Topics and Speakers Neeraj Badjatia, MD
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Synopsis
Consciousness is such a fundamental part of normal life that it defies facile description. Yet when consciousness is impaired, such as in coma, the subtle distinctions between levels of awareness, arousal, and consciousness become critical diagnostic and prognostic tools. In this lecture, Dr Neeraj Badjatia discusses the pathophysiology of coma. The majority of the lecture is devoted to a detailed examination of the clinical approach to comatose patients, including the neurological exam, the differential diagnoses, and prognostic indicators.
The physiology of arousal emerges from the action of the reticular activating system (RAS), a poorly localized network of cells in the rostral brainstem and the diencephelon. The RAS receives stimulations from the environment via the somatosensory pathways, the autonomic pathways and the limbic system inputs. In turn, the RAS stimulates the brain, activating the cortex. Because it is a diffuse network of cells, there is no single transmitter system involved with the RAS. Neurologists try to induce arousal in comatose patients by stimulating the RAS.
Awareness and arousal exist along a dynamic continuum from full consciousness to a vegetative state. The cerebral cortex mediates awareness; disruption of the cortical activity can lead to altered awareness. The highest level of altered consciousness is lethargy, in which there is decreased responsiveness although the patient remains arousable. Stupor is a slightly more diminished level of awareness, there is less meaningful cortical interaction. The eyes remain open in stupor allowing stimulation of the reticular activating system. Coma refers to an even more diminished state of consciousness, in which the patient is unarousable to external stimuli of any kind. Sleep-wake cycles are absent in coma. A hallmark of coma is the lack of eye opening.
After detailing the spectrum of consciousness, Dr Badjatia turns to the clinical approach to coma. As he describes it, treating a comatose patient involves detective work. Combining the principles of emergency medicine and clinical neurology, the proper management of coma involves integrating the findings from the bedside examination with laboratory tests. First, the physician must determine that the patient is clinically stable. The next step is to determine the cause of the altered level of consciousness, by looking at electrolyte abnormalities, oxygen levels and possible toxin consumption. Trauma, infectious disease and drug ingestion could all lead to coma. Neuroimaging can help determine whether the altered mental status is due to structural or nonstructural causes. Interviewing an eyewitness, such as a family member or paramedic, can help yield a detailed history of what led up to the patient's admission.
The neurologic examination involves deciding which of four levels of arousal best describes the patient: alert, lethargic, stuporous, or comatose. Dr Badjatia describes how to use the Glasgow coma scale to make that determination. Other important tests are the blink threat and eye movements. The appearance of the pupils varies with different states of injury. Symmetry is extremely important to assess. A unilateral change to one of the pupils may indicate dangerous brain swelling and increased intracranial pressure. In assessing motor movements, it is important to look for symmetry and purpose. If the patient does not demonstrate spontaneous movement, noxious stimuli can be applied.
The overarching goal of the clinical approach to coma, Dr Badjatia concludes, is to maximize the likelihood of neurologic recovery. Determining prognosis may require a combination of neurologic assessment, EEG or other electrophysiologic tests, and further neuroimaging. Time and duration of coma are the most telling signs of which patients will improve and which will not.
