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A shock artifact is virtually always seen if the recording electrodes are near the stimulating electrode, or if the leads to either of them are near or touching each other. In some cases, slow, gradual reorientation of the two stimulating electrodes to each other will reduce the artifact by changing the current flow paths on the skin. Examples include the 60cycle signal caused by electromagnetic radiation from power lines; the modified 60-cycle signal of fluorescent lights; the high-frequency, complex discharges from cautery and diathermic equipment; and the irregular waveforms from radio sources, and magnetic resonance imaging power16. Artifacts sometimes are referred to as interference because they interfere with recording the activity of interest. By recognizing the nature and source of an artifact, clinical neurophysiologists can often reduce or eliminate it by changing the electrodes or by changing the location of the equipment or its relationship to the power source. Differential amplification that is used in all modern recording equipment markedly reduces external artifacts. This ratio determines the likelihood of eliminating the artifact by averaging the signal. Changes in amplitude, frequency, and distribution of waveforms occur in continuous waveforms. Frequency change may include the addition of new, abnormal frequencies, the loss of normal frequencies, and either an increase or a decrease in amplitude. The configuration, distribution, size, and pattern of normally occurring discrete events may be changed by disease. The waveforms recorded in clinical neurophysiology are divided into continuous waveforms and discrete waveforms, or events. Continuous waveforms are described by their frequency components, amplitudes, and distributions. Discrete waveforms are described by their individual amplitudes, durations, and configurations as well as by their patterns of occurrence and distribution. A digital averaging method for removal of stimulus artifacts in neurophysiologic experiments. A convenient method for detecting electrolyte bridges in multichannel electroencephalogram and event-related potential recordings. Application of fractal theory in analysis of human electroencephalographic signals. A novel method for automated classification of epileptiform activity in the human electroencephalogram-based on independent component analysis. The characteristics of the waveforms and their alteration with disease are a function of the neural generators producing the waveform. A particular modality of recording in clinical neurophysiology reflects only the alteration in the area of the nervous system generating the activity. These patterns of responses can provide important clues to the underlying disease process. Longer recordings are needed to document infrequent episodes and to define their nature, character, and spread. For abnormal electric activity that occurs only in an outpatient setting or under specific circumstances, ambulatory recordings from a few scalp electrodes are made continuously during activities at home or work (Chapter 12) to obtain a full picture of their nature. Electroencephalograms can also be recorded in other specialized situations, such as in the intensive care unit or operating room, or with computerized quantitation, as described in Chapter 14. Patients being considered for epilepsy surgery require highly specialized recordings, including new correlations with magnetic resonance imaging (Chapter 15). Cortical function can also be assessed with potentials that occur before a planned movement or in response to external stimulation (Chapter 16). The activating procedures consist of hyperventilation, photic stimulation, and sleep recordings. The degree of the slowing depends on age, the vigor of hyperventilation, whether the patient is hypoglycemic, and posture.

