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Hemiplegia Hemiplegia By Dr. Osman Sadig Bukhari By Dr. Osman Sadig Bukhari
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Page 1: Hemiplegia

HemiplegiaHemiplegiaBy Dr. Osman Sadig BukhariBy Dr. Osman Sadig Bukhari

Page 2: Hemiplegia

11 - -lecture at 8:30lecture at 8:30

22 - -No student is allowed to attend za No student is allowed to attend za lecturelecture

after 8:45 & is considered as absenafter 8:45 & is considered as absen

Page 3: Hemiplegia

- -HemiplegiaHemiplegia: : CompleteComplete loss of power or weakness on loss of power or weakness on

one side of za bodyone side of za body

- -HemiparesisHemiparesis:: IncompleteIncomplete loss of power or weakness on loss of power or weakness on

one side of za bodyone side of za body

Hemiplegia & hemiparesis are most Hemiplegia & hemiparesis are most

commonly due to commonly due to stroke stroke i.e. i.e. CVACVA..

Page 4: Hemiplegia
Page 5: Hemiplegia
Page 6: Hemiplegia

Stroke isStroke is:: - - is za is za 33rdrd commonest cause of death commonest cause of death and and

disability in za developed worlddisability in za developed world

- - mortality from stroke is 20-30% in themortality from stroke is 20-30% in the

11stst month & 60% of survivors are month & 60% of survivors are dependantdependant..

- - prevalence is2- 5 /1000/year & it is rising prevalence is2- 5 /1000/year & it is rising because of the aging population because of the aging population . .

- - male > femalesmale > females

Page 7: Hemiplegia

Risk factors for hemiplegiaRisk factors for hemiplegia 11 - -Non modifiable factorsNon modifiable factors

- - age - genderage - gender - - race - hereditaryrace - hereditary

22 - -Modifiable factorsModifiable factors - - Arterial HT - Cardiac diseasesArterial HT - Cardiac diseases - - DM - Cigarette smokingDM - Cigarette smoking

- - Hyperlipidaemia - ThrombocythemiaHyperlipidaemia - Thrombocythemia - - Polycythemia - Physical inactivityPolycythemia - Physical inactivity

- - Obesity - OCPsObesity - OCPs - - High alcohol intake - TraumaHigh alcohol intake - Trauma

- - Peripheral vascular diseasePeripheral vascular disease

Page 8: Hemiplegia

Stroke isStroke is:: uncommon uncommon before 40yearsbefore 40years except with except with : :

- -traumatrauma

- - cardiac diseases e.g RHDcardiac diseases e.g RHD

- - congenital vascular abncongenital vascular abn

- - inflammatory arteritisinflammatory arteritis

- - vascular diseasevascular disease

- - SS anaemiaSS anaemia

Page 9: Hemiplegia

Hemiplegia Hemiplegia is either due to:is either due to: 1- 1-Thromboembolic infarction (ischemic) Thromboembolic infarction (ischemic)

(80%): thrombosis/embolism(80%): thrombosis/embolism 22 - -HaemorrhageHaemorrhage (15%) (15%)::

intracerebral/ subarachnoidintracerebral/ subarachnoid 33 - -Dissection of carotid & vertebral arteriesDissection of carotid & vertebral arteries

44 - -Cortical venous or dural venous sinus Cortical venous or dural venous sinus thrombthromb

55 - -Subdural & extradural bleedingSubdural & extradural bleeding

Site of strokeSite of stroke - -internal capsule - brainsteminternal capsule - brainstem

- - cerebral cortex - basal gangliacerebral cortex - basal ganglia - - cerebellumcerebellum

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Mechanism of strokeMechanism of stroke::

11 - -Cerebral infarctionCerebral infarction (Ischemic) (Ischemic) - - thrombosis at za site of atheromathrombosis at za site of atheroma

