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Biomedical subjects

B Kaada

Publications and source records attributed to B Kaada.

At least 19 recordsLinked to original sources
PubMed1995

[Fear paralysis--still a possible cause of crib death].

There is overwhelming evidence that prone sleeping entails more risk of sudden infant death than supine sleeping does. However, no generally accepted biological explanation of this phenomenon has been found. In a viewpoint article in Acta Paediatrica in 1994 the author has re-emphasized that the fear paralysis reflex (tonic immobility) could be a cause of sudden infant death. The response consists of immobility, apnea, profound bradycardia and vasoconstriction. The bradycardia may proceed to irreversible asystole and silent death within a few minutes. In infant monkeys, this innate, atavistic reflex, which is prompted by aversive environmental fear-producing events, has the same age distribution as sudden infant death syndrome between the 2nd and 5th month of life. Main triggering stimuli are: restraint of movement (preventing flight) and sudden exposure to unfamiliar environments and persons, events for which the organism appears to be unprepared. Movements of the extremities are more restrained in the prone than in the supine position with greater chance of eliciting fear paralysis responses and death in prone sleepers. This biological mechanism presumably also applies to the winter peak (restraint due to overwrapping), sleeping outdoors (overwrapping) and co-sleeping in the same bed as another (parent).

Animals↗
PubMed1994

Why is there an increased risk for sudden infant death in prone sleeping? Fear paralysis and atrial stretch reflexes implicated?

A number of recent reports have indicated a higher risk of sudden infant death syndrome (SIDS) in the prone sleeping position, compared with the supine position. However, the biological mechanisms for this increased risk have not been established. For this report, two biological explanations are proposed, each of which may be influenced by altered sleeping position in such a way that they may create conditions for increased triggering of SIDS.

Adrenergic Fibers↗
PubMed1993

[The Chinese runners' revolution].

Scientists are discussing possible explanations of the fantastic improvement in physical performance achieved by Chinese female runners in 1993. Some untraditional procedure must have been used in addition to intense training. The author points out that a study conducted almost a decade ago, and reported in Acupuncture and Electro-Therapeutics Research (1984; 9: 165-80), showed a marked increase in physical performance following low-frequency (2 Hz) transcutaneous electrical nerve stimulation (TENS) in athletes competing in swimming, running and cycling events. This study was known to the Chinese, and TENS could be one of the methods used. Neither this method nor acupuncture are regarded as doping, since at present it is impossible to demonstrate that the athletes have received such treatment.

Acupuncture Therapy↗
PubMed1991

Low-frequency transcutaneous nerve stimulation in mild/moderate hypertension.

Low-frequency peripheral nerve stimulation may induce widespread cutaneous and muscular vasodilatation in animals and humans due to sympatho-inhibition. This response has in humans been shown to be associated with a lowering of the systemic vascular resistance and arterial pressure. In the present study the effectiveness of low-frequency (2 Hz) transcutaneous electrical nerve stimulation (TNS) has been examined in 46 patients, all 41-43 years of age, with a primary diagnosis of uncomplicated mild/moderate hypertension (90-115 mmHg diastolic pressure). The study was designed blind with matched controls in a TNS group and a placebo group. The blood pressure was measured objectively with an automatic monitor. In a short-term experiment TNS produced a significant lowering of systolic, mean arterial, and diastolic pressures amounting to 8 mmHg (P less than 0.01), 6 mmHg (P less than 0.01), and 4 mmHg (P less than 0.02), respectively. In a long-term study, after 2 weeks of daily stimulation, a similar depression was recorded with no stimulation on the day of examination. An eventual clinical use of the depressor effect of TNS demands further clinical research.

Adult↗
PubMed1990

[Sudden infant death--an emotional trigger mechanism].

Southall and coworkers have demonstrated in a recent study that attacks of lifelessness with sudden and severe hypoxemia and cyanosis are caused by a combination of respiratory arrest in expiration, and a right-to-left shunting of the blood through the lungs due to increased pulmonary vascular resistance. This mechanism is thought to be the cause of death. They have also defined the precipitating factors which are sudden, naturally occurring stimuli causing fear, anger or pain. They underline the importance of elements of surprise and unexpectedness. These observations lend strong support to the "fear paralysis" hypothesis proposed in 1986 by Kaada and Gabrielsen. We stressed that the process leading to death was triggered on by emotional factors (first and foremost fear). Stimuli evoking fear are any threat perceived as a danger. Actual stimuli in infants are restrained movement, sudden and unexpected noises, sudden exposure to strange environments and persons. Elements of surprise and novelty were similarly emphasized. The reflex is suppressed by the administration of anxiolytic drugs like clonidine and amitriptyline.

