Miopatía y polineuropatía en el paciente crítico. Estudio PEC : parálisis del enfermo crítico

Alguns pacients ingressats en la Unitat de Cures Intensives (UCI) desenvolupen una debilitat muscular en grau variable que pot arribar fins a la tetraparesia o tretraplejia. Aquesta condició és deguda a una disfunció neuromuscular perifèrica. No existeix consens internacional per al diagnòstic. En aquest treball s'estudien, de manera prospectiva, les alteracions en l'electromiograma i la seva correlació amb l'anatomia patològica del múscul com a mètode diagnòstic de miopatia i/o neuropatia del pacient crític. A més s'avaluen diversos factors predisponents i pronòstics, conseqüències d'aquesta malaltia i el seu moment d'inici.Algunos pacientes ingresados en la Unidad de Cuidados Intensivos (UCI) desarrollan una debilidad muscular en grado variable que puede llegar hasta la tetraparesia o tretraplejia. Esta condición es debida a una disfunción neuromuscular periférica. No existe consenso internacional para el diagnóstico. En este trabajo se estudian las alteraciones en el electromiograma y su correlación con la anatomía patológica del músculo como método diagnóstico de miopatía y/o nueropatía del paciente crítico. Además se evalúan diversos factores predisponentes y pronósticos, consecuencias de esta enfermedad y su momento de inicio

Prognostic Accuracy of N20 Somatosensory Potential in Patients With Acute Ischemic Stroke and Endovascular Thrombectomy

Background Somatosensory evoked potentials may add substantial prognostic value in patients with acute ischemic stroke and contribute to the selection of patients who may benefit from revascularization therapies beyond the accepted therapeutic time windows. We aimed to study the prognostic accuracy of the N20 somatosensory evoked potential component of the ischemic hemisphere in patients with anterior large‐vessel occlusion undergoing endovascular thrombectomy (EVT). Methods Presence and amplitude of the N20 response were recorded before and after EVT. Its adjusted predictive value for functional independence (modified Rankin scale score, ≤2) at day 7 was analyzed by binary logistic regression adjusting by age, mean arterial blood pressure, National Institute of Health Stroke Scale, Alberta Stroke Program Early CT Score, and serum glucose. N20 predictive power was compared with that of clinical and imaging models by using receiver operating characteristics curve analysis. Results A total of 223 consecutive patients were studied (mean age, 70 years; median National Institute of Health Stroke Scale score, 18). Somatosensory evoked potential recordings identified the presence of N20 in 110 (49.3%), absence in 58 (26%), and not assessable in 55 patients due to radiofrequency interferences in the angiography room. Before EVT, N20 predicted functional independence with a sensitivity of 93% (95% CI, 78%–98%) and negative predictive value of 93% (95% CI, 80%–98%). The adjusted odds ratio for functional independence was 9.9 (95% CI, 3.1–44.6). In receiver operating characteristics curve analysis, N20 amplitude showed a higher area under the curve than prehospital or in‐hospital variables, including advanced imaging. Sensitivity increased to 100% (95% CI, 0.85–1) when N20 was present after EVT. Conclusion Somatosensory evoked potential monitoring is a noninvasive and bedside technique that could help eligibility of patients with acute ischemic stroke for EVT and predict functional recovery

Manifesting heterozygotes in McArdle disease:a myth or a realityrole of statins

McArdle disease is an autosomal recessive condition caused by deficiency of the PYGM gene-encoded muscle isoform of glycogen phosphorylase. Some cases of “manifesting” heterozygotes or carriers (i.e., patients who show some McArdle-like symptoms or signs despite being carriers of only one mutated PYGM allele) have been reported in the literature but there is controversy, with misdiagnosis being a possibility. The purpose of our study was to determine if there are actually “manifesting” heterozygotes of McArdle disease and, if existing, whether statin treatment can trigger such condition. Eighty-one relatives of McArdle patients (among a total of 16 different families) were studied. We determined whether they were carriers of PYGM mutations and also collected information on exercise tests (second wind and modified Wingate anaerobic test) and statin intake. We found 50 carriers and 31 non-carriers of PYGM mutations. Although we found existence of heterozygotes manifesting some exercise-related muscle problems such as exacerbated myalgia or weakness, they only accounted for 14% of the carriers and muscle symptoms were milder than those commonly reported in patients. Further, no carrier (whether reporting symptoms or not) showed the second wind phenomenon or a flat blood lactate response to maximal-intensity exercise, both of which are hallmarks of McArdle disease. On the other hand, statin myotoxicity was not associated with muscle symptom onset