Conrad M. Swartz

Electroconvulsive Therapy Emergence Agitation and Succinylcholine Dose

In this prospective study, five patients who had repeatedly shown troublesome restless emergence agitation after each of 20 sessions of electroconvulsive therapy (ECT) with a succinylcholine dose about .7 mg/kg showed no agitation after 15 ECT sessions in which the succinylcholine dose was increased to about 1.0 mg/kg. The probability that the pattern of response to higher succinylcholine dose resulted from random processes is less than .005. This provides evidence that patients predisposed to emergence agitation are sensitive to seizure-induced metabolic changes in skeletal muscle tissue and that the likelihood of emergence agitation rises with the ratio of skeletal muscle mass to succinylcholine dose. Because ECT-inducted serum lactate elevations are blocked by succinylcholine, emergence agitation might be essentially the same phenomenon as lactate-induced panic.

Postictal prolactin elevations in rats.

Electrically induced seizures were followed by temporary elevations in serum prolactin over baseline in rats, while electrical irritation made no change. Naloxone 4 mg/kg i.p. pretreatment preserved this pattern but attenuated all levels including baseline by about 50%. While atropine 0.1 mg/kg s.c. did not change baseline levels, the prolactin levels after electrical irritation without seizure were about the same as those following a genuine seizure; atropine apparently facilitated stress-induced prolactin release. Seizures did not raise post-haloperidol prolactin levels above their high baseline levels.

Multiple muscle enzyme release with psychiatric illness.

Associations (p<.001) between serum concentrations of lactate dehydrogenase (LDH) and glutamic oxaloacetic transaminase (SGOT) were observed in physically well patients with mania (N =100, r=.70), depression (N= 138, r=.51), chronic schizophrenia (N=85, r=.68), and schizoaffective or atypical psychosis (N =39, r=.52) discharged from 1978 through 1981. In contrast, there was a negligible association between these enzymes in 90 nonpsychiatric inpatient control subjects. Patients with mania (229.0 ± 106.1 IU/1) showed significantly (t=3.16, p<.002, two-tailed) higher lactate dehydrogenase (LDH) levels than control subjects (191 ± 41.7 IU/1) and a 14% incidence of abnormally high serum LDH levels vs. 1% among control subjects. Results were unchanged when patients taking neuroleptics were excluded. These results indicate that psychiatric illness, especially mania, induces release of LDH and SGOT, occasionally to unusually high levels. This is similar to previous reports of muscle creatine phosphokinase release in psychiatric patients. Presumably, these enzymes are released from skeletal muscle in association with agitation, with muscle tension, or with blood stasis and local tissue hypoxia consequent to hypoactivity.

Clozapine Treatment of Euphoric Mania

Four patients with treatment-resistant euphoric mania characterized by elevated mood, hyperactivity, and rapid speech, refractory to standard treatments and anticonvulsants, showed dramatic improvement in symptoms when treated with clozapine. All developed enhanced functioning and new insight into previous psychopathology. This degree of improvement suggests that clozapine can be considered in the treatment of not only schizophrenia, schizoaffective disorder, and dysphoric mania but also classic euphoric mania unresponsive to traditional treatments.

Encephalopathy Associated with Rapid Decrease of High Levels of Lithium

A case is described in which a highly detailed time course of serum lithium levels and mental status observations was consistent with neurotoxicity from the rapid decrease in high lithium levels rather than from the high lithium levels alone. The highest lithium level observed was 4.89 mEq/L; the patient remained oriented until about 40 h after hospital admission and the serum lithium level fell below 1.65 mEq/L. An EEG taken during the 2-day period of gross disorientation showed focal sharp epileptiform waves and paroxysmal bursts of slowing without full seizure. In view of these and previous complementary observations, and a rationale of similarity between hyperlithemia and hyponatremia, the potential toxicities of dialysis and abrupt lithium dose discontinuation should be considered in patients who develop high lithium levels after taking regular doses.

