Gerardo Guinto Balanzar

Diaphragma Sellae: A Surgical Reference for Transsphenoidal Resection of Pituitary Macroadenomas

OBJECTIVE To classify patterns of descent of the diaphragma sellae (DS) to the sella turcica after transsphenoidal resection of pituitary macroadenomas and to determine whether there is any correlation between type of descent and volume or growth pattern of the tumor, as well as the presence of any postoperative hormone alteration, cerebrospinal fluid leak, and/or residual tumor. METHODS One hundred patients with pituitary macroadenomas in which microsurgical transsphenoidal approach was indicated were prospectively included. We classified patterns of descent of the DS into four types: type A: symmetrical descent with a central fold corresponding to the pituitary stalk; type B: asymmetrical with a lateralized fold; type C: symmetrical and uniform descent without any fold; and type D: minimal or no descent in absence of visible residual tumor. A correlation was made between these types of descent and clinical and radiological findings. RESULTS The largest tumors were types A and B; endocrine deficit was more frequent in types A and C, whereas the possibility of residual tumor was more elevated in types B and D. No statistically significant differences were found regarding tumor morphology and cerebrospinal fluid leakage. CONCLUSIONS Our results suggest that pattern of descent of the DS may serve as a reference to determine the risk of leaving residual tumor as well as the possibility of developing postoperative endocrine deficit. It is apparent that tumor volume, more than morphology, is the main factor determining type of descent of the DS.

Vasospasm in subarachnoid hemorrhage.

ubarachnoid hemorrhage (SAH) secondary to cerebral aneurysm rupture occurs with an approximate frequency S of 10 cases per 100,000 adults annually. Half of the patients who die do so before receiving medical attention. In approximately half of the patients who survive, a complication occurs that is known as focal and/or cognitive deficit secondary to cerebral vascular narrowing, or simply vasospasm (V). This complication usually appears between the fourth and ninth day of the hemorrhagic event and has a high index of morbidity and mortality, even when the aneurysm has been successfully excluded from the circulation. It is known that the risk factors most related to the presence of V are a greater quantity of blood in the subarachnoid space (SAS), particularly in the basal cisterns; poor neurological status; female gender; history of smoking; hydrocephalus; or increased intracranial pressure. Among those factors, the presence of blood in the SAS is undoubtedly the most important one associated with the genesis of this vascular narrowing. The precise pathophysiological mechanism by which V is generated has not yet been fully elucidated, but has been linked with the release of oxyhemoglobin and other vasoactive substances by the clot. The factors that have been mentioned are neuronal apoptosis; scavenging or reduction in the production of nitric oxide; increase in the levels of endothelin-1; direct oxidative stress on smooth muscle cells of the arterial wall; production of free radicals; lipid peroxidation of cell membranes; modification of calcium and potassium channels; and differential

Nontraumatic Subarachnoid Hemorrhage: Clinical Outcome

ontraumatic subarachnoid hemorrhage (SAH) represents 3%e6% of all cases of cerebrovascular disease, N which translates to an annual incidence of 8e10 cases/ 100,000 population. The most common cause is a rupture of a cerebral aneurysm, which occurs with a frequency of approximately 90%. However, in some cases, the exact cause cannot be determined. Although many theories have been formulated, uncertainty currently exists regarding the exact mechanism by which a cerebral aneurysm forms or ruptures. It is highly probable that the problem is multifactorial, with involvement of structural elements of the arteries, angiogenic factors, and vasoactive substances. Some theories have been postulated to explain the cause of bleeding in cases of spontaneous SAH without aneurysm. Arterial hypertension is one of the most accepted theories; another is the presence of a small thrombosed aneurysm, which is impossible to visualize in initial imaging studies.