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Effect of clozapine and in neuroleptic-free schizophrenics generic 25mg fildena visa popular erectile dysfunction drugs. Neuropsychopharmacology adjunctive high-dose glycine in treatment-resistant schizophre- 1997;17:141–150 discount fildena 50mg amex erectile dysfunction surgical treatment options. D-serine added to clozapine matergic neurotransmission by ketamine: a novel step in the for the treatment of schizophrenia. Am J Psychiatry 1999;156: pathway from NMDA receptor blockade to dopaminergic and 1822–1825. Single photon emis- aspartate receptor-mediated neurotransmission in rat prefrontal sion computed tomography in phencyclidine and related drug cortical neurons in vitro. NMDA-depen- mography study of phencyclidine users as a possible drug model dent modulation of CA1 local circuit inhibition. Glutamate modula- cognitive deficits and cortical dopamine dysfunction in monkeys tion of dopamine measured in vivo with positron emission to- after long-term administration of phencyclidine. Science 1997; mography (PET) and 11C-raclopride in normal human sub- 277:953–955. Impaired recruitment of cortical dopamine activation induced by phencyclidine: con- the hippocampus during conscious recollection in schizophre- trasting pattern to striatal response. Activation of fore- mediated N-methyl-D-aspartate receptor antagonism cause brain dopamine systems by phencyclidine and footshock stress: schizophrenia-like oculomotor abnormalities? Reversal of phencyclidine effects the effects of aging on cognition. Annu Rev Psychol 1997;48: by a group II metabotropic glutamate receptor agonist in rats. Autoimmune encephalomyeli- long-term stability of new hippocampal place cell maps by tis ameliorated by AMPA antagonists. Normal aging: regionally specific changed in hippo- tive symptoms in schizophrenia by glycine. Multistability of cognitive placebo-controlled, crossover trial of glycine adjuvant therapy maps in the hippocampus of old rats. Efficacy of high- amino acid receptors in two mouse strains. Neurobiol Aging dose glycine in the treatment of enduring negative symptoms 1993;14:197–206. Declines in mRNA expression of different sub- 90 Neuropsychopharmacology: The Fifth Generation of Progress units may account for differential effects of aging on agonist 252. Circuit-specific and antagonist binding to the NMDA receptor. J Neurosci 2000; alterations in hippocampal synaptophysin immunoreactivity 20:1666–1674. Hippocampal depen- of aged long-evans rats: relationship to spatial learning. Neurosci- dent learning ability correlates with N-Methyl-D-Aspartate ence 1996;74:741–756. Proc Natl Acad Sci USA 1996; receptors and apoptotic neurodegeneration in the developing 3121–3125. GRIGORIADIS HISTORICAL PERSPECTIVES CHARACTERISTICS OF THE CRF PEPTIDE AND GENE SEQUENCES In 1948 Sir Geoffrey Harris first proposed the concept that Amino Acid Sequence and Structure of the hypothalamus plays a primary role in the regulation of CRF the pituitary-adrenocortical axis. Subsequently,during the 1950s,Guillemin and Rosenberg,and Saffran and Schally The sequence of CRF has been determined in a variety of independently observed the presence of a factor in hypo- species including sheep,humans,rats,pigs,goats,and cows. Rat and human CRFs are identical tropic hormone (ACTH,corticotropin) from anterior pi- to one another and differ from ovine CRF by seven amino tuitary cells in vitro. All three CRFs have close amino acid homol- lamic hypophysiotropic factor to be recognized,its ogy and share some biological properties with sauvagine,a chemical identity remained elusive until 1981,when Wylie 40-amino acid peptide that exists in frog skin,and urotensin Vale and colleagues at the Salk Institute reported the I,a 41-amino acid peptide derived from fish urophysis. Just over a decade later,Vale and col- bles rat and human CRF. This initial discovery led to the identification of a ity of the peptide. Studies to determine the solution struc- second receptor subtype (termed CRF2),which has now ture of CRF using proton nuclear magnetic resonance sug- been localized and characterized in a variety of species gest that human CRF comprises an extended N-terminal (see the following). An -helical oCRF(9-41) has been and its related receptor targets. More detailed and compre- demonstrated to be an antagonist of CRF (8),which under- hensive information on CRF is available in recent reviews scores the necessity of the -helical conformation for recep- (3,4) and books (5,6) on the topic. Detailed descriptions of the organization of CRF immunoreactive cells and fibers in rat brain have been published (11–13). Morphologic data clearly indicate that the paraventricu- lar nucleus of the hypothalamus (PVN) is the major site of CRF-containing cell bodies that influence anterior pituitary hormone secretion. These neurons originate in the parvocel- lular portion of the PVN and send axon terminals to the capillaries of the median eminence. CRF is also present in a small group of PVN neurons that project to the lower brainstem and spinal cord; this group of neurons may be FIGURE 7.

