Plasma tryptophan and musculoskeletal pain in non-articular rheumatism ("fibrositis syndrome").

Plasma-free tryptophan is inversely related to the severity of subjective pain in 8 patients who fulfilled criteria for a variety of non-articular rheumatism, the "fibrositis syndrome". The observation is consistent with animal and human studies suggesting a relationship between reduced brain serotonin metabolism and pain reactivity.     

Sleep and fibrositis syndrome

Chronic diffuse myalgia, localized areas of tenderness, fatigue, and unrefreshing sleep are related to a physiologic arousal disorder within sleep, that is, the alpha EEG NREM sleep anomaly. This sleep physiologic disorder, nonrestorative sleep, and symptoms of fibrositis syndrome are shown to occur with psychologic, environmental, and physiologic distress conditions. Pathogenic mechanisms that link nonrestorative sleep physiology to pain and fatigue may involve metabolic dysfunction of the brain with sleep-related alteration in immunologic and neurotransmitter functions (serotonin, substance P, endorphins). These sleep-related mechanisms have important implications for the understanding and treatment of fibrositis/fibromyalgia syndrome.     

A spectral method for removing eye movement artifacts from the EEG.

A frequency-domain technique for compensating for eye artifacts in mid-line scalp EEG when power spectra are to be calculated is reported. It has been tested in 12 subjects during voluntary and random eye movements. The method which involves calculating the ratio of EEG and EOG spectra adequately controls for low-frequency components in the EEG due to eye artifacts and allows recovery of the dominant peaks in the scalp EEG spectrum.     

Seasonal symptom severity in patients with rheumatic diseases: a study of 1,424 patients

OBJECTIVE: To examine the nature of seasonal symptoms, their prevalence, and differences among rheumatic disorders by examining longitudinal data over a period of up to 24 years. METHODS: We used a questionnaire assessment of seasonal symptoms using the Seasonal Pattern Assessment Questionnaire (SPAQ) in 1,424 patients with rheumatoid arthritis (RA), osteoarthritis (OA), and fibromyalgia (FM). Clinical status was evaluated with standard assessment measures, and reported symptoms were compared with actual seasonal differences measured for periods of up to 24 years. RESULTS: About 50% of patients with rheumatic disease reported exacerbation of rheumatic symptoms (pain, global severity, and fatigue) by seasonal changes. The presence of seasonal symptoms was not related to diagnosis or to seasonal affective disorder (SAD) symptoms, and symptoms were less common in older patients and in men. The number of symptoms and the severity of allied factors (depression, anxiety, pain, global severity, number of months with seasonal symptoms) were increased in persons with FM and/or complete SAD symptoms. Using circular statistics, the modal months for worse symptoms were December and January, and for best symptoms was July. Bimodal patterns of seasonality were identified for global severity, joint pain, fatigue, and socialization. Seasonal symptoms differed as to the degree at which they were dispersed around the 12 month circle. When pain and global severity measurements obtained over a 24 year period were analyzed, pain was slightly increased in the summer and global severity was not related to season at all. Even when patients who specifically reported worse symptoms in winter and best symptoms in summer were examined, no effect of season could be found. CONCLUSION: Seasonal rheumatic symptoms are commonly reported across all rheumatic diseases, but appear to reflect perception rather than reality since reported symptoms do not agree with measured clinical scores. In addition, regardless of seasonal complaints, measured pain and global severity scores are not worse in winter. Although patients with FM and Season (+) patients report more severe symptoms, their pattern of reporting and their actual scores do not differ according to season compared to persons without FM or positive seasonality.     

Alpha EEG sleep and morning symptoms in rheumatoid arthritis

We studied the influence of disturbed sleep physiology on morning symptoms in 15 patients with classical rheumatoid arthritis (RA) who were experiencing an acute flare. All were found to have an alpha frequency (7 to 11.5 Hz) EEG sleep anomaly, an overnight increase in tenderness in their peripheral joints and in "fibrositic" regions, as well as increased weakness and diminished energy. One patient experienced remission in symptoms and improvement in sleep physiology. The morning symptoms may relate to a nonrestorative sleep disorder associated with the alpha EEG sleep anomaly.     

EEG frequency patterns associated with hallucinations in schizophrenia and "creativity" in normals

This study attempts to define EEG power spectral patterns associated with hallucinatory behaviors in schizophrenia. Six unmedicated schizophrenics with Schneiderian criteria were interviewed and their tongue potentials were monitored and recorded on FM tape. Eye movements and tongue potentials were monitored and segments with artifacts were not used. Consecutive 4-sec intervals of EEG were analyzed in the frequency domain using fast Fourier transorm methods and serial power spectra plots obtained. The intrusiveness of the hallucinatory experience may be similar to the sudden internal experience of perceptual resolution in a creative task. Six normal controls were similarly monitored and analyzed while responding to tests of "creativity." In the 4-sec interval prior to reports of hallucinatory experiences, a frequency pattern of predominatly delta and theta power was found in 71.7% of the EEG segments. In the control group, 78.1% of the EEG segments preceding a creative response demonstrated a similar low frequency pattern which also differed significantly from the base line EEG frequency pattern.     

Periodic movements in sleep and sleep-wake complaint

Periodic movements during sleep (PMS) are frequent, involuntary movements, usually of the lower extremities, that disrupt sleep. Twelve patients (nine men and three women, mean age 53.9 years) with a complaint of persistent insomnia (DIMS) were compared with 11 patients (eight men and three women, mean age 53.0 years) complaining of excessive daytime sleepiness (DOES). DIMS patients had more PMS (both absolute and relative), a longer delay to sleep onset and to REM onset, more wakefulness after sleep onset, and less total sleep time. Although the fragmentation of physiological sleep was more severe in the DIMS patients, those individuals with DOES reported cognitive intrusions during their sleep. While DOES patients may be regarded as "sleeping through" the brief arousals associated with leg activity during sleep, there appears to be sufficient cognitive awareness of the nocturnal interruption to precipitate a complaint of daytime sleepiness. Insomnia patients, however, appear to experience longer and more frequent awakenings, which are proportional to increased fragmentation of sleep.     

Sleep, cytokines and immune function

Bi-directional communication pathways exist between the brain and the cytokine-immune-endocrine systems. The hypothalamic-pituitary axis, the efferent neuronal hypothalamus-autonomic nervous system axis, and the direct drainage of macromolecules from the brain into the blood and the lymphatic system provide a network by which the sleeping/waking brain influence bodily functions. Similarly, changes in cytokine levels in the periphery modulate the central nervous system either directly or via the vagal nerve and influence the sleeping/waking brain. In humans, circadian nocturnal sleep-daytime wakefulness is associated with changes in peripheral cytokines, cellular immune functions, and endocrines. Progesterone levels influence sleep and cellular immune functions during the menstrual cycle. The interaction between the circadian sleeping/waking brain and the cytokine-immune-endocrine system are integral to preserving homeostasis. Disorganization or loss of sleep disrupts the harmonious integration of the circadian cytokine-immune-endocrine system. However, the mechanisms of circadian sleep/wakefulness-related cytokine-immune-endocrine functions in host defence against disease remain to be determined.