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Biomedical subjects

K Ricker

Publications and source records attributed to K Ricker.

At least 73 records · Page 4Linked to original sources
PubMed1984

The stiff-man syndrome: new pathophysiological aspects from abnormal exteroceptive reflexes and the response to clomipramine, clonidine, and tizanidine.

Neurophysiological investigations of a patient suffering from the stiff-man syndrome revealed that exteroceptive reflexes, in particular those elicited from the skin, were excessively enhanced. In contrast, no abnormalities were found within the monosynaptic reflex arc. Clomipramine injection severely aggravated the clinical symptoms whereas diazepam, clonidine, and tizanidine decreased both muscular stiffness and abnormal exteroceptive reflexes. The hypothesis is put forward that the stiff-man syndrome is a disorder of descending brain-stem systems which exert a net inhibitory control on axial and limb girdle muscle tone as well as on exteroceptive reflex transmission. Detection of abnormal exteroceptive reflex activity in conjunction with neuropharmacological testing might help in the diagnosis of this rare disease.

Adult↗
PubMed1983

Two cases of adynamia episodica hereditaria: in vitro investigation of muscle cell membrane and contraction parameters.

Membrane potentials, current-voltage relationships, and contractile parameters were studied in intact muscle cell bundles obtained from two patients with adynamia episodica hereditaria. In a normal extracellular medium, the cell membranes had resting potentials of about -80 mV and their current-voltage relationships were not significantly different from control curves. In contrast to normal muscles the afflicted cells were paralyzed in a medium having 6-10 mmol/liter potassium. The mechanisms of paralysis in the two specimens were different from each other. Many fibers from one patient were spontaneously active even in normal solution. In high potassium solution spontaneous activity was increased and the cells gradually depolarized to values at which excitatory sodium current is normally inactivated. This depolarization was connected with an increased sodium conductance and was reversed by the application of tetrodotoxin (TTX). The fibers from the other patient were not spontaneously active. In high potassium solution they were paralyzed at membrane potential values at which normal fibers would still contract. The reason for this paralysis was a reduced excitability.

Adolescent↗
PubMed1983

Different effectiveness of tocainide and hydrochlorothiazide in paramyotonia congenita with hyperkalemic episodic paralysis.

We investigated the effectiveness of tocainide and hydrochlorothiazide on muscular symptoms in a patient with paramyotonia congenita and episodic attacks of hyperkalemic paralysis. Generalized weakness was evoked by exercise and potassium loading. Myotonia and weakness were evoked by local muscle cooling. Tocainide prevented myotonia and weakness induced by cooling, but failed to prevent hyperkalemic weakness. Hydrochlorothiazide prevented hyperkalemic weakness, but did not influence symptoms evoked by cooling. These results suggest that, in this disorder, two different mechanisms cause muscular weakness.

Adult↗
PubMed1983

A dominantly inherited myopathy with excessive tubular aggregates.

We studied a family in which seven individuals in three generations had slowly progressive weakness without atrophy, myalgia, cramps, or episodic weakness. Creatine kinase was normal, and EMG showed only slight "myopathic" changes. Neuromuscular transmission was undisturbed. Muscle biopsies were performed in three patients. About 60 to 90% of all fibers contained tubular aggregates. There was a marked variation in fiber size and a marked type II fiber atrophy. Biopsy of an asymptomatic family member was normal. The nature of the underlying disease was obscure.

Adult↗
PubMed1981

Somatosensory cerebral evoked potentials in spinal cord diseases.

Cortical-evoked potentials (CEPs) induced by the stimulation of the tibial nerve, were investigated in 16 patients with localized myelopathy, and in five patients with generalised myelopathy, and compared with the results obtained in 30 healthy test subjects. The investigations show that the pulses that give rise to the CEP, are conducted mainly by the posterior columns. Damage to the ventrolateral tracts, in contrast, leads only to a reduction in the amplitude of the CEPs. If account is taken of possible artefacts and misinterpretations, the method described is highly suitable for determining the level of a lesion in complete paraplegia and for obtaining information as to the size and extent of spinal cord damage in myelopathies.

Adolescent↗
PubMed1981

Thyroid function and circulating antithyroid antibodies in myasthenia gravis.

Evaluation of thyroid function in 104 patients with myasthenia gravis by T3, T4, TBG, and TSH radioimmunoassays and the TRH-stimulation test in 47 patients disclosed thyrotoxicosis in 5.7%, preclinical hyperthyroidism probably due to autonomously functioning thyroid tissue in about 10% of patients stimulated with TRH, hypothyroidism in 1.9%, and preclinical hypothyroidism in 3.4%. Eighty-four percent were euthyroid. Antithyroid antibody activity was detected by hemagglutination tests. Twelve patients had antithyroglobulin antibodies (Tab), and 28 had antimicrosomal antibodies (Mab). Among the euthyroid myasthenic patients, 7 were Tab-positive and 20 were Mab-positive. Euthyroid antibody-positive patients had a significantly higher TSH response in the TRH stimulation test and may be at high risk for hypothyroidism.

Adolescent↗
PubMed1981

[T3, T4, TSH and circulating antithyroglobulin antibodies in myasthenia gravis].

