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physostigmine/atrofia

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Neuropathy-induced apoptosis: protective effect of physostigmine.

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Traumatic, infectious, metabolic, and chemical noxa to the nervous system are the etiology of a crippling disease generally termed neuropathy. Motor disorders, altered sensibility, and pain are the pathognomonic traits. Cellular alterations induced by this chronic pathology include mitochondrial

Physostigmine in familial ataxias.

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Physostigmine was given to 12 patients with various spincerebellar degenerations, and neurologic examinations were recorded on video tapes and assessed on a semiquantitative scale. Forty minutes after a single dose, the scores improved by 35.7 +/- 4.7 percent (means +/- SEM). Eight patients were

Long-term outpatient treatment of senile dementia with oral physostigmine.

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The authors describe five patients with senile dementia of the Alzheimer type (SDAT) who were treated with oral physostigmine from 1 to 3 3/4 years. An abbreviated form of the Buschke selective reminding test was used to assess the patients' short-term verbal memory at periodic clinic visits.

Oral physostigmine as treatment for dementia of the Alzheimer type: a long-term outpatient trial.

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Six patients with dementia of the Alzheimer type (DAT), treated with oral physostigmine and followed from 9 to 27 months (mean +/- SD, 17.8 +/- 7.3 months), were matched for sex, age, initial degree of dementia, and length of follow-up with six control patients who did not receive oral
Dry mouth produces a deterioration in oral health and impairs quality of life. There is a need for a novel approach to the pharmacological treatment of dry mouth. With a view to enhancing the cholinergic drive on minor salivary glands, whilst at the same time minimising adverse systemic effects, the

Physostigmine reverses cognitive dysfunction caused by moderate hypoxia in adult mice.

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BACKGROUND Cognitive changes associated with moderate hypoxia in rodents may result from the diminished functioning of central cholinergic neurotransmission. We designed this study to examine whether treatment with physostigmine (PHY), an acetylcholinesterase inhibitor, could improve the impairment
Degeneration of the cholinergic magnocellular neurons in the basal forebrain and their cortical projections is a major feature of the neuropathology of Alzheimer's disease. In the present study, two experiments examined the disruptive effects on visual attentional performance of two different
Light microscopy was undertaken on sections from the caudal flexure of the duodenum and the terminal ileum proximal to the ileocaecal fold in 5 control horses, 5 horses with acute grass sickness (AGS), and 5 horses with chronic grass sickness (CGS). With the exception of the ileal submucous plexus

Determination of physostigmine in plasma and cerebrospinal fluid by liquid chromatography with electrochemical detection.

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Physostigmine (Phy) was determined in plasma and cerebrospinal fluid (CSF) by HPLC with electrochemical detection, with use of a normal-phase column and methanolic sodium acetate buffer, pH 4.6. The detection limit of the method was 0.5 micrograms/L for a 2-mL sample of plasma or 0.5 mL of CSF.
Delirium is a common problem in ICU patients, resulting in prolonged ICU stay and increased mortality. A cholinergic deficiency in the central nervous system is supposed to be a relevant pathophysiologic process in delirium. Acetylcholine is a major transmitter of the parasympathetic nervous system

Hyperactive vestibulo-ocular reflex in cerebellar degeneration: pathogenesis and treatment.

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We studied a patient with a cerebellar degeneration and hyperactive vestibulo-ocular reflex (VOR). He complained of oscillopsia and blurred vision with head movement. A twofold increase in VOR gain (peak eye velocity/peak head velocity) at high frequencies was associated with a VOR time constant of

Neuroendocrine responses to physostigmine in Alzheimer's disease.

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To assess central nervous system cholinergic neuroendocrine regulation in Alzheimer's disease (AD), we measured plasma arginine vasopressin, beta-endorphin, and epinephrine responses to a cholinergic challenge elicited by intravenous administration of the acetylcholinesterase inhibitor physostigmine

Acetylcholinesterase inhibitors reduce neuroinflammation and -degeneration in the cortex and hippocampus of a surgery stress rat model.

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Exogenous stress like tissue damage and pathogen invasion during surgical trauma could lead to a peripheral inflammatory response and induce neuroinflammation, which can result in postoperative cognitive dysfunction (POCD). The cholinergic anti-inflammatory pathway is a neurohumoral mechanism that

Histology of the iris in geese and ducks photosensitized by ingestion of Ammi majus seeds.

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Geese and ducks were photosensitized by the ingestion of Ammi majus seeds, and exposure to sunlight. Mydriasis was a characteristic clinical feature of this syndrome in both species. Histologically the iris of the affected birds showed vacuolisation and varying degrees of atrophy of the muscle of

Pharmacological evaluation of the cholinergic system in progressive supranuclear palsy.

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Severe cholinergic loss occurs in the brains of patients with progressive supranuclear palsy. To evaluate the functional implications of this neuronal deficit, dose-response curves were obtained in patients with progressive supranuclear palsy and normal control subjects undergoing intravenous
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