Search PubMed⌕ Search

Biomedical subjects

S Kuwabara

Publications and source records attributed to S Kuwabara.

At least 73 records · Page 4Linked to original sources
PubMed1999

Acute motor axonal neuropathy and acute motor-sensory axonal neuropathy share a common immunological profile.

Griffin and colleagues (Griffin JW, Li CY, Ho TW, Tian M, Gao CY, Xue P, Mishu B, Cornblath DR, Macko C, McKhann GM, Asbury AK. Pathology of motor-sensory axonal Guillain-Barré syndrome. Ann Neurol 1996;39:17-28 [4]) proposed that acute motor axonal neuropathy (AMAN) and acute motor-sensory axonal neuropathy (AMSAN) are part of the spectrum of a single type of immune attack on the axon. In contrast, IgG anti-GM1 antibody is associated closely with AMAN, but whether other IgG anti-ganglioside antibodies are associated with this neuropathy is not clear. We investigated whether IgG anti-ganglioside antibodies can be used as immunological markers to differentiate AMAN from acute inflammatory demyelinating polyneuropathy (AIDP) and whether these autoantibodies are present in AMSAN. The frequencies of anti-GM1, anti-GM1b, and anti-GD1a IgG antibodies in 21 AMAN patients were significantly higher than in 19 AIDP patients. Anti-GM1b and anti-GD1a IgG, as well as anti-GM1 IgG antibodies, therefore are immunological markers for AMAN. The patients with AMSAN had anti-GM1, anti-GM1b, and anti-GD1a IgG antibodies, indicative that AMAN and AMSAN share a common immunological profile.

Adolescent↗
PubMed1999

Haemophilus influenzae has a GM1 ganglioside-like structure and elicits Guillain-Barré syndrome.

The authors report a patient with an axonal Guillain-Barré syndrome (acute motor axonal neuropathy) associated with anti-GM1 antibody after Haemophilus influenzae infection. The result of ELISA inhibition studies and cytochemical staining with cholera toxin suggest the presence of a GM1-like structure on the surface of H. influenzae isolated from the patient. A particular strain of H. influenzae may have a GM1-like structure and may elicit an axonal Guillain-Barré syndrome.

Adult↗
PubMed1999

Axonal involvement at the common entrapment sites in Guillain-Barré syndrome with IgG anti-GM1 antibody.

If anti-GM1 antibody plays a role in the axonal damage in Guillain-Barré syndrome, the common entrapment sites may be preferentially involved with evidence of axonal dysfunction. To assess this hypothesis, we studied nerve conduction across the cubital tunnel in 44 patients. Abnormal amplitude reduction of compound muscle action potentials (CMAPs) was found in 45% of 20 immunoglobulin G (IgG) anti-GM1-positive and in 29% of 24 anti-GM1-negative patients. The time course and sequel were distinct between the two groups. In the former group, the amplitude reduction was prominent in weeks 1 to 2 and was followed by a decrease in distal CMAPs (axonal degeneration) or an increase in proximal CMAPs (resolution of conduction block). In contrast, anti-GM1-negative patients showed slower resolution with temporal dispersion. In anti-GM1-positive cases, amplitude reduction at the common entrapment site is frequent and may reflect wallerian degeneration or physiological conduction block at the nodes of Ranvier, both suggesting axonal involvement.

Action Potentials↗
PubMed1999

Dissociated small hand muscle involvement in amyotrophic lateral sclerosis detected by motor unit number estimates.

In some patients with amyotrophic lateral sclerosis (ALS), the thenar hand is more severely affected than the hypothenar hand. To quantify the dissociated involvement, we examined the motor unit number estimate (MUNE) of both the abductor pollicis brevis (APB) and abductor digiti minimi (ADM) muscles in 23 patients with ALS. Whereas ALS patients had significantly smaller MUNEs than normal subjects in both muscles, the extent of motor unit loss was significantly greater in the APB than ADM. Moreover, a simple comparison of the amplitude of compound muscle action potentials (CMAPs) showed that ALS patients had significantly smaller APB/ADM ratios than normal subjects and patients with cervical spondylotic amyotrophy, bulbospinal muscular atrophy, or peripheral neuropathy. The more severe involvement of the APB probably reflects the specific pathophysiology in ALS, and possible mechanisms for the dissociated involvement are discussed.

Action Potentials↗
PubMed1999

Activity-dependent excitability changes in chronic inflammatory demyelinating polyneuropathy: A microneurographic study.

