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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A clinically relevant sleep-wake disturbance is found in up to half the patients with dementia, and the sundowning agitation is a common cause of institutionalisation of demented geriatric patients. The circadian rhythm of demented patients is levelled off with increased daytime sleep and disrupted night sleep. Particularly in vascular dementia, Korsakow syndrome, Parkinson's disease, and depression the alteration of sleep architecture may be pronounced, whereas in Alzheimer's disease prominent hypersomnolence or insomnia is typically only found in later stages of the diseases. Greatly increased daytime sleepiness or striking insomnia at the very beginning of suspected dementia should thus prompt the search for other, possibly treatable causes of dementia. Neuropathological and neurophysiological studies support the hypothesis of a deteriorated hypothalamic suprachiasmatic nucleus (harbouring the biological clock) as a cause for the deranged circadian sleep-wake system in dementia. Management of sundowning behaviour includes restriction of daytime sleep, exposure to bright lights, and social interaction schedules during the day. The benzodiazepines and analogues usually not being sufficiently effectual, low doses of mild neuroleptics are often needed. Whether recent reports on efficacy of melatonin in elderly insomniacs also apply to demented patients is yet uncertain. The careful search and treatment of possible extracerebral physiologic factors causing reversible hypersomnia or insomnia is an important requisite. Polysomnographic studies are needed to recognise treatable sleep disturbance which could deteriorate or mimic dementia and sundowning. Particularly, a sleep-apnea-hypopnea syndrome must be searched for at the beginning of a suspected dementia, when successful treatment is still possible. Sleep studies should also identify periodic leg movements of sleep with restless legs and/or increased daytime sleepiness, and hyperkinetic parasomnias such as REM sleep behaviour disorder which may complicate or imitate sundowning.
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PMID:[Sleep disorders and dementia]. 938 Oct 26

The pedunculopontine (PPN) region of the upper brainstem is recognized as a critical modulator of activated behavioral states such as wakefulness and rapid eye movement (REM) sleep. The expression of REM sleep-related physiology (e.g. thalamocortical arousal, ponto-geniculate-occipital (PGO) waves, and atonia) depends upon a subpopulation of PPN neurons that release acetylcholine (ACh) to act upon muscarinic receptors (mAChRs). Serotonin's potent hyperpolarization of cholinergic PPN neurons is central to present working models of REM sleep control. A growing body of experimental evidence and clinical experience suggests that the responsiveness of the PPN region, and thereby modulation of REM sleep, involves closely adjacent glutamatergic neurons and alternate afferent neurotransmitters. Although many of these afferents are yet to be defined, dopamine-sensitive GABAergic pathways exiting the main output nuclei of the basal ganglia and adjacent forebrain nuclei appear to be the most conspicuous and the most likely to be clinically relevant. These GABAergic pathways are ideally sited to modulate the physiologic hallmarks of REM sleep differentially (e.g. atonia versus cortical activation), because each originates from a functionally unique forebrain circuit and terminates in a unique pattern upon brain stem neurons with unique membrane characteristics. Evidence is reviewed that changes in the quality, timing, and quantity of REM sleep that characterize narcolepsy, REM sleep behavior disorder, and neurodegenerative and affective disorders (depression and schizophrenia) reflect 1) changes in responsiveness of cells in the PPN region governed by these afferents; 2) increase or decrease in PPN cell number; or 3) mAChRs mediating increased responsiveness to ACh derived from the PPN. Auditory evoked potentials and acoustic startle responses provide means independent from recording sleep to assess pathophysiologies affecting the PPN and its connections and thereby complement investigations of their role in affecting daytime functions (e.g. arousal and attention).
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PMID:Contributions of the pedunculopontine region to normal and altered REM sleep. 970 83

