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Biomedical subjects

Takamichi Hattori

Publications and source records attributed to Takamichi Hattori.

At least 19 recordsLinked to original sources
PubMed2007

Urinary retention and sympathetic sphincter obstruction in axonal Guillain-Barré syndrome.

A 62-year-old woman with axonal Guillain-Barré syndrome developed weakness and urinary retention simultaneously. The retention failed to recover for 10 months even after she regained the ability to walk. The patient exhibited no postural hypotension. Videourodynamics showed that the retention was caused not by the bladder paralysis but rather by internal (sympathetic) sphincter obstruction, which is extremely uncommon in peripheral neuropathies. We started the patient on an alpha-adrenergic antagonist, urapidil, at 30 mg/day, and this led to successful relaxation of the urethra and reduced the postvoid residual from 200 ml to less than 30 ml. The underlying mechanisms of urinary retention in our patient appeared to involve hyperactive lumbosacral sympathetic nerves. Urinary retention and sympathetic sphincter obstruction can thus be features of axonal Guillain-Barré syndrome.

Adrenergic alpha-Antagonists↗
PubMed2007

Time course of axonal regeneration in acute motor axonal neuropathy.

Patients with acute motor axonal neuropathy (AMAN) generally recover well. We reviewed clinical and electrophysiologic recovery in 13 patients for up to 5 years. Twelve patients showed rapid recovery over 12 months, whereas in the remaining one the recovery was slow and incomplete at 5 years. In AMAN, axonal degeneration appears to develop predominantly in the motor nerve terminals, and only occasionally more proximally in the nerve roots. Nerve terminal degeneration-regeneration presumably provides a mechanism for good recovery.

Adolescent↗
PubMed2006

The effects of physiological fluctuation of serum potassium levels on excitability properties in healthy human motor axons.

OBJECTIVE: Previous axonal excitability studies suggest hyperkalemia or hypokalemia can significantly alter membrane potential and thereby, excitability properties. We studied whether physiological fluctuation of serum potassium levels affects axonal excitability in normal human axons. METHODS: Threshold tracking was used to measure strength-duration properties, refractory periods, supernormality, and threshold electrotonus in median motor axons of 12 normal volunteers. In each subject, the excitability indices and serum potassium levels were measured three times (baseline, 2h later, and 2 weeks later). RESULTS: The pooled data (n=36) showed significant correlation of the relative refractory period, supernormality, and depolarizing threshold electrotonus with potassium levels. Among each trial (12 subjects) the correlation did not reach statistical significance occasionally. Strength-duration properties, refractoriness, late subnormality, and hyperpolarizing threshold electrotonus were not significantly affected by serum potassium levels. CONCLUSIONS: Even in the normal range, serum potassium levels could slightly alter axonal excitability of human axons. Among excitability indices, the relative refractory period, supernormality, and threshold electrotonus are sensitive to potassium levels. SIGNIFICANCE: Physiological fluctuation of serum potassium levels could partly be responsible for inter- and intra-subject variability of excitability indices.

Adult↗
PubMed2006

Mechanism of constipation in familial amyloid polyneuropathy: a case report.

Previously no functional study has been available for the mechanism of constipation in familial amyloid polyneuropathy (FAP). We performed a gut function test in a 78-year-old woman with transthyretin-type FAP who had severe constipation. The gut function test showed a prolonged colonic transit time, a low anal pressure at rest and upon squeezing, loss of the spontaneous phasic rectal contractions, and weak abdominal strain. All these abnormalities suggested a peripheral autonomic dysfunction, corresponding to the enteric neuropathy that was confirmed upon autopsy.

Aged↗
PubMed2006

Increased nodal persistent Na+ currents in human neuropathy and motor neuron disease estimated by latent addition.

OBJECTIVE: To investigate the changes in nodal persistent Na(+) currents in human neuropathy and motor neuron disease. In human motor axons, approximately 1.0% of total Na(+) channels are active at rest, termed "persistent" Na(+) channels, and the conductance can be non-invasively estimated by the technique of latent addition in vivo. METHODS: Latent addition was performed in median motor axons of 93 patients with axonal neuropathy (n=38), lower motor neuron disorder (LMND; n=19) or amyotrophic lateral sclerosis (ALS; n=36) and in 27 age-matched normal subjects. Brief hyperpolarizing conditioning current pulses were delivered, and threshold change at the conditioning-test interval of 0.2 ms was measured as an estimator of the magnitude of persistent Na(+) currents. Threshold electrotonus and supernormality were also measured as indicators of resting membrane potential. RESULTS: Threshold changes at 0.2 ms were significantly greater in patients with neuropathy or LMND (p<0.05), and tended to be greater in ALS patients (p=0.075) than in normal controls. Threshold electrotonus and supernormality did not differ in each patient group and normal controls, suggesting that membrane potential is not altered in patients. In the recovery phase of axonal neuropathy, the threshold changes increased in parallel with an increase in amplitudes of compound muscle action potential. CONCLUSIONS: Persistent Na(+) currents appear to increase commonly in disorders involving lower motor neurons, possibly associated with axonal regeneration or collateral sprouting or changes in Na(+) channel gating. SIGNIFICANCE: The increased axonal excitability could partly be responsible for positive motor symptoms such as muscle cramping frequently seen in lower motor neuron disorders.

