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Biomedical subjects

Josef Finsterer

Publications and source records attributed to Josef Finsterer.

At least 37 records · Page 2Linked to original sources
PubMed2003

Increased CSF protein in chloroquine-induced axonal polyneuropathy and myopathy.

OBJECTIVES: Few data are available about myopathy and polyneuropathy as rare side effects of chloroquine treatment. Even more rarely are cerebrospinal fluid (CSF) abnormalities in chloroquine polyneuropathy/myopathy. CASE DESCRIPTION: The patient is an 81-year-old woman with a 30-year history of chronic polyarthritis. As a basic therapy, she received chloroquine (250 mg per day) since 1997. Already, 1 year later she developed slowly progressive gait disturbance, which led to recurrent falls, and forced her to use crutches and other orthotic devices. Since March 2001, she was no longer able to climb stairs. Since then she also developed sensory disturbances in both lower limbs. Clinical neurological investigation revealed weakness and wasting of all four limbs and reduced tendon reflexes and stocking-type sensory disturbances. Nerve conduction studies were indicative of an axonal polyneuropathy. Electromyography was non-specifically abnormal. Muscle biopsy of the gastrocnemius muscle disclosed neuropathic and myopathic features and frequent fibers with partially rimmed vacuoles, containing concentrically or parallelly sliced inclusions. CSF investigations disclosed increased protein but otherwise normal findings. Five months after discontinuation of chloroquine and replacement by leflunomid, there was marked clinical improvement. CONCLUSIONS: Chloroquine polyneuropathy/myopathy may go along with increased CSF protein. Discontinuation of the causative agent results in prompt recovery of the described abnormalities.

Aged↗
PubMed2003

Quantification of concentric-needle-induced insertional activity by turn/amplitude analysis.

Quantification of needle-induced insertional activity (IA) by means of the turn/amplitude analysis (TAA) has not been attempted so far. IA was recorded from the right brachial biceps and right anterior tibial muscle of 29 healthy subjects, 17 woman, 12 men, aged 24-79 years and 51 patients with neuromuscular disorders (29 neuropathies and 22 myopathies), 24 woman, 27 men, aged 17-81 years. IA was analyzed with regard to IA duration (IAD), turns/second (T/S), amplitude/turn (A/T), T/S:IAD and A/T:IAD. IAD was not significantly different between healthy and diseased subjects in either of the two investigated muscles. On the contrary, T/S, A/T, T/S:IAD and A/T:IAD were significantly increased in the brachial biceps and anterior tibial muscle of patients with neuropathies. In myopathies T/S were increased in both muscles and the T/S:IAD in the anterior tibial muscle. Quantification of IA by TAA increases the sensitivity of conventional EMG from 38 to 69% in neuropathies and from 41 to 73% in myopathies. It is concluded that quantification of IA by TAA is of diagnostic support in the detection of neuromuscular disorders. The most useful parameter in this respect is the T/S, which, contrary to IAD, is increased in patients with neuropathies as well as patients with myopathies.

Action Potentials↗
PubMed2003

Reproducibility of the lactate stress test.

Although the lactate stress test has been shown to be a powerful tool to screen for respiratory chain disorders, little is known about the reproducibility of this test. The aim of the present study was thus to look for the reliability of the lactate stress test in disease controls and patients with primary respiratory chain disorders. In 23 patients with respiratory chain disorder, 16 women and 7 men, aged 36-81 years, and 18 disease controls, 5 women and 18 men, aged 37-70 years, the lactate stress test was carried out when respiratory chain disorder was suspected for the first time and at the first follow-up. The sensitivity of the first lactate stress test was 81% and the specificity 72%. The sensitivity of the second lactate stress test was 74% and the specificity 61%. The reproducibility of the lactate stress test was 65% in patients with respiratory chain disorders and 78% in disease controls. In conclusion, this study shows that the sensitivity, specificity, and reproducibility of the lactate stress test is high enough to warrant its application as a reliable, supplementary method to search for respiratory chain disorders.

Adult↗
PubMed2003

Long lasting impaired cerebral blood flow after ecstasy intoxication.

