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Updated: Jul 17, 2026

Spinal Hernia Repair and Cauda Equina Repositioning After Lumbar Decompression under Three-Dimensional Microscopy: A Case Report and Literature Review

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[Neurogenic bladder dysfunction a main disability of decompression sickness: a case report].

P Decavel¹, V Bonniaud, R Joassin

¹Service de rééducation neurologique, centre hospitalier universitaire de Dijon, 23, rue Gaffarel, 21079 Dijon cedex, France.

Annales De Readaptation Et De Medecine Physique : Revue Scientifique De La Societe Francaise De Reeducation Fonctionnelle De Readaptation Et De Medecine Physique

|January 24, 2007

Summary

Decompression sickness can cause prolonged neurogenic bladder dysfunction, even after motor recovery. This case highlights urinary retention as a primary symptom, emphasizing the need for awareness in divers.

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Spinal Hernia Repair and Cauda Equina Repositioning After Lumbar Decompression under Three-Dimensional Microscopy: A Case Report and Literature Review

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A Single Cell Dissociation Approach for Molecular Analysis of Urinary Bladder in the Mouse Following Spinal Cord Injury

A Single Cell Dissociation Approach for Molecular Analysis of Urinary Bladder in the Mouse Following Spinal Cord Injury

Published on: June 17, 2020

Area of Science:

Neurology
Diving Medicine
Urology

Background:

Bladder dysfunction is a frequent, often early, symptom of decompression sickness.
Persistence of urinary issues and neurogenic bladder are rarely reported in decompression sickness literature.

Observation:

A 21-year-old female scuba diver developed dysbaric myelitis after deep dives, presenting with tetraparesia, paraparesia, and urinary retention.
Neuro-urodynamic testing revealed detrusor sphincter dyssynergia and detrusor overactivity.
Despite rapid motor recovery, the patient experienced persistent urinary and fecal urgencies a year later.

Findings:

Dysbaric myelitis, a form of neurological decompression, affects half of affected individuals, likely due to venous ischemia.
Foramen ovale is identified as a significant risk factor for dysbaric myelitis.
Neurogenic bladder dysfunction can be a prolonged and primary manifestation of decompression sickness.

Implications:

This case underscores the potential for persistent bladder dysfunction following decompression sickness.
Healthcare providers should consider neurogenic bladder in the differential diagnosis of urinary retention in divers.
Further research is needed to elucidate the pathophysiology and long-term management of bladder dysfunction in decompression sickness.