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Psychosomatics 47:170-174, March-April
doi: 10.1176/appi.psy.47.2.170
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Case Report

HIV-Associated Mania Treated With Electroconvulsive Therapy and Highly-Active Antiretroviral Therapy

Stephen J. Ferrando, M.D., and Chloe Nims, M.D.

Received January 26, 2005; accepted March 30, 2005. From the New York-Presbyterian Hospital, Weill Medical College of Cornell University. Address correspondence and reprint requests to Dr. Ferrando, New York-Presbyterian Hospital, 525 E. 68th St., Box 181, New York, NY 10021. e-mail: sjferran{at}med.cornell.edu


  INTRODUCTION

 
TOP
 INTRODUCTION
Case Report
 Discussion
 Conclusion
 REFERENCES
 
The past 10 years has witnessed a shift in the HIV epidemic in the developed world, with dramatic reductions in morbidity and mortality associated with the use of combination antiretroviral therapy.1 Despite this shift, neuropsychiatric presentations of central nervous system (CNS) HIV continue to be an important component of the differential diagnosis of new-onset neuropsychiatric symptoms. The following case presentation provides a basis for discussion of current issues in HIV neuropsychiatry that should be important components of clinical teaching in medicine and psychiatry.


  Case Report

 
TOP
 INTRODUCTION
 Case Report
Discussion
 Conclusion
 REFERENCES
 
Mr. A is a 34-year-old African American gay man with no previous personal or family psychiatric history and no active or past substance abuse who was transferred to the emergency room for treatment of mania and neuroleptic malignant syndrome (NMS).

Mr. A was in his usual state of health, employed as director of his department, when he began to exhibit irritability, religious preoccupation, grandiosity, increased goal-directed activity, and an increased interest in sex. Friends called an ambulance when they found him smashing things in his apartment, and he was taken to a city hospital. Upon the family's request, he was subsequently transferred to a psychiatric facility for treatment of presumed primary bipolar disorder. He received olanzapine up to 15 mg and intramuscular (IM) haloperidol up to 20 mg per day over a 3-day period. He was transferred to our emergency room with symptoms of NMS 15 days after his initial presentation.

Upon arrival, Mr. A was found to be febrile, tachycardic, rigid, and delirious. He was admitted to the general-medicine service, where a complete work-up was initiated. Admission labs were notable for lymphopenia, elevated liver enzymes, a creatine phosphokinase level that peaked at 2,298, normal renal function, and a negative urine toxicology screen. A brain computerized tomographic (CT) scan without contrast revealed atrophy inappropriate for age.

A psychiatric consultation was requested. An HIV test was recommended by the psychiatric consultation team, and the test was positive. Further work-up revealed a CD4 + lymphocyte count of 33 cells/mm3, an HIV-1 viral load of 337,000 copies/ml, a serum total testosterone level of 183 ng/dl, and no evidence of opportunistic infection. Complete cerebrospinal fluid studies were unrevealing. An MRI scan of the brain, with and without gadilinium, revealed diffuse cortical atrophy, and an EEG in the awake, agitated state, was unremarkable. Serum was negative for hepatitis A, B, and C. Serum VDRL was negative, and thyroid studies were within normal limits.

Treatment of the NMS consisted of discontinuation of all neuroleptics, along with hydration and monitoring. Bromocriptine was ordered but was discontinued after 2 days because of worsening of the agitation. Treatment of the agitation, compounded by NMS, was limited to intravenous (IV) lorazepam, wrist restraints, constant observation, and a private room with minimal stimulation. The patient's mother rarely left the bedside.

On Hospital Day 11, a combination of antiretroviral medications, consisting of lamivudine, zidovudine, lopinavir, and ritonavir was initiated to treat presumed AIDS mania. Ultimately, the patient became completely uncooperative with oral medication, necessitating antiretroviral treatment interruption after 14 days. His mental status deteriorated over the next several days to groaning, posturing, facial grimacing, echolalia, and, finally, muteness, while, physically, the patient remained combative.

