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At least 1,243 records · Page 69Linked to original sources
PubMed2003

Costs of thalamic deep brain stimulation for movement disorders in patients with multiple sclerosis.

Several studies have shown that thalamic deep brain stimulation (DBS) reduces tremor and improves hand performance in patients with multiple sclerosis (MS). The purpose of this paper is to describe the cost implications of DBS in MS patients and to highlight postoperative medical requirements that can be associated with this therapy. In a prospective study of thalamic DBS in MS patients the mean equipment costs were pounds 4769 (median pounds 7010, Medtronic, 1998 prices); mean neurosurgical inpatient costs per operated patient (n = 15) were pounds 4848 (range pounds 1982-8920, median pounds 5110); and mean in-patient postoperative rehabilitation cost pounds 4602 (range pounds 0-32,225, median pounds 1783). In addition there were transport and follow up costs. Mean neurosurgical inpatient stay following stereotactic DBS implantation was 15 days (median 12 days); and mean inpatient, postoperative rehabilitation stay 54 days (median 25 days). Although there were significant improvements in hand function and tremor reduction at 12 months postoperation, the level of patient performance in activities of daily living, their perception of their handicap and ipse facto the amount of home support required were unchanged from preoperative levels. This study has highlighted significant unforeseen medical requirements and costs that can occur in MS patients who have thalamic DBS surgery.

Activities of Daily Living↗
PubMed1996

Behavioral and neurochemical dysfunction in the circling (ci) rat: a novel genetic animal model of a movement disorder.

One of the crucial breakthroughs in research on parkinsonism was the observation of circling behaviour in rodents after unilateral intranigral injection of 6-hydroxydopamine. This Ungerstedt model remains one of the basic animal models of Parkinson's disease. We report here the first mutant rat strain with abnormal circling behaviour and several other features reminiscent of the Ungerstedt Parkinson model. The neurological disorder in the novel mutant rat strain is determined monogenetically by a recessive autosomal gene termed circling (ci). Mutant rats of both genders exhibit an intense asymmetric circling in an open-field or rotometer, which is enhanced by treatment with amphetamine. Neurochemical determinations show that mutants of both genders have significantly lower concentrations of dopamine and dopamine metabolites in the striatum ipsilateral to the preferred direction of rotation. Furthermore, in a forelimb-reaching test for assessing the skilled motor capacities of rats, ci rats show a marked deficit on the side contralateral to the preferred direction of turning, which is analogous to motor deficits previously described for rats subjected to unilateral 6-hydroxydopamine lesions. The new mutant rat strain thus exhibits remarkable similarities to the Ungerstedt model and could be used to study the endogenous processes, particularly the genetic components, that might eventually lead to progressive motor dysfunctions.

Amphetamine↗
PubMed2006

Operative and hardware complications of deep brain stimulation for movement disorders.

The objective of this investigation was to present the operative and hardware complications encountered during follow-up of patients with in situ deep brain stimulators. The study took the form of a retrospective chart review on a series of consecutive patients who were treated successfully with insertion of deep brain stimulators at a single centre by a single surgeon between 1999 and 2005. During the study period, a total of 60 patients underwent 96 procedures for implantation of unilateral or bilateral DBS electrodes. The mean follow-up period was 43.7 months (range 6-78 months) from the time of the first procedure. No patients were lost to follow-up or died. Eighteen patients (30%) developed 28 adverse events, requiring 28 electrodes to be replaced. Seven patients developed two adverse events and two patients developed three adverse events. The rate of adverse events per electrode-year was 8%. We observed a higher proportion of early complications (<6 months postoperatively) in patients with Parkinson's disease, while dystonic patients had more late complications (>6 months postoperatively) and no early complications. Thirty per cent of our patients developed an adverse event that could potentially lead to revision of the implanted hardware. In patients with Parkinson's disease most of the complications tend to occur during the first 6 months postoperatively, while in dystonic patients most occur between 12 and 24 months postoperatively.

Adult↗
PubMed2005

Risk factors for hemorrhage during microelectrode-guided deep brain stimulator implantation for movement disorders.