Alcohol risk for developing alcohol-related disorders effective fildena 25 mg erectile dysfunction treatment nasal spray, Part 1 buy generic fildena 100mg on-line tramadol causes erectile dysfunction. Benefits and pitfalls encountered in alcohol sensitivity and the inheritance of alcoholism risk. Biol Psychiatry 1999; Psychol Med 1999;29:1069–1081. Does tumor necrosis factor play a role in alco- of ethanol on punished responding in the P and NP rats. The potential pitfalls of a case-controlled Clin Exp Res 1991;15:700–704. Alcohol and the brain: pharmacological insights for ethanol sensitivity in BXD recombinant inbred mice. Biological, psychological and environmental pre- 31. Ethanol intoxication in dictors of the alcoholism risk: a longitudinal study. J Stud Alcohol Drosophila: genetic and pharmacological evidence for regulation 1998;59:485–494. Selective genotyping studies in human and animal models. Am J Addict 1999;8: for the role of 5-HT2A, 5-HT2C, and GABAA6 receptors and 261–278. Pharmacogenetics of responses to alcohol and genes pilot study. General and specific inheritance of substance abuse search for genes that relate to a low level of response to alcohol. Arch Gen Psychiatry 1998;55: Alcohol Clin Exp Res 2001;25:323–329. An 8-year follow-up of 450sons of sons of alcoholics. The relationships of a family history Alcohol Clin Exp Res 1999;23:1312–1319. The EEG after six domains of life functioning to the development of alcohol alcohol administration in men at risk for alcoholism. EEG, autonomic and subjective tween self-rating of the effects of alcohol and alcohol challenge correlates of the risk for alcoholism. J Stud Alcohol 1993;54: results in ninety-eight young men. Meta-analysis of subjective sensitivity to alcohol in electroencephalogram (EEG) and event-related brain potentials sons of alcoholics. A twin study of genetic in daughters of alcoholics: a pilot study and a comparison with influences on the acute adaptation of the EEG to alcohol. The relationship of hol Clin Exp Res 1999;23:494–501. Identification of a Alcohol Clin Exp Res 2000;24:27A. Ser857-Asn857 substitution in DRK1 (KCNB1), population 20. Alcohol chal- frequencies and lack of association to the low voltage alpha EEG lenges in young men from alcoholic pedigrees and control fami- trait. Children of alcoholics exhibit attenu- brain development. Clinical importance of age to alcohol in sons of alcoholics. Alcohol Clin Exp Res 1991;15: at onset in type 1 and type 2 primary alcoholics. Common genetic to alcohol in young adult Jewish men: a pilot study. J Stud risk factors for conduct disorder and alcohol dependence. Behavioral out- graphic responses to alcohol challenge in Native American Mis- comes among children of alcoholics: during the early and middle sion Indians. Genetic-environ- Chapter 98: Vulnerability Factors for Alcoholism 1409 mental interaction in the genesis of aggressivity and conduct to naloxone in sons of alcohol-dependent men. Int J Neuropsychopharmacol tary adrenal axis functioning and cerebrospinal fluid cortico- 1998;1:153–168.

