• Title of article

    Clinical correlates and prognosis in early spindle coma

  • Author/Authors

    Peter W. Kaplan، نويسنده , , Didier Genoud، نويسنده , , Tony W. Ho، نويسنده , , Pierre Jallon، نويسنده ,

  • Issue Information
    روزنامه با شماره پیاپی سال 2000
  • Pages
    7
  • From page
    584
  • To page
    590
  • Abstract
    Objective: To determine the prognostic significance of spindle coma (SC) according to etiology and EEG reactivity. Methods: We reviewed 15 patients with SC due to various causes within 8 days of coma to determine the prognostic significance of this EEG pattern. Results: The outcome among survivors was favorable: among 13 survivors, 9 were independent in all activities of daily living (ADLs) at 6 months; 3 were dependent in all ADLs; and one remained in coma. EEG reactivity to noxious stimuli best predicted outcome: All patients (whatever the coma etiology) with EEG reactivity survived; conversely, not all patients without EEG reactivity died. Conclusion: In our patients, EEG reactivity independent of etiology predicted survival, neurological examination did not predict outcome. Most SC survivors had a meaningful recovery achieving all ADLs. From the literature, the cause of SC was predictive of outcome: encephalopathy, seizures and trauma had the best prognosis while hypoxia, CRA and structural lesions carried the worst. Literature review revealed that 23% of patients [56/242] died or remained in a persistent vegetative state (PVS). Best outcomes occurred when SC was due to drugs, encephalopathy or seizures: (0/14 died or were in a PVS). With trauma 15% [25/169] died or were in a PVS). Intermediate outcomes occurred with hypoxia and cardio-respiratory arrest (CRA): 33% [7/21] died or were in a PVS. The gravest outcomes occurred with brain-stem and cerebral infarctions, and tumors: 73% [22/30] died or were in a PVS.
  • Keywords
    Spindle coma , cardiac arrest , EEG , drugs , Etiology , prognosis
  • Journal title
    Clinical Neurophysiology
  • Serial Year
    2000
  • Journal title
    Clinical Neurophysiology
  • Record number

    521869