Electroconvulsive therapy (ECT) has been an effective treatment for psychiatric disorders for more than fifty years. Practitioners have reported that ECT may have beneficial effects on medical disorders, including neuroleptic malignant syndrome, hypopituitarism, status epilepticus, and Parkinson's disease (PD).^1,2 Until 1991, only two reviews summarized reports of ECT on PD and other movement disorders,^3,4 and more recent reviews have offered guidelines for administration of ECT in PD.^4,5 Increasing numbers of reports have noted the effects of ECT in parkinsonian syndromes, particularly those without psychiatric comorbidity, as well as other movement disorders. This review evaluates this new data, as such, and provides a summary of the mechanisms of action by which ECT may influence individual movement disorders.

Articles were identified through a literature search of the MEDLINE database via the National Library of Medicine (PubMed). Searches were conducted using "electroconvulsive therapy and movement disorders," "electroconvulsive therapy and dystonia," and "electroconvulsive therapy and dyskinesia" as keywords. All English language articles between January 1990 and December 2000 were selected, and articles appearing in the previously mentioned review³ were excluded. This yielded a total of 110 articles. These were then examined to identify case reports or case series describing patients with preexisting movement disorders who underwent ECT treatment for any reason. Additionally, bibliographies of these articles were inspected to identify any further reports.

A total of 51 separate reports were found for acute ECT treatment in a variety of movement disorders.^6—56 Ten of these reports detailed maintenance ECT treatments.^{10,11,16,23,27,29,39,47,48,53} The effects of ECT on motor symptoms are summarized in t1a and t2.

Parkinson’s Disease and Parkinsonian Syndromes

A reasonable amount of literature now exists documenting the positive effects of ECT in patients with PD. During this review period, there have been 21 new reports of patients with PD undergoing ECT,^{8—24,26,27,29,30} and four additional reports describing ECT and parkinsonian syndromes (totaling 25 reports).^6,7,25,28 There were 135 patients total, with 76 having sufficient comment on motor scores to determine efficacy. Including data from the previous review,³ there are now 52 reports, with a total of 213 patients.

Seventeen of the 25 reports, described above, were case reports or case series.^{6—11,13,15—18,23—25,27—29} Two retrospective reviews have also been reported.^12,26 One of these¹² focused on the safety of ECT with organic brain disorders and made no comment on the outcome of movement disorders. The second²⁶ described the effect of ECT on parkinsonian symptoms in 25 patients, with 14 responding positively. There were four prospective, open trials during this review period.^{14,19—22,30} One¹⁴ focused on the incidence of delirium in PD patients receiving ECT, with no comment on the movement disorder. Three reports^20—22 described the same group of patients, one with acute treatment and two with long-term followup; the overall response rate was nine out of 13 patients. In two additional trials,^19,30 benefits were observed in 16 out of 16 patients and six out of six patients respectively. There were no controlled trials during this review period.

Information on electrode placement or motor response could not be determined for 74 patients.^{6,8,10,12,14—18,25,26} For patients treated with unilateral ECT,^{7,9—11,19—24,28—30} 38 of 44 (86%) demonstrated improvement in motor symptoms. Five of six (83%) patients who began with unilateral treatment but switched to bilateral treatment,^{9,10,13,19,23} demonstrated motor improvement. For bilateral treatment,^9—11,18,27 10 out of 11 patients (91%) had motor improvement. Including cases from the previous review,³ there have been 42 out of 52 patients (81%) undergoing unilateral ECT with improvement in parkinsonian symptoms and 54 out of 81 (67%) undergoing bilateral ECT.

We found 41 patients with no coexisting psychiatric disorder who were undergoing ECT to treat the motor symptoms of PD.^{16,19—23,27,29,30} Among these patients, 36 (88%) had motor improvement. Together with patients in the previous review,³ 58 of 75 patients (77%) with PD and without psychiatric illness improved.

Since previous reports often do not provide detailed assessment of patients, little information exists regarding the symptoms of PD that respond to treatment. Fall and colleagues¹⁹ showed statistically significant improvement in gait, upper extremity swing, rigidity, and tremor subscales of the Webster test. Pridmore and colleagues²⁰ showed statistically significant reductions in akinesia, tremor, and rigidity subscales of the Unified Parkinson's Disease Rating Scale (UPDRS). Specific motor effects could be determined in 26 patients from case reports or case series. Nine patients had improvements in motor scores on UPDRS scores.^6,10,11,29 Twelve patients demonstrated improvement in gait and mobility.^{8—10,18,23,24,29} Seven patients had improvement in tremor,^9,11,13,27 and 12 showed reductions in on/off time.^{11,16,23,27,29} Five patients showed improvement in rigidity,^8,11 and one had decreased cogwheeling.⁹ There is also little information regarding patient factors that might predict response. Fall and colleagues¹⁹ noted that responders demonstrated slightly less preexisting impairment than nonresponders. In contrast, Pridmore and colleagues²¹ reported that responders tended to be older and have more severe symptoms.

