Primary progressive freezing gait
Identifieur interne : 001C63 ( Istex/Corpus ); précédent : 001C62; suivant : 001C64Primary progressive freezing gait
Auteurs : Achiron ; I. Ziv ; M. Goren ; H. Goldberg ; Y. Zoldan ; H. Sroka ; E. MelamedSource :
- Movement Disorders [ 0885-3185 ] ; 1993.
English descriptors
- KwdEn :
Abstract
Freezing gait is an incapacitating symptom often observed in patients with Parkinson's disease. It has been less frequently described in association with multi‐infarct state, multisystem atrophies, and normotensive hydrocephalus. In our movement disorder clinic, we have diagnosed (and followed up to 3 years; median, 16 months), 18 patients in whom progressive freezing gait was the sole neurological dysfunction. These 15 men and 3 women (aged 60−82 years; 74 ± 6) were subjected to an extensive neurological workup that included clinical evaluation, videotaping for grading of gait disability, comprehensive blood and cerebrospinal fluid (CSF) analysis, and brain computed tomography (CT) and magnetic resonance imaging (MRI). Mean disease duration was 2.5 ± 1.9 years (range, 0.5−6). Neurological examination disclosed freezing gait, often associated with varying degrees of postural instability. The degree of freezing gait ranged from sudden motor blocks only when confronted with obstacles to severe disability with total inability to start walking requiring a walker, massive assistance, or a wheelchair. However, patients could mimic gait movements with absolutely no freezing when seated or lying prone, and most of them could overcome arrests by the “walking‐over‐lines” maneuver. Otherwise, neurological examination was normal with no signs of bradykinesia, rigidity, or tremor. Blood chemistry and CSF analysis were normal. Brain CT and MRI were normal or showed mild cortical atrophy in 12 and putative lacunes in 6 patients. Therapy with levodopa or dopamine agonists was ineffective. During the follow‐up period, a gradual progression of the freezing gait was observed. However, it remained unaccompanied by any other neurological findings. We therefore conclude that primary progressive freezing gait should be recognized as a distinct neurological entity, unique in its clinical presentation and natural course. The lack of response to levodopa raises the possibility that nondopaminergic pathways might be involved.
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DOI: 10.1002/mds.870080307
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<titleGroup><title type="main" xml:lang="en">Primary progressive freezing gait</title>
<title type="short" xml:lang="en">PRIMARY PROGRESSIVE FREEZING GAIT</title>
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<familyName>Goldberg</familyName>
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<creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>H.</givenNames>
<familyName>Sroka</familyName>
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<creator xml:id="au7" creatorRole="author" affiliationRef="#af1"><personName><givenNames>E.</givenNames>
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<affiliationGroup><affiliation xml:id="af1" countryCode="IL" type="organization"><unparsedAffiliation>Department of Neurology, the Felsenstein Research Center, Beilinson Medical Center, and Sackler School of Medicine, Tel‐Aviv University, Petah‐Tiqva, Israel</unparsedAffiliation>
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<affiliation xml:id="af2" countryCode="IL" type="organization"><unparsedAffiliation>Department of Radiology, the Felsenstein Research Center, Beilinson Medical Center, and Sackler School of Medicine, Tel‐Aviv University, Petah‐Tiqva, Israel</unparsedAffiliation>
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<keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Freezing gait</keyword>
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<p>Freezing gait is an incapacitating symptom often observed in patients with Parkinson's disease. It has been less frequently described in association with multi‐infarct state, multisystem atrophies, and normotensive hydrocephalus. In our movement disorder clinic, we have diagnosed (and followed up to 3 years; median, 16 months), 18 patients in whom progressive freezing gait was the sole neurological dysfunction. These 15 men and 3 women (aged 60−82 years; 74 ± 6) were subjected to an extensive neurological workup that included clinical evaluation, videotaping for grading of gait disability, comprehensive blood and cerebrospinal fluid (CSF) analysis, and brain computed tomography (CT) and magnetic resonance imaging (MRI). Mean disease duration was 2.5 ± 1.9 years (range, 0.5−6). Neurological examination disclosed freezing gait, often associated with varying degrees of postural instability. The degree of freezing gait ranged from sudden motor blocks only when confronted with obstacles to severe disability with total inability to start walking requiring a walker, massive assistance, or a wheelchair. However, patients could mimic gait movements with absolutely no freezing when seated or lying prone, and most of them could overcome arrests by the “walking‐over‐lines” maneuver. Otherwise, neurological examination was normal with no signs of bradykinesia, rigidity, or tremor. Blood chemistry and CSF analysis were normal. Brain CT and MRI were normal or showed mild cortical atrophy in 12 and putative lacunes in 6 patients. Therapy with levodopa or dopamine agonists was ineffective. During the follow‐up period, a gradual progression of the freezing gait was observed. However, it remained unaccompanied by any other neurological findings. We therefore conclude that primary progressive freezing gait should be recognized as a distinct neurological entity, unique in its clinical presentation and natural course. The lack of response to levodopa raises the possibility that nondopaminergic pathways might be involved.</p>
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<abstract lang="en">Freezing gait is an incapacitating symptom often observed in patients with Parkinson's disease. It has been less frequently described in association with multi‐infarct state, multisystem atrophies, and normotensive hydrocephalus. In our movement disorder clinic, we have diagnosed (and followed up to 3 years; median, 16 months), 18 patients in whom progressive freezing gait was the sole neurological dysfunction. These 15 men and 3 women (aged 60−82 years; 74 ± 6) were subjected to an extensive neurological workup that included clinical evaluation, videotaping for grading of gait disability, comprehensive blood and cerebrospinal fluid (CSF) analysis, and brain computed tomography (CT) and magnetic resonance imaging (MRI). Mean disease duration was 2.5 ± 1.9 years (range, 0.5−6). Neurological examination disclosed freezing gait, often associated with varying degrees of postural instability. The degree of freezing gait ranged from sudden motor blocks only when confronted with obstacles to severe disability with total inability to start walking requiring a walker, massive assistance, or a wheelchair. However, patients could mimic gait movements with absolutely no freezing when seated or lying prone, and most of them could overcome arrests by the “walking‐over‐lines” maneuver. Otherwise, neurological examination was normal with no signs of bradykinesia, rigidity, or tremor. Blood chemistry and CSF analysis were normal. Brain CT and MRI were normal or showed mild cortical atrophy in 12 and putative lacunes in 6 patients. Therapy with levodopa or dopamine agonists was ineffective. During the follow‐up period, a gradual progression of the freezing gait was observed. However, it remained unaccompanied by any other neurological findings. We therefore conclude that primary progressive freezing gait should be recognized as a distinct neurological entity, unique in its clinical presentation and natural course. The lack of response to levodopa raises the possibility that nondopaminergic pathways might be involved.</abstract>
<subject lang="en"><genre>Keywords</genre>
<topic>Freezing gait</topic>
<topic>Festinations</topic>
<topic>Instability</topic>
<topic>Falls</topic>
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<relatedItem type="host"><titleInfo><title>Movement Disorders</title>
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<identifier type="ISSN">0885-3185</identifier>
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<part><date>1993</date>
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