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Materials and Methods Eighty‐eight PD patients participating in a rehabilitation course were studied. The Clinical Dementia Rating (CDR) was used to assess cognitive impairment.
Sixty‐six patients were cognitively intact and 22 had cognitive impairment (≥1 in two or more domains or a sum of boxes score of ≥3). The Finnish CERAD test battery was used to measure cognitive functions in seven different domains (language functions, verbal learning, visuospatial functions, delayed recall, memory consolidation, recognition memory, and executive functions).
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THE first descriptions of the syndrome that would eventually be named malignant hyperthermia (MH) were made in the early 1960s. By 1970, it became clear that alterations in skeletal muscle constituted the primary defect in MH. Through the collaboration of an outstanding pharmacologist, Werner Kalow, and a thoughtful clinical anesthesiologist, Beverly Britt, the basic elements of the common test for MH were described. Kalow and Britt subjected biopsied muscle to graded increments of caffeine, demonstrating a leftward shift of the dose–response curve in muscle from patients who had experienced an episode of MH. Described how muscle from these patients developed contractures to clinical concentrations of halothane in vitro. Between 1970 and 1985, testing was standardized ( e.g., which muscle to biopsy, exposure regimens, diagnostic thresholds) to develop an accurate diagnostic test for MH. Two slightly different protocols emerged: a European version and a North American version, both using halothane alone and caffeine alone as the testing reagents.
Meanwhile, in Japan, a slightly different approach was developed using muscle fibers that were chemically or mechanically “skinned.” This review summarizes the clinical evaluation of the patient with presumed MH susceptibility (MHS) and describe tests that are used in this evaluation. In general, suitable patients for biopsy include those with a family history of MH or who display unexplained hypercarbia, and those who exhibit perioperative rhabdomyolysis (). By itself, massive rhabdomyolysis in association with hyperkalemia and cardiac arrest is usually not MH. Nonetheless, some experts advise muscle biopsy, as much for histology and analysis for dystrophin to detect muscular dystrophy as to exclude MH. Exercise-induced rhabdomyolysis has also been associated with MH.
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Blood collection device problems may go unnoticed by laboratorians since routine quality control (QC) practice typically does not assess all aspects of laboratory testing from blood collection, including specimen processing, analytical testing, and test reporting (7,8). Write something about yourself. No need to be fancy, just an overview. No Archives Categories.
MH is a hypermetabolic disorder, and many other diseases and conditions can mimic it. Modern anesthetic techniques and drugs seem to retard the development of an MH episode, relative to the classic fulminant episode, e.g., marked hypermetabolism, hyperthermia, acidosis, rhabdomyolysis, and cardiac arrhythmias. This led to the development of a clinical grading scale to estimate the likelihood that an MH episode has occurred. The scale incorporates six clinical criteria: evidence of muscle rigidity, muscle breakdown, respiratory acidosis, temperature increase, cardiac involvement, and family history (). The likelihood of MH increases if the patient has manifested multiple signs of MH.