Biomedical subjects

F Birklein

Publications and source records attributed to F Birklein.

9 recordsLinked to original sources

PubMed2000

Sudomotor testing discriminates between subjects with and without antibodies against botulinum toxin A--a preliminary observation.

With an increasing number of patients being treated with botulinum toxin A (BTX A), the incidence of neutralizing anti-BTX antibodies (ABA) is rising. Because BTX A is known to inhibit sweating, sudometry seems to be a promising tool to test the efficacy of BTX A. We injected BTX A subcutaneously in normal control subjects and four patients with spasmodic torticollis, two responders and two nonresponders with proven ABA. Sweating was visualized using iodine starch staining and quantified used capacitance hygrometry. BTX A inhibited sweating completely at the injection site in both control subjects and all responders without evidence for ABA. However, continued sweating was recorded when the nonresponders with proven ABA were tested. We conclude that sudomotor testing is able to discriminate between subjects with and without clinically important ABA.

Antibodies↗

PubMed1999

[Complex regional pain syndrome. Clinical and autonomic disorders during acute and chronic illness stages].

In order to describe autonomic dysfunction and clinical outcome in complex regional pain syndrome (CRPS) 20 patients were followed-up. First investigation was performed in the acute stage of CRPS and the second investigation two years later after therapy (individual, not standardized). Skin temperature and sudomotor function (thermoregulatory sweating (TST) and quantitative sudomotor axon reflex (QSART)) were assessed, and a clinical follow-up was performed carefully. Skin temperature was warmer on the affected side at first investigation (p < 0.001) and colder at follow-up (p < 0.02). Sudomotor output was enhanced on the affected side both after TST (p < 0.005) and QSART (p < 0.05) at first investigation. At follow-up, however, while thermoregulatory sweating was still increased (p < 0.04) QSART was not different. While autonomic failure improves as assessed by clinical examination, therapy failed to alleviate pain significantly. But patients' self-assesment of therapy was mostly positive (16 of 20, p < 0.001). The present study has shown that the autonomic failure may be probably the result of central disturbances of thermoregulation, but secondary peripheral mechanisms also contribute to our findings. Individual based therapy seems to be efficacious for long term treatment, but for final judge controlled studies are required.

Adult↗

PubMed1999

Patterns of hyperalgesia in complex regional pain syndrome.

Complex regional pain syndrome (CRPS) is characterized by a triad of sensory, motor and autonomic dysfunctions, with long-standing pain and temperature differences of the affected and contralateral limb as predominant symptoms. The pathogenesis of the disorder still remains unclear. Among the main hypotheses of an underlying pathophysiology we find inflammatory processes and dysfunction of the sympathetic nervous system. Whether the main site of dysfunction is found centrally or peripherally is not known. With psychophysical methods we studied patterns of hyperalgesia to obtain a better understanding of the neuropathic pain component in CRPS. Forty patients in an acute phase of CRPS and a median duration of the disease of 10 weeks, were included in the study. Hyperalgesia to heat was tested with a thermode providing feedback-controlled temperature increases. Two forms of mechanical hyperalgesia were examined: phasic mechanical stimuli by using a custom-made impact stimulator for the determination of individual pain thresholds, tonic mechanical stimuli were applied using a pinch-device. Additionally a 'wind-up' paradigm was used to study a pain phenomenon of presumed central origin: a defined impact stimulus was given once and five times in repetition. A subpopulation of patients was reevaluated for mechanical hyperalgesia after i.v. injection of 500 mg acetyl-salicylic acid. Hyperalgesia to heat was insignificant. We found, however, a marked mechanical hyperalgesia to phasic impact stimuli (P < 0.005), whereas, static stimulation (squeezing skin folds) results were insignificant again. Wind-up related pain was also significantly enhanced in the affected limb (P < 0.02). The anti-inflammatory agent had no effect. These results indicate a non-inflammatory pathogenesis in CRPS presumably central in origin.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1999

[The assessment of sudomotor function for diagnosis of autonomic diseases. Principles and methods].

