MEG measurement of event-related brain activity evoked by emotional prosody recognition.

Cortical areas involved in processing of emotional prosody (EP) in spoken language, such as joy or sadness, have been found in functional magnetic resonance imaging (fMRI) studies bilaterally or dominantly in the right frontal or temporal lobes. In this study, we investigated spatiotemporal patterns of cortical activity related to EP processing using magnetoencephalography (MEG). In this experiment, a joyful face (JF) or a sad face (SF) was displayed after voices which had emotional features of joy (joy prosody: JP) or sadness (sad prosody: SP) were presented. Subjects were requested to judge whether emotional features of the voice and the face were identical or not. MEG signals evoked by emotional voices were measured and significant differences of cortical activities associated with processing of emotional feature were observed between the right and left hemisphere during the latency of 100-150 ms that includes the N1m component. Our study suggests that MEG is a useful method, in addition to fMRI and event-related scalp potentials (ERP) for studying non-invasively EP processing in the human brain.

CD4 cross-linking (CD4XL) induces RAS activation and tumor necrosis factor-alpha secretion in CD4+ T cells.

CD4 molecules are the primary receptors for human immunodeficiency virus (HIV) and bind the envelope glycoprotein gp120 of HIV with high-affinity. We have previously shown that cross-linking of CD4 molecules (CD4XL) in normal peripheral blood mononuclear cells (PBMC) results in secretion of cytokines tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma), but not of interleukin-2 (IL-2) or IL-4. To investigate the intracellular signaling events associated with CD4-gp120 interaction, we incubated CD4+ T cells from peripheral blood of HIV-negative healthy donors with HIV envelope protein gp160 alone or performed CD4XL with gp160 and anti-gp160 antibody. This procedure resulted in tyrosine phosphorylation of intracellular substrates p59fyn, zap 70, and p95vav and also led to ras activation, as assessed by conversion of rasGDP to rasGTP. The role of ras in CD4 signaling was further investigated using CD4+ Jurkat cells transfected with a dominant negative ras mutant. CD4+ T cells expressing dn-ras secreted significantly reduced levels of TNF-alpha in response to CD4XL. These studies indicate that interaction of HIV gp160 with CD4 molecules activates the ras pathway in T cells, which may result in the cells becoming unresponsive to subsequent stimulation.

Simultaneous bleeding from multiple lenticulostriate arteries in hypertensive intracerebral haemorrhage.

Angiography within 1 h of the onset of an intracerebral haematoma in a hypertension man showed active bleeding from at least two lenticulostriate arteries. We discuss the pathophysiological significance of this finding.

Angiographic extravasation of contrast medium in acute "spontaneous" subdural hematoma.

Acute spontaneous subdural hematoma is very rare. We have encountered four such cases and verified the arterial origin of the bleeding at operation. None of the patients had a history of head trauma, and each had developed sudden onset of headache and other neurologic deficits, which simulate other cerebrovascular diseases. CT directly revealed subdural hematoma but gave no indication as to the source of the bleeding. Cerebral angiography was performed in all cases, with three of them showing localized extravasation of the contrast material into the subdural space. The extravasation was noted usually in the late arterial phase. This is a useful finding for diagnosing this disease and localizing the bleeding point. It is expected that with more routine use of cerebral angiography in cases of acute spontaneous subdural hematoma, extravasation of the contrast medium will be seen more frequently.

[Rebleeding of ruptured intracranial aneurysms in the acute stage].

Among the cases of ruptured aneurysms we have handled, some patients have rebled before surgery was performed. In this study, we examine the factors that contribute to the rerupture of cerebral aneurysms in the acute stage and suggest measures to prevent rerupture prior to surgery. We have encountered 32 cases of rebleeding prior to surgery. The rebleeding occurred within six hours of the initial subarachnoid hemorrhage (SAH) in 26 patients, among whom 21 rebled within three hours. Thirteen patients rebled during bed rest, 10 patients during angiography, 4 patients during CT scan and 5 patients in various other circumstances. Nine of the 10 patients who rebled during angiography had undergone the procedure within three hours of the initial SAH. Overall, the patients' condition deteriorated substantially after rebleeding. Considering these circumstances surrounding aneurysmal rerupture, we suggest the following measures for the prevention of preoperative rerupture in the acute stage: 1) maintenance of lowered blood pressure during the risky period; 2) intentional delay of performance of angiography until at least hours after the initial rupture, and 3) performance of surgery on an emergency basis.