On Hospital Day 24, the patient was transferred to the medical intensive-care unit, where he was placed on a midazolam drip up to 55 mg/hour. He remained tachycardic, with no suppression of his respiratory rate, afebrile, with no signs of infection, and in an intractable state of agitated delirium. On Hospital Day 31, a course of bilateral electroconvulsive therapy (ECT) was initiated. The IV midazolam drip of 55 mg/hour was interrupted for 30 minutes before delivery of the stimulus. With this strategy, the patient achieved robust EEG seizures, with dramatic improvement after the third session. Slow taper of the midazolam was initiated. Mr. A completed a course of seven bilateral treatments. Care was given to avoid depolarizing anesthetic agents, given the recent history of NMS. Of note, the patient was rechallenged with 25 mg of oral chlorpromazine on Hospital Day 35 and developed his only episode of fever (38.4°C) within 2 hours of being given this dose. The fever work-up was negative; further neuroleptics were held; and the patient defervesced and remained afebrile. On Hospital Day 44, the patient was transferred out of the ICU to the medical floor. The remaining midazolam was replaced by chlordiazepoxide, which was tapered and discontinued, and then antiretroviral therapy was restarted. Lamotrigine was initiated for prophylactic maintenance therapy for mixed mania. The patient was discharged to his apartment under his mother's supervision on Hospital Day 51. At the time of discharge, his agitation had subsided totally; his mood was mildly depressed; and there were some residual cognitive deficits that improved significantly over the weeks after discharge. At 3-month follow-up, CD4 lymphocyte count was 91 cells/mm3, and HIV-1 viral load was below the limit of detection (<50 viral copies/ml).


  Discussion

 
TOP
 INTRODUCTION
 Case Report
 Discussion
Conclusion
 REFERENCES
 
This extraordinary case of HIV-associated mania illustrates four important issues. First, although HIV infection should be considered in the differential diagnosis of new-onset neuropsychiatric presentations, reduced HIV-associated morbidity and mortality and a lack of recent epidemiological data regarding HIV seroprevalence in the general hospital have led to a reduced index of suspicion and, likely, missed diagnosis. Second, CNS HIV, now more completely understood, continues to be prevalent and is a modern "great imitator" of psychiatric illness, including mania. Third, because of the subcortical neuropathology of HIV, these patients are highly susceptible to neuroleptic-induced extrapyramidal symptoms, including neuroleptic malignant syndrome (NMS). Finally, conventional psychiatric treatments, including ECT, can be used in conjunction with potent antiretroviral therapy to quell the fire of HIV-associated neuropsychiatric conditions.

Index of Suspicion
Since the first protease inhibitor, saquinavir, was approved in 1995, combination antiretroviral therapy (commonly called Highly-Active Antiretroviral Therapy, or HAART) has become the standard of HIV treatment in the developed world, leading to dramatic reductions in HIV-related morbidity and mortality.1 The prevailing view of HIV to the public and the medical community is that of a chronic, treatable, if not curable, illness. This relative truism has led, however, to an underestimation of the ongoing impact of HIV. HIV risk-behavior remains prevalent, particularly among young, gay men and persons of color,2 and HIV remains endemic in the United States, with the rate of new HIV infections remaining steady at approximately 40,000 per year.2,3 Because of reduced hospitalization rates of patients with known infection, medical staff may be less familiar with HIV complications, particularly those related to CNS disease. The current patient, a gay African American man with a new-onset neuropsychiatric condition, brain atrophy, and lymphopenia, traversed three emergency rooms, a psychiatric unit, and initial inpatient medical evaluation before HIV testing was suggested. Before this, he was slotted for transfer to another psychiatric inpatient setting once the NMS was cleared. The notion of a manic presentation of HIV, although common 10–20 years ago and, hopefully, familiar to psychiatrists in psychosomatic medicine, appeared both novel and fascinating to the medical and psychiatric house-staff. It is difficult to assess the current rates of HIV infection in the general hospital, and rates of undiagnosed HIV, since all blinded HIV seroprevalence studies in this setting preceded 1995.4,5 Such studies documented HIV seroprevalence rates ranging from 0.1% to 14%, with up to 10% of cases going undiagnosed at discharge. With the currently reduced awareness of HIV-related complications brought about by improved therapies and with the delivery of HIV care occurring primarily in HIV specialty clinics, it is likely that cases of HIV continue to go undiagnosed and untreated, particularly when neuropsychiatric presentations are involved.

