A prospective study of the early postsurgical psychiatric associations of epilepsy surgery

OBJECTIVES— To examine prospectively the frequencyand nature of psychiatric symptoms seen in patients during the firstthree months after temporal lobe surgery for chronic intractableepilepsy and in addition to study the relation between presurgicalmental state, laterality of surgery, and postsurgical seizure andpsychiatric course.
METHOD—A consecutive series of 60 patients beingassessed for temporal lobe surgery for intractable epilepsy werestudied. They were interviewed before surgery and at six weeks andagain at three months after operation.
RESULTS—At six weeks after surgery half of thosewith no psychopathology preoperatively had developed symptoms ofanxiety or depression and 45% of all patients were noted to haveincreased emotional lability. By three months after surgery emotionallability and anxiety symptoms had diminished whereas depressive statestended to persist. Patients with a left hemispheric focus were morelikely to experience persisting anxiety.
CONCLUSION—The early months after surgery forepilepsy are characterised by the relatively common presence ofpsychiatric symptoms. It is proposed that presurgical and earlypostsurgical neuropsychiatric involvement in programmes of surgery forepilepsy will help to improve the quality of the treatment packageoffered to patients.

     

Temporal lobe abnormalities in dementia and depression: a study using high resolution single photon emission tomography and magnetic resonance imaging

OBJECTIVES—Perfusion SPECT and MRI were used totest the hypothesis that late onset depression is associated with brain abnormalities.
METHODS—Forty depressed patients (DSM-III-R majordepressive episode, not demented at two year follow up) were recruitedwho were either drug free, or on a stable dose of antidepressants forat least three weeks, as well as 22 demented patients (DSM-IIIR and NINCDS/ADRDA criteria for probable Alzheimer's disease). Patients wereimaged at rest with a high resolution single slice 12 detector headscanner (SME-Neuro 900) and the cerebral perfusion marker ^99mTc-exametazime (HM-PAO). Temporal lobe templates werefitted with brains pitched by 20°-30°. A subgroup of 41 patients(22 depressed) were also scanned using a Siemens Magnetron 1.0 Teslamagnetic resonance imager, using a FLAIR imaging sequence for theassessment of white matter hyperintensities, and a Turbo FLASH sequencefor the measurement of medial temporal lobe width.
RESULTS—Demented patients showed reducedperfusion, particularly in the left temporoparietal cortex. In theseregions of interest, patients with late onset depression tended to haveperfusion values intermediate between patients with early onsetdepression and demented patients. Differences in changes in whitematter between demented and early and late onset depressive patientsdid not reach conventional levels of significance. Temporal lobe width differed between demented and depressed patients, but not between earlyand late onset depressed patients. Perfusion and temporal lobe widthwere not associated, but reductions of perfusion were associated withperiventricular white matter changes. Mini mental state examinationscores were associated with temporal perfusion in demented patients andwith changes in deep white matter in depressed patients. Finally,severity of depressive symptoms was associated with decreased perfusionin frontotemporal and basal ganglia regions of interest.
CONCLUSION—A cumulative effect of duration ofillness on regional cerebral perfusion could not be confirmed. Lateonset depression may show more abnormalities of deep whitematter and of left temporoparietal perfusion than early onsetdepression, but the underlying pathology remains to be established.

     

Decreased capacity for mental effort after single supratentorial lacunar infarct may affect performance in everyday life

OBJECTIVES—The long term outcome after a singlesymptomatic lacunar infarct may be less favourable than is generallyassumed. Patients often present with complaints such as fatigue or"being different from before the stroke", for which there are noobvious physical explanations. Although cognitive functioning isconsidered normal in most patients with lacunar infarction in theinternal capsule or corona radiata, a study was carried out todetermine if subclinical changes in mental or emotional function canexplain these vague complaints characteristic for their disablement.
METHODS— Sixteen patients, each with asingle symptomatic supratentorial lacunar infarct, and 16 matchedhealthy controls were examined with an extensive neuropsychologicalscreening battery and a standardised questionnaire aimed at emotionalproblems. The mean number of correct responses was calculated for eachsubject and averaged within each group.
RESULTS—Although, on the whole, there wereno differences in performance, patients' results on the followingtasks in different modalities showed evidence for decreased performanceunder relatively more demanding conditions: line orientation task (meandifference (MD) 261 ms; 95% confidence interval (95%CI) 94 to 428),Rey-Osterrieth delayed recall (MD−3.8, 95% CI −7.5 to0.0), visual elevator subtest of the everyday attention task (EAT) (MD−0.7, 95% CI −1.5 to 0.1), lottery subtest of the EAT (MD −0.6,95% CI −1.3 to 0.1) and WAIS similarities (MD −3.2 95% CI −6.3to 0.1). Patients also more often had emotional disturbances than controls.
CONCLUSION—Both subtle cognitive impairments andemotional disturbances may play a part in the decreased competence ineveryday life of patients with a supratentorial lacunar infarct.

