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H Nukada

Publications and source records attributed to H Nukada.

At least 19 recordsLinked to original sources
PubMed2000

Skin wrinkling for the assessment of sympathetic function in the limbs.

BACKGROUND: Wrinkling of the skin of the palm and sole is considered to be dependent on the presence of intact sympathetic nervous activity. Loss of sympathetic integrity could be simply and usefully assessed by the absence of wrinkling. To test this hypothesis, the skin wrinkle test was compared with the starch-iodine sweat test and sympathetic skin response (SSR) in patients with abnormal sympathetic function. METHODS: The three tests were carried out in 34 patients (68 limbs) undergoing temporary or permanent disruption of the sympathetic chain to upper or lower limbs. Included in this group were six diabetics undergoing chemical or surgical sympathectomy, lumbar epidural infusions following vascular surgery, and patients for whom sympathectomy was being considered. Sensitivity and specificity analysis and predictive values of the wrinkling response and the starch-iodine test were related to the SSR as the standard. RESULTS: The wrinkle test showed a sensitivity of 97% and specificity of 95%, and bore good correlation to the SSR. The starch-iodine test showed sensitivity of 55% and specificity of 93%. A hypothesis for the mechanism of wrinkling based on the observations of the present study is proposed. CONCLUSION: The wrinkle test is a reliable test of sympathetic function, is inexpensive and is easy to perform at the bedside. The sweat gland myo-epithelial cells and absence of sebum could play an important role in the wrinkling response. It can be used to select patients who will benefit from sympathectomy, and can adequately evaluate sympathetic blockade.

Adolescent↗
PubMed2000

Acute inflammatory demyelination in reperfusion nerve injury.

We investigated the pathological appearance of acute inflammation and its role in the development of demyelination in reperfused rat sciatic, tibial, and peroneal nerves after a 5-hour period of near-complete ischemia. Polymorphonuclear neutrophil migration was seen early in the endoneurial lesion. After 18 hours of reperfusion, there was maximal intercellular adhesion molecule-1 expression on endoneurial vessels, and polymorphonuclear neutrophil accumulation was then prominent, reaching a peak 24 hours after reperfusion. Endoneurial mononuclear macrophages increased nearly fourfold after 48 to 72 hours of reperfusion. Macrophages were observed invading Schwann cells and myelin lamellae with associated demyelination. Thus, this study provides evidence of macrophage-associated demyelination after reperfusion similar to that seen in inflammatory neuropathies.

Acute Disease↗
PubMed1999

Endoneurial microvascular abnormalities of sural nerve in non-diabetic chronic atherosclerotic occlusive disease.

Neuropathic abnormalities are found in chronically ischaemic limbs associated with non-diabetic atherosclerotic peripheral vascular disease (PVD). In chronic ischaemic neuropathy, microvascular alterations play a key role in its development. We undertook morphometric assessment of endoneurial microvessels in the sural nerves, taken from severely ischaemic amputated legs in nine chronic non-diabetic PVD. These subjects had threatened ischaemic limbs and revealed clinical, physiological and pathological evidence of neuropathy. For comparison, sural nerves taken from amputated legs due to non-ischaemic disorders (n=4) and chronic PVD associated with diabetes (n=3) were also assessed. We evaluated the areas of vascular lumen, endothelial cells and whole vessel, as well as the percentage of closed capillaries. Endothelial area of sural nerve microvessels in non-diabetic PVD nerves was significantly greater than in non-ischaemic control nerves. Periendothelial cell area containing pericytes and basement membranes was also significantly increased in non-diabetic PVD nerves when compared with control nerves. Vascular lumen area was significantly less in non-diabetic PVD nerves than in non-ischaemic control nerves. Endoneurial microvessels in diabetic PVD nerves showed similar results: thickened vessel wall and smaller lumen. Periendothelial area in diabetic nerves was significantly greater than in non-diabetic PVD nerves. We demonstrated swollen endothelial cells and increased periendothelial area associated with narrowed lumen in sural nerve endoneurial microvessels of severe chronic PVD. Basement membrane reduplication of endoneurial capillaries was seen in non-diabetic PVD nerves. These microvascular abnormalities could play an important role in the development of chronic ischaemic neuropathy in PVD limbs.

