Distinct diurnal temperature rhythm patterns in critical illness myopathy: secondary analysis of two prospective trials

Diurnal rhythms of body temperature, drinking and activity over reproductive cycles

To the Editor: Widrick et al. ([18][1]) have published data from a 12-day unilateral lower limb suspension (ULLS) study conducted in 1994 using the methods originally published by Berg et al. in 1991 ([3][2]). Analyses included the morphology and contractile behavior of skinned skeletal muscle

Diurnal rhythm in body temperature and heart rate of 12 healthy athletes were recorded during a TransPacific voyage from Japan to the west coast of the United States. The speed of the ship was 14-16 knots which caused shortening of the actual length of a day by 32 minutes. The ratio of the lag of change in diurnal body temperature rhythm did not seem to be constant throughout the voyage. The adjustment of the rhythm to a new local time seemed to occur slowly during the first few days but fairly fast after the second week on the ship. During the voyage the rhythm was approximately 2 hours behind the typical temperature rhythm of the local time, and the rhythm could follow the new environmental routines in 3 or 4 days after arrival in USA. The results obtained suggest that the intrinsic biological rhythm formed during a longer period of time resists greatly distortion by a new environmental rhythm even with moderate speeds in trans·position. The diurnal rhythm in body function appears to adapt fairly rapidly to new environmental routines, although there are some literatures showing that the rhythm is hardly disturbed by a displacement or an inversion of the daily routines of living 1 ' 2 '· Sasaki 3 ' reported that there was apparently no difference between the diurnal change in body temperature and the external periodicity of living with a slower transposition across the longitudes, but with a faster speed of transposition which resulted in change of a day by approximately 30 minutes one could see a disparity between the external periodicity and the diurnal rhythm. In this latter case, apparently three days seem to be neces­ sary before the subjects' diurnal body rhythm is adjusted to the new environmental routine. Data observed for quickest transposition by a jet flight

To review the medical literature on critical illness polyneuropathy and myopathy in childhood. Medline and EMBASE were searched using the following terms: critical illness (neuropathy, polyneuropathy, and myopathy), critical care (neuropathy, polyneuropathy, and myopathy), acute myopathy, acute necrotizing myopathy, children, and pediatric. The references listed in publications thus identified were also reviewed. All studies relating to pediatric critical illness polyneuropathy and myopathy were included. The adult literature was also reviewed as to the current understanding of critical illness polyneuropathy and myopathy. Critical illness polyneuropathy and critical illness myopathy are well recognized in adults, in whom they commonly cause generalized weakness and muscle wasting, with failure to wean from mechanical ventilation. Critical illness polyneuropathy and critical illness myopathy are reported in 32-100% of critically ill adult patients ventilated for >3 days. There is significant clinical and neurophysiologic overlap between the two conditions, such that the term critical illness polyneuropathy and myopathy (CIPNM) is often used. Critical illness polyneuropathy and critical illness myopathy have only occasionally been reported in childhood, and little is known of their prevalence or clinical significance in this population. This article summarizes the pediatric literature on critical illness polyneuropathy and critical illness myopathy and highlights areas for future research in critically ill children. Critical illness polyneuropathy and myopathy may cause significant morbidity in critically ill children. These conditions seem to be clinically and electrophysiologically similar in children and adults, but prospective studies of these entities are required to better characterize their frequency, natural history, and clinical significance in pediatric practice.

The paraventricular nucleus of the thalamus alters rhythms in core temperature and energy balance in a state-dependent manner

A wireless measuring device for long term measurements of the diurnal temperature rhythm on unrestrained rats is presented. Up to 5 rats could be tested simultaneously. The electronic units, the coating problems for the implanted transmitter, and the tissue reaction are described. It is observed that the circadian temperature rhythm in subcutis and in mammary cancer is almost in phase. The consequence of this is discussed.

