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At least 1,351 records · Page 75Linked to original sources
PubMed1984

'Dystonia'-like postural asymmetry after microinjection of ACTH N-terminal fragments but not after ACTH1-39 in rat brainstem suggests role of neuropeptide mutation in genetic movement disorder.

N-terminal fragments of adrenocorticotropin (ACTH) was reported to exert potent 'dystonia'-like effects on posture and locomotion following a unilateral microinjection into the rat brainstem. The high reliability of this phenomenon provided a suitable animal model for the study of these actions. The present structure-activity study showed that ACTH1-39, in contrast to its N-terminal fragments, did not have any 'dystonic' actions, however transient or slight. Thus, the folded conformation of [1-39] in vivo may prevent its N-terminal region from interacting with those CNS sites that trigger 'dystonic' actions. These results suggest that genetically-linked human dystonia may have originated in part as a consequence of a mutation in the processing of the ACTH molecule, resulting in an aberrantly-folded conformation that allows its N-terminal region to trigger the dystonic syndrome.

Adrenocorticotropic Hormone↗
PubMed2006

Basal ganglia oscillations and pathophysiology of movement disorders.

Low frequency rest tremor is one of the cardinal signs of Parkinson's disease and some of its animal models. Current physiological studies and models of the basal ganglia differ as to which aspects of neuronal activity are crucial to the pathophysiology of Parkinson's disease. There is evidence that neural oscillations and synchronization play a central role in the generation of the disease. However, parkinsonian tremor is not strictly correlated with the synchronous oscillations in the basal ganglia networks. Rather, abnormal basal ganglia output enforces abnormal thalamo-cortical processing leading to akinesia, the main negative symptom of Parkinson's disease. Parkinsonian tremor has probably evolved as a downstream compensatory mechanism.

Animals↗
PubMed2005

Cholinergic nicotinic receptor involvement in movement disorders associated with Lewy body diseases. An autoradiography study using [(125)I]alpha-conotoxinMII in the striatum and thalamus.

The presence of alpha6 subunit containing nicotinic acetylcholine receptors on nigrostriatal dopaminergic neurons has been demonstrated in rodents and monkeys. [(125)I]alpha-conotoxinMII is a radioligand that binds to alpha6, and also alpha3 subunits of nicotinic acetylcholine receptors (nAChRs). In the present study, we have compared the distribution of [(125)I]alpha-conotoxinMII binding in post mortem human tissue from four groups of patients: individuals with dementia with Lewy bodies displaying extra-pyramidal features (DLB + EPF), DLB without extra-pyramidal features (DLB - EPF) Parkinson's disease without dementia (PD) and age-matched controls. Reduced binding was observed in the putamen and caudate in PD and both DLB groups. In DLB patients, the decline was greater in DLB + EPF compared to DLB - EPF group. The declines in nicotinic receptor binding in the striatum were in part paralleled by reductions in the striatal dopamine transporter. In the thalamus, [(125)I]alpha-conotoxinMII binding was significantly reduced in the centromedian nucleus in both DLB groups, and also in the parafascicular nucleus in the DLB - EPF group. In DLB + EPF and PD patients, there was decreased binding in the ventral lateral nucleus. This study demonstrates alterations of alpha6 and/or alpha3 nAChRs binding in DLB and PD, which are likely to relate to extra-pyramidal symptoms.

Aged↗
PubMed2005

Alzheimer's disease: an intracellular movement disorder?

Axonal transport is essential for maintaining the structure and function of nerve cells. Deficient axonal transport has been implicated in several neurodegenerative diseases, including Alzheimer's disease (AD). In addition to a disturbed cytoskeleton and other abnormalities observed in AD that are suggestive of axonal transport deficits, several AD-related proteins are implicated in the regulation of axonal transport. A recent study has demonstrated that the axonal transport deficit occurs early in the course of AD, preceding amyloid pathology substantially in mouse models of AD; more importantly, the study showed that reduced axonal transport leads to increased amyloid beta production and deposition. These data place axonal transport deficits at a central point in the pathogenesis of AD.

Alzheimer Disease↗
PubMed2005

Parasomnias and other sleep-related movement disorders.

Parasomnias are common clinical complaints. Formal sleep evaluation including PSG is indicated for parasomnias that are violent and potentially injurious; disruptive to the bed partner or other household members; accompanied by excessive daytime sleepiness; or associated with medical,psychiatric, or neurologic symptoms or findings [2]. Multiple sleep latency testing should be considered for patients who have complaints of excessive daytime sleepiness. An extensive history, including medical, neurologic,psychiatric, and sleep disorder, and a review of medication, alcohol, illicit drug use, and family history of parasomnias, may provide useful clues. Distinguishing between a parasomnia and a seizure may be difficult as both can present as recurrent, stereotypical behaviors. Evaluation may be aided by an expanded EEG montage during overnight PSG studies.

Humans↗
PubMed1994

Choreoathetotic movement disorder in a boy with Mycoplasma pneumoniae encephalitis.

We present a case of a 10-year-old boy who presented to the emergency department with high fever, acute choreoathetosis, weakness, and dysarthria. An EEG showed generalized slowing, and serologies defined an acute case of Mycoplasma pneumoniae encephalitis. This report describes the most common presentations, therapy, and outcomes of M pneumoniae encephalitis.

Acute Disease↗
PubMed2002

Isolated orofacial dyskinesia: a methylphenidate-induced movement disorder.

We report a case of orofacial dyskinesia in a 6-year-old female with attention-deficit-hyperactivity disorder who received a low dose of methylphenidate. The orofacial dyskinesia appeared immediately and subsided rapidly on the same day in an "on-off" fashion and on 3 separate days when methylphenidate was taken. To our knowledge this particular side effect has not been described previously and might represent an unusual type of brain response or sensitivity.

Attention Deficit Disorder with Hyperactivity↗