Circadian rhythm of periodic limb movements and sensory symptoms of restless legs syndrome

The symptoms of restless legs syndrome (RLS) worsen while patients are sitting or lying and also worsen at night. The current study was designed to determine if the periodic limb movements (PLMs) and sensory symptoms of RLS are modulated by an independent circadian factor. We recorded sleeping and waking PLMs and waking sensory symptoms in eight volunteers with RLS for 3 successive nights and days, starting with a polysomnographic recording of 2 nights, followed by a third night of sleep deprivation and the day after sleep deprivation. This study showed that both the PLMs and sensory symptoms were worst at night with a maximum for both between midnight and 1:00 AM and a minimum between 9:00 and 11:00 AM. Sleep and drowsiness had a tendency to worsen PLMs and sensory symptoms after the night of sleep deprivation. Circadian temperature curves were normal in all four patients with adequate data collection. The highest PLM counts occurred on the falling phase of the circadian temperature curve whereas the lowest PLM counts occurred on the rising phase of the curve. We conclude that the PLM and sensory symptoms in RLS are influenced by a circadian rhythm, and that the "worsening at night" criterion of the RLS Definition Criteria is, at least in part, distinct from the "worsening while lying or sitting" criterion.     

A controlled study of additional sr-L-dopa in L-dopa-responsive restless legs syndrome with late-night symptoms

OBJECTIVE: To investigate whether a combination treatment of regular-release levodopa (rr-L-dopa) and sustained-release levodopa (sr-L-dopa) compared with monotherapy of rr-L-dopa improves sleep quality and reduces periodic limb movements (PLM) in patients with restless legs syndrome (RLS) and problems with maintaining sleep. BACKGROUND: Reappearance of RLS symptoms during the second half of the night while being treated with rr-L-dopa is a common problem in the treatment of sleep disturbances caused by RLS. METHODS: A randomized, controlled, double-blind crossover trial was undertaken. Eligible patients fulfilled the diagnostic criteria of the International RLS Study Group, and met an actigraphically confirmed higher number of PLM per hour time in bed (PLM index) during the second half compared with the first half of the night under treatment with rr-L-dopa. During the crossover periods the patients received 100 to 200 mg rr-L-dopa plus either placebo or 100 to 200 mg sr-L-dopa at bedtime for 4 weeks each period. RESULTS: Thirty patients with RLS (11 men and 19 women) were assessed by actigraphy and subjective sleep quality, and showed a significant improvement in PLM index (p < 0.0001), in "time in bed without movements" (p < 0.0001), and in subjective sleep quality (p < 0.001). Eight of 30 patients reported an altered pattern of RLS symptoms, characterized by a time shift of RLS symptoms into the afternoon or evening, five of these during monotherapy with rr-L-dopa. CONCLUSIONS: A combination therapy of rr-L-dopa and sr-L-dopa is better than monotherapy with rr-L-dopa in reducing the frequency of PLM and problems maintaining sleep, even in patients who are severely affected.     

Polysomnographic sleep measures in patients with uremic and idiopathic restless legs syndrome

In the present study, the nocturnal electroencephalographic sleep pattern, the number of periodic leg movements (PLM) during sleep and wakefulness, and the subjective sleep parameters of patients with uremic (n = 10) and idiopathic (n = 17) restless legs syndrome (RLS) were compared. The main finding was that the total number of PLM (p = 0.019), the PLM index (p = 0.018), and the PLM index while awake (p = 0.003) were significantly higher in patients with uremic RLS compared with patients who had idiopathic RLS. Additionally, both groups showed a distinct time-of-night pattern of PLM activity. Polysomnographic measures of sleep continuity (total sleep time, sleep efficiency, sleep onset latency, time awake) and sleep architecture (amount of nonrapid eye movement sleep stages 1, 2, 3, and 4 and the amount of rapid eye movement sleep) did not differ between uremic and idiopathic RLS patients. With regard to subjective parameters, sleep quality was estimated to be worse in uremic RLS (p = 0.033), whereas other parameters (for example, severity of RLS, quality of life) did not differ between the two groups. It is suggested that uremia itself worsens the motor symptoms of RLS, probably as a result of increased excitability.     