Behavioral disturbances in Parkinson's disease (PD) are a common source of disability to both patients and their families, but there is a considerable controversy regarding their frequency and their neuropathological and neurochemical bases. Since they are so common, the disorders associated with PD should be well recognized, and proper management by neurologists is required. The most frequent behavioral disturbances encountered in patients with PD are depression, anxiety, cognitive impairment and dementia. Also frequent are sleep disorders such as sleep fragmentation, REM sleep behavior disorder, insomnia and altered dreaming. The most troublesome situations come from drug-induced psychiatric states, such as delusional states, hallucinations, paranoid ideation, delirium, and confusion. The treatment of these behaviors is reviewed here.
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PMID:Therapy of behavioral disorders in Parkinson's disease. 1034 4

The frequency of sleep complaints in patients with Parkinson's disease (PD) is estimated to be between 60-90% and a variety of either disease-related or secondary mechanisms and the dopaminergic treatment itself contributes to the development of different sleep disturbances. These comprise slight, fragmented sleep with increased number of arousals and awakenings, and PD-specific motor phenomena such as nocturnal immobility, rest tremor, eye-blinking, dyskinesias, and other phenomena such as periodic and nonperiodic limb movements in sleep, restless legs syndrome, fragmentary myoclonus, and respiratory dysfunction in sleep. Depression and hallucinations/psychosis further complicate the picture. The incidence of REM sleep behavior disorder (RBD) with nightmares and violent behavior is increased in PD and may occur as a preclinical disease-related symptom. A careful sleep history of patients and their partners, polysomnograms when necessary, motor and psychiatric assessments should precede individual treatment strategies, which include adjusting dopaminergic daytime treatment, benzodiazepines for RBD, reduction of anticholinergic drugs, and, if necessary, clozapine for nocturnal psychosis.
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PMID:Sleep dysfunction in Parkinson's disease. 1078 36

Dementia with Lewy bodies (DLB) is the second most frequent neuropathologically diagnosed degenerative dementing illness. The clinical characteristics are progressive dementia, parkinsonian syndrome, fluctuations of cognitive functions, alertness, and attention, visual hallucinations (usually detailed and well described), depression, REM sleep behavior disorder, adverse responses to standard neuroleptics doses, falls, syncopes, systematized delusions, and other modalities of hallucinations. Specificity of the clinical diagnostic criteria is high (95%), and sensitivity is considerably lower. Mean age at disease onset ranges between 60 and 68 years. The male gender prevails. Disease duration is 6 to 8 years. The differential diagnoses of DLB are dementia of the Alzheimer type, Parkinson's disease, subcortical arteriosclerotic encephalopathy, progressive supranuclear palsy, multiple system atrophy, and rarely Creutzfeldt-Jakob disease. The genetic background of the disease is unclear. Magnetic resonance imaging and single photon emission tomography can contribute to the diagnosis. Controlled pharmacological studies have so far not been published. The disease is treated with L-dopa, atypical neuroleptics, acetylcholine esterase inhibitors, antihypotensive agents, and peripheral anticholinergic and alpha receptor-blocking medications to improve neurogenic bladder dysfunction.
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PMID:[Dementia with Lewy bodies]. 1113 88

