[Hypnosis in the control of pain].
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Humans↗
Biomedical subjects
R L Carasso
Publications and source records attributed to R L Carasso.
The effects of DSIP on pain threshold during light and dark periods in rats are not naloxone-sensitive.
The effects of Delta-Sleep-Induced Peptide (DSIP) were examined in rats kept at 12:12 light:dark schedule. The peak of the circadian pain threshold of saline-treated rats occurred at 10:00. Rats treated with 0.1 mg/kg, i.p. DSIP exhibited a significantly higher pain threshold level (as measured by hot plate) both in the light and dark periods. Prior to the treatment the peak was at 10:00. With treatment the peak shifted to 18:00. A dose of 1.0 mg/kg DSIP increased the pain threshold level only during the dark period. The analgesia induced by DSIP is insensitive to naloxone pretreatment.
Animals↗
Effects of dietary fats on learning, pain threshold, thermoregulation and motor activity in rats: interaction with the length of feeding period.
The effects of both a semisynthetic diet containing 20% fat from various sources (soybean oil, sunflower oil and lard) and a control diet on learning capacity, motor activity, pain threshold and thermoregulation were studied in rats which were fed on these diets for various lengths of feeding periods (1, 2, 3 and 4 weeks). Two weeks feeding period of soybean oil source induced an improvement in learning capacity, which was further enhanced by increasing the length of the feeding period. A 3-week feeding period was required to obtain an increase in the pain threshold, by which time the rats were also protected from d-amphetamine induced hypothermia. The analgesia induced by the diet is naloxone-dependent. None of the other diets, including the sunflower oil diet, which is richer in polyunsaturated fatty acids, differed from control diet. While the mode of action of this diet is still unknown, the effects of the soybean oil source diet cannot be attributed to nutritional factors such as changes in energy consumption or body weight.
Animals↗
Treatment of cervical headache with hypnosis, suggestive therapy, and relaxation techniques.
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Cervical Vertebrae↗
Flufenamic acid in prostaglandin migraine.
A new class of migraine symptomatology is suggested which consists of major signs of migraine related to disturbances in the menstrual cycle. Not only are these patients different from other migraine patients, they are most responsive to an antiprostaglandin drug. This drug is less useful in other forms of migraine. We suggest that this type of migraine be called prostaglandin migraine.
Adult↗
The prevention and treatment of migraine with an analgesic combination.
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Acetaminophen↗
Vasoconstriction and d-amphetamine-induced hypothermia.
The hypothermic effect of d-amphetamine was investigated in rats in which vasoconstriction or vasodilation was induced by pharmacological agents: aramine as vasoconstrictor and neprasol as vasodilator. The d-amphetamine-induced hypothermia was enhanced by both drugs among rats kept at 4 degrees C, and both drugs were unable to modify the d-amphetamine-induced hypothermia. These results indicate that although vasoconstriction and vasodilation play a major role in thermoregulation, d-amphetamine-induced hypothermia is not mediated peripherally by vasoconstriction. Since changes in basal metabolic rate, motor activity, food intake and vasoconstriction are not the peripheral mechanisms by which d-amphetamine induced hypothermia, the mechanisms is still unknown.
Animals↗
Physiological evidence (hypothermia) for central effects of beta-blocker agents.
In recent studies carried out during the last decade, it has been found that beta-blocker agents have many central effects. These findings raise the question how beta-blocker agents act when they influence central effects. In spite of intensive research efforts on this subject, no answer has been offered so far. Several studies indicate that the effect of beta-blocker agents on the dopaminergic receptors in the brain is very similar to their effect on beta-adrenergic receptors. In a set of experiments we checked the effect of two beta-blocker agents: oxprenolol and dl-propranolol, and the effect of d-propranolol on hypothermia induced by d-amphetamine and apomorphine at an ambient temperature of 4 degrees C. It was found that the two beta-blockers and the d-propranolol significantly potentiated the effect of hypothermia induced by d-amphetamine and apomorphine, an effect which is mediated by the central dopaminergic system. However, the activity of the beta-blockers was agonistic. Furthermore, the influence of d-propranolol on hypothermia shows that this dopaminergic agonistic activity of the beta-blockers is not related to peripheral or central beta-receptor blockage.
Animals↗
A comparison of the hypothermic effects of methylphenidate and d-amphetamine.
