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Coma has many causes but there are a few urgent ones in clinical practice. Management must start with establishing the cause and an attempt to reverse or attenuate some of the damage. This may include early neurosurgical intervention, efforts to reduce brain tissue shift and raised intracranial pressure, correction of markedly abnormal laboratory abnormalities, and administration of available antidotes. Supporting the patient's vital signs, susceptible to major fluctuations in a changing situation, remains the most crucial aspect of management. Management of the comatose patient is in an intensive care unit and neurointensivists are very often involved. This chapter summarizes the principles of caring for the comatose patient and everything a neurologist would need to know. The basic principles of neurologic assessment of the comatose patient have not changed, but better organization can be achieved by grouping comatose patients according to specific circumstances and findings on neuroimaging. Ongoing supportive care involves especially aggressive prevention of medical complications associated with mechanical ventilation and prolonged immobility. Waiting for recovery-and many do- is often all that is left. Neurorehabilitation of the comatose patient is underdeveloped and may not be effective. There are, as of yet, few proven options for neurostimulation in comatose patients., (© 2017 Elsevier B.V. All rights reserved.)

Objective: To systematically review outcomes in comatose survivors after cardiac arrest and cardiopulmonary resuscitation (CPR)., Methods: The authors analyzed studies (1966 to 2006) that explored predictors of death or unconsciousness after 1 month or unconsciousness or severe disability after 6 months., Results: The authors identified four class I studies, three class II studies, and five class III studies on clinical findings and circumstances. The indicators of poor outcome after CPR are absent pupillary light response or corneal reflexes, and extensor or no motor response to pain after 3 days of observation (level A), and myoclonus status epilepticus (level B). Prognosis cannot be based on circumstances of CPR (level B) or elevated body temperature (level C). The authors identified one class I, one class II, and nine class III studies on electrophysiology. Bilateral absent cortical responses on somatosensory evoked potential studies recorded 3 days after CPR predicted poor outcome (level B). Burst suppression or generalized epileptiform discharges on EEG predicted poor outcomes but with insufficient prognostic accuracy (level C). The authors identified one class I, 11 class III, and three class IV studies on biochemical markers. Serum neuron-specific enolase higher than 33 microg/L predicted poor outcome (level B). Ten class IV studies on brain monitoring and neuroimaging did not provide data to support or refute usefulness in prognostication (level U)., Conclusion: Pupillary light response, corneal reflexes, motor responses to pain, myoclonus status epilepticus, serum neuron-specific enolase, and somatosensory evoked potential studies can reliably assist in accurately predicting poor outcome in comatose patients after cardiopulmonary resuscitation for cardiac arrest.

Background and Purpose: The prognosis of comatose survivors is determined by clinical examination. Early laboratory indicators of poor prognosis (such as evoked potentials) have low sensitivity. The role of MR imaging as a confirmatory study was investigated., Methods: We studied fluid-attenuated inversion recovery (FLAIR) and diffusion-weighted (DW) imaging in 10 patients comatose after cardiac arrest., Results: None of the 10 comatose patients had myoclonus status epilepticus or fixed, dilated pupils on neurologic examination, and none had abnormal somatosensory-evoked potentials. Eight patients showed diffuse signal abnormalities, predominantly in the cerebellum (n = 5), the thalamus (n = 8), the frontal and parietal cortices (n = 8), and the hippocampus (n = 9). One patient showed normal MR imaging results, and one patient had abnormalities in the thalamus and cerebellum and minimal abnormality on DW images; both later awakened. None of the patients with abnormal cortical structures on FLAIR MR images recovered beyond a severely disabled state., Conclusion: MR imaging in comatose survivors may parallel the pathologic findings in severe anoxic-ischemic injury, and extensive abnormalities may indicate little to no prospects for recovery. If confirmed, MR imaging may have a role as a prognosticating test in anoxic-ischemic coma.

We report a 45-year-old man with fulminant pneumococcal meningitis. Fluid attenuated inverse ratio MR images showed the ravaging consequences of occlusive vasculopathy and a transient purulent basal exudate. Bilateral thalamic lesions may have explained the failure to awaken despite appropriate antibiotic therapy.

Generalized myoclonus status is common in comatose patients after cardiac resuscitation, but its prognostic value is uncertain. We studied the clinical, radiologic, and pathologic findings in 107 consecutive patients who remained comatose after cardiac resuscitation. Myoclonus status was present in 40 patients (37%). Features more prevalent in patients with myoclonus status were burst suppression on electroencephalograms, cerebral edema or cerebral infarcts on computed tomography scans, and acute ischemic neuronal change in all cortical laminae. All patients with myoclonus status died. Of 67 patients without myoclonus, 20 awakened. We conclude that myoclonus status in postanoxic coma should be considered an agonal phenomenon that indicates devastating neocortical damage. Its presence in comatose patients after cardiac arrest must strongly influence the decision to withdraw life support.