Evidence map›Paper›PMID 8568522›Full record

ArticleJournal of neurology1995

Clinico-pathophysiological features of acute autonomic and sensory neuropathy: a long-term follow-up study.

T Yasuda, G Sobue, K Mokuno, S Hakusui, T Ito, Y Hirose, T Yanagi

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In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

T YasudaDepartment of Neurology, Nagoya Daini Red Cross Hospital, Japan.
G Sobue
K Mokuno
S Hakusui
T Ito
Y Hirose
T Yanagi

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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

Action PotentialsAdultAgedAutonomic Nervous System DiseasesBiopsyEvoked Potentials, SomatosensoryFemaleFollow-Up StudiesHumansMagnetic Resonance ImagingNerve Growth FactorsPhosphopyruvate HydrataseS100 Calcium Binding Protein beta SubunitS100 ProteinsSensation DisordersSpinal CordNerve Growth FactorsPhosphopyruvate HydrataseS100 Calcium Binding Protein beta SubunitS100 Proteins

Identifiers

PMID8568522

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.