Pesticide-Induced Quadriplegia in a 55-Year-Old Woman

Abstract

Acephate is a commercial organophosphate pesticide formerly used in households and now used primarily for agriculture. Poisoning symptoms include salivation, lacrimation, urination, defecation, gastrointestinal illness, and emesis. In addition to these classic symptoms, neurodegeneration can result from increased and continued exposure of organophosphates. This 55-year-old woman presented with organophosphate-induced delayed neuropathy in the form of quadriplegia due to the commonly used pesticide acephate. She was exposed to this pesticide through multiple sprayings in her work office with underrecognized poisoning symptoms. She presented to her primary care physician with neuropathic pain and paralysis in her arm following the sprayings and eventual complete paralysis. The patient lived for 2 years following her toxic exposure and quadriplegia. A complete autopsy after her death confirmed a transverse myelitis in her spinal cord. We conclude that in susceptible individuals, acephate in excessive amounts can produce severe delayed neurotoxicity as demonstrated in animal studies.

Anticonvulsant discovery through animal models of status epilepticus induced by organophosphorus nerve agents and pesticides

“…Individuals who survive an acute toxic exposure are subject to the long‐term consequences of central nervous system damage caused by SE. Additionally, in cases of OP poisoning, survivors often experience peripheral polyneuropathies and general multifaceted health problems …”

“…Additionally, in cases of OP poisoning, survivors often experience peripheral polyneuropathies and general multifaceted health problems. [8][9][10][11][12] Anticholinergic drugs have proven effective for treatment of peripheral effects of NA/OP exposure, but neurological symptoms like SE have been much harder to ameliorate. The current standard of care for SE is treatment with benzodiazepines, which aims to reduce neuronal excitation by enhancing inhibitory GABAergic signaling.…”

Organophosphate neurotoxicity to the voluntary motor system on the trail of environment-caused amyotrophic lateral sclerosis: the known, the misknown, and the unknown

“…The question we initially posed with this review was: “what can we learn from acute exposure to high doses of neurotoxicants (OPIDN) that may be useful in understanding chronic diseases resulting from silent exposure (ALS)?” The answer we found is: “a lot.” The resemblances between OPIDN and ALS are striking at clinical, etiological, neuropathological, cellular, and potentially molecular levels. During our journey through the OPIDN literature, we found that some of the field was still “frozen” in the original definition of non-cholinergic neuropathic compounds, and regardless of whether semantic or classification changes are needed, scientists need to increase awareness pertaining to the multiplication of OPIDN (or OPIDN-like) cases flourishing in the recent literature of acute poisoning with cholinergic OPs (Meggs 2003; Thivakaran et al 2012; Beavers et al 2014). As highlighted by several experts in the field (Abou-Donia and Lapadula 1990; Lotti and Moretto 2005), AchE and NTE cannot account for all the neurotoxic clinical expressions of OP poisoning.…”

“…OPIDN is a relatively rare, non-lethal (with the exception of very severe cases (Beavers et al 2014), but potentially extremely debilitating neurodegenerative disorder observed after repeated or acute intoxication with different types of OPs (Abou-Donia 2003). More than 70,000 cases of OPIDN have been documented over the last 70 years (Johnson and Glynn 2001).…”

“…TOCP) and associated mainly with axonal degeneration, and “type II” caused by trivalent phosphines and which also involves neuronal cell body degeneration (Abou-Donia and Lapadula 1990). However, a growing number of studies have reported clear neuronal necrosis, chromatolysis, apoptosis, and cell body loss of ventral horn motor neurons with exposure to type I OPs in animals (Funk et al 1994; Konno et al 1999; Mou et al 2006; Zou et al 2013) and humans (Beavers et al 2014). If different classes of OPs cannot account for these data discrepancies in the literature, the dissociation of soma loss from axon degeneration could depend on alternative factors: first, other variables related to the exposure itself (e.g.…”