Periodic limb movement disorder in neuroleptic-induced akathisia

We recorded all-night polysomnograms of four schizophrenic patients with neuroleptic-induced akathisia (NIA) before and during treatment with clonazepam. Also, four non-akathitic schizophrenic patients were recorded all-night polysomnograms as control subjects. Daily treatment with 1.5 to 3 mg clonazepam improved subjective complaints of all the 4 patients with NIA. Three of 4 patients with NIA exhibited periodic limb movements (PLM) on bilateral legs, but none of 4 control subjects showed PLM. Total number of PLM and PLM per hour decreased during clonazepam treatment. Moreover, mean inter-movement intervals of PLM of 3 patients were prolonged on bilateral legs. NIA might change its feature as PLM during night sleep.     

Sleep changes after 4 consecutive days of venlafaxine administration in normal volunteers

BACKGROUND: The purpose was to examine the effect of the antidepressant drug venlafaxine on sleep architecture and periodic leg movements of sleep (PLMS) in normal volunteers. METHOD: Eight normal volunteers were studied under laboratory sleep conditions as follows: 1 acclimatization night, 1 baseline night, and 4 consecutive nights of venlafaxine p.o. administration (75 mg during the first 2 nights and 150 mg the last 2 nights). RESULTS: Venlafaxine increased both wake time and sleep stage I. Sleep stages II and III were reduced. REM sleep time was reduced after the first venlafaxine dose, and, by the fourth night, REM sleep was completely suppressed in all volunteers. Six of the eight volunteers showed PLMS at a frequency above 25 per hour. CONCLUSION: Venlafaxine produces several sleep disturbances, which include abnormal leg movements.     

Effect of flurenizide on adaptive reactions in patients with chronic obstructive pulmonary disease

Studies on the wake-sleep cycle with participation of eight female volunteers were performed before, during, and after a 120-day bed rest with the head-end of bed tilted down at 6 degrees (HDT). Methods of polysomnography and actography were applied. The test-subjects were assigned into 2 groups. Group A was prescribed to use countermeasures throughout the experiment; no countermeasures was administered by group B. Evidence of significant alteration in sleep structure at different time points in HDT is given in comparison with data about females of the control group under the conditions of everyday activity. Sleep deviations in the subjects were reordered at each of the three points of investigation and differed from those in control. HDT was shown to modify the sleep structure in experimental groups A and B. A supposition is made that under these conditions the dynamics of physical activity during night sleep had an adaptive character.     

Patients with alcohol problems

The effects of mental and physical daytime activities upon REM sleep cycle (REM cycle) during 1 night was studied in five university students (aged 19-25 years). Mental activity with high tension has effects upon the timing of REM sleep periods in the later part of the night. Physical activity has effects upon the timing of REM sleep in the early part of the night. The result suggests that mental and/or physical activities during daytime modulate REM cycle during the night.     

Brain-derived neurotrophic factor stimulates hindlimb stepping and sprouting of cholinergic fibers after spinal cord injury

Neurotrophic factors have been proposed as a therapeutic treatment for traumatic brain and spinal cord injury. The present study determined whether exogenous administration of one such factor, brain-derived neurotrophic factor (BDNF), could effect behavioral recovery and/or histopathological changes after spinal cord injury. Adult rats received a mild or moderate contusion injury or complete transection of the mid-thoracic spinal cord. Immediately thereafter, they were infused intrathecally with vehicle or BDNF for 28 days. Behavioral recovery was evaluated for 6 weeks after injury, at which time the rats were sacrificed and the spinal cord tissue was examined histologically. The infusion of BDNF resulted in acute stimulation of hindlimb activity. These effects included activation of alternating airstepping in injured rats when the hindlimbs were unloaded as well as slight improvements in the rate of recovery in open field locomotion score. BDNF infusion was also associated with enhanced growth of cholinergic fibers at the injury epicenter, but did not affect white matter sparing or density of serotonergic axons at or below the injury site. Based on immunohistochemical detection of BDNF protein distribution, these described effects are likely to be mediated by the activation of cells and axons within the central injury region and the along the peripheral rim of the spinal cord. Together, these findings demonstrate that the exogenous infusion of BDNF after spinal trauma can influence postinjury outcome through mechanisms that include acute stimulation of hindlimb activity and neuritogenesis at the injury site.     

