The mechanism of thermal and painful dysesthesias is not fully understood. It has been theorized that a loss of large touch-pressure fibers disinhibits the pain-receiving nerve cells in the posterior horns of the spinal cord. An argument against this explanation is the lack of pain in Friedreich ataxia, in which the larger neurons degenerate, and also in certain purely sensory polyneuropathies, where only the perception of tactile stimuli (large fibers) is lost. A more likely explanation, supported by microneurographic recordings, is that dysesthetic pain results from ectopic discharges arising at many sites along surviving intact or regenerating nerve fibers or their terminal receptors. It has been postulated, on uncertain grounds, that the deep, aching neuropathic pain of sciatica or brachial neuritis (nerve trunk pain) arises from irritation of the normal endings (nervi nervorum) in the sheaths of the nerve trunks themselves (Asbury and Fields). These considerations are discussed in Chap. 7.
Proprioceptive deafferentation with retention of a reasonable degree of motor function may give rise to ataxia of gait and of limb movement as discussed in Chap. 8. Dysfunction of the spinocerebellar fibers of the peripheral nerves is probably the source of the ataxia. Some of the most severe ataxias of this type occur with sensory ganglionopathy, as commented further on.
Ataxia without weakness is also characteristic of tabes dorsalis, a purely posterior root disease, but this syndrome  can be duplicated by a type of diabetic polyneuropathy, which affects posterior roots (diabetic pseudotabes) and by a variant of GBS (termed Fisher syndrome). The ataxia is indistinguishable from that caused by cerebellar diseases, but other features of cerebellar dysfunction such as dysarthria and nystagmus are lacking. Characteristic of the sensory-ataxic gait are brusque, flinging, slapping movements of the legs. Loss of proprioception may also give rise to small wavering, fluctuating movements of the outstretched fingers—called pseudoathetotic, or “dancing fingers.”
An action tremor of fast-frequency type may also appear during certain phases of a polyneuropathy;
Shahani and coworkers had the impression that it is a result of loss of input from the muscle-spindle afferents. Corticosteroid therapy enhances this fast tremor. A particularly severe form of slower action tremor is combined with clumsiness of movement in the neuropathies caused by the autoimmune, anti-myelin-associated glycoprotein (anti-MAG) polyneuropathy and in some cases of chronic inflammatory demyelinating polyneuropathy (CIDP). The tremor may be so coarse as to resemble the intention tremor of cerebellar disease and all movements are rendered useless. However, a tremor at rest is not found in these afferent-sensory neuropathies. The neuropathic type of tremor is also discussed in Chap. 4.