ArticleJournal of neurology1995
Clinico-pathophysiological features of acute autonomic and sensory neuropathy: a long-term follow-up study.
Article in Journal of neurology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Acute Sensory and Autonomic Neuronopathy: A Devastating Disorder Affecting Sensory and Autonomic Ganglia.Seminars in neurology · 2020Pooled it
- Article
- The spectrum of clinicopathological features in pure autonomic neuropathy.Journal of neurology · 2012Article
- Sensory neuropathies including painful and toxic neuropathies.Journal of neurology · 1997Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We evaluated the clinico-pathophysiological features of three patients with acute autonomic and sensory neuropathy (AASN) who were followed for over 3 years. Signs of an autonomic disturbance including vomiting, anhidrosis, urinary disturbances, orthostatic hypotension and reduced coefficient of variation of the R-R interval on electrocardiography gradually improved about 1 year after onset. However, all three exhibited severe generalized sensory impairment for all modalities with the development of persistent sensory ataxia. No sensory nerve action potentials could be elicited and no somatosensory evoked potentials could be obtained. Sural nerve biopsy revealed severe axonopathy. In two patients, a high-intensity area was observed in the posterior column of the spinal cord on T2*-weighted axial magnetic resonance images. The level of neuron-specific enolase in cerebrospinal fluid was markedly elevated in two patients, indicating spinal nerve root or sensory neuron damage. Motor nerve function was well preserved in all patients. Our findings suggests that the major lesion in patients with AASN, particularly those with a sensory deficit, is present in the dorsal root ganglion neurons, that is there is a ganglioneuronopathy.
Indexed as
Identifiers
8568522What OpenQuestion holds
Registered trials
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