Microvascular Decompression for Glossopharyngeal Neuralgia in the Semi-Sitting Position: A Report of Two Cases.

The semi-sitting position is well known to neurosurgeons. However, there are few reports of microvascular decompression surgery for glossopharyngeal neuralgia performed using the semi-sitting position. The semi-sitting position is not widely adopted in Japan, but it is considered to be a very useful neurosurgical position. Microvascular decompression surgery for glossopharyngeal neuralgia is a relatively rare procedure, and the semi-sitting position is very effective, considering the possibility of intraoperative cardiac arrest and postoperative complications of lower cranial nerve palsy. This report describes two cases of glossopharyngeal neuralgia operated in the semi-sitting position. Microvascular decompression was performed on both patients, and postoperative pain controls were good and no complications were observed. We show that the use of the semi-sitting position to perform microvascular decompression for glossopharyngeal neuralgia provides an excellent surgical view of the brainstem.

Limitations of median nerve somatosensory evoked potential monitoring during carotid endarterectomy.

OBJECTIVE: Hypoperfusion during carotid artery cross-clamping (CC) for carotid endarterectomy (CEA) may result in the major complication of perioperative stroke. Median nerve somatosensory evoked potential (MNSSEP) monitoring, which is an established method for the prediction of cerebral ischemia, has low sensitivity in detecting such hypoperfusion. In this study the authors sought to explore the limitations of MNSSEP monitoring compared to tibial nerve somatosensory evoked potential (TNSSEP) monitoring for the detection of CC-related hypoperfusion. METHODS: The authors retrospectively analyzed data from patients who underwent unilateral CEA with routine shunt use. All patients underwent preoperative magnetic resonance angiography and were monitored for intraoperative cerebral ischemia by using MNSSEP, TNSSEP, and carotid stump pressure during CC. First, the frequency of MNSSEP and TNSSEP changes during CC were analyzed. Subsequently, variables related to stump pressure were determined by using linear analysis and those related to each of the somatosensory evoked potential (SSEP) changes were determined by using logistic regression analysis. RESULTS: A total of 94 patients (mean age 74 years) were included in the study. TNSSEP identified a greater number of SSEP changes during CC than MNSSEP (20.2% vs 11.7%; p < 0.05). Linear regression analysis demonstrated that hypoplasia of the contralateral proximal segment of the anterior cerebral artery (A1 hypoplasia) (p < 0.01) and hypoplasia of the ipsilateral precommunicating segment of the posterior cerebral artery (P1 hypoplasia) (p = 0.02) independently and negatively correlated with stump pressure. Both contralateral A1 hypoplasia (OR 26.25, 95% CI 4.52-152.51) and ipsilateral P1 hypoplasia (OR 8.75, 95% CI 1.83-41.94) were independently related to the TNSSEP changes. However, only ipsilateral P1 hypoplasia (OR 8.76, 95% CI 1.61-47.67) was independently related to MNSSEP changes. CONCLUSIONS: TNSSEP monitoring appears to be superior to MNSSEP in detecting CC-related hypoperfusion. Correlation with stump pressure and SSEP changes indicates that TNSSEP, and not MNSSEP monitoring, is a reliable indicator of cerebral ischemia in the territory of the anterior cerebral artery.

Delayed Postoperative Spinal Epidural Hematoma after Cervical Laminoplasty.

A 56-year-old man underwent cervical laminoplasty for cervical spondylosis. On the 7th postoperative day, he suddenly felt severe neck pain, and tetraplegia developed rapidly over 1.5 hrs. Computed tomography demonstrated a huge hematoma compressing the cervical spinal cord. Clot was evacuated 3 hrs after the onset of symptoms. The patient's postoperative course was uneventful. His blood pressure could not be properly controlled in the perioperative period. Surgeons should keep in mind that delayed postoperative spinal epidural hematoma (DPSEH) can occur more than a week after surgery, and meticulous blood pressure control is important for more than a week after a spinal operation.

[Intra-tumoral hemorrhage caused by foramen magnum meningioma: a case report].

