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BACKGROUND: The evolution from free muscle-sparing transverse rectus abdominis myocutaneous flap to deep inferior epigastric perforator (DIEP) flap leads to less donor-site morbidity. However, rectus fascia is usually incised longitudinally from perforator(s) to iliac vessels, often exceeding 15 cm when including longitudinal muscle spreading. By using a limited fascia incisional (LFI-) technique, we try to diminish abdominal wall functional decrease. METHODS: Twenty-seven patients who underwent unilateral breast reconstructions using free DIEP-flap with limited fascia incision between December 2014 and October 2017 were included in the study. Each patient received a periumbilical electromyogram (EMG) preoperatively, at 6 and 14 weeks postoperatively. They were compared with 27 patients having unilateral breast reconstructions using classic free DIEP-flap, performed at the same department between November 2009 and May 2011. RESULTS: In our LFI-technique, one vertical (4 cm) incision is made where the pedicle exits the muscle. A second, oblique (3 cm) incision is made more distally where the pedicle runs into the iliac vessels. After release, the pedicle is tunneled through the incisions, leaving all fascia, and therefore muscle, intact. In the LFI-group small neurogenic changes were noticed in only 26% and 11% of the patients at, respectively, 6 and 14 weeks postoperatively. By contrast, in the control group, postoperative neurogenic deviations remained in 37% of the patients at 14 weeks postoperatively; significant different compared to the LFI-group. CONCLUSION: This study shows the importance of preserving anterior rectus fascia. Nerve supply and abdominal rectus muscle function are less endangered using small segmental fascia incisions. We believe that our technique diminishes donor-site morbidity significantly and improves the postoperative recovery.

The etiopathogenesis of fibromyalgia (FM) and chronic fatigue syndrome (CFS) is not yet elucidated. Hypothalamo-pituitary-adrenal (HPA) axis dysfunction is reflected in the hormonal disturbances found in FM and CFS. Some study groups have introduced a novel hypothesis that moderate or intermittent intracranial hypertension may be involved in the etiopathogenesis of FM and CFS. In these conditions, hormonal disturbances may be caused by the mechanical effect of increased cerebrospinal fluid pressure, which hampers blood flow in the pituitary gland. Severe intracranial pressure may compress the pituitary gland, resulting in primary empty sella (ES), potentially leading to pituitary hormone deficiencies. The aim of this narrative review was to explore whether similar hormonal changes and symptoms exist between primary ES and FM or CFS and to link them to cerebrospinal fluid pressure dysregulation. A thorough search of the PubMed and Web of Science databases and the reference lists of the included studies revealed that several clinical characteristics were more prevalent in primary ES, FM or CFS patients than in controls, including increased cerebrospinal fluid pressure, obesity, female sex, headaches and migraine, fatigue, visual disturbances (visual acuity and eye motility abnormalities), vestibulocochlear disturbances (vertigo and neurosensorial hearing loss), and bodily pain (radicular pain and small-fiber neuropathy). Furthermore, challenge tests of the pituitary gland showed similar abnormalities in all three conditions: blunted adrenocorticotropic hormone, cortisol, growth hormone, luteinizing hormone, and thyroid stimulating hormone responses and an increased prolactin response. The findings of this narrative review provide further support for the hypothesis that moderately or intermittently increased cerebrospinal fluid pressure is involved in the pathogenesis of FM and CFS and should stimulate further research into the etiopathogenesis of these conditions. ispartof: JOURNAL OF PAIN RESEARCH vol:16 pages:205-219 ispartof: location:New Zealand status: published

Purpose Increasing evidence suggests that fibromyalgia most likely represents a neurological dysfunction. We previously hypothesized that at least some fibromyalgia cases may be caused by irritation of nerve root fibers and sensory neurons due to moderately increased cerebrospinal pressure. Because of the rostro-caudal hydrostatic pressure gradient, neurogenic abnormalities are expected to be most pronounced in sacral nerve roots. The purpose was to review electrodiagnostic tests of patients with fibromyalgia. Methods A retrospective review of electrodiagnostic test results, including the lumbar and sacral nerve root myotomes of patients diagnosed with fibromyalgia according to the 1990 criteria of the American College of Rheumatology was done. Results All 17 patients were female. Sural nerve responses could not be elicited in 12% and S1-Hoffmann reflex latencies were increased in 41%. In 12% of the patients, fibular motor nerve distal latency and conduction velocity were outside normal limits. Needle-EMG revealed neurogenic motor unit potentials in 0% of L2, 6% of L3, 29% of L4, 71% of L5, 47% of S1, 94% of S2, and 76% of S3-S4 myotomes. S3-S4 nerve-supplied anal reflexes were delayed in 94%. Conclusion This is the first time that electrodiagnostic data of both lumbar and sacral nerve root myotomes in fibromyalgia patients are presented. All patients showed neurogenic abnormalities that were more pronounced in the sacral than in the lumbar myotomes with a rather patchy distribution pattern. We propose that, in addition to skin punch biopsies to assess small fiber neuropathy, assessment of the anal reflex may be a useful part of the diagnostic pathway in patients with fibromyalgia.

