Delayed arousal

Abstract

Elderly patients have medical and psychological problems affecting all major organ systems. These problems may alter the pharmacokinetics and/or pharmacodynamics of medications, or expose previous neurologic deficits simply as a result of sedation. Delayed arousal, therefore, may arise from structural problems that are pre-existent or new, or metabolic or functional disorders such as convulsive or nonconvulsive seizures. Determining the cause of delayed arousal may require clinical, chemical, and structural tests. Structural problems that impair consciousness arise from a small number of focal lesions to specific areas of the central nervous system, or from pathology affecting the cerebrum. In general, focal or multifocal lesions can be identified by computerized tomography, or diffusion-weighted imaging. An algorithm is presented that outlines a workup for an elderly patient with delayed arousal.

Figure 1

The ascending arousal system in the brainstem consists of two branches: the first is an ascending pathway to the thalamus and cerebral cortex (yellow), and the second bypasses the thalamus, activating neurons in the lateral hypothalamic area and basal forebrain, and throughout the cerebral cortex (red).

Figure 2

The regional effects of anesthetics on brain function are shown in humans who were given various anesthetic agents at doses that produced loss of consciousness. The data are a composite of results from different groups of investigators and encompass the study of eight different agents. All images show regional decreases in activity caused by anesthesia compared to the awake state, except the propofol correlation image, which shows where increasing anesthetic dose correlates with decreasing blood flow. The suppressive effects on the thalamus is a common anesthetic effect.

Figure 3

The ventrolateral preoptic nucleus projects to the monoaminergic nuclei (red), including the tuberomammillary nucleus (TMN), the raphe cell groups and the locus coeruleus (LC). It also innervates neurons in the lateral hypothalamus (green), including the perifornical (PeF) orexin (ORX) neurons, and interneurons in the cholinergic (ACh) cell groups (yellow), the pedunculopontine (PPT) and laterodorsal tegmental nuclei (LDT).

Figure 4

The relationship between delta and the recovery from an infusion of fentanyl maintaining a constant concentration of 10 ng/ml for 60 minutes. Recovery in 50% of patients (C₅₀) is assumed to occur at concentration of 5 ng/ml. If delta = 10, almost all patients recover at a concentration of 5 ng/ml at roughly the context-sensitive half-time (approximately 23 min.). However, when delta = 2, the mean effect time, derived by integrating the probability of effect curve rises to 130 minutes, with approximately 10% of patients not recovering for 5 hours. From: Bailey JM: Technique for quantifying the duration of intravenous anesthetic effect. Anesthesiology 83:1095–1103, 1995

Figure 5

Age related changes in MAC of inhalational anesthetics, normalized to MAC at 40 years of age. From: Eger EI, 2nd: Age, minimum alveolar anesthetic concentration, and minimum alveolar anesthetic concentration-awake. Anesth Analg 93:947–53, 2001

Figure 6

Context-sensitive 50%, 80% and 90% decrement times for inhalational anesthetics. Note that context-sensitive half-time is analogous to context-sensitive 50% decrement time. From: Bailey JM: Context-sensitive half-times and other decrement times of inhaled anesthetics. Anesth Analg 85:681–6, 1997

Figure 7

Triphasic waves occurring in clusters are evident in the EEG of a patient with hepatic encephalopathy. Electrodes are placed in the 10–20 International electrode convention. All electrodes are referred to C_Z. The electrode positions are in pairs, left then right, from midline anterior to posterior in the upper 10 traces, and from lateral anterior to posterior in the lower 8 traces. Reprinted by permission from Brenner RP. EEG in Encephalopathy and Coma. American Journal of Electroneurodiagnostic Technology 2003;43(3):164–184.

Figure 8

BIPLEDs are evident in the EEG in patient with prolonged hypoglycemia. Electrodes are placed in the 10–20 International electrode convention. The electrodes are arranged in a bipolar montage. The first and third set of 4 electrodes are on the left side of the head, and the second and fourth set of 4 electrodes are on the right side of the head. Within each set the electrodes are arranged anterior to posterior with the first and second sets representing midline electrodes, and the third and fourth sets representing lateral electrodes. The bottom 2 electrode pairs are F_z to C_z, and C_z to P_z. Reprinted by permission from Brenner RP. EEG in Encephalopathy and Coma. American Journal of Electroneurodiagnostic Technology 2003;43(3):164–184.

Figure 9

Generalized non-convulsive status epilepticus in the EEG in patient following cerebral anoxia. Electrodes are placed in the 10–20 International electrode convention. Electrodes are placed in the 10–20 International electrode convention. The electrodes are arranged in a bipolar montage. The first and third set of 4 electrodes are on the left side of the head, and the second and fourth set of 4 electrodes are on the right side of the head. Within each set the electrodes are arranged anterior to posterior with the first and second sets representing midline electrodes, and the third and fourth sets representing lateral electrodes. The bottom 3 electrode pairs are F_z to C_z, and C_z to P_z with the bottom trace the electrocardiogram (ECG). Reprinted by permission from Brenner RP. EEG in Encephalopathy and Coma. American Journal of Electroneurodiagnostic Technology 2003;43(3):164–184.

Figure 10

An algorithm to work-up a patient with delayed arousal. CT, computerized tomography; MRI, magnetic resonance imaging; DWI, diffusion weighted imaging; LFT, liver function tests; Mg, magnesium levels; Mn, manganese levels; and EEG, electroencephalogram.