Recovery, from depression

Methohexital [18652-93-2] (Brevital), C 4H gN202, (2) is a barbiturate iv anesthetic iaduction agent that has a slightly faster onset than thiopentone and less accumulation. The recovery from anesthesia is also slightly faster and better. However, iaduction is associated with an iacreased iacidence of excitatory phenomena. Methohexital also causes respiratory and cardiovascular depression and is unstable ia solution, necessitating reconstitution before use (99). 

Clarkson CW, Hondeghem LM (1985) Mechanism for bupivacaine depression of cardiac conduction fast block of sodium channels during the action potential with slow recovery from block during diastole. Anesthesiology 62 396-405... 

Antidepressant drugs are used to manage depressive episodes such as major depression or depression accompanied by anxiety. These drugs may be used in conjunction with psychotherapy in severe depression. The SSRIs also are used to treat obsessive-compulsive disorders. The uses of individual antidepressants are given in the Summary Drug Table Antidepressants. Treatment is usually continued for 9 months after recovery from the first major depressive episode. If the patient, at a later date, experiences another major depressive episode, treatment is continued for 5 years, and with a third episode, treatment is continued indefinitely. 

All the jellyfish venoms are toxic but also stimulate the cell mediated and humoral immunological systems of man. After injection of large doses of jellyfish venom into human skin, a perivascular mononuclear cell infiltration appears within the dermis. This infiltration is composed predominantly of helper inducer cells which produce suppressor activity. It appears that the NK enhancement of human leukocytes in patients envenomated by Chrysaora quinquecirrha is depressed when the clinical lesion is inflammatory (10). Recovery from this suppression follows the amelioration of the acute cutaneous reaction. In other instances, envenomated patients have abnormal macrophage migration tests (11). 

There is, however, a unique risk in the bipolar form that antidepressant treatment may trigger a switch into mania. This may occur either as the natural outcome of recovery from depression or as a pharmacological effect of the drug. Particular antidepressants (the selective serotonin reuptake inhibitors) seem less liable to induce the switch into mania than other antidepressants or electroconvulsive therapy. Treatment for mania consists initially of antipsychotic medication, for instance the widely used haloperidol, often combined with other less specific sedative medication such as the benzodiazepines (lorazepam intramuscularly or diazepam orally). The manic state will usually begin to subside within hours and this improvement develops further over the next 2 weeks. If the patient remains disturbed with manic symptoms, additional treatment with a mood stabilizer may help. 

A schematic flowsheet for molybdenum recovery from porphyry coppers is shown in Figure 2.34. Here the important role is played by flotation. The first stage involves collective flotation of copper and molybdenum. The floated product is upgraded through two or three cleaning flotations. Finally, molybdenum is recovered by depressing copper values. In order to depress a mineral, some kind of oxidation should be implied on its surface, or re-... 

This is a rather bleak picture of the effects of antidepressant treatment. In the best of circumstances - which is what the trial was designed to evaluate - only one out of three depressed patients showed a lasting recovery from depression, and since there was no evaluation of what the recovery rate might have been with placebo treatment, there is no way of knowing whether their recovery was actually due to the medication they had been given. 

The nice thing about the neural-plasticity hypothesis is that it seems to explain so much. In fact, it is a better explanation of the effects of psychotherapy than of drugs. If recovery from depression depends on learning new ways of thinking, then psychotherapy - and especially cognitive behavioural psychotherapy - ought to be effective, and indeed it is, as we shall see in Chapter 7. The... 

In depressed patients, cortical-hypothalamic-pituitary-adrenal axis hyperactivity can be explained by the hypersecretion of CRF, and secondary pituitary and adrenal gland hypertrophy. Impaired negative feedback at various CNS sites, including the hippocampus and pituitary are also likely to contribute. Downregulation of hippocampal mineralocorticoid receptors and expression is reported in depressed suicides [50]. In bipolar disorder, hyperactivity of the cortical-hypothalamic-pituitary-adrenal axis has been observed [51]. This increase in cortical-hypothalamic-pituitary-adrenal axis activity has also been observed in mixed mood states, mania and in depression in rapidcycling patients. Partial reversal of HPA overactivity is associated with treatment and recovery from depression. 

Firing rate of substantia nigra DA neurons increased Recovery from depressed firing rate of VTA DA neurons D 1-like antagonist in amygdala doesn t precipitate withdrawal Reduced amygdala central nucleus DA... 

The full spectrum of depressive symptoms including depressed mood, anhedonia, lack of energy, and even suicidal thoughts may strike as many as 25% of patients who experience a TBL Depression in these patients not only exacts a tremendous psychosocial toll but also interferes with their participation in physical and occupational rehabilitation. As a result, long-term functional recovery from TBl can be sorely compromised by depression. Potential treatments for post-TBl depression include conventional antidepressants and stimulants (see Table 12.1). 

Concomitant narcotic administration - The respiratory depressant effect of fentanyl may persist longer than the analgesic effect. Consider the total dose of all opioid analgesics used before ordering narcotic analgesics during recovery from anesthesia. Use opioids in reduced doses initially, %to 1/3 those usually recommended. 