Tarlov cysts (TCs) are dilations of nerve roots arising from pathologically increased hydrostatic pressure (HP) in the spinal canal. There is much controversy regarding whether these cysts are a rare source of pain or often produce symptoms. The aim of this review was to identify the reasons that symptomatic TCs (STCs) are easily overlooked. The literature was searched for data regarding pathogenesis and symptomatology. TCs may be overlooked for the following reasons: (1) STCs are considered clinically irrelevant findings; (2) it is assumed that it is clinically difficult to ascertain that TCs are the cause of pain; (3) MRI or electromyography studies only focus on the L1 to S1 nerves; (4) TCs are usually not reported by radiologists; (5) degenerative alterations of the lumbosacral spine are almost always identified as the cause of a patient’s pain; (6) it is not generally known that small TCs can be symptomatic; (7) examinations and treatments usually focus on the cysts as an underlying mechanism; however, essentially, increased HP is the main underlying mechanism for producing symptoms. Consequently, STCs may relapse after surgery; (8) bladder, bowel and sphincter dysfunction are not inquired about during history taking. (9) Unexplained pain is often attributed to depression, whereas depression is more likely the consequence of debilitating neuropathic pain. (10) The recognition of STCs is subject to gender bias, confirmation bias and cognitive dissonance and unconscious bias in publishing. There are several reasons STCs are underdiagnosed, mostly due to persistent misconceptions and biases. These slides can be retrieved under Electronic Supplementary Material.

Background Tarlov cysts (TCs) are expanded nerve root sheaths that occur near the dorsal root ganglion and result from increased intraspinal hydrostatic pressure. TCs most frequently affect the lumbosacral plexus and therefore may cause specific symptoms such as perineal pain and neurogenic bladder, bowel, and sphincter problems. It has been estimated that 1% of the population has symptomatic Tarlov cysts (STCs). However, STCs appear to be underdiagnosed, with the pain reported by patients commonly attributed to degenerative alterations seen on MRI. The aim of the present study is to investigate the utility of a comprehensive questionnaire for use by physicians in establishing the diagnosis of STCs. Methods We compared questionnaire responses regarding patient history between 33 patients diagnosed with symptomatic TCs and 42 patients with chronic low back pain and sciatica due to disc problems or degenerative or inflammatory disorders. The diagnosis of STCs was confirmed using nerve conduction studies (NCS) and electromyography (EMG) of the sacral myotomes by an expert neurophysiologist. Results The questionnaire responses revealed specific differences in perineal symptoms (perineal pain, dyspareunia,coccygodynia), bowel symptoms (constipation, diarrhea), bladder symptoms (hesitation, retention, frequency), and anal sphincter problems (anal pain, mild fecal incontinence). Additionally, sitting, walking, and straining aggravated pain more frequently inSTC patients, and STC patients were more often forced to stop working and/or reduce their social activities. Conclusions Including the above-listed items in the patient history might facilitate differentiation of low back pain and sciatica due to STCs from that due to disc problems or degenerative or inflammatory disorders. ispartof: Acta Neurochirurgica vol:160 issue:4 pages:839-844 ispartof: location:Austria status: published

PURPOSE: To assess the independent association between ICU-acquired neuromuscular complications and 5-year mortality and morbidity. To explore the optimal threshold of the Medical Research Council (MRC) sum score, assessing weakness, for the prediction of 5-year outcomes. METHODS: Sub-analyses of a prospective, 5-year follow-up study including 883 EPaNIC patients (Early versus Late Parenteral Nutrition in Intensive Care) (Clinicaltrials.gov:NCT00512122), systematically screened in ICU for neuromuscular complications with MRC sum score ('MRC-cohort', N = 600), electrophysiology on day 8 ± 1 to quantify compound muscle action potential ('CMAP-cohort', N = 689), or both ('MRC&CMAP-cohort', N = 415). Associations between ICU-acquired neuromuscular complications and 5-year mortality, hand-grip strength (HGF, %predicted), 6-min-walk distance (6-MWD, %predicted) and physical function of the SF-36 quality-of-life questionnaire (PF-SF-36) at 5-years were assessed with Cox regression and linear regression, adjusted for confounders. The optimal threshold for MRC at ICU discharge to predict 5-year outcomes was determined by martingale residual plots (survival) and scatterplots (morbidity). RESULTS: Both lower MRC sum score at ICU discharge, indicating less strength [HR, per-point-increase: 0.946 (95% CI 0.928-0.968), p = 0.001], and abnormal CMAP, indicating nerve/muscle dysfunction [HR: 1.568 (95% CI 1.165-2.186), p = 0.004], independently associated with increased 5-year mortality. In the MRC&CMAP-cohort, MRC [HR: 0.956 (95% CI 0.934-0.980), p = 0.001] but not CMAP [HR: 1.478 (95% CI 0.875-2.838), p = 0.088] independently associated with 5-year mortality. Among 205 survivors, low MRC independently associated with low HGF [0.866 (95% CI 0.237-1.527), p = 0.004], low 6-MWD [105.1 (95% CI 12.1-212.9), p = 0.043] and low PF-SF-36 [- 0.119 (95% CI - 0.186 to - 0.057), p = 0.002], whereas abnormal CMAP did not correlate with these morbidity endpoints. Exploratory analyses suggested that MRC ≤ 55 best predicted poor long-term morbidity and mortality. Both MRC ≤ 55 and abnormal CMAP independently associated with 5-year mortality. CONCLUSIONS: ICU-acquired neuromuscular complications may impact 5-year morbidity and mortality. MRC sum score, even if slightly reduced, may affect long-term mortality, strength, functional capacity and physical function, whereas abnormal CMAP only related to long-term mortality. ispartof: INTENSIVE CARE MEDICINE vol:46 issue:6 pages:1184-1193 ispartof: location:United States status: published

