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Biomedical subjects

F Petzke

Publications and source records attributed to F Petzke.

17 recordsLinked to original sources
PubMed2006

[Central pain processing in chronic low back pain. Evidence for reduced pain inhibition].

INTRODUCTION: A study of patients with low back pain (LBP) had revealed altered central pain processing. At an equal pain level LBP patients had considerably more neuronal activation in the somatosensory cortices than controls. In a new analysis of this dataset, we further investigated the differences in central pain processing between LBP patients and controls, looking for possible pathogenic mechanisms. METHODS: Central pain processing was studied by functional magnetic resonance imaging (fMRI), using equally painful pressure stimuli in a block paradigm. In this study, we reanalyzed the fMRI data to statistically compare pain-elicited neuronal activation of both groups. RESULTS: Equally painful pressure stimulation resulted in a significantly lower increase of regional cerebral blood flow (rCBF) in the periaqueductal gray (PAG) of the LBP patients. The analysis further revealed a significantly higher increase of rCBF in LBP than in HC in the primary and secondary somatosensory cortex and the lateral orbitofrontal cortex (LOFK), elicited by these same stimuli. CONCLUSIONS: These findings support a dysfunction of the inhibitory systems controlled by the PAG as a possible pathogenic mechanism in chronic low back pain.

Adult↗
PubMed2006

Assessing cognition and psychomotor function under long-term treatment with controlled release oxycodone in non-cancer pain patients.

BACKGROUND: The therapeutic use of opioids can be associated with altered cognition and impaired psychomotor function. Several studies have demonstrated the impact of opioid therapy on psychomotor performance and cognition, but no data exist about the effect of long-term treatment with controlled release oxycodone (CRO) on driving ability. METHODS: Thirty patients suffering from chronic non-cancer pain who had been treated with stable doses of CRO where included in a prospective trial and compared with 90 healthy volunteers (matched pairs). A computerized test battery that was developed to assess the driving ability of traffic delinquents in Germany was employed. Attention reaction, visual orientation, motor coordination and vigilance were evaluated. The data from a total of 11 parameters were assessed and for each test a relevant score was defined. As the primary endpoint the sum score of the three relevant scores was determined. A weaker statistical means to assess the patients' performance is to compare the test results with an age-independent control group. Individuals performing worse than the 16th percentile of this control group are considered to be unable to drive according to German legislation. RESULTS: Significant non-inferiority could not be demonstrated for the primary endpoint. However, driving ability as defined as a result above the 16th percentile did not differ significantly between the patients receiving CRO and the age-independent control group. CONCLUSION: The use of CRO does not prohibit driving, but individual assessment is necessary.

Adult↗
PubMed2005

Propofol attenuates responses of the auditory cortex to acoustic stimulation in a dose-dependent manner: a FMRI study.

BACKGROUND: Functional magnetic resonance imaging (fMRI) using blood-oxygen-level-dependent (BOLD) contrasts is a common method for studying sensory or cognitive brain functions. The aim of the present study was to assess the effect of the intravenous anaesthetic propofol on auditory-induced brain activation using BOLD contrast fMRI. METHODS: In eight neurosurgical patients, musical stimuli were presented binaurally in a block design. Imaging was performed under five conditions: no propofol (or wakefulness) and propofol plasma target concentrations of 0.5, 1.0, 1.5, and 2.0 microg ml(-1). RESULTS: During wakefulness we found activations in the superior temporal gyrus (STG) corresponding to the primary and secondary auditory cortex as well as in regions of higher functions of auditory information processing. The BOLD response decreased with increasing concentrations of propofol but remained partially preserved in areas of basic auditory processing in the STG during propofol 2.0 microg ml(-1). CONCLUSIONS: Our results suggest a dose-dependent impairment of central processing of auditory information after propofol administration. These results are consistent with electrophysiological findings measuring neuronal activity directly, thus suggesting a dose-dependent impairment of central processing of auditory information after propofol administration. However, propofol did not totally blunt primary cortical responses to acoustic stimulation, indicating that patients may process auditory information under general anaesthesia.

Acoustic Stimulation↗
PubMed2004

Pain catastrophizing and neural responses to pain among persons with fibromyalgia.