Acute dissociation after 1 night of sleep loss.

Recent research has shown that dissociative symptoms are related to self-reports of deviant sleep experiences. The present study is the 1st to explore whether sleep loss can fuel dissociative symptoms. Twenty-five healthy volunteers were deprived of sleep for 1 night. Sleepiness and dissociative symptoms were assessed every 6 hr. The authors measured both spontaneous dissociative symptoms and dissociative symptoms induced by dot-staring during sensory deprivation. Sleepiness as well as spontaneous and induced dissociative symptoms were stable throughout the day but increased during the night. These findings provide further evidence for a robust relationship between disruptions in sleep patterns and dissociative symptoms. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

A test of the 1992 International Standards for Neurological and Functional Classification of Spinal Cord Injury

This study was designed to test the 1992 International Standards for Neurological and Functional Classification of Spinal Cord Injury. One hundred and six professionals in the field of spinal cord injury attending an instructional course at the 1994 ASIA Meeting participated in the test. Participants completed a pretest and posttest in which they classified two patients who had a spinal cord injury (one with complete tetraplegia and one with incomplete paraplegia) by sensory and motor levels, zone of partial preservation (ZPP), ASIA Impairment Scale and completeness of injury. Between tests, three members of the ASIA Standards Executive Committee gave presentations on the neurological assessment, scoring, scaling and classification of spinal cord injury and a video of the actual examinations of the two cases was viewed. Percent 'correct' (as defined by the ASIA Standards Committee) was calculated for sensory and motor levels, ZPP, ASIA Impairment and completeness. Overall, the analyses showed that participants had very little difficulty in correctly classifying the patient with complete tetraplegia. Pretests scores ranged from 72% (left motor level) to 96% (complete injury), posttest scores from 73% (left motor level) to 100% correct (complete injury). For the patient with incomplete paraplegia (Case 2), scores were considerably lower. Pretest scores ranged from 16% (right motor level) to 95% correct (incomplete injury); posttest scores from 21% (right motor level) to 97% correct (incomplete injury). The results showed that further revisions of the 1992 Standards and more training is needed to ensure accurate classification of spinal cord injury.     

Intermediate-term outcome of cervical spinal cord-injured patients older than 50 years of age

STUDY DESIGN: This study retrospectively reviewed the intermediate-term clinical outcome of patients who were 50 years of age or older at the time they experienced their cervical spinal cord injury. OBJECTIVES: To establish reasonable expectations for the functional outcome in the older patient with cervical spinal cord injury. BACKGROUND DATA: The long-term morbidity and mortality of large groups of patients with spinal cord injury have been reported. The specific functional ability, disposition, morbidity, and mortality of this group of older patients injured after 50 years of age, however, have been less well defined. METHODS: Forty-one consecutive patients older than 50 years of age at the time of cervical cord injury were studied, and functional abilities, independence, need for assistance in activities of daily living, disposition, morbidity, and mortality were assessed. All patients had more than 2 years of follow-up examinations (mean, 5.5 years) by the same spine injury service. RESULTS: There were 13 complete and 28 incomplete cervical cord lesions. The mean age of the patients at follow-up examination was 67.5 years. The average follow-up period was 5.5 years after injury. None of the patients with complete cord injury improved, and all required extensive care. Twenty-one (80%) of 26 of the patients with incomplete cord injury were able to ambulate with some assistance. Nineteen of 26 patients had independent or near-independent abilities with activities of daily living. Twenty (77%) of 26 were able to return home. All patients with complete cord injury (13 of 13) had died by the time of the follow-up visit. Seventy-seven percent (10 of 13) of this patient group had died within the first year. Those surviving lived an average of 3.5 years after their injury. Fourteen of 28 patients with incomplete cord injury (50%) had died by the time of the follow-up visit. Six (43%) of the 14 deaths were attributed to complications of their spinal cord injury. CONCLUSION: The functional outcome of the person older than 50 years with a complete cervical cord injury is poor. Of the 14% who survived the first year, all required extensive attendant care, and no neurologic improvement was seen. The patient with an incomplete cord injury has an overall good outcome regarding ambulation and returning to home.     

