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Biomedical subjects

A Ferbert

Publications and source records attributed to A Ferbert.

At least 37 records · Page 2Linked to original sources
PubMed1998

Safety, pharmacokinetics and biological activity of enlimomab (anti-ICAM-1 antibody): an open-label, dose escalation study in patients hospitalized for acute stroke.

BACKGROUND AND PURPOSE: To obtain information on the safety, pharmacokinetics and biological activity of enlimomab (anti-ICAM-1 antibody) in stroke patients. METHODS: An open, uncontrolled, dose titration study was conducted in 32 patients hospitalized for stroke. Patients received one of four fixed dose regimens of enlimomab. A loading dose of enlimomab administered within 24 h of the onset of stroke symptoms was followed by four daily maintenance doses; total doses ranged from 140 to 480 mg. RESULTS: The pharmacokinetic target levels (enlimomab serum levels of >/=10 microg/ml) were consistently achieved in all patients receiving dose regimens III and IV. Non-serious adverse events thought to be causally related to enlimomab administration included headache, vomiting and extrasystoles. Serious events occurred in 14 patients, including pneumonia, sepsis, cardiac failure and cardiac arrest. The only serious adverse event considered to be related to enlimomab administration was an anaphylactoid reaction, in a patient who received an unfiltered loading dose of antibody; the patient recovered. The overall mortality in the study was 15.6% and the 30-day mortality was 12.5%. There was no increase in the frequency of adverse events with increasing doses of enlimomab. CONCLUSIONS: Doses of enlimomab between 140 and 480 mg administered over 5 days did not increase the risk of adverse events in patients with ischaemic or haemorrhagic stroke during an observation period of 30 +/- 10 days. A loading dose of 160 mg followed by four daily maintenance doses of 40 mg appears to be suitable for further study.

Acute Disease↗
PubMed1998

Cortical representation of proximal and distal arm muscles as assessed by focal transcranial magnetic stimulation.

In 21 healthy volunteers, a mapping of cortical areas from which motor evoked potentials in deltoid muscle and first dorsal interosseal muscle (FDI) could be elicited by focal transcranial magnetic stimulation was performed. For this purpose, magnetic stimuli were applied using a figure-of-eight shaped magnetic coil and a Magstim 200 stimulator at an intensity of 15% above motor threshold for the deltoid muscle. There was a considerable overlap between the cortical areas from which motor responses of the two muscles could be evoked with the FDI represented more laterally than the deltoid muscle. The cortical location from which maximal amplitudes of motor evoked potentials were elicited was 4-8 cm lateral of Cz with the FDI and 2-6 cm lateral of Cz with the deltoid muscle. Calculated centres of cortical points with maximal muscle responses were significantly separated with the FDI represented 5.7 cm lateral of Cz and deltoid muscle 4.3 cm lateral of Cz. The anterior-posterior extension of the cortical maps did not show significant differences between the proximal and distal arm muscle. In no subject an ipsilateral representation of either muscle could be found even when stimulating at maximal intensity.

Adult↗
PubMed1997

Transcranial magnetic double stimulation: influence of the intensity of the conditioning stimulus.

The influence of stimulus parameters on compound muscle potentials evoked by transcranial magnetic double stimulation was systematically investigated. Two magnetic stimulators were discharged via a figure-of-eight-shaped magnetic coil (outer diameter of each circular coil, 7 cm) over the left hemisphere, 6 cm lateral to Cz, using a Bistim interface. Recordings were made from the right first dorsal interosseus muscle. In experiment I, in 12 healthy volunteers the intensity of the conditioning subthreshold stimulus was varied from 0 to 100% of the relaxed motor threshold at an interstimulus interval of 1 ms. In experiment II, interstimulus intervals of 1, 3 and 5 ms were used to investigate the effect of conditioning stimuli of 3 fixed intensities. Maximal reduction of the amplitude of motor evoked potentials was found at a conditioning stimulus intensity of 65% of the relaxed motor threshold (and at an interstimulus interval of 1 ms). Because intensities of the conditioning stimulus higher than 65% reduced amplitudes of motor evoked potentials less effectively than at this intensity, refractoriness of pyramidal neurons can be ruled out as the main mechanism contributing to the observed inhibition. Activation of inhibitory interneurons by intensities lower than is necessary to activate pyramidal neurons is discussed as a possible mechanism for the inhibitory effects evoked by transcranial magnetic stimulation.

