Hemiplegia


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INTRODUCTION

Paralysis of one side of the body due to Pyramidal tract lesion at any point from its origin in the cerebral cortex down to the fifth Cervical segment ( beginning of origin of cervical plexus ) .

ETIOLOGY

VASCULAR - Cerebral hemorrhage , Stroke , Diabetic Neuropathy.

INFECTIVE - Encephalitis , Meningitis , Brain abscess.

NEOPLASTIC - Glioma - meningioma

DEMYLINATION - Disseminated sclerosis , lesions to the Internal capsule .

TRAUMATIC - Cerebral lacerations , Subdural Hematoma . Rare cause of hemiplegia is due to local anaesthsia injections given intra arterially rapidly , instead of given in a nerve branch .

CONGENITAL - Cerebral palsy

DISSEMINATED - Multiple Sclerosis

PSYCHOLOGICAL - Parasomnia (Nocturnal hemiplegia ).

MECHANISM -

Damage to the corticospinal tract leads to the injury on the opposite side of the body. This happens because the motor fibres of the corticospinal tract , which take origin from the motor cortex in brain , cross to the opposite side in the lower part of medulla oblongata and then descend down in spinal cord to supply their respective muscles.

Depending on the site of lesion in brain , the severity of hemiplegia varies.

SITE OF LESION	SIGNS AND SYMPTOMS
INTERNAL CAPULE	Dense and uniform Hemiplegia ( UMN Facial ) Hemisensory blunting Homonymous hemianopia
CORTEX	Non dense non uniform weakness Monoplegia Cortical signs ( Dysphasia , Apraxia , Cortical sensory loss , Convulsions )
SUBCORTEX	Pattern of weakness similar to cortical
BRAINSTEM	Crossed hemiplegia Ipsilateral LMN CN Palsy and contralateral hemiplegia Cerebellar signs.
MIDBRAIN	Crossed cerebellar ataxia with Ipsilateral Third nerve palsy ( Claude `s syndrome ) Weber`s syndrome - Third nerve palsy and contralateral hemiplegia Contralateral hemiplegia - Cerebral peduncle Contralateral rhythmic , ataxic action tremor ; rhythmic postural or holding tremor (rubral tremor)
PONS	LMN Facial and contralateral hemiplegia Fifth nerve and contralateral hemiplegia Lateral Gaze palsy and contralateral hemiplegia
MEDULLA - Lateral medullary syndrome	Same side ( Horner `s syndrome , Loss of pain and touch on the face , Cerebellar signs , Palate weakness ) Opposite side ( Loss of pain and temperature sensation on the body and limbs )
MEDULLA - Medial medullary syndrome	Same side ( wasting and weakness of the tongue ) Opposite side ( hemiplegia without facial palsy )
SPINAL CORD	Rare No facial Brown sequard Syndrome

MEDICAL DIAGNOSIS

HISTORY AND EXAMINATION

An accurate history profiling the timing of neurological events is obtained from the patient or from family members in the case of the unconscious or noncommunicative patient . Of particular importance are the exact time and pattern of symptom occurs . The most common , slowest in hours , wakes up in the morning with weakness , history of TIA , old age is typical with thrombosis . An embolus occurs rapidly with no warning , history of heart disease , younger age group , no progression (maximum deficit occurs at onset) . An abrupt onset with worsening symptoms , history of prolonged hypertension , severe headache described as "worst headache of my life " , altered consciousness , convulsions , vomiting is suggestive of haemorrhage. The patient 's past history , including episodes of TIAs or head trauma , presence of major or minor risk factors and medications , pertinent family history and recent alterations in patient function ( either transient or permanent ) are thoroughly investigated.

The physical examination of the patient includes an investigation of vital signs ( heart rate , respiratory rate , blood pressure , clubbing ) , signs of cardiac decompensation, and function of the cerebral hemispheres , cerebellum , cranial nerves , eyes and sensorimotor system.

OUTCOME MEASURES

NIH Stroke Scale

Dynamic Gait Index, the 4-item Dynamic Gait Index, and the Functional Gait Assessment show sufficient validity, responsiveness, and reliability for assessment of walking function in patients with stroke undergoing rehabilitation, but the Functional Gait Assessment is recommended for its psychometric properties^[7].

