The authors present a critical review of the literature on the hemorrhagic complications of pituitary adenomas, especially those leading to apoplexy. They emphasize the distinction between pituitary apoplexy, hemorrhages leading to sudden endocrine alterations, and asymptomatic hemorrhages. Moreover, they speculate upon the possible pathophysiology of pituitary apoplexy and its predisposing factors. The clinical presentation, natural history, radiological findings, and differential diagnosis are also discussed. Finally, the historical evolution of the treatment of pituitary apoplexy is reviewed, with emphasis on the surgical treatment.

The authors investigated the pharmacokinetics of mannitol administered for treatment of vasogenic cerebral edema. A cortical cold injury was produced in 23 cats maintained under general anesthesia for 5 or 21 hours. Control animals received no mannitol, while treatment groups received either a single dose or five doses administered at 4-hour intervals of 0.33 gm/kg radiolabeled mannitol. Liquid scintillation counting was carried out to determine the concentrations of mannitol in the cerebral tissue, cerebrospinal fluid, plasma, and urine. Cerebral water content and linear progression of edema were also measured. Rapid plasma clearance prevented accumulation of mannitol after multiple intravenous injections, as 84% +/- 2% (mean +/- standard error of the mean) of the infused mannitol was excreted through the urine. However, there was progressive accumulation of mannitol within the cerebral tissue, especially in the edematous white matter where it reached a level of 0.33 +/- 0.03 mg/gm after five doses, exceeding the trough plasma concentrations by a ratio of 2.69:1. Water content measurement showed that a single dose of mannitol failed to reduce cerebral water content or edema progression at 4 hours postinjection, while multiple doses produced a 3% increase in water content in edematous regions (p greater than 0.0003). The results of this study demonstrated a reversal of the osmotic concentration gradient between edematous brain and plasma following multiple mannitol injections, associated with exacerbation of vasogenic cerebral edema.

The configuration of the intracranial pressure (ICP) pulse wave represents a complex sum of various components. Amplitude variations of an isolated component might reflect changes in a specific intracranial structure. Fifteen awake patients suffering from hydrocephalus, benign intracranial hypertension, or head injury underwent ICP monitoring through a ventricular catheter and were subjected to three standardized maneuvers to alter the intracranial dynamics: head elevation, voluntary hyperventilation, and cerebrospinal fluid (CSF) withdrawal. A 12 degrees head elevation and fractionated CSF withdrawal caused a mild ICP drop and a proportionate amplitude reduction of all the wave components. Voluntary hyperventilation caused a comparable fall in ICP, and a disproportionate reduction in the amplitude of the wave components, especially the P2 component. It is postulated that the decrease in amplitude of the P2 component reflects the reduction of the cerebral bulk caused by hyperventilation. Head elevation and CSF withdrawal caused a decrease of global ICP but no specific changes in any intracranial structure, and consequently the configuration of the pulse wave remained unchanged. The establishment of relationships between anatomical substrate and particular wave components is promising since potentially it could be useful for monitoring conditions such as vasoparalysis, impaired cerebrovascular reactivity, and cerebral edema.

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