Minimally invasive management of ependymoma of the aqueduct of Sylvius: therapeutic considerations and management.

A major concern in the neuroendoscopic approach to an intraventricular tumor is the histological confirmation from a limited biopsy. However, the effort to excise the whole bulk of the tumor should be made for the minimally invasive management of selected intraventricular tumors. The case of an adult male with focal aqueductal ependymoma who presented with the clinical syndrome of hydrocephalus is reported. This may be of particular interest because it represents the first case of aqueductal ependymoma that has been successfully treated with endoscopic surgery.

Dementia with Lewy bodies showing advanced Lewy pathology but minimal Alzheimer pathology--Lewy pathology causes neuronal loss inducing progressive dementia.

The present study concerns an autopsied case of dementia with Lewy bodies (DLB) showing advanced Lewy pathology but minimal Alzheimer pathology. The patient was a 50-year-old Japanese male without inheritance. His initial symptoms at the age of 43 suggested the diagnosis ofjuvenile idiopathic Parkinson's disease (PD), but were followed by memory disturbance 1 year later. He showed parkinsonism, dementia, personality change, fluctuating cognition and visual hallucinations 3 years later. Neuroradiological examination revealed moderate brain atrophy, predominantly in the frontal and temporal lobes. Neuropathological examination demonstrated a widespread occurrence of Lewy bodies (LB) with LB-related neurites not only in the brainstem but also in the cerebrum. The present case showed Lewy pathology which corresponded to stage IV by our staging and was parallel to neuronal loss. There was marked neuronal loss with many LB-related neurites in the CA2 of the hippocampus. Neurofibrillary tangles (NFT) were almost restricted to the entorhinal cortex, while senile plaques were absent. Consequently, the present case was pathologically diagnosed as having DLB of the neocortical type, pure form. In the present study, we suggest that Lewy pathology in the cerebral cortex could be responsible for progressive dementia.

Extrusion of intracellular calcium ion after in vitro ischemia in the rat hippocampal CA1 region.

Simultaneous recordings of intracellular Ca(2+) ([Ca(2+)](i)) signal and extracellular DC potential were obtained from the CA1 region in 1-[6-amino-2-(5-carboxy-2-oxazolyl)-5-benzofuranyloxy]-2-(2-amino-5-methylphenoxy)-ethane-N,N,N',N'-tetraacetic acid penta-acetoxymethyl ester (Fura-2/AM)-loaded rat hippocampal slices. Superfusion with oxygen- and glucose-deprived medium (in vitro ischemia) for 5-6 min produced a rapid rise of the [Ca(2+)](i) level in the stratum radiatum (rising phase of the [Ca(2+)](i) signal), which occurred simultaneously with a rapid negative DC potential (rapid negative potential). When oxygen and glucose were reintroduced, the increased [Ca(2+)](i) signal diminished rapidly (falling phase of the [Ca(2+)](i) signal) during the generation of a slow negative DC potential (slow negative potential), which occurred within 1 min from the onset of the reintroduction. Thereafter, the [Ca(2+)](i) signal partially and the slow negative potential completely returned to the preexposure level approximately 6 min after the reintroduction. The changes in [Ca(2+)](i) signal during and after in vitro ischemia were very similar to the changes in the membrane potential of glial cells. The rising and falling phases of [Ca(2+)](i) signal corresponded to the rapid depolarization and a depolarizing hump, respectively, in the repolarizing phase of glial cells. A prolonged application of in vitro ischemia or a reintroduction of either glucose or oxygen suppressed the falling phase after ischemic exposure. The application of ouabain (30 microM) generated both a rapid negative potential and a rapid elevation of [Ca(2+)](i), but no slow negative potential or rapid reduction in [Ca(2+)](i) were observed. When oxygen and glucose were reintroduced to slices in the Na(+)-free or ouabain- or Ni(2+)-containing medium, the falling phase was suppressed. The falling phase was significantly accelerated in Ca(2+)- and Mg(2+)-free with EGTA-containing medium. In contrast, the falling phase was significantly slower in the Ca(2+)-free with high Mg(2+)- and EGTA-containing medium. The falling phase of the [Ca(2+)](i) signal after ischemic exposure is thus considered to be primarily dependent on the reactivation of Na(+), K(+)-ATPases, while the extrusion of cytosolic Ca(2+) via the forward-mode operation of Na(+)/Ca(2+) exchangers in glial cells is thought to be directly involved in the rapid reduction of [Ca(2+)](i) after ischemic exposure.

Cervical myelopathy due to compression by bilateral vertebral arteries--case report.

A 69-year-old man presented with progressive cervical myelopathy due to vascular compression of the upper cervical spinal cord. Vertebral angiography and magnetic resonance imaging revealed that the elongated bilateral vertebral arteries (VAs) had compressed the spinal cord at the C-2 level. The spinal cord was surgically decompressed laterally by retracting the VAs with Gore-Tex tape and anchoring them to the dura. The patient's symptoms improved postoperatively. Decompression and anchoring of the causative vessels is recommended due to the large size of the VAs.

Na+/Ca2+ exchanger activity induces a slow DC potential after in vitro ischemia in rat hippocampal CA1 region.

In rat hippocampal CA1 neurons recorded intracellularly from tissue slices, a rapid depolarization occurred approximately 5 min after application of ischemia-simulating medium. In extracellular recordings obtained from CA1 region, a rapid negative-going DC potential (rapid DC potential) was recorded, corresponding to a rapid depolarization. When oxygen and glucose were reintroduced after generating the rapid depolarization, the membrane further depolarized and the potential became 0 mV after 5 min. Contrary, the DC potential began to repolarize slowly and subsequently a slow negative-going DC potential (slow DC potential) occurred within 1 min. A prolonged application of ischemia-simulating medium suppressed the slow DC potential. Addition of a high concentration of ouabain in normoxic medium reproduced a rapid but not a slow DC potential. The slow DC potential was reduced in low Na+- or Co2+-containing medium, but was not affected in low Cl-, high K+ or K+-free medium, suggesting that the slow DC potential is Na+-and Ca2+-dependent. Ni2+ (Ca2+ channel blocker as well as the Na+/Ca2+ exchanger blocker) and benzamil hydrochloride (Na+/Ca2+ exchanger blocker) reduced the slow DC potential dose-dependently. These results suggest that the slow DC potential is mediated by forward mode operation of Na+/Ca2+ exchangers in non-neuronal cells, and that reactivation of Na+, K+-ATPase is necessary to the Na+/Ca2 +exchanger activity.

[A case of crushing head injury with bilateral abducens and facial nerve palsies].

A 20-year-old male was admitted to our hospital suffering from a crushing head injury. At accident, his head had been compressed by the printing machine on both temporal regions. He remained at dull conscious. On admission one hour after the injury, he showed bilateral sixth-nerve and seventh nerve palsies and bleeding from the nose. CT scan showed marked pneumocephalus, traumatic subarachnoid hemorrhage, fluid collections in the bilateral sphenoid sinuses and right mastoid air cells. Bone CT disclosed bilateral temporal bone fractures. MRI did not show cerebral parenchymal damage. He recovered fully conscious at four hours after the injury, but cranial nerve palsies sustained over 30 days after the injury. Bilateral decompression of the facial canal were performed at day 31. At one year after the injury, bilateral abducens nerve palsies and facial nerve palsies recovered incompletely (grade III). The case report and the mechanism of such cranial nerve injuries by low-velocity crushing head injury is described.