- - embolism to a cerebral artery fromembolism to a cerebral artery from

- - extracranial vesselsextracranial vessels

- - heartheart

* * cerebral oedema may complicate cerebral oedema may complicate infarctioninfarction

and impair blood supply & cause and impair blood supply & cause furtherfurther

damagedamage

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22 - -Cerebral haemorrhageCerebral haemorrhage

- -subarachnoid haemorrhagesubarachnoid haemorrhage

- - ruptured beri aneurysmruptured beri aneurysm

- - ruptured AVMruptured AVM

- - intracerebral haemorrhageintracerebral haemorrhage

- - rupture of perforating vessels rupture of perforating vessels weakenedweakened

by HT or atheromatous degenerationby HT or atheromatous degeneration

) ) micro aneurysm= 0.8-1.0 mmmicro aneurysm= 0.8-1.0 mm((

- - rupture of aneurysms or AVMrupture of aneurysms or AVM

* * SAH arterial spasm & cerebral infarctionSAH arterial spasm & cerebral infarction

* * ICH may extend to subarachnoid spaceICH may extend to subarachnoid space..

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* * Disability from stroke depends on theDisability from stroke depends on the

site & extent of damagesite & extent of damage

* * Cerebellar hage can be fatal if there isCerebellar hage can be fatal if there is

compression of brain stemcompression of brain stem..

Page 13: Hemiplegia

Clinical classification of strokeClinical classification of stroke

11 - -Transient ischemic attackTransient ischemic attack (TIA): (TIA): suddensudden

loss of focal neurological fn lasting < loss of focal neurological fn lasting < 24hrs. 24hrs. 2- 2- Completed stroke :Completed stroke :loss of loss of focal neurological fn with focal neurological fn with symptoms symptoms lasting > 24hrslasting > 24hrs..

- - Major strokeMajor stroke

- - Minor stroke ( recovery in 1-2Ws), Minor stroke ( recovery in 1-2Ws), RINDRIND..

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33 - -Evolving stroke Evolving stroke (stroke –in-evolution(stroke –in-evolution)) symptoms worsening gradually or insymptoms worsening gradually or in

stepwise fashion over hrs or days or Ws stepwise fashion over hrs or days or Ws involving adjacent motor or involving adjacent motor or sensory sites within za distribution sensory sites within za distribution of a major cerebral artery (DD= of a major cerebral artery (DD=

tumour, SDH)tumour, SDH) . .

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Disorders causing stroke Disorders causing stroke comprisescomprises::

11 - -Thromboembolic diseaseThromboembolic disease (infarction) (infarction) - - atherosclerosisatherosclerosis

- - arteriosclerosis (HT, degenerative)arteriosclerosis (HT, degenerative)

- - embolism (20%)embolism (20%)

- - arteritis (syph, TA, PAN, SLE)arteritis (syph, TA, PAN, SLE)

- - dissection (spontaneous, traumatic)dissection (spontaneous, traumatic)

- - Vasospasm (migraine, SAH, angiogr)Vasospasm (migraine, SAH, angiogr)

- - hyper viscosity (PRV)hyper viscosity (PRV)

- - anti phospholipid syndromeanti phospholipid syndrome

- - SS disease - hypotension - OCPsSS disease - hypotension - OCPs

Page 16: Hemiplegia

22 - -Haemorrhage( Haemorrhage( intracerebral in 50% & 50% intracerebral in 50% & 50% SAHSAH

- - rupture of a vessel or micro aneurysm in rupture of a vessel or micro aneurysm in HTHT

- - AVMAVM

- - Beri aneurysmsBeri aneurysms

- - Degenerative aneurysmsDegenerative aneurysms

- - HT arteriolar aneurysmsHT arteriolar aneurysms

- - Mycotic aneurysmsMycotic aneurysms

- - Anticoagulants, thrombolytic therapyAnticoagulants, thrombolytic therapy

- - Bleeding disorders (ITP, DIC, haemophilia)Bleeding disorders (ITP, DIC, haemophilia)

- - Alcohol, cocaine, amphetamineAlcohol, cocaine, amphetamine..