The side effects of treatment also deserve comment. Fifty-nine of the total 135 patients (44%) developed significant delirium or confusion during the course of treatment.^{9—11,13,14,18—20,24,26,29} In one prospective study,¹⁴ the incidence was reported as 85%, although duration was not specified for 25 patients.^13,18 ,^20,26 Six patients had delirium lasting 2 days or less, when the next ECT treatment was administered,^10,19,24,29 , and 28 patients experienced delirium for longer periods, up to 3 months in some cases.^9,11,14,19 Often, these reports incompletely describe ECT parameters or other potential etiologies of delirium. In four reports,^11,13,19,26 the characteristics of individual patients could not be ascertained. In the remaining studies, 26 patients who developed delirium were treated with unilateral ECT,^{9,14,20,24,29} and four were treated with bilateral ECT.^9,10,18 Two started on unilateral ECT but switched to bilateral ECT.⁹ Three studies did not specify the number of treatments,^14,24,26 and in the remaining studies, patients received three to 12 treatments.^{9—11,13,18—20,29} The onset of delirium was specified for nine patients, ranging from 1 to 9 days after the start of ECT.^9,24,29 All studies specifying stimulus type noted the use of brief pulse stimulation.^{9—11,13,14,19,29} Studies specifying treatment frequency noted a 3-times-per-week schedule,^{9,14,19,24,26,29} except one study where four ECT treatments were administered for more than 8 days.²⁰ Most studies did not specify the electrical energy delivered, and two noted the use of "moderate suprathreshold" dosing.^9,14 One study used dosing based on age,^20,21 and another had a setting of 75% on the Thymatron device.²⁴ Another study used a dose titration of 2.5x seizure threshold for unilateral ECT and a 1.5x seizure threshold for bilateral treatment.²⁶ Finally, one study noted a current of 0.8 Amperes but did not specify energy.¹⁹ In two reports,^11,24 reduced L-dopa dosage appeared to minimize delirium. However, one case series⁹ and one prospective study¹⁴ showed no relationship between the development of delirium and L-dopa dosage or the duration of PD. Another prospective study¹⁹ showed no correlation between delirium and age, duration of PD, duration of L-dopa treatment, dosage of L-dopa, physical disability, number of ECT treatments, or duration of ECT stimulation. Patients with delirium had preexisting evidence of blood/brain barrier compromise. A retrospective review²⁶ found no association between delirium and age, medications administered during ECT, electrode placement, preexisting dementia, or the presence of neuroimaging/EEG abnormalities, which contrasts with previously identified risk factors for postical delirium.² However, this finding is potentially confounded by the fact that 10 of 13 patients were on L-dopa at the time of ECT, and five of 13 patients had L-dopa instituted or increased prior to ECT.

Other side effects were less common. Six patients developed dyskinesias during the course of treatment, and four of these responded to decreased doses of L-dopa.^16,20,26,27 One patient had worsening of parkinsonian symptoms during treatment,²⁶ and one developed transient agitation after ECT.²⁷ Another patient developed hallucinations and delusions, which also occurred during previous treatment with pergolide.²⁷

Most patients were receiving medications concurrent with ECT, although the precise number could not be determined. Almost all were taking L-dopa preparations.^{6,9—11,13,18,19,23,24,27,29,30} A smaller number were on other antiparkinsonian medications, typically in combination with L-dopa.^{6,8—10,13,19,25,27,30} Many were taking more than two medications.^{6,9,10,19,25,27,30} Two patients^8,25 were not taking L-dopa therapy at the time of ECT but were receiving other antiparkinsonian medications. One of the two had good motor response to ECT⁸ and the other was not specified.²⁵ Finally, four patients^9,10 were not on any antiparkinsonian medications at the time they received ECT. Of the four, two had noticeable improvement,¹⁰ one demonstrated mild improvement,⁹ and one remained unchanged.¹⁰

