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Biomedical subjects

T Bartsch

Publications and source records attributed to T Bartsch.

At least 19 recordsLinked to original sources

Selective affection of hippocampal CA-1 neurons in patients with transient global amnesia without long-term sequelae.

The aetiology, pathomechanisms and anatomical correlates of transient global amnesia (TGA) still remain obscure. Recently, focal MR-signal diffusion-weighted imaging (DWI) changes in the hippocampus have been described in patients with TGA, but the exact localization, long term outcome and pathophysiological nature of these lesions still remain unknown. The topography and time course of hippocampal DWI lesions in 41 TGA patients was studied using serial 3 T high-resolution MR-imaging and correlated to clinical and neuropsychometric results. Of these, 29 patients showed 36 DWI lesions with corresponding T(2) lesions in the hippocampus within a time window of 48 h after onset. Almost all lesions (94%; 34/36) were selectively found in the CA-1 sector (Sommer sector) of the hippocampal cornu ammonis. Most DWI lesions (8/10) were already detectable in the peri-acute phase <6 h after onset of symptoms. A follow-up study 4-6 months after the episode did not show evidence for residual structural sequelae of these lesions (n = 20/20). A venous MR angiography of the intracranial dural sinus showed an asymmetric venous drainage in 21/24 (88%) patients. In 11/16 (69%) patients with unilateral lesions, the asymmetry corresponded to the side of the DWI lesion. Significant episodic verbal memory deficits in the acute phase (n = 14/18) were associated with lesions of the dominant hemisphere while impairment of visuospatial memory was associated with lesions of the non-dominant hemisphere. Persistent neuropsychological sequelae were not detected 4-6 months after the episode (n = 16). This is the first prospective study combining high-resolution imaging and neuropsychometry analysing the detailed functional anatomy and outcome of hippocampal DWI/T(2) lesions in TGA supporting the view the TGA being a benign transient disorder. The TGA can be considered a model for a focal transient perturbation of memory circuits in the temporo-mesial region.

Adult↗

[Intra-arterial and intramuscular transplantation of adult, autologous bone marrow stem cells. Novel treatment for therapy-refractory peripheral arterial occlusive disease].

HISTORY AND CLINICAL FINDINGS: A 62-year-old man had limb ischemia in stage IIb (Fontaine's classification). After surgical and interventional measures the right superficial femoral artery had remained occluded for more than one year. The patient's walking distance was only 100 meters. It was therefore decided to do a combined intraarterial and intramuscular transplantation of stem cells into the right limb. INVESTIGATIONS: Before and 10 weeks after the transplantation noninvasive tests, namely walking distance, ankle-brachial index at rest and during exercise, occlusion plethysmography and capillary venous oxygen saturation were measured. The patient was also asked to fill in a questionnaire of his symptoms. THERAPY AND RESULTS: After harvesting the patient's bone marrow the mononuclear cell fraction was separated (109.8 x 10(6)). Afterwards 10 ml of the cell suspension were injected into the right superficial femoral artery and 5 ml each of the suspension was injected into 5 different locations of the quadriceps femoris and the gastrocnemius muscles. After 10 weeks" follow-up a seven-fold improvement of walking distance and an increase of tissue oxygen saturation of more then 50% were recorded. The ankle-brachial index at rest remained unchanged, but on exercise it increased by 24%. CONCLUSION: The combined intraarterial and intramuscular transplantation of human autologous bone marrow stem cells may be a novel and clinically feasible treatment for patients with severe chronic limb ischemia. The success of this approach may be the result of increased neo-angiogenesis, especially of the small muscle-supplying vessels.

Arterial Occlusive Diseases↗

Animal models of migraine: looking at the component parts of a complex disorder.

Animal models of human disease have been extremely helpful both in advancing the understanding of brain disorders and in developing new therapeutic approaches. Models for studying headache mechanisms, particularly those directed at migraine, have been developed and exploited efficiently in the last decade, leading to better understanding of the potential mechanisms of the disorder and of the action for antimigraine treatments. Model systems employed have focused on the pain-producing cranial structures, the large vessels and dura mater, in order to provide reproducible physiological measures that could be subject to pharmacological exploration. A wide range of methods using both in vivo and in vitro approaches are now employed; these range from manipulation of the mouse genome in order to produce animals with human disease-producing mutations, through sensitive immunohistochemical methods to vascular, neurovascular and electrophysiological studies. No one model system in experimental animals can explain all the features of migraine; however, the systems available have begun to offer ways to dissect migraine's component parts to allow a better understanding of the problem and the development of new treatment strategies.

Animals↗

Inhibition of nociceptive dural input in the trigeminal nucleus caudalis by somatostatin receptor blockade in the posterior hypothalamus.

