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From the Biology of Dreaming to the Biology of Mind
... For an interesting epistemological viewpoint on the scientic framework of psychoanalysis, see also [290], in which the Author considers it as a natural science. ...
Some main historiographic aspects of R.G. Collingwood historicism are considered as basic elements for certain epistemological discussions about possible relationships between theoretical and social-humanistic sciences. Moreover, further remarks on creative mathematical thought are made in the light of what established.
... Some investigators question a direct causal link between sleep biology and psychology (Foulkes & Cavallero, 1993;Moffitt & Hoffmann, 1987). Other investigators have constrained their views of sleep psychology based on our current knowledge of sleep neurobiology (Hartmann, 1982;Hobson & McCarley, 1977;Kahn et al., 1997;Koukkou & Lehmann, 1983). Clearly, the brain undergoes significant changes during sleep, and it would be unreasonable to believe that this cannot directly alter the psychological functioning, and even gross function, of the sleeping brain. ...
... (1988), this paper compares conscious and unconscious processes across waking, nonlucid, and lucid dreams. Sleep psychology can display gross functional dissociation between perceptual and cognitive consciousness. We utilize this observation to develop models of sleep experience and dream generation. These models accommodate Hunt’s (1989) “multiplicity of dreams”, as well as the intrinsic variation of perceptual and cognitive activity during dreaming. Lucid dreams are suggested to result from the presence of a skill-based mental set, the lucid dream context, which allows voluntary interaction with the spontaneous dream process. Our view of dreaming provides an explanation of the tendency of lucid dreams to either fade or revert to nonlucid dreams. Neurobiological considerations lead us to hypothesize that, in the sleeping brain, a reversal of information flow from medial temporal lobe mnemonic structures to thalamocortical perceptual circuits imparts parameterization to dream perceptual consciousness. A consequence of our thinking is that dreaming results in a “mental recombination” of cerebral information networks, which contributes to the ability of waking consciousness to generate novel and adaptive
Samples consisting of 10 patients out of each of the following diagnostic groups are compared to each other, as well as to a selected control group, with regard to their sleep polygram: narcisssistic depression resp. MDD, schizophrenia, psychosomatic and borderline disease and anorexia nervosa. The different and common aspects of the standard parameters of sleep (quantitative proportions of the sleep stages) and the parameters of structure (segmentation of time) are illustrated in a synopsis. Furthermore the authors attempt to compare the sleep structure of individual diseases with those of other diseases and with those of the selected control group in terms of delimitative entities. On the background of sleep sturctures, which also entails comparisons of ectreme groups with regard to the allocation of NREM 3 and the length of REM latency, the attempt is made to investigate how far aspects of sleep structure coincide with aspects of human-structure as described by Ammon, on the basis of his human-structural concept with respect to the various psychiatric diseases.
Therapists inevitably feel more gratified in their work when their cases have better treatment outcomes. This book is designed to help them achieve that by providing practical solutions to problems that arise in psychotherapy, such as:
This article offers a holistic evolutionary perspective on dreaming and early sexual development. Going beyond Freud, and more in line with recent psychoanalysis and academic research, oedipality becomes part of understanding the development of sexual strategy, while dreaming is viewed as an evolved mechanism for moderating and updating affectively charged approach-avoidance conflicts associated with self-preservation and reproduction. The article suggests plausible evolutionary assumptions for interpretations of politics and expressive culture.
This report presents data from three experiments investigating the effects of agents which change brain serotonin levels upon the length of the sleep-dream cycle in the rat.
The most challenging objections to the Threat Simulation Theory (TST) of the function of dreaming include such issues as whether the competing Random Activation Theory can explain dreaming, whether TST can accommodate the apparently dysfunctional nature of post-traumatic nightmares, whether dreams are too bizarre and disorganized to constitute proper simulations, and whether dream recall is too biased to reveal the true nature of dreams. I show how these and many other objections can be accommodated by TST, and how several lines of new supporting evidence are provided by the commentators. Accordingly TST offers a promising new approach to the function of dreaming, covering a wide range of evidence and theoretically integrating psychological and biological levels of explanation.
