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 1,387 records · Page 77Linked to original sources
PubMed1982

[Encephalitis of the basel ganglia associated with mumps].

Two weeks after epidemic parotitis a 10-year old boy developed an acute extrapyramidal syndrome together with pyramidal tract signs but without impairment of consciousness. The CSF showed mild pleocytosis. The CT of the brain exhibited a well defined circumscribed and symmetrical swelling and hypodensity of the basal ganglia and of the internal capsule. Only slight and transient dysrhythmia was to be found in the EEG. Therapy with Prednisolone, Biperidene and Tiapride resulted in regression of symptoms. But one year later rigor and pyramidal tract signs remained evident in spite of intensive physiotherapy and logopaedic measures. Residual symmetric atrophia of the basal ganglia became evident in the CT by dilatation of the anterior horns of the lateral ventricles caused by lacking of the vault of the caudate nuclei heads.

Basal Ganglia Diseases↗
PubMed1977

Aging and extrapyramidal function.

Measurements on human brain samples of some enzymes concerned with neurotransmitter synthesis suggest serious losses with age. The most severe loss found was that in striatal tyrosine hydroxylase activity, the rate-controlling enzyme in the synthesis of dopamine. Cell counts in the substantia nigra where this dopaminergic tract originates suggest that the decrease in enzyme activity is partly due to cell loss, but must largely reflect decreased activity of residual cells. It is possible that this loss may account for some of the difficulties in movement seen in aged individuals and that it might be less if pigment formation in these cells could be inhibited.

Adolescent↗
PubMed1985

[An autopsy case with peculiar acidophilic bodies in the dentate nucleus and brain stem, associated with degeneration of the pyramidal-extrapyramidal systems].

Case S.S. 59 years of age, male. At the age of 25, he had admitted to sanatorium for 7 years because of pulmonary tuberculosis. After his discharge, at the age of 45, he had started complaining of depressive mood or the idea of suicide and admitted to a mental hospital. Psychiatric diagnosis was depression and slight mental retardation. Shortly after, his depressive mood was improved, but his hypochondriac attitude was unchanged. No tendency toward dementia was proven. At the age of 54, he became enable to walk. Neurologically, pyramidal and some sort of extrapyramidal signs, dysarthria, disturbance of swallowing, fecal and urinary incontinence became apparent. Laboratory data showed scarcely any abnormality. At the age of 59, he died of bronchopneumonia. Neuropathologically, moderate degeneration of dentate nucleus, slight degeneration of pyramidal tract from medulla oblongata to spinal cord, striatum, substantia nigra were found. Neither senile plaques nor neurofibrillary changes could be seen throughout central nervous system. The most important finding is the presence of peculiar acidophilic bodies. They are round or oval, 10 approximately 20 mu in diameter and distributed in dentate nucleus, oculomotor nucleus, central grey of midbrain, superior colliculus, putamen, pallidum, subthalamic nucleus, Zona incerta, hypothalamus, Locus coeruleus, reticular formation of midbrain and pons, pontine nucleus, raphe nucleus, vestibular nucleus, inferior olive in order of number of the bodies. These bodies are scattered in so-called ground substance, and have no relations to any cell bodies or cell processes.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain Stem↗
PubMed1987

Pedunculopontine tegmental nucleus of the rat: cytoarchitecture, cytochemistry, and some extrapyramidal connections of the mesopontine tegmentum.