Biologically derived depression and the dexamethasone suppression test

ORMAL in essentially all people who have no psychiatric or medical illness,‘.’ the dexamethasone suppression test is abnormal in about half of patients with an endogenous depressive illness. That this fraction is not li 10 or 9/10 has made its potential role in the diagnostic process less obvious. On the other hand, since the endogenous depressions which have been studied with this test were so classified with only clinical symptoms and signs, it is easy to wonder if patients with genuine biochemically derived depressions would be nearly unanimous in showing abnormal dexamethasone suppression tests. Under such a hypothesis, essentially all depressed patients with normal suppression of serum cortisol might be thought of as having a severe psychogenic depression which clinically mimics the symptoms and signs by which endogenous depression is diagnosed. It is also conceivable (but not proven) that in some psychogenic depressives abnormal results of dexamethasone suppression tests might develop from somatic stresses of poor nutrition 01 changes in the circadian pattern of activity and sleep, for example. To test the hypothesis that essentially all patients with biochemically derived depressions have abnormal dexamethasone suppression tests, the selection of suitable patients must be rigorous. Childbirth is a somatic experience which generates severe depressive psychoses which would not otherwise 0ccur.j In particular, the frequency of onset of depressive illness during the period between two days and two weeks after parturition is so much larger than the expected incidence among non-postpartum females that essentially all of the depressive illness beginning during this interval can be regarded as depression generated by parturition. In this study it will be regarded that an incapacitating postpartum depression of onset between 2 days and 2 weeks after delivery is a biochemically derived depressive illness. A study of the dexamethasone suppression test among postpartum women would probably be complicated by the effects on cortisol regulation of the many stressful somatic experiences surrounding childbirth. This hormonal test of excess cortisol secretion can be abnormal from surgery or hypoglycemia.‘.’ The stress of labor itself generates high levels of ACTH and cortisol.‘.’ The puerperium is a time of rapid large changes in levels of various hormones. such as progesterone, the estrogens, prolactin, and oxytocin; there are many possibilities of effects of hormones on each other which might interfere with

Melancholia with onset during treatment with SSRIs.

A defined group of medical records was surveyed for patients who showed onset of major depression with melancholic features while taking an antidepressant medication. Nine cases resulted. In all the antidepressants being taken while melancholia began were SSRIs and the melancholic depression remitted rapidly with the first treatment given, bupropion in five males, nortriptyline with triiodothyronine in two females, and ECT in one male and one female. This suggests that patients who take SSRIs and are melancholic respond well to bupropion, nortriptyline, or ECT These observations complement reports of low responsivity of melancholic depression to SSRIs and distinctions between melancholic and nonmelancholic depressions.

Mitigating acute skin rashes and nausea from lithium

Abstract Effective in treating and preventing particular types of mental illness, lithium has recently been reported to cut the costs of medical care and improve the quality of life of many appropriately selected patients. 1 Unfortunately, some patients who are selected as appropriate for starting lithium are greatly discomforted by some of its side effects. Prominent among the discomforting effects are resting tremors, nausea and vomiting, and excessive thirst and urination; these are rarely severe enough for the physician to recommend lithium discontinuance. On the other hand, it is common to see patients who have quit their lithium on their own complaining of annoying side effects. Among the few circumstances in which physicians recommend lithium discontinuance is when an intense skin rash appears within a few hours of administration. The life prospects for many patients who cannot or will not take lithium are gloomy: they will likely experience repeated episodes and exacerbations of their psychiatric illness and their careers and personal lives will suffer the discouragements of interruptions. Those who take neuroleptics in place of lithium experience a more subtle handicap, that of mental inertia and emotional blunting from tranquilization. As good medical practice it seems prudent to try to help patients accommodate to lithium with various pharmacological maneuvers when these side effects interfere with reliable lithium administration. In this report some cases will be reviewed in which side effects of an acute skin reaction or nausea threatened to take precedence over lithiums therapeutic effects.

Dose Effect on Dexamethasone Suppression Testing with Electroconvulsive Therapy

AbstractTo determine if accelerated dexamethasone elimination underlies dexamethasone suppression test (DST) Cortisol level increases reported with electroconvulsive therapy (ECT), 1- and 2-mg DSTs were compared in 12 consecutive male melancholies. Post-ECT nonsuppression occurred in none with 2 mg but in four ECT responders with 1 mg (p = 0.0192). Combining subjects from our prior 2-mg DST study, nonsuppression occurred in one sixth pre-ECT and none post-ECT, while mean DST Cortisol levels decreased (p = 0.043) from 4.00 μ/dL to 1.76 μ/dL. In contrast, mean 1-mg DST Cortisols were 6.04 μ/dL pre-ECT but 6.63 μ/dL post-ECT. With ECT, DST Cortisol variability should decrease as DST nonsuppression converts to suppression; variability indeed fell by 75% with μ(p < 0.0001), but showed no fall with 1 mg. These differences between DST doses indicate that, after ECT, 2 mg is adequate but 1 mg is not. Presumably, ECT anesthesia medications accelerate dexamethasone elimination.

Benzodiazepines Affect Dexamethasone Suppression Testing

AbstractIn ten hospitalized depressives, dexamethasone suppression test (DST) 8 am Cortisol levels were 54% lower (p = 0.05) and less variable (p = 0.013) after 3 days on lorazepam (2.4, SD 5.3 μ/dl) than after lorazepam discontinuation (5.2, SD 8.5 μ/dl). All three DST nonsuppressors showed strikingly lower DST Cortisol levels under the influence of lorazepam. This is evidence that benzodiazepines can affect DST results. Clinical research DST studies that allowed benzodiazepines may have been affected by them.