Annotated Abstracts of Journal Articles
2015, 1st Quarter
Annotations by Nicholas Kontos, MD
ANNOTATION (Nicholas Kontos)
The Finding: Assuming certain ideas about “appropriate” or “acceptable” risks of seizure recurrence while driving, an 8-month seizure-free period was determined to be necessary following an unprovoked first seizure. Five seizure-free months may be sufficient following a provoked first-seizure.
Strengths and Weaknesses: Drawing on a large regional (West Australian) database, this study was able to prospectively follow 1386 patients following their first seizure. Seizure recurrence risk while driving was looked at in terms of actual events, expected events based on expected time spent driving per day (assumed 1hr, but did you know that the average Australian drives 90min daily?), and stratified based on provoked (including with CNS lesion vs systemic cause) vs unprovoked (including idiopathic vs with existing CNS vulnerability factor) seizure etiology. The study was necessarily based on self-reports of seizure recurrence, not to mention on honesty about going against medical advice on driving restrictions. For what it’s worth, the results were consistent with prior work in this area.
Relevance: There is a high incidence of psychopathology in epilepsy, and of seizure-inducing events (TBI, intoxication, withdrawal) in the psychiatrically ill. Psychiatrists may not expect to advise patients on driving restrictions, but are not uncommonly faced with this anxiety-provoking issue. This study helps put matters into statistical perspective, and offers some preliminary advice to providers who do not live in jurisdictions with strict rules.
Objectives: The risk of recurrence following a first-ever seizure is 40-50%, warranting driving restriction during the early period of highest risk. This restriction must be balanced against the occupational, educational and social limitations that result from patients being ineligible to drive. The recommended duration of non-driving after a first seizure varies widely between jurisdictions, influenced by various factors including the community perception of an acceptable relative level of risk for an accident (the accident risk ratio; ARR). Driving restrictions may be based on individualised risk assessments or across-the-board guidelines, but these approaches both require accurate data on the risk of seizure recurrence.
Methods: 1386 patients with first-ever seizure were prospectively analysed. Seizure recurrence was evaluated using survival analysis. The duration of non-driving required for a range of risks of seizure recurrence and ARRs was calculated. Additionally, the actual occurrence of seizures while driving was prospectively determined during follow-up.
Results: For a risk of seizure recurrence to fall to 2.5% per month, corresponding to a monthly risk of a seizure while driving of 1.04 per thousand and an ARR of 2.6, non-driving periods of 8 months are required for unprovoked first-ever seizure, and 5 months for provoked first-ever seizure. Of patients with a seizure recurrence, 14 (2%) occurred while driving, with the monthly risk falling to less than 1/1000 after 6 months.
Conclusions: Our data provide a quantitative approach to decisions regarding a return to driving in patients with first-ever provoked or unprovoked seizure.
ANNOTATION (Nicholas Kontos)
The Finding: Deep brain stimulation of the subthalamic nucleus (and globus pallidus interna) can be associated with significant psychiatric side effects. It also involves dealing with the positive and negative neuropsychiatric consequences of antiparkinsonian medication reductions. Impulse control disturbances, affective syndromes (of both types), cognitive impairment, and psychological impact on the patient and social circle are all affected by deep brain stimulation, medication use/reduction/cessation, and Parkinson’s disease itself.
Strengths and Weaknesses: This excellent review is well-structured and judiciously referenced to provide information and guidance based on not just symptoms, but their context in terms of cause (disease, medication, stimulation) and type. It could have done with a figure or two and a table, but overall it is a nice entry point into this subject.
Relevance: Psychosomatic medicine specialists have long been involved in the management of patients with Parkinson’s disease. The efficacy, trajectory, and complications of subthalamic nucleus stimulation use make it a necessary new area to become familiar with.
Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is an established treatment for the motor symptoms of Parkinson’s disease (PD). Nonmotor features of PD, however, may not improve with STN DBS, and a specific constellation of neuropsychiatric symptoms may emerge in the postoperative period. Mania, impulsivity, depression, and apathy may curtail the potential gains from surgery. In this paper, the authors discuss surgical candidacy, postoperative management of neuropsychiatric issues, and clinical dilemmas for the psychiatrist at the DBS center. A paradigm that considers stimulation effects and dopamine replacement therapy to be key drivers of postoperative neuropsychiatric problems is presented.
ANNOTATION (Nicholas Kontos)
The phenomenologic similarities between delirium and dementia with Lewy bodies (DLB), most prominently including waxing and waning mental status (perhaps only also shared in an overlapping way by catatonic syndromes), provide challenges for differential diagnosis and opportunities for understanding certain types of neuropsychiatric impairment.
Strengths and Weaknesses: This comprehensive review of phenomenologic, chemical, and structural findings in the delirium-DLB overlap not only addresses the question in the paper’s title, but also provides a review and update on both of these entities. In the end, not much in the way of a meaningful conclusion is reached, but this paper calls attention to a difficult task of differential diagnosis that may not be at the tip of every consultant’s brain as often as it should.
Relevance: The delirium-DLB differential is consequential because pharmacologic treatment of the former is almost incompatible with the latter, and because autopsy studies have long told us that DLB is underdiagnosed clinically.
Dementia with Lewy bodies (DLB) is recognised as the second most common form of dementia in older people. Delirium is a condition of acute brain dysfunction for which a pre-existing diagnosis of dementia is a risk factor. Conversely delirium is associated with an increased risk of developing dementia. The reasons for this bidirectional relationship are not well understood. Our aim was to review possible similarities in the clinical presentation and pathophysiology between delirium and DLB, and explore possible links between these diagnoses. A systematic search using Medline, Embase and Psychinfo was performed. References were scanned for relevant articles, supplemented by articles identified from reference lists and those known to the authors. 94 articles were selected for inclusion in the review. Delirium and DLB share a number of clinical similarities, including global impairment of cognition, fluctuations in attention and perceptual abnormalities. Delirium is a frequent presenting feature of DLB. In terms of pathophysiological mechanisms, cholinergic dysfunction and genetics may provide a common link. Neuroimaging studies suggest a brain vulnerability in delirium which may also occur in dementia. The basal ganglia, which play a key role in DLB, have also been implicated in delirium. The role of Cerebrospinal fluid (CSF) and serum biomarkers for both diagnoses is an interesting area although some results are conflicting and further work in this area is needed. Delirium and DLB share a number of features and we hypothesise that delirium may, in some cases, represent early or ‘prodromal’ DLB. Further research is needed to test the novel hypothesis that delirium may be an early marker for future DLB, which would aid early diagnosis of DLB and identify those at high risk.