Somatostatin is a neuromodulator in the central nervous system and is involved in the regulation of metabolic and neuroendocrine functions. Recent experimental and clinical findings point to a role for somatostatin in the central processing of nociception. We studied the effects of somatostatin receptor modulation in the posterior hypothalamic area (PH) of the rat on dural nociceptive input. Somatostatin (10 microg/microl) and the somatostatin antagonist cyclo-somatostatin (50 microg/microl) were microinjected into the PH and the effects on responses of neurons in the trigeminal subnucleus caudalis studied. Injection of somatostatin (n=11) did not affect A- and C-fibre responses to dural electrical stimulation, nor was spontaneous activity altered (P>0.05). Injection of cyclo-somatostatin (n=10) into the PH reduced A-(-35.5+/-5.8%) and C-fibre (-43.1+/-7.5%) responses to dural stimulation and resulted in decreased spontaneous activity (-38.1+/-7.3%, P<0.05). Responses to facial thermal stimulation were decreased by 51.2+/-5.8% (n=5). Control injections had no significant effect (n=9). Blockade of somatostatin receptors in the PH has an anti-nociceptive effect on dural and facial input, probably mediated via GABAergic mechanisms. As somatostatin is also involved in hypothalamic regulation of metabolic, neuroendocrine and autonomic functions, somatostatin receptor mechanisms in the PH may play a role in the pathophysiology of primary headache disorders, such as migraine or cluster headache.

Action Potentials↗

Activation of 5-HT(1B/1D) receptor in the periaqueductal gray inhibits nociception.

It is considered that the site of action of the abortive antimigraine compounds acting at serotonin, 5-HT(1B/1D,) receptors (triptans) is the trigeminovascular system. We tested whether there is a non-trigeminal site of action. The 5-HT(1B/1D) agonist, naratriptan, was microinjected into the ventrolateral periaqueductal gray (vlPAG), and activity in the trigeminal nucleus caudalis (TNC) was monitored. Recordings were made from 20 nociceptive neurons in the dorsal horn of the TNC that received convergent input from the dura mater and face. Responses of neurons to dural, facial cutaneous and corneal stimulation were studied before and after injection of naratriptan. Naratriptan decreased the excitability to electrical stimulation of the dura mater as the A-fiber response decreased by 24 +/- 4.1% (p < 0.001) and the C-fiber response decreased by 42 +/- 8.2% (p < 0.001). Spontaneous activity was decreased by 38 +/- 7.5% (p < 0.001). After injection, the mechanical thresholds of the dura mater increased from (n = 14, p < 0.01). Responses to stimulation of the face and cornea were not altered by injection of naratriptan. These results suggest that 5-HT(1B/1D) receptor activation in the vlPAG activates descending pain-modulating pathways that inhibit dural, but not facial and corneal nociceptive input. These findings have implications for the understanding of the action of triptans in migraine and cluster headache, suggesting that brain loci other than the trigeminal nucleus may play a role in the clinical action of triptans.

Animals↗

[The trigemino-cervical complex. Integration of peripheral and central pain mechanisms in primary headache syndromes].

The activation of the trigeminal nociceptive system is the neural substrate of pain in primary headache syndromes such as migraine and cluster headache. The nociceptive inflow from the meninges to the spinal cord is relayed in brainstem neurones of the trigemino-cervical complex (TCC). Two important mechanisms of pain transmission are reviewed: convergence of nociceptive trigeminal and cervical afferents and sensitization of trigemino-cervical neurones. These mechanisms have clinical correlates such as hyperalgesia, allodynia, spread and referral of pain to trigeminal or cervical dermatomes. Neurones in the TCC are subject to a modulation of pain-modulatory circuits in the brainstem such as the periaqueductal grey (PAG). Recent experimental and clinical findings of a modulation of these pain processes are discussed. The review focuses on TCC neurones as integrative relay neurones between peripheral and central pain mechanisms. The understanding of these mechanisms has implications for the understanding of the clinical phenomenology in primary headache syndromes and the development of therapeutical options.

Brain↗

Differential modulation of nociceptive dural input to [hypocretin] orexin A and B receptor activation in the posterior hypothalamic area.