- - Sub dural or extra dural bleedingSub dural or extra dural bleeding

Page 17: Hemiplegia

Clinical features of strokeClinical features of stroke

Depends on za site & extent & Depends on za site & extent & involves a combination of features involves a combination of features that may includethat may include::

- -hemiparesis hemiparesis - loss of speech - loss of speech

- - hemianaethesiahemianaethesia

Page 18: Hemiplegia

- - - The clinical The clinical onset is often rapidonset is often rapid and and reaches max within few hoursreaches max within few hours - Unilateral weakness +/- - Unilateral weakness +/- dysphasia is the commonest dysphasia is the commonest

presentationpresentation . .

- - Hypotonia, depressed reflexes and Hypotonia, depressed reflexes and extensor reflex occur initially, extensor reflex occur initially, followed later by hypertonia, followed later by hypertonia, hyper reflexia & extensor planterhyper reflexia & extensor planter

responseresponse

- - There may be impaired consciousness There may be impaired consciousness because of brain oedema (+/- because of brain oedema (+/-

papilloedema)papilloedema) . .

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- - With severe strokes flaccid paralysis isWith severe strokes flaccid paralysis is

accompanied by HA, vomiting, seizuresaccompanied by HA, vomiting, seizures

gaze paresis, impaired consciousness +/- gaze paresis, impaired consciousness +/- papilloedema 2ndry to cerebral papilloedema 2ndry to cerebral oedema - - Ataxia & hemisensory loss oedema - - Ataxia & hemisensory loss occur with deeplyoccur with deeply

seated lacunar infarctsseated lacunar infarcts..

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- - Monoparesis or dysphasia occur wz Monoparesis or dysphasia occur wz cortical lesions cortical lesions - Hemianaethesia & visual - Hemianaethesia & visual

fields defectsfields defects - - With brain stem lesions C/f depends on the With brain stem lesions C/f depends on the

structures involved. The cardinal structures involved. The cardinal feature is ipsilateral nuclear signs and feature is ipsilateral nuclear signs and contralateral pyramidal and S/T tract contralateral pyramidal and S/T tract lesions signs (lesions signs (crossedcrossed). Coma ). Coma may occur due to damage to reticular may occur due to damage to reticular

activating systemactivating system . . - - Recovery from stroke takes days, weeks orRecovery from stroke takes days, weeks or

monthsmonths..

Page 21: Hemiplegia

** ** In In cerebral hagecerebral hage there is there is profound profound hemiplegiahemiplegia

from the startfrom the start

** ** The The onset in cerebral emboli is abrupt onset in cerebral emboli is abrupt withwith

clear predisposing factorclear predisposing factor

** ** In cerebral thrombosis there is usually noIn cerebral thrombosis there is usually no

comacoma

** ** In HT encephalopathy the BP is very highIn HT encephalopathy the BP is very high

** ** Always consider head injury & intra Always consider head injury & intra cranialcranial

bleeding in pts with hemiplegiableeding in pts with hemiplegia..

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Differential diag of acute strokeDifferential diag of acute stroke 11 - -cerebral tumourscerebral tumours

22 - -subdural haematomasubdural haematoma 33 - -cerebral abscess, cystscerebral abscess, cysts

44 - -Todd's paralysisTodd's paralysis 55 - -demyelinating disordersdemyelinating disorders

66 - -hypoglycemiahypoglycemia 77 - -encephalitisencephalitis

88 - -hysterical conversionhysterical conversion - - eye lids firmly shut, pt resisting eye lids firmly shut, pt resisting

openingopening - - normal corneal reflexnormal corneal reflex

- - normal caloric response is diagnosticnormal caloric response is diagnostic..