     

Parkinson's disease and depression: evidence for an alteration of the basal limbic system detected by transcranial sonography

OBJECTIVES—Depression is a frequent symptom inParkinson's disease. Compelling evidence suggests a role of thebrainstem in the control of mood and cognition. In patients withunipolar depression transcranial sonography (TS) studies have shownstructural alteration of the mesencephalic brainstem raphe which couldsuggest an involvement of the basal limbic system in the pathogenesisof primary mood disorders. The objective of the present study was toevaluate whether a similar alteration could be found in depressedpatients with Parkinson's disease using TS.
METHODS—Thirty patients with Parkinson's diseaseand 30 age and sex adjusted controls were examined by TS. Rapheechogenicity was rated semiquantitatively. The severity of motorsymptoms and depression was rated using standard research instruments.
RESULTS—Raphe echogenicity was significantlyreduced in depressed patients with Parkinson's disease compared withnon-depressed patients with Parkinson's disease and control subjects.Raphe echogenicity correlated negatively with degree of motorimpairment, and differences in raphe echo between depressed andnon-depressed patients with Parkinson's disease were upheld when motorimpairment was controlled for.
CONCLUSION—These preliminary findings suggestthat, as in unipolar depression, a morphological alteration of thebrainstem raphe might be involved in the pathogenesis of depression inParkinson's disease. This raphe alteration may reflect involvement inthe basal limbic system in the pathogenesis of secondary depression.This concept is in line with current knowledge on the pathogenesis ofboth depression in Parkinson's disease and primary depressive disorders.

     

Relation between psychiatric disorder and abnormal illness behaviour in patients undergoing operations for cervical discectomy

OBJECTIVE—To test the hypothesis that depressionin patients being considered for cervical disc surgery is associatedwith severe organic pathology. Secondly, to test whether depression andabnormal illness attitudes recorded preoperatively would predict poorer recovery.
METHODS—Seventy four patients with pain anddisability from cervical arthrosis were examined during investigationsbefore potential cervical surgery. The prevalence of psychiatricdisorder was assessed using the SCAN, and attitude to illness using theillness attitude scale.
RESULTS—There was a rate of depressive disorderin the sample of 37%. The depressed patients did not have more severeorganic pathology, more neurological symptoms or signs, or moredisablement. They reported more pain and displayed more abnormalillness behaviour. Fifty patients went on to cervical surgery. Outcomefour to eight months postoperatively was not related to the presence ofpsychiatric disorder or illness attitude recorded preoperatively.
CONCLUSION—Depressive disorder is not secondaryto severe pathology; the outcome of surgery is predominantly determinedby physical factors.

     

Effects of exercise on cognitive and motor function in chronic fatigue syndrome and depression

OBJECTIVES—Patients with chronic fatigue syndromecomplain of physical and mental fatigue that is worsened by exertion.It was predicted that the cognitive and motor responses to vigorousexercise in patients with chronic fatigue syndrome would differ fromthose in depressed and healthy controls.
METHODS—Ten patients with chronic fatiguesyndrome, 10 with depressive illness, and 10 healthy controls completedcognitive and muscle strength testing before and after a treadmillexercise test. Measures of cardiovascular functioning and perceivedeffort, fatigue, and mood were taken during each stage of testing.
RESULTS—Depressed patients performed worst oncognitive tests at baseline. During the treadmill test, patients withchronic fatigue syndrome had higher ratings of perceived effort andfatigue than both control groups, whereas patients with depressionreported lower mood. After exertion, patients with chronic fatiguesyndrome showed a greater decrease than healthy controls on everydaytests of focused (p=0.02) and sustained (p=0.001) attention, as well asgreater deterioration than depressed patients on the focused attentiontask (p=0.03). No between group differences were found incardiovascular or symptom measures taken during the cognitive testing.
CONCLUSIONS—Patients with chronic fatigue syndromeshow a specific sensitivity to the effects of exertion on effortfulcognitive functioning. This occurs despite subjective and objectiveevidence of effort allocation in chronic fatigue syndrome, suggestingthat patients have reduced working memory capacity, or a greater demandto monitor cognitive processes, or both. Further insight into thepathophysiology of the core complaints in chronic fatigue syndrome islikely to be realised by studying the effects of exercise on otheraspects of everyday functioning.

