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Biomedical subjects

F Erbguth

Publications and source records attributed to F Erbguth.

At least 19 recordsLinked to original sources

Botulinum Toxin A reduces neurogenic flare but has almost no effect on pain and hyperalgesia in human skin.

Botulinum toxin A (BoNT/A) has been used therapeutically to treat muscular hypercontractions and sudomotor hyperactivity. There is increasing evidence that BoNT/A might also have analgesic properties, in particular in headache. In the present investigation we tested the often cited hypothesis that BoNT/A-induced analgesia can be attributed to inhibition of neuropeptide release from nociceptive nerve fibers. In 15 healthy volunteers BoNT/A (5, 10, 20 mouse units BOTOX) or saline (contralateral side) was injected intracutaneously on the volar forearm. On day zero, the day of injection, no further tests were performed. We repeatedly elicited pain, mechanical hyperalgesia and neurogenic flare by transcutaneous electrical stimulation simultaneously on the BoNT/A and saline treated side on day 1, 2, 3, 7 and 14 after injection. Before each session, sweating and local anhidrosis was assessed by iodine starch staining.BoNT/A suppressed sweating as early as from the second day after injection (p < 0.001). The size of electrically induced flare was smaller on the BoNT/A treated arm (BoNT/A side: 21.46 cm(2) +/- 3.58, saline side 24.80 +/- 3.46, p < 0.005) and BoNT/A reduced electrically-induced pain by about 10 % (p < 0.001). However, hyperalgesia to pin-prick and allodynia after electrical stimulation were unchanged. In conclusion our results indicate that peripheral neuropeptide release is attenuated by BoNT/A. In contrast, the analgesic effect of BoNT/A was very limited. Therefore we assume that other than neuropeptide mechanisms must be important for BoNT/A induced pain relief in clinical pain syndromes.

Adult↗

[Neurological complications of inflammatory intestinal diseases].

A number of neurological symptoms have been described as complications of inflammatory bowel disorders such as coeliac disease, Whipple's disease, Crohn's disease and ulcerative colitis. The neurology of coeliac disease includes disorders of the central nervous system encompassing cerebellar ataxia, epilepsy, myoclonus, dementia and multifocal leukoencephalopathy. Peripheral neuropathies, of axonal and demyelinating types, and myopathies have also been reported. The pathomechanisms are more related to immunological-inflammatory processes than to a malresorptive vitamin deficiencies. While CNS symptoms of coeliac disease show a poor response to gluten restriction, peripheral symptoms may respond to elimination of gluten from the diet. There are few reports of a successful corticosteroid treatment in patients showing inflammatory findings in the CSF or bioptic material. Whipple's disease is caused by the gram-positive bacillus Tropheryma whipplei. Patients with a central nervous system manifestation of Whipple's disease may develop a variety of symptoms including dementia, supranuclear gaze palsy, movement disorders, hypothalamic dysfunction and myorhythmia. The CNS-infection is diagnosed by PCR of the CSF. Long-term antibiotic treatment is required, and relapses may occur after withdrawal of antimicrobial therapy. Crohn's disease and ulcerative colitis are complicated by various forms of polyneuropathies, and arterial and venous cerebrovascular diseases. In most cases with neurological complications of inflammatory gastrointestinal diseases an immune mediated inflammatory process is suspected to be the underlying pathomechanism.

Aged↗

Serum procalcitonin monitoring for differential diagnosis of ventriculitis in adult intensive care patients.

The objective of our study was to assess the value of serum procalcitonin (PCT) monitoring in the differential diagnosis of ventriculitis in adult intensive care (ICU) patients. We analyzed 15 consecutive patients with ventriculitis in which a ventricular catheter had been inserted and contrasted these data with the observations in 10 patients with community-acquired bacterial meningitis. Cerebrospinal fluid (CSF) and blood samples were collected daily to assess serum PCT, C-reactive protein (CRP) and CSF leukocyte count. PCT levels were normal or slightly elevated in patients with ventriculitis with either positive or negative CSF bacterial culture but elevated in patients with bacterial meningitis. A PCT cut-off value of 1.0 ng/ml or more showed a specificity of 77% and a sensitivity of 68% for ventriculitis with positive CSF bacterial culture. Serum PCT levels reflected more accurately the time phases of disease during therapy. We conclude that the monitoring of serum PCT alone is not helpful for the differential diagnosis of ventriculitis, in contrast to that of bacterial meningitis. The value of PCT as an additional marker with which to assess the efficacy of therapy in ventriculitis is suggested, but requires further assessment.

