul><ul><li>1- carotid endarterectomy in TIAs and </li></ul><ul><li>minor stroke when stenosis is > 70%. It </li></ul><ul><li>reduces incidence of stroke by 75%. </li></ul><ul><li>Avoided over in pts 65 years. </li></ul><ul><li>2 - surgical evacuation of haematoma if </li></ul><ul><li>accessible & if pat continue to deteriorate e.g cerebellar hage to prevent brainstem compression. </li></ul>
  33. 35. <ul><li>Rehabilitation: </li></ul><ul><li>- identify risk factors & treat </li></ul><ul><li>- TR 2ndry depression </li></ul>
  34. 36. <ul><li>Secondary prevention of stroke </li></ul><ul><li>1- control of cardiovascular risk factors </li></ul><ul><li>2- control of HT </li></ul><ul><li>3- long term anti platelet therapy unless the </li></ul><ul><li>stroke was hagic </li></ul><ul><li>4- Pts with atrial fibrillation should be considered </li></ul><ul><li>for anti coagulation & if there is a major </li></ul><ul><li>CI should receive anti platelets </li></ul>
  35. 37. <ul><li>Primary prevention of stroke </li></ul><ul><li>1- control of HT </li></ul><ul><li>2- control of DM </li></ul><ul><li>3- stopping of smoking </li></ul><ul><li>4- lowering of lipid levels </li></ul><ul><li>5- anti coagulation in atrial fibrillation if no CI </li></ul><ul><li>6- reducing Hb in polycythemia vera </li></ul><ul><li>7- diagnosis & surgical TR of carotid atheroma </li></ul>
  36. 38. <ul><li>Complications of acute stroke </li></ul><ul><li>- pneumonia - dehydration </li></ul><ul><li>- hyponatraemia - hypoxaemia </li></ul><ul><li>- hypoglycemia - DVT </li></ul><ul><li>- seizures - subluxation of joints </li></ul><ul><li>- frozen shoulder - pressure sores </li></ul><ul><li>- UTI - constipation </li></ul>
  37. 39. <ul><li>Prognosis: </li></ul><ul><li>- 25% die as a direct result of stroke. </li></ul><ul><li>More in hagic stroke. </li></ul><ul><li>- 50-75% who survive stroke achieve functional </li></ul><ul><li>independency in 3Ms </li></ul><ul><li>- poor outcome in pts wz deep coma and </li></ul><ul><li>dense hemiplegia </li></ul><ul><li>- mortality during za 1 st month is about 40-50% </li></ul><ul><li>from extension of za cerebral damage, aspirat </li></ul><ul><li>pneumonia & DVT wz pulmonary embolism. </li></ul><ul><li>- recurrent stroke occur in 5-10%/ year </li></ul><ul><li>- patient may die of cardiovascular disease. </li></ul>

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