Letters to the Editor Pregnancy in Parkinson’s Disease: A Review of the Literature and a Case Report We read with interest the article by Hagell et al. 1 The authors revise the literature on pregnancy in Parkinson’s disease (PD) and report the case of a woman with PD who was treated with L-dopa-benserazide throughout an uncomplicated pregnancy. She gave birth to a healthy baby without any worsening of her PD. We want to add a similar case with the difference being that our patient was treated with bromocriptine monotherapy during her pregnancy. A 40-year-old woman developed progressive PD and began treatment with L-dopa-carbidopa in March 1982. Two years later, a bilateral tubal ligation was performed. In May 1986, she began experiencing nausea and vomiting which were attributed to levodopa. Despite treatment with domperidone and the re- duction of the levodopa dose, the nausea and vomiting contin- ued. At the end of May 1986, her physician changed her levo- dopa therapy to bromocriptine alone at doses of 20 mg per day. Within the following months, other symptoms of pregnancy occurred, and the diagnosis was finally confirmed by ultraso- nographic examination. Throughout the pregnancy the patient’s parkinsonian symptoms remained stable and the same dose of bromocriptine was continued. She gave birth to a normal term infant in January 1987. The baby showed no evidence of ab- normal findings and is now a healthy boy. To our knowledge, we are unaware of any reports of women with PD receiving bromocriptine monotherapy during their pregnancy. Our patient had an uncomplicated pregnancy and gave birth to a normal boy. The dopamine agonist bromocriptine has been widely used to facilitate pregnancy in hyperprolactinemic women and as an antiparkinsonian drug. There has been no evidence of a tera- togenic effect of bromocriptine in people or animals, and no disturbances in the physical, psychomotor, and intellectual de- velopment of the offspring have been observed. 2,3 In animal studies there have been reports of teratogenicity of levodopa in rats. 4 However, no major complications of unsuc- cessful pregnancy or teratogenicity during pregnancy have been reported with L-dopa monotherapy or in combination with a peripheral decarboxylase inhibitor, except for one case of spontaneous abortion after 2 months of gestation for which the cause is unknown. 5 Cessation of antiparkinsonian treatment increases the dis- abilities of patients and causes harmful effects on pregnancy and labor. Although there are no reasons to withdraw L-dopa or its combination with a peripheral carboxylase, it is impossible to assume that there is an absolute guarantee for its use in pregnancy. We suggest that bromocriptine monotherapy is a good alter- native to L-dopa, at least during pregnancy, because there are more studies that demonstrate its safe use during pregnancy in animals and people. 2,3 Furthermore, bromocriptine mono- therapy has been effective in a majority of patients for treat- ment periods of less than 1 year. 6 Julia ´n Benito-Leo ´n, MD, PhD Services of Neurology Hospital General de Mo ´stoles Mo ´stoles (Madrid), Spain Fe ´lix Bermejo, MD, PhD Jesu ´s Porta-Etessam, MD Hospital Universitario 12 de Octubre Madrid, Spain References 1. Hagell P, Odin P, Vinge E. Pregnancy in Parkinson’s disease: a review of the literature and a case report. Mov Disord 1998;13: 34–38. 2. Narburgh LJ, Turner J, Freeman SJ. Evaluation of the teratogenic potential of the dopamine agonist bromocriptine in rats. Toxicol Lett 1990;50:189–194. 3. Weil C. The safety of bromocriptine in hyperprolactinemic female infertility: a literature review. Curr Med Res Opin 1986;10:172– 195. 4. Ball MC, Sagar HJ. Levodopa in pregnancy. Mov Disord 1995; 10:115. 5. Gershanik OS, Leist A. Juvenile onset of Parkinson’s disease. Adv Neurol 1986;45:213–216. 6. Watts RL. The role of dopamine agonists in early Parkinson’s disease. Neurology 1997;49(suppl 1):S34–S48. Cervical Stenosis and Dystonic Cerebral Palsy Pollack et al.’s 1 recent article emphasized the high risk of cervical disk disease among dystonic cerebral palsy (CP) pa- tients. Although the authors alluded to ‘‘aggravators of pre- existing spondylotic changes’’ in this subpopulation of CP pa- tients, cervical spondylosis and stenosis alone may result in myelopathy as illustrated in the following patient. A 19-year-old man was the product of a 33-week gestation. At 8 months of age a diagnosis of cerebral palsy was made. He was healthy and was considered normal aside from motor im- pairment. He had always done well in school with the assis- tance of an aide. He was able to ambulate with a walker. At age 11, he started to develop dystonia which became progressive. Severe leg spasms and marked lower extremity scissoring then developed. The patient’s symptoms were uncontrolled on di- azepam and baclofen at dosages of up to 180 mg daily. His leg spasms progressed to the point that he was no longer able to walk. These were initially diagnosed as clonus and therefore at age 15 he underwent dorsal rhizotomy involving L2 to S1 bilaterally without any relief. He experienced no weakness from this operation but did develop numbness in his feet. After this operation, the family and the patient noted that his dystonia worsened; daily he experienced hours of painful dystonia with both legs extended parallel to the floor, the left arm extended backward, and the neck flexed. He was then evaluated for the first time by one of the authors (JHF) and a diagnosis of par- Movement Disorders Vol. 14, No. 1, 1999, pp. 194–195 © 1999 Movement Disorder Society 194