Adolescent↗

Severe neurological complications of ulcerative colitis.

A 37 year old man presented with a 15 year history of ulcerative colitis. On examination he had weakness of the right arm, slurred speech and progressive confusion, followed by a rapid deterioration of consciousness and motor functions resulting in coma, tetraparesis and bilateral Babinski responses. Magnetic resonance imaging of the brain and spinal cord revealed multiple hyper- and hypointense white matter lesions. Clinical symptoms, history and neuroradiological findings led to the diagnosis of an ulcerative colitis-associated CNS disorder. An autoimmune vasculitic process may have played an important pathophysiological role, considering the vasculitic changes observed by skin biopsy as well as the rapid clinical improvement following immunosuppressive therapy with corticosteroids and azathioprine. During a follow up period of more than one year we observed continuous and complete recovery of neurologic symptoms.

Adult↗

Transcutaneous and intra-arterial blood gas monitoring--a comparison during apnoea testing for the determination of brain death.

Intra-arterial (i.a.) and transcutaneous (t.c.) blood gas monitoring were compared with in vitro blood gas analysis (abg) during apnoea testing for the determination of brain death in a prospective observational study. All three methods were used simultaneously in 19 patients in whom brain death was suspected. Brain death was confirmed in each case adhering to the recommendations of the Scientific Advisory Board of the German Federal Chamber of Physicians which demand a PCO2 of at least 60 mmHg. In vitro parameters ranged from 23.2 to 80.4 mmHg (PCO2), 52.7 to 509.9 mmHg (PO2), and 7.072 to 7.591 (pH). The intra-individual correlations between both monitoring methods (rPCO2=0.958, rPO2=0.859) and between each of them and abg (r>0.960) were high. Absolute deviations from abg for the corrected as well as uncorrected measurements were similar for both methods, except with regard to group bias where an advantage for the i.a. values emerged. Since many of the i.a. measurements failed and the disposable i.a. probes cost much more than the t.c. electrodes, the i.a. technique at present holds no advantage over t.c. measurements in testing for apnoea in suspected brain death except where simultaneous monitoring of pH and temperature are desired.

Adolescent↗

[Cerebral tuberculosis in a patient with Sharp's syndrome].

HISTORY AND ADMISSION DIAGNOSIS: A 57-year-old female patient with fever and impaired consciousness was admitted to the department of neurology after her first epileptic seizure. She had a 9-year history of mixed connective tissue disease (MCTD, Sharp's syndrome) predominantly presenting with pulmonary symptoms and destructive arthritis. Endoprothetic surgery had to be performed several times and she was given long-term immunosuppressive therapy. INVESTIGATIONS: Cerebrospinal fluid analysis showed pleocytosis (59/mm3), high protein concentration (2540 mg/l) and low glucose level (31 mg/dl) compared to blood glucose level (122 mg/dl) the indicating possible tuberculous meningoencephalitis. DIAGNOSIS, TREATMENT AND COURSE: Tuberculostatic therapy was initiated, but despite extensive testing Mycobacterium tuberculosis could initially not be detected by microscopy, culture or amplification techniques (TMA; transcription mediated amplification). Clinical response to antituberculous therapy was poor and the patient developed cerebral ischaemia and hydrocephalus. Because of earlier histological findings from the synovialectomy showing epitheloid cell granuloma a knee joint specimen from a wound drainage was tested and extracerebral tuberculosis was finally confirmed by mycobacterial culture so that tuberculosis as the reason for the meningoencephalitis became highly probable. Despite slight improvements the patient still had hemiparesis and lethargy as neurological sequalae at the end of therapy. CONCLUSION: The case demonstrates the difficulties in the diagnosis of tuberculosis in patients with signs and symptoms similar for those caused by other multisystemic diseases. When tuberculous meningitis is considered, therapy should be initiated even in cases with negative microbiological tests because of severe consequences when treatment is delayed.

