Urinary disorders in amyotrophic lateral sclerosis subjects.

14:22 EDT 21st October 2014 | BioPortfolio

Summary of "Urinary disorders in amyotrophic lateral sclerosis subjects."

Abstract Amyotrophic lateral sclerosis (ALS) related disorders are considered to be uncommon. We hypothesize that urinary dysfunction may occur in ALS patients in the context of spasticity of pelvic floor musculature. We recorded data on 54 subjects with ALS. All subjects were evaluated with ALSFRS and M-Ashworth Scale for lower limbs. Bladder scan procedure was performed to asses post void residual (PVR) in all subjects. Forty-one percent of subjects were symptomatic for urinary disorders and 35% of subjects had a PVR > 50 ml. Linear correlation was found between PVR and ALSFRS with a R(2) 0.95 and p = 0.025; a linear correlation was also noted between PVR and lower limbs Ashworth Scale. We conclude that urinary retention is common in ALS. Urological evaluation is indicated in ALS patients with prominent spasticity.

Affiliation

Italian MS Society, AISM Rehabilitation Centre, Genova, Italy.

Journal Details

This article was published in the following journal.

Name: Amyotrophic lateral sclerosis : official publication of the World Federation of Neurology Research Group on Motor Neuron Disease
ISSN: 1471-180X
Pages:

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Medical and Biotech [MESH] Definitions

A glutamate antagonist (RECEPTORS, GLUTAMATE) used as an anticonvulsant (ANTICONVULSANTS) and to prolong the survival of patients with AMYOTROPHIC LATERAL SCLEROSIS.

Diseases characterized by a selective degeneration of the motor neurons of the spinal cord, brainstem, or motor cortex. Clinical subtypes are distinguished by the major site of degeneration. In AMYOTROPHIC LATERAL SCLEROSIS there is involvement of upper, lower, and brainstem motor neurons. In progressive muscular atrophy and related syndromes (see MUSCULAR ATROPHY, SPINAL) the motor neurons in the spinal cord are primarily affected. With progressive bulbar palsy (BULBAR PALSY, PROGRESSIVE), the initial degeneration occurs in the brainstem. In primary lateral sclerosis, the cortical neurons are affected in isolation. (Adams et al., Principles of Neurology, 6th ed, p1089)

Diseases characterized by the presence of abnormally phosphorylated, ubiquitinated, and cleaved DNA-binding protein TDP-43 in affected brain and spinal cord. Inclusions of the pathologic protein in neurons and glia, without the presence of AMYLOID, is the major feature of these conditions, thus making these proteinopathies distinct from most other neurogenerative disorders in which protein misfolding leads to brain amyloidosis. Both frontotemporal lobar degeneration and AMYOTROPHIC LATERAL SCLEROSIS exhibit this common method of pathogenesis and thus they may represent two extremes of a continuous clinicopathological spectrum of one disease.

A degenerative disorder affecting upper MOTOR NEURONS in the brain and lower motor neurons in the brain stem and SPINAL CORD. Disease onset is usually after the age of 50 and the process is usually fatal within 3 to 6 years. Clinical manifestations include progressive weakness, atrophy, FASCICULATION, hyperreflexia, DYSARTHRIA, dysphagia, and eventual paralysis of respiratory function. Pathologic features include the replacement of motor neurons with fibrous ASTROCYTES and atrophy of anterior SPINAL NERVE ROOTS and corticospinal tracts. (From Adams et al., Principles of Neurology, 6th ed, pp1089-94)

A motor neuron disease marked by progressive weakness of the muscles innervated by cranial nerves of the lower brain stem. Clinical manifestations include dysarthria, dysphagia, facial weakness, tongue weakness, and fasciculations of the tongue and facial muscles. The adult form of the disease is marked initially by bulbar weakness which progresses to involve motor neurons throughout the neuroaxis. Eventually this condition may become indistinguishable from AMYOTROPHIC LATERAL SCLEROSIS. Fazio-Londe syndrome is an inherited form of this illness which occurs in children and young adults. (Adams et al., Principles of Neurology, 6th ed, p1091; Brain 1992 Dec;115(Pt 6):1889-1900)

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