If nerves, sensory roots, or spinal tracts are damaged or partially interrupted, the patient may complain of tingling or prickling feelings (“like Novocain” or like the feelings in a limb that has “fallen asleep,” the colloquialism for nerve compression), cramp-like sensations, or burning or cutting pain occurring either spontaneously or in response to stimulation.
The clinical description of a sensation may divulge the particular sensory fibers involved (see Table 8-1). It is known that stimulation of touch fibers gives rise to a sensation of tingling and buzzing; of muscle proprioceptors, to pseudocramp (the sensation of cramping without actual muscle contraction); of thermal fibers, to heat (including burning) and coldness; and of A-δ fibers, to prickling and pain. Paresthesia arising from ectopic discharges in large sensory fibers can be induced by nerve compression, hypocalcemia, hypomagnesemia, certain medications (niacin foremost among them), and diverse diseases of nerves. Band-like sensations on a limb or the trunk are the result of dysfunction in large sensory fibers, either in the periphery or their continuation in the posterior columns. Certain sensory symptoms suggest an anatomic location of nerve disease; for example, lancinating pains that radiate to the back or neck implicate root or, less often, sensory ganglion disease.
Persistent paresthesias incriminate a lesion involving sensory pathways in nerves, spinal cord, or higher structures. Most often, the large diameter, heavily myelinated fibers in the peripheral nerves or posterior columns are involved. Evanescent paresthesia, of course, is usually of no significance. Every person has had the experience of resting a limb on the ulnar, sciatic, or peroneal nerve and having the extremity “fall asleep.” This is because of compressive interruption of axonal transport and not of ischemia of the nerves or other structures of the limb as is commonly assumed. The hyperventilation of anxiety may cause paresthesia of the lips and hands (sometimes unilateral) from diminution of CO2 and thereby of ionized calcium; tetany may also occur, with carpopedal spasms. However, these sensory experiences are transient and should not be confused with the persistent, albeit sometimes fluctuating, paresthesias of structural disease of the nervous system. Severe acral and peripheral paresthesias with perversion of hot and cold sensations are characteristic of certain neurotoxic shellfish poisonings (ciguatera) and other toxins, such as mercury.
Also worth comment are vibratory paresthesias, which we have encountered in only a handful of patients. One articulate physician described the sensation as a high-amplitude, low-frequency “buzz” that was distinctly different from the more common prickling paresthesia, burning, numbness, etc. We have the impression that these sensations are almost always a manifestation of central sensory disease, in one case probably attributable to the posterior columns and in another to cerebral disease. Beyond this, little is known about this symptom.
Effect of Age on Sensory Function
A matter of importance in the testing of sensation is the progressive impairment of sensory perception that occurs with advancing age. This requires that sensory thresholds, particularly in the feet and legs, be assessed in relation to age standards. The effect of aging is most evident in relation to vibratory sense, but proprioception, the perception of touch, and fast pain are also diminished with age. Sweating and vasomotor reflexes are reduced as well. These aging changes, which are discussed further in Chap. 28, are probably caused by neuronal loss in dorsal root ganglia and are reflected in a progressive depletion of fibers in the posterior columns. Receptors in the skin and special sense organs (taste, smell) also atrophy with age. On the other hand, it is too facile to attribute sensory loss to aging alone because it risks overlooking important disorders, some treatable.
Testing of Sensory Function