The novel neuropeptides orexin A and B are selectively synthesised in the lateral and posterior hypothalamus and are involved in hypothalamic regulation of autonomic and neuroendocrine functions. Recent findings point also to a role in nociception. As the posterior hypothalamus is involved in the central modulation of nociception we studied the effects of hypocretin/orexin receptor activation in the posterior hypothalamic area (PH) of the rat on dural nociceptive input. Orexins were microinjected into the PH and the effects on responses of neurones in the caudal trigeminal nucleus studied. Injection of orexin A decreased the A- and C-fibre responses to dural electrical stimulation as well as spontaneous activity. Responses to noxious thermal stimulation of the facial skin were also decreased by orexin A. Injection of orexin B into the PH, however, elicited increased responses to dural stimulation in A- and C-fibre responses and resulted in increased spontaneous activity. Responses to facial thermal stimulation were also increased by orexin B. Control injection of saline into the PH had no significant effect. The results show a differential modulation of dural nociceptive input by orexin A and B receptor activation in the PH. The results support the role of the PH in the nociceptive processing of meningeal input. As both peptides are also involved in hypothalamic regulation of neuroendocrine and autonomic functions, orexinergic mechanisms in the PH may provide a link for endocrine and autonomic changes as well as nociceptive phenomena seen in primary headache disorders.

Action Potentials↗

Precise determination of the 2s(1/2)-2p(1/2) splitting in very heavy lithiumlike ions utilizing dielectronic recombination.

The 2s(1/2)-2p(1/2) energy splittings DeltaE(L) of the lithiumlike ions 19779Au76+, 20882Pb79+, and 23892U89+ have been measured at the Experimental Storage Ring, utilizing low energy dielectronic recombination. The resonance energies in total 41 different 1s(2) 2p(1/2)nl(j(')) (n > or =20) autoionizing Rydberg states populated in the dielectronic capture process have been determined. The 2s(1/2)-->2p(1/2) excitation energies have been obtained by extrapolation of these resonance energies to the associated series limits n--> infinity. The combined analysis of the experimental data for all three ions yields DeltaE(L)=216.134(96) eV for Au76+, 230.650(81) eV for Pb79+, and 280.516(99) eV for U89+.

Journal Article↗

Increased responses in trigeminocervical nociceptive neurons to cervical input after stimulation of the dura mater.

Pain referral and spread in headache patients may be attributed to a sensitization of central nociceptive neurons with an increased excitability to afferent input. We investigated if noxious dural stimulation evokes sensitization of second-order neurons that leads to an increased responsiveness to stimulation of cervical afferents. Recordings were made from 29 nociceptive neurons in the C2 dorsal horn of the rat that received convergent synaptic input from trigeminal and cervical afferents. Trigeminal afferents of the supratentorial dura mater were activated by mustard oil (MO) and the responses of second-order neurons to stimulation of the greater occipital nerve (GON) were studied before and after dural stimulation. Projection sites to the contralateral thalamus were determined by antidromic stimulation. After dural application with MO, mechanical thresholds of the dura significantly decreased (P < 0.05) and an enlargement of the trigeminal and cervical cutaneous mechanoreceptive fields was observed in 71% of neurons. The responses to noxious mechanical stimulation of deep paraspinal muscles increased after MO application (P < 0.001). Similarly, an increase in the excitability to electrical stimulation of the GON was observed in C-fibre responses (P < 0.001). These results suggest that stimulation of nociceptive afferent C-fibres of the dura mater leads to a sensitization of second-order neurons receiving cervical input. This mechanism might be involved in the referral of pain from trigeminal to cervical structures and might contribute to the clinical phenomena of cervical hypersensitivity in migraine and cluster headache. Understanding this interaction is likely to be pivotal in characterizing the physiology of treatment with manipulations involving cervical input, such as GON injection.

Afferent Pathways↗

The trigeminocervical complex and migraine: current concepts and synthesis.

Neurones in the trigeminocervical complex are the major relay neurones for nociceptive afferent input from the meninges and cervical structures; therefore, they are the neural substrates of head pain. This review highlights the importance of two basic mechanisms in headache physiology: convergence of nociceptive afferents and sensitization of trigeminocervical neurones. These physiologic findings have clinical correlates such as hypersensitivity and spread and referral of pain frequently seen in patients with primary headache, such as migraine. Special reference is made to the influence of structures from the upper cervical spine in generating and contributing to migraine headaches. The pathophysiology and functional relevance of these basic mechanisms to headaches is discussed in the context of recent experimental findings with regard to pain processing.

Calcium↗

High Rydberg resonances in dielectronic recombination of pb(79+).

Dielectronic recombination resonances of Pb (79+) associated with 2s(1/2)-->2p(1/2) excitations were measured at the heavy-ion storage ring ESR at GSI. The fine structure of the energetically lowest resonance manifold Pb (78+)(1s(2)2p(1/2)20l(j)) at around 18 eV could partially be resolved, and rate coefficients on an absolute scale were obtained. A comparison of the experimental data with results of a fully relativistic theoretical approach shows that high-angular-momentum components up to j=31/2 significantly contribute to the total resonance strength demonstrating the necessity to revise the widespread notion of negligible high-angular-momentum contributions at least for very highly charged ions.