OBJECTIVE: Although hemorrhage is a well-known complication of microelectrode-guided deep brain stimulation (DBS) surgery, risk factors for the development of hemorrhage have not been well defined. We analyzed the risk factors for symptomatic and asymptomatic hemorrhage in a large series of DBS implantations into the subthalamic nucleus, ventrolateral thalamus, and internal globus pallidus. METHODS: All DBS procedures performed by a single surgeon at our institution between June 1998 and May 2004 were included in this study. All patients had postoperative imaging (magnetic resonance imaging or computed tomography) 4 to 24 hours after surgery. Hematomas were noted and scored as symptomatic or asymptomatic. Statistical correlation of factors affecting risk of hematoma formation was performed by use of logistic regression analysis. RESULTS: The total number of lead implantations was 481. There were 6 symptomatic hematomas and 10 asymptomatic hematomas. Three of the symptomatic hematomas resulted in permanent new neurological deficit. The risk of hematoma (of any type) per lead implantation was 3.3%, whereas the risk of permanent deficit from hematoma was 0.6%. Patients who developed hematomas had a slightly greater number of microelectrode recording penetrations than patients who did not have hematomas, but this difference did not reach statistical significance. There was not a statistically significant relationship between risk of hematoma and patient age or diagnosis. There was a significant effect of brain target (P = 0.001), with only 1 hemorrhage detected after thalamic DBS. CONCLUSION: DBS is generally safe, with only 0.6% of implantations associated with permanent neurological deficit. The incremental risk of successive serial microelectrode penetrations is small.

Aged↗
PubMed2006

Tandospirone, a 5-HT1A agonist, ameliorates movement disorder via non-dopaminergic systems in rats with unilateral 6-hydroxydopamine-generated lesions.

Serotonin 1A (5-HT1A) receptors are distributed throughout the brain with their highest concentrations in the frontal cortex, subthalamic nucleus and entopeduncular nucleus as well as the dorsal and median raphe nucleus. There is growing evidence that 5-HT1A receptor agonists have an antidepressant effect in individuals with major depressive disorders. Recent clinical studies suggest that tandospirone, a highly potent and selective 5-HT1A receptor agonist used clinically as an antidepressant in Japan and China, may act as an antiparkinsonian drug. In the present study, we investigated the effect of tandospirone on contralateral rotational behavior in a unilateral hemiparkinsonian rat model produced with 6-hydroxydopamine (6-OHDA). Tandospirone, as well as 8-hydroxy-2-(di-n-propylamino) tetralin (8-OHDPAT), significantly increased contralateral turnings in a dose-dependent manner (0.5-10 mg/kg). Tandospirone also remarkably potentiated the contralateral turning induced by 0.025 mg/kg of apomorphine. Pretreatment with WAY-100635, a 5-HT1A receptor antagonist, almost completely blocked the contralateral turning behavior evoked by tandospirone and 8-OHDPAT, but not that by apomorphine. SCH-23390, a selective dopamine D1 receptor antagonist, did not affect on the tandospirone-induced rotational behavior. These results suggested that tandospirone could act on postsynaptic 5-HT1A receptors and modulate excitatory amino acid pathways in the basal ganglia. Thus, tandospirone could have therapeutic potential for the treatment of Parkinson's disease by modulating neuronal activities of non-dopaminergic pathways.

Analysis of Variance↗
PubMed1997

Non-functional CYP2D6 alleles and risk for neuroleptic-induced movement disorders in schizophrenic patients.

The use of classic anti-psychotic drugs in the long-term treatment of schizophrenia is associated with risk for extrapyramidal side-effects, such as akathisia, parkinsonism and tardive dyskinesia (TD). Approximately 5-10% of European Caucasians lack the cytochrome P450 enzyme CYP2D6 (so-called poor metabolizers; PM), which normally metabolizes several drugs including many neuroleptics. PM subjects may achieve high or toxic plasma levels upon standard drug therapy. In this study we have examined 100 subjects from the Nithsdale cohort of schizophrenic patients in South-west Scotland receiving long-term neuroleptic medication, which enabled us to perform both a cross-sectional and longitudinal evaluation of extrapyramidal side-effects in relation to the genetically impaired CYP2D6 metabolism. We identified ten (10%) schizophrenic subjects with the PM genotype. In the cross-sectional study, the prevalence of TD, parkinsonism and akathisia was 51%, 38% and 15%, respectively. Patients with TD or parkinsonism were significantly older than patients without these side-effects. In contrast, patients with akathisia were significantly younger than patients without akathisia. There was a non-significant tendency for PM subjects to have more severe ratings for TD and parkinsonism. In the long-term evaluation based on repeated ratings since 1981, there was a non-significant 3-fold higher frequency of PM subjects among schizophrenic patients with longitudinal TD, as compared with the group of patients with fluctuating or no TD. These results indicate that genetically impaired CYP2D6 metabolism may be a contributing factor for the development of persistent TD.

Adult↗
PubMed2004

Behavior-related alterations of striatal neurochemistry in a mouse model of stereotyped movement disorder.

