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Biomedical subjects

Mitsuru Kawamura

Publications and source records attributed to Mitsuru Kawamura.

At least 37 records · Page 2Linked to original sources
PubMed2005

Increased norepinephrine-associated adrenomedullary inclusions in Parkinson's disease.

The association with Parkinson's disease (PD) of adrenomedullary inclusions, known as 'hyaline globules' or 'adrenal bodies', has been reported for over 35 years. However, the common perception has been that adrenomedullary chromaffin cells cannot be recognized as pathological cells in PD. In the present study, we discovered that the number of adrenomedullary inclusions per unit area of the adrenal medulla was larger in PD and other Lewy body disorders (LBD) than in other neurological diseases and controls without any autonomic dysfunctions, and correlated with the duration of LBD. We also showed that the cells with adrenomedullary inclusions are all norepinephrine-secreting chromaffin cells. This was detected by PAS reaction following peroxidase immunohistochemistry of four proteins: chromogranin A, phenylethanolamine N-methyltransferase, S-100 protein and neurofilament protein. We also proved that the components of adrenomedullary inclusions are immunocytochemically different from those of Lewy bodies and Lewy-related neurites, as adrenomedullary inclusions were immunonegative to ubiquitin and alpha-synuclein as well as to the above four proteins. Therefore, contrary to current opinion, the norepinephrine-secreting adrenomedullary chromaffin cell is indeed another type of pathological cell in PD and other LBD.

Adrenal Medulla↗
PubMed2005

[Impairment of social cognition in Parkinson's disease].

The characteristic four symptoms of motor deficits, bradykinesia, rigidity, resting tremor and impairment of postural reflex with Parkinson's disease (PD) are accompanied by specific cognitive deficits. Deficits of executive functions, skill learning, and visuospatial cognition are well known. The results of our recent studies show the deficit of social cognition which include facial expression recognition, sensation of gaze direction, "theory of mind" in comprehension, and decision making. These symptoms can be explained by the damage of the amygdala and/or its connection, which are known to play a crucial role in social cognition, it is attributed to the involvement of amygdala and it's connection to the frontal lobe in PD. The impairment of social cognition is an important mental change associated with PD.

Cognition Disorders↗
PubMed2005

[An autopsied case of medullary glioma with an abrupt onset of headache and hemiparesis].

We describe an 89-year-old woman who presented with an abrupt onset of headache and right hemiparesis. With the initial diagnosis of cerebral infarction, we started therapy using sodium ozagrel. The right hemiparesis worsened, however, and a continuous intravenous heparin injection showed no effect. Furthermore, nystagmus in the bilateral eyes, dysphagia, left hemiparesis, and central ventilation disorder appeared one after another in three weeks. A magnetic resonance images (MRI) of the head, performed on the fifth hospital day with regular intervals of axial sections, disclosed no lesion responsible for right hemiparesis. MRI of the brainstem and upper cervical cord, performed after two weeks with smaller intervals of axial sections, revealed a T2 high signal lesion in the left side of the medulla oblongata and upper cervical cord. After about five weeks from the onset of the disease, she died of pneumonia. With the pathological examination, we diagnosed as glioma originated in the left ventral part of medulla oblongata. Five similar cases of brainstem glioma have been reported so far. Our patient, the oldest one, showed an exceptionally rapid clinical course, instructing us to consider the possibility of medullary glioma even in the elderly patients presenting with acute onset hemiparesis followed by rapid and progressive appearance of brainstem signs.

Aged↗
PubMed2005

[An autopsied case of paraneoplastic neurologic syndrome (limbic encephalitis, cerebellar degeneration, and pseudohypertrophy in the inferior olivary nuclei) associated with T cell lymphoma].

