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Neuropathies can develop as complications of toxic effects of various drugs and other environmental exposures (Table 18 1)1 Toxic neuropathies due to chemotherapeutic agents are discussed in 17 This chapter deals with toxic neuropathies related to other medications thesia in a length-dependent pattern Motor strength is typically normal
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Nerve conduction studies (NCS) reveal reduced amplitudes or absent sensory nerve action potentials (SNAPs) in the legs worse than in the arms, along with normal motor conduction studies
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MISONIDAZOLE Clinical Features
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Misonidazole is used as an adjuvant agent in the treatment of various malignancies1 3 Some patients develop painful paresthesias and sometimes distal weakness in a length-dependent pattern after approximately 3 5 weeks of therapeutic drug administration (total dose greater than 18 g) Vibratory and temperature perception are usually reduced, but muscle stretch re exes are preserved The neuropathy usually improves following discontinuation of the drug
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Nerve biopsies reveal loss of myelinated nerve bers
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Pathogenesis
The pathogenic basis of the neuropathy is not known
CHLOROQUINE Clinical Features
Chloroquine is used in the treatment of malaria, sarcoidosis, systemic lupus erythematosus, scleroderma, and rheumatoid arthritis7 9 Chloroquine can cause a toxic myopathy characterized by slowly progressive, painless, proximal weakness and atrophy, which are worse in the legs than in the arms (discussed in 32) A neuropathy can also develop with or without the myopathy, leading to sensory loss, distal weakness, and reduced muscle stretch re exes The neuromyopathy usually appears in patients taking 500 mg for a year or more but has been reported with doses as low as 200 mg/d The signs and symptoms of the neuropathy and myopathy are usually reversible following discontinuation of chloroquine
Laboratory Features
Sensory nerve conduction studies (NCS) reveal reduced amplitudes or unobtainable responses in the legs more than the arms Motor conduction studies are typically normal
Histopathology
A reduction in the large myelinated bers with axonal degeneration and segmental demyelination and remyelination is apparent on sural nerve biopsies Accumulation of neuro laments with axonal swellings can be found on electron microscopy (EM)
Pathogenesis
The pathogenic basis of the neuropathy is not known
Laboratory Features
Serum creatine kinase (CK) levels are usually elevated due to the superimposed myopathy NCS reveal mild slowing of motor and sensory nerve conduction velocities (NCVs) with a mild to moderate reduction in the amplitudes, although NCS may be normal in patients with only the myopathy7 9 Electromyography (EMG) demonstrates myopathic motor unit action potentials (MUAPs), increased insertional activity in the form of positive sharp waves, brillation potentials, and occasionally myotonic potentials, particularly in the proximal muscles
METRONIDAZOLE Clinical Features
Metronidazole is used to treat a variety of protozoan infections and Crohn disease4 6 As with misonidazole, metronidazole is a member of the nitroimidazole group and has been associated with hyperalgesia and hypes-
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SECTION II
SPECIFIC DISORDERS
TABLE 18 1 TOXIC NEUROPATHIES
Drug Misonidazole
Mechanism of Neurotoxicity Unknown
Clinical Features Painful paresthesias and loss of large and small ber sensory modalities and sometimes distal weakness in lengthdependent pattern Painful paresthesias and loss of large and small ber sensory modalities and sometimes distal weakness in lengthdependent pattern Loss of large and small ber sensory modalities and distal weakness in lengthdependent pattern; superimposed myopathy may lead to proximal weakness
Nerve Histopathology Axonal degeneration of large myelinated bers; axonal swellings; segmental demyelination
EMG/NCS Low-amplitude or unobtainable SNAPs with normal or only slightly reduced CMAP amplitudes
Metronidazole
Unknown
Axonal degeneration
Low-amplitude or unobtainable SNAPs with normal CMAP
Chloroquine and hydroxychloroquine
Amphiphilic properties may lead to drug lipid complexes that are indigestible and result in accumulation of autophagic vacuoles
Axonal degeneration with autophagic vacuoles in nerves as well as muscle bers
Amiodarone
Amphiphilic properties may lead to drug lipid complexes that are indigestible and result in accumulation of autophagic vacuoles
Paresthesia and pain with loss of large and small ber sensory modalities and distal weakness in lengthdependent pattern; superimposed myopathy may lead to proximal weakness
Axonal degeneration and segmental demyelination with myeloid inclusions in nerves and muscle bers
Colchicine
Inhibits polymerization of tubulin in microtubules and impairs axoplasmic ow
Numbness and paresthesia with loss of large ber modalities in a length-dependent fashion; superimposed myopathy may lead to proximal in addition to distal weakness
Nerve biopsies demonstrate axonal degeneration; muscle biopsies reveal bers with vacuoles
Podophyllin
Binds to microtubules and impairs axoplasmic ow
Sensory loss, tingling, muscle weakness, and diminished muscle stretch re exes in length-dependent pattern; autonomic neuropathy
Axonal degeneration
Low-amplitude or unobtainable SNAPs with normal or reduced CMAP amplitudes; distal denervation on EMG; irritability and myopathic appearing MUAPs proximally in patients with superimposed toxic myopathy Low-amplitude or unobtainable SNAPs with normal or reduced CMAP amplitudes; can also have prominent slowing of CVs; distal denervation on EMG; irritability and myopathic appearing MUAPs proximally in patients with superimposed toxic myopathy Low-amplitude or unobtainable SNAPs with normal or reduced CMAP amplitudes; irritability and myopathic appearing MUAPs proximally in patients with superimposed toxic myopathy Low-amplitude or unobtainable SNAPs with normal or reduced CMAP amplitudes
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