Adaptation, Physiological↗
PubMed1996

[Periodic paralysis as the first manifestation of hyperthyroidism].

HISTORY AND CLINICAL FINDINGS: A 19-year-old man had mild diarrhoea at the time that suddenly one night he was unable to turn in his bed and the following morning could not move his arms and legs for 4 hours. Neither he nor any family members had previously had any paralysis. Physical examination was unremarkable except for mild tachycardia and first-degree goitre. INVESTIGATIONS: A provocation test with glucose (3 g/kg) and insulin (0.1 IU/kg) caused renewed paralysis for several hours, serum potassium falling from 4.3 to 3.4 mmol/l. The paralysis was reversed on oral potassium (40 mmol) Thyroid function tests revealed hyperthyroidism with an increased concentration of free thyroxine (25.5 pg/ml) and free triiodothyronine (9.7 pg/ml), while thyroid-stimulating hormone was decreased (0.07 mU/I), supporting the diagnosis of autoimmune thyroiditis. TREATMENT AND COURSE: Thyrostatic treatment was started with thiamazole (10 mg every other day). There was no further periodic paralysis and another provocation test was negative. CONCLUSION: Fleeting paralysis is often misdiagnosed as being psychogenic. Potassium abnormalities are the most common cause but are only rarely associated with hyperthyroidism. This case of thyrotoxic hypokalaemic paralysis was probably based on a genetic defect of muscle fibre membrane manifesting itself only in the presence of hyperthyroidism.

Adult↗
PubMed1996

[Follow-up and immunologic findings in drug-induced myasthenia].

PATIENT AND METHOD: We report 5 patients, who developed myasthenia, four of them after treatment on D-penicillamine, one after treatment on chloroquine. 3 patients suffered from rheumatoid arthritis, one from a psoriatic arthritis and one from cirrhosis of the liver. Three patients developed an ocular myasthenia, one patient an oculopharyngeal and one patient has had generalized myasthenic syndrome. RESULTS: Four patients showed an improvement of clinical status within days up to 18 months following discontinuation of the therapy, whereas one patient deteriorated. The quickest improvement was observed in the patient with chloroquine induced myasthenia. Four patients had raised acetylcholine-receptor antibody titers. The patient with chloroquine induced myasthenia had had a normal acetylcholin-receptor antibody titer. The human leucocyte antigen type was compared with the results of literature. CONCLUSION: To what extent human leucocyte antigen type HLA DR 4 has a correlation with the development of myasthenia following treatment on chloroquine can not yet be answered with respect to the very small number of cases at the moment.

Aged↗
PubMed1996

Pure stimulus-sensitive truncal myoclonus of propriospinal origin.

The clinical and electrophysiological features of stimulus-sensitive truncal myoclonus are described in a 49-year-old woman. Touching the skin of the back and abdomen would evoke jerks in both ipsilateral and contralateral axial muscles; there was no spontaneous jerking. Multichannel EMG recordings showed bilateral short-latency muscle bursts at truncal recording sites both rostral and caudal to stimulus sites. The short latencies of muscle bursts in adjacent segments give evidence of a spinal origin of myoclonus; the pattern of recruitment and the velocity of spread suggest the involvement of propriospinal pathways. The presence of intrathecal IgG synthesis and of oligoclonal bands in the CSF point towards an inflammatory process which may underly the unusual type of myoclonus in this patient.

Abdominal Muscles↗
PubMed1996

Botulinum toxin in the therapy of gustatory sweating.

Three patients suffering from gustatory sweating following trauma to the preauricular region from a bullet wound or parotid gland surgery were treated by intracutaneous injection of botulinum toxin A. Within 2 weeks, gustatory sweating in the area injected completely ceased in all patients with no side-effects. The efficacy of treatment was confirmed by repeated Minor's iodine starch tests. So far, sweating has not recurred during a follow-up period of up to 8 months. Botulinum toxin appears to be a promising new drug for the treatment of this autonomic disorder.

Adult↗
PubMed1996

Effects of carbamazepine on cortical excitatory and inhibitory phenomena: a study with paired transcranial magnetic stimulation.