Methylphenidate is a central nervous system stimulant with a spectrum of action similar to the effects of d-amphetamine. d-Amphetamine-induced hypothermia is mediated via release of dopamine in the DA mesolimbic pathway. Methylphenidate causes hypothermia among rats kept at 4 degrees C, but d-amphetamine is twice as potent as methylphenidate. Dose-response relationship of methylphenidate thermal effects exhibits a U-shape curve. The hypothermic effects of 5-15 mg/kg methylphenidate are mediated by central dopaminergic neurons, as pretreatment with haloperidol inhibits these effects. The hypothermia produced by larger doses of methylphenidate is not blocked by pretreatment with haloperidol and hypothermia induced by d-amphetamine is blocked by pretreatment with haloperidol.
Animals↗
Clomipramine and amitriptyline in the treatment of severe pain.
Clomipramine is the most potent 5-HT reuptake blockade agent among the antidepressants. A comparison between the effect of clomipramine and a less powerful 5-HT reuptake blockade agent (amitriptyline) could test the hypothesis that brain 5-HT is a mediator of pain sensation. Groups of patients of either sex, with pain indication of trigeminal neuralgia, tension headache or postherpatic neuralgia, received doses of clomipramine or amitriptyline in a single blind clinical experiment. The results after three months of treatment showed that clomipramine: (1) was better than amitriptyline in treating trigeminal neuralgia; (2) tended to be better in the treatment of tension headache; and (3) amitriptyline is better in treating postherpatic neuralgia. Clomipramine was better tolerated. The results support the hypothesis that in certain pain situations, clomipramine exerts a beneficial effect, not only because of its effect on the depression and anxiety level of the patient, but also via its effects on the 5-HT brain system.
Adult↗
Habituation and transfer during sleep in cats.
In order to test the concept of "sleep learning", cats were exposed to habituation treatment of auditory stimuli during different stages of the sleep-waking cycle. While it was possible to demonstrate that habituation to an auditory stimulus can take place in paradoxical sleep (PS) and slow-wave sleep (SWS) as well as during periods of wakefulness, it was not always possible to demonstrate a transfer of habituation from the training period to other periods. A complete transfer of habituation occurred between the two sleep periods (PS and SWS); a partial transfer of habituation occurred between the waking period and both of the two sleep stages (PS and SWS), but only a minimal transfer of habituation was found between any one of the sleep stages and the waking period. When the cats were able to transfer the habituation, they also were able to discriminate between the habituating tone and a novel tone. The findings that only minimal transfer of habituation could occur between each of the sleep stages and the waking period do not lend support to the concept of "sleep learning".
Animals↗
Measurement of prostaglandin E2 in cerebrospinal fluid in patients suffering from stroke.
In 16 patients suffering from cerebrovascular events, prostaglandin (PG) E2 was measured in their cerebrospinal fluid and correlated with their clinical status and evolution. Prostaglandin E2 ranged from 200-3000 pg (picogram)/ml of cerebrospinal fluid. A positive correlation was found between PG E2 levels and the severity and clinical outcome of the stroke.
Adult↗
The effects of d-amphetamine and temperature on p-cresol and pentylenetetrazol induced convulsions.
Each of twelve (12) rats were subjected to temperatures of 37c, 20c, and 4c in an environmental chamber. Seizure responses to p-cresol injections produced a U-shaped function, with minimal seizures occuring at 20c. Subsequent administration of d-amphetamine eliminated seizures, except at 4c, at which temperature only stereotyped behavior was observed. Environmental temperature effects on metrazol injections in a second group (N=72) seemed to increase linearly with respect to seizure susceptibility and mortality, although latency to first seizure was also a U-shaped function. The findings are discussed in the context of developing a model of epilepsy appropriate for behavioral research.
Animals↗
Modification of d-amphetamine- or chlorpromazine-induced hypothermia by beta-endorphin, MIF-I, and alpha-MSH: mediation by the dopaminergic system.
