Methocarbamol]]>

Risk Factor: C
Class: Autonomics/ Skeletal muscle relaxants

Contents of this page:
Fetal Risk Summary
Breast Feeding Summary
References

Fetal Risk Summary

The centrally acting muscle relaxant, methocarbamol, is not teratogenic in animals (personal communication, A.H. Robins Company, 1987). The agent crosses the placenta to the fetus in dogs (1) but, apparently, placental transfer in humans has not been studied.

One manufacturer has an unpublished case on file relating to a mother who consumed methocarbamol, 1 g 4 times/day, throughout gestation (personal communication, A.H. Robins Company, 1987). The mother also used marijuana, and possibly other illicit substances, during her pregnancy. No physical or developmental abnormalities were noted at birth, but the infant did exhibit withdrawal symptoms consisting of prolonged crying, restlessness, easy irritability, and seizures. The infant was hospitalized for 2 months following birth to treat these symptoms. No further withdrawal symptoms or seizures were observed following discharge from the hospital. Follow-up neurologic examination indicated that developmental patterns were normal.

The above manufacturer also has informal data on file obtained from the Boston Collaborative Drug Surveillance Program (personal communication, A.H. Robins Company, 1987). These data, compiled between 1977 and 1981, relate to the use of methocarbamol by pregnant patients of the Puget Sound Group Health Cooperative in Seattle, Washington. During the data collection interval, 27 1st trimester exposures to the muscle relaxant were documented. None of the exposed infants had a congenital malformation.

The Collaborative Perinatal Project monitored 50,282 mother-child pairs, 22 of which were exposed to methocarbamol during the 1st trimester (2, pp. 358, 360). One of these infants had an inguinal hernia. For use anytime during pregnancy, 119 exposures were recorded (2, p. 493). In this latter group, six infants had an inguinal hernia. An association between the drug and the defect cannot be determined from these data.

In a surveillance study of Michigan Medicaid recipients involving 229,101 completed pregnancies conducted between 1985 and 1992, 340 newborns had been exposed to methocarbamol during the 1st trimester (F. Rosa, personal communication, FDA, 1993). A total of 13 (3.8%) major birth defects were observed (14 expected), including (observed/expected) 1/1 polydactyly and 1/1 limb reduction defect. No anomalies were observed in four other defect categories (cardiovascular defects, oral clefts, spina bifida, and hypospadias) for which specific data were available. These data do not support an association between the drug and congenital defects.

The authors of a 1982 study of 350 patients with congenital contractures of the joints (arthrogryposis) concluded that only 15 had been exposed to a possible teratogen (3). One of the 15 cases involved a 24-year-old woman who had consumed, at 2 months of gestation, methocarbamol and propoxyphene, 750 mg and 65 mg, respectively, 23 times/day for 3 days to treat severe back pain. The term female infant was noted at birth to have multiple joint contractures involving the thumbs, wrists, elbows, knees, and feet. The latter was described as a bilateral equinovarus deformity. There were practically no foot creases. Other abnormalities present were frontal bosselation, a midline hemangioma, and weak abdominal musculature. Development was normal at 3 years of age except for the joint contractures, which had improved with time, and a grade I/VI systolic murmur.

Because of the muscle relaxant properties of methocarbamol, the authors of the above study attributed the defect to this drug. Their review of the literature and of the records of the Centers for Disease Control and Prevention failed to find any other cases of arthrogryposis with maternal methocarbamol ingestion. Moreover, no reports have appeared since then relating the defect to maternal use of the drug. A case of arthrogryposis, however, had been previously described with propoxyphene ingestion (see Propoxyphene for details) (4). Thus, based on the present information, it is unlikely that a relationship exists between maternal use of methocarbamol and congenital contractures in the newborn.

Breast Feeding Summary

Methocarbamol is excreted in the milk of dogs (1), but human studies have not been located. Because newborns have been directly treated for tetanus with methocarbamol, any amounts excreted in milk are probably not clinically significant. The American Academy of Pediatrics classifies methocarbamol as compatible with breast feeding (5).

References

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  1. Campbell AD, Coles FK, Eubank LL, Huf EG. Distribution and metabolism of methocarbamol. J Pharmacol Exp Ther 1961;131:1825.
  2. Heinonen OP, Slone D, Shapiro S. Birth Defects and Drugs in Pregnancy. Littleton, MA: Publishing Sciences Group, 1977.
  3. Hall JG, Reed SD. Teratogens associated with congenital contractures in humans and in animals. Teratology 1982;25:17391.
  4. Barrow MV, Souder DE. Propoxyphene and congenital malformations. JAMA 1971;217:15512.
  5. Committee on Drugs, American Academy of Pediatrics. The transfer of drugs and other chemicals into human milk. Pediatrics 1994;93:13750.

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