Akio Kotani

Giant basilar artery aneurysm with intramural hemorrhage and then disastrous hemorrhage: case report.

OBJECTIVE AND IMPORTANCE Intracranial giant aneurysms have been considered to grow by recurrence of intramural hemorrhage of the aneurysmal wall. However, it remains uncertain whether rupture of giant aneurysms is brought about by the same mechanism that causes the rupture of smaller saccular aneurysms. It is also unclear whether intramural hemorrhage is correlated with the rupture of giant aneurysms. CLINICAL PRESENTATION A 67-year-old woman was admitted with symptoms of gait disturbance and dementia. Computed tomographic scans revealed a large mass located in the prepontine region and extending into the third ventricle as well as moderate dilatation of the lateral ventricles. Angiography demonstrated a giant basilar tip aneurysm and multiple aneurysms located in the bilateral anterior and middle cerebral arteries. INTERVENTION Ventriculoperitoneal shunting was scheduled, but subarachnoid and intraventricular hemorrhage occurred and the patient died. Computed tomographic scans, performed immediately before the disastrous hemorrhage, displayed intramural hemorrhage in the wall of the giant basilar tip aneurysm. Ventricular drainage was performed, but the patient died. CONCLUSION It seems probable that intramural hemorrhage of the aneurysmal wall may cause both the growth and rupture of intracranial giant aneurysms.

Acute aggravation of subdural fluid collection associated with dural metastasis of malignant neoplasms: case report and review of the literature

A 63-year-old woman was admitted to our hospital with serious headache and vomiting. Five months before admission, she had undergone surgery for a primary advanced gastric cancer. Neuroradiological examinations revealed subdural fluid collection. We twice performed evacuation of the subdural fluid collection. However, aggravation of her state of consciousness progressed and she passed away. Histological examinations demonstrated that the dural veins were infiltrated by numerous tumor cells that produced mucus; however, ruptured vessels were not found. Furthermore, the subdural fluid collection increased shortly after the initial operation. We infer that the cause of the collection, which was associated with the dural metastasis of malignant tumors, was not only mucin secretion by tumor cells but also a rapid increase in perfusion pressure in the vessels of the dura mater, resulting in extravasation of plasma components into the subdural space. Our case demonstrates that the pathogenetic mechanism that is specific for subdural fluid collection caused by dural metastasis of malignant tumors differs from the mechanism of production of subdural hematoma associated with dural metastasis.

Emotional Slow Negative Potential Shift (CNV) in the Thalamus

In order to know the functional relationship between CNV recorded at the vertex and activity of the thalamic nucleus, the CNV at the vertex and the intrathalamic slow potentials responding to an S1-S2-R paradigm were recorded during thalamotomy under local anesthesia. It might be concluded that the activity of the medial thalamus and medial parts of the subthalamic area not only generate slow potential shifts corresponding to S1-S2-R, but also play an important role in controlling the CNV at the vertex.

Primary central nervous system malignant lymphoma in a patient with rheumatoid arthritis receiving low-dose methotrexate treatment

Abstract We report the first case of primary central nervous system lymphoma (PCNSL) developing in a patient with rheumatoid arthritis (RA) undergoing low-dose methotrexate therapy (LD-MTX). The characteristic clinical management and course in our experience of the present case illustrate the important points about PCNSL in methotrexate-associated lymphoproliferative disorders (MTX-LPD). The number of cases of MTX-LPD in RA patients may increase in the future, since current treatment strategies for RA recommend starting MTX use in early stage RA, and recent insights have tended to show an increase with higher doses.

Thalamic Relay Nucleus Stimulation as a Preventive Method against Recurrent Tendency following Thalamotomy for Intractable Pain

Recurrence of intractable pain was observed following basomedial thalamotomy, in spite of making a lesion as wide as possible at both the neo and paleo-spinothalamic pathway. As a last resort for prevention of recurrence, the relay nucleus stimulation for selection of the candidate among the cases suffered from intractable pain was applied in clinical cases. The mechanism of inhibitory modulating effect of relay nucleus stimulation upon the medial thalamic neuron responding to noxious stimuli was also studied in experimental animals. Experimental Results: The neurons responded to noxious stimuli in the medial thalamic nucleus are divided into 2 types; one group (F-type neuron) shows activation of action potentials with about 20 msec. latency; the other (I-type neuron) shows inhibition upon the spontaneous activities. The F-type cell is pre or post-synaptically inhibited while the I-type cell disinhibited by conditioning stimulation in the thalamic relay nucleus, although the relay nucleus does not directly connect with the medial nucleus. The inhibitory modulating effect by stimulation of the thalamic relay nucleus is suppressed following the sensori-motor cortical ablation, or making lesion in the anteromedial thalamic area. It may be concluded that the conditioning stimulation of the thalamic relay nucleus produces the inhibitory modulating effect through the cortical or intrathalamic fiber connections upon pain perceptive activity at the medial thalamic nucleus. Clinical Observations: In clinical cases whose intractable pains were suppressed by conditioning stimulation of thalamic relay nucleus, the medial thalamotomy had excellent long lasting pain killing effects. It is concluded that the pain relief effects of medial thalamotomy can be predicted before the destruction of thalamic nucleus by application of conditioning stimulation in the thalamic relay nucleus.