The purpose of this study was to investigate activity-dependent excitability changes in polyneuropathy and their correlation with symptomatology. First, we recorded sensory nerve action potentials (SNAPs) with an intraneural microelectrode during impulse trains in 11 patients with chronic inflammatory demyelinating polyneuropathy. When the stimulus frequency was increased to >/=20 Hz, all patients showed marked decreases in the amplitudes of averaged SNAPs (128 responses) associated with latency increases. The amplitude decreases were much greater than those in patients with axonal neuropathies. In single-unit recordings, responses showed latency increases, which were small but sufficient to cause decreases in the averaged responses. Clinical sensory impairment was correlated with the degree of preexisting conduction block or axonal loss, but not with the degree of rate-dependent amplitude decreases. Activity-dependent changes occur preferentially in demyelinating neuropathy and are a sensitive measure of demyelination. The mechanism responsible for the amplitude decreases could be conduction slowing or block caused by activity-dependent hyperpolarization.

Action Potentials↗
PubMed1999

Special sensory ataxia in Miller Fisher syndrome detected by postural body sway analysis.

To investigate whether ataxia in Miller Fisher syndrome (MFS) is caused by loss of proprioception or cerebellar dysfunction, we studied the power spectrum peak of the body sway frequency in 10 MFS patients, and compared the results with those of patients with cerebellar or sensory ataxia. The cerebellar patients had a peak at 2.4 Hz, whereas sensory ataxia patients had a 1-Hz peak. Nine of the MFS patients had a distinct 1-Hz peak. Clinical sensory loss or abnormal sensory nerve potentials were present in only 3 patients, whereas soleus H-reflexes were absent in all the MFS patients. MFS patients have dysfunction of the proprioceptive afferent system, and the special sensory ataxia may be caused by the selective involvement of muscle spindle afferents.

Adult↗
PubMed1999

Hyperreflexia in Guillain-Barré syndrome: relation with acute motor axonal neuropathy and anti-GM1 antibody.

OBJECTIVES: To investigate the incidence of hyperreflexia in patients with Guillain-Barré syndrome (GBS), and its relation with electrodiagnosis of acute motor axonal neuropathy (AMAN), antiganglioside GM1 antibody, and Campylobacter jejuni infection. It was reported that patients with AMAN in northern China often had hyperreflexia in the recovery phase. METHODS: In 54 consecutive Japanese patients with GBS, sequential findings of tendon reflexes were reviewed. By electrodiagnostic criteria, patients were classified as having AMAN or acute inflammatory demyelinating polyneuropathy (AIDP). Anti-GM1 and anti-C jejuni antibodies were measured by enzyme linked immunosorbent assays. RESULTS: Seven (13%) patients developed hyperreflexia with the spread of the myotatic reflex to other segments in the early recovery phase, one of whom already had hyperreflexia in the acute progressive phase. Of the seven patients, six had AMAN and all seven had anti-GM1 antibodies, whereas only two had anti-C jejuni antibodies. Hyperreflexia was more often found in patients with AMAN than AIDP (6/23 v 1/18, p=0. 002), and in patients with anti-GM1 antibodies than without them (7/26 v 0/28, p=0.01). Hyperreflexic patients had milder peak disabilities than patients without hyperreflexia (p=0.03). Increased motor neuron excitability in the hyperreflexic patients was supported by increased soleus H-reflex amplitudes and the appearance of H-reflexes in the small hand or foot muscles. CONCLUSIONS: Hyperreflexia often occurs in patients with GBS especially with AMAN, anti-GM1 antibodies, and milder disease. Increased motor neuron excitability further characterises the subgroup of patients with GBS with AMAN and anti-GM1 antibodies.

Acute Disease↗
PubMed1999

IgG anti-GQ1b positive acute ataxia without ophthalmoplegia.

IgG anti-GQ1b antibody was present in a patient with acute ataxia and areflexia without ophthalmoplegia or elementary sensory loss. Sensory nerve conduction studies and somatosensory evoked potentials were normal, but postural body sway analysis showed dysfunction of the proprioceptive afferent system. The clinical presentation and laboratory results for this patient resemble those of Miller Fisher syndrome, except for the lack of ophthalmoplegia. This case may represent part of an IgG anti-GQ1b syndrome.

Acute Disease↗
PubMed1999

n-Hexane neuropathy caused by addictive inhalation: clinical and electrophysiological features.