The pedunculopontine tegmental nucleus (PPTn) was originally defined on cytoarchitectonic grounds in humans. We have employed cytoarchitectonic, cytochemical, and connectional criteria to define a homologous cell group in the rat. A detailed cytoarchitectonic delineation of the mesopontine tegmentum, including the PPTn, was performed employing tissue stained for Nissl substance. Choline acetyltransferase (ChAT) immunostained tissue was then analyzed in order to investigate the relationship of cholinergic perikarya, dendritic arborizations, and axonal trajectories within this cytoarchitectonic scheme. To confirm some of our cytoarchitectonic delineations, the relationships between neuronal elements staining for ChAT and tyrosine hydroxylase were investigated on tissue stained immunohistochemically for the simultaneous demonstration of these two enzymes. The PPTn consists of large, multipolar neurons, all of which stain immunohistochemically for ChAT. It is present within cross-sections that also include the A-6 through A-9 catecholamine cell groups and is traversed by catecholaminergic axons within the dorsal tegmental bundle and central tegmental tract. The dendrites of PPTn neurons respect several nuclear boundaries and are oriented perpendicularly to several well-defined fiber tracts. Cholinergic axons ascend from the mesopontine tegmentum through the dorsal tegmental bundle and a more lateral dorsal ascending pathway. A portion of the latter terminates within the lateral geniculate nucleus. It has been widely believed that the PPTn is reciprocally connected with several extrapyramidal structures, including the globus pallidus and substantia nigra pars reticulata. Therefore, the relationships of pallidotegmental and nigrotegmental pathways to the PPTn were investigated employing the anterograde autoradiographic methodology. The reciprocity of tegmental connections with the substantia nigra and entopeduncular nucleus was investigated employing combined WGA-HRP injections and ChAT immunohistochemistry. The pallido- and nigrotegmental terminal fields did not coincide with the PPTn, but, rather, were located just medial and dorsomedial to it (the midbrain extrapyramidal area). The midbrain extrapyramidal area, but not the PPTn, was reciprocally connected with the substantia nigra and entopeduncular nucleus. We discuss these results in light of other cytoarchitectonic, cytochemical, connectional, and physiologic studies of the functional anatomy of the mesopontine tegmentum.

Animals↗
PubMed1966

Neurochemical bases of tremor and other disorders of movement.

Monkeys inflicted with specific unilateral electrolytic lesions in the upper brain stem developed extrapyramidal disorders. Hypokinesia of the limbs was associated contralaterally with a lesion of the substantia nigra and depletion of striatal dopamine. Choreiform movements were observed in animals that had, contralaterally, a lesion severing the most dorsomedial fibres of the cerebral peduncle and the rubro-tegmentospinal tract, associated with depletion of striatal serotonin. Monkeys showing sustained postural tremor and hypokinesia had lesions affecting these three tracts contralaterally and loss of striatal dopamine and serotonin on the lesion side. Of many drugs tested, only harmaline and harmine affected the dyskinesias. The nigrostriatal fibres appear to be dopaminergic; the cerebral peduncular (dorsomedial) fibres, serotoninergic. The role of striatal dopamine and serotonin in the control of normal movements and posture of the limbs represents the first directly demonstrated function of these amines in the central nervous system.

Alkaloids↗
PubMed1988

Medullary and spinal efferents of the pedunculopontine tegmental nucleus and adjacent mesopontine tegmentum in the rat.

The medullary and spinal efferents of the pedunculopontine tegmental nucleus and adjacent mesopontine tegmentum were investigated by employing (1) the anterograde autoradiographic methodology and (2) the retrograde transport of HRP and/or WGA-HRP in combination with choline acetyltransferase immunohistochemistry. The anterograde experiments identified five descending pathways from the mesopontine tegmentum: (1) Probst's tract, which descends in the dorsolateral reticular formation in close relation to the nucleus of the solitary tract; (2) a ventrolateral branch of Probst's tract that extends ventrolaterally alongside the spinal trigeminal nucleus; (3) a ventromedial branch of Probst's tract that extends ventromedially through the gigantocellular field of the medulla; (4) the medial reticulospinal tract, which descends in parallel with the medial longitudinal fasciculus and turns ventrolaterally along the dorsal surface of the inferior olive to enter the ventrolateral funiculus of the spinal cord; and (5) a crossed ventromedial pathway, which descends in a ventral paramedian position through the magnocellular field of the medulla. The origins of these pathways reflected a rough lateral-to-medial topography of mesopontine tegmental cell groups. The parabrachial nucleus, situated furthest laterally, for example, projected primarily through Probst's tract and its ventrolateral branch. The pedunculopontine tegmental nucleus, midbrain extrapyramidal area, and the subceruleal region, situated more medially, projected descending axons largely through the ventromedial branch of Probst's tract. The pontine tegmental field, situated furthest medially and ventromedially, was the largest contributor to the medial reticulospinal tract. The retrograde transport experiments confirmed these general organizational features. The combination of retrograde transport with choline acetyltransferase immunohistochemistry established that the cholinergic pedunculopontine tegmental nucleus contributes a large portion to the mesopontine tegmental innervation of the medullary reticular formation. A much smaller number of cholinergic pedunculopontine neurons project as far as the spinal cord. Spinal projections from the mesopontine tegmentum originate largely from non-cholinergic neurons of the midbrain extrapyramidal area, subceruleal region, Kölliker-Fuse division of the parabrachial nucleus, and pontine tegmental field.

