✓ The authors report their experience with nine cases of acute pituitary apoplexy; eight had proven chromophobe adenomas, and two of these patients had the clinical stigmata of Cushing's syndrome. One patient who displayed acromegalic features was treated with x-ray, and no pathological specimen was obtained. The outstanding clinical features of acute pituitary apoplexy were sudden headache, depressed consciousness, ophthalmoplegia, meningismus, and signs of compression of the optic nerve or chiasma. Clinical or laboratory evidence of severe hypopituitarism was rare. The apoplectic syndrome was the first indication of the presence of a pituitary tumor in all nine cases. In one case anticoagulant therapy (for an acute myocardial infarction) appeared to have precipitated hemorrhage in an unrecognized chromophobe adenoma. The authors suggest that acute pituitary apoplexy is a surgical emergency resulting from sudden ischemia, necrosis, and hemorrhage when an expanding pituitary neoplasm has become impacted at the diaphragmatic notch.

An aneurysmal bone cyst originating from the squamous portion of the left temporal bone is reported. The lesion presented in a 62-year-old nonhypertensive man as a spontaneous, intraparenchymal left temporal lobe hematoma. No evidence of trauma, hermorrhagic diathesis, or concurrent systemic disease was found. Previous case reports of aneurysmal bone cysts of the skull are reviewed.

The purpose of this study was to determine the primary effects of subarachnoid hemorrhage (SAH) on cerebral oxidative metabolism and energy balance. Rhesus monkeys were prepared so that cerebral metabolic consumption rates of oxygen, glucose and the lactate/pyruvate ratios of CSF were estimated after isobarically and hyperbarically induced SAH. A regional analysis was performed on brain sections after similarly induced SAH in the rat, for levels of tissue, glucose, lactate, pyruvate, ATP, ADP, AMP, PCr and the partition of hexokinase between soluble and mitochondrial bound forms. The presence of intracranial hypertension was associated with an immediate ischemia, and increased cerebral glucose extraction was initially noted. Specific tissue substrate concentrations in rat brain indicated that fresh intracisternal hemorrhage is associated with decreased glycosis at a time when high energy phosphate levels are normal. It is concluded that intracranial hypertension hastens the onset of ischemia after SAH. SAH alone produces a decrease in cerebral energy requirements which secondarily depresses the rates of consumption of energy yielding substrates. The depression in metabolic rates may be mediated through a brain stem mechanism.

Ischemia-provoking factors such as vasospasm, decreased cerebral perfusion pressure, and intravascular thrombosis may be present after subarchnoid hemorrhage (SAH). When these factors were not present during controlled SAH, a primary depression of cerebral glycolysis associated with normal stores of energy-rich phosphates was found. Although cerebral blood flow usually changes in response to changes in cerebral metabolic needs, this influence on the circulation was not evident in the early hours after SAH. After 3 to 4 hours an erratic decrease in blood flow occurred, probably related to vasospasm, and there were measurable decreases in energy-rich phosphates similar to those occurring after more severe and prolonged ischemias. These findings are indicative of abnormally erratic vascular responses to metabolic cues and may play a role in producing the encephalopathy of SAH.