Thallium salts, when taken in sufficient amount, produce a clinical picture resembling that of GBS or an acute sensory polyneuropathy. If the salts are taken orally, there is first abdominal pain, vomiting, and diarrhea, followed within a few days by pain and tingling in the toes and fingertips and then rapid weakening of muscles of the limbs, initially the distal ones. As the weakness progresses, the tendon reflexes diminish. Pain sensation is reduced more than tactile, vibratory, and position sense. Persistent acral pain with allodynia has been a major feature in 3 of the 5 patients we have examined; in 2 of our patients there was no weakness, only sensory loss and ataxia. All cranial nerves except the first 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 first 10 days as a result of 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 1 or 2 weeks), all serve to differentiate this neuropathy from GBS, porphyria, and other acute polyneuropathies. Relative preservation of reflexes 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. 41, 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, many instances are imputed to toxins by both patients and unskeptical physicians with little substantiation. 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 are present; if other individuals similarly exposed are affected; and whether symptoms stabilize or improve once the patient is removed from the presumed source of exposure. Failure to satisfy these precepts generally signifies some other disorder.
On occasion, a vasculitic polyneuropathy as an isolated process or associated with lupus erythematosus, polyarteritis nodosa, and related disorders may develop as rapidly as GBS and careful clinical and electrophysiologic testing are needed to distinguish them. 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 caused by vasculitis evolve more slowly, with the syndrome assuming 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, and renal transplantation develop 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. An unusual neuropathy in burn patients has been described by Marquez and colleagues; separating it from the category of critical illness polyneuropathy is difficult.