Hemiplegia

Pyramidal Pathway

I) Cortico spinal tract:
It arises from Betz cells in area 4, and then descends:
1- In the corona radiata.
2- In the internal capsule:
It occupies the posterior 1/3 of the anterior limb, genu &
the anterior 2/3 of the posterior limb.
3- In the mid brain:
It occupies the middle 3/5 of the cerebral peduncle.
4- In the pons:
It occupies the basis pontis & is traversed by 6 & 7 nerves.
5- In the medulla:
It occupies the pyramid.
6- In the lower part of the medulla 90% of the fibres cross to
the opposite side and descend as the crossed pyramidal
tract in the lateral column of the spinal cord
7- 10% of the fibres descend as direct pyramidal tract,
and gradually cross to the opposite side.
8- The cortico-spinal tract terminates at the anterior horn
cells of different spinal segments.
II) Cortico-bulbar tract:
• The motor cranial nerve nuclei in the brain stem receive bilateral
pyramidal supply through this tract,
• except: the lower part of the 7^th nucleus and the 12^th nucleus
which are supplied by fibres from the opposite tract only.
 

Hemiplegia

 

Definition

Paralysis of half the body due to interruption of the pyramidal tract at any point from the cerebral cortex down to 5^th cervical segment of the spinal cord (beginning of brachial plexus).
 

Etiology

I) Vascular: the most common cause.
A. Thrombosis: resulting in cerebral infarction.
1. Vessel wall disease:
• Cerebral atherosclerosis.
• Vasculitis e.g.: PAN & SLE.
2. Hyperviscosity:
• Polycythaemia vera.
• Secondary polycythaemia.
3. Slow circulation:
• Heart failure.
• Hypotension e.g.
- Myocardial infarction & shock.
- Severe blood loss.
- Excess antihypertensive drugs.
B. Embolism: resulting in cerebral infarction.
The source of embolism may be:
1. Heart:
• Mitral stenosis with AF.
• Infective endocarditis of aortic or mitral valve.
• Mural thrombi on top of myocardial infarction.
• Left atrial myxoma.
• Mitral valve prolapse.
• Prosthetic valves.
2. Distal vessels:
• Arterial: detached atheromatous plaque.
• Venous: DVT may lead to paradoxical embolism.
3. Rare causes:
• Air, tumour, fat or parasitic emboli.
C. Hemorrhage:
1. Intra-cerebral haemorrhage due to:
• Severe hypertension.
• Purpura, haemophilia or anticoagulants.
2. Subaracnoid haemorrhage due to:
Aneurysm or angioma in the circle of Willis.
II) Traumatic;
Cerebral laceration & sub-dural haematoma.
III) Inflammatory:
Brain abscess & encephalitis.
IV) Brain tumors:
Glioma & meningioma.
V) Disseminated:
MS & DEM.
VI) Congenital.
Cerebral palsy.
VII) Hysterical.
Patient suffers from paralysis in the absence of organic lesion.
 

Clinical Picture

The typical picture is Spastic Hemiplegia.
This picture may be modified according to:
I. The level of the lesion.
II. The etiology.
III. The stage of hemiplegia.
 

The typical Spastic Hemiplegia

1. Paralysis or paresis of one side of the body.

• It affects the progravity more than the antigravity muscles.
- In UL: the extensors are weaker than the flexors.
- In LL: the flexors are weaker than the extensors.
• It affects the distal more than the proximal muscles.
- The hand is weaker than the shoulder.
- The foot is weaker than the hip.
2. Clasp knife spasticity.
• It affects the antigravity more than the progravity muscles.
- In UL: the flexors are more spastic than the extensors.
- In LL: the extensors are more spastic than the flexors.
• It affects the adductors more than the abductors.
3. Exaggerated deep reflexes.
• Deep reflexes are exaggerated on the paralysed side.
• Pathological reflexes may appear.
• Clonus may be elicited in the ankle, the knee or the wrist.
4. Lost superficial reflexes.
Abdominal & cremasteric reflexes are lost on paralysed side.
5. Positive Babinski’s sign.
Dorsiflexion of big toe with or without fanning of other toes.
6. Gait:
Circumduction, if the patient can walk.

The clinical picture changes according to the level of the lesion, the aetiology and the stage.

Leveling Of Hemiplegia

I) Cerebral hemiplegia:
1- Cortical:
- Starts as monoplegia.
- May be preceded by convulsions.
- May be coma.
- May be aphasia or cortical sensory loss.
- May be affection of conjugate movements of eyes.
2- Subcortical:
- Starts as monoplegia.
- No convulsions.
- No coma.
- No aphasia, sensory loss or conjugate affection.
3- Capsular:
- Starts as complete hemiplegia.
- Cortical sensory loss in the same side of hemiplegia.
- Homonymous hemianopia.
- No convulsions, coma, aphasia, or conjugate affection.
II) Brain stem Hemiplegia: (crossed hemiplegia)
1- Mid Brain:
Weber syndrome:
- 3^rd nerve paralysis on the side of the lesion. (ipsilateral)
- Hemiplegia on the opposite side. (contralateral)
Benedict syndrome:
- 3^rd nerve paralysis on the side of the lesion.
- Hemipareses on the opposite side.
- Hemiataxia on the opposite side (red nucleus affection).
2- Pons:
Millard- Gobbler syndrome:
- 6^th & 7^th nerves paralysis on the side of the lesion.
- Hemiplegia on the opposite side.
Foville syndrome:
- Affection of conjugate movements of the eyes.
- Hemiplegia on the opposite side.
- May be 6^th and 7^th on the side of the lesion.
3- Medulla:
Avellis syndrome:
- 9^th &10^th nerve paralysis on the side of the lesion.
- Hemiplegia on the opposite side.
Jackson syndrome:
- 10^th and 12^th nerves paralysis on the side of the lesion.
- Hemiplegia on the opposite side.