Action Potentials↗
PubMed2006

Chronic inflammatory demyelinating polyneuropathy associated with idiopathic hemochromatosis.

We describe a 50-year-old woman who developed chronic inflammatory demyelinating polyneuropathy (CIDP) one year after onset of hemochromatosis. Electrodiagnostic studies showed evidence of multifocal demyelination. Marked hypergammaglobulinemia with positive anti-nuclear and anti-DNA antibodies was found. Corticosteroid treatment resulted in a significant lessening of neurological symptoms. This is the first case of CIDP with hemochromatosis. The association may be coincidental, but the altered immune system by hemochromatosis was possibly related to the development of CIDP in this patient.

Adrenal Cortex Hormones↗
PubMed2006

High-dose intravenous immunoglobulin for the treatment of MuSK antibody-positive seronegative myasthenia gravis.

We treated two patients with anti-muscle specific tyrosine kinase (MuSK)-antibody positive seronegative myasthenia gravis (MG) with high-dose intravenous gammaglobulin (IVIg) and evaluated their clinical courses. Both patients were Japanese women, MuSK-positive seronegative MG, and were unresponsive to conventional treatments, including thymectomy, steroids, and tacrolimus. The patients required frequent hospitalization for plasmapheresis. In case 1, a 45-year-old woman, it was difficult to obtain blood access for plasmapheresis. High-dose IVIg, 400 mg/kg per day for 5 days, was administered in cases 1 and 2. In both cases, clinical improvement was observed 3 days after the start of IVIg therapy and lasted for 2 to 3 months. We propose that IVIg therapy is an effective treatment for MuSK-positive seronegative MG, when conventional treatments have failed.

Adult↗
PubMed2006

Cerebral blood flow and oxygenation during head-up tilt in patients with multiple system atrophy and healthy control subjects.

To assess cerebral hemodynamics in patients with multiple system atrophy (MSA), cerebral blood flow and oxygenation were evaluated in 7 MSA patients and 9 healthy controls during a head-up tilt test (HUT) by means of transcranial Doppler ultrasonography and near-infrared spectrophotometry. In the MSA patients examined, the perfusion pressure reduction during HUT was marked, but severe reduction in blood flow velocity was prevented because of a decrease in cerebrovascular resistance. The MSA patients showed no severe reduction in cerebral oxygenation during HUT. These findings indicate that our MSA patients exhibited a compensatory cerebral vasodilatation response to orthostatic hypotension.

Aged↗
PubMed2006

Distal excitability changes in motor axons in amyotrophic lateral sclerosis.

OBJECTIVE: Previous axonal excitability studies in amyotrophic lateral sclerosis (ALS) have suggested that impaired potassium channel function could be responsible for the generation of fasciculations, but the ectopic activity arises predominantly from the motor nerve terminals. This study tested the hypothesis that dysfunction of potassium channels is more pronounced in the more distal parts of axons. METHODS: Threshold electrotonus was used to compare accommodation at the motor point of abductor pollicis brevis, and at the wrist portion of the median nerve, between 22 patients with ALS and 19 normal subjects. As target responses for motor point stimulation, movement-related potentials were recorded using an accelerometer. RESULTS: Compared to normal subjects, ALS patients showed greater threshold changes to depolarizing conditioning currents at both the motor point and wrist, suggesting less accommodation by potassium currents. Differences in the threshold electrotonus curves between the normal and ALS groups were much more prominent at the motor point than at the wrist. CONCLUSIONS: In ALS, axonal potassium channels are impaired more prominently in distal portions of axons than at the nerve trunk, and this is consistent with evidence that fasciculations mostly arise from the nerve terminals. SIGNIFICANCE: Excitability testing at the motor point provides additional information about the pathophysiology of ALS.

Action Potentials↗