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H C Sabelli

Publications and source records attributed to H C Sabelli.

At least 19 recordsLinked to original sources
PubMed1991

Process theory as a framework for comprehensive psychodynamic formulations.

In this article, we have proposed a method for developing integrative psychiatric formulations based on process theory, as contrasted to eclectic attempts to combine separate, often disparate, theories. Congruent with chaos theory and "far from equilibrium" thermodynamics, process theory proposes that normal development and psychopathology are creative processes open to chance, choice, and meaningful coincidences and governed by harmonious and conflictual interactions between opposites. We have illustrated our method by discussing a case, previously described by Perry, Cooper, and Michels (1987) from three psychoanalytic perspectives. We interpret this case to result from a possible neuroamine depletion, poor family life, social defects, and habitual conflictual/depressive patterns of interaction.

Brain↗
PubMed1990

Septic encephalopathy. Evidence for altered phenylalanine metabolism and comparison with hepatic encephalopathy.

We elected to test the hypothesis that the metabolic encephalopathy associated with systemic sepsis may have a pathogenesis that is similar to hepatic encepathology, ie, as the consequence of hepatic dysfunction that induces alterations in synthesis of catecholic and noncatecholic neurotransmitters. Eleven patients with septic encephalopathy were compared with nine patients with septic encephalopathy and nine normal controls with respect to blood and cerebrospinal fluid (CSF) amino acid profile, phenylethylamine and its metabolite phenylacetic acid, and blood ammonia. Blood and CSF levels of phenylacetic acid increased markedly in septic and hepatic encephalopathy while CSF phenylethylamine levels were not increased in either condition, presumably due to rapid turnover. The CSF concentrations of all the aromatic amino acids were increased in hepatic encephalopathy, whereas in the patients with sepsis, only phenylalanine levels were increased. Evidence of stimulated neutral amino acid transport into brain was demonstrated in hepatic not septic encephalopathy and appeared to correlate with the CSF glutamine concentration. Blood ammonia levels were increased in hepatic but not in septic encephalopathy. Our data support the hypothesis that metabolites of phenylethylamine contribute to encephalopathy in systemic sepsis and hepatic failure; however, the entities differ in other respects.

Ammonia↗
PubMed1990

The thermodynamics of bipolarity: a bifurcation model of bipolar illness and bipolar character and its psychotherapeutic applications.

Two models dominate current formulations of bipolar illness: the homeostatic model implicit in Freud's psychodynamics and most neuroamine deficit/excess theories; and the oscillatory model of exaggerated biological rhythms. The homeostatic model is based on the closed systems approach of classic thermodynamics, while the oscillatory model requires the open systems approach of modern thermodynamics. Here we present a thermodynamic model of bipolarity that includes both homeostatic and oscillatory features and adds the most important feature of open systems thermodynamics: the creation of novel structures in bifurcation processes. According to the proposed model, bipolarity is the result of exaggerated biological energy that augments homeostatic, oscillatory and creative psychological processes. Only low-energy closed systems tend to rest ("point attractor") and entropic disorder. Open processes containing and exchanging energy fluctuate between opposite states ("periodic attractors"); they are characteristic of most physiological rhythms and are exaggerated in bipolar subjects. At higher energies, their strong fluctuations destroy pre-existing patterns and structures, produce turbulence ("chaotic attractors"), which sudden switches between opposite states, and create new and more complex structures. Likewise, high-energy bipolars develop high spontaneity, great fluctuations between opposite moods, internal and interpersonal chaos, and enhanced creativity (personal, artistic, professional) as well as psychopathology (personality deviations, psychotic delusions). Offered here is a theoretical explanation of the dual--creative and destructive--nature of bipolarity in terms of the new enantiodromic concept of entropy generalized by process theory. Clinically, this article offers an integrative model of bipolarity that accounts for many clinical features and contributes to a definition of the bipolar personality.

Adult↗
PubMed1990

Urinary phenylacetic acid in panic disorder with and without depression.