III) Spinal Hemiplegia:
· Cause: Stab wound, disc prolapse, MS or tumour.
· Clinical picture: Brown Sequard syndrome.
a. At the level of the lesion:
• Ipsilateral LMNL:
In the muscles supplied by the affected segments.
• Ipsilateral hyposthesia:
In dermatomes supplied by the affected segments.
b. Below the level of the lesion:
• Ipsilateral UMNL.
• Ipsilateral deep sensory loss.
• Contralateral superficial sensory loss.
• Touch diminishes on both sides.
 

II. Clinical Modification according to aetiology

1) Embolic hemiplegia:

• Young age.
• Acute onset (seconds).
• MS murmur and irregular heart.
• No increased ICT.
• Rapid improvement.
2) Haemorrhagic hemiplegia:
• Middle age.
• Acute onset (minutes).
• Hypertensive.
• Left ventricular enlargement.
• Increased ICT.
• Bad prognosis (death).
3) Thrombotic hemiplegia:
• Old age.
• Slow onset (hours).
• Normotensive or hypertensive.
• Normal or enlarged heart.
• No increased ICT.
• Slow improvement.
4) Brain abscess:
• Any age.
• Gradual onset (days).
• Increased ICT.
• Severe toxemia.
• Gradually progressive course.
5) Brain tumor:
• Any age.
• Gradual onset (weeks).
• Increased ICT.
• Mild toxemia.
• Gradually progressive course.
6) Multiple sclerosis:
• Acute onset and exacerbations & remissions.
• Affection of multiple sites in the CNS.
7) Hysterical hemiplegia:
• Usually female.
• Disturbed psychological make up.
• Acute psychic trauma.
• Hysterical cries.
• Atypical hypertonia.
• Symmetrical exaggeration of deep reflexes.
• Hysterical clonus (continues after release of stretch).
• Normal BP, Heart and pupils.

	Thrombosis	Embolism	Haemorrhage
1. Age	Old age.	Young age.	Middle or old age.
2. Onset	Taking hours	Taking seconds	Taking minutes
3. Prodromata	TIAs	Absent.	Absent.
4. Vomiting	Absent.	Absent.	Common.
5. Consciousness	Usually preserved.	Usually preserved.	Lost, with deepening coma.
6. Convulsions	May occur.	May occur.	Frequent.
7. Pupils	Normal & equal.	Normal & equal.	Dilated & fixed
8. Fever	Absent.	Absent.	Present.
9. Blood pressure	May be high.	Normal.	Usually high.
10 Heart	May be L.V. enlargement.	Usually valvular lesion.	Left ventricular enlargement.
11. C.S.F.	Clear.	Clear.	Bloody, ↑ tension.
12. CT scan, MRI	Hypodense area.	Hypodense area.	Hyperdense area.

III. Spastic hemiplegia may be preceded by one of 2 stages

1. Flaccid or shock stage:
• Occurs in acute lesions (hemorrhage & embolism).
• It lasts for 2-6 weeks.
• Hypotonia & hyporeflexia in the paralyzed side.
• May be coma with lateralization if the lesion is cortical.

2. Premonitory stage:
• Occurs in thrombotic hemiplegia due to atherosclerosis.
• There is headache, and lack of concentration.
• There is weakness and numbness in one side.
• Thrombotic hemiplegia may follow in hours or.
• The patient returns normal & the attacks may be repeated
(TIAs) before he develops hemiplegia one day.

	Investigation

1. MRI & CT: Will diagnose the cause.
2. CSF: will show blood in cases of haemorrhage.
 

Management Of Hemiplegia

I. Care of bed reddin patient:
1. Care of the skin:
• Use air mattress to alternate pressure points.
• Frequent change of the patient’s position.
• Wash of the back by alcohol followed by powder.
2. Care of respiration:
• Suction of nasal and pharyngeal secretions.
• O₂ inhalation via catheter or mask especially in coma.
• Tracheostomy in urgent cases.
3. Care of nutrition and fluid balance:
Tube or parentral feeding in comatosed patients.
4. Care of the urinary bladder:
• Self-retaining catheter in case of retention or incontinence.
• Urinary antiseptics.
5. Care of the bowels:
Daily enema.
II. Symptomatic measures:
1. Dehydrating measures: for brain oedema.
2. Tranquilizers: for insomnia & irritability.
3. Muscle relaxants: for spasticity.

III. Specific
A) Cerebral Thrombosis:
1- Care of BP:
a. Antihypertensives: for hypertension.
b. Vasopressors: for hypotension.
2- Antiplatelets:
a. Acetyl salicylic acid (Aspirin): 75-300 mg daily.
b. Dipyridamole (Persantin): 75 mg tds.
c. Teclopedine (Teclid): 250 mg tds.
3- Anticoagulants: indicated in
a. Stroke in evolution.
b. Recurrent TIAs.
4- Other drugs may be used:
Nootropil, Trental & Trivastal.
B) Cerebral Embolism:
1- Treatment of the source of emboli.
2- Anticoagulants to prevent further embolization.
C) Cerebral Haemorrhage:
1- Antihypertensives: for hypertension.
2- Antifibrinolytic drugs: as tranexamic acid.
IV. Physiotherapy:
• Proper positioning of the hemiplegic side.
• Massage and passive & active exercises.