Cases That Test Your Skills

Depressed, delusional, and ‘dead’

Current Psychiatry. 2006 July;5(7):105-113

References

1. McCall WV, Mann SC, Shelp FE, et al. Fatal pulmonary embolism in the catatonic syndrome: two case reports and a literature review. J Clin Psychiatry 1995;56:21-5.

2. Rosebush PI, Hildebrand AM, Furlong BG, Mazurek MF. Catatonic syndrome in a general psychiatric inpatient population: frequency, clinical presentation, and responses to lorazepam. J Clin Psychiatry 1990;51:357-62.

3. Diagnostic and statistical manual of mental disorders, 4th ed, text rev. Washington, DC: American Psychiatric Association; 2000.

4. Fink M, Taylor MA. Catatonia: a clinician’s guide to diagnosis and treatment. Cambridge, UK: Cambridge University Press; 2003.

5. Mann SC, Caroff SN, Bleier HR, et al. Electroconvulsive therapy of the lethal catatonia syndrome. Convuls Ther 1990;6:239-47.

6. Yamada K, Katsuragi S, Fujii I. A case study of Cotard’s syndrome: stages and diagnosis. Acta Psychiatr Scand 1999;100:369-99.

7. Enoch MD, Ball H. Uncommon psychiatric syndromes, 4th ed. London: Arnold Publishers; 2001.

8. Nejad AG, Toofani K. Co-existence of lycanthropy and Cotard’s syndrome in a single case. Acta Psychiat Scand 2005;111:250-2.

9. Beers MH, Passman LJ. Antihypertensive medications and depression. Drugs 1990;40:792-9.

10. Baumeister AA, Hawkins MF, Uzelac SM. The myth of reserpine-induced depression: role in the historical development of the monoamine hypothesis. J Hist Neurosci 2003;12:207-20.

11. Drug facts and comparisons. St. Louis: Wolters Kluwer; 2006.

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13. Caroff SN, Mann SC, Francis A, Fricchionne GL. Catatonia: from psychopathology to neurobiology. Washington, DC: American Psychiatric Publishing; 2004.

14. Mahgoub NA, Hossain A. Cotard’s syndrome and electroconvulsive therapy. Psychiatr Serv 2004;51:1319-20.

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16. Schwartz CM, Nelson AL. Rational electroconvulsive therapy electrode placement. Psychiatry 2005;2:37-43.

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Characteristics of Cotard’s syndrome

Delusional belief that one’s body parts, friends, family, money, or the world do not exist Can accompany major depression, schizophrenia, dementia, or a general medical condition Relatively rare, with unknown incidence and prevalence. More common during late middle life and among women Sudden onset with no history of psychiatric disorder Associated with nondominant parietal lobe lesions and catatonia

Delusional belief that one’s body parts, friends, family, money, or the world do not exist
Can accompany major depression, schizophrenia, dementia, or a general medical condition
Relatively rare, with unknown incidence and prevalence. More common during late middle life and among women
Sudden onset with no history of psychiatric disorder
Associated with nondominant parietal lobe lesions and catatonia

The authors’ observations

Mr. P.’s episode appears to have been idiopathic.

Reserpine could have caused his decompensation, though precisely how is unclear. The medication is alleged to cause depression by depleting serotonin, dopamine, and norepinephrine, but some researchers believe it exacerbates pre-existing depression.^9,10

When treating any patient with a history of depression, find out if he or she is taking reserpine. Advise the primary care physician to discontinue the drug if the patient is self-deprecating or despondent, or reports early morning insomnia, loss of appetite, or impotence.¹¹

Treatment: False Start

To address Mr. P’s catatonia, we stop quetiapine and mirtazapine and start IM lorazepam, 2 mg qid. After 4 days his condition is stable, but he still believes that he and everyone else is dead.

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The authors’ observations

Parenteral benzodiazepines typically are used to treat patients with catatonia and Cotard’s syndrome while the clinician searches for a toxic or medical cause. Most patients with nonemergent catatonia respond to a benzodiazepine.¹²

Although opinion differs on starting dosages of IM lorazepam in retarded catatonia, we recommend 2 mg IM and repeat doses every 3 hours if the patient does not respond.^4,13 Lack of response after 20 mg (10 doses) warrants ECT.⁴

Consider ECT—which has shown effectiveness for treating both catatonia and Cotard’s syndrome in case reports^6-8,14,15—as first-line treatment in emergent catatonia. Do not try a first- or second-generation neuroleptic, which can worsen clinical outcome.

Treatment: a Three-Week Trial

We receive informed consent from Mr. P’s brother to try 10 ECT treatments over 3 weeks. We choose left anterior right temporal electrode placement to minimize cognitive interference,¹⁶ and give Mr. P glycopyrrolate, 0.2 mg before each treatment, to manage bradycardia resulting from enhanced vagal tone after electrical stimulation. According to ECT protocol, we administer the anesthetic methohexital, 0.75 to 1.0 mg/kg, and the muscle relaxant succinylcholine, 0.5 to 1 mg/kg, to shorten seizure duration during ECT.

Mr. P also receives forced ventilation at each treatment to counteract brief succinylcholine-induced paralysis of the diaphragm and other muscle tissue. Stimulus intensity begins at 35% and is increased to 50% as the patient’s seizure threshold increases. Each morning, Mr. P also receives extended-release venlafaxine, 225 mg, for depressive symptoms, and hydrochlorothiazide, 25 mg.

After the first ECT treatment, Mr. P’s affect starts to brighten. He speaks a few words after the third treatment and begins eating larger portions by the fifth treatment. After the last treatment, he is performing activities of daily living, talking readily and coherently, and playing basketball with peers. He shows no adverse cognitive effects or other complications from ECT.

The authors’ observations

Although little evidence guides treatment of catatonia in the developmentally disabled,¹⁷ we support early use of ECT in those with serious refractory mental illness.¹⁸ Some clinicians hesitate to administer ECT to patients with mental retardation because they might be particularly vulnerable to adverse medication effects.¹⁹ ECT, however, has been found to cause minimal side effects in this population²⁰ and does not cause or exacerbate brain damage.²¹

If the patient is mentally incapable of consenting to ECT, obtain informed consent from his or her legal guardian.

Conclusion: Leaving the Hospital

We discharge Mr. P after 25 days. He shows no evidence of psychosis, suicidality, or intent to harm others. He continues hydrochlorothiazide and venlafaxine at the same dosages. He returns home with his brother, and 6 months later is functioning well.

Related resources

National Mental Health Association. Electroconvulsive therapy. www.nmha.org/infoctr/factsheets/ect.cfm.

Drug brand names

Bupropion • Wellbutrin
Disulfiram • Antabuse
Glycopyrrolate • Robinul
Hydrochlorothiazide • Various
Lorazepam • Ativan
Methohexital • Brevital
Mirtazapine • Remeron
Quetiapine • Seroquel
Reserpine • Serpasil
Succinylcholine • Anectine
Venlafaxine XR • Effexor XR

Disclosures

The authors report no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.