Motor and Sensory Functions of the Nervous System
The motor cortex, a vertical band within each cerebral hemi-sphere, controls the voluntary movements of the body. The exact locations within the brain at which the voluntary movements of the muscles of the face, thumb, hand, arm, trunk, and leg origi-nate are known (Fig. 60-13). To initiate muscle movement, these particular cells must send the stimulus down along their fibers. Stimulation of these cells with an electric current will also result in muscle contraction. En route to the pons, the motor fibers converge into a tight bundle known as the internal capsule. A com-paratively small injury to the capsule causes paralysis in more muscles than does a much larger injury to the cortex itself.
Within the medulla, the motor axons from the cortex form the motor pathways or tracts, notably the corticospinal or pyramidal tracts. Here, most of the fibers cross (or decussate) to the oppo-site side, continuing as a crossed pyramidal tract. The remaining fibers enter the spinal cord on the same side as the direct pyrami-dal tract. Each fiber in this tract finally crosses to the opposite side of the cord and terminates within the gray matter of the anterior horn on that side, in proximity to a motor nerve cell. Fibers of the crossed pyramidal tract terminate within the anterior horn and make connections with anterior horn cells on the same side. All of the motor fibers of the spinal nerves represent extensions of these anterior horn cells, with each of these fibers communicat-ing with only one particular muscle fiber.
The motor system is complex, and motor function depends on the integrity of the corticospinal tracts, the extrapyramidal system, and cerebellar function. A motor impulse consists of a two-neuron pathway (described below). The motor nerve pathways are contained in the spinal cord. Some represent the pathways of the so-called extrapyramidal system, establishing connections be-tween the anterior horn cells and the automatic control centers located in the basal ganglia and the cerebellum. Others are components of reflex arcs, forming synaptic connections between anterior horn cells and sensory fibers that have entered adjacent or neighboring segments of the cord.
The voluntary motor systemconsists of two groups of neurons: upper motor neurons and lower motor neurons. Upper motor neurons originate in the cere-bral cortex, the cerebellum, and the brain stem and modulate the activity of the lower motor neurons. Upper motor neuron fibers make up the descending motor pathways and are located entirely within the CNS. Lower motor neurons are located either in the anterior horn of the spinal cord gray matter or within cranial nerve nuclei in the brain stem. Axons of both extend through pe-ripheral nerves and terminate in skeletal muscle. Lower motor neurons are located in both the CNS and the peripheral nervous system.
The motor pathways from the brain to the spinal cord, as well as from the cerebrum to the brain stem, are formed by upper motor neurons. They begin in the cortex of one side of the brain, descend through the internal capsule, cross to the opposite side in the brain stem, descend through the corticospinal tract, and synapse with the lower motor neurons in the cord. The lower motor neurons receive the impulse in the posterior part of the cord and run to the myoneural junction located in the periph-eral muscle. The clinical features of lesions of upper and lower motor neurons are discussed in the sections that follow and in Table 60-4.
Upper Motor Neuron Lesions. Upper motor neuron lesions can involve the motor cortex, the internal capsule, the spinal cord, and other structures of the brain through which the corticospinal tract descends. If the upper motor neurons are damaged or de-stroyed, as frequently occurs with stroke or spinal cord injury, paralysis (loss of voluntary movement) results. However, because the inhibitory influences of intact upper motor neurons are now impaired, reflex (involuntary) movements are uninhibited, and hence hyperactive deep tendon reflexes, diminished or absent superficial reflexes, and pathologic reflexes such as a Babinski re-sponse occur. Severe leg spasms can occur as the result of an upper motor neuron lesion; the spasms result from the preserved reflex arc, which lacks inhibition along the spinal cord below the level of injury.
There is little or no muscle atrophy, and muscles remain per-manently tense, exhibiting spastic paralysis or paresis (weakness). Paralysis associated with upper motor neuron lesions usually af-fects a whole extremity, both extremities, and an entire half of the body. Hemiplegia (paralysis of an arm and leg on the same side of the body) can be the result of an upper motor neuron lesion. If hemorrhage, an embolus, or a thrombus destroys the fibers from the motor area in the internal capsule, the arm and the leg of the opposite side become stiff and very weak or paralyzed, and the reflexes are hyperactive. When both legs are paralyzed, the condition is called paraplegia; paralysis of all four extremities is quadriple-gia.
A patient is considered to havelower motor neuron damage if a motor nerve is severed between the muscle and the spinal cord.
The result of lower motor neu-ron damage is muscle paralysis. Reflexes are lost, and the muscle becomes flaccid (limp) and atrophied from disuse. If the patient has injured the spinal trunk and it can heal, use of the muscles connected to that section of the spinal cord may be regained. If the anterior horn motor cells are destroyed, however, the nerves cannot regenerate and the muscles are never useful again. Flac-cid paralysis and atrophy of the affected muscles are the princi-pal signs of lower motor neuron disease. Lower motor neuron lesions can be the result of trauma, infection (poliomyelitis), tox-ins, vascular disorders, congenital malformations, degenerative processes, and neoplasms. Compression of nerve roots by herni-ated intervertebral disks is a common cause of lower motor neu-ron dysfunction.
The smoothness, accuracy, andstrength that characterize the muscular movements of a normal person are attributable to the influence of the cerebellum and the basal ganglia.
The cerebellum (refer to Fig. 60-2), described earlier, is located beneath the occipital lobe of the cerebrum; it is responsible for the coordination, balance, and timing of all muscular move-ments that originate in the motor centers of the cerebral cortex. Through the action of the cerebellum, the contractions of op-posing muscle groups are adjusted in relation to each other to maximal mechanical advantage; muscle contractions can be sus-tained evenly at the desired tension and without significant fluc-tuation, and reciprocal movements can be reproduced at high and constant speed, in stereotyped fashion and with relatively little effort.