To assess the clinical and electrophysiological features of n-hexane neuropathy caused by addictive inhalation, 4 patients were studied in the progressive phase. The neurological manifestations were characterized by subacute predominantly motor polyneuropathy and disease progression despite discontinuance of the chemicals, which were similar to those reported in industrial exposure, although with a severer degree associated with anorexia and body weight loss. Electrophysiological studies showed that all showed multifocal conduction block and profound conduction slowing, as well as features of axonal degeneration. Sural nerve biopsy showed axonal loss, axonal swelling, and thin myelin probably due to retraction by axonal swelling. n-Hexane abuse causes severe subacute polyneuropathy. The mixed axonal and demyelinating electrophysiological features were consistent with peculiar pathological findings. Conduction block, probably due to paranodal myelin retraction or ongoing wallerian degeneration, is very frequent and could be responsible for the clinical deficits, especially in the early phase of illness.

Administration, Inhalation↗
PubMed1999

Intravenous methylcobalamin treatment for uremic and diabetic neuropathy in chronic hemodialysis patients.

OBJECT: To study the effects of the intravenous administration of methylcobalamin, an analogue of vitamin B12, for uremic or uremic-diabetic polyneuropathy in patients who are receiving maintenance hemodialysis. An ultra-high dose of vitamin B12 has been reported to promote peripheral nerve regeneration in experimental neuropathy. METHODS: Nine patients received a 500 microg methylcobalamin injection 3 times a week for 6 months. The effects were evaluated using neuropathic pain grading and a nerve conduction study. RESULTS: Serum concentrations of vitamin B12 were ultra-high during treatment due to the lack of urinary excretion. After 6 months of treatment, the patients' pain or paresthesia had lessened, and the ulnar motor and median sensory nerve conduction velocities showed significant improvement. There were no side effects. CONCLUSION: Intravenous methycobalamin treatment is a safe and potentially beneficial therapy for neuropathy in chronic hemodialysis patients.

Action Potentials↗
PubMed1999

[Electrophysiology of juvenile muscular atrophy of unilateral upper limb (Hirayama's disease)].

To examine the validity of electrodiagnostic tests to help diagnosis and to evaluate disease activity of juvenile atrophy of unilateral upper limb (Hirayama's disease), we reviewed the results of nerve conduction studies, motor unit number estimates, electromyography, and somatosensory evoked potentials in consecutive 38 patients. There was selective involvement of the C8-T1 myotomes, in which motor unit loss was more prominent in the abductor digiti minimi than in the abductor pollicis brevis muscles, and F wave persistency was decreased out of proportion to the motor unit loss. These findings may help diagnosis. With respect to the disease activity and treatment, denervation potentials in the flexor carpi radialis muscle were more frequent in patients with shorter disease duration than those with longer duration. Median F wave persistency was greater in patients treated with neck brace than in patients without the treatment. These parameters can monitor the disease activity and efficacy of treatment.

Adolescent↗
PubMed1998

IgG anti-GM1 antibody is associated with reversible conduction failure and axonal degeneration in Guillain-Barré syndrome.

To investigate the pathophysiological role of anti-GM1 antibody in Guillain-Barré syndrome (GBS), we reviewed sequential nerve conduction studies of 345 nerves in 34 GBS patients. Statistically significant correlation between IgG anti-GM1 antibodies and electrodiagnoses was found. Sixteen IgG anti-GM1-positive patients were classified as having acute motor or acute motor sensory axonal neuropathy (AMAN or AMSAN) (12 patients), as having acute inflammatory demyelinating polyneuropathy (AIDP) (3 patients), or as undetermined (1 patient) by electrodiagnostic criteria. Besides axonal features, there was rapid resolution of conduction slowing and block. In 3 patients initially diagnosed as having AIDP, conduction slowing was resolved within days, and 1 of them and 3 AMAN patients showed markedly rapid increases in amplitudes of distal compound muscle action potentials that were not accompanied by prolonged duration and polyphasia. The time courses of conduction abnormalities were distinct from those in IgG anti-GM1-negative AIDP patients. Rapid resolution of conduction slowing and block, and the absence of remyelinating slow components, suggest that conduction failure may be caused by impaired physiological conduction at the nodes of Ranvier. Reversible conduction failure as well as axonal degeneration constitutes the pathophysiological mechanisms in IgG anti-GM1-positive GBS. In both cases, immune-mediated attack probably occurs on the axolemma of motor fibers.

Adult↗
PubMed1998

Esophageal intramural metastasis from an adenocarcinoma of the gastric cardia: report of a case.