     

Abnormal response to negative feedback in unipolar depression: evidence for a diagnosis specific impairment

OBJECTIVES—To assess in further detail thespecific form of motivational impairment influencing neuropsychologicalperformance in depression—oversensitivity to perceived failure. Thepresent study considers two questions: firstly whether this is specificto depression and secondly how the effect relates to clinical features.
METHODS—Unipolar depressed patients and matchedcontrols were assessed on two neuropsychological tests giving explicitperformance feedback. The data were analysed in two separate studies toconsider the questions above. The first study considered thespecificity of the effect to depressed patients, using data on the sametests collected from other patient groups. The second study was alongitudinal assessment of the depressed patients on clinical recoveryto determine whether the effect is specific to the depressed state.
RESULTS—The effect was not seen in non-depressedpatient groups, either neurological or psychiatric groups. Thelongitudinal study showed a residual abnormal response to negativefeedback on clinical recovery.
CONCLUSIONS—Abnormal response to negativefeedback is specific to a primary diagnosis of depression and may be atrait rather than a state factor of the disorder. These results arediscussed in relation to the putative neuropathology of depression andalso to cognitive and behavioural accounts of the disorder. Thefindings presented here have important implications for establishing alink between mood and cognition in unipolar depression.

     

Apathy and hypersomnia are common features of myotonic dystrophy

OBJECTIVES—Myotonic dystrophy is a diseasecharacterised by myotonia and muscle weakness. Psychiatric disorder andsleep problems have also been considered important features of theillness. This study investigated the extent to which apathy, majordepression, and hypersomnolence were present. The objective was toclarify if the apathy reported anecdotally was a feature of CNSinvolvement or if this was attributable to major depression,hypersomnolence, or a consequence of chronic muscle weakness.
METHODS—These features were studied in 36 adultswith non-congenital myotonic dystrophy and 13 patients withCharcot-Marie-Tooth disease. By using patients with Charcot-Marie-Toothdisease as a comparison group the aim was to control for the disablingeffects of having an inherited chronic neurological disease causingmuscle weakness. Standardised assessment instruments were used whereverpossible to facilitate comparison with other groups reported in themedical literature.
RESULTS—There was no excess of major depression oncross sectional analysis in these patients with mild myotonicdystrophy. However, apathy was a prominent feature of myotonicdystrophy in comparison with a similarly disabled group of patientswith Charcot-Marie-Tooth disease (clinician rated score;Mann Whitney U test, p=0.0005). Rates of hypersomnolencewere greater in the myotonic dystrophy group, occurring in 39% ofmyotonic dystrophy patients, but there was no correlation with apathy.
CONCLUSION—These data suggest that apathyand hypersomnia are independent and common features of myotonicdystrophy. Apathy cannot be accounted for by clinical depression orperipheral muscle weakness and is therefore likely to reflect CNSinvolvement. These features of the disease impair quality of life andmay be treatable.

     

Lightning stroke and neuropsychological impairment: cases and questions

OBJECTIVE—To objectify neuropsychological impairments in survivors of lightning stroke with lasting complaints about poor concentration and inability to divide their attention.
DESIGN—A series of six cases of lightning stroke were studied. All patients had lost consciousness and reported amnesia of varying length. Assessment took place between one and four years after injury, ensuring that their neurological state had stabilised. They were tested with a neuropsychological battery with an emphasis on attention and memory. Personality and emotional reaction to the accident were assessed with questionnaires and a lightning fear scale. Complaints were recorded by means of a trauma complaints list including 10 questions on symptoms of the post-traumatic stress disorder.
RESULTS—Patients reported fatigue and lack of energy as their main complaints. In addition, poor concentration, irritability, and emotional lability were mentioned often. Neuropsychological tests disclosed mild impairments in memory, attention, and visual reaction times. Two patients could be classified as depressed, and one of these also showed convincing signs of the post-traumatic stress disorder.
CONCLUSION—As the lasting complaints and impairments could not be explained, for all six cases, as resulting from head injury concomitant with lightning stroke, cerebral hypoxia or a post-traumatic stress syndrome, it is concluded that lightning stroke can result in subtle cognitive impairments. It is speculated that most complaints of these survivors are caused by a vegetative dysregulation, a disorder that has often been noted in the literature on the effects of electrical injury to the nervous system. Such a dysregulation might cause both the main complaint of fatigue and the mild cognitive impairments identified with the present test battery.

