There is a spectrum of alterations of mental status, ranging from confusion or delirium (disorders in perception) to lethargy, stupor, and coma (states of decreased awareness). A lethargic pediatric patient has decreased awareness of self and the environment. In an emergency setting, this translates to decreased eye contact with family members, nursing, and physician personnel.2 A stuporous pediatric patient has decreased eye contact, decreased motor activity, and unintelligible vocalization. Stuporous patients can be aroused with vigorous noxious stimulation. Comatose patients are unresponsive and cannot be aroused by verbal or physical stimulation, such as phlebotomy, arterial catheterization, or lumbar puncture.3 4 and 5
Irrespective of the cause, AMS is indicative of either depression of the cerebral cortex or localized abnormalities of the ascending reticular activating system. Both cerebral cortices must be affected in order to cause AMS. Classic causes of bilateral cortical impairment are toxic and metabolic states that deprive the brain of normal substrates. Altered mental status can also be produced through dysfunction of the reticular activating system that is housed in the brainstem and midbrain. This system connects cranial nerve nuclei and extends from the brainstem to the thalamus. It governs respirations, cardiovascular functions, and many aspects of homeostasis, as well as daily wake-sleep cycles. Any abrupt interruption or selective destruction of the reticular activating system may result in AMS. 13
The pathologic conditions that effect awareness and arousal can be described using three broad pathologic categories: supratentorial mass lesion, subtentorial mass lesion, and metabolic encephalopathy.36
Supratentorial mass lesions cause AMS by compressing the brainstem and/or diencephalon. Signs and symptoms of this type of lesion include focal motor abnormalities that are often present from the onset of the altered level of consciousness. The progression of neurologic dysfunction is from rostral to caudal with sequential failure of midbrain, pontine, and medullary function. Compromise by supratentorial lesions causes slow nystagmus toward and fast nystagmus from a cold stimulus during caloric testing.
Subtentorial mass lesions lead to reticular activating system dysfunction, in which prompt loss of consciousness is generally the rule. There is a discrete level of dysfunction. Cranial nerve abnormalities are frequently found due to the highly packed neurologically eloquent anatomy. Abnormal respiratory patterns such as Cheyne-Stokes respiration, neurogenic hyperventilation, and ataxic breathing are common. With brainstem injury, asymmetric and/or fixed pupils are found. No eye movements occur despite cold stimuli to both auditory canals.
Metabolic encephalopathy usually causes depressed consciousness before depressed motor signs, which, when present, are typically symmetric. 37 Respiratory function is involved relatively early, and abnormalities are often secondary to acid-base imbalance. Pupillary reflexes are generally preserved. Pupils may be sluggish, but the movement is intact and symmetric. Exceptions occur with profound anoxia and the influence of cholinergics, anticholinergics, opiates, and barbiturates.
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