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C Sommer

Publications and source records attributed to C Sommer.

At least 37 records · Page 2Linked to original sources
PubMed2004

Association analysis of the functional monoamine oxidase A gene promotor polymorphism in migraine.

Migraine affects about 15% of the adult population. Serotonergic and dopaminergic systems are believed to be involved in its pathophysiology. One of the key enzymes in the degradation of serotonin and to a lesser extent of dopamine is monoamine oxidase A (MAO-A). In this study we investigated a functionally relevant gene-linked polymorphic repetitive sequence (LPR) located approximately 1.2 kb upstream of the ATG codon in the MAO-A-promotor gene. 119 patients with migraine and 229 controls were tested. The allelic distribution of the controls and the migraine patients did not show significant differences with respect to the low- and high-activity alleles. Moreover, effectiveness of the potent serotonergic antimigraine agents, triptans, which are metabolized by MAO-A, was clinically not affected by the MAO-A-LPR in our patients. These findings thus indicate that there is no association between the functional MAO-A-LPR and susceptibility to migraine.

Adult↗
PubMed2004

The extent of cytokine induction in peripheral nerve lesions depends on the mode of injury and NMDA receptor signaling.

We compared cytokine and chemokine induction in mice after sciatic nerve crush and chronic constriction injury (CCI) by quantitative reverse transcriptase polymerase chain reaction. In both nerve lesion paradigms, transcripts for tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-1beta, IL-10, and monocyte chemoattractant protein-1 (MCP-1) were significantly increased in degenerating nerve stumps already at day 1, with a greater magnitude and longer duration in CCI. NMDA receptor blockade significantly reduced cytokine expression after CCI on the mRNA and protein level. In dorsal root ganglia, only IL-10 mRNA levels were modified after nerve injury. Our study indicates that the mode of nerve injury influences the extent of cytokine expression, and identifies NMDA-mediated signaling as one mechanism of cytokine induction in peripheral nerves.

Analysis of Variance↗
PubMed2004

Lipomas of the internal auditory canal--report of two cases and review of the literature.

OBJECTIVE: Lipomas of the internal auditory canal are extremely rare. So far, only 21 cases have been described in the literature. We present here two of our own cases and review the literature to date with special emphasis on the diagnostic and therapeutic options. METHOD: During the last seven years two lipomas of the internal auditory canal were surgically treated in our department. Despite native and gadolinium-enhanced MRI and a thin-sliced temporal bone CT scan they were misdiagnosed as intracanalicular acoustic neurinomas. RESULTS: Total tumour removal could be achieved, the facial nerve function was conserved, but both patients were rendered functionally deaf after surgery. CONCLUSION: Lipomas' radiological behaviour may mimic acoustic neurinomas; without fat-suppressed T(1)-weighted images they are often preoperatively misdiagnosed as acoustic neurinomas. Although the postoperative morbidity with respect to cochlear and facial nerve function is much higher than in small acoustic schwannomas, early surgery may be justified, because complete removal is only possible in this stage. No reliable data are available concerning the natural history of this kind of lesion.

Adult↗
PubMed2004

Locking compression plate loosening and plate breakage: a report of four cases.

The Locking Compression Plate (LCP) system offers a number of advantages in fracture fixation combining angular stability through the use of locking screws with traditional fixation techniques. This makes the implant particularly suitable for use in poor bone stock and complex joint fractures, especially in the epimetaphyseal area. However, the system is complex, requiring careful attention to biomechanical principles, and a number of potential pitfalls need to be considered. These pitfalls are illustrated in the 4 cases described herein, in which treatment was unsuccessful due to implant breakage or loosening. In each case, treatment failure could be attributed to the choice of an inappropriate plate and/or fixation technique, rather than to the features of the Locking Compression Plate system itself. Such experiences highlight the importance of detailed understanding of the biomechanical principles of plate fixation as well as careful preoperative planning for the successful use of the Locking Compression Plate system.

