Detection of current-sheet and bipolar ion flows in a self-generated antiparallel magnetic field of laser-produced plasmas for magnetic reconnection research.

Magnetic reconnection in laser-produced magnetized plasma is investigated by using optical diagnostics. The magnetic field is generated via the Biermann battery effect, and the inversely directed magnetic field lines interact with each other. It is shown by self-emission measurement that two colliding plasmas stagnate on a midplane, forming two planar dense regions, and that they interact later in time. Laser Thomson scattering spectra are distorted in the direction of the self-generated magnetic field, indicating asymmetric ion velocity distribution and plasma acceleration. In addition, the spectra perpendicular to the magnetic field show different peak intensity, suggesting an electron current formation. These results are interpreted as magnetic field dissipation, reconnection, and outflow acceleration. Two-directional laser Thomson scattering is, as discussed here, a powerful tool for the investigation of microphysics in the reconnection region.

High-power laser experiment forming a supercritical collisionless shock in a magnetized uniform plasma at rest.

We present an experimental method to generate quasiperpendicular supercritical magnetized collisionless shocks. In our experiment, ambient nitrogen (N) plasma is at rest and well magnetized, and it has uniform mass density. The plasma is pushed by laser-driven ablation aluminum (Al) plasma. Streaked optical pyrometry and spatially resolved laser collective Thomson scattering clarify structures of plasma density and temperatures, which are compared with one-dimensional particle-in-cell simulations. It is indicated that just after the laser irradiation, the Al plasma is magnetized by a self-generated Biermann battery field, and the plasma slaps the incident N plasma. The compressed external field in the N plasma reflects N ions, leading to counterstreaming magnetized N flows. Namely, we identify the edge of the reflected N ions. Such interacting plasmas form a magnetized collisionless shock.

[Pure sensory stroke due to a pontine lesion: a study of clinical symptomatology and somatosensory evoked potential findings].

We studied clinical symptomatology and somatosensory evoked potentials(SEP) of 7 pure sensory stroke patients due to pontine lesions. Clinical symptoms were examined by modality(pinprick, touch, vibration and joint position sense), intensity and distribution of the sensory disturbance. SEP were recorded by the median nerve stimulation in the upper extremities, and the posterior tibial nerve stimulation in the lower extremities. Patients 1-4 were characterized by decreased contra-lesional fingers or fingers, toes joint position sense, normal pinprick and vibration sense. We think that these patients' lesions were localized in the lemniscus medialis. Patients 5-7 were characterized by decreased contra-lesional upper extremity or upper and lower extremity vibration sense, decreased pinprick sense and normal joint position sense. We think that these patients' lesions involved spinothalamic tract. There was no abnormal finding of SEP with upper extremity stimulation, but disappearance or very low amplitude of P38 with lower extremity stimulation in 4 of the 7 patients. We conclude that 1) the vibration sense may be conducted also through the spinothalamic tract, 2) SEP findings are abnormal only with lower extremity stimulation in pontine pure sensory infarction.

[A case of acute type adult T cell leukemia and human T-lymphotropic virus type I associated myelopathy who presented meningitis and polyradiculoneuropathy and improved with steroid treatment].

We reported a 35-year-old male patient with acute type adult T cell leukemia(ATL) and human T-lymphotropic virus type I associated myelopathy. He presented meningitis and polyradiculoneuropathy and improved with steroid treatment. He presented headache and sensory ataxia and these symptoms responded to steroid treatment. The usual clinical features of ATL were absent at onset. There existed ATL-like cells in the cerebrospinal fluid and HTLV-I proviral DNA in the blood. Therefore, we surmised that there was monoclonal hyperplasia of the infected cells. He presented ATL after 2 years remission. We pointed out that there was acute type of ATL in patients with meningitis and polyradiculoneuropathy, for which steroid treatment could be effective.

[Amnesia following herpes simplex encephalitis].