Journal Article↗

The ORL-1 (NOP1) receptor ligand nociceptin/orphanin FQ (N/OFQ) inhibits neurogenic dural vasodilatation in the rat.

The effects of the ORL-1 (NOP(1)) receptor ligand nociceptin (N/OFQ) and the nociceptin antagonists [Nphe(1)]N/OFQ-(1-13)-NH(2) (Nphe) and nocistatin (NST) on neurogenic dural vasodilatation (NDV) in the rat dura mater evoked by electrical stimulation of a closed cranial window were studied. The middle meningeal artery was visualised using intravital microscopy, and the vessel diameter analysed using a video dimension analyser. N/OFQ (1, 10, 100 nmol kg(-1); i.v., n=10) significantly and dose-dependently suppressed NDV maximally by 65% (P<0.01). Neither Nphe (100 nmol kg(-1); n=5) nor NST (100 nmol kg(-1); n=4) alone had an effect on NDV (P>0.05). Baseline vessel diameter was not significantly affected by application of N/OFQ, NST or Nphe. Application of the selective N/OFQ antagonist Nphe (10, 100 nmol kg(-1) i.v., n=8) dose-dependently and significantly (P<0.01) reversed the inhibition of NDV induced by application of N/OFQ (10 nmol kg(-1)). NST (10, 100 nmol kg(-1); n=7) failed to reverse the effects elicited by N/OFQ. Application of N/OFQ elicited a dose-dependent transient decrease in arterial blood pressure (P<0.01). Nphe dose-dependently reversed the cardiovascular effects induced by application of N/OFQ (10 nmol kg(-1)) (P<0.01),while NST did not alter the blood pressure reaction elicited by N/OFQ. The results show that N/OFQ inhibits NDV, an effect which is antagonised by Nphe, but not by NST. ORL-1 (NOP(1)) receptors located on trigeminal sensory fibres may be involved in the regulation of dural vessel diameter and hence may play a role in migraine pathophysiology.

Analysis of Variance↗

Semiclassical quantization by harmonic inversion: comparison of algorithms.

Harmonic inversion techniques have been shown to be a powerful tool for the semiclassical quantization and analysis of quantum spectra of both classically integrable and chaotic dynamical systems. Various computational procedures have been proposed for this purpose. Our aim is to find out which method is numerically most efficient. To this end, we summarize and discuss the different techniques and compare their accuracies by way of two example systems.

Journal Article↗

Cervico-thoracic disc protrusions in controlled compressed-air diving: clinical and MRI findings.

Prevalence of cervical and thoracic disc protrusions was investigated by MRI in 24 military long-term compressed-air divers and 24 controls. A total of 26 disc protrusions (17 cervical disc protrusions) were detected in 58% of the divers whereas 18 protrusions were detected in 38 % of the controls (13 disc cervical protrusions). There was no significant difference between groups and no correlation with the diving experience. Neurological examination revealed no clinical abnormalities. In contrast to a recent study, our results suggest that long-term divers are at no increased risk for accumulating spinal disc protrusions or intramedullary abnormalities.

Adult↗

Neurologic outcome of controlled compressed-air diving.

The authors compared the neurologic, neuropsychological, and neuroradiologic status of military compressed-air divers without a history of neurologic decompression illness and controls. No gross differences in the neuropsychometric test results or abnormal neurologic findings were found. There was no correlation between test results, diving experience, and number and size of cerebral MRI lesions. Prevalence of cerebral lesions was not increased in divers. These results suggest that there are no long-term CNS sequelae in military divers if diving is performed under controlled conditions.

Adult↗

Respiratory rhythmicity in the activity of postganglionic neurones supplying the rat tail during hyperthermia.

It has been suggested that thermoregulatory stimulation changes respiration-related rhythmicity in the activity of postganglionic sympathetic neurones supplying the rat tail to a distinct modulation independent of respiration. To study this possibility, single and few fibre recordings were made from ten filaments split from the ventral collector nerves of the rat during whole body warming. Sympathetic activity was analysed by autocorrelation and phrenic-triggered summation. All neurones except one were gradually inhibited and lost their on-going activity above a core temperature of 39-39.5 degrees C while the frequency of the phrenic bursts increased significantly. During hyperthermia, all neurones tested exhibited a prominent respiratory modulation in their activity which, compared to normothermia, was significantly increased in strength, or even newly acquired. No other rhythm emerged. These results speak against the hypothesis that in the rat sympathetic pathways controlling the tail vasculature and thus involved in thermoregulation, during hyperthermia become controlled by central oscillators distinct from the respiratory rhythm generator. Rather, respiratory modulation appears to remain the dominant rhythm as is common for sympathetic neurones supplying other cardiovascular targets.

Action Potentials↗