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HILLYARD AND MARTA KUTAS To uncover the neural bases of a cognitive process it is extracellular fluid produce ERPs purchase prednisone 40mg mastercard allergy list, the flow of synaptic cur- important both to identify the participating brain regions rent through neuronal processes produce ERFs prednisone 20mg without a prescription allergy symptoms and headaches, thereby giv- and determine the precise time course of information trans- ing rise to concentric magnetic fields surrounding the cell. Although neu- When a sufficient number of neurons having a similar ana- roimaging techniques based on cerebral blood flow or me- tomic configuration are synchronously active, their sum- tabolism (e. Noninvasive recordings of the lation of generator locations from surface field distributions electrical and magnetic fields generated by active neuronal is known as the inverse problem, which typically has no populations, however, can reveal the timing of brain activity unique solution. However, the validity of inverse source related to cognition with a very high, msec-level resolution. In general, sensory, motor, or cognitive events are known as event- the localization of active neural populations is more straight- related potentials (ERPs) and the corresponding magnetic forward with surface recordings of ERFs than with ERPs, field changes are termed event-related fields (ERFs). Both because magnetic fields, unlike electrical fields, are mini- ERPs and ERFs consist of precisely timed sequences of mally distorted by the physical properties of the intervening waves of varying field strength and polarity (Fig. The general research strategy has been to discover whereas others consider ERP/ERF components to be those the mapping between the components of the waveform and waveform features that are associated with a particular cog- specific cognitive processes that are engaged by a particular nitive process or manipulation (2). When an ERP/ERF component can be shown to be are generated primarily by the flow of ionic currents in a valid index of the neural activity underlying a cognitive elongated nerve cells during synaptic activity. Whereas syn- operation, that component can yield valuable information aptic currents flowing across nerve cell membranes into the about the presence or absence of that operation and its tim- ing with respect to other cognitive events. In many cases, such data have been related to psychological models of the Steven A. Hillyard: Department of Neurosciences, University of Califor- underlying processing operations and used to test alternative nia, San Diego, La Jolla, California. Marta Kutas: Department of Cognitive Science, University of California, theoretical positions. In addition, by localizing the neural San Diego, La Jolla, California. The characteristic waveform of the auditory event-re- latedpotentialfollowingabriefstim- ulus such as a click or tone. The indi- vidual components (peaks and troughs) are evoked with specific time delays (latencies) after stimulus onset. Note the logarithmic time base, which makes it possible to visu- alize the earliest waves (I–VI) gener- ated in the auditory brainstem path- ways. Longer latency negative (N) and positive (P) components are gen- erated in different cortical areas. Dashedlineshowsincreasednegativ- ityelicitedbyattendedsounds(nega- tive difference) or by deviant sounds (mismatch negativity), and dotted line shows N2 and P3 components to task-relevanttargetstimuli. The use of ERP/ERF recordings to evaluate cognitive disorders associated with The P50 and SensoryGating neurobehavioral and psychopathologic syndromes also is re- The refractory properties of the auditory P50 (P1) compo- viewed. In the standard paradigm, pairs of PREATTENTIVE SENSORY PROCESSING auditory stimuli are presented with an ISI of 0. In nents as well, represent sensory-evoked neural activity in general, schizophrenic subjects do not show as large a reduc- modality-specific cortical areas. These evoked components tion in the P50 amplitude to S2 relative to S1 as do normal vary with the physical parameters of the stimuli and in many controls. This refractory reduction of P50 amplitude to S2 cases are associated with the preattentive