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Biomedical subjects

I Akiguchi

Publications and source records attributed to I Akiguchi.

At least 235 records · Page 13Linked to original sources
PubMed1989

Spontaneous spongy degeneration of the brain stem in SAM-P/8 mice, a newly developed memory-deficient strain.

A spontaneous spongy degeneration of the brain stem and spinal cord was discovered in a murine model of accelerated senescence (SAM), cared for under both conventional (SAM-P/8) and specific pathogen-free (SAM-P/8/Ta) conditions. SAM-P/8 and SAM-P/8/Ta showed no clinical neurological abnormalities, yet there was a deterioration in learning and memory abilities. Light microscopic examination revealed a spongy degeneration in the brain stem and spinal cord, in the reticular formation, and proliferation of hypertrophic astrocytes in the spongy area. The spongiform degeneration progressed with advancing age from four to eight months, after which the entire brain was involved. Astrocytosis increased with advancing degeneration. Ultrastructurally, mild dendritic swelling occurred at one month of age. At two months of age, moderate postsynaptic swelling and a widening of intracellular membrane structure were observed, and at age five months there were large vacuoles circumscribed by membranous lamellae, identifiable as myelin. Vacuoles in SAM-P/8 proved to be swollen neuronal processes and oligodendroglial processes. These SAM-P/8 and SAM-P/8/Ta strains of mice are new memory-deficient strains with spontaneous spongy degeneration associated with aging.

Animals↗
PubMed1989

[Left antero-medial thalamic infarction and symptoms of amnesia, aphasia, and dementia].

Three cases of left antero-medial thalamic infarction who showed amnesia, aphasia and dementia were studied comparatively in terms of clinical features and the MRI findings. Case 1 and Case 2, who showed transient amnesia and aphasia respectively, had a single lesion in the left antero-medial thalamus. Case 1 had a lesion in a more ventral part than Case 2, suggesting that Case 1 had a lesion of the bundles into the anterior and dorsomedial thalamic nuclei while Case 2 had a lesion of the ventrolateral thalamic nucleus. On the other hand, Case 3 who showed persistent dementia had multiple lesions in addition to the left antero-medial thalamic infarction. A review of the previous reports and investigations of the present cases suggest that a single ischemic lesion in the left antero-medial thalamus will cause amnesia and/or aphasic symptom while in cases with other multiple lesions it may cause persistent dementia.

Aged↗
PubMed1989

[Catecholaminergic systems in the amygdaloid complex of SDAT and aged controls: tyrosine hydroxylase immunohistochemistry].

Catecholaminergic systems in the amygdaloid complex in patients with senile dementia of Alzheimer type (SDAT) and aged controls have been studied with tyrosine hydroxylase (TH) immunohistochemistry. TH-immunoreactivity was found in fibers in all subnuclei of human amygdala, although varying in density in the subnuclei. The most dense catecholaminergic innervation was observed in the central, basal, and cortical nuclei of amygdala. The prominent finding in the amygdaloid complex of SDAT was that swollen and bulbous TH-immunoreactive neurites were found in association with neuritic plaques, which have not, rarely if any, been found in controls. The numerical density of neurites was mostly in parallel with that of TH-immunoreactive fibers except for the central nucleus. Thus, it is suggested that a class of populations of TH-immunoreactive neurons are selectively affected in the amygdaloid complex in SDAT.

Aged↗
PubMed1989

[The cause of paradoxical growth of intracranial tuberculomas during anti-tuberculous chemotherapy].

A case of multiple intracranial tuberculomas diagnosed by enhanced brain CT scan and MRI, which developed during the course of miliary tuberculosis under anti-tuberculous chemotherapy was experienced. Chemotherapy with an increased dose of each agent and corticosteroid was administered, and eventually intracranial tuberculomas nearly disappeared. After 1970, there have been 29 reported cases of intracranial tuberculomas in Japan, which were diagnosed by brain CT and treated with anti-tuberculous agents. Among them, 27 evaluable cases were classified into 3 groups. Group A: Intracranial tuberculomas were proved by CT before chemotherapy in 7 cases. Four of them enlarged during chemotherapy. Group B: During chemotherapy of tuberculous meningitis, neurological symptoms worsened or prolonged, and finally intracranial tuberculomas were found by CT in 9 cases. In 5 of them, after meningitis was improved by chemotherapy, neurological symptoms worsened and intracranial tuberculomas were found. Group C: During chemotherapy of pulmonary tuberculosis or miliary tuberculosis, neurological symptoms appeared and intracranial tuberculomas were found by CT in 11 cases (including our own case). Getting 3 groups together, intracranial tuberculomas seem to have worsened during chemotherapy in 24 out of 27 evaluable cases. In view of response to chemotherapy, these 24 cases can be divided into 2 categories: 1) non-responders to chemotherapy; 2) cases finally cured by chemotherapy ("transient worsening").(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

[Xeroderma pigmentosum presenting clinical features of spinocerebellar degeneration].

