Return
Primary Psychiatry. 2005;12(7):25-28
Dr. Ginsberg is director of outpatient services in Tisch Hospital’s Department of Psychiatry at New York University Medical Center in New York City.
Disclosure: Dr. Ginsberg is a speaker for Forest, GlaxoSmithKline, Organon, and Ortho-McNeil; is a consultant for Bristol-Myers Squibb, Eli Lilly, and Pfizer; and has received research support from Cyberonics and UCB Pharma.
Lamotrigine-Induced Neutropenia
Lamotrigine is a Food and Drug Administration-approved anticonvulsant for partial and Lennox-Gestaut syndrome-associated seizures, as well for the maintenance phase of bipolar I disorder. Previous Psychopharmacology Reviews columns have discussed the off-label use of lamotrigine for posttraumatic stress disorder,1 frontal lobe dementia,2 refractory unipolar depression,3,4 and treatment-resistant schizophrenia.5 Other than the uncommon occurrence of a serious drug-associated rash, in general, the side-effect profile of lamotrigine is favorable, which has led to its growing use among clinicians. Now comes a report of lamotrigine-induced neutropenia.6
A 23-year-old woman was hospitalized with bipolar II depression. Her history was also remarkable for polysubstance abuse and eating disorder not otherwise specified. Two months previously, topiramate had been initiated, with which the patient had been partially compliant. On the first day of admission, topiramate 50 mg/day was initiated, then increased to 100 mg at bedtime on day 10. Subsequently, topiramate was decreased to 75 mg/day on day 15, then further decreased to 50 mg on day 26. Lamotrigine 12.5 mg at bedtime was added on day 15, then increased to 25 mg/day on day 19 and to 50 mg/day on day 26.
A complete blood count (CBC) on day 2 was normal. A random CBC on day 29 revealed neutropenia (1.0 X 109/L), so topiramate 50 mg at bedtime and lamotrigine 50 mg/day, were discontinued. Subsequently, over the next 2 weeks, the patient’s neutrophil count increased to 2.0 X 109/L on day 43 and to 2.4 X 109/L on day 44. On day 46, lamotrigine 5 mg at bedtime was initiated. Two days later, neutrophils dropped to 1.8 X 109/L, so lamotrigine was discontinued. The following day, neutrophils rose to 2.2 X 109/L and then to 2.4 X 109/L on the day after that (ie, day 50).
The temporal sequence of events of initiation, discontinuation, rechallenge, then discontinuation again is consistent with lamotrigine-induced neutropenia, which, in the patient described, did not result in any adverse complications. There are several prior reports of lamotrigine-induced neutropenia, all reversible upon drug discontinuation.7-11 According to the manufacturer’s package insert for lamotrigine, leukopenia is an infrequent event (1/100 to 1/1000 incidence).12 Moreover, the absence of systemic signs such as fever, rash, or lymphadenopathy would seem to rule out a hypersensitivity reaction as the etiology of this patient’s neutropenia. While the incidence is low, lamotrigine may result in neutropenia. While there is no recommendation for regular monitoring of CBC in lamotrigine-treated patients, clinicians ought to be aware of the possibility of this uncommon but potentially serious adverse event. PP
References
1. Hertzberg MA, Butterfield MI, Feldman ME, et al. A preliminary study of lamotrigine for the treatment of posttraumatic stress disorder. Biol Psychiatry. 1999;45:1226-1229.
2. Devarajan S, Dursun SM. Aggression in dementia with lamotrigine treatment [letter]. Am J Psychiatry. 2000;157:1178.
3. Maltese TM. Adjunctive lamotrigine treatment for major depression [letter]. Am J Psychiatry. 1999;156:1833.
4. Barbee JG, Jamhour NJ. Lamotrigine as an augmentation agent in treatment-resistant depression. J Clin Psychiatry. 2002;63:737-741.
5. Dursun SM, McIntosh D. Clozapine plus lamotrigine in treatment-resistant schizophrenia [letter]. Arch Gen Psychiatry. 1999;56:950.
6. LeDrew K, Phillips L, Hogan M, et al. Lamotrigine-induced neutropenia [letter]. Can J Psychiatry. 2005;50:242.
7. Fadul CE, Meyer LP, Jobst BC, et al. Agranulocytosis associated with lamotrigine in a patient with a low grade glioma. Epilepsia. 2002;43:199-200.
