Neurological manifestations in Japanese Ama divers.

Repetitive breath-hold (BH) diving can lead to accumulation of nitrogen (N2) in blood and tissues, which may give rise to decompression illness (DCI). An unusual condition is "Taravana", the diving syndrome reported by Cross in the 1960s. That report generated wide discussion as to whether BH diving can cause DCI. Paulev was the first person to suggest the link between DCI and BH diving. He, a submarine medical officer developed symptoms of DCI after a series of BH dives, having proceeded the dives by spending time in a hyperbaric chamber at 20 meters for 8 minutes. Recently four professional Japanese BH divers (Ama) with histories of diving accidents were reported. Magnetic resonance imaging of these divers detected cerebral infarcts localized in the watershed areas of the brain. A survey conducted on their island revealed that many Ama divers had experienced stroke-like events. A clinical feature of DCI in BH diving is that the damage is limited to the brain. Although the mechanisms of brain damage in BH diving are unclear, N2 bubbles passing through the lungs or the heart so as to become arterialized are most likely to be the etiological factor.

Radiotherapy after hyperbaric oxygenation improves radioresponse in experimental tumor models.

We examined the effect of radiotherapy after hyperbaric oxygen (HBO) breathing in experimental tumors using a tumor growth delay assay. Tumor models used were SCCVII (radiobiological hypoxic fraction: approximately 10%) and 9L tumors (containing less hypoxic cells) subcutaneously transplanted into C3H/He mice and Fisher 344 rats, respectively. Irradiation using X-rays was locally administered to the tumors immediately after decompression. HBO breathing enhanced the radiation response in SCCVII tumors but not in 9L ones. In the next experiment using SCCVII tumors, irradiation was administered 5, 15, 30, and 90 min after decompression. A significant growth delay was seen in the treated animals within 30 min after HBO breathing, and the tumor growth delay time was prolonged 1.61 times as long as that in radiotherapy alone. We concluded that: (1) radiotherapy after HBO breathing is effective for tumors with hypoxic cells; and (2) the time lapse from decompression to irradiation is an important factor in improving radiosensitivity. Radiotherapy after HBO breathing can be used to enhance the efficacy of clinical treatments.

Simultaneous hypertensive intracerebral hematomas: two case reports.

We describe two patients (76- and 54-year-old females) with multiple hypertensive intracerebral hematomas occurring simultaneously. One patient had a right thalamic hematoma extending into the internal capsule and basal ganglia together with an other one in the left putamen. The other patient had two hematomas located ipsilaterally in the left putamen and thalamus. Their neurological examinations showed only unilateral deficits. Their magnetic resonance angiograms revealed no vascular malformations. Neuroradiological procedures are essential for the diagnosis of these multiple brain events.

Preservation of tumour oxygen after hyperbaric oxygenation monitored by magnetic resonance imaging.

Hyperbaric oxygen (HBO) has been proposed to reduce tumour hypoxia by increasing the dissolved molecular oxygen in tissue. Using a non-invasive magnetic resonance imaging (MRI) technique, we monitored the changes in MRI signal intensity after HBO exposure because dissolved paramagnetic molecular oxygen itself shortens the T1 relation time. SCCVII tumour cells transplanted in mice were used. The molecular oxygen-enhanced MR images were acquired using an inversion recovery-preparation fast low angle shot (IR-FLASH) sequence sensitizing the paramagnetic effects of molecular oxygen using a 4.7 tesla MR system. MR signal of muscles decreased rapidly and returned to the control level within 40 min after decompression, whereas that of tumours decreased gradually and remained at a high level 60 min after HBO exposure. In contrast, the signal from the tumours in the normobaric oxygen group showed no significant change. Our data suggested that MR signal changes of tumours and muscles represent an alternation of extravascular oxygenation. The preserving tumour oxygen concentration after HBO exposure may be important regarding adjuvant therapy for cancer patients.

Effects of radiotherapy after hyperbaric oxygenation on malignant gliomas.

The purpose of this non-randomized trial was to evaluate the efficacy of radiotherapy combined with hyperbaric oxygen (HBO) in patients with malignant glioma. Between 1987 and 1997, 29 patients in whom computerized tomography (CT) or magnetic resonance imaging (MRI) scans showed post-operative residual tumours were locally irradiated with nitrosourea-based chemotherapy. Treatments were consecutively combined with HBO at two institutions since 1991 and 1993. Fifteen patients were irradiated daily after HBO, and the periods of time from decompression to irradiation were within 15 and 30 min in 11 and four patients respectively. Fourteen other patients were treated without HBO. Tumour responses were assessed by CT or MRI scans and survival times were compared between the treated groups. In the HBO group, 11 of 15 patients (73%) showed > or = 50% tumour regression. All responders were irradiated within 15 min after decompression. In the non-HBO group, four of 14 patients (29%) showed tumour regression. The median survivals in patients with and without HBO were 24 and 12 months, respectively, and were significantly different (P < 0.05). No serious side-effects were observed in the HBO patients. In conclusion, irradiation after HBO seems to be a useful form of treatment for malignant gliomas, but irradiation should be administered immediately after decompression.