We describe a patient with paraneoplastic neurologic syndrome confirmed on postmortem examination. This 42-year-old man was admitted due to general fatigue, emaciation and acute-onset disorientation. Neurological examination revealed disorientation, moderate cognitive impairment, cerebellar ataxia, bilateral limitations and nystagmus in all directions during external ocular movement, swallowing disorder, bilateral Babinski sign, sensory disturbance in the distal parts of all extremities, and Romberg's sign. T-cell lymphoma was diagnosed following biopsy of the cervical lymph node. Neurological condition improved slightly after chemotherapy, but subsequently deteriorated. At about 6 years after the disease onset, brain magnetic resonance imaging (MRI) revealed atrophy of bilateral hippocampi and the upper vermis of the cerebellum. The patient died of pneumonia after a clinical course of about 6 years and 6 months. Pathologically, neuronal loss, reactive gliosis and perivascular lymphocytic infiltration were observed in the hippocampi, cerebellum, and inferior olivary nuclei. Lymphocytes around the vessels were positive for LCA and UCHL-1, but negative for CD8 and L26, and thus were considered to be T cells. No lymphoma cell was observed in the central nervous system or lymphatic organs. Based on the pathological findings, paraneoplastic neurologic syndrome (limbic encephalitis, cerebellar degeneration and olivary pseudohypertrophy) associated with T-cell type malignant lymphoma was diagnosed. Only three other cases of paraneoplastic neurologic syndrome associated with T-cell lymphoma have been reported. In those cases, death occurred due to the deterioration of malignant lymphoma, whereas the present patient died about 6 years after the remission of malignant lymphoma. Prognosis may thus depend on the course of the malignant lymphoma. In the present patient, neurological symptoms deteriorated after remission of malignant lymphoma, and no pathological lesion were found in the lymphatic organs. Lesions in the central nervous system in paraneoplastic neurological syndromes may follow a course independent of the original malignant disease.

Humans↗
PubMed2005

[A case report of acute neuromyopathy induced by concomitant use of colchicine and bezafibrate].

We report a patient of acute neuromyopathy induced by concomitant use of colchicine and bezafibrate. A 75-year-old man with chronic renal failure and hyperlipidemia treated with bezafibrate (400 mg/day) for 1.5 years had developed watery diarrhea followed by acute tetraparesis, 14 days after the administration of colchicine for recurrent gout. Neurological examination showed proximal muscle weakness with myalgia, distal mild numbness (dysesthesia) of four limbs and generalized decreased or absent reflexies. The findings including elevated serum muscle enzymes, myogenic patterns with widespread myotonic discharge on the electromyography and delayed latency of F-wave on nerve conduction study indicated that the patient's clinical features were consistent with neuromyopathy. Soon after both colchicine and bezafibrate were stopped, the patient's symptoms resolved rapidly, therefore we made a diagnosis of drug-induced neuromyopathy, although rhabdomyolysis with Guillain-Barré syndrome was initially suspected. Recently, there had been reported acute and severe neuromuscular disorder induced by combination therapy with colchicine and anti-hyperlipidemic drugs, and there were clinical similarities between the cases of these reports and our case. Co-administration of colchicine with bezafibrate might accelerate the onset of neuromyopathy in connection with chronic renal failure in this case. Extreme caution is warranted when the patient with renal insufficiency concomitant use of colchicine and bezafibrate.

Acute Disease↗
PubMed2004

An autopsied case of Sjogren's syndrome with massive necrotic and demyelinating lesions of the cerebellar white matter.

A 69-year-old woman developed subacute cerebellar ataxia and tremors in all four limbs in April 1996. Laboratory examination showed elevated antibodies against Ro and La. Head magnetic resonance imaging showed T(2) high-intensity lesions in the cerebellar white matter bilaterally and later in the pons. In April 2000, she died of multiple organ failure with incidental colon cancer. The autopsy showed atrophic parotid glands with an accumulation of lymphocytes around the ducts, confirming the diagnosis of Sjogren's syndrome histopathologically. The neuropathological examination revealed severe necrotic lesions in the cerebellar white matter bilaterally with several foci of perivenous demyelination in the periphery of the lesions and similar demyelinated areas in the pons. Immunohistochemistry with anti-JC virus antibody demonstrated no positive inclusions. A single focus of granulomatous arteritis was observed in one subarachnoid artery. The combination of Sjogren's syndrome, granulomatous angitis, and foci of perivenous demyelination suggests that an autoimmune mechanism played an important role in causing the necrotic lesions in the cerebellar white matter in this case.