Survival from critical illness has improved in recent years, leading to increased attention to the sequelae of such illness. Neuromuscular weakness in the intensive care unit (ICU) is common, persistent, and has significant public health implications. The differential diagnosis of weakness in the ICU is extensive and includes critical illness neuromyopathy. Prolonged immobility and bedrest lead to catabolism and muscle atrophy, and are associated with critical illness neuromyopathy and ICU-acquired weakness. Early mobilization therapy has been advocated as a mechanism to prevent ICU-acquired weakness. Early mobilization is safe and feasible in most ICU patients, and improves outcomes. Implementation of early mobilization therapy requires changes in ICU culture, including decreased sedation and bedrest. Various technologies exist to increase compliance with early mobilization programs. Drugs targeting muscle pathways to decrease atrophy and muscle-wasting are in development. Additional research on early mobilization in the ICU is needed.

Background and Aims:Intensive care unit acquired weakness (ICUAW) is a common occurrence in patients who are critically ill. It is most often due to critical illness polyneuropathy (CIP) or to critical illness myopathy (CIM). ICUAW is increasingly being recognized partly as a consequence of improved survival in patients with severe sepsis and multi-organ failure, partly related to commonly used agents such as steroids and muscle relaxants. There have been occasional reports of CIP and CIM in children, but little is known about their prevalence or clinical impact in the pediatric population. This review summarizes the current understanding of pathophysiology, clinical presentation, diagnosis and treatment of CIP and CIM in general with special reference to published literature in the pediatric age group.Subjects and Methods:Studies were identified through MedLine and Embase using relevant MeSH and Key words. Both adult and pediatric studies were included.Results:ICUAW in children is a poorly described entity with unknown incidence, etiology and unclear long-term prognosis.Conclusions:Critical illness polyneuropathy and myopathy is relatively rare, but clinically significant sequelae of multifactorial origin affecting morbidity, length of intensive care unit (ICU) stay and possibly mortality in critically ill children admitted to pediatric ICU.

To investigate the impact of critical illness polyneuropathy and critical illness myopathy on short-term and long-term patient outcome. In the acute-care setting, critical illness polyneuropathy and critical illness myopathy are important causes of acute paralysis in critically ill comatose patients, and may cause inappropriately pessimistic prognoses. Duration of weaning from artificial ventilation is 2 to 7 times greater in patients with critical illness polyneuropathy than in patients without critical illness polyneuropathy. After intensive care unit and hospital discharge, many patients diagnosed with critical illness polyneuropathy or critical illness myopathy are reported to complain of profound muscle weakness. Chronic disability was a common finding among them. Complete functional recovery with patients regaining the ability to breathe spontaneously and to walk independently was reported in 180 of 263 patients (68.4%); severe disability with tetraparesis, tetraplegia, or paraplegia was reported in 74 patients (28.1%). Persisting milder disabilities were common even in patients with complete functional recovery, and included reduced or absent deep tendon reflexes, stocking and glove sensory loss, muscle atrophy, painful hyperesthesia, and foot drop. An association of critical illness polyneuropathy and critical illness myopathy with increased intensive care unit and hospital mortality has been demonstrated only in selected intensive care unit populations; data are insufficient to demonstrate any association with long-term mortality. Intensive care unit-acquired critical illness polyneuropathy and critical illness myopathy influence the evaluation of acutely ill comatose patients and may instigate unreasonably pessimistic prognosis. Critical illness polyneuropathy and critical illness myopathy are an important cause of difficult weaning of patients from the ventilator and of persisting muscle weakness and disability after intensive care unit discharge.

