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What Is the Evidence for Using Anti-Epileptic Drugs to Treat Agitation and Irritability in Huntington's Disease?
- Kok Keong Leong, Mark Paramlall
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- Journal:
- BJPsych Open / Volume 8 / Issue S1 / June 2022
- Published online by Cambridge University Press:
- 20 June 2022, p. S182
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Aims
Background: Huntington's disease (HD), due to the pathological expansion of CAG trinucleotide repeats within the Huntington's gene on chromosome 4p (1), is an autosomal dominant progressive neurodegenerative disease with motor, cognitive and neuropsychiatric symptoms that includes irritability and agitation in an estimated 38–73% of HD patients (2) which is characterized by impatience and a tendency to become angry in response to minimal provocation. Expert consensus recommends implementation of environmental and behavioural strategies then commencing treatment with SSRI's, Neuroleptics or Anti-Epileptic Drugs (AED) (3). No previous papers, to our knowledge, have examined the newest antiepileptic agents or have identified the most efficacious antiepileptics for this use. Aim: We present a review of the literature describing antiepileptic treatments for agitation and irritability in HD focusing on identification of the most efficacious antiepileptics and the role of newer antiepileptic agents for this use.
MethodsA search in the main database sources (EMBASE, MEDLINE, Allied and Complementary medicine) was performed in order to obtain a comprehensive evaluation of available antiepileptic psychopharmacological treatments in HD for agitation and irritability.
ResultsAntiepileptic (AED) agents described in consensus statements and case studies have included sodium valproate, carbamazepine and lamotrigine, which work by inhibition of voltage gated Na and Ca channels, and are often combined with antipsychotic agents for improvement of pathological mood swings and irritability. However, none of the papers identified were Level III or better.
ConclusionNo specific mood stabilizing antiepileptic psychopharmacological treatment of the Psychiatric symptoms of irritability and agitation in HD was identified. Overall, the use of AED have weak evidence base with no quantifiable outcome measures, such as such as the Disruptive or Aggressive Behavior behavioural subscale of the Unified Huntington's Disease Rating Scale or the Neuropsychiatric Inventory, indicating improvement of symptoms identified. Surveys and expert opinions were based on their personal knowledge of the HD populations and the selection of the experts surveyed was not systematic which could influence the practice pattern results. The review indicates a pressing need for treatment studies to determine which psychopharmacological and behavioral treatments are most efficacious.
How does self-report of anxiety symptoms compare with observer assessments after acquired brain injury?
- Alex Seelochan, Mark Paramlall, Himanshu Tyagi, Rohan Kandasamy, Ida Bakar, Cameron Holloway, Samantha Harding, Anna Gadhvi
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- Journal:
- BJPsych Open / Volume 7 / Issue S1 / June 2021
- Published online by Cambridge University Press:
- 18 June 2021, p. S288
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Comorbid anxiety and mood disorders occur in 30% and 60% of individuals post-ABI (acquired brain injury), respectively (Juengst et al, 2014). The presence of psychiatric symptoms correlate to poorer outcomes in post-stroke rehabilitation, worsened quality of life (QoL), and deficits in memory, attention, and processing speed that persists years following the index event. Despite this, it is unclear whether to what degree anxiety impacts cognition. Furthermore, the literature on this topic is inconsistent when comparing subjective and clinician measurements. This study seeks to ameliorate this gap in literature by analyzing how clinicians’ measures of anxiety and cognitive performance correlate with subjective assessments of patient's own anxiety symptoms.
MethodIndividuals with an ABI who were seen in a clinical neuropsychiatry outpatient clinic between 2019 and 2020 completed a GAD-7 (Generalized Anxiety Disorder-7) questionnaire (patient's self-report of the severity of anxiety symptoms) and an observer completed a Neuropsychiatric Inventory Questionnaire (NPIQ) including a subscale for anxiety (NPIQ-A). Participants also underwent a formal cognitive examination with the Montreal Cognitive Assessment (MoCA). A total of 24 ABI patients (depressed ABI and non-depressed ABI) were analyzed for variation, statistical agreement and correlation. Here, total anxiety scores (using GAD-7 scores), anxiety severity (correlating category based on total GAD-7 score) were compared against the objective measures for anxiety (NPI-QA) and cognition (MoCA). In order to standardize MoCA scores, z scores were used in the statistical analysis.
ResultThe patient's subjective raw scores of anxiety were statistically significantly different from the corresponding scores from objective observers on Wilcoxon-Rank Sum tests (p < 0.01), however, there was a statistical correlation between GAD (categorized by severity level) and NPI-QA (p = 0.75). Spearman Rank Correlation did show positive, but, statistically insignificant correlation between dyads of these independent variables (including GAD7/NPIQ-A, GAD 7 categorised/NPIQ-A, GAD7/MoCA, GAD 7 categorised/MoCA).
ConclusionThese findings indicate (1) self-reported measures of anxiety (GAD7) in ABI were inconsistent with objective measures of anxiety in this cohort, (2) anxiety measures did not demonstrate significant correlation when compared to objective measures for cognitive function, and (3) ABI patients did not display good insight into the severity of their anxiety symptoms as measured by the GAD7. Further research should focus on utilizing other subjective measurement tools for anxiety and/or clinician evaluation tools with NPIQ-A.