Aged↗
PubMed2003

Diagnostic value of sural nerve matrix metalloproteinase-9 in diabetic patients with CIDP.

Patients with diabetes mellitus (DM) may develop chronic inflammatory demyelinating polyneuropathy (CIDP), which may be difficult to distinguish from diabetic neuropathy (DNP). Here the authors show that immunoreactivity for matrix metalloproteinase-9 on sural nerve biopsies may help to identify CIDP-DM. In a pilot study on 10 CIDP-DM patients with IV immunoglobulins and tight glycemic control, the CIDP-DM patients had a better outcome than DNP patients treated with tight glycemic control only.

Adult↗
PubMed2003

Neuropathology and binding studies in anti-amphiphysin-associated stiff-person syndrome.

The authors report a 71-year-old woman with amphiphysin-associated paraneoplastic stiff-person syndrome, opsoclonus, and encephalopathy. The patient's symptoms temporarily responded to plasmapheresis in parallel with a decline of serum anti-amphiphysin antibody titers. Later, the encephalopathy progressed rapidly and the patient died. Binding studies and the detection of autoantibodies in the patient's CNS as well as the treatment response suggest a pathogenic role of the anti-amphiphysin antibodies.

Aged↗
PubMed2003

[Determining the diagnosis from the pain pattern. Brief and stabbing or chronic and dull?].

For the neurological differential diagnosis of facial pain, symptomatic pain must be differentiated from the so-called primary pain syndromes. Trigeminal neuralgia is usually readily diagnosed on the basis of the typical history. The treatment of choice is carbamazepine. If this fails, invasive options are available. Atypical facial pain should be diagnosed only when all known primary and secondary pain syndromes have been excluded. Treatment is difficult and comprises the administration of tricyclic antidepressants. Cluster headache and chronic paroxysmal hemicrania each has an unmistakable temporal course. Although the etiology remains unknown, specific therapeutic options are available. The Tolosa-Hunt syndrome is presumably caused by a granuloma in the cavernous sinus, and treatment is effected with corticosteroids. Painful craniomandibular dysfunction (CMD) is often misinterpreted as atypical facial pain.

Cluster Headache↗
PubMed2003

Neuroprotective effect of granulocyte colony-stimulating factor after focal cerebral ischemia.

BACKGROUND AND PURPOSE: The potential neuroprotective effect of the granulocyte colony-stimulating factor (G-CSF) after glutamate-induced excitotoxicity in cell culture and after focal cerebral ischemia in rats was studied. We hypothesized the existence of the G-CSF receptor (G-CSFR) as a main G-CSF effector on neurons, and immunohistochemistry, immunoblotting, and polymerase chain reaction were performed. The G-CSFR-mediated action was studied by activation of signal transducer(s) and activator(s) of transcription-3 (STAT3) in the periphery of the infarction. METHODS: Neuroprotection of various G-CSF concentrations on glutamate-induced excitotoxicity was studied in cell culture. In vivo, ischemia was induced by use of a suture occlusion model of the middle cerebral artery (90-minute occlusion) in the rat. Thirty minutes after the induction of ischemia, the animals (n=12 per group) received G-CSF at 60 microg/kg body wt IV for 90 minutes or vehicle (saline). Infarct volume was calculated on the basis of 2,3,5-triphenyltetrazolium chloride staining 24 hours after ischemia. Expression of the G-CSFR was studied by immunohistochemistry and verified by reverse transcription-polymerase chain reaction and immunoblotting. Expression of STAT3 was determined by immunohistochemistry. RESULTS: In cell culture, G-CSF exhibited a significant neuroprotective effect after glutamate-induced excitotoxicity (P<0.05). A G-CSF concentration of 10 ng/mL was maximally effective, resulting in a nearly complete protection. In vivo, G-CSF reduced infarct volume to 47% (132.0+/-112.7 mm3 versus 278.9+/-91.6 mm3 [P<0.05] in the control group). Immunohistochemistry, Western blotting, and reverse transcription-polymerase chain reaction revealed the existence of G-CSFRs in neurons and glial cells. Animals treated with G-CSF significantly upregulated STAT3 in the periphery of the infarction compared with control animals (P<0.05). CONCLUSIONS: G-CSF achieved a significant neuroprotective effect in cell culture and after intravenous administration after stroke. Increased STAT3 expression in the penumbra of G-CSF-treated rats suggests mediation by G-CSFR.

