Objective-Prolonged improvement in neurological and mental disorders has been seen after only cranioplasty in patients initially treated with external decompression for high intracranial pressure. The objective was to evaluate, using 133Xe CT and 31P magnetic resonance spectroscopy (MRS), how restoring the bone itself can influence cerebral blood flow and cerebral energy metabolism after high intracranial pressure is attenuated. Methods-Seven patients (45-65 years old) who had undergone external decompression to prevent uncontrollable intracranial hypertension after acute subarachnoid haemorrhage were evaluated. Cerebral blood flow and metabolic changes were evaluated before and after cranioplasty. Results-The ratio of phosphocreatine to inorganic phosphate (PCr/Pi), which is a sensitive index of cerebral energy depletion, was calculated and ,3-ATP was measured. The cerebral blood flow value in the thalamus was normalised, from 44 (SD 9) to 56 (SD 8) ml/100 g/min (P < 0.01) and the value in the hemisphere increased from 26 (SD 3) to 29 (SD 4) ml/100 g/min on the side with the bone defect. The PCr/Pi ratio improved greatly from 2 53 (SD 0'45) to 3'01 (SD 0.24) (P < 0.01). On the normal side, the values of cerebral blood flow and PCr/Pi increased significantly (P < 0'01) after cranioplasty, possibly due to transneural suppression. The pH of brain tissue was unchanged bilaterally after cranioplasty. Conclusion-Cranioplasty should be carried out as soon as oedema has disappeared, because a bone defect itself may decrease cerebral blood flow and disturb energy metabolism.(7 Neurol Neurosurg Psychiatry 1996;61: 166-171) pressive craniotomy remains controversial. Some authors found that morbidity was increased in survivors although decompressive craniectomy reduced the mortality rate, probably because it reduced the adverse effects of severe cerebral oedema and swelling.i"2 Many patients with severe head injury or massive cerebral infarction undergo external decompression as a treatment.However, little is known about how a bone defect itself can influence cerebral blood flow and cerebral energy metabolism after high intracranial pressure is normalised. Prolonged improvement in neurological and mental disorders has been seen only after cranioplasty in patients treated initially with external decompression for high intracranial pressure.'3-'7 The objective of the present study was to measure cerebral blood flow and metabolic changes, using '33Xe CT and 31P magnetic resonance spectroscopy (MRS), before and after cranioplasty to evaluate whether the brain would recover after attenuation of high intracranial pressure, by restoration of the bone itself. Materials and methodsSeven patients (45-65 years old) were selected who had undergone clipping and external decompression to prevent uncontrollable

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To evaluate the current status of the management of hypertensive patients in Japan, we investigated 907 treated hypertensive patients (486 females and 421 males; mean age, 66.7 years) followed by cardiologists.

Sensitivity may improve with combined reading of nonselective MIP and source images.

It is concluded that the skeletal muscles of hypertensive patients released deltaHX in excess by activation of muscle-type adenosine monophosphate (AMP) deaminase, depending on the degree of hypoxia. The modification of deltaHX by angiotensin-converting enzyme inhibitors and alpha1-blockers influenced the level of serum uric acid, suggesting that the skeletal muscles may be an important source of uric acid as well as of the substrate of xanthine oxidase in hypertension.