Visceral Hypersensitivity

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

  • Visceral and somatic hypersensitivity are present in some patients with functional gastrointestinal disorders
  • Injury to visceral afferents is the most common underlying cause of visceral hypersensitivity that is maintained by either peripheral and/or central nervous system mechanisms
  • Animal models of hypersensitivity have been used to examine the neural mechanisms of hypersensitivity following inflammatory injury, such as alterations in the N-methyl, D-aspartate receptor, dorsal horn neurons or c-Fos
  • Increased intestinal permeability might lead to hypersensitivity and abdominal pain in patients with functional gastrointestinal disorders
  • Functional gastrointestinal disorders are similar to other chronic pain disorders in which persistent nociceptive mechanisms are activated

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Lance-Adams syndrome

Marcellino C, Wijdicks EF. Posthypoxic action myoclonus (the Lance Adams syndrome). BMJ Case Rep. 2020 Apr 16;13(4):e234332.

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  • Action myoclonus is exceptionally rare (less than 0.5% in a series of patients who have a cardiac arrest).
  • Myoclonus occurring after hypoxic brain injury from cardiac arrest, characterised by abrupt irregular muscle contractions. (1)
    • Acute: starting within 48 hours after the arrest (when isolated, sometimes terms acute Lance-Adams syndrome). (2)
    • Chronic: Lance-Adams syndrome, which may start from days to weeks after arrest and progressively worsen, with or without other neurological symptoms.
  • Potentially confused with myoclonus status in a comatose patient, yet the examination, imaging, degree of disability and prognosis are very divergent.
  • Typically, no EEG seizure correlates.

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Cefepime-induced neurotoxicity

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.

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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.

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