Intratumoral bleeding from a meningioma is very rare. We herein report a case of a foramen magnum meningioma which presented in association with intratumoral bleeding. A 49-year-old female who had been suffering from occipital headache and shoulder pain on neck motion was referred to our hospital to undergo treatment for a tumor located in the posterior fossa. Magnetic resonance imaging (MRI) demonstrated a foramen magnum meningioma which originated at the lower clivus and extended to the C2 level of the vertebral column. Marked compression and distortion of the medulla oblongata and spinal cord was also noted. Surgery was therefore planned. The patient thereafter suffered from a sudden onset of headache, vomiting and hoarseness, and was transferred to our hospital. A computed tomography (CT) showed intratumoral bleeding, which extended to the subarachnoid space and the fourth ventricle. The tumor, as well as the massive hematoma, were both immediately removed. The histological diagnosis was meningothelial meningioma. We also reviewed the pertinent literature and propose the possible mechanism for such tumor bleeding in this particular location in which the blockage of the cerebrospinal fluid caused a craniovertebral pressure gradient, which thus resulted in intratumoral bleeding.

Angiotensin II impairs neurovascular coupling in neocortex through NADPH oxidase-derived radicals.

Angiotensin II (Ang II) exerts detrimental effects on cerebral circulation, the mechanisms of which have not been elucidated. In particular, Ang II impairs the increase in cerebral blood flow (CBF) produced by neural activity, a critical mechanism that matches substrate delivery with energy demands in brain. We investigated whether Ang II exerts its deleterious actions by activating Ang II type 1 (AT1) receptors on cerebral blood vessels and producing reactive oxygen species (ROS) through NADPH oxidase. Somatosensory cortex CBF was monitored in anesthetized mice by laser-Doppler flowmetry. Ang II (0.25 microg/kg per minute IV) attenuated the CBF increase produced by mechanical stimulation of the vibrissae. The effect was blocked by the AT1 antagonist losartan and by ROS scavenger superoxide dismutase or tiron and was not observed in mice lacking the gp91phox subunit of NADPH oxidase or in wild-type mice treated with the NADPH oxidase peptide inhibitor gp91ds-tat. Ang II increased ROS production in cerebral microvessels, an effect blocked by the ROS scavenger Mn(III)tetrakis (4-benzoic acid) porphyrin and by the NADPH oxidase assembly inhibitor apocynin. Ang II did not increase ROS production in gp91-null mice. Double-label immunoelectron microscopy demonstrated that AT1 and gp91phox immunoreactivities were present in endothelium and adventitia of neocortical arterioles. Collectively, these findings suggest that Ang II impairs functional hyperemia by activating AT1 receptors and inducing ROS production via a gp91phox containing NADPH oxidase. The data provide the mechanistic basis for the cerebrovascular dysregulation induced by Ang II and suggest novel therapeutic strategies to counteract the effects of hypertension on the brain.

Abeta-induced vascular oxidative stress and attenuation of functional hyperemia in mouse somatosensory cortex.

We investigated the role of vascular oxidative stress in the mechanisms of the impairment in cerebrovascular regulation produced by the amyloid-beta peptide (Abeta). In particular, we sought to provide evidence of vascular oxidative stress in mice overexpressing the amyloid precursor protein (APP) and to determine whether the Abeta-induced attenuation in functional hyperemia is mediated by free radical overproduction. Oxidative/nitrosative stress was assessed by 3-nitrotyrosine immunoreactivity, while free radical production was determined in cerebral microvessels by hydroethidine microfluorography. To study functional hyperemia the somatosensory cortex was activated by whisker stimulation while local blood flow was monitored by laser-Doppler flowmetry. It was found that APP mice show signs of oxidative/nitrosative stress in pial and intracerebral blood vessels well before they develop oxidative stress in neurons and glia or amyloid plaques. Treatment of cerebral microvessels isolated from wild-type mice with Abeta (1 microM) increased free radical production as assessed by the hydroethidine technique. The Abeta-induced attenuation of the increase in somatosensory cortex blood flow produced by whisker stimulation was prevented by treatment with the free radical scavengers MnTBAP or tiron. These data provide evidence that in APP mice vascular oxidative stress precedes the development of parenchymal oxidative stress, and that Abeta-produced vascular reactive oxygen species are involved in the attendant attenuation in functional hyperemia. Thus, vascular oxidative stress is an early event in the course of the brain dysfunction produced by APP overexpression and Abeta, and, as such, could be the target of early therapeutic interventions based on antioxidants.