Animals↗
PubMed2006

Efficacy and adverse effects of atypical antipsychotics for dementia: meta-analysis of randomized, placebo-controlled trials.

OBJECTIVE: Atypical antipsychotic medications are widely used to treat delusions, aggression, and agitation in people with Alzheimer disease (AD) and other dementia. Several clinical trials have not shown efficacy, and there have been concerns about adverse events. The objective of this study was to assess the evidence for efficacy and adverse events of atypicals for people with dementia. METHODS: MEDLINE, the Cochrane Register of Controlled Trials, meetings, presentations, and information obtained from sponsors were used in this study. Published and unpublished randomized, placebo-controlled, double-blind, parallel-group trials in patients with AD or dementia of atypical antipsychotics marketed in the United States were studied. Clinical and trials characteristics, outcomes, and adverse events were extracted. Data were checked by a second reviewer. Fifteen trials including 16 contrasts of atypical antipsychotics with placebo met selection criteria: aripiprazole (k = 3), olanzapine (k = 5), quetiapine (k = 3), and risperidone (k = 5). A total of 3,353 patients were randomized to drug and 1,757 to placebo. Standard meta-analysis methods were used to summarize outcomes. RESULTS: Quality of the reporting of trials varied. Efficacy on rating scales was observed by meta-analysis for aripiprazole and risperidone, but not for olanzapine. Response rates were frequently not reported. There were smaller effects for less severe dementia, outpatients, and patients selected for psychosis. Approximately one-third dropped out without overall differences between drug and placebo. Adverse events were mainly somnolence and urinary tract infection or incontinence across drugs, and extrapyramidal symptoms or abnormal gait with risperidone or olanzapine. Cognitive test scores worsened with drugs. There was no evidence for increased injury, falls, or syncope. There was a significant risk for cerebrovascular events, especially with risperidone; increased risk for death overall was reported elsewhere. CONCLUSIONS: Small statistical effect sizes on symptom rating scales support the evidence for the efficacy of aripiprazole and risperidone. Incomplete reporting restricts estimates of response rates and clinical significance. Dropouts and adverse events further limit effectiveness. Atypicals should be considered within the context of medical need and the efficacy and safety of alternatives. Individual patient meta-analyses are needed to better assess clinical significance and effectiveness.

Aged↗
PubMed1995

In vivo diagnosis of Hallervorden-Spatz disease.

The authors present the MRI findings of two children with insidious walking difficulties, signs of corticospinal tract involvement, and signs and symptoms of extrapyramidal dysfunction such as rigidity and generalized dystonia, the latter with predominance of oromandibular involvement. In one child, MRI revealed prominent hypo-intensity in the globus pallidus and in the substantia nigra on T2-weighted spin echo images, consistent with iron deposition and thus with previous post-mortem findings of Hallervorden-Spatz disease. In the other case, the hypo-intensity was restricted to the globus pallidus, in which a small area of hyperintensity in its internal segment was demonstrated--the so called 'eye-of-the-tiger' sign. The authors propose that a combination of previously mentioned neurological signs with these specific MRI findings is highly suggestive of an in vivo diagnosis of the late infantile type of HSD.

Fatal Outcome↗
PubMedDate not supplied

[Neurological examinations of workers with chronic exposure to manganese dioxide during the production of piles and batteries].

The authors examined 118 workers making piles and batteries under conditions of exposure to toxic action of manganese dioxide dust. Neurological and EEG investigations showed presence of pyramidal tract lesion signs in 16.9% of workers, extrapyramidal syndromes in 6.8%, peripheral nervous system involvement in 13.5% and neurotic complaints in 42.4%. The frequency of neurological manifestations was directly proportional to the duration of work in exposure. The difference in the frequency of neurotic complaints and signs of peripheral and central nervous system damage was statistically significant between the group exposed to manganese dioxide and the control group. EEG investigations were performed in 51 workers and abnormalities were found in 21 cases.

