Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “EXTRAPYRAMIDAL TRACTS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 667 records · Page 37Linked to original sources
PubMed2005

Gait instability and fractal dynamics of older adults with a "cautious" gait: why do certain older adults walk fearfully?

Many older adults walk with a cautious and impaired gait of unknown origin, however, the relationship between fear of falling and the observed gait changes is not well understood. To better understand the "cautious" gait of the elderly, we tested the hypothesis that temporal gait variability, putatively a marker of intrinsic walking unsteadiness, is increased among older adults with a cautious gait and a higher-level gait disorder (HLGD), an altered gait that cannot be attributed to a well-defined cause. Twenty-five older adults (mean age: 78 years) with a HLGD were compared to healthy controls of similar age and sex (n=28). The clinical characteristics (e.g., neurological status, fear of falling), the magnitude of the stride-to-stride variations in gait cycle timing (a measure of temporal gait variability), and a fractal index of gait (a measure of the stride dynamics independent of the magnitude of the variability) were studied in both groups. Gait variability was significantly increased (P<0.0001) in HLGD subjects (52+/-26 ms) compared to controls (27+/-9 ms). Changes in frontal lobe and extra-pyramidal function were also found in the patient group. Among HLGD subjects, gait variability was not associated (P>0.05) with age, gender, MMSE score, muscle strength, # of co-morbidities, balance, cerebellar signs, or pyramidal signs, but was significantly associated with scores on the Geriatric Depression Scale (r=0.46, P<0.02) and fear of falling (r=0.69, P<0.0001). Among HLGD subjects, only a fractal index was significantly different in fallers and non-fallers. These findings underscore the idea that the gait changes in older adults who walk with fear may be an appropriate response to unsteadiness, are likely a marker of underlying pathology, and are not simply a physiological or psychological consequence of normal aging.

Accidental Falls↗
PubMed2006

Amisulpride-induced tardive dyskinesia.

Tardive dyskinesia (TD) is a movement disorder that develops during the course of long-term treatment with neuroleptic agents and is characterized primarily by choreiform and athetotic movements. We report the case of a 34-year-old man suffering from schizophrenia, disorganized type. He received amisulpride (400 mg daily) and the result was much improvement. 20 months later, he was presented with TD, which resolved almost completely after change of treatment to 1200 mg quetiapine without any relapsing. To our knowledge, his is the first case report in the literature of tardive dyskinesia induced by amisulpride.

Adult↗
PubMed1995

Neuroleptic drug exposure and treatment of parkinsonism in the elderly: a case-control study.

PURPOSE: Despite the widespread use of neuroleptic medications for the elderly, little is known about the frequency of treatment for drug-induced parkinsonian syndromes in this age group, particularly with L-dopa-type drugs, which are more appropriate for the treatment of true idiopathic Parkinson's disease. PATIENTS AND METHODS: We identified 3,512 patients aged 65 to 99 enrolled in a large state Medicaid program who were newly prescribed a drug to treat parkinsonian symptoms. Controls were comparable program enrollees of similar age who had not been prescribed an antiparkinsonian drug. In a case-control study, we evaluated the use of neuroleptic drugs in the 90 days before initiation of antiparkinsonian therapy. RESULTS: Patients taking neuroleptics were 5.4 times more likely to begin antiparkinsonian medication than were nonusers (95% confidence interval [CI] 4.8 to 6.1). They also had a greater than two-fold increase in risk of beginning therapy with a dopaminergic drug specific for idiopathic Parkinson's disease, not generally indicated for treatment of drug-induced parkinsonism (adjusted odds ratio 2.2, 95% CI 1.9 to 2.7). Clear dose-response relationships were demonstrated, as were differences among neuroleptics. Among all patients started on dopaminergic drugs in this population, 37% of such therapy was attributable to prior neuroleptic use. Continuation of the neuroleptic persisted in 71% of patients so treated. CONCLUSION: Neuroleptic use is a common cause of extrapyramidal dysfunction in the elderly, and the side effect is frequently treated by adding an anticholinergic or dopaminergic drug to the regimen. The use of anticholinergic drugs presents risks of additional drug side effects; the use of dopaminergic drugs, generally not appropriate for drug-induced parkinsonian syndrome, suggests that extrapyramidal neuroleptic side effects may often be mistaken for idiopathic Parkinson's disease in older patients.

