Objective: To prospectively validate the Montreal Cognitive Assessment (MoCA) in a UK memory clinic. Method:We administered the MoCA and Mini-Mental State Examination (MMSE) to 32 subjects fulfilling diagnostic criteria for dementia, to 23 subjects fulfilling diagnostic criteria for mild cognitive impairment (MCI), and to 12 memory clinic comparison subjects, at baseline and then at 6-month follow-up. Clinical diagnoses for dementia and MCI were made according to ICD-10 and Petersen criteria. The sensitivity and specificity of both measures were assessed for detection of MCI and dementia.Results: With a cut-off score of 26, the MMSE had a sensitivity of 17% to detect subjects with MCI, whereas the MoCA detected 83%. The MMSE had a sensitivity of 25% to detect subjects with dementia, whereas the MoCA detected 94%. Specificity for the MMSE was 100%, and specificity for the MoCA was 50%. Of subjects with MCI, 35% developed dementia within 6 months, and all scored less than 26 points on the MoCA at baseline. Conclusions:The MoCA is a useful brief screening tool for the detection of mild dementia or MCI in subjects scoring over 25 points on the MMSE. In patients already diagnosed with MCI, the MoCA helps identify those at risk of developing dementia at 6-month follow-up. Clinical Implications· The MoCA is a useful screening tool for the detection of mild dementia and MCI. · The MoCA is a useful predictive screening tool for the development of dementia in subjects with MCI. · Compared with the MMSE, the MoCA has no advantage in detecting change in cognition over a 6-month period. Limitations· The study size was small, with a short follow-up period of 6 months. · The memory clinic comparision group had a high proportion of subjects with functional psychiatric illness. · The conclusions regarding validity are restricted to a memory clinic setting.

Alzheimer's disease (AD) is a significant public health concern. The incidence continues to rise, and it is set to be over one million in the UK by 2025. The processes involved in the pathogenesis of AD have been shown to overlap with those found in cognitive decline in patients with Obstructive Sleep Apnoea (OSA). Currently, the standard treatment for OSA is Continuous Positive Airway Pressure. Adherence to treatment can, however, be an issue, especially in patients with dementia. Also, not all patients respond adequately, necessitating the use of additional treatments. Based on the body of data, we here suggest that excessive and prolonged neuronal activity might contribute to genesis and acceleration of both AD and OSA in the absence of appropriately structured sleep. Further, we argue that external factors, including systemic inflammation and obesity, are likely to interfere with immunological processes of the brain, and further promote disease progression. If this hypothesis is proven in future studies, it could have far-reaching clinical translational implications, as well as implications for future treatment strategies in OSA.

The treatment approach to effective treatment of the patients with Non-REM parasomnias or POD offering first sleep hygiene advice, next treatment of concurrent sleep disorders and management of other priming factors like stress and anxiety, and lastly pharmacotherapy for Non-REM parasomnia is supported by our results. Non pharmacological interventions were effective in one third of our patients, and CBT/MBSR and melatonin appeared promising new treatments.

Obstructive sleep apnea (OSA) causes daytime fatigue and sleepiness, and has an established relationship with cardiovascular and metabolic disease. Recent years have seen the emergence of an evidence base linking OSA with an increased risk of degenerative neurological disease and associated cognitive impairment, an accelerated rate of decline in kidney function with an increased risk of clinically significant chronic kidney disease (CKD), and with a significantly higher rate of cancer incidence and death. This review evaluates the evidence base linking OSA with these seemingly unrelated co-morbidities, and explores potential mechanistic links underpinning their development in patients with OSA, including intermittent hypoxia (IH), sleep fragmentation, sympathetic excitation, and immune dysregulation.

BackgroundSodium oxybate is licensed in Europe for the treatment of narcolepsy with cataplexy in adults. The aim of this study was to assess the efficacy and safety of sodium oxybate in clinical practice in patients with narcolepsy and cataplexy refractory to other treatments.Materials and methodsThis was a retrospective single centre study including patients with severe narcolepsy with cataplexy refractory to other treatments, who were initiated on sodium oxybate between 2009 and 2015. Patients were allowed to be on other stimulants or/and anti-cataplectic agents. Epworth sleepiness scale (ESS) and weekly cataplexy events were recorded. Side effects (SEs) were recorded at every follow-up visit.Results90 patients were prescribed sodium oxybate, with a total of 3116 patient-months of drug exposure. ESS and weekly cataplexy events were significantly reduced by sodium oxybate for all patients (ΔESS = 4.3 ± 4.4 and Δcataplexy = 21.8 ± 18.5 events/week; p < 0.0001, respectively). The required maintenance dose could not be predicted based upon gender, body mass index, or clinical factors. 60% of patients were able to reduce or come off other medications. Half of the patients experienced at least one SE, and 26.6% had to stop treatment due to limiting SEs. Nausea, mood swings and enuresis were the most commonly reported SEs. SEs that led to drug discontinuation, particularly psychosis, were associated with increasing age and were observed early after the initiation of the drug.ConclusionsSodium oxybate provides a good clinical efficacy and acceptable safety profile in routine clinical practice for the treatment of patients suffering from narcolepsy with cataplexy. A quarter of patients experience SEs requiring withdrawal of the drug with older patients being more vulnerable to the more serious SEs.

In the largest series of catathrenia patients reported to date, we found that this rare disorder is characterized by a distinct breathing pattern and arises predominantly from REM sleep, with arousals almost uniformly preceding or coinciding with the onset of CPs.

Background Exploding head syndrome is a rarely reported benign sensory parasomnia that may nonetheless have significant impact on patients’ quality of life and their perceived well-being. To date, the mechanisms underlying attacks, characterised by a painless perception of abrupt, loud noises at transitional sleep-wake or wake-sleep states, are by and large unclear. Methods and results In order to address the current gap in the knowledge of potential underlying pathophysiology, a retrospective case-control study of polysomnographic recordings of patients presenting to a tertiary sleep disorders clinic with exploding head syndrome was conducted. Interictal (non-attack associated) electroencephalographic biomarkers were investigated by performing macrostructural and event-related dynamic spectral analyses of the whole-night EEG. In patients with exploding head syndrome, additional oscillatory activity was recorded during wakefulness and at sleep/wake periods. This activity differed in its frequency, topography and source from the alpha rhythm that it accompanied. Conclusion Based on these preliminary findings, we hypothesise that at times of sleep-wake transition in patients with exploding head syndrome, aberrant attentional processing may lead to amplification and modulation of external sensory stimuli.

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