8. De Camargo O, Bode H. Agranulocytosis associated with lamotrigine. BMJ. 1999;318:11.
9. Nicholson RJ, Kelly KP, Grand IS. Leukopenia associated with lamotrigine. BMJ. 1995;310:504.
10. Normann C, Hummel B, Scharer LO, et al. Lamotrigine as an adjunct to paroxetine in acute depression. J Clin Psychiatry. 2002;63:337-344.
11. Lambert O, Veryac G, Armand C, et al. Lamotrigine-induced neutropenia following two attempts to increase dosage above 50 mg/day with recovery between episodes. Adverse Drug Reacti Toxicol Rev. 2002;1:57-59.
12. Lamictal (package insert). Research Triangle Park, Nc: GlaxoSmithKline; 2004.
Adjunctive Rivastigmine Reduces Negative Symptoms of Schizophrenia
While traditional neuroleptics are effective for the positive symptoms of schizophrenia, their efficacy in treating the negative symptoms is more limited. Negative symptoms such as flat affect, alogia, and avolition, typically appear early in the course of illness and often are chronic, treatment refractory, and may interfere with quality of life. With the advent of atypical antipsychotics, it is now possible to treat both positive and negative symptoms, as well as affective/cognitive and depressive symptoms, resulting in a greater ability for those afflicted with schizophrenia to function in daily life. However, despite the increased use of atypical neuroleptics, most patients with schizophrenia still suffer with residual negative symptoms of the disease. As a result, there remains a need for additional medications to target these persistent symptoms. Now comes a case of residual schizophrenia with predominantly negative symptoms that responded to the addition of rivastigmine to risperidone.1
A 45-year-old Indian woman had residual schizophrenia of 6 years’ duration. Despite treatment with risperidone 6 mg/day, over the prior 18 months she had developed progressive passivity, lack of initiative, marked psychomotor retardation, poverty of speech, and poor facial expression. With the support of her family, she maintained good compliance with risperidone, which completely controlled her positive symptoms. At the time of evaluation, the patient was assessed with the following inventories: the Scale for the Assessment of Negative Symptoms (SANS); the Instrumental Activities of Daily Living (IADL), the Satisfaction With Life Scale (SWLS), the Halstead-Reitan Battery for psychomotor speed, attention, and scanning; the Rey Auditory Verbal Learning Test; and the Wechsler Memory Scale-Third Edition for learning and memory. Subsequently, she began rivastigmine tartrate 1.5 mg twice daily, titrated to 6 mg/day after 2 months. She continued risperidone 6 mg/daily. A second SANS evaluation, done after 4 weeks of drug therapy, showed 10% improvement in negative symptoms. After 6 months of combined drug treatment, the SANS score had decreased by 41% from baseline. Similarly, baseline IADL and SWLS scores improved by 36% and 28%, respectively. Neuropsychological testing revealed appreciably improved cognitive function that was directly related to the improvement in her quality of life.
Neurotransmitters involved in the pathophysiology of schizophrenia include dopamine, serotonin, glutamate, and acetylcholine. Cognitive impairment in schizophrenia results, at least in part, from diminished acetylcholine activity in the brain cortex. Combined with neuroleptics, rivastigmine, an acetylcholinesterase and butyrylcholinesterase inhibitor widely used in treating Alzheimer’s disease and subcortical vascular dementias, has shown efficacy in improving negative schizophrenia symptoms.2,3 Previous research has also demonstrated benefits in cognitive functioning in schizophrenic patients adjunctively treated with the acetylcholinesterase inhibitor donepezil.4,5
These findings point to a possible role for adjunctive use of acetylcholinesterase inhibitors, in combination with atypical neuroleptics, in the treatment of residual schizophrenia. Additional studies with randomized, double-blind, placebo-controlled designs, are needed to more fully assess these treatments for this condition. PP
References
1. Raguraman J, Sagar JV, Chandrasekaran R. Effects of rivastigmine in a case of residual schizophrenia [letter]. Can J Psychiatry. 2005; 50:243-244.
2. Van de Graff K, Loonen A, Hovens JE, et al. Pilot study of the effects of rivastigmine in Schizophrenia. J Eur Coll Neuropsychopharmacol. 2003;13(suppl 4):S315.