Motor stereotypy is a common component of several developmental, genetic, and neuropsychiatric disorders. In animals, these behaviors can be induced or attenuated via pharmacological manipulation of specific neural loci comprising cortico basal ganglia-cortical feedback circuits, including the striatum. The present study employed the deer mouse model of spontaneous and persistent stereotypy to assess the involvement of several endogenous neurotransmitters and neuromodulators in mediating the expression of the stereotypic behaviors (i.e., repetitive hindlimb jumping) exhibited by these mice. This was accomplished by employing a microdialysis sampling system coupled on-line to capillary electrophoresis with laser-induced fluorescence (CE-LIF) detection apparatus. Given the 13-s temporal resolution for analyte measurement afforded by this system, discrete behavior-related alterations in striatal neurochemical concentrations were detected. Rearing behavior was found to be associated with significant and selective elevations of striatal glutamate (Glu) and aspartate (Asp) concentrations. Moreover, rearing was found to most frequently precede repetitive jumping. The results also indicated that alterations in striatal serine (Ser) concentrations were involved in the modulation of locomotor activity. The present findings support a role of the striatal glutamatergic system in the mediation of spontaneous stereotypic behavior and suggest a potential neuronal mechanism by which transition to stereotypy occurs in these mice. Moreover, the present findings demonstrate the usefulness of the microdialysis system employed in studying the neurochemical substrates of rapidly transitioning behavior.

Amino Acids↗
PubMed2005

Deep brain stimulation in movement disorders: stereotactic coregistration of two-dimensional electrical field modeling and magnetic resonance imaging.

OBJECT: Adjusting electrical parameters used in deep brain stimulation (DBS) for dystonia remains time consuming and is currently based on clinical observation alone. The goal of this study was to visualize electrical parameters around the electrode, to correlate these parameters with the anatomy of the globus pallidus internus (GPI), and to study the relationship between the volume of stimulated tissue and the electrical parameter settings. METHODS: The authors developed a computer-assisted methodological model for visualizing electrical parameters (the isopotential and the isoelectric field magnitude), with reference to the stereotactic target, for different stimulation settings (monopolar and bipolar) applied during DBS. Electrical field values were correlated with the anatomy of the GPI, which was determined by performing stereotactic magnetic resonance imaging in one reference patient. By using this method it is possible to compare potential and electrical field distributions for different stimulation modes. In monopolar and bipolar stimulation, the shape and distribution of the potential and electrical field are different and depend on the stimulation voltage. Distributions visualized for patient-specific parameters can be subsequently correlated with anatomical information. The application of this method to one patient demonstrated that the 0.2-V/ mm isofield line fits best with the lateral GPI borders at the level of the stimulated contacts. CONCLUSIONS: The electrical field is a crucial parameter because it is assumed to be responsible for triggering action potentials. Electrical field visualization allows the calculation of the stimulated volume for a given isoline. Its application to an entire series of patients may help determine a threshold for obtaining a therapeutic effect, which is currently unknown, and consequently may aid in optimizing parameter settings in individual patients.

Adolescent↗
PubMed1977

[Simple examination of spastic movement disorders of the lower limbs in the infant age].

In 334 children active dorsiflexion of the feet was tested in order to screen for spasticity of the lower limbs. The conditions were: 1. The child lying supine. 2. The head turned actively and if this is not possible passively to the side of the examined foot. 3. Passive extension of the child's hip and knee of the examined side by the examinator. 4. Stimulation of the skin at the lateral and lower part of the shin, or the dorsum pedis or the anterior part of the toes and the planta pedis to provoke active dorsiflexion of the foot. Stimulation is done by the fingers of the examinator or by a slight touch with an ordinary handbrush. Dorsiflexion of the foot is graded "normal" if it surpasses 90--100 degrees, "suspicious" if it only reaches 90 degrees and "pathologic" if 90 degrees cannot be reached or if this can be done only on the medial side or if there is constant clawing of the toes even with sufficient dorsiflexion. We have examined 334 children; 260 of these were younger than one year. The results of this kind of stimulated dorsiflexion of the foot were compared with the results of the usual extensive neurological examination with regard to spasticity of the lower limbs (see literature) and with both of VOJTA's most sensible postural reactions. The following conclusions are drawn: 1. Spasticity of the lower limbs can be excluded with a high degree of probability when dorsiflexion of the feet is graded "normal". 2. If the dorsiflexion is graded "suspicious" or "pathologic" a more thorough neurological examination is warranted and if necessary short-term controls. 3. The results of this examination are in good agreement with the one of VOJTA's most sensitive postural reactions to indicate spasticity of the lower limbs.

Age Factors↗
PubMed1994

Clinical usefulness of apomorphine in movement disorders.