Chedoke-McMaster Stroke Assessment

Chedoke Arm and Hand Activity Inventory

CRS-R Coma Recovery Scale Revised is used to assess patients with a disorder of consciousness, commonly coma.

Take a look at our Stroke Outcome Measures Overview for more information

CEREBROVASCULAR IMAGING

Cerebrovascular imaging is the main tool to establish the diagnosis of suspected hemiplegia. Advanced neuroimaging can rapidly indentify the occluded artery and estimate the size of the core and the penumbra.

COMPUTER TOMOGRAPHY AND MRI SCANS

For acute care of stroke patients, a number of computed tomography (CT) and magnetic resonance (MR) techniques are essential. Noncontrast CT excludes other causes of acute neurologic defi cits and intracranial hemorrhage. CT and MR angiography can identify intravascular clots, and the CT angiography source images improve detection of acute infarction over plain CT. Diffusion MRI estimates the size, location, and age of infarcted core more precisely, and perfusion imaging estimates the ischemic penumbra.CT and MR imaging techniques are used to provide four types of information that are essential to the care of acute stroke patients.

1. They establish the diagnosis of ischemic stroke and exclude other potential causes of an acute neurologic defi cit.

2. They identify intracranial hemorrhage.

3. They identify the vascular lesion responsible for the ischemic event.

4. They provide additional characterization of brain tissue that may guide stroke therapy by determining the viability of different regions of the brain and distinguishing between irreversibly infarcted tissue and potentially salvageable tissue.

When a stroke has been diagnosed, determining the underlying aetiology is important with regard to secondary stroke prevention. Common techniques include:

• ultrasound of the carotid arteries to determine carotid stenosis

• electrocardiogram (ECG) to detect arrhythmias of the heart which may send clots in the heart to the blood vessels of the brain

• Holter monitor to identify intermittent arrhythmias

• angiogram of the blood vessels of the brain to detect possible aneurysms or arteriovenous malformations and

• blood test to examine the presence of hypercholesterolemia (high cholesterol).

EXAMINATION

The selection of examination procedures will vary based on a number of factors including patient age , location and severity of stroke , stage of recovery , data from initial screenings , phase of rehabilitation and home /community / work situation , as well as other factors.

GENERAL EXAMINATION

General appearance including posture , motor activity

Vital signs - Level of consciousness ,pulse , BP , look for pupil size , conjugate deviations of eyes , Meningeal signs.

Neurocutaneous markers-

• Neurofibroma over the skin ( may have associated Tuberous sclerosis of brain )
• Sebaceous adenoma
• Sturge Weber syndrome - facial nerve (port wine stain ) involving one half of face with upper eyelid - associated with atrophy and calcification of ipsilateral cerebral hemisphere.
• Lymphadenopathy
• Cyanosis
• Clubbing
• Shortening of hemiplegic limb - indicates it is dating from early childhood
• Irregular pulse of atrial fibrillation

HIGHER FUNCTION

A. CONSCIOUSNESS - Check level of altered sensorium . for this refer Glasgow Coma Scale

B. ORIENTATION -in time , place , space , person are tested.

C. MEMORY

D. INTELLIGENCE

E. SPEECH - Speech disturbances APHASIA may occur

F. EMOTION

G. JUDGEMENT

H. BEHAVIOUR

I. PRESENCE OF HALLUCINATION / DELUSION / ILLUSION

GAIT

In hemiparesis, facial paresis may not be obvious. In mild cases, subtle features of facial paralysis (eg, flattening of the nasolabial fold on 1 side compared to the other, mild asymmetry of the palpebral fissures or of the face as the patient smiles) may be sought. The shoulder is adducted; the elbow is flexed; the forearm is pronated, and the wrist and fingers are flexed. In the lower extremities, the only indication of paresis may be that the ball of the patient's shoe may be worn more on the affected side.

In severe cases, the hand may be clenched; the knee is held in extension and the ankle is plantar flexed, making the paralyzed leg functionally longer than the other. The patient therefore has to circumduct the affected leg to ambulate.

