Biomedical subjects

Satoshi Kuwabara

Publications and source records attributed to Satoshi Kuwabara.

59 records · Page 4Linked to original sources

PubMed2002

Patterns of nerve conduction abnormalities in POEMS syndrome.

Polyneuropathy, organomegaly, endocrinopathy, M protein, and skin changes (POEMS) syndrome is a rare cause of demyelinating and axonal neuropathy. POEMS syndrome and chronic inflammatory demyelinating polyneuropathy (CIDP) cause peripheral nerve demyelination, and the electrodiagnostic findings may therefore be similar, but the two disorders are distinct. To elucidate the electrodiagnostic features of POEMS syndrome, we reviewed nerve conduction studies of 8 patients, and compared their results with those in 42 patients with CIDP. The patients with POEMS syndrome showed (1) slowing of nerve conduction that was more predominant in the intermediate than distal nerve segments, (2) rare conduction block (6% of the tested nerves), and (3) more severe attenuation of compound muscle action potentials in the lower than upper limbs. Findings in the CIDP patients were characterized by multifocal conduction slowing that was occasionally dominant distally, frequent conduction block (44% of tested nerves), and less discrepancy between upper and lower limb nerves. The pattern of nerve conduction abnormalities differs between these disorders. Recognition of these typical patterns may be helpful for early diagnosis of POEMS syndrome.

Adult↗

PubMed2002

Fisher syndrome or Bickerstaff brainstem encephalitis? Anti-GQ1b IgG antibody syndrome involving both the peripheral and central nervous systems.

We describe a 27-year-old woman who showed the clinical triad of Fisher syndrome (ophthalmoplegia, ataxia, and areflexia), a disturbance of consciousness, facial diplegia, and hemisensory loss. Her serum was positive for anti-GQ1b immunoglobulin G (IgG) antibody. The electroencephalographic findings (diffuse slow activity), median somatosensory evoked potential (absent cortical N20 with normal cervical N13), and blink reflex studies (absent R2) suggested central dysfunction, whereas results of facial nerve conduction studies (low amplitudes of compound muscle action potentials), F-wave and H-reflex studies (absent F-waves and soleus H-reflexes), and brainstem auditory evoked potentials (prolongation of wave I latency) suggested peripheral abnormalities. This case supports the hypothesized continuity between Fisher syndrome and Bickerstaff brainstem encephalitis. These two conditions may represent a single autoimmune disease mediated by anti-GQ1b antibody, usually involving the peripheral and occasionally the central nervous systems.

Adult↗

PubMed2002

Abnormalities of axonal excitability are not generalized in early multifocal motor neuropathy.

The clinical and neurophysiological features of multifocal motor neuropathy (MMN) indicate selective involvement of motor axons, but pathological abnormalities in sensory axons suggest a more widespread disease process. The present study was undertaken to determine whether the focal abnormalities are associated with widespread subclinical abnormalities in motor axons. Threshold tracking was used to measure excitability properties (stimulus-response curves, strength-duration properties, recovery cycle, and threshold electrotonus) of the median nerve in five patients with MMN with lesions proximal to the site of testing. Patients were compared with 25 healthy controls. The changes in excitability indices were similar to those in controls, and in one patient there was no alteration after treatment with intravenous gammaglobulin. In this patient, indices of axonal excitability were also measured before, during, and after ischemia of the arm for 10 min. Again no differences were detected. This study provides no evidence for a generalized subclinical abnormality in MMN, at least when disease duration is less than 6 years.

Action Potentials↗

PubMed2002

Conduction block during and after ischaemia in chronic inflammatory demyelinating polyneuropathy.

A previous study suggested that axonal hyperpolariza tion produced by maximal voluntary contraction could accentuate conduction block in symptomatic patients with chronic inflammatory demyelinating polyneuropathy (CIDP). If this is so, conduction block should occur with hyperpolarization due to other causes such as the release of ischaemia. The effects of ischaemia on axonal excitability and on impulse conduction were therefore studied in 12 healthy control subjects and seven patients with symptomatic CIDP. The compound muscle action potential (CMAP) of abductor pollicis brevis was recorded in response to supramaximal stimuli to the median nerve at the wrist alternating with measurements of axonal excitability before, during and after ischaemia for 10 min produced by inflation of a sphygmomanometer cuff around the arm. During ischaemia, the amplitude/area of the maximal CMAP was reduced in the patients by 10% and, after release of ischaemia, it was attenuated by 19%. There were only slight changes in the CMAPs in the healthy controls. The attenuation of the CMAP during ischaemia presumably results from depolarization-induced inactivation of Na(+) channels in axons critically dependent on the number of functioning Na(+) channels for action potential generation. The attenuation of the CMAP after release of ischaemia paralleled the post-ischaemic hyperpolarization and was probably precipitated by it. This study provides suggestive evidence that axonal depolarization can produce conduction block in CIDP, in addition to providing confirmation that axonal hyperpolarization can also do so. In patients with chronic demyelinating disorders, conduction block can probably result from a wider range of physiological stresses than previously appreciated, such as natural activity, ischaemia or recovery from transient ischaemia--all of which could produce fluctuations in symptoms.

Action Potentials↗

PubMed2002

The acute effects of glycemic control on axonal excitability in human diabetic nerves.

OBJECTIVE: To investigate whether glycemic control is associated with reversible changes in axonal excitability in human diabetic nerves. It is known that voluntary contraction or compression ischemia alters nerve Na+/K+ pump activity, and axonal excitability changes due to the pump activity can be estimated by threshold tracking. METHODS: Threshold, the current required to produce a compound muscle action potential 50% of maximum, was determined from the stimulus-response curve, and threshold changes produced by maximal voluntary contraction or ischemia were measured before and after insulin treatment in 10 diabetic patients. RESULTS: Within 3 weeks of the start of treatment, the threshold changes became greater following voluntary contractions (+13+/-4% versus +23+/-5%; mean+/-SEM; p=0.04) and during ischemia (-5+/-2% versus -11+/-2%; p=0.04). CONCLUSIONS: The extent of threshold fluctuation depends on multiple metabolic factors associated with diabetes such as decreased Na+/K+ ATPase activity, increased anaerobic glycolysis, and tissue acidosis, and nerve excitability can respond quickly to glycemic control in diabetic patients.

Action Potentials↗