The efficacy of an implementation intention intervention for promoting physical activity among individuals with spinal cord injury: A randomized controlled trial.

Objective: To evaluate the efficacy of an 8-week implementation intention intervention for promoting physical activity among individuals with spinal cord injury. Study Design: Randomized clinical trial. Method: Participants were randomly assigned to an implementation intention intervention (n = 26) or control (n = 28) condition and were asked to engage in 30 min of moderate to heavy intensity physical activity 3 times per week. Results: Participants who formed implementation intentions followed through with their physical activity intentions, engaging in more physical activity than participants in the control condition. Participants in the intervention condition also experienced sustained motivation and greater confidence to schedule physical activity compared with participants in the control condition. Implications: These findings suggest a role for implementation intentions in health promotion programs for people with spinal cord injury. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Pattern of prehension in patients with high cervical injuries (author's transl)

After explaining the tertiary patterns of prehension the possibilities of restoring prehensile function in patients after high cervical spinal injury (C4-C6) by means of orthotics or operation are discussed. Absolute indication for the application of electrical orthotics in patients with complete spinal cord injuries below C4 and C5 and the relative indication below C6 with a motoric orthotic or operation are cleared out.     

Identification of macrophage migration inhibitory factor (MIF) in rat spinal cord and its kinetics on experimental spinal cord injury

BACKGROUND: Among spinal cord injuries, secondary injury is considered to be a "reversible" process and seems to be a key target for the treatment of spinal cord injury. Recently, macrophage migration inhibitory factor (MIF) has been reevaluated as being one of the most important cytokines which act during wound healing, proliferation and differentiation of cells. However, the expression of MIF in the spinal cord has not been investigated yet. PURPOSE: The purpose of this paper is to demonstrate the MIF expression in normal rat spinal cord and to evaluate the kinetics of MIF after spinal cord injury. MATERIALS & METHODS: Female Wistar (280-320 g) rats were studied. Spinal cord injury was made by the clip compression method at the level of C7/Th1 (56 g, For 1 min.). The expression of MIF was examined by immunohistochemistry and northern blot analysis. MIF content in the cerebrospinal fluid (CSF) was measured by enzyme-linked immunosorbent assays (ELISA). Furthermore, to examine the MIF function on neuronal cell, cell proliferation assay (MTS assay) was carried out using PC12, pheochromocytoma cell line, and LN444, glioblastoma cell line, in the presence of anti-MIF monoclonal antibody. RESULTS: MIF stain was positive in normal rat spinal cord white matter. The expression of MIF decreased between 1 hour and 6 hours after injury. It was found to have re-appeared 24 hours after injury. The kinetics of MIF mRNA expression showed reverse-correlation with those of the MIF positive stain. MIF content in CSF was found to be elevated soon after injury. MTS assay suggested that MIF had some proliferative function on neuronal cells. CONCLUSION: MIF exists in the rat white matter. And it's immediately released into the CSF and then re-synthesized 24-hr after injury. MIF shows a cell proliferative function on neuronal cells. These results suggest that MIF plays an important role for secondary spinal cord injury.     