Imipramine (Tofranil) [Antidepressant/TCA] WARNING Close observation for suicidal thinking or unusual changes in behavior Uses Depres-sion, enuresis, panic attack, chronic pain Action TCA t CNS synaptic serotonin or norepinephrine Dose Adults. Hospitalized Initial 100 mg/24 h PO in doses T over several wk 300 mg/d max Output Maint 50-150 mg PO hs, 300 mg/24 h max Peds. Antidepressant 1.5-5 mg/kg/24 h daUy-qid Enuresis >6 y 10-25 mg PO qhs T by 10-25 mg at 1-2-wk int vals (max 50 mg for 6-12 y, 75 mg for >12 y) Rx for 2-3 mo, then tap Caution [D, /-] Contra Use w/ MAOIs, NAG, acute recovery from MI, PRG, CHF, angina, CVD, arrhythmias Disp Tabs, caps SE CV Sxs, dizziness, xerostomia, discolored urine Interactions t Effects W/ amiodarone, anticholinergics, BBs, cimetidine, diltiazem, Li, OCPs, quinidine, phenothiazines, ritonavir, verapamil, EtOH, evening primrose oil t effects OF CNS depressants, hypoglycemics, warfarin T risk of serotonin synd W/MAOIs 4-... 

Neuromuscular paralysis occurs 12 to 36 hours after ingestion of the toxin. Early symptoms include diplopia, dysphagia, and dysarthria. Paralysis may descend to include proximal and limb muscles and result in dyspnea and respiratory depression. The toxins do not cross the placental barrier but do enter the central nervous system (CNS). PupU size may or may not be normal, but mental and sensory functions are not impaired. Recovery from paralysis requires days to weeks. 

Puig-Antich, J., Lukens, E., Davies, M., Goetz, D., Brennan-Quattrock, J., and Todak, G. (1985) Psychosocial functioning in prepubertal depressive disorders. II. Interpersonal relationships after sustained recovery from the affective episode. Arch Gen Psychiatry 42 511-517. 

Animal behavioral models can be used to evaluate the effect of antidepressants on depression [Thiebot et al. 1992]. If TMS and ECT exert antidepressant effects by a similar mechanism, animal models for depression that are sensitive to electroconvulsive shock [ECS] should also be sensitive to TMS. ECS has effects on known animal models for depression. These effects may be displayed after recovery from the immediate effects of the convulsions [Thiebot et al. 1992]. We evaluated the effects of TMS on the forced swimming test and on apomorphine-induced stereotypy, a sensitive behavioral measure for the effects of repeated ECS. 

Anderson DN, Wilkinson AM, Abou-Saleh MT, et al Recovery from depression after electroconvulsive therapy is accompanied by evidence of increased tetra-hydrobiopterin-dependent hydroxylation. Acta Psychiatr Scand 90 10-13, 1994 Anderson IM, Cowen PJ Effect of pindolol on endocrine and temperature responses to buspirone in healthy volunteers. Psychopharmacology 106 428-432, 1992 Anderson IM, Tomenson BM Treatment discontinuation with selective serotonin reuptake inhibitors compared with tricyclic antidepressants a meta-analysis. BMJ 310 1433-1438, 1995... 

Nasrallah HA, Varney N, Coffman JA, et al Opiate antagonism fails to reverse post-ECT cognitive deficits. J Clin Psychiatry 47 555-556, 1986 Nasrallah HA, Coffman JA, Olson SC Structural brain-imaging findings in affective disorders an overview. J Neuropsychiatry Clin Neurosci 1 21-26, 1989 Naylor GJ, Smith AHW Defective genetic control of sodium-pump density in manic depressive psychosis. Psychol Med 11 257-263, 1981 Naylor GJ, McNamee HB, Moody JP Erythrocyte sodium and potassium in depressive illness. J Psychosom Res 14 173-177, 1970 Naylor GJ, McNamee HB, Moody JP Changes in erythrocyte sodium and potassium on recovery from depressive illness. Br J Psychiatry 118 219-223, 1971 Naylor GJ, Dick DAT, Dick EG, et al Lithium therapy and erythrocyte membrane cation carrier. Psychopharmacologia 37 81-86, 1974 Naylor GJ, Smith AHW, Dick EG, et al Erythrocyte membrane cation carrier in manic-depressive psychosis. Psychol Med 10 521-525, 1980... 

Mueller Tl, Leon AC, Keller MB, et al. Recurrence after recovery from major depressive disorder during 15 years of observational follow-up. Am J Psychiatry 1999 156 1001-1006. 

Lidocaine blocks activated and inactivated sodium channels with rapid kinetics (Figure 14-9) the inactivated state block ensures greater effects on cells with long action potentials such as Purkinje and ventricular cells, compared with atrial cells. The rapid kinetics at normal resting potentials result in recovery from block between action potentials and no effect on conduction. The increased inactivation and slower unbinding kinetics result in the selective depression of conduction in depolarized cells. 

Etomidate is a carboxylated imidazole that can be used for induction of anesthesia in patients with limited cardiovascular reserve. Its major advantage over other intravenous anesthetics is that it causes minimal cardiovascular and respiratory depression. Etomidate produces a rapid loss of consciousness, with minimal hypotension even in elderly patients with poor cardiovascular reserve. The heart rate is usually unchanged, and the incidence of apnea is low. The drug has no analgesic effects, and coadministration of opioid analgesics is required to decrease cardiac responses during tracheal intubation and to lessen spontaneous muscle movements. Following an induction dose, initial recovery from etomidate is less rapid (< 10 minutes) compared with recovery from propofol. 

Dysthymia is a low-grade but very chronic form of depression, which lasts for more than 2 years (Fig. 5—7). It may represent a relatively stable and unremitting illness of low-grade depression, or it may indicate a state of partial recovery from an episode of major depressive disorder. When major depressive episodes are superimposed on dysthymia, the resulting condition is sometimes called double depression (Fig. 5—8) and may account for many of those with poor interepisode recovery. 

If pathological and generalized anxiety is a state of incomplete recovery from depression or from anxiety disorder subtypes, it would not be surprising if highly... 

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