A case of group D xeroderma pigmentosum is reported. This 26-year-old woman was normal delivery, and showed a normal psychomotor development. Her parents noted a patchy brownish pigmentation on her limbs, face and trunk soon after the birth. Gait disturbance appeared at 17 years old and progressed over 9 years. Neurological examination disclosed a severe loss of deep sensation, spastic weakness and mild cerebellar ataxia. Slight involvement of peripheral nerves was revealed by the elecrophysiological investigations. CT and MRI brain scans showed a cerebellar atrophy, however no atrophy was seen in the cerebrum. Adrenocortical hypo-function was noted by decreased 17 KS and 17 OHCS. Unscheduled DNA synthesis of the patient's skin fibroblast was 45% of normal controls, and the result was consistent with group D xeroderma pigmentosum. The neurological findings of this patient are well characterized by the degeneration of the posterior and lateral column of the spinal cord, cerebellum and peripheral nerves. We discussed symptomatological and etiological similarities of the present case to spinocerebellar degeneration. It may be necessary to consider the possibility of xeroderma pigmentosum in the differential diagnosis of spinocerebellar degeneration.

Adult↗
PubMed1989

[Paramedian thalamic and midbrain infarcts associated with palilalia].

We report a case with paramedian thalamic and midbrain infarcts associated with palilalia. A 62-year-old man fell into a comatose state, and was admitted to an emergency hospital. Two days later, his consciousness level began to improve. Neurological examination revealed bilateral cerebellar ataxia, oculomotor nerve palsy, lack of spontaneity, and amnesia. Deep tendon reflexes were normal on all extremities, and no muscular weakness was observed. Babinski sign was noted on the right side. Muscle tone was decreased. No sensory disturbance was found. Two months later, he began to show compulsive repetition of syllables, words, or phrases, and was transferred to our hospital. He involuntarily repeated one syllable or a word five to ten times in spontaneous speech, repetition of phrases being not so frequent as that of syllables or words. This speech abnormality was considered as palilalia, which Souques first reported in 1908. The palilalia of this patient was rarely noted when he repeated words spoken to him by the examiner. As he spoke, the rate of speech gradually increased, the loudness reduced, and finally he began to whisper (palilalie aphone). The palilalia continued for four months. MRI showed infarcts in the medial thalami, subthalamic and midbrain on both sides. Auditory brainstem response showed delayed latency of bilateral V waves, and EEG revealed bilateral theta waves. In this patient no lesion other than thalamus, subthalamus and midbrain was detected by MRI. It is suggested that bilateral lesion of the thalami and their projection areas caused palilalia in this patient.

Cerebral Infarction↗
PubMed1989

[A case of venous dural sinus thrombosis presenting dementia syndrome. An autopsy case].

We report clinical and pathological features of a case of dementia syndrome due to dural sinus thrombosis. In three years before admission, the patient, a 64-year old man, had had four convulsive attacks; scattered calcification shadows were disclosed by plain CT. Ten months before the admission, he complained of progressive memory disturbance and dyscalculia. General physical examination showed no remarkable abnormalities except for bruit at the left mastoid process. Although his time orientation was poor, he was otherwise fully awake. Neurologically, memory disturbance, finger agnosia, and dyscalculia were observed. Right Barré's sign, and exaggerated right patellar tendon reflex were observed. Plain X-ray CT revealed calcification-like, scattered high-density areas in the floor of the cerebral cortical sulci. Enhanced CT showed abnormal vessel high-density areas in both the cerebrum and brainstem. Cerebral angiography showed thrombosis of bilateral transverse sinuses, arterio-venous fistula in the left transverse sinus, and remarkably dilated cortical veins over both cerebral hemispheres. Positron emission tomography revealed misery perfusion areas in bilateral cerebral hemispheres. We presume that the mass effect of venous engorgement and chronic ischemia due to the arterio-venous fistula caused the dementia syndrome. These clinical manifestations were improved by amantadine and the patient was discharged. During follow-up, he died of subarachnoid hemorrhage, and an autopsy was performed. Pathological findings were as follows: 1) cortical and subcortical multiple-infarction in the cerebrum, 2) hematoma in the subarachnoid space, 3) venous dilatation of the cortical veins and pseudocalcification of their walls, and 4) thrombus in the transverse dural sinus.

