What Is Brain Damage and Does Electroconvulsive Therapy Cause It?

ABSTRACT: Surveys show public misperceptions and confusion about brain damage and electroconvulsive therapy (ECT). Fictional movies have misrepresented ECT to suggest brain damage and to ridicule mental illness and psychiatric patients. "Brain damage" has become a colloquial expression without consistent meaning. In contrast, brain injury is the medical term for destruction of brain cells, such as from kinetic impact (concussion), hypoxia, or infection. Studies of both high-resolution magnetic resonance imaging (MRI) and enzyme assays find that causes of brain injury are accompanied by observable structural changes on MRI and elevated blood and cerebrospinal fluid levels of brain enzymes that leak from injured brain cells. Concussion is also followed by intracerebral bleeding, progressive brain atrophy, diffuse axonal injury, cranial nerve injury, and 2-4 fold increased risk for dementia. In contrast, there is no evidence that ECT produces any of these. Studies of ECT patients find no brain edema, structural change persisting 6 months, or elevated levels of leaked brain enzymes. Statistical comparisons between brain injury and ECT effects indicate no similarity ( P < 0.00000001). Moreover, the kinetic, thermal, and electrical effects of ECT are far below levels that could possibly cause harm. This robust evidence shows that there is no basis to claim that ECT causes brain injury.

A mechanism of seizure induction by electricity and its clinical implications.

A model of ECT seizure induction by rapid kindling is described. The electrical stimulus as a series of pulses progressively disrupts neuronal cell membranes, with corresponding progressive increases in intracellular concentrations of sodium, calcium, and voltage. Eventually, the intracellular voltage rises to trigger neuronal firing in waves from seizure foci. The quantity of seizure foci produced is expressed by the stimulus charge multiplied by the current cubed. Differences in implications are described between this model and the traditional model that extrapolates from an isolated single neuron undergoing immediate electrical depolarization by a single pulse. Total brain exposure to seizure neurotransmitter release in ECT is analogous to body exposure to medication in drug therapy and may be expressed by a physiological measurement such as electroencephalographic postictal suppression or peak seizure heart rate.

Age-based seizure threshold determination.

OBJECTIVE: The intent was to improve seizure threshold titration by decreasing stimuli number. METHOD: An age-based method of titration for initial seizure threshold bilateral electroconvulsive therapy was constructed and used in 15 women and 9 men aged 35 to 80 years. Titration steps were one eighth, one fourth, three eighths, one half, five eighths, three fourths, 1, and 1.2 times age, expressed as "% Energy." RESULTS: Male thresholds were a significantly (P < 0.05, t(22) = 2.18) higher percentage of age (61.9%; SD, 32.6%) than female thresholds (41.2%; SD, 15.2%). Four women (27%) and 4 men (44%) showed seizure thresholds more than 50% of age. On average, women received 3.2 stimuli and men received 4.4 stimuli. No patient seized at one-eighth age. All patients who seized at one-fourth age were women and younger than 65 years. CONCLUSIONS: For women younger than 65 years, these data suggest that titration starting at one-fourth age should require 1.8 stimuli on average. For older women, starting at three-eighths age should average 1.8 stimuli. For men, starting at three-eighths age should require 2.4 stimuli, but with steps at three fourths, 1, and 1.25 age titration should average 1.8 stimuli. Age-based dosing should succeed in women younger than 65 years at one-half age and older than 65 years at five-eighths age. For men, dosing at one-half age should succeed among one half and is a reasonable initial titration dose.

Clinically insubstantial cognitive side effects of bitemporal electroconvulsive therapy at 0.5 msec pulse width.

BACKGROUND: We measured cognitive side effects from bitemporal electroconvulsive therapy (ECT) using stimuli of 0.5 msec pulse width 900 milliamperes (mA). METHODS: Mini-Mental State Exam (MMSE) and 21-item Hamilton Rating Scale for Depression (HRSD-21) were rated within 36 hours before and 36 hours after a series of 6 bitemporal ECT sessions on 15 patients age ≥45. RESULTS: MMSE remained high after ECT (pre-ECT mean 29, standard deviation [SD] 1.60, post-ECT mean 28.53, SD 1.36) with no significant change. The mean HRSD-21 fell from 27.5 to 16.3. Post-ECT MMSE was significantly and markedly higher than in previous studies of bitemporal ECT; all had used ECT stimuli of pulse width at least 1 msec. CONCLUSIONS: With stimuli of 0.5 msec pulse width and 900 mA, 6 bitemporal ECTs did not decrease MMSE score. This result leaves no opportunity for further decrease in basic cognitive side effects, and complements published reports of stronger physiological effects with stimuli of 0.5 msec pulse width and 900 mA. ECT stimuli of 0.5 msec pulse width and 900 mA are more desirable than wider pulse widths. Six bitemporal ECT sessions using these stimuli generally will not have more cognitive side effects than treatments with other placements, allowing maintenance of full efficacy with clinically insubstantial side effects.

Propofol interruption of ECT seizure to reduce side-effects: a pilot study.

Fifteen depressed subjects received six bitemporal electroconvulsive therapy (ECT) treatments under etomidate anesthesia. They were randomized to blindly either receive propofol 0.5mg/kg 15s post-stimulus or not. Propofol infusion significantly prevented long seizures, and prevented cognitive decrements in most neuropsychological tests, several significantly. Propofol interruption may clinically help reduce ECT side-effects.

ECT generalized seizure drives heart rate above treadmill stress test maximum.