Aged↗
PubMed2004

Deficits in long-term retention of learned motor skills in patients with cortical or subcortical degeneration.

We investigated the acquisition and long-term retention of new skills in patients with cortical (Alzheimer's disease, AD) and subcortical (progressive supranuclear palsy, PSP; Parkinson's disease, PD) degeneration. The motor skill task performance of the PD and PSP patients improved with training, but the improvement disappeared within a few months, whereas AD patients retained learned skills for 3-18 months. The results of our experiments show that subcortical dysfunction induces a retention deficit for newly learned motor skills. Our present study suggests that a normal striatum is necessary for the formation of long-lasting motor skills, and that the striatum plays an important role as a motor skill consolidation system.

Alzheimer Disease↗
PubMed2004

[Detection of micro mutation in dystrophin gene of DMD female carrier].

We attempted to identify a mutation in dystrophin gene in a female patient who was suspected a Duchenne muscular dystrophy (DMD) carrier with muscle weakness of upper limbs and congestive heart failure. We examined the mutation hot spots in DMD gene, exon 3, 6, 8, 13, 17, 19, 43, 44, 45, 47, 48, 49, 50, 52, 60 by multiplex PCR which had been a diagnostic screening strategy, and detected an extra band in exon 43 product. We also detected an extra band in exon 43 products by SSCP analysis for detection of small mutations which could not be detected by multiplex PCR. As a result of sequencing a PCR product of an exon 43, we confirmed an allele having the insertion of a 2 base of AT in Intron42, which is described for the first time. Although we can not conclude that this insertion is responsible for DMD, but it may cause abnormal splicing. In carrier detection of DMD without genetic information of proband, it is difficult to detect mutations by multiplex PCR solely. Therefore, SSCP of PCR products are recommended to detect mutation in DMD carrier.

Aged↗
PubMed2003

Musical alexia for rhythm notation: a discrepancy between pitch and rhythm.

In the process of reading music, the reading of rhythm and pitch might be differentiated, although there is no evidence of this to date. There have been cases of disorders restricted to the reading of pitch, but none in which the disorder has been restricted to the reading of rhythm. We present a case of musical alexia and agraphia with Wernicke's aphasia. An in-depth assessment of the subject's musical reading ability showed that her musical alexia was restricted to unfamiliar melodies. When a melody was divided into rhythm elements and pitch elements, pitch reading was preserved, but rhythm reading was severely disturbed. This is the first case reported of a disorder restricted to rhythm reading, and suggests the independence of rhythm reading and pitch reading.

Aphasia, Wernicke↗
PubMed2003

[A case of cerebral deep venous and venous sinus thromboses with anti-cardiolipin antibody].

We describe a case of cerebral deep venous and venous sinus thromboses with anti-cardiolipin antibody. A 62-year-old male with no previous illness of thrombosis but with alcohol abuse was admitted with acute onset unconsciousness. He recovered two days after with no severe sequela. Laboratory findings suggested the preceding conditions of dehydration and inflammation. X-ray CT of the head revealed symmetrical low density areas in the thalami and basal ganglia, high density signs in the cerebral deep veins, and dilation of the lateral ventricles. MRI on the second hospital day showed abnormal intensities in the thalami and basal ganglia (high signal on T 2-weighed and FLAIR image, low signals on T 1-weighed image, but almost isointensity on diffusion weighed image) and acute to subacute phase thrombus in the superior sagittal sinus. Abnormal intensities observed on MRI disappeared gradually in the following studies. Venous phase images of cerebral angiography performed in chronic phase disclosed occlusion of the superior sagittal sinus and stenosis of the vein of Galen. These radiological findings support the diagnosis of cerebral deep vein and venous sinus thromboses. Hematological examination revealed positive anti-cardiolipin IgG antibody. Several cases of cerebral deep venous thrombosis with anti-cardiolipin antibody have been reported. In our case, dehydration induced by alcohol abuse would have been the trigger of thrombosis, while the existence of anti-cardiolipin antibody might contribute to the risk of thrombosis as an underlying condition.

