Some aspects of higher motor disorders and their relationship to movement disorders associated with disease of subcortical nuclei.
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Animals↗
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Homozygosity for a missense mutation in the 67 kDa isoform of glutamate decarboxylase in a family with autosomal recessive spastic cerebral palsy: parallels with Stiff-Person Syndrome and other movement disorders.
BACKGROUND: Cerebral palsy (CP) is an heterogeneous group of neurological disorders of movement and/or posture, with an estimated incidence of 1 in 1000 live births. Non-progressive forms of symmetrical, spastic CP have been identified, which show a Mendelian autosomal recessive pattern of inheritance. We recently described the mapping of a recessive spastic CP locus to a 5 cM chromosomal region located at 2q24-31.1, in rare consanguineous families. METHODS: Here we present data that refine this locus to a 0.5 cM region, flanked by the microsatellite markers D2S2345 and D2S326. The minimal region contains the candidate gene GAD1, which encodes a glutamate decarboxylase isoform (GAD67), involved in conversion of the amino acid and excitatory neurotransmitter glutamate to the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). RESULTS: A novel amino acid mis-sense mutation in GAD67 was detected, which segregated with CP in affected individuals. CONCLUSIONS: This result is interesting because auto-antibodies to GAD67 and the more widely studied GAD65 homologue encoded by the GAD2 gene, are described in patients with Stiff-Person Syndrome (SPS), epilepsy, cerebellar ataxia and Batten disease. Further investigation seems merited of the possibility that variation in the GAD1 sequence, potentially affecting glutamate/GABA ratios, may underlie this form of spastic CP, given the presence of anti-GAD antibodies in SPS and the recognised excitotoxicity of glutamate in various contexts.
Cerebral Palsy↗
THE DISORDERED MOVEMENT IN PARKINSONISM AND THE EFFECT OF DRUG TREATMENT.
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Atropine↗
Neuropathology of movement disorders.
This article reviews the cytoskeletal abnormalities, morphologic lesion patterns, and resulting pathophysiology of the most frequent neurodegenerative movement disorders caused by dysfunction of the basal ganglia and related neuronal loops. The following topics are discussed: Among the akinetic-rigid Lewy body disorders is idiopathic Parkinson's disease, which reveals specific lesion patterns of pathophysiologic and therapeutic relevance. Dementia with Lewy bodies characterized by cortical Lewy bodies appears intermediate between Parkinson's and Alzheimer's diseases. Tau pathologic disorders may show some clinical and morphologic overlap. Multiple system atrophy has ubiquitous oligodendroglial inclusions as a cytopathologic hallmark. Secondary parkinsonism includes drug-related, toxic, and other symptomatic disorders. Hyperkinetic disorders include CAG-related inherited diseases, showing specific genetic defects and morphologic lesions. Dystonia syndromes show inconsistent pathologic findings, and myoclonus may be related to a variety of disorders. Consensus data on clinical and neuropathologic criteria already existing for some disorders, together with molecular genetic and biochemical data will provide further insight into the complex pathophysiology and pathogenesis of movement disorders.
Humans↗
Treatment of movement disorders with trihexyphenidyl.
The clinical efficacy of the trihexyphenidyl was investigated in 100 patients with movement disorders. The study group consisted of 54 women and 46 men. Their ages ranged from 18 to 70 years, and their duration of illness varied from a few months to 36 years. Each patient had a videotape of the movements and a neurological examination, before administration of the drug, at the time of maximum or effective dosage, and one week after withdrawal from trihexyphenidyl. The drug was administered at an initial total daily dose of 2 mg and gradually increased to a total daily dose of 60 mg over a period of 4-6 weeks. Improvements were rated both clinically and from the videotapes. Three groups of movement disorders demonstrated a significant response to trihexyphenidyl: (1) dystonia 37%; tonic torticollis demonstrated a significantly better response than the clonic variant (80% vs. 22%). (2) rhythmic-oscillatory movements of brainstem-cerebellar origin (palatal myoclonus, pendular nystagmus, facial myokymia) 90%; (3) cerebellar tremor 75%. Among 32 responders, 17 (56%) continued taking trihexyphenidyl beyond 24 months. Side effects consisted of dryness of the mouth, jitteriness, stomatitis, blurred vision, and forgetfulness.
Adolescent↗
Algorithms for neuroleptic-associated tardive movement disorders.