encoding of stimu- has been interpreted as a sign of preattentive sensory gating, lus features. In the visual modality, for example, the early which occurs because the initial S1 automatically activates C1 component (onset latency 50 to 60 msec) originates an inhibitory system that suppresses responsiveness to S2 (9, in retinotopically organized visual cortex (5) and varies in 10). This inhibitory system presumably prevents irrelevant amplitude according to the spatial frequency of the stimulus information from ascending to higher levels of cortical pro- (6). Similarly, the early auditory cortical components P50 cessing. The abnormally large S2/S1 amplitude ratio for and N100 (and their magnetic counterparts, M50 and P50 seen in schizophrenics was thus considered evidence M100) arise in part from generators in tonotopically organ- for impaired sensory gating, which was suggested to be the ized supratemporal auditory cortex and reflect the encoding principal sensory deficit of the disease process. This pattern of more rapid P50 recovery in schizophrenia In general, ERP amplitudes decrease when the time be- has been widely reported, but there have been some notable tween successive stimulus presentations is made shorter than exceptions that raise questions about the exact conditions the refractory or recovery period of the component under needed to produce the effect (13–15). Although the neural processes underlying ERP refrac- tion, however, is whether existing studies have, in fact, dem- tory effects are not well established, some candidate mecha- onstrated a reliably abnormal S2/S1 ratio of the auditory nisms include synaptic fatigue, active inhibition, and the P50 in schizophrenics. This concern stems from the way the Chapter 32: Event-Related Potentials and Magnetic Fields 429 P50 has typically been measured—as the maximal positive parator process that contrasts current auditory input against amplitude within a time window (e. Such peak measures may be features held in preperceptual sensory memory. This mis- artificially inflated by increased levels of background noise match detection process may represent an early stage in the in the EEG recordings, originating from either intracranial alerting and orienting of the organism toward novel and or extracranial sources. Thus, if a patient group has higher potentially important changes in the acoustic environment. This type of error is more the memory traces of the preceding sounds (23). Indeed, pronounced when measuring the P50 to S2, because its the maximal interstimulus interval (ISI) at which the MMN amplitude is diminished relative to the noise owing to re- can be maintained is of the order of 10 sec, corresponding fractory effects. Reports of increased variability and lower well with behavioral estimates of the duration of echoic reliability of P50 measures in schizophrenics (12,16) suggest memory (19,20). The MMN also can be used to study more that background noise levels are indeed higher in the patient permanent auditory memory traces, such as those for the groups.

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Continue Re-evaluate allograft antihypertensive therapy function and drug therapy Reassess periodically Consider TRAS FIGURE 13-19 Transplant renal artery stenosis (TRAS) buy prednisone 5 mg low price allergy symptoms pressure in head. TRAS accounts for less than 5% of cases of hypertension after transplantation buy generic prednisone 20mg allergy shots grass. N onetheless, TRAS should always be considered in patients with refractory hypertension who develop renal insufficiency after addition of an ACEI to the therapeutic regim en. Although noninvasive studies (such as a renal scan with captopril) m ay be helpful in diagnosing TRAS, angiography rem ains the gold standard for diagnosis. Revascularization of the allograft by either surgical or angioplastic techniques m ay im prove renal function and am eliorate hypertension [33,34]. Both tacrolim us and m ycophenolate m ofetil (M M F) cause bloating, nausea, vom iting, and diarrhea in a dose-dependent m anner, particularly when used Nausea and in combination [15,16,25]. Some authors have noted that this rather nonspecific GI toxicity occurs m ore com m only with N eoral® than Drug