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The Trigeminocardiac Reflex in Electroconvulsive Therapy
... reflex in humans and other mammals." 7 Consequently, "Acute poststimulus bradycardia and asystole are common during ECT." 7 E. Though ECT devices can potentially trigger the TCR, irreversible electroporation, augment drug delivery, acquired channelopathies, and the Abscopal Effect, ECT device manufacturers chose not to complete Premarket Approval (PMA) safety testing or Product Development Protocols (PDP) to establish electrical dosing consensus standards, essentially creating heuristic electrical dosing. For example, the US manufactured Thymatron device dose is configured using the following independent parameters to calculate electrical output duration from 0.14 to 8 seconds: i. ...
... Last year, The Journal of ECT acknowledged acute slowing of heart rate and heart attack are common in ECT because pulsing nearly an ampere current through the trigeminal nerve for up to 8 seconds triggers the trigeminocardiac reflex. 7 One in 50 patients have major cardiac Events during ECT. 8 One in 93 patients die within 30 days; the leading cause of death is cardiac failure. ...
Testimony opposing CT SB 898 to extend forced electroconvulsive therapy (ECT) based on Long-Term Consequences of Electroconvulsive Therapy/Electrical Injury's neurological sequalae's association with neurodegenerative diseases.
Original research discussing acquired communication disorders caused by electrical trauma which pose unique communication barriers due to their evolving symptom manifestation. As the person ages away from the initial injury, communication barriers can become more pronounced with age.
This presentation provides details explaining how electrical trauma, repeated electrical trauma and lengthy exposure to other forms of non-ionizing radiation can impact speech and communication. Following both UK's National Radiological Protection Board and United States Gulf War Hearing recommendations to study electroconvulsive therapy recipients to better understand the heterogeneity of amyotrophic lateral sclerosis (ALS) and other neurodegenerative diseases. I present four different case studies: Functional NeuroCognitive Imaging results and videos of ECT recipients now living with the neurological sequela of electrical injury which impacts speech and communication. It provides insights into the potential interventions which successfully work for the presenter who lives with speech and communication disorders as a result of chronic electroconvulsive therapy. It identifies strategies to make alternative augmentative communication (AAC) less fatiguing for people who live with a history of chronic exposure to non-ionizing radiation. The presentation concludes with ideas for future research.
-Non-ionizing radiation exposures and subsequent neurodegenerative diseases (Progressive supranuclear palsy and Myoneural Disorders: Amyotrophic Lateral Sclerosis, Motor Neuron Disease and Muscular Sclerosis).
-Immediate and delayed consequences of Electrical Injury/Electromagnetic injury
-Repetitive mild to moderate Traumatic Brain Injuries
-Cognitive communication disorder
-Anoxia/Hypoxia
-Trigeminal, vagal and other cranial nerve dysfunction.
-Electroporation
-Motor Neuron Dysfunction/Motor Neuron Loss
-Demyelination
-Episodic Paroxysmal Neuromuscular Disorders
-Acquired Channelopathies
-Thiols
-Aphasia
-Verbal Apraxia
-Dysarthria, Anarthria
-Preserving residual voice
-Barriers to accessing AAC
-Voice Banking
-AAC Recommendations
The presentation is available with 1.0 CEU through "AAC in the Cloud" website (https://presenters.aacconference.com/videos/UXpVd1FUSXk=)
Background:
The trigeminocardiac reflex (TCR) is defined as sudden onset of parasympathetic dysrhythmias including hemodynamic irregularities, apnea, and gastric hypermotility during stimulation of sensory branches of the trigeminal nerve. Since the first description of the TCR 1999, there is an ongoing discussion about a more flexible than the existing clinical definition. Aim of this work was to create a clinical surrogate definition through a systematic review of the literature.
Methods:
In this meta-analysis study, literature about TCR occurrences was, according to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis statement, systematically identified through various search engines including PubMed (Medline), Embase (Ovid SP), and ISI Web of Sciences databases from January 2005 to August 2015. TCR was defined as a drop of heart rate (HR) below 60 bpm or 20% to the baseline. We extracted detailed data about hemodynamic changes and searched for connections between arterial blood pressure (BP) and HR changes during such episodes.
Results:
Overall 45 studies harboring 57 patients were included in the study but only 32 patients showed sufficient data for final analyze. HR showed a nonlinear behavior with a "tipping point" phenomena that differs in variance from the central/peripheral (20-30% drop) to ganglion (40-49% drop). BP showed a linear behavior with a "central limit" phenomena not differing in variance in the whole subgroup (30-39% drop). An analyzation of the correlation between BP and HR showed a trend to a linear correlation.
Conclusions:
We can show for the first time that HR is the dominant variable in the TCR and present a new surrogate definition model. This model and the role of BP must be better investigated in further studies.
Trigemino-cardiac reflex (TCR) is a well-established phenomenon that is mainly reported in the various surgical specialties. However, the role of this unique reflex is entirely unknown in other medicine domains. Therefore, the present mini-review aims to explore the role of TCR in such unusual cases and also highlights the importance of case reports for knowledge creation in such context.