Apomorphine, the first dopamine agonist to be synthesized, has received a renewed interest in the last few years. This compound acts powerfully on D1 and D2 dopamine receptors and has the most complete pharmacological profile of all clinically available dopamine agonists. When given subcutaneously, apomorphine consistently reverses levodopa-resistant "off" periods in parkinsonian subjects: thus, it is used in cases with severe motor fluctuations, either by continuous infusion with a portable pump or by multiple injections. Studies based on this approach have been highly encouraging, as they have shown a significant reduction in off time and a good drug tolerability. The main side effect has been the occurrence of nodular skin lesions, especially when continuous infusions were used. At variance with other dopamine agonists, a low incidence of psychiatric morbidity has been reported with apomorphine. The few available comparative reports have shown that this compound is more potent and better tolerated than lisuride. Parenteral apomorphine has been used in Parkinson's disease (PD) to replace levodopa after surgery or to treat the malignant syndrome brought about by sudden levodopa withdrawal. Acute challenge with apomorphine has been used to test dopaminergic responsiveness in parkinsonian syndromes and in dystonia. The clinical response to apomorphine may predict the effect of a chronic therapy with levodopa in approximately 90% of PD cases. Further studies are still necessary to evaluate the exact relationship between the acute response to apomorphine and a chronic therapy. In addition, apomorphine has been used to conduct clinical pharmacological studies in PD, for it is particularly well suited for research on the pharmacodynamics of central dopamine receptors. In summary, apomorphine appears to be an efficacious and safe drug for the treatment of advanced PD. It must still be considered under clinical evaluation as a test drug for acute challenge in PD and dystonia. Finally, in our opinion, the available data suggest apomorphine (in conjunction with domperidone) as a first-choice treatment for the neuroleptic malignant syndrome and the temporary replacement of levodopa (e.g., after gastrointestinal surgery).

Antiparkinson Agents↗
PubMed1993

Specificity of behavioral and neurochemical dysfunction in the chakragati mouse: a novel genetic model of a movement disorder.

The chakragati (ckr) mouse is a transgenic insertional mutant that displays lateralized circling behavior, locomotor hyperactivity, hyperexcitability as well as body weight deficits. The mutation is autosomal and recessive. We have previously found that ckr mice have bilateral asymmetric elevations in striatal dopamine (DA) D2-like (D2, D3 and/or D4), but not D1-like (D1 and/or D5) receptors. Predictably, these mice increase turning in response to the D2-like agonist quinpirole and spontaneously rotate contralateral to the striatal side with the higher D2-like receptors. The overall objective of the present study was to assess the neurochemical specificity of the mutation in ckr mouse, particularly since motor behaviors can be elicited by a multitude of brain regions and neurotransmitter systems within the basal ganglia. Using quantitative receptor autoradiography, we examined the regional distribution of DA uptake sites and 5-HT1A, 5-HT1B/1D, GABAA and mu opioid receptors. Also, we wanted to determine whether increased behavioral laterality as seen in rotation is evident with another test of laterality, such as lateral paw preference. The ckr mice showed greater paw preferences than normal mice; however, neither the degree nor direction of these preferences correlated with rotational behavior. The ckr mice showed moderate decreases in the density of DA uptake sites in all subregions of the striatum, but not in the nucleus accumbens or olfactory tubercle. Interestingly, these decreases in ckr mice were not accompanied by a reduction in striatal tissue DA content. 5-HT1 and mu opiate receptor populations were normal in ckr mice. However, GABAA sites in the mediodorsal thalamus and superior colliculus were bilaterally and asymmetrically elevated in ckr mice. These data are consistent with the idea that the motor phenotypes of the ckr mouse result from specific disturbances within nigro-striatal, striato-pallido-thalamic and striato-nigro-collicular circuitry. The implications of these and past findings are discussed in relation to current thinking about hyperkinetic motor syndromes in humans involving reduced basal ganglia outflow.

Animals↗
PubMed2003

Injectable neuromuscular blockade in the treatment of spasticity and movement disorders.