Purpose Increasing evidence suggests that fibromyalgia most likely represents a neurological dysfunction. We previously hypothesized that at least some fibromyalgia cases may be caused by irritation of nerve root fibers and sensory neurons due to moderately increased cerebrospinal pressure. Because of the rostro-caudal hydrostatic pressure gradient, neurogenic abnormalities are expected to be most pronounced in sacral nerve roots. The purpose was to review electrodiagnostic tests of patients with fibromyalgia. Methods A retrospective review of electrodiagnostic test results, including the lumbar and sacral nerve root myotomes of patients diagnosed with fibromyalgia according to the 1990 criteria of the American College of Rheumatology was done. Results All 17 patients were female. Sural nerve responses could not be elicited in 12% and S1-Hoffmann reflex latencies were increased in 41%. In 12% of the patients, fibular motor nerve distal latency and conduction velocity were outside normal limits. Needle-EMG revealed neurogenic motor unit potentials in 0% of L2, 6% of L3, 29% of L4, 71% of L5, 47% of S1, 94% of S2, and 76% of S3-S4 myotomes. S3-S4 nerve-supplied anal reflexes were delayed in 94%. Conclusion This is the first time that electrodiagnostic data of both lumbar and sacral nerve root myotomes in fibromyalgia patients are presented. All patients showed neurogenic abnormalities that were more pronounced in the sacral than in the lumbar myotomes with a rather patchy distribution pattern. We propose that, in addition to skin punch biopsies to assess small fiber neuropathy, assessment of the anal reflex may be a useful part of the diagnostic pathway in patients with fibromyalgia.

Mieke Hulens,1 Ricky Rasschaert,2 Greet Vansant,3 Ingeborg Stalmans,4,5 Frans Bruyninckx,6 Wim Dankaerts1 1Department of Rehabilitation Sciences, Faculty of Kinesiology and Rehabilitation Sciences, Musculoskeletal Rehabilitation Research Unit, University of Leuven, Leuven, Belgium; 2Department of Neurosurgery, Sint-Jozefziekenhuis, Bornem, Belgium; 3Department of Social and Primary Health Care, Public Health Nutrition, University of Leuven, Leuven, Belgium; 4Department of Neurosciences, Ophthalmology Research Group, University of Leuven KU Leuven, Leuven, Belgium; 5Department of Ophthalmology, University Hospitals UZ Leuven, Leuven, Belgium; 6Clinical Electromyography Laboratory, Department of Academic Consultants, Faculty of Medicine, University Hospitals UZ Leuven, Leuven, Belgium Purpose: Idiopathic intracranial hypertension (IICH) is a condition characterized by raised intracranial pressure (ICP), and its diagnosis is established when the opening pressure measured during a lumbar puncture is elevated >20 cm H2O in nonobese patients or >25 cm H2O in obese patients. Papilledema is caused by forced filling of the optic nerve sheath with cerebrospinal fluid (CSF). Other common but underappreciated symptoms of IICH are neck pain, back pain, and radicular pain in the arms and legs resulting from associated increased spinal pressure and forced filling of the spinal nerves with CSF. Widespread pain and also several other characteristics of IICH share notable similarities with characteristics of fibromyalgia (FM) and chronic fatigue syndrome (CFS), two overlapping chronic pain conditions. The aim of this review was to compare literature data regarding the characteristics of IICH, FM, and CFS and to link the shared data to an apparent underlying physiopathology, that is, increased ICP.Methods: Data in the literature regarding these three conditions were compared and linked to the hypothesis of the shared underlying physiopathology of increased cerebrospinal pressure.Results: The shared characteristics of IICH, FM, and CFS that can be caused by increased ICP include headaches, fatigue, cognitive impairment, loss of gray matter, involvement of cranial nerves, and overload of the lymphatic olfactory pathway. Increased pressure in the spinal canal and in peripheral nerve root sheaths causes widespread pain, weakness in the arms and legs, walking difficulties (ataxia), and bladder, bowel, and sphincter symptoms. Additionally, IICH, FM, and CFS are frequently associated with sympathetic overactivity symptoms and obesity. These conditions share a strong female predominance and are frequently associated with Ehlers-Danlos syndrome.Conclusion: IICH, FM, and CFS share a large variety of symptoms that might all be explained by the same pathophysiology of increased cerebrospinal pressure. Keywords: chronic pain, fatigue, headache, Ehlers-Danlos, sympathetic activity, lymphatic olfactory pathway, small fiber neuropathy, Ménière’s disease, Tarlov cysts

Tarlov cysts (TCs) are dilations of nerve roots arising from pathologically increased hydrostatic pressure (HP) in the spinal canal. There is much controversy regarding whether these cysts are a rare source of pain or often produce symptoms. The aim of this review was to identify the reasons that symptomatic TCs (STCs) are easily overlooked.The literature was searched for data regarding pathogenesis and symptomatology.TCs may be overlooked for the following reasons: (1) STCs are considered clinically irrelevant findings; (2) it is assumed that it is clinically difficult to ascertain that TCs are the cause of pain; (3) MRI or electromyography studies only focus on the L1 to S1 nerves; (4) TCs are usually not reported by radiologists; (5) degenerative alterations of the lumbosacral spine are almost always identified as the cause of a patient's pain; (6) it is not generally known that small TCs can be symptomatic; (7) examinations and treatments usually focus on the cysts as an underlying mechanism; however, essentially, increased HP is the main underlying mechanism for producing symptoms. Consequently, STCs may relapse after surgery; (8) bladder, bowel and sphincter dysfunction are not inquired about during history taking. (9) Unexplained pain is often attributed to depression, whereas depression is more likely the consequence of debilitating neuropathic pain. (10) The recognition of STCs is subject to gender bias, confirmation bias and cognitive dissonance and unconscious bias in publishing.There are several reasons STCs are underdiagnosed, mostly due to persistent misconceptions and biases. These slides can be retrieved under Electronic Supplementary Material.

