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Fluoxetine and placebo were compared in 89 outpatients with major depression with (n = 45) or without (n = 44) a reduced or shortened rapid eye movement latency (SREML) (< or = 65 minutes) to determine whether rapid eye movement latency (REML) predicted placebo and/or antidepressant response. Men and women were stratified based on polysomnographic recordings and then randomly assigned to receive double-blind fluoxetine (20 mg/day) or placebo for 8 weeks after a 2-week, single-blind, placebo lead-in period. Fluoxetine-treated patients demonstrated a significantly greater reduction in the Hamilton Rating Scale for Depression total score and a significantly greater response rate than placebo-treated patients in both the SREML and the combined strata. Treatment differences in the non-SREML stratum were not statistically significant. Results supported REML as a predictor of placebo nonresponse but did not predict a differential fluoxetine response in patients with SREML compared with patients without SREML.

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Circadian rhythm abnormalities have been implicated in winter seasonal affective disorder. We examined the circadian temperature rhythm of 22 patients with winter depression and 10 normal controls who had participated in various high-intensity light treatment experiments. We did not find abnormalities in the baseline phase or amplitude of the temperature rhythm in patients compared to controls. Nor did we find abnormalities in the phase-shifting response to morning light. There was some evidence that the "phase-delayed" half of the patients responded poorly to phase advances produced by morning light, whereas the "phase-advanced" half of the patients responded poorly when their rhythms delayed. However, the antidepressant responses during the best week (week of lowest depression score) were unrelated to temperature rhythm phase shifts. In general, there was not strong support for a relationship between circadian rhythms changes and antidepressant response.

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We studied 32 patients with winter seasonal affective disorder (SAD) in a counterbalanced crossover design comparing 1 h of morning light treatment (about 7000 lux) to 1 h of morning placebo treatment (deactivated negative ion generator). Both treatments significantly reduced depression ratings, but there was no difference between the antidepressant response to light and to placebo. Several possible explanations for this result were discussed including an inadequate 'dose' of light (e.g., ineffective duration or intensity), an unusual sample of patients, and a placebo mechanism.

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The transition from well to depressed offers a window to the mechanisms which underlie depressive symptoms. We examined the onset of each of 15 symptoms in 53 patients with winter depression. Three symptoms had a risk of onset closely associated with the onset of the episode itself and may represent a core syndrome. The risk of onset for the remaining symptoms was unrelated to the onset and the course of the episode. The symptoms were equally likely to begin at any time during the episode and suggest a different pathological mechanism. A dual vulnerability hypothesis is proposed; research and treatment implications are discussed.

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This chapter will focus on the office management of psychiatric patients with sleep disorders. Psychiatric aspects of insomnia, the parasomnias, circadian rhythm disorder and disorders of excessive sleepiness will be reviewed. The antidepressants, electroconvulsive therapy, amino acids and bright lights.

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Seasonal affective disorders is a form of recurrent depression that appears to be precipitated by a specific stressor (i.e., winter) and resolves spontaneously in spring or summer. The elements of winter that must contribute to SAD are unknown at this time although light deficiency most likely plays a role. It is similar to late luteal dysphoric disorder because of the circumscribed time course, range of severity and female predominance. Atypical anergic symptoms usually dominate the clinical picture but more typical anxious and agitated symptoms can be present. Onset and offset of symptoms and severity varies greatly. Fall onset is usually gradual while spring remission can be more startling and abrupt producing hypomania in some patients. Full summer remission occurs in most patients when followed prospectively and is associated with improvement in personality and biological measures. Most patients improve with light therapy but it is not known how sustained this effect is or whether it is comparable to treatment with antidepressants in similarly affected patients. BL treatment also implies a single etiological mechanism of SAD, but this is still unproven. Lights, while effective do not appear to be as effective as summer. This could be because most BL clinical trials have been too brief to actually simulate summer or because of the significant heterogeneity in population. It is important to remember that lights alone cannot replicate summer conditions. Summer light is up to ten times stronger than currently available light boxes and the season produces many other environmental and social changes. Most likely SAD will prove similar to other forms of depression in that it is a multidimensional problem which requires a variety of treatments to alleviate various aspects of the syndrome.

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The authors administered the Diagnostic Interview Schedule to 21 patients with borderline personality disorder. The patients met criteria for various other DSM-III diagnoses, meeting exclusion criteria in some cases, and not in other cases. Frequency distribution of each diagnosis and the diagnoses of each individual patient, are presented. Affective disorder was the most common diagnosis (85%). Of these, 62% had primary major depression, and 23% had secondary depression. Other diagnoses include bipolar disorder, dysthymia, panic, agoraphobia, alcohol and Drug abuse, somatization disorder, and many others. The authors conclude that while borderline disorder may be a sub-affective disorder, a specific diagnostic profile for this disorder that accounts for the presence of other Axis I and Axis II syndromes has yet to be delineated.

