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Introduction to dementia
Published in Joanne Brooke, Dementia in Prison, 2020
Sleep disturbance is another common symptom of DLB, which includes violent movements as the person with DLB tries to act out nightmares, which is diagnosed as rapid eye movement sleep behaviour disorder (Chan et al., 2018). People with DLB will have movement difficulties when the condition is diagnosed. These symptoms are similar to those of Parkinson’s disease and include slow and stiff (rigid) movement with a blank facial expression, and difficulty with their balance as their limbs may sometimes tremble (Gomperts, 2016). As the disease progresses, symptoms become similar to those of Alzheimer’s disease. The life expectancy of a person with DLB varies considerably; on average, it is estimated to be from six to 12 years after the first symptoms, similar to a person with Alzheimer’s disease (Gill et al., 2011).
Specific causes of automatism
Published in John Rumbold, Automatism as a Defence in Criminal Law, 2018
Rapid eye movement sleep behaviour disorder (RBD) was first described as a distinct clinical entity in 1986 (Schenck et al., 1986). It consists of REM sleep without atonia (RSWA) with abnormal dreams which are then acted out. This discovery had been predicted by a condition induced in cats by surgical lesions of the brainstem near to the locus coeruleus. It usually occurs in males over 50 years of age, and often precedes the diagnosis of a neurodegenerative disorder (e.g. Parkinson’s disease, dementia with Lewy bodies or multiple system atrophy) by several years. It can be induced by drugs such as propranolol, tricyclic antidepressants, selective serotonin re-uptake inhibitors, venlafaxine and caffeine. RBD can also be induced by stress, and there are reports of an association with post-traumatic stress disorder (Husain, Miller and Carwile, 2001). The discontinuation of REM suppressant agents such as alcohol, amphetamines, cocaine and imipramine can induce RBD, possibly via a rebound increase in REM sleep. Narcolepsy is often associated with RBD, where the prerequisite RWSA is present in 50 per cent according to one study (Dauvilliers et al., 2007). It is also common in narcolepsy to go straight into REM sleep, which can also happen after extreme REM deprivation. One estimate of the incidence of RBD from Ohayon’s study of sleep violence is 0.5 per cent (Ohayon, Caulet and Priest, 1997). Despite the high frequency of harmful behaviour, the average diagnostic delay in one study was 8.7 years (White et al., 2012).
The Psychiatric Interview
Published in Mohamed Ahmed Abd El-Hay, Essentials of Psychiatric Assessment, 2018
The use of electroencephalography in the differentiation of psychiatric disorders is fairly limited. However, an electroencephalogram can be very useful when a patient has altered mental status, such as delirium or encephalopathy. It can be useful for distinguishing between possible diagnoses, e.g.: It can diagnose complex partial status epilepticus, in cases of altered consciousness and abnormal behavior. However, normal EEG does not exclude seizure disorder from the differential diagnosis, because 20 percent of patients with epilepsy will have normal EEGs, and 2 percent of patients without epilepsy will have spike and wave formation.The EEG is also useful for distinguishing some specific etiologies of encephalopathy; it might show the di- and triphasic waves characteristic of renal failure, hepatic failure, or anoxia.In comatose patients, the EEG can be very valuable for identifying the level of nervous system impairment; it can show an alpha coma pattern or a theta coma pattern characteristic of brainstem lesions producing coma or it may show a delta coma pattern characteristic of bihemispheric disease. In catatonic patients, the EEG has a normal awake-look.The EEG may detect sleep abnormalities consistent with sleep apnea, rapid eye movement sleep behavior disorder, or narcolepsy.