Aged↗
PubMed1999

Protein carbonyl formation and tyrosine nitration as markers of oxidative damage during ischaemia-reperfusion injury to rat sciatic nerve.

We have investigated the role of oxidative damage in peripheral nerve ischaemia-reperfusion injury using a rat sciatic nerve model. After 5 h ischaemia blood flow to the sciatic nerve was restarted and markers of oxidative damage measured after various times of reperfusion. As a marker of protein oxidative damage, protein carbonyl formation was measured using a sensitive enzyme-linked immunosorbent assay. Protein carbonyl content was unaffected by ischaemia alone, but increased by 55% after 12-18 h reperfusion, correlating with the onset of nerve pathology. Pretreatment with the xanthine oxidase inhibitor allopurinol prevented these abnormalities, suggesting that xanthine oxidase activity is proximal to oxidative damage during reperfusion injury. To determine whether formation of the potent oxidant peroxynitrite from nitric oxide and superoxide contributed to ischaemia-reperfusion injury, we measured the accumulation of 3-nitrotyrosine residues in proteins. Only one protein of 49,000 mol. wt contained significant amounts of 3-nitrotyrosine residues which was shown to be glial fibrillary acidic protein, an abundant cytoskeletal protein in Schwann cells. However glial fibrillary acidic protein contained 3-nitrotyrosine residues prior to ischaemia-reperfusion, and the amount of nitrated tyrosine residues in total glial fibrillary acidic protein did not increase significantly during reperfusion, therefore it was not possible to draw conclusions about the role of peroxynitrite in nerve reperfusion injury.

Animals↗
PubMed1998

Preservation of skin vasoconstrictor responses in chronic atherosclerotic peripheral vascular disease.

Peripheral neuropathy is often found in ischemic limbs with nondiabetic atherosclerotic peripheral vascular disease (PVD). Sensory symptoms such as burning pain are common in severely ischemic limbs, and sympathectomy has been undertaken for ischemic rest pain. The authors assessed noninvasive quantitative skin vasomotor reflexes in toes and standard systemic cardiovascular autonomic tests in 44 PVD subjects with varying severity of limb ischemia, 30 age-matched control subjects, and nine PVD subjects associated with diabetes. Skin vasoconstrictor reflexes to inspiratory gasp, Valsalva maneuver, and postural change, and the postischemic reactive hyperemic response, were evaluated by the measurement of skin blood flow on toe pads by use of a laser Doppler flowmeter. Vasoconstrictor responses were not significantly different between PVD toes, even in severely ischemic limb, and age-matched controls. Reactive hyperemia was significantly less in PVD than in controls. Cardiovagal and systemic vasoconstrictor reflexes were also evaluated. All PVD subjects showed normal systemic cardiovascular reflexes. In contrast, these reflexes were severely impaired in diabetic PVD. The authors demonstrated that skin vasoconstrictive sympathetic reflex is preserved in chronically ischemic limbs with PVD, suggesting that sympathetic nerve fibers are relatively resistant to chronic ischemia.

Aged↗
PubMed1997

Carbonyl histochemistry in rat reperfusion nerve injury.