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The use of biologic markers in the evaluation of borderline personality disorder (BPD) patients is reviewed. Many patients with Axis II BPD have coexisting Axis I diagnoses of which depression is the most commonly reported. Biologic markers have not aided in the diagnosis of BPD, but some markers, particularly EEG sleep, are not only abnormal in BPD, but also appear to discriminate Axis I depression from other Axis I codiagnoses. Monoamine oxidase, in vitro red blood cell lithium ratio, and P300 auditory evoked potential when used alone or in a combined diagnostic approach, show promise in identifying these codiagnoses as well. Dexamethasone suppression and thyrotropin-releasing hormone tests appear nonspecific in this population. Pharmacologic trials have demonstrated that some BPD patients have good therapeutic response to antipsychotics and tranylcypromine and poor response to alprazolam.

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Twenty-one patients who met DSM-III criteria for borderline personality disorder (BPD) and also scored at least 7 on the Diagnostic Interview for Borderlines (DIB) were assessed on four biological markers: electroencephalographic (EEG) sleep, in vitro lithium ratio, platelet monoamine oxidase (MAO), and dexamethasone suppression test (DST). REM latency averaged 58.66 (SD 14.39); platelet MAO averaged 21.74 (SD 10.33); and lithium ratio was 0.357 (SD 0.139) in the BPD patients. All of those values were significantly abnormal. Many patients had abnormalities on three or four measures. These patients in general had multiple Axis I diagnoses from the Diagnostic Interview Schedule (DIS), and these Axis I diagnoses tended to produce patient clusters. Patients with a DIS diagnosis of schizophrenia, mania, hypomania, or schizoaffective mania had elevated lithium, low MAO, and normal EEG sleep, while those patients with coexisting major depression tended to have short rapid eye movement (REM) latency, high REM density, and normal MAO and lithium ratio. Only two patients were nonsuppressors on the DST, confirming recent reports of normal DST results in personality disorders.

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Two craniopagus twins sharing some common cerebral circulation but no common brain structures were recorded polygraphically and continuously observed for behavioral sleep states and wakefulness. The observations lasted 9.5 h when the twins were 12 weeks postgestation and for 24 h at 16 weeks post gestation, or approximately 4 weeks postterm. Sleep onsets were synchronous 67% of the time (+/- 5 min), but arousals were synchronous only 38% of the time (+/- 5 min) at 16 weeks postgestation. The recordings reported here are the longest ever made of craniopagus twins. This report is consistent with some interdependence of the sleep of each twin on the other. Possible reasons for this are discussed.

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1. Bright fluorescent Vitalite (TM) (2000-2500 lux) was presented to 2 subjects with Seasonal Affective Disorder (SAD) and 3 normal controls 2 hours prior to bedtime for one week. Oral temperature and heart rate were measured during this time in the two groups and compared to 7 days of baseline measurements made the week before where the subjects sat quietly in dim light and monitored their temperature and pulse. Bright evening light prevented the fall in oral temperature in both SAD subjects and one normal control. Bright light also prevented the normal fall of heart rates in SAD subjects but not in normal controls. 2. Bright evening lights also produced a significant delay in sleep onset that was cumulative over the seven days in SAD subjects but was also present but less pronounced in 2 normal controls. 3. Evening light produced "activation" that was generally pleasant but produced significant irritability in one SAD subject.

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Pentazocine, in combination with the antihistamine tripelennamine, was a popular drug of intravenous abuse in many large cities in the late 1970s and early 1980s. To stem the abuse of pentazocine, naloxone was added to the tablet. This would presumably allow oral activity, but naloxone would block the euphoria if the pills were injected. Abuse of pentazocine appears to have diminished, but we have recently treated three addicts who continued to inject pentazocine, despite its naloxone content. Two patients experienced no overall decrease in the drug-induced euphoria. The third patient became acutely psychotic with each injection. Hypotheses are advanced to explain these findings.

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Heart rate and heart rate regulation during sleep and wakefulness was studied in 28 patients with major depressive disorder and in 19 control subjects. Heart rate during quiet wakefulness was greater in the depressed group (H.R. = 73.04) than in the control group (H.R. = 65.35) (t = 3.06, p less than 0.005). Heart rate remained elevated throughout sleep in the depressed group as measured in Stage II (H.R. = 67.81) compared with the control group (H.R. = 60.84) (t = 2.49, p less than 0.01). Heart rate increased during movements in sleep in all subjects. The heart rate increases were attenuated in the depressed subjects compared with nondepressed controls (p less than 0.001). The effect was independent of sleep stage or baseline heart rate. All effects were independent of subject age. These findings point to a change in autonomic regulation of heart rate in depression.

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A 64-year-old man ingested 4500 mg of maprotiline hydrochloride. He developed major motor myoclonic seizures, first-degree AV block, intraventricular conduction delay, hypotension, and urinary retention. Myoclonic seizures have not been previously reported with maprotiline toxicity.

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Sleep disturbances, including disturbances in REM sleep, are common among depressed adults; it is unclear if the same is true for depressed adolescents. The authors monitored the sleep of 13 depressed adolescents and 13 normal age-matched controls. They found that, as with depressed adults, REM latency was significantly shorter and REM density significantly greater in the depressed group. There was no correlation between reduced REM latency and severity of depression, but there was a significant negative correlation between REM latency and age.

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