Clinical Note

Lesions and Motor Reflex Abnormalities

Specific lesions within the neuronal components of the somatic motor system can cause characteristic abnormalities in motor reflexes. Flaccid paralysis usually denotes the loss of peripheral nerve innervation. Without input from alpha motor neurons of the spinal cord, there is no voluntary movement of the muscle and no resistance to passive movement. No reflexes can be elicited, and atrophy of the muscle will be observed. Unlike components of the central nervous system (CNS), axonal processes of peripheral nerves can regenerate in some cases, particularly if the lesion is localized to peripheral regions of the nerve. Reinnervation can take a year or more, after which time patients may experience a partial or (in rare cases) complete return of function and a reversal in the process of muscle atrophy.

Muscle rigidity is seen in patients with damage to descending spinal tracts that normally inhibit alpha motor neurons or, more commonly, with damage to motor areas in the brain from which these inhibitory tracts originate. Without normal inhibitory input, motor neurons are overly active and cause heightened contraction in somatic muscles. The patient may have difficulty in performing most voluntary and involuntary movements because the balanced (inhibitory versus excitatory) nature of the motor command system will be disturbed (see Chapter 57). Examination of the patient will demonstrate increased resistance to passive motion in all directions in all muscles because the lesion is central in origin and thus will affect all levels of the spinal cord. A common cause of rigidity is Parkinson's disease, which affects certain motor regions of the basal ganglia (see Chapter 58).

Muscle spasticity is clinically defined as an abnormal increase in muscle tone due to loss of inhibition of gamma motor neurons. Because gamma motor neurons normally regulate the output of muscle stretch receptors, disinhibition of these neurons will lead to an exaggerated (spastic) stretch reflex in the affected muscles. Like muscle rigidity, spasticity reflects loss of descending tracts to the spinal cord. However, in this case the abnormal reflexes characteristically result from a general lesion of the cord, such as spinal transection, which destroys all CNS input to alpha and gamma motor neurons below the level of the lesion. Patients with a severed spinal cord will initially undergo a period of spinal shock, characterized by flaccid paralysis of muscles below the transection. Voluntary control of these muscles is permanently lost, but over time the flaccid paralysis will be followed by muscle spasticity evidenced by a much increased response in tendon reflexes.

tract acts in conjunction with the vestibulospinal tract, particularly the medial portion, in order to bring about this orientation response. Because of its relatively small size, the tectospinal tract may be the less important of the two tracts involved in the orientation response.

Two other descending motor tracts originate from the reticular formation in the brain stem. Located in the central core of the pons and medulla just anterior to the cerebral aqueduct, the reticular formation is composed of a highly interconnected meshwork of neurons that is not organized in discrete nuclei. This reticular organization serves a number of coordinating functions. As previously described, gaze centers of the oculomotor system are located within the reticular formation. Two motor centers regulating spinal motor neurons are also recognized. Cells in the pontine reticular formation give rise to the pontine reticulospinal tract, which projects ipsilater-ally along with other fibers in the MLF to terminate on alpha and gamma motor neurons, innervating axial muscles and extensor muscles of the limbs. Through its excitatory input it serves to increase muscle tone.

The medullary reticulospinal tract originates in the medullary reticular formation, projects bilaterally, and terminates on motor neurons innervating axial and extensor muscles of the limbs. This pathway serves to balance the excitatory drive from the pontine reticulospinal tract by inhibiting motor neurons and decreasing axial and extensor muscle tone. Having separate pathways for excitation

FIGURE 5 Driving forces to lower motor neurons. (A) Inputs and outputs from alpha and gamma motor neurons in the spinal cord: (1) Sensory input enters the dorsal aspects of the cord; (2) excitatory and inhibitory interneurons are concentrated in the central gray of the spinal cord and brain stem; (3) medial tracts are comprised of the uncrossed neurons of the corticospinal tract and neurons descending from the brain stem; (4) lateral tracts arise in the cerebellum (relayed through the red nucleus) and the cortex. (B) Coronal section of the brain through the precentral gyrus shows the origin of the descending medial tracts. (C) Coronal section shows the origin of the descending lateral tracts.

and inhibition of the same motor units may seem unnecessary and redundant; nevertheless, there are numerous examples of this type of dual-control organization within the nervous system, leading to the conclusion that the enhanced control and sensitivity it provides must offer significant advantages. The motor cortex provides strong input to the reticular formation and in this way indirectly regulates the ongoing tone of the same motor units that it activates directly through the corticospinal tract.