Neuromuscular blockade via injection of alcohol, phenol, or botulinum toxin reduces the tone of overactive muscles in order to restore the appropriate balance between agonists and antagonists. Such a restoration allows improved stretch and increased resting length and can reduce the likelihood of contracture. Alcohol or phenol, injected onto the motor nerve, denatures proteins and promotes axonal degeneration. The onset of action is within hours, whereas the duration of action is variable, ranging from 2 weeks to 6 months and beyond. The advantages of alcohol or phenol chemodenervation lie in their low cost and lack of antigenicity. The disadvantages include the technical difficulty of the injections and significant risk for pain as a result of treatment. Botulinum toxins, purified forms of Clostridium botulinum exotoxins, are injected directly into muscle, where they cleave one or more vesicle fusion proteins, thus blocking release of acetylcholine at the neuromuscular junction. Three commercial products--two of serotype A and one of B--are available. Each differs in its unit potency, side effects, and duration of action. On average, botulinum toxin has a clinical onset of action approximately 12 to 72 hours after injection, with a peak effect at 1 to 3 weeks. Effects then plateau for 1 to 2 months, with patients often requiring reinjection approximately every 3 months. Side effects may include local discomfort at the site of the injection and excessive weakness of the injected or nearby muscles, although more distant effects may occur. Antibody formation is a significant clinical concern and eventually obviates treatment benefit in approximately 5% of patients. Switching serotypes may be effective, at least temporarily. Consensus dosing guidelines have been developed and are presented within. Numerous studies have suggested that botulinum toxin has a role in the care of children with spasticity or dystonia related to cerebral palsy, and may improve equinus, gait, upper extremity use, comfort, and care. Evidence of functional improvement remains equivocal in the severely impaired child; however, there is evidence for improvement in less impaired children. The optimal candidate for injectable neuromuscular blockade is one who has a limited number of muscles that need treatment, who does not have fixed contracture, and who retains selective motor control. The ultimate goal of treatment for the hypertonic child is to maximize function, comfort, and independence. Hypertonia is only one aspect of the upper motoneuron syndrome, which includes both positive and negative symptoms. The treatment program, in which chemodenervation is only one tool, requires a multidisciplinary evaluation and individualized plan to address the whole patient.

Anti-Dyskinesia Agents↗
PubMed2001

Movement disorder, memory, psychiatric symptoms and serum DHEA levels in schizophrenic and schizoaffective patients.

OBJECTIVE: Reports of low levels of dehydroepiandrosterone (DHEA) or its sulphate (DHEA-S) in some schizophrenic patients and in some persons with poorer motoric and cognitive functioning led us to examine clinical correlates of serum DHEA and DHEA-S levels in schizophrenic patients. METHOD: Ratings of abnormal movements, memory and psychiatric symptoms in 17 medicated chronic schizophrenic or schizoaffective inpatients at a state hospital were correlated with serum DHEA and DHEA-S levels, and their ratios with serum cortisol. RESULTS: Controlling for age, higher DHEA levels and/or higher DHEA/cortisol ratios were significantly correlated with lower symptom ratings on the Brief Psychiatric Rating Scale, better performance on some measures of memory, and lower ratings of parkinsonian symptoms. CONCLUSION: Relatively low DHEA levels or DHEA/cortisol ratios may identify a particularly impaired subgroup of medicated patients with chronic schizophrenia. Potential implications are discussed.

Adult↗
PubMedDate not supplied

Movement disorder with abnormal copper metabolism--a case report and review of the literature.

We describe a neurological disease, seen in the elder sister of identical twins, with dysarthria, involuntary movements, spastic gait, slightly low serum copper, borderline low to normal serum ceruloplasmin, normal urinary copper, and a high hair copper concentration. This neurological disorder appears to differ from others associated with abnormal copper metabolism such as Wilson's or Menkes' kinky hair disease.

Adult↗
PubMed1995

Strychnine-insensitive glycine site antagonists attenuate a cardiac arrest-induced movement disorder.

Male Sprague-Dawley rats underwent experimentally induced cardiac arrest and resuscitation, subsequently exhibiting involuntary jerking movements (myoclonus) with salient features similar to the human form of the disorder. The novel strychnine-insensitive glycine site antagonists ACEA-1011 (5-chloro-7-trifluoromethyl-1,2,3,4-tetrahydroquinoxaline-2,3,-dio ne) and ACEA-1021 (5-nitro-6,7-dichloro-quinoxalinedione) significantly attenuated the myoclonus in cardiac-arrested rats. (+)-HA-966, (+/-)-HA-966 (3-amino-1-hydroxy-2-pyrrolidinone), and felbamate (2-phenyl-1,3-propanediol dicarbamate) were also effective. Although the drugs vary in their selectivity for strychnine-insensitive glycine sites, they all possess antagonist activity at these sites. Vehicle injections (saline, dimethyl sulfoxide, water) were without effect and no obvious side effects were observed with any of the ligands tested in this study. Since hyperexcitability in the central nervous system is thought to underlie myoclonus, the attenuation of excitatory amino acid neurotransmission through antagonism of strychnine-insensitive glycine sites provides a logical mechanism of action for the antimyoclonic effects observed herein.

Animals↗