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Biomedical subjects

M Matsunaga

Publications and source records attributed to M Matsunaga.

At least 73 records · Page 4Linked to original sources
PubMed1995

Recurrent Guillain-Barré syndrome in Japan.

The clinical profiles of 11 Japanese patients with recurrent episodes of Guillain-Barré syndrome (GBS), including 3 of our cases out of a total of 76 patients (48 males and 28 females), are reviewed. The recurrence rate was estimated as 4%. Among the 11 Japanese patients, 10 were male. Various viral infections had been confirmed in 1 case. No patients showed recurrent ophthalmoplegia. Sensory involvement varied from one episode to the next. These findings suggest the changing distribution of the demyelinating lesions and possibly a different reaction to the unknown pathogens in the recurrence of GBS.

Adolescent↗
PubMed1995

[A case of Guillain-Barré syndrome with ophthalmoplegia showing high titers of anti-GQ1b and -GD1b antibodies in the serum].

A 24-year-old housewife developed double vision, tingling sensation, and weakness in the legs following a flu-like illness. She then developed dysphagia and difficulty in standing. On admission her eyes were fixed in midline due to ophthalmoplegia. Doll's eye sign was negative. She had severe generalized muscle weakness and no sensory deficits. All tendon reflexes were lost. CSF protein was 58 mg/dl with cell count of 2/mm3. Antibodies to campylobacter jejuni, mycoplasma, EBV, and other microbes were negative. We treated her with plasmapheresis after which she showed rapid clinical recovery, although the ophthalmoplegia improved slightly later. Increased titer of IgG class antibodies to GD1b and to GQ1b, and of IgM antibody to GQ1b, were detected in the serum taken during the acute phase of the illness. In parallel with clinical amelioration, both the anti-GD1b and -GQ1b antibodies decreased in titer, or became negative. Since there is no common epitope to GD1b and GQ1b gangliosides, we speculated that the anti-GD1b and -GQ1b antibodies were induced independently by different antigens in this patient. Moreover, the presence of high titer IgM antibody to GQ1b possible indicates that this patient was at the relatively early stage of infection of unknown microbe, which then induced the IgG antibodies to GD1b and GQ1b by cross sensitization, which might correlate with the tetraplegia and the ophthalmoplegia, respectively.

Adult↗
PubMed1995

[Relationship between insulin secretion and insulin resistance in nondiabetic subjects with myotonic dystrophy--a case control study].

Hyperinsulinemia in myotonic dystrophy (MyD) is generally considered as a result of insulin resistance. However, as a consequence of abnormality in systemic membrane fluidity in this disease, abnormal insulin clearance or intrinsic pancreatic beta-cell dysfunction could also contribute to the hyperinsulinemia. To clarify the cause of hyperinsulinemia in MyD, we examined the insulin resistance, insulin clearance and the capacity of insulin secretion in 6 patients with MyD. They received a euglycemic hyperinsulinemic (insulin 40 mU/m2/min) clamp study for the quantification of insulin resistance by the glucose infusion rate (GIR). We evaluated their capacity of insulin secretion by the ratio of increment of serum insulin level to that of plasma glucose level 30 minutes after a 75 g oral glucose load (insulinogenic index; I.I.) and the ratio of area under the curve of serum insulin levels to that of plasma glucose levels during a 75 g oral glucose load (AUCIRI/AUCPG). The I.I. (1.1 +/- 0.6 vs 0.4 +/- 0.3, p < 0.05) and the AUCIRI/AUCPG (0.5 +/- 0.2 vs 0.2 +/- 0.1, p < 0.01) in MyD were significantly greater than those of GIR, body mass index and sex matched 6 non-diabetic controls respectively. Insulin clearance, estimated by the level of insulin and C-peptide before and during a euglycemic clamp study did not differ between the two groups. These results indicate that the postload hyperinsulinemia observed in MyD is not solely resulted from insulin resistance. Other factors, such as intrinsic beta-cell disorder may be involved.

