corticobasal degeneration


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corticobasal degeneration

a rare, progressive disease (considered by some a variant of Parkinson disease) involving both cerebral cortex and extrapyramidal structures; clinically manifest as disturbances of voluntary movements and rigidity; pathologic characteristics include degeneration of the cerebral cortex with balloon neurons and degeneration of the substantia nigra; apraxia, cortical sensory loss, myoclonus, and phantom limb syndrome have been reported.

corticobasal degeneration

A rare idiopathic cerebrodegenerative “tauopathy” which is difficult to diagnose in vivo (less than 25% are correctly diagnosed), as many patients carry the diagnosis of progressive supranuclear palsy whilst alive. Of those with a clinical diagnosis of corticobasal degeneration in vivo, 75% had another diagnosis at autopsy; again, many had progressive supranuclear palsy.

cor·ti·co·ba·sal de·gen·er·a·tion

(kōr'ti-kō-bā'săl dĕ-jen'ĕr-ā'shŭn)
A rare, progressive disease involving both cerebral cortex and extrapyramidal structures; clinically manifested as disturbances of voluntary movements and rigidity; pathologic characteristics include degeneration of the cerebral cortex with balloon neurons and degeneration of the substantia nigra.

corticobasal degeneration

A neurological disorder in which brain cells atrophy and die in the basal ganglia and the cortex of the brain. The disease produces symptoms similar to those found in Parkinson's disease but does not respond to parkinsonian medications.
See also: degeneration
References in periodicals archive ?
Duffy, "Apraxia of speech and non-fluent aphasia: a new clinical marker for corticobasal degeneration and progressive supranuclear palsy," Current Opinion in Neurology, vol.
Office of Rare Diseases neuropathologic criteria for corticobasal degeneration. J Neuropathol Exp Neurol.
Other types of atypical Parkinsonism including dementia with Lewy bodies (DLB), corticobasal degeneration (CBD), and multiple system atrophy (MSA) and secondary Parkinsonism, as well as patients with difficulty in completing this NMSS questionnaire (e.g.
They first address specific conditions and basic mechanisms in dementia and cognitive decline, including Alzheimer's disease, amyotrophic lateral sclerosis, corticobasal degeneration, Creutzfeldt-Jakob disease, frontotemporal lobar degeneration, Gaucher disease, Huntington's disease, dementia with Lewy bodies, normal pressure hydrocephalus, Parkinson's disease, Pick's disease, posterior cortical atrophy, progressive supranuclear palsy, cognitive vascular impairment, Wernicke-Korsakoff syndrome, risk factors, malnutrition, the role of diet in chronic inflammation and innate immunity in Alzheimer's, pathophysiological mechanisms and nutrition, and body composition.
These conditions include multiple system atrophy, progressive supranuclear palsy, corticobasal degeneration, Lewy body dementia, stroke, encephalitis (inflammation of the brain), and head trauma.
Neocortical neuronal loss and gliosis is usually most prominent in frontal and temporal regions, but in corticobasal degeneration (FTLD-tau [CBD]), for example, there is often prominent, and sometimes asymmetric, parietal and motor cortex neuronal loss and gliosis as well.
However, patients with those symptoms most frequently have a type of frontotemporal lobar degeneration (FTLD), such as FTLD with the deposition of TAR-DNA binding protein-43 (TDP-43), corticobasal degeneration pathology, Pick's disease pathology, or progressive supranuclear palsy pathology.