Amantadine↗
PubMed1988

Age-related deterioration of ability of acquisition in memory and learning in senescence accelerated mouse: SAM-P/8 as an animal model of disturbances in recent memory.

Memory, learning and behavior of senescence accelerated mouse (SAM-P/8) were investigated by using passive avoidance response, T-maze and open field and the findings were compared with those from senescence resistant mouse (SAM-R/1 control). SAM-P/8 mice showed a remarkable age-related deterioration in ability of memory and learning in passive avoidance response. This age-related memory and learning deficit was linked to a deterioration in the ability of acquisition and was not due to impairment in the ability of retention and hyperactivity, as observed in the open field. In the alternation T-maze tests, SAM-P/8 showed as high a rate of alternations as did the SAM-R/1 and in the T-maze avoidance tests, SAM-P/8 also showed as intact a memory ability as seen in the SAM-R/1, despite a memory deficit in the passive avoidance response. Thus, SAM-P/8 may prove to be a pertinent model for researching mechanisms related to the memory deficit seen in senile humans.

Aging↗
PubMed1988

Direct projections of non-pyramidal neurons of Ammon's horn to the supramammillary region in the cat.

Non-pyramidal neurons in cat Ammon's horn were shown to send their axons to the supramammillary regions (SMR), i.e. the supramammillary nucleus and its vicinities including the supramammillary nucleus and the lateral, posterior and dorsal hypothalamic areas: wheat germ agglutinin-horseradish peroxidase (WGA-HRP) injection into Ammon's horn resulted in labeling of presumed axon terminals in the SMR; and after injecting HRP into the SMR, retrogradely labeled non-pyramidal neurons were seen in Ammon's horn.

Animals↗
PubMed1988

Reduced nicotinamide adenine dinucleotide phosphate-diaphorase histochemistry in the pontomesencephalic region of the human brainstem.

Reduced nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-diaphorase), which is specifically localized in neurons, has been histochemically demonstrated in human brain by using a perfusion-fixation procedure. With such fixed human brainstem, it was possible to study the topographic organization of NADPH-diaphorase-containing neurons that were visualized in fine detail for the first time. In the pontomesencephalic region, positive neurons were observed in nuclei around the decussation and arm of the superior cerebellar peduncle. These nuclei included the pedunculopontine tegmental, lateral parabrachial and oral pontine reticular nuclei. The positive somata were mainly multipolar in shape and medium to large in size. The positive neurons appeared to correspond to cholinergic neurons, at least partly in the brainstem, in terms of both the patterns of distribution and the cellular morphology.

Brain Stem↗
PubMed1988

Prolonged disturbance of consciousness with periodic EEG discharges after fulminant hepatitis.

Prolonged disturbance of consciousness associated with periodic EEG discharges developed in a 57-year-old male after fulminant hepatitis. He had repeated episodes with mutism and depersonalization, each lasting for 1-2 days. There were periodic EEG discharges during each episode. The atypical triphasic wave was a constituent of periodic EEG discharges together with spike and sharp waves, which suggests that the atypical triphasic wave has an epileptogenic factor as do spike and sharp waves. The effectiveness of anticonvulsants on the disturbance also suggests that there was an epileptogenic factor in the causation of the disturbance of consciousness.

Cognition Disorders↗
PubMed1988

Bilateral cheiro-oral syndrome following pontine haemorrhage.

Cheiro-oral syndrome is a peculiar sensory disturbance observed around the corner of the mouth and the palm of the hand on the same side, usually occurring unilaterally. A male patient with bilateral cheiro-oral syndrome following pontine haemorrhage is reported. CT, MRI and neurological findings showed that the syndrome was due to a lesion in the medial lemniscus and ventral secondary ascending tract of the trigeminal nerve on both sides. Although unilateral cheiro-oral syndrome has been reported with a lesion in the parietal lobe, thalamus or brain stem, a bilateral syndrome could be caused only by a lesion of the brain stem.

Cerebral Hemorrhage↗
PubMed1988

Human T cell lines established from the cerebrospinal fluid of patients with human T lymphotropic virus type I-associated myelopathy (HAM).