The basal ganglia, masses of gray matter in the midbrain be-neath the cerebral hemispheres, border the lateral ventricles and lie in proximity to the internal capsule. The basal ganglia play an important role in planning and coordinating motor movements and posture. Complex neural connections link the basal ganglia with the cerebral cortex. The major effect of these structures is to inhibit unwanted muscular activity; disorders of the basal ganglia result in exaggerated, uncontrolled movements.
Impaired cerebellar function, which may occur as a result of an intracranial injury or some type of an expanding mass (eg, a hemorrhage, abscess, or tumor), results in loss of muscle tone, weakness, and fatigue. Depending on the area of the brain af-fected, the patient has different motor symptoms or responses. The patient may demonstrate decorticate, decerebrate, or flaccid posturing, usually as a result of cerebral trauma (Bateman, 2001). Decortication (decorticate posturing) is the result of lesions of the internal capsule or cerebral hemispheres; the patient has flexion and internal rotation of the arms and wrists and extension, inter-nal rotation, and plantar flexion of the feet. Decerebration (de-cerebrate posturing), the result of lesions at the midbrain, is more ominous than decortication. The patient has extension and ex-ternal rotation of the arms and wrists and extension, plantar flex-ion, and internal rotation of the feet. Flaccid posturing is usually the result of lower brain stem dysfunction; the patient has no motor function, is limp, and lacks motor tone.
Flaccidity preceded by decerebration in a patient with cerebral injury indicates severe neurologic impairment, which may herald brain death. However, before the declaration of brain death, the patient must have spinal cord injury ruled out, the effects of all neuromuscular paralyzing agents must have worn off, and any other possible treatable causes of neurologic impairment must be investigated.
Tumors, infection, or abscess and increased intracranial pres-sure can all affect the cerebellum. Cerebellar signs, such as ataxia, incoordination, and seizures, as well as CSF obstruction and com-pression of the brain stem may be seen. Signs of increased in-tracranial pressure, including vomiting, headache, and changes in vital signs and level of consciousness, are especially common when CSF flow is obstructed.
Destruction or dysfunction of the basal ganglia leads not to paralysis but to muscle rigidity, with disturbances of posture and movement. Such patients tend to have involuntary movements. These may take the form of coarse tremors, most often in the upper extremities, particularly in the distal portions; athetosis, movement of a slow, squirming, writhing, twisting type; or chorea, marked by spasmodic, purposeless, irregular, uncoordi-nated motions of the trunk and the extremities, and facial gri-macing. Disorders due to lesions of the basal ganglia include Parkinson’s disease, Huntington’s disease, and spasmodic torticollis.
The thalamus, a major receivingand transmitting center for the afferent sensory nerves, is a large structure connected to the midbrain. It lies next to the third ven-tricle and forms the floor of the lateral ventricle (see Fig. 60-3). The thalamus integrates all sensory impulses except olfaction. It plays a role in the conscious awareness of pain and the recogni-tion of variation in temperature and touch. The thalamus is re-sponsible for the sense of movement and position and the ability to recognize the size, shape, and quality of objects.
Afferent impulses travel from theirpoints of origin to their destinations in the cerebral cortex via the ascending pathways directly, or they may cross at the level of the spinal cord or in the medulla, depending on the type of sensation that is registered. Sensory information may be integrated at the level of the spinal cord or may be relayed to the brain. Knowledge of these pathways is important for neurologic assessment and for understanding symptoms and their relationship to various lesions.
Sensory impulses enter the spinal cord by way of the posterior root. These axons convey sensations of heat, cold, and pain and enter the posterior gray column of the cord, where they make connections with the cells of secondary neurons. Pain and tem-perature fibers cross immediately to the opposite side of the cord and course upward to the thalamus. Fibers carrying sensations of touch, light pressure, and localization do not connect immedi-ately with the second neuron but ascend the cord for a variable distance before entering the gray matter and completing this con-nection. The axon of the secondary neuron crosses the cord and proceeds upward to the thalamus.
Position and vibratory sensation are produced by stimuli aris-ing from muscles, joints, and bones. These stimuli are conveyed, uncrossed, all the way to the brain stem by the axon of the pri-mary neuron. In the medulla, synaptic connections are made with cells of the secondary neurons, whose axons cross to the opposite side and then proceed to the thalamus.
Destruction of a sensory nerve results in totalloss of sensation in its area of distribution. Transection of the spinal cord yields complete anesthesia below the level of injury. Selective destruction or degeneration of the posterior columns of the spinal cord is responsible for a loss of position and vibratory sense in segments distal to the lesion, without loss of touch, pain, or temperature perception. A lesion, such as a cyst, in the center of the spinal cord causes dissociation of sensation—loss of pain at the level of the lesion. This occurs because the fibers carrying pain and temperature cross within the cord immediately on en-tering; thus, any lesion that divides the cord longitudinally di-vides these fibers. Other sensory fibers ascend the cord for variable distances, some even to the medulla, before crossing, thereby by-passing the lesion and avoiding destruction.
Lesions affecting the posterior spinal nerve roots may cause im-pairment of tactile sensation, including intermittent severe pain that is referred to their areas of distribution. Tingling of the fingers and the toes can be a prominent symptom of spinal cord disease, presumably due to degenerative changes in the sensory fibers that extend to the thalamus (ie, belonging to the spinothalamic tract).
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