     

Hallucinosis in idiopathic Parkinson's disease

BACKGROUND—Hallucinosis is a complication ofthe treatment of idiopathic Parkinson's disease commonly thought toafflict older, chronically medicated, cognitively impaired patients.However, patients with idiopathic Parkinson's disease of shortduration experiencing hallucinosis on relatively low doses ofdopaminergic medication have been found. The aim, therefore,was to investigate the homogeneity of a population of patients withidiopathic Parkinson's disease and hallucinosis.
METHODS—The clinical, demographic, and cognitivecorrelates of hallucinosis were investigated in a sample of 129 patients with idiopathic Parkinson's disease.
RESULTS—There were two subgroups of patientswith idiopathic Parkinson's disease experiencing hallucinosis. Inpatients with a disease duration of five years or less, hallucinosiswas associated with rapid progression of the motor component of thedisease but not cognitive impairment. In patients with idiopathicParkinson's disease of longer than five years duration, hallucinosiswas associated with postural instability, global cognitiveimpairment, and lack of depressive affect. In all patients withidiopathic Parkinson's disease, hallucinosis was more prevalent whenthey were treated with a direct acting dopamine receptor agonist.Hallucinosis was not associated with age at onset of idiopathicParkinson's disease or dosage of dopaminergic medication.
CONCLUSION—Hallucinosis in idiopathic Parkinson'sdisease is heterogeneous, falling into two groups. The difference inthe pathophysiological basis of hallucinosis in these two groups ofpatients is discussed.

     

Anosognosia: examining the disconnection hypothesis

OBJECTIVE—To test the hypothesis thatanosognosia for hemiparesis results from intrahemispheric disconnection.
METHODS—Using right carotid barbiturate injectionas a model for anosognosia for hemiparesis, systematic attempts weremade to modify deficit awareness by providing the left hemisphere withexplicit information regarding left upper extremity function.
RESULTS—Experimental interventions failed tomodify deficit awareness in 19 of 32 patients. In those patients whodiscovered their weakness, attempted movement of the weak limb seemsmore important than explicit observation of the extremity by the left hemisphere.
CONCLUSIONS—The results fail tosupport Geschwind's disconnection hypothesis for anosognosia for hemiparesis.

     

Mood-congruent amygdala responses to subliminally presented facial expressions in major depression: associations with anhedonia

Background

Anhedonia has long been recognized as a key feature of major depressive disorders, but little is known about the association between hedonic symptoms and neurobiological processes in depressed patients. We investigated whether amygdala mood-congruent responses to emotional stimuli in depressed patients are correlated with anhedonic symptoms at automatic levels of processing.

Methods

We measured amygdala responsiveness to subliminally presented sad and happy facial expressions in depressed patients and matched healthy controls using functional magnetic resonance imaging. Amygdala responsiveness was compared between patients and healthy controls within a 2 (group) × 2 (emotion) design. In addition, we correlated patients’ amygdala responsiveness to sad and happy facial stimuli with self-report questionnaire measures of anhedonia.

Results

We included 35 patients and 35 controls in our study. As in previous studies, we observed a strong emotion × group interaction in the bilateral amygdala: depressed patients showed greater amygdala responses to sad than happy faces, whereas healthy controls responded more strongly to happy than sad faces. The lack of automatic right amygdala responsiveness to happy faces in depressed patients was associated with higher physical anhedonia scores.

Limitations

Almost all depressed patients were taking antidepressant medications.