Phenylacetic acid (PAA) excretion was measured in 39 patients who met criteria for panic disorder; 9 of these also had major depression, and 30 did not. Patients with panic and depression excreted 66 +/- 23 mg/day of PAA, an amount significantly lower than in normal controls; patients with panic disorder but without depression excreted 104 +/- 23 mg/day of PAA (not significantly lower than controls). The results support previous studies indicating that PAA excretion is a marker for depressive disorder.

Adolescent↗
PubMed1989

Biological priority and psychological supremacy: a new integrative paradigm derived from process theory.

Process theory is a comprehensive theory of physical and psychological processes that can serve to integrate biological, social, and psychodynamic psychiatry. Process theory uses concepts derived from mathematical dynamics and Heraclitus's process philosophy. It provides three novel and clinically applicable concepts: 1) biological priority and psychological supremacy (as contrasted to theories of biological or psychological primacy), 2) union of opposites (as contrasted to psychoanalytic and dialectic conflicts and to systems homeostasis), and 3) creative bifurcations (as contrasted to determinism and developmental theories).

Biological Psychiatry↗
PubMed1989

High phenylacetic acid differentiates schizoaffective from schizophrenic patients.

Twenty-four hour urinary phenylacetic acid was high in 12 acutely psychotic schizoaffective patients (240.3 +/- 51.9 mg/day) and low in 16 acutely psychotic schizophrenic patients (53.6 +/- 15.1 mg/day). These results indicate a biochemical difference between these two types of acute psychoses and indicate alterations in phenylalanine metabolism.

Adult↗
PubMed1978

Lithium prevention of amphetamine-induced 'manic' excitement and of reserpine-induced 'depression' in mice: possible role of 2-phenylethylamine.

Repeated treatment of mice with lithium chloride (45 mg/kg, i.p., daily for 8 days) reduced the jumping, fighting, stereotypies, and hyperactivity induced by d-amphetamine (5 mg/kg, i.p.). Lithium also reduced the hypoactivity observed 1--3 h after reserpine (0.75 mg/kg, i.p.). In biochemical studies we found that 8-day treatment with lithium markedly reduced (to 45% of control) the recovery from brain of labelled 2-phenylethylamine (PEA) following i.p. injection of labelled L-phenylalanine, while decreasing recovery from brain of labelled PEA following its i.p. injection of 63% of control. In saline-treated mice, d-amphetamine appeared to increase PEA synthesis and to accelerate its disposition, whereas reserpine enhanced PEA synthesis and reduced disposition; all of these effects were antagonized by lithium pretreatments. Since PEA appears to be one of the most powerful behavioral stimulants among endogenous neuroamines, and because its deaminated metabolites are behavioral depressants, such antagonism of brain PEA metabolism may significantly contribute to the prophylactic action of lithium against both manic and depressive behavior.

Animals↗
PubMed1976

Biochemical plasticity of synaptic transmission: a critical review of Dale's Principle.

"Dale's Principle" states that each neuron releases one and only one synaptic transmitter. Mental disorders and behavioral drug effects are attributed to activation or blockade of one or more of these specific transmitters. A series of biochemical, electrophysiological, and behavioral studies suggests the alternative view that at each monoaminergic synapse the action of the transmitter is modulated by several metabolically related substances: amine analogs (2-phenylethylamine [PEA], p-tyramine, etc.), deaminated products (aldehydes, acids, and alcohols), and possibly also amino acid precursors. In support of this view, the authors present evidence for the presence, synthesis, metabolism, and biological activity (at the cellular level, using microelectrode techniques) of amino acid, amines, and deaminated compounds metabolically related to catecholamines and sorotonin. That neuroamino acids exert direct effects (not mediated via their amine metabolites) is illustrated by the rapid effects of microiontophoretic dopa upon cortical unit activity, and by the observation that neither the lethargic effect of 5-hydroxytryptophan (considered to support Jouvet's serotonergic theory of sleep) nor the behavioral stimulant effects of dopa (considered to support the catecholamine theory of affective behavior) are significantly prevented by L-aromatic amino acid decarboxylase inhibitors. The biological activity of the deaminated metabolites of catecholamines and serotonin is illustrated by the effects of their microiontophoretic administration upon cortical units. Further, probenecid (an inhibitor of acid transport across the blood-brain barrier) is shown to qualitatively alter the effects of intraventricularly administered PEA and of its metabolite phenylacetic acid upon visual evoked potentials. Rabbit brain is shown to synthesize a series of pharmacologically active noncatecholic phenylethylamines as by-products of catecholamine metabolism. Amine modulators such as PEA differ from typical transmitters by their ability to cross biological barriers; inhibition of decarboxylase in peripheral tissues only (using alpha-methyldopa hydrazine) markedly depletes brain PEA (but not catecholamines). Because of the homeostatic control of the rate of transmitter synthesis and disposition, physiological, pharmacological, and pathological changes may be expected to affect more the tissue levels of related modulators. This modulator theory of drug action is illustrated by the effect of several psychotropic drugs upon the brain levels of PEA and of norepinephrine. For instance, amphetamine initially decreases and then increases brain PEA levels, without altering brain norepinephrine levels. The authors propose an expanded "Dale's Principle": each neuron is specific in that it releases at all its endings the same pool of chemical messengers, composed of one transmitter and metabolically related modulators, the relative proportion of which is determined by the physiological state of the cell (biochemical plasticity)...

