A polysomnographic and clinical report on sleep-related injury in 100 adult patients.

In 100 consecutive adults who came to a sleep disorders center complaining of repeated nocturnal injury, polysomnographic study identified five disorders: night terrors/sleepwalking (N = 54), REM sleep behavior disorder (N = 36), dissociative disorders (N = 7), nocturnal seizures (N = 2), and sleep apnea (N = 1). Ninety-five patients sustained ecchymoses, 30 had lacerations, and nine had fractures. DSM-III axis I disorders (past or current) were found in 48.1% of the group with night terrors/sleepwalking and in 30.6% of the group with REM sleep behavior disorder; these were mainly affective disorders. In these two groups, clonazepam controlled the symptoms of 51 of the 61 patients to whom it was given.

Delayed emergence of a parkinsonian disorder in 38% of 29 older men initially diagnosed with idiopathic rapid eye movement sleep behaviour disorder.

We report longitudinal data on a group of 29 male patients 50 years of age or older who were initially diagnosed as having idiopathic REM sleep behavior disorder (RBD) after extensive polysomnographic and neurologic evaluations. Thirty-eight percent (11/29) were eventually diagnosed as having a parkinsonian disorder (presumably Parkinson's disease) at a mean interval of 3.7 +/- 1.4 (SD) years after the diagnosis of RBD+, and at a mean interval of 12.7 +/- 7.3 years after the onset of RBD. To date, only 7% (2/29) of patients have developed any other neurologic disorder. At the time of RBD diagnosis, data from the RBD group with eventual Parkinson's disease (n = 11) and the current idiopathic RBD group (n = 16) were indistinguishable, with two exceptions: the RBD-Parkinson's disease group had a significantly elevated hourly index of periodic limb movements of non-REM sleep and an elevated REM sleep percentage. RBD was fully or substantially controlled with nightly clonazepam treatment in 89% (24/27) of patients in both groups. Thus, RBD can be the heralding manifestation of Parkinson's disease in a substantial subgroup of older male RBD patients. However, a number of presumed Parkinson's disease patients may eventually be diagnosed with multiple system atrophy (striatonigral degeneration subtype). Our findings indicate the importance of serial neurologic evaluations after RBD is diagnosed and implicate the pedunculopontine nucleus as a likely site of pathology in combined RBD-Parkinson's disease, based on experimental and theoretical considerations rather than on autopsy data.

Sleep-related eating disorders: polysomnographic correlates of a heterogeneous syndrome distinct from daytime eating disorders.

Over a 5-yr period, 19 adults presented to our sleep disorders center with histories of involuntary, nocturnal, sleep-related eating that usually occurred with other problematic nocturnal behaviors. Mean age (+/- SD) at presentation was 37.4 (+/- 9.1) yr (range 18-54); 73.7% of the patients (n = 14) were female. Mean age of sleep-related eating onset was 24.7 (+/- 12.9) yr (range 5-44). Eating occurred from sleep nightly in 57.9% (n = 11) of patients. Chief complaints included excessive weight gain, concerns about choking while eating or about starting fires from cooking and sleep disruption. Extensive polysomnographic studies, clinical evaluations and treatment outcome data identified three etiologic categories for the sleep-related eating: (a) sleepwalking (SW), 84.2% (n = 16); (b) periodic movements of sleep (PMS), 10.5% (n = 2) and (c) triazolam abuse (0.75 mg hs), 5.3% (n = 1). DSM-III Axis 1 psychiatric disorders (affective, anxiety) were present in 47.4% (n = 9) of the patients, and only two patients had a daytime eating disorder (anorexia nervosa), each in remission for 3-7 yr. Nearly half of all patients fulfilled established criteria for being overweight, based on the body mass index. Onset of sleep-related eating was linked directly to the onset of SW, PMS, triazolam abuse, nicotine abstinence, chronic autoimmune hepatitis, narcolepsy, encephalitis or acute stress. In the SW group, 72.7% (8/11) of patients had nocturnal eating and other SW behavior suppressed by clonazepam (n = 7) and/or bromocriptine (n = 2) treatment. Both patients with PMS likewise responded to treatment with combinations of carbidopa/L-dopa, codeine and clonazepam. Thus, sleep-related eating disorders can generally be controlled with treatment of the underlying sleep disorder.