Chronic subdural hematoma associated with middle meningeal arteriovenous fistula treated by a combination of embolization and burr hole drainage.

A rare case of chronic subdural hematoma associated with a middle meningeal arteriovenous fistula was treated by a combination of embolization and burr hole drainage. This clinical situation might be missed in this era of computed tomography, when cerebral angiography is seldom indicated for the diagnosis of neuro-traumatic diseases. We should bear in mind the possibility of this clinical situation of a chronic subdural hematoma associated with a linear skull fracture crossing the middle meningeal groove in order to avoid possible hemorrhagic complications during surgery for chronic subdural hematoma.

"Kissing aneurysms" of the internal carotid artery.

Five patients with kissing aneurysms (adherent internal carotid-posterior communicating artery and ipsilateral internal carotid-anterior choroidal artery aneurysms) are reported. There was female predominance and the subarachnoid hemorrhage was commonly due to rupture of the proximal posterior communicating artery aneurysm. Despite the demonstration of angiographic cleavage, the two aneurysms adhere to each other, which makes surgical dissection difficult. Meticulous dissection of the aneurysmal necks and preservation of the blood flow in the anterior choroidal artery are of vital importance.

[Surgical treatment of arteriovenous malformations in the brain stem].

The authors report the surgical removal of four arteriovenous malformations (AVM's) in the brain stem causing hemorrhage. These included two intra-axial and two extra-axial AVM's. Three of the four were situated at the pons, and the remaining one in the posterior medullary velum. Complete surgical removal was obtained in the two extra-axial cases and in one of the intra-axial cases. The patient in whom complete removal was not obtained received partial embolization therapy with the remaining feeder being coagulated surgically. No patient was made permanently worse after surgery. One patient, in a comatose state on admission, died, while the remaining three patients showed useful recovery. These data indicate that surgical therapy with or without endovascular surgery appears to be possible for some AVM's and can be performed at an acceptable risk.

Aneurysmal rupture during angiography.

The aim of the present study was to analyze the clinical data on rebleeding in cerebral aneurysms during angiography and to evaluate the importance of the time interval between the latest rupture and angiography. Fourteen personal cases and 202 patients reported in the literature are reviewed. Rebleeding during angiography occurred most often (78%) on Day O; 89% bled when angiography was performed within 6 hours of the latest rupture. The prognosis in such ruptures was poor, with a mortality of 79%. Intentional delay in angiography of at least 6 hours from the latest rupture is recommended if the associated hematoma is not large.

[Neurological deterioration induced by giant intracranial aneurysms even though these aneurysms had not ruptured; mural hemorrhage and intraluminal thrombosis].

The authors report two cases of intracranial giant aneurysms inducing acute neurological deterioration even though rupture of the aneurysms had not occurred. Neurological aggravation was attributable to the acute swelling of the aneurysmal mass after intramural hemorrhage in one case, and the formation of rapid and massive intraluminal thrombosis in another case. MRI confirmed these mechanisms in both cases. MRI is very useful for demonstrating mural and intraluminal pathologies involving giant aneurysms.

Mechanism of acute deterioration of the neurological status following rapid and massive intraluminal thrombosis in case of a giant intracavernous carotid artery aneurysm: demonstration by MR imaging.

A case is reported of a thrombosed giant aneurysm of the intracavernous carotid artery. Transient neurological deterioration was attributable to the acute swelling of the aneurysmal mass after rapid and massive intraluminal thrombosis. Characteristics on the magnetic resonance imaging of this case are reported and discussed.