Fibromyalgia (FM) exhibits characteristics of a neurological disorder, and similarities have been identified between FM and idiopathic intracranial hypertension (IICH). When intracranial pressure rises, the drainage of excess cerebrospinal fluid (CSF) through the subarachnoid space of the cranial and spinal nerves increases. Higher CSF pressure irritates nerve fibers inside nerve root sheaths and may consequently cause radicular pain, as was reported in patients with IICH. Moreover, the cut-off of 20-25 cm H20 used to define IICH may be too high, as has been suggested in patients with chronic fatigue syndrome. We hypothesize that the neurological symptoms of FM are caused by the dysregulation of cerebrospinal pressure (CSP) and that spinal fluid drainage can relieve this pain. Exploring the processes underlying increased CSP may provide an alternative explanation for the generation of unexplained widespread pain (WSP) and FM as opposed to central sensitization. Additionally, when performing a lumbar puncture for diagnostic reasons, it is useful to measure opening pressure in patients with chronic WSP. ispartof: MEDICAL HYPOTHESES vol:118 pages:55-58 ispartof: location:United States status: published

Fibromyalgia (FM) is a debilitating, widespread pain disorder that is assumed to originate from inappropriate pain processing in the central nervous system. Psychological and behavioral factors are both believed to underlie the pathogenesis and complicate the treatment. This hypothesis, however, has not yet been sufficiently supported by scientific evidence and accumulating evidence supports a peripheral neurological origin of the symptoms. We postulate that FM and several unexplained widespread pain syndromes are caused by chronic postural idiopathic cerebrospinal hypertension. Thus, the symptoms originate from the filling of nerve root sleeves under high pressure with subsequent polyradiculopathy from the compression of the nerve root fibers (axons) inside the sleeves. Associated symptoms, such as bladder and bowel dysfunction, result from compression of the sacral nerve root fibers, and facial pain and paresthesia result from compression of the cranial nerve root fibers. Idiopathic Intracranial Hypertension, Normal Pressure Hydrocephalus and the clinical entity of symptomatic Tarlov cysts share similar central and peripheral neurological symptoms and are likely other manifestations of the same condition. The hypothesis presented in this article links the characteristics of fibromyalgia and unexplained widespread pain to cerebrospinal pressure dysregulation with support from scientific evidence and provides a conclusive explanation for the multitude of symptoms associated with fibromyalgia. ispartof: Medical Hypotheses vol:110 pages:150-154 status: published

Tarlov cysts (TCs) consist of dilated nerve root sheaths filled with cerebrospinal fluid (CSF) and are most frequently found in the sacrum. It is estimated that 25% of detected TCs cause chronic pain and intestinal and urogenital symptoms due to compression of the sacral nerve root fibers inside the TC. Unfortunately, symptomatic TCs are frequently overlooked. It is assumed that TCs result from pathologically increased hydrostatic pressure (HP) in the dural sac that forces CSF into the nerve root sheaths. We hypothesize that in patients with TCs, increased spinal hydrostatic pressure is always associated with increased intracranial pressure. This hypothesis of increased cerebrospinal pressure might explain why patients with sacral TCs frequently report distant symptoms, such as headaches and pain in the neck and arms. In this paper, we describe a case report that provides evidence for this hypothesis. A 30-year-old man presented for the first time in our clinic complaining of lower back, leg, thoracic, neck, and arm pain; headaches; and bladder, bowel, and sphincter symptoms. He was born prematurely and suffered cerebral intraventricular bleeding followed by progressive hydrocephalus. Progression was stabilized with acetazolamide and lumbar punctures. At 19 years of age, his head circumference had further increased and he reported back pain and headaches. Fundoscopy showed no papilledema, and lumbar puncture for CSF evacuation improved the headaches and back pain. The former medical team chose not to insert a ventriculo-external shunt. Brain magnetic resonance imaging (MRI) showed significant dilation of all the ventricles. No CSF flow obstruction between the ventricles was observed. Surprisingly, MRI of the lumbar and sacral spine showed multiple large TCs. This case report indicates that hydrocephalus with a patent aqueduct may be associated with TCs because the increased intracranial pressure is transferred to the spinal canal. While increased intracranial pressure causes dilation of the ventricles, the associated increased spinal pressure may cause dilation of multiple spinal nerve root sheaths to form TCs. Furthermore, while the increased volume of the ventricles gradually compresses the neurons and axons of the brain against the bony skull, simultaneously, the increased pressure inside the nerve sheaths may also gradually compress the neurons and axons located inside the dorsal root ganglia and spinal nerves, resulting in neuropathic pain, sensory abnormalities, and neurogenic bladder and bowel symptoms. Hydrocephalus patients reporting neuropathic pain should be screened for the presence of TCs. ispartof: Medical Hypotheses vol:130 ispartof: location:United States status: Published online