Six reports^{10,11,16,23,27,29} include detailed maintenance ECT treatment in 12 patients. Three patients suffered from depression,¹⁰ ,^23,29 and seven had no psychiatric disorder and received maintenance ECT solely for parkinsonian symptoms.^16,23,27 Two subjects did not have psychiatric comorbidity specified.¹¹ Patients received single ECT treatments every 2 to 6 weeks. Seven subjects maintained their improvement during the entire time of treatment, which ranged from 12 weeks to 12 months.^11,16,27,29 For one patient, maintenance ECT provided additional improvement beyond that of acute treatment.²⁹ However, some subjects failed to maintain benefit. One patient²⁹ received ECT for 14 months, with the interval between treatments gradually decreasing to weekly; by the end of this period, the improvement from ECT lasted only 1 day. Another patient¹⁶ had good initial response but lost benefit during maintenance treatment. One¹⁰ lost benefit with maintenance ECT but improved when the interval between treatments was shortened until the time of publication. Finally, one subject²⁷ showed positive response to maintenance ECT, but this was lost after a prolonged period between treatments. Subsequent response after resuming ECT was not as robust as the initial response, and ECT was discontinued due to deteriorating cognition. In the previous review,³ there were three patients with PD who underwent maintenance ECT treatment. Two patients with PD and comorbid depression had continued remission of their parkinsonian symptoms with monthly ECT. A third patient with PD and psychotic depression had motor improvement with initial ECT treatments but failed to maintain benefit despite twice-weekly maintenance ECT.

Drug-induced Syndromes

There were four reports involving eight patients with drug-induced parkinsonism who underwent ECT.^26,31—33 Outcome could be ascertained for three patients in three reports.^31—33 One had improvement in parkinsonian symptoms.³² A second had a return of motor symptoms that had previously occurred with neuroleptic treatment,³¹ while a third had significant worsening of preexisting parkinsonian symptoms.³³ One patient in the previous review³ also had motor improvement. Other reports, which reported group trends but not individual results, were favorable.⁵⁷

There were six reports involving 34 patients with tardive dyskinesia (TD) who received ECT.^35—40 Outcome could be determined on fifteen patients in five of these reports.^{34,35,37,39,40} Seven patients experienced improvement in dyskinesia, ranging from mild improvement to complete remission.^{34,35,37,39,40} The remaining eight were unchanged.⁴⁰ In the previous review,³ 22 additional patients were identified. Nine were documented to show improvement in dyskinesia and four were unchanged. Nine patients experienced worsening or development of dyskinesias after ECT, though the causal link was often not clear.

There were five reports involving five patients with tardive dystonia who underwent ECT treatment.^{33,38,41—43} Three of five experienced improvement in dystonic symptoms, lasting from 1 week to several years.^41—43 One patient experienced worsening of symptoms,³³ and one was not specified.³⁸ Additionally, two reports were identified in the previous review,³ with both patients showing improvement in dystonic symptoms.

Other Movement Disorders

There have been three reports involving seven patients with progressive supranuclear palsy (PSP) who received ECT.^22,44,45 Two patients had comorbid depression,^44,45 which was alleviated in one patient with treatment.⁴⁵ The other five underwent ECT solely for their movement disorder.^22,45 One patient had significant benefit in motor symptoms as measured by UPDRS scores,⁴⁵ and three others demonstrated mild benefit.^22,45 Three patients had worsening of bulbar symptoms, with one also having decline in UPDRS motor scores.^44,45 Also, six of seven reported cases had significant confusion and cognitive deterioration.^44,45

There have been three reports involving five patients with multiple system atrophy (MSA) receiving ECT.^46—48 All five patients had comorbid depression. Four of these five patients experienced some motor improvement,^47,48 with the only nonresponder being the only patient receiving unilateral ECT.⁴⁶ The motor symptoms showing improvement differed across patients, with some patients improving in areas that other patients did not (e.g. gait). Benefits in tremor and rigidity were most consistently reported.^47,48 Deterioration in cognition were noted in two patients, though only one required discontinuation of treatment.⁴⁸ Two patients began maintenance treatment. One sustained improvement over four months, receiving six treatments.⁴⁷ The second had remission over 2 months with maintenance treatments every 4 weeks.⁴⁸

There have been two reports involving two patients with Wilson's disease receiving ECT.^49,50 One was diagnosed with paranoid schizophrenia and the other major depression with psychotic features and cognitive impairment. Neither patient had worsening of motor symptoms during treatment, with one patient⁵⁰ having his first manifestation of movement disorder 2 months after ECT completion. The patient with depressive features had a switch to mania after one treatment.⁴⁹

