Both decompression sickness (DCS) and cerebral arterial gas embolism (CAGE) in divers and others who work at raised environmental pressures may affect the central nervous system (CNS) The range of symptoms and signs encompasses all aspects of function of the CNS Usually readily detectable clinically as significant alterations In sensory and motor function there may be subtle changes to higher cerebral functions which are more difficult to detect There is accumulating evidence which suggests that damage to the CNS may be more widespread than previously thought and in excess of that detectable clinically, even by skilled expert examination (1) This may be true even after aggressive and thorough treatment The possibility of covert damage to the CNS is of concern to physicians involved with divers as much as their employers

For the past year and a half, the Royal Navy has applied a new technique to the investigation of acute dysbarism of the CNS The patients involved have been predominantly sports divers suffering from neurological DCS but some cases of CAGE have also been investigated.

The technique involves radio-isotope imaging of the brain using the radiopharmaceutical agent Technesium 99m-labelled hydroxymethylpropyleneamine oxime (Tc99m-HMPA0) and single photon emission tomography (SPET) to demonstrate cerebral perfusion (2)


Our patients Included military and sports divers. A total of 28 cases were selected from over 50 available according to strict criteria chosen to minimise confusing factors such as misdiagnosis and inappropriate treatment Our cases ranged in severity from vague feelings of ill-health, through transient neurological symptoms and signs and also included some patients with severe and potentially disabling disease.

The results, published in full elsewhere (3) indicate that there are significant abnormalities of cerebral blood flow following diving accidents Of the 23 patients with serious or Type II DCS 19 had motor or sensory symptoms or signs, 7 bilaterally and 12 unilaterally. In the latter patients abnormalities were found in the contralateral parietal lobe. Of those patients with bilateral symptoms 3 had abnormalities in one parietal lobe only Major symptoms were reported on the contralateral side 8 patients were found to have changes to mentation. All 8 had parietal abnormalities and 6 had frontal lobe changes. One patient, with joint pain only, Type I DCS had normal cerebral perfusion.

There were 4 patients diagnosed with CAGE 3 had unilateral symptoms and signs and one bilateral. In each of the three patients with unilateral symptoms or signs there was a corresponding abnormality noted in the contralateral parietal lobe Only a right sided deficit was reported in the patient with bilateral symptoms and signs.

Limited follow-up studies have been performed on 18 patients from this and a larger study. Of those with DCS (14) a total of 33 deficits were noted initially Rescanned between 1 and 14 months later 32 deficits were found Two had returned to normal and two to nearly normal. A further 13 had improved but 12 remained unchanged 2 patients showed new perfusion deficits

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