Disease relevance of Gait Disorders, Neurologic

• OBJECTIVE: To analyze the SPG3A coding sequence in an individual with childhood-onset spastic gait, who, prior to the birth of her similarly affected child, had no previous family history of hereditary spastic paraplegia [1].
• Injection of 5 mg Rolipram/kg provoked transient slackening and unsteady gait while chronic application of 6 mg/kg/day strongly accelerated the weight gain in adolescent rats [2].
• Hereditary spastic paraplegia (HSP) is a neurodegenerative disease characterized by lower-limb spasticity, hyperreflexia, progressive spastic gait abnormalities, and an extensor-plantar response [3].
• Each patient had spastic gait, dysarthria, dystonic posturing of both arms and generalized hyperreflexia, but no Kayser-Fleischer rings or retinitis pigmentosa [4].

High impact information on Gait Disorders, Neurologic

• The disease phenotype in K313 is characterized by hyperreflexia and a spastic gait, but intelligence is normal [5].
• PMCA2-null mice grow more slowly than heterozygous and wild-type mice and exhibit an unsteady gait and difficulties in maintaining balance [6].
• Neurologic evaluation 24 h after successful resuscitation revealed only an unsteady gait in all vasopressin-treated animals; after 96 h, magnetic resonance imaging revealed no cerebral pathology [7].
• Five patients, age 54 to 80 years, presented between 3 weeks and 18 months after symptomatic onset of progressive cognitive decline, psychosis, and unsteady gait that proved to be due to a steroid-responsive nonvasculitic autoimmune inflammatory meningoencephalitic syndrome [8].
• For many subjects with an SPG3A mutation, spastic gait begins in early childhood and does not significantly worsen even over many years [1].

Chemical compound and disease context of Gait Disorders, Neurologic

• When compared with control rats, rats with unilateral dopamine depletion displayed a shuffling gait and short stride lengths [9].
• The technique of polarised light goniometry was used to quantify objectively parameters of the spastic gait during a double-blind cross-over trial comparing the spasmolytic effects of DS103-282, baclofen and placebo [10].
• 6 h after irradiation, behavioural and histological evaluations revealed that exposure to 2.5 Gy caused hypolocomotion, stumbling gait and somnolence, which was significantly reduced, from the dose of 4 mg/kg i.p. of riluzole [11].
• Neurologic evaluation 24 h after successful resuscitation revealed only an unsteady gait and was normal 5 days after the experiment in all vasopressin/epinephrine-treated animals [12].
• Amantadine increases gait steadiness in frontal gait disorder due to subcortical vascular encephalopathy: a double-blind randomized placebo-controlled trial based on quantitative gait analysis [13].

Anatomical context of Gait Disorders, Neurologic

• Hereditary spastic paraplegia (HSP) linked to the spastic gait gene 4 (SPG4) is controversial, as the "pure" form traditionally has been considered confined to the long axons of the spinal cord [14].

Gene context of Gait Disorders, Neurologic

• These results suggest that vestibular dysfunction is a symptom that develops very early in MJD and may contribute to unsteady gait as the initial symptom [15].
• A 63-year-old NPC patient had intermittent dizziness and unsteady gait 3 years after irradiation [16].
• Treatment with a steroid improved the deep sensory disturbance, unsteady gait, and CRP level [17].

References