Pain catastrophizing, or characterizations of pain as awful, horrible and unbearable, is increasingly being recognized as an important factor in the experience of pain. The purpose of this investigation was to examine the association between catastrophizing, as measured by the Coping Strategies Questionnaire Catastrophizing Subscale, and brain responses to blunt pressure assessed by functional MRI among 29 subjects with fibromyalgia. Since catastrophizing has been suggested to augment pain perception through enhanced attention to painful stimuli, and heightened emotional responses to pain, we hypothesized that catastrophizing would be positively associated with activation in structures believed to be involved in these aspects of pain processing. As catastrophizing is also strongly associated with depression, the influence of depressive symptomatology was statistically removed. Residual scores of catastrophizing controlling for depressive symptomatology were significantly associated with increased activity in the ipsilateral claustrum (r = 0.51, P < 0.05), cerebellum (r = 0.43, P < 0.05), dorsolateral prefrontal cortex (r = 0.47, P < 0.05), and parietal cortex (r = 0.41, P < 0.05), and in the contralateral dorsal anterior cingulate gyrus (ACC; r = 0.43, P < 0.05), dorsolateral prefrontal cortex (r = 0.41, P < 0.05), medial frontal cortex (r = 0.40, P < 0.05) and lentiform nuclei (r = 0.40, P < 0.05). Analysis of subjects classified as high or low catastrophizers, based on a median split of residual catastrophizing scores, showed that both groups displayed significant increases in ipsilateral secondary somatosensory cortex (SII), although the magnitude of activation was twice as large among high catastrophizers. Both groups also had significant activations in contralateral insula, SII, primary somatosensory cortex (SI), inferior parietal lobule and thalamus. High catastrophizers displayed unique activation in the contralateral anterior ACC, and the contralateral and ipsilateral lentiform. Both groups also displayed significant ipsilateral activation in SI, anterior and posterior cerebellum, posterior cingulate gyrus, and superior and inferior frontal gyrus. These findings suggest that pain catastrophizing, independent of the influence of depression, is significantly associated with increased activity in brain areas related to anticipation of pain (medial frontal cortex, cerebellum), attention to pain (dorsal ACC, dorsolateral prefrontal cortex), emotional aspects of pain (claustrum, closely connected to amygdala) and motor control. These results support the hypothesis that catastrophizing influences pain perception through altering attention and anticipation, and heightening emotional responses to pain. Activation associated with catastrophizing in motor areas of the brain may reflect expressive responses to pain that are associated with greater pain catastrophizing.

Adaptation, Psychological↗
PubMed2003

Intracranial placement of a nasotracheal tube after transnasal trans-sphenoidal surgery.

Intracranial misplacement of a tracheal tube during attempted nasotracheal intubation is a rare, usually lethal complication. Such incidents are associated with fractures of the face and base of the skull. We report inadvertent intracranial placement of a nasotracheal tube in a patient who had 2 weeks previously undergone transnasal trans-sphenoidal surgery for a pituitary tumour. One should be aware that transnasal trans-sphenoidal surgery leaves a bony defect in the skull, which is susceptible to perforation by nasally introduced tubes.

Adenoma↗
PubMed2001

Slow-release tramadol for treatment of chronic malignant pain--an open multicenter trial.

Patients with moderate to severe cancer pain and insufficient pain relief from nonopioid analgesics were treated with slow-release tramadol for initial dose finding and as a long-term treatment. Immediate-release tramadol was provided for the treatment of breakthrough pain and a standard nonopioid analgesic (1000 mg naproxen daily) was given as suggested for step 2 of the WHO analgesic ladder. Ninety of 146 patients (62%) completed the 6-week trial period. Drop-outs were due to adverse events (20%), inadequate pain relief (9%), or both (2.5%), death due to the underlying disease (4%), low patient compliance (2%) or other reasons. Average and maximal pain intensity decreased from day 1 to day 4. The number of patients with good and complete pain relief increased from 43% after week 1 to 71% after week 6 with maximum daily doses of tramadol up to 650 mg. However, 70% of the patients still needed less than 400 mg tramadol per day in week 6. Most patients (86%) experienced adverse events during the study period. Some common side effects of opioids, such as fatigue, dizziness, and constipation, decreased in frequency over the 6 weeks. The frequency of other adverse events such as nausea, vomiting and sweating did not change. Slow-release tramadol provided fast and efficient pain relief in almost two-thirds of patients both during initial dose finding and during long-term treatment, improving treatment options in step 2 of the WHO analgesic ladder.