[Surgical treatment of ruptured dissecting aneurysms: proximal clipping vs trapping].

The best surgical treatment for ruptured dissecting aneurysms of the vertebral artery is still controversial. Four patients (1 male, 3 female), age ranging from 43 to 62, were operated upon in our department during the last 6 years. Duration from rupture to the operation was 0 to 4 days. In 2 cases, proximal clipping was the primary treatment, while 2 had a trapping. Antiplatelet agents were given to prevent vasospasm in all cases postoperatively. In proximal clipping cases, one patient had suffered from fatal rerupture on the sixth postoperative day. In trapping cases, Wallenberg syndrome developed in one patient. These results suggest that a proximal clipping may not allow the treatment for the vasospasm because of the danger of rebleeding and also a trapped segment of vertebral artery should be as short as possible to avoid compromised perforators.

[MR findings in traumatic cerebrospinal fluid leakage with special reference to indications of the need for dural repair].

Eleven cases of traumatic cerebrospinal fluid (CSF) leakage (8 cases of rhinorrhea and 3 cases of otorrhea) were reviewed to discuss magnetic resonance (MR) findings and surgical indications of the need for dural repair. Five patients had delayed onset of CSF rhinorrhea, 12 to 66 days (mean 28 days) after the trauma, and in the remaining 6 patients (3 rhinorrhea and 3 otorrhea) CSF leakage was noted on admission. MR study was carried out within 7 days after the onset of CSF leakage using a 0.5 tesla imager. In 7 cases of rhinorrhea, MR images demonstrated brain herniation into the ethmoid or frontal sinuses and the dural defects were repaired with the vascularized periosteum flap taken from the frontal bone or the fascia lata. In the operations, brain parenchyma was found to be plugged into the fracture line as MR images showed, and also to adhere to the margin of dural fistula. In the remaining 4 patients (without the MR findings of brain herniation into the paranasal sinuses) spontaneous cessation of CSF leakage occurred and their clinical course was good. Spontaneous cessation of CSF leakage in these cases may suggest the complete healing of the lacerated dura. However, in cases with the brain herniated into the paranasal sinuses CSF leakage may not be observed, and natural healing of the dural defect cannot be expected. Therefore, such brain herniation indicates the absolute need for dural repair even if CSF leakage is not observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Pontine hemorrhages presenting as trigeminal neuropathy--report of three cases.

Three patients with pontine hemorrhages presenting clinically as trigeminal neuropathy are described. No patient was hypertensive and angiograms were normal. Magnetic resonance (MR) imaging showed heterogeneous lesions, suggesting cavernous malformation, in one patient, but no definite diagnosis could be made in the other two patients. Such cases are rare and should be evaluated using serial MR imaging to differentiate angiographically occult vascular malformation from spontaneous hemorrhage.

HIV-gp 160-induced T cell-dependent B cell differentiation. Role of T cell-B cell activation molecule and IL-6.

The HIV envelope glycoprotein gp160 has been previously demonstrated to induce differentiation of normal B lymphocytes into Ig-secreting cells; the response is T cell-dependent, and T cells pretreated with gp160 can support B cell differentiation. This study investigates the cell surface molecules and cytokines that play a role in the gp160-induced T-B cell interaction. Utilizing CD4+CD45RO+ cloned T cells as the source of helper cells, we observed that physical contact with B cells is essential for the gp160-induced B cell response; no IgG-secretion occurred if T cells were separated from the B cells by culturing them in Transwell chambers. The expression of T cell-B cell activation molecule, a novel surface molecule associated with T cell activation, was moderately increased by gp160, and antibody to T cell-B cell activation molecule abrogated the gp160-mediated Th cell function. Cell surface molecules LFA-1, ICAM-1, HLA-DR, CD28, and B7 were also involved in the T-B cell interaction since mAb to any of these molecules inhibited the gp160-induced B cell differentiation response. gp160 also induced IL-6R and CD23 molecule expression on B cells when added to cultures of T plus B cells; there was CD23 expression only in cells that formed conjugates with T cells. Paraforamaldehyde-fixed, gp160-pretreated T cells failed to elicit IgG responses in B cells, but did induce CD23 and IL-6R up-regulation on B cells. Addition of exogenous IL-6, but not IL-2 or IL-4, restored the IgG secretion. These findings indicate that the T cell dependence for gp160-induced B cell differentiation responses involves two steps: one requires contact-dependent interaction of several cell surface molecules, and the second requires IL-6 secretion.

