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Biomedical subjects

J Gert van Dijk

Publications and source records attributed to J Gert van Dijk.

9 recordsLinked to original sources
PubMed2003

Two approaches to measure amplitude changes of the sensory nerve action potential over a length of nerve.

Changes in amplitude of sensory nerve action potentials (SNAPs) over a length of nerve have not been used for diagnostic purposes. We measured such changes for median and ulnar nerves in 25 healthy subjects in two ways. The multiple-stimulation method involved three stimulation sites (palm, wrist, elbow) and one recording site on a finger. The multiple-recording method involved stimulation at the wrist and simultaneous recording from two adjacent sites on a finger. Percentile changes in amplitude could be measured in all subjects for the median nerve, but not for the ulnar nerve due to submaximal stimulation in the palm. For the median nerve, the multiple-recording method resulted in a mean amplitude change of 79% +/- 13%, whereas comparison of wrist to palm stimulation in the multiple-stimulus method resulted in a change of 73% +/- 10%. These values are high enough to encourage study into practical applications of such methods in detecting peripheral nerve disease.

Action Potentials↗
PubMed2003

Water drinking as a potential treatment for idiopathic exercise-related syncope: a case report.

We report a 20-year-old sportsman with frequent attacks of lightheadedness, chest pain, blurred vision and falls during and shortly after exercise. Cardiac and pulmonal evaluation and routine autonomic function tests were normal apart from a relatively high resting heart rate (70 bpm) compared to endurance-trained men. In view of the relation to exercise, the patient was asked to cycle with maximal effort on an ergometer with continuous blood pressure (BP), heart rate (HR) and electroencephalogram (EEG) registration. Immediately after cessation of exercise a brief hypotensive period (75/45 mmHg) occurred together with sinus tachycardia (180 bpm) during which the patient experienced his typical complaints. We hypothesized that our patient's symptoms were primary related to sympathetic failure. As water drinking has been demonstrated to raise sympathetic activity rapidly, we undertook a second cycling test after ingestion of 1000 mL tap water. Symptoms nor hypotension recurred. Because of the short lasting pressor effect and its minimal side effects, we suggest water drinking as simple and possible effective therapy for idiopathic exercise-related syncope.

Adult↗
PubMed2003

Fainting in animals.

Fainting (syncope) is unconsciousness due to insufficient cerebral circulation in the context of a temporary failure of the systemic circulation. This paper firstly aims to discuss fainting in animals, and secondly to discuss animal physiology to broaden the understanding of human fainting. Of the three major syncope types (cardiac, orthostatic and reflex syncope), only cardiac syncope occurs in animals as in man, through arrhythmia or output failure. Man's orthostatic fainting tendency has been blamed on his upright posture. A comparison with animals shows that giraffes, tree climbing snakes, and animals that quickly raise and lower their heads face more serious gravitational circulatory challenges than man, but do not appear to faint. Merely carrying the brain above the heart does not explain a fainting tendency, as the human heart-to-brain height is smaller than that of many mammals with similar blood pressure. Two evolutionary novelties may be to blame: the proportion of cardiac output going upwards to the brain is much larger than in apes, and man's large legs suggest that the volume lost to venous pooling is also larger. Emotional factors play a role in many reflex syncope events. Tonic immobility ('feigning death','playing possum') is not a good model, as it concerns immobility as a survival strategy of an attentive brain, rather than unconsciousness due to circulatory breakdown. Whether orienting and defense responses form a valid model remains to be proven. Emotional fainting may be uniquely human; how mental processes can shut down the circulation and thereby the brain needs serious study, as it may hold the key to syncope prevention.

Animals↗
PubMed2002

Major and minor form of hereditary hyperekplexia.