Adult↗
PubMed2001

Transdermal fentanyl for the management of cancer pain: a survey of 1005 patients.

Transdermal fentanyl was released in Germany in 1995. From October 1996 to February 1998 transdermal treatment was documented for 1005 patients (506 men and 499 women with a mean age of 60 years, range 20-92 years) with chronic pain in an open survey including 290 physicians from hospitals and general practitioners throughout Germany. Most patients suffered from cancer pain and only 11 patients had chronic pain from non-malignant disease. Physicians were asked to complete a questionnaire for patients treated with transdermal fentanyl on initiation of therapy (day 0), and days 3, 6, 18, 30 thereafter, followed by monthly follow-up intervals. Patients were asked to complete a pain diary. Transdermal therapy was documented from day 0 for 824 patients, while 181 patients had been treated with transdermal fentanyl before admission in the survey. Most of the other 824 patients had been treated with other step 3 opioids (55% of the patients) or step 2 opioids (23%) before conversion to transdermal fentanyl, whereas 8% had been treated only with non-opioids and 14% had received analgesics only as required or not at all before initiation of transdermal therapy. The most important reasons for switching to transdermal opioid therapy were insufficient pain relief with the previous medication followed by a variety of gastrointestinal symptoms impeding oral analgesic therapy. Initial fentanyl doses ranged from 0.6 to 9.6 mg/day (25 to 400 microg/h) with a median of 1.2 mg/day (50 microg/h). Median doses slowly increased throughout the observation period to 2.4 mg/day (100 microg/h) after 4 months of treatment. Most patients continued transdermal therapy until the time of death (47% of patients). Other reasons for discontinuation were inadequate pain relief (10%), pain relief with other analgesic regimens (10%), other symptoms than pain (5%), rejection of transdermal therapy by the patient (6%) or miscellaneous (16%). Adverse events were documented as the reason for discontinuation of transdermal therapy in 49 patients (5%). Dyspnoea was documented for seven patients as the reason for discontinuation. One of these patients, as well as another patient with an episode of apnoea, had to be treated with artificial respiration for several hours, but both patients recovered without sequelae. Transdermal therapy with fentanyl was safe and efficient in this national survey. Transdermal fentanyl can be recommended for treatment of moderate to severe cancer pain and probably may even be used as a first-line drug on step 3 of the World Health Organization recommendations in selected patient groups.

Administration, Cutaneous↗
PubMed2000

Sympathetic nervous system function in fibromyalgia.

This review focuses on studies of the sympathetic nervous system in fibromyalgia (FM). First, a brief review of the sympathetic system, and its relationship to the human stress response, is outlined. Then various studies of functional assessment of sympathetic function in FM are highlighted. Certain methods of assessment (eg, heart rate variability, biochemical, and psychophysical responses to various stressors) that we believe to be of specific importance for future research are discussed in greater detail. Finally, findings on autonomic function in related disorders--specifically, chronic fatigue syndrome, irritable bowel syndrome, and migraine--will be briefly presented.

Female↗
PubMed1999

Temporal presentation of chronic cancer pain: transitory pains on admission to a multidisciplinary pain clinic.

Transitory flares of pain are well-recognized events in both untreated and treated patients suffering from chronic cancer pain. For the purpose of this survey, we refer to transitory pain (TP) as any event subjectively characterized by transience and pain intensity over a baseline pain. In Part I, TP was reported by 243 (39%) of 613 consecutive cancer pain patients. Gender, age, tumor site, stage, and therapy were not related to the presence of TP. Neuropathic baseline pain was associated with a higher prevalence of TP (P < 0.0001). TP was somatic in 39%, visceral in 22%, and neuropathic in 36% of patients. TP intensity was severe or worse in 92% of patients. Neuropathic TP was briefer and occurred more frequently than nociceptive TP. In Part II, further features of TP were surveyed in 55 patients. Patients reported spontaneous occurrence of TP (40%), a relationship to movement (36%), to the analgesic regimen (35%), to coughing (11%), and to various other factors (18%). Only half of the movement-related TP were predictable. Rescue medication was at least partially effective in 75% of patients. Change in position, rest, diversion, and physiotherapy were commonly employed to alleviate TP. This survey outlined a framework to characterize TP that may prove useful to clarify the definition, pathophysiology, and prevalence of these pains.

