Motor system
Movements result from coordinated contraction and relaxation of groups of muscles. The prime movers contract with reciprocal relaxation of the antagonists. Synergists are those muscles which stabilize the proximal joints and maintain appropriate postures to make the movement most effective. Voluntary activity is initiated by the upper moter neuron (UMN) which consists of neurons of the motor cortex (precentral area) and its fiber connections. The relaxation of the antagonists and activity of the synergists are coordinated by the cerebellum. The maintenance of posture is mediated largely through the extrapyramidal system and the vestibular and spinal reflexes. The influences from the upper motor neuron, extrapuramidal system and cerebellum act upon the anterior horn cell of the spinal cord or the motor nuclei of the brain stem, which have connections to groups of muscle fibers. The lower motor unit which is the final common path consists of the anterior horn cell and its efferent connections. Whereas the lower motor neuron (LMN) innervates groups of muscle fibers, the upper motor neuron mediates movements.
The upper motor neuron (UMN)
This consists of the cortical cells (pyramidal cells) which are located in the motor area (pre-central gyrus) and their axons which pass down the brain stem and spinal cord to reach the brain stem nuclei or anterior horn cells of the opposite side. In the motor area, which represents the opposite side of the body parts are represented from above downwards in the order of perineum, foot, leg, thigh, trunk, arm, of representation is proportional to the functional importance of the part, so that the hand, face, and foot receive a wider area of the motor cortex than the other parts.
From the motor cortex, the fibers project down through the subcortical region to reach the internal capsule where the motor fibres come into close contact and they occupy the anterior two-thirds of the posterior limb of the internal capsule. In the internal capsule, the fibers for the head are in front and those for the lower limbs are behind. Still further behind in the posterior limb of the internal capsule are the sensory fibers, visual fibers, and auditory fibers. From the internal capsule, the motor ibers pass through the midbrain (where they are held in the cerebral penduncles), the pons (where they break up into smaller fasciculi and are criss-crossed by other fiber tracts), and the medualla (where they aggregate to form the medullary pyramids). In the mid-brain, the pyramid tract is in close relation with the 3rd nerve nucleus, in the pons it is close to the 7th nerve nucleus, and in the medulla it is close to the 12th nerve nucleus. Therefore lesions at these levels also involve the corresponding cranial nerve nuclei. In the brain stem (mid-brain, pons, and medulla) the pyramidal tract gives UMN fibers to the cranial nerve nuclei of the opposite side. At the lower end of the medulla, the major portion of the pyramidal tract (about 80%) crosses over to the opposite side and this crossed pyramidal tract descends in the lateral corticospinal tract along the full length of the spinal cord to supply the anterior horn cells. The uncrossed fibers descend in the spinal cord as the anterior corticospinal tract and at different spinal segments they also cross to the opposite side to supply the anterior horn cells. Thus it can be seen that the upper motor neuron controls the brain stem and spinal nuclei of the opposite side.
Lesions of the pyramidal tract result in loss of voluntary activity. since the UMN normally carries fibres which inhibit the stretch reflexes mediated by the LMN lesions of the UMN result in exaggeration of these stretch reflexes. The superficial reflexes (cutaneous protective reflexes) also are altered. Upper motor neuron lesions are clinically characterised by the following signs:
1. Loss of voluntary power
2. Increase in tone-clasp knife rigidity also known as spasticity. In this the resistance to passive movement. Muscles relax, once this phase is overcome. The flexor muscles of the upper limb and extensor muscles of the lower limb are maximally affected.
3. Exaggerated deep tendon reflexes: When the deep tendon reflexes are exaggerated, simple increased in amplitude may occur even without neurological disorders, eg. anziety. Inequality between corresponding reflexes on either side is of great diagnostic value. In bilateral UMN lesions above the level of the Pons, the jaw jerk is also exaggerated. When the UMN lesion is well established, clonus may develop. In clinical practice, patellar clonus and ankle clonus are the ones commonly looked for.
4. Alteration in superficial reflexes: The abdomina and cremasteric reflexes are lost.
The plantar response: This becomes extensor. This is referred to as the Babinski's sign. Normally on stroking the lateral aspect of the foot from the heel to the ball of the big toe with a sharp object a set of responses occurs. The big toe flexes, the lateral four toes also flex and crowd together. Minimal contraction of the tensor fascia lata, the adductors of the thigh and sartorius occurs. This whole response is referred to as the 'flexor' plantar response.
