Ketamine and strychnine treatment of an infant with nonketotic hyperglycinaemia

Tegtmeyer-Metzdorf, H.; Roth, Bernhardt; G�nther, M.; Theisohn, M.; Heinemann, Uwe; Adams, H. A.; Sticht, G

doi:10.1007/s004310050365

Cited by 2 publications

(3 citation statements)

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“…[6][7][8] Others have used dextromethorphan, ketamine or strychnine as non-competitive antagonists of one of the glycine receptors in the CNS. 9,10 Although these case reports support the use of such strategies, the evidence is anecdotal only and none have been consistently effective. 4 Other therapies are aimed at symptom control, in particular seizure management and currently advocated anticonvulsants include carbemazepine, lamotrigine and topiramate.…”

Section: Discussionmentioning

confidence: 98%

“…Most therapies have been aimed at decreasing the glycine load in the CNS by reducing dietary glycine intake and by conjugating glycine to benzoate or salicylate, in a mechanism similar to that employed for hyperammonaemia 6−8 . Others have used dextromethorphan, ketamine or strychnine as non‐competitive antagonists of one of the glycine receptors in the CNS 9,10 . Although these case reports support the use of such strategies, the evidence is anecdotal only and none have been consistently effective 4 .…”

Section: Discussionmentioning

confidence: 99%

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Seizures and a hiccup in the diagnosis

Wallace

Manikkam

Maxwell

2004

J Paediatrics Child Health

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CASE REPORTA female infant was born by normal vaginal delivery at Waikato Hospital at 40 weeks gestation to a 17-year-old primigravida following an uneventful pregnancy. Labour was complicated by the presence of thick meconium. Apgar scores were 6 and 8 at 1 and 5 minutes, birthweight 2920 g and head circumference 34 cm. Neonatal intensive care unit admission was not required in the immediate postnatal period. As it was Christmas day, at 14 h of age mother and baby transferred to a peripheral hospital to be closer to home. There were comments in the infant's notes that she had not fed well and was very sleepy but this was not thought to be significantly abnormal. However, midwifery staff attending the child following this transfer were also concerned about her poor feeding, floppiness and lethargy. Thus, at 36 h of age, the infant was referred back to the tertiary institution where she was admitted to the neonatal intensive care unit. Examination revealed a non-toxic child with moderate hypotonia and poor reactivity. Deep tendon reflexes were normal. There were no dysmorphic features. On review of the antenatal history, there was no alcohol or drug use in pregnancy and the parents were not related. Mother reported a history of Chlamydia and genital herpes prior to this pregnancy.Complete blood count, electrolytes, urea, glucose, liver function tests, serum lactate and arterial blood gas were normal. Serum ammonia was 97 µ mol/L (0-50). A urine toxicology screen for amphetamines, opiates, benzodiazepines and cannabinoids was negative. Cerebral ultrasound showed unusual grey-white matter differentiation with slit like ventricles. The initial impression was of an unrecognized asphyxial insult. On day 3, the infant began to have short generalized seizures and apnoeas. In addition, her level of consciousness had deteriorated further and hypotonia worsened. Phenobarbitone was commenced but a midazolam infusion was also required to control seizure activity. CSF cell count, protein and glucose were normal however, penicillin, cefotaxime and acyclovir were given until CSF culture and Herpes simplex virus (HSV) DNA were reported as negative. Her apnoeas were managed initially with nasal prong oxygen but by 6 days of age she required intermittent positive pressure ventilation.The infant was discussed with a metabolic paediatrician and although an underlying metabolic diagnosis was considered unlikely, a more extensive metabolic work up was initiated. Tests performed included urinary organic and amino acids, plasma very long chain fatty acids, plasma and CSF glycine, serum uric acid and plasma carnitine and acylcarnitine.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Seizures and a hiccup in the diagnosis

Wallace

Manikkam

Maxwell

2004

J Paediatrics Child Health

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“…Ketamin ist ein nichtkompetitiver N-Methyl-D-Aspartat-Rezeptor-Antagonist, dessen praktische Bedeutung durch pharmakokinetische Besonderheiten limitiert ist, aber bei therapierefraktären zerebralen Anfällen in Erwä-gung gezogen werden kann [18,27]. Auch Benzodiazepine wie Diazepam, die die GABAerge Inhibition verstär-ken und möglicherweise auch mit der glutamatergen Transmission interferieren [18], werden eingesetzt [9].…”

Section: Diskussionunclassified