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phates, and industrial solvents As a rule, the neuropathies induced by these agents fall into the chronic category (to be discussed further on) Certain drugs, however notably triorthocresylphosphate (TOCP) and other organophosphates (see page 1037), thallium, and rarely arsenic produce a polyneuropathy that may be fatal in a matter of days It should be stressed that organophosphate neuropathy can be identi ed in almost all instances by the severe anticholinergic effects that are apparent immediately after exposure Severe and permanent motor paralysis is caused by TOCP; this ultimately proves to be due to involvement of both upper and lower motor neurons Thallium salts, when taken in suf cient amount, may produce a clinical picture resembling that of GBS or an acute sensory polyneuropathy If the salts are taken orally, there is rst abdominal pain, vomiting, and diarrhea, followed within a few days by pain and tingling in the toes and ngertips and then rapid weakening of muscles of the limbs, initially the distal ones As the weakness progresses, the tendon re exes diminish Pain sensation is reduced more than tactile, vibratory, and position sense Persistent acral pain with allodynia has been a major feature in three of the ve patients we have examined; in two of our patients there was no weakness, only sensory loss and ataxia All cranial nerves except the rst and eighth may be affected; facial palsies, ophthalmoplegia, nystagmus, optic neuritis with visual impairment, and vocal cord palsies are additional abnormalities, but only in the most severely affected patients The CSF protein rises to more than 100 mg Death may occur in the rst 10 days, due to cardiac arrest The early onset of painful paresthesias, sensory loss, and pain localized to joints, back, and chest as well as rapid loss of hair (after a week or two) all serve to differentiate this neuropathy from GBS, porphyria, and other acute polyneuropathies Relative preservation of re exes is noteworthy, and rapidly evolving, complete alopecia is a striking feature Patients with lesser degrees of intoxication may recover completely within weeks or months Thallium salts act like potassium, and a high intake of potassium chloride hastens the excretion of thallium Chelating agents are of unproven value but are usually included in treatment Some cases of arsenical and possibly mercurial polyneuropathy may also develop acutely More often these conditions evolve subacutely, for which reason they are discussed further on As alluded to earlier and in Chap 43, certain other toxic neuropathies, such as those related to organophosphate or diethylene chloride (Sterno) poisoning, may have an acute onset and progress over days In regard to this category of polyneuropathy, it must be pointed out that many instances are imputed with little substantiation to a toxic cause by both patients and unskeptical physicians Before making such an attribution, it is useful to ask whether the clinical features are compatible with the known neurotoxicity of an environmental agent or drug; whether the severity of symptoms is consistent with degree of presumed exposure (real or imagined); whether the associated systemic signs of an intoxication were present; if other individuals similarly exposed had been affected; and whether symptoms stabilized or improved once the patient had been removed from the presumed source of exposure Failure to satisfy these precepts generally signi es some other disorder.

velop as rapidly as GBS, and careful clinical and electrophysiologic testing may be needed to distinguish these disorders Three of our patients with polyarteritis and one with Churg-Strauss disease became completely paralyzed within a week, and one died of intestinal perforation However, most cases of neuropathy due to vasculitis evolve more slowly, and the syndrome then assumes an asymmetrical and multifocal distribution, for which reason it is described in the next section There is no doubt that paraneoplastic neuropathies, discussed further in the subacute category, can evolve more rapidly than is typical for this process and thereby simulate GBS We have observed a few patients with alcoholism, occult carcinoma, Hodgkin disease, or renal transplantation who developed an acute polyneuropathy, as rapid in its evolution as GBS, and acute episodes of this type have also been described in patients with Refsum disease

Acute Autonomic Polyneuropathy ( Pure Pandysantonomia )

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Since the rst description of such a case by Young, Adams, and colleagues, a number of others have been recorded as summarized by Low et al The condition, probably a type of postinfectious polyneuropathy within the category of GBS, is described in detail in Chap 26 Some success has been achieved by treatment with IVIG A subacute and more chronic form, also immune in nature, is described further on under Idiopathic Autonomic Neuropathy

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