Nobuyoshi Matsushima

Reversible splenial lesion in the corpus callosum following rapid withdrawal of carbamazepine after neurosurgical decompression for trigeminal neuralgia

Reversible splenial lesions (RSL) of the corpus callosum have been described in various clinical conditions, and some are attributed to the action of antiepileptic drugs (AED). Abrupt withdrawal of an AED in preparation for surgical treatment can result in RSL of the corpus callosum in patients with trigeminal neuralgia who do not have epilepsy. We report two patients who developed RSL following surgical treatment of trigeminal neuralgia. Since our two patients did not have epilepsy, it is strongly suggested that the AED, rather than convulsive status epilepticus, could be a contributing factor in RSL. The pathogenesis of AED-associated RSL is not clear. Similar RSL can appear under various circumstances, implying that factors other than AED can influence a common end-point mechanism that results in RSL. Nevertheless, delirium after surgery may be a cue for inquiring about RSL. This condition is transient and represents a clinicoradiological syndrome with an excellent prognosis. We should consider this phenomenon in the perioperative period after surgery for trigeminal neuralgia to avoid invasive diagnostic and therapeutic procedures.

MRI findings of atypical meningioma with microcystic changes

A 54-year-old woman presented with visual disturbance and consulted with a physician at our hospital. Neurological examination revealed left hemianopsia. MRI of the brain revealed an extraaxial tumor with a markedly low T1 signal and a markedly high T2 signal in the right occipital region (Figs. 1a, 1b). Peritumoral edema was visible on the T2-weighted images (Fig. 1b). Contrast-enhanced T1-weighted images showed inhomogeneous and less intense enhancement (Fig. 1c). Diffusion-weighted imaging (DWI) was performed and an apparent diffusion coefficient (ADC) map (Fig. 1d) revealed much higher diffusion of the tumor (1.41 · 10 mm/s) than normal white matter (0.70 · 10 mm/s), equivalent to that of adjacent peritumoral edema (1.40 · 10 mm/s). A diagnosis of microcystic meningioma was considered. Subsequently, the patient underwent total tumor resection. Intraoperatively, the tumor attached to the dura matter was soft and moist, resembling a jellyfish. No invasion into adjacent brain parenchyma was apparent. Histological examination showed that the tumor comprised neoplastic meningothelial cells with abundant cysts of various size (Fig. 2a). Histological diagnosis was atypical meningioma with microcystic changes (WHO grade II) because the tumor features increased cellularity and prominent nucleoli (Fig. 2b), and foci of geographic necrosis (Fig. 2c). However, mitotic activity was not high and the MIB1 labeling index was 3%. The patient had a good postoperative course and has been under follow-up for six months.

Dermal spindle cell lipoma of the posterior neck: CT and MR findings

Accepted: 2 January 2003 Published online: 1 May 2003

Source localization of posterior slow waves of youth using dipole modeling

Posterior slow waves of youth have a well‐known electroencephalographic pattern that peaks in adolescence and usually disappears in adulthood. In general, posterior slow waves of youth are regarded as normal, but some reports have suggested that their presence is related to immature personalities or inappropriate social behavior. The physiological significance of this electroencephalographic pattern, however, remains unclear. The purpose of this study was to investigate the neural origins of posterior slow waves of youth using dipole source modeling.

Electroencephalographic Dipole Source Modeling of Frontal Intermittent Rhythmic Delta Activity

Background: Frontal intermittent rhythmic delta activity (FIRDA) on electroencephalography (EEG) consists of a run of rhythmic delta waves with frontal predominance. Although FIRDA is a relatively common abnormal EEG finding, the underlying mechanisms that produce FIRDA remain unclear. The aim of this study was to investigate the cortical source of FIRDA using dipole source modeling. Methods: We selected EEG epochs, including typical FIRDAs, from EEG recordings obtained using 25 scalp electrodes on 5 subjects. We averaged these epochs by arranging the negative peaks of the delta waves at the Fp electrodes and estimated dipoles for nine averaged waveforms. Results: Averaged waveforms were explained by a single-dipole model in seven FIRDAs and by a two-dipole model in the remaining two FIRDAs with high reliability. Estimated dipoles had a radial orientation with respect to the frontal pole and were located in the medial frontal region. The anterior cingulate cortex was the most common dipole location. Conclusions: This is the first study to approach the fundamental FIRDA mechanism by dipole source modeling and to clarify that FIRDA may be generated from the medial frontal region, particularly from the anterior cingulate cortex.