Adult↗
PubMed1995

[Sensory nerve conduction velocity determined by somatosensory evoked potentials in patients with hereditary motor and sensory neuropathy type I].

We evaluated sensory nerve conduction velocity (SCV) determined by somatosensory evoked potentials (SEPs) components in 2 cases of hereditary motor and sensory neuropathy whose sensory nerve action potentials (SNAPs) were not evoked. SEPs elicited by median or ulnar nerve stimulation at the wrist or elbow were recorded from 5 scalp electrodes with ear reference. In both cases, no parietal N20 or frontal P20 component was identified, but a clear parietal P27 component was noted. The onset latency of the P27 component elicited by wrist or elbow stimulation was identified as the point where the superimposed 5 waves diverged. Then, the SCV was obtained by dividing the distance between the wrist and elbow by the onset latency difference. Tibial SCV was also determined by a similar method in one patient. The SCVs of the median, ulnar and tibial nerves were markedly decreased but 10-30% faster than the motor nerve conduction velocities measured concomitantly. We showed that a multichannel scalp recording of SEPs makes it possible to determine the onset latencies of the cortical components. So, SEP testing should be applied to obtain the SCVs in patients whose SNAPs were unrecordable.

Adult↗
PubMed1994

Reduction of GABAA and GABAB receptor densities in the cerebellar cortex from 3-acetylpyridine-induced ataxic rats.

We measured GABAA and GABAB receptor densities in the cerebellar cortex from 3-acetylpyridine-induced ataxic rats using receptor autoradiography. GABAA and GABAB receptor densities were significantly reduced both in the molecular layer and the granule cell layer. Reduction of GABA receptor densities may be induced by loss of GABA receptors on the degenerated climbing fibers or by secondary or compensatory changes of neuronal activities in the cerebellum.

Animals↗
PubMed1994

Quantitative autoradiographic distribution of glutamate receptors in the cervical segment of the spinal cord of the wobbler mouse.

The reduction of glutamate content has been observed in the spinal cord of the wobbler mouse, a purported model of amyotrophic lateral sclerosis (ALS). To elucidate glutamate receptors in the wobbler spinal cord, we measured densities of N-methyl-D-aspartate (NMDA), kainate, alpha-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid (AMPA) and metabotropic glutamate (mGlu) binding sites using in vitro autoradiography. In wobbler mice, NMDA, kainate, and AMPA binding sites were increased in the dorsal horn and kainate binding sites were also increased in the intermediate zone. However, mGlu binding was unchanged. These results disagree with those observed in ALS spinal cords, in which NMDA and kinate binding sites are decreased. The wobbler mouse may have the glutamate dysfunction, but in a different way from ALS.

Animals↗
PubMed1994

Correlation of somatosensory central conduction time with height.

To study the correlation between somatosensory central conduction time (CCT) and the subject's height, we recorded somatosensory evoked potentials (SEPs) from the neck and scalp elicited by median nerve stimulation in 72 normal young adults. We determined the CCT in each subject from peak-to-peak and onset-to-onset measurements. The mean value for the onset CCT was 6.2 +/- 0.4 msec and for the peak CCT, 5.7 +/- 0.5 msec. The peak CCT was significantly shorter but showed a wide range. There was a significant correlation between the onset CCT, but not the peak CCT, and height. Our findings confirm that the length of the central somatosensory pathway is proportional to the subject's height and indicate that the "conventional" peak CCT measurement of median nerve SEPs is inadequate.

Adolescent↗
PubMed1994

[A case of benign intracranial hypertension associated with systemic lupus erythematosus (SLE) showing diffuse white matter lesions on MRI].