Cyanosis↗
PubMed1990

Effects of an angiotensin converting enzyme (ACE) inhibitor on plasma endorphin level.

1. In addition to their antihypertensive effect, ACE inhibitors have been reported to increase general well-being, general health and vitality and work performance. The cause of these effects is not known. A possible mechanism may be release of beta-endorphins. 2. In the present study changes in plasma concentration of beta-endorphins on days with ACE inhibitor treatment (n = 12) and on non-treatment control days (n = 12) were compared in 6 patients. 3. Both on control and treatment days the beta-endorphin level fell, by 7.1 and 10.0%, respectively, from 8.00 a.m. to 8.00 p.m., reflecting the known diurnal rhythm of this opioid. This difference between the control and treatment days is not statistically significant. 4. The study should be extended to determine endorphin concentration in the cerebrospinal fluid, and other opioids should be looked for.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

Sudden infant death syndrome during weekends and holidays in Norway in 1967-1985.

A few previous studies have revealed an increased risk for sudden infant death syndrome (SIDS) during weekends and holidays suggesting environmental factors as potential trigger mechanisms for death. In the present study, the weekend/holiday effect has been assessed on the basis of 1480 SIDS cases in 19 Norwegian counties during a 19-year period (1967-85). The phenomenon has been confirmed for 17 of the 19 counties. Special attention has been attached to differences in the geographical and seasonal distribution of the phenomenon. Deaths of other causes in infancy did not display such a dependency on the day of the week.

Age Factors↗
PubMed1990

Transcutaneous nerve stimulation in patients with coronary arterial disease: haemodynamic and biochemical effects.

Low-frequency transcutaneous nerve stimulation (TNS) is known to produce widespread and prolonged vasodilation in skin and muscles. In the present study the effects of low-frequency TNS on coronary and systemic haemodynamics, myocardial blood flow, myocardial oxygen consumption, myocardial free fatty acid and lactate uptake were measured at rest in 16 normotensive patients, with coronary heart disease, undergoing diagnostic cardiac catheterization. In addition, vasoactive intestinal polypeptides (VIP) and noradrenaline were measured in the coronary sinus and the aorta. The study was randomized and double-blind, with half of the patients serving as placebo controls. A stimulation period of 20 min caused a significant lowering of mean femoral arterial pressure and systemic vascular resistance measured at 15 and 30 min after the start of TNS (P less than 0.01). There was no significant change in the other parameters mentioned. The hypotonic effect is considered to be due to increased peripheral microcirculation resulting from sympatho-inhibition.

Coronary Circulation↗
PubMed1989

[Treatment of fibromyalgia by low-frequency transcutaneous nerve stimulation].

Fibromyalgia is a syndrome of a non-inflammatory nature characterized first and foremost by great pain in a number of tendons and muscles. The syndrome has only recently been delineated as a separate entity, the criteria for which are still being discussed. Recent studies have revealed reduced oxygenation in the trigger points, apparently a result of reduced microcirculation due to sympatho-inhibition (5). Since low-frequency TNS is known to increase microcirculation in skin and muscles in widespread areas, and since such stimulation also produces widespread pain-relief through the activation of endogenous opioids, this appears to be a rational therapy for this syndrome. In the present study, 40 patients with fibromyalgia received low-frequency TNS. The effects were beneficial in about 70% of the cases.

Fibromyalgia↗
PubMed1989

[Nocebo--the opposite of placebo].

It is well documented that placebo represents Pavlovian conditioned reflexes activated by positive anticipation of healing. The pain-relieving effects of placebo are due to a psychical activation of the endogenous opioid-serotonergic, pain-inhibitory descending system. The opposite effect is nocebo, a term introduced in 1961 by Kennedy (10). Nocebo-effects similarly appears to be produced by conditioned reflexes, but are activated by negative expectations (fig 1). A number of examples of nocebo are given. Nocebo-stimuli, such as anxiety, fear, mistrust and doubt, may reduce a placebo-effect; it may induce negative side-effects in placebo-treatment; it may produce new aversive symptoms; and it may reverse symptoms from positive ones to negative ones (e.g. revert an analgesic response to hyperalgesia). In its most extreme, nocebo-stimuli may cause death, as in voodoo-death in primitive societies, an example of the fear-paralysis reflex. Whether the outcome is positive or negative is determined, inter alia, by the subject's possibility of coping with the situation. In a setting where the animal has no control over an aversive stimulus, as in inescapable foot shocks, nocebo-effects predominate. It is postulated that noradrenergic neurons in locus coeruleus in the brain stem are involved in the production of nocebo-effects. The "placebo-system" and the "nocebo-system" exert a reciprocal inhibition at a brainstem level (fig 3).