Muscle weakness contributes to prolonged rehabilitation and adverse outcome of critically ill patients. Distinction between a neurogenic and/or myogenic underlying problem is difficult using routine diagnostic tools. Preferential loss of myosin has been suggested to point to a myogenic component. We evaluated markers of muscle atrophy and denervation, and the myosin/actin ratio in limb and abdominal wall skeletal muscle of prolonged critically ill patients and matched controls in relation to insulin therapy and known risk factors for intensive care unit-acquired weakness.Secondary analysis of two large, prospective, single-center randomized clinical studies.University hospital surgical and medical intensive care unit.Critically ill patients and matched controls.Intensive care unit patients had been randomized to blood glucose control to 80-110 mg/dL with insulin infusion or conventional glucose management, where insulin was only administered when glucose levels rose above 215 mg/dL.As compared with controls, rectus abdominis and vastus lateralis muscle of critically ill patients showed smaller myofiber size, decreased mRNA levels for myofibrillar proteins, increased proteolytic enzyme activities, and a lower myosin/actin ratio, virtually irrespective of insulin therapy. Increased forkhead box O1 action may have played a role. Most alterations were more severe in patients treated with corticosteroids. Duration of corticosteroid treatment, independent of duration of intensive care unit stay or other risk factors, was a dominant risk factor for a low myosin/actin ratio. The immature acetylcholine receptor subunit γ messenger RNA expression was elevated in vastus lateralis, independent of the myosin/actin ratio.Both limb and abdominal wall skeletal muscles of prolonged critically ill patients showed downregulation of protein synthesis at the gene expression level as well as increased proteolysis. This affected myosin to a greater extent than actin, resulting in a decreased myosin/actin ratio. Muscle atrophy was not ameliorated by intensive insulin therapy, but possibly aggravated by corticosteroids.

Summary Background Long-term functional outcome of diaphragm paralysis is largely unknown. Methods A retrospective study was conducted in 23 consecutive patients (21 males, 56±9 years) with uni- or bilateral diaphragm paralysis to examine whether functional respiratory recovery can be predicted from the compound motor action potential (CMAP) of the diaphragm at the time of diagnosis. Pulmonary function and CMAP were evaluated at baseline and at follow-up. CMAP amplitude and latency were recorded by surface electromyography with percutaneous electrical stimulation of the phrenic nerve. Patients were followed for (median) 15 months up to 131 months (range 5–131). Functional respiratory recovery was defined as an increase in forced vital capacity >400ml. Results Functional recovery occurred in 43% of the patients after 12 months (10 out of 23) and in 52% after 24 months (12 out of 23). Type and etiology of paralysis did not influence recovery. CMAP, anthropometric characteristics and baseline pulmonary function did not predict functional respiratory recovery. Whether respiratory muscle training improved pulmonary function is uncertain. Moreover, it did not result in a greater percentage functional respiratory recovery. Relapse after an initial improvement was observed in 26% of the patients. Conclusions The present study indicates that functional recovery of diaphragm paralysis is difficult to predict and may occur years after the onset of the paralysis.

Tarlov, or perineural cysts (TC) are commonly overlooked as a cause of sacroischialgia and urogenital and bowel problems. TC can be seen on MRI, but are often considered asymptomatic. This is especially true for smaller cysts. Moreover, there are only few diagnostic characteristics that can be used to confirm that the cysts are the cause of the symptoms. As a consequence, a lot of controversy remains regarding the clinical importance of TC. Because of this underdiagnosed condition, patients often suffer for several years from unrecognized chronic neuropathic pain and neurological conditions. In this paper, case reports of three patients with giant and smaller symptomatic sacral cysts are presented, in which electromyographic testing was performed in order to demonstrate nerve damage. We conclude that electromyography of the sacral nerve roots can be a reasonable tool for the diagnosis of symptomatic TC, as well as for the differentiation from other pathological entities causing sacroischialgia. Moreover, using electromyography it was also documented that smaller cysts of less than 1 cm can cause nerve damage. Therefore incidence of symptomatic TC may be higher than initially thought. ispartof: Pain Practice vol:16 issue:5 pages:E81-E88 ispartof: location:United States status: published

Hyperglycemia and insulin resistance are common in critically ill patients, even if they have not previously had diabetes. Whether the normalization of blood glucose levels with insulin therapy improves the prognosis for such patients is not known.We performed a prospective, randomized, controlled study involving adults admitted to our surgical intensive care unit who were receiving mechanical ventilation. On admission, patients were randomly assigned to receive intensive insulin therapy (maintenance of blood glucose at a level between 80 and 110 mg per deciliter [4.4 and 6.1 mmol per liter]) or conventional treatment (infusion of insulin only if the blood glucose level exceeded 215 mg per deciliter [11.9 mmol per liter] and maintenance of glucose at a level between 180 and 200 mg per deciliter [10.0 and 11.1 mmol per liter]).At 12 months, with a total of 1548 patients enrolled, intensive insulin therapy reduced mortality during intensive care from 8.0 percent with conventional treatment to 4.6 percent (P0.04, with adjustment for sequential analyses). The benefit of intensive insulin therapy was attributable to its effect on mortality among patients who remained in the intensive care unit for more than five days (20.2 percent with conventional treatment, as compared with 10.6 percent with intensive insulin therapy, P=0.005). The greatest reduction in mortality involved deaths due to multiple-organ failure with a proven septic focus. Intensive insulin therapy also reduced overall in-hospital mortality by 34 percent, bloodstream infections by 46 percent, acute renal failure requiring dialysis or hemofiltration by 41 percent, the median number of red-cell transfusions by 50 percent, and critical-illness polyneuropathy by 44 percent, and patients receiving intensive therapy were less likely to require prolonged mechanical ventilation and intensive care.Intensive insulin therapy to maintain blood glucose at or below 110 mg per deciliter reduces morbidity and mortality among critically ill patients in the surgical intensive care unit.

