Hemiplegia

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

Acute bleeding and hemorrhagic transformation are visible on CT scanning . In the subacute phase CT scan can delineate the development of cerebral edema (within 3 days) , which then fades over the next 2 to 3 weeks. Cerebral infarction (within 3 to 5 days) is visible with the addition of contrast material by showing areas of decreased density. Long term parenchymal changes consistent with scar formation are also visible on CT.

MAGNETIC RESONANCE IMAGING

MRI is more sensitive in the diagnosis of acute stroke , allowing detection of cerebral ischemia as early as 30 minutes after vascular occlusion and infarction within 2 to 6 hours. It is also able to detail the extent of infarction or haemorrhage and can detect smaller lesion than a CT scan . Use of contrast enhancement allows documentation of changes in an infarct over the first 2 to 3 weeks.

MAGNETIC RESONANCE ANGIOGRAPHY

Magnetic resonance angiography (MRA) is a type of magnetic resonance image that uses special software to create an image of the arteries in the brain. It is used to identify vascular abnormalities (e.g.,stenosis) and alterations in blood flow as a result of embolus or thrombosis.

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.

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).

SENSATION

Specific localization areas of dysfunction are common with cortical lesions , whereas diffuse involvement throughout one side of the body suggests deeper lesions involving the thalamus and adjacent structures. Impairment in touch sensation (64% to 94%), proprioception (17%to 52%) , vibration (44%) and loss of pinprick sensation (35% to 71%) have been reported. Symptoms of crossed anesthesia (ipsilateral facial impairments with contralateral trunk and limb involvement ) typify brainstem lesions.

A sensory examination should include testing of superficial sensations (touch , temperature , pressure , sharp or dull discrimination ) and deep sensations (proprioception ,kinesthesia , vibration ). Combined cortical sensation such as stereognosis , tactile localization , two point discrimination , texture recognition should also be examined . Comparison with the intact side should bee viewed with caution because impairment may exist in the supposedly "normal" extremities due to aging and co- morbidities.

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

Flaccidity is present immediately after stroke and is due primarily to the effects of cerebral shock. It is generally short lived , lasting a few days or weeks . Flaccidity may persist in a small number of patients with lesions restricted to the primary motor cortex or cerebellum. UE spasticity is frequently strong in scapular retractors ; shoulder adductors , depressors , and internal rotators ; elbow flexors and forearm pronators ; and wrist and finger flexors. In the neck spasticity may cause increased lateral flexion to the hemiplegic side. In the LE , spasticity is often strong in the pelvic retractors, hip adductors and internal rotators , hip and knee extensors , plantarflexors and supinators , and toe flexors.

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.

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.

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 .