Chronic behavioral disorders of human REM sleep: a new category of parasomnia.

Four men, aged 67-72 years, had 4-month to 6-year histories of injuring themselves or their spouses with aggressive behaviors during sleep, often during attempted dream enactment. A 60-year-old woman had disruptive though nonviolent sleep and dream behaviors. Polysomnography did not detect seizures but did document REM sleep pathology with variable loss of chin atonia, extraordinarily increased limb-twitch activity, and increased REM ocular activity and density. A broad range of REM sleep behaviors was recorded on videotape, including stereotypical hand motions, reaching and searching gestures, punches, kicks, and verified dream movements. Stage 3-4 slow wave sleep was elevated for age in all patients. NREM sleep was devoid of harmful behaviors, although three men had periodic myoclonus. There was no associated psychiatric disorder, whereas serious neurologic disorder was closely associated in four cases: olivo-ponto-cerebellar degeneration, Guillain-Barré syndrome, subarachnoid hemorrhage, and an atypical dementia. Two patients had immediate and lasting sleep behavioral suppression induced by clonazepam, and another patient had the same response with desipramine. All instances of drug discontinuation prompted immediate relapse. In four cases there was associated dream hyperactivity, which resolved with behavioral control. These REM sleep neurobehavioral disorders constitute another category of parasomnia, replicate findings from 21 years ago in cats receiving pontine tegmental lesions, and offer additional perspectives on human behavior, neurophysiology, pharmacology, and dream phenomenology.

Polysomnographic studies in amyotrophic lateral sclerosis.

We retrospectively reviewed 17 polysomnograms (PSG) in symptomatic amyotrophic lateral sclerosis (ALS) patients to assess the type and frequency of sleep disordered events and correlated these findings with pulmonary function tests (PFTs), presenting complaints, presence of bulbar dysfunction, and response to bi-level positive airway pressure (PAP) treatment. PSG revealed abnormalities in 16 patients. Complaints of orthopnea, daytime sleepiness (but not morning headaches) and a low negative inspiratory force (NIF) correlated with sleep disruption. However, neither the forced vital capacity (FVC) nor the NIF reliably predicted any specific PSG finding. Twelve of 13 patients treated with bi-level PAP responded favorably. Since the response to bi-level PAP is frequently gratifying, PSG should strongly be considered in ALS patients with suspected sleep disturbances.

Sleep in aging.

Sleep-related complaints, particularly insomnia and wakefulness at night, are common. The causes are multiple, and include normal, if not ideal, changes in sleep stages and organization with age. The prevalence of sleep disorders is also known to increase with advancing age. These factors are even more exaggerated in the sleep of older individuals who suffer from dementia, and may account for nocturnal agitation in this group.

Sleep violence--forensic science implications: polygraphic and video documentation.

During the past century, infrequent, anecdotal reports of sleep-related violence with forensic science implications have appeared. Recent rapid developments in the field of sleep-disorders medicine have resulted in greater understanding of a variety of sleep-related behaviors, and formal sleep-behavior monitoring techniques have permitted their documentation and classification. Sleep-related violence can be associated with a number of diagnosable and treatable sleep disorders, including (1) night terrors/sleepwalking, (2) nocturnal seizures, (3) rapid eye movement (REM) sleep-behavior disorder, (4) sleep drunkenness, and (5) psychogenic dissociative states occurring during the sleep period. Potentially violent automatized behavior, without consciousness, can and does occur during sleep. The violence resulting from these disorders may be misinterpreted as purposeful suicide, assault, or even homicide. Sleep-related violence must be added to the list of automatisms. A classification system of both waking and sleep-related automatic behavior is proposed, with recommendations for assessment of such behavior.

Ischemic stroke. How to keep the first one from happening.

The prevention of stroke has undenied merit. Recognition of stroke-inducing conditions (eg, cardiac diseases associated with embolism, polycythemia) provides opportunities for specific prevention strategies. For a larger number of patients, however, risk factors for degenerative vascular disease should be addressed. The evidence for efficacy is strongest for treatment of hypertension, and smoking cessation also reduces the risk of stroke. The value of treatment of hyperlipidemia in reducing the incidence of a first stroke remains to be demonstrated. Optimal management of carotid bruit and asymptomatic stenosis will be clarified by results of ongoing clinical trials. On the basis of available data, use of aspirin by healthy persons without risk factors cannot be recommended as a method for preventing a first ischemic stroke.