Prolonged neuroleptic exposure is often associated with several forms of tardive movement disorders, conditions adversely affecting the patient's quality of life. Risk factors for individual tardive movement disorders is noted. Once they develop, one should modify neuroleptic regimen with preferential replacement of conventional neuroleptics with lower potency ones. The subsequent algorithm is difficult to formulate, and its success is sometimes hampered by coexisting psychiatric disease. Several suggestions to be tried are as follows: high doses of anticholinergics and/or dantrolene sodium against tardive dystonia, and reduction of anticholinergic dose and/or clonidine, a alpha2 agonist, against tardive dyskinesia and tardive akathisia.
Algorithms↗
Drug-induced parkinsonism and other movement disorders.
This is a review of reserpine, haloperidol, and various phenothiazines that produce parkinsonism and other movement disorders. The by-products of illicit meperidine synthesis, MPTP and its more sinister companion, MPP, are also discussed. Movement disorders, transient or fixed, frank parkinsonism and/or dyskinesia, due to a variety of other medications and toxic agents are included. These are methanol, lithium, methyldopa, antimetabolites, antidepressants, sympathomimetic anorexiants, some types of antihistamines, and various combinations of agricultural chemicals.
Haloperidol↗
Beneficial effect of donepezil in the treatment of elderly patients with tardive movement disorders.
BACKGROUND: Tardive dyskinesia and other delayed-onset abnormal involuntary movement disorders may occur as a result of the use of psychotropic drugs. A distinction is usually made between classic tardive dyskinesia (TD) (orobuccal-lingual-facial) and tardive dystonia, tardive tremor (TT), tardive akathisia, and other related syndromes. In spite of the development of atypical antipsychotics with fewer side effects, tardive movement disorders nevertheless continue to present a significant clinical and therapeutic challenge. Several reports have suggested that donepezil may be helpful in the treatment of TD. METHOD: A preliminary study was conducted of 7 patients (5 women and 2 men) enrolled over a period of 6 months who had been experiencing TT for a period of at least 1 year. The ages of the patients ranged from 64 to 79 years, and all patients were on stable antipsychotic therapy. Donepezil was added to their usual treatment for 8 weeks. The severity of patients' extrapyramidal symptoms was assessed using the tremor subscale of the Simpson-Angus Scale (SAS) and self-rated with a modification of the Clinical Global Impressions scale, the Subjective Clinical Improvement Impression scale. The clinical response was evaluated by comparing the rating scores at baseline prior to donepezil treatment and every 2 weeks thereafter. RESULTS: The addition of donepezil (up to 10 mg/day) was associated with a clinically significant improvement (from 37.5% to 63.6%) on the SAS tremor subscale following 4 weeks of therapy. Only 1 patient discontinued follow-up due to side effects. CONCLUSION: The results suggest that donepezil may be effective in the treatment of TT, and this finding should be evaluated further by a randomized controlled study.
Aged↗
Ictal movement disorders and hypothalamic hamartoma.
We report the case of a woman presenting with unusual, symptomatic epilepsy related to a hypothalamic hamartoma, in the absence of mental retardation or precocious puberty. The seizures manifested themselves clinically as characteristic, paroxysmal movement disorders, such as choreic/ballistic movement. This type of phenomenon is rarely of epileptic origin: we thus suggest that the movement disorder observed here could be due to functional disorganization of the basal ganglia network by the epileptic discharge, causing loss of the inhibition of thalamic activity and thus allowing the occurrence of abnormal movements.
Adult↗
Subclinical eye movement disorders in patients with multiple sclerosis.
Eye movements were quantitatively evaluated in 16 patients with well-documented multiple sclerosis who had minimal or no clinically apparent eye movement disorder. Induced saccade and pursuit eye movements were recorded with electro-oculography and analyzed with newly developed programs on a laboratory digital computer. Thirteen of the 16 patients had significant (p less than 0.05) impairment of saccades and/or smooth pursuit when compared with 25 normal subjects tested in our laboratory. The type and frequency of abnormalities were as follows: saccade dysmetria, eight; delayed saccade reaction time, five; bilateral saccade slowing, four; slowing of adducting saccades only (medial longitudinal fasciculus syndrome), one; and impaired smooth pursuit, both directions, three, and one direction only, three. In addition, four patients had vestibular nystagmus with eyes closed, and one patient had typical rebound nystagmus. These data suggest that quantitative assessment of eye movements in patients with suspected multiple sclerosis can help in identifying the important "second lesion."
