Psychiatric Annals

UPDATING ECT 

Medical Indications for Electroconvulsive Therapy

Teresa A Rummans, MD

Abstract

Among the nonpsychiatric conditions treated with ECT are catatonia, NMS, hypopituitarism, intractable seizure disorders, and Parkinson's disease.

Abstract

Among the nonpsychiatric conditions treated with ECT are catatonia, NMS, hypopituitarism, intractable seizure disorders, and Parkinson's disease.

In 1990, the American Psychiatric Association Task Force on Electroconvulsive Therapy (ECT)1 published its recommendations on the practice of ECT. In this report, they outlined both the psychiatric and medical conditions for which ECT is indicated. Among the psychiatric indications for ECT are major depression, mania, and acute psychosis. Medical disorders that may benefit from ECT include:

* catatonia secondary to medical conditions,

* neuroleptic malignant syndrome (NMS),

* hypopituitarism,

* intractable seizure disorder, and

* Parkinson's disease (particularly with the on-off phenomenon).

Despite the theoretical potential benefits for the use of ECT in these medical conditions, few clinical studies have examined the use of ECT in their treatment. This article reviews the clinical usage of ECT in these five disorders.

CATATONIA SECONDARY TO MEDICAL CONDITIONS

Catatonia is a complex syndrome. We have suggested that it be divided into two categories - simple and malignant2 - according to whether or not severe medical and neurologic manifestations develop. Both types of catatonia can be divided further according to their etiology, which includes psychiatric, medical and neurologic, drug-related, and idiopathic causes.

Catatonia, whether simple or malignant, is seen most commonly in patients with psychiatric disorders, especially schizophrenia and affective disorders. When catatonia results from one of these disorders, ECT has been shown to be quite effective. However, when catatonia is the direct result of a specific medical or neurologic disorder, then the effectiveness and safety of ECT is often unclear.

Taylor' composed an extensive list of medical and neurologic conditions causing catatonia. Among them are structural brain disorders, such as tumors and strokes, and nonstructural brain disorders, such as infections and epilepsy. Catatonia may also be caused by systemic illnesses, such as lupus erythematosus; metabolic abnormalities that occur with diabetic ketoacidosis, renal, and hepatic dysfunction; and toxic reactions to drugs that occur with neuroleptics, alcohol, amphetamines, and phencyclidine. When catatonia develops as a result of one of these conditions, treatment is often difficult until the underlying medical disorder is reversed.

The use of ECT in treating the catatonic symptoms secondary to a medical and/or neurologic disorder has been reported in only a few cases. In fact, to my knowledge, catatonia secondary to only three of these conditions (lupus erythematosus, multiple sclerosis, and typhoid fever) has been treated with ECT3·4 In these three cases, the catatonic symptoms responded dramatically to ECT; but most were also receiving medical treatment for their underlying medical condition in conjunction with ECT. Therefore, it is unclear whether ECT alone would have been as effective or safe in treating their catatonia. Unfortunately, no controlled studies exist.

On the other hand, when medical and neurologic symptoms are secondary to the catatonic process as seen with malignant (or near-lethal) catatonia, ECT may be lifesaving. In Mann and associates'5 review of ECT in the treatment of malignant catatonia, they found that malignant catatonia responded quite favorably to ECT. In our experience6 and that of others,7 in patients with malignant catatonia with severe medical and neurologic sequelae, ECT not only reversed the catatonic symptoms but completely reversed the severe life-threatening medical and neurologic abnormalities that developed secondary to the illness.

When Mann et al5 compared the cases of ECT-treated malignant catatonia with similar cases not treated with ECT, the outcome was significantly different. Those not treated with ECT had a very high mortality rate compared with those who received ECT Unfortunately, the mechanism by which this condition develops and the mechanism by which ECT works remain unknown. Despite our intellectual shortcomings, when these cases are recognized and treated, the results can be quite dramatic.

In summary, although the APA Task Force on ECT lists catatonia secondary to medical conditions as one of the indications for ECT, caution is warranted. In these circumstances, the medical and/or neurologic disorders underlying catatonia should be addressed and treated as aggressively as possible. Only when the catatonic symptoms are refractory to psychopharmacologic interventions or are more life-threatening than the underlying medical/neurologic disorders should ECT be considered. On the other hand, in patients with malignant catatonia where the catatonic process produces severe and life-threatening medical/neurologic complications, ECT should be considered a first-line therapy.

