36 terms



Terms in this set (...)

paralysis of one side of the body dt pyramidal tract lesion (unilateral) at any point f its origin in the cerebral cortex down to the 5 th cervical segment
weakness of one side of the body
- psychogenic or functional
- organic : congenital or infantile , acquired
@ features of psychological hemiplegia
f> m
-hysterical personality, preceeded by emotional upset
- -ve angle: negative neurological signs on examination
- bizarre distribution ( not a hemiplegic pattern)
- bizzare gait
- normal reflexes
- no wasting
- + ve babinski rising up test
- + ve platysma sign
congenital hemiplegia
hemiplegia dated since birth
- dt intrauterine: measles, drugs; natal: trauma, asphyxia ; postnatal: asphyxia
infantile hemiplegia dt
hemiplegia developing during infancy & childhood
dt: inflammation : encephalitis ; vascular: thrombosis
@ features of congenital and infantile hemiplegia
- restricted growth (mal or under development) of the involved side e.g. shorter hand or leg
- spasticity and contractures
- epilepsy ( fits)
- involuntary movement over the hemiplegic side ( chorea, athetosis)
- mental changes : mental retardation or behavior changes
- no aphasia : LT hemisphere affection as the speech function will be taken over by Rt hemisphere
it is not ..... , but a lot can be done, as the brain in thus age is flexible & any function lost in damaged part can be substituded by the undamaged part. this can't happen in the acquired type
- usually parents do not notice hemiplegia in their child unless after several months
curable, infantile and congenital hemiplegia
acquired hemiplegia with rapid onset
- vascular ( M/C) : 2nd cause of death after heart dis, 5 th cause of disability ; embolism seconds, hge minutes, thrombosis hours
- traumatic minutes or hours: brain contusion, subdural haematoma, intracranial hge
- inflammation hours or days : meningitis, encephalitis
- demyelinating dis (acute onset 90%; chronic onset 10%)
acquired hemiplegia with gradual onset(wk or month) and @ by?
- SOL ( tumour) like meningioma or glioma
- traumatic ( ch. subdural haematoma)
- chronic inflammation ( ch. brain abscess)
@ by: the presence of general manifestations of inc intracranial pressure
causes of recurrent hemiplegia
- hysterical
- vascular : TIAs, hypertension encephalopathy, sickle cell crisis
- demyelinating disease: remission & relapse
- postepilectic Todd's paralysis ( dt neuronal exhaustion)
- hemiplegic migraine
- traumatic, cerebral hge, embolism
- thrombosis (hours), miningitis, encephalitis (days to weeks), dyemelinating (days-weeks)
- ch. inflammation (brain abscess), subdural haematoma, tumour
-acute infection, embolism, thrombosis
- - hysterical; vascular : TIAs, hypertension encephalopathy, sickle cell crisis; demyelinating disease: remission & relapse; postepilectic Todd's paralysis ( dt neuronal exhaustion); hemiplegic migraine
acute lesion c/p (2 stages)
- stage of flacidity (shock st)
- st of spasticity ( established hemiplegia)
c/p of gradual lesion (1stage)
hemiplegia passes directly into the st of spasticity
st of flaccidity (shock st)
1. happen in acute sudden causes
2. duration: 3-6 wk then pass to usual spasticity. the shorter the duration the better px. this st are prolonged by general poor condition of the pt's health, infections (eg: chest or urinary tract infection)
3. conciousness +- confusion or coma
4. motor system (on the paralysed side)
- hypotonia of pyramidal diatribution => complete loss of ms tone (flaccidity)
. skilled > gross
. UL : extrnsor > flexor
. LL: flexor > extensor
. deep reflexes : lost
. no plantar reflex
- sensory system: hemi anaesthesia mb present
- speech: +- aphasia or dysphasia ( if the dominant hemisphere is affected) & ( the pt is concious)
- cranial nerve:
. conjugAte deviation of the eye towards the paralysed side in capasular hemiplegia (dt irritation)
. the tongue is deviated to the hemiplagic side (unilateRal pyramidal supply in 50%)
- during recovery f the shock st : the ms tone & deep reflexes reappear & gradually inc. babinski sign bcome +ve . the st of spasticity sets in
- if the onset is ass w coma, the paralysed side is determined by tge following:
. the limbs ob the paralysed side are more flaccid & drop passively
. the cheekon the paralysed sides moves in and out w respiration
st of spasticity
1. this occur f the start in ch causes or in acute st after the flaccid st
2. conciousness: regained
3. motor dystem:
- power: weakness of pyramudal distribution w hemiplegic position:
. it affects the DISTAL more than the proximal ms
. in UL: the extensor are weaker than FLEXOR (flexed elbow, wrist, MCP, IPJ, semiprone forearm, adducted shoulder)
. in LL : flexors are weaker than EXTENSIRS
- tone: clasp knife spasticity in anti gravity ms
. flexors of UL
. extensors of LL
. adductors> abductors
- reflexes:
. deep reflexes: in both UL& LL are exaggerated on the paralysed side (biceps, triceps, brachioradialis, knee& ankle reflexes)
. sup reflexes: abd and cremasteric reflexes are lost on the paralysed side
. pathological deep reflexes (normally absent) mb : finger reflex, patellar r, adductor r)
. clonus mb elicited in the ankle, less frequently in the knee or wrist
. +VE babinski sign: exte planter r => on eliciting the plantar response on the paralysed side, there is dorsiflexion of the big toe w or w/o fannning of the other toes
. gait: circumduction dt spasticity of the extensors & adductors of LL
- sensory system: +- hemianasthesia
- speech : +- if in dominant hemisphere
. aphasia
. dysphasia (diff reading)
. dysarthria
. dysgraphia

