# Hyperbaric oxygen-assisted neurological recovery in a patient with classic heat stroke: a case report

**Authors:** Xin-xin Zheng, Liu-xu Chen, Ren Cheng-Han Fan, Zhi-qiang Zhang, Sheng Chen, Xiao-yang Wang, Guo-xin He

PMC · DOI: 10.3389/fmed.2026.1726603 · 2026-02-19

## TL;DR

A patient with heat stroke and brain injury showed neurological recovery after hyperbaric oxygen therapy, though its exact role is unclear.

## Contribution

This case report explores the potential of hyperbaric oxygen therapy in neurological recovery from heat stroke.

## Key findings

- The patient showed progressive neurological improvement after 27 hyperbaric oxygen therapy sessions.
- Hyperbaric oxygen therapy was associated with recovery of consciousness, limb strength, and partial speech.
- Neurological deficits persisted despite standard treatments, suggesting a possible role for HBOT.

## Abstract

Heat stroke (HS) is a critical condition involving severe central nervous system injury. While standard treatments—such as cooling, ventilation, and fluid resuscitation—can stabilize patients, they are often inadequate in addressing long-term neurological complications, including impaired consciousness and paralysis. The persistent deficits in neurological function remain a major clinical challenge. Hyperbaric oxygen therapy (HBOT), which improves brain oxygenation and supports neural repair, offers a potential solution. In the case we present of a patient with HS and brain injury, HBOT was associated with neurological recovery, although its specific contribution relative to conventional treatment remains uncertain.

A 35-year-old male laborer was admitted to the hospital following 5 h of outdoor exertion in high ambient temperatures. He presented comatose with a GCS of 3 (E1V1M1), with sluggish pupillary light reflexes and absent Babinski signs. Initial management in the intensive care unit included active cooling, mechanical ventilation, and supportive therapy. Despite these measures, the patient remained unconscious with quadriparesis. Cranial CT and MRI indicated signal abnormalities in the bilateral cerebellar hemispheres and basal ganglia, which were consistent with HS-induced encephalopathy. Upon stabilization of core temperature, the patient started HBOT at 0.20 MPa for 60–80 min daily in 10-day cycles. After 27 sessions, the patient exhibited progressive neurological improvement, including recovery of consciousness, restoration of limb strength, assisted ambulation, and partial return of speech. The patient was ultimately discharged in accordance with medical advice.

In this case of classic heatstroke with cerebral involvement, HBOT was introduced after partial neurological improvement had already occurred, and was associated with further recovery. The precise role of HBOT in addition to supportive care remains to be clarified.

## Linked entities

- **Diseases:** encephalopathy (MONDO:0005560)

## Full-text entities

- **Genes:** NFE2L2 (NFE2 like bZIP transcription factor 2) [NCBI Gene 4780] {aka IMDDHH, NRF2, Nrf-2}, NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548] {aka AGTAVPRL, AII, AVP, C1orf7, CIAS1, CLR1.1}, SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, CALCA (calcitonin related polypeptide alpha) [NCBI Gene 796] {aka CALC1, CGRP, CGRP-I, CGRP-alpha, CGRP1, CT}, GPT (glutamic--pyruvic transaminase) [NCBI Gene 2875] {aka AAT1, ALT, ALT1, GPT1, SGPT}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}
- **Diseases:** effusion (MESH:D000080324), infection (MESH:D007239), ischemic stroke (MESH:D002544), impaired consciousness (MESH:D003244), brain injury (MESH:D001930), brain dysfunction (MESH:D001927), death (MESH:D003643), spasms (MESH:D013035), lacunar infarction (MESH:D059409), neurological sequelae (MESH:D009422), coma (MESH:D003128), cognitive dysfunction (MESH:D003072), basal ganglia abnormalities (MESH:D001480), motor dysfunction (MESH:D000068079), HS (MESH:D018883), neuronal loss (MESH:D009410), TBI (MESH:D000070642), cortical edema (MESH:D004487), CNS injury (MESH:D002493), neuroinflammation (MESH:D000090862), pleural thickening (MESH:D010995), unconsciousness (MESH:D014474), peripheral nerve or muscle injury (MESH:D059348), pain (MESH:D010146), muscle contractions (MESH:C536214), trauma (MESH:D014947), neurodegenerative diseases (MESH:D019636), inflammation (MESH:D007249), cerebral lesions (MESH:D002539), cerebral hypoperfusion (MESH:D002547), quadriparesis (MESH:D011782), deficits in neurological function (MESH:D009461), ischemia (MESH:D007511), seizures (MESH:D012640), cerebellar atrophy (MESH:D002526), fever (MESH:D005334), paralysis (MESH:D010243), delirium (MESH:D003693), stroke (MESH:D020521), cerebral edema (MESH:D001929), carbon monoxide poisoning (MESH:D002249), lesions (MESH:D009059), multi-organ dysfunction (MESH:D009102), pulmonary infiltrates (MESH:D017254), cerebral hypoxia (MESH:D002534)
- **Chemicals:** Oxygen (MESH:D010100)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12960640/full.md

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Source: https://tomesphere.com/paper/PMC12960640