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 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.

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.

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.

[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.

[A case of acute mountain sickness with bilateral lesion of pallidum].

The patient was 56-year-old female, who suffered from ataxia and then fell into coma on the next day after she had moved from the sea level to an altitude of 4,200 m. After she was brought to lower altitude, consciousness recovered within several hours. For about 2 days thereafter, disorientation was observed, and she was diagnosed as AMS (acute mountain sickness). Only insomnia continued in chronic stage. The results of X-ray computed tomography (CT) on 25th day after the onset of the disease revealed no abnormal finding except the slightly increasing uptake of contrast material. Symmetrical low density regions were seen in bilateral basal ganglia after one year, and the globus pallidus lesions were confirmed by magnetic resonance imaging. In the past, cerebral edema has been reported in most cases of AMS, and the neurotic symptoms of AMS have been attributed to cerebral edema, while the essential condition of this disease is not yet elucidated. In the present case, the globus pallidus lesions could be identified through the following-up of the central nervous system by X-ray CT and MRI as the first attempt for the case of AMS. There has been no report of globus pallidus lesions in the cases of AMS. Whereas low oxygen partial pressure is the primary cause of AMS, and it is highly probable that the disorders in globus pallidus as reported in the cases of carbon monoxide poisoning, anesthetic accident, etc. are related to the occurrence of AMS.

[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.

[Paroxysmal cerebellar ataxia--an evaluation using the findings from magnetic resonance imaging, positron emission tomography, and acetazolamide treatment].

Paroxysmal cerebellar ataxia (PCA) is a specific disease which exhibits spasmodic cerebellar ataxia but rarely shows abnormal neurological findings in the intermission. Verger first described an isolated case. Subsequent reports of the disease included mostly cases with autosomal dominant inheritance, but the reports have been limited to about 20 families. Although both the lesion and the cause have not been clearly identified, since Vighetto et al. demonstrated the atrophy of the anterosuperior region of the cerebellar vermis using magnetic resonance imaging (MRI), the lesion of PCA captured the attention of researchers. The patient was a 40-year-old male, who exhibited spasmodic inarticulation and dizziness during walking when he was 10 years old. The symptoms gradually became aggravated in both frequency and duration. Abnormal findings were observed by electroencephalography and Hydantol F was given with no successful effect. The results of a CT scan of the head revealed no abnormality, whereas those of MRI revealed the atrophy in the folia of anterosuperior region of the cerebellar vermis by MRI as in the case of Vighetto et al., and PCA was suspected. Findings from positron emission tomography (PET) for the first time disclosed the abnormality in the cerebellar vermis and brainstem, and suggested an organic disorder in the cerebellar vermis and a functional abnormality in the cerebellum and brainstem. Since the report by Griggs et al., it has been known that acetazolamide is effective for PCA although the pharmacological mechanism is not yet clear. In our present case, the attack was improved in both frequency and duration by the administration of acetazolamide, and the effectiveness of acetazolamide in the patient was confirmed.(ABSTRACT TRUNCATED AT 250 WORDS)

[Antemortem diagnosis of Marchiafava-Bignami disease].

Marchiafava-Bignami disease (M-B disease) is a peculiar disease, observed in hardened drinkers and resulting in demyelinization and necrosis of the corpus callosum. The clinical symptoms are diverse, and it is difficult to diagnose accurately while the patient is alive. Almost all reports in the past have been based on necropsy. Only three cases of M-B disease have been reported in Japan so far, none of which was based on a diagnosis while the patient was alive. We have been able to perform diagnosis of M-B disease while the patients were still alive by means of X-ray computed tomography (CT) and magnetic resonance imaging (MRI), and to study the clinical symptoms from the acute stage. In addition to the study on our own patients, we also conducted a neurosymptomatic study on the clinical symptoms of 6 cases, for which details of the symptomatology have been described-out of about 150 cases reported in the past. In the acute stage of M-B disease, we observed psychic symptoms, such as clouding of consciousness, mnemonic disorders and disorders and disorientation, or various frontal lobe symptoms, such as change in personality, raptus nervorum, dysphemia, pyramidal signs and astasia-abasia. These are non-specific symptoms and it is necessary to differentiate from encephalitis and other encephalopathy. In the chronic stage, dysphemia becomes sustained and, in addition, symptoms of transection of the corpus callosum are noted among the disorders of higher cerebral functions. If M-B disease is suggested from clinical symptoms, it is advisable to confirm the lesions in the corpus callosum by X-ray CT and MRI.(ABSTRACT TRUNCATED AT 250 WORDS)

[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.

[Alexia with agraphia produced by localized infarction in the inferior posterior region of the left temporal lobe].

There have been several reports on alexia with agraphia due to hemorrhage or trauma in the inferior posterior region of the left temporal lobe since Yamadori (1982) first reported a case of cerebral hemorrhage. We presented the first case of alexia with agraphia due to a circumscribed infarct in the inferior posterior region of the left temporal lobe. A 65-year-old right-handed man had an acute onset of inability to read Japanese "kana" letters and to write any letters. He had no difficulty in speaking or understanding. Neurological examination on admission was normal except for homonymous quadrantanopia in the right upper field. Neuropsychological findings: Spontaneous speech was fluent without dysprosody. There were no disturbances in auditory understanding or in repetition. He could read Japanese "kanji" characters correctly, however, he could not read any "kana" letters. Writing was also disturbed severely even as to his address, name or telephone number. Calculation was also difficult. There were no disturbances in naming colors, no ideomotor or constructional apraxia nor visual agnosia. X-ray computed tomography (CT) scan showed a faint low density area with ring enhancement suggesting a cerebral infarct in the inferior posterior region of the left temporal lobe. Patient's hospital course was characterized by a marked improvement of alexia, especially of "kana" letters as compared with that of "kanji" characters. Dissociative improvement of alexia compared with agraphia in this case could be explained by the fact that the lesion was in close contact with the occipital lobe and that he also had pure alexia in the early stage.

[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.

[A case of multiple sclerosis with pure alexia].

We report here a case of multiple sclerosis (MS) showing pure alexia. The patient was a 28 year-old, right-handed male student of medicine. He had been healthy prior to college, but when he tried to read the newspaper one morning in January of 1983, he suddenly became aware that he could not. He could speak fluently and had no disturbances of auditory comprehension. No signs of abnormality were noted in his writing ability. Thereafter, the patient occasionally experienced difficulty in reading, together with right homonymous hemianopsia. These symptoms, however, usually vanished following sleep. In April, 1984, the patient experienced headache and ataxia when walking, followed by repeated remission and exacerbation of the symptoms. Corticosteroid therapy produced complete disappearance of the headache and ataxia. In September of 1985, he was hospitalized at our department due to the clouding of consciousness accompanied by convulsions. Neurologically, no abnormalities of the ocular fundus were noted and Babinski's sign was negative, but left hemiplegia was observed. Neuropsychologically, his intelligence was normal and he had no difficulty in writing, but paralexia was noted. There were no disorders of spontaneous speech or auditory comprehension. Examination by CT scan and magnetic resonance imaging revealed a number of lesions in the white substance of the cerebrum, including the left occipital lobe. The abnormal signs seen radiographically vanished when cortical hormones were administered. It has been thought that the symptoms of multiple sclerosis are due mainly to disorders of the white substance, and that MS seldom produces symptoms of aphasia, due to the fact that the lesions in this disease are generally small.(ABSTRACT TRUNCATED AT 250 WORDS)

[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.

[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.