OBJECTIVES: Heart rate (HR) accelerates with the electroconvulsive therapy (ECT) seizure and decelerates when it ends. The peak HR during ECT seizure has been reported to reflect clinical impact. We aimed to identify the expected range for ECT peak HR and how it varies with age and sex, as a reference in clinical use. METHODS: We examined medical records for the maximum peak seizure HR over the ECT course for all ECT patients over defined periods at 2 clinical sites. Methohexital-succinylcholine anesthesia was usually used. Subject totals were 87 men and 90 women. RESULTS: Electroconvulsive therapy peak HR was 140 to 180 bpm and did not fall with age through 80 years, separately for men and women. A few patients lay outside this cluster and showed age-related decrease. Overall and including the extreme elderly, peak HR fell by 0.29 bpm/yr. CONCLUSIONS: Electroconvulsive therapy seizure peak HR less than 140 bpm points to weakness of the ECT seizure (and need to increase stimulus dose), cardiac disease, or medication effect limiting HR. Electroconvulsive therapy peak HR exceeds treadmill exercise maximum HR after 60 years and falls significantly less with age than the 0.7 to 1 bpm/yr reported for maximum HR with treadmill exercise stress. These comparisons suggest that ECT peak HR and treadmill maximum HR are limited by different aspects of physiology, and that exercise HR is limited by metabolic demand and humoral activity rather than the heart itself.

Carvedilol suppresses intractable hiccups.

Carvedilol (6.25 mg, 4 times daily) relieved 2 years of constant hiccupping, marked tardive dyskinesia, compulsive self-induced vomiting, and feelings of hopelessness and low mood in a 59-year-old African-American man. He previously failed trials of ranitidine, chlorpromazine, promethazine, tegaserod, ondansetron, metoclopramide, pantoprazole, pyloric injections of botulinum toxin A, and a vagal nerve stimulator. At a 5-month follow-up, improvement was maintained; there had been several instances of rapid relapse on carvedilol discontinuation.

Electroconvulsive therapy stimulus dose expressed as volume of seizure foci.

BACKGROUND: Electrical stimulus dose is typically stated as charge in millicoulombs (mC), representing the number of electrons. However, by overlooking the voltage threshold for neuronal depolarization, charge alone is inappropriate. Any charge can accumulate from subthreshold voltage over time. Stimulus energy represents heat content; without a delivery rate, it is not related to depolarization voltage. The objective was to formulate stimulus dose in accordance with seizure induction physiology. METHOD: Stimulus dose was expressed as volume of generated seizure foci, a variable dependent on current and charge. A second more detailed model considers brain voltages as related to clinical deep brain stimulation. RESULTS: For the constant current stimuli characteristic of widely available American stimulators, stimulus dose is proportional to current cubed multiplied by charge. This relationship corresponds to the 3 dimensions of a voltage field in space, where the volume above a certain voltage increases with the cube of the voltage radius. As a consequence, any particular charge at 0.9 A (ampere) current has a seizure foci dose approximately 50% higher than the same charge at 0.8 A. CONCLUSIONS: The modeling offers an explanation for published measurements comparing instruments of maximum current 0.8 and 0.9 A. The modeling also suggests compensation approaches to be applied to the age-based bilateral stimulus dosing method. An electrical dosing strategy based on "half-age" (2.5 mC/y) is reasonable for 0.9-A stimulation but a "three-quarters age" (3.7 mC/y) is more appropriate for 0.8-A stimulation. The present results can allow doses and seizure thresholds to be compared between different currents, as when substituting one electroconvulsive therapy instrument for another.

Dystonic rabbit syndrome from citalopram.

OBJECTIVE: Two cases are described of dystonic rabbit syndrome induced by citalopram. This syndrome is a movement disorder with a 5-Hz rhythmic vertical motion of the mouth and lips without involvement of the tongue. METHOD: The patients were interviewed and examined, and additional history was taken from the medical records. The Naranjo adverse drug reaction rating scale was applied. Relevant literature was reviewed. RESULTS: Two patients developed dystonic rabbit syndrome soon after starting escitalopram 10 mg/day or citalopram 5 mg/day. Neither patient had any past or current exposure to a dopamine-blocking drug or any history of movement disorder. [Es]citalopram discontinuation led to disappearance of the movement disorder. The Naranjo scale indicates high probability of dystonic rabbit syndrome from citalopram. CONCLUSION: Citalopram can rapidly induce dystonic rabbit syndrome. This effect suggests that for some patients citalopram has neuropsychiatric effects similar to those of a dopamine-blocking antipsychotic drug. This might be of concern with patients who cannot communicate well (eg, young children; patients with dementia, developmental disabilities, or aphasia).

Rational electroconvulsive therapy electrode placement.

Expertise in medicating depression requires experience with all types of antidepressants, including several medications within each type. Likewise, electroconvulsive therapy (ECT) proficiency includes experience with each of the modern electrode placements, of which there are four. Besides traditional bilateral and right unilateral placements, ECT electrode placement includes bifrontal and left anterior right temporal (LART) placements. In comparing antidepressant drugs, clinical trials have proven few differences of statistical significance, and useful proven differences are still more unusual. Analogously, few differences have been proven between ECT electrode placements, and many reported differences can be accounted for by large differences in electrical stimulus dosage. Still, the absence of proven differences does not show that there are no useful variations. This paper reviews the meaningful differences that are generally appreciated from clinical experience and biomedical principles for ECT electrode placement as well as antidepressant drugs.