MRI has facilitated diagnostic assessment of the corpus callosum. Diagnostic classification of solitary or multiple lesions of the corpus callosum has not attracted much attention, although signal abnormalities are not uncommon. Our aim was to identify characteristic imaging features of lesions frequently encountered in practice. We reviewed the case histories of 59 patients with lesions shown on MRI. The nature of the lesions was based on clinical features and/or long term follow-up (ischaemic 20, Virchow-Robin spaces 3, diffuse axonal injury 7, multiple sclerosis 11, hydrocephalus 5, acute disseminated encephalomyelitis 5, Marchiafava-Bignami disease 4, lymphoma 2, glioblastoma hamartoma each 1). The location in the sagittal plane, the relationship to the borders of the corpus callosum and midline and the size were documented. The 20 ischaemic lesions were asymmetrical but adjacent to the midline; the latter was involved in new or large lesions. Diffuse axonal injury commonly resulted in large lesions, which tended to be asymmetrical; the midline and borders of the corpus callosum were always involved. Lesions in MS were small, at the lower border of the corpus callosum next to the septum pellucidum, and crossed the midline asymmetrically. Acute disseminated encephalomyelitis and the other perivenous inflammatory diseases caused relatively large, asymmetrical lesions. Hydrocephalus resulted in lesions of the upper part of the corpus callosum, and mostly in its posterior two thirds; they were found in the midline. Lesions in Marchiafava-Bignami disease were large, often symmetrically in the midline in the splenium and did not reach the edge of the corpus callosum.

Peritumoural brain oedema was examined retrospectively in 175 patients with 179 intracranial meningiomas. The influence of tumour size, location and histology were investigated. Tumour volume and localization, and the presence of peritumoural brain oedema (PTBOe) were determined by computed tomography (CT). The oedema-tumour volume ratio was defined as Oedema Index (Oel). All patients underwent microsurgical removal of the tumour. Surgically resected meningiomas were classified histopathologically based on criteria of the new World Health Organization (WHO) classification. A close relationship was found between the tumour size and the incidence of peritumoural oedema: with increasing size of the tumour the incidence of oedema also rises, the oedema index, however decreases. Frontobasal and temporobasal meningiomas showed a significant increase in the oedema incidence and the mean oedema index. If major parts of the surface of meningiomas were adjacent to subarachnoid cisterns only a slight tendency for the development of oedema was observed. WHO-III-meningiomas showed a significantly higher oedema incidence (61.1% vs. 94.4%; p < 0.004) and mean oedema index (Oel = 2.7 vs. 3.7; p < 0.0009) than WHO-I-meningiomas. Brain tissue was affected in 59 cases. 19 meningiomas with infiltration into adjacent brain parenchyma revealed a statistically significant increase in oedema incidence (94.7% vs. 51.7%; p < 0.0003) and mean oedema index (Oel = 3.9 vs. Oel = 2.2; p < 0.0001) when compared to tumours without any brain tissue involvement in the histopathological specimens. Tumours with large volume, fronto-temporo-basal location and anaplastic histology were not only associated with the highest incidence of oedema formation but also presented with an overproportionate infiltrative growth. Thus, a disruption of the arachnoid or a true brain infiltration may be an essential factor for the development of a PTBOe.

The pulsation in the lower spine seems to be related to a second motor of CSF movement because there is a rising respiratory influence and a reappearance of pulsation waves. Physiological spinal CSF pulsation contains a relevant respiratory component.

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Spontaneous spinal hematomas are frequently located in the thoracic spine. Subdural spinal haemorrhage is more frequent than epidural. Epidural haemorrhage is frequently located dorsal to the spinal cord because of the tight fixation of the dura to the vertebral bodies.

Image fusion is a helpful tool for accurate determination of target point co-ordinates in DBS. In combination with intraoperative, electrophysiological recordings and stimulation which are still considered to be the most reliable localisation methods, image fusion may help to discern the anatomical and functional three-dimensionality of the target nuclei. Image fusion may reduce the number of trajectories needed for intraoperative electrophysiological determination of the optimal electrode localisation and thus lower the risk of complications.

Thrombotic occlusion of the internal cerebral veins is a particularly dangerous form of cerebral venous thrombosis (CVT) as it causes venous infarction of the thalami. Because both thalami drain into the vein of Galen and straight sinus, bilateral thalamic involvement is frequently encountered in internal CVT. However, unilateral thalamic edema may also occur, even if all internal cerebral veins are occluded. This suggests collateral venous drainage of the thalami, which is commonly insufficient in internal CVT. Patients with unilateral congestion of the thalamus, including 3 patients reported here, had mostly left-sided involvement, indicating that right-sided unilateral thalamic involvement in CVT may be clinically silent.

The etiology, pathogenesis, histopathologic diagnosis, prognosis, and treatment of giant cell reparative granulomas of the skull are controversial. We report a 14-year-old girl with an advanced recurrent giant cell reparative granuloma of the skull base and paranasal sinuses whose only clinical manifestation was a loss of vision. After undergoing endovascular catheter embolization, the patient underwent repeated surgical resections of the mass via a combined frontobasal and modified infratemporal approach followed by radiation therapy. Histopathologic examination confirmed the diagnosis of giant cell reparative granuloma. A traumatic event in the patient's history-a fossa canina abscess followed by tooth extraction 14 months before admission-supports the theory of a reactive reparative process as a pathogenetic mechanism for this disease. Histopathologic criteria and clinical aggressiveness must be considered to achieve adequate treatment of giant cell lesions of the skull.