Linked Life Data

17886476

Source:http://linkedlifedata.com/resource/pubmed/id/17886476

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2007-9-24
pubmed:abstractText
In Parkinson disease patients who receive long-term antiparkinsonian medication, their original symptoms of rigidity, tremor and related motor disturbances markedly improve or disappear. However, the condition is still far from satisfactory in terms of maintaining independence in daily life activities even in these patients in whom the drug treatment is for improving motor disturbances. The reason is that they show abnormal behavior characterized by "spending the entire day in an idle state, which is perceived as laziness."This behavior is very annoying for the patient and the family. Despite the excellent effectiveness of drug treatment, this propensity toward idleness in mental and motor functions is not improved. Despite the denial of the depressive state and the absence of obvious cognitive disorder, such patients lack ambition and spend their time idly. However, although their motor function remains subliminal, such patients can carry out motor activities when the situation requires, but usually they do not have the drive to move. If we use the current nosological descriptions, the former is called "bradyphrenia" or psychic akinesia or slowness of thinking and the latter is called "akinesia". Akinesia is composed of two cardinal elements "bradykinesia" and "hypokinesia". Bradykinesia is the evaluation of quality of appeared motor behavior, and hypokinesia is the poverty of movement behavior. These two symptoms differ essentially. Hypokinesia is much more essential and is a cardinal element of akinesia. It indicates that the current drug treatment is ineffective for the improvement of hypokinesia and bradyphrenia. That is, these symptoms are a result of a dysfunction different from that causing residual motor symptoms or a result of other additional dysfunctions developing during the pathophysiological course of the disease. The dopamine (DA) system of the dorsal striatal pathway projecting from the substantia nigra pars compacta (A9) to the dorsal part of the striatum (motor striatum) functions in the control of speed and dexterity of movement. On the other hand, the DA system through the medial forebrain bundle projecting from the ventral tegmental area (VTA-A10) to the nucleus accumbens, ventral striatum (limbic striatum) and the cortex is associated with hypokinesia and bradyphrenia. This association can be confirmed by a long-term follow-up of Parkinson disease patients and experimental animal models lesioned in the ventral DA pathway (mesolimbic and mesocortical pathways).
pubmed:language
jpn
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1881-6096
pubmed:author
pubmed:issnType
Print
pubmed:volume
59
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
943-51
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
[Mesolimbic and mesocortical pathways in Parkinson disease].
pubmed:affiliation
Department of Neurology, Tokyo Metropolitan HMTC Ebara Hospital, 4-5-10 Higashiyukigaya, Ota-ku, Tokyo 145-0065, Japan.
pubmed:publicationType
Journal Article, English Abstract, Review