We describe a 35-year-old woman with benign intracranial hypertension (BIH) secondary to systemic lupus erythematosus (SLE). She had low grade fever and skin eruptions, but neurological examination revealed no abnormal findings. Antinuclear and anti ds-DNA antibodies were positive, and complements were decreased. MRI demonstrated diffuse hyperintense white matter lesions on T2-weighted imaging. Mild bilateral papilledemas developed in the fundi, when her headache was exacerbated. The cerebrospinal fluid (CSF) pressure was 550 mmH2O. Cerebral angiography showed no cerebral sinus thrombosis. She was diagnosed as BIH secondary to SLE. Since RI cisternography revealed remarkably delayed absorption of the CSF, it was speculated that the CSF absorption by arachnoid villi would be probably disturbed in association with some autoimmune mechanisms by SLE. The subsequent rise of intraventricular pressure may result in retrograde transependymal flow of the CSF and the diffuse hyperintense white matter lesions on MRI.

Adult↗
PubMed1994

Posterior interosseous syndrome in acute Guillain-Barré syndrome.

Four cases presenting with posterior interosseous nerve syndrome (PIS) in the early period of acute Guillain-Barré syndrome (GBS) are described. The characteristic signs of PIS, consisting of finger extension inability, partial loss of power in wrist extension, and radial deviation during attempted wrist extension were demonstrated bilaterally. Radial nerve conduction study revealed a fall in of compound muscle potential amplitude after proximal stimulation. The signs of PIS became indistinguishable during the course of the illness; this was due to further progression of the forearm weakness veiling the syndrome in some patients, or recovery following plasmapheresis in others. Three of them were amateur sportsmen, in whom active supination-pronation of the forearm was probably responsible for this particular presentation.

Action Potentials↗
PubMed1994

[A case of convexity arachnoid cyst associated with chronic subdural hematoma and intracystic hemorrhage].

Arachnoid cysts account for about 1% of all intracranial tumors, in which about 50% arise from the middle cranial fossa, and rarely occur at the cerebral convexity. They sometimes are associated with chronic subdural hematoma (CSDH) but the exact mechanism of their development is still unclear. A 15-year-old boy was admitted to our hospital with an arachnoid cyst at the right frontal convexity. When he experienced recurrent generalized seizure, CT and MRI revealed CSDH localized at the surface of the arachnoid cyst. Radical operation for the cyst with CSDH was successfully performed. As far as we know, it is rare that CSDH and hematoma are colocalized over an arachnoid cyst at the cerebral convexity. In this report, the operative findings of this patient and possible mechanism of CSDH formation were reported.

Adolescent↗
PubMed1993

A case of tachycardia-induced cardiomyopathy due to chronic ectopic atrial tachycardia.

Only a few reports exist that chronic supraventricular tachycardia causes ventricular dilation and poor left ventricular contraction--so-called "tachycardia-induced cardiomyopathy." Clinical and electrophysiologic features of chronic supraventricular tachycardia including chronic persistent ectopic atrial tachycardia (EAT) in adults have also been described by a few investigators. We report a rare case of long follow-up of chronic EAT-induced severe cardiomyopathy and mitral regurgitation that was well controlled after medical treatment.

Cardiac Catheterization↗
PubMed1993

Recurrence of thyrotoxicosis after attack of allergic rhinitis in patients with Graves' disease.

Graves' disease is frequently aggravated during antithyroid drug therapy; however, little is known of its aggravating factors. We studied 83 patients with Graves' disease who were euthyroid for at least 6 months under antithyroid maintenance therapy, and we examined the relationship between thyrotoxicosis relapse, attack of allergic rhinitis, and peripheral eosinophil increase. Forty-one patients showed thyrotoxicosis relapse; of these, 22 (54%) showed peripheral eosinophil increase, and 14 (34%) had attacks of allergic rhinitis. In the remaining 42 patients without thyrotoxicosis relapse, only 4 (10%, P < 0.001) showed an increase in peripheral eosinophils, and only 3 (7%, P < 0.01) had allergic rhinitis. Recurrence of thyrotoxicosis was observed with the increase in serum levels of TSH-receptor antibodies and increase in eosinophils 2 months after the attack of allergic rhinitis. Three patients with seasonal allergic rhinitis showed thyrotoxicosis relapse at the same time of year within 2 consecutive years. Our findings indicate that allergic rhinitis can be an aggravating factor of Graves' disease and suggest that the preceding increase in peripheral eosinophils can be a predictive indicator of recurrence of thyrotoxicosis during antithyroid drug therapy.