Passagere und leichtgradige Störungen der Einschlafens bzw. des Durchschlafens, störende Ereignisse im Ablauf einer Nachtschlafperiode
oder Einbußen in der Vigilanz am Tage gehören zu den häufigsten Beschwerden des menschlichen Lebens. Immerhin hat jeder 4.
Einwohner der industrialisierten Staaten im Verlauf seines Lebens mindestens einmal Schlafschwierigkeiten, die so schwer ausgeprägt
sind, dass eine manifeste, eindeutig diagnostizierbare Krankheit festzustellen ist. Psychische Erkrankungen gehen mit unterschiedlicher
Häufigkeit, jedoch fast ausnahmslos mit Störungen des Schlafes einher, die allein schon ein therapeutisches Problem für den
Psychiater werden können.
In this article, in an attempt to integrate recent findings with existing knowledge, we provide an overview of issues related to nightmares that could be useful as a guide to clinical work. After defining what should be considered as a nightmare, we look into the relationship of nightmares with issues such as normal development and maturation, as well as culture. Issues of stress and personality are then discussed in their relation to situational and chronic nightmares. State and trait factors are further elaborated on as we explore the relationship of nightmares and psychopathology. A brief review of organic and pharmacological causes of nightmares follows before we embark on a discussion of issues that relate nightmares to psychological trauma. Some final remarks on treatment conclude our review.
Postmortem brain specimens from 18 schizophrenic patients and 12 normal controls were assayed for dopamine-beta-hydroxylase (DBH), the enzyme responsible for the final step in norepinephrine biosynthesis. There was a significant reduction in the DBH activity of the schizophrenic group in all brain regions examined. Enzyme deficits in hippocampus and diencephalon were somewhat larger than that in pons-medulla. Since various extraneous factors, such as non-specific deterioration, drug treatment, duration of hospitalization, cause of death, sex, and age could be ruled out, the deficits in DBH mnay be associated with the schizophrenic disease process. These findings are consistent with the hypothesis that noradrenergic "reward" pathways are damaged in schizophrenia.
Single or repeated intraventricular injections of 6-hydroxydopamine caused marked and long-lasting deficits in brain self-stimulation
and other rewarded behaviors in the rat. The behavioral deficits, as well as the depletion of brain norepinephrine induced
by 6-hydroxydopamine, were prevented by prior treatment with chlorpromazine. Episodic or continuous formation of endogenous
6-hydroxydopamine in man as a result of a genetically determined enzymatic error could selectively damage the binding capacity
and, eventually, the structural integrity of the noradrenergic reward mechanism. Such damage might cause the fundamental symptoms
and long-term downhill course of schizophrenia.
Experimental data, based upon a total of 212 hypnagogic awakenings contributed by 9 Ss, are presented on the incidence of reports of various forms of hypnagogic mentation and on the relationship of such reports to EEG activity. It was found that mental activity in some form or another was invariably reported throughout the hypnagogic period. Content reported was predominantly visual and lacking in affective intensity and it became increasingly hallucinatory and unamenable to voluntary control as EEG patterns shifted from an alpha EEG to a spindling EEG. Dreamlike reports very similar to RFM reports (i.e., dramatic, hallucinatory episodes) were quite common during descending EEG Stages 1 and 2, and also occurred with an alpha rhythm. (28 ref.)
Twelve subjects were studied for a total of 30 nights of uninterrupted sleep by simultaneous recording of EEG, eye movements, heart rate, respiration, and systolic blood pressure. In agreement with previous reports, progressive decreases in heart and respiratory rates and an early fall followed by a sustained rise in systolic blood pressure were found to be consistent base-line trends. Superimposed upon these trends and coinciding with the regular recurrence of stage I rapid eye movements (REM) there were periodic changes in these three functions of two kinds: a) slight increases in average level and b) marked increases in minute-to-minute variability. The changes in average level of blood pressure and of both blood pressure and heart rate variability were more conspicuous during the later REM periods of the night. Alternative interpretations and possible medical implications of these findings are discussed.
dreaming; sleep and EEG; eye movements and sleep
Submitted on October 11, 1963
This chapter presents a preliminary study on 5-hydroxytryptophan (5-HTP) and chronic schizophrenia. On a functional level, the way in which the serotonin effector cell is functioning has to be known. If there is an abnormality in its function, a direct or indirect relationship between that malfunction and the disease seems probable. A pharmacological test of this might be achieved by determining if an alteration of brain serotonin concentrations can cause a change in schizophrenic behavior. In such a test described in the chapter, the 5-HTP-L-alphahydrazinomethyldopa (MK-486) combination was compared with placebo. This comparison revealed that the drug combination was better than placebo in at least seven patients and worse than placebo in two. Although 5-HTP is converted to serotonin within cells that contain serotonin, it has been shown that other cells containing aromatic decarboxylase can also convert 5-HTP to serotonin.