Rapid eye movement sleep behavior disorder. A treatable parasomnia affecting older adults.

Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia defined by intermittent loss of electromyographic atonia during REM sleep with emergence of complex and vigorous behaviors. Punching, kicking, and leaping from bed during attempted dream enactment caused repeated injury in nine of our first ten adult patients. Mean age at onset was 62 years; nine of the patients were male. All patients underwent standard polysomnographic studies with videotaping of behaviors and extensive neurologic and psychiatric evaluations. The RBD was unrelated to psychopathologic conditions but in five cases was closely linked with major neuropathologic disorders: dementia (two), olivopontocerebellar degeneration, subarachnoid hemorrhage, and the Guillain-Barré syndrome. Other common polysomnographic abnormalities were high REM density, increased stage 3/4 (slow-wave) sleep, and both periodic and aperiodic limb twitching in non-REM sleep. Eight patients had dream changes involving motor overactivity and violent confrontations of dream characters. Clonazepam induced rapid and sustained improvement of dream and sleep behavior problems in seven patients, as did desipramine hydrochloride in one patient.

Sleep fragmentation in rheumatoid arthritis.

Fatigue is commonly reported by patients with rheumatoid arthritis (RA), and it is frequently used to evaluate disease activity and response to therapy. We theorized that the feeling of fatigue in patients with RA may be a manifestation of disturbance of sleep. Sixteen patients with chronic, active RA, who were selected for early onset of fatigue (less than 6 hours after morning awakening), were extensively evaluated by formal all-night polysomnographic recording and multiple sleep latency testing (MSLT). Although no sleep deprivation was found, all patients had some type of marked disturbances of sleep, including unanticipated sleep apnea (2 patients), frequent movement of extremities (all 16 patients), and frequent arousal (all 16 patients). The alpha-delta sleep pattern was present in 13 patients, and 7 were found by MSLT to be hypersomnolent. None of the patients accurately recognized the degree of their sleep disruption. Our findings from the MSLT indicate that fatigue in patients with RA may be a manifestation of sleep fragmentation, rather than a nonspecific constitutional symptom.

A retrospective outcome study and review of hypnosis as treatment of adults with sleepwalking and sleep terror.

Hypnosis has been described anecdotally to be effective in the treatment of sleepwalking and sleep terror, potentially dangerous parasomnias. The authors report the use of hypnosis in the treatment of 27 adult patients with these disorders. A total of 74% of these individuals reported much or very much improvement when followed over substantial periods after instruction in self-hypnotic exercises that were practiced in the home. Hypnosis, often preferred over pharmacotherapy by patients, required one to six office visits (mean = 1.6). This represents a very cost-effective and noninvasive means of treatment, especially when constrasted with lengthy psychotherapy and pharmacotherapy.

Mannitol pharmacokinetics and serum osmolality in dogs and humans.

The relationship between mannitol pharmacokinetics and changes in serum osmolality were studied in dogs and humans. Four human subjects each received between 0.5 and 0.7 g/kg of mannitol as an i.v. infusion given over 15 min. Intravenous bolus doses of 0.5, 1.0 and 1.5 g/kg were given to each of five animals. Serial determinations of serum osmolality and serum mannitol concentrations were then performed. Mannitol disposition was best described using a biexponential equation and assuming a two-compartment, open model with elimination from the central compartment. For human subjects, the mean (+/- S.D.) distribution half-life was 2.11 +/- 2.67 min and the elimination half-life was 71.15 +/- 27.02 min. The volume of distribution was 0.47 +/- 0.50 liters/kg and total body clearance was 7.15 +/- 10.23 ml X min-1 X kg-1. The disposition of mannitol in dogs is similar to that observed in humans. Mannitol clearance was independent of dose whereas the central compartment volume was significantly larger (P less than .005) in animals receiving the 1.5-g/kg dose. The volume change is probably due to a rapid, uncompensated shift of water from intracellular to extracellular space. There was a strong positive correlation (r = 0.90) between mannitol concentration and serum osmolality changes. However, neither maximum serum mannitol concentration nor maximum serum osmolality increased proportionately with dose. Only the 1.5-g/kg dose produced a sustained elevation of serum osmolality, confirming that larger doses are more likely to result in prolonged hypertonic dehydration.