Conclusion

We replicated our previous finding of depressed patients showing automatic amygdala mood-congruent biases in terms of enhanced reactivity to negative emotional stimuli and reduced activity to positive emotional stimuli. The altered amygdala processing of positive stimuli in patients was associated with anhedonia scores. The results indicate that reduced amygdala responsiveness to positive stimuli may contribute to an-hedonic symptoms due to reduced/inappropriate salience attribution to positive information at very early processing levels.     

MELAS: a new disease associated mitochondrial DNA mutation and evidence for further genetic heterogeneity

OBJECTIVES—To define the molecular genetic basisof the MELAS phenotype in five patients without any known mutation ofmitochondrial DNA.
METHODS—Systematic automated mitochondrial DNAsequencing of all mitochondrial transfer RNA and cytochrome c oxidasegenes was undertaken in five patients who had the MELAS phenotype.
RESULTS— A novel heteroplasmic mitochondrial DNAmutation was identified in the transfer RNA gene for phenylalanine inone case (patient 3). This mutation was not detected in the patient'sblood or in her mother's blood. No pathogenic mutations wereidentified in the other four patients.
CONCLUSIONS—This is the first point mutation inthe transfer RNA gene for phenylalanine to be associated with MELAS.The absence of mutations in the remaining four patients suggests thatthere is further genetic heterogeneity associated with thismitochondrial phenotype.

     

Forgetting rates in neuropsychiatric disorders

OBJECTIVE—Previous studies have attributedaccelerated forgetting rates on recognition memory tasks to temporallobe pathology, but findings in some patient groups may have beenattributable to metabolic disruption. Findings in psychiatric disorderssuch as schizophrenia are conflicting. The purpose of the present study was to compare forgetting rates in patients with confusional states (post-elecroconvulsive therapy (post-ECT), delirium), with those obtained in schizophrenic patients (with putative temporal lobe pathology), non-ECT depressed patients, and healthy controls. Thefindings could also be compared with previous reports in patients withhead injury, focal structural lesions, and Alzheimer's dementia.
METHODS—Two studies employed a picture recognitiontask to examine forgetting rates, the first between delays of 1 minute,15 minutes, and 30 minutes, and the second between delays of 10 minutes, 2hours, and 24hours.
RESULTS—There were no significant differences inforgetting rates between 1 minute and 30 minutes, but the ECT groupshowed accelerated forgetting between 10 minutes and 2 hours comparedwith healthy controls, associated with a rapid decline in "hitrate". This was not attributable to differential changes in eitherdepression or severity of memory impairment. There were no differencesin forgetting rates across the other subject groups.
CONCLUSION—Post-ECT confusional state patients(similarly to "within post-traumatic amnesia" patients with headinjury) show accelerated forgetting on a recognition memory task and,in this, they contrast with patients who have focal structural lesionsor widespread cortical atrophy. Accelerated forgetting may reflect theeffect of disrupted cerebral metabolism on either "consolidation"or memory "binding" processes.

     

Neuropsychological deficits in multiple sclerosis after acute relapse

OBJECTIVES—To examine cognitive and neurologicalchanges and their relation to brain pathology in patients with multiplesclerosis during acute relapse.
METHODS—Thirteen patients with multiple sclerosiswere examined with a battery of neuropsychological tests during acuterelapse and six weeks later. Their performance was compared with theperformance of 10 controls matched for age and premorbid IQ. Gadolinium(Gd) enhanced MRI was also performed in patients on both occasions.
RESULTS—The patients with multiple sclerosisperformed significantly worse than controls on most tests of attentionand memory during acute relapse and in remission. At follow up therewas a significant or trend of improvement in performance on some testsof attention for patients in whom the Gd enhanced lesion load haddecreased. In this subgroup of patients, their improvement alsocorrelated significantly with the reduction in acute lesion load.
CONCLUSIONS—The findings suggest that certainneuropsychological deficits detected during an acute relapse may bereversible, particularly in patients who initially have mild cognitive impairment.

     

Intracranial aneurysms in three patients with disseminated Lyme borreliosis: cause or chance association?

METHODS—Three patients with Borreliaburgdorferi infection and intracranial aneurysms are described.
RESULTS—All three patients had neurologicalsymptoms. Perivascular and vasculitic lymphocytic inflammation weredetected in the brain biopsy specimen of one patient. The aneurysm waslocated in the internal carotid arteries in two patients and in thebasilar artery in one patient. The aneurysm ruptured in two patients.
CONCLUSIONS—Cerebral lymphocytic vasculitis andintracranial aneurysms may be associated with B burgdorferiinfection. It is suggested that inflammatory changes caused byB burgdorferi in vessel walls may be a pathogeneticmechanism for the formation of aneurysms.