The present article is meant to suggest an approach to the guidelines for the therapy of sleep disturbances in Parkinson's Disease (PD) patients.The factors affecting the quality of life in PD patients are depression, sleep disturbances and dependence. A large review of the literature on sleep disturbances in PD patients, provided the basis for the following classification of the sleep-arousal disturbances in PD patients. We suggest a model based on 3 steps in the treatment of sleep disturbances in PD patients. This model allowing the patient, the spouse or the caregiver a quiet sleep at night, may postpone the retirement and the institutionalization of the PD patient. I. Correct diagnosis of sleep disorders based on detailed anamnesis of the patient and of the spouse or of the caregiver. One week recording on a symptom diary (log) by the patient or the caregiver. Correct diagnosis of sleep disorders co morbidities. Selection of the most appropriate sleep test among: polysomnography (PSG), multiple sleep latency test (MSLT), multiple wake latency test (MWLT), Epworth Sleepiness Scale, actigraphy or video-PSG. II. The nonspecific therapeutic approach consists in: a) Checking the sleep effect on motor performance, is it beneficial, worse or neutral. b) Psycho-physical assistance. c) Dopaminergic adjustment is necessary owing to the progression of the nigrostriatal degeneration and the increased sensitivity of the terminals, which alter the normal modulator mechanisms of the motor centers in PD patients. Among the many neurotransmitters of the nigro-striatal pathway one can distinguish two with a major influence on REM and NonREM sleep. REM sleep corresponds to an increased cholinergic receptor activity and a decreased dopaminergic activity. This is the reason why REM sleep deprivation by suppressing cholinergic receptor activity ameliorates PD motor symptoms. L-Dopa and its agonists by suppressing cholinergic receptors suppress REM sleep. The permanent adjustment according to the progression of the degenerative process of the disease will diminishe aggravation. The following types of sleep-arousal disturbances have to be considered in PD patients: - Sleep Disturbances, Light Fragmented Sleep (LFS), Abnormal Motor Activity During Sleep (AMADS), REM Behavior Disorders (RBD), Sleep Related Breathing Disorders (SRBD), Sleep Related Hallucinations (SRH), Sleep Related Psychotic Behavior (SRPB). - Arousal Disturbances, Sleep Attacks (SA), Excessive Daytime Sleepiness (EDS), Each syndrome has to receive a score according to its severity. III. The specific therapy consists in: LFS: Benzodiazepines & Nondiazepines. AMADS: Clonazepam, Opioid, Apomorphine infusion; RBD: Clonazepam and dopaminergic agonists; SRBD: CPAP, UPPP, nasal interventions, losing weight; SRH: Clozapine, Risperidone; SRPD: Nortriptyline, Clozapine, Olanzepine; SA-adjustment; EDS-arousing drugs. Each therapeutic approach must be tailored to the individual PD patient.
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PMID:Sleep disturbances in Parkinsonism. 1258 74

The syndrome of dementia with Lewy bodies (DLB) is characterised by the clinical triad of fluctuating cognitive impairment, recurrent visual hallucinations and spontaneous motor features of Parkinsonism. In an attempt to define DLB as a distinct clinical syndrome separate from Alzheimer's disease (AD) and Parkinson's disease (PD) with dementia, a consensus workshop in 1995 established a new set of diagnostic criteria. Dementia that precedes or accompanies the onset of spontaneous (i.e., not neuroleptic-induced) Parkinsonism is termed DLB. In addition, fluctuations in alertness, cognition and function and visual hallucinations are emphasised and included as core features of DLB. The degree to which an individual patient exhibits cognitive impairment, behavioural problems and Parkinsonian features is variable. Therefore, treatment must be individualised. Although there are no officially approved drugs for DLB, limited experience from clinical trials, as well as past experience with the treatment of AD and PD patients, provide some basis for making drug choices. The cholinergic deficit seen in DLB makes cholinesterase inhibitor drugs the mainstay of treatment for cognitive impairment. This class of drugs has also shown therapeutic benefit in reducing hallucinations and other neuropsychiatric symptoms of the disease. Because of their relatively greater therapeutic window, cholinesterase inhibitors are also used as first-line therapy for the treatment of psychosis in DLB. Patients with DLB are extremely sensitive to the extrapyramidal side effects of neuroleptic medications. Thus, only atypical antipsychotic agents such as quetiapine, should be considered as alternative treatment for psychosis. Anxiety and depression are best treated with selective serotonin re-uptake inhibitors, whereas REM sleep behaviour disorder may be treated with low dose clonazepam. Parkinsonism responds to dopaminergic agents; however, precipitation or aggravation of hallucinosis may occur. Levodopa is preferred over dopamine agonists due to its lower propensity to cause hallucinations and somnolence. As the diagnostic criteria for DLB become more refined and validated by postmortem studies, it is hoped that rigorous, well-designed trials will be performed, aimed at alleviating the primary target symptoms of dementia, psychosis and Parkinsonism.
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PMID:Pharmacotherapy of dementia with Lewy bodies. 1459 56