Animals↗
PubMed1989

[Sudden infant death--the QT interval in ECG and bradyarrhythmias].

Prolongation of ventricular repolarization, as evidenced from an increased QT-interval, makes the ventricles more susceptible to fibrillation. The theory has previously been advanced that some cases of sudden infant death syndrome may be due to a non-hereditary QT-prolongation, resulting in fibrillation and cardiac death. This theory has been seriously doubted, since in subsequent long series of recordings in newborns the QT-interval has been found normal at rest. However, the QT-theory has recently been revived by a report that in some babies with sudden infant death syndrome the ability to shorten the QT-interval as the heart rate increases is impaired, an observation which is consistent with the QT-theory. The present experiments on infant and adult rodents have shown that during the innate fear paralysis reflex, elicited by a variety of frightening stimuli of a type that commonly occur during ordinary daily life, the QT-interval may be transiently prolonged and is usually associated with bradycardia and changes of the ST-segment and T-wave. The fear paralysis reflex has previously been proposed as a triggering mechanism for SIDS. These findings lend support both to the fear paralysis theory and the QT-theory. The reflex may represent an external cause of QT-prolongation which adds to the intrinsic impairment of repolarization resulting in a condition which favours ventricular fibrillation. A second unfavourable intrinsic factor is chronic hypoxia.

Arrhythmias, Cardiac↗
PubMed1989

Increase of plasma beta-endorphins in connective tissue massage.

1. Connective tissue massage produces relief of pain and increases microcirculation in a number of vascular beds. 2. The concentration of plasma beta-endorphins has been measured in 12 volunteers before and 5, 30 and 90 min after a 30-min session of connective tissue massage. 3. There was a moderate mean increase of 16% in beta-endorphin levels from 20.0 to 23.2 pg/0.1 ml (P = 0.025), lasting for about 1 hr with a maximum in the test 5 min after termination of the massage. 4. It is assumed that the release of beta-endorphins is linked with the pain relief and feeling of warmth and well-being associated with the treatment.

Adult↗
PubMed1989

Transcutaneous nerve stimulation (TNS) in tinnitus.

Low-frequency (2 Hz) TNS applied distally to peripheral nerves of the upper extremity is known to induce a wide-spread, non-segmental and prolonged relief of pain and an increased microcirculation due to sympatho-inhibition in a number of vascular beds. Such stimulation was administered in 29 tinnitus patients of various etiology. Reduction of tinnitus was encountered in 9 subjects in response to a 45-min TNS-session. The improvement was mainly seen in tinnitus characterized by lower frequencies (125-500 Hz). In 7 of the 9 patients, the tinnitus reduction was associated with improvement of hearing, predominantly in the low-frequency band. The effects were still present after one week following daily stimulation at home. On continued treatment, the effects were found to be transitory in 4 of the patients, whereas the remaining 5 patients are still using the stimulator after 2 to 5 years. It is suggested that the mechanism behind the beneficial effects is increased microcirculation in part of the auditory pathways.

Auditory Threshold↗
PubMed1989

[Nocebo--the antipode to placebo].

It is well documented that placebo represents Pavlovian conditioned reflexes activated by positive anticipation of healing. The pain-relieving effects of placebo are due to a psychical activation of the endogenous opioid-serotonergic, pain-inhibitory descending system. The opposite effect is nocebo, a term introduced in 1961 by Kennedy. Nocebo-effects similarly appear to be produced by conditioned reflexes, but are activated by negative expectations (Figure 1). A number of examples of nocebo are given. Nocebo-stimuli, such as anxiety, fear, mistrust and doubt, may reduce a placebo-effect; it may induce negative side-effects in placebo-treatment; it may produce new aversive symptoms; and it may reverse symptoms from positive ones to negative ones (e.g. revert an analgesic response to hyperalgesia). In its most extreme, nocebo-stimuli may cause death, as in voodoo-death in primitive societies, an example of the fear-paralysis reflex. Whether the outcome is positive or negative is determined, inter alia, by the subject's possibility of coping with the situation. In a setting where the animal has no control over an aversive stimulus, as in inescapable foot shocks, nocebo-effects predominate. It is postulated that noradrenergic neurons in locus coeruleus in the brain stem are involved in the production of nocebo-effects. The "placebo-system" and the "nocebo-system" exert a reciprocal inhibition at a brainstem level (Figure 3).

Drug-Related Side Effects and Adverse Reactions↗