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West Nile virus encephalitis most commonly affects the basal ganglia, thalami, medial temporal lobes, and brainstem. Electroencephalography may show various degrees of generalized slowing or other nonspecific abnormalities. A brain biopsy should be considered in an unexplained case of presumed encephalitis, especially where there are enhancing lesions on T1 post-contrast imaging. High-risk exposures to B virus (Cercopithecine herpesvirus 1 associated with macaque monkeys) should be treated with oral valacyclovir 1 gram given three times daily. Suspected cases of rabies must be immediately treated with human rabies immune globulin and rabies vaccine. Finally, arboviral and tick-transmitted infections are reportable to either local health officials or the Centers for Disease Control and Prevention. Prognosis Symptoms of acute encephalitis usually last from a few days to weeks, but recovery can occur slowly over months, and long-term neurologic deficits can persist for years. Frequent sequelae include personality change, cognitive impairment, including short-term memory loss and impaired concentration, headache, anxiety, irritability, tremor, dizziness, and fatigue. Focal neurologic injury sustained during encephalitis can later become a nidus for localization-related epilepsy. Recommendations for prevention of and therapy for exposure to B virus (cercopithecine herpesvirus 1). The management of encephalitis: Clinical practice guidelines by the Infectious Diseases Society of America. In many cases, the viral agent is never isolated but rather presumed based on the season of infection, exposures (eg, swimming pools; laboratory animals, rodents, and insects; sick contacts; travel), and existence of concomitant systemic symptoms (eg, rash, parotitis, diarrhea, or pharyngitis). Symptoms and Signs Fever, headache, and nuchal rigidity are the cardinal symptoms. Deep tendon reflexes may be transiently increased; otherwise, the examination is notable for the absence of abnormal findings on the neurologic examination. Flaccid paralysis with associated meningitis suggests a possible enteroviral infection of West Nile virus. Saliva, throat washings, and stool can be examined for virus, although the diagnostic yield is low except for some enteroviruses. Treatment Viral meningitis is a self-limited disease that requires only supportive treatment with analgesics, antiemetics, and intravenous hydration. Approximately two-thirds of patients have a history of zoster or varicella rash within the last few months prior to presentation. A modest pleocytosis, usually fewer than 100 cells/mm3, predominantly mononuclear cells, is seen in approximately two-thirds of patients. The pathogenesis of viral myelitis is similar to viral encephalitis, and most viruses that cause encephalitis also cause myelitis. Myelitis can concomitantly occur with radiculitis (termed myeloradiculitis) and rarely encephalitis (encephalomyelitis), or both (encephalomyeloradiculitis). Good epidemiologic data on viral myelitis are lacking, in part because it is relatively uncommon and because the underlying cause of most cases is not often determined. Patients should be treated for a minimum of 14 days, with close monitoring of clinical and neuroimaging findings.

Myopathy in Cushing disease is identical to that seen in chronic corticosteroid myopathy (discussed earlier). Symptoms and Signs Patients may have proximal muscle weakness, atrophy, hyperactive deep tendon reflexes, and fasciculations, and in severe cases, this combination may resemble amyotrophic lateral sclerosis. Muscle cramps are occasionally present, and respiratory failure, presumably due to severe hypercalcemia, has been reported. Laboratory Findings Hypercalcemia and hypophosphatemia are usually present and may worsen clinical weakness. Exercise intolerance Muscle weakness Muscle fatigability Myalgias and muscle cramps Myoglobinuria Treatment In primary hyperparathyroidism, surgical removal of the oversecreting gland or adenoma often restores muscle strength. In secondary hyperparathyroidism resulting from chronic renal disease, treatment is more difficult, although administration of vitamin D and reduction in phosphorus intake may be beneficial. Symptoms include progressive proximal muscle weakness often associated with musculoskeletal pain involving the back, hips, or lower limbs and metabolic and radiographic findings consistent with osteomalacia. Low levels of 25-hydroxyvitamin D in the blood are seen, and oral Primary metabolic myopathies are rare conditions caused by a biochemical defect of skeletal muscle energy systems. The biochemical defect may involve carbohydrate metabolism (glycogen storage), lipid metabolism, mitochondria, or the purine nucleotide cycle. Most metabolic myopathies become symptomatic during activities that require increased muscle energy consumption such as exercise (exercise intolerance). Chief symptoms include muscle weakness or fatigability, myalgias, cramps, and myoglobinuria. The patient then immediately begins repetitive, rapid grip exercises (eg, squeezing a ball or hand ergometer) for as long as possible. The test is aborted if the patient develops a cramp or contracture during cuff inflation or exercise. When the patient fatigues, the cuff is released and blood is drawn at 1, 3, 5, 10, and 15 minutes postexercise for evaluation of elevated lactate and ammonia levels. The test should be performed with caution, however, because of the risk of compartment syndrome with ulnar nerve damage or severe rhabdomyolysis that may lead to renal failure. In patients with coenzyme Q10 deficiency, complete recovery may occur with oral coenzyme Q10 supplementation at a dose of 150 mg/d. Acute myoglobinuric renal failure and life-threatening electrolyte disturbances are the most dreaded complications. In severe cases, treatment may require peritoneal dialysis or hemodialysis; patients with milder disease can be treated with aggressive hydration, alkalinization of urine with sodium bicarbonate, and correction of electrolyte disturbances. Patients with myoglobinuria typically present with weakness, myalgias, and edema involving affected muscles. Urine is characteristically brownish to dark red and tests positive for heme by the dipstick test despite the absence of red blood Channelopathies are rare diseases caused by functional disturbances of ion channel proteins as a result of specific mutations. These disorders include the familial periodic paralyses and disorders with myotonia. General Considerations Congenital muscular dystrophies can be separated into two groups: those associated with mental retardation and those associated with normal mental development. There is no specific treatment for the congenital muscular dystrophies, and management focuses on supportive care and rehabilitation therapy. Special Tests for Periodic Paralysis In all forms of periodic paralysis, muscle biopsy may show vacuoles within muscle fibers during severe attacks. These conditions can be distinguished from muscular dystrophies, which are caused by defects of the muscle membrane. Congenital myopathies usually manifest in infancy with delayed milestones or occur in the neonatal period (floppy infant syndrome) or, less commonly, in adulthood. Patients with central core myopathy, even in the absence of clinical weakness, are at risk for malignant hyperthermia during general anesthesia. Most cases are X-linked recessive, although 30% involve spontaneous new mutations.

