Stroke : Rapidly developing clinical signs of focal or global distribution of the cerebral function

 
Hemiplegia : paralysis of one side of the body duo to pyramidal tract lesion at any point from its
origin in the cerebral cortex down to the 5th segment .
 
Causes
1. Vascular
 Thrombotic
o Vessel wall disease : atherosclerosis or vasculitis
o Blood disease : polycythemia , thrombocytosis , hyergammaglobulinemaia
o Heart disease : heart failure , systemic hypotension (in cases of myocardial
infraction , shock )
 Embolic
o Heart : mitral stenosis with AF , subacute bacterial endocarditis , atrial myoxoma
o Distal vessel : arterial or venous
o Rare sources : lung , tumor, bone
 Hemorrhagic
o intracerebral : the leak in the brain substance , may leak to the ventricles (this is
very serious as it may compress on the vital centers ) the commonest artery causing
intracerebral damage is lenticulo_striate branch of the middle cerebral artery
o Subarachnoid
o Intradural or extradural
 Causes of hemorrhage are
 Hyper tension
 Rapture of aneurysm
 Hemorrhagic blood disease
 Anticoagulants
 Trauma
 
2. Infective : encephalitis , brain abscess
3. Neoplastic : meningioma or glioma
4. Traumatic
5. Congenital : CP
6. Demyelinating
7. Hysterical
 
Clinical picture
 Onset and course
o Acute , regressive in cases of infection , vascular , traumatic lesions
o Chronic progressive in case of neoplastic lesion
o Fluctuating in cases of D.S
 Signs and symptoms
 o In acute stages the clinical pictures passes through two stages Flaccid and spastic
stages
o In progressive stages the patient passes to the spastic stage directly
Stage Flaccidity Spasticity

  1. It lasts from 2 to 6 weeks 1. Paralysis of one side of

1. On the paralyzed side there is the body showing pyramidal
complete loss of muscle tone and deep distribution and it affects the
reflexes and absence of planter reflex progravity muscles more than the
1. During recovery there is a antigravity
gradual increase in MS tone and In UL extensor are weaker than flexor
appearance of deep reflexes and +ve In LL flexor are weaker than flexor
Babinski sign  
1. If the onset is associated with 1. Hypertonia affects the
coma the paralyzed side is determined by antigravity muscles more than
 The limbs are more progravity
flaccid and drop passively In UL flexor more
 The cheek on the In LL extensor more
paralyzed side moves with  
respiration 1. Exaggerated deep
  reflexes and appearance of
Note that the length of the stage depends pathological reflexes
on the general health condition of the  
patient 1. Lost superficial reflexes
1. Positive Babinski sign
2. Gait (discussed in detail
later )
 
Signs and symptoms according to the level of the lesion
 
Spinal
The lesion is in one side of the cord , it is situated between the C1 andC5 segments resulting in
Brown Sequrd syndrome
 
a. At the level of the lesion
Ipsilateral loss of sensation in the areas supplied by the affected sensations
Ipsilateral localized L.M.N.L lesion in the muscles supplied by the affected segment
 
b. Below the level of the lesion
Contralateral hemiplegia
Ipsilateral deep sensory loss
Contralateral loss of pain and temp.
Touch is diminished in both sides
 
Brain stem
 
Midbrain Pontine Medullary

Weber's Millurd gubler's Avellis

     
Contralateral hemiplegia Contralateral hemiplegia Contralateral hemiplegia
3rd cranial nerve affection 6,7 cranial nerve affection 9,10 cranial nerve affection

Benedict's Foville Jackson

     
Contralateral hemiplegia Contralateral hemiplegia Contralateral hemiplegia
3rd cranial affection Medial longitudinal bundle 11,12 cranial nerve affection
Hemi ataxia duo to red nucleus affection leading to loss of  
affection conjugate deviation to the same
side of the eye
 
Cerebral
 
Associated with upper motor neuron lesion of the facial and hypoglossal paralysis on the opposite side
of the lesion
 
Cortical Subcortical Capsular

1. Coma The same as Contralateral hemiplegia with

1. Convulsions cortical but U.M.N
1. Contralateral homonymous more Hemihyposthesia
hemianopia extensive Hemianopia
2. Contralateral cortical sensory loss No convulsions or aphasia
1. Aphasia and agraphia if the  
dominant hemisphere is involved  
1. Usually represented with
monoplegia
 
Management of Stroke
 
Medical management
Stroke is a syndrome not a disease so the first step in treatment is proper diagnosis and determination
of cause of the attack
 
 Care of vital signs
 Symptomatic treatment
 Cerebral dehydration : Mannitol or Glycerol or steroids
 Antiemetic drugs : premperan , largactil
 Tranquilizers and sedatives
 Muscle relaxant
 Vitamins and tonics
 Specific treatment
 o Thrombotic
 Care of blood pressure : capotopril ………….. Avoid sudden marked reduce in
B.P which decrease the blood flow to the brain
 Antiplatelet : Aspirin , persantin , ticlid
 Anticoagulant in cases of embolic hemiplegia or T.I.A
 Piracetam improve brain metabolism
 Trental improve microcirculation of the brain
o Embolic
o Cerebral as before but surgical evacuation may be needed
 Physiotherapy