Myasthenia gravis (MG) is a rare neuromuscular disease which is known to be associated with hyperthyroidism at high frequency (3-10%). These investigations, however, are basing on studies of the basal metabolic rate, protein bound iodine (PBI) and the thyroidal radioiodine uptake. In our study (104 MG patients, 104 control subjects) we wanted to evaluate thyroid function on the basis of T3, T4, TBG and TSH radioimmunoassays and in addition we looked for the presence of circulating antithyroglobulin antibodies (Tab) and antimicrosomal antibodies (Mab). The following thyroidal states were disclosed: Thyrotoxicosis (5.8%), hypothyroidism (1.9%), preclinical hypothyroidism (3.8%) and euthyroidism (88.5%). Twenty-eight myasthenic patients were Mab-positive and twelve in addition Tab-positive. Comparing the twenty euthyroid antibody-positive MG-patients with euthyroid antibody-negatives no statistically significant differences were found in thyroid function parameters. It is discussed that part of the thyroid antibody-positive patients may have a symptomless autoimmune thyroiditis which is finally resulting in hypothyroidism via a preclinical hypothyroid status.

Adolescent↗
PubMed1979

Influence of temperature on isometric contraction and passive muscular tension in paramyotonia congenita (Eulenburg).

Four patients without symptoms of episodic hyperkalemic weakness from two families with paramyotonia congenita (Eulenburg) are described. 1. Maximum voluntary muscle contraction of the upper and lower arm was studied under isometric conditions at different temperatures. If the temperature was lowered stepwise, distinct paresis occured at 32--31 degrees C which increased with the amount of muscular effort. The upper arm muscles, however, developed weakness gradually after cooling. 2. During cooling of the resting muscle, the EMG showed dense spontaneous activity of the fibrillary type, which decreased again at about 30 degrees C. It can be assumed that in paramyotonia congenita cooling produces muscle cell membrane depolarization which at a critical level causes the firing of action potentials and finally muscular paresis. 3. Increasing muscular stiffness can be interpreted as abnormally slow muscular relaxation after isometric contraction. In the forearm muscles the time to 3/4 relaxation after cooling was about six times normal, in the upper arm muscles only two times normal. As an additional parameter the mechanical resistance to passive stretching of a muscle has been studied. This passive muscular tension increased simultaneously with the onset of weakness. 4. The close relation between weakness and stiffness suggest that both symptoms are caused by the same basic defect which is probably located in the sarcolemma. It is suggested that a defect of the sodium channel causes a cooling-dependent increase in sodium conductance. Raised intracellular sodium causes in the first place membrane depolarization, and in the second place depression of calcium reuptake through competition by sodium for calcium binding sites. This would explain muscle stiffness and delayed relaxation as well.

Arm↗
PubMed1979

[Basic conditions for electromyographic examination. Part I: EMG, nerve conduction velocity and test of motor end-plate function (author's transl)].

The purpose of the following contribution is to give a survey about the basic conditions of electromyographic examination. The necessary apparatus will be described as well as the course of examination. Moreover the parameter for the evaluation will be explained together with exogenous falsifying influences. This contribution is thought to be a guide for orientation to improve electromyographic recording and evaluation.

Electric Stimulation↗
PubMed1978

Fenoterol precipitating myotonia in a minimally affected case of recessive myotonia congenita.

Fenoterol is used in patients with premature labor to delay delivery. A young women treated with fenoterol developed severe generalized myotonia. Symptoms disappeared after medication had been stopped. In a later study myotonic discharges were found electromyographically in the muscles of the patient and her brother. Both suffered from subclinical recessive myotonia congenita (Becker). A heterozygous manifestation may be supposed.

Adult↗
PubMed1978

Transient muscular weakness in severe recessive myotonia congenita. Improvement of isometric muscle force by drugs relieving myotomic stiffness.

The maximum force of voluntary muscle contraction was registered under isometric conditions in nine patients with recessive myotonia congenita. The recordings were made on the upper arm. Five patients with severe myotonia had a transient weakness after muscle rest. Electromyographic registrations with wire electrodes showed that the myotonic muscle fiber discharges disappeared during the transient weakness. Medication improving myotonic stiffness also improved the weakness. The cause of transient weakness seems to be similar to that of myotonic stiffness. It is known that an increasing depolarization of the myotonic muscle fiber membrane leads to the myotonic discharges and myotonic stiffness. In severe myotonia the progressing depolarization could cause a loss of excitability of the muscle fiber membrane and thereby a transient paresis of a more or less large number of muscle fibers.

Adult↗
PubMed1977

The influence of local cooling on neuromuscular transmission in the myasthenic syndrome of Eaton and Lambert.

The effect of local cooling was studied in two patients with the Eaton-Lambert syndrome. We stimulated the ulnar nerve and registered the compound muscle action potential, the twitch force, and the maximum tetanic force. A distinct improvement of neuromuscular transmission occurred after cooling. The amplitude of the muscle action potential and the twitch force were larger and the time of the postactivation facilitation was longer. This effect of cooling is similar to the effect of guanidine on neuromuscular transmission. The release of acetylcholine at the nerve terminal is probably enhanced by cooling.

Aged↗
PubMed1977

Influence of temperature on neuromuscular transmission in myasthenia gravis.

The effect of local cooling was studied in 28 patients with myastenia gravis. We stimulated the ulnar nerve with single stimuli and trains at 3/s for 2s and at 50/s for 1.5 s. The compound muscle action potential (MAP), the muscle twitch and the isometric tetanic force of the adductor pollicis were registered. 1. At 3/s stimulation the pathological decrement of the MAP decreased after slight cooling. 2. The amplitude of the single MAP was higher at lower temperature when compared to normal temperature. The same increase is however to be found in healthy subjects. 3. After slight cooling, the maximum tetanic force was higher. However, the decrement of the force was higher also, therefore ruling out a practicable application of cooling for the patient. 4. After severe cooling (18-22 degrees C) the tetanic force was much lower and in many cases a complete failure of the neuromuscular transmission occured.

Action Potentials↗