There have been three reports involving eight patients with Huntington's disease (HD) who received ECT.^51—53 All but one of these had comorbid unipolar or bipolar depression. One patient with no psychiatric illness had improvement in motor symptoms;⁵³ six had no change;^51,52 and one had worsening of motor symptoms, possibly due to agitated catatonia associated with bipolar mania.⁵¹ One patient, who required multiple attempts to induce seizures during treatment, also developed prolonged delirium.⁵¹ The single patient with improvement began a course of maintenance ECT, with one treatment every 3 months.⁵³ This patient had further improvement in his movement disorder during the maintenance phase. There have been four other reports,⁵¹ comprising a total of eight patients, which were made before this review and not included in the previous review.³ None of these reports commented on the effect of ECT on the movement disorder. Three of these patients had depression that improved with ECT; the remaining five had unspecified psychoses, with no comment on psychiatric outcome.

There was a single report of one patient with tic disorder who received ECT,⁵⁴ with subsequent reduction in tics. Three other cases were described in the previous review.³ One of the three cases experienced reduction in tics. In both cases of improvement, the authors speculated that the reduction in tics might be directly related to resolution of depression, even though one patient had remission of tics before improvement in depressive symptoms.^54,58 One other case described resolution of mood symptoms with no change in tics.⁵⁹

There was one report⁵⁵ of a single patient with Meige's syndrome with comorbid major depression and anxiety receiving ECT. She underwent bilateral ECT for depression, with remission being achieved. With each ECT treatment, she was noted to have decreased involuntary movements and increased mobility, but the effects only lasted 48 to 72 hours.

There was a single report⁵⁶ of one patient with polycythemia vera and a mixed movement disorder receiving ECT. Her movement disorder consisted of dystonia of the trunk and pelvis, bucco-linguo-masticatory syndrome, akathisia, and hyperventilation. She also suffered from organic depressive disorder with psychotic features, attributed to her polycythemia. She received ECT treatments on 12 occasions, with no improvement in her depressive symptoms. Effects of ECT on her movement disorder were not specified.

ECT remains an effective treatment for a variety of psychiatric illnesses, particularly depression. These disorders occur frequently in patients with movement disorders, and ECT does appear effective for alleviating mood symptoms in this population. Due to the uncontrolled nature of these reports, it is not known whether comorbid movement disorders adversely affect the response of depression to ECT. ECT may also be effective in treatment of drug-induced psychotic states in PD.

ECT also shows some promise in treating motor manifestations of movement disorders, though these data must be interpreted cautiously. The majority of reports address ECT and Parkinson's disease, with many of them being favorable. Based on these reports, some ECT experts have advocated general usage of ECT in Parkinson's disease. One editorial recommended "a therapeutic trial of ECT for every patient with intractable or drug-resistant Parkinson's disease, particularly those with the on-off syndrome."⁶⁰ Another editorial⁶¹ advocated a therapeutic trial of ECT before such procedures as neuronal transplantation were considered. Experts in PD have been less encouraging,⁶² and recent neurological guidelines for management fail to mention this as a treatment option for motor symptoms.⁶³ Experts in PD note publication bias to report only positive results and the small number of well documented studies. Furthermore, they raise concerns about the biological basis of response, induction of confusional states, and the need for maintenance treatment for continued response. These criticisms must be addressed if one advocates ECT as a treatment for the motoric symptoms of PD.

The concern about possible publication bias overemphasizing positive results is well justified, as most of the data concerning ECT and PD consist of case reports. Practitioners are less likely to publish negative results or to pursue further study of a treatment modality when initial results are not encouraging.⁶² Retrospective reviews and open prospective trials may provide a better view of response rates by including nonresponders, and these studies have been positive. Although data concerning ECT and PD do not rely solely on case reports, the lack of further controlled studies is a serious limitation.

