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Biomedical subjects

J Schattschneider

Publications and source records attributed to J Schattschneider.

9 recordsLinked to original sources
PubMed2006

Endothelial dysfunction in cold type complex regional pain syndrome.

The authors examined endothelial function in cold type chronic complex regional pain syndrome (CRPS) I using acetylcholine- and sodium nitroprusside-induced vasodilation combined with laser Doppler flowmetry in 14 patients and 10 controls. On the affected side, acetylcholine-induced vasodilation was significantly reduced in comparison to controls and the unaffected extremity. No significant differences were found after application of sodium nitroprusside. The results demonstrate impaired endothelial function in chronic CRPS I.

Acetylcholine↗
PubMed2004

Interaction between histamine-induced itch and experimental muscle pain.

Itch sensation can be inhibited by simultaneously applied cutaneous pain at the same skin site via a central mechanism. Deep muscle pain is often associated with sensory changes in the corresponding dermatome. We investigated whether experimentally induced muscle pain has any influence on histamine-induced itch and vice versa in a double blind placebo-controlled study. Experiments were performed in 18 healthy subjects. In nine individuals control iontophoresis of histamine into the forearm produced a distinct itch sensation. Another nine individuals participated in an additional experiment in which histamine and saline were iontophoresed on the forearm in a randomized double-blinded two-way crossover design after intramuscular injection of capsaicin into the ipsilateral brachioradial muscle. Capsaicin-induced muscle pain reduced itch sensation significantly. In contrast, capsaicin-induced muscle pain increased significantly after cutaneous histamine application compared to muscle pain after iontophoresis of saline (placebo). These novel data indicate that muscle pain inhibits itch and histamine increases muscle pain. A bi-directional interaction between cutaneous histamine-sensitive afferents and nociceptive muscle afferents via central mechanisms is suggested.

Adult↗
PubMed2003

[Recent trends in understanding and therapy of complex regional pain syndromes].

Since the term "complex regional pain syndromes" (CRPS) was introduced based on a revised taxonomy for disorders previously called reflex sympathetic dystrophy and causalgia in 1995, much knowledge grew up on the understanding and therapy of the disease. This review gives an overview on the clinical characteristics, pathophysiology, diagnostic tools and therapeutic options in CRPS. It will especially focus on recent findings on the role of the sympathetic nervous system, the central nervous system and peripheral inflammatory processes as underlying mechanisms. Although there is no diagnostic gold standard, careful clinical evaluation and additional apparative test procedures are very helpful for the diagnosis. An early and interdisciplinary approach is the basis for an optimal and successful treatment.

Causalgia↗
PubMed2003

[The symptom sympathetic maintained pain].

Sympathetically maintained pain is a symptom which occurs in neuropathic pain syndromes of different etiologies. From animal experiments it is known that nociceptive afferents after partial nerve lesions develop adrenergic sensitivity at the site of the injury. In addition, a sympathetic-afferent coupling takes place in the dorsal root ganglia. It is still controversial if these pathophysiological mechanisms are responsible for the developing of SMP in humans. Clinical studies support the idea that also in humans the application of adrenergic substances in pharmacological doses is capable to influence nociception, but a direct interaction between the sympathetic system and the nociceptive system had not been demonstrated so far. By using a thermal suit for whole body cooling and warming, which produces low and high activity of sympathetic vasoconstrictor neurons, it was possible for the first time to demonstrate an interaction between physiological changes in sympathetic activity and nociception.

Afferent Pathways↗
PubMed2003

Complex regional pain syndrome--diagnostic, mechanisms, CNS involvement and therapy.

Complex regional pain syndromes (CRPS, formerly reflex sympathetic dystrophy and causalgia) are neuropathic pain conditions of one extremity developing inadequately after a trauma. The initiating trauma affects primarily the extremity, but can also be a central lesion (e.g., spinal cord injury, stroke). CRPS is clinically characterized by sensory, autonomic and motor disturbances. Pathophysiologically there is evidence for functional changes within the central nervous system and for involvement of peripheral inflammatory processes. The sympathetic nervous system plays a key role in maintaining pain and autonomic dysfunction in the affected extremity. After a primary central lesion, secondary peripheral changes in the paretic extremity are suggested to be important in initiating a CRPS. Though there is no diagnostic gold standard, careful clinical evaluation and additional test procedures should lead to an adequate diagnosis. An early diagnosis and an interdisciplinary approach are important for optimal and successful treatment.

Central Nervous System↗
PubMed2002

Relation between sympathetic vasoconstrictor activity and pain and hyperalgesia in complex regional pain syndromes: a case-control study.