vomiting Diarrhea Other complications with Sandim m une® (both from Sandoz Pharm aceuticals, East Cyclosporine 4 3 Hepatotoxicity, constipation H anover, N J). Tacrolimus 30 32 Hepatotoxicity, constipation MMF 20 31 Constipation, dyspepsia Azathioprine 12 Rare Hepatotoxicity, pancreatitis FIGURE 13-21 (See Color Plate) Endoscopic image of candida esophagitis with diffuse white exudate (panel A) and colitis induced by cytomegalovirus infection with submucosal hemorrhage, ulcers, and diffuse mucosal edema (panel B). The avail- ability and common use of effective prophy- laxis against acid-peptic disease (eg, H2 block- ers, omeprazole, and antacids) have signifi- cantly reduced the frequency of upper gastrointestinal bleeding. However, infectious agents such as cytomegalovirus and candida continue to be problematic, particularly in the setting of the more intense immunosup- pression afforded by drugs such as mycophe- A B nolate mofetil (M M F) and tacrolimus. FIGURE 13-22 H istologic im age of chronic active hepatitis secondary to infection with the hepatitis C virus (H CV). N ote the periportal distribution of the lymphocytic infiltrate. Recent identification of HCV has caused intense reevaluation of the causes, frequency, and natural history of liver disease in renal allograft recipients. As the percentage of patients with end-stage renal disease who are infected with the hepatitis B virus has diminished, HCV has become the most problematic cause of liver disease. In recipients with H CV antibodies, im m unosup- pressive therapy m ay potentiate liver injury from the virus and accelerate the course of tim e over which cirrhosis develops. Nonetheless, in patients who desire transplantation and have well- preserved liver function, little evidence exists of better longevity on dialysis. HCV can be transmitted easily from donor to recipient in solid organ transplantation. Because kidney transplantation is not a life-saving procedure, m ost transplant centers choose not to use kidneys from donors who are infected with H CV. Previously, liver disease was thought to be a com m on cause of death in renal allograft recipients. As blood transfusions have becom e less com m on in the dialysis population and hepatitis B virus less prevalent, the risk of death owing to hepatic disease seems to have diminished. Unfortunately, therapies for HCV-related hepatitis (interferon- ) have proved to be of questionable efficacy and m ay stim ulate rejection of the renal allograft [35–37]. Bone densitom etry M agnetic resonance imaging of osteonecrosis. H ere, a renal transplant fem oral head but can affect any weight- early after transplantation. M etabolic bone recipient dem onstrates m arked osteoporosis, bearing bone. The m ost debilitating com pli- disease in this setting is usually multifactorial. This decrease reflects better have som e degree of renal osteodystrophy, options (including bisphosphonates, estrogens, management of calcium and bone homeostasis exacerbated in som e cases by the im pact of and thiazides) have offered hope of preserving during long-term dialysis and less intense alum inum toxicity or 2-m icroglobulin or even increasing bone m ass [38,39]. Patients with diabetes are BM D— bone m ass density. Administration of corticosteroids lim ited (pain m anagem ent while awaiting and cyclosporine also contributes to bone progression to the need for joint replacement). Although biochemical evidence of M agnetic resonance im aging is a sensitive secondary hyperparathyroidism usually diagnostic m ethod, allowing detection of resolves during the first year after transplan- osteonecrosis at a very early stage. Asterisk— values significantly different from those at the time of transplantation. Gout is the clinical m anifestation of hyperuricem ia. After transplantation, cyclosporine can exacerbate hyperuricem ia, and severe gout can be problematic even in the presence of chronic immunosuppression. M anagement of gouty arthritis usually involves some com bination of colchicine and judicious use of short courses of nonsteroidal anti-inflammatory drugs. Concomitant administration of allopurinol and azathioprine can cause profound bone m arrow suppression and is avoided by m ost physicians who treat transplant recipients.