Four hours after having taken 10 ecstasy tablets a Grand Mal seizure occurred in a 19-year-old woman followed by coma, hyperthermia, tachycardia, tachypnea, and renal failure. After awakening she was oriented but presented with helplessness, disconcertion, hallucinations, panic attacks, and amnesic syndrome. Computed tomography and magnetic resonance imaging scans of the brain were normal. [99Tc]-hexamethylpropyleneamine oxime (HMPAO)-single photon emission computed tomography (SPECT), 20 days after intoxication, showed reduced, inhomogeneous, supratentorial tracer uptake bilaterally. Electroencephalography (EEG) disclosed diffuse slowing and occasionally generalized sharp waves. Valproic acid was begun. Except for slight amnesia, neuropsychological deficits had disappeared and [99Tc]-HMPAO-SPECT normalized, 29 days later. Decreased cortical blood flow was explained by vasoconstriction following ecstasy-induced depletion of serotonin.

Adult↗
PubMed2003

Thrombocytosis under ciprofloxacin and tazobactam/piperacillin.

Whether the simultaneous administration of ciprofloxacin or tazobactam/piperacillin increases the risk of thrombocytosis is unknown. Broncho-pulmonary infection in a 50-year-old male with acute, hypertensive, intracerebral bleeding, necessitated therapy with cefpirome (2 g/day, 6 days), ciprofloxacin (800 mg/d, 11 days) and tazobactam/piperacillin (9 g/day, 11 days). Starting with the 8th hospital day, the thrombocyte count steadily increased from 410000/microl to a maximum of 1132000/microl on hospital day 16. Afterwards the thrombocyte count continuously decreased to normal values. Primary thrombocytosis and secondary causes were excluded. Since the thrombocyte count started to increase immediately after initiation and dropped immediately after discontinuation of ciprofloxacin and tazobactam/piperacillin and all other drugs were discontinued already before or were started after the nadir of the thrombocyte count, these two antibiotics were regarded causative. It is concluded that simultaneous administration of ciprofloxacin and tazobactam/piperacillin may cause marked thrombocytosis. Discontinuation of these two antibiotics results in an immediate decline of the thrombocyte count to normal values within three weeks.

Anti-Bacterial Agents↗
PubMed2003

Favorable outcome of long-lasting thoracic spondylodiscitis with spinal epidural abscess induced by Staphylococcus aureus.

A favorable outcome in chronic spondylodiscitis with epidural abscess is rare. A 65-year-old woman developed recurrent, localized, thoracic back pain over 2.5 years. Nine months after the onset of the pain, sensory disturbances of the left lower leg occurred. Fourteen months before admission, she developed recurrent fever, bladder dysfunction, and weakness and numbness of both lower legs. An incomplete sensory transverse syndrome with paraparesis was diagnosed. Magnetic resonance imaging of the spine suggested destruction of the T11 vertebral body, with spondylodiscitis of the adjacent discs and an epidural abscess between levels T4 and T9. Laminectomy was immediately performed and the abscess was drained. Culture revealed infection with Staphylococcus aureus. After 10 weeks of therapy, recovery was almost complete. Spondylodiscitis with epidural abscess may have a favorable outcome, even if symptoms start more than 2 years before treatment.

Abscess↗
PubMed2003

Reflux esophagitis in the pathogenesis of paroxysmal atrial fibrillation: results of a pilot study.

BACKGROUND: We sought to assess whether proton pump inhibitor (PPI) therapy of gastroesophageal reflux disease (GERD) in patients with lone paroxysmal atrial fibrillation (PAF) leads to a reduction of PAF-related symptoms. METHODS: The records of patients with reflux esophagitis were screened for the diagnosis of lone PAF. All patients with reflux esophagitis and lone PAF were invited for a follow-up visit, at which PAF- and GERD-related symptoms, medication, and electrocardiogram were recorded. RESULTS: Among 89 patients, 18 (6 women, aged 39-69 years) had lone PAF. Decrease or disappearance of at least one PAF-related symptom occurred in 14 of 18 patients (78%) after PPI therapy. In two of the remaining four patients, GERD-related symptoms persisted. Antiarrhythmic drugs were discontinued in five patients, and none had to be increased in dosage or newly prescribed. The electrocardiogram showed sinus rhythm in all patients. CONCLUSION: In lone PAF, GERD should be investigated as a potential pathogenetic mechanism. PPI therapy reduces not only GERD-related but also PAF-related symptoms.

