Toxins neurologic

Souayah, N., Karim, H., Kamin, S.S., McArdle, J., and Marcus, S. 2006. Severe botulism after focal injection of botuhnum toxin. Neurology 67 1855-1856. 

Narahashi T Northwestern University Medical School, Chicago, IL The effects of therapeutic drugs and toxins on neuronal ion channels National Institute of Neurological Disorders and Stroke... 

Botulism also affects animals, where intoxication is caused by C. botulinum types C and D. A bovine disease visceral botulism was reported in Germany (Bohnel et al., 2001). It was caused by a long-lasting exposure to low quantities of botulin toxin that interfered with the neurological control of intestinal physiology. Visceral botulism in cows may pose a health risk for milk consumers, although to date there are no precise data on how serious the problem is (Cobb et al., 2002). 

The onset of botulism occurs generally between 18 and 36 hours after consumption of food products containing botulin toxin. However, it may affect patients earlier or later, even on the tenth day after food consumption. The first symptoms include stomach ache, nausea, vomiting, and diarrhea, followed by neurological disorders. Other symptoms include, skin, mouth and throat dryness, diplopia, blurred vision, dysphonia, dysarthria, dysphagia, and peripheral weakness. In lethal cases of botulism, respiratory muscles are involved. This leads to respiratory failure and death. Because all the symptoms are connected with toxemia, the first step of medical treatment is to provide a patient with antiserum. 

Toxicology. Hexachlorobenzene (HCB) causes porphyria, enlarged liver and thyroid, and neurological symptoms it is a developmental toxin, and in experimental animals it is carcinogenic. 

Tetanus immunoglobulin is an example of an antibody preparation used to induee passive immunization against a mierobial toxin. Tetanus (lockjaw) is an infectious disease caused by the bacterium, Clostridium tetani. Bacterial spores can commonly contaminate surface wounds and the resulting bacterial cells produce a toxin as they multiply. The toxin interferes with normal neurological function, particularly at neuromuscular junctions. The result is spasmodic contraction of muscles and, if untreated, mortality rates are high. Treatment with antibiotics and anti-toxin, however, is highly effective if administered promptly. 

Marras, C., Andrews, D., Sime, E., and Lang, A.E. (2001) Botulinum toxin for simple motor tics a randomized, double-blind, controlled clinical trial. Neurology 56 605-610. 

Medical and neurological evaluations of an aggressive youth (to rule out toxins, infections, medical conditions, substance use, seizure disorders, and head trauma) followed by a full psychiatric assessment... 

The cockle, Austrovenus stutchburyi from New Zealand contained brevetoxin Bi (225) [230] and the greenshell mussel, Pema canaliculus contained brevetoxin B3 (226) [231]. A further brevetoxin analogue, brevetoxin B2 (227) was isolated from the hepatopancreas of P. canaliculus [232], while the major toxin in neurological shellfish poisoning (NSP) associated with P. canaliculus was identified as brevetoxin B4 (228) [233]. 

Cornelia CL, Pullman SL. Botulinum toxins in neurological disease. Muscle Nerve. 2004 29 628-644. 

Gordon MF, Brashear A, Elovic E, et al. Repeated dosing of botulinum toxin type A for upper limb spasticity following stroke. Neurology. 2004 63 1971-1973. 

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