Objective Critically ill patients often develop intensive care unit–acquired weakness. Reduction in muscle mass and muscle strength occurs early after admission to the intensive care unit (ICU). Although early active muscle training could attenuate this intensive care unit–acquired weakness, in the early phase of critical illness, a large proportion of patients are unable to participate in any active mobilization. Neuromuscular electrical stimulation (NMES) could be an alternative strategy for muscle training. The aim of this study was to investigate the safety and feasibility of NMES in critically ill patients. Design This is an observational study. Setting The setting is in the medical and surgical ICUs of a tertiary referral university hospital. Patients Fifty patients with a prognosticated prolonged stay of at least 6 days were included on day 3 to 5 of their ICU stay. Patients with preexisting neuromuscular disorders and patients with musculoskeletal conditions limiting quadriceps contraction were excluded. Intervention Twenty-five minutes of simultaneous bilateral NMES of the quadriceps femoris muscle. This intervention was performed 5 days per week (Monday-Friday). Effective muscle stimulation was defined as a palpable and visible contraction (partial or full muscle bulk). Measurements The following parameters, potentially affecting contraction upon NMES, were assessed: functional status before admission to the ICU (Barthel index), type and severity of illness (Acute Physiology And Chronic Health Evaluation II score and sepsis), treatments possibly influencing the muscle contraction (corticosteroids, vasopressors, inotropes, aminoglycosides, and neuromuscular blocking agents), level of consciousness (Glasgow Coma Scale, score on 5 standardized questions evaluating awakening, and sedation agitation scale), characteristics of stimulation (intensity of the NMES, number of sessions per patient, and edema), and neuromuscular electrophysiologic characteristics. Changes in heart rate, blood pressure, oxygen saturation, respiratory rate, and skin reactions were registered to assess the safety of the technique. Results In 50% of the patients, an adequate quadriceps contraction was obtained in at least 75% of the NMES sessions. Univariate analysis showed that lower limb edema ( P P = .008), admission to the medical ICU ( P = .041), and treatment with vasopressors ( P = .011) were associated with impaired quadriceps contraction. A backward multivariate analysis identified presence of sepsis, lower limb edema, and use of vasopressors as independent predictors of impaired quadriceps contraction ( R 2 = 59.5%). Patients responded better to NMES in the beginning of their ICU stay in comparison with after 1 week of ICU stay. There was no change in any of the safety end points with NMES. Conclusions Critically ill patients having sepsis, edema, or receiving vasopressors were less likely to respond to NMES with an adequate quadriceps contraction. Neuromuscular electrical stimulation is a safe intervention to be administered in the ICU.

SummaryThe ilioinguinal-iliohypogastric nerve entrapment syndrome is a recognised cause of, usually chronic, lower abdominal pain. Diagnosis is based upon a typical clinical triad and relief of pain by injection of a local anaesthetic. In the present study we assessed the value of abdominal muscle electromyography in 41 patients with a clinical syndrome suggestive of ilioinguinal-iliohypogastric nerve entrapment.Electromyographic abnormalities were detected in 15 of 25 cases (60%) with definite diagnosis and in 6 of 16 (37%) of those with probable diagnosis of ilioinguinal-iliohypogastric nerve entrapment syndrome.The rather low sensitivity and the clinical value of this technique are discussed.

The aim of the functional magnetic resonance imaging (fMRI) study was to investigate brain activation associated with active and passive movements, and tactile stimulation in 17 children with right-sided unilateral cerebral palsy (CP), compared to 19 typically developing children (TD). The active movements consisted of repetitive opening and closing of the hand. For passive movements, an MRI-compatible robot moved the finger up and down. Tactile stimulation was provided by manually stroking the dorsal surface of the hand with a sponge cotton cloth. In both groups, contralateral primary sensorimotor cortex activation (SM1) was seen for all tasks, as well as additional contralateral primary somatosensory cortex (S1) activation for passive movements. Ipsilateral cerebellar activity was observed in TD children during all tasks, but only during active movements in CP children. Of interest was additional ipsilateral SM1 recruitment in CP during active movements as well as ipsilateral S1 activation during passive movements and tactile stimulation. Another interesting new finding was the contralateral cerebellum activation in both groups during different tasks, also in cerebellar areas not primarily linked to the sensorimotor network. Active movements elicited significantly more brain activation in CP compared to TD children. In both groups, active movements displayed significantly more brain activation compared to passive movements and tactile stimulation.