BACKGROUND: Complex regional pain syndromes can be relieved by sympathetic blockage. The mechanisms of sympathetically maintained pain (SMP) are unclear. We aimed to establish the effect of physiological sympathetic cutaneous vasoconstrictor activity on pain and hyperalgesia in patients with complex regional pain syndromes. METHODS: High and low cutaneous vasoconstrictor activity was produced by whole-body cooling and warming (thermal suit) in 13 patients with type I disease and in ten controls. The degree of cutaneous vasoconstrictor discharge was monitored by measurement of skin blood flow and temperature at the arm and leg. Local skin temperature at the affected region was fixed at 35 degrees C. Pain was quantified during high and low cutaneous vasoconstrictor activity (intensity of spontaneous pain, area of mechanical hyperalgesias, heat-pain thresholds). Furthermore, pain was measured before and after diagnostic sympathetic blockage to identify patients with SMP and sympathetically independent pain. FINDINGS: In patients with SMP, intensity of spontaneous pain significantly increased, by 22%, and spatial distribution of mechanical dynamic and punctate hyperalgesia increased by 42% and 27%, respectively, during high sympathetic activity compared with low activity. Heat-pain thresholds did not differ during high and low cutaneous vasoconstrictor activity (cold and warm state, 43.6 degrees C vs 44.6 degrees C). Pain relief after sympathetic blockage correlated with augmentation of spontaneous pain after experimental stimulation of cutaneous vasoconstrictor activity (r=0.6, p=0.0244). INTERPRETATION: We have shown that in complex regional pain syndromes with SMP, physiological activation of cutaneous vasoconstrictor neurons projecting to the painful arm or leg enhances spontaneous pain and hyperalgesia. We postulate that there is a pathological interaction between sympathetic and afferent neurons within the skin.

Adult↗
PubMed2001

Histamine-induced itch converts into pain in neuropathic hyperalgesia.

Physiologically, itch and pain are transmitted in separate specific peripheral C-units and central afferent pathways. Some neuropathic pain patients with intact but sensitized (irritable) primary C-nociceptors have spontaneous pain, heat hyperalgesia, static and dynamic mechanical hyperalgesia. The question was whether cutaneous histamine application induces pain in these patients. For comparison histamine was applied into normal skin experimentally sensitized by capsaicin. Histamine application in the capsaicin-induced primary or secondary hyperalgesic skin did not change the intensity and quality of capsaicin pain. Itch was profoundly inhibited. Conversely, histamine application in neuropathic skin induced severe increase in spontaneous burning pain but no itch. In neuropathies irritable nociceptors may express histamine receptors or induce central sensitization to histaminergic stimuli so that itch converts into pain.

Histamine↗
PubMed2001

Vascular abnormalities in reflex sympathetic dystrophy (CRPS I): mechanisms and diagnostic value.

Complex regional pain syndrome type I (CRPS I, formerly known as reflex sympathetic dystrophy) is a painful neuropathic disorder that develops after trauma affecting the limbs without overt nerve injury. Clinical features are spontaneous pain, hyperalgesia, impairment of motor function, swelling, changes in sweating, and vascular abnormalities. In this study, the pathophysiological mechanisms of vascular abnormalities were investigated. Furthermore, the incidence, sensitivity and specificity of side differences in skin temperature were defined in order to distinguish patients with definite CRPS I from patients with extremity pain of other origin. In 25 CRPS I patients and two control groups (20 healthy subjects and 15 patients with other types of extremity pain), cutaneous sympathetic vasoconstrictor activity was altered tonically by the use of controlled thermoregulation. Whole-body temperature changes were induced with a thermal suit in which cold or hot water circulated. The vascular reflex response (skin blood flow, laser Doppler flowmetry, skin temperature, infrared thermometry) was analysed to quantify sympathetic outflow. Measurements were performed during a complete thermoregulatory cycle, i.e. during the entire spectrum of sympathetic vasoconstrictor activity from high (whole-body cooling) to low sympathetic activity (whole-body warming). Venous noradrenalin levels were determined bilaterally in five CRPS patients. (i) Three distinct vascular regulation patterns were identified related to the duration of the disorder. In the "warm" (acute) type of regulation, the affected limb was warmer and perfusion values were higher than in the contralateral limb during the entire spectrum of sympathetic activity. In the "intermediate" type of regulation the limb was either warmer or colder. In the "cold" (chronic) type of regulation, skin temperature and perfusion values were lower on the affected side during the entire spectrum of sympathetic vasoconstrictor activity. (ii) Noradrenalin levels were lower on the affected side, even in chronic patients with considerable cutaneous vasoconstriction. (iii) Temperature and blood flow differences between the two sides were dynamic and most prominent at a high to medium level of vasoconstrictor activity. (iv) In both control groups, there were only minor side differences in flow and temperature. In conclusion, it is suggested that, in CRPS I, unilateral inhibition of sympathetic vasoconstrictor neurones leads to a warmer affected limb in the acute stage. Secondary changes in neurovascular transmission may lead to vasoconstriction and cold skin in chronic CRPS I, whereas sympathetic activity is still depressed. Vascular abnormalities are dynamic. The maximal skin temperature difference that occurs during the thermoregulatory cycle distinguishes CRPS I from other extremity pain syndromes with high sensitivity and specificity.

Adult↗