We describe three patients presenting themselves with amnesia following herpes simplex encephalitis. All three patients showed anterograde amnesia. Moreover, one patient showed retrograde amnesia extending about fifty years prior to the onset of the illness. Two patients revealed semantic memory disorder, disinhibitory behaviors and confabulations, which suggested the existence of frontal lobe dysfunction. MRI of all three patients disclosed uni- or bilateral temporal lesions. SPECT images showed decreased uptake not only in the temporal lobes but also in the frontal lobes. Amnesia following herpes simplex encephalitis has been thought to be caused by the temporal lobe disorder. However, we postulate that the frontal lobe dysfunction might contribute to the appearance of amnesia.

[A clinico-pathological study of so-called "acute multiple sclerosis" mimicking a brain tumor on the MRI findings].

We are reporting an autopsy case of so-called "acute multiple sclerosis" that was difficult to differentiate from a brain tumor on MRI findings. This case was a 69-year-old man, whose initial symptoms consisted of headache and unsteadiness in walking. Neurological findings included mild ataxia of the left upper extremity and positive Romberg sign. T 2-weighted MRI showed high intensity areas in the posterior limb of the right internal capsule and white matter near the posterior horn of the right lateral ventricle. Although the headache improved, the unsteadiness was exacerbated and the patient became unable to keep standing. Psychiatric symptoms and left hemiparesis were added to the clinical picture. The following MRI proved expansion of the previous lesions and the diffusely enhanced lesion spreading into the contralateral side through the corpus callosum. Stereotaxic biopsy showed the perivascular accumulation of small lymphocytes and a large number of bizarre astrocytes. Primary brain malignant lymphoma was diagnosed and radiation therapy was carried out. However, he developed perforation of the intestinal tract and died. Autopsy findings revealed scattered and disseminated small lesions in the cerebral white matter and the corpus callosum. There were a large number of lipid-laden macrophages, no stainable myelin and preserved axis cylinders in those lesions. Thus, those were interpreted as demyelinting lesions. They were scattered and multiple. This case was radiologically characterised by the diffusely enhanced, expanding butterfly-shaped lesion in bilateral cerebral hemisphere through the corpus callosum, and pathologically proven to be acute demyelination associated with severe perivascular infiltration of inflammatory cells. Multiple sclerosis may mimic neoplastic processes as trans-callosal hyperplastic neuroimage on neuroimaging like the present case.

Pure topographic disorientation due to right retrosplenial lesion.

We report three patients with selective topographic disorientation due to small, focal hemorrhages extending from the right retrosplenial region to the medial parietal lobe. All three could discriminate and identify familiar buildings and landscapes, but had great difficulty remembering spatial positional relationships between two distant locations (i.e., the direction from one location to another) in familiar areas. These symptoms were different than the perception and memory deficits for buildings and landscapes caused by the medial temporo-occipital lesion. These findings suggest that the directional orientation between two locations within a familiar area ("sense of direction") is closely associated with the right retrosplenial region and the medial parietal lobe in humans.

Primary progressive apraxia in Pick's disease: a clinicopathologic study.

A 62-year-old right-handed man gradually experienced increasing difficulty with speech and manual dexterity. He had apraxia of speech, buccofacial apraxia, and complex limb apraxia as well as terminal dementia. At autopsy, focal cortical atrophy, neuronal loss, and neuropil rarefaction in the second and third cortical layers were most prominent in the left opercular, lower precentral, superior parietal, and left temporal pole. Numerous Pick bodies were diffusely present in the temporal and posterior frontal lobes and, to a lesser degree, in the superior parietal lobule. This report demonstrates an association between the distribution of Pick's pathology and several apraxic impairments.

An autopsy case of Marchiafava-Bignami disease with peculiar chronological CT changes in the corpus callosum: neuroradiopathological correlations.

