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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The neuropathology of human sleep remains an ill-defined issue. The data concerning the main structures of human brain areas involved, or supposed to be implicated, in sleep organisation are reviewed. Five levels of organisation can be schematically recognized: (i) the ascending arousal system, (ii) the non REM and REM systems (iii) regulated by hypothalamic areas, (iv) and the biological clock, (v) modulated by a number of "allostatic" influences. These are briefly described, with emphasis on the location of structures involved in humans, and on the recently revised concepts. Current knowledge on the topography of lesions associated with the main sleep disorders in degenerative diseases is recalled, including REM sleep behavior disorders, restless legs syndrome and periodic leg movements, sleep apneas, insomnia, excessive daily sleepiness, secondary narcolepsy and disturbed sleep-wake rhythms. The lesions of sleep related structures observed in early and late stages of four degenerative diseases are then reviewed. Two synucleinopathies (Lewy lesions associated disorders, including Parkinson's disease and Dementia with Lewy bodies, and Multiple System Atrophy) and two tauopathies (Progressive Supranuclear Palsy and Alzheimer's disease) are dealt with. The distribution of lesions usually found in affected patients fit with that expected from the prevalence of different sleep disorders in these diseases. This confirms the current opinion that these disorders depend on the distribution of lesions rather than on their biochemical nature. Further studies might throw insight on the mechanism of normal and pathological sleep in humans, counterpart of the increasing knowledge provided by animal models. Specially designed prospective clinicopathological studies including peculiar attention to sleep are urgently needed.
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PMID:[The neuropathology of sleep in human neurodegenerative diseases]. 1876 Apr 29

To clarify the profile of depressive symptoms in major depressive episodes in patients with Alzheimer's disease (AD-MD), we compared AD-MD with major depressive disorder in non-demented elderly patients (MDD) matched for age, using the 17-item Hamilton Rating Scale for Depression (HAM-D(17)). In addition, to clarify which depressive symptoms of AD patients respond to treatment with the selective serotonin and noradrenaline reuptake inhibitor (SNRI) milnacipran, we compared the HAM-D(17) average score and the score of each HAM-D item, the mini-mental state examination (MMSE) score, and GAF score according to the DSM-IV evaluation of AD-MD patients at baseline and at the endpoint (12 weeks). Depressive mood, loss of interest in hobbies and social activities and anxiety (psychic) scored the highest in both AD-MD and MDD groups, while psychomotor retardation scored significantly higher in AD-MD, and insomnia and anxiety (somatic) significantly did so in MDD. We also found that depressive mood, suicidal tendency, loss of interest, psychomotor retardation, anxiety (psychic), gastrointestinal symptoms, general somatic symptoms, and hypochondriasis remarkably improved in patients of AD-MD treated with milnacipran. Our results suggest that in general the profiles of depression in AD-MD and MDD are similar, despite some different clinical features between both conditions. Our study also suggests that milnacipran is promising to treat a broad range of depressive symptoms in AD-MD patients.
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PMID:Therapeutic effects of the selective serotonin noradrenaline reuptake inhibitor milnacipran on depressive symptoms in patients with Alzheimer's disease. 1916 99

Sleep disturbances are widespread among older adults. Degenerative neurologic disorders that cause dementia, such as Alzheimer's disease and Parkinson's disease, exacerbate age-related changes in sleep, as do many common comorbid medical and psychiatric conditions. Medications used to treat chronic illness and insomnia have many side effects that can further disrupt sleep and place patients at risk for injury. This article reviews the neurophysiology of sleep in normal aging and sleep changes associated with common dementia subtypes and comorbid conditions. Current pharmacologic and nonpharmacologic evidence-based treatment options are discussed, including the use of light therapy, increased physical and social activity, and multicomponent cognitive-behavioral interventions for improving sleep in institutionalized and community-dwelling adults with dementia.
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PMID:Current treatments for sleep disturbances in individuals with dementia. 1918 4