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Preliminary findings of antistreptococcal antibody titers and basal ganglia volumes in tic order 50mg fildena with visa erectile dysfunction drug overdose, obsessive-compulsive discount 150 mg fildena erectile dysfunction protocol video, and attention deficit/hyperactivity disorders. Multivariate analysis of variance assessing the strength of the association of diagnosis-by-antibody interactions with basal ganglia volumes. Increased anterior cingulate volumes were in- posterior cingulate or dorsolateral prefrontal cortical vol- versely correlated with reduced striatal volumes in OCD umes between pediatric OCDpatients and controls (88). Oculomotor response inhibition abnormalities Thus, prefrontal cortical abnormalities in pediatric OCD also correlated with increased anterior cingulate volumes may be localized to ventral prefrontal anterior cingulate cir- and reduced striatal volumes in pediatric OCDpatients cuits, particularly in younger patients. Chapter 113: Imaging and Neurocircuitry of OCD 1629 FIGURE 113. Mean response suppression failures for nondepressed, psychotropic medication-naive pediatric patients with obsessive-compulsive disorder (OCD) and normal controls performing the antisaccadic task. Lines through distributions represent the mean value. Oculomotor response inhibition abnormalities in pediatric obsessive- compulsive disorder. Temporal Cortex subtle abnormalities in this circuitry. It should be noted that it is often difficult to distinguish the amygdala and The temporal limbic structures, comprising the amygdala hippocampus even at the histologic level (132). This function Thalamus undergoes striking changes throughout childhood, adoles- cence, and early adulthood (126,127). Medial orbital frontal Volumetric abnormalities in ventral prefrontal cortex and cortex, anterior cingulate cortex, and ventral striatum re- the striatum in pediatric OCDpatients led to our studying ceive dense afferent projections from limbic regions, includ- the thalamus, the final subcortical input to frontal cortex. Jenike and co-workers (84) reported no significant differ- Initial MRI investigation in adult OCDpatients and ences in thalamic volume in adult OCDpatients, many of healthy controls revealed no significant differences in mesio- whom had been treated with psychotropic medication and temporal lobe brain structures (84,95,105). In contrast, Gilbert and co- investigation by Szesko and colleagues (107) using criteria workers (76) demonstrated significantly increased thalamic from postmortem histologic analysis (129) with a semiauto- volume as measured by volumetric MRI in 21 treatment- mated computerized system (130) demonstrated bilateral naive, pediatric OCDpatients compared to 21 age- and reductions in amygdala volume in OCDpatients as com- sex-matched healthy controls (Fig. No significant differences be- callosum and anterior cingulate cortex, volumetric abnor- tween OCDpatients and controls were observed in the hip- malities in the thalamus were particularly pronounced in pocampus. After mono- Recent investigation in pediatric OCDpatients has also drug therapy with the SSRI, paroxetine, thalamic volumes implicated the amygdala (87,91). Specifically, Rosenberg decreased to levels comparable to those observed in healthy and associates (87) reported reduced putamen but not cau- children. Reduction in thalamic volume was positively cor- date volumes in treatment-naive pediatric OCDpatients. In contrast, served after temporal lobe lesions (131). In pediatric OCD thalamic volume did not decrease after 12 weeks of CBT patients, a positive correlation was observed between puta- in 11 treatment-naive pediatric OCDpatients who received men and amygdala volumes but not amygdala and caudate no adjunctive medication treatment (133). Subsequent investigation also revealed signifi- changes were observed in total brain volume, the striatum, cant differences between pediatric OCDpatients and con- or anterior cingulate cortex with either CBT or paroxetine trols in the size of the splenium, the region of the corpus treatment. How- tical development and activity (134), thalamic volumetric ever, direct measurement of whole temporal lobe, amygdala, reductions in pediatric OCDpatients may be specific to and hippocampal and superior temporal gyrus volumes SSRI treatment as opposed to a generalized treatment re- failed to reveal any significant differences between pediatric sponse or spontaneous resolution of symptoms. Per- It should be noted that the techniques utilized in these haps, volumetric abnormalities of the amygdala only be- investigations were unable to discriminate specific subdivi- come apparent later in development. Thus, we were unable to localize methods may not have been sensitive enough to distinguish changes to specific thalamic target fields. The dorsomedial 1630 Neuropsychopharmacology: The Fifth Generation of Progress A B C FIGURE 113. A: Corpus callosum area (A) in pediatric (left [•, MMM, normal controls; , ----------, OCD patients. Reprinted from Rosenberg DR, Keshavan MS, Dick EL, et al. Corpus callosal morphology in treatment naive pediatric obsessive-compulsive disorder. Prog Neuropsychopharmacol Biol Psychiatry 1997;21: 1269–1283. Retrocallosal white matter abnormalities in patients with obsessive-com- pulsive disorder. B: Anterior cingulate volume in pediatric (left [ , ⋅⋅⋅⋅⋅⋅⋅⋅⋅⋅, controls (r. Toward a neurodevelopmental model of obsessive-compulsive disorder. Orbital frontal and amygdala volume reduc- tions in obsessive-compulsive disorder.

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Research using rodents adminis­ tered electroconvulsive shock (ECS) and examining the CSF Salzman asserts that the psychiatric community continues of patients receiving ECT has supported a relationship be- to show ambivalence toward ECT and ECT research has tween increases in neuropeptides during the convulsive suffered as a consequence (10) order fildena 100 mg amex erectile dysfunction boyfriend. According to the diencephalic hypothesis fildena 150 mg generic beta blocker causes erectile dysfunction, steps within the NIMH to address these issues and provide ECT seizures that have a longer duration, and ECT param­ more focused research in ECT (10), an understanding of eters that are more effective at stimulating the diencephalic the basic mechanisms by which ECT exerts its effect is still structures (i. This fact is an irony given that ECT is one of the and high-dose greater than low-dose ECT), therefