A juvenile case of cerebellar arteriovenous malformation with gradual onset of dysphoria and headache.

A 25-year-old woman was admitted because of frequent vomiting and headache which had lasted over one week. She had initially clear consciousness but slowly progressive mild headache and dysphoria. Emergency cranial CT revealed a 4 cm haematoma in the left cerebellar hemisphere. CT angiography showed a 2×2 cm nidus of an arteriovenous malformation (AVM) in the left hemisphere fed from the left posterior inferior cerebellar artery and draining into the inferior hemispheric vein. We performed a surgical resection of the AVM after decompression therapy to counteract the brain oedema. She recovered completely without any neurological deficits. This case recalls the importance of cooperation between diagnostic neuroradiology and neurosurgery in emergency, considering AVM, even if infrequent, among possible diseases.

Cerebral blood flow autoregulation during intracranial hypertension: a simple, purely hydraulic mechanism?

OBJECTIVE: In this paper, we re-propose the role of a hydraulic mechanism, acting where the bridging veins enter the dural sinuses in cerebral blood flow (CBF) autoregulation. MATERIALS AND METHODS: We carried out an intraventricular infusion in ten albino rabbits and increased intracranial pressure (ICP) up to arterial blood pressure (ABP) levels. We measured CBF velocity by an ultrasound probe applied to a by-pass inserted in a carotid artery and recorded ICP by an intraventricular needle. Diastolic and pulsatile ICP and ABP values were analyzed from basal conditions up to brain tamponade and vice versa. CONCLUSIONS: A biphasic pattern of pulsatile intracranial pressure (pICP) was observed in all trials. Initially, until the CBF velocity remained constant, pICP increased (from 1.2 to 5.4 mmHg) following a rise in diastolic intracranial pressure (dICP); thereafter, in spite of a further rise in dICP, pICP decreased (2.87 mmHg) following CBF velocity reduction until intracranial circulation arrest (pICP=1.2 mmHg). A specular pattern was observed when the intraventricular infusion was stopped and CBF velocity returned to basal levels. These findings can be interpreted as indicating a hydraulic mechanism. Initially, when CBF is still constant, pICP rise is due to an increase in venous outflow resistance; subsequently, when CBF decreases following a further increase in venous outflow resistance, the vascular engorgement produces an arteriolar vasodilation. This vasodilation determines an increase in vascular wall stiffness, thus reducing pulse transmission to surrounding subarachnoid spaces.

Spontaneous regression of a symptomatic pineal cyst after endoscopic third-ventriculostomy.

With the advent of modern diagnostic tools for neuroimaging, the incidental detection of pineal cysts in asymptomatic subjects has increased. Only rarely do pineal cysts present with the clinical signs and symptoms of increased intracranial pressure or with neurological deficits in relation to compression and distortion of the adjacent nervous structures and cerebrospinal fluid pathways. While asymptomatic cysts are considered to be normal variants for which no further investigations are usually required, surgical treatment is suggested for symptomatic cysts, with the goal of eliminating the block in the cerebrospinal fluid circulation and/or the mass effect exerted by the lesion. In this report we describe a pediatric case of symptomatic pineal cyst, revealed by repeated episodes of headache caused by secondary obstructive hydrocephalus. Following an endoscopic third-ventriculostomy, serial magnetic resonance imaging studies demonstrated that not only had the ventriculomegaly resolved but also that the pineal cyst had regressed over time. A to-and-fro movement of fluid through the cyst wall, the direction of which depends on the equilibrium existing between the inner pressure of the cyst and the outer cerebrospinal fluid pressure, is suggested as a possible mechanism accounting for this unexpected result--to our knowledge, the first reported in literature.

Blood salvage in craniosynostosis surgery.

In the history of surgery, every single step forward in the development of complex surgical techniques has been sustained by the acquisition of more reliable and effective methods for controlling hemostasis. For many years, in fact, uncontrolled hemorrhages, together with infections, represented the most deadly hazard of surgical procedures. In the last century, technical advances in surgical hardware and homologous blood transfusions have been utilized to counteract operative and postoperative anemia and hypovolemia. At the end of this millennium, however, new revelations about the infective and noninfective risks of allogeneic blood transfusions have led to a new acceleration in patients' and physicians' demands for autologous transfusions and more efficient blood conservation techniques. Specific surgical protocols, based on the preoperative administration of r-HuEPO, preoperative autologous blood donation, acute preoperative normovolemic hemodilution and intraoperative blood salvage techniques, have been designed by pediatric neurosurgeons to minimize the exposure of patients affected by craniosynostoses to allogeneic blood and blood components even when the surgical procedure is to be realized at an early age. In spite of the evolution expected in this area in the immediate future, the implementation of these blood concentration methodologies may prove to be highly effective only when associated with a concerned attitude of the surgeon toward blood-sparing intraoperative strategies.

"No allogeneic blood transfusion" protocol for the surgical correction of craniosynostoses. II. Clinical application.

The authors describe the results obtained in 13 consecutive cases of craniosynostosis operated on according to a protocol devised at avoiding allogeneic blood transfusion. The protocol is based on pre- and postoperative treatment with erythropoietin, preoperative autologous blood donation, preoperative normovolemic hemodilution and intraoperative blood salvage. Nine subjects were affected by simple forms of craniosynostosis, whereas the remaining 4 presented with oxycephaly or craniofacial syndromes. Five of the 13 children were under 7 months and a further 3, under 10 months of age at the time of the surgical operation. Seven children weighed less than 10 kg. Allogeneic blood transfusion was avoided in 11 of the 13 children considered. Two failures - defined as the necessity to reinfuse the patient with an allogeneic blood transfusion - were recorded, 1 of them resulting from an unexpected hemorrhage during surgery. The results obtained indicate that this protocol designed to avoid allogeneic blood transfusion can be safely applied in the great majority of children with craniosynostosis, even when the surgical correction is carried out early in life.

"No allogeneic blood transfusion" protocol for the surgical correction of craniosynostoses. I. Rationale.

Improved anesthesiological and surgical care has resulted in a progressively declining need for allogeneic blood transfusion. In infants with craniosynostosis, however, allogeneic blood transfusion is still performed as a routine procedure. In the present paper, the authors describe a protocol they have devised with the aim of limiting or even avoiding allogeneic blood transfusion even in very young patients, consequently avoiding the risks of infective or immunologic reactions associated with the procedure. The protocol is based on stimulation of the hematopoietic system with erythropoietin, selection of an appropriate age for operation when a favorable balance between fetal and adult-type hemoglobin is established (that is after 4-6 months), preoperative preparation of the autologous blood supply, and intraoperative blood salvage.