3. Lenzi A, Maltinti E, Poggi E, et al. Effects of rivastigmine on cognitive function and quality of life in patients with schizophrenia. Clin Neuropharmacol. 2003;26:317-321.
4. Stryjer R, Strous RD, Bar F, et al. Beneficial effect of donepezil augmentation for the management of comorbid schizophrenia and dementia. Clin Neuropharmacol. 2003;26:12-17.
5. Tugal O, Yazici K. A double-blind, placebo-controlled, cross-over trial of adjunctive donepezil for cognitive impairment in schizophrenia. J Eur Coll Neuropsychopharmacol. 2003;13(suppl 4):S294.
Itraconazole-Tadalafil Interaction Results in Priapism
Priapism, characterized by abnormal, prolonged, painful erection of the penis, is a urological emergency. If not treated in time, complications may occur including difficulty urinating, urinary retention, impotence, cavernosa fibrosis, and gangrene. Even with surgery, about 40% to 50% of patients with priapism will become impotent.1 Causes of priapism include blood dyscrasias, solid tumors, trauma, spinal cord injuries, and stroke. Medications may also cause priapism. The ones most commonly associated with priapism among the latter are antihypertensives, anticoagulants, antidepressants, and antipsychotics.2,3 Now comes a report of priapism resulting from an interaction between the phosphodiesterase type-5 enzyme (PDE-5) inhibitor tadalafil, and the antifungal agent itraconazole.4
A 56-year-old white man with erectile dysfunction (ED) but with an otherwise benign medical history had been using sildenafil 100 mg as needed, from 1999 to 2003, without adverse effects. In an effort to achieve improved and more sustained efficacy, he later switched to tadalafil 10 mg. He was not taking any concomitant medications and denied any undesirable side effects. In September 2003, due to recurrent onychomycosis of the foot, he started taking itraconazole 400 mg/day for 7 days/month. In the past, he had taken itraconazole, including in addition to the PDE-5 inhibitor sildenafil, without experiencing any adverse effects. During the first day of monthly itraconazole therapy in October 2003, he took a dose of tadalafil. Within several hours, priapism occurred, lasting over 4 hours but without impeding urinary flow. The next month, during weekly itraconazole treatment, the patient took the same dose of tadalafil, and again experienced priapism lasting over 4 hours. He reported it to his physician, adding that painful erections had occurred repeatedly over 72 hours. Over the next 7 months, the patient did not use tadalafil. However, upon use of sildenafil in the context of ongoing itraconazole therapy, he did not experience any recurrences of priapism.
Based on the temporal sequence of events, it is likely that the combination of tadalafil and itraconazole was the cause of this patient’s priapism. Until now, there have not been any published reports of tadalafil resulting in priapism. However, there are reports of an association between sildenafil and priapism.5-7 It is likely that a pharmacokinetic interaction between tadalafil, a substrate of the cytochrome P450 3A4 (CYP) isoenzyme, and itraconazole, a potent CYP inhibitor, resulted in elevated serum levels of tadalafil and as a consequence, priapism. According to the package insert for Tadalafil,8 another CYP inhibitor, ketoconazole, at doses of 200 mg/day, causes an increase of tadalafil (10 mg) area-under-the-curve and maximum concentration 107% and 15%, respectively, relative to the values of the same dose of tadalafil alone.8 While no drug-drug interaction studies between tadalafil and itraconazole have been conducted, it is likely that a similar relationship exists. Interestingly, the patient did not experience priapism when sildenafil, another substrate of CYP, was combined with itraconazole. Given the potential seriousness of priapism, a medical emergency requiring prompt urological intervention to prevent complications such as impotence and gangrene, clinicians who prescribe tadalafil need to be aware of the potential for precipitating priapism in patients taking concomitant medications that inhibit CYP. PP
References
1. Thompson JW, Ware MR, Blashfield RK. Psychotropic medication and priapism: a comprehensive review. J Clin Psychiatry. 1990;51:430-433.
2. Patel AG, Mukherji K, Lee A. Priapism associated with psychotropic drugs. Br J Hosp Med. 1996;55:315-319.
3. Heckers S, Anick D, Boverman JF, et al. Priapism following olanzapine administration in a patient with multiple sclerosis. Psychosomatics. 1998;39:288-290.
4. Galatti L, Fioravanti A, Salvo F, et al. Interaction between tadalafil and itraconazole [letter]. Ann Pharmacother. 2005;39:200.