Several mechanisms of action have been proposed for ECT in PD. Some researchers have argued that the improvement in motor symptoms is due to resolved depression, with reduced psychomotor retardation.⁶⁴ Our review, as well as the previous review,³ argues against this. A substantial number of patients without any discernible psychiatric disease have had improvement in motor symptoms. Also, as previously noted by Young,⁶⁵ one report⁸ describes a dissociation between improvement in mood and motor symptoms, with the latter occurring earlier in treatment. Other authors have argued that improvement is due to disruption of the blood-brain barrier that is known to occur with ECT treatment.⁶⁶ This would allow increased levels of L-dopa to enter the brain, potentially alleviating motor symptoms even though the oral drug dosage remained constant.⁶⁴ The above reports, documenting patients with improvement who were not on L-dopa, indicate other mechanisms are at least partly responsible. The most commonly accepted explanation is a neurochemical one. Animal and human studies have suggested that ECT enhances dopaminergic transmission. Since serum and CSF levels of dopamine metabolites are not consistent in studies, it is thought that the effects may be enhancement at the receptor or postreceptor level.⁶⁷ However, some of the evidence for this comes from the improvement in PD following ECT.⁶⁷ Fochtmann and colleagues⁶⁸ have shown that electroconvulsive shock in rats increases dopamine type 1 receptor binding in the substantia nigra. They hypothesize that this may be associated with other changes in the dopamine system, including upregulation of dopamine type 2 receptors in the striatum. The latter may be the mechanism by which ECT exerts an antiparkinsonian effect. Only two studies^19,30 during this review period addressed this issue. These confirmed an increase in cerebrospinal fluid dopamine metabolites after ECT, indicating increased dopamine neurotransmission. These changes did not appear to be mediated by alterations in the dopamine transporter protein, indicating other mechanisms for the efficacy of ECT.

ECT has significant effects on both noradrenergic and serotonergic transmission.⁶⁷ Although these changes likely play a role in the alleviation of depression, their role in the motor changes are unclear.^69,70 Finally, animal studies have shown upregulation of the GABAergic system, although this has not been demonstrated in humans.⁶⁷ Changes in the GABAergic system may influence the abnormal movements in PD, although evidence is still controversial.⁷¹

Concerns about delirium or confusional states are also justified but should not prevent use of ECT. Continued delirium or cognitive dysfunction (defined in most reports as lasting more than 24 hours) is thought to be a rare side effect of ECT. One study⁷² indicated that post-ECT delirium occurred in approximately 10% of patients at some time during treatment. Given that some authors have postulated a subcortical mechanism for delirium,⁷³ it is not surprising that patients with impaired subcortical function such as PD would be more vulnerable. Although precise incidence figures are not ascertainable due to the uncontrolled nature of many reports, the above figures for delirium are concerning. The prolonged periods of delirium in many patients adds further weight to this. In vulnerable patients, several strategies can minimize post-ECT delirium.⁷⁴ These include twice-weekly ECT instead of thrice weekly, use of unilateral ECT, using the minimally effective electrical dose, using brief pulse stimulation, and avoiding potentially deliriogenic medications. For PD patients undergoing ECT, reducing the dosage of L-dopa has been effective for some, but not all, patients who developed delirium. Current recommendations to reduce L-dopa dosages by half⁴ should be followed unless clinical symptoms of PD are too severe to allow reductions. Right unilateral electrode placement should be used initially.⁴ Previous recommendations³ against unilateral treatment due to limited experience are no longer justified, given the number of patients benefitting with this modality. Strong consideration should be given to twice-weekly treatments. This is clearly an area needing further research, both in depressed and nondepressed PD patients, to determine the overall incidence of delirium and the effectiveness of these strategies to minimize it.

Several issues also remain in the use of maintenance ECT for PD. With only 15 patients undergoing such treatment, it is difficult to generalize results. However, it is clear that some patients have continued benefit in motor symptoms with maintenance ECT, both with and without comorbid affective disorders. Other patients have required progressively shorter intervals between treatments until the frequency of ECT was no longer feasible. The reasons for this phenomenon are unknown at present. The optimal interval between ECT treatments is also not known. Previous guidelines⁴ suggest that this intertreatment interval should be initially short, such as once a week, and progressively increased to the longest interval that sustains the improvement. This approach is reasonable. However, with some patients having prolonged symptom-free intervals after the initial ECT series (up to 35 months has been reported²²), this approach may expose a small number of patients to a higher number of ECT treatments than is necessary.

Continued investigation of ECT for the motoric symptoms of PD is indeed warranted. A recent report⁷⁵ describes the long-term outcome of pallidotomy for PD, with sustained improvements in off-period contralateral signs and in on-period dyskinesias noted. In this study, however, one-half of the original cohort was excluded for various reasons. These patients had similar baseline characteristics but worse response to surgery at 6 months compared to the study group, potentially biasing the latter toward positive outcome. Another report⁷⁶ described the outcome for transplantation of embryonic dopamine neurons for severe PD. Small amounts of motor improvement, measured using standardized scales, was noted in some younger patients but no improvement in older patients. Thus, the treatment for advanced or refractory PD remains unsatisfactory, and other novel treatments may yet play a role. Furthermore, patients may prefer the option of ECT over other treatment modalities for refractory symptoms. Pridmore and Pollard²² reported that more than half of their patients who could give an opinion would consider a future course of ECT. Another survey⁷⁷ of PD patients showed that 28% would consider ECT in their current state and another 32% would consider it if their condition worsened.