Tyrosine phosphorylation of guanosine triphosphatase activating protein by activation via surface IgG in human B cells.

In this study, we analyzed tyrosine phosphorylation of guanosine triphosphatase (GTPase) activating protein in human B cells stimulated through surface IgG, using Western blot and immunoprecipitation. Stimulation through surface IgG induced the tyrosine phosphorylation of GTPase-activating protein (GAP) and two associated proteins, a 190-Kd protein and a 62-Kd protein, within 1 minute and in a dose-dependent manner. This tyrosine phosphorylation was blocked by Genistein (Extrasynthese, Genay, France). These data suggest that GTPase-activating protein is involved in a signal transduction pathway initiated from surface IgG in human B cells.

Functional expression of interleukin 2 receptor in a human factor-dependent megakaryoblastic leukemia cell line: evidence that granulocyte-macrophage colony-stimulating factor inhibits interleukin 2 binding to its receptor.

Human interleukin 2 (IL-2) is a member of the class of crucial regulators of lymphocyte proliferation. The action of IL-2 is known to be mediated through binding to a specific IL-2 receptor (IL-2R) which comprises at least two distinct proteins: IL-2R alpha (p55) and IL-2R beta (p70-75). However, the expression and function of IL-2R are largely unknown in acute myeloblastic leukemia cells. In a human granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-3, or stem cell factor-dependent myeloid leukemia cell line (M07E), IL-2 was found to stimulate proliferation in a dose-dependent manner and to augment GM-CSF- and stem cell factor-induced proliferation of M07E cells. The expression of IL-2R beta on M07E cells was detectable with 125I-IL-2 binding and affinity cross-linking analyses and with a monoclonal antibody against IL-2R beta, Mik-beta 1. Although the expression of IL-2R beta was not down-regulated but somewhat up-regulated by treatment with GM-CSF in both mRNA and protein levels, GM-CSF was found to compete (75%) with radiolabeled IL-2 for binding to IL-2R on M07E cells, whereas no competition of GM-CSF binding was observed with IL-2 even at a 400-fold molar excess. These results suggest that IL-2R may be functionally expressed in some cases of acute myeloblastic leukemia cells and raise the possibility that IL-2 may have some effects on human myelopoiesis.

[Ischemic complications following parent artery occlusion with detachable balloons in the treatment of large carotid aneurysms: effectiveness of 99mTc-HMPAO SPECT and importance of postoperative management].

Three patients with large carotid aneurysms were treated by parent artery occlusion with detachable balloons. Of these, 2 had intracavernous carotid artery aneurysms and one had a carotid-ophthalmic aneurysm. All patients underwent a formal balloon occlusion test and tolerated it well. One patient with a carotid-ophthalmic aneurysm, however, developed postoperative ischemic effects. This case was that of a 55 year-old female with right visual disturbance. Her middle cerebral artery flow had been compromised during test occlusion under induced hypotension. Although initially intact after balloon occlusion, she was found to be hemiplegic 24 hours later. She subsequently developed multiple small infarcts which were shown on MRI and which corresponded exactly to the previously demonstrated region of decreased flow during testing. This ischemic complication is possibly due to hypoperfusion, but embolism from the thrombosed aneurysm can not be denied. To prevent these complications, an extracranial-intracranial artery anastomosis prior to parent artery occlusion should be considered if the preoperative 99mTc-HMPAO SPECT shows a compromised cerebral blood flow. In addition to this, postoperative anticoagulant therapy should be given even if test occlusion was well tolerated clinically.