Adult↗
PubMedDate not supplied

["Abnormal" neurologic findings in the "healthy" elderly].

Neuropathological changes and clinical neurological findings of the nervous system of healthy, old people (more than 80 years old) are referenced according to the literature. In addition, the results of a clinical neurological examination of 86 healthy senior citizens (average age: 83.6 years) are demonstrated. The respective findings are summarized in a table according to their frequency. The involution of the human nervous system with age results neuropathologically and clinically-neurologically in damage to the frontal lobe (disinhibition of archaic reflexes), the extrapyramidal system (Parkinsonian walking pattern), the posterior tract of the spine (unsteadiness of walking), and the peripheral nervous system (e.g. loss of the achilles tendon reflex). The Parkinsonian-like walking pattern of the healthy old-aged human is thought to be a disinhibition of an archaic pattern of posture and movement. Brief suggestions for differential diagnosis and therapy are presented.

Aged↗
PubMed1993

Proximal and distal impairments in rat forelimb use in reaching follow unilateral pyramidal tract lesions.

Although it was once thought that the corticospinal (pyramidal) tract was the main substrate of voluntary movement, the extent to which it is involved in the control of proximal vs. distal musculature, independent finger movements, and movements characteristic of different species of animals now is unclear. The objective of this study was to examine the effects of pyramidal tract lesions on skilled forelimb use in rats. In addition, cell morphology in motor cortex following lesions was examined. Naive and trained rats received unilateral pyramidal sections just rostral to the pyramidal decussation. Performance was assessed and filmed on two reaching tasks. Measures of reaching consisted of success in obtaining food, kinematic analysis of limb trajectory and velocity, and qualitative evaluation of 10 movement components comprising a reach. Pyramidal tract lesions only impaired reaching for single food pellets. Almost all movements comprising a reach, except digit opening, were impaired, including lifting, aiming, pronating and supinating the limb, and releasing food. Although success in limb use was unchanged over the 180 day observation period, there were significant improvements in the qualitative features of limb use. Histologically, the morphology of pyramidal cells in the forelimb area ipsilateral to the lesion seemed normal. Rats with additional damage to adjacent structures, such as the medial lemniscus and olivary complex, were much more severely impaired on the reaching tasks, and displayed similar impairments as judged by qualitative and kinematic measures. The results demonstrate that a number of movements involved in independent limb use are chronically impaired by pyramidal tract lesions in the rat. Nevertheless, significant use of the limb is possible, due perhaps to both the contribution of extrapyramidal motor systems and the influence of the remaining pyramidal system through its extrapyramidal connections. The results not only show that the rat pyramidal tract supports functions very similar to those of primates and thus might provide a good model for some aspects of pyramidal tract dysfunctions, but also they argue that the pyramidal tract is involved in both proximal and distal limb movements.

Animals↗
PubMed1999

Olanzapine: a basic science update.

Olanzapine, an atypical antipsychotic, has a broad receptor binding profile, which may account for its pharmacological effects in schizophrenia. In vitro receptor binding studies showed a high affinity for dopamine D2, D3, and D4 receptors; all 5-HT2 receptor subtypes and the 5-HT6 receptor; muscarinic receptors, especially the M1 subtype: and alpha 1-adrenergic receptors. In vivo studies showed that olanzapine had potent activity at D2 and 5-HT2A receptors, but much less activity at D1 and muscarinic receptors, and that it inhibited dopaminergic neurons in the A10 but not the A9 tract, suggesting that this agent will not cause extrapyramidal side-effects (EPS). Microdialysis studies showed that olanzapine increased the extracellular levels of norepinephrine and dopamine, but not 5-HT, in the prefrontal cortex, and increased extracellular dopamine levels in the neostriatum and nucleus accumbens, areas of the brain associated with schizophrenia. Studies of gene expression showed that olanzapine 10 mg/kg also increased Fos expression in the prefrontal cortex, the dorsolateral striatum, and the nucleus accumbens. These findings are consistent with the effectiveness of olanzapine on both negative and positive symptoms and suggest that, with careful dosing, olanzapine should not cause EPS.

Animals↗
PubMed1975

Pallido-pyramidal syndrome treated with levodopa.

