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Dextromethorphan for the Treatment of Parkinson's Disease and Similar Conditions of the Nervous System

11:14 EDT 25th May 2013 | BioPortfolio

Summary

This study is designed to determine whether dextromethorphan, a drug commonly found in cough medicine, is beneficial and safe for the treatment of Parkinson's disease and other diseases that might share biochemical abnormalities with Parkinson's disease.

Patients with Parkinson's disease are missing the chemical neurotransmitter dopamine. This occurs as a result of destructive changes in an area of the brain responsible for making dopamine, the basal ganglia. Rhythmical muscular tremors, rigidity of movement, shuffling footsteps, droopy posture, and a mask-like expression on the face characterize Parkinson's disease.

Researchers believe that dextromethorphan may be able to safely modify psychomotor function of patients with Parkinson's Disease.

Description

The ability of the putative excitatory amino acid receptor antagonist, dextromethorphan, to modify psychomotor function safely in patients with neurodegenerative disease will be evaluated using a modified double-blind placebo-controlled design. Therapeutic activity will be rated at various doses by means of standard motor and cognitive performance scales. Safety will be assessed at frequent intervals by clinical observation and laboratory tests.

Study Design

Endpoint Classification: Safety/Efficacy Study, Primary Purpose: Treatment

Conditions

Neurodegenerative Disease

Intervention

dextromethorphan

Location

National Institute of Neurological Disorders and Stroke (NINDS)
Bethesda
Maryland
United States
20892

Status

Completed

Source

National Institutes of Health Clinical Center (CC)

Results (where available)

View Results

Links

Medical and Biotech [MESH] Definitions

Sandhoff Disease

An autosomal recessive neurodegenerative disorder characterized by an accumulation of G(M2) GANGLIOSIDE in neurons and other tissues. It is caused by mutation in the common beta subunit of HEXOSAMINIDASE A and HEXOSAMINIDASE B. Thus this disease is also known as the O variant since both hexosaminidase A and B are missing. Clinically, it is indistinguishable from TAY-SACHS DISEASE.

Lewy Body Disease

A neurodegenerative disease characterized by dementia, mild parkinsonism, and fluctuations in attention and alertness. The neuropsychiatric manifestations tend to precede the onset of bradykinesia, MUSCLE RIGIDITY, and other extrapyramidal signs. DELUSIONS and visual HALLUCINATIONS are relatively frequent in this condition. Histologic examination reveals LEWY BODIES in the CEREBRAL CORTEX and BRAIN STEM. SENILE PLAQUES and other pathologic features characteristic of ALZHEIMER DISEASE may also be present. (From Neurology 1997;48:376-380; Neurology 1996;47:1113-1124)

Dextrorphan

Dextro form of levorphanol. It acts as a noncompetitive NMDA receptor antagonist, among other effects, and has been proposed as a neuroprotective agent. It is also a metabolite of DEXTROMETHORPHAN.

Sialic Acid Storage Disease

Autosomal recessive neurodegenerative disorders caused by lysosomal membrane transport defects that result in accumulation of free sialic acid (N-ACETYLNEURAMINIC ACID) within the lysosomes. The two main clinical phenotypes, which are allelic variants of the SLC17A5 gene, are ISSD, a severe infantile form, or Salla disease, a slowly progressive adult form, named for the geographic area in Finland where the kindred first studied resided.

Neuronal Ceroid-lipofuscinoses

A group of severe neurodegenerative diseases characterized by intracellular accumulation of autofluorescent wax-like lipid materials (CEROID; LIPOFUSCIN) in neurons. There are several subtypes based on mutations of the various genes, time of disease onset, and severity of the neurological defects such as progressive DEMENTIA; SEIZURES; and visual failure.

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