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Conrad M Swartz

Publications and source records attributed to Conrad M Swartz.

10 recordsLinked to original sources

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.

Electroconvulsive Therapy↗

Diminished ECT response in catatonia due to chronic neurologic condition.

A series of four clinical cases suggests that catatonic disorder due to a chronic neurologic condition does not respond as reliably to electroconvulsive therapy (ECT) as functional catatonia does. Cases reported in the medical literature show a similar pattern. Presumably this form of catatonia is intrinsically less responsive to ECT, although the possibility remains that a more intense quality of treatment and prophylaxis is needed. Conversely, catatonia resistant to ECT suggests an underlying medical condition.

Adult↗

Postictal asystole during ECT.

BACKGROUND: Asystole is an uncommon but potentially fatal complication of electroconvulsive therapy (ECT). Several risks for poststimulus asystole have been described, but risks for asystole at other times have not. METHOD: Two instances of ECT postictal asystole in healthy adult males are reported. Features in common are identified. RESULTS: features shared differ from risk factors for poststimulus asystole. In common were adult but not geriatric age, male sex, good physical and cardiac health, mesomorphic habitus, anticholinergic pretreatment, vigorous ECT seizure, and low resting heart rate. Both patients showed postictal bradyarrhythmia at the previous ECT. CONCLUSIONS: Postictal asystole has apparent similarities to postexertional asystole in athletes. The combination of higher pretreatment doses of an atropinic agent, a sympatholytic agent, and close monitoring of postictal cardiac rhythm should be considered with patients similar to ours, especially after occurrence of postictal bradyarrhythmia.

Adult↗

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).

Adult↗

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.

Carbazoles↗

Suppression of catatonia-like signs by lorazepam in nonconvulsive status epilepticus without seizure termination.

Nonconvulsive status epilepticus (NCSE) cannot be reliably distinguished from catatonia by signs or symptoms. The authors report on a 68-year-old man with endogenous major depression who displayed catatonia-like psychopathology, which temporarily disappeared with lorazepam. An EEG then revealed NCSE. Presumably, lorazepam suppressed seizure in areas where it had caused clouding of consciousness, but it did not suppress all seizure activity. When lorazepam was stopped, the catatonia-like delirium returned; it disappeared again with valproate administration. This case illustrates that the reduction of signs consistent with catatonia by benzodiazepines does not by itself confirm catatonia, even in patients with endogenous depression.

Aged↗