depend on what and where is the lesion
cerebral hemiplegia:
a) cortical lesion: @ by
- more restricted to one limb (monoplegia)
- contralateral cortical sensory loss (if the parietal lobe is involved)
- coma (if the lesion is extensive)
- convulsions (if the lesion is irritative)
- if in the dominant hemisphere: language changes (aphasia)
- mental changes
b) internal capsule lesion
- usually there is hemiplegia
- if extends backward=> sensory affection
- if extends more backward=> hemianopia
brain stem
a) mid brain:
- weber s
. ipsilat 3rd nerve affection
. contralat hemiplegia
- bendict's s (red nucleus lesion)
. ipsilateral 3rd nerve affection
. contralat hemiplegia
. crossed hemiataxia if the red nucleus is affected
b) pons
-millard gubbler s
. contralat hemiplegia
. ipsilat 6th & 7th affection
- fovile,s s
. contralat hemiplegia
. loss of conjugate eye deviation to the side of the lesion
. 5th palsy
c) medulla
- avellis s
. contralat h
. ipsilateral 9th & 10th cranial n paralysis
- jackson's s
. contral h
. ipsilateral 10 & 12th cranial n paralysis
spinal cord
- the lesion is on one side of the cord & is situated btw C1 & C 5 segments
- it is caused by: stab wound, disc prolapse, DS, or tumour => brown-sequard s @ by:

1. at the level of the lesion:
. ipsilat localised LMNL of the ms supplied by the affected segments
. ipsilater loss of all sensations in the area supplied by the dorsal roots of the affected segments
2. below the level of the lesion:
. ipsilateral hemiplegia
. ipsilateral deep sensory loss
. contralateral superficial sensory loss for pain & temp
. touch diminishes on both side
- > 50 y/o
- hx of artherosclerosis or vasculitis, hx of bl dis like polycythemia, DIC, leukemia
- onset is rapid within hours
- absent: vomiting, fever
- -+ convulsions
- pupils is N and equal
- impaired and regressive conciousness
- BP mb high dt IHD
- N pulse and CSF
- CT and MRI = hypodrnse area
- px is better
- in any age
- hx of rheumatic heart , AF, SBE, MI, atheroma f carotid or badilar artery, air ir fat embolism
- onset is sudden (within s)
- absent vomiting, fever
- -+ convulsion
- pupils is N and equal
- conciousness is impaired and regressive dt resolution of edema Vd of contricted vessels
- BP and CSF in N
- pulse: AF
- CT MRI : hupodense area
- px best unless IHD
->40 y
- hx of htn
- onset is sudden (within minutes) & occurs on action
- vomiting common, fever present, frequent convulsion
- pupils are dilated and irreactive
- conciousness : coma and progressive
- BP usually high
- pulse: bradycardia dt high ICP
- CSF mb bloody
- CT MRI : hyperdense area
- px is worst
dx clinically
1. sudden onset = s to min= vascular/trauma
2. acute onset = hours to days= inflammatory, vascular
3. subacute = days -< 4 weeks as acute = infla, vascular
4. ch onst= > 4wks = degenerative & SOL (tumour)

