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of an acute or subacute limb weakness with paresthesias and distal loss of vibratory and position sense The weakness characteristically involves all extremities at the same time or may descend from arms to legs After a few days to a week or more, the patient may be unable to stand or walk and occasionally the paralysis is so extensive as to impair respiration The CSF protein is usually elevated (50 to 200 mg/dL) Diphtheritic deaths that occur after the pharyngeal infection has subsided are due to cardiomyopathy or, less often, to severe polyneuropathy with respiratory paralysis This type of polyneuropathy, now quite rare, should be suspected in the midst of an outbreak of diphtheritic infection, as occurred recently in Russia (Logina and Donaghy) The important pathologic change is one of segmental demyelination without in ammatory reaction of spinal roots, sensory ganglia, and adjacent spinal nerves Anterior horn cells, axons, peripheral nerves distally, and muscle bers remain normal (Fisher and Adams) Treatment Diphtheria antitoxin, given within 48 h of the onset of the infection reduces the incidence and severity of neuropathic complications Antitoxin is probably of little value once the polyneuropathy begins Thereafter, treatment is purely symptomatic, along the lines indicated for GBS The prognosis for full recovery is excellent once respiratory paralysis is circumvented

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A severe, rapidly advancing, more or less symmetrical and mainly motor polyneuropathy often with abdominal pain, psychosis (delirium or confusion), and convulsions may be a manifestation of acute intermittent porphyria This type of porphyria is inherited as an autosomal dominant trait and is not associated with cutaneous sensitivity to sunlight The metabolic defect is in the liver and is marked by increased production and urinary excretion of porphobilinogen and of the porphyrin precursor -amino-levulinic acid The peripheral and central nervous systems may also be affected in another hepatic type of porphyria (the variegate type) In the latter, the skin is markedly sensitive to light and trauma, and porphyrins are at all times found in the stools Both of these hepatic forms of porphyria are to be distinguished from the rarer erythropoietic (congenital photosensitive) porphyria, in which the nervous system is not affected The classic study of acute intermittent porphyria was made by Waldenstrom in 1937 The initial and often the most prominent symptom is moderate to severe colicky abdominal pain It may be generalized or localized and is unattended by rigidity of the abdominal wall or tenderness Constipation is frequent and radiographs show intestinal distention (ileus) Attacks last for days to weeks and repeated vomiting may lead to inanition In latent forms, the patient may be asymptomatic or complain only of slight dyspepsia The disease can be identi ed after some time by its characteristic recurrent attacks, often precipitated by drugs such as sulfonamides, griseofulvin, estrogens, barbiturates, phenytoin, and the succinimide anticonvulsants The possibility of sensitivity to these drugs must always be kept in mind when convulsions are being treated in the porphyric patient The rst attack rarely occurs before puberty, and the disease is most likely to threaten life during adolescence and early adulthood In contrast, acute polyneuropathy that appears for the rst time in mid- or late adult life is not likely to be porphyric The neurologic manifestations are usually those of an acute polyneuropathy involving the motor nerves more severely than the.

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