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A basic understanding of simple electronics is vital for the student of clinical neurophysiology to better understand how we begin to analyze neurobiological systems. The elements of basic circuits have relevant and tangible application to the way in which we model the behavior of neural systems in the laboratory. This chapter helps to define and assemble these varied circuit elements for the student. This base of understanding is then used to illustrate how simple electronic circuits can filter and amplify biological data. The composition and behavior of commonly used electrodes are discussed, as are the varied montages we use to record and/or display the measured data, as in an EEG. Attention is devoted to digital signal analysis because modern clinical neurophysiology increasingly relies on digitasampling for ease of data analysis and storage. Lastly, electrical safety issues are considered, particularly as they apply to the clinical neurophysiology arena.

Clinical neurophysiological studies are based on the recording of both spontaneous electrical activity, as with the EEG, or with stimulated responses, such as evoked potentials. The electrical signaling within these neuronal circuits is responsible for both the spontaneous and evoked electrical activity that is routinely measured in the clinical neurophysiology laboratory. This chapter will review some of the basic concepts of neuronal signaling that are important to the understanding of clinical neurophysiology.

The neuron is uniquely suited for the transmission of electrical impulses. The neuronal membrane itself allows for charge separation; depending on the permeability of the membrane to a given type of ion, that ion will distribute across the membrane, producing a resting membrane potential, described by the Nernst equation. However, via the sodium-potassium (Na-K) pump, an active electrochemical gradient is maintained across the cell membrane, the magnitude of which can be calculated by knowing the relative concentrations of all the relevant ions, both in the intracellular fluid (ICF) and extracellular fluid (ECF), via the Goldman-Hodgkin-Katz equation. The development of action potentials are dependent on the presence of voltage-gated sodium channels, which open when the membrane itself is partially depolarized through mechanical, electrical, or chemical means. The initiation of an action potential creates a spreading area of voltage change, causing additional nearby channels to open, ultimately leading to the propagation of the action potential down the entire length of the axon. Myelin dramatically speeds the process of neuronal depolarization by producing salutatory conduction. Together, with the complex set of processes at the neuromuscular junction, neural transmission is effectively achieved.

The term “volume conduction” refers to the complex effects of measuring electrical potentials a distance from their source generators. Near-field potentials refer to those recorded in relative close proximity to the detector, whereas far-field potentials refer to those recorded at a considerable distance, as is most commonly the case in evoked potentials. A relative straightforward model of volume conduction can be worked through to assist in better understanding how volume conduction effects can impact the shape of a recorded neuronal potential. In fact, all motor and sensory nerve conduction waveforms are substantially impacted by volume conductive effects. The recording setup of sensory studies (i.e., whether they are bipolar or referential) also impacts the size and morphology of the recorded signals. In addition, the compound motor action potential actually represents a composite of both near- and far-field activity. The morphology of both spontaneous discharges and the motor unit potentials themselves evaluated during needle EMG are, in part, caused by the complex effects of volume conduction.

When an experienced electroencephalographer sits down to review an EEG, whether obtained on a pen/ink-based analog machine or from the cathode ray tube screen of a digital device, a number of mental integrations take place seamlessly. This chapter addresses the “normal” EEG observed in people older than 18 yr of age. Topics to be covered include the normal waking background rhythm (alpha rhythm); beta activity; mu, theta, and lambda waves; activation effects on the EEG; and features of normal sleep.

Various procedures are commonly used in the recording of the EEG in an effort to increase the diagnostic yield of the test. Common methods, such as hyperventilation (HV), photic stimulation, and sleep deprivation, referred to collectively as activation techniques, are traditionally used toward this end. Less common techniques, such as withdrawal of antiepileptic medications, use of specific triggers reported by the patient, and other idiosyncratic methods can be tried as well. This chapter will review methods of activation of the EEG, including HV, photic stimulation, and sleep deprivation. Historical background, physiological mechanisms, standard techniques, and clinical significance will also be reviewed.

The object of this chapter is to familiarize the reader with a number of commonly encountered normal variants of brain-derived EEG activity. The term “normal variant pattern” refers to those rhythms or waveforms that have features reminiscent of either interictal or ictal EEG abnormalities. However, these patterns have been found in a substantial proportion of tracings from healthy subjects and, therefore, are not currently thought to represent pathological entities. It is, therefore, vital that such patterns be appropriately recognized by the EEG reader as normal variants and not erroneously confused for pathological patterns. This chapter addresses four main categories of variant EEG activity:

Despite the advances in neuroimaging technology in recent decades, the EEG is still the cornerstone of diagnostic testing for patients with epilepsy, and it remains the best real-time assessment of cerebral physiological function available. For patients with suspected seizure disorders, the routine EEG is used by clinicians to identify the presence of interictal epileptiform discharges that serve as a marker for epilepsy, and more prolonged ambulatory or inpatient EEG monitoring is used to record completseizures. This chapter reviews interictal epileptiform abnormalities, ictal patterns observed in association with seizures, and periodic epileptiform discharge patterns.

This chapter addresses the related topics of focal and generalized slowing, coma, and brain death. These EEG abnormalities are encountered in a wide range of clinical situations of variable severity. Focal and generalized slowing are both common and highly nonspecific findings in the EEG laboratory. Despite their lack of etiological specificity, EEG slowing and related patterns often bear important implications for both the location of CNS abnormalities and/or the prognosis for neurological recovery.

This chapter provides an overview of the developmental changes in the pediatric EEG from early prematurity through adolescence. The early development of recognizable sleep-wake cycles in the premature infant, the changes that occur around term and the maturation of the EEG in the awake, drowsy, and sleep states are described. Changes in response to routine activation procedures are also described. Figures are provided throughout the text. Discussion of common variant patterns observed in childhood is also provided.