Animals↗
PubMed2003

Pronounced arterial collateralization was induced after permanent rat cerebral four-vessel occlusion. Relation to neuropathology and capillary ultrastructure.

The present study investigates chronic changes in cerebral arterial vessel system, microvasculature, and brain histopathology using an adult rat model based on permanent and stepwise occlusion of four cerebral vessels. Digital subtraction angiography (DSA) was performed to study chronic changes in arterial cerebral vessel system after permanent vessel occlusion. Long-lasting functional changes such as NMDA-, AMPA- and GABA(A)-receptor binding were detected in hippocampus and dentate gyrus using autoradiography. Structural changes in cerebral capillaries were investigated using light- and electron microscopy. Chronic cerebral oligemia did not cause any significant changes in the densities of excitatory glutamate and inhibitory GABA(A) receptors. By electron microscopy we could document, however, that most capillaries in vessel-occluded animals shrank, the endothelial cells were prominent with enlarged nuclei and increased cytoplasm, and the basal membrane was thickened. In contrast to the degenerative changes in brain capillaries, pronounced arterial collateralization was disclosed by DSA after chronic brain vessel occlusion. The model of chronic occlusion of four cerebral vessels is characterized by capillary degeneration and arterial collateralization proceeding in parallel. Thus, this rat model may be useful in investigations of long-lasting compensatory mechanisms contributing to cerebrovascular or neurodegenerative disorders.

Angiography, Digital Subtraction↗
PubMed2003

[Retinopathy of prematurity screening and follow-up with Retcam120: expertise of a team of neonatologists concerning 145 patients].

OBJECTIVES: The high incidence of retinopathy in very premature infants requires strict evaluation and follow-up in neonatal intensive care. The strict organization required in each center, under the responsibility of ophthalmologists, is sometimes puzzling. Therefore, we tested the hypothesis that the introduction of the Retcam allows the neonatologist under the control of ophthalmologist to diagnose retinopathy of prematurity then preventing sequelae, by comparison of pictures interpretations between neonatologists and ophthalmologists. METHODS: The Retcam gives a 120 degrees picture of the retina which is captured digitally. Then, the interpretation of the neonatologist can be reviewed by the ophthalmologist. We screened premature babies less than 32 weeks of gestation and less than 1500 g, during 1 year, including learning experience. We compared pictures interpretation by neonatologists and ophthalmologists of Retcam recordings. RESULTS: One hundred and forty-five patients were included. Eight cases of retinopathy were diagnosed with an exact correlation : 3 grade III in zone 2 form plus disease, 1 stage III zone 2 unilateral, 1 stage II in zone 3, 2 stage II en zone 2, 1 grade I zone 3 on at least 5 h contiguous. We had neither false positive, nor false negative. Five infants were treated without significant sequelae. CONCLUSIONS: Retcam 120 allows an easy diagnosis and follow-up for the retinopathy of prematurity by the neonatologist. We advocate to spread Retcam to the wards where the screening of retinopathy is difficult for the ophthalmology department. As every case requiring therapy is diagnosed, prevention of severe visual handicap is completed. The cost of this apparatus is equivalent to the cost of the care for a congenital blindness.

Female↗
PubMed2003

Regulation of PDGF and PDGF receptor in cultured dermal papilla cells and follicular keratinocytes of the human hair follicle.