We report herein the rare case of a 65-year-old man found to have esophageal intramural metastasis from cancer of the gastric cardia. Endoscopic examination initially revealed an infiltrating ulcerative tumor of the gastric cardia involving the esophagogastric junction, as well as a submucosal tumor of the lower esophagus. A total thoracic esophagogastrectomy with lower mediastinal lymphadenectomy was performed, and the resected specimen demonstrated that both the cardia and esophageal tumors were adenocarcinomas with the same cellular differentiation. As lymphatic invasion and metastases to the paracardial and mediastinal lymph nodes were observed, the esophageal submucosal tumor was considered to be an intramural metastasis from the carcinoma of the gastric cardia resulting from extensive lymphatic spread. The patient died of recurrent disease 9 months after the resection. This case report serves to demonstrate that intramural metastasis may be a local indicator of the systemic spread of disease in patients with gastric carcinoma, as it is in esophageal carcinoma.

Adenocarcinoma↗
PubMed1998

Demyelinating polyneuropathy with preferentially-proximal involvement.

A 47-year-old man showed progressive, symmetrical weakness in the limbs for 6 months. There was muscle atrophy, fasciculations, and acute denervation without motor conduction abnormalities below the elbows or knees, and motor neuron disease had once been suspected. However, compound muscle action potentials (CMAPs) after proximal stimulation showed an amplitude reduction between axilla and Erb's point for the median and ulnar nerves on both sides. His weakness as well as the amplitude reduction improved after administration of prednisolone. Demyelinative conduction abnormalities can be limited to the proximal segments for at least several months in a conduction equivalent to chronic inflammatory demyelinating polyneuropathy (CIDP).

Demyelinating Diseases↗
PubMed1998

Sensory impairments in spinal multiple sclerosis: a combined clinical, magnetic resonance imaging and somatosensory evoked potential study.

Thirty-one cases (26 patients) of clinically definite multiple sclerosis with predominant spinal cord involvement were studied retrospectively, focusing in particular on the results of sensory testings which were compared with the findings of spinal cord magnetic resonance imaging (MRI) and somatosensory evoked potentials (SEPs). Factor analysis of the sensory impairments showed two factors corresponding to superficial (pain and light-touch) and deep (position and 'thumb/big toe localizing') sensations. Vibratory sense depended on both factors, but more on deep sensations. Multiple regression analysis of the SEP abnormalities and sensory deficits showed that impaired deep sensations contributed to abnormal SEPs, but the results of clinical sensory testings and SEPs were dissociated in 31% of the extremities examined. The MRI sagittal images correlated well with the levels of sensory impairments, whereas the axial images showed a poor relationship to the extent of sensory impairments. We concluded that the use of SEPs as well as MRI is not always superior to such clinical sensory tests as the 'thumb/big toe localizing tests'.

Adolescent↗
PubMed1998

Outcomes of extended radical esophagectomy for thoracic esophageal cancer.

BACKGROUND: Great controversy exists concerning the adequate extent of esophagectomy for cure in patients with esophageal cancer. Extended radical esophagectomy combined with three-field lymphadenectomy has been performed to improve the cure rates for patients with the disease in Japan. The purposes of this study were to assess the mortality and morbidity rates after extended radical esophagectomy and to determine the oncologic indications for this procedure. STUDY DESIGN: We reviewed 190 patients who underwent extended radical esophagectomy for invasive esophageal cancer. The procedures were performed prospectively between 1982 and 1996. RESULTS: The 30-day mortality, in-hospital mortality, and morbidity rates were 1.6%, 4.7%, and 58.4%, respectively. The most common postoperative complication was vocal-cord paralysis (45.3%), followed by major pulmonary complications (21.6%). The overall survival rate for the 190 patients was 41.5% at 5 years, with a median followup period of 61 months. Some subgroups of patients had an extremely poor prognosis despite extended radical esophagectomy. Survival was < or = 5 years in all patients with five or more positive nodes; all patients with simultaneous metastases to the cervical, mediastinal, and abdominal lymph nodes; and all patients with cervical metastases from a lower esophageal tumor. CONCLUSIONS: Extended radical esophagectomy is potentially associated with high morbidity rates although the mortality rates are acceptable, suggesting the necessity of careful patient selection. This procedure is indicated oncologically only for patients with four or fewer metastatic nodes or with metastases confined to one or two of the three anatomic compartments (neck, mediastinum, and abdomen) from upper or midesophageal tumors.

Carcinoma, Squamous Cell↗