Lower body parkinsonism: Evidence for vascular etiology
Identifieur interne : 006448 ( Main/Exploration ); précédent : 006447; suivant : 006449Lower body parkinsonism: Evidence for vascular etiology
Auteurs : Patricia M. Fitzgerald [États-Unis] ; Jankovic [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 1989.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
- Aged, Arteriosclerotic parkinsonism, Binswanger's disease, Cerebrovascular Disorders (complications), Degenerative disease, Etiopathogenesis, Female, Gait, Gait aplaxia, Gait disorder, Human, Humans, Lower limb, Male, Movement, Nervous system diseases, Nuclear magnetic resonance imaging, Parkinson Disease (etiology), Parkinson Disease (physiopathology), Parkinson disease, Parkinson's disease, Senile gait, Vascular parkinsonism.
- MESH :
- complications : Cerebrovascular Disorders.
- etiology : Parkinson Disease.
- physiopathology : Parkinson Disease.
- Aged, Female, Gait, Humans, Male, Movement.
Abstract
We studied 10 patients with marked gait difficulty and no or only minimal upper limb involvement, defined here as lower body parkinsonism (LBP). They were compared to a control group of 100 patients with otherwise typical Parkinson's disease (PD). Both groups were of comparable age, but the mean duration of symptoms was significantly shorter in the LBP group (2.6 ± 1.5 years versus 7.5 ± 4.9 years). Gait disturbance was the initial symptom in 90% of LBP patients, as opposed to 7% of controls. Hypertension was present in 70% of LBP patients, and only 22% responded to levodopa. In contrast, only 21% of controls had a history of hypertension, and 96% improved with levodopa. We conclude that these 10 LBP patients constitute a homogenous group, distinct from typical PD. Besides their disproportionate gait disturbance, they are distinguished from PD patients by more rapid progression, higher incidence of hypertension, and a poor response to levodopa. Ischemic etiology for LBP is supported by abnormal neuroimaging studies.
Url:
DOI: 10.1002/mds.870040306
Affiliations:
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Fitzgerald</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Texas</region></placeName><wicri:cityArea>Department of Neurology, Baylor College of Medicine, Houston</wicri:cityArea></affiliation></author><author><name sortKey="Jankovic" sort="Jankovic" uniqKey="Jankovic" last="Jankovic">Jankovic</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Texas</region></placeName><wicri:cityArea>Department of Neurology, Baylor College of Medicine, Houston</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1989">1989</date><biblScope unit="vol">4</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="249">249</biblScope><biblScope unit="page" to="260">260</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">5D34CD9D3629E4124D68BBA491156E89A1D48E7C</idno><idno type="DOI">10.1002/mds.870040306</idno><idno type="ArticleID">MDS870040306</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Arteriosclerotic parkinsonism</term><term>Binswanger's disease</term><term>Cerebrovascular Disorders (complications)</term><term>Degenerative disease</term><term>Etiopathogenesis</term><term>Female</term><term>Gait</term><term>Gait aplaxia</term><term>Gait disorder</term><term>Human</term><term>Humans</term><term>Lower limb</term><term>Male</term><term>Movement</term><term>Nervous system diseases</term><term>Nuclear magnetic resonance imaging</term><term>Parkinson Disease (etiology)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson disease</term><term>Parkinson's disease</term><term>Senile gait</term><term>Vascular parkinsonism</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Cerebrovascular Disorders</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Female</term><term>Gait</term><term>Humans</term><term>Male</term><term>Movement</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Etiopathogénie</term><term>Homme</term><term>Imagerie RMN</term><term>Maladie dégénérative</term><term>Membre inférieur</term><term>Parkinson maladie</term><term>Système nerveux pathologie</term><term>Trouble marche</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We studied 10 patients with marked gait difficulty and no or only minimal upper limb involvement, defined here as lower body parkinsonism (LBP). They were compared to a control group of 100 patients with otherwise typical Parkinson's disease (PD). Both groups were of comparable age, but the mean duration of symptoms was significantly shorter in the LBP group (2.6 ± 1.5 years versus 7.5 ± 4.9 years). Gait disturbance was the initial symptom in 90% of LBP patients, as opposed to 7% of controls. Hypertension was present in 70% of LBP patients, and only 22% responded to levodopa. In contrast, only 21% of controls had a history of hypertension, and 96% improved with levodopa. We conclude that these 10 LBP patients constitute a homogenous group, distinct from typical PD. Besides their disproportionate gait disturbance, they are distinguished from PD patients by more rapid progression, higher incidence of hypertension, and a poor response to levodopa. Ischemic etiology for LBP is supported by abnormal neuroimaging studies.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Texas</li></region></list><tree><country name="États-Unis"><region name="Texas"><name sortKey="Fitzgerald, Patricia M" sort="Fitzgerald, Patricia M" uniqKey="Fitzgerald P" first="Patricia M." last="Fitzgerald">Patricia M. Fitzgerald</name></region><name sortKey="Jankovic" sort="Jankovic" uniqKey="Jankovic" last="Jankovic">Jankovic</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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