Adult↗
Therapeutic stereotactic procedures on the thalamus for motor movement disorders.
The value of functional neurosurgery in the treatment of motor movement disorders is emphasized. The two methods of stereotactic procedures, namely a destructive one with small lesions centered on specific targets, and a non-destructive one with chronically inserted electrodes connected with an also implanted programmable neuropacemaker are described in detail. The results in Parkinsonian tremor, essential tremor, tremor of multiple sclerosis, post-traumatic tremor and in other involuntary movement disorders are reported and demonstrate that stereotactic neurosurgical treatment of these conditions is a safe and efficacious method.
Adult↗
Neuroimaging and therapeutics in movement disorders.
In this review, we discuss the role of neuroimaging in assessing treatment options for movement disorders, particularly Parkinson's disease (PD). Imaging methods to assess dopaminergic function have recently been applied in trials of potential neuroprotective agents. Other imaging methods using regional metabolism and/or cerebral perfusion have been recently introduced to quantify the modulation of network activity as an objective marker of the treatment response. Both imaging strategies have provided novel insights into the mechanisms underlying a variety of pharmacological and stereotaxic surgical treatment strategies for PD and other movement disorders.
Animals↗
Thalamic stimulation for choreiform movement disorders in children. Report of two cases.
Surgery for movement disorders is most commonly performed in patients with dyskinesia and tremor associated with Parkinson's disease or in those with essential tremor. The role of ablative surgery or deep brain stimulation in patients with choreiform movements is poorly defined. The authors placed thalamic stimulation systems in two children with disabling choreiform disorders due to intracerebral hemorrhage or cerebral palsy. Each patient displayed choreiform movements in the upper extremities both at rest and with intention, which interfered with daily activities and socialization. Both children obtained significant improvement in their choreiform movements, and their upper extremity function improved with no incidence of morbidity. Thalamic stimulation appears to be a promising and nonablative approach for children with choreiform movement disorders.
Activities of Daily Living↗
Long-term tolerability of tetrabenazine in the treatment of hyperkinetic movement disorders.
We sought to review the long-term tolerability of tetrabenazine (TBZ) and seek determinants of tolerability in the treatment of hyperkinetic movement disorders. A retrospective chart review was performed on patients treated with TBZ between 1997 and 2004. Efficacy of TBZ was assessed by a 1- to 5-point response scale (1 = marked reduction in abnormal movements, 5 = worsening). All adverse events (AEs) were captured according to their relationship with study drug. A total of 448 patients (42% male) were treated for a variety of hyperkinesias, including tardive dyskinesia (n = 149), dystonia (n = 132), chorea (n = 98), tics (n = 92), and myoclonus (n = 19). The mean age at onset of the movement disorder was 43.0 +/- 24.2 years, with TBZ starting at a mean age of 50.0 +/- 22.3 years. Patients remained on treatment for a mean of 2.3 +/- 3.4 years. An efficacy response rating of 1 or 2 was sustained in the majority of patients between the first and last visit. Common AEs included drowsiness (25.0%), Parkinsonism (15.4%), depression (7.6%), and akathisia (7.6%). Comparison of log-likelihood ratios revealed that age was a reliable predictor of Parkinsonism (P < 0.0001). TBZ is a safe and effective drug for the long-term treatment of hyperkinetic movement disorders.
Adult↗
Neuropsychiatric assessment of Gilles de la Tourette patients: comparative study with other hyperkinetic and hypokinetic movement disorders.
