[Occipital encephalocele and epilepsy].

We report the incidence of epilepsy in 7 patients with occipital encephalocele (meningocele: 6 cases, meningoencephalocystocele: 1 case). Two cases had epilepsy and a case without the history of epileptic seizure had an epileptic pattern on the EEG. All these 3 cases had cortical dysplasia(CD) such as schizencephaly and subcortical gray matter, and two of them were associated with mental retardation. The location of the prominent CD was correlated with the EEG abnormalities and clinical epileptic pattern in each case. Associated hydrocephalus and placement of VP shunt had no significant influence on the occurrence of the epilepsy. Thus, complicated CD is thought to be epileptogenic in patients with occipital encephalocele.

Magnetoencephalographic analysis of periodic lateralized epileptiform discharges (PLEDs).

OBJECTIVE: To clarify the spatial and temporal distribution of the electroencephalographic (EEG) pattern termed 'periodic lateralized epileptiform discharges' (PLEDs), we performed magnetoencephalography (MEG) to analyze PLEDs in a patient with a right parietal metastasis associated with meningeal carcinomatosis. METHODS: A 37-channel biomagnetometer was used to simultaneously record the EEG and MEG. Equivalent current dipole (ECD) source localization was calculated based on a single-dipole model and mapped onto a magnetic resonance image. Single-photon emission computed tomography with technetium-99-hexamethyl-propyleneamine oxime (HMPAO-SPECT study) was also performed during both presence and absence of PLEDs according to an EEG monitor. RESULTS: By EEG the PLEDs, predominantly right-sided, consisted of a typical negative triphasic spike followed by a slow negative wave. By MEG the PLEDs had a sequence with 3 distinct components. ECDs in the 3 components were localized to the cortex around the lesion, although exact localization and dipole direction varied between components. HMPAO-SPECT demonstrated hypoperfusion of the lesion and adjacent cortex during both quiescence and appearance of PLEDs. CONCLUSION: Our results indicate that PLEDs originated from the hypoperfused cortex surrounding the lesion.

Effect of intracarotid bradykinin infusion on cerebral blood flow in dogs.

We examined whether intracarotid infusion of bradykinin altered circulation in the normal canine brain. Twenty-four anesthetized dogs were divided into four groups receiving different doses of bradykinin (1, 2.5, 5, and 10 micrograms kg-1 min-1). Regional cerebral blood flow (rCBF) was measured continuously using laser Doppler flowmetry through a burr hole in the frontal bone. Systemic blood pressure (SBP) and heart rate (HR) were monitored simultaneously. Higher doses of bradykinin significantly but temporarily decreased rCBF and SBP immediately after the start of infusion; these parameters rapidly recovered and then were stable through the rest of the infusion. During this period, percent change in rCBF and SBP was small, and differences between groups were not significant. On the other hand, HR increased during infusion and remained high. SBP, rCBF, and HR returned to pre-infusion levels after bradykinin was stopped. The results suggest that intracarotid infusion of bradykinin for treatment of brain tumors would be safe in terms of circulation to the uninvolved brain.

Distribution of brainstem somatosensory evoked potentials following upper and lower limb stimulation.

OBJECTIVE: Because somatosensory evoked potentials (SEP) to lower limb stimulation have not been recorded from the brainstem to the extent that upper limb SEPs have been studied, we compared brainstem recordings in response to both median nerve (MN) and posterior tibial nerve (PTN)stimulation. METHODS: SEPs were recorded directly from the dorsal surface of the brainstem in four patients with fourth ventricle tumors. RESULTS: Following MN stimulation, medullary SEPs were characterized by a major negativity (N1) preceded by a small positivity (P1) and followed by a large positivity (P2). In the pons, triphasic waves with predominant negativity were obtained. With PTN stimulation, similar medullary SEPs with a P1'-N1'-P2' configuration and pontine SEPs with a triphasic waveform were obtained. CONCLUSIONS: Since the distribution of PTN SEP was identical to that of MN SEP, PTN SEPs are thought to be generated by mechanisms similar to those for MN SEP. Thus, the P1' and N1' of medullary SEP would be generated by the dorsal column fibers that terminate in the nucleus, with P2' possibly arising postsynaptically in the nucleus. The triphasic PTN SEP from the pons reflects an axonal potential generated in the medial lemniscal pathway.

Intrinsic epileptogenicity of focal cortical dysplasia as revealed by magnetoencephalography and electrocorticography.