NEUROLEPTIC MALIGNANT SYNDROME

Neuroleptic malignant syndrome (NMS) is characterized by a triad of fever, rigidity, and mental status changes in patients receiving neuroleptics. The exact etiology is unknown but appears to be related to abnormalities in dopaminergic transmission. We, and others, have speculated that this syndrome actually may be a subcategory of malignant catatonia that is drug-induced.2 If this is so, one would expect ECT to be effective in reversing this syndrome.

In 1991, Davis et al8 reviewed the cases of NMS treated with ECT. They found that 48 of 655 cases of NMS had received ECT, 29 of whom received ECT during the acute phase of NMS. Of the 29, 24 improved significantly; the five who did not improve were continuing to receive neuroleptics. Only three of the patients receiving ECT died, and those patients were three of the five receiving concomitant neuroleptics. When patients receiving ECT were compared with patients receiving one of the pharmacotherapies (amantadine, bromocriptine, dantrolene, or L-dopa) for NMS, the outcome was similar. However, both treatment groups had a lower mortality rate than the group receiving nonspecific supportive therapy alone.

In summary, NMS may be just one form of malignant catatonia. If so, any sign that the patient is not rapidly improving with support and/or pharmacotherapy should be a clear indication for intervention with ECT

HYPOPITUITARISM

Dysregulation of the hypothalamicpituitary axis occurs in patients with depression. Although the exact mechanism by which this occurs is obscure, these abnormalities usually reverse with successful treatment of the underlying depressive disorder. Several studies reviewed by Kamil and Joffee in 199 19 have shown that there is a transient rise in levels of Cortisol, adrenocorticotropin hormone (ACTH), thyroid-stimulating hormone, and prolactin. The rise most likely results from an enhancement in dopaminergic and serotonergic transmission that directly modifies the hypothalamic-pituitary axis. The clinical significance of these changes remains uncertain.

Theoretically, treatment of depression may also alter the hypothalamicpituitary axis. This speculation has led to at least one case report by Pitts and Patterson in 197910 in which ECT was reported to effectively treat persistent hypothalamic-pituitary suppression in a patient with concurrent chronic depression. This report of ECT's effectiveness in treating hypothalamic-hypopituitarism - especially the hypothalamic-pituitary adrenal axis dysfunction - is confounded by a number of variables. One is the patient's concurrent depressive illness and the effects that the depressive illness has on the neuroendocrine abnormalities. Another variable is the effect of chronic dexamethasone (used as an adjuvant agent for treating this patient's depression). The use of this agent contributed to the development of the neuroendocrine changes, and its discontinuation contributed to at least partial improvement in these abnormalities. Therefore, it is unclear whether ECT alone was responsible for the improvement seen in the hypothalamicpituitary-adrenal axis.

In summary, animal research implies that ECT affects neuroendocrine pathways. How they are affected in humans is not as clearly defined. Furthermore, jumping from theoretical assumptions that ECT may affect hypothalamicpituitary dysfunction in humans, to the assumption that it may treat patients with hypothalamic-pituitary abnormalities (independent of co-existing psychiatric disorders) is not supported in any clinical literature to my knowledge. Therefore, I would be cautious in considering the use of ECT in treating primary hypopituitarism.

INTRACTABLE SEIZURE DISORDERS

Electroconvulsive therapy produces changes in the actual electrically induced seizures over a course of treatment. The two major effects are on the seizure threshold and duration. Seizure threshold is gradually increased, and seizure duration is gradually reduced.11 Theoretically, both of these properties can have a beneficial effect on the frequency and intensity of epileptic seizures.

In addition to the indirect anticonvulsant effects on seizure threshold and duration, electrically induced seizures may also have a direct anticonvulsant effect. Abrams11(PP68'691 reviewed the literature on this topic and found several authors who demonstrated a marked protective anticonvulsant effect in animals, which lasted from minutes to several days after receiving ECT. The mechanism for this effect is unclear, but it has been hypothesized that it inhibits the development and suppresses the expression of kindling similarly to anticonvulsant medication.

It has also been suggested that ECT may actually release an endogenous anticonvulsant. This hypothesis was tested by Tortella and Long12 in the mid-1980s. They found that if they injected CSF from ECT-treated rats into non-ECT-treated rats, subsequent flurothyl-induced seizures were significantly more difficult to achieve.

These observations of direct and indirect anticonvulsant properties of ECT have led some to consider its usage in treating patients with epilepsy with and without psychiatric symptoms. 111P"1 Although ECT may have been considered as a treatment for patients with intractable epilepsy without psychiatric symptoms before anticonvulsant medications were available, I do not believe it would be considered now. However, in epilepsy patients with severe depression and/or psychosis, ECT with its anticonvulsant properties may be a good treatment choice.

Before ending this section on the effects of ECT on epilepsy, a few comments should be made regarding the potential for ECT to spontaneously kindle seizure production or for ECT to generate prolonged seizures. Although a few reports exist of patients spontaneously developing status epilepticus or other electroencephalogram abnormalities, almost all of these patients had concurrent factors contributing to the development of their problems. These additional factors included structural neurologic abnormalities, metabolic abnormalities, or coadministration of a seizure thresholdlowering agent. The only cases of reported spontaneous seizures following ECT in patients without preexisting abnormalities have been in patients receiving multiple ECT treatments in a single sessjon llippl71-172)

ECT produces both direct and indirect anticonvulsant effects over a treatment course. These effects have been helpful to patients with intractable epilepsy in some cases. However, no prospective randomized study exists to fully evaluate the use of ECT in intractable seizure patients. Therefore, ECT should be considered of theoretical benefit in this patient population and used only when the patients' psychiatric problems dictate its use.

PARKINSON'S DISEASE

Since 1947, observations have been recorded about the use of ECT in treating the psychiatric and/or neurologic symptoms of Parkinson's disease. The mechanism of action of ECT on both the psychiatric and neurologic symptoms associated with Parkinson's disease has not been clearly defined. Existing research implicates changes in the dopaminergic system, possibly by altering the dopaminergic receptors. However, modifications in other neurotransmitter systems, such as the cholinergic system, may be responsible for some of the adverse effects on cognition that are commonly associated with ECT.13

Psychiatric morbidity is common in Parkinson's disease. Depression alone occurs in approximately 40% of the patients.14 As one would expect, many reports document the efficacy of ECT in treating the depressive symptoms in this group.

What is less clear is the impact of ECT on both the motor abnormalities and cognitive decline associated with Parkinson's disease. In Faber and Trimble's review of ECT in Parkinson's patients in 199 1,13 they found a total of 33 patients with Parkinson's disease who had been treated with ECT for their movement disorder alone. Of this group, 21 of 33 had slight-to-marked improvement in their symptoms. There was no note of worsening of their symptoms.

Only one of these studies, by Anderson et al in 1987, was a prospective randomized trial.15 They reported that 9 of the 11 patients improved with ECT The response duration lasted from hours to months. Rasmussen and Abrams16 note that advanced age and severe disability may be favorable features that predict response to the change in motor function seen with ECT Occasionally, dyskinesias develop in patients concurrently receiving levodopa; however, this problem can be addressed by reducing the levodopa dosage. Therefore, it appears that ECT may have a transient beneficial effect on the movement disorder aspect of Parkinson's disease.

Dementia occurs in approximately 30%, and subtle neuropsychological deficits not associated with overt dementia occur in up to 40% of patients with Parkinson's disease.14 In our experience, we found that those patients with definite cognitive decline associated with Parkinson's disease experienced more ECT morbidity in the form of post-ECT delirium.17 Speculations as to the cause of this side effect include a particular vulnerability of those with basal ganglia abnormality and a rapid change in CNS dopamine levels.

Whether the cognitive changes are transient or permanent is not known. Therefore, it is important to identify those Parkinson's patients with cognitive abnormalities who may be more susceptible to developing morbidity associated with ECT prior to initiating treatment. They should be monitored closely during the treatment course. When cognitive changes occur from ECT treatment, the therapy should be discontinued.

In summary, ECT is an effective and relatively safe form of antidepressant therapy for those Parkinson's patients with depression. Additional beneficial ef1 fects may be seen in controlling the patients' movement disorder symptoms. However, when patients have cognitive impairment prior to ECT, ECT should be used cautiously and patients observed closely for signs of worsening cognitive status. If this occurs, ECT should be postponed, if not terminated.

CONCLUSION

Electroconvulsive therapy is a relatively safe treatment modality that is generally recognized and accepted as a beneficial tool in the treatment armamentarium for severe psychiatric disorders. In patients with mixed neuropsychiatrie disorders, such as catatonia - simple catatonia or malignant catatonia (associated with or without neuroleptics), or Parkinson's disease - ECT is an important treatment option. In these circumstances, ECT may be an avenue for helping those patients who otherwise may continue to deteriorate or even die from their underlying illness. However, the use of ECT in patients with hypopituitarism and intractable seizure disorders remains theoretical.

REFERENCES

1. American Psychiatric Association Task Force on ECT. The Practice of ECT: Recommendations for Treatment. Training, and Privileging. Washington, DC: American Psychiatric Press Ine; 1990.

2. Philbrick K, Rummans T. Malignant catatonia: sequelae and treatment. i992 American Psychiatric Association Annual Meeting New Research Programs and Abstracts. Washington, DC: American Psychiatric Association: 1992:57.

3. Taylor M. Catatonia: a review of a behavioral neurologic syndrome. Neuropsychiatry. Neuropsychology and Behavioral Neurology. 1990; 3111:48-72.

4. Fucchione G, Kaufman L. Gruber B, Tenk M. Electroconvulsive therapy and cyclophosphomide in combination for severe neuropsychiatrie lupus with catatonia. Am J Med. 1990; 88:442-443.

5. Mann SC, CaroffSN, Bleier HR. Antelo E, Un H. Electroconvulsive therapy of the lethal catatonia syndrome: case report and review. Convulsive Therapy. 1990; 6(31:239-247.

6. Rummans T. Bassingthwaigthe M. Severe medical and neurologic complications associated with near-lethal catatonia treated with ECT Convulsive Therapy. 1991: 7(2): 121-124.

7. Geretsegger C. Rochowanski E. Electroconvulsive therapy in acute life-threatening catatonia with associated cardiac and respiratory decompensation. Convulsive Therapy. 1987; 3(41:291-295.

8. Davis JM, Janicak PG, Sakkas P, Gilmore C, Wang Z. Electroconvulsive therapy in treatment of the neuroleptic malignant syndrome. Convulsive Therapy. 1991; 7(2): ? 1-120.

9. Kamil R, Joffee RT. Neuroendocrine testing in electroconvulsive therapy. Psychiatr Clin North Am. 1991; 14(41:961-970.

10. Pitts FN, Patterson CW. Electroconvulsive therapy for hypothalamic-hypopituitarism (CRFACTH type). Am J Psychiatry. 1979; 136(81:1074-1077.

11. Abrams R. Electroconvulsive Therapy. 2nd ed. Cambridge. England: Oxford University Press; 1992:68-69.

12. Tortella FC, Long JB. Endogenous anticonvulsant substance in rat cerebrospinal Huid after a generalized seizure. Science. 1985; 228:1106-1108.

13. Faber B, Trimble MR. Electroconvulsive therapy in Parkinson's disease and other movement disorders. ??? Disord. 1991; 6(41:293-303.

14. Cummings J. Depression and Parkinson's disease: a review. Am d Psychiatry. 1992; 149(4 1:443-454.

15. Anderson K, BaNdin J. Gottpries CG, et al. A double-blind evaluation of electroconvulsive therapy in Parkinson's disease with "on-off phenomena. Acta Neurol Scand. 1987; 76:191-199.

16. Rasmussen K, Abrams R. Treatment of Parkinson's disease with ECT Psychiatr Clin North Am. 1991; 14(41:925-933.

17. Oh J, Rummans T O'Connor MK, Ahlskog JE. Cognitive impairment after ECT in patients with Parkinson's disease and psychiatric illness. Am J Psychiatry. 1992; 149(2):271.

10.3928/0048-5713-19930101-09

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