Background Critical illness polyneuropathy or myopathy (CIP/CIM) is a frequent complication in the intensive care unit (ICU) and is associated with prolonged mechanical ventilation, longer ICU stay and increased mortality. This is an interim update of a review first published in 2009 (Hermans 2009). It has been updated to October 2011, with further potentially eligible studies from a December 2013 search characterised as awaiting assessment. Objectives To systematically review the evidence from RCTs concerning the ability of any intervention to reduce the incidence of CIP or CIM in critically ill individuals. Search methods On 4 October 2011, we searched the Cochrane Neuromuscular Disease Group Specialized Register, CENTRAL, MEDLINE, and EMBASE. We checked the bibliographies of identified trials and contacted trial authors and experts in the field. We carried out an additional search of these databases on 6 December 2013 to identify recent studies. Selection criteria All randomised controlled trials (RCTs), examining the effect of any intervention on the incidence of CIP/CIM in people admitted to adult medical or surgical ICUs. The primary outcome was the incidence of CIP/CIM in ICU, based on electrophysiological or clinical examination. Secondary outcomes included duration of mechanical ventilation, duration of ICU stay, death at 30 and 180 days after ICU admission and serious adverse events from the treatment regimens. Data collection and analysis Two authors independently extracted the data and assessed the risk of bias in included studies. Main results We identified five trials that met our inclusion criteria. Two trials compared intensive insulin therapy (IIT) to conventional insulin therapy (CIT). IIT significantly reduced CIP/CIM in the screened (n = 825; risk ratio (RR) 0.65, 95% confidence interval (CI) 0.55 to 0.77) and total (n = 2748; RR 0.70, 95% CI 0.60 to 0.82) population randomised. IIT reduced duration of mechanical ventilation, ICU stay and 180-day mortality, but not 30-day mortality compared with CIT. Hypoglycaemia increased with IIT but did not cause early deaths.One trial compared corticosteroids with placebo (n = 180). The trial found no effect of treatment on CIP/CIM (RR 1.27, 95% CI 0.77 to 2.08), 180-day mortality, new infections, glycaemia at day seven, or episodes of pneumonia, but did show a reduction of new shock events.In the fourth trial, early physical therapy reduced CIP/CIM in 82/104 evaluable participants in ICU (RR 0.62. 95% CI 0.39 to 0.96). Statistical significance was lost when we performed a full intention-to-treat analysis (RR 0.81, 95% CI 0.60 to 1.08). Duration of mechanical ventilation but not ICU stay was significantly shorter in the intervention group. Hospital mortality was not affected but 30- and 180-day mortality results were not available. No adverse effects were noticed.The last trial found a reduced incidence of CIP/CIM in 52 evaluable participants out of a total of 140 who were randomised to electrical muscle stimulation (EMS) versus no stimulation (RR 0.32, 95% CI 0.10 to 1.01). These data were prone to bias due to imbalances between treatment groups in this subgroup of participants. After we imputed missing data and performed an intention-to-treat analysis, there was still no significant effect (RR 0.94, 95% CI 0.78 to 1.15). The investigators found no effect on duration of mechanical ventilation and noted no difference in ICU mortality, but did not report 30- and 180-day mortality.We updated the searches in December 2013 and identified nine potentially eligible studies that will be assessed for inclusion in the next update of the review. Authors' conclusions There is moderate quality evidence from two large trials that intensive insulin therapy reduces CIP/CIM, and high quality evidence that it reduces duration of mechanical ventilation, ICU stay and 180-day mortality, at the expense of hypoglycaemia. Consequences and prevention of hypoglycaemia need further study. There is moderate quality evidence which suggests no effect of corticosteroids on CIP/CIM and high quality evidence that steroids do not affect secondary outcomes, except for fewer new shock episodes. Moderate quality evidence suggests a potential benefit of early rehabilitation on CIP/CIM which is accompanied by a shorter duration of mechanical ventilation but without an effect on ICU stay. Very low quality evidence suggests no effect of EMS, although data are prone to bias. Strict diagnostic criteria for CIP/CIM are urgently needed for research purposes. Large RCTs need to be conducted to further explore the role of early rehabilitation and EMS and to develop new preventive strategies.

Critical illness polyneuropathy/myopathy causes limb and respiratory muscle weakness, prolongs mechanical ventilation, and extends hospitalization of intensive care patients. Besides controlling risk factors, no specific prevention or treatment exists. Recently, intensive insulin therapy prevented critical illness polyneuropathy in a surgical intensive care unit.To investigate the impact of intensive insulin therapy on polyneuropathy/myopathy and treatment with prolonged mechanical ventilation in medical patients in the intensive care unit for at least 7 days.This was a prospectively planned subanalysis of a randomized controlled trial evaluating the effect of intensive insulin versus conventional therapy on morbidity and mortality in critically ill medical patients. All patients who were still in intensive care on Day 7 were screened weekly by electroneuromyography. The effect of intensive insulin therapy on critical illness polyneuropathy/myopathy and the relationship with duration of mechanical ventilation were assessed.Independent of risk factors, intensive insulin therapy reduced incidence of critical illness polyneuropathy/myopathy (107/212 [50.5%] to 81/208 [38.9%], p = 0.02). Treatment with prolonged (or = 14 d) mechanical ventilation was reduced from 99 of 212 (46.7%) to 72 of 208 (34.6%) (p = 0.01). This was statistically only partially explained by prevention of critical illness polyneuropathy/myopathy.In a subset of medical patients in the intensive care unit for at least 7 days, enrolled in a randomized controlled trial of intensive insulin therapy, those assigned to intensive insulin therapy had a reduced incidence of critical illness polyneuropathy/myopathy and were treated with prolonged mechanical ventilation less frequently.