Glutamate neurotoxicity during spinal cord ischemia--development of a delayed-onset paraplegia model

The incidence and severity of spinal cord dysfunction are related to both the depth and duration of the resulting ischemic state. Evidence is accumulating that glutamate, a major neurotransmitter, has potent neurotoxic activity during ischemia. In our laboratory, it has been confirmed that exogenous glutamate has detrimental effects on spinal cord neurons during brief ischemia in vivo. We hypothesized that glutamate neurotoxicity is associated with delayed-neuronal dysfunction. Delayed-onset paraplegia is defined as a neurologic deficit which develops after initial recovery. Infrarenal aortic segments from 12 New Zealand white rabbits, were isolated for 5 minutes and perfused at a rate of 2 ml/min. Group I (n = 6) received normothermic saline (39 degrees C). Group II (n = 6) received normothermic L-glutamate (20 mM). Neurologic function was assessed at 6, 24, and 48 hours after surgery according to the modified Tarlov scale. After 48 hours, the rabbits were euthanized and their spinal cords were harvested for histologic examination. The neurologic function of all group I was fully intact, whereas three rabbits in group II showed acute paraplegia and the other three showed delayed-onset paraplegia. Histologic examination of spinal cords from rabbits in group I revealed no evidence of cord injury, whereas spinal cords from those in group II had evidence of moderate spinal cord injury with central gray matter and adjacent white matter necrosis and axonal swelling. These results indicate that dose-dependent glutamate neurotoxicity is associated with delayed neuronal dysfunction following ischemia in vivo. The severity of the ischemic event, i.e., extracellular glutamate overload, is suspected to be the etiology of delayed-onset paraplegia which, in turn, is thought to be the result of borderline ischemia. This model may allow a pharmacologic approach to the prevention of ischemic spinal cord injury.     

Companionable sleep: Social regulation of sleep and cosleeping in egyptian families.

This exploratory study examined family sleep patterns and quality in a setting of normative napping and cosleeping. Participants were 78 members of 16 families from 2 locales in Egypt (Cairo and a village). Each family member provided a history of sleeping arrangements, 1 week of continuous activity records, and details of each sleep event. Sleep records documented late-onset and dispersed sleep patterns with extensive cosleeping. Of recorded sleep events, 69% involved cosleeping, 24% included more than 1 cosleeper, and only 21% were solitary. Mid-late afternoon napping occurred on 31% of days, and night sleep onsets averaged after midnight. Age and gender structured sleep arrangements and, together with locale, extensively explained sleep behavior (onset, duration, total) and quality. Cosleepers had fewer night arousals, shorter and less variable night sleep duration, and less total sleep. Increased solitary sleep in adolescents and young adults was associated with increased sleep dysregulation, including exaggerated phase shifts in males and more nighttime arousals in females. Where normative, cosleeping may provide psychosensory stimuli that moderate arousal and stabilize sleep. Such moderating features may address important self-regulatory developmental needs during adolescence. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Spinal cord evoked potentials and edema in the pathophysiology of rat spinal cord injury. Involvement of nitric oxide

The possibility that nitric oxide is somehow involved in the early bioelectrical disturbances following spinal cord injury in relation to the later pathophysiology of the spinal cord was examined in a rat model of spinal cord trauma. A focal trauma to the rat spinal cord was produced by an incision of the right dorsal horn of the T 10-11 segments under urethane anaesthesia. The spinal cord evoked potentials (SCEP) were recorded using epidural electrodes placed over the T9 and T12 segments of the cord following supramaximal stimulation of the right tibial and sural nerves in the hind leg. Trauma to the spinal cord significantly attenuated the SCEP amplitude (about 60%) immediately after injury which persisted up to 1 h. However, a significant increase in SCEP latency was seen at the end of 5 h after trauma. These spinal cord segments exhibited profound upregulation of neuronal nitric oxide synthase (NOS) immunoreactivity, and the development of edema and cell injury. Pretreatment with a serotonin synthesis inhibitor drug p-chlorophenylalanine (p-CPA) or an anxiolytic drug diazepam significantly attenuated the decrease in SCEP amplitude, upregulation of NOS, edema and cell injury. On the other hand, no significant reduction in SCEP amplitude, NOS immunolabelling, edema or cell changes were seen after injury in rats pretreated with L-NAME. These observations suggest that nitric oxide is somehow involved in the early disturbances of SCEP and contribute to the later pathophysiology of spinal cord injury.     

