BackgroundParkinson disease (PD) is associated with a high prevalence of insomnia, affecting up to 88% of patients. Pharmacotherapy studies in the literature addressing insomnia in PD reveal disappointing and inconsistent results. Cognitive behavioral therapy (CBT) is a novel treatment option with durable effects shown in primary insomnia. However, the lack of accessibility and expense can be limiting. For these reasons, computerized CBT for insomnia (CCBT-I) has been developed. The CCBT-I program is a 6-week web-based course consisting of daily “lessons” providing learnable skills and appropriate recommendations to help patients improve their sleep habits and patterns.MethodsWe conducted a single-center, pilot, randomized controlled trial comparing CCBT-I versus standardized sleep hygiene instructions to treat insomnia in PD. Twenty-eight subjects with PD experiencing insomnia, with a score > 11 on the Insomnia Severity Index (ISI) were recruited. Based on a 6-point improvement in ISI in treatment group when compared to controls and an alpha = 0.05 and beta of 0.1 (power = 90%) a sample size of 11 patients (on active treatment) were required to detect this treatment effect using a dependent sample t-test.ResultsIn total, 8/14 (57%) subjects randomized to CCBT-I versus 13/14 (93%) subjects randomized to standard education completed the study. Among completers, the improvement in ISI scores was greater with CCBT-I as compared to standard education (−7.9 vs −3.5; p = 0.03). However, in an intention-to-treat analysis, where all enrolled subjects were included, the change in ISI between groups was not significant (−.4.5 vs −3.3; p = 0.48), likely due to the high dropout rate in the CCBT-I group (43%).ConclusionThis pilot study suggests that CCBT-I can be an effective treatment option for PD patients with insomnia when the course is thoroughly completed. High drop-out rate in our study shows that although effective, it may not be a generalizable option; however, larger studies are needed for further evaluation.
Posterior spinal artery (PSA) aneurysms are a rare cause of subarachnoid hemorrhage (SAH). The commonly abused street drug 3,4-methylenedioxymethamphetamine (MDMA) or ‘Ecstasy’ has been linked to both systemic and neurological complications. A teenager presented with neck stiffness, headaches and nausea after ingesting ‘Ecstasy’. A brain CT was negative for SAH but a CT angiogram suggested cerebral vasculitis. A lumbar puncture showed SAH but a cerebral angiogram was negative. After a spinal MR angiogram identified abnormalities on the dorsal surface of the cervical spinal cord, a spinal angiogram demonstrated a left PSA 2 mm fusiform aneurysm. The patient underwent surgery and the aneurysmal portion of the PSA was excised without postoperative neurological sequelae. ‘Ecstasy’ can lead to neurovascular inflammation, intracranial hemorrhage, SAH and potentially even de novo aneurysm formation and subsequent rupture. PSA aneurysms may be treated by endovascular proximal vessel occlusion or open surgical excision.
Posterior spinal artery (PSA) aneurysms are a rare cause of subarachnoid hemorrhage (SAH). The commonly abused street drug 3,4-methylenedioxymethamphetamine (MDMA) or 'Ecstasy' has been linked to both systemic and neurological complications. A teenager presented with neck stiffness, headaches and nausea after ingesting 'Ecstasy'. A brain CT was negative for SAH but a CT angiogram suggested cerebral vasculitis. A lumbar puncture showed SAH but a cerebral angiogram was negative. After a spinal MR angiogram identified abnormalities on the dorsal surface of the cervical spinal cord, a spinal angiogram demonstrated a left PSA 2 mm fusiform aneurysm. The patient underwent surgery and the aneurysmal portion of the PSA was excised without postoperative neurological sequelae. 'Ecstasy' can lead to neurovascular inflammation, intracranial hemorrhage, SAH and potentially even de novo aneurysm formation and subsequent rupture. PSA aneurysms may be treated by endovascular proximal vessel occlusion or open surgical excision.
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