engine system
Movements are the result of coordinated contraction and relaxation of muscle groups. The prime movers contract with reciprocal relaxation of the antagonists. Synergists are those muscles that stabilize the proximal joints and maintain proper postures for more efficient movement. Voluntary activity is initiated by the upper motor neuron (UMN), which consists of neurons from the motor cortex (precentral area) and their fiber connections. The relaxation of the antagonists and the activity of the synergists are coordinated by the cerebellum. Postural maintenance is largely mediated by the extrapyramidal system and vestibular and spinal reflexes. Influences from the upper motor neuron, extrapuramidal system, and cerebellum act on the anterior horn cell of the spinal cord or the motor nuclei of the brainstem, which have connections to groups of muscle fibers. The lower motor unit, which is the final common pathway, consists of the anterior horn cell and its efferent connections. While the lower motor neuron (LMN) innervates groups of muscle fibers, the upper motor neuron mediates movements.
The upper motor neuron (UMN)
It consists of cortical cells (pyramidal cells) found in the motor area (precentral gyrus) and their axons that travel down the brainstem and spinal cord to reach the brainstem nuclei or anterior horn cells on the opposite side. In the motor area, which represents the opposite side of the body, the parts are represented from top to bottom in the order of perineum, foot, leg, thigh, trunk, arm, the representation is proportional to the functional importance of the part, from so that the hand, face, and foot receive a wider area of motor cortex than the other parts.
From the motor cortex, the fibers project downward through the subcortical region to reach the internal capsule where the motor fibers come into close contact and occupy the anterior two-thirds of the posterior arm of the internal capsule. In the internal capsule, the fibers of the head are in front and those of the lower limbs are behind. Even further back, in the posterior arm of the internal capsule, are the sensory fibers, the visual fibers, and the auditory fibers. From the internal capsule, the motor fibers pass through the midbrain (where they are held in the cerebral stalks), the pons (where they divide into smaller tracts and are traversed by other fiber tracts), and the medulla (where they join). . aggregates to form the medullary pyramids). In the midbrain, the pyramidal tract is closely related to the nerve nucleus 3, in the pons it is close to the nerve nucleus 7, and in the medulla it is close to the nerve nucleus 12. Therefore, lesions at these levels they also involve the corresponding cranial nerve nuclei. In the brain stem (midbrain, pons, and medulla oblongata), the pyramidal tract supplies UMN fibers to the cranial nerve nuclei on the opposite side. At the lower end of the medulla oblongata, most of the pyramidal tract (about 80%) crosses to the opposite side, and this crossed pyramidal tract descends in the lateral corticospinal tract along the entire length of the spinal cord to supply the anterior horn. cells. The uncrossed fibers descend into the spinal cord as the anterior corticospinal tract and in different spinal segments also cross to the opposite side to innervate the anterior horn cells. Thus, the upper motor neuron can be seen to control the brainstem and spinal nuclei on the opposite side.
Injuries to the pyramidal tract result in loss of voluntary activity. since the UMN normally carries fibers that inhibit stretch reflexes mediated by UMN lesions in the UMN result in an exaggeration of these stretch reflexes. Superficial reflexes (cutaneous protective reflexes) are also impaired. Upper motor neuron lesions are clinically characterized by the following signs:
1. Loss of voluntary power
2. Increased stiffness of the tone-closing scalpel, also known as spasticity. In this resistance to passive movement. The muscles relax, once this phase is over. The flexor muscles of the upper extremity and the extensor muscles of the lower extremity are affected the most.
3. Exaggerated deep tendon reflexes: When deep tendon reflexes are exaggerated, a simple increase in amplitude may occur even without neurological disturbances, e.g. anxiety The inequality between the corresponding reflexes on each side has great diagnostic value. In bilateral UMN lesions above the level of the pons, the jaw reflex is also exaggerated. When the UMN lesion is well established, clonus may develop. In clinical practice, patellar clonus and ankle clonus are commonly sought.
4. Alteration of superficial reflexes: Abdominal and cremasteric reflexes are lost.
The plantar response: This becomes extender. This is known as the Babinski sign. Normally, stroking the lateral aspect of the foot from the heel to the tip of the big toe with a sharp object elicits a series of responses. The big toe is flexed, the four lateral toes are also flexed and bunched. There is minimal contraction of the tensor fascia latae, the adductors of the thigh, and the sartorius. This entire response is known as the ‘flexor’ plantar response.