Adolescent↗
PubMed1998

Neuroendocrine dysfunction in African trypanosomiasis. The role of cytokines.

Sleeping sickness (SS; African trypanosomiasis) is an anthropozoonosis transmitted by the tsetse fly. Infection with Trypanosoma brucei in humans is associated with adynamia, lethargy, anorexia, and more specifically amenorrhea/infertility in women and loss of libido/impotence in men. Recent evidence suggests that experimental infection in animals with Trypanosoma brucei species causes polyglandular endocrine failure by local inflammation of the pituitary, thyroid, adrenal, and gonadal glands. In a cross-sectional study we investigated the prevalence and significance of neuroendocrine abnormalities in 137 Ugandan patients with SS. In the untreated stage of the disease, there was a high prevalence of adrenal insufficiency (27%), hypothyroidism (50%) and hypogonadism (85%). Pituitary function tests suggested an unusual combined central (hypothalamic/pituitary) and peripheral defect in hormone secretion. Specific therapy resulted in a rapid recovery of adrenal/thyroid function, whereas hypogonadism persisted for years in a substantial portion of patients. We did not detect pituitary, thyroid, adrenal, and gonadal autoantibodies in patients with endocrine dysfunction, ruling out an autoimmune origin of the endocrine abnormalities. However, the presence of hypopituitarism correlated with high cytokine concentrations (TNF-alpha, IL-6) which--together with direct parasitic infiltration of the endocrine glands--are involved in the pathogenesis of SS-associated endocrine dysfunction.

Animals↗
PubMed1996

Hypogonadism in Rhodesian sleeping sickness: evidence for acute and chronic dysfunction of the hypothalamic-pituitary-gonadal axis.

OBJECTIVE: To investigate acute and long-term effects of Rhodesian sleeping sickness on the function of the hypothalamic-pituitary-gonadal (HPG) axis in men. DESIGN: An observational, cross-sectional study. SETTING: Primary health care centers under care of the National Sleeping Sickness Control Program in southeast Uganda. PARTICIPANTS: Fifty-two male patients with sleeping sickness at different stages of treatment and 11 clinically healthy male volunteers recruited from health care personnel. INTERVENTIONS: Patients and controls were questioned about loss of libido and impotence. All received 100 micrograms GnRH i.v. Blood was drawn before and 30 minutes after GnRH administration. MAIN OUTCOME MEASURES: Frequency of loss of libido and impotence. Baseline T and sex hormone-binding globulin baseline and GnRH- stimulated serum LH and FSH concentrations. RESULTS: Loss of libido and/or impotence were present in 39% of men with active disease before therapy, whereas 84% were biochemically hypogonadal. After cure, 45% of men still were symptomatic and 45% were biochemically hypogonadal. Compared with controls (806 +/- 59 pg/mL [conversion factor to SI unit, 0.03467]; mean +/- SEM), T concentrations were decreased substantially in patients before (249 +/- 48 ng/dL), during treatment (429 +/- 56 ng/dL), and after cure (431 +/- 58 ng/dL). Corresponding baseline LH concentrations were inappropriately low and the relative LH response to GnRH was reduced both before and during treatment (794% +/- 131% versus 322% +/- 68%). Follicle-stimulating hormone concentrations increased gradually up to 8.0 +/- 1.3 mIU/mL (conversion factor to SI unit, 1.00) at the end of treatment, returning to 4.2 +/- 0.6 mIU/mL after cure. CONCLUSIONS: Rhodesian sleeping sickness causes acute and chronic HPG axis dysfunction. The clinical and biochemical picture suggest a combined central and peripheral hypogonadism. This is only in part reversible after cure and most likely due to direct parasitic infiltration and/or secondary inflammation causing necrosis and/or fibrosis at the pituitary and gonadal levels.