Focal cortical dysplasia (FCD) is often associated with severe partial epilepsy. In this study, we performed magnetoencephalography (MEG) and electrocorticogrsphy (ECoG) on four patients with FCD-associated epilepsy to confirm the 'intrinsic' epileptogenicity of FCD. In all patients, we determined the three-dimensional locations of the magnetic sources of the interictal paroxysmal activities by a single dipole model, and then the estimated dipole localization was superimposed on the magnetic resonance image. The dipole clusters were located in the T2-prolonged lesions, namely in the FCD lesions themselves. All patients underwent surgery for their medically intractable epilepsy, and the acute and/or chronic ECoG were thereafter recorded. Either frequent or continuous paroxysmal activities were recorded from the ECoG electrodes which were placed over the surface of the FCD lesion, while few paroxysmal activities were observed on the normal appearing adjacent cortex. Intraoperative depth recordings were performed in a patient with the needle electrode inserted into the FCD lesion and they revealed these paroxysmal foci to be located not on the cortical surface but at a depth of 15 mm from the cortical surface where both abnormal giant neurons and bizarre large eosinophilic cells (so-called balloon cells) were also prominently observed on the postoperative histological sections. Following a lesionectomy combined with the removal of the underlying white matter, three patients demonstrated a favorable seizure outcome. Our findings thus suggest the FCD lesions to be highly and intrinsically epileptogenic lesions.

[Clinical experience of image-guided neurosurgery with a frameless navigation system (StealthStation)].

We have applied the frameless navigation system (StealthStation) to various neurosurgical procedures to examine its usefulness. The system consists of a UNIX based workstation that creates triplanar and 3-dimensional images; an infrared optical digitizer with camera array; a reference-light-emitting diode (LED) array (e.g., reference array); and pointer probe modified by the addition of LEDs. This system was used to assist in placing a minimal skin incision and craniotomy in 4 cases, to determine the tumor/brain interface in 2 cases, to target the subcortical lesion in one case, and to correlate bony structure with a skull base tumor in 3 cases. The combined use with magnetic source imaging of the somatosensory cortex allowed a fast orientation of eloquent areas in 2 cases with peri-Rolandic tumor. This system, thus, was proved to be a useful adjunct to open-tumor biopsy or resection.

[Carbamazepine induced hyponatremia].

Carbamazepine (CBZ) is a drug which can induce the syndrome of inappropriate antidiuretic hormone (SIADH). Until 1980's, there were reports regarding CBZ-induced SIADH, but it is rarely reported these days. We here report two cases of CBZ-induced SIADH. Hyponatremia in these cases was rapidly improved by withdrawal of administration of CBZ. According to the previous reports, the rate of hyponatremia in patients receiving CBZ is not small. It ranges from 48% to 31%. As CBZ is frequently used for patients with epilepsy and neuralgia, not only their blood CBZ concentration but also their serum Na level should be monitored.

[Two cases of mesial temporal lobe epilepsy associated with old intracerebral hemorrhage in the lateral temporal lobe without "dual pathology"].

Two cases of intractable temporal lobe epilepsy associated with old intracerebral hemorrhage in the lateral temporal lobe were reported. Although preoperative magnetic resonance imaging (MRI) failed to reveal hippocampal atrophy with T2 hyperintensity, electrocorticographic (ECoG) recording with chronic invasive subdural electrodes indicated the mesial temporal lobe to be an ictal onset zone. After anterior temporal lobectomy involving the lesion and hippocampectomy, the patients became seizure-free. Hippocampal sclerosis, namely "dual pathology", was not noted on histological examination. Careful ECoG recording with chronic subdural electrodes is mandatory even when the preoperative MRI does not demonstrate the radiological hippocampal sclerosis.

[Efficacy of the fluid attenuated inversion recovery (FLAIR) sequence of MRI as a preoperative diagnosis of hippocampal sclerosis].

A newly advanced MRI pulse sequence, the FLAIR (fluid attenuated inversion recovery) imaging, in which a long TE spin echo sequence is used with suppression of the CSF with an inversion pulse, displays the CSF space as a no-signal intensity area. There have been only a few reports on the FLAIR pulse sequence of temporal lobe epilepsy (TLE) as yet. We examined 9 cases of intractable TLE by FLAIR images and analyzed the advantages and disadvantages of the FLAIR pulse sequence for decision making on temporal lobectomy. All patients underwent anterior temporal lobectomy with hippocampectomy, and the diagnoses were confirmed histologically after surgery. Abnormally high T2 signals (HT2S) were more conspicuous with the FLAIR sequence than with any of the conventional sequences. Tilted axial plane, orientated along to the long axis of the hippocampal body, clearly demonstrated hippocampal atrophy (HA). Selection of a FLAIR sequence into the routine MR examination of patients with TLE is recommended.