Free radical mediated, site-specific lipid and protein oxidation has been implicated in the pathophysiology of an ischaemic/reperfusion injury. The aim of the present study was to determine whether carbonyl formation could be detected histochemically in reperfused rat sciatic nerves. We also examined the effects of preischaemic alpha-tocopherol supplementation on carbonyl formation in reperfused nerves. Seven hours of near-complete ischaemia was induced in rat right hindlimb by occlusion of major arteries using microvascular clips. Histochemical detection of carbonyl compounds, applying naphthoic acid hydrazide (NAH) and Fast Blue B (FBB), was undertaken at thigh, knee and calf levels of sciatic, tibial and peroneal nerves. NAH-FBB reactivity was confined to vessels in reperfused nerves. Positively stained epi-, peri- and endoneurial vessels were invariably observed after 2 h of reperfusion at all levels examined. After 24 and 48 h and 7 days of reperfusion, NAH-FBB-positive vessels were more frequently found at knee and calf levels than at the thigh level. Following preischaemic alpha-tocopherol supplementation, no vessels were stained positively with NAH-FBB, except for some epineurial vessels at knee and calf levels after 2 h of reperfusion. Morphometry in endoneurial vessels at the knee level revealed that endothelial cell area in alpha-tocopherol-treated reperfused nerves was significantly less when compared with those in reperfused nerves without alpha-tocopherol. In conclusion, we have demonstrated histochemical evidence of carbonyl formation in vessels, but not with nerve fibres, in ischaemic/reperfused rat sciatic nerves. These abnormalities were prevented with preischaemic supplementation of alpha-tocopherol.

Animals↗
PubMed1997

Auditory and inspiratory gasp-evoked sympathetic skin response: age effects.

The sympathetic skin response (SSR) has been employed to assess peripheral neuropathy as an index of sympathetic sudomotor activity. A variety of stimuli can be used to elicit the SSR, but their relative ease of use and reliability have not been studied. In addition, the extent to which age affects the SSR remains unresolved. We compared two different stimuli, a sudden loud noise and an inspiratory gasp, whilst recording SSRs from the hand and foot. We also investigated the effects of age on SSR amplitude and latency in 58 healthy volunteers (ages 13-79). SSRs evoked by the auditory stimulus were recorded in all subjects, while gasp-induced SSRs were not elicited in two subjects. We found that SSRs evoked by the auditory stimulus had less inter- and intra-subject latency and waveform variability than the gasp-induced response. The increased latency variability associated with the inspiratory gasp technique was probably due to triggering errors. Our results confirmed that the amplitude of the SSR is extremely variable and appears to be affected by many factors. Auditory-evoked SSR latencies revealed a significant non-linear increase with age, while SSRs evoked by an inspiratory gasp did not demonstrate age dependence. We conclude that an auditory stimulus is superior to an inspiratory gasp in evoking SSRs, both in terms of consistent appearance and reduced latency variability. As the SSR latency increases significantly with age, this effect should be carefully considered when interpreting the response.

Acoustic Stimulation↗
PubMed1997

Reperfusion nerve injury: pathology due to reflow and prolonged ischaemia.

Ischaemia plays an important role in the development of pathological changes in various neuropathies. Nerve pathology in acute ischaemic injury has been delineated longitudinally in peripheral nerve and reperfusion injury could amplify ischaemic pathology. We examined ischaemia/reperfusion-induced pathological changes along the length of sciatic, tibial and peroneal nerves from pelvic to ankle levels. Pathological features were correlated with the degree of postischaemic nerve blood flow (NBF) restoration, measured by a laser Doppler flowmeter, and the blood-nerve barrier function by a horseradish peroxidase (HRP) technique. Major arteries which supply rat hindlimb were occluded for 3, 5, or 7 hours, and reperfusion was accomplished by the removal of vascular clips. Nerve pathology was assessed after 12, 24 and 48 hours, and 5 and 7 days of reperfusion. Pathological alterations at the thigh level included vascular swelling, endoneurial and intramyelinic oedema, demyelination, thrombosis, and red blood cell (RBC) extravasation. A paucity of axonal degeneration was also characteristic at this level. By contrast, the distal nerve from knee to ankle showed evidence of extensive axonal changes, occluded vessels, and panfascicular nerve fibre and vascular degeneration. Postischaemic NBF reflow was confirmed at the thigh level immediately, 24 and 48 hours after reperfusion, whereas NBF restoration at the knee to calf level was less than preischaemic values. HRP leakage was found in both proximal and distal nerve segments. In conclusion, we demonstrated different types of structural changes along the length of ischaemic/reperfused rat sciatic nerves. The present study suggests that pathological abnormalities at the thigh level are most likely due to reoxygenation of ischaemia-inflicted endothelial cells, and distal morphological changes could be induced by prolonged ischaemia resulting from occluded vessels.