Adolescent↗
PubMed1993

Sinus and atrioventricular nodal re-entrant tachycardia.

A case of a 42-year-old woman who had combined sinus and atrioventricular nodal tachycardia is reported. Programmed atrial stimulation study showed the induction of the two types of paroxysmal supraventricular tachycardia. The mechanisms of these supraventricular tachycardias were both sinus nodal and atrioventricular re-entrant tachycardia. Sinus nodal re-entrant tachycardia could be induced only after injection of atropine. The tachycardias could no longer be induced after the administration of verapamil.

Adult↗
PubMed1993

[A case of NIDDM associated with oculomotor palsy due to atypical carotid cavernous sinus fistula].

Partial ophthalmoplegia due to third nerve palsy with an intact pupil is a frequent cause of diploplia observed in diabetic patients. Pupillary muscle involvement, such as anisocoria and loss of light reflex, is usually uncommon in this diabetic cranial mononeuropathy. A 65-year-old woman with non-insulin dependent diabetes mellitus (NIDDM) suddenly developed a severe headache and diplopla. Right oculomotor nerve palsy was observed in association with anisocoria, ptosis of the right lid, and a defective light reflex. No exophthalmos or vascular bruit was observed in the right orbital region. Computed tomography and magnetic resonance images of the head were negative. Cerebral angiography revealed a carotid cavernous sinus fistula (CCF). The patient was successfully treated with external carotid artery embolization combined with radiation. It is well known that pupil sparing in oculomotor nerve palsy predicts an extraaxial ischemic lesion, while pupil involvement predicts an extraaxial compression lesion. Therefore, pupillary involvement in oculomotor nerve palsy in diabetic patients necessitates cerebrovascular investigation to rule out ICPC aneurysm or tumor. In this circumstance, a variant type of CCF without characteristic ocular signs should be included in the differential diagnosis.

Aged↗
PubMed1993

[Phenylketonuria with adult-onset neurological manifestation].

We report a male patient with phenylketonuria (PKU) who developed multisystem neurological manifestation in his fourth decade. He was born in 1957 when a neonatal mass screening had not been available. His neuropsychological development was entirely normal and he was a good athlete during his high school days. He was in good health until the age of 32, when his vision was blurred. In four months his gait progressively deteriorated to bind him to a wheel chair. On physical examination he had red hair and gray eyes. IQ was 68. Visual field showed concentric narrowing and his visual acuity was 0.2/0.3 (2.0/2.0). The limbs were spastic and weakened. He complained of pain in the extremities. He suffered from pollakisuria. Routine blood tests and CSF findings were normal. He was also found to be normal in peripheral nerve conduction studies and central conduction studies of SEP and VEP. EEG showed diffuse slowing in background activities. T2-weighted MRI of the head revealed widespread high-intensity areas in the deep white matter especially in bilateral occipital lobes. Serum aminogram disclosed the remarkably elevated phenylalanine (Phe) level to 1663 nmol/ml (normal range 50-90) and reduced tyrosine. Urinary secretion of endogenous tetrahydroxy-biopterin (BH4; coenzyme of Phe hydroxylase) remained in a normal range, and oral administration of 100 mg/kg of BH4 failed to normalize the serum Phe level. Despite a strict dietary control (oral intake of Phe less than 0.5 g/day), the serum Phe level remained high around 500 nmol/ml and his neurological deficits still deteriorated.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