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Biomedical subjects

Masato Asahina

Publications and source records attributed to Masato Asahina.

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↗
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

Hemodynamic effects of clonidine in two contrasting models of autonomic failure: multiple system atrophy and pure autonomic failure.

We assessed the effects of clonidine on blood pressure (BP) and heart rate (HR) in multiple system atrophy (MSA), where the autonomic nervous system lesion site is preganglionic, and in pure autonomic failure (PAF), where it is postganglionic. In normal subjects, intravenous infusion of the selective alpha2-adrenoceptor agonist clonidine reduces BP and plasma noradrenaline (NA) levels by means of central alpha2-adrenoceptor action, as well as inducing growth hormone (GH) release. Clonidine-induced GH release is impaired in MSA but spared in PAF. However, the hemodynamic effects of clonidine have not been studied extensively in these disorders. We examined intravenous clonidine test results (performed in our autonomic laboratories using the London Autonomic Units protocol) in 58 patients: 39 with probable MSA and 19 with PAF. Systolic BP (SBP), diastolic BP (DBP), HR, and NA levels were measured supine at baseline and for up to 60 minutes after clonidine. Clonidine resulted in a significant BP fall in MSA patients, which occurred earlier (within 15 minutes of clonidine) and to a greater extent than seen in PAF patients. MSA and PAF patients showed reduction in HR after clonidine administration, although this finding was significantly greater in MSA than in PAF patients. NA levels decreased significantly after clonidine administration in both groups. Although basal NA levels were lower in PAF than in MSA patients, there was no difference in NA reduction relative to baseline between groups. MSA patients showed significant negative correlation between basal NA levels and BP response to clonidine. Clonidine infusion reduces BP and HR in both MSA and PAF groups but to a greater extent in MSA patients. The greater vasodepressor action of clonidine in MSA patients suggests that there is partial preservation of brainstem sympathetic outflow pathways in MSA and may reflect its action at sites in the brainstem and spinal cord that were in part functionally preserved in MSA. Despite similar degrees of NA reduction after clonidine administration, the vasodepressor effect of clonidine was attenuated in PAF compared with MSA patients. This attenuation in PAF patients may reflect greater peripheral alpha2-adrenoceptor denervation supersensitivity due to the postganglionic lesion site. These BP differences, thus, may reflect the underlying lesion site in MSA and PAF, and the hemodynamic data after clonidine infusion may help differentiate these conditions.

Adrenergic alpha-Agonists↗
PubMed2006

Urinary dysfunction and autonomic control in amyloid neuropathy.

Uro-neurological assessment was performed in four patients with small-fiber neuropathy due to amyloidosis (2 transthyretin-type/2 immunoglobulin light-chain-type). Voiding difficulties were due to detrusor weakness and impaired bladder sensation. In two patients cholinesterase inhibition treatment caused urge incontinence, indicating detrusor denervation supersensitivity. The underlying mechanisms of urinary dysfunction seem to involve postganglionic cholinergic and afferent somatic nerves.

Aged↗
PubMed2005

Mosapride citrate, a novel 5-HT4 agonist and partial 5-HT3 antagonist, ameliorates constipation in parkinsonian patients.

Mosapride citrate is a novel selective 5-HT4 receptor agonist. It facilitates acetylcholine release from the enteric cholinergic neurons. In contrast to cisapride, mosapride does not block K(+) channels or D2 dopaminergic receptors. The objective of this study is to perform an open study of mosapride citrate's effects on constipation, a prominent lower gastrointestinal tract disorder in parkinsonian patients. A total of 14 parkinsonian patients (7 with Parkinson's disease, 7 with multiple system atrophy; 10 men, 4 women; mean age, 67 years) with constipation (10 with bowel movement < 3 times/week; 14 with difficulty in defecation) were treated with 15 mg/day of mosapride citrate for 3 months. Pre- and posttreatment objective parameters in colonic transit time (CTT) and rectoanal videomanometry were obtained. Statistical analysis was made by Student's t test. Mosapride was well tolerated by all patients except for 1, who discontinued use of the drug because of epigastric discomfort. None had a worsening of parkinsonism or other adverse events. Thirteen patients reported subjective improvements in bowel frequency (>3 times/week, 13) and difficult defecation (13). Mosapride shortened CTT of the left colon (P < 0.01) and the total colon (P < 0.05). During rectal filling, mosapride lessened the first sensation (P < 0.05) and augmented the amplitude in phasic rectal contraction. During defecation, mosapride augmented the amplitude in rectal contraction (P < 0.05) and lessened the volume of postdefecation residuals. The present study showed for the first time that mosapride citrate augmented lower gastrointestinal tract motility, as shown in CTT and videomanometry, and thereby ameliorated constipation in parkinsonian patients without serious adverse effects.

Aged↗
PubMed2005

Differences in overshoot of blood pressure after head-up tilt in two groups with chronic autonomic failure: pure autonomic failure and multiple system atrophy.

On head down tilt to the supine horizontal position (tilt reversal) after head up tilt (HUT), patients with orthostatic hypotension may show an increase in blood pressure (BP) relative to baseline readings. We assessed this BP overshoot in 8 patients with pure autonomic failure (PAF, 64+/-13 years) and 8 patients with multiple system atrophy (MSA, 66+/-10 years). BP was intermittently measured during pre-tilt supine, HUT (60 degrees , 10 min), and post-tilt supine periods. In addition, beat-to-beat BP was measured continuously using the Portapres model 2 device to calculate stroke volume (SV), cardiac output (CO) and total peripheral resistance (TPR). There was systolic BP overshoot of > or = 15 mmHg after tilt reversal in 5 out of 8 PAF, but in only one of 8 MSA. A mean increase of systolic BP in PAF was significantly higher than that in MSA (p<0.01). TPR increased over baseline level after tilt reversal, although there was no significant difference. SV and CO levels during the post-tilt supine period were similar to baseline levels. In conclusion, BP overshoot was prominent in the PAF group but not in the MSA group. The phenomenon of BP overshoot while supine, especially in PAF, may have implications for long term cardiac and vascular damage in such patients.

