Strychnine Sulfate


💊 Chemical information

Estricnina, sulfato de; Strychninae Sulphas; Strychnine Sulphate; Strychninum Sulfuricum; Sulfato de Estricnina.
Chemical formula: (C21H22N2O2)2,H2SO4,5H2O = 857.0.
CAS — 60-41-3 (anhydrous strychnine sulfate); 6049110-3 (strychnine sulfate pentahydrate).


In Fr. and Viet.

💊 Adverse Effects

The symptoms of strychnine poisoning are mainly those arising from stimulation of the CNS. Early signs occurring within 15 to 30 minutes of ingestion include tremors, slight twitching, and stiffness of the face and limbs. Painful convulsions develop and may be triggered by minor sensory stimuli; since consciousness is not impaired patients may be extremely distressed. All forms of sensation are heightened. The body becomes arched backwards in hyperextension with the head retracted, arms and legs extended, fists clenched, and the feet turned inward. The jaw is rigidly clamped and contraction of the facial muscles produces a characteristic grinning expression known as ‘risus sardonicus’. The convulsions may recur repeatedly and are interspersed with periods of relaxation. If not treated adequately, few patients survive more than 5 episodes of convulsions, death usually occurring due to respiratory and cardiac arrest. Fatalities in adults have occurred with doses as little as 16 mg. Secondary effects arising from the severe spasms include lactic acidosis, rhabdomyolysis, renal failure, hyperthermia, hyperkalaemia, and dehydration.


1. O’Callaghan WG, et al. Unusual strychnine poisoning and its treatment: report of eight cases. BMJ 1982; 285: 478
2. Blain PG, et al. Strychnine poisoning: abnormal eye movements. J Toxicol Clin Toxicol 1982; 19: 215–17
3. Boyd RE, et al. Strychnine poisoning: recovery from profound lactic acidosis, hyperthermia, and rhabdomyolysis. Am J Med 1983; 74: 507–12
4. Burn DJ, et al. Strychnine poisoning as an unusual cause of convulsions. Postgrad Med J 1989; 65: 563–4
5. Yamarick W, et al. Strychnine poisoning in an adolescent. J Toxicol Clin Toxicol 1992; 30: 141–8
6. Heiser JM, et al. Massive strychnine intoxication: serial blood levels in a fatal case. J Toxicol Clin Toxicol 1992; 30: 269–83
7. Nishiyama T, Nagase M. Strychnine poisoning: natural course of a nonfatal case. Am J Emerg Med 1995; 13: 172–3
8. Katz J, et al. Strychnine poisoning from a Cambodian traditional remedy. Am J Emerg Med 1996; 14: 475–7
9. Hernandez AF, et al. Acute chemical pancreatitis associated with nonfatal strychnine poisoning. J Toxicol Clin Toxicol 1998; 36: 67–71
10. Greene R, Meatherall R. Dermal exposure to strychnine. J Anal Toxic ol 2001; 25: 344–7
11. Wood D, et al. Case report: survival after deliberate strychnine self-poisoning, with toxicokinetic data. Crit Care 2002; 6: 456–9
12. Scheffold N, et al. Strychninvergiftung. Dtsch Med Wochenschr 2004; 129: 2236–8
13. Shadnia S, et al. A case of acute strychnine poisoning. Vet Hum Toxic ol 2004; 46: 76–9.

💊 Treatment of Adverse Effects

The main aim of therapy in strychnine poisoning is the prompt prevention or control of convulsions and asphyxia. Activated charcoal should be given if the patient presents within 1 hour of ingestion. Convulsions should be controlled or prevented by diazepam or lorazepam. Intubation and assisted respiration may be required. Should benzodiazepines fail then phenytoin or phenobarbital may be tried. All unnecessary external stimuli should be avoided and if possible the patient should be kept at rest in a quiet darkened room. Patients should be monitored for any secondary effects such as metabolic acidosis so that appropriate symptomatic treatment can be given.

💊 Uses and Administration

Strychnine competes with glycine, which is an inhibitory neurotransmitter; it thus exerts a central stimulant effect by blocking an inhibitory activity. Strychnine was formerly used as a bitter and analeptic but is now mainly used under strict control as a rodenticide. It has also been used as a mole poison, although this use is banned in some countries including the UK. Strychnine has been used in multi-ingredient preparations for the treatment of ophthalmic and urinarytract disorders. It has also been tried in the treatment of nonketotic hyperglycinaemia.

