Phrenic nerve conduction studies in acute organophosphate poisoning

Singh, Gagandeep; Sidhu, U.; Mahajan, Ramit; Avasthi, G; Whig, J

doi:10.1002/(sici)1097-4598(200004)23:4<627::aid-mus23>3.3.co;2-j

Cited by 5 publications

(12 citation statements)

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“…Low amplitude of the diaphragmatic CMAP correlates well with the need for assisted mechanical ventilation and the reduced amplitude improves with amelioration of the neuromuscular transmission deÞ cit [ Figure 3a-d]. [28] Treatment…”

Section: Organophosphate-induced Respiratory Failure -Clinical Neuropsupporting

confidence: 52%

“…Respiratory failure is an important manifestation of the acute OP poisoning [20,[28][29][30] and is multifactorial: Respiratory muscle weakness in, particularly the diaphragm, central respiratory depression, and pulmonary factors (pulmonary edema, bronchoconstriction, bronchorrhea). [28] Electrodiagnostic tests can be of help in differentiating between neuromuscular and nonneuromuscular causes of respiratory failure in acute OP poisoning.…”

Section: Organophosphate-induced Respiratory Failure -Clinical Neuropmentioning

confidence: 99%

“…[28] Electrodiagnostic tests can be of help in differentiating between neuromuscular and nonneuromuscular causes of respiratory failure in acute OP poisoning. Low amplitude of the diaphragmatic CMAP correlates well with the need for assisted mechanical ventilation and the reduced amplitude improves with amelioration of the neuromuscular transmission deÞ cit [ Figure 3a-d].…”

Section: Organophosphate-induced Respiratory Failure -Clinical Neuropmentioning

confidence: 99%

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Neurology of acute organophosphate poisoning

2009

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Acute organophosphate (OP) poisoning is one of the most common poisonings in emergency medicine and toxicological practice in some of the less-developed nations in South Asia. Traditionally, OP poisoning comes under the domain of emergency physicians, internists, intensivists, and toxicologists. However, some of the complications following OP poisoning are neurological and involve neurologists. The pathophysiological basis for the clinical manifestations of OP poisoning is inactivation of the enzyme, acetylcholinesterase at the peripheral nicotinic and muscarinic and central nervous system (CNS) nerve terminals and junctions. Nicotinic manifestations occur in severe cases and late in the course; these comprise of fasciculations and neuromuscular paralysis. There is a good correlation between the electrophysiological abnormalities and the severity of the clinical manifestations. Neurophysiological abnormalities characteristic of nicotinic junctions (mainly neuromuscular junction) dysfunction include: (1) single, supramaximal electrical-stimulus-induced repetitive response/s, (2) decrement-increment response to high frequency (30 Hz) repetitive nerve stimulation (RNS), and (3) decremental response to high frequency (30 Hz) RNS. Atropine ameliorates muscarinic manifestations. Therapeutic agents that can ameliorate nicotinic manifestations, mainly neuromuscular, are oximes. However, the evidence for this effect is inconclusive. This may be due to the fact that there are several factors that determine the therapeutic effect of oximes. These factors include: The OP compound responsible for poisoning, duration of poisoning, severity of poisoning, and route of exposure. There is also a need to study the effect of oximes on the neurophysiological abnormalities.

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Section: Organophosphate-induced Respiratory Failure -Clinical Neuropsupporting

confidence: 52%

Section: Organophosphate-induced Respiratory Failure -Clinical Neuropmentioning

confidence: 99%

Section: Organophosphate-induced Respiratory Failure -Clinical Neuropmentioning

confidence: 99%

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Neurology of acute organophosphate poisoning

2009

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“…Electrophysiological studies have been performed on a few patients with intermediate syndrome Sedgwick and Senanayake, 1997;Senanayake and Karalliedde, 1987;Singh et al, 2000;Wadia et al, 1987). Nerve conduction velocity was normal and distal latencies were either normal or slightly reduced.…”

Section: Electrophysiologymentioning

confidence: 99%

Clinical Toxicology of Anticholinesterase Agents in Humans

Lotti

2010

Hayes' Handbook of Pesticide Toxicology

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“…In one animal study, it was shown the decrement response worsened with administration of edrophonium and recovered with D-tubocurarine (17). In one study reduced diaphragmatic CMAP amplitudes correlated with the need for mechanical ventilation in acute organophosphate poisoning (20). Likewise long thoracic nerve studies may also be useful in predicting such patients (19).…”

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confidence: 97%

The role of clinical neurophysiology in bioterrorism

Prakash

2005

Acta Neurol Scand

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Chemical and biological agents have been used as weapons of mass destruction for a long time and presents as a serious threat to mankind. They have been used in many great wars and terrorist attacks with devastating results. The knowledge about these weapons of mass destruction is crucial to health care providers. Early recognition of the clinical characteristics of poisoning as a result of these chemical and biological agents is important to initiate appropriate therapy and minimizing casualties. Neurophysiological investigations when integrated with clinical features are helpful in early identification of some of these agents, especially when serological confirmation is not rapidly available. In this review, we have focused on chemical and biological weapons, which affect the nervous system and the role of clinical neurophysiology in such conditions.

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Phrenic nerve conduction studies in acute organophosphate poisoning

Cited by 5 publications

References 0 publications

Neurology of acute organophosphate poisoning

Neurology of acute organophosphate poisoning

Clinical Toxicology of Anticholinesterase Agents in Humans

The role of clinical neurophysiology in bioterrorism

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