Patients with COVID-19 may develop a range of neurological disorders. We report here 4 COVID-19 subjects with intensive care unit-acquired weakness and their functional outcome. In addition, a scoping review of COVID-19 literature was performed to investigate this issue. Of the post-COVID-19 patients admitted to our Neuro-Rehabilitation Unit, 4 (3 males, 1 female; mean age 59.2 ± 8.62 years) had intensive care unit-acquired weakness, diagnosed with electromyography. Muscle strength and functional evaluation were performed on all patients with Medical Research Council, Disability Rating Scale and Functional Independence Measure, respectively, at admission, discharge and 6-month follow-up after discharge. Electromyography revealed that 3 subjects had critical illness polyneuropathy and 1 had critical illness polyneuropathy/critical illness myopathy. At follow-up, the 3 subjects with critical illness polyneuropathy reached full recovery. The patient with critical illness polyneuropathy/critical illness myopathy showed moderate disability requiring bilateral ankle foot-orthosis and support for ambulation. The scoping review retrieved 11 studies of COVID-19 patients with intensive care unit-acquired weakness, concerning a total of 80 patients: 23 with critical illness myopathy (7 probable), 21 with critical illness polyneuropathy (8 possible), 15 with critical illness polyneuropathy and myopathy (CIPNM) and 21 with intensive care unit-acquired weakness. Of 35 patients who survived, only 3 (8.5%) reached full recovery. All 3 had critical illness myopathy, but 2 of these had a diagnosis of probable critical illness myopathy. Intensive care unit-acquired weakness commonly occurred in subjects with COVID-19. Recovery was variable and a low percentage reached full recovery. However, the heterogeneity of studies did not allow definitive conclusions to be drawn.LAY ABSTRACTPatients with COVID-19 may develop a range of neurological disorders. We report here 4 cases of COVID-19 patients with intensive care unit-acquired weakness and their functional outcome. In addition, a scoping review of the COVID-19 literature was performed to investigate the occurrence of, and recovery from, intensive care unit-acquired weakness and sub-types (critical illness polyneuropathy, critical illness myopathy and critical illness polyneuropathy/critical illness myopathy) in subjects with COVID-19. Of these 4 patients, the 3 patients with critical illness polyneuropathy reached full recovery. The patient with critical illness polyneuropathy/critical illness myopathy showed moderate disability, requiring use of a bilateral device (ankle foot-orthosis). The scoping review of studies of COVID-19 patients with intensive care unit-acquired weakness retrieved a total of 80 patients: 21 with intensive care unit-acquired weakness, 23 with critical illness myopathy, 21 with critical illness polyneuropathy, and 15 with critical illness polyneuropathy/critical illness myopathy. Intensive care unit-acquired weakness commonly occurred in COVID-19 subjects, but the outcome was variable and a low percentage reached full recovery. COVID-19 subjects can develop long-term consequences and limitations, particularly those with intensive care unitacquired weakness, who need more rehabilitation. New rehabilitative strategies and well-designed studies investigating the benefit of rehabilitation are necessary.

SUMMARYAlzheimer’s disease (AD) is characterised, not only by cognitive deficits and neuropathological changes, but also by several non-cognitive behavioural symptoms that can lead to a poorer quality of life. Circadian disturbances in core body temperature and physical activity are reported in AD patients, although the cause and consequences of these changes are unknown. We therefore characterised circadian patterns of body temperature and activity in male triple transgenic AD mice (3xTgAD) and non-transgenic (Non-Tg) control mice by remote radiotelemetry. At 4 months of age, daily temperature rhythms were phase advanced and by 6 months of age an increase in mean core body temperature and amplitude of temperature rhythms were observed in 3xTgAD mice. No differences in daily activity rhythms were seen in 4- to 9-month-old 3xTgAD mice, but by 10 months of age an increase in mean daily activity and the amplitude of activity profiles for 3xTgAD mice were detected. At all ages (4–10 months), 3xTgAD mice exhibited greater food intake compared with Non-Tg mice. The changes in temperature did not appear to be solely due to increased food intake and were not cyclooxygenase dependent because the temperature rise was not abolished by chronic ibuprofen treatment. No β-amyloid (Aβ) plaques or neurofibrillary tangles were noted in the hypothalamus of 3xTgAD mice, a key area involved in temperature regulation, although these pathological features were observed in the hippocampus and amygdala of 3xTgAD mice from 10 months of age. These data demonstrate age-dependent changes in core body temperature and activity in 3xTgAD mice that are present before significant AD-related neuropathology and are analogous to those observed in AD patients. The 3xTgAD mouse might therefore be an appropriate model for studying the underlying mechanisms involved in non-cognitive behavioural changes in AD.