Two siblings are reported who developed classical signs and symptoms of Parkinsonism in the first decade of life. In addition, they had evidence of cortical spinal tract disease, thus putting them in the category of Davison's pallido-pyramidal syndrome. Both deteriorated to the point of a non-productive existence until the institution of levodopa treatment, at the ages of 18 and 20 years. The response of the extrapyramidal signs plus the lack of response of the pyramidal tract signs demonstrate the specificity of a pharmacological agent in certain areas of the nervous system. The rapid response of the female patient to very low doses of levodopa is unusual in our experience. Both patients have remained well for eight months after initiation of treatment.

Adolescent↗
PubMed1986

Intracortical stimulation in pyramidotomized monkeys.

In order to examine, separately, the organizations of pyramidal and extrapyramidal projections from the primary motor cortex, efforts were made to map the forelimb area of two rhesus monkeys with microstimulation before and after unilateral pyramidotomy. However, microstimulation was not effective in evoking motor responses following complete pyramidal tract section. Movements were evoked using a modified intracortical electrode with a large exposed tip and using stimulation parameters similar to those used for surface stimulation. The results from this modified intracortical stimulation generally agree with those from surface stimulation studies in that: (1) the extrapyramidal topography is similar to the normal motor cortex topography and (2) while peripheral responses can be evoked from the cortex following pyramidotomy, greater spatial and temporal summation are necessary to evoke these responses. In addition, the modified intracortical technique revealed a more widespread post-pyramidotomy digit representation than observed previously with surface stimulation. Results from an incomplete pyramidal tract lesion suggest that recovery of motor function may include plastic changes in surviving corticospinal axons.

Animals↗
PubMed1976

Familial unusual encephalopathy of Binswanger's type without hypertension.

Clinical and pathological studies have been conducted on two brothers with unusual encephalopathy of Binswanger's type. The disease started in the third decade with steady progressive course leading to death in eight or nine years. The clinical picture was summarized as a combination of organic dementia, extrapyramidal disorders associated with pseudobulbar symptoms and marked pyramidal tract signs. The blood pressure remained always normal during the course. Pathologically, there were diffuse and focal demyelination with sparing of U-fibers, multiple small foci of perivascular softening in the cerebral white matter and in the basal ganglia and severe arteriosclerotic changes of memingeal small arteries and long arteries with 100 to 400 micron caliber in the cerebral white matter. Vessel changes consisted of fibrous intimal proliferation, severe hyalinosis and splitting of intima and/or internal elastic membrane. The histopathological process belonged to the category of subcortical arteriosclerotic encephalopathy of Binswanger's type. There has been some discussion as to differential diagnosis among various forms of vasculitis such as cerebral endangiitis obliterans, periarteritis nodosa, systemic lupus erythematosus, rheumatic vascular disease and giant cell arteritis.

Adult↗
PubMed1991

Clozapine-induced neuroleptic malignant syndrome.

Neuroleptic malignant syndrome (NMS), a rare but serious side effect of psychotropic drugs, is usually attributed to blockade of striatal and hypothalamic dopaminergic tracts. Clozapine is an atypical antipsychotic that has minimal extrapyramidal effects and might not be expected to cause NMS. The authors report the development of NMS in a 30-year-old white man after three 25-mg clozapine doses. To their knowledge, this is the first case of NMS linked with clozapine in which concurrent psychotropic medications cannot be implicated.

Adult↗
PubMedDate not supplied

[Dyskinetic-athetosic syndrome in a patient with prior radiculo-myelo-encephalopathy of probable viral origin. Therapeutic guidelines with levodopa and preliminary results].

The regulation of skeletal muscle tone and of the automatic and half-automatic movements by the extrapyramidal system in briefly discussed. The essential importance to keep separated the akinetic-hypertonic syndromes from the hypotonic-hyperkinetic ones is further confirmed. In fact two different chemical mediating agents work separately in these two cases: the Dopamine for the Nigro-Striatal system and the Ach for other tracts whose anatomy is still not well known, but which surely belong to the extrapyramidal system. Further more a clinical case of dyskinetic-athetosic post-infective syndrome, successfully treated with L.D., is discussed. The effectiveness of neuroleptic drugs in these hypotonic-hyperkinetic syndrome is stressed while they cause and worsen extra-pyramidal symptoms such as hypertonia and akynesia (hypertonic akinetic s.).

Athetosis↗