A 35-year-old woman with childhood-onset parasomnia, marked by arm waving with talking and shouting, developed marital discord solely because her parasomnia disrupted her husband's sleep. She became progressively depressed after her husband began to sleep in a separate bedroom, eventually becoming acutely suicidal. There had been no psychiatric history prior to her marriage. An evaluation with a sleep specialist-neurologist and polysomnographic monitoring confirmed the diagnosis of idiopathic REM sleep behavior disorder (RBD). Treatment with clonazepam, 1.0-1.5 mg at bedtime controlled her RBD and she again slept with her husband, which fully resolved their marital discord and her secondary depression.
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PMID:A case of marital discord and secondary depression with attempted suicide resulting from REM sleep behavior disorder in a 35-year-old woman. 1503 35

Parkinson's disease is a progressive disorder of the central nervous system. Degeneration of the dopaminergic neurons is the main cause of the disease. The basic symptoms of Parkinson's disease are bradykinesia, rigidity and resting tremor. Disturbances of the autonomous nervous system, depression, dementia and sleep disorders are common, too. People with Parkinson's disease suffer from insomnia, excessive daytime sleepiness, "sleep attacks", nightmares, REM sleep behaviour disorder, periodic limb movement in sleep, restless legs syndrome and sleep apnea syndrome. The main cause of sleep disorders in Parkinson's disease are age-connected changes in sleep architecture, disturbances of neurotransmission, movement disturbances in sleep, medications and concomitant diseases. The authors present the current state of knowledge on sleep disorders in Parkinson's disease, especially, the role of dopaminergic therapy, methods of diagnostics and treatment as well as the influence of sleep disturbances on patient's quality of life.
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PMID:[Sleep disturbances in Parkinson's disease]. 1627 62

Synucleinopathies, with and without dementia, encompass a wide range of diseases including Parkinson's disease, multiple system atrophy, rapid eye movement (REM) sleep behavior disorder, and dementia with Lewy bodies (DLB). DLB is a neurodegenerative disorder resulting in slowly progressive and unrelenting dementia until death. Prevalence studies suggest that it is the second most common dementing illness in the elderly. The neuropathologic findings of DLB show a wide anatomic range. Lewy bodies and Lewy-related pathology are found from the brain stem to the cortex and, in many cases, associated with concurrent Alzheimer's disease pathology. A recent international consortium on DLB has resulted in revised criteria for the clinical and pathological diagnosis of DLB incorporating new information about the core clinical features and improved methods for their assessment. The presentation of DLB is typically one of cortical and subcortical cognitive impairments, with worse visuospatial and executive dysfunction than Alzheimer's disease. There may be relative sparing of memory especially in the early stages. Core clinical features of DLB include fluctuating attention, recurrent visual hallucinations, and parkinsonism. Suggestive features include REM sleep behavior disorder, severe neuroleptic sensitivity, and low dopamine transporter uptake in the basal ganglia on functional neuroimaging. Additional supportive features that commonly occur in DLB, but with lower specificity, include repeated falls and syncope, transient, unexplained loss of consciousness, severe autonomic dysfunction, hallucinations in other modalities, systematized delusions, depression, relative preservation of medial temporal lobe structures on structural neuroimaging, reduced occipital activity on functional neuroimaging, prominent slow wave activity on electroencephalogram, and low uptake myocardial scintigraphy. Management of DLB includes pharmacological and nonpharmacological interventions for its cognitive, neuropsychiatric, motor, and sleep disturbances.
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PMID:Dementia with Lewy bodies. 1722 40


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