“Myasthenia gravis (MG), an antibody-mediated autoimmune disease of the neuromuscular junction, is characterized by muscle weakness and fatigability and is caused by autoantibodies against muscle nicotinic acetylcholine receptor (AChR). The anti-AChR antibody is produced by T cell-dependent and B cell-mediated pathogenic mechanisms, activates the complement system and leads to inflammation of the postsynaptic muscle membrane.” (Uzawa)
Clinical diagnosis of brain death: Prerequisites and criteria (UpToDate – login required.)
| Prerequisites |
| Clinical or neuroimaging evidence of an acute central nervous system (CNS) catastrophe (eg, traumatic brain injury, subarachnoid hemorrhage) Exclusion of complicating medical conditions that may confound clinical assessment (no severe electrolyte, acid-base, endocrine, or circulatory [ie, shock] disturbance) No drug intoxication or poisoning, including any sedative drug administered in hospital, which may confound the clinical assessment Core temperature >36°C (97°F) Systolic blood pressure >100 mmHg; vasopressors may be required |
| Examination findings |
| Coma Absent brain-originating motor response, including response to pain stimulus above the neck or other brain-originating movements (eg, seizures, decerebrate or decorticate posturing) Absent pupillary light reflex; pupils are midposition (3.5 to 4 mm) Absent corneal reflexes Absent oculocephalic (doll’s eyes) and oculovestibular reflexes (caloric responses) Absent jaw jerk Absent gag reflex Absent cough with tracheal suctioning Absent sucking or rooting reflexes (in neonates) Apnea as demonstrated by apnea test |
| Observation period |
| At least 6 hours; longer time periods recommended in children and for certain conditions such as after cardiac arrest |
Zhou Q, Verne GN. New insights into visceral hypersensitivity–clinical implications in IBS. Nat Rev Gastroenterol Hepatol. 2011 Jun;8(6):349-55.
Key points
Marcellino C, Wijdicks EF. Posthypoxic action myoclonus (the Lance Adams syndrome). BMJ Case Rep. 2020 Apr 16;13(4):e234332.
Free full-text. (Includes video.)
Lau C, et al. A retrospective study to determine the cefepime-induced neurotoxicity threshold in hospitalized patients. J Antimicrob Chemother. 2020 Mar 1;75(3):718-725.
Full-text for Emory users.
Results: In total, 206 patients were administered 259 courses of cefepime, with an overall CIN incidence of 6% (16/259 courses). A total of 64 courses had a cefepime trough concentration measured (24.7%). A cefepime trough concentration of 36 mg/L provided the best differentiation between patients who experienced neurotoxicity and those who did not. No other patient covariates were identified to be significantly associated with neurotoxicity occurring.
Conclusions: A cefepime trough plasma concentration ≥36 mg/L appears to be the most sensitive and specific cut-off to predict CIN occurring. No patient factors were associated with the development of CIN when accounting for cefepime trough plasma concentrations.
Surgical Focus 