Marcia C. da Silva

Reduced local cerebral blood flow in periventricular white matter in experimental neonatal hydrocephalus-Restoration with CSF shunting

The extent to which the reduction in CBF occurring in hydrocephalus is a primary or secondary event in the pathogenesis of the brain injury that ensues has not been clearly established. This is particularly true in neonatal hydrocephalus, where the disorder is most common, and where timing of the treatment of the developing nervous system is so important. We investigated the changes in local CBF (lCBF) in an animal model of severe progressive neonatal hydrocephalus before and after CSF shunting. Hydrocephalus was induced in 27 1-week-old kittens by percutaneous injection of 0.05 ml of 25% kaolin into the cisterna magna. Fourteen littermates acted as controls. The lCBF was measured by 14C-iodoantipyrine quantitative autoradiography after 1 week in 15 animals (8 hydrocephalic, 7 controls) and after 3 weeks in 26 animals (19 hydrocephalic, 7 controls) following induction of hydrocephalus. Twelve of the 3-week hydrocephalic group received a ventriculoperitoneal shunt 10 days following kaolin injection. At 1 week following induction of hydrocephalus, lCBF was globally reduced in cortical gray matter and white matter as well as deep subcortical structures. The maximum reduction was in the parietal white matter, to 37% of control levels. At 3 weeks a significant reduction in lCBF persisted only in the white matter (parietal, occipital, and corpus callosum; average, 42% of control levels), whereas cortical gray and deep subcortical structures had returned to normal levels spontaneously. lCBF was normal in 3-week hydrocephalic shunted animals in all areas. CSF shunting restores the fall in lCBF in the periventricular white matter in this model. These findings are consistent with previous studies in the same model demonstrating derangement of high-energy phosphate metabolism and white matter anaerobic glycolysis with hydrocephalus and resolution with shunting.

Functional Obstruction of an Antisiphon Device by Raised Tissue Capsule Pressure

The proper function of an antisiphon device (ASD) requires that it be exposed externally to atmospheric pressure and that its mobile membrane be free to move. A 4-year-old boy who had an ASD placed for postshunt subdural hematomas presented with functional obstruction of the ASD-symptomatic ventriculomegaly despite evidence of patency of the shunt system by radionuclide flow study. At surgery, the distal shunt system including the ASD was infused with normal saline before and after surgical exposure of the device. The pressures required to maintain a flow rate of 5 ml/h and 50 ml/h were 27 mm Hg and 30 mm Hg, respectively. After surgical exposure, these pressures fell to 0 mm Hg and 5 mm Hg, respectively, for the same infusion rates. Surgical exposure removes the effects of the tissue capsule, including the overlying skin and a collagenous sheath, restoring the external pressure to atmospheric pressure. Functional obstruction of ASDs occurs because of raised ambient pressure from the tissue capsule acting to depress the mobile membrane of the ASD, increasing its resistance to flow. This case confirms previously reported effects of subcutaneous implantation of ASDs in experimental animals and is the probable explanation for reported functional obstruction of ASDs in other patients.

Effect of Subcutaneous Implantation of Anti-Siphon Devices on CSF Shunt Function

Anti-siphon devices (ASD) were initially bench tested at flow rates between 10 and 50 cm3/h and with the distal catheter height between 0 and -60 cm. There was a small increase in pressure with increased flow rate in the horizontal position (p less than 0.001). The inflow pressure initially dropped with the distal catheter height at -20 cm; it then rose progressively with distal catheter heights of -40 and -60 cm (p less than 0.001). To determine the effect of ambient pressure the devices were placed in a barometric chamber at pressures between -200 and +200 mm H2O. Positive pressures caused a linear increase in inflow pressure; negative chamber pressure reduced the anti-siphon effect. Eight ASDs were implanted subcutaneously in piglets and tested in situ weekly for 4 weeks. Implantation caused a mean increase in inflow pressure of 93.5 mm H2O 7 days after implantation (p less than 0.001) and which persisted for 4 weeks. Incision of the capsule surrounding the ASD at the end of 4 weeks caused a drop in pressure. The capsule consisted of an outer layer of collagen fibres with an inner layer of histiocytes. Subcutaneous implantation of ASDs causes an increase in the ambient pressure of the device which significantly increases their resistance to flow.

Fourth ventriculostomy: an alternative treatment for hydrocephalus due to atresia of the Magendie and Luschka foramina

Atresia of the foramina of Magendie and Luschka is a rare cause of obstructive hydrocephalus. Although this condition has been classically treated by CSF shunting, recent treatments have also included endoscopic third ventriculostomy. In the present study, the authors present the case of a patient with hydrocephalus in whom an alternative method was used following a CSF shunt malfunction. A young female patient in whom a shunt was placed during the patients 1st year of life was faring well until she was 8 years old. She was admitted to the emergency department 5 times with signs of CSF shunt malfunction. Each time, the CT scan showed a slight dilation of the lateral and third ventricles and a large increase in the size of the fourth ventricle. In comparison, ventricles were smaller in a previous imaging study obtained when the patient was asymptomatic. Magnetic resonance imaging showed the same slight dilation of all the ventricles and a significant increase in the fourth ventricle. There was no aqueductal stenosis. An important enlargement of both lateral recesses of the fourth ventricle suggested the possibility of an atresia of the foramina. The foramen of Monro and the width of the third ventricle would not allow the passage of an endoscope. The decision was made to open those foramina endoscopically through the fourth ventricle. After induction of general anesthesia, with the patient in the prone position, a bur hole was made in the left paramedian and suboccipital region. The endoscope was introduced underneath the cerebellar hemisphere. The authors were then able to distinguish the floor of the fourth ventricle and other anatomical landmarks. Navigation through the lateral recesses allowed them to see the fine membranes closing the foramina. These membranes were opened with a monopolar cautery as a blunt instrument. The orifice was then enlarged with a 3 Fr Fogarty catheter. The authors also opened a bulging thin membrane located at the foramen of Magendie. During the postoperative period, the authors observed a marked improvement in the state of the patients alertness as well as a disappearance of her headaches and cessation of vomiting. In addition, the patients gait ataxia improved slowly. Six-month postoperative MR imaging demonstrated an unequivocal reduction in the size of the fourth ventricle. The patient was still doing well 36 months after the surgery. Endoscopic fourth ventriculostomy, the opening of the 3 foramina of the fourth ventricle, may be an alternative treatment in cases in which these structures are congenitally closed.

Spontaneous acute subdural hematoma contralateral to an arachnoid cyst

Arachnoid cysts (AC) are extra-cerebral cerebrospinal fluid collections of unknown origin. They correspond to 1% of all intracranial nontraumatic space-occupying lesions and appear more frequently in the middle fossa (50%). More than 25% of these cysts are incidental findings and the majority of patients are asymptomatic. Seizures, intracranial hypertension signs, neurological deficits, macrocrania, developmental delay and bulging of the skull are the main signs and symptoms of the lesion. AC rupture and bleeding are rare, usually occurring in young adults and associated with trauma. The risk of hemorrhage does not exceed 0.04% / year. We describe the case of a ten-year-old boy who presented with acute signs of intracranial hypertension secondary to a spontaneous acute subdural hematoma, contralateral to an AC of the middle fossa. Three factors were significant in this case: signs and symptoms occurred spontaneously; the presence of an acute subdural hematoma exclusively contralateral to the AC; successful outcome of the conservative treatment.