Roberto C. Heros

Origin, growth, and rupture of saccular aneurysms: A review

Pathological and hemodynamic concepts regarding the origin, growth, and rupture of intracranial saccular aneurysms are reviewed. Aneurysms form as a result of an interplay between hemodynamic factors, such as axial stream impingement and the water hammer effect, and structural weaknesses at apices of arterial bifurcations, such as congenital and acquired medial defects, funnel-shaped dilatations, and areas of thinning. Hypertension and time aid the formation of aneurysms. Unknown factors in women and in some families also play a role. Enlargement of aneurysms results from an interplay between mechanical factors, such as self-excitation and resonance, that produce structural fatigue and pathological processes of repair of the aneurysmal wall. Rupture of aneurysms is caused by the same hemodynamic factors that effect growth and is also influenced by extramural pressure. Pathologically, a major rupture may be preceded by fibrinous and leukocytic infiltration of the wall, bleb formation, and a minor hemorrhage. Such minor leaks can be followed by healing and growth. Aneurysms that escape major hemorrhage or heal successfully after a hemorrhage can grow to giant proportions, but remain susceptible to rupture despite their size, unless they become completely thrombosed. Intramural thrombosis may be stimulated by minor leaks and is dependent upon the physical characteristics of aneurysms. Experimental, angiographic, and clinical studies that pertain to the origin, growth, and rupture of aneurysms are also reviewed.

Intraoperative hypoxia detected by evoked potential monitoring.

Somatosensory cortical evoked potentials (SCEP) are used to monitor spinal cord function during operations on the spine and spinal cord (1-3). These intermediate latency responses to stimulation of peripheral nerves originate in the cerebral cortex (4). They are subject to alteration by anesthetics (5,6) and by perturbations of physiologic state that may occur during surgery (7, 8). If SCEP monitoring is to reflect reliably surgical trespass on sensory pathways, potentially confounding factors that also affect SCEP must be monitored and kept as constant as possible. SCEP recording may detect not only physical encroachment on conducting pathways at the operative site but also systemic physiologic changes that require correction. We have observed SCEP alterations as the presenting manifestation of intraoperative hypoxia.

Monitoring of cortical somatosensory evoked potentials to determine the safety of sacrificing the anterior cerebral artery

Cortical somatosensory evoked potentials (SSEPs) reflect the functional integrity of somatosensory pathways from the site of stimulation to the primary somatosensory cortex. We used intraoperative monitoring of cortical SSEPs to determine whether the right anterior cerebral artery (RACA), the major feeding vessel of a large arteriovenous malformation (AVM), could be sacrificed without compromising sensorimotor function in the left lower extremity. The SSEPs recorded after test occlusion of the RACA showed preservation of the initial cortical positivity, and the RACA was divided. The AVM was excised completely, and the patient suffered no neurological deficit.

Intracranial lipoma with hematopoietic elements (myelolipoma). Report of a case with successful surgical resection

A 74‐year‐old woman presented with a symptomatic posterior fossa mass which was successfully resected. Histologic examination revealed that the tumor was composed primarily of adipose and hematopoietic tissues warranting the diagnosis of myelolipoma. This represents the first case report of intracranial myelolipoma as well as the first reported successful surgical resection of this tumor in this location. A review of this subject indicates that the term myelolipoma denotes tumors with at least two different etiologies. The first represents metaplastic differentiation within a lipoma and the second appears to be a response of adrenal tissue to noxious stimuli.

An experimental study of the influence of antifibrinolytic therapy on post-subarachnoid-hemorrhagic cerebral vasospasm and hydrocephalus

The incidence and severity of cerebral vasospasm and hydrocephalus following induced subarachnoid hemorrhage in an experimental group of animals that subsequently received epsilon-aminocaproic acid was compared to that seen in a control group that received no antifibrinolytic therapy. No augmentation of either vasospasm or hydrocephalus could be attributed to the epsilon-aminocaproic acid in the treated as compared to the control group.