Kaplan + Sadock's Synopsis of Psychiatry, 11e

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Chapter 1: Neural Sciences

Table 1.8-5 Electroencephalography (EEG) Alterations Associated with Psychiatric Disorders

▲▲ 1.9 Chronobiology Chronobiology is the study of biological time. The rotation of the Earth about its axis imposes a 24-hour cyclicity on the biosphere. Although it is widely accepted that organisms have evolved to occupy geographical niches that can be defined by the three spa- tial dimensions, it is less appreciated that organisms have also evolved to occupy temporal niches that are defined by the fourth dimension—time. Much like light represents a small portion of the electromagnetic spectrum, the 24-hour periodicity represents a small time domain within the spectrum of temporal biology. A broad range of frequencies exist throughout biology, ranging from millisecond oscillations in ocular field potentials to the 17-year cycle of emergence seen in the periodic cicada ( Magici- cada spp.). Although these different periodicities all fall within the realm of chronobiology, circadian (Latin: circa, about; dies, day) rhythms that have a period of about one day are among the most extensively studied and best understood biological rhythms. A defining feature of circadian rhythms is that they persist in the absence of time cues and are not simply driven by the 24-hour environmental cycle. Experimental animals housed for several months under constant darkness, temperature, and humidity continue to exhibit robust circadian rhythms. Mainte- nance of rhythmicity in a “timeless” environment points to the existence of an internal biological timing system that is respon- sible for generating these endogenous rhythms. The site of the primary circadian oscillator in mammals, including humans, is the suprachiasmatic nucleus (SCN), located in the anterior hypothalamus. The mean circadian period gener- ated by the human SCN is approximately 24.18 hours. Like a watch that ticks 10 minutes and 48 seconds too slowly per day, an individual with such a period gradually comes out of synchrony with the astronomical day. In slightly more than 3 months, a normally diurnal human would be in antiphase to the day–night cycle and thus would become transiently nocturnal. Therefore, a circadian clock must be reset on a regular basis to be effective at maintaining the proper phase relationships of behavioral and physiological processes within the context of the 24-hour day. Although factors such as temperature and humidity exhibit daily fluctuations, the environmental parameter that most reli- ably corresponds to the period of Earth’s rotation around its axis is the change in illuminance associated with the day–night cycle. Accordingly, organisms have evolved to use this daily change in light levels as a time cue or zeitgeber (German: zeit, time; geber, giver) to reset the endogenous circadian clock. Regulation of the circadian pacemaker through the detection of changes in illumi- nance requires a photoreceptive apparatus that communicates with the central oscillator. This apparatus is known to reside in the eyes, because surgical removal of the eyes renders an animal incapable of resetting its clock in response to light. The circadian clock drives many rhythms, including rhythms in behavior, core body temperature, sleep, feeding, drinking, and hormonal levels. One such circadian-regulated hormone is the indoleamine, melatonin. Melatonin synthesis is controlled through a multisynaptic pathway from the SCN to the pineal gland. Serum levels of melatonin become elevated at night and return to baseline during the day. The nocturnal rise in melato- nin is a convenient marker of circadian phase. Exposure to light elicits two distinct effects on the daily melatonin profile. First,

Panic disorder

Paroxysmal EEG changes consistent with partial seizure activity during attack in one third of patients; focal slowing in about 25% of patients Usually normal, but EEG indicated in new patient presenting with catato- nia to rule out other causes High prevalence (up to 60%) of EEG abnormalities versus normal con- trols; spike or spike-wave discharges Increased incidence of EEG abnormali- ties in those with aggressive behavior

Catatonia

Attention-deficit/

hyperactivity disor- der (ADHD) Antisocial personality disorder Borderline personality disorder

Positive spikes: 14 and 6 per second seen in 25% of patients Chronic alcoholism Prominent slowing and periodic later- alized paroxysmal discharges Alcohol withdrawal May be normal in patients who are not delirious; excessive fast activity in patients with delirium

Dementia

Rarely normal in advanced dementia; may be helpful in differentiating pseudodementia from dementia

hyperactivity disorder (ADHD), and learning disability subpopulations. QEEG findings in ADHD show that increased theta abnormality fron- tally may be a strong predictor of response to methylphenidate and other psychostimulants and that favorable clinical responses may be associated with a normalization of the EEG abnormality. Cerebral Evoked Potentials Cerebral EPs are a series of surface (scalp) recordable waves that result from brain visual, auditory, somatosensory, and cognitive stimulation. They have been shown to be abnormal in many psychiatric conditions, including schizophrenia and Alzheimer’s disease, thus creating difficulty in using cerebral EPs for differential diagnosis purposes. R eferences Alhaj H, Wisniewski G, McAllister-Williams RH. The use of the EEG in measur- ing therapeutic drug action: Focus on depression and antidepressants. J Psycho- pharmacol. 2011;25:1175. André VM, Cepeda C, Fisher YE, Huynh MY, Bardakjian N, Singh S, Yang XW, Levine MS. Differential electrophysiological changes in striatal output neurons in Huntington’s disease. J Neurosci. 2011;31:1170. Boutros NN, Arfken CL. A four-step approach to developing diagnostic testing in psychiatry. Clin EEG Neurosci. 2007;38:62. Boutros NN, Galderisi S, Pogarell O, Riggio S, eds. Standard Electroencephalography in Clinical Psychiatry:A Practical Handbook. Hoboken, NJ:Wiley-Blackwell; 2011. Boutros NN, Iacono WG, Galderisi S. Applied electrophysiology. In: Sadock BJ, Sadock VA, Ruiz P, eds. Kaplan & Sadock’s Comprehensive Textbook of Psy- chiatry. 9 th ed. Philadelphia: Lippincott Williams & Wilkins; 2009:211. Gosselin N, Bottari C, Chen JK, Petrides M, Tinawi S, de Guise E, Ptito A. Elec- trophysiology and functional MRI in post-acute mild traumatic brain injury. J Neurotrauma. 2011;28:329. HoranWP, Wynn JK, KringAM, Simons RF, Green MF. Electrophysiological corre- lates of emotional responding in schizophrenia. J Abnorm Psychol. 2010;119:18. Hunter AM, Cook IA, Leuchter AF. The promise of the quantitative electroenceph- alogram as a predictor of antidepressant treatment outcomes in major depres- sive disorder. Psychiatr Clin North Am. 2007;30:105. Jarahi M, Sheibani V, Safakhah HA, Torkmandi H, Rashidy-Pour A. Effects of pro- gesterone on neuropathic pain responses in an experimental animal model for peripheral neuropathy in the rat: A behavioral and electrophysiological study. Neuroscience . 2014;256:403–411. Winterer G, McCarley RW. Electrophysiology of schizophrenia. In: Weinberger DR, Harrison PJ. Schizophrenia. 3 rd ed. Hoboken, NJ: Blackwell Publishing Ltd; 2011:311.