In UMN lesion when a nociceptive stimulus is applied to the lateral aspect of the foot, the big toe extends (dorsiflexes), and the other toes fan out and dorsiflex. With stronger stimuli, the ankle dorsiflexes and hip and knee flex. If the UMN lesion is small, this abnormal response is elicitable only from the lateral margin of the sole of the foot. As the lesion extends, the response can be elicited by applying the stimulus over a wider area, such as the medial aspect of the foot and the leg. These are known by different names.
Oppenheim's sign: Extensor plantar response elicited by stroking the shin of the leg.
Gordon's sign: Squeezing the tendo-Achilles to elicit the extensore plantar response.
Chaddock's sign: A light stroke applied to the lateral aspect of the dorsum of the foot to elicit the extensor response.
The student shold learn to elicit the plantar response carefully since it is of great value in deciding upon the presence or absence of an UMN lesion. The plantar response is normally extenosr in babies till the age of one year by which time the corticospinal tacts become myelinated. When the baby learns to walk, the plantar response becomes flexor. The plantar response is bilaterally extensor in deep sleep and coma.
5.Absence of wasting: In UMN lesion, unlike LMN lesion, wasting is absent. This is because the lower motor unit is intact, so that reflex activity and trophic influences are preserved. prolonged disuse may give rise to slight atrophy.
6. Electrical reactions of the affected muscles are unaltered.
Since the UMN starts in the cortex and comes down a long way it is essential to determine the level at which it is interrupted.
Cortical lesions: These are characterized by localized paralysis of one side of the face, or one limb etc. Sine the moro area of the cortex is extensive, only large lesions produce total hemiplegia. Presence of other cortical dysfunctions such as aphasia and Jacksonian epilepsy is suggestive of cortical lesions.
Internal Capsule: Since all the pyramidal fibers are held within a small area in this structure, lesions at this level produce extensive paralysis of the opposite side resulting in hemiplegia in which the face upper and lower limbs and half of the trunk are paralysed. Extension of the lesion posteriorly results in hemianaesthesia and hemianopia as well.
Brainstem lesions:
Lesions in the midbrain, pons and medulla lead to lower motor neuron paralysis of the corresponding cranial nerve and upper motor neuron lesion on the opposite side (crossed hemiplegia).
Midbrain lesion- ipsilateral 3rd nerve lesion and hemiplegia of the opposite side.
Pontine Lesion-ipsilateral 7t nerve lesion and hemiplegia of the opposite side.
Medullary lesion-ipsilateral 12th nerve lesion and hemiplegia of the opposite side.
Spinal Cord lesions: since the major portion of the pyramidal tract has crossed at the lower margin of the medula, lesions below this level produce ipsilateral UMN lesions. In many cases the lesions are bilateral. The level of lesion is determined by the presence of other accompanying signs such as sensory loss and lower motor neuron involvement at the affected segment. In pure pyramidal tract lesions, the upper level is determined by the loss of voluntary power and reflex abnormalities.
Lower motor neuron (LMN): The motor cells of the cranial nerve nuclei of the brain stem and the anterior horn cells of the spinal cord from the lower motor neurons. The axons from these cells reach the mixed peripheral nerve (from the spinal cord they emerge as the anterior nerve root) and supply the motor end plates of a group of muscles. The anterior horn cell, its axon and the group of muscle fibers it supplies comprise a lower motor unit. All muscles are supplied by several such motor units. The anterior horn cell is influence by umpulses cerebellum, and sensory afferents from the posterior nerve roots. The lower motor neuron is an integral part of the spinal reflex arc. It is the final common path for all motor activity (both voluntary and reflex) of all muscles. Integrity of the lower motor neuron is essential for maintaining the normal nutrition and size of the muscle fibre and when the lower motor neuron is damaged, the corresponding muscles undergo atrophy.
Signs of lower motor neuron lesion
1. Loss of all movements-voluntary and reflex.
2. Loss of tone-flaccidity
3. Wasting-which appears within 2-3 weeks of the lesion.
4. Loss of deep tendon reflexes and the corresponding superficial reflexes
5. Denervated muscle fibers contract spontaneously. Contraction of single muscle fibers is called fibrillation. This is not visible, but can be detected by electromyography. Groups of muscle fibers which are damaged, but which are still capable of contracting spontaneously give rise to visible fasciculations.
6. The atrophic muscles undergo contractures.
7. Electrical activity of the muscle is altered and this can be detected by electromagnyography. The pattern of motor loss depends on the site of affection of the lower motor neuron.
Lesions of the anterior horn cells or the anterior root give rise to segmental loss of function. Lesions in the peripheral nerve give rise to paralysis of the muscles supplied by that nerve. often peripheral nerve lesions are associated with sensory disturbances.
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