Adult↗
PubMed2003

Ischemic stroke and splenic rupture in a case of Streptococcus bovis endocarditis.

A 58-year-old man with an acute stroke suffered from splenic rupture. Streptococcus bovis was found in blood cultures, and gram-negative cocci were found in the infarcted spleen. Hemorrhagic transformation of the stroke occurred. Echocardiography showed aortic endocarditis. Cardiac surgery was not performed because of concern about cerebral bleeding. The patient died due to cerebral rehemorrhage after 3 weeks.

Blood↗
PubMed2003

The heart in human dystrophinopathies.

Dystrophinopathies are due to mutations in the dystrophin gene on chromosome Xp21.1 and comprise the allelic entities Duchenne muscular dystrophy (DMD), Becker muscular dystrophy (BMD) and X-linked dilative cardiomyopathy (XLDCM). In all three entities, the heart is affected to various degrees, depending on the stage of the disease and the type of the mutation (cardiac involvement, CI). The pathoanatomic evidence of CI in dystrophinopathies is the replacement of myocardium by connective tissue or fat. In DMD/BMD, the left ventricular posterobasal and lateral walls are most extensively affected, sparing the right ventricle and the atrium. Degree and dynamics of CI vary among the three entities. In DMD/BMD, CI usually remains subclinical in the early stages of the disease. Typical initial manifestations of CI in DMD/BMD are sinus tachycardia, tall R1 in V1, prominent Q in I, aVL, V6 or in II, III, and aVF, increased QT dispersion and possibly autonomic dysfunction. Initially, echocardiography is normal or shows regional wall motion abnormalities in areas of fibrosis. With spreading of fibrosis, left ventricular dysfunction and ventricular arrhythmias additionally occur. In the final stages of the disease, systolic function may lead to heart failure and sudden death. Subclinical or clinical CI is present in about 90% of the DMD/BMD patients but is the cause of death in only 20% of the DMD and 50% of the BMD patients. XLDCM is a rapidly progressive, almost exclusively myocardial disorder, starting in teenage males as heart failure due to dilative cardiomyopathy (CMP), leading to death from intractable heart failure within 1-2 years after diagnosis. Therapy of arrhythmias and CMP in all three disorders follows the established cardiological recommendations. Due to its protective effect, ACE inhibitors are recommended already at the early stages of the disease. Beta-blockers may be an additional option if indicated.

Atrial Natriuretic Factor↗
PubMed2003

Primary and secondary stroke prevention in nonrheumatic atrial fibrillation by oral anticoagulation.

The risk of stroke or embolism in atrial fibrillation (AF) patients can be reduced by 68% by oral anticoagulation (OAC). This review is aimed to (1) summarize indications for OAC in patients with AF, (2) give an overview of the current knowledge of risk factors for bleeding complications of OAC and (3) give practical recommendations for an optimal OAC therapy in the neurological setting. Indications for OAC are increased age (>75 years), arterial hypertension, diabetes mellitus, previous thromboembolism, heart failure and, probably, coronary heart disease. Risk factors for bleeding complications are overanticoagulation with international normalized ratios (INRs) >3.0, increased age, arterial hypertension, diabetes mellitus, previous thromboembolism, polypharmacy, the early phase of OAC therapy and a lack of patients' education. Before initiation of OAC, the patient should be screened for potential bleeding sites. Careful monitoring of OAC comprises fixed appointments for the INR value determination, tracking for the patient, if he does not attend, advices about pain therapy, information about the influence of diet on the INR value and drug interaction, unscheduled INR determination in case of acute disorders and regular assessment if OAC is still indicated. Monitoring of OAC needs an effort, which has to be adequately estimated by the health care system.

Administration, Oral↗
PubMed2003

Elimination of the left atrial appendage to prevent stroke or embolism? Anatomic, physiologic, and pathophysiologic considerations.