Diseases

• Yoshimura Takeshita syndrome
• Multiple sclerosis ichthyosis factor VIII deficiency
• Pulmonary venous return anomaly
• Complex regional pain syndrome
• Polyneuritis
• Amelogenesis imperfecta hypomaturation type
• Doyne honeycomb retinal dystrophy
• Oculocutaneous albinism type 2
• Mental retardation multiple nevi

Mask or mouthpiece used with a portable volume ventilator, set in the assist-control mode. The respiratory rate is set on the lowest possible to allow the child to take breaths as needed. Disordered breathing patterns Central apnoea Central hypoventilation syndrome is defined as persistent alveolar hypoventilation and/or apnoea during sleep, and impaired ventilatory responses to hypercapnia. Cessation of breathing occurs for >20 seconds, at times accompanied by bradycardia and cyanosis. Generally, a problem of infancy, but may be seen later in childhood due to acquired brain injury. Idiopathic congenital central hypoventilation syndrome Unexplained by any of the listed possible causes. Seen with autonomic dysfunction-very low heart rate and respiratory rate variability, abrupt asystole, abnormal pupillary reactivity, temperature dysregulation, profuse sweating, swallowing difficulties, and/or oesophageal dysmotility. Late-onset central hypoventilation syndrome Presents following respiratory infection or anaesthesia, which may trigger the need for nocturnal ventilator support. Often preceded by chronic pulmonary hypertension, right heart failure, or respiratory infections with seizures or need for mechanical ventilation. Counsel parents Consider acetazolamide, non-invasive/long-term ventilation as appropriate. History and examination give diagnostic clues, but endoscopy is usually, and imaging may be required. Inspiratory stridor suggests a laryngeal obstruction, expiratory stridor implies tracheobronchial obstruction, and a biphasic stridor suggests a subglottic or glottic abnormality. Most neurological stridor is chronic; other causes include congenital or acquired stenosis or other compressive abnormalities, including webs, rings aberrant vessels, etc. Reduce numbers of unfamiliar bystanders to the minimum consistent with safety of personnel. Ensure any sensory impairments are minimized (find misplaced hearing aids, glasses, etc. Establish a rapport and attempt to reassure verbally and calm down: preferably consistently by the same member of staff. If medication is necessary, oral medication (haloperidol or risperidone) is preferable to parenteral administration. If parenteral administration is considered necessary, intramuscular administration is usually safer and more practicable than intravenous administration in an acute situation. Parenteral haloperidol can cause acute oculogyric crisis or dystonia (treat with procyclidine). Drug treatment Drug treatment of delirium should only be used when essential and then with care, especially in children. Antipsychotics and benzodiazepines can aggravate delirium, exacerbate underlying causes (for example, benzodiazepines worsening respiratory failure) and cause significant unwanted effects. In severe behavioural disturbance, haloperidol may be given intramuscularly or intravenously. Note resting pupil size and symmetry, and briskness and symmetry of the response to light. Do not mistake a dilated non-reactive pupil due an afferent pupillary defect (optic nerve involvement in fracture of the bony orbit) for a fixed dilated pupil due to third cranial nerve involvement in a herniation syndrome (the consensual response is present in the former, absent in the latter. The normal response is to maintain eye orientation in space (eyes move relative to the head and orbits). Intubation and ventilation of the unconscious child will be either for the purpose of securing a safe airway due to an inadequate cough and gag reflex, or for the management of raised intracranial pressure.