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Biomedical subjects

J Chevrel

Publications and source records attributed to J Chevrel.

7 recordsLinked to original sources
PubMed1997

Buprenorphine withdrawal syndrome in a newborn.

A pregnant woman who was addicted to heroin rapidly withdrew from illicit drugs after the onset of a 4 mg/day buprenorphine treatment. In the newborn's blood, urine, and meconium 20 hours after birth, high concentrations of buprenorphine and its metabolite norbuprenorphine were detected, with a higher buprenorphine/norbuprenorphine ratio than in adults, possibly as a consequence of immature hepatic function; no illicit drugs were found. The child had a weak withdrawal syndrome on the second day of life and recovered rapidly. The measured buprenorphine daily dose ingested by the newborn through mother's milk was very low (3.28 micrograms) and probably had little pharmacologic effect because no withdrawal signs could be noted when maternal feeding was later abruptly interrupted. Further investigations are required to determine whether buprenorphine can be considered to be a good alternative to methadone in the treatment of pregnant heroin addicts to prevent marked withdrawal syndromes in newborns.

Adult↗
PubMed1995

[Hyperexplexia].

Hyperexplexia is a disease of neonatal onset characterized by an exaggerated startle reflex. Early diagnosis is important to rule out epilepsy. Clinical findings are mainly hypertony and generalized startle reflex which is exaggerated by tiredness and some exogenous stimuli. Electroencephalogram is normal. The expression of the disease is variable including minor forms that may be unnoticed and major forms with arthrogryposis-like symptoms, orthopedic complications, false passages, apnea and even sudden infant death (SID). The evolution is generally benign and symptoms disappear within 2 or 3 years. A neuromotor retardation is often present, without intellectual deficit. In severe forms, the risk of SID requires a multidisciplinary follow-up including monitoring and treatment with clonazepam. A low GABA level in cerebrospinal fluid has been reported. Present etiological hypotheses include neuromediator and/or receptor dysfunction.

Humans↗
PubMed1994

Possible involvement of a gamma-hydroxybutyric acid receptor in startle disease.

Startle disease or hyperreflexia is an autosomal dominant neurological disorder, with a neonatal onset, characterized by muscular hypertonia and myoclonic jerks, exaggerated by the slightest stimulus. Low concentrations of free gamma-aminobutyric acid (GABA) have been found in the cerebrospinal fluid of two affected infants. The involvement of GABA or its receptors has been raised and the use of GABA-agonist drugs has been suggested. We report a newborn with startle disease who also had a low concentration of GABA in the cerebrospinal fluid. No clinical improvement was observed with progabide, a GABA agonist. Furthermore, a high dose (100 mg/kg) of gamma-hydroxybutyrate (GHB) did not improve muscular stiffness and failed to induce general anesthesia. GHB, currently used as an effective general anaesthetic, is a structural analogue of GABA. It is present naturally at low concentrations in the brain and is regarded as an inhibitory neurotransmitter. Two specific GHB receptors, distinct from the GABA receptors, have been identified in rat brain. Failure to induce general anesthesia with a high dose of GHB suggests that one of these receptors could be involved in startle disease.

Anesthetics↗