Will they wake up?
Clinical Indicators
Better prognostic factors:
> Young age
> Less comorbidity
> Not alcoholic
> No history of mental illness
> Shorter duration of time unconscious
> Traumatic aetiology – pts with an Unresponsive Wakefulness Syndrome post TBI much more likely to continue to improve compared to a non-tarumatic cause e.g. hypoxic brain injury
> Minimally Conscious State better than Unresponsive Wakefulness Syndrome
LAB INDICATORS
> Serum Neuron Specific Enolase
> Serum and CSF protein S-100B
Never used alone to prognosticate
Electrophysiology
EEG: Alpha coma or burst suppression associated with poor prognosis
EEG reactive to stimulation (e.g. clap) carries better prognosis
SSEP used after a hypoxic brain injury (see RCA SSEP section) but not accurate in TBI or mass lesions
Imaging
The structural damage seen on CT and MRI informs prognosis
Still only used in research:
- Functional MRI
- PET imaging
- Transcranial magnetic stimulation with EEG
Is Coma Curable?
The Neurocritical Care Society think so!
They’ve outlined a bold plan: the Curing Coma Campaign. It’s a signature clinical, scientific, and public health effort, aspiring to be the first global public health initiative to tackle the unifying concept of coma as a treatable medical entity.
This campaign is certainly driving research in this area.
Obviously the aetiology of the coma is an important factor in it’s “curability”.
Outlined in this article, they propose the nomenclature of Disorder of Consciousness (DOC) “endotypes”:
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DOC endotype without commensurate structural damage In principle, these could be reversible using traditional treatment approaches (e.g., seizures, drug overdose) and are recognized based on metabolic or electrical instability.
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DOC endotype with structural or functional damage that is amenable to replacement or bypass therapy This would include damage that could potentially be replaced by surrogate brain function such as stimulant medications or brain-machine interfaces. Even if interventions are not present today, this endotype would represent a high-priority and fertile target for identifying and testing new interventions. Except in the most severe cases, hypoxic-ischemic injury and traumatic brain injury would fit in this category.
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DOC endotype that is not amenable to pharmacologic or anatomic replacement or repair therapy Essentially, this would be untreatable conditions based on the underlying biology, such as end-stage prion or Alzheimer disease. This endotype may progress from endotype 1 or 2 when metabolic, electrical, or structural disease is not reversed. It would be hoped that this endotype might be a “moving target” in which novel therapies emerge that can arrest disease progression and move patients into endotype 1 or 2 by virtue of more successful therapies to reverse metabolic or electrical instability or provide replacement or bypass therapy.
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DOC mimics endotype in which structural damage results in a syndrome that mimics or is mistaken for a DOC. Examples could include severe aphasia, abulia, or locked-in syndrome. Such endotyping could allow targeted treatment for these alternate impairments with similarly profound functional impact.
The hope is this will allow:
- Improvement in the accuracy of early neuro-prognostication
- Identification of patients amenable to interventions at specific time points
- Clinical trials of targeted treatments to accelerate emergence from coma and improve cognitive and functional outcome.
- Improved communication between the patient, family members, and clinicians.