Age Distribution↗
PubMed1997

Effects of amisulpride, an atypical antipsychotic which blocks preferentially presynaptic dopamine autoreceptors, on integrated functional cerebral activity in the rat.

Amisulpride, a benzamide derivative with an atypical neuroleptic profile relieves the negative symptoms of schizophrenia when administered at low doses (50-150 mg). In an attempt to define the anatomical substrates involved in this action we have studied the effects of amisulpride on regional cerebral glucose utilisation (RCGU) in the awake lightly restrained rat, by quantitative autoradiography using [14C]2-deoxyglucose ([14C]2-DG). Amisulpride was administered 1 h before [14C]2DG i.v. injection, at a dose of 5 mg/kg which resulted in a striatal D2 receptor occupancy of 10% similar to that induced by doses of this compound used for the treatment of negative symptoms of schizophrenia. Amisulpride induced significant RCGU increases in cortical areas, in visual relays, in auditory structures and in several limbic structures. The pattern of changes in RCGU seen with amisulpride clearly differs from that of haloperidol, given at a dose resulting in a similar occupancy of striatal D2 receptors (0.01 mg/kg), which was mostly ineffective. The amisulpride-induced activation of RCGU in specific brain areas involved in the control of cognitive functions and motivational and emotional behavior, may at least in part, explain the efficacy of this compound in the treatment of negative symptoms of schizophrenia.

Amisulpride↗
PubMed1999

Differential responses by neurotensin systems in extrapyramidal and limbic structures to ibogaine and cocaine.

Ibogaine (Endabuse) is a psychoactive indole alkaloid found in the West African shrub, Tabernanthe iboga. This drug interrupts cocaine and amphetamine abuse and has been proposed for treatment of addiction to these stimulants. However, the mechanism of action that explains its pharmacological properties is unclear. Since previous studies demonstrated differential effects of psychotomimetic drugs (cocaine and methamphetamine) on neuropeptides such as neurotensin (NT), the present study was designed to determine: (1) the effects of ibogaine on striatal, nigral, cortical, and accumbens neurotensin-like immunoreactivity (NTLI); (2) the effects of selective dopamine antagonists on ibogaine-induced changes in NT concentrations in these brain areas; and (3) the effects of ibogaine pretreatment on cocaine-induced changes in striatal, nigral, cortical and accumbens NTLI content. Ibogaine treatments profoundly affected NT systems by increasing striatal, nigral, and accumbens NTLI content 12 h after the last drug administration. In contrast, NTLI concentrations were not significantly increased in the frontal cortex after ibogaine treatment. The ibogaine-induced increases in NTLI in striatum, nucleus accumbens and substantia nigra were blocked by coadministration of the selective D1 receptor antagonist, SCH 23390. The D2 receptor antagonist, eticlopride, blocked the ibogaine-induced increase in nigral NTLI, but not in striatum and nucleus accumbens. Ibogaine pretreatment significantly blocked the striatal and nigral increases of NTLI resulting from a single cocaine administration. Whereas many of the responses by NT systems to ibogaine resembled those which occur after cocaine, there were also some important differences. These data suggest that NT may contribute to an interaction between ibogaine and the DA system and may participate in the pharmacological actions of this drug.

Animals↗
PubMed1997

Differential effect of haloperidol on release of neurotensin in extrapyramidal and limbic systems.