1st STEP: to dx ischemic f hgic stroke:
1. CT scan of the brain within 3 hrs
- to visualize hge (intracerebral or subarachoid)
- CT is better than MRI for hge
- CT scan :
. in hgic hemiplegia=> +ve from the start
. in infarction => -ve 1st then after 48 hours => +ve
2. MRI of brain : MRI is better than CT in
. lacunar infarction
. infarction of small art
. infarction in post fossa
. infarction in brain stem

2nd step: dx of brain tumour: MRI & CT scan
also MRI can exlude other causes (subdural harmatoma, epilepsy, mygranus hemiplegia, HTN encephalopathy, meningitis, encephalitis)
3rd STEP: ix to know the site of lesion
. US = non invasive for carotid or vertebral art
. transcranial doppler
. invasive as angiogram
4th STEP: look for RF
. routine lab ix
. xray= cardimegaly
. ECG, ECHO: to know the source of emboli
. trans esophageal is dx for source of emboli
. lipid profile
. collagenic tests
1. general care of a comatosed pt
2. symptomatic rx & physiotherapy
3. sp therapy
- tx of ischemic infarction
- tx of hgic infarction
criteria for TPA
- not more than 80 years old or less than 12 y/o
- bp < 180/100
- CT brain free in 1st 3 hours of cerebral insult
- No hx of intake of heparin and salicylate
- no hx of recent MI
- bleeding (internal hge or an any body cavities)
TAKE consent from family (20% went to hgic stroke = death)



1. Previous intracranial He at anytime

2. Hgic stroke <6months

3. Closed head/facial trauma within 3 months

4. Suspected aortic dissection

5. Ischemic stroke within 3 months

6. Active bleeding diathesis

7. Uncontrolled high BP

8. Known structural cerebral vascular lesion

9. AVM

10. Thrombocytopenia

11. Blood coagulation disorder

12. Aneurysm

13. Brain tumor

14. Pericardial effusion

RELATIVE:1. Current anticoagulant use2. Surgery last 2 weeks3. Prolonged CPR >10min4. Bleeding diathesis5. Diabetic/Hgic retinopathy6. Pregnancy 7. Active peptic ulcer8. Controlled severe HTN
restoration of cerebral BF in ischemic infarction
- thrombolytic therapy (tissue plasminogen activator)
tx for prevention of recurrence of ischemic infarction
- anticoagulant therapy(heparin)
- oral anticoagulant
- antiplatelets (aspirin, clopidogrel, ticlopidin)
mx in general for hemiplegia
- general care of comatosed pt
- symptomatic tx and physiotherapy (antiemetic, antihypertension, ms relaxants, pysiotherapy)
- sp therapy for ischasemic infarction(restoration BF, prevention of recurrence, deal w brain edema, improve cerebral circulation, improve brain metabolism, maintain N BP)
- OR sp therapy for hgic infartion( control BP, surgical evacuation of operable cases, drugs: coagulants (vit K), antifibrinolytic drugs (aminocaproic acid)
- deal w RF( treat DM, treat dyslipidemia)
- long term therapy (antiplatelets, pentoxyfilline)
deal w brain edema
- mannitol - diuretics - corticosteroids
antidote for heparin?
- protamine sulphate
CI of heparin?
- septic embolization (endocarditis)
- hgic infarction
- large infarction
- very high BP
- bleeding tendency
- liver disease
antidote for oral anticoagulant

(oral anticoagulant not use now as routine therapy in stroke dt high risk of hgic. only indicated in: -embolic cardiac source- venous infarction: dev over days not like art hours- post circulation )
- parenteral vit k
how to improve cerebral blodd circulation?
- good hydratio
- pentoxy-filline
a) general care of a comatosed pt
- skin care : change the pt position /2hours & frequently wash then apply vaseline or talc powder in the P points
- repiratory care: o2 inhalation, suction of secretion & aireay mb needed
- fluid & nutrition : NG tube feeding or IV fluids & TPN (total parentral nutrition)
- bowel & bladder care: urinary catheter & daily enema
improve brain metabolism & antiplatelets => protection of the partially recoverable zone around the edge of the infact (penumbra) & interferes w the cytotoxic nechanism tiggered bu ischemia