Animals↗
PubMed1996

Pathology of acute and chronic ischaemic neuropathy in atherosclerotic peripheral vascular disease.

The peripheral nerve pathology in ischaemic limbs with atherosclerotic peripheral vascular diseases (PVD) is difficult to ascertain because of the limited number of reports. In addition, it has been debated whether chronic ischaemia per se could cause morphological abnormalities in peripheral nerves. In this prospective study, we examined pathological findings in the sural, saphenous, deep peroneal, superficial peroneal and tibial nerves, taken from seven acutely and nine chronically ischaemic amputated legs in which ischaemia was due to non-diabetic severe PVD. For morphological comparison, nerves were also taken from amputated legs without ischaemic disease and those in which PVD was associated with diabetes. In acutely ischaemic nerves, pathological changes were dependent upon the duration of ischaemia. Axonal degeneration of both myelinated and unmyelinated nerve fibres (MFs and UMFs) with occluded vessels was prominent, if acute ischaemia was present for > 24 h. Focal lesions, a hallmark of acute ischaemic neuropathy, were seen in both acute and chronic PVD nerves. Chronic PVD nerves also revealed considerable variations in the density of MFs between the fascicles of individual nerves and between the nerves of individual subjects: demyelination and remyelination, endoneurial oedema particularly at the subperineurial region, swollen endothelial cells, various but infrequent axonal changes, and relative preservation of UMFs were also seen. All pathological changes found in acute and chronic PVD nerves, except for a high rate demyelinated and remyelinated nerve fibres, have been described in experimental models of acute ischaemic/reperfusion injury. Demyelination could be induced by chronic ischaemia. Thus, pathological alterations in chronic ischaemic neuropathy may be due to the combined effects of acute ischaemia/reperfusion and chronic hypoxia.

Aged↗
PubMed1996

Isolated triceps weakness in exercise-induced radial neuropathy.

OBJECTIVE: We report a case of isolated triceps weakness resulting from radial neuropathy. PATIENT: A middle-aged healthy man, a keen athlete, developed acute weakness of the triceps brachii muscle due to radial neuropathy. No other radial nerve innervated muscles were involved. Triceps function completely recovered in six weeks clinically and electrophysiologically suggesting focal conduction block secondary to demyelination. DISCUSSION: Acute radial neuropathy after strenuous arm exercise resulting from a compression lesion with acute conduction block, has been previously described. However, all reported cases involved severe weakness of radial nerve innervated distal muscles with wrist drop, while isolated weakness of the triceps brachii muscle in radial neuropathy has never been previously described. CONCLUSIONS: We suggest that selective weakness in the triceps could be the sole manifestation of an exercise-related radial neuropathy. This particular type of radial neuropathy could be a variant of neuralgic amyotrophy.

Action Potentials↗
PubMed1995

Gosha-jinki-gan (herbal medicine) in streptozocin-induced diabetic neuropathy.

