Atrophy of weak or paralyzed muscles is characteristic of chronic disease of the motor neuron or motor axon and conversely, demyelinating neuropathies relatively spare muscle bulk because of the absence of denervation. Atrophy proceeds slowly over several weeks and months, the degree being proportional to the number of damaged motor nerve fibers. The maximum degree of denervation atrophy after an acute injury to the axons occurs in 90 to 120 days and reduces muscle volume by 75 to 80 percent. Atrophy may also be a consequence of disuse; it occurs over many weeks but in itself does not reduce muscle volume by more than 25 to 30 percent. In chronic axonal neuropathies, the degrees of paralysis and atrophy tend to correspond. As mentioned previously, atrophy does not coincide with weakness in acute paralysis caused by the demyelinative neuropathies in which the nerve fiber is relatively less affected than is the myelin. Ultimately in muscle atrophy, there is degeneration and loss of the denervated muscle fibers. This process begins in 6 to 12 months; in 3 to 4 years, most of the denervated fibers will have degenerated. If reinnervation takes place within a year or so, motor function and muscle volume may be restored.
As a rule, neuropathies are associated with a reduction or loss of tendon reflexes. Most often, this is the result of an interruption of the afferent (sensory) portion of the monosynaptic reflex arc. The reflexes may be diminished if muscular function is impaired, but this occurs mainly in the case of extreme atrophy, in which there are too few muscle fibers to manifest a contraction. There are, of course, many other processes that reduce the tendon reflexes, but it is the neuropathies with which loss of reflexes is most closely associated. An exception is the group of small-fiber neuropathies, in which tendon reflexes may be retained, even with marked loss of perception of painful stimuli. This discrepancy is attributable to the dependence of the afferent component of the tendon reflex arc on the large, heavily myelinated fibers that originate in muscle spindles. Conversely, in neuropathies that affect the largest diameter and most heavily myelinated fibers, the tendon reflexes are diminished early and disproportionately to weakness. Slowing of conduction in sensory fibers may also abolish the reflex by dispersing the afferent volley of impulses initiated by the tendon tap. There is generally a concordance between areflexia and a loss of proprioceptive and joint-position senses; that is, the large nerve fibers from spindle afferents are of the same type and size as those mediating these forms of sensation. Furthermore, loss of sensory functions that are dependent on these large fibers in the presence of preserved reflexes implicates the central projections of the sensory ganglion cells, that is, a lesion in the posterior columns of the spinal cord that does not interrupt the afferent tendon reflex arc. Regional loss of a reflex is usually a sign of a radiculopathy.
in Chap. 8)
Most polyneuropathies cause impairment of both motor and sensory functions, but one is often affected more than the other. In the toxic and metabolic neuropathies, sensory loss usually exceeds weakness. These differences are emphasized in the descriptions of individual peripheral nerve diseases in later parts of the chapter.