The trigeminocardiac reflex (TCR) is defined as the sudden onset of parasympathetic dysrhythmia, sympathetic hypotension, apnea, or gastric hypermotility during stimulation of any of the sensory branches of the trigeminal nerve. Clinically, the TCR has been reported in all the surgical procedures in which a structure innervated by the trigeminal nerve is involved. Although, there is an abundant literature with reports of incidences and risk factors of the TCR; the physiological significance and function of this brainstem reflex has not yet been fully elucidated. In addition, there are complexities within the TCR that requires examination and clarification. There is also a growing need to discuss its cellular mechanism and functional consequences. Therefore, the current review provides an updated examination of the TCR with a particular focus on the mechanisms and diverse nature of the TCR.
Background
This observational study documented heart rate over the entire course of electrically induced seizures and aimed to evaluate the effects of stimulus electrode placement, patients' age, stimulus dose, and additional predictors.
Method
In 119 consecutive patients with 64 right unilateral (RUL) and 55 bifrontal (BF) electroconvulsive treatments, heart rate graphs based on beat-to-beat measurements were plotted up to durations of 130 s.
Results
In RUL stimulation, the initial drop in heart rate lasted for 12.5 ± 2.6 s (mean ± standard deviation). This depended on stimulus train duration, age, and baseline heart rate. In seizures induced with BF electrode placement, a sympathetic response was observed within the first few seconds of the stimulation phase (median 3.5 s). This was also the case with subconvulsive stimulations. The mean peak heart rate in all 119 treatments amounted to 135 ± 20 bpm and depended on baseline heart rate and seizure duration; electrode placement, charge dose, and age were insignificant in regression analysis. A marked decline in heart rate in connection with seizure cessation occurred in 71% of treatments.
Conclusions
A significant independent effect of stimulus electrode positioning on cardiac action was evident only in the initial phase of the seizures. Electrical stimulation rather than the seizure causes the initial heart rate increase in BF treatments. The data reveal no rationale for setting the stimulus doses as a function of intraictal peak heart rates (‘benchmark method’). The marked decline in heart rate at the end of most seizures is probably mediated by a baroreceptor reflex.
Electroconvulsive therapy (ECT) remains stigmatized in the broader medical community because of misunderstandings about treatment procedures, mortality rates, and cardiovascular complications. Electroconvulsive therapy causes periprocedural hemodynamic variability because of the surges in parasympathetic and sympathetic nervous systems after the administration of the electrical charge. Patients experience an increase in cardiac workload, which is potentially dangerous for patients with preexisting heart disease. Several findings suggest that cardiac complications occur most frequently in patients with underlying cardiovascular disease. We describe the cardiovascular complications that may result from ECT treatment and offer insight on how to mitigate these concerns if they occur. PubMed was queried using terms "electroconvulsive therapy" and "cardiovascular adverse effects." A table is provided with the common cardiovascular side effects of ECT and the most recent evidence-based treatment strategies to manage them. Generally, ECT is a safe procedure in which complications are minor and manageable. Most major complications caused by ECT are related to the cardiovascular system; however, with an appropriate pre-ECT evaluation and a comprehensive multidisciplinary team approach, the cardiovascular complications can be well managed and minimized. Providing proper cardiac clearance can prevent cardiac complications and provide timely care to treatment-resistant populations who are at risk for excessive morbidity and suicide.
We present a case of transient right hemifacial rash after right unilateral electroconvulsive therapy. This phenomenon may have similarities with the cranial dysautonomia, Harlequin syndrome.
The trigemino-cardiac reflex (TCR) is clinically defined as the sudden onset of parasympathetic activity, sympathetic hypotension, apnea, or gastric hypermotility during central or peripheral stimulation of any of the sensory branches of the trigeminal nerve. Clinically, the TCR has been reported to occur during craniofacial surgery, manipulation of the trigeminal nerve/ganglion and during surgery for lesion in the cerebellopontine angle, cavernous sinus, and the pituitary fossa. Apart from the few clinical reports, the physiologic function of this brainstem reflex has not yet been fully explored. The manifestation of the TCR can vary from bradycardia and hypotension to asystole. From the experimental findings, the TCR represents an expression of a central reflex leading to rapid cerebrovascular vasodilatation generated from excitation of oxygen-sensitive neurons in the rostral ventro-lateral medulla oblongata. By this physiologic response, the systemic and cerebral circulations may be adjusted in a way that augments cerebral perfusion. This review summarizes the current state of knowledge about TCR.
The individual time-course of the seizure threshold (ST) in electroconvulsive therapy is mostly unknown. It is assumed that a typical seizure is followed by a short refractory period and that ST increases in the long run. We hypothesize ST to be lowered immediately after the refractory period, particularly after inadequate or abortive seizures where risk for prolonged seizures is generally higher. Ketamine anesthesia does not possess pronounced anticonvulsive properties like propofol, etomidate, thiopental, or methohexital. It is therefore ideal to test such a hypothesis. We report the case of a geriatric patient with a major depressive episode, who received 5 consecutive electroconvulsive therapies with S-ketamine, all with identical right unilateral high-energy stimulation and restimulation. Whereas all primary stimulations were inadequate, all restimulations showed significantly improved seizure parameters such as midictal amplitude, maximal postictal heart rate, and average seizure energy index. In this patient, the refractory period turned out to be longer than 1 minute, and ST was lower in all 5 instances of restimulation. This ST decrease could be clinically useful in one-session restimulations.
