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Biomedical subjects

Josef Finsterer

Publications and source records attributed to Josef Finsterer.

At least 19 recordsLinked to original sources
PubMed2003

Ptosis: causes, presentation, and management.

Drooping of the upper eyelid (upper eyelid ptosis) may be minimal (1-2 mm), moderate (3-4 mm), or severe (>4 mm), covering the pupil entirely. Ptosis can affect one or both eyes. Ptosis can be present at birth (congenital) or develop later in life (acquired). Ptosis may be due to a myogenic, neurogenic, aponeurotic, mechanical or traumatic cause. Usually, ptosis occurs isolated, but may be associated with various other conditions, like immunological, degenerative, or hereditary disorders, tumors, or infections. Besides drooping, patients with ptosis complain about tired appearance, blurred vision, and increased tearing. Patients with significant ptosis may need to tilt their head back into a chin-up position, lift their eyelid with a finger, or raise their eyebrows. Continuous activation of the forehead and scalp muscles may additionally cause tension headache and eyestrain. If congenital ptosis is not corrected, amblyopia, leading to permanently poor vision, may develop. Patients with ptosis should be investigated clinically by an ophthalmologist and neurologist, for blood tests, X-rays, and CT/MRI scans of the brain, orbita, and thorax. Treatment of ptosis depends on age, etiology, whether one or both eyelids are involved, the severity of ptosis, the levator function, and presence of additional ophthalmologic or neurologic abnormalities. Generally, treatment of ptosis comprises a watch-and-wait policy, prosthesis, medication, or surgery. For minimal ptosis, Müller's muscle conjunctival resection or the Fasanella Servat procedure are proposed. For moderate ptosis with a levator function of 5-10 mm, shortening of the levator palpebrae or levator muscle advancement are proposed. For severe ptosis with a levator function <5 mm, a brow/frontalis suspension is indicated. Risks of ptosis surgery infrequently include infection, bleeding, over- or undercorrection, and reduced vision. Immediately after surgery, there may be temporary difficulties in completely closing the eye. Although improvement of the lid height is usually achieved, the eyelids may not appear perfectly symmetrical. In rare cases, full eyelid movement does not return. In some cases, more than one operation is required.

Blepharoplasty↗
PubMed2003

Familial left ventricular hypertrabeculation in myotonic dystrophy type 1.

BACKGROUND: Familial left ventricular hypertrabeculation (LVHT)has not been described in myotonic dystrophy type 1 (MD1). CASE REPORT: Two MD1 patients are described, father and daughter, both presenting with LVHT. The father was a 45-year-old man with the typical MD1 phenotype starting in 1992. DNA analysis revealed a heterozygous expansion of 300 CTG repeats in the myotonic dystrophy protein kinase (DMPK) gene on chromosome 19q13.3. He had a history of successful electrocardioversion of atrial flutter into sinus rhythm. Cardiac history and clinical cardiologic examination were otherwise normal. On ECG, ST elevation was found exclusively. Transthoracic echocardiography revealed LVHT, previously described only in Becker's muscular dystrophy, metabolic myopathy, Barth syndrome, and other rare genetic disorders. In the 13-year-old daughter, occasional muscle cramps since 1998, discrete weakness of the left triceps brachii muscle, and discrete distal wasting of the upper limbs were found. Serum creatine kinase (CK) and electromyography were normal. The daughter carried an expansion of 140 CTG repeats in the DMPK gene. Clinical cardiologic examination as well as the ECG were normal. Echocardiography revealed LVHT,which was also confirmed by cardiac MRI. Neither the father nor the daughter required any cardiac medication. CONCLUSION: This study demonstrates that LVHT in MD1 may bea cardiac manifestation of the underlying skeletal muscle disorder, may show a familial occurrence, or may be associated with other cardiac abnormalities or isolated.

Adolescent↗
PubMed2003

Influence of tiapride on platelet counts in healthy volunteers and patients with movement disorders.

BACKGROUND: The selective D2 antagonist tiapride is administered in various movement disorders. Furthermore, there are indications that tiapride increases platelet counts. AIM: To characterize tiapride's potential to increase platelet counts in healthy subjects and patients with movement disorders. METHODS: In Part A, 10 healthy volunteers received tiapride (300 mg/day) for 21 days in a longitudinal, prospective, open trial. One hundred healthy subjects served as controls. Part B was a retrospective analysis of 15 patients with movement disorders on tiapride [Huntington's disease (n=6), Morbus Little (n=3), hyperkinetic syndromes of undetermined etiology (n=3), blepharospasm (n=1), cervical dystonia (n=1), perioral dyskinesia (n=1)] and 15 age- and sex-matched controls. RESULTS: Part A: Although serum prolactin levels increased by 526+/-14%, confirming good drug compliance, tiapride elicited only minor changes in platelet counts. Part B: Platelet counts correlated positively with the dose of tiapride (100-800 mg/day; r=.67; P=.007). Platelet counts were significantly higher in patients on tiapride compared to healthy age-matched controls (P<.001). Four patients responded to an increase in the tiapride dosage with an increase in platelet count by 97-173 cells/nl. CONCLUSION: Three weeks of treatment with tiapride (300 mg/day) is insufficient to elevate platelet counts to a clinically relevant extent in young healthy volunteers. However, in elderly patients with movement disorders tiapride treatment is associated with markedly increased platelet counts.

Administration, Oral↗
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

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

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↗