Long-established systems of traditional medicine have evolved from systematic recordings of human experience over several millennia. Although not strictly based on concepts of modern science, they nevertheless are founded on a corpus of organised knowledge written in documents, and the evident conclusion is that the alleged "trial and error" methodology has provided useful drugs for humans. Herbal medicine should be investigated as a potential regimen for diabetic neuropathy for the following reasons: (1) diabetic neuropathy remains an important clinical problem affecting a significant proportion of diabetic subjects without satisfactory treatment; (2) there are multiple pathogenetic mechanisms in diabetic neuropathy; and (3) herbal medicine which is a combination prescription has unique synergistic and synthetic effects that result from interactions between individual herbal components, and may induce a wide range of therapeutic potential and utility. Gosha-jinki-gan (GJK), consisting of 10 herbs, has been widely used for a regimen of diabetic complications, including neuropathy, in Japan. However, the effect of GJK on experimental diabetic neuropathy has never been previously evaluated. We examined nerve conduction velocity (NCV) and nerve glucose, sorbitol, fructose and myo-inositol levels in streptozocin (STZ)-induced diabetic rats that were treated with GJK. After 1 week of the STZ injection in 7-9-week-old rats, GJK treatment (100 mg/100 g body weight/day) was started orally. At 16 weeks after the STZ injection, the sciatic NCV of GJK-treated diabetic rats improved significantly when compared to non-treated diabetic rats, although they were not yet normalised.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Sciatic nerve morphology and morphometry in mature rats with streptozocin-induced diabetes.

Controversy exists as to the morphological and morphometric changes seen in experimental diabetic neuropathy (EDN). Most previous studies have utilized immature animals, with controversy as to whether the observed changes are due to maturational delays induced by hyperglycemia, or to diabetes per se. This study utilizes mature 9-month-old Sprague-Dawley rats. Six control and six hyperglycemic rats were examined 24 weeks after streptozocin injection. No morphological abnormalities were seen in the sciatic nerve at the light microscopy level. Total fascicular area and myelinated fiber density showed no significant differences (ANOVA, P > 0.05). No significant differences [ANOVA, P > 0.05 and Kolmogorov-Smirnoff (K-S), P > 0.05] between control and diabetic groups were shown for fiber, axon, and myelin areas, fiber and axon diameters, and myelin thickness. Fiber index of circularity, axon index of circularity, and g ratio were not significantly different with ANOVA (P > 0.05), but the diabetic group showed significantly lower values (P < 0.001) with K-S testing. Regression analyses of axonal area and log(n) axonal area plotted against myelin thickness showed no significant differences between the control and diabetic animals. This study in mature rats confirms the relative lack of morphological and morphometric changes in EDN which have previously been reported in studies involving immature rats. It highlights the difficulties in trying to extrapolate from EDN to human diabetic neuropathy where severe morphological and morphometric abnormalities may be present.

Animals↗
PubMed1994

Vascular and metabolic factors in the pathogenesis of experimental diabetic neuropathy in mature rats.

The complex interrelationships between metabolic factors (increased nerve glucose, fructose and sorbitol and decreased nerve myo-inositol levels) and ischaemic-hypoxic vascular factors [decreased nerve blood flow (NBF) and increased nerve vascular resistance (NVR)] in the pathogenesis of diabetic neuropathy are incompletely understood. This study evaluates, in mature animals, the time course and magnitude of changes in factors postulated to be of importance in the pathogenesis of experimental diabetic neuropathy (EDN). Hyperglycaemia was induced in mature 9-month-old male Sprague-Dawley rats with streptozocin (as in studies utilizing immature rats it has been difficult to separate effects which are due to the growth retardation and maturational delay induced by hyperglycaemia from those arising from diabetes per se). Groups of age-matched control and diabetic animals were compared 1, 2, 4, 8, 16 and 24 weeks after injection. In diabetic animals NBF was decreased and NVR was increased after 1 week (P < 0.05); sciatic nerve glucose, sorbitol and fructose levels were increased after 1 week (P < 0.05). These changes were maintained for the duration of the experiment. Sciatic and caudal nerve conduction velocities were significantly decreased after 16 weeks (P < 0.05), although trends were apparent after 4 weeks. Diabetic animals showed decreased sciatic nerve myo-inositol levels between 2 and 16 weeks (P < 0.05), but there was no significant difference at 24 weeks. There were no significant differences in sciatic nerve total (Na+K+)ATPase concentrations. Early and sustained alterations in vascular indices (NBF and NVR) support the postulate that ischaemic-hypoxic factors may play a role in the causation of EDN. The ischaemic-hypoxic postulates do not, however, diminish the obvious importance of the multitude of metabolic alterations which also occur very early after the onset of hyperglycaemia.

