Clinical review: neuromonitoring - an update

Abstract

Critically ill patients are frequently at risk of neurological dysfunction as a result of primary neurological conditions or secondary insults. Determining which aspects of brain function are affected and how best to manage the neurological dysfunction can often be difficult and is complicated by the limited information that can be gained from clinical examination in such patients and the effects of therapies, notably sedation, on neurological function. Methods to measure and monitor brain function have evolved considerably in recent years and now play an important role in the evaluation and management of patients with brain injury. Importantly, no single technique is ideal for all patients and different variables will need to be monitored in different patients; in many patients, a combination of monitoring techniques will be needed. Although clinical studies support the physiologic feasibility and biologic plausibility of management based on information from various monitors, data supporting this concept from randomized trials are still required.

Figures

Figure 1

Some of the pathological cascades contributing to aggravate neuronal injury after acute brain injury. Initial mechanisms, such as excitotoxicity and mitochondrial dysfunction, initiate damage in the very early minutes/hours; other factors, such as energy dysfunction, edema, and inflammation come into play later in the process. CBF, cerebral blood flow.

Figure 2

Intracranial pressure curve in conditions of normal and reduced compliance. Valuable information on intracranial buffering mechanisms can be extracted from the shape of the curves: when all normal components (peaks) of the intracranial pressure (ICP) curve are clearly evident (left panel), the intracranial system is behaving normally and small increases in volume can still be compensated for. However, when a P2-predominant pattern is displayed (right panel), the intracranial system is less compliant and compensatory abilities are reduced.

Figure 3

Intracranial pressure (ICP), mean arterial pressure (MAP), and cerebral perfusion pressure (CPP) in a patient with traumatic brain injury undergoing bronchoscopy under general anesthesia with myorelaxants. ICP increased to 45 mmHg and CPP decreased concomitantly to 40 mmHg. Broncoscopy was stopped, further sedation given and manual hyperventilation administered briefly. ICP and CPP returned to normal levels.

Figure 4

Transformation of raw electroencephalogram (EEG) into quantitative EEG (qEEG). The center top panel shows a 10 second segment of raw EEG. This EEG segment can be transformed using mathematical processing to separate the waves into major frequency bins with the height of each bin indicating the relative percentage (that is, power) of that frequency during the 10 second epoch (lower left panel). Each bandwidth can be trended on a minute by minute basis to create a variability histogram for that bandwidth for each channel (lower right panel). The alpha bandwidth variability trend is shown (lower center panel).

Figure 5

Lack of variability over time of the percent alpha trend (PAV) is associated with poor clinical outcomes. The daily PAV scores are graphed for those brain injured patients who eventually had a good outcome (top panel) and those that had a poor outcome (bottom panel). The PAV scores tend to remain good or improve day by day in those patients with a good outcome, whereas they remain poor or worsen day by day in those patients with a bad outcome.