Neurological Aspects of Biological and Chemical Terrorism

Martin, Coleman; Adams, Harold P.

doi:10.1001/archneur.60.1.21

Cited by 44 publications

(37 citation statements)

References 27 publications

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“…Cerebrospinal fluid (CSF) shows neutrophilic pleocytosis often greater than 500 ml, elevated erythrocyte count, and elevated protein [14], which are findings similar to the profile expected in herpes simplex virus (HSV) encephalitis or subarachnoid hemorrhage [30]. Gram-stain shows copious largegram positive rods with or without endospores.…”

Section: Neurological Manifestationmentioning

confidence: 67%

“…It is resistant to ceftriaxone and other 3 rd generation cephalosporins. Treatment for anthrax consists of a multi-drug regimen of ciprofloxacin, and at least one other agent of vancomycin, chloramphenicol, or penicillin [14]. For inhalational anthrax, the recommended regimen is ciprofloxacin or doxycycline, plus clindamycin and rifampin.…”

Section: Neurological Manifestationmentioning

confidence: 99%

“…Doxycycline and clindamycin, however, exhibit poor cerebrospinal fluid penetration and should be avoided in cases of anthrax meningoencephalitis. The addition of rifampin serves for the prevention or treatment of neurological manifestations [14] in cases treated with doxycycline or clindamycin. Treatment duration is long; a 60-day course is not unusual, given that spores can remain dormant for a long time.…”

Section: Neurological Manifestationmentioning

confidence: 99%

“…Therefore, preparedness among neurologists is as important as it is for emergency, infectious diseases, and critical care personnel [14]. The main challenge is to be cognizant of the clinical syndromes and to be able to distinguish diseases caused by bioterrorism from more commonly occurring natural disorders [15].…”

Section: Introductionmentioning

confidence: 99%

“…Of the many agents that may be used, prominent neurological features occur with cyanide, cholinesterase inhibitors, botulinum toxin, anthrax [14], and paralyzing toxins, as well as nerve agents (Table 3).…”

Section: Introductionmentioning

confidence: 99%

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Treatment of Neuroterrorism

Busl

Bleck

2012

Neurotherapeutics

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Bioterrorism is defined as the intentional use of biological, chemical, nuclear, or radiological agents to cause disease, death, or environmental damage. Early recognition of a bioterrorist attack is of utmost importance to minimize casualties and initiate appropriate therapy. The range of agents that could potentially be used as weapons is wide, however, only a few of these agents have all the characteristics making them ideal for that purpose. Many of the chemical and biological weapons can cause neurological symptoms and damage the nervous system in varying degrees. Therefore, preparedness among neurologists is important. The main challenge is to be cognizant of the clinical syndromes and to be able to differentiate diseases caused by bioterrorism from naturally occurring disorders. This review provides an overview of the biological and chemical warfare agents, with a focus on neurological manifestation and an approach to treatment from a perspective of neurological critical care.

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Section: Neurological Manifestationmentioning

confidence: 67%

Section: Neurological Manifestationmentioning

confidence: 99%

Section: Neurological Manifestationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Treatment of Neuroterrorism

Busl

Bleck

2012

Neurotherapeutics

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The Vitamin B12 Analog Cobinamide Is an Effective Antidote for Oral Cyanide Poisoning

et al. 2016

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Introduction Cyanide is a major chemical threat, and cyanide ingestion carries a higher risk for a supra-lethal dose exposure compared to inhalation but provides an opportunity for effective treatment due to a longer treatment window and a gastrointestinal cyanide reservoir that could be neutralized prior to systemic absorption. We hypothesized that orally administered cobinamide may function as a high-binding affinity scavenger and that gastric alkalinization would reduce cyanide absorption and concurrently increase cobinamide binding, further enhancing antidote effectiveness. Methods Thirty New Zealand white rabbits were divided into five groups and were given a lethal dose of oral cyanide poisoning (50 mg). The survival time of animals was monitored with oral cyanide alone, oral cyanide with gastric alkalinization with oral sodium bicarbonate buffer (500 mg), and in combination with either aquohydroxocobinamide or dinitrocobinamide (250 mM). Red blood cell cyanide concentration, plasma cobinamide, and thiocyanate concentrations were measured from blood samples.Results In cyanide ingested animals, oral sodium bicarbonate alone significantly prolonged survival time to 20.3 ± 8.6 min compared to 10.5 ± 4.3 min in saline-treated controls, but did not lead to overall survival. Aquohydroxocobinamide and dinitrocobinamide increased survival time to 64 ± 41 (p < 0.05) and 75 ± 16.4 min (p < 0.001), respectively. Compared to aquohydroxocobinamide, dinitrocobinamide showed greater systemic absorption and reduced blood pressure. Dinitrocobinamide also markedly increased the red blood cell cyanide concentration. Under all conditions, the plasma thiocyanate concentration gradually increased with time. Conclusion This study demonstrates a promising new approach to treat high-dose cyanide ingestion, with gastric alkalinization alone and in combination with oral cobinamide for treating a supra-lethal dose of orally administered cyanide in rabbits.

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