Level of consciousness can be determined by applying verbal, tactile, visual, and painful stimuli. Initially, the patient should be observed for the presence of spontaneous movement or postures. Spontaneous purposeful movement suggests intact brainstem pathways. The degree of stimulus that is necessary to evoke a response should be recorded. One initially attempts verbal stimuli, followed by tactile stimuli, then painful stimuli, which include sternal rub or fingernail or toenail pressure. The type of movements evoked with these maneuvers also should be noted. Patient movements may include appropriate withdrawal, which indicates intact spinal cord, brainstem, and cortical pathways. One should consider corticospinal tract dysfunction if movement is asymmetric. Decerebrate or decorticate posturing is also of localizing significance (see Motor and Reflex Activity, p. 82).

The Glasgow Coma Scale is an objective scale that may prove useful for measuring the depth of coma or the level of consciousness in patients who have had stroke. This scale (Appendix B) has a score range from 3 (minimum score, deepest coma) to 15 (maximum score, normal consciousness). The FOUR Score is another clinical grading scale used for the assessment of coma. Four domains including eye responses, motor responses, brainstem reflexes, and breathing pattern are evaluated, and the score range is 0 to 16. Assessment of the level of coma alone does not establish the cause, but documentation of progression or regression of the level of coma is vitally important.

Generally, normal respiration is characterized by rhythmic breathing with a frequency of approximately 10 to 15 breaths per minute (a normal breath is approximately 500 mL of inspired air). Some respiratory patterns can have a localizing significance and help in the diagnosis of coma (Fig. 6-2).

Cheyne-Stokes respiration is a periodic pattern in which episodes of hyperpnea alternate with apnea and suggests bilateral, deep hemispheric lesions or diffuse cortical and brainstem dysfunction. This respiration pattern may be the first sign of transtentorial herniation in patients with a unilateral supratentorial lesion. The pattern may also be seen in normal individuals and in those with metabolic disorders and other causes of diffuse cortical and brainstem dysfunction. Central neurogenic hyperventilation, a regular, rapid, deep, machinery-like breathing, usually indicates a lesion of the brainstem tegmentum between the low midbrain and the middle third of the pons or diffuse cortical or brainstem dysfunction. A systemic, acid-base imbalance must also be considered if hyperventilation is noted. Central neurogenic hyperventilation that results in metabolic acidosis may be caused by pneumonia (often accompanied by an expiratory grunt, cyanosis, and fever), neurogenic pulmonary edema, or diabetic or uremic acidosis and may occur in hepatic coma and salicylate poisoning. Apneustic breathing consists of a prolonged inspiratory cramp followed by an expiratory pause and usually denotes a lesion (especially infarction or primary hemorrhage) in the pons. Ataxic breathing, which is irregular and variable, and cluster breathing, with irregular pauses between breaths, are often terminal patterns that signify a high medullary dysfunction. With further depression of the medulla, respiration becomes more erratic and may eventually decrease (suppression) and then stop (apnea).

Pupillary size, symmetry, and reactivity to light (Fig. 6-3) are all important in the evaluation of the comatose patient. The response of the pupils to light in a comatose patient should be tested with a bright light to be certain of the response. Pupillary light response is relatively resistant to metabolic abnormalities, and the preservation of light response in association with other signs of midbrain dysfunction indicates a probable metabolic cause. Although the presence of the light reflex is the single most important physical sign that differentiates diffuse (cortical and brainstem dysfunction) from structural brain disease, metabolic disorders can mimic structural brain disease. Glutethimide, scopolamine, and atropine may cause fixed and dilated pupils; opiates may cause constricted pupils.

Bilateral dilated (6-7 mm) and fixed pupils usually signify brain death but may also occur with barbiturate intoxication or severe hypothermia. Midposition (4-5 mm), equal, and reactive pupils usually occur in patients with diffuse cortical and brainstem dysfunction; midposition pupils that are fixed to light indicate a midbrain lesion. Unilateral pupillary dilation may indicate uncal herniation through the tentorial notch or a third cranial nerve compressive lesion. Bilateral very small (pinpoint) and reactive pupils suggest pontine hemorrhage, infarction, or narcotic use.

Careful assessment of eye position and movements in comatose patients is often very helpful for localizing the offending lesion(s) (Fig. 6-4). Spontaneous, roving, conjugate eye movements indicate intact brainstem pathways. Dysconjugate ocular movements typically indicate abnormal brainstem function. Lateral gaze deviation is also localizing, as noted later.