5. Sur RL, Kane CJ. Sildenafil citrate-associated priapism. Urology. 2000;55:950.
6. Kassim AA, Fabry ME, Nagel RL. Acute priapism associated with the use of sildenafil in a patient with sickle cell trait. Blood. 2000;95:1878-1879.
7. Goldmeier D, Lamba H. Prolonged erections produced by dihydrocodeine and sildenafil. BMJ. 2002;324:1555.
8. Cialis (package insert). Indianapolis, IN: Eli Lilly; 2005.
Diazepam-Associated Gynecomastia
Drug-induced gynecomastia in men is believed to result from an altered ratio between testosterone and estrogen concentrations.1 In some cases, however, the mechanism of drug-induced gynecomastia is unknown. Benzodiazepine-associated gynecomastia has been reported at least as far back as the early 1980s.2,3 Now comes another report of diazepam-induced gynecomastia.4
An obese, 47-year-old man with an otherwise unremarkable medical history presented with breast enlargement that had first become apparent to him 2 months previously, which was 8 months after he had begun self-medicating with diazepam for anxiety. In his country, Serbia, diazepam is available over the counter. Initially, he took diazepam 5–10 mg on an as-needed basis. Dissatisfied with the results, he increased the dose to 10–30 mg/day. Two weeks prior to presentation, he had increased his dosage to 40–50 mg/day. He denied being sedated or even feeling tired, instead reporting that over time he seemed to feel more nervous and aggressive, which in his view necessitated his increasing his dosage of diazepam.
Over the last few months of diazepam treatment, his breasts had become gradually enlarged, measured at 10.6 cm in width, 2.7 cm above the middle line of the chest, with no secretion or nodes. The patient was obese, with a body mass index (BMI) of 32.19 kg/m2. He attributed his breast enlargement to obesity, although it was not reported how much weight he had gained during the time interval during which his breast size increased. Other than one use of cotrimoxazole over 6 months prior to his presentation, he denied using any medications other than diazepam.
Three weeks after being advised to gradually taper off the diazepam, the patient described using the medication only occasionally, at a dosage of 5–15 mg/day. Over this period, while the patient’s BMI decreased slightly, to 31.2 kg/m2, he experienced a significant breast dimension reduction, reaching near normal size, measured at 7.2 cm in width, 1.6 cm above the middle line of the chest. He also reported that he was less nervous and aggressive.
The presentation appears consistent with diazepam associated gynecomastia. Whether this was a primary effect, or secondary to drug-induced weight gain, cannot be ascertained based on the information reported. In addition, the patient appeared to have developed possible tolerance and withdrawal to diazepam. Given the widespread use of diazepam, as well as other benzodiazepines, it is important for clinicians to recognize that gynecomastia may sometimes be an adverse effect of this class of medications. PP
References
1. Ismail AA, Barth JH. Endocrinology of gynaecomastia. Ann Clin Biochem. 2001;38(pt 6):596-607.
2. Bergman D, Futterweit W, Segal R, et al. Increased oestradiol in diazepam related gynecomastia. Lancet. 1981;2:1225-1226.
3. Llop R, Gomez-Farran F, Figueras A, et al. Gynecomastia associated with enalapril and diazepam [letter]. Ann Pharmcother. 1994;28:671-672.
