CMT, Depression + Electroconvulsive Therapy

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Am J Psychiatry 165:776-a-777, June 2008

Electroconvulsive Therapy in a Patient With Concomitant Depression

and Charcot-Marie-Tooth Disease

ANNA LAENGER, M.D., GREGOR LEICHT, M.D., CORNELIUS SCHULE, M.D.,

THOMAS C. BAGHAI, M.D., STEFFEN LINDHAUS, M.D., and RAINER RUPPRECHT,

M.D. Munich, Germany

Charcot-Marie-Tooth disease is a severe neurological disorder

affecting both motor and sensory peripheral nerves. In patients with

peripheral autonomic nervous or respiratory system involvement,

anesthesia management can be difficult. A higher risk for malignant

hyperthermia and succinylcholine-induced hyperkalemia during

anesthesia in patients with Charcot-Marie-Tooth disease is under

discussion (1, 2). These issues may limit the possibility for

psychiatric patients with Charcot-Marie-Tooth disease to undergo

electroconvulsive therapy (ECT). We present the first case of a

successful performance of ECT in a patient suffering from both severe

treatment-resistant depression and Charcot-Marie-Tooth disease.

" Mr. T, " a 70-year-old man suffering from Charcot-Marie-Tooth disease

type I, with pronounced muscle atrophy in the upper and lower

extremities, was referred to our department with severe, delusional,

first-episode depression. For almost 2 years, a loss of drive,

delusions of poverty, and near mutism were the most prominent

symptoms. Since the patient had previously been resistant to any

antidepressant (citalopram, clomipramine, duloxetine, mirtazapine,

paroxetine, reboxetine, tranylcypromine) or antipsychotic

(haloperidol, olanzapine, quetiapine, risperidone), we decided to

perform ECT.

Electroencephalography and magnetic resonance imaging did not reveal

any pathology. Blood gas analysis showed a slight compensated

respiratory acidosis (PaO2=83 mmHg, PaCO2=44 mmHg, pH=7.41, HCO3 =27

mmol/l, BE= –0.9 mmol/l). Both body plethysmographic and spirometric

measurements were normal, with regular vital capacity (4.27 l, 102%

predicted) and Tiffeneau index (85%, 114% predicted).

The patient received eight unilateral and seven bitemporal

electroconvulsive treatments (bidirectional: 309 to 622 mC; length of

stimulus train: 5.2 to 8 seconds) over a period of 6 weeks.

Concomitant antidepressant and antipsychotic medications (reboxetine,

4 mg; risperidone 2 mg per day) were continued during ECT. Anesthesia

was induced with intravenous propofol (2.5 mg/kg) and mivacurium (0.1

mg/kg), followed by oxygenation, with 100% oxygen for 4 minutes.

Severity of depression was assessed using the 21-item Hamilton

Depression Rating Scale (HAM-D) every 14 days during ECT treatment.

Except for several short episodes of bradycardia (minimum 42 bpm)

during anesthesia and a delayed recovery phase after ECT

(approximately 10 minutes), no significant complications occurred

during anesthesia and ECT, nor were there any cognitive disturbances.

Within a few sessions, the patient showed improved mood and a clear

increase in drive and social activity. His HAM-D score decreased from

36 at baseline to 22 by the end of ECT treatment. This effect has

been sustained with lithium and bupropion following ECT for more than

6 months.

To our knowledge, this is the first report of ECT in a patient

suffering from concomitant Charcot-Marie-Tooth disease. Thus, with

adequate prearrangement, ECT can safely be performed in patients

suffering from both Charcot-Marie-Tooth disease and pharmacotherapy-

resistant psychiatric disorders. Nevertheless, ECT anesthesia

procedures should be standardized based on systematic evaluations.