Muscle Relaxant
PREGNANCY RECOMMENDATION: Human Data Suggest Low Risk
BREASTFEEDING RECOMMENDATION: No Human Data—Probably Compatible
PREGNANCY SUMMARY
No evidence of human developmental toxicity attributable to methocarbamol has been located.
FETAL RISK SUMMARY
The centrally acting muscle relaxant, methocarbamol, is not teratogenic in animals (A.H. Robins Company, personal communication, 1987). It is not known if the drug crosses the human placenta. The agent crosses the placenta of dogs (1).
One manufacturer has an unpublished case on file relating to a mother who consumed methocarbamol, 1 g 4 times/day, throughout gestation (A.H. Robins Company, personal communication, 1987).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 (A.H. Robins Company, personal communication, 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 whom 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 at 2 months of gestation had consumed methocarbamol and propoxyphene, 750 and 65 mg, respectively, 2–3 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.
The authors of the above study attributed the multiple joint contractures in the infant to methocarbamol because of its muscle relaxant properties. However, 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.
BREASTFEEDING SUMMARY
No reports describing the use of methocarbamol during human lactation have been located. Because newborns have been directly treated for tetanus with methocarbamol, any amount excreted in milk is probably clinically insignificant.
References
1.Campbell AD, Coles FK, Eubank LL, Huf EG. Distribution and metabolism of methocarbamol. J Pharmacol Exp Ther 1961;131:18–25.
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;25:173–91.
4.Barrow MV, Souder DE. Propoxyphene and congenital malformations. JAMA 1971;217:1551–2.