Other manifestations of autonomic paralysis are small or medium-sized unreactive pupils that are unusually sensitive to certain drugs (see Chap. 13); lack of sweat, tears, and saliva; erectile dysfunction; weak bowel and bladder sphincters with urinary retention or overflow incontinence; and weakness and dilation of the esophagus and colon. As a result of vagal and other parasympathetic dysfunction, the normal variability of heart rate with respiration (sinus arrhythmia) is lost and there may be paralytic ileus or dyscoordinated peristalsis, as well as achlorhydria and hyponatremia. Some of these abnormalities are found in diabetic and amyloid polyneuropathy. They correspond to degeneration of small unmyelinated autonomic fibers in the peripheral nerves.
In any neuropathy involving sensory nerves, there is loss of autonomic function in the same zones as sensory loss. This is not true of radicular diseases because the autonomic fibers join the spinal nerves from the sympathetic chain and parasympathetic ganglia more distally. Changes in sweating and cutaneous blood flow may be demonstrated by a number of special tests described in Chap. 25.
Fasciculations, Cramps, and Spasms (See Also Chap. 46)
Fasciculations and cramps are not prominent features in most polyneuropathies and in this respect there is a difference from diseases of the anterior horn cells where they are important features. There are exceptions, however. Chronic spinal motor root compression leads to fasciculations or painful spasms in the innervated muscles. Occasionally one observes a state of mild motor polyneuropathy that, upon recovery, leaves the muscles in a state variably referred to as myokymia, continuous muscular activity, and neuromyotonia as discussed in Chap. 46. The affected muscles ripple and quiver and occasionally cramp. Use of the muscles increases this activity and there is a reduction in their contractile efficiency, which the patient senses as a stiffness and heaviness. In some instances this apparently constitutes the entire neuropathic syndrome and may be relieved by carbamazepine or phenytoin.
Other closely related phenomena are spasms or involuntary movements of the toes and feet. The latter, when the sole manifestation of disease, was referred to by
Spillane and colleagues as the syndrome of painful legs and moving toes. It has been attributed by Nathan to ectopic discharges in sensory roots, ganglia, or nerves, evoking both pain and organized movements. This is but one of many causes of the nocturnal restless leg syndrome, but it does not explain the more common type of idiopathic restless leg nocturnal syndrome described in Chap. 18. Other possible mechanisms for cramps and spasms are ephaptic cross-transmission between adjacent axons denuded of myelin, segmental hyperactivity from deafferentation, and neuronal sprouting during reinnervation. Infrequently, the muscle activity induces odd postures or slow writhing movements that Jankovic and van der Linden have likened to dystonia. The pathophysiology of these asynchronous activities of motor neurons is not known. Stimulation of a motor nerve in these cases, instead of causing a brief burst of action potentials in the muscle, results in a prolonged or dispersed series of potentials lasting several hundred milliseconds. Evidently, branched axons involved in collateral innervation have unstable polarization that may last for years.