In the UMN lesion, when a nociceptive stimulus is applied to the lateral aspect of the foot, the great toe extends (dorsiflexion) and the other toes fan out and dorsiflexion. With stronger stimuli, the ankle dorsiflexes and the hip and knee flex. If the UMN lesion is small, this abnormal response can only be obtained from the lateral margin of the sole. As the lesion spreads, the response can be elicited by applying the stimulus over a wider area, such as the medial aspect of the foot and lower 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 Achilles tendon to elicit the extensor plantar response.
Chaddock’s sign: a light blow applied to the lateral aspect of the dorsum of the foot to elicit the extensor response.
The student must learn to elicit the plantar response carefully, as it is of great value in deciding on the presence or absence of a UMN lesion. The plantar response is normally greatest in infants up to the age of one year, at which time corticospinal touches 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 emaciation: in the UMN lesion, unlike the LMN lesion, there is no emaciation. This is because the lower motor unit is intact, so reflex activity and trophic influences are preserved. prolonged disuse may lead to slight atrophy.
6. The electrical reactions of the affected muscles are altered.
Since UMN starts in the cortex and goes very low, it is essential to determine the level at which it is discontinued.
cortical lesions: These are characterized by localized paralysis of one side of the face, or a limb, etc. Since the moro area of the cortex is extensive, only large lesions produce full hemiplegia. The presence of other cortical dysfunctions, such as aphasia and Jacksonian epilepsy, suggests 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 upper and lower extremities of the face and head are paralyzed. half of the trunk The extent of the lesion subsequently produces hemianesthesia and also hemianopsia.
brain stem lesions:
Lesions in the midbrain, pons, and medulla oblongata cause lower motor neuron palsy of the corresponding cranial nerve and upper motor neuron lesion on the opposite side (crossed hemiplegia).
Midbrain lesion: ipsilateral third nerve lesion and hemiplegia on the opposite side.
Pontine lesion: ipsilateral nerve 7t lesion and hemiplegia on the opposite side.
Spinal cord injury: ipsilateral injury to the XII nerve and hemiplegia on the opposite side.
spinal cord injuries: Since most of the pyramidal tract has been crossed at the lower margin of the medulla, lesions below this level produce ipsilateral UMN lesions. In many cases the lesions are bilateral. The level of the lesion is determined by the presence of other accompanying signs, such as sensory loss and lower motor neuron involvement in the affected segment. In pure pyramidal tract lesions, the upper level is determined by loss of voluntary force and reflex abnormalities.
Lower motor neuron (LMN): Motor cells of the cranial nerve nuclei of the brain stem and anterior horn cells of the spinal cord of lower motor neurons. The axons of these cells reach the mixed peripheral nerve (from the spinal cord they emerge as the anterior nerve root) and innervate the motor end plates of a group of muscles. The anterior horn cell, its axon, and the group of muscle fibers it innervates comprise a lower motor unit. All muscles are innervated by several of these motor units. The anterior horn cell is influenced by impulses from the cerebellum and sensory afferent fibers from the posterior nerve roots. The lower motor neuron is an integral part of the spinal reflex arc. It is the final common pathway for all motor activity (both voluntary and reflex) of all muscles. Lower motor neuron integrity is essential for maintaining normal muscle fiber nutrition and size, and when the lower motor neuron is damaged, the corresponding muscles atrophy.
Signs of lower motor neuron injury
1. Loss of all movements-voluntary and reflexes.
2. Loss of tone-flabbiness
3. Emaciation: appearing within 2-3 weeks after injury.
4. Loss of deep tendon reflexes and corresponding superficial reflexes
5. The denervated muscle fibers contract spontaneously. The contraction of individual muscle fibers is called fibrillation. This is not visible, but can be detected by electromyography. Muscle fiber groups that are damaged but still capable of spontaneous contraction give rise to visible fasciculations.
6. Atrophic muscles suffer from contractures.
7. The electrical activity of the muscle is altered and this can be detected by electromagnography. The pattern of motor loss depends on the site of lower motor neuron involvement.
Lesions of the anterior horn or anterior root cells result in segmental loss of function. Injuries to the peripheral nerve result in paralysis of the muscles supplied by that nerve. Peripheral nerve lesions are often associated with sensory disturbances.