The effect of the antipsychotic drug haloperidol on extracellular neurotensin-like immunoreactivity was investigated by microdialysis and compared with the time-dependent response of tissue neurotensin-like immunoreactivity content in brain structures containing dopamine nerve cell bodies and terminals. A single administration of haloperidol (1 mg/kg) increased the extracellular neurotensin-like immunoreactivity levels in nucleus accumbens as measured by microdialysis, but decreased its extracellular concentration in the caudate regions surrounding the probe. The same treatment increased the tissue content of neurotensin-like immunoreactivity in both the nucleus accumbens core and all caudate regions examined within 24 h after the injection. Interestingly, although the neurotensin-like immunoreactivity concentration in the substantia nigra was not altered by the haloperidol treatment, neurotensin-like immunoreactivity levels decreased significantly in the ventral tegmental area. These findings suggest that varied neurotensin systems are associated with nigrostriatal and mesolimbic dopamine pathways and these systems have different responses to haloperidol. The changes in the release of neurotensin may contribute to altered caudate and accumbens neurotensin-like immunoreactivity tissue content induced by haloperidol treatment, but other factors, such as variation in synthesis also likely influence these effects. Differential actions of haloperidol on neurotensin release might be due to regional differences in dopamine or sigma receptor subtypes associated with the neurotensin-containing neurons.

Animals↗
PubMed2000

Responses of the extrapyramidal and limbic substance P systems to ibogaine and cocaine treatments.

Ibogaine is an indolamine found in the West Africa shrub, Tabernanthe iboga, and has been proposed for the treatment of addiction to central nervous system (CNS) stimulants such as cocaine and amphetamine. The mechanism of ibogaine action and its suitability as a treatment for drug addiction still remains unclear. Since previous studies demonstrated differential effects of stimulants of abuse (amphetamines) on neuropeptide systems such as substance P, we examined the impact of ibogaine and cocaine on extrapyramidal (striatum and substantia nigra) and limbic (nucleus accumbens and frontal cortex) substance P-like immunoreactivity. Ibogaine and cocaine treatments altered substance P systems by increasing striatal and nigral substance P-like immunoreactivity concentration 12 h after the last drug treatment. However, substance P-like immunoreactivity content was not significantly increased in nucleus accumbens after treatment with either drug. The ibogaine- and cocaine-induced increases in substance P-like immunoreactivity in striatum and substantia nigra were blocked by coadministration of selective dopamine D(1) receptor antagonist (SCH 23390; R(+)-7-Chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4, 5-tetrahydro-1H-3-benzazepine hydrochloride) or dopamine D(2) receptor antagonist (eticlopride; S(-)-3-Chloro-5-ethyl-N-[(1-ethyl-2-pyrrolidinyl)methyl]-6-hydroxy-2- methoxy-benzamide hydrochloride). Most of the responses by substance P systems to ibogaine administration resembled those caused by cocaine, except in cortical tissue where multiple administration of cocaine, but not ibogaine increased substance P-like immunoreactivity. These data suggest that substance P systems may contribute to the effects of ibogaine and cocaine treatment.

Animals↗
PubMed1976

Iron deficiency and behavior.

The literature bearing on the behavioral correlates of sideropenia in animals and man is reviewed. There is evidence to support the contention that sideropenia, per se, is causally related to the subjective complaints of the iron-deficient and/or anemic individual. And, although important biochemical pathways involving electron transport, catecholamine catabolism, and porphyrin synthesis have been shown to be deranged in iron-deficient animals and human beings, the role of these alterations in any putative behavioral aberration is conjectural at present. Given the high prevalence of iron deficiency in the world's population, these issues should be addressed by appropriate biochemical and psychologic studies in animals and human beings.

Adult↗
PubMedDate not supplied

New atypical antipsychotic medications.