In hemiplegic patients in whom all the paralysis is on the same side of the body, the lesion is of the contralateral upper motor neuron. In most cases, the lesion lies in the cortical, subcortical, or capsular region (therefore above the brainstem). In the alternating or crossed hemiplegias, CN paralysis is ipsilateral to the lesion, and body paralysis is contralateral. In such cases, CN paralysis is of the lower motor neuron type, and the location of the affected CN helps determine the level of the lesion in the brainstem. Therefore, paralysis of CN III on the right side and body paralysis on the left (Weber syndrome) indicates a midbrain lesion, whereas a lesion of CN VII with crossed hemiplegia (Millard-Gubler syndrome) indicates a pontine lesion, and CN XII paralysis with crossed hemiplegia (Jackson syndrome) indicates a lower medullary lesion.

CRANIAL NERVE INTEGRITY

The therapist examines for facial sensation (CN 5) , facial movements (CN 5 and 7), and labrynthine / auditory function (CN 8 ) . The presence of swallowing and drooling necessitates an examination of the motor nuclei of the lower brainstem cranial nerves (CN 9 , 10 and 12) affecting the muscles of the face , tongue , pharynx and larynx. The visual system should be carefully investigated , including tests for visual field defects (CN 2 , optic radiation , visual cortex ), acuity (CN 2 ) ,Pupillary reflexes (CN 2 and 3 ) and extraocular movements (CN 3 , 4 and 6).

CRANIAL NERVE SYNDROME ASSOCIATED WITH HEMIPLEGIA

SYNDROME	SITE	TRACT	SIGNS	USUAL CAUSE
1.WEBER`S	BASE OF MIDBRAIN	CORTICOSPINAL TRACT +3rd NERVE NUCLEUS	IPSILATERAL 3rd NERVE PALSY + CONTRALATERAL HEMIPLEGIA	VASCULAR , TUMOR
2. BENEDIKT`S	MIDBRAIN	CORTICOSPINAL TRACT , 3rd NERVE NUCLEUS + RED NUCLEUS	IPSILATERAL 3rd NERVE PALSY + CONTRALATERAL HEMIPLEGIA + TREMORS + ATAXIA	VASCULAR , TUMOR
3.MILLARD GUBLAR'S	PONS	CORTICOSPINAL TRACT + 6th AND 7th NERVE NUCLEUS	IPSILATERAL LMN 6th AND 7th NERVE PALSY + CONTRALATERAL HEMIPLEGIA	VASCULAR, TUMOR
4. MEDIAL MEDULLARY SYNDROME	MEDIAL MEDULLA	CORTICOSPINAL TRACT + 12th NERVE NUCLEUS	IPSILATERAL TONGUE PARALYSIS +CONTRALATERAL HEMIPLEGIA	VASCULAR

SENSATION

Sensory integration is the ability of the brain to organise , interpret , and use sensory information . Examination of sensory function involves testing patient's ability to interpret and discriminate among incoming sensory information.

Pattern of sensory loss	Site of lesion
1.Mono-neural 2.Stock and glove 3.Maculo-anesthetic (leprosy)	Peripheral nerve
4.Radicular sensory loss	Root
5.Saddle area loss	Conus
6.Dissociated sensory loss (Brown-Sequard syndrome) joint position / vibration / light touch on same side and pain / temperature on opposite side	Unilateral cord lesion
7.Sensory level	Extra-medullary lesion
8.Jacket sensory loss (dissociated)	Intra-medullary lesion
9.Crossed hemihyposthesia	Lateral medullary syndrome
10.Hemi-hyposthesia	Capsular & brain stem lesions
11.Corticalsensory loss numbness , agnosia , loss of two point discrimination , astereognosis , graphanaesthesia ,sensory inattention	Area(1, 2, 3) of parietal lobe

FLEXIBILITY AND JOINT INTEGRITY

An examination of joint flexibility should include passive ROM using a goniometer , joint hypermobility/hypomobility , and soft tissue changes (swelling ,inflammation or restriction). The shoulder and wrist should be examined closely because joint malalignment problems are common. Edema of the wrist often produces malaligned carpal bones with resulting impingement during wrist extension. Active ROM may be limited or impossible for the patient in early or middle recovery in the presence of paresis , spasticity , or obligatory synergies that can preclude isolated voluntary movements.