Brain Ischemia↗

[Polyradiculopathy and ataxia: clinical manifestation of late recurrence of pilocytic astrocytoma with cerebral and spinal dissemination].

A 14-year-old girl underwent surgery for cerebral pilocytic astrocytoma. Eighteen years later she developed acute ataxia and a polyneuropathic syndrome. A recurrence with cerebral and spinal leptomeningeal dissemination of the tumor was discovered. Treatment of these cases is always difficult, and no standard therapy scheme has been established so far.

Adolescent↗

Critical illness polyneuropathy: clinical findings and cell culture assay of neurotoxicity assessed by a prospective study.

OBJECTIVE: First, to evaluate the role of typical intensive care-related conditions like sepsis, prolonged ventilation, drug effects and metabolic disorders in the pathogenesis of critical illness polyneuropathy (CIP); second, to investigate the possible significance of patient serum neurotoxicity assessed by an in vitro cytotoxicity assay with respect to CIP development. DESIGN: Prospective study. SETTING: Neurological intensive care unit. PATIENTS AND PARTICIPANTS: Twenty-eight patients who were on mechanical respiratory support for at least 4 days during a 21-month study period. RESULTS: Diagnosis of CIP was established by clinical and electrophysiological examination in 16 (57%) of 28 patients. Patients were investigated on days 4, 8 and 14 of mechanical ventilation. Two of 16 CIP patients had clinical signs of polyneuropathy at initial examination. Factors that correlated significantly with the development of CIP were: the multiple organ failure score on day 8 of ventilation, the total duration of respiratory support, the presence of weaning problems and the manifestation of complicating sepsis and/or lung failure. The in vitro toxicity assay showed serum neurotoxicity in 12 of 16 CIP patients. Electrophysiological investigations yielded false positive results of the toxicity assay in six patients (not developing CIP) and false negative results in four patients (developing clinical and electrophysiological signs of CIP). Statistical analysis did not reveal a significant correlation between the diagnosis of CIP and the finding serum neurotoxicity. CONCLUSION: The results support the hypothesis of a multi-factorial aetiopathogenesis of CIP. We observed serum neurotoxicity in the majority of CIP patients, indicating the possible involvement of a so far unknown, low-molecular-weight neurotoxic agent in CIP pathogenesis.

Adrenal Cortex Hormones↗

Cerebral vein thrombosis and prothrombin gene (G20210A) mutation.

Recently, prothrombin gene mutation G20210A has been associated with elevated thrombosis risk and rarely with cerebral vein thrombosis (CVT). Three patients are described who had this genetic predisposition and who developed CVT in an unusual constellation with other factors. In the first patient, the intake of valproic acid (VPA) may have played an aggravating role in the development of CVT; in the second patient diagnosis of coagulation disorder was made during pregnancy consultation 6 years after CVT; in the third patient the CVT occurred at the age of 78 years. In patients with CVT, coagulation-examinations should include tests for the prothrombin gene (G20210A) mutation.

Adult↗

Dose thresholds and duration of the local anhidrotic effect of botulinum toxin injections: measured by sudometry.

BACKGROUND: Local injections of botulinum toxin type A (BTX-A) have been used successfully to treat focal hyperhidrosis, but because experimental data were lacking, doses have been chosen arbitrarily or empirically. OBJECTIVES: To analyse dose dependency and duration of BTX-A-derived suppression of sweat gland activity. METHODS: Employing a standardized scheme (four injections, square 2 x 2 cm), different doses of BTX-A [Dysport(R); 2.5-120 mouse units (MU)] were injected subcutaneously at the lateral aspects of both of the lower legs in 15 healthy volunteers. Sweat tests were performed before, and 3 weeks and 6 months after, BTX-A injections. Sweating was visualized by staining with iodine starch, and quantified by capacitance hygrometry after carbachol iontophoresis, the quantitative sudomotor axon reflex test (QSART). RESULTS: Iodine starch staining indicated a threshold dose of 10 MU (2.5 MU cm-2) leading to visible anhidrotic skin spots after 3 weeks in all subjects. This was maintained for 6 months with doses of 50 MU (12.5 MU cm-2) or higher, but the size of the anhidrotic skin area decreased over time (P < 0.001) indicating partial recovery at the edges. After 3 weeks QSART was significantly reduced (P < 0.02) and completely suppressed by doses of 80 MU (20 MU cm-2) or more, although after 6 months QSART increased again to pre-BTX-A levels (P < 0.001). Both methods indicated that the suppression of sweating is dose dependent (QSART: r = -0.70, P < 0.001; iodine starch staining: r = 0.74, P < 0.001). CONCLUSIONS: Our findings suggest that BTX-A effectiveness can be quantified by testing sudomotor function. For the first time threshold doses for the suppression of sweating have been defined.