The production of all the major symptoms of parkinsonism is attributed chiefly to the loss of the normal dopaminergic input into the striatum. This loss of dopaminergic input is due to degeneration of the cell bodies of the substantia nigra. An analogous loss of serotonin (5-hydroxytryptamine) may be of significance in the production of parkinsonian tremor. L-dopa ameliorates the symptoms of parkiusonism as a result of reinstitution of dopamine inhibition of the striatal neurons. L-dopa induced dyskinesias are felt to be related to denervation hypersensitivity of striatal neurons to dopamine produced by dopaminergic denervation. Failure to respond to L-dopa is related to degeneration of striatal dopaminergic receptors. The efficacy of amantadine hydrochloride is felt to be related to a block of the presynaptic reuptake of dopamine and thereby a prolongation of dopamine's effect at the receptor site.
Dreams, drug-induced hallucinations, and certain aspects of psychosis share common psychic and behavioural properties. Research in our laboratory, and in other laboratories throughout the world, has led us to the conclusion that these phenomenological similarities are based on common neurochemical mechanisms. Based on a multidisciplinary approach employing neurochemical, electrophysiological, neuropharmacological, and behavioural techniques, we have conducted experiments which indicate that decreased serotonergic neurotransmission, possibly coupled with increased dopaminergic function, may be responsible for the manifestation of these common events.
THERE is evidence that biogenic amines are involved in the mechanisms of sleep1,2. Although the exact relationship is not clear, recent results suggest that decreases in the concen-tration of catecholamines (noradrenaline or dopamine) in the brain cause increased desynchronized sleep (D) (sleep with rapid desynchronized cortical activity, also known as paradoxical or REM sleep), whereas increases in the concentration of catecholamines decrease D3-5. Not all the results, however, are in agreement1,2,6.
This chapter consists of eleven letters from Sigmund Freud to Wilhelm Fliess dated between November 11th, 1887 through August 2nd, 1893. These letters discuss client's background and diagnosis, Freud's family, professional meetings, and brain anatomy, neurosis, sexual functioning and hysteria. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
IN RECENT years levodopa has proved to be the most effective agent presently available for the treatment of parkinsonism.1-6 Among the side effects of levodopa therapy, psychiatric disturbances have been noted.3-6Levodopa is not only the precursor of dopamine hydrochloride but also of norepinephrine.7 Although the action of these two catecholamines upon the central nervous system is incompletely understood, evidence has been accumulated in the last two decades upon their action in behavior.8,9 In this context we would like to report 16 cases of psychiatric disturbances which occurred among 45 patients treated with levodopa.Method
Levodopa was administered to 45 patients (31 men and 14 women) with Parkinson's syndrome. Forty-one patients had primary parkinsonism or Parkinson's disease, three had postencephalitic parkinsonism, and one had arteriosclerotic parkinsonism. Of the patients willing to enter the program, only those with decompensated cardiovascular disease, renal disease, psychosis
Recent research in the neurobiology of dreaming sleep provides new evidence for possible structural and functional substrates of formal aspects of the dream process. The data suggest that dreaming sleep is physiologically determined and shaped by a brain stem neuronal mechanism that can be modeled physiologically and mathematically. Formal features of the generator processes with strong implications for dream theory include periodicity and automaticity of forebrain activation, suggesting a preprogrammed neural basis for dream mentation in sleep; intense and sporadic activation of brain stem sensorimotor circuits including reticular, oculomotor, and vestibular neurons, possibly determining spatiotemporal aspects of dream imagery; and shifts in transmitter ratios, possibly accounting for dream amnesia. The authors suggest that the automatically activated forebrain synthesizes the dream by comparing information generated in specific brain stem circuits with information stored in memory.
