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Related Experiment Videos

Sustained upgaze in coma

J R Keane

    Annals of Neurology
    |April 1, 1981
    PubMed
    Summary
    This summary is machine-generated.

    Severe hypoxic encephalopathy can cause sustained upward gaze deviation in coma patients. This sign, often seen after cardiac arrest, may stem from cerebellar pathway damage, not midbrain lesions.

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    Area of Science:

    • Neurology
    • Neuroscience
    • Pathology

    Background:

    • Sustained upward gaze deviation is a clinical sign observed in patients with severe hypoxic encephalopathy.
    • This sign has been anecdotally associated with cardiac arrest and systemic hypotension.
    • The precise anatomical localization and underlying pathophysiology remain unclear.

    Purpose of the Study:

    • To investigate the clinical presentation and neuropathological findings in patients with coma and sustained upward gaze deviation.
    • To determine the relationship between upward gaze deviation and hypoxic brain injury.
    • To explore potential anatomical correlates of this neurological sign.

    Main Methods:

    • Retrospective analysis of 15 patients with coma and upward gaze deviation following cardiac arrest and 2 patients with prolonged systemic hypotension.

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  • Review of neuropathological examinations, focusing on cerebral, cerebellar, and brainstem damage.
  • Correlation of clinical signs such as facial myoclonic jerks and nystagmus with gaze deviation.

    • Main Results:

    • Neuropathological examination revealed diffuse cerebral and cerebellar damage with relative brainstem sparing.
    • No focal lesions were identified in the upper midbrain or pretectum.
    • Six patients developed downward-beating nystagmus as upward gaze resolved; 4 of 6 with posthypoxic facial myoclonic jerks showed synchronous upward gaze.

    Conclusions:

    • Forced upgaze in coma is typically a consequence of severe hypoxic encephalopathy.
    • The sign does not indicate a structural lesion in the pretectum or midbrain.
    • Damage to cerebellar pathways is a potential cause of forced upward gaze in this clinical context.