Platelet-derived growth factor (PDGF) is a potent mitogenic factor for many cell types and has been shown to be important in follicular development and vasculogenesis. In this study, we examined the expression pattern of both PDGF factors and their corresponding receptors in mesenchyme-derived dermal papilla cells (DPCs) and epithelial follicular keratinocytes (FKs). Both types of PDGF receptors are expressed in FKs, whereas DPCs only express PDGF receptor beta on the protein level, a finding also seen in whole organ cultures. By examining the expression of PDGF ligands, we were able to show that cultured FKs synthesize both PDGF-A and PDGF-B, whereas, DPCs only express PDGF-A. As immunomodulatory cytokines were shown to affect hair growth, we investigated the effects of IL-1beta, IL-4, TNF-alpha, TGF-beta and IFN-gamma on the expression levels of PDGF factors in cultured DPCs and FKs. Interestingly, we could show a significant down-regulatory effect by catagen-inducing cytokines like IL-1beta or IFN-gamma, suggesting a possible involvement of PDGF signaling in the induction of catagen. The question concerning the latter hypothesis remains to be elucidated in further studies on whole organ cultures.

Autocrine Communication↗
PubMed2003

[Diagnosis and therapy of vasculitic neuropathy. Consensus statement of the German Centers for Neuromuscular Disease].

Vasculitic neuropathies are immune mediated diseases of the peripheral nervous system, in which inflammation of the blood vessels causes damage to the nerves. We distinguish neuropathies associated with primary and secondary systemic vasculitis, with rheumatic diseases, with malignant disorders, drug-induced vasculitis and the non-systemic vasculitic neuropathies (NSVN). The typical clinical picture consists in an asymmetric or multifocal, painful sensorimotor neuropathy with an acute, subacute or chronic course and acute relapses. Neurophysiology reveals an active, asymmetric, axonal sensorimotor neuropathy. The disorders usually respond to immunosuppressive treatment. A diagnosis of definite vasculitis can be made with evidence of vasculitis in a biopsy specimen. The absence of positive morphological evidence, however, does not exclude the diagnosis. There is no single laboratory test that can prove or exclude vasculitis, in NSVN even an elaborate panel of blood tests can show normal findings. Systemic vasculitis has an incidence of 4/100,000 per year and, untreated, has a poor prognosis, which is greatly improved by the use of immunosuppressive treatment. The prognosis of NSVN is generally better, although many patients need long term immunosuppression. Current treatment recommendations for vasculitic neuropathies are presented.

Humans↗
PubMed2002

Small fibre neuropathy in sarcoidosis.

Some patients with sarcoidosis have unexplained pain and dysaesthesia. We did quantitative sensory testing in 31 sarcoidosis patients with pain or autonomic dysfunction. 25 patients had reduced warmth sensitivity, cold sensitivity, or both. Intraepidermal nerve fibre density (IENFD) was measured in punch biopsy skin samples in seven consecutive patients. All seven patients had reduced IENFD compared with controls, which confirmed the presence of small fibre neuropathy in these patients. Some patients with sarcoidosis may have small fibre neuropathy with autonomic involvement.

Adult↗
PubMed2002

Epidermal innervation density after partial sciatic nerve lesion and pain-related behavior in the rat.

The epidermis is innervated by fine nerve endings that are thought to have important sensory functions including nociception. Their role in neuropathic pain is as yet unclear. We used rats with a chronic constriction injury (CCI) of the sciatic nerve, a model of painful partial nerve injury, to examine the temporal course of the epidermal innervation density in correlation with corresponding nerve fiber numbers in the sciatic nerve and with pain-related behavior of the rats. A significant reduction of protein gene product 9.5 (PGP 9.5)-immunoreactive (ir) fibers and a nearly complete loss of calcitonin gene-related peptide (CGRP)-ir fibers was found after CCI in the epidermis as well as in the sciatic nerve. Reappearance of epidermal fibers was delayed compared to the regeneration of nerve fibers in the sciatic nerve. The maximum of pain-related behavior occurred at the time of maximal reduction of epidermal nerve fiber density. Possible explanations for this apparent discrepancy could be the presence of abnormal electrophysiological properties in the few remaining epidermal fibers, the lack of inhibition by intact fibers, or the generation of hyperalgesia in deeper layers of the skin. The number of PGP 9.5-ir Langerhans cells was increased after CCI, and this increase also temporally correlated with the presence of thermal hyperalgesia and mechanical allodynia, supporting a role of Langerhans cells in the generation of pain.

