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Biomedical subjects

I M Zervas

Publications and source records attributed to I M Zervas.

14 recordsLinked to original sources
PubMed2006

Set shifting deficits in melancholic vs. non-melancholic depression: preliminary findings.

Twenty-two patients with major depressive disorder, 11 of them with melancholic features, and 11 controls were investigated with CANTAB subtests focusing in visual memory/learning and executive functions. Melancholic patients performed worse than the other groups in all tasks and manifested a significant impairment in set shifting. The results are discussed in association with prefrontal dysfunction.

Cognition Disorders↗
PubMed2006

Hip dysplasia following a case of olanzapine exposed pregnancy: a questionable association.

This is a case report of a 33 year old woman with a history of psychosis, who presented to the women's mental health clinic for consultation at the 12(th) week of gestation, having already received olanzapine throughout the first trimester. She was followed from that point on at our clinic and remained on small doses of olanzapine for the rest of her pregnancy, which was uncomplicated. She gave birth to a healthy female, which at the age of three months was diagnosed with developmental dysplasia of the hip and subsequently received appropriate treatment with favorable outcome. The possibility of the association of this congenital dysplasia with the use of olanzapine during pregnancy is further discussed in this paper.

Adult↗
PubMed2000

Olanzapine and obsessive-compulsive symptoms.

Clozapine and risperidone have been implicated in the development of obsessive-compulsive symptoms. We present three cases in which olanzapine caused a significant exacerbation of obsessive-compulsive symptoms in schizophrenia (two cases) and obsessive-compulsive disorder (one case).

Adult↗
PubMed2000

Administration of citalopram before ECT: seizure duration and hormone responses.

From theoretical and clinical perspectives, it is important to know if selected serotonin-reuptake inhibitors (SSRIs), often administered concurrently with electroconvulsive therapy (ECT), modify seizure duration. In a study with a double-blind, cross-over design, the authors evaluated the effect of citalopram, the most selective SSRI available, on the length of electrically induced seizures and on hormone secretion during ECT. Ten depressed women were given either 20 mg citalopram or placebo orally 2 hours before the third and fourth ECT sessions. Seizure duration was assessed by the cuff technique and from electroencephalographic recordings, whereas blood for prolactin, thyrotropin, and cortisol assessment was sampled before ECT and 5, 10, 20, 30, 40, and 60 minutes after ECT. No adverse effects after the administration of citalopram were recorded. The length of seizures was not statistically different in the citalopram (29.3+/-8.4 seconds) and placebo sessions (28.2+/-9.4 seconds). Neither pre-ECT plasma hormone levels measured 2 hours after citalopram or placebo administration nor the patterns of ECT-induced hormone secretions differed between the two drug and placebo conditions. The lack of effect of citalopram on hormones in this study may be a result of possible deficiencies of the monoaminergic (i.e., serotoninergic) systems in depression. Although safety and efficacy issues were not fully addressed by coadministering citalopram for the long term and throughout the course of ECT, these findings support the view that challenges the typical clinical practice of discontinuing SSRIs before ECT.

Administration, Oral↗
PubMed1999

Blunted TSH response to TRH and seizure duration in ECT.

The relationship between the thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH) and the duration of seizures induced by electroconvulsive therapy (ECT) in depressed patients was investigated. In a balanced-order cross-over design, 16 depressed women were given 0.4 mg TRH or placebo intravenously, 20 min before ECT in the first two sessions. In the third ECT session TRH was given just prior to ECT. Thyrotropin (TSH) levels at various sampling times, as well as the duration of seizures, were measured. There was a significant inverse correlation between plasma TSH concentrations 20 min after TRH administration (deltaTSH) and seizure duration. Furthermore, when patients were categorized according to their TSH response to TRH, the group with blunted responses (deltaTSH <6 microIU/ mL, n = 7) had a longer seizure time during ECT than the group with non-blunted responses (deltaTSH > 6 microIU/mL, n = 9). Finally, the seizure duration in the group with blunted TSH responses was reduced significantly when TRH was co-administered, while it remained unchanged in the group with non-blunted TSH responses. It is concluded that a blunted TSH response to TRH might indicate a seizure susceptibility as measured by the duration of seizures induced by ECT. The fact that TRH pre-administration had a reducing effect suggests that this substance might be involved in the pathophysiology of ECT-induced seizures.

Adult↗
PubMed1998

Effects of TRH administration on orientation time and recall after ECT.