Antibodies, Anticardiolipin↗
PubMed2003

[A case of amyotrophic lateral sclerosis with dementia presenting long clinical course].

We describe a patient with amyotrophic lateral sclerosis with dementia (ALS-D) displaying a long clinical course. A 68-year-old Japanese male with no family history of note was admitted complaining of severe dysarthria and dysphagia. At 63 years old, Pick's disease was diagnosed on the basis of abnormal behavior, such as "Denkfaulheit" and moria, and temporal lobe atrophy observed on magnetic resonance imaging (MRI). Five years after onset, dysarthria and dysphagia emerged, and gradually worsened. On admission, muscular weakness of the upper extremities, fasciculation, and exaggerated tendon stretch reflexes were noted. Needle electromyography performed on the left upper and lower extremities revealed neurogenic pattern changes. Based on these findings and clinical course, ALS-D was diagnosed. Due to severe bulbar palsy, verbal communication was impossible. However, neither specific symptoms of dementia nor abnormal behavior was demonstrated, although this latter had been observed 5 years ago, with only short-term memory impairment apparent. MRI disclosed severe knife-edge atrophy of bilateral temporal lobes, most prominently in the anterior regions. SPECT images revealed decreased uptake of tracer in bilateral inferior temporal lobes, predominantly on the left side. The patient died suddenly 4 months after admission, and post-mortem examination was not conducted. Total clinical course was about 8 years. Several cases of ALS-D have displayed similar clinical courses to the presented case. Some of these would also have initially been diagnosed as Pick's disease. We speculate that cases displaying psychiatric symptoms for several years and initially diagnosed as Pick's disease may finally be diagnosed as ALS-D upon the eventual emergence of motor symptoms(bulbar palsy).

Aged↗
PubMed2003

[A case presenting with trochlear nerve palsy and segmental sensory disturbance due to circumscribed midbrain and upper pontine hemorrhage].

We describe a patient presenting with trochlear nerve palsy and segmental sensory disturbance due to circumscribed mesencephalic hemorrhage. A 36-year-old man with no past illness visited our hospital complaining of sudden onset of diplopia, dysesthesia of the left face and upper extremity, and acuphenes of the left ear. Neurological examination revealed left trochlear nerve palsy and segmental sensory disturbance of the left side almost above T11 level. Pain and temperature sensation were disturbed, but vibration, joint position, graphesthesia, kinesthesia, and discrimination sensation were spared. Magnetic resonance imaging of the head, performed 7 days after onset, revealed acute to subacute phase hemorrhage at the right inferior colliculus. No abnormalities were identified on cerebral angiography. Symptoms gradually improved with conservative therapy. After about ten weeks, diplopia disappeared and area of sensory disturbance was reduced (disturbance of pain sensation reduced to about T4 level, temperature sensation to about T9). Segmental sensory disturbance usually accompanies spinal cord lesion. However, several cases of similar symptoms following cerebrovascular disease of the brainstem have been reported. Conversely, some reports have indicated that trochlear nerve palsy due to midbrain hemorrhage accompanies sensory disturbance contralateral to the lesion. The nature of sensory disturbance is thus variable. The present case suggests that segmental sensory disturbance might accompany trochlear nerve palsy caused by hemorrhage of the inferior colliculus, as intramedullary fibers of the trochlear nerve and spinothalamic tract are located nearby and somatotopy of the spinothalamic tract is preserved even at the level of the midbrain.

Adult↗