Page 23: Hemiplegia

Investigation of strokeInvestigation of stroke 11 - -Investigations to confirm the diagnosisInvestigations to confirm the diagnosis

Is it Is it ischemicischemic or or haemorrhagicgic??haemorrhagicgic?? - CT brain - MRI - CT brain - MRI

- - MRA - L punctureMRA - L puncture..

* * Exclusion of hage is important if any form Exclusion of hage is important if any form ofof

anti thrombotic therapy is contemplatedanti thrombotic therapy is contemplated..

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Rt cerebral haemorrhage

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Rt cerebral infarction

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Subdural haematoma

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22 - -Investigations to establish za underlyingInvestigations to establish za underlying

disease and the possibility of a treatabledisease and the possibility of a treatable

causecause::

a/ embolism from the hearta/ embolism from the heart b/ embolism from large arteries b/ embolism from large arteries c/ temporal arteritis c/ temporal arteritis d/surgical treatable hage. d/surgical treatable hage. - ECG - CXR - ECG - CXR - Echo Doppler US - - Echo Doppler US - Carotid angiographyCarotid angiography

Page 28: Hemiplegia

33 - -Investigations to identify risk factorsInvestigations to identify risk factors::

CBC, blood sugar, lipid profile, serologyCBC, blood sugar, lipid profile, serology

for syphilis, clotting studies, serology forfor syphilis, clotting studies, serology for

collagen diseases, blood cultures forcollagen diseases, blood cultures for

SBE is suspected, sickling test, tests forSBE is suspected, sickling test, tests for

thrombophilia (protein C & S, anti thrombophilia (protein C & S, anti thrombin 3)thrombin 3)

Page 29: Hemiplegia

Management of HemiplegiaManagement of Hemiplegia The aim isThe aim is-:-:

11 - -To To minimize brain damageminimize brain damage 22 - -To To reduce disabilityreduce disability through through

rehabilitationrehabilitation 33 - -To To prevent complicationsprevent complications

44 - -To To treat za underlying causetreat za underlying cause.. 55--To To prevent za recurrence of strokeprevent za recurrence of stroke

66 - -To To refer pts wz SAH to neurosurgeryrefer pts wz SAH to neurosurgery.. ** ** To admit or not depends on za clinicalTo admit or not depends on za clinical state & facilities at home ( TIAs & minstate & facilities at home ( TIAs & min

stroke at homestroke at home))

Page 30: Hemiplegia

No specific treatment is available for most pts No specific treatment is available for most pts with stroke, so their immediate with stroke, so their immediate management is supportive withmanagement is supportive with General General measuresmeasures::

- - ABCABC

- - nursing carenursing care

- - fluid balance & nutrition= NG feeding andfluid balance & nutrition= NG feeding and

hydration. TR of infectionshydration. TR of infections . .

- - urinary cath if not continenturinary cath if not continent

- - physiotherapy, occupational, speechphysiotherapy, occupational, speech

and psychotherapyand psychotherapy..

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Med treatmentMed treatment::

11 - -Anti hypertensivesAnti hypertensives not given at the not given at the

start unless very high (> 180/110)start unless very high (> 180/110)

as some pts show reactive increase in as some pts show reactive increase in BPBP..

It is gradually lowered after za 1It is gradually lowered after za 1stst week week

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22 - -Anti plateletsAnti platelets reduce za incidence of reduce za incidence of

stroke by 25% e.g. aspirin 75-300mgstroke by 25% e.g. aspirin 75-300mg

dipyridamol 75 tds, clopidogreldipyridamol 75 tds, clopidogrel

33 - - Anti coagulantsAnti coagulants only if there is a only if there is a

source of emboli & avoided in za 1source of emboli & avoided in za 1stst

2Ws following infarction. It may be2Ws following infarction. It may be

used in evolving stroke, but C/I inused in evolving stroke, but C/I in

intra cranial hage & cerebral tumoursintra cranial hage & cerebral tumours

which should be rouled out by CTwhich should be rouled out by CT

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44 - -ThrombolysisThrombolysis (tpA) in USA given (tpA) in USA given withinwithin

33 hours of cerebral infarctionhours of cerebral infarction . .