The effects of beta-endorphin, MIF-I, and alpha-MSH on d-amphetamine- a CPZ-induced hypothermias in rats kept at 4 degrees C were tested in three experimental groups: (a) intact; (b) rats with lesions of the olfactory tubercle; and (c) rats in which the link between the DA mesolimbic pathway and the striatum was disconnected. All drugs tested alone (except MIF-I) caused significant hypothermia. Pretreatment with CPZ, MIF-I, and alpha-MSH potentiated d-amphetamine-induced hypothermia in intact rats. Pretreatment with alpha-MSH potentiated CPZ-induced hypothermia. beta-Endorphin partially blocked d-amphetamine-induced hypothermia, but did not interact with CPZ, MIF-I, or alpha-MSH. All potentiations were either reduced or disappeared in the incisioned rats. CPZ and alpha-MSH caused hypothermia in olfactory tubercle-lesioned rats. The results indicate that: (a) the DA mesolimbic pathway is involved in the hypothermic response of all drugs tested; (b) an intact feedback loop is required for the potentiation of the hypothermic response of CPZ on d-amphetamine, MIF-I on d-amphetamine, and alpha-MSH on d-amphetamine and CPZ; (c) beta-endorphin acts as a partial blocker of d-amphetamine; MIF-I is a weak potentiator of d-amphetamine, alpha-MSH acts as a negative modulator of the DA system, most probably in the striatum.
Animals↗
Changes in circadian rhythms of thermoregulation and motor activity in rats as a function of aging: effects of d-amphetamine and alpha-MSH.
Thermoregulatory and motor activity circadian cycles are age-dependent. While the level of thermoregulation and motor activity remained almost at the same level during the first 1-15 months during the light portion of the 24-hr cycle, a significant decrease in the level of both rhythms was observed during the dark period. Therefore, older rats exhibited reversed cycles compared with younger rats. Treatments with d-amphetamine resulted in the enhancement of reversal of the cycles. Rats treated with alpha-MSH failed to exhibit a reversal of the cycles. While the effects of d-amphetamine are mediated by the brain DA mesolimbic pathway, it seems that alpha-MSH acts on the dopaminergic system at different sites of action.
Aging↗
The facilitative effects of alpha-MSH and melanin on learning, thermoregulation, and pain in neonatal MSG-treated rats.
Administration of monosodium glutamate (MSG) in the neonatal period renders the rat to be alpha-MSH deficient later in life. In this study rats received MSG in their neonatal period and were examined at the age of 60 days. alpha-MSH caused hypothermia, potentiated induced hypothermia, blocked paradoxical behavioral thermoregulation, improved performance in the Morris water tank, but had no effect on pain threshold. Melanin only caused an increase in pain threshold. It is suggested that the differential effect of alpha-MSH and melanin is governed by the dopaminergic system.
Animals↗
A comparison of dopamine agonists and catechol-O-methyltransferase inhibitors in Parkinson's disease.
To compare the efficacy and tolerability of three dopamine agonists--pergolide (PRG), pramipexole (PRX), and ropinirole (ROP)-and two catechol-O-methyltranferase (COMT) inhibitors-tolcapone (TOL) and entacapone (ENT)-as add-on therapies to levodopa (L-Dopa) in Parkinson's disease, we analyzed randomized, double-blind, placebo-controlled, multicenter studies. To our knowledge, they had not yet been evaluated in comparison with each other. Statistical analyses used odds ratios, numbers needed to harm, and Fisher's inverse chi2 method. Seven studies meeting the inclusion criteria included treatment of 1,756 patients. The common efficacy measures were the reduction of L-Dopa dose and "off' duration. The reported reduction in L-Dopa dose was significant for all drugs in relation to placebo, but was most significant for PRX and ENT (p < 0.0001). The most significant reduction in "off' duration was with PRG, PRX, and ENT (p < 0.001). The common tolerability measures were the percentage of patients withdrawn because of side effects, because of any reason, and because of the development of dyskinesias. Ropinirole, PRX, and ENT caused fewer withdrawals related to side effects. Pergolide was better than other analyzed drugs concerning withdrawals for any reason. All drugs caused more dyskinesias than placebo (p < 0.0001), with overlapping confidence intervals, except for TOL 600 mg, which caused more dyskinesias than dopamine agonists and ENT. Pramipexole and ENT had the best efficacy and tolerability profile in this analysis.
Catechol O-Methyltransferase Inhibitors↗
Acute mania and hemichorea.
A 61-year-old man suddenly became euphoric and talkative. Later the same day, he developed hemichoreic movements of the left limbs. The patient fulfilled the DSM-IV criteria for a manic episode by abnormally and persistently elevated mood, decreased need for sleep, high distractibility, pressured speech, increased goal-directed activity, and hypersexuality. The mood changes persisted for several weeks. Magnetic resonance imaging of the brain showed a right thalamic infarction. The co-occurrence of hemichorea and mania caused by focal thalamic lesion is very rare. It may be explained by dysfunction in basal ganglia thalamocortical circuitry.
Acute Disease↗