The effect of a single dose of oral carbamazepine on cortical facilitatory and inhibitory phenomena was investigated in 13 healthy human subjects by focal transcranial magnetic stimulation. Paired stimulation was performed via a figure-of-eight shaped magnetic coil using two Magstim-200 stimulators and a Bistim-interface at interstimulus intervals of 3, 10, and 17 ms. In addition, the silent period evoked by single focal transcranial stimuli during sustained voluntary muscle contraction was investigated without and with carbamazepine. Recordings of compound muscle action potentials (CMAP) were taken from the left first dorsal interosseus muscle. Carbamazepine significantly reduced the facilitatory effect of conditioning stimuli of 85% of motor threshold at an interstimulus interval of 10 ms on the CMAP-amplitude from 162% to 127%, whereas under all other conditions no significant depression of CMAP-amplitudes occurred. This effect is discussed in the context of carbamazepine's use-dependent inhibition of neuronal high-frequency discharges. The mean relative duration of the silent period was longer with carbamazepine at all 6 stimulus intensities investigated, the absolute effect being very low in relation to the interindividual variability of silent period duration. The study demonstrates the applicability of transcranial magnetic stimulation as an in vivo method in the assessment of drug effects on cortical facilitatory as well as inhibitory phenomena.

Adult↗
PubMed1996

Transcallosal inhibition in cortical and subcortical cerebral vascular lesions.

The excitability of the motor cortex after transcranial magnetic stimulation was investigated in 10 patients with purely subcortical, and in 22 patients with cortical-subcortical cerebrovascular lesions. In the first investigation we applied magnetic double stimuli over both motor cortices with different inter-stimulus intervals. The first (conditioning) stimulus was applied to the affected hemisphere and the second stimulus (test stimulus) to the unaffected side. The responses of the first dorsal interosseal (FDI) muscle, contralateral to the test stimulus, were recorded after applying the test stimulus alone and at inter-stimulus intervals of 5 ms, 7 ms, 15 ms, 30 ms and 60 ms. In a second investigation the patients were asked to activate their non-paretic first dorsal interosseus muscle and the magnetic stimulus was applied over the affected hemisphere. The EMG responses were rectified and averaged. Patients with subcortical cerebral lesions below the centrum semiovale (i.e., having no effect on the transcallosal fibres) displayed a pronounced inhibition of one motor cortex after the stimulation of the contralateral side, comparable with normal subjects. Patients with cortical-subcortical cerebral lesions displayed only partly less inhibition of their motor cortex but the results in this group were not uniform. Since inhibition was preserved in patients with subcortical lesions, which had destroyed the corticospinal tract, we conclude that this inhibition is not mediated through an ipsilateral projection but via a transcallosal route.

Adult↗
PubMed1995

A unique case of tardive dystonia induced by short-term therapy with perazin.

Perazin is a piperazine derivative of phenothiazine with higher affinity for the D2 than the D1 receptor. We observed a 43-year-old woman who developed blepharospasm and oral hyperkinesia as a tardive dystonic syndrome after short-term treatment with perazin. She had never taken any other neuroleptic medication and all known forms of secondary dystonia were ruled out. We were unable to find any previous reports of perazin-induced tardive dystonia.

Adult↗
PubMed1994

[Severe "late" dystonia after neuroleptic anxiolysis with fluspirilene].

The development of severe tardive dystonia after short-term use of low-dose Fluspirilen is described. A 39-year-old woman was treated with Fluspirilen IM by her family doctor for reactive depression. She did received no other neuroleptic agents and no risk factors for the development of tardive dyskinesia (e.g. old age or organic brain damage) were present. For the first time a relation between short-term monotherapy with Fluspirilen and tardive dyskinesia appears highly probable. The use of Fluspirilen for the treatment of psychogenic disturbances should therefore be considered carefully.

Adjustment Disorders↗
PubMed1993

Tremor due to stroke.

We report on four patients with unilateral tremor stemming from cerebrovascular accidents. In two patients with proven lesions of the thalamus, the tremor was irregular and, in addition, there was dystonic posturing of the affected arm. Tremor and dystonic posturing had appeared after the stroke. In the other two patients tremor had occurred immediately at the onset of the stroke and lasted only a few days. The tremors were of small amplitude and high frequency, and lesions could not be found on CT or MRI in these two patients. None of our patients showed signs of the so-called rubral tremor.

Aged↗
PubMed1993

Blink reflex in patients with an ischaemic lesion of the brain-stem verified by MRI.