Mania as a Manifestation of CNS HIV Infection
In order to understand the neuropathological basis of this patient's presentation, it is vital to understand the spectrum of HIV infection in the CNS. Since the beginning of the epidemic, the neuropsychiatric manifestations of this retroviral infection have been recognized. HIV can produce a range of cognitive and behavioral symptoms that become more frequent and severe as the immune system declines and symptomatic illness and AIDS ensue. In 1991, the American Academy of Neurology defined two clinical disorders: HIV-associated Minor Cognitive Motor Disorder (MCMD) and HIV-associated Dementia (HAD).6 Both disorders present with cognitive and behavioral symptoms associated with functional impairment (mild in MCMD, moderate-to-severe in HAD) and have been found to predict shorter survival.7,8 The cognitive symptoms usually seen are characteristic of other subcortical-frontal disorders; these include impairment in psychomotor processing speed, executive functioning, and verbal memory. Behavioral symptoms range from apathy and depression to mania and psychosis.

Neuropathologically, HIV traverses the blood–brain barrier primarily via infected blood mononuclear cells, which become activated macrophages once they enter the brain. Neuropathological changes appear to be a result of toxic cytokines (including tumor necrosis factor-{alpha}, interferon-{gamma}) and metabolites (e.g., quinolinic acid) resulting from this immune activation.9 Subcortical brain structures, such as the basal ganglia and periventricular white matter, are most affected. If unchecked, this immune cascade leads to neuronal cell apoptosis. However, effective suppression of CNS viral replication and the resulting immune activation has the potential to reverse at least some of the neuropathological changes.

HIV-associated neuropathology has received heightened attention in recent years because of two associated developments: First, simultaneous plasma and CSF HIV-1 viral load monitoring has demonstrated that the CNS is an independent site of viral replication, especially in the later stages of AIDS.10 In other words, the virus may replicate separately in the CNS and plasma. Second, we now recognize that antiretroviral medications have differing levels of penetration into the CNS. It was initially hypothesized that poorly-penetrating antiretrovirals might treat CNS infection inadequately, despite being effective peripherally. This led to concerns that actively-replicating virus in the CNS could cause progressive cognitive decline in otherwise-healthy HIV+ individuals and could also lead to a "re-seeding" of drug-resistant virus into the peripheral circulation. Small clinical studies have shown that antiretrovirals with the highest degree of CNS penetration, such as zidovudine and indinivir, are associated with the greatest cognitive improvement.10,11 However, from an epidemiological perspective, concerns regarding rising rates of HAD have been unsupported. There has been an approximately 50% reduction in the incidence of HAD from the pre- to the post-HAART era.12 Heterogeneous HAART regimens have been shown to reduce CSF viral load to undetectable levels,13 to reverse white-matter lesions on MRI,14 to reverse brain-metabolic abnormalities detected by proton MR spectroscopy,15 and also to improve neuropsychological test performance.16,17 Despite these hopeful findings, however, functionally significant cognitive and behavioral disturbances, without frank dementia, may persist in up to 22% of HAART-treated patients,18 impeding adherence to treatment19 and ability to work.20