Electroconvulsive therapy (ECT) is a highly effective treatment for severe depressive disorder. Efficacy and cognitive outcomes have been shown to depend on variations in electrode placement and other stimulus parameters, presumably because of differences in the pattern of neuronal activation. This latter effect, however, is poorly understood.
In this study, we present an anatomically accurate human head computational model to stimulate neuronal excitation during ECT, to better understand the effects of varying electrode placement and stimulus parameters.
Electric field and current density throughout the head, as well as direct neural activation within the brain, were computed using the finite element method. Regions representing passive volume conductors (skin, skull, cerebrospinal fluid) were extracellularly coupled to an excitable neural continuum region representing the brain. The skull was modeled with anistropic electrical conductivity.
Simulation results indicated that direct activation of the brain occurred immediately beneath the electrodes on the scalp, consistent with existing imaging studies. In addition, we found that the brainstem was also activated using a right unilateral electrode configuration. Simulation also demonstrated that a reduction in stimulus amplitude or pulse width led to a reduction in the spatial extent of brain activation.
The novel model described in this study was able to simulate direct excitation of the brain during ECT, was useful in characterizing differences in neuronal activation as electrode placement, pulse width, and amplitude were altered, and is proposed as a tool for further exploring the effects of variations in ECT stimulation approaches. Results from the simulations assist in understanding recently described clinical phenomena, in particular, the reduction in cognitive side effects with ultrabrief pulse width stimulation, and greater effects of the ECT stimulus on cardiovascular function with unilateral electrode placement.
Temporary asystole can be detected at various time points during electroconvulsive treatment. We carefully monitored and documented its incidence during stimulation to evaluate currently known and assumed predictors.
All treatments over a 20-month period in 2 separate institutions were recorded prospectively. Data from 119 patients comprising 720 treatments were suitable for multiple regression analysis.
Electrode placement was the most influential determinant. Treatment series using right unilateral placement (64 patients and 291 traces) produced a mean (SD) asystole duration of 5.64 (2.88) seconds (range, 1.21-11.20 seconds), compared to a duration of 0.80 (0.21) seconds (range, 0.47-1.71 seconds) in bifrontal series (55 patients, 429 traces). Multiple regression analysis showed no independent effect of body weight, age, β-blocker medication, or preexisting heart block. Stimulus dose and succinylcholine dose had no influence in univariate analyses. Cardiac action in bifrontal treatment series was highly predictable using baseline values. During unilateral stimulation, between-subject differences accounted for 79% of the observed variation.
The heart rate during stimulation depends mainly on electrode positioning. A yet unidentified, probably constitutional factor is responsible for the broad range of asystole duration brought about by right unilateral electrode placement. Any assessment using interindividual analysis will therefore be biased as long as that factor remains unknown.
Electroconvulsive therapy (ECT) is the most effective treatment for severe depression, and different forms are increasingly used in clinical practice. This study investigated the acute cardiac effects of different forms of ECT: bitemporal and bifrontal (1.5 times seizure threshold), and right unilateral (RUL) (five times seizure threshold). For RUL ECT, the effect of stimulus pulsewidth (1.0 or 0.3 ms) was also examined. Electrocardiograms recorded just prior to and during the ECT stimulus in 476 ECT treatments in 114 patients were examined. The degree of bradycardia (any slowing of heart rate) and incidence of asystole (absence of heart beats for ≥5 s) during the ECT stimulus were measured from these traces. Regression analyses estimated the contribution of patient and ECT treatment factors to the risk of bradycardia and asystole. Bifrontal ECT was associated with less severe bradycardia than bitemporal or RUL ECT (p<0.001). Modelling showed, for a mean pre-ECT heart rate of 85 beats per minute (bpm), expected heart rates during the stimulus were 78 bpm (bifrontal), 46 bpm (bitemporal) and 35 bpm (RUL). Bifrontal ECT was also associated with a lower incidence of asystole than RUL ECT (corrected odds ratio 1:207) and bitemporal ECT (corrected odds ratio 1:24). Ultrabrief pulsewidth stimulation resulted in lesser bradycardia and asystole than standard pulsewidth stimulation for RUL ECT. Modelling showed, for a mean pre-ECT heart rate of 86 bpm, expected heart rates were 43 bpm (ultrabrief RUL) and 26 bpm (RUL). Bradycardia and asystole were relatively common side-effects during the ECT stimulus. Bifrontal ECT was associated with the lowest risk of bradycardia and asystole during ECT and should be considered for patients at risk of arrhythmias and prolonged asystole during ECT.
A hypertensive patient with a history of diabetes and ischemic heart disease was given propranolol before ECT and experienced cardiac arrest after subconvulsive electrical stimulation. The authors suggest exercising caution when combining beta-adrenergic blockade and ECT.
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.
Two instances of ECT postictal asystole in healthy adult males are reported. Features in common are identified.
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.
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.