The role of the basal ganglia in conditions with co-occurring movement disorders and neuropsychiatric symptoms is not well known. It has been hypothesized that hyperkinesia -disinhibited behaviors and hypokinesia-inhibited behaviors result from an imbalance between the direct and indirect striatal output pathways, and that differential involvement of these pathways could account for the concurrent abnormalities in movement and behavior observed in these disorders. This study aimed to evaluate whether the pattern and the extent of the neuropsychiatric manifestations of patients with GTS, a hyperkinetic movement disorder of basal ganglia origin, differs from that of patients with other basal ganglia hyperkinetic (e.g., HD) or hypokinetic (e.g., PSP) movement disorders, and to determine whether patients with GTS show a greater frequency of hyperactive behaviors (e.g., agitation, irritability, euphoria, or anxiety) than PSP patients, and are comparable to patients with HD. The Neuropsychiatric Inventory (NPI), a scale with established validity and reliability, was administered to 26 patients with GTS (mean age, 30.2 +/- 2.2 years), and the results were compared with that of 29 patients with HD (mean age, 43.8 +/- 2 years) and 34 with PSP (mean +/- S.D. age, 66.6 +/- 1.2 years). There was no difference between the groups in the total NPI scores. However, there was a double dissociation in behaviors: patients with hyperkinetic disorders (HD and GTS) exhibited significantly more agitation, irritability, anxiety, euphoria, and hyperkinesia, whereas hypokinetic patients (PSP) exhibited more apathy. Patients with GTS showed greater scores than HD patients in all those scores differentiating HD and GTS from PSP patients (e.g., agitation, irritability, anxiety and euphoria), and were differentiated in a logistic regression analysis from both HD and PSP patients in having significantly more anxiety. We found that patients with GTS manifested predominantly hyperactive behaviors similar but more pronounced than those presented by patients with HD, while those with PSP manifested hypoactive behaviors. Based on our findings and the proposed models of basal ganglia dysfunction in these disorders, we suggest that the hyperactive behaviors in GTS are comparable to those observed in HD, being both secondary to an excitatory subcortical output through the medial and orbitofrontal cortical circuits, while in PSP the hypoactive behaviors are secondary to hypostimulation of these circuits. Abnormalities of other brain structures (e.g., amygdala, brainstem nuclei) may account for the significantly higher anxiety scores differentiating GTS from HD patients.
Adult↗
Lifetime antipsychotic-drug exposure, dyskinesia and related movement disorders in the developmentally disabled.
The relationship between dyskinesia and related movement disorders was examined as a function of cumulative exposure to antipsychotic drugs (APD). Lifetime drug-exposure histories were obtained for 162 developmentally disabled (DD) persons; drug-exposed groups were compared to nondrug-exposed groups. There were no statistically significant relationships between dyskinesia and the amount of lifetime APD exposure, nor between dyskinesia and the number of long-term APDs, mean exposure, peak exposure, recency of exposure, duration of exposure, changes in medication levels, number of drug interruptions, age, gender, cerebral palsy, epilepsy, or IQ. Of the other movement disorders, a positive relationship was noted only between akathisia and long-term APD exposure; the increased prevalence of akathisia persisted beyond four years after APD withdrawal.
Adolescent↗
Coexistence of movement disorders and epilepsia partialis continua as the initial signs in probable Creutzfeldt-Jakob disease.
Movement disorders and epilepsy rarely occur in the early stage of Creutzfeldt-Jakob disease (CJD) but have not been reported concurrently. We report on a 47-year-old patient with probable CJD who presented with generalized chorea and focal dystonia with myoclonic jerks on the right hand. Myoclonic jerks progressed to epilepsia partialis continua within 5 days of admission to the hospital. The diagnosis of our patient was compatible with probable CJD on the basis of clinical course, electroencephalogram, and diffusion-weighted magnetic resonance imaging findings, and presence of 14-3-3 protein in cerebrospinal fluid. To our knowledge, this is the first report of a case developing both movement disorders and epilepsia partialis continua in the early stage of the disease.
Basal Ganglia↗
[Pathophysiology of restless leg syndrome and periodic leg movement disorder in view of the latest research findings].
Both restless leg syndrome and periodic leg movement disorder have been classified as primary sleep disorders by the International Classification of Sleep Disorders. Considering the characteristic clinical symptoms, it is supposed that their pathomechanism involves the peripheral and central stimulus-processing mechanisms of the nervous system as well as several elements of the motor system. During the last couple of years many new elements of the pathomechanism have been discovered, in particular the dysfunction of the postsynaptic dopamine receptors related to the iron metabolism of the central nervous system, the role of opiate receptors, and the involvement of subclinical small fiber neuropathy. Many of these findings have been incorporated into the diagnostic and treatment protocols used in the management of patients with restless leg syndrome or periodic leg movement disorder. Considering the rapidly increasing number of publications on their pathomechanism and the various fields it involves, the authors found it necessary to evaluate these data and to interpret their relationships within the frame of sleep-wake regulation.
Central Nervous System↗