Results 251 to 260 of about 81,081 (302)
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Neurodegenerative Cerebellar Ataxia
Continuum, 2022Neurodegenerative cerebellar ataxia is a diverse collection of diseases that are unified by gait and balance abnormalities, appendicular incoordination, and abnormalities of eye movement and speech. The differential diagnosis is broad, ranging from paraneoplastic syndromes that progress quite rapidly to unidentified genetic disorders that progress ...
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Australian and New Zealand Journal of Medicine, 1989
AbstractThis report describes the clinical features of 13 cases of periodic, paroxysmal cerebellar ataxia. A family history suggestive of an autosomal dominant disorder was present in 10 cases, the first two reported Australian families involved with this disorder. Variation in the age of onset, frequency of attacks and the presence of distinct symptom
G F, Feeney, R S, Boyle
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AbstractThis report describes the clinical features of 13 cases of periodic, paroxysmal cerebellar ataxia. A family history suggestive of an autosomal dominant disorder was present in 10 cases, the first two reported Australian families involved with this disorder. Variation in the age of onset, frequency of attacks and the presence of distinct symptom
G F, Feeney, R S, Boyle
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Non-cerebellar ataxias: posterior column-like ataxia and cerebellar-like ataxia
Rinsho Shinkeigaku, 2023Ataxia is not only due to cerebellar lesions, but also due to non-cerebellar lesions such as those in the brain, spinal cord, dorsal root (DR), peripheral nerve. In this article, optic ataxia is excluded and 'vestibular ataxia' is briefly referred. Non-cerebellar ataxias are generically called sensory ataxia or posterior column ataxia.
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Seminars in Neurology, 2014
This review broadly covers the commoner genetic ataxias, concentrating on their clinical features. Over the last two decades there has been a potentially bewildering profusion of newly described genetic ataxias. However, at least half of dominant ataxias (SCAs) are caused by (CAG)n repeat expansions resulting in expanded polyglutamine tracts (SCAs 1, 2,
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This review broadly covers the commoner genetic ataxias, concentrating on their clinical features. Over the last two decades there has been a potentially bewildering profusion of newly described genetic ataxias. However, at least half of dominant ataxias (SCAs) are caused by (CAG)n repeat expansions resulting in expanded polyglutamine tracts (SCAs 1, 2,
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2018
The cerebellum plays an integral role in the control of limb and ocular movements, balance, and walking. Cerebellar disorders may be classified as sporadic or hereditary with clinical presentation varying with the extent and site of cerebellar damage and extracerebellar signs.
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The cerebellum plays an integral role in the control of limb and ocular movements, balance, and walking. Cerebellar disorders may be classified as sporadic or hereditary with clinical presentation varying with the extent and site of cerebellar damage and extracerebellar signs.
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Cerebellar stimulation in acute cerebellar ataxia
Clinical Neurophysiology, 2001To report follow-up studies of cerebellar stimulation in patients with acute cerebellar ataxia (ACA).We studied two patients with ACA. One patient also had decreased deep sensations in the feet due to combined diseases such as diabetic polyneuropathy and lumbosacral radiculopathies. We applied the technique of electrical stimulation over the cerebellum
K, Matsunaga +3 more
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Nonparaneoplastic autoimmune cerebellar ataxias
Current Opinion in Neurology, 2019Purpose of review The current review develops the clinical presentations of nonparaneoplastic autoimmune cerebellar ataxia (ACA) and analyzes the association with autoantibodies. Recent findings Emerging evidence suggests that autoimmunity is involved in a significant proportion of ...
Bastien, Joubert, Jerome, Honnorat
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Pathophysiology of cerebellar ataxia
Movement Disorders, 1992AbstractHuman and animal experiments performed recently have resulted in a more detailed understanding of limb movement and body posture disorders associated with cerebellar dysfunction. The delay in movement initiation can be explained by a delay in onset of phasic motor cortex neural discharge owing to decreased input from the cerebellar hemispheres.
H C, Diener, J, Dichgans
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Journal of Clinical Neuroscience, 2006
1. Clinical backgroundA 58-year-old man presented with a four-year history ofgradually increasing gait unsteadiness, urinary inconti-nence and erectile dysfunction. His daughter complainedthat he snored loudly at night, but on further questioningit was apparent that this was an inspiratory stridor.
K, Kee, P J, Hand
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1. Clinical backgroundA 58-year-old man presented with a four-year history ofgradually increasing gait unsteadiness, urinary inconti-nence and erectile dysfunction. His daughter complainedthat he snored loudly at night, but on further questioningit was apparent that this was an inspiratory stridor.
K, Kee, P J, Hand
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