Nonketotic hyperglycinaemia.

Nonketotic hyperglycinaemia (also known as glycine encephalopathy) is an inborn defect in the enzyme system responsible for the metabolism of glycine. It is characterised by raised concentrations of glycine in plasma, CSF, and urine. Symptoms of glycine accumulation include respiratory distress, muscular hypotonia, seizures, vomiting, and extreme lethargy. Mental retardation and early infant death are common. Sodium benzoate can reduce plasma-glycine concentrations to near normal1 but is relatively ineffective in reducing CSF levels or in preventing mental retardation.2 Strychnine, a glycine antagonist, has been of some benefit in counteracting its CNS effects.3-5 However, even treatment with both drugs may be ineffective in severe cases6 and may ultimately have little effect on the course of the disease.7 Glycine is reported to stimulate NmethylD-aspartate (NMDA) receptors in the CNS and the combination of strychnine and ketamine (an NMDA receptor antagonist) was of some benefit in a newborn infant with severe non-ketotic hyperglycinaemia.8 Addition of low-dose dextromethorphan (an NMDA receptor antagonist) to treatment with sodium benzoate, arginine, carnitine, diazepam, and phenobarbital in an infant with nonketotic hyperglycinaemia9 was associated with resolution of nystagmus and improvement in eye contact and interactive behaviour, without altering serum- or CSF-glycine concentrations. Dextromethorphan with sodium benzoate alone may also be helpful, although the combination is not uniformly effective.10 Treatment with sodium benzoate and dextromethorphan was beneficial in a 6-month-old child with mild atypical nonketotic hyperglycinaemia,11 although it was later shown that it was sodium benzoate that had the greatest effect on EEG and behavioural changes. A partial response to low-protein diet and sodium benzoate occurred in a patient with late-onset nonketotic hyperglycinaemia; there was a more dramatic response when imipramine was added to therapy.12
1. Van Hove JLK,et al. Benzoate treatment and the glycine index in nonketotic hyperglycinaemia. J Inherit Metab Dis 2005; 28: 651–63
2. Krieger I, et al. Cerebrospinal fluid glycine in nonketotic hyperglycinemia: effect of treatment with sodium benzoate and a ventricular shunt. Metabolism 1977; 26: 517–24
3. Ch’ien LT, et al. Glycine encephalopathy. N Engl J Med 1978; 298: 687
4. Gitzelmann R, et al. Strychnine for the treatment of nonketotic hyperglycinaemia. N Engl J Med 1978; 298: 1424
5. Arneson D, et al. Strychnine therapy in nonketotic hyperglycinemia. Pediatrics 1979; 63: 369–73
6. Sankaran K, et al. Glycine encephalopathy in a neonate. Clin Pediatr (Phila) 1982; 21: 636–7
7. MacDermot KD, et al. Attempts at use of strychnine sulfate in the treatment of nonketotic hyperglycinemia. Pediatrics 1980; 65: 61–4
8. Tegtmeyer-Metzdorf H, et al. Ketamine and strychnine treatment of an infant with nonketotic hyperglycinaemia. Eur J Pediatr 1995; 154: 649–53
9. Alemzadeh R, et al. Efficacy of low-dose dextromethorphan in the treatment of nonketotic hyperglycinemia. Pediatrics 1996; 97: 924–6
10. Hamosh A, et al. Long-term use of high-dose benzoate and dextromethorphan for the treatment of nonketotic hyperglycinemia. J Pediatr 1998; 132: 709–13
11. Neuberger JM, et al. Effect of sodium benzoate in the treatment of atypical nonketotic hyperglycinaemia. J Inherit Metab Dis 2000; 23: 22–6
12. Wiltshire EJ, et al. Treatment of late-onset nonketotic hyperglycinaemia: effectiveness of imipramine and benzoate. J Inherit Metab Dis 2000; 23: 15–21.

💊 Preparations

Proprietary Preparations

Multi-ingredient: Chile: Vigofortal; Hung.: Artin†; Israel: Te s o p a l m e d Forte cum Yohimbine; Ital.: Neuroftal†; Pol.: Cardiamid-Coffein; Port.: Hipersex†; Thai.: Hemo-Cyto-Serum.
Published May 08, 2019.