Contractures can develop anywhere but are particular apparent in the paretic limbs. As contractures progress , edema and pain may develop and further restrict mobility . In the UE ,limitations in the shoulder motion of flexion , abduction and external rotation are common. Contractures are likely in the elbow and finger flexors , and forearm pronators. In the LE , plantarflexion contractures are common.

MOTOR FUNCTION

TONE

An examination of tone is essential . Passive motion testing can be done to determine the presence of hypertonicity or spasticity. Severity of spasticity can be graded on the basis of resistance to passive stretch using the Modified Asthworth Scale.

STAGE OF FLACCID PARALYSIS: It is also known as shock stage . It lasts from 2-6 weeks , the shorter the duration better the prognosis. On the paralysed side there is complete loss of muscle tone (flaccidity) , absence of deep reflexes and no plantar reflex.This stage is prolonged by general poor condition of the patients health , infections (e.g. chest or urinary tract infection ) and bed sores. During recovery from the shock stage , the muscle tone and deep reflexes reappear and gradually increase. Babinski sign becomes positive . The stage of spasticity sets in .If the onset is associated with coma , the paralysed side is determined by the following :

1. The limb on the paralysed side are more flaccid and drop passively.
2. The cheek on the paralysed side moves in and out with respiration.

STAGE OF SPASTIC PARALYSIS : Stage of established hemiplegia where there is :

1.Paralysis of one side of the body . This paralysis shows a pyramidal distribution .

It affects the progravity more than the antigravity muscles as the former are normally weaker than the latter.

• In upper limb , the extensors are weaker than the flexors.
• In lower limb, the flexors are weaker than the extensors.

It affects the distal more than the proximal muscles.

• The hand is weaker than the shoulders.
• The foot is weaker than the hip

2. Hypertonia (spasticity) of the paralysed muscle of clasp knife:

It affects the antigravity more than the progravity muscles as the former normally have a stronger muscle tone :

• In upper limb, the flexors are more spastic than the extensors.
• In lower limb , the extensors are more spastic than the flexors.

CLONUS - Series of rythmical contraction occuring in response to maintenance of tension in muscle tone . It is due to gamma neuronal discharge. Sustained clonus is a sign of pyramidal tract lesion.

REFLEXES

Reflexes are altered and also vary according to the stage of recovery . Initially , stroke result in hyporeflexia with flaccidity . When spasticity and synergy emerges , hyperreflexia is seen . Deep tendon reflexes are hyperactive and patient may demonstrate clonus , claspknife response and positive Babinski , all consistent finding of upper motor neuron syndrome.There are certain pathological reflexes looked for in hemiplegia . In upper limb clinically significant - if markedly active and asymmetrical are Hoffmann's sign , Wartenberg's sign . Superficial reflexes in hemiplegia are loss of Abdominal reflex and cremastric reflex which is a sign of UMN Lesion .

VOLUNTARY MOVEMENTS

Abnormal and highly stereotyped obligatory synergies emerge with spasticity following stroke . Thus the patient is unable to perform an isolated movements of a single limb segment without producing movements in the remainder of the limb. Two distinct abnormal synergy patterns have been described for each extremity : flexion and extension synergy.

File:Limb Synergies.png

Chedoke-McMaster Stroke Assessment

An inspection of synergy components reveals that certain muscles are not involved in either synergies . These muscles include the 1. latissimus dorsi 2. teres major 3. serratus anterior 4. finger extensors and 5. ankle evertors. These muscles are therefore generally difficult to activate while the patient are exhibiting these patterns.

For assessment Fugl-Meyer Assessment of Motor Recovery after Stroke

COORDINATION

Proprioceptive loses can result in sensory ataxia . Strokes affecting the cerebellum typically produce cerebellar ataxia and motor weakness. The resulting problem with timing and sequencing of muscles can significantly impair function and limit adaptability to changing task and environmental demands.

The therapist focuses on e↑lements of speed / rate control , steadiness , response orientation , and reaction and movement times.Fine motor control and dexterity should be examined using writing , dressing and feeding tasks .