     

Dermatome variations in patients with transitional vertebrae

OBJECTIVES—To test whether the position oflumbosacral dermatomes varies in the presence of transitional vertebrae.
MATERIAL AND METHODS—Fifty consecutive malepatients were tested for thoracolumbar and lumbosacral transitionalvertebrae by radiography and for the position of the dermatome gapbetween the lumbar dermatomes Ll, L2, L3, and the sacral dermatomes S2and S3. The dermatome gap was documented with the use of thecremasteric reflex, the receptive field of which ends sharply at thegap which allows its delineation.
RESULTS—Thirty two of 50 patients had a normalthoracolumbosacral spinal configuration, 10 patients had transitionalvertebrae. The patients with a cranial displacement of thethoracolumbar or lumbosacral vertebral transition showed a dermatomegap which lay significantly more ventrally than in the patients with anormal spinal configuration.
CONCLUSION—The finding supports the notion of avariant position of lumbosacral dermatomes in the presence oftransitional vertebrae in males.

     

Disturbed striatoprefrontal mediated visual behaviour in moderate to severe parkinsonian patients

OBJECTIVES—To study visuospatial and visualmemory functions in moderate to severe parkinsonian patients.
METHODS—Visual antisaccades (AS) and rememberedsaccades (RS) were examined in 30 patients with moderate to severeParkinson's disease and in 44 age matched controls. AS are saccades inthe direction opposite to the target. RS are saccades towards theremembered position of a target that is no longer visible.
RESULTS—Patients with Parkinson's disease hadserious difficulties in suppressing a reflex saccade ("visualgrasping") or they made no saccade at all ("visual akinesia").The remembered saccade was often wrongly directed.
CONCLUSIONS—These types of errors point to adysfunction in the striatoprefrontal loop. The discrepancy of theresults with those in the literature, which are mostly normal, could beexplained by the more advanced stage of our patients. This mightcorrespond to the development of unresponsiveness to levodopa or ofnon-dopaminergic lesions.

     

Dopaminergic stimulation in unilateral neglect

OBJECTIVE—To explorethe hypothesis that dopaminergic circuits play a part in the premotorcomponents of the unilateral neglect syndrome, the effects of acutedopaminergic stimulation in patients with neglect were studied.
METHODS—Two tasks wereevaluated before and after subcutaneous administration of apomorphineand placebo: a circle crossing test and a test of target exploration (amodified version of the bell test), performed both in perceptual(counting) and in perceptual-motor (pointing) conditions.
SUBJECTS—Four patientswith left neglect.
RESULTS—Afterdopaminergic stimulation, a significant improvement was found comparedwith placebo administration and baseline evaluation, in the performanceof the two tests. Three of the patients had a more marked improvementin the perceptual-motor condition (pointing) of the task than theperceptual condition (counting).
CONCLUSIONS—Thefindings suggest that dopaminergic neuronal networks may mediate, indifferent ways, both perceptive and premotor components of theunilateral neglect syndrome.

     

GTP cyclohydrolase I mutations in patients with dystonia responsive to anticholinergic drugs

OBJECTIVES—to investigate the hypothesis that GTPcyclohydrolase I (GCH1) mutations are responsible for the phenotype ofhighly anticholinergic responsive dystonia in patients with apparentprimary torsion dystonia.
METHODS—from 107 British patients with clinicallydiagnosed primary torsion dystonia, seven patients were identified withan excellent response to anticholinergic drugs. All six exons of theGCH1 gene were sequenced in these patients to identify mutations.
RESULTS—three novel GCH1 mutations wereidentified in two patients. One patient was a compound heterozygotewith asymptomatic carrier parents. The clinical phenotype ofpatients with and without GCH1 mutations was similar.
CONCLUSIONS—these findings show that a proportionof patients with apparent primary torsion dystonia and a good responseto anticholinergic drugs have GCH1 mutations and therefore have avariant of dopa responsive dystonia. The difficulty in distinguishingclinically between patients with and without mutations underscores theimportance of considering the diagnosis of a levodopa responsivedystonia in all such patients.