Clinical presentations and electromyographical aspects in toxic neuropathies
Peripheral nerves are likely to be damaged by a wide array of toxins and medications causing different types of neuropathies mainly affecting distal nerves. Toxic neuropathies are often misdiagnosed due to the lack of available specific evidence. However, they can be suspected through clinical exami...
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Published in: | Neurophysiologie clinique Vol. 48; no. 3; p. 139 |
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Elsevier Masson SAS
01-06-2018
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Abstract | Peripheral nerves are likely to be damaged by a wide array of toxins and medications causing different types of neuropathies mainly affecting distal nerves. Toxic neuropathies are often misdiagnosed due to the lack of available specific evidence. However, they can be suspected through clinical examination and electrodiagnostic features. We aimed to determine the pattern of clinical and electroneuromyographic disorder in toxic neuropathies.
A retrospective study was carried out on patients who had history of neurotoxin exposure and diagnosed with toxic neuropathy. All cases underwent detailed neurological examination and appropriate investigations needed to exclude other causes of neuropathy, as well as electrophysiological studies (EMG).
Over the 21 patients we selected: 9 were alcoholic, 4 glue-sniffing addicts, 2 received medication with metronidazole and 3 had chemotherapy. Two had a professional exposure to N-Hexane and 1 did a suicide attempt with organophosphate. Neurological examination showed motor deficit predominating in distal limbs (61.9%), areflexia (85.7%) amyotrophy (19%) as well as proprioceptive ataxia (42.8%) and hypoesthesia (33.3%). Electrophysiological studies showed a symmetric sensorial dominant sensory-motor axonal type polyneuropathy (90%) with greater involvement of lower extremities (100%). Therefore, demyelinating features were detected in 40% with increased distal and F wave latencies (35%), decreased motor and sensory nerve conduction velocities (40%), motor conduction block (15%) and temporal dispersion (5%) defining the polyradiculoneuropathy electromyographic criteria (20%). Denervation signs were revealed in 30%. Most of patients (57.14%) regained their sensory and motor capacities within few months.
Peripheral neuropathies secondary to toxins are increasingly considered but can be difficult to definitively diagnose especially when it presents with a subacute severe form mimicking Guillain-Barré syndrome. Yet, detecting the syndromic presentation and a history of toxin exposure can facilitate prompt and accurate diagnosis. |
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AbstractList | Objectives: Peripheral nerves are likely to be damaged by a wide array of toxins and medications causing different types of neuropathies mainly affecting distal nerves. Toxic neuropathies are often misdiagnosed due to the lack of available specific evidence. However, they can be suspected through clinical examination and electrodiagnostic features. We aimed to determine the pattern of clinical and electroneuromyographic disorder in toxic neuropathies. Methods: A retrospective study was carried out on patients who had history of neurotoxin exposure and diagnosed with toxic neuropathy. All cases underwent detailed neurological examination and appropriate investigations needed to exclude other causes of neuropathy, as well as electrophysiological studies (EMG). Results: Over the 21 patients we selected: 9 were alcoholic, 4 glue-sniffing addicts, 2 received medication with metronidazole and 3 had chemotherapy. Two had a professional exposure to N-Hexane and 1 did a suicide attempt with organophosphate. Neurological examination showed motor deficit predominating in distal limbs (61.9%), areflexia (85.7%) amyotrophy (19%) as well as proprioceptive ataxia (42.8%) and hypoesthesia (33.3%). Electrophysiological studies showed a symmetric sensorial dominant sensory-motor axonal type polyneuropathy (90%) with greater involvement of lower extremities (100%). Therefore, demyelinating features were detected in 40% with increased distal and F wave latencies (35%), decreased motor and sensory nerve conduction velocities (40%), motor conduction block (15%) and temporal dispersion (5%) defining the polyradiculoneuropathy electromyographic criteria (20%). Denervation signs were revealed in 30%. Most of patients (57.14%) regained their sensory and motor capacities within few months. Conclusion: Peripheral neuropathies secondary to toxins are increasingly considered but can be difficult to definitively diagnose especially when it presents with a subacute severe form mimicking Guillain-Barré syndrome. Yet, detecting the syndromic presentation and a history of toxin exposure can facilitate prompt and accurate diagnosis. Peripheral nerves are likely to be damaged by a wide array of toxins and medications causing different types of neuropathies mainly affecting distal nerves. Toxic neuropathies are often misdiagnosed due to the lack of available specific evidence. However, they can be suspected through clinical examination and electrodiagnostic features. We aimed to determine the pattern of clinical and electroneuromyographic disorder in toxic neuropathies. A retrospective study was carried out on patients who had history of neurotoxin exposure and diagnosed with toxic neuropathy. All cases underwent detailed neurological examination and appropriate investigations needed to exclude other causes of neuropathy, as well as electrophysiological studies (EMG). Over the 21 patients we selected: 9 were alcoholic, 4 glue-sniffing addicts, 2 received medication with metronidazole and 3 had chemotherapy. Two had a professional exposure to N-Hexane and 1 did a suicide attempt with organophosphate. Neurological examination showed motor deficit predominating in distal limbs (61.9%), areflexia (85.7%) amyotrophy (19%) as well as proprioceptive ataxia (42.8%) and hypoesthesia (33.3%). Electrophysiological studies showed a symmetric sensorial dominant sensory-motor axonal type polyneuropathy (90%) with greater involvement of lower extremities (100%). Therefore, demyelinating features were detected in 40% with increased distal and F wave latencies (35%), decreased motor and sensory nerve conduction velocities (40%), motor conduction block (15%) and temporal dispersion (5%) defining the polyradiculoneuropathy electromyographic criteria (20%). Denervation signs were revealed in 30%. Most of patients (57.14%) regained their sensory and motor capacities within few months. Peripheral neuropathies secondary to toxins are increasingly considered but can be difficult to definitively diagnose especially when it presents with a subacute severe form mimicking Guillain-Barré syndrome. Yet, detecting the syndromic presentation and a history of toxin exposure can facilitate prompt and accurate diagnosis. |
Author | Sakka, Salma Farhat, Nouha Dammak, Mariem Hdiji, Olfa Mhiri, Chokri Zouari, Rania Bouattour, Nadia Kacem, Hanen Haj |
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SubjectTerms | Addicts Ataxia Chemotherapy Demyelination Denervation Electromyography Metronidazole Mimicry n-Hexane Nerve conduction Organophosphates Peripheral nerves Peripheral neuropathy Polyneuropathy Proprioception Suicide Toxic neuropathy Toxicity |
Title | Clinical presentations and electromyographical aspects in toxic neuropathies |
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