A theory is developed along the following lines: Schizophrenia is basically an illness; the variety of clinical syndromes can perhaps be understood as adaptations to a single deficit; and the multiplicity of causes or aggravating factors can be seen as factors producing acute or chronic stress. Thus both apparent complexities could be compatible with a single basic deficit which includes vulnerability to stress.The deficit may be in the area of feedback processing. Evidence of subtle neuromuscular dysfunction in schizophrenia compatible with a feedback processing deficit is presented. It is suggested that deficient functioning of brain norepinephrine systems may underlie this feedback processing deficit. Since both the feedback processing deficit and the norepinephrine deficiency have previously been postulated as characteristic of desynchronized or dreaming sleep (REM sleep), this view provides a possible biological basis for the similarities between dreaming and schizophrenia.Data concerning the behavioral and psychological effects of dopamine are examined, it is suggested that dopamine plays a role as the biological substrate of un-neutralized psychic energy, which in vulnerable individuals produces psychotic pressure. This may involve dopamine released from noradrenergic neurons in the brain, and acting at these norepinephrine synapses or at dopamine synapses in close proximity, for instance in the cerebral cortex. If so, the basic, probably genetic, deficit producing susceptibility to schizophrenia could be at the dopamine-beta-hydroxylase step. This could explain the schizophrenic's acute sensitivity to stress since at times of stress norepinephrine would be reduced and synthesis of dopamine but not of norepinephrine would be increased.
Cats injected with LSD (d-lysergic acid diethylamide) exhibit a group of behaviors that appear to be specific to hallucinogenic
drugs. Two of these behaviors, limb flick and abortive grooming, have an extremely low frequency of occurrence in normal cats,
but often dominate the behavior of LSD-treated cats. The frequency of occurrence of this group of behaviors is related to
the dose of LSD. The behavioral changes are long-lasting following a single injection of LSD, and exhibit tolerance following
the repeated administration of LSD. They are not elicited by a variety of control drugs, but are elicited by other indole
nucleus hallucinogens. Because the behavioral effects are specific, reliable, easy to score, and quantifiable, they represent
an animal model that can be used in studies of the effects of LSD and related hallucinogens.
During the sleep cycle in cats, neurons localized to the posterolateral pole of the nucleus locus coeruleus and the nucleus
subcoeruleus undergo discharge rate changes that are the opposite of those of the pontine reticular giant cells. The inverse
rate ratios and activity curves of these two interconnected populations are compatible with reciprocal interaction as a physiological
basis of sleep cycle oscillation.
Postmorten brain specimens from nine chronic schizophrenic patients and nine control were assayed for activity of dopamine beta-hydroxylase, the enzyme responsible for the conversion of dopamine to norepinephrine. Unlike the results of previous reports, there was no statistically significant difference in enzyme activity between the patient and control groups. There were, however, significant negative correlations between dopamin beta-hydroxylase activity and the tim spent in the morgue before autopsy, and between enzyme activity of schizophrenics and dosage of chlorpromazine or its equivalent.
The electrograms of neck, limb and respiratory muscles were studied in unrestrained cats sleeping at different environmental temperatures. 1. 1. Thermal neutrality. Slow wave sleep: postural activity is present in neck and intercostal records; diaphragmatic and intercostal electrograms show respiratory activity; limb muscles are inactive. Fast wave sleep: neck and intercostal postural activity disappears; intercostal respiratory activity is weak; respiratory activity of the diaphragm persists. 2. 2. Low environmental temperature. Slow wave sleep: postural activity is present in neck and intercostal electrograms; shivering activity is clearly observed in all records except that of the diaphragm; shivering intensity increases from waking to slow wave sleep; interaction occurs between respiratory and shivering rhythms. Fast wave sleep: postural and shivering activities disappear. 3. 3. High environmental temperature. Slow wave sleep: neck and intercostal postural activity is weak; diaphragmatic and intercostal electrograms show panting activity; frequency of panting increases from waking to slow wave sleep. Fast wave sleep: postural and panting activities disappear. Summing up, fast wave sleep is associated with changes in the regulation of postural, respiratory and thermoregulatory muscle activities.
