Since the first description of such a case by Young and colleagues and Adams and associates, a number of others have been recorded and summarized by Low and colleagues. The condition, probably a type of postinfectious polyneuropathy in the category of GBS, is described in detail in Chap. 25. Some success has been achieved by treatment with IVIg. A subacute and more chronic form, also immune in nature, is described later under “Idiopathic Autonomic Neuropathy” and a paraneoplastic variety is known.
Placed in this category are neuropathies that evolve over several weeks to months and, after reaching their peak of severity, tend to persist for a variable period. Admittedly, the dividing line between such cases and those that evolve over somewhat shorter or longer periods is indistinct; there are many diseases of nerve that overlap both the acute and the early chronic categories. In contrast to the acute polyneuropathies, however, most that are subacute have prominent sensory features and are of axonal type. The main exception is a subacute inflammatory–demyelinative type, essentially a slow form of GBS, evolving over 4 to 8 weeks, as described by Hughes and coworkers. Similarly, some instances of diphtheritic neuropathy evolve subacutely. Despite these qualifications, in the end, a symmetrical polyneuropathy syndrome of subacute type most often proves to be caused by nutritional deficiency (often complicated by alcoholism), by a remote effect of cancer (paraneoplastic, as described later), by poisoning with arsenic, lead, or by the toxic effects of any number of drugs used for therapeutic purposes (cisplatin, nitrofurantoin, isoniazid, etc.). Occasionally other drugs, metals, and industrial solvents are incriminated; these are discussed in Chap. 41.
(See Chap. 40)
In the Western world, nutritional polyneuropathy is usually associated with chronic alcoholism. As indicated in earlier discussions, all data point to the identity or at least close relationship between alcoholic neuropathy and neuropathic beriberi. A nutritional factor is responsible for both, although in any given case it remains unclear whether the deficiency is one of thiamine, nicotinic acid, pyridoxine, pantothenic acid, folic acid, or a combination of these B vitamins. Our colleague M. Victor, who devoted considerable attention to this subject, was never persuaded of the existence of a form of polyneuropathy attributable solely to the toxic effect of alcohol, although claims of such an entity continue to be made and the perception persists among most physicians that alcohol is directly damaging to nerves. Nutritional neuropathy and other neurologic complications of deficiency disorders (Strachan syndrome, pellagra, vitamin B12 deficiency, and malabsorption syndromes) are described fully in Chap. 40. A predominantly sensory neuropathy with burning pain is typical of most forms of severe nutritional deprivation.
Paraneoplastic Polyneuropathy and Sensory Ganglionopathy (See Chap. 30)
Although capable of producing diverse clinical presentations, most often the remote effect of cancer takes the form of a predominantly distal, symmetrical sensory, or sensorimotor polyneuropathy. Weakness and atrophy, ataxia, and sensory loss of the limbs may advance over several weeks or months to the point where the patient is confined to a wheelchair or bed; usually the CSF protein concentration is mildly elevated. All these symptoms may occur months or even a year or longer before a malignant tumor is found, although usually the tumor is apparent and most often is a lung cancer.