The electrically elicited blink reflex was investigated in 25 patients with ischaemic lesions of the pons or the medulla oblongata. Only patients with a lesion on MRI appropriate to the clinical syndrome were included. Twenty patients had an infarction of the pons, bilateral in 5. Additional 5 patients had an infarction of the dorsolateral medulla oblongata. Patients with hemispheric lesions were excluded. Four of the 5 patients with Wallenberg's syndrome showed delayed R2 components to stimulation ipsilateral to the lesion. Additional loss of the ipsilateral R1 component was observed in 1 patient. Fifteen of the 20 patients with pontine infarctions had pathological blink reflexes. All 6 patients with a unilateral pons lesion and an abnormality of R1 had this abnormality on the side contralateral to the lesion. In 3 cases with bilateral pontine infarction R1 was abnormal on one side or on either side. Of 11 patients with a normal R1, 6 had isolated abnormalities of R2 without consistent correlation to the side of the lesion. We conclude that abnormalities of the blink reflex are of minor localizing value in pontine infarction. This may be explained by the fact that a pontine infarction affects either the reflex arch itself or descending pathways that have a modulating influence on the reflex arch. Infarctions of the medulla oblongata, however, have characteristic abnormalities that have already been described.

Adult↗
PubMed1993

Simulation of the conduction velocity properties of nerve fibres by an electrical model.

The paper presents a simple electrical circuit model from which the relationship between the diameter of the axon and its conduction velocity can be derived. The model is primarily intended for the larger myelinated fibres in peripheral nerves. However, a simplified model is also shown for nonmyelinated fibres, where the relationship is quite different. In the conclusion some qualitative considerations are presented for thin myelinated fibres with a slow velocity of conduction. The conduction velocity/diameter relationship of these fibres gradually approaches that for nonmyelinated fibres with decreasing diameter.

Axons↗
PubMed1993

Corticocortical inhibition in human motor cortex.

1. In ten normal volunteers, a transcranial magnetic or electric stimulus that was subthreshold for evoking an EMG response in relaxed muscles was used to condition responses evoked by a later, suprathreshold magnetic or electric test shock. In most experiments the test stimulus was given to the lateral part of the motor strip in order to evoke EMG responses in the first dorsal interosseous muscle (FDI). 2. A magnetic conditioning stimulus over the hand area of cortex could suppress responses produced in the relaxed FDI by a suprathreshold magnetic test stimulus at interstimulus intervals of 1-6 ms. At interstimulus intervals of 10 and 15 ms, the test response was facilitated. 3. Using a focal magnetic stimulus we explored the effects of moving the conditioning stimulus to different scalp locations while maintaining the magnetic test coil at one site. If the conditioning coil was moved anterior or posterior to the motor strip there was less suppression of test responses in the FDI. In contrast, stimulation at the vertex could suppress FDI responses by an amount comparable to that seen with stimulation over the hand area. With the positions of the two coils reversed, conditioning stimuli over the hand area suppressed responses evoked in leg muscles by vertex test shocks. 4. The intensity of both conditioning and test shocks influenced the amount of suppression. Small test responses were more readily suppressed than large responses. The best suppression was seen with small conditioning stimuli (0.7-0.9 times motor threshold in relaxed muscle); increasing the intensity to motor threshold or above resulted in less suppression or even facilitation. 5. Two experiments suggested that the suppression was produced by an action on cortical, rather than spinal excitability. First, a magnetic conditioning stimulus over the hand area failed to produce any suppression of responses evoked in active hand muscles by a small (approximately 200 V, 50 microsecond time constant) anodal electric test shock. Second, a vertex conditioning shock had no effect on forearm flexor H reflexes even though responses in the same muscles produced by magnetic cortical test shocks were readily suppressed at appropriate interstimulus intervals. 6. Small anodal electric conditioning stimuli were much less effective in suppressing magnetic test responses than either magnetic or cathodal electric conditioning shocks.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1993

[Clinical course of paraneoplastic limbic encephalitis].

A 49-year-old woman presented with increasing memory loss without dementia. The EEG showed slow activity over the temporal lobe. MRT revealed temporal areas of increased signal intensity without gadolinium enhancement. The diagnosis of limbic encephalitis was made after detection of a bronchial carcinoma. A MRT control examination after chemotherapy showed resolution of the abnormalities. This observation may indicate that chemotherapy has modified that part of the immunological system responsible for induction of limbic encephalitis.

Carcinoma, Bronchogenic↗