This article describes a sleep education program (SEP) designed to teach owner/operators and direct-care staff working in adult family homes (AFHs) how to improve the sleep and nighttime behavior of older residents with dementia. There have been no sleep intervention studies conducted in AFHs, and strategies that are known to improve sleep in community-dwelling older adults or nursing home residents may not be feasible or effective in AFHs because of their unique care environment. The SEP was developed on the basis of experiences treating sleep disturbances in community-dwelling older adults with dementia (the Nighttime Insomnia Treatment and Education in Alzheimer's Disease study). In this article, we address both the clinical and empirical challenges faced by researchers recruiting and intervening in AFHs, raise issues pertinent to assessment of residents and staff, and discuss implications for evaluating the impact of behavioral treatments for sleep-wake disturbances in AFH residents.
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PMID:Managing sleep disturbances in adult family homes: recruitment and implementation of a behavioral treatment program. 1921 11

Excessive daytime somnolence (EDS) is associated with age-related changes, environment, circadian rhythm or sleep pattern disorder, insomnia, medications, lifestyle factors, depression, pain, and illness. The notion of "sleep architecture" connotes a structure that describes the sleep cycle (i.e., stages) and wakefulness during a single sleep period-that is, rapid eye movement (REM) and non-REM sleep. Circadian rhythms perform a variety of functions including regulation of the quality and distribution of the stages of sleep. Insomnia includes delayed sleep onset as well as premature wakening; sleep is nonrestorative. Comorbidities associated with insomnia are Alzheimer's disease and other dementias, delirium, depression, congestive heart failure, chronic obstructive pulmonary disease, gastroesophageal reflux disease, pain, degenerative diseases of the neurological system, and sleep apnea. Continuous inadequate sleep affects cognitive function, physical performance, overall well-being, and quality of life. There is a greater risk of falls from insomnia than is the use of hypnotics to manage it. Sleep disruption among older adults is underrecognized and undertreated. Assessment using valid tools can be performed rapidly. There are a variety of treatment options, including sleep hygiene and pharmacological and alternative modalities.
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PMID:Sleepiness or excessive daytime somnolence. 1921 14

Changing sleep architecture in the elderly may increase their vulnerability to comorbid insomnia. Common comorbid conditions include chronic pain, depression, nocturia, and neurologic conditions such as Parkinson's and Alzheimer's disease. Diagnosing and treating comorbid insomnia in an older population poses special challenges for clinicians given the variety of coexisting medical and psychological conditions, polypharmacy, and the potential adverse effects of the most commonly used medications for insomnia in this population. Thus, the use of nonpharmacologic treatments, such as cognitive behavior therapy and relaxation techniques, is recommended before any medical approaches.
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PMID:Late-life comorbid insomnia: diagnosis and treatment. 1929 2

Increased attention to the prevalence of excessive sleepiness has led to a clear need to treat this symptom, thus reinforcing the need for a greater understanding of the neurobiology of sleep and wakefulness. Although the physiological mechanisms of sleep and wakefulness are highly interrelated, recent research reveals that there are distinct differences in the active brain processing and the specific neurochemical systems involved in the two states. In this review, we will examine the specific neuronal pathways, transmitters, and receptors composing the ascending arousal system that flow from the brainstem through the thalamus, hypothalamus, and basal forebrain to the cerebral cortex. We will also discuss the mutually inhibitory interaction between the core neuronal components of this arousal system and the sleep-active neurons in the ventrolateral preoptic nucleus, which serves as a brainstem-switch, regulating the stability of the sleep-wake states. In addition, we will review the role of homeostatic and circadian processes in the sleep-wake cycle, including the influence of the suprachiasmatic nucleus on coordination of sleep-wake systems. Finally, we will summarize how the above processes are reflected in disorders of sleep and wakefulness, including insomnia, narcolepsy, disorders associated with fragmented sleep, circadian rhythm sleep disorders, and primary neurological disorders such as Parkinson's and Alzheimer's diseases.
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PMID:Neurophysiology of sleep and wakefulness: basic science and clinical implications. 1958 57