This patient presented with HIV-associated mania, which has been described in the literature as a late-onset mania that is secondary to HIV brain infection.21–25 HIV-associated mania meets criteria for a classical secondary mania, characterized by an identifiable medical cause, later-than-average age at onset, and lack of previous personal or family history of mania.26 This secondary mania has a prevalence of 1.2% in HIV+ patients (similar to the general population), and 4.3%–8% in AIDS patients seen in HIV specialty clinics in the pre-HAART era.23,25 This untreated patient had profound immunosuppression, elevated plasma HIV viral load (CSF viral-load testing was not commercially available), and no personal or family history of mania. Clinically, HIV-associated mania has been differentiated from bipolar mania in manifesting more dysphoria, irritability, and cognitive impairment, which were prominent features of this patient's initial presentation. Furthermore, this patient's condition progressed to include paranoid psychosis and, eventually, catatonia, characterized by mutism, posturing, and catatonic excitement. Such features have been reported in association with mania, NMS, and advanced HIV-associated dementia,27 underscoring the many etiological mechanisms of the clinical presentation of catatonia.28

Neuroleptic Sensitivity
This patient's presentation with NMS highlights the sensitivity of HIV patients to extrapyramidal side effects of neuroleptic medications, including NMS, particularly when high potency and multiple neuroleptics are administered.29–31 In one study of patients with HIV-related psychosis, all haloperidol-treated patients developed extrapyramidal symptoms (EPS).32 However, cases of EPS and NMS have been reported in HIV patients in association with low-potency agents, such as phenothiazine antiemetics.33–35 This patient developed NMS as a result of combined neuroleptics (olanzapine and haloperidol), which is a risk factor documented in the literature.36 Furthermore, during his hospital course, he developed a fever, perhaps a harbinger of NMS exacerbation, within hours after a single dose of a chlorpromazine challenge. Most psychiatrists choose atypical neuroleptics for HIV and other patients with subcortical neuropathology. However, these agents are not without risk for EPS in HIV patients,37 including the risk for metabolic inhibition of some agents by protease inhibitors.38

Concurrent Treatment With HAART and ECT
The treatment of this patient involved the use of ECT in combination with potent antiretroviral medication. Theoretically, given the fact that the patient's neuropsychiatric symptoms were caused by productive HIV CNS infection, the utilization of psychiatric treatment alone in this case would be akin to attempting to douse a fire while allowing gasoline to leak into its base. It is likely that 2 weeks of potent HAART helped to reduce the stimulus for this patient's symptoms. Potent antiretroviral therapy has been documented to protect against the development of HIV-associated mania39 via suppression of CNS HIV replication. In terms of psychiatric treatment, ECT was chosen because of the refractoriness of this patient's progressive catatonic manic presentation, his inability to cooperate with treatment, and concern for recurrent NMS and other psychotropic-induced toxicities. Although ECT has been documented to be effective in the treatment of severe depression in HIV+ patients40,41 and in medically healthy patients with bipolar mania,42 to our knowledge, this is the first documented case of ECT for the treatment of HIV-associated mania. Furthermore, to the extent that residual symptoms of NMS might have been an ongoing component of this patient's presentation, ECT has also been documented to reduce morbidity and mortality associated with NMS in the general psychiatric population.43


  Conclusion

 
TOP
 INTRODUCTION
 Case Report
 Discussion
 Conclusion
REFERENCES
 
This extraordinary case of AIDS mania that went initially undetected but was ultimately successfully treated with ECT and HAART, underscores the endemic persistence of HIV and the potential for this virus to present with neuropsychiatric symptoms. It is essential to make education regarding HIV and its neuropsychiatric presentations an integral part of residency and continuing education for medical and psychiatric staff. Fortunately, as was the case with this patient, highly effective antiretroviral and psychiatric treatment interventions can reverse at least some of the havoc wreaked by this virus and result in gratifying clinical outcomes.


  REFERENCES

 
TOP
 INTRODUCTION
 Case Report
 Discussion
 Conclusion
 REFERENCES
 

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