Temporal Associations between Sleep and Daytime Functioning in Parkinson’s Disease: A Smartphone-Based Ecological Momentary Assessment
Published in Behavioral Sleep Medicine, 2020
Jade Q. Wu, Alice Cronin-Golomb
The first possibility calls for future studies that either exclude sleep disorders (e.g., rapid eye movement sleep behavior disorder [RBD]), or has sufficiently large subgroups to compare the effect of sleep disorders on temporal relationships between basic sleep variables and daytime function. The second and third possibilities, if valid, suggest that modifiable psychological targets may exist for improving daytime function. For example, misattribution of daytime symptoms to sleep problems may directly increase anxiety or cause misperception of sleep quality (e.g., “if I feel poorly now, it must be because I didn’t sleep well last night”). In turn, high anxiety may lead to hypervigilance of nighttime awakenings, which are then perceived as poor sleep. Hence, this bidirectional association may be driven by dysfunctional beliefs about sleep and misperception of sleep, which are hallmark mechanisms underlying psychophysiological insomnia (Hiller, Johnston, Dohnt, Lovato, & Gradisar, 2015). Fortunately, these mechanisms respond well to cognitive and behavioral therapy for insomnia (CBT-I) (Eidelman et al., 2016). One study has reported that this brief, nonpharmacological intervention is efficacious for treating insomnia in PD, but CBT-I was combined with light therapy in this trial (Romenets et al., 2013). Future trials are needed to assess CBT-I’s independent effectiveness, and to assess related improvements in mood and cognitive function.
Clinical characteristics and quality of life in Chinese patients with Parkinson’s disease beyond 20 years
Published in Neurological Research, 2018
Ruwei Ou, Yanbing Hou, Wei Song, Qianqian Wei, Yongping Chen, Bei Cao, Xiaoqin Yuan, Huifang Shang
At baseline, we collected clinical data regarding age, sex, age at onset, disease duration, diagnosis delay, personal history, chronic disease history, treatment regimen and motor complications through a standardized personal interview. The total levodopa equivalent daily dose (LEDD) (mg/day) was calculated according to a previous systematic review [11]. Rapid eye movement sleep behavior disorder (RBD) was diagnosed according to the international classification of sleep disorders (ICSD). Unified PD Rating Scale (UPDRS) part III and H&Y stage were utilized to evaluate the severity of motor symptoms [2,12]. The annual decline rate for the UPDRS III score was calculated as the mean point loss per year from symptom onset to the time of interview. For the CPD patients, survival time (years) was measured as the interval from the onset of motor symptoms to death. The severity of non-motor symptoms (NMSs) was assessed with the Non-Motor Symptom Scale (NMSS) [13], which includes 9 domains and 30 items [14]. Cognitive function was evaluated with the mini-mental state examination (MMSE). The QoL of PD patients was evaluated with the Chinese version of the PD Questionnaire 39 (PDQ-39) [15].
Changing the treatment paradigm for Parkinson’s disease psychosis with pimavanserin
Published in Expert Review of Clinical Pharmacology, 2019
Kelly E. Lyons, Rajesh Pahwa, Neal Hermanowicz, Thomas Davis, Fernando Pagan, Stuart Isaacson
Historically, PDP has been considered primarily an adverse effect of dopaminergic and other PD therapies (i.e. drug-induced psychosis) [10,17]. However, the consensus diagnostic criteria describe dopaminergic therapy as neither necessary nor sufficient for the emergence of PDP [10]. Indeed, some studies found that PDP symptoms occurred independently of medication factors (dose, duration) [12,24,25] and were not triggered by high-dose levodopa infusion challenge [26]. Other studies, however, have reported an association of antiparkinsonian drug treatment with PDP symptoms, although not necessarily of a causal nature [14,17,27]. The currently available data suggest that PDP is most likely a consequence of PD neurodegeneration coupled with drug treatment, comorbidities, and other extrinsic factors [17]; indeed, PDP rarely occurs in the absence of drug treatment. Other PDP risk factors and correlates reported in the literature include increased age, older age at PD onset, duration of PD and treatment, PD disease severity, cognitive dysfunction and dementia, depression, daytime somnolence, sleep disorders, including rapid eye movement sleep behavior disorder, and visual disorders [9,11,14,15,18,24,25,28,29]. Studies that have assessed pathologic risk factors for early PDP have identified reduced cerebrospinal fluid amyloid Aβ1-42 [28], gray matter loss in occipitotemporal regions, and hypometabolism in parietal and temporal areas [30] as potential biomarkers. Increased density of serotonergic 5-HT2A receptors in the inferolateral temporal cortex has also been identified [31–33] in post-mortem studies of people with PDP compared with PD patients without psychosis and compared with normal controls.