Animals↗
PubMed2002

Impaired sensory function in heterozygous P0 knockout mice is associated with nodal changes in sensory nerves.

Mice heterozygously deficient in the major myelin component P0 are an established model of an inherited neuropathy and show signs of myelin degeneration in motor nerves. Unlike the case in patients, the sensory nerves are only mildly affected in the mouse mutants and do not show features indicative of myelin degeneration. Unexpectedly, by applying established behavioral tests, we found sensory deficits, as reflected by raised withdrawal thresholds to mechanical and thermal stimuli, whereas behavioral signs of a painful neuropathy were not detectable. By electron microscopy of longitudinal sections of sensory nerves, we found abnormalities in nodes of Ranvier comprising enlarged nodal gaps and poorly developed nodal Schwann cell microvilli. These alterations might be causally linked to the sensory deficits in the absence of profound myelin degeneration in the sensory nerves of the mutants.

Animals↗
PubMed2002

[Pharmacotherapy of orofacial pain].

OBJECTIVES: Pharmacotherapy of chronic orofacial pain is unsatisfactory. Here we set out to prepare a systematic review of randomized controlled clinical trials (RCTs) on pharmacotherapy of facial pain. METHODS: The diagnostic groups "temporomandibular disorders" (TMDs), "atypical facial pain", and "trigeminal neuralgia" were included. RCTs published between 1966 and August 2001 were identified by Medline search, from review articles, and from the Cochrane and Bandolier databases. The quality of the trials was judged according to established criteria. Good or excellent pain reduction or >50% pain reduction were used as endpoints for successful treatment. Numbers needed to treat (NNTs) and their 95% confidence intervals were calculated where dichotomous data were available. RESULTS: Twelve studies were identified for the TMDs, 11 for trigeminal neuralgia, four for atypical facial pain. Many studies had methodological problems and small numbers of patients. There was sufficient evidence of efficacy of carbamazepin in trigeminal neuralgia, also for baclofen and lamotrigine. In the TMD studies, there was evidence of a moderate effect of muscle relaxants/tranquilizers. Two studies of atypical facial pain showed a moderate effect of antidepressants. CONCLUSIONS: Apart from studies in trigeminal neuralgia, there is little evidence of efficacy of pharmacotherapy in orofacial pain. High quality studies with sufficient numbers of patients using operational definitions of disease entities are warranted.

Analgesics↗
PubMed2002

[Effects of Repetitive Exposure to Hyperbaric Oxygen (HBO) on Leukocyte Function].

OBJECTIVE: Despite favourable clinical data on the successful use of hyperbaric oxygen (HBO), only limited investigations have been carried out to date regarding the influence of hyperoxia on leukocyte function. In a murine model, CD4+ T-cell population remained unchanged after repeated HBO exposure, however CD8+ cells were found to be increased. The aim of this study was to investigate whether repetitive exposure to hyperoxia would affect human monocyte and lymphocyte function. METHODS: Methods: After Ethics Committee approval the effects of elevated partial oxygen pressure were studied in the course of a ten-day HBO therapy (2.5 atmospheres absolute over a daily period of 90 min). Monocytes and lymphocytes of 30 patients with acute hearing loss were determined by flow cytometry before, throughout and after HBO therapy using monoclonal antibodies to CD3, CD4, CD8, CD14, CD25, CD45 and HLA-DR. Statistical analysis was made by ANOVA (analysis of variance). RESULTS: The relative percentage of CD3+, CD4+, CD8+, CD25+, CD14+, and HLA-DR+ cells remained unchanged during the course of and after HBO therapy. CONCLUSIONS: We conclude that repetitive exposure to hyperoxia does not influence human monocyte and lymphocyte functions in contrast to experimental data.

Adult↗