Neural correlates of sure influences local cerebral blood flow in the rat hippocampus discount 5mg prednisone with visa allergy symptoms to eggs. Participation of the dorsal hippocam- tron emission tomography study buy prednisone 40mg with amex allergy fatigue. Biol Psychiatry 1999;45: pus in the glucocorticoid feedback effect on adrenocortical activ- 806–816. Brain correlates of of response to behavioral therapy versus pharmacotherapy in an unexpected panic attack: a human positron emission tomo- obsessive-compulsive disorder. Hippocampal remodeling habituation to repeated complex visual stimulation studied with and damage by corticosteroids: implications for mood disorders. Brain systems mediating robbery re-experience: affective memories studied with PET. Classical fear conditioning in functional presentations of facial stimuli on human brain function: an neuroimaging. Temporal lobe abnormali- involvement in human aversive trace conditioning revealed ties in panic disorder: an MRI study. Biol Psychiatry 1990;27: through event-related functional magnetic resonance imaging. Amygdala activity at encoding neural networks in humans: a PET study of pavlovian condi- correlated with long-term, free recall of emotional information. Psychophysiology 1993;30: substrates for anxiety and fear: clinical associations based on 126–130. Functional neuroanatomy macology: the fourth generation of progress. New York: Raven, of visually elicited simple phobic fear: additional data and theo- 1995:387–396. The amygdala and individ- Psychiatry 1998;44:1264–1276. Current approaches to etiology and pathophysiology with panic disorder and comparison subjects. Brain activity during 964 Neuropsychopharmacology: The Fifth Generation of Progress transient sadness and happiness in healthy women. Brain activation in PTSD regional cerebral blood flow during transient self-induced sad- in response to trauma-related stimuli. Differential limbic- and extinction of freezing and fear-potentiated startle following cortical correlates of sadness and anxiety in healthy subjects: electrolytic lesions of medial prefrontal cortex in rats. Decreased brain bat-related posttraumatic stress disorder. Biol Psychiatry 1996; GABA(A)-benzodiazepine receptor binding in panic disorder: 40:1091–1099. Patterns in behavioral neuroanatomy: associa- tary-adrenocortical axis. Phila- tine on regional cerebral blood flow in obsessive-compulsive delphia: FA Davis, 1985:1–70. Brain mechanisms glutamatergic changes with paroxetine therapy for pediatric ob- in human classical conditioning: a PET blood flow study. Am Acad Child Adolesc Psychiatry roreport 1995:6:1723–1728. Differential contribution of dorsal and vation detected with echo-planar functional magnetic resonance ventral medial prefrontal cortex to the acquisition and extinction imaging. Extinction of emo- malities in obsessive-compulsive disorder: a quantitative mor- tional learning: contribution of medial prefrontal cortex. A differential neural tive serotonin reuptake inhibitors in the spectrum of anxiety. Conscious and unconscious mediation of procaine-induced emotional and psychosensory emotional learning in the human amygdala. Positron emission ity during transient self-induced anxiety and anger in healthy tomographic evaluation of cerebral blood flow during state anxi- adults. Cerebral glucose benzodiazepine receptor uptake in the prefrontal cortex in pa- metabolic rates in obsessive-compulsive disorder. Human amygdala activa- metabolic differences in patients with panic disorder. Neuropsy- tion during conditioned fear acquisition and extinction: a chopharmacology 1990;3:261–272. Neural activation during metabolic asymmetries replicated in an independent group selective attention to subjective emotional responses. Cerebral blood relates of happiness, sadness, and disgust.

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It appears cheap 20 mg prednisone mastercard allergy medicine cetirizine, can trigger symptoms of PMS cheap prednisone 20mg without a prescription allergy report oklahoma, an observation that at first therefore, that like women with PMS, women with a history glance appears discordant with the lack of differences in of PPD experience mood state destabilization in association gonadal steroid levels between women with PMS and con- with changes in levels of gonadal steroids that are without trols. The reconciliation of these observations is found in effect on mood in women lacking a history of PPD. The the second part of the aforementioned study, in which a hormonal changes can trigger the mood state change, but comparison group of women with confirmed absence of only in a context of increased susceptibility to affective dys- PMS received the same protocol of Lupron and hormone regulation. The control women showed no perturbation of mood during Lupron-induced hypogonadism or during Context hormone addback with either progesterone or estradiol, de- spite achieving hormone levels comparable with those seen The differential sensitivity to gonadal steroids seen in in the women with PMS. Women with