4. Jelenkovic AV, Macukanovic-Golubovic LD. Diazepam-associated gynecomastia [letter]. Ann Pharmacother. 2005;39:201.
Gabapentin-Induced Dystonia
Gabapentin is a γ-aminobutyric acid (GABA)ergic anticonvulsant indicated for adjunctive therapy in the treatment of partial seizures, with and without secondary generalization, in adults with epilepsy. It is also approved for the treatment of postherpetic neuralgia. As is well known, gabapentin has been used off-label to treat a number of neuropsychiatric conditions including bipolar disorder,1 anxiety disorders,2-5 somatization disorder,6 behavioral dyscontrol,7-9 cocaine and alcohol withdrawal,10,11 antipsychotic-induced movement disorders,12 neuropathic pain,13,14 ciguatera poisoning,15 nicotine16 and benzodiazepine dependence,17 tinnitus,18 and hot flashes in postmenopausal women and in men taking hormone therapy for prostate cancer.19,20 Gabapentin is well absorbed, renally excreted, does not bind to plasma proteins, and has few, if any, drug interactions. The most frequent adverse effects are drowsiness, dizziness, ataxia, and gastrointestinal upset.21 In addition, gabapentin may also be associated with sexual dysfunction.22-28 Now comes a report of a woman who on two occasions experienced recurrent acute gabapentin-induced dystonic reactions that resolved with drug discontinuation.29
A 72-year-old woman was referred to the Neurology Unit due to complaints of tremors of both arms. She had a history of depression and hypertension, the latter treated with amiloride 5 mg/day plus hydrochlorothiazide 50 mg/day. She denied use of any other medications, and had been on an adequate low-sodium diet for the past 5 years. At the time of presentation, she presented with postural and intention tremor of both arms and cephalic resting tremor without other neurologic symptoms. There was no observable rigidity or bradykinesia. Standard laboratory testing, including serum creatinine and thyroid hormones, was normal.An electrocardiogram did not show any rhythm disorders. Diagnosed with essential tremor, she was treated with propranolol 120 mg/day. However, symptomatic bradycardia made it necessary to withdraw the drug.
Gabapentin was initiated, with slow dosage escalation, to 2,100 mg/day after 7 weeks of treatment. Shortly after starting the medication, the patient developed abruptly repetitive rotatory and sustained movements of the neck, as well as proximal contractions in the arms. She stopped gabapentin on her own, with resolution of the dystonic reaction. There was no family history of dystonia. A computed tomography scan of the brain and an electroencephalogram revealed no abnormalities.
Gabapentin was restarted at a lower dose than before and was titrated to a total of 1,800 mg/day in the sixth week. Subsequently, the patient developed a recurrence of her dystonic reaction. Gabapentin was discontinued, with resolution of the dystonia, without further recurrence, 2 days later. Next the patient was started on primidone, 250 mg twice daily, with significant improvement of her tremor.
The case described is consistent with gabapentin-induced dystonia. There are several prior published case reports of this adverse event in association with dystonia.30-32 In addition, other movement disorders have also been reported in association with gabapentin, including myoclonus,33 choreoathetosis,34,35 and ataxia.36 Interestingly, there is a report of significant improvement in a 4-year-old child suffering from familial paroxistic dystonia who significantly improved after administration of gabapentin at a dose of 10 mg/kg/day.37 The conflicting data suggests that gabapentin may be efficacious in the treatment of some types of movement disorders but in other patients may actually precipitate movement disorders. Whether the outcome is a function of dosage used, individual predisposing factors, or some combination of factors at present is not known. PP
References
1. Stanton SP, Keck PE Jr, McElroy SL. Treatment of acute mania with gabapentin [letter]. Am J Psychiatry. 1997;154:287.
2. Chouinard G, Beauclair L, Belanger MC. Gabapentin: long-term antianxiety and hypnotic effects in psychiatric patients with comorbid anxiety-related disorders [letter]. Can J Psychiatry. 1998;43:305.
3. Pollack MH, Matthews J, Scott EL. Gabapentin as a potential treatment for anxiety disorders [letter]. Am J Psychiatry. 1998;155:992-993.
4. Pande AC, Davidson JRT, Jefferson JW, et al. Treatment of social phobia with gabapentin: A placebo-controlled study. J Clin Psychopharmacology. 1999;19:341-348.
5. Brannon N, Labbate L, Huber M. Gabapentin treatment for posttraumatic stress disorder. Can J Psychiatry. 2000;45:84.
6. Garcia-Campayo J, Sanz-Carrillo C. Gabapentin for the treatment of patients with somatization disorder [letter]. J Clin Psychiatry. 2001;62:474.
7. Ryback R, Ryback L. Gabapentin for behavioral dyscontrol [letter]. Am J Psychiatry. 1995;152:1399.
8. Herrmann N, Lanctot K, Myszak M. Effectiveness of gabapentin for the treatment of behavioral disorders in dementia. J Clin Psychopharmacol. 2000;20:90-93.
9. Low RA Jr., Brandes M. Gabapentin for the management of agitation [letter]. J Clin Psychopharmacol. 1999;19:482-483.
10. Markowitz JS, Finkenbine R, Myrick H, et al. Gabapentin abuse in a cocaine user: implications for treatment? J Clin Psychopharmacol. 1997;17:423-424.