Thermoregulatory and emotional sweating can be distinguished in humans. While the first is organized via feed back mechanisms involving thermoreceptors, thermoregulatory centers in the brain and the effector system (sympathetic nervous system and sweat glands), the latter is generated directly by cortical and limbic mechanisms without any feed back. Sweat glands on the hairy skin can be stimulated by thermoregulatory mechanisms (rising body temperature), the emotional sweating on the glabrous skin as a result of an arousal reaction and they can be stimulated by peripheral acting cholinergic agents, which initiate direct or axon reflex mediated sweating. To evaluate sweating there are qualitative methods that visualize the sweat response or indirect methods like the registration of skin potentials. Alternatively sweat output can be quantified by evaporative measurement. For best results these methods should be combined. In this way autonomic dysfunction e.g. after nerve lesions, in polyneuropathies, central lesions and certain pain disorders can be assessed. The sudomotor function tests complete the conventional electrophysiological methods.

Animals↗

PubMed1998

Spatial extension of sudomotor axon reflex sweating in human skin.

Acetylcholine (ACh) applied to human skin is known to elicit a sweat response, which consists of a direct muscarinergic (M3) activation of sweat glands and a nicotinic axon reflex response from sudomotor terminals. To visualize the extent of axon reflex sweating after ACh-iontophoresis, iodine starch staining was used. Iontophoresis was performed under occlusion at the peroneal aspects of the lower leg and the center of the foot dorsum of healthy volunteers (n = 10). Ten minutes after stimulation, the area of dark blue staining was recorded by a video camera. Control experiments were performed with saline, histamine, pilocarpine and nicotine iontophoresis. The stained area was measured and the maximum and minimum distance of its boundary from the edge of the iontophoresis probe was determined (maximum/minimum radius). Sizes of stained areas and maximum radii were significantly greater on the lower leg compared to the foot (P < 0.01). The median sizes of the stained areas on the leg were 14.6 cm2 and on the foot dorsum 8.0 cm2. The respective median maximum radii were 3.1 cm on the leg and 2.3 cm on the foot dorsum (median minimum, leg 1.1 cm, foot 0.8 cm). These results match microneurographic findings of innervation territories of sympathetic efferent units. Area sizes of stained skin showed a close correlation between both stimulation sites (R = 0.96, P < 0.01), i.e. the sizes of sweat responses on leg and foot show a constant relation (foot/leg = 0.57) in spite of their great interindividual variability. This novel technique of establishing sweat responses provides information on the size of sudomotor innervation territories and may be useful for clinical studies in patients with suspected impairment of sympathetic functions.

Acetylcholine↗

PubMed1998

Pattern of autonomic dysfunction in time course of complex regional pain syndrome.

The objective of the present investigation was to describe and localize autonomic dysfunction in acute and chronic stages of complex regional pain syndrome (CRPS). Patients were investigated twice: the first investigation was performed as soon as diagnosis was established during the acute stage of CRPS and the second investigation was performed about 2 years later. Twenty-one patients completed the follow-up investigation. The median duration of CRPS was 5 (range 2-21) weeks at first investigation and 94 weeks (22-148) at follow-up. Skin temperature was recorded by thermography, sudomotor function was assessed by thermoregulatory sweat test (TST) and quantitative sudomotor axon reflex test (QSART). Skin temperature was warmer on the affected side at the first investigation (P < 0.001) and colder at follow-up (P < 0.02) compared with the contralateral limb. Sudomotor output was enhanced after both TST (P < 0.005) and QSART (P < 0.05) at the first investigation on the affected side. However, at follow-up, sweating after TST was still increased (P < 0.04) while QSART responses were not different between the affected and unaffected limbs. As compared to controls there was no statistically significant difference, neither in skin temperature nor sweating, neither on the affected nor on the unaffected side. In conclusion, the present investigation proved that vasomotor and sudomotor control are substantially altered in CRPS. In the acute stage vasomotor control is decreased in the affected limb whereas sudomotor function is enhanced. This may be the result of disturbances of thermoregulation, but different secondary peripheral mechanisms, concerning vasomotor and sudomotor function, contribute to clinical presentation of CRPS and affect autonomic function at all stages of CRPS.

Adult↗

PubMed1997

Effects of cutaneous histamine application in patients with sympathetic reflex dystrophy.