T cell lines were established from the cerebrospinal fluid (CSF) lymphocytes of two patients with human T lymphotropic virus type I (HTLV-I)-associated myelopathy (HAM). These two interleukin-2 (IL-2)-dependent T cell lines have been cultured for more than 8 months without any accessory cells. The surface phenotype of these cells was CD2(+), CD4(+), CD8(-), Ia(+) and Tac(+). Southern blot hybridization analysis revealed the presence of HTLV-I provirus in these cells and C-type retrovirus particles were identified by electron microscopy. These findings indicate the presence of HTLV-I infected helper T lymphocytes in the CSF of the patients with HAM. These HTLV-I(+) T cell lines may be valuable for investigating the possible neutrotropism of HTLV-I and the role of HTLV-I in the pathogenesis of HAM.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1988

Analysis of the provirus genome integrated in T cell lines established from the cerebrospinal fluid of patients with human T lymphotropic virus type I-associated myelopathy (HAM).

T cell lines were established from the cerebrospinal fluid (CSF) lymphocytes of three patients with human T lymphotropic virus type I (HTLV-I)-associated myelopathy (HAM). To elucidate the possible changes of the provirus nucleotide sequences integrated in HAM-derived T cell line cells, DNA from these cells was digested with PstI, which cleaved the provirus genome of HTLV-I at several sites, and three common bands were detected by Southern blot analysis in all cases. These bands were identical in size to those detected in T cell lines established from peripheral blood lymphocytes of adult T cell leukemia (ATL) patients. These results were confirmed with restriction enzymes HindIII and BamHI. These findings suggest that the provirus genome detected in T cell lines derived from CSF of HAM patients is identical to HTLV-I.

Adult↗
PubMed1988

The imbalance in CSF T cell subsets in active multiple sclerosis.

We determined the percentage of each lymphocyte subpopulation in the cerebrospinal fluid (CSF) and the peripheral blood of 7 patients with active multiple sclerosis (MS), 7 with inactive MS, 5 with other inflammatory diseases in the central nervous system, and 12 with non-inflammatory neurological diseases, using fluorescein-labelled monoclonal antibodies (anti-Leu7, anti-HLA-DR, and those that recognize such surface antigens as CD3, CD4, CD8, and CD19), and by laser flow cytometry to clarify the clinical usefulness of their measurement in the assessment of disease activity in MS. In CSF, a significant increase in the percentage of CD4+ cells and a significant decrease in the percentage of CD8+ cells were observed in the active MS group compared with the other 3 groups, while none of the percentages of the 6 subsets studied in the peripheral blood were significantly different among these groups. Our preliminary study indicated that evaluation of the percentages of CD4+ and CD8+ cells in CSF by flow cytometry could be a useful indicator of disease activity in MS.

Adult↗
PubMed1988

Evidence of hypovitaminosis D in patients with mitral ring calcification.

In order to evaluate the role of calcium regulating hormones in the pathogenesis of mitral ring calcification, we have studied the serum levels of PTH and vitamin D metabolites in aged females both with and without mitral ring calcification (MRC). In the patients with MRC (n = 17), significantly lower levels of serum total protein (6.6 +/- 0.2 in the MRC group vs 7.1 +/- 0.1 g/dl in the control group, mean +/- SEM), BUN (15.7 +/- 0.9 vs 18.3 +/- 0.9 mg/dl), creatinine (0.7 +/- 0.02 vs 0.9 +/- 0.02 mg/dl) and calcium (8.4 +/- 0.1 vs 9.2 +/- 0.1 mg/ml) were observed as compared with those in the controls (n = 32). Significantly higher PTH levels (0.57 +/- 0.07 vs 0.38 +/- 0.04 ng/ml) were found in the MRC group. Levels of all three vitamin D metabolites in the MRC group were significantly lower than those in the control group (25-OHD; 11.2 +/- 1.4 vs 19.6 +/- 1.2 ng/ml, 24,25(OH)2D; 0.7 +/- 0.1 vs 1.3 +/- 0.1 ng/ml and 1,25(OH)2D; 12.5 +/- 2.4 vs 43.0 +/- 3.5 pg/ml). The correlation coefficient between PTH and 1,25(OH) 2D was -0.382(n = 49, p less than 0.01). Thus, the significantly higher PTH levels in the MRC group might result in hypovitaminosis D. In conclusion, evidence of hypovitaminosis D in the patients with mitral ring calcification was demonstrated.

Aged↗