Biomedical subjects

T Suppes

Publications and source records attributed to T Suppes.

64 records · Page 4Linked to original sources

PubMed1991

Risk of recurrence following discontinuation of lithium treatment in bipolar disorder.

Episode recurrence in bipolar disorder following discontinuation of stable maintenance treatment with lithium salts was analyzed from 14 studies involving 257 patients with bipolar I disorder. More than 50% of new episodes of illness occurred within 10 weeks of stopping an average of 30 months of treatment. By survival analysis of 124 cases in which the time to a new episode was known, the computed time to 50% failure of remission was 5.0 months after stopping therapy; the time to 25% recurrence of mania was 5.2 times earlier than for depression (2.7 vs 14 months). In 16 patients with a mean cycle length before treatment of 11.6 months, the time to a new episode when off lithium therapy was only 1.7 months. Risk of early recurrence of bipolar illness, especially of mania, evidently is increased following discontinuation of lithium use and may exceed that predicted by the course of the untreated disorder. The basis and management of risks associated with discontinuing effective long-term mood-stabilizing treatment require further study.

Bipolar Disorder↗

PubMed1987

Sensitivity of neuronal dopamine response in the substantia nigra and ventral tegmentum to clozapine, metoclopramide and SCH 23390.

The activity of neurones in the substantial nigra and ventral tegmentum was recorded extracellularly in vitro. Dopamine produced depression of spontaneous firing in a dose-dependent manner. Antagonism of these neuronal responses to dopamine by metoclopramide, SCH 23390 and clozapine was examined. Metoclopramide antagonised the responses to dopamine in the manner expected; SCH 23390 had little effect on the response to dopamine as would be predicted for a selective dopamine "D1" antagonist. Clozapine did not produce the expected antagonism of the response to dopamine. The results at the single neurone level are compared with behavioural and biochemical data.

Action Potentials↗

PubMed1987

Cellular and synaptic physiology and epileptogenesis of developing rat neocortical neurons in vitro.

The cellular and synaptic physiology of developing rat neocortical neurons was studied using the in vitro slice method. Rats aged 1-28 days were used for analysis. During the first two postnatal weeks several sequential changes occur in membrane properties and evoked synaptic potentials. Immature neurons had higher input resistances, more linear I-V characteristics, longer membrane time constants, and slower rising and falling phases of action potentials. The developmental increase in rate of rise of the action potential suggests an increasing density of voltage-dependent Na+-channels are inserted in neuronal membranes during postnatal development. The higher input resistance of young cells might be due to their small size and differences in membrane properties. The long time constant indicates a higher specific membrane resistivity of immature neurons. Postsynaptic potentials (PSPs) recorded in young neurons were longer in latency, longer in duration, and more fragile during repetitive activation than their mature counterparts. In addition, PSPs evoked in neurons of animals less than 1 week old did not contain inhibitory postsynaptic components. These physiological features of immature neocortical neurons help explain the pattern of epileptogenesis in young animals. When neonatal cortical slices were exposed to the gamma-aminobutyric acid (GABA) antagonists penicillin or bicuculline, the frequency of occurrence of discharges resembling epileptiform depolarization shifts approached that found in mature slices only during the second postnatal week. Depolarization shifts at younger ages were less stereotyped and more sensitive to stimulus parameters than those in mature neurons.

Animals↗

PubMed1985

The influence of dopamine on epileptiform burst activity in hippocampal pyramidal neurons.

Dopamine (DA) application to guinea pig hippocampal CA1 neurons in vitro causes hyperpolarization of the resting potential, increase in conductance, and increase in amplitude and duration of the afterhyperpolarization (AHP). Since these changes could influence repetitive firing, we performed experiments to determine whether DA-induced effects would suppress epileptogenesis in the hippocampus. Epileptiform bursts were induced by adding penicillin (3.4 mM) to the perfusion medium. Focal application of DA (40-160 microns) onto CA1 cells (n = 15) produced a hyperpolarization averaging 4.5 mV beginning in 5-20 s and lasting up to 3 min. DA also caused an increase in the amplitude and duration of slow AHPs. The frequency of spontaneous epileptiform events however was not affected. CA3 neurons (n = 6) responded to DA application with an initial 1-3 mV depolarization beginning within 5-30 s and lasting 1-2 min. In 3 cases a small hyperpolarization lasting several minutes subsequently developed. AHP duration increased 70% and amplitude increased 35% (n = 4). Along with these membrane changes the frequency of epileptiform bursting in CA3 cells slowed for 1-3 min. We added DA (10-80 microM) to the perfusion medium to see whether a significant decrease in epileptiform burst frequency might occur in the follower CA1 region if greater numbers of pacemaker CA2 and CA3 cells were exposed to DA. Spontaneous CA1 bursting was reversibly slowed, the interburst interval became variable and increased from a mean of 4 to a mean of 5-7 s (n = 6). These results suggest that DA may play a role in decreasing the incidence or frequency of epileptogenic discharges in vivo.

Animals↗

PubMed1984

A late slow depolarization unmasked in the presence of tetraethylammonium in neonatal rat sympathetic neurons in vitro.