Adolescent↗

A randomized, double-blind, placebo-controlled study of the efficacy and safety of botulinum toxin type A in upper limb spasticity in patients with stroke.

OBJECTIVE: To study the efficacy and safety of botulinum toxin type A (BtxA) in the treatment of upper limb muscle spasticity, caused by stroke. METHODS: This was a randomized, controlled trial. Patients received either placebo injections or a total of 1000 IU of BtxA (Dysport) into five muscles of the affected arm. Muscle tone was assessed using the Modified Ashworth Scale (MAS). Other outcome measures were the change in the joint range of motion (ROM), the Barthel index, pain score, goal attainment and the subjective evaluation of benefit by patients and investigators. The patients were assessed blind to randomization at baseline and 4, 8, 12 and 16 weeks after treatment. RESULTS: Fifty nine patients were recruited and received treatment. One patient was lost to follow-up before the last scheduled visit of the study. The group of patients who received BtxA had a significant reduction in the summed MAS score at week 4 compared with the placebo group (P=0.004). The magnitude of benefit over the 16 week follow-up period was significantly reduced for the BtxA group in the wrist (P=0.004) and the finger joints (P=0.001) when compared with the placebo. There was no statistically significant difference between the groups in the joint ROM, muscle pain, goal-attainment or the Barthel index scores at week 4 of the study. At week 16, the BtxA group showed significantly greater improvement in the passive ROM at the elbow (P=0.036). The patients' global assessment of benefit at the end of the study showed that 16 (50%) patients in the placebo group had 'much improved' or had 'some improvement' compared with 24 (92.3%) patients in the BtxA group (P=0.007). The investigators' rating for the same item was 16 (50%) and 23 (88.4%) patients, respectively (P=0.002). Sixteen and twenty patients in the BtxA and placebo groups, respectively, had an adverse event. The most frequently reported adverse events were accidental injury, respiratory and urinary tract infections and muscle pain. CONCLUSION: The findings of the present study suggest that treatment with BtxA in a dose of 1000 units reduces muscle tone in patients with post-stroke upper limb spasticity. This effect is sustained for at least 16 weeks. BtxA is safe in the dose used in this study. IMPORTANT NOTE: The authors wish to emphasize that the botulinum toxin preparation used in this study was Dysport (Ipsen Ltd) which has a different therapeutic equivalence from other commercially available product, Botox (Allergan Inc.).

Aged↗

Acute stroke management in the local general hospital.

BACKGROUND AND PURPOSE: The majority of stroke patients are treated in local general hospitals. Despite this fact, little is known about stroke care in these institutions. We sought to investigate the status quo of acute stroke management in nonspecialized facilities with limited equipment and resources. METHODS: Four general hospitals located in smaller cities of a rural area in Germany participated in this study. The 4 hospitals were similar in structure and technical equipment; none had a CT scanner in-house. We reviewed the medical records of every stroke patient hospitalized in 1 of the 4 hospitals within a period of 8 weeks within 1 year. RESULTS: We collected data of a total of 95 patients at all 4 hospitals. The frequency of diagnostic tests was low: at least 1 CT scan was obtained in only 36.8% of all cases, whereas diagnostic methods available in-house were used more frequently, such as Doppler ultrasound (49.0%), echocardiography (42.3%), and 24-hour ECG registration (48.4%). Each hospital had a different therapeutic approach. Main therapeutic options were the use of pentoxyfilline (0% to 90.5%), osmodiuretics (0% to 90%), piracetam (0% to 93.3%), and hydroxyethylstarch (4.8% to 30%). Medication for long-term secondary prevention was given to 69.8% of all patients. CONCLUSIONS: This study provides one of the few data samples reflecting stroke care in smaller general hospitals. The findings demonstrate a partially suboptimal level of care in these institutions. To achieve future improvements, extended human and technical resources as well as research for stroke care should not be restricted to academic stroke centers.