Conventional antipsychotics were the first treatments effective in controlling psychotic symptomatology and revolutionized management of psychotic disorders when introduced in the 1950's. The use of these agents has, however, been marked by several shortcomings, including limited efficacy in treating the negative and cognitive symptoms of schizophrenia, and by significant extrapyramidal and other side-effects. There appears to be justifiable excitement about the introduction of the newer atypical antipsychotics, which may represent the second pharmacological revolution in the treatment of psychotic disorders. But how are these agents really different from their neuroleptic predecessors? How is their pharmacological profile different? Are there clear differences in efficacy? How do side-effect profiles differ? These issues are reviewed in this manuscript. Atypical agents are pharmacologically distinct from their neuroleptic predecessors. Their primary advantage is their superior side effect profiles, particularly with regard to EPS. The implications of EPS reduction touch virtually every domain of pathology in schizophrenia, including short- and long-term movement disorders, negative symptoms, noncompliance, relapse rate, cognitive dysfunction, and dysphoria. It should be emphasized that while atypical antipsychotics share some clinical attributes, there are substantial clinical differences between them as well. These differences are reviewed in this article as well. The drugs' unique profiles with regard to other side effects may make it possible to tailor treatment more individually to patients. Further refinement of our understanding of the clinical utility of these drugs awaits their widespread use in mainstream clinical settings. Controlled studies comparing them to one another should be of particular interest.

Antipsychotic Agents↗
PubMed2001

H reflex behavior in Parkinson's disease patients and patients with extrapyramidal and pyramidal signs combined.

The H reflex was elicited in 21 normal subjects, 48 patients with Parkinson's disease (PD) and 22 patients with pyramidal and extrapyramidal signs combined (PESC). In most normal subjects (90.5%), in 29.2% of PD patients and 54.5% of patient with PESC the threshold for sensory fibers was lower than for motor fibers, and the H reflex was obtained before the M response for all duration stimuli in both legs. In 9.5% of normal subjects, 39.6% of PD patients with mild and moderate rigidity (according to the motor part of UPDRS) and 31.8% of patients with PESC, the threshold for the H reflex and M response was the same or the M response threshold was lower in at least one of the legs for short stimulus duration (0.1-0.2 ms). In 31.2% of PD patients (most of them with severe rigidity) and 13.7% of patients with PESC, the threshold for M response was lower for all stimulus duration in at least one of the legs, and it was obtained before H reflex. These very significant differences in behavior of the H reflex in PD patients (Fisher exact test, p<0.0001) that almost disappear in patients with PESC, could be possibly explained by changes in agonist-antagonist inhibition.

Adult↗
PubMed1999

Extrapyramidal and neuroendocrine effects of AM404, an inhibitor of the carrier-mediated transport of anandamide.

A selective inhibitor of the carrier-mediated transport of endogenous cannabinoids, N-(4-hydroxyphenyl)-arachidonylethanolamide (AM404), has been recently synthesized and proposed as a useful tool for studying the physiological effects of endogenous cannabinoids and as a potential therapeutic agent in a variety of diseases. In the present study, we have examined the effects of this compound in two important brain processes in which a role for anandamide and other endogenous cannabinoids has been claimed: neuroendocrine regulation and extrapyramidal motor activity. A single and well-characterized dose of AM404, which presumably resulted in a significant elevation of the levels of endogenous cannabinoids, produced a marked decrease in plasma prolactin (PRL) levels, with no changes in luteinizing hormone (LH) levels. This decrease in PRL levels was accompanied by an increase in the activity of tyrosine hydroxylase (TH) in the medial basal hypothalamus. Both decreased PRL secretion and increased hypothalamic TH activity have been reported to occur after the administration of anandamide. Administration of AM404 also produced a marked motor inhibition in the open-field test, as also reported for anandamide, with a decrease in ambulatory and exploratory activities and an increase in the time spent in inactivity. This was accompanied by a decrease in the activity of TH in the substantia nigra, an effect also previously observed for anandamide.

3,4-Dihydroxyphenylacetic Acid↗