Adult↗
PubMed1996

[An innovative procedure of oxygen detection in medicine, biology, environmental research and biotechnology based on luminescence quenching].

For most (aerobic) animal organisms, oxygen is a mandatory and global substrate. The accurate measurement of oxygen is therefore of importance in the fields of medicine, biology, environmental research and biotechnology. The fact that oxygen is not readily soluble in aqueous media makes its detection more difficult. In contrast to the technique of polarography, the use of luminescence quenching by paramagnetic oxygen, does not consume the oxygen. Another problem of oxygen detection in connection with respiration is the need for very short response times. A third problem, which is associated with luminescence itself, is the fading of the dyes, which results in long-term signal instability. The last two problems can be optimally resolved by adsorbing the luminescence dye onto chromatographic materials--in particular hydrophobic material--having a very large internal surface area, and using the decay time in accordance with the Stern-Volmer equation as oxygen signal. For this, continuous evaluation of the signal is necessary. The carrier material doped with dye is incorporated in a single-grain layer. For measurements in liquids, the detector layer is protected by a black silicone membrane. Two designs are possible for the oxygen detector: (I) a special form using glass fibres, and (II) a miniature detector utilizing optoelectronic solid state technology. Both fluorescence and phosphorescence can be employed, the dye used being excited by light, obviating the need for quartz. The detector layers may be either of high sensitivity for small oxygen concentrations, or have equal sensitivity over the entire oxygen concentration range. There is an optimal figure for the specific amount of adsorbed dye. Application examples are given for respiration and for the determination of oxygen uptake by suspended cells.

Animals↗
PubMed1994

Impairment of adrenocortical function associated with increased plasma tumor necrosis factor-alpha and interleukin-6 concentrations in African trypanosomiasis.

African sleeping sickness (SS) is a severe, potentially lethal parasitic disease. The treatments of choice are the antiparasitic agents suramin, which is adrenotoxic, and/or melarsoprol. We evaluated the functional integrity of the hypothalamic-pituitary-adrenal (HPA) axis of patients with SS before, during, and after therapy with suramin and/or melarsoprol, in two sequential stages. First, we employed the standard adrenocorticotropic hormone (ACTH) 1-24 stimulation test (250 micrograms i.v.) to assess the maximal adrenocortical responsiveness of 69 patients with SS and 38 normal controls. We demonstrated paradoxically subnormal cortisol responses before suramin therapy [net cortisol response 60 min after stimulation: 10.5 +/- 2.9 (mean +/- SE) vs. 17.5 +/- 1.0 micrograms/dl for controls, p = 0.004], with 27% of the patients falling within the adrenal insufficiency range (stimulated cortisol concentration < 20 micrograms/dl). These responses subsequently and unexpectedly improved with suramin and/or melarsoprol therapy. Second, we performed a human corticotropin-releasing hormone (hCRH) test (100 micrograms i.v.) in 68 additional patients with SS and 14 control subjects to examine whether the glucocorticoid deficiency observed was primary and/or secondary. Compared to controls, the ACTH and cortisol responses to hCRH were blunted (ACTH after 60 min: 29 +/- 7 vs. 58 +/- 8 pg/ml in controls, p = 0.014; cortisol: 15.2 +/- 1.5 vs. 19.6 +/- 0.7 micrograms/dl, p = 0.018), suggesting the presence of secondary adrenal insufficiency. There was improvement of both ACTH and cortisol responsiveness to hCRH with therapy, with cortisol recovery occurring before ACTH, suggesting an additional primary component of adrenal dysfunction in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Thyroid dysfunction in African trypanosomiasis: a possible role for inflammatory cytokines.

