Psychosomatics 49:67-72, January-February 2008
doi: 10.1176/appi.psy.49.1.67
© 2008 Academy of Psychosomatic Medicine
ECT in Patients With Psychopathology Related to Acute Neurologic Illness
Keith G. Rasmussen, M.D.,
Dionne A. Hart, M.D., and
Timothy W. Lineberry, M.D.
Received September 13, 2006; revised October 30, 2006; accepted November 1, 2006. From the Mayo Clinic, Dept. of Psychiatry and Psychology, Rochester, MN. Send correspondence and reprint requests to Keith G. Rasmussen, M.D., Mayo Clinic Dept. of Psychiatry and Psychology, 200 First St. SW, Rochester, MN 55905. e-mail: rasmussen.keith{at}mayo.edu
© 2008 The Academy of Psychosomatic Medicine
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ABSTRACT
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Psychiatrists are occasionally called upon to assist in the management of patients with severe psychopathologic syndromes resulting from acute neurologic illness. In the absence of other options for treating the underlying neurological disorder or with persistence of the psychopathology after resolution of the neurologic illness, electroconvulsive therapy (ECT) may be considered. The authors treated four such patients, two of whom experienced no benefit and two of whom experienced dramatic benefit. The authors provide recommendations for the approach to acutely ill neurologic patients with regard to the use of ECT.
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INTRODUCTION
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Electroconvulsive therapy (ECT) is often used to treat psychopathologic syndromes that occur during the course of chronic neurologic illnesses such as dementia, Parkinson’s disease, and epilepsy.1 Psychiatrists may also be called upon to assist in the management of patients with acute, fulminant neurological illnesses manifesting psychopathologic features such as agitation, psychosis, and catatonia. There are many etiologies, including toxic, metabolic, structural, infectious, or other syndromes. Occasionally, no further specific treatment options are available for the underlying medical or neurologic condition, or the precise etiology of the underlying condition is unknown, or the psychopathologic features persist after the acute phase of the underlying illness has abated. In such cases, ECT may present one treatment option if the patient manifests an agitated psychotic state, mania, melancholic depression, or catatonia. We utilized ECT for four patients who appeared to suffer acute, severe neurologic deteriorations with associated psychopathology. We describe these cases and derive clinically useful recommendations from them.
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Case 1
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This patient was a 22-year-old woman previously in good health and without psychiatric history. She presented to a local emergency room with an approximately 1-week history of headache, and she was found to be febrile. Cerebrospinal fluid (CSF) analysis revealed a count of 700 white blood cells (WBCs) per microliter, with 98% lymphocytes. An electroencephalogram (EEG) showed diffuse slowing. Over the next few days, without specific treatment, her mental status deteriorated, and she became unresponsive. She was started empirically on acyclovir before the results of herpes simplex virus polymerase chain-reaction testing were back, and she was transferred to our facility.
Upon initial evaluation at transfer, she was obtunded and required mechanical ventilation. She was admitted to an intensive care unit. Repeat CSF analysis was negative for herpes simplex virus (as was the sample from the outside facility). Her WBC count was 583 per microliter, with 96% lymphocytes. Extensive work-up included three serial EEGs, which showed dysrhythmia, Grade 3, and atypical triphasic waves. Serial head magnetic resonance imaging (MRI) and head computerized tomographic (CT) scans were unremarkable. Neuro-SPECT revealed decreased tracer uptake bilaterally in the temporal lobes. Conjunctival biopsy was negative for neurosarcoidosis. Cerebral angiogram was negative for vasculitis. Serologies and CSF analysis for multiple infectious agents were all negative, including bacterial cultures, Epstein-Barr virus, Creutzfeldt-Jakob disease, acid fast stain, varicella zoster virus, fungal serologies, cytomegalovirus, Legionella antibody, diphtheria, tetanus, B. henselae, B. quintana, C. pneumonia, C. psittaci, C. trachomatis, S. pneumoniae, anti-D-nase b, antistrept-O, spirochetal, Lyme disease, viral serologies, hepatitis serologies, human immunodeficiency virus (HIV), and parasite serologies. Other blood tests in addition to the complete blood count, electrolytes, liver-function tests, and renal-function tests, were all unremarkable. Creatine kinase approximately 10 days into the hospitalization was slightly elevated, at 222 U/liter. Thyroid-stimulating hormone, total T4, and antithyroid peroxidase titers were normal. Tests for heavy metals, paraneoplastic antibodies, organic acids in the urine, and a variety of other antibodies (c-ANCA, p-ANCA, rheumatoid factor, myeloperoxidase, proteinase, antinuclear, antidouble-stranded DNA, extractable nuclear antigen) were all negative. Ceruloplasmin was nonsignificantly elevated. Angiotensin-converting enzyme levels were normal. Coagulation studies were normal, as were tests of T- and B-cell surface-marker antigens.