Hyperekplexia is a hereditary neurological disorder characterized by excessive startle responses. Within the disorder two clinical forms can be distinguished. The major form is characterized by continuous generalized stiffness in the first year of life and an exaggerated startle reflex, accompanied by temporary generalized stiffness and falls, whereas in the minor form only excessive startle and hypnic jerks have been described. Mutations in the gene encoding the alpha-1 subunit of the glycine receptor (GLRA1) are responsible for the major form of hyperekplexia but no mutation was detected in patients with the minor form in the large Dutch pedigree originally described by Suhren and colleagues. Here we describe the genetic analysis of the GLRA1 gene of two English families in which both forms of hyperekplexia were present. Mutation analysis revealed no genetic defect in the GLRA1 gene in patients carrying either the minor or major forms. This is further evidence that the minor form of hyperekplexia is seldom due to a genetic defect in the GLRA1 gene.

Adolescent↗
PubMed2002

Repetitive nerve stimulation of the nasalis muscle: technique and normal values.

A technique of repetitive nerve stimulation of the facial nerve with recording from the nasalis and orbicularis oculi muscles was developed and tested in 15 healthy subjects. Quality criteria were that the stimulus artifact should return to baseline before the onset of the compound muscle action potential (CMAP), and that the CMAP should begin with a negative phase, be biphasic in shape, and have an amplitude of over 1 mV. Repetitive nerve stimulation was only performed if all four criteria were met, which was the case in all 15 subjects for the nasalis muscle, but in only 5 subjects for the orbicularis oculi muscle. The largest observed decrement was 9% in area. Reptitive nerve stimulation of the nasalis muscle is thus feasible, but its diagnostic utility remains to be established in patients with disorders of neuromuscular transmission.

Action Potentials↗
PubMed2002

Cataplexy: 'tonic immobility' rather than 'REM-sleep atonia'?

BACKGROUND: Cataplexy, a sudden loss of muscle tone in response to strong emotions, is the most specific symptom of narcolepsy. It is currently thought to be due to disturbed rapid eye movement (REM) sleep regulation, and portrayed as REM sleep atonia occurring at the wrong time. However, there are several arguments against including cataplexy in the 'state boundary control' hypothesis. It does not explain why cataplexy is triggered by emotions, and recent studies in narcoleptic dogs showed that REM sleep regulatory mechanisms were in fact intact in these animals. METHODS: We review the literature on the REM sleep dissociation theory, discuss the merits and demerits of the theory, and propose an alternative hypothesis explaining cataplexy. RESULTS: Cataplexy may represent an atavism (recurrence of an ancestral characteristic) of tonic immobility. Tonic immobility (TI) denotes a condition in which an animal is rendered immobile when faced with danger. Arguments in favor of the TI hypotheses are that it explains the emotional triggering. Furthermore, centers regulating narcolepsy and TI are both located in the lateral hypothalamic area. Finally, several drugs known for their ameliorating effect on cataplexy reduce the frequency and duration of TI in animals. CONCLUSION: Cataplexy may be due to a mechanism different from the other clinical symptoms of narcolepsy.

Journal Article↗
PubMed2002

Neurophysiologic aspects of patients with generalized or multifocal tonic dystonia of reflex sympathetic dystrophy.

Reflex sympathetic dystrophy (RSD) is a syndrome dominated by sensory, autonomic, and motor features of the extremities. In this study, 10 severely affected RSD patients who progressed to multifocal or generalized tonic dystonia underwent H-reflex evaluation, needle electromyography (EMG), polysomnography, somatosensory evoked potentials, and transcranial magnetic stimulation. H-reflex evaluation revealed an impaired vibratory inhibition of the H-reflex and a higher facilitation peak in the recovery curve between 200 to 350 msec. Needle EMG revealed an impaired reciprocal inhibition, and many patients were unable to alter the amount of muscle activity voluntarily. Evaluations of the stretch reflex showed a markedly decreased threshold and abnormal responses to tonic and phasic changes. Polysomnography performed in five patients revealed no abnormal EMG activity during nonrapid eye movement and rapid eye movement sleep, but EEG arousal phenomena provoked abnormally high and brief bursts of surface EMG activity in all registered muscle groups. Somatosensory evoked potentials and transcranial magnetic stimulation were normal. Taken together, the findings in these patients with tonic dystonia of RSD are in accordance with an impairment of inhibitory interneuronal circuits at the level of the brainstem or spinal cord.

Adult↗