One of the largest and most important descending tracts in the spinal cord is the lateral corticospinal tract or pyramidal tract (Fig. 6). It contains 1 million fibers, half of which originate from large pyramidal cells within the primary motor cortex located just anterior to the central left cerebral cortex left cerebral cortex

A. Striatum caudate putamen internal capsule

B. Thalamus

FIGURE 6 Targets of corticofugal projections. The CNS is shown in coronal section (left), the striatum and thalamus are shown in lateral view, and the brain stem and spinal cord are shown in cross section (right). Descending corticofugal fibers (shown in blue) originate from widespread areas of the motor cortex and coalesce into fiber bundles called the internal capsule. They then penetrate nuclear groups in the diencephalon (caudate and putamen) and project through the brain stem. They undergo partial decussation in the medulla and project through the spinal cord. Specific tracts within the main fiber bundles are named according to their targets: The corticostriate tract (A, to the caudate and putamen) and the corticothalamic tract (B, to the thalamus) are involved in "motor loops'' that coordinate movement commands (see Chapter 58). The corticorubro tract (C, to the red nucleus) and the corticopontine tract (D, to the pontine nuclei) influence cerebellar function (see Chapter 59). The corticoreticular tract (E) acts on many of the motor nuclei of the brain stem. The cortico-olivary tract (F) and corticocuneate/gracile tract (G) modify sensory processing. The lateral corticospinal tract (H, descending contralaterally) influences motor control of distal muscles by terminating on neurons in the dorsal, intermediate, and ventral parts of the spinal cord. The ventral corticospinal tract (I) descends ipsilaterally and controls proximal muscles spinal cord.

A. Striatum caudate putamen internal capsule

B. Thalamus

C. Red nucleus

D. Pontine nuclei

E. Reticular formation

F. Inferior olive

- G Dorsal column nuclei

H. lateral spinal cord

I. Medial spinal cord

FIGURE 6 Targets of corticofugal projections. The CNS is shown in coronal section (left), the striatum and thalamus are shown in lateral view, and the brain stem and spinal cord are shown in cross section (right). Descending corticofugal fibers (shown in blue) originate from widespread areas of the motor cortex and coalesce into fiber bundles called the internal capsule. They then penetrate nuclear groups in the diencephalon (caudate and putamen) and project through the brain stem. They undergo partial decussation in the medulla and project through the spinal cord. Specific tracts within the main fiber bundles are named according to their targets: The corticostriate tract (A, to the caudate and putamen) and the corticothalamic tract (B, to the thalamus) are involved in "motor loops'' that coordinate movement commands (see Chapter 58). The corticorubro tract (C, to the red nucleus) and the corticopontine tract (D, to the pontine nuclei) influence cerebellar function (see Chapter 59). The corticoreticular tract (E) acts on many of the motor nuclei of the brain stem. The cortico-olivary tract (F) and corticocuneate/gracile tract (G) modify sensory processing. The lateral corticospinal tract (H, descending contralaterally) influences motor control of distal muscles by terminating on neurons in the dorsal, intermediate, and ventral parts of the spinal cord. The ventral corticospinal tract (I) descends ipsilaterally and controls proximal muscles spinal cord.

C. Red nucleus

D. Pontine nuclei

E. Reticular formation

F. Inferior olive

- G Dorsal column nuclei

H. lateral spinal cord

I. Medial spinal cord

midbrain medulla medulla spinal cord midbrain pons medulla medulla spinal cord sulcus. The fibers coalesce as they descend in the internal capsule, traveling ipsilaterally through the course of the brain stem. They form a pair of thick, pyramidal-shaped bundles on the posterior aspect of the lower medulla. At the junction of the brain stem and spinal cord, most of these fibers decussate and move to the lateral funiculus of the cord. Fibers leave the main fiber bundle at all levels of the brain stem and spinal cord, providing conscious control over all cranial nerve motor nuclei and motor segments of the cord. Their role is to initiate voluntary movement.

The cerebellum and the basal ganglia also provide important input to spinal motor neurons, both directly and indirectly through projections involving the motor cortex. These pathways will be described in succeeding chapters after first considering the organization of the motor cortex in more detail.

Suggested Readings

Boyd IA. The isolated mammalian muscle spindle. Trends Neurosci 1980; 3:258-265.

Grillner S, Wallen P. Central pattern generators for locomotion, with special reference to vertebrates. Annu Rev Neurosci 1985; 8:233-261.

Hullinger M. The mammalian muscle spindle and its central control.

Rev Physiol Biochem Pharmacol 1984; 101:1-110. Pearson K. The control of walking. Sci Am 1976; 235(6):72-86. Stein RB. What muscle variable does the nervous system control in limb movements? Behav Brain Sci 1992; 5:535.

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