Intensive insulin therapy (IIT) improves the outcome of prolonged critically ill patients, but concerns remain regarding potential harm and the optimal blood glucose level. These questions were addressed using the pooled dataset of two randomized controlled trials. Independent of parenteral glucose load, IIT reduced mortality from 23.6 to 20.4% in the intention-to-treat group (n = 2,748; P = 0.04) and from 37.9 to 30.1% among long stayers (n = 1,389; P = 0.002), with no difference among short stayers (8.9 vs. 10.4%; n = 1,359; P = 0.4). Compared with blood glucose of 110-150 mg/dl, mortality was higher with blood glucose150 mg/dl (odds ratio 1.38 [95% CI 1.10-1.75]; P = 0.007) and lower with110 mg/dl (0.77 [0.61-0.96]; P = 0.02). Only patients with diabetes (n = 407) showed no survival benefit of IIT. Prevention of kidney injury and critical illness polyneuropathy required blood glucose strictly110 mg/day, but this level carried the highest risk of hypoglycemia. Within 24 h of hypoglycemia, three patients in the conventional and one in the IIT group died (P = 0.0004) without difference in hospital mortality. No new neurological problems occurred in survivors who experienced hypoglycemia in intensive care units (ICUs). We conclude that IIT reduces mortality of all medical/surgical ICU patients, except those with a prior history of diabetes, and does not cause harm. A blood glucose target110 mg/day was most effective but also carried the highest risk of hypoglycemia.

PURPOSE: Muscle weakness in long-stay ICU patients contributes to 1-year mortality. Whether electrophysiological screening is an alternative diagnostic tool in unconscious/uncooperative patients remains unknown. We aimed to determine the diagnostic properties of abnormal compound muscle action potential (CMAP), sensory nerve action potential (SNAP), and spontaneous electrical activity (SEA) for Medical Research Council (MRC)-defined weakness and their predictive value for 1-year mortality. METHODS: Data were prospectively collected during the EPaNIC trial (ClinicalTrials.gov: NCT00512122). First, sensitivity, specificity, positive (PPV) and negative predictive values (NPV) of abnormal CMAP, SNAP, and SEA for weakness were determined. Subsequently, association between 1-year mortality and abnormal findings on electrophysiological screening was assessed by univariate and multivariate analyses correcting for weakness and other risk factors and the prediction model involved only a development phase. RESULTS: A total of 730 patients were electrophysiologically screened of whom 432 were tested for weakness. On day 8, normal CMAP excluded weakness with a high NPV (80.5 %). By day 15, abnormal SNAP and the presence of SEA had a high PPV (91.7 and 80.0 %, respectively). Only a reduced CMAP on day 8 was associated with higher 1-year mortality [35.6 vs 15.2 % (p < 0.001)]. This association remained significant after correction for weakness and other risk factors [OR 2.463 (95 % CI 1.113-5.452), p = 0.026]. Also among conscious/cooperative patients without weakness, reduced CMAP was independently associated with a higher likelihood of death occurring during 1 year [HR 2.818 (95 % CI 1.074-7.391), p = 0.035]. CONCLUSIONS: The diagnostic properties of electrophysiological screening vary over time. Abnormal CMAP documented early during critical illness carries information about longer-term outcome, which should be further investigated mechanistically. ispartof: INTENSIVE CARE MEDICINE vol:41 issue:12 pages:2138-2148 ispartof: location:United States status: published

Motor axons supplying lumbrical muscles are less severely affected than axons supplying thenar muscles in the carpal tunnel syndrome; sometimes lumbrical motor fibers are less affected than digit 2 sensory fibers. This pattern is consistent with compression of both the anterior and posterior aspects of the median nerve in the carpal tunnel because nerve fibers responsible for thenar, lumbrical, and digit 2 functions lie in an anterior-posterior gradient within the distal median nerve. Recognition of lumbrical sparing supports the electrodiagnosis of carpal tunnel syndrome when the distal latency to thenar muscles or the palm-to-wrist mixed median nerve conduction velocity is normal.

Objective: To investigate the effectiveness of maintaining blood glucose levels below 6.1 mmol/L with insulin as prevention of secondary injury to the central and peripheral nervous systems of intensive care patients. Methods: The authors studied the effect of intensive insulin therapy on critical illness polyneuropathy (CIPNP), assessed by weekly EMG screening, and its impact on mechanical ventilation dependency, as a prospectively planned subanalysis of a large randomized, controlled trial of 1,548 intensive care patients. In the 63 patients admitted with isolated brain injury, the authors studied the impact of insulin therapy on intracranial pressure, diabetes insipidus, seizures, and long-term rehabilitation at 6 and 12 months follow-up. Results: Intensive insulin therapy reduced ventilation dependency (p 0.0007; Mantel-Cox log rank test) and the risk of CIPNP (p 0.0001). The risk of CIPNP among the 405 long-stay (7 days in intensive care unit) patients was lowered by 49% (p 0.0001). Of all metabolic and clinical effects of insulin therapy, and corrected for known risk factors, the level of glycemic control independently explained this benefit (OR for CIPNP 1.26 (1.09 to 1.46) per mmol blood glucose, p 0.002). In turn, prevention of CIPNP explained the ability of intensive insulin therapy to reduce the risk of prolonged mechanical ventilation (OR 3.75 (1.49 to 9.39), p 0.005). In isolated brain injury patients, intensive insulin therapy reduced mean (p 0.003) and maximal (p 0.0001) intracranial pressure while identical cerebral perfusion pressures were obtained with eightfold less vasopressors (p 0.01). Seizures (p 0.0001) and diabetes insipidus (p 0.06) occurred less frequently. At 12 months follow-up, more brain-injured survivors in the intensive insulin group were able to care for most of their own needs (p 0.05). Conclusions: Preventing even moderate hyperglycemia with insulin during intensive care protected the central and peripheral nervous systems, with clinical consequences such as shortening of intensive care dependency and possibly better long-term rehabilitation. NEUROLOGY 2005;64:1348-1353