We investigated the effect of thyrotropin-releasing hormone (TRH) on orientation time and recall, in nine depressed female inpatients undergoing electroconvulsive therapy (ECT). In a balanced order crossover design, an intravenous bolus of 0.4 mg TRH or placebo was administered 20 min before ECT in the first two sessions. Orientation time and retrograde and anterograde components of the memory dysfunction, immediately and 24 h later, were assessed. Administration of TRH did not influence orientation time, word recall, or immediate short story recall compared with placebo. We did find, however, an improvement in the number of short story items recalled after 24 h when patients were given TRH compared with placebo. This indicates that TRH may have a protective role against the specific negative effect of ECT on delayed recall.

Adult↗
PubMed1996

Effects of thyrotropin-releasing hormone administration on the electroconvulsive therapy induced prolactin responses and seizure time.

The effects of thyrotropin-releasing hormone (TRH) administration on electroconvulsive therapy (ECT)-induced prolactin (PRL) secretion and the duration of the seizure were studied in 14 depressed women. In a balanced order crossover design the patients were given 0.4 mg TRH or placebo intravenously 20 min before ECT during the first two sessions. In the third ECT session TRH was given just prior to ECT. ECT elicited the expected PRL response when given alone and when given 20 min after TRH when PRL plasma levels were high. During the coadministration design (third ECT session) PRL levels were raised not as a sum of the two stimuli but even significantly more. TRH failed to modify the duration of the seizure induced by ECT. Therefore, if TRH is involved in seizure modulation during ECT, our findings suggest a postictal rather than ictal role for TRH.

Adult↗
PubMed1995

Effects of methysergide and ritanserin on the prolactin and thyrotropin responses to TRH in depressed patients.

Despite extensive study of the effects of various pharmacological agents on the thyrotropin (TSH) and prolactin (PRL) responses to TRH challenge, the effect of serotoninergic agents remains inconclusive. We studied the effect of the serotonin antagonists methysergide (non-selective 5-HT1/5-HT2 blocker with dopaminergic properties) and ritanserin (selective 5-HT2 blocker) on the TSH and PRL responses to TRH stimulation in two groups of medication-free female depressed patients in a double-blind, within-subject design. Methysergide was found to decrease significantly the PRL response to TRH, while ritanserin had no effect. Neither compound influenced the TSH response. Results suggest that 5-HT2 mechanisms do not mediate the PRL and TSH responses to TRH challenge in depression. The reduction in PRL observed after methysergide is probably due to either 5-HT1 or dopaminergic mechanisms.

Aged↗
PubMed1995

ECT and non-memory cognition: a review.

The literature on the effects of electroconvulsive therapy (ECT) on non-memory cognitive functions is reviewed. It is concluded that with early methods of ECT administration (sine wave, high dose), these effects are larger than those of depression. They are less pronounced, and usually do not exceed the effects of depression, when modern methods of ECT administration (brief pulse, moderate or low dose) are used. Following ECT, these functions progressively improve. At one week to seven months after ECT, performance is better than before ECT, probably because of the alleviation of both the effects of depression and of ECT. The time course to full recovery of the non-memory effects resembles that of the recovery of amnesic effects, although the latter are more pronounced. With bilateral ECT, as with right unilateral ECT, there is evidence that right hemisphere effects are more pronounced. The results of this review argue that clinicians should take the non-memory cognitive effects of ECT into account, and patients should be informed of their existence before they sign consent for ECT.

Cognition Disorders↗
PubMed1993

Patient delay in cancer. A view from the crisis model.

Despite widespread cancer awareness programs, deleterious delays in seeking diagnosis and care for cancer are as prominent now as as they were 50 years ago. These delays may be seen as attempts to resolve or postpone the crisis brought on an individual by the suspicion of terminal illness. The use of denial-like processes in the cognitive appraisal employed to assess this crisis is influenced by a variety of personal, social, and physical factors. Case material is examined to discuss the integration of these factors by the crisis model of physical illness and to examine the implications of such an approach for earlier detection and treatment of cancer.

Adaptation, Psychological↗
PubMedDate not supplied

Presbyophrenia: a possible subtype of dementia.

Presbyophrenia is characterized by memory impairment, disorientation, confabulation, hypomanic features, and a preserved social facade. These occur in the absence of prior history of alcoholism or affective illness. We present three cases with presbyophrenia and suggest that the syndrome is a recognizable subtype of dementia, possibly related to disruption of aminergic pathways in frontal and subcortical structures.

Aged↗