55 - -Manitol 200ml 20% & dexamethazoneManitol 200ml 20% & dexamethazone

reduce mortality in pts with brain reduce mortality in pts with brain oedemaoedema

2ndry to severe stroke (dilating pupils2ndry to severe stroke (dilating pupils , ,

increasing BP & reduced PR= Cushing’sincreasing BP & reduced PR= Cushing’s

signsign.).)

66 - -BaclofeBaclofenn (GABA antagonist) for (GABA antagonist) for spasticityspasticity

Page 34: Hemiplegia

Surgical treatmentSurgical treatment::

11 - -carotid endarterectomycarotid endarterectomy in TIAs and in TIAs and

minor stroke when stenosis is > 70%. Itminor stroke when stenosis is > 70%. It

reduces incidence of stroke by 75%reduces incidence of stroke by 75%..

Avoided over in pts 65 yearsAvoided over in pts 65 years..

22 - - surgical evacuation of haematomasurgical evacuation of haematoma if if

accessible & if pat continue to accessible & if pat continue to deteriorate e.g cerebellar hage to deteriorate e.g cerebellar hage to prevent brainstem prevent brainstem compressioncompression . .

Page 35: Hemiplegia

RehabilitationRehabilitation::

- - identify risk factors & treatidentify risk factors & treat

- - TR 2ndry depressionTR 2ndry depression

Page 36: Hemiplegia

Secondary prevention of strokeSecondary prevention of stroke 11 - -control of cardiovascular risk factorscontrol of cardiovascular risk factors

22 - -control of HTcontrol of HT

33 - -long term anti platelet therapy unless long term anti platelet therapy unless thethe

stroke was hagicstroke was hagic

44 - -Pts with atrial fibrillation should be Pts with atrial fibrillation should be consideredconsidered

for anti coagulation & if there is a majorfor anti coagulation & if there is a major

CI should receive anti plateletsCI should receive anti platelets

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Primary prevention of strokePrimary prevention of stroke 11 - -control of HTcontrol of HT

22 - -control of DMcontrol of DM

33 - -stopping of smokingstopping of smoking

44 - -lowering of lipid levelslowering of lipid levels

55 - -anti coagulation in atrial fibrillation if no anti coagulation in atrial fibrillation if no CICI

66 - -reducing Hb in polycythemia verareducing Hb in polycythemia vera

77 - -diagnosis & surgical TR of carotid diagnosis & surgical TR of carotid atheromaatheroma

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Complications of acute strokeComplications of acute stroke - -pneumonia - dehydrationpneumonia - dehydration

- - hyponatraemia - hypoxaemiahyponatraemia - hypoxaemia

- - hypoglycemia - DVThypoglycemia - DVT

- - seizures - subluxation of jointsseizures - subluxation of joints

- - frozen shoulder - pressure soresfrozen shoulder - pressure sores

- - UTI - constipationUTI - constipation

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PrognosisPrognosis:: - - 25%25% die as a direct result of strokedie as a direct result of stroke..

More in hagic strokeMore in hagic stroke.. - - 50-75%50-75% who survive stroke achieve functionalwho survive stroke achieve functional

independency in 3Msindependency in 3Ms - - poor outcome in pts wz deep coma andpoor outcome in pts wz deep coma and

dense hemiplegiadense hemiplegia - - mortality during za 1mortality during za 1stst month is about 40-50% month is about 40-50% from extension of za cerebral damage, aspiratfrom extension of za cerebral damage, aspirat

pneumonia & DVT wz pulmonary embolismpneumonia & DVT wz pulmonary embolism.. - - recurrent stroke occur in 5-10%/ yearrecurrent stroke occur in 5-10%/ year

- - patient may die of cardiovascular diseasepatient may die of cardiovascular disease..