Spinal cord poisons

Injection - Heart failure secondary to chronic lung disease cardiac arrhythmias brain tumor acute alcoholism delirium tremens idiosyncrasy to the drug increased intracranial or CSF pressure head injuries acute bronchial asthma upper airway obstruction. Because of its stimulating effect on the spinal cord, morphine should not be used in convulsive states (eg, status epilepticus, tetanus, strychnine poisoning) concomitantly with MAOIs or in those who have received such agents within 14 days. 

Strychnine, a very poisonous alkaloid to animals, binds to glycine receptors. Applications of strychnine can be considered only in clinical doses. Their purpose is to activate neurotransmitters in the spinal cord, which is generally suppressed by glycine. Strychnine competes only with glycine in the receptor. This alkaloid may be used to stimulate respiration and circulation in cases of physical weakness. Moreover, strychnine products are used in the treatment of eye and optic nerve disorders. Larger doses are lethal. 

The aminopyridines (4-aminopyridine 3,4-diaminopyri-dine) accelerate spontaneous exocytosis at central and peripheral synapses. There is also an increase in the number of transmitter quanta released by a nerve action potential. This is probably the result of increased Ca++ inflow at the terminals due to a reduction of K+ conductance and prolongation of the nerve action potential. Muscle strength is increased in patients with the Lambert-Eaton myasthenic syndrome and in others poisoned with botuUnum E toxin (discussed later). Improvement in uncontrolled spasms, muscle tone, and pulmonary function is noted in patients with multiple sclerosis or long-standing spinal cord damage. Side effects that limit clinical utility include convulsions, restlessness, insomnia, and elevated blood pressure. Of the two agents, 3,4-diaminopyridine is the more potent and crosses the blood-brain barrier less readily. 

GABA and glycine. Glycine receptors are pentameric structures that are selectively permeable to . Strychnine, which is a potent spinal cord convulsant and has been used in some rat poisons, selectively blocks glycine receptors. 

A potential source of cyanide poisoning is cassava, a starch from the root of Manihot esculenta, used as food in much of Africa. The root contains cyanogenic linamarin, which is normally removed in processing the root for food. Widespread cases of a spinal cord disorder called konzo and characterized by spastic paralysis have been attributed to ingestion of linamarin from inadequately... 

Palmer-Jones T (1965) Poisonous Honey Overseas and in New Zealand. NZ Med J 64 631 Kudo Y, Niwa H, Tanaka A, Yamada K (1984) Action of Picrotoxinm and Related Compounds on the Spinal Cord the Role of a Hydroxyl-group at the 6-Position in Antagonizing the Actions of Amino acids and Presynaptic Inhibition. Br J Pharmacol 81 373 Lowe MD, White EP (1972) Tutin in Coriaria Species - Identification and Estimation. NZ J Sci 15 303... 

A similar plant is water hemlock, which contains a different toxin, called cicutoxin. This is very potent and exposure to it is often fatal. One study of poisonings with this plant found that 30 per cent of victims died. It affects primarily the brain and the spinal cord, causing seizures and epileptic fits, possibly by overstimulating certain nerves (cholinergic pathways). 

The cyanide in cassava that is not properly prepared can be released by the action of enzymes in our gut and can poison an individual. It does this by binding to an enzyme in the mitochondria inside the cell which blocks the production of energy. In vulnerable tissues, like the nerves of the spinal cord, this causes damage. The detoxication of cyanide with sulphur, derived from sulphur-containing amino acids in protein, produces thiocyanate, which is excreted into the urine, but this system is easily overwhelmed especially in those deficient in sulphur. Drought and poor soil seem to increase the production of linamarin in cassava, and it is possible that other dietary deficiencies may contribute to the nerve damage. 

The limited neuropachologic information available from studies of affected persons deanonstrates that OP poisoning Induces degeneration of nerve fibers in spinal cord and peripheral nerves (122). 

In poisoning by a cerebral depressant or after spinal cord trauma, the principal cause of hypotension is low peripheral resistance due to reduced vascular tone. The cardiac output can be restored by simply tilting the patient head-down and by increasing the venous filling pressure by infusing fluid. Vasoactive drugs (noradrenaline, dobutamine) may be beneficial. 

Tetanus toxin poisoning produces tetanus, i.e. muscle contractions resulting in spastic paralysis. In contrast, Botulinum neurotoxins cause botulism, which is characterized by flaccid paralysis. This difference reflects differences in the anatomical level of action of these toxins. TeTx acts primarily on the CNS where it blocks exocytosis from inhibitory glycinergic synapses in the spinal cord. Loss of inhibitory control results in motoneuron firing. BoNTs act primarily in the periphery where they inhibit acetylcholine release at the neuromuscular junctions. 

Thiomerosal is metabolized to ethylmercury and thiosalicylate. Toxicologists have assumed that ethylmercury poisoning is similar to the toxicity of me-thylmercury. Flowever, ethylmercury cannot bypass the blood-brain barrier as easily as methylmercury. The entry of methylmercury into the brain relies on an active transport system. Ethylmercury on the other hand is a larger molecule and cannot use this system. Furthermore, it is more rapidly decomposed. Because of these limitations, when the same dose of both mercurial compounds is administered, the concentrations of methylmercury are greater in the brain when compared to ethylmercury. Due to the limited entry of the latter into the brain, this compound is more likely to cause damage to the spinal cord, myocardium and skeletal muscle. 

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