Brain biopsy from the left temporal lobe revealed a lymphocytic infiltrate consistent with meningoencephalitis. Cultures of brain tissue were negative. There were no viral inclusions, glial nodules, granulomas, or signs of vasculitis. Because of the inflammation in the brain and lack of apparent infective agent, a trial of high-dose steroids was undertaken, without success.
Care for the first month or so consisted of antibiotic trials (ceftriaxone and vancomycin), as well as completion of a full course of acyclovir. She developed abnormal involuntary movements requiring sedation with propofol, and she remained on mechanical ventilation. Attempts to wean her off this were unsuccessful. She was given short trials each of benztropine, amantadine, and L-dopa for the abnormal involuntary movements, all without success. Haloperidol in doses up to 60 mg per day was administered for approximately 2.5 weeks about midway through the hospitalization to help suppress the movements, which were felt to be choreiform at that point. Of note, the full syndromal manifestations of her neurologic deterioration had occurred by the time she was administered the first dose of haloperidol, and the severity did not worsen after it was administered.
The possibility of malignant catatonia was raised approximately 3 weeks into the hospitalization because of her mutism and stupor and lack of response to any of the measures undertaken. After psychiatric consultation and discussion with family, an empiric trial of ECT was undertaken. Of note, the patient continued on a propofol drip and did not receive benzodiazepines. She received 10 bitemporal ECT treatments, with perhaps minimal improvement in her hyperkinetic movements, but this was not substantial enough to warrant continued treatment. She did not recover from her stupor or engage in purposeful behavior or speech, and she remained on a propofol drip. A trial of plasma exchange was undertaken without success. She had great autonomic instability, especially with asystolic periods, and a pacemaker was implanted. Approximately 3 months after admission (about 1 month after the last ECT treatment), she suffered a cardiorespiratory arrest and was resuscitated, but upon review of her status with her family, she was withdrawn from life support, and she expired. Autopsy confirmed the neuropathological findings of the brain biopsy and did not reveal any previously undiagnosed medical problems.
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Case 2
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This patient was an 18-year-old young man without any psychiatric or significant medical history. Approximately 1 month before his transfer to our facility, he was in his usual health when he suffered an apparent seizure after complaining of eye pain and paresthesias. In the hospital, he was noted to have a fever of 103°F. Neuroimaging was unremarkable. CSF examination, the specifics of which are not available, showed an abnormal increase in lymphocytes. Tests for a variety of viral and other infectious agents were negative. He developed severe behavioral agitation and psychosis. He was treated with acyclovir and psychotropic agents and was released after approximately 1 week. Less than 1 week later, he was readmitted because of persistence of psychosis and behavioral agitation. He failed to respond to several antipsychotic medication trials, and he was transferred to our facility.
An extensive neurological work-up was again undertaken, including CSF examination, head MRI, EEG, conjunctival biopsy (to rule out neurosarcoidosis), and multiple blood studies. CSF was negative for H. influenza, S. pneumoniae, N. meningitidis, brucellosis, mycobacteria, fungi, cytomegalovirus, Epstein-Barr virus, tropherma whipplei, varicella zoster virus, and viral culture. The gram stain was negative, and acid fast was negative. Lymphocytes were present on CSF cytology but were not malignant. Other CSF tests, all negative or normal, included angiotensin levels, 14-3-3 protein, CRMP-5, neuron-specific enolase, total protein, and amphiphysin. Total nucleated cells were 4.0 (normal: <5.0), 91% lymphocytes (normal: 40%–80%). Blood studies were negative for antinuclear, antidouble-stranded DNA, and extractable nuclear antigen antibodies. A paraneoplastic antibody cascade screen was negative, as was myoglobin. Infectious blood studies were negative for Anaplasma, B. henselae, B. quintana, Lyme, E. chaffeensis, syphilis, hepatitis, HIV, human T-cell lymphatic virus (HTLV) I and II, parasites, various viral agents (adenovirus, California virus, Epstein-Barr virus, cytomegalovirus, mumps, rubella, rubeola, St. Louis, MO, encephalitis, West Nile virus, Western equine and Eastern equine encephalitis). Head MRI showed T2 signal abnormalities in the deep white matter of the left frontal lobe and posterior frontal lobe near the abutment of the white and gray matter. Conjunctival biopsy was normal. EEG showed dysrhythmia, Grade 2, generalized.