Neonatal rat superior cervical ganglia were mechanically dissociated, and the sympathetic neurons grown in dispersed cell cultures. Intracellular microelectrodes were used to study the effects of tetraethylammonium (TEA+), a blocker of outward K+ currents, on the excitable properties of these neurons. Addition of TEA+ to the perfusion media (TEA+-media) caused the resting potential to depolarize and the action potential to increase in duration. In TEA+-media (20-60 mM), a late delayed depolarization (LDD) followed the falling phase of the action potential with a delay of 1.5-2 s (n = 95). The LDD peak amplitude was in the range of 4-26 mV and the duration, to full return of the resting potential, was in the range of 18-90 s. For a given cell the amplitude and duration of the LDD were constant. The LDD was associated with a conductance increase. No LDD could be elicited in the presence of calcium channel blockers. Evidence was found for a Ca2+-dependence of the LDD: increasing the extracellular Ca2+ concentration caused increases in the amplitude and duration of the LDD. The significance of an endogenous LDD-like potential and possible explanations for the origin of the LDD are discussed.

Animals↗

PubMed1983

Cholinergic enhancement of penicillin-induced epileptiform discharges in pyramidal neurons of the guinea pig hippocampus.

Acetylcholine (1-20 mM) was applied to guinea pig hippocampal slices bathed in normal and penicillin-containing media. Recordings in the CA 1 pyramidal cell layer in the presence of penicillin showed that acetylcholine caused a prolonged enhancement of the extracellular field potential. Intracellular recordings documented an increase in duration of cell bursting, a decrease in burst afterhyperpolarization, and a membrane depolarization lasting 1-5 min. These results suggest that the actions of acetylcholine to increase membrane excitability interact with penicillin-induced disinhibition to enhance hippocampal epileptogenesis.

Acetylcholine↗

PubMedDate not supplied

Comparison of the internal state scale to clinician-administered scales in asthma patients receiving corticosteroid therapy.

Mood symptoms are reported frequently in asthma patients, particularly during corticosteroid therapy. This investigation compared the Internal State Scale (ISS), a self-report measure of symptoms of mania and depression, to the Hamilton Rating Scale for Depression (HRSD), Young Mania Rating Scale (YMRS), and Brief Psychiatric Rating Scale (BPRS) in a group of asthma patients (n=60 at baseline) before, during, and after a 1-2 week burst of prednisone. The depression and well being subscales of the ISS correlated well with HDRS scores. The perceived conflict subscale correlated with the BPRS scores. However, none of the ISS subscales correlated consistently and specifically with the YMRS in this population. Possible explanations for differences observed in bipolar versus asthma patients given the ISS are discussed. These data suggest the ISS may be a useful tool for depression symptoms and overall psychopathology in asthma patients and in patients receiving corticosteroid therapy. However, its ability may be attenuated outside of the population for which it was designed.

Anti-Inflammatory Agents↗

PubMedDate not supplied

Discontinuation of maintenance treatment in bipolar disorder: risks and implications.

There is abundant evidence for substantial long-term prophylactic efficacy of lithium in bipolar manic-depressive disorders. Interruption of such treatment carries an extraordinarily high risk of recurrence within several months, even after several years of stability. Even a sharp reduction in dose may carry some risk. Gradual discontinuation of lithium was accompanied by markedly reduced risk of early recurrence. There is suggestive evidence that the phenomenon of high risk of recurrence after abrupt interruption of maintenance treatment may occur with other disorders and treatments, including neuroleptics in schizophrenia and possibly antidepressants in recurrent depression. The phenomenon of discontinuation-associated iatrogenic risk of early recurrence of major psychiatric illness has clear clinical implications. These include the need to evaluate safer methods of interrupting long-term maintenance treatment, particularly when clinical indications for rapid cessation are compelling and gradual discontinuation is not feasible. Questions also arise concerning interpretation of existing experimental studies of maintenance treatments that require interruption of treatment, reduction of dose, or crossover to a placebo, as well as the ethical and scientifically unambiguous design of future studies of this kind.

Antimanic Agents↗

PubMedDate not supplied

Pediatric-onset bipolar disorder: a neglected clinical and public health problem.

Bipolar disorder (BPD), probably the most prevalent psychotic disorder in adults, has been relatively neglected or controversial in children and adolescents over the past century. We reviewed the literature on early-onset BPD. Estimates of prevalence, particularly before puberty, are limited by historical biases against pediatric mood disorders and by formidable diagnostic complexity and comorbidity. Although clinical features of pediatric and adult BPD have similarities, pediatric cases probably cannot be defined solely by features characteristic of adult cases. Onset was before age 20 years in at least 25% of reported BPD cases, with some increase in this incidence over the past century. Pediatric BPD is familial more often than is adult-onset BPD, may be associated with a premorbid cyclothymic or hyperthymic temperament, and can be precipitated by antidepressant treatment. Pediatric BPD episodes frequently include irritability, dysphoria, or psychotic symptoms; they are commonly chronic and carry high risks of substance abuse and suicide. BPD is often recognized in adolescents, but the syndrome or its antecedents are almost certainly underrecognized and undertreated in children. Controlled studies of short- and long-term treatment, course, and outcome in this disorder remain strikingly limited, and the syndrome urgently requires increased clinical and scientific interest.

Adolescent↗

PubMedDate not supplied

Mood symptoms during corticosteroid therapy: a review.

Corticosteroids such as prednisone are commonly prescribed for a variety of illnesses mediated by the immune system. This paper reviews the available literature on mood symptoms during corticosteroid treatment. Few studies have used well-recognized measures of symptoms or clearly defined diagnostic criteria to characterize such mood changes. The limited data available suggest that symptoms of hypomania, mania, depression, and psychosis are common during therapy. Symptoms appear to be dose dependent and generally begin during the first few weeks of treatment. Risk factors for the development of mood instability or psychosis are not known. The similarities of the psychiatric symptoms resulting from corticosteroid treatment to the symptoms of bipolar disorder are discussed.

Adrenal Cortex Hormones↗