Pharmacotherapy. 2004 Dec;24(12):1804-6.
Carisoprodol withdrawal syndrome.

Reeves RR, Beddingfield JJ, Mack JE.
G.V. (Sonny) Montgomery VA Medical Center, School of Medicine, University of Mississippi, Jackson, Mississippi, USA.

A 43-year-old man with chronic back and shoulder pain was treated with hydrocodone. He began taking excessive amounts of the drug, so his physicians stopped prescribing it. The patient then obtained the muscle relaxant carisoprodol on his own from several sources. He was consuming up to 30 or more tablets/day (> or =10,500 mg/day) for several weeks, then abruptly stopped taking the drug. Within 48 hours he developed anxiety, tremors, muscle twitching, insomnia, auditory and visual hallucinations, and bizarre behavior. The symptoms intensified and peaked on the fourth day after carisoprodol cessation. The patient required brief treatment with olanzapine and tapering dosages of lorazepam while the symptoms gradually resolved. To our knowledge, this is the first documented case of a withdrawal syndrome with carisoprodol. The symptoms most likely resulted because of accumulation of meprobamate, the active metabolite of carisoprodol in humans. Clinicians prescribing carisoprodol should be aware of the possibility for abuse or addiction. Further, we recommend that carisoprodol be designated a controlled substance at the federal level.

Source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract soma carisoprodol &list_uids=15585447





Psychopharmacology (Berl). 2004 May 5 [Epub ahead of print]
Stimulant and relaxant drugs combined with stimulant and relaxant information: a study of active placebo.

Flaten MA, Simonsen T, Zahlsen K, Aamo T, Sager G, Olsen H.

Department of Psychology, University of Tromso, Breivika, 9037, Tromso, Norway.

RATIONALE. The active placebo hypothesis states that placebo effects are potentiated when an active drug is administered. OBJECTIVE. This hypothesis was tested in an experiment where information about the effect of a drug was combined with administration of an active drug or placebo. METHODS. Information that a drug acted as a relaxant, a stimulant, or as a placebo was crossed with oral administration of a relaxant drug (700 mg carisoprodol), a stimulant drug (400 mg caffeine) or placebo (lactose) in healthy volunteers ( n=94). Dependent variables were subjective and physiological measures of arousal, as well as serum carisoprodol and caffeine levels. Data were collected from 15 to 280 min after administration of drug or placebo. RESULTS. Caffeine increased alertness, systolic and diastolic blood pressure, startle blink reflexes, and skin conductance responses. Subjects were calmer after carisoprodol, and heart rate was increased. There was a positive correlation between increased arousal and carisoprodol levels when stimulant information had been provided. However, this was only seen when carisoprodol levels were very low. There was no evidence that caffeine modulated the placebo response. CONCLUSIONS. Active placebo responses were seen only transiently when carisoprodol levels were low, and only in the subjective arousal data. Caffeine did not support active placebo responses. The overall findings did not favour the active placebo hypothesis.

Source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15133576&dopt=Abstract soma carisoprodol




Drug Alcohol Depend. 2004 Jun 11;74(3):311-8.
Impairment due to intake of carisoprodol.

Bramness JG, Skurtveit S, Morland J.

Norwegian Institute of Public Health, Division of Forensic Toxicology and Drug Abuse, Nydalen, 0403 Oslo, Norway. jorgen.bramnesabmed.uio.no

BACKGROUND: Carisoprodol is a centrally acting muscle relaxant commonly used for lower back pain. It is a drug of abuse and has been detected among impaired drivers. Carisoprodol's active metabolite meprobamate is thought to act through the GABA(A) receptor complex and produces a well-known impairing effect. It is unclear whether therapeutic intake of carisoprodol leads to impairment, and the effect of supratherapeutic doses has not been investigated. Possible impairment could further be a product of the parent drug and/or the metabolite meprobamate. The present study aimed to investigate if carisoprodol had an impairing effect by it self. METHODS: From the database at the Norwegian Institute of Public Health, Division for Forensic Toxicology and Drug Abuse 62 cases containing carisoprodol and meprobamate as only drugs were identified. These cases constituted our material. RESULTS: Impaired drivers (73%) had higher blood carisoprodol concentration than not impaired drivers (27%), but no difference in blood meprobamate concentration was found for all the drivers viewed together. Amongst occasional users of carisoprodol, however, there was difference in blood meprobamate concentration between not impaired and impaired drivers. The risk of being judged impaired rose with increasing blood carisoprodol concentration, but not with increasing blood meprobamate concentration. The clinical effects of carisoprodol as measured by the clinical test for impairment (CTI) resembled those of benzodiazepines with some important differences such as tachycardia, involuntary movements, hand tremor and horizontal gaze nystagmus, which may be specific carisoprodol effects. CONCLUSION: Carisoprodol probably has an impairing effect by itself, at least at b