There is no specific antidote for<unk>  but recovery from exposure is possible with early supportive medical treatment.<unk>  poisoning demands aggressive management with early control of muscle spasms, intubation for loss of airway control, toxin removal (decontamination), intravenous hydration and potentially active cooling efforts in the context of hyperthermia as well as hemodialysis in kidney failure (to note,<unk>  has not been shown to be removed by hemodialysis).<unk>  poisoning in today's age generally results from herbal remedies and<unk> -containing rodenticides. Moreover, management should be tailored to the patient's history of chief complaint and workup to rule out other causes. If a poisoned person is able to survive for 6 to 12 hours subsequent to initial dose, they have a good prognosis. The patient should be kept in a quiet and darkened room, because excessive manipulation and loud noises may cause convulsions. Because these convulsions are extremely painful, appropriate analgesics should be administered. Treatment of<unk>  poisoning involves oral administration of activated charcoal which adsorbs<unk>  within the digestive tract; unabsorbed<unk>  is removed from the stomach by gastric lavage, along with tannic acid or potassium permanganate solutions to oxidize<unk> . Activated charcoal may be beneficial, but its benefit remains unproven, to note its use should be avoided in any patient with a tenuous airway or altered mental status. Seizures are controlled by anticonvulsants, such as phenobarbital or diazepam, along with muscle relaxants such as dantrolene to combat muscle rigidity. Historically chloroform or heavy doses of chloral, bromide, urethane or amyl nitrite were used to restrain the convulsions. Because medications such as diazepam are not effective to relieve convulsions in all cases, concurrent use of barbiturates and/or propofol can be utilized. The sine qua non of<unk>  toxicity is the "awake" seizure, in which tonic-clonic activity occurs but the patient is alert and oriented throughout and afterwards. Accordingly, George Harley (1829–1896) showed in 1850 that curare (wourali) was effective for the treatment of tetanus and<unk>  poisoning. Curare causes paralysis, and it is important to note that, if seizure activity is present, the use of muscle paralysis will only mask the signs of ongoing seizure activity despite otherwise ongoing present brain damage.
Strychnine
Cromoglicic acid
Deoxypyridinoline
Pyridinoline
Phenibut
Thiotepa
Charybdotoxin
Beta-Zearalenol