HBOT for Multiple Sclerosis Symptom Management in Concord, CA

Multiple sclerosis (MS) is a chronic autoimmune demyelinating disease in which the immune system attacks myelin — the protective sheath surrounding axons in the central nervous system — causing plaques of demyelination throughout the brain and spinal cord. Approximately one million Americans are currently living with MS, with an estimated 5,000 new diagnoses each year. The disease most commonly appears between ages 20 and 40 and affects approximately three times as many women as men.

The most common form, relapsing-remitting MS (RRMS), is characterized by discrete attacks (relapses) of neurological dysfunction followed by partial or complete recovery, interspersed with periods of clinical stability. Over time, many RRMS patients transition to secondary progressive MS (SPMS), characterized by gradual neurological worsening. Primary progressive MS (PPMS) begins with gradual decline from the outset without discrete relapses.

The Bay Area has active MS patient communities and access to world-class neurological care at UCSF, John Muir Health, and other Bay Area centers. Despite excellent access to disease-modifying therapies — medications that reduce relapse frequency and slow structural progression — a majority of MS patients continue to experience significant symptom burden that these therapies do not address. MS fatigue, cognitive impairment, bladder dysfunction, spasticity, and pain are common targets for adjunctive therapies including HBOT.

HBOT addresses two of the core pathological processes in MS: the metabolic vulnerability of demyelinated axons to hypoxia, and the ongoing neuroinflammation that drives lesion expansion and axonal loss. These are precisely the mechanisms that current disease-modifying therapies — which primarily target immune cell trafficking and relapse frequency — do not adequately address.

Demyelinated axons are significantly more oxygen-dependent than healthy myelinated fibers, because they must maintain sodium pump activity along their entire length rather than relying on the energy-efficient saltatory conduction that intact myelin enables. In MS patients with CNS hypoperfusion (which imaging studies confirm is present throughout the disease course), this increased metabolic demand cannot be met, contributing to conduction failure, fatigue, and progressive axonal degeneration. At 1.5 to 2.5 atmospheres of 100% oxygen, HBOT raises tissue oxygen concentrations to levels that restore energetic sufficiency in these metabolically stressed axons, directly reducing conduction fatigue and supporting the viability of oligodendrocyte precursor cells that mediate remyelination.

The evidence base for HBOT in MS is most robust for fatigue. A systematic review and multiple randomized controlled trials — including the series of studies conducted at the MS Research and Treatment Centre in Dundee, Scotland — have documented significant reductions in fatigue severity in MS patients treated with HBOT, with benefits maintained over extended follow-up periods. Additional evidence supports improvements in bladder function, cognitive performance, and quality of life measures. HBOT is used as an adjunct to — not a replacement for — disease-modifying therapies, and Dr. Toth coordinates care closely with patients' neurologists. Protocols typically involve an induction phase of 20 daily sessions followed by maintenance sessions on a schedule individualized to each patient's response and functional needs.