Aged↗
PubMed2005

The effect of different physiological stimuli on skin vasomotor reflexes above and below the lesion in human chronic spinal cord injury.

OBJECTIVE: Spinal cord injury (SCI) results in disruption of descending tonic activation of sympathetic circuits in the spinal cord. The authors determined whether different stimuli that increase sympathetic activity induced cutaneous vasoconstriction (skin vasomotor reflex, SkVR) above and below the level of lesion in subjects with clinically complete SCI. METHODS: Baseline skin blood flow (SkBF) and SkVR reduction rate in the pulp of the finger and great toe was measured by laser Doppler probes in chronic complete SCI and in controls. RESULTS: In the finger, baseline SkBF was similar in SCI and controls. The SkVR was elicited by all stimuli in controls but was significantly diminished to gasp, mental arithmetic, tactile stimulation, cutaneous cold, and deep breathing in high SCI compared to controls. In the toe, baseline SkBF was less stable in both controls and SCI. SkVR trends were identified in controls, and responses were not present or greatly reduced in high and low SCI. CONCLUSIONS: Measurements of skin vasomotor reflexes to physiological stimuli may be a noninvasive method to evaluate the extent of sympathetic adrenergic pathways in chronic SCI. This is of clinical relevance in monitoring recovery of sympathetic adrenergic function either spontaneously or following repair interventions.

Adult↗
PubMed2004

Putaminal hemorrhage disrupts thalamocortical projection to secondary somatosensory cortex: case report.

Putaminal hemorrhage presenting pure sensory stroke is rare. We describe a case of left putaminal hemorrhage presenting contralateral hemisensory disturbance without hemiparesis. A 52-year-old man developed analgesia and thermoanesthesia in the right half of his body, but deep sensation was relatively well preserved. Neuroradiological and somatosensory evoked potential findings suggested that thalamocortical sensory pathways to the secondary somatosensory cortex (S2) were involved, whereas those to the primary somatosensory cortex (S1) were spared. In experimental animals, spinothalamic projections from the thalamic nucleus input directly to S2. In humans, thalamocortical pathways are still a subject of debate, but results of recent functional imaging studies suggest that the pathway of pain inputs directly to S2 and that of tactile sensation to S2 via S1. Our findings support these reports.

Evoked Potentials, Somatosensory↗
PubMed2004

Novel PINK1 mutations in early-onset parkinsonism.

PINK1 was recently found to be associated with PARK6 as the causative gene. We performed mutation analysis in eight inbred families whose haplotypes link to the PARK6 region. We identified six pathogenic mutations (R246X, H271Q, E417G, L347P, and Q239X/R492X) in six unrelated families. All sites of mutations were novel, suggesting that PINK1 may be the second most common causative gene next to parkin in parkinsonism with the recessive mode of inheritance.

Adolescent↗
PubMed2004

Colonic transit time, sphincter EMG, and rectoanal videomanometry in multiple system atrophy.

Both constipation and fecal incontinence are prominent lower gastrointestinal tract (LGIT) dysfunctions that occur frequently in multiple system atrophy (MSA). We investigated the mechanism of constipation and fecal incontinence in MSA. Colonic transit time (CTT), sphincter electromyography (EMG), and rectoanal videomanometry were performed in 15 patients with MSA (10 men, 5 women; mean age, 63.5 years; mean duration of disease, 3 years; decreased bowel frequency [< 3 times a week] in 9; difficulty in expulsion in 11; fecal incontinence in 3) and 10 age-matched healthy control subjects (7 men and 3 women; mean age, 62 years; decreased bowel frequency in 2; mild difficulty in expulsion in 2; fecal incontinence in none). Compared to the control subjects, MSA patients had significantly prolonged CTT in the rectosigmoid segment and total colon. Sphincter EMG showed neurogenic motor unit potentials in none of control subjects but in 93% of MSA patients. At the resting state, MSA patients showed a lower anal squeeze pressure (external sphincter weakness) and a smaller increase in abdominal pressure on coughing. During rectal filling, MSA patients showed smaller amplitude in phasic rectal contraction, which was accompanied by an increase in anal pressure that normally decreased, together with leaking in 3 patients. During defecation, most MSA patients could not defecate completely and had larger postdefecation residuals. MSA patients had weak abdominal strain, smaller rectal contraction on defecation, and larger anal contraction on defecation (paradoxical sphincter contraction on defecation), although these differences were not statistically significant. These findings in MSA patients were similar to those in Parkinson's disease patients in our previous study, except for the sphincter denervation and weakness in MSA. Constipation in MSA most probably results from slow colonic transit, decreased phasic rectal contraction, and weak abdominal strain, and fecal incontinence results from weak anal sphincter due to denervation. The responsible sites for these dysfunctions seem to be both central and peripheral nervous systems that regulate the LGIT.

Aged↗
PubMed2003

Amezinium metilsulfate, a sympathomimetic agent, may increase the risk of urinary retention in multiple system atrophy.

In 5 patients with multiple system atrophy, administration of 15 mg/day of amezinium metilsulfate, an adrenergic agent, during 6 months for the treatment of postural hypotension exacerbated post-micturition residuals as compared to that before treatment (178 ml versus 113 ml for a change of 37 %, p < 0.05). Amezinium metilsulfate most probably stimulates both alpha1B-receptors in the vascular wall and alpha1A/D-receptors in the proximal urethra.

Aged↗