Drug-induced movement disorders also appear responsive to ECT, although data are mostly case reports and case series. ECT is thought to reduce drug-induced parkinsonism by upregulating postsynaptic dopamine receptors, similar to its effects in idiopathic PD. A previous review³ and an additional case have confirmed its utility. Another case series⁵⁷ has suggested that ECT may prevent drug-induced parkinsonism in patients who have not developed this complication. However, two patients in the case series had worsened symptoms, which had not previously been reported. The reasons for this are unclear, but caution is warranted in such patients undergoing ECT. With the widespread usage of atypical antipsychotics, which have lower rates of parkinsonism, such issues may not be particularly pressing.

Tardive dyskinesia and dystonia appear responsive to ECT, although overall results are mixed. ECT is thought to prevent supersensitization of postsynaptic dopamine receptors that play a role in development of tardive states.⁷⁸ Such effects only occurred with concurrent neuroleptic administration, which may account for the efficacy of ECT in both hypo- and hyperdopaminergic states. Some patients improve, many remain unchanged, and a small number experience worsening of symptoms. The single prospective study⁴⁰ found improvement in one patient, with eight remaining unchanged. The reason as to why some patients experience worsening of symptoms is unclear. However, Hay and colleagues³⁴ note the difficulties in attributing worsened TD to ECT, as many patients concurrently have alterations in their medication regimen. These alterations may cause withdrawal dyskinesias that spontaneously remit with time. If medications are discontinued in order to begin administration of ECT, these withdrawal dyskinesias may be erroneously attributed to ECT. Similar issues may exist for tardive dystonia, as the single case with worsened symptoms also involved the discontinuation of medications prior to ECT.³³ However, this patient also developed aspiration from dysphagia and dystonia, illustrating that these effects cannot be completely ignored even if transient. Finally, three reports^79—81 have documented lower prevalence of TD in patients who received ECT. Given that treatments for tardive dyskinesia are generally disappointing,⁸² the possible protective role of ECT with tardive dyskinesia deserves further study.

There is much less data regarding movement disorders other than PD, consisting only of case reports and case series. Disorders with parkinsonian or dystonic symptoms, such as PSP and MSA, have the most reports of improvement. Since the effects of ECT on dopamine are primarily postsynaptic,⁶⁷ improvement might be expected even if L-dopa administration is not useful. As previously noted, ECT also affects a variety of other neurotransmitters, such as gamma-aminobutyric acid (GABA). Movement disorders involving these transmitters, such as HD, are largely unaffected by ECT, though occasional patients may benefit. Resolution of mood symptoms may also contribute to improvement.⁵⁴ These patients should not be denied ECT based solely on the above reports noting delirium and worsening of the movement disorder. However, these reports should be considered in the risk/benefit ratio and the decision to prescribe ECT. Such patients should be treated as clinically indicated by their psychiatric condition. The risk of delirium may be minimized using the above strategies.

Overall, a substantial amount of data support the positive effects of ECT on the motor symptoms of Parkinson's disease. However, almost all of these data are from case reports or case series, with only one randomized, controlled trial in the literature. This, together with concerns over side effects, may raise doubts among neurologists. Further research and collaboration with neurological colleagues should be encouraged to address these concerns, as ECT may be a viable option that is acceptable to many patients. Initial reports suggest that other movement disorders, particularly those with parkinsonism, may improve with ECT. Further observation of patients with these disorders who undergo ECT will be needed to clarify the potential role for ECT.

Dr. Mittal was supported in part by the Mental Illness Research Education and Clinical Center, Veterans Integrated Service Network 16 (MIRECC-VISN 16), Department of Veterans Affairs. No other support was received in the preparation of this manuscript by any author. The authors would like to thank Stuart Yablon, M.D., Victor Dostrow, M.D., and Amelia Nasrallah, M.A., for their review of the manuscript and for editorial assistance.

Portions of this work were presented in poster form at the 11th Annual Meeting of the Association for Convulsive Therapy, New Orleans, Louisiana, May 6, 2001; and the 48th Annual Meeting of the Academy of Psychosomatic Medicine, San Antonio, Texas, November 15, 2001.