11. Myrick H, Malcolm R, Brady KT. Gabapentin treatment of alcohol withdrawal [letter]. Am J Psychiatry. 1998;155:1632.
12. Hardoy MC, Carta MG, Cabras PL. Gabapentin as a promising treatment for antipsychotic-induced movement disorders in schizoaffective and bipolar disorder patients. J Affect Disord. 1999;54:315-317.
13. Morris GL. Gabapentin. Epilepsia. 1999;40(suppl 5):S63-S70.
14. Laird MA, Gidal BE. Use of gabapentin in the treatment of neuropathic pain. Ann Pharmacother. 2000;34:802-807.
15. Perez CM, Vasquez PA, Perret CF. Treatment of ciguatera poisoning with gabapentin [letter]. N Engl J Med. 2001;344:692-693.
16. Myrick H, Malcolm R, Henderson S, et al. Gabapentin for misuse of homemade nicotine nasal spray [letter]. Am J Psychiatry. 2001;158:498.
17. Crockford D, White WD, Campbell B. Gabapentin use in benzodiazepine dependence and detoxification [letter]. Can J Psychiatry. 2001;46:287.
18. Zapp JJ. Gabapentin for the treatment of tinnitus: a case report. ENT. 2001;80:114-116.
19. Guttuso TJ Jr. Gabapentin’s effects on hot flashes and hypothermia. Neurology. 2000;54:2161-2163.
20. Jeffery SM, Pepe JJ, Popovich LM, et al. Gabapentin for hot flashes in prostate cancer. Ann Pharmacother. 2002;36:433-436.
21. Dichter MA, Brodie J. New antiepileptic drugs. N Engl J Med 1996; 334:1583-1590.
22. Clark JD, Elliott J. Gabapentin-induced anorgasmia. Neurology. 1999; 53:2209.
23. Labbate LA, Rubey RN. Gabapentin-induced ejaculatory failure and anorgasmia [letter]. Am J Psychiatry. 1999;156:972.
24. Husain AM, Carwile ST, Miller PP, et al. Improved sexual function in three men taking lamotrigine for epilepsy. South Med J. 2000;93:335-336.
25. Brannon GE, Rolland PD. Anorgasmia in a patient with bipolar disorder type 1 treated with gabapentin. J Clin Psychopharmacol. 2000;20:379-381.
26. Montes JM, Ferrando L. Gabapentin-induced anorgasmia as a cause of noncompliance in a bipolar patient [letter]. Bipolar Disord. 2001;3:52.
27. Grant AC, Oh H. Gabapentin-induced anorgasmia in women [letter]. Am J Psychiatry. 2002;159:1247.
28. Physicians Desk Reference. 56th ed. Montvale, NJ: Medical Economics Company, Inc., 2002.
29. Pina MA, Modrego PJ. Dystonia induced by gabapentin [letter]. Ann Pharmacother. 2005; 39:380-382.
30. Reeves AL, So EL, Sharbrough FW, et al. Movement disorders associated with the use of gabapentin. Epilepsia. 1996;37:988-990.
31. Bernal M, Arcocha J, Peralta P, et al. Dystonic movements: a possible secondary effect of gabapentin [letter] [Spanish]. Rev Neurol. 1999;28:1215.
32. Palomeras E, Sanz P, Cano A, et al. Dystonia in a patient treated with propranolol and gabapentin. Arch Neurol. 2000;57:570-571.
33. Asconape J, Diedrich A, DellaBadia J. Myoclonus associated with the use of gabapentin. Epilepsia. 2000;41:479-481.
34. Buetefisch CM, Gutierrez A, Gutmann L. Choreoathetotic movements: a possible side effect of gabapentin. Neurology. 1996;46:851-852.
35. Chudnow RS, Dewey RB Jr, Lawson CR. Choreoathetosis as a side effect of gabapentin therapy in severely neurologically impaired patients. Arch Neurol. 1997;54:910-912.
36. Steinhoff BJ, Herrendorf G, Bittermann HJ, et al. Isolated ataxia as an idiosyncratic side-effect under gabapentin. Seizure. 1997;6:503-504.
37. Chudnow RS, Mimbela RA, Owen DB, et al. Gabapentin for familial paroxysmal dystonic choreoathetosis. Neurology. 1997;49:1441-1442.
Return