We conducted a comparative analysis of the autopsy findings in a case of Marchiafava-Bignami disease with the X-ray computed tomography (CT) and magnetic resonance imaging (MRI) findings obtained while the patient was alive. Histologically, massive deposits of hemosiderin were demonstrated in the astrocytes and macrophages located in the walls of the callosal cystic lesion, suggesting that the transient increase in density during the subacute stage observed on X-ray CT is secondary to significant hemorrhage.

Prosopagnosia: a clinical and anatomical study of four patients.

We tested in great detail face perception and face memory in four cases of prosopagnosia. Three of them showed deficits of face perception and/or of familiar faces memory. There was one prosopagnosic patient, however, who showed no abnormality in face perception and discrimination and could recall familiar faces. This case suggests that a form of prosopagnosia may exist, which is due to the disconnection between face perception and face memory. X-ray CT, MRI and PET studies revealed that two patients did not have damage of the left hemisphere, supporting the view that prosopagnosia can arise from unilateral right-sided lesion.

[Mirror movements observed in patients skilled in playing the piano--symptomatological study].

We investigated mirror movements observed in two patients skilled in playing the piano and compared these symptoms with those reported in patients associated with frontal lobe, corpus callosum or cervical cord lesion. We found the following common features in our two patients: 1) mirror movements were observed during skilled finger movements such as playing the piano, 2) these were observed in distal parts of the bilateral upper extremities, 3) contralateral imitative associated movements were seen concomitantly, 4) frontal lobe symptoms and callosal disconnection syndrome were not seen, 5) both patients recalled having mirror movements in their infancy, and one had family history. These characteristics of mirror movements in our patients were similar to those in patients associated with cervical cord lesion, but were different from those in patients associated with frontal lobe or corpus callosum lesion. It is suggested that abnormal pathways in the pyramidal tract or cervical cord lesion elicited mirror movements in our patients.

[Hypoxic encephalopathy with quadriplegia and cortical blindness].

We report a 63-year-old woman with quadriplegia and cortical blindness due to hypoxic encephalopathy. She was hospitalized with a fever of 40 degrees C. After injection of an antipyretic drug, she suddenly entered a state of shock. Artificial breathing was induced, but she did not regain consciousness. She was admitted to this hospital in a state of coma. One month later, she regained consciousness, and her quadriplegia and decreased visual acuity became apparent. Neurological examination revealed cortical blindness (initially with Anton sign), geotropic ocular deviation, forced weeping, flaccid quadriplegia, and bilateral pyramidal tract signs (generalized hyperreflexia, positive bilateral Babinski sign). Magnetic resonance imaging of the brain, on a T2 weighted image, showed high-intensity areas in the bilateral precentral gyri and bilateral calcarine cortex. In this case, artificial breathing was induced immediately after shock, and respiratory arrest occurred for a very short time, suggesting that the cause of this hypoxia may be due to mild hyproperfusion. Among previously reported cases, there are 5 cases with relative selective lesions in the bilateral precentral gyri and bilateral calcarine cortex. Findings in all cases were by autopsy, revealing oligemic hypoxia. The onsets of these cases were cardiogenic or peripheral shock from cardiac arrest or arrhythmia, etc., during surgery. Two cases died in a coma state. The other 3 cases regained consciousness with quadriplegia. Among these 3 cases, the case reported by Murayama had quadriplegia and cortical blindness, as in this case.(ABSTRACT TRUNCATED AT 250 WORDS)

[Pure anterograde amnesia due to bilateral fornix lesions].

The patient was a right-handed 59-year-old female technician who was admitted to our hospital with a complaint of memory loss. Clinical examination revealed pure anterograde amnesia regarding episodic memory, while semantic and procedural memory was intact. Radiological procedures (CT scan and MRI) revealed a tumor of the septum pellucidum, which localized from the lower part of the corpus callosum to the anterior parts of the bilateral fornices. Transcallosal total removal was performed (pathological examination revealed that it was astrocytoma). Radiological and operative findings showed that the thalamus, the mammillary bodies, the hippocampus, and the basal forebrain, which are closely related to memory, were spared. After the operation, she reported no further memory disturbance. Preoperative neuropsychological tests revealed anterograde amnesia for verbal and visual stimuli, but postoperatively the former disappeared and the latter improved. Pre- and postoperatively, she was nonaphasic, and her immediate memory, intelligence, and frontal functions were intact. Cases of amnesia due only to fornix lesions are rare, and have not been reported yet in Japan. Our case is valuable in terms of showing that only the fornix lesion was responsible for memory disturbance. The main symptom resulting from fornix lesion is thought to be anterograde amnesia.