This study investigated the relationship between self-reported sleep factors (sleep duration, insomnia, use of sleeping medicine, probable sleep apnoea and feelings of fatigue and tiredness) with cognitive functioning in 5177 people aged 30 years or older from a cross-sectional representative sample of the adult population in Finland (The Finnish Health 2000 Survey). Previous studies have indicated a U-shaped association between increased health risks and sleep duration; we hypothesized a U-shaped association between sleep duration and cognitive functioning. Objective cognitive functioning was assessed with tasks derived from the Consortium to Establish a Registry for Alzheimer's Disease test battery (verbal fluency, encoding and retaining verbal material). Subjective cognitive functioning and sleep-related factors were assessed with questionnaires. Health status was assessed during a health interview. Depressive and alcohol use disorders were assessed with the Composite International Diagnostic Interview. Medication was recorded during the health examination. Short and long sleep duration, tiredness and fatigue were found to be associated with both objectively assessed and self-reported decreased cognitive functioning. The association was stronger between sleep factors and subjective cognitive function than with objective cognitive tests. These data suggest that self-reported habitual short and long sleep duration reflect both realization of homeostatic sleep need and symptom formation in the context of the individual's health status.
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PMID:Self-reported sleep duration and cognitive functioning in the general population. 1994 91

In this study we report a case of valproate-induced delirium in a patient affected with Alzheimer's disease (AD). A 75-year-old woman with AD presented moderate cognitive impairment associated to behavioral disorders, characterized by aggression, agitation, severe insomnia. She was treated with galantamine, promazine, acetylsalicylic acid and pantoprazole. Since behavioral disorders worsened more and more, home neurological consultation was asked. The neurologist prescribed a mood stabilizer, sodium valproate 500 mg daily for the first week and then, twice a day and stopped promazine. After an apparent initial benefit, about 16 days later, patient suddenly developed hyperactive delirium. It was characterized by worsening of insomnia and agitation, severe confusion, delusions, visual hallucinations alternated to sedation. She became progressively unable to walk and completely dependent in daily living activities. An urgent geriatric consultation was performed at patient's home; physical examination showed mild dehydration, normal blood pressure. Oxygen saturation and electrocardiogram were normal. Sodium valproate was immediately stopped and rehydration was performed. The patient was admitted to a Geriatric Unit, where organic and metabolic damages were excluded. During the hospital stay the patient was agitated, aggressive, confused; intramuscular haloperidol 5mg and saline intravenous infusion 1500 cc daily were performed, they were partly successful. Three days after she was discharged and continued treatment with oral haloperidol 5mg daily. One week later the patient recovered and she is at present healthy. This is a case report of valproate-induced delirium. The Naranjo scale scored 7, classifying this drug-related event as probable. The present case report suggests the need for minimizing the use of psychoactive drugs in elderly demented patients, whether possible; age-related changes in pharmacokinetics and pharmacodynamics suggest the opportunity of a careful evaluation and a slow titration of treatments in these patients.
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PMID:Valproate-induced delirium in a demented patient. 1983 23

Following a 48-week, double-blind, randomized, placebo-controlled trial of donepezil in 821 patients with amnestic mild cognitive impairment (aMCI), safety and tolerability of donepezil (10 mg) were further evaluated in a 28-week extension study. Of 499 participants who completed the double-blind phase, 145 enrolled in the open-label study. Adverse events (AEs) were recorded throughout. Overall, 57.4% of participants in the donepezil/donepezil group and 62.3% in the placebo/donepezil group experienced an AE, with the most frequent treatment-emergent AEs being diarrhea, muscle spasms, insomnia, and nausea. Most were mild to moderate in severity and were more common in the first several weeks after treatment initiation. More participants in the placebo/donepezil group (22.1%) discontinued donepezil due to an AE compared with the donepezil/donepezil group (10.3%). These findings support the safety of donepezil in patients with aMCI. When compared with other studies, however, the data suggest that patients with Alzheimer's tolerate donepezil better than patients with MCI.
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PMID:Safety and tolerability of donepezil in mild cognitive impairment: open-label extension study. 1994 65


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