Residency · Residency · Neurology

Neurological Assessment in the ICU: Coma and Consciousness

Introduction

Neurological assessment in the intensive care unit demands a systematic and reproducible approach to evaluating patients with impaired consciousness. The neurologist must distinguish between disorders of arousal and disorders of awareness, as these distinctions have profound implications for diagnosis, management, and prognosis.

Defining Consciousness

The Two Dimensions of Consciousness

Consciousness has two distinct dimensions. Arousal (wakefulness) is mediated by the ascending reticular activating system (ARAS) in the brainstem tegmentum, hypothalamus, and thalamus. Awareness (content) is mediated by widespread thalamocortical and corticocortical networks. Consciousness requires both intact arousal and awareness functioning together, and lesions disrupting either dimension produce clinically distinct syndromes.

Spectrum of Impaired Consciousness

Coma is eyes-closed unresponsiveness with no evidence of arousal or awareness. The vegetative state (unresponsive wakefulness syndrome) involves return of sleep-wake cycles without reproducible awareness. The minimally conscious state (MCS) shows inconsistent but reproducible evidence of awareness such as visual tracking, command following, or intelligible verbalization. The confusional state or delirium has preserved arousal with fluctuating and disorganized awareness.

The Structured Neurological Examination in the ICU

Glasgow Coma Scale (GCS)

The GCS evaluates eye opening (E1-E4), verbal response (V1-V5), and motor response (M1-M6) with a total score range of 3 to 15. Its limitations include inability to assess verbal response in intubated patients and failure to evaluate brainstem reflexes.

FOUR Score (Full Outline of UnResponsiveness)

DomainScore 4Score 3Score 2Score 1Score 0
Eye (E)Eyelids open, tracking or blinking to commandEyelids open, not trackingEyelids closed, open to loud voiceEyelids closed, open to painEyelids remain closed with pain
Motor (M)Thumbs up, fist, peace sign to commandLocalizing to painFlexion response to painExtension response to painNo response or generalized myoclonus
Brainstem (B)Pupil and corneal reflexes presentOne pupil wide and fixedPupil OR corneal reflexes absentPupil AND corneal reflexes absentAbsent pupil, corneal, and cough reflexes
Respiration (R)Not intubated, regular breathingNot intubated, Cheyne-Stokes patternNot intubated, irregular breathingIntubated, breathes above ventilator rateIntubated, breathes at ventilator rate or apnea

The FOUR score evaluates four domains: eye response, motor response, brainstem reflexes, and respiration, each scored 0 to 4 (total 0-16). Its advantages over GCS include testability in intubated patients, capture of brainstem function, and ability to detect locked-in syndrome.

Brainstem Reflex Assessment

The pupillary light reflex tests the afferent CN II and efferent CN III pathways; clinicians assess pupil size, symmetry, and reactivity. The corneal reflex tests the afferent CN V1 and efferent CN VII. The oculocephalic reflex (doll's eyes) demonstrates intact brainstem function when conjugate contralateral eye deviation occurs with head rotation. The oculovestibular reflex (cold calorics) produces tonic eye deviation toward the irrigated ear in comatose patients with an intact brainstem when ice water is used. The gag and cough reflexes assess CN IX and X integrity.

Motor Response Patterns

Localizing refers to purposeful movement toward a noxious stimulus that crosses the midline. Flexion withdrawal is a stereotyped flexion without localizing. Decorticate posturing (abnormal flexion) produces upper extremity flexion and lower extremity extension, suggesting hemispheric or internal capsule dysfunction. Decerebrate posturing (extension) produces extension and internal rotation of all extremities, suggesting midbrain or pontine dysfunction. No response suggests extensive brainstem injury.

Ancillary Studies

Electroencephalography (EEG)

Continuous EEG (cEEG) is the gold standard for detecting nonconvulsive seizures and nonconvulsive status epilepticus. Background patterns correlate with depth of encephalopathy, ranging from alpha through theta, delta, burst-suppression, to electrocerebral silence. Reactivity of EEG to stimulation is a favorable prognostic indicator.

Neuroimaging

CT head without contrast provides emergent evaluation of structural causes including hemorrhage, herniation, and hydrocephalus. MRI with diffusion-weighted imaging (DWI) detects ischemic injury, diffuse axonal injury, and posterior reversible encephalopathy.

Evoked Potentials

Somatosensory evoked potentials (SSEPs) are particularly valuable: bilateral absence of cortical N20 responses strongly predicts poor outcome after cardiac arrest. Brainstem auditory evoked potentials (BAEPs) assess brainstem integrity from the cochlear nerve to the midbrain.

Etiological Approach to Coma

Structural Causes

Structural causes include supratentorial mass lesions causing transtentorial herniation, infratentorial lesions directly compressing or destroying the ARAS, and bilateral thalamic lesions (as in top-of-the-basilar syndrome or deep cerebral venous thrombosis).

Metabolic and Toxic Causes

These include hypoglycemia, hepatic encephalopathy, uremia, electrolyte derangements, drug intoxication (opioids, benzodiazepines, barbiturates), septic encephalopathy, thyroid storm, and myxedema coma.

Clinical Pearls

Reversible causes of coma must always be ruled out first: hypoglycemia, opioid overdose (naloxone trial), and nonconvulsive status epilepticus (urgent EEG). The FOUR score is superior to the GCS in the ICU because it can be applied to intubated patients and captures brainstem function. Asymmetric pupils in a comatose patient should prompt emergent imaging to evaluate for uncal herniation. A comatose patient who yawns, coughs, or swallows spontaneously has intact lower brainstem function, which is prognostically important. The neurological examination should be documented serially and precisely because trend changes are more informative than any single assessment.

References

  • Posner JB, Saper CB, Schiff ND, Claassen J. Plum and Posner's Diagnosis and Treatment of Stupor and Coma. 5th ed. Oxford University Press; 2019.
  • Wijdicks EFM, Bamlet WR, Maramattom BV, Manno EM, McClelland RL. Validation of a new coma scale: the FOUR score. Ann Neurol. 2005;58(4):585-593.
  • Claassen J, Taccone FS, Horn P, et al. Recommendations on the use of EEG monitoring in critically ill patients. Clin Neurophysiol. 2013;124(10):1948-1957.
  • Edlow JA, Rabinstein A, Traub SJ, Wijdicks EFM. Diagnosis of reversible causes of coma. Lancet. 2014;384(9959):2064-2076.

Read this lecture as Markdown