A unique murine CD43 epitope Lp-3: distinct distribution from another CD43 epitope S7.

In foregoing studies, we found a unique B cell differentiation antigen Lp-3 which is expressed on pre-B and premature B cells in the bone marrow, but is negative on bone marrow mature B cells and peripheral resting B cells. Nonetheless, Lp-3 was clearly positive on the majority of CD5 B(B1) cells. When we examined the biochemical nature and partial amino acid sequences of purified 132-kDa Lp-3 molecules and the nucleotide sequence of the cDNA clones, we found that Lp-3 is an epitope of CD43. Thus, the monoclonal antibody (mAb) Lp-3 may be the first mAb to murine CD43 defined by primary target structure analysis. Comparison of tissue distribution of Lp-3 and S7, an epitope previously suggested to associate with murine CD43, showed that they were similarly distributed on thymocytes, peripheral B and T cells, granulocytes, and platelets. In the bone marrow, while both Lp-3 and S7 were negative on mature B cells, the former was positive on all B lineage cells at an early ontogeny and the latter was positive only on the minor population of pre-B cells and pro-B cells. Lp-3 and S7 epitopes also showed different distributions on basement membranes of renal glomerulus, bronchus, and endometrium, lining cells of choroid plexus and muscular cells of arterioles in a variety of tissues. As CD43 has various isoforms generated by different degrees of glycosylation of the common core peptide, it is likely that Lp-3 and S7 are associated with different CD43 isoforms.

[Hypoglycemic encephalopathy demonstrating generalized multiple cortical infarctions--sequential CT findings].

A fifty-nine-year-old alcoholic man with severe hypoglycemic encephalopathy was examined using sequential CT scans of the brain (CT). Twenty-seven hours after the attack, which resulted in a comatose state, CT disclosed multiple low density areas throughout the cerebral cortex which resembled multiple cortical infarctions. CT obtained four days after the ictus demonstrated more prominent low density areas in the cerebral cortex, diffuse cerebral edema and partial cortical enhancement after administration of contrast medium. Sixteen days after the ictus, the multiple low density areas in the cerebral cortex disappeared. Enhanced CT on day 23 demonstrated marked gyral enhancement throughout the cerebral cortex. Thereafter diffuse brain atrophy progressed rapidly as demonstrated by MRI on day 82 which showed extensive cortical and subcortical atrophy particularly in the frontoparietal and parieto-occipital regions bilaterally with dilated lateral ventricles. Hypoglycemia and anoxia have long been thought to give rise to similar types of brain damage based on neuropathological observations. But it has recently been shown that they are quite different based on neurochemical and neurophysiological findings. Numerous previously reported autopsy cases of hypoglycemia confirm these findings which are neuropathologically similar to the multiple infarction seen in the present case. We conclude that the acute cortical changes of the present case are specific for hypoglycemic encephalopathy. The findings indicate that the basic mechanisms operating in hypoglycemia and anoxia are different.

Cheiro-oral topography of sensory disturbances due to lesions of thalamocortical projections.

Sensory disturbance in the unilateral hand and ipsilateral mouth region, the cheiro-oral syndrome, may be due to cortical, thalamic, or brainstem lesions. We report five patients with this syndrome due to infarction at the border of the posterior limb of the internal capsule and the corona radiata. The sensory fibers from the mouth area and hand probably travel to the cortical sensory areas in close proximity after leaving the posterior ventral thalamic nucleus.