1. 1. In this series of experiments we have shown that depletion of serotonin (5-HT) by the tryptophan hydroxylase inhibitor, para-chlorophenylalanine (PCPA) in cats is attended by a marked loss of sleep. 2. 2. Cats chronically supplied with electrodes to record the EEG, neck EMG and eye movements were contained and observed around the clock in screened, sound-attenuated rooms for up to 19 days. Their "vigilance profile" consisting of a three-level graph (PS = paradoxical sleep; SS = slow sleep; W = waking) was determined and total W-times, SS-times, and PS-times calculated for every 4 and 24 h periods. 3. 3. PCPA was administered in various doses i.p. A single dose of 200 mg/kg was sufficient to reduce sleep to close to zero level. The minimal sleep level occurred about 3 days after injection. Sleep was back, or close, to control level after about 16 days. With smaller doses, lesser sleep reductions were obtained. 4. 4. PS over total sleep ratio remained constant except for a relative increase of PS in those cases where total sleep approached zero level. 5. 5. 5-Hydroxytryptophan (5-HTP; 30 mg/kg i.p.) given 48 h after PCPA restored slow sleep temporarily to levels above control within 10 min after injection. PS started to occur about 5-6 h after 5-HTP. 6. 6. Biochemical analysis for 5-HT of the brains of cats treated with various doses of PCPA confirmed the observations in rats, mice and rabbits; various brain-stem and cortical areas were found to be markedly depleted of (total) 5-HT. 7. 7. It is suggested that discrepancies in the time course of sleep deprivation and total 5-HT content are due to such additional factors as negative feedback. Also, free 5-HT may show time courses of depletion and restoration different from those of total 5-HT.
Oral administration of the serotonin precursor L-5-hydroxytryptophan with a peripheral decarboxylase inhibitor produced Mild
to moderate improvement in six of seven chronic undifferentiated schizophrenic patients who were resistant to phenothiazine
treatment, as compared to an oral administration of a placebo. Two of four chronic paranoid schizophrenic patients who were
resistant to phenothiazine treatment became worse with 5-hydroxytryptophan, one improved. It is presumed that these psychological
changes were directly or indirectly produced from increases in brain serotonin. Indirect data from animals and humans indicate
that there may be an abnormality in serotonin metabolism in some schizophrenics. While our data are consistent with this hypothesis,
other explanations for our data must be entertained.
As part of an investigation of the possible role of dopaminergic mechanisms in some psychoses, the behavioral effects of administration of l-Dopa to schizophrenic patients was assessed. l-Dopa was administered in dosages of 3–6 g/day to 10 such patients who had been maintained off neuroleptic drugs for approximately a week. Behavioral worsening occurred in all 10 patients. Three showed non-specific stimulation while the remaining 7 showed a combination of both stimulation and worsening of pre-existent symptoms or the development of new symptomatology. The significance of these findings is discussed with regard to those of other investigators.
l-Alpha-methylparatyrosine administered orally in doses of 50, 75 and 100 mg/kg produced a significant increase in desynchronized sleep time (D-time) in the rat. However, 75 mg/kg of l-AMPT, administered intraperitoneally resulted in disturbed sleep and reduced D-time; this may explain some discrepancies in previous studies. Over a 24-h period, the time of maximum increase in D-time after oral l-AMPT coincided closely with the time of maximum decrease in brain norepinephrine levels; both occurred 7–10 h after drug administration.
Through psychiatric interviews and psychological tests the authors studied 38 adults who reported experiencing at least one nightmare per week. Nearly all of the subjects had a lifelong history of frequent nightmares. Four of the subjects met DSM-III criteria for schizophrenia, 9 met the criteria for borderline personality, and 6 met the criteria for schizotypal personality. The others had no specific diagnosis, and none of the subjects had a diagnosis of typical neurosis. Many had mentally ill relatives. Most had artistic interests and talents. These nightmare sufferers may be seen as unusually vulnerable, with a potential for mental illness--especially schizophrenia--as well as a potential for artistic achievement.
Various meanings have been given to the word "metapsychology" by its opponents and proponents in the psychoanalytic literature. These are discussed and compared with the meaning Freud intended the word to have. The question of the place of psychoanalytic psychology in science--whether it is or is not in natural science--is also considered.
Institute of Psychiatry, Maudsley Monogr
- P H Connell
- Solomon P.
Amphetamine Psychosis. Institute of Psychiatry, Maudsley Monogr
- P H Connell