Sepsis may cause not only failure of parenchymal organs but can also cause damage to peripheral nerves and skeletal muscles. It is now recognized that sepsis-mediated disorders of the peripheral nerves and the muscle, called critical illness polyneuropathy (CIP) and critical illness myopathy, are responsible for weakness and muscle atrophy occurring de novo in intensively treated patients. CIP represents an acute axonal neuropathy that develops during treatment of severely ill patients and remits spontaneously, once the critical condition is under control. The course is monophasic and self-limiting. Among the critical illness myopathies, three main types have been identified: a non-necrotizing "cachectic" myopathy (critical illness myopathy in the strict sense), a myopathy with selective loss of myosin filaments ("thick filament myopathy") and an acute necrotizing myopathy of intensive care. Clinical manifestations of both critical illness myopathies and CIP include delayed weaning from the respirator, muscle weakness, and prolonging of the mobilization phase. The pathogenesis of these neuromuscular complications of sepsis is not understood in detail but most authors assume that the inflammatory factors that mediate systemic inflammatory response and multiple organ failure are closely involved. In thick filament myopathy and acute necrotizing myopathy, administration of steroids and neuromuscular blocking agents may act as triggers. Specific therapies have not been discovered. Stabilization of the underlying critical condition and elimination of sepsis appear to be of major importance. Steroids and muscle relaxants should be avoided or administered at the lowest dose possible.

Sepsis may cause not only failure of parenchymal organs but can also cause damage to peripheral nerves and skeletal muscles. It is now recognized that sepsis‐mediated disorders of the peripheral nerves and the muscle, called critical illness polyneuropathy (CIP) and critical illness myopathy, are responsible for weakness and muscle atrophy occurring de novo in intensively treated patients. CIP represents an acute axonal neuropathy that develops during treatment of severely ill patients and remits spontaneously, once the critical condition is under control. The course is monophasic and self‐limiting. Among the critical illness myopathies, three main types have been identified: a nonnecrotizing “cachectic” myopathy (critical illness myopathy in the strict sense), a myopathy with selective loss of myosin filaments (“thick filament myopathy”) and an acute necrotizing myopathy of intensive care. Clinical manifestations of both critical illness myopathies and CIP include delayed weaning from the respirator, muscle weakness, and prolonging of the mobilization phase. The pathogenesis of these neuromuscular complications of sepsis is not understood in detail but most authors assume that the inflammatory factors that mediate systemic inflammatory response and multiple organ failure are closely involved. In thick filament myopathy and acute necrotizing myopathy, administration of steroids and neuromuscular blocking agents may act as triggers. Specific therapies have not been discovered. Stabilization of the underlying critical condition and elimination of sepsis appear to be of major importance. Steroids and muscle relaxants should be avoided or administered at the lowest dose possible.

BackgroundCritical illness polyneuropathy (CIP) and critical illness myopathy (CIM) are complications causing weakness of respiratory and limb muscles in critically ill patients. As an important differential diagnosis of Guillain-Barré syndrome (GBS), CIP and CIM should be diagnosed with caution, after a complete clinical and laboratory examination. Although not uncommon in ICU, CIP and CIM as severe complications of percutaneous nephrostolithotomy (PNL) have not been documented in literature.Case presentationA 48-year-old Chinese woman was referred to our hospital, complaining of occasional pain in the right lower back for one month. Lithiasis was diagnosed by ultrasonographical and radiological examinations on the urinary system. PNL was indicated and performed. The patient developed CIP and CIM on the fourth day after PNL. Early recognition and treatment of the severe complications contributed to a satisfactory recovery of the patient.ConclusionThis case expands our understanding of the complications of PNL and underscores the importance of differentiating CIP/CIM from GBS in case of such patients developing weakness after the treatment. Clinical characteristics and examination results should be carefully evaluated to make the diagnosis of CIP or CIM. Both anti-septic prophylaxis and control of hyperglycemia might be effective for the prevention of CIP or CIM; aggressive treatment on sepsis and multiple organ failure is considered to be the most effective measure to reduce the incidence of CIP/CIM.

The effects of ambient temperature on the body temperature rhythm of rats, hamsters, gerbils, and tree shrews