Diuretics↗

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↗

Sensory tricks in cervical dystonia: perceptual dysbalance of parietal cortex modulates frontal motor programming.

Cervical dystonia is a disabling basal ganglia disorder characterized by an involuntary head deviation to one side. A typical but also mysterious feature is the impressive improvement of muscle spasms and involuntary head posture by application of a sensory facial stimulus (sensory trick). Here, we report the effect of a sensory trick on cortical activation patterns in 7 patients with cervical dystonia by using H2(15)O positron emission tomography. The application of the sensory trick stimulus, resulting in a near-neutral head position, led to an increased activation mainly of the superior and inferior parietal lobule (ipsilateral to the original head turn) and bilateral occipital cortex and to a decreased activity of the supplementary motor area and the primary sensorimotor cortex (contralateral to the head turn). We propose that a perceptual dysbalance induced by a sensory trick maneuver leads to a relative displacement of the egocentric midvertical reference to the opposite side and a decrease in motor cortex activity. This modulation of motor programming gives novel insights into the mechanisms involved in sensorimotor integration in movement disorders.

Adult↗

[Nosocomial pneumonias in a neurology intensive care unit].

BACKGROUND AND OBJECTIVE: Nosocomial pneumonia in patients in an intensive care unit (ICU) are a great problem as a cause of increased morbidity and mortality as well as the resulting high cost of treatment. This study was aimed at determining the incidence of nosocomial pneumonia and the risk factors for its occurrence in patients with severe neurological disease. PATIENTS AND METHODS: Between 1.1. and 31.12.1997, 217 patients (125 men, 92 women; average age 63.4 years) were prospectively included if they were treated for more than 48 hours in the ICU of the Neurology Department of Erlangen University. The occurrence of nosocomial pneumonia (NP) was noted, using the criteria of the Center of Disease Control and Prevention (CDC). Incidence of the diseases was related to age, sex, initial state of consciousness, type of ventilation, duration of stay in the ICU and any associated medical condition. RESULTS: NP was diagnosed in 68 patients (31.4%). Statistically significant relative risks were male sex (2.4 fold, P < 0.01), clouded consciousness with a Glasgow coma score < 8 (6.2 fold, P < 0.001), mechanical ventilation (8.4 fold, P < 0.001), time in ICU > or = 8 days (9.3 fold, P < 0.001) and associated medical condition (3.3 fold, P < 0.005). In 17.7% of cases no relevant pathogen was identified microbiologically. A mixed infection was present in 36.8% of cases. The most common Gram-positive organism was Staph, aureus (35.3%), the most common Gram-negative ones were Ps. aeruginosa (25%), Kl. pneumoniae and Kl. oxytoca (11.8%), E. Coli (10.3%) and Acinetobacter species (7.4%). There was also a high rate of infection or infestation with Candida albicans or glabrata (41.2%). NP played a clinically decisive role in the fatal course of 13 of the 47 patients who died. CONCLUSION: These data (incidence, relative risk) can, by taking into consideration various aspects of specialist and hospital hygienic practices, contribute to a continuing optimization of the prevention and treatment of disease.

Aged↗

[Renal tubular acidosis with severe hypokalemic tetraparesis after ibuprofen intake].

HISTORY: A 72-year-old woman was admitted because of severe acute tetraparesis, more marked proximally. For six months she had been taking ibuprofen, up to 4800 mg daily, for a painful ulcer of the lower leg. INVESTIGATIONS: Biochemical tests revealed marked hypokalaemia (serum potassium 1.4 mmol/l) with a metabolic acidosis (pH 7.29). The ECG showed changes of hypokalaemia (ST-segment depression and U wave). TREATMENT AND COURSE: Within two days of administering potassium and bicarbonate the pareses completely regressed. Transitorily abnormal renal functions also rapidly normalized after ibuprofen had been discontinued. CONCLUSION: The biochemical findings suggest renal tubular acidosis, type 2, most likely caused by the excess intake of ibuprofen, a drug which can cause renal dysfunctions with life-threatening electrolyte abnormalities.

Acidosis, Renal Tubular↗