PMS, therefore, are women with a history of PMS or PPD emphasizes that the differentially sensitive to gonadal steroids such that they response to a biological signal cannot be inferred absent an experience mood destabilization with levels or changes in understanding of the context in which the signal occurs. Gonadal steroids, then, ronments, prior experience, past history of exposure to the are necessary but not sufficient for PMS. With the imminent mapping PMS, but only in women, who, for undetermined reasons, of the human genome, this last contextual determinant be- are otherwise vulnerable to experience mood state destabili- comes of great practical interest as a potential explanation zation (199). In other words, PMS represents an abnormal for the differential response to steroids. Data already exist response to normal hormone levels. Similarly, strain/genetic (and task-dependent) differ- PMS. This literature, however, may be similarly distilled; ences in behavioral sensitivity to allopregnanolone were ob- the evidence for a reproductive hormone abnormality in served by Finn et al. Nonetheless, demonstrated not only intraperson stability of baseline cor- it is difficult to regard as irrelevant the enormous hormonal tisol and feedback sensitivity (to dexamethasone), which excursions occurring during the puerperium (with precipi- suggests a genetic influence (209), but also a higher sensitiv- tous drops of estradiol and progesterone from levels of up ity to exogenously administered glucocorticoid (dexametha- to 15,000 pg/mL and 150 ng/mL, respectively, to hypogon- sone) in association with a polymorphism in exon 2 of the adal levels in just 1 to 3 days). Analagous to our observations glucocorticoid receptor. Association studies suggest a pro- with PMS, it is possible that women with and those without gressively increased rate and severity of prostate cancer as PPD differ in sensitivity to puerperal hormone changes, not the number of cytosine–adenine–guanosine (CAG) tri- in the degree to which they occur. To test this hypothesis, nucleotide repeats in exon 1 of the androgen receptor de- we created a scaled-down model of the puerperium in which creases (210). This observation is accompanied by the recent women received high-dose estradiol and progesterone for 2 observation that androgen receptors with decreased CAG months (superimposed on Lupron-induced gonadal repeats demonstrate increased transcriptional efficiency suppression to permit comparability and stability of levels (211). Steroid receptor polymorphisms, then, may alter the achieved), followed by a blinded, precipitous withdrawal of steroid signaling pathway in such a way as to produce or 1172 Neuropsychopharmacology: The Fifth Generation of Progress contribute to a different behavioral/phenotypic response to forts to illuminate the neurobiology of mood and mood a hormone signal. Androgens: biochemistry, physiology, and clinical significance. New York: John Wiley and Sons, 1956: may yield markedly different phenotypic expressions of the 9. The effects produced on man by subcuta-´ neous injections of a liquid obtained from the testicles of ani- Hormones as Therapeutic Agents mals. An emerging area of interest is the use of gonadal steroids 4. Basic guides to the mechanism of in PPD, the evidence for a reproductive hormonal abnor- estrogen action. A receptor molecule for estrogens: isolation (214–216; Schmidt et al. Some from the rat uterus and preliminary characterization. Estrogen receptor- studies have observed lower plasma LH levels in postmeno- associated proteins: possible mediators of hormone-induced pausal depressed women, but no consistent group-related transcription. Co-activator and co-repres- Similarly, despite claims for the antidepressant efficacy of sor regulation of the agonist/antagonist activity of the mixed antiestrogen 4-hydroxytamoxifen. Mol Endocrinol 1997;11: estrogen dating back to the nineteenth century (4,221), re- 657–666. The partial agonist and postmenopausal women (222–226) have been inconsis- activity of antagonist-occupied steroid receptors is controlled tent (227–229) and have been compromised by the failure by a novel hinge domain-binding co-activator L7/SPA and the to diagnose depression (as opposed to depressive symptoms, co-repressors N-COR or SMRT. Transcriptional activi- teristics), the failure (with one exception; see ref. Endocrinology 1997; ment of psychotropic efficacy, and the failure to assess effi- 138:2900–2908. Steroid hormone receptors compete for factors that mediate their enhancer func- tentially important distinction identified by Montgomery tion. Differential effect of forms A and B of that demonstrated the antidepressant efficacy of estradiol in human progesterone receptor on estradiol-dependent transcrip- perimenopausal women with major and minor depression tion. The antidepressant effects were further shown gen receptor subtype: a novel mediator of estrogen action in the subsample of women with no hot flushes, so that in neuroendocrine systems.

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