The "elimination" of the left atrial appendage (LAA) seems to be an attractive alternative to oral anticoagulation in the treatment of atrial fibrillation, especially in patients with contraindications to oral anticoagulation therapy. The LAA, however, plays an important role in the maintenance and regulation of the cardiac function, in arterial hypertension, atrial fibrillation, coronary heart disease, valvular heart disease, and heart failure. Data, mainly from animal studies, indicate that elimination of the LAA may impede thirst in patients with hypovolemia, may impair hemodynamic response to volume or pressure overload, may decrease cardiac output, and may promote heart failure. It may have adverse effects in humans as well. Further studies on the hemodynamic and neurohumoral consequences of left atrial appendage elimination are required to advance our understanding of LAA physiology and pathophysiology.

Aged↗
PubMed2003

Non-compaction on echocardiography and autopsy.

In an 80-year old woman with chronic heart failure due to cardiomyopathy, left ventricular non-compaction, also termed left ventricular hypertrabeculation, in the apex, the lateral wall, the posterior wall and proximally to the papillary muscles was diagnosed on echocardiography, two days before decease. Autopsy three days after echocardiography revealed thin and thick, red and white threads closely interwoven to an irregular meshwork. Echocardiography correctly localised non-compaction, but did not detect the fine meshwork and could not differentiate between the compacted and non-compacted layer of the myocardium. Cardiomyopathy was attributed to cardiac involvement in metabolic myopathy, retrospectively diagnosed upon the clinical presentation, recurrent creatine-kinase elevation, lactacidosis, and the presence of non-compaction, frequently associated with neuromuscular disorders.

Aged↗
PubMed2003

Oral anticoagulation for ECG tremor artefact simulating atrial fibrillation.

That tremor simulates atrial fibrillation and causes oral anticoagulation has not been reported. In a 69-year-old patient with diabetes, arterial hypertension and recurrent strokes, hand tremor developed since 1998. In September 2000 atrial fibrillation was diagnosed upon a routine and 24-hour ambulatory ECG. Because of the additional risk factors for stroke/embolism, phenprocoumon was begun. The diagnosis was changed to paroxysmal AF upon the following ECGs, showing sinus rhythm. Not earlier than 1 year after establishing the diagnosis,"atrial fibrillation" was identified as being due to a tremor artefact. Phenprocoumon was discontinued. Neurological investigations revealed Parkinson's disease as the cause of the tremor. Three weeks after initiation of pramipexol, the tremor artefact was no longer visible on ECG. Misinterpreting an ECG-artefact due to Parkinsons's tremor as atrial fibrillation may be followed by unnecessary diagnostic and therapeutic procedures, including long-term oral anticoagulation. Upon adequate treatment of Parkinson's disease, the tremor artefact immediately disappears from the ECG.

Aged↗
PubMed2003

Antineutrophil cytoplasmic autoantibody-negative antiproteinase 3 syndrome presenting as vasculitis, endocarditis, polyneuropathy and Dupuytren's contracture.

Antiproteinase 3 antibodies (antiPR3) are assumed to be subtypes of antineutrophil cytoplasmic autoantibodies (ANCA), with a high specificity for active Wegener's granulomatosis and microscopic polyangiitis. Thus, antiPR3 positivity in ELISA, together with negativity in indirect immunofluorescence (IIF) is a rare finding. A 56-year-old man with Dupuytren's contracture and polyneuropathy was admitted for leukocytoclastic vasculitis. Echocardiography, performed because of fever and dyspnea, detected aortic valve endocarditis. Because of severe aortic insufficiency the valve was replaced. Blood cultures and bacteriologic investigations of the explanted valve were negative. AntiPR3 were elevated (123-163 U/ml; normal <6 U/ml), together with negativity in IIF. This case shows that antiPR3 elevation with negative ANCA may be associated with vasculitis, endocarditis, polyneuropathy and Dupuytren's contracture. A causal relationship between the clinical presentation and antiPR3 elevation is likely. In order not to miss such cases of vasculitis, combined screening by IIF and ELISA is recommended in selected cases.

Antibodies, Antineutrophil Cytoplasmic↗