Влияние различных антидепрессантов на фазы сна

A clinical consequence of REM suppression can be a change in frequency and intensity of dreaming, as well as a pronounced exacerbation of intense, disturbing dreams related to “REM rebound” on discontinuation. Pulmonary specialists sometimes advocate use of an activating TCA such as protriptyline because it may help suppress REM sleep—when sleep apnea episodes may be accentuated—and also provide benefit for the daytime somnolence that many patients with sleep apnea experience.

The Effects of Antidepressants on Sleep

Оксибутинин в качестве корректора гипергидроза вызванного приёмом антидепрессантов

Patient A is a 59-year-old man with a history of recurrent episodes of panic disorder, for which he had used paroxetine, venlafaxine, and escitalopram as well as high doses of oxazepam in the past. He was admitted to the hospital because of a severe depressive episode with suicidal ideation. The depression was successfully treated with clomipramine, 100 mg/day, which was effective for the treatment of panic attacks as well. Although he sweated all over his body, he was willing to continue clomipramine monotherapy after discharge. Lowering the dosage did not change the situation, nor did treatment with cognitive-behavioral therapy. Finally, a trial with oxybutynin, 2.5 mg b.i.d., relieved the hyperhidrosis completely, without any side effects.

Patient B is a 60-year-old man with recurrent severe depressive episodes with psychotic symptoms and agitation. Typical for his disorder are the rapid onset of relapse and the severity of agitation, which in the past required hospitalization and seclusion. In the latest episode he was treated with clomipramine, 75 mg/day, and olanzapine, 15 mg/day, but he suffered from severe hyperhidrosis. A switch from olanzapine to haloperidol did not change the hyperhidrosis. Later, 800 mg/day of lithium was successfully added for the treatment of his depressive symptoms. Oxybutynin, 5 mg t.i.d., was added to his treatment and relieved his hyperhidrosis without side effects.

There are several preferential strategies to treat hyperhidrosis, such as lowering the dosage or altering the dosing schedule, changing clothing or food habits, or regulating anxiety (2). In the present two cases, these strategies were unsuccessful and oxybutynin maintenance treatment was introduced. With its rapid, short-term effect (within an hour), oxybutynin could also be considered "as needed" in specific social situations. One should be careful in dosing to avoid anticholinergic side effects such as constipation, urinary retention, and blurred vision. Although placebo-controlled research is necessary, the cases reported here suggest that adding oxybutynin to antidepressants can be a simple and effective treatment option for hyperhidrosis.

Oxybutynin for Antidepressant-Induced Hyperhidrosis

Потенциирование трийодтиронином при недостаточном ответе на терапию ТЦА

"The exact mechanism of action of T3 augmentation remains largely unknown. In depressed patients, the circulating plasma levels of free T4 appear to be normal,
but levels of free T3 may be decreased. Approximately one third of depressed patients show blunting of the TSH response to thyrotropin releasing hormone.
Approximately 15% of depressed patients have elevated basal TSH levels, probably indicating subclinical hypothyroidism, and thyroid autoantibodies
are found in a similar percentage of patients.11
Thyroid abnormalities are found at a higher frequency among TCA nonresponders and this may link with the underlying mechanism of T3 augmentation.In most case reports, patients had normal thyroid function, as in our second case. There seems to be no
relationship between thyroid state and the efficacy of T3 augmentation. In the first case, the patient had sick euthyroid syndrome, which is sometimes seen in
depressed patients. In this condition, peripheral deiodination of T4 to T3 is reduced, although the TSH level is normal.
One proposed mechanism of T3 augmentation is that T3 may raise peripheral thyroid hormone concentrations in patients with covert or borderline hypothyroidism. Other authorities believe that there is no difference in the thyroid state of the
responders and nonresponders to T3 augmentation. 12 L-triiodothyronine may act in euthyroid patients through augmentation of the β-adrenergic system.13 Alternatively, T3 may also affect thyroid utilisation and local neuronal deiodination in the brain."

"The usual dose of T3 in augmentation therapy is 25 µg/d to 50 µg/d. A starting dose of 20 µg increasing to 40 µg was given to the patients in this study. Initial improvement in mood is usually apparent within several days. Goodwin et al reported that there was improvement in all aspects of the depressive syndrome within 1 to 3 days. For the two patients in this study,initial responses were noted after 3 and 7 days. An adequate trial of T3 augmentation should last for 7 to 14 days to reach its full effect. If T3 augmentation is effective, most studies recommend a maintenance
period of 2 months before gradually reducing the dose at the rate of 10 µg every 3 to 7 days."

Triiodothyronine augmentation for the treatment of depression in substance misusers unresponsive to tricyclic antidepressants.