Substance abuse and medical complications following spinal cord injury.

This study examined relationships between medical complications resulting in hospital stays and alcohol and illicit substance use in 71 persons with recent spinal cord injury (SCI). At 5 intervals after injury, medical records were reviewed for pressure ulcers and urinary tract infections (UTIs). Abstainers with histories of drinking problems before SCI were at greater risk for UTIs from 7 to 12 months after injury and for longer hospital stays. Former drinkers may not have implemented the self-care skills that were a focus during inpatient rehabilitation. Preinjury illicit substance abuse was related to an increased risk of pressure ulcers 30 months after SCL Clinical implications are clear: Psychologists should inquire about substance use patterns, monitor psychological well-being, and explore the ways in which self-care habits are related to substance use. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effect of intrathecal nimodipine on spinal cord blood flow and evoked potentials in the normal or injured cord

A method was developed for administering intrathecal pharmacotherapy in a rat model of spinal cord injury. The effects of intrathecal administration of nimodipine on spinal cord blood flow (SCBF) and evoked potentials (EPs) were measured in the normal and injured spinal cord. It had previously been shown that systemic nimodipine caused severe hypotension after spinal cord injury. After baseline SCBF and EPs, 15 uninjured rats were blindly allocated to one of three groups: one placebo group (n = 5); and two groups with intrathecal nimodipine, 0.05 mg/kg (n = 5), or 0.2 mg/kg (n = 5). Ten other rats received a 35 g acute clip compression injury of the spinal cord for 1 minute and, were allocated to one of two groups: placebo (n = 5); and intrathecal nimodipine 0.05 mg/kg (n = 5) given 60 min after injury. In the uninjured groups, neither 0.05 nor 0.2 mg/kg of nimodipine increased SCBF during, or 30 min after, intrathecal infusion. However, the mean arterial blood pressure (MABP) decreased significantly to 69.73.1% after the infusion of 0.2 mg/kg nimodipine and did not recover by 98 min. In all three groups of uninjured rats, the amplitude of the cerebellar EP was decreased 30 min after infusion. After spinal cord injury, there were significant decreases in MABP, SCBF and EP amplitude in both placebo and treatment groups, but there was no therapeutic benefit from nimodipine. Thus, intrathecal infusion of nimodipine did not prevent the hypotension encountered with systemic administration and exerted no beneficial effect on SCBF or EPs after acute spinal cord injury.     

Relationship between sleep patterns and human colonic motor patterns

BACKGROUND/AIMS: The precise relationships among colonic motor patterns, depth of sleep, and awakening are incompletely understood. The aim of this study was to correlate human colonic motor patterns with sleep stage, nocturnal arousals, and waking. METHODS: We monitored sleep and correlated sleep stage, arousals, and waking with pressures (area under curve and propagating contractions) recorded from the entire colon in 11 healthy volunteers. RESULTS: Propagating contraction frequency (P = 0.01) and area under the curve (P = 0.001) were significantly reduced at night. There was a highly significant correlation between depth of sleep and suppression of area under curve (P = 0.001) and propagating contraction frequency (P = 0.0001). Propagating contractions were eliminated during slow-wave sleep. During rapid eye movement sleep, colonic pressure and propagating contraction frequency increased sharply to levels comparable with those found in stage 2 sleep. Transient arousal from stable sleep, with or without waking, was a potent and immediate stimulus for colonic propagating contractions. CONCLUSIONS: Sleep per se has a profound inhibitory effect on propagating and nonpropagating activity and is the major determinant of diurnal variation of colonic motility. Propagating contractions are eliminated in slow-wave sleep. Rapid eye movement sleep, arousals, and waking have immediate stimulatory effects on colonic motility.