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NCS demonstrate reduced amplitudes or absent SNAPs and CMAPs102 104
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stimulation, the CMAP amplitudes initially decrement but then recover approaching the baseline amplitudes In OPIDP, NCS reveal decreased amplitudes of SNAPs and CMAPs consistent with an axonal sensorimotor polyneuropathy
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Autopsy studies have demonstrated a distal axonopathy and degeneration of the gracile fasciculus and the corticospinal tract70 In addition, marked loss of both myelinated and unmyelinated nerve bers in the sural nerve and a moderate loss of nerve bers in the sciatic nerve were observed on autopsy of a patient who died from exposure to sarin gas105
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The pathogenic basis for OPIDP is not clear Organophosphates bind to and inhibit an enzyme called neuropathy target esterase (NTE)112 However, inhibition of NTE is not suf cient for the development of OPIDP The organophosphate NTE complex must age, whereby a lateral side chain of NTE is cleaved Downstream this leads to the toxic neuropathy
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Figure 18 2 Hexacarbon toxicity Giant axons are appreciated on this nerve biopsy in an individual who developed a severe neuropathy associated with chronic glue snif ng (With permission from Amato AA, Dumitru D Acquired neuropathies In Dumitru D, Amato AA, Swartz MJ (eds) Electrodiagnostic Medicine, 2nd edn Philadelphia: Hanley & Belfus, 2002, pp 937 1041, Fig 23 10, p 1008)
Pathogenesis
The exact mechanism by which hexacarbons cause a toxic neuropathy is not known Hexacarbon exposure may lead to covalent cross-linking between axonal neuro laments, which results in their aggregation, impaired axonal transport, swelling of the axons, and eventual axonal degeneration70
HEXACARBONS (n-HEXANE, METHYL n-BUTYL KETONE)/GLUE SNIFFER S NEUROPATHY Clinical Features
n-Hexane and methyl n-butyl ketone are water-insoluble industrial organic solvents, which are also present in some glues Exposure through inhalation, accidentally or intentionally (glue snif ng), or through skin absorption can lead to a profound subacute sensorimotor polyneuropathy progressing over the course of 4 6 weeks70,116 119 The neuropathy presents with numbness and tingling in the feet and later involves the proximal legs and arms Progressive weakness also develops Respiratory muscles are usually spared
VINYL BENZENE (STYRENE)
Vinyl benzene or styrene is used to make some plastics and synthetic rubber Toxic exposure leads to a primarily sensory neuropathy with burning pain and paresthesia in the legs129 Neurological examination demonstrates a reduction in pain and temperature, with relatively good preservation of proprioception and vibration and muscle stretch Strength is normal NCS demonstrate a mild reduction in motor conduction velocities in the lower limbs
Laboratory Features
NCS demonstrate decreased amplitudes of the SNAPs and CMAPs with slightly slow CVs117,120 127 Partial conduction block has also been appreciated in motor conduction studies in some patients128
NEUROPATHIES CAUSED BY HEAVY METAL INTOXICATION
Heavy metals toxicity can be associated with axonal polyneuropathies130 The severity of the neuropathy is usually related to the amount of metal that entered the patient s system either acutely or chronically Clinical improvement is dependent on cessation of the exposure and supportive measures Multiple organ systems can be involved besides the peripheral nervous system
Histopathology
Nerve biopsy reveals a loss of myelinated and giant axons (Fig 18 2)70,116,119 Segmental demyelination is also seen EM reveals that the swollen axons are lled with 10-nm neuro laments
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TOXIC NEUROPATHIES
LEAD Clinical Features
Lead neuropathy is uncommon, but it can be seen in children who accidentally ingest lead-based paints in older buildings and in industrial workers exposed to containing lead products130,131 The most common presentation of lead poisoning is an encephalopathy; however symptoms and signs of a primarily motor neuropathy can also occur130,132 136 The neuropathy is characterized by an insidious and progressive onset of weakness usually beginning in the arms, particularly involving the wrist/ nger extensor weakness such that it resembles a radial neuropathy Foot drop can be seen Weakness can be asymmetric Sensation is generally preserved; however, the autonomic nervous system can be affected, leading to constipation Muscle stretch re exes are diminished and plantar responses are exor Bluish-black discoloration of gums near the teeth may be appreciated
ethyl mercury Organic mercury poisoning presents with paresthesias in hands and feet, which progress proximally and may involve the face and tongue Also, patients may have dysarthria, ataxia, reduced mentation, and visual and hearing loss The inorganic mercury compounds are primarily used for industrial purposes and consist of various mercury salts Toxicity may arise from ingestion or inhalation of the compounds Gastrointestinal symptoms and nephrotic syndrome are the primary clinically features associated with acute toxicity with inorganic mercury, but encephalopathy and sensorimotor polyneuropathy can also develop
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