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Serum and urine levels of thallium are increased Routine laboratory testing can reveal anemia, renal insuf ciency, and abnormal liver function tests CSF protein levels are also elevated NCS demonstrate features of a primarily axonal, sensorimotor polyneuropathy152,154,155 Within the rst few days of intoxication NCS can be normal After 1 2 weeks, the SNAPs and CMAPs in the legs have reduced amplitudes and H-re exes are lost
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Because arsenic is cleared from blood rapidly, serum concentration of arsenic is not diagnostically helpful However, arsenic levels are increased in the urine, hair, or ngernails of patients exposed to arsenic Anemia with stippling of erythrocytes is common and occasionally pancytopenia and aplastic anemia can develop Increased CSF protein levels without pleocytosis can be seen, which again can lead to misdiagnosis as Guillain Barre syndrome NCS are usually more suggestive of an axonal sensorimotor polyneuropathy; however, demyelinating features can be present130,158 168 Sensory NCS reveal low-amplitude or absent SNAPs with relatively preserved distal latencies and CVs Motor conduction studies may demonstrate possible conduction block and prolongation of F-wave latencies Serial studies demonstrate progressive deterioration of the CMAP
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Autopsy studies and nerve biopsies demonstrate chromatolysis of cranial and spinal motor nuclei and dorsal spinal ganglia and axonal degeneration of motor and sensory nerves152,156,157
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The pathogenic basis for the toxicity not known
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With acute intoxication, potassium ferric ferrocyanide II may be effective in preventing absorption of thallium from the gut130 However, there may be no bene t
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TOXIC NEUROPATHIES
amplitudes to distal stimulation associated with slowing of the conduction velocities Needle EMG demonstrate positive sharp waves and brillation potentials with reduced numbers of motor units in the distal muscles progressing proximally in patients exposed to signi cant amounts of arsenic
Pathogenesis
The pathogenic basis for the neuropathy is not known It may be related to an immunological reaction triggered by the gold therapy130
Treatment
Treatment consists of stopping the gold therapy British anti-Lewisite has been tried as well in a few patients, but it is unclear if this therapy is effective130
Histopathology
Nerve biopsies demonstrate axonal degeneration, reduced large- and small-diameter myelinated bers, occasional onion-bulb formations, and an increase in interstitial Autopsy studies have revealed a loss of anterior horn cells
SUMMARY
Many drugs can be associated with a toxic neuropathy and thus the need for taking an extensive medication history in any patient being evaluated for a neuromuscular disorder The mechanisms by which these agents cause neuropathy are variable These may have a primary effect on the neuronal cell body (ganglionopathy, the Schwann cells and myelin sheath, or axons) Most of the time, the neuropathies stabilize and improve after discontinuing the offending agent However, there can be a coasting effect such that the neuropathy clinically worsens for a few months even after stopping the medication
Pathogenesis
The pathogenic basis of arsenic toxicity is not known Arsenic may react with sulfhydryl groups of enzymatic (eg, pyruvate dehydrogenase complex) and structural proteins in the neurons leading to their degeneration130
Treatment
Chelation therapy with British anti-Lewisite has yielded inconsistent results and its effect is not dramatic; therefore, it is not generally recommended130
GOLD Clinical Features
Gold therapy (eg, sodium aurothiomalate) is sometimes used to treat rheumatoid arthritis Some patients treated with gold salts develop a sensorimotor neuropathy several months following drug initiation manifesting as distal paresthesias in the hands and feet and occasionally mild weakness130,170 172 In addition, a systemic reaction (eg, rash and pruritis) to the gold usually accompanies the neuropathic symptoms Examination reveals reduced sensation to all modalities and diminished muscle stretch re exes Fasciculations or myokymia may be evident on examination It may be impossible to distinguish the toxic neuropathy related to gold to the other more common neuropathies associated with rheumatoid arthritis (see 14)
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