Thirty-six patients suffering from acute reflex sympathetic dystrophy (RSD) were examined in order to evaluate nociceptive C-fibers. Axon reflex vasodilatation was induced by iontophoresis of histamine and recorded (laser Doppler flux). The strength of concomitant sensation was rated on a visual analogue scale, and the quality was characterized as itching or burning pain. Skin temperature was recorded by infrared thermography. The results were compared with investigations of unaffected limbs of patients and volunteers. The histamine-induced sensation on the symptomatic side was more often burning pain than itching (P < 0.001), and skin temperature was increased on the affected limb (P < 0.001). Axon reflex vasodilatation and the strength of sensations were unaltered. In conclusion, this study rules out a significant deterioration of afferent C-fibers in RSD, but gives evidence of sensitization of nociceptive function. This nociceptive sensitization has to be taken into consideration for effective treatment of RSD.

Adult↗

PubMed1997

Sudomotor function in sympathetic reflex dystrophy.

Sudomotor functions were studied in 27 patients suffering from reflex sympathetic dystrophy (RSD) according to the criteria established by Bonica (18 women, 9 men; mean age 50 +/- 12.3 years; median duration of disease 8 weeks, range 2-468 weeks). To measure local sweating rates, two small chambers (5 cm2) were affixed to corresponding areas of hairy skin on the affected and unaffected limbs. Dry nitrogen gas was passed through the chambers (270 ml/min) and evaporation was recorded at both devices with hygrometers. Thermoregulatory sweating (TST) was induced by raising body temperature (intake of 0.5 1 hot tea and infra-red irradiation). Local sweating was also induced through an axon reflex (QSART) by transcutaneous iontophoretic application of carbachol (5 min, 1 mA). In addition, skin temperature was measured on the affected and unaffected side by infra-red thermography. Mean skin temperature was significantly higher on the affected side (P < 0.003). In spite of the temperature differences, there was no difference in basal sweating on the affected and unaffected side. However, both methods of sudomotor stimulation lead to significantly greater sweating responses on the affected compared to the unaffected side (TST: P < 0.05, QSART: P < 0.004). Latency to onset of sweating was significantly shorter on the affected side under both test conditions (P < 0.04 and P < 0.003, respectively). Sweat responses were not correlated to absolute skin temperature but were probably related to the increased blood flow on the affected side. Our findings imply a differential disturbance of vasomotor and sudomotor mechanisms in affected skin. Whereas vasoconstrictor activity is apparently lowered, sudomotor output is either unaltered or may even be enhanced.

Axons↗

PubMedDate not supplied

Cardiac autonomic involvement and peripheral nerve function in patients with diabetic neuropathy.

The aim of our study was to investigate the relationship between cardiac autonomic neuropathy and dysfunction of myelinated and unmyelinated nerve fibres in the peripheral nerve. We measured nerve conduction velocities, warmth/cold perception thresholds at the foot dorsum, sympathetic skin response (SSR), and performed the quantitative sudomotor axon reflex test (QSART). Forty-three diabetic patients with distal-symmetric polyneuropathy were included. According to the results of heart rate variation, 20 patients had cardiac autonomic neuropathy (CAN+). Apart from motor nerve conduction velocities, all tests were more often abnormal in CAN+ patients. Warmth thresholds (afferent C-fibres) and reduced compound muscle action potentials (CMAPs) of the tibial and peroneal nerve, indicating axonal damage, were more often abnormal in CAN+. Cold threshold and sural nerve conduction velocity were indicators of involvement of myelinated small and large nerve fibres, but not of the cardiac autonomic system. Ninety-four percent (94%) of patients with absent SSR and 78% of patients with abnormal QSART had CAN+. SSR and QSART may be useful for assessment of autonomic neuropathy in diabetic patients with cardiac arrhythmia where direct measurement of heart rate variability is not possible. In the majority of our patients with CAN+, the vagal-cardiac and the sudomotor-sympathetic systems were involved simultaneously, although two entirely different systems were tested. This may reflect a C-fibre directed selectivity of the pathological process in autonomic diabetic neuropathy. In conclusion our results show that diabetics with and without cardiac autonomic neuropathy have a different profile of involvement of peripheral nerve fibres.

Adult↗