OBJECTIVE: Sleeping sickness (African trypanosomiasis) is an anthropozoonosis transmitted by the tsetse fly. The treatments of choice are the antiparasitic agents suramin and/or melarsoprol. Experimental infection of animals with Trypanosoma brucei results in inflammatory lesions in the pituitary and/or the thyroid gland. In biochemical terms, these animals have hypothyroidism. We evaluated the functional integrity of the hypothalamic-pituitary-thyroid axis in patients with African trypanosomiasis before, during and after specific therapy. DESIGN: Prospective, controlled, cross-sectional study. PATIENTS AND MEASUREMENTS: Sixty-five patients with sleeping sickness (31 female, 34 male; aged 18-66; 32 with haemolymphatic sleeping sickness receiving suramin i.v., 33 with cerebral sleeping sickness receiving melarsoprol) and 13 control subjects (6 female, 7 male; aged 21-60) were enrolled in a cross-sectional study after giving informed consent. Fourteen patients were studied shortly after admission for sleeping sickness, 19 in the middle of the course of treatment, 18 at the end of the 5-week treatment period, and 14 patients after cure. All subjects underwent a TRH stimulation test at 1200 with bolus injection of 400 micrograms TRH i.v. Blood was drawn for determination of fT3, fT4, TSH, rT3, TNF-alpha, IL-1 and IL-6 at 0 minutes and TSH at 60 minutes. All hormones and cytokines were determined by RIA or ELISA. RESULTS: Baseline TSH concentrations (mean +/- SEM) were elevated in unmedicated patients with sleeping sickness compared to normal subjects (2.6 +/- 0.4 vs 1.4 +/- 0.2 mU/l; P = 0.01), whereas fT3 (2.7 +/- 0.5 vs 5.8 +/- 0.3 pmol/l; P = 0.0002) and fT4 concentrations (10.3 +/- 1.2 vs 15.4 + 0.8 pmol/l; P = 0.007) were low. Stimulated TSH concentrations did not significantly differ from normal controls. Reverse T3 concentration in patients with sleeping sickness were normal (2.2 +/- 0.3 vs 2.4 +/- 0.2 nmol/l; P = NS). During the course of treatment, baseline TSH, fT3 and fT4 concentrations slowly returned to normal and were indistinguishable from controls after cure. Plasma concentrations of TNF-alpha (16.0 +/- 4.1 vs 2.9 +/- 1.4 ng/l in controls; P = 0.003) and interleukin-6 (19.2 +/- 7.3 vs 1.3 +/- 0.2 ng/l; P = 0.0001), but not interleukin-1 beta (2.0 +/- 0.2 vs 0.9 +/- 0.2, ng/l P = NS), were elevated, when thyroid function impairment and disease activity were at their maximum, but gradually decreased into the normal range with therapy. We found a negative correlation between baseline cytokine concentrations and fT3 concentrations (TNF-alpha: r = -0.34, P = 0.003; IL-6: r = -0.43, P = 0.0001). CONCLUSIONS: We conclude that unmedicated sleeping sickness is associated with significant impairment of thyroid function, which is reversed with specific therapy. Elevated TSH concentrations and low fT3 and fT4 concentrations suggest primary hypothyroidism in patients with sleeping sickness. However, an additional pituitary and/or hypothalamic component cannot be excluded. This impairment may be due to the elevated plasma cytokine concentrations found in these patients or may be the result of parasitic thyroiditis.

Adolescent↗
PubMedDate not supplied

Adrenocortical insufficiency in Rhodesian sleeping sickness is not attributable to suramin.

Suramin, a polysulphonated naphthylurea used in the treatment of human African trypanosomiasis (HAT), is known to cause adrenocortical insufficiency in doses exceeding the quantity used for treatment of HAT. We have previously reported that Trypanosoma brucei rhodesinese infection causes a combined central and peripheral adrenal insufficiency. To evaluate whether suramin therapy acts as an additional adrenotoxic factor, we assessed adrenocortical function in 72 patients suffering from HAT at different times during treatment with either suramin or melarsoprol by a rapid adrenocorticotropic hormone test. We found a significantly diminished peak cortisol response to stimulation in the acutely ill patients (P = 0.001), indicating impaired adrenocortical function, as well as a high incidence of partial adrenocortical insufficiency (27%). During and after trypanocidal therapy the incidence of partial adrenal insufficiency gradually declined (to 25% and 18% respectively). Stimulated peak cortisol levels did not differ significantly between patients receiving suramin and those given melarsoprol. No correlation was found between serum suramin concentration and the cortisol response to stimulation (r = 0.09, P = 0.47). Thus we conclude that suramin in trypanocidal doses neither causes nor worsens the adrenocortical dysfunction observed in Rhodesian HAT.

Addison Disease↗