July 16, 2009
My father was a US Navy diver/Submarine Service from the late 40′s to the early 70′s. His duties included escape training tank instructor and saturation diving as a member of the original Deep Submergence Group. He is currently 77 years old and previously diagnosed with Alzheimers. Recently, that diagnosis was changed to “shrunken brain” due to lack of oxygen from diving. Is this common in divers?
July 19, 2009
I’m sorry to hear that.
There is no formal diagnosis termed “shrunken brain.” It is not a recognized condition in either divers or non-divers. And I don’t know on what basis your father’s diagnosis was altered. Or to what end.
In some diseases of brain the outer layer of gray matter, called the cerebral cortex, thins and makes the brain appear “shrunken.” This is known as cortical atrophy and can be observed in a number of neurodegenerative disorders. It is seen in Alzheimer’s as the disease advances. I suspect something like this is the issue.
There is an increasing body of literature indicating that scuba may be associated with damage to gray and white matter areas of the brain and with neuropsychological deficits. This damage does seem to be the result of obstruction of sements of the cerebral circulation. The area of brain blocked from receiving an adequate blood supply may die of hypoxia.
While these abnormalities appear to occur in both professional and amateur divers, they are more common and pronounced in professional divers, especially those who frequently dive extreme profiles. Those with long diving careers extending into advanced age well might be expected to be the most effected.
Divers known to have patent foramen ovale (PFO) seem to have an increased likelihood of such lesions and divers with a history of decompression illness (DCI) also could be at increased risk.
In any event, the issue at hand appears to be largely academic as neither Alzheimer’s disease nor its variants, or areas of white or gray matter death from whatever cause, can be healed or reversed to any meanigful extent. The loss is essentially permanent. Given that all potentially reversible or materially treatable causes for the signs and symptoms have been ruled out, further pursuit of fine-grained differential diagnosis is unlikely to significantly contribute to the patient’s care.
Treatment for such conditions is at present limited to a few only very modestly effective drugs. The most important steps in managing such brain states are a clear understanding by caregivers of what to expect and how to structure both their own lives and that of the patient so as to maximize the functioning and well-being of all involved.
If the patient has not yet been evaluated by a recognized expert in the senile dementias, such examination would be prudent.
This is educational only and does not constitute or imply a doctor-patient relationship. It is not medical advice to you or any other individual, and should not be construed as such.