Animals↗
PubMed1994

Sport and exercise headache: Part 1. Prevalence among university students.

Sport- and exercise-related headaches have been recognized over the last 20 years, but their prevalence is unknown. A nine-page questionnaire was used to study the prevalence of sports headaches among two contrasting populations of Otago University students: medical students (n = 178) and physical education students (n = 190). Both populations had a similar response rate of approximately 80%. It was found that 35% of respondents had experienced sport- and exercise-related headaches among the two populations, with similar rates for men and women seen in both. Comparison of the two populations showed no significant difference in the rate of sports headache among women, whereas the men physical education students has a significantly higher rate of sports headache than the men medical students. A high frequency of trauma-related headaches in contact sports accounted for this higher rate among the men physical education students. This study demonstrated that sport-and exercise-related headaches are a common problem among university students.

Adolescent↗
PubMed1994

Sport and exercise headache: Part 2. Diagnosis and classification.

A group of 129 subjects (67 men and 62 women) experiencing sports headache was established using a questionnaire. A wide range of information was gathered, focusing on the mode of onset, time course, characteristic features and associated symptoms of sports-related headache. Criteria for the varieties of sports headaches were established using head trauma and then migraine to divide subgroups of sports headaches. Cases were classified into four categories: effort migraine, trauma-triggered migraine, effort-exertion headache, and post-traumatic headache. The percentages of each sports-related headache found were: effort migraine 9%, trauma-triggered migraine 6%, effort-exertion headache 60%, post-traumatic headache 22% and miscellaneous 3%. Sports migraine accounted for 15% of the total sports headache sample. Effort-exertion headache was the most common type of sports headache. Although effort-exertion headache could be separated into subjects who had an acute severe headache induced by anaerobic exercise (exertion headache) from those having a substantial headache lasting hours initiated by aerobic exercise (effort headache), most subjects with effort-exertion headache in this study appeared not to fall into any discrete subgroups. Trauma-related headaches were experienced mainly by men in contact sports, while women more commonly had non-trauma-related headache in running and jogging.

Adolescent↗
PubMed1994

Perivascular demyelination and intramyelinic oedema in reperfusion nerve injury.

Nerve ischaemia plays a major role in the development of pathological alterations in various neuropathies, and the effects of ischaemia are amplified by reperfusion in various tissues. While pathological alterations in acutely ischaemic nerve have been established, nerve pathology resulting from reperfusion injury has never been elucidated. To evaluate what cell type in peripheral nerve is affected by reoxygenation following a hypoxic episode, we developed an animal model of transient severe limb ischaemia. Near-complete ischaemia, confirmed by the measurement of nerve blood flow, was achieved by clamping multiple arteries of supply to rat hindlimb. After 3, 5 or 7 h of limb ischaemia, vascular clips were released to reperfuse blood flow. Pathology in sciatic, tibial and peroneal nerves at the lower thigh level was examined at 7 d after reperfusion. All reperfused nerves developed demyelinated nerve fibres, particularly in perivascular regions. Although 3 h of ischaemia followed by reperfusion caused demyelination, perivascular demyelination was more prominent after a longer period of ischaemia with reperfusion. Two types of nerve oedema were observed; endoneurial oedema especially in perivascular and subperineurial spaces, and intramyelinic oedema. Nerve fibres with intramyelinic oedema were not confined to the perivascular region. Swollen endothelial cells in endoneurial vessels were also invariably observed. Nerve ischaemia per se, without reperfusion, did not induce these pathological changes. Because myelin appears to be particularly susceptible to activated free radicals, oxidative stress, activated neutrophils, and cytokine formation seem to be important underlying mechanisms in the development of perivascular demyelination and intramyelinic oedema in ischaemic/reperfused nerves.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