5-Hydroxytryptophan↗
PubMed1975

Behavioral and electrophysiological effects of phenylethanolamine and 2-phenylethylamine.

The electrophysiological and behavioral effects of phenylethanolamine (OHPEA) and of its precursor 2-phenylethylamine (PEA) were studied in mice and rabbits. In animals pretreated with MAOI, PEA was found to exert strong amphetamine-like effects, EEG alerting, reduction of visual evoked responses, increased locomotor activity, and blockade of tonic seizures induced by electroshock. OHPEA exerted weaker amphetamine-like effects. Inhibition of dopamine-beta-hydroxylase increased most of the effects of PEA. In non-pretreated animals, OHPEA was found to shorten electroshock latency and to prolong the duration of visual evoked responses. PEA (but not OHPEA) potentiated the excitement induced by delta9-tetrahydrocannabinol in MAOI-pretreated mice. Reserpine pretreatment reduced but did not abolish the CNS effects of OHPEA and PEA. One may speculate that endogenous PEA is more likely to serve as a modulator for ergotropic functions than is endogenous OHPEA.

Animals↗
PubMed1975

Differential membrane effects of general and local anesthetics.

The authors studied the effects of varying Na+ and Ca++ concentrations and of replacing H2O with D2O in Ringer's solution upon the actions of general and local anesthetics on isolated frog sciatic nerves. This experimental model was used to study whether general anesthetics affect excitable membranes in a manner similar to that of typical membrane stabilizers (local anesthetics). Procaine (2.5-7.5 mM), halothane (9, 18, and 36 mM), enflurane (8 mM), and ketamine (0.15 and 0.73 mM) raised threshold and lowered spike amplitude, and their effects were facilitated by reducing Na+ concentration in the Ringer's solution. The local anesthetic effects of procaine (2.5-7.5 mM) and ketamine (0.73 mM) were antagonized by Ca++, while the axonal depressant effect of halothane was facilitated by increasing Ca++ concentration in the Ringer's solution, indicating a different mode of action. General anesthetics also differed from local anesthetics in their interaction with water: replacement by D2O of H2O in the Ringer's solution selectively increased the axonal depressant effects of halothane and enflurane but not those of ketamine or procaine. Since D2O differs from H2O in its greater ice-likeness, these results are consistent with the view that general anesthetics stabilize excitable membranes via stabilization of the water-biopolymer lattice, as predicted by the hydrate-microcrystal theory of anesthesia. In contrast, local anesthetics may stabilize excitable tissues by binding to the same fixed negative charges of the membrane to which Ca++ is normally bound. (Key words: Theories of anesthesia, hydrate-microcrystal; Nerve, mode of action of anesthetics; Anesthetics, volatile, halothane; Anesthetics, volatile, enflurane; Anesthetics, local, procaine; Anesthetics, intravenous, ketamine.)

Anesthesia, General↗