[New approaches in neurosurgery and hyperbaric medicine--the importance of preventive and industrial medicine].

Neurosurgical patients have been mainly treated by surgical procedures over the past decades. In addition, hyperbaric oxygen (HBO) therapy in neurosurgery has been used in patients with ischemic cerebrovascular diseases, head trauma, spinal damage, postoperative brain edema and others. However, the main therapeutic methods for neurosurgical diseases have changed dramatically due to developments in radiological techniques, such as radiosurgery and intravascular surgery. With changes in therapeutic methods, HBO therapy may become a very important treatment option for neurosurgical patients. For example, HBO therapy combined with radiotherapy (UOEH regimen) and anticoagulant therapy appear to be very effective in the treatments of malignant brain tumors and ischemic cerebrovascular diseases, respectively. On the other hand, medical examinations under hyper- and hypobaric environments have not yet been fully studied in the central nervous system compared to those in the cardiopulmonary systems. Moreover, the mechanisms of cerebral lesions in decompression sickness and acute mountain sickness remain unclear. Clinical neurologic approaches are very important in these fields. Hence, clinicians and researchers skilled in both neurosurgery and hyperbaric medicine will be required for advanced treatment and preventive and industrial medicine.

Radiotherapy after hyperbaric oxygenation for malignant gliomas: a pilot study.

The results of radiotherapy combined with hyperbaric oxygen in 9 patients with malignant glioma were compared with those of radiotherapy without hyperbaric O2 in 12 patients. This is the first report of a pilot study of irradiation immediately after exposure to hyperbaric O2 in humans. All patients receiving this treatment showed more than 50% regression of the tumor, and in 4 of them, the tumors disappeared completely. Only 4 out of 12 patients without hyperbaric O2 showed decreases in tumor size, and all 12 patients died within 36 months. So far, this new regimen seems to be a useful form of radiotherapy for malignant gliomas.

Hyperbaric oxygen therapy adjunctive to mild hypertensive hypervolemia for symptomatic vasospasm.

The efficacy of hyperbaric oxygen (HBO) therapy was evaluated retrospectively in 43 patients who developed symptomatic vasospasm following acute aneurysm surgery. HBO therapy was given as an adjunct to mild hypertensive hypervolemia in 24 patients. Before HBO therapy, 17 patients had no infarct (Group 1), and seven had infarcts (Group 2) caused by vasospasm. A further 19 patients received mild hypertensive hypervolemia alone (Group 3). Cerebral infarcts developed in four Group 1 and 12 Group 3 patients. A good outcome 1 month after surgery was achieved by 13 Group 1 (76%), one Group 2, and seven Group 3 patients (37%). Fifteen of the 24 patients who received HBO therapy responded to HBO exposure, and 12 responding patients (80%) had a good outcome. During HBO exposure, electroencephalographic improvements were all accompanied by neurological improvements. There were no complications related to HBO therapy. HBO therapy adjunctive to mild hypertensive hypervolemia is helpful in preventing cerebral infarction associated with symptomatic vasospasm.

Intracranial pressure responses during hyperbaric oxygen therapy.

The responses of intracranial pressure (ICP) to hyperbaric oxygen (HBO) therapy and arterial gas pressures were investigated. ICP was measured through a ventricular or spinal drainage catheter in patients with brain tumor or cerebrovascular disease. Changes in ICP, heart rate (HR), arterial blood pressure (ABP), and transcutaneous partial pressure of carbon dioxide (PtcCO2) or oxygen (PtcO2) were recorded continuously during air or 100% O2 breathing at 1 and 2.5 atmospheres absolute (ATA). HR and PtcCO2 decreased and mean ABP was unchanged during HBO inhalation. ICP was reduced at the beginning and tended to increase gradually during HBO inhalation. The change from air to O2 without altering respiratory frequency and volume caused a gradual increase of ICP and PtcCO2 with a transient ICP reduction in an artificially respirated patient. Intentionally reduced respiration to maintain PtcCO2 at the value at 2.5 ATA with air caused the ICP to return to near the value at 2.5 ATA with air even during HBO inhalation. These findings suggest that reduced ICP is initially due to direct cerebral vasoconstriction caused by hyperoxia and is maintained mainly by induced hypocapnia during HBO inhalation. Care is required when giving HBO therapy to patients with a high ICP and/or who are respirated artificially.