Angiotensin II attenuates functional hyperemia in the mouse somatosensory cortex.

We investigated whether angiotensin II (ANG II), a peptide that plays a central role in the genesis of hypertension, alters the coupling between synaptic activity and cerebral blood flow (CBF), a critical homeostatic mechanism that assures adequate cerebral perfusion to active brain regions. The somatosensory cortex was activated by stroking the facial whiskers in anesthetized C57BL/6J mice while local CBF was recorded by laser-Doppler flowmetry. Intravenous ANG II infusion (0.25 mug.kg-1.min-1) increased mean arterial pressure (MAP) from 82 +/- 2 to 102 +/- 3 mmHg (P < 0.05) without affecting resting CBF (P > 0.05). ANG II attenuated the CBF increase produced by whisker stimulation by 65% (P < 0.05) but did not affect the response to hypercapnia or to neocortical application of the nitric oxide donor S-nitroso-N-acetyl penicillamine (P > 0.05). The effect of ANG II on functional hyperemia persisted if the elevation in MAP was offset by controlled hemorrhage or prevented by topical application of the peptide to the activated cortex. ANG II did not reduce the amplitude of the P1 wave of the field potentials evoked by whisker stimulation (P > 0.05). Infusion of phenylephrine increased MAP (P > 0.05 from ANG II) but did not alter the functional hyperemic response (P > 0.05). The data suggest that ANG II alters the coupling between CBF and neural activity. The mechanisms of the effect are not related to the elevation in MAP and/or to inhibition of the synaptic activity evoked by whisker stimulation. The imbalance between CBF and neural activity induced by ANG II may alter the homeostasis of the neuronal microenvironment and contribute to brain dysfunction during ANG II-induced hypertension.

Cerebrovascular autoregulation is profoundly impaired in mice overexpressing amyloid precursor protein.

The amyloid-beta (A beta) peptide, which is derived from the amyloid precursor protein (APP), is involved in the pathogenesis of Alzheimer's dementia and impairs endothelium-dependent vasodilation in cerebral vessels. We investigated whether cerebrovascular autoregulation, i.e., the ability of the cerebral circulation to maintain flow in the face of changes in mean arterial pressure (MAP), is impaired in transgenic mice that overexpress APP and A beta. Neocortical cerebral blood flow (CBF) was monitored by laser-Doppler flowmetry in anesthetized APP(+) and APP(-) mice. MAP was elevated by intravenous infusion of phenylephrine and reduced by controlled exsanguination. In APP(-) mice, autoregulation was preserved. However, in APP(+) mice, autoregulation was markedly disrupted. The magnitude of the disruption was linearly related to brain A beta concentration. The failure of autoregulation was paralleled by impairment of the CBF response to endothelium-dependent vasodilators. Thus A beta disrupts a critical homeostatic mechanism of the cerebral circulation and renders CBF highly dependent on MAP. The resulting alterations in cerebral perfusion may play a role in the brain dysfunction and periventricular white-matter changes associated with Alzheimer's dementia.

Alterations in cerebral blood flow and glucose utilization in mice overexpressing the amyloid precursor protein.

We have used quantitative autoradiographic techniques to study the relationship between cerebral blood flow (CBF) and glucose utilization (CGU) in two lines of transgenic mice overexpressing Swedish mutant amyloid precursor protein (APP) and APP-derived Abeta peptides. Mice were studied at an age when there are no amyloid plaques. In the 2123 line, CBF was reduced only in telencephalic regions with no corresponding decrease in CGU. In 2576 transgenics, a line with higher levels of Abeta peptide, both CBF and CGU were reduced throughout the brain. The data indicate that Abeta induces alterations in resting CBF that are either associated with or independent of alterations in CGU and that occur in the absence of amyloid deposition in neuropil of blood vessels. These observations support the hypothesis that cerebrovascular and metabolic abnormalities are early events in the pathogenesis of Alzheimer's disease.