Whereas no specific infectious etiology could be confirmed, it was believed that he probably had suffered an acute viral encephalitis. He had elevated creatine kinase levels (peaking at 3,932 U/liter at mid-hospital stay, but progressing downward to 127 by discharge), suggesting possible neuroleptic malignant syndrome, but he had no other stigmata of that syndrome (i.e., no rigidity) and had received numerous intramuscular injections.
Mental status exam revealed echolalia, perseveration, and cognitive slowing. He tended to be combative and required seclusion. He also evinced hyper-religious themes and persecutory delusions. Extensive psychotropic medication trials failed to achieve more than temporary sedation. Psychotropics administered during the hospitalization included, at various times, aripiprazole 15 mg per day for 5 days, haloperidol 5-mg injections a total of 10 times during a 4-day period (along with 3 po doses), lorazepam up to 6 mg/day throughout the hospitalization by mouth as well as a total of 19 injections on an as-needed basis, olanzapine 10 mg–25 mg per day for a 3-day period, paroxetine 10 mg–30 mg/day for the first 3 days of hospitalization, quetiapine 300 mg/day for a 5-day period, ziprasidone 80 mg–240 mg/day over a 9-day period, and occasional doses of trazodone, diphenhydramine, chloral hydrate, and zolpidem. With consent from his parents, an emergent course of ECT was undertaken. He received 11 bitemporal ECT treatments with complete resolution of the psychopathologic changes, and he was discharged taking lorazepam 1 mg tid. The various neuroleptics were administered relatively early during the hospitalization and were not needed as he started to respond to ECT. They provided little if any relief from his agitation and psychosis but did not seem to worsen these signs, either.
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Case 3
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This patient was a 65-year-old married woman who had a remote history of left thalamic infarct, with residual right facial pain syndrome, obstructive sleep apnea, hypothyroidism, and depression. She was fully functional and not currently depressed when she had an outpatient bladder surgical procedure for stress incontinence. She was discharged home, and the next day, apparently several hours after her husband administered her prescribed opiate pain medications, she was found unresponsive. She was transferred from the local emergency room to our facility. After 3 days, she was discharged recovered. The diagnosis was oversedation from the medications with a contribution of hypoventilation from her sleep-related breathing disorder.
Approximately 3 weeks later, she was brought to our emergency room by family with an approximately 1-week history of not tending to her own activities of daily living, decreased speech, occasional frank unresponsiveness, and weight loss. Of note, her husband had recently been admitted to our hospital with a terminal illness, and she was left at home to care for herself for the first time in decades. A neurological consultation was arranged in our emergency room and a head CT scan was performed. The conclusion was that the presentation was "not neurologic," and she was admitted to a medical service. An EEG revealed Grade 2 dysrhythmia, with generalized slowing. A thorough metabolic profile was unremarkable. She was felt to be catatonically depressed and was transferred to the psychiatric unit.
With the family’s permission, and continued lack of verbal responsiveness or goal-directed behavior, a course of ECT was undertaken. Psychotropics administered up to that point included continuation of her longstanding escitalopram, lorazepam in two separate doses of 1 mg, and haloperidol in two doses of 5 mg intramuscularly on 2 consecutive days. These medications failed either to effect improvement or cause apparent worsening. She received a course of 8 bitemporal treatments, with no improvement and even worsening of her functional status. The ECT was halted, and a specialist consultation with a behavioral neurologist was arranged. At this point, she was poorly communicative, answering in yes/no answers that were not always relevant to the subject of conversation. She was mumbling incomprehensibly and agitated at night. She did not attend to hygiene. A new diagnostic work-up was undertaken. Head MRI showed dramatic white-matter hyperintensities ascribed by the neuroradiologist to small-vessel ischemic changes. FLAIR images did not suggest prion-related changes or hippocampal damage (and thus did not suggest hypoxic injury). Repeat EEG showed dysrhythmia, Grade 3, with new onset of atypical triphasic waves and multifocal spikes. Laboratory studies revealed antithyroid peroxidase antibodies of 89 (normal: <40), but normal TSH and T4 levels). CSF showed elevated protein but was otherwise unremarkable (studies for prion disease could not be undertaken because of a shortage of CSF in the sample). A preliminary diagnosis of SREAT (steroid-responsive encephalopathy associated with thyroiditis) was made, and the patient was placed on a 5-day regimen of high-dose glucocorticoids (4 days of intravenous methylprednisolone and 1 day of oral prednisone). There was minimal improvement, but the myoclonus was no longer present. Repeat EEG was unchanged except for the disappearance of the spikes. Repeat head MRI was unchanged.
She was transferred to the neurology service and underwent a cerebral angiogram, which showed no evidence of vasculitis. A right frontal lobe brain and meningeal biopsy was nondiagnostic, showing only reactive gliosis and moderate amyloid angiopathy. It was negative for tests of prion disease. She received another 5-day course of high-dose methylprednisolone followed by daily oral prednisone. She was discharged to a nursing home. Outpatient follow-up several weeks later revealed her to have made steady progress. She was more conversant and could follow simple but not complex demands. There were no behavioral disruptions at the nursing home. She seemed brighter and more attentive during conversation. She had no rigidity or myoclonus. There was a postural and left resting tremor of the upper extremity. The behavioral neurologist on follow-up 3 months post-discharge assessed the case as possible SREAT based on the improvement attributed to the steroids as well as resolution of signal abnormalities on head MRI in the caudate heads and thalami. CADASIL and amyloid angiopathy were other considerations.
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Case 4
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A 31-year-old woman, previously in good health and without psychiatric history, had an acute onset of headache and fever, with progressive behavioral changes consisting of agitation and delusions. She was hospitalized, and CSF analysis revealed excessive lymphocytes. Extensive serological and CSF tests failed to identify a specific infective agent; the working diagnosis was viral encephalitis, and she was given intravenous acyclovir. Behavioral agitation was treated with lorazepam in doses ranging from a few milligrams per day to a 2-day period in which she received 19 mg 1 day and 40 mg the next, without significant improvement. Eventually, propofol was used. On the fourth hospital day, a total of 1 mg intravenous haloperidol was administered, with resultant acute rigidity. A few other sporadic haloperidol doses, ranging from 0.5 mg to 5 mg, were administered without apparent worsening of her condition.
Autonomic lability occurred; she had periods of atrial fibrillation and some several-second asystolic events. Catatonic signs, including waxy flexibility, stupor, and mutism, were prominent. Intensive care as described for approximately 1 week was met with no success, and ECT was initiated. Over the next 3 weeks, she received 10 bitemporal ECT treatments with progressive improvement in all behavioral spheres. She was removed from the propofol drip and transferred to the physical medicine service for rehabilitation. Cognitive testing on follow-up 5 months later was normal; she was off psychotropic medications, and the catatonia had not recurred.
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DISCUSSION
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Discussion of the extensive differential diagnosis of medical, neurologic, or toxic causes of psychopathology, as well as the appropriate diagnostic work-up, is well beyond the scope of this communication. Our limitations include the obviously small sample size and the lack of systematic identification of cases. The four cases in this series included all patients in the authors’ tenure at Mayo since 1999 and all recalled cases by ECT colleagues in the department. It is possible that there may have been other patients treated with ECT who had sustained acute neurologic deterioration and had a presumed neurologic diagnosis, such as an infection or metabolic abnormality, not included in this report.
In this report, we focus on the following scenario: 1) a patient has a severe psychopathologic syndrome that is usually responsive to ECT, such as mania, psychosis, catatonia, or depression; 2) these features are believed to be secondary to a known or suspected acute neurological condition; 3) there are felt to be no further specific therapies for the underlying condition or, after resolution of such, the psychopathologic features persist.
Ordinarily, case report literature contains only successes, leading to selection bias. We felt it was important to report negative outcomes, as well. In two of our cases, ECT was of no benefit. It is probably the case that the more closely the psychopathologic features mimic those of the classic ECT-responsive syndromes (i.e., melancholia, psychosis, catatonia, and mania), the more likely ECT is to be successful. In our series, the two patients with dramatic benefit (Cases 2 and 4) suffered a classic catatonic syndrome. It is well known that such patients respond well to ECT.2
The other two patients suffered what were thought to be catatonic syndromes. Of course, catatonia responds well to ECT.3 The challenge for the diagnosis is to decide whether, in fact, the patients are catatonic. For example, the acutely ill neurologic patient may be minimally responsive or obtunded, and, especially in the absence of a known etiology, one may wonder whether it is a catatonic presentation or simply the direct effects of a neuropathological process on level of arousal. Until such time as laboratory tests can be used to confirm the presence or absence of a presumed neurobiologic substrate of catatonia, the use of criteria sets for catatonia4 should help the clinician make a determination. It is probably true that catatonia in the face of bipolar disorder or schizophrenia responds better to ECT than does catatonia due to known brain disease,5 especially if, in the latter case, the underlying neuropathologic process is unresolved.
A further confounding factor may be the presence of cognitive disturbance. Neurologic illnesses frequently cause cognitive dysfunction or even frank delirium, but in a patient with a known history of depression (such as our Case 3) and some indication of current depressive features, one may speculate that it is a severe catatonic depressive syndrome causing the cognitive disturbance, further leading one in the direction of ECT. Finally, even though catatonia induced by medical causes may respond to ECT, it is probably the case that it responds less well if the underlying medical condition is still active and untreated, as in our two patients who did not benefit from ECT.
It is our proposition that ECT is justified in a patient who appears or is known to have suffered an acute neurologic illness resulting in ECT-responsive psychopathologic features when there is either no further treatment option for the presumed underlying condition or the psychopathologic features have persisted beyond its resolution. One may wonder what special risks ECT presents in this scenario. Presumably, such patients have already had evaluations excluding masses or increased intracranial pressure. Also, gross metabolic disturbances that one usually looks for with pre-ECT blood work, such as electrolyte abnormalities or hypo- or hyperglycemia, have been excluded, as well. Furthermore, by the time ECT is considered, fever, if present on initial presentation, has abated; empiric courses of antimicrobial agents have been administered; and the patient does not have signs of currently active infection on the basis of blood or CSF examination. With these considerations in mind, and with the acknowledgment that we are referring to a large, heterogeneous group of patients with multiple possible etiologies, we still feel that ECT is, in general, a very safe treatment option. The typical "worst-case scenario" is probably lack of response, versus active worsening, caused by the induced seizures. Although one obviously would like to have a precise neurologic diagnosis before proceeding with ECT, the dictates of patient safety may indicate a course of ECT before that diagnosis is reached, especially in cases of malignant catatonia.6
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ACKNOWLEDGMENTS
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Case 2 was presented in abstract form at the annual meeting of The Association for Convulsive Therapy, May 2004. Case 4 was presented in abstract form at the annual meeting of The Academy of Psychosomatic Medicine, November 1999.
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REFERENCES
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- Rasmussen KG, Rummans TA, Tsang TSM, et al: ECT in the medically ill, in American Psychiatric Publishing Textbook of Psychosomatic Medicine. Edited by Levenson J. Washington, DC, American Psychiatric Publishing, 2004, pp 957-978
- American Psychiatric Association Committee on ECT: Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging, 2nd Edition. Washington, DC, American Psychiatric Association, 2001, Chapter 2
- Philbrick KL, Rummans TA: Malignant catatonia. J Neuropsychiatry Clin Neurosci 1994; 6:1–13[Abstract/Free Full Text]
- Bush G, Fink M, Petrides G, et al: Catatonia I: rating scale and standardized examination. Acta Psychiatr Scand 1996; 93:129–136[Medline]
- Swartz CM, Acosta D, Bashir A: Diminished ECT response in catatonia due to chronic neurologic condition. J ECT 2003; 19:110–114[CrossRef][Medline]
- Taylor MA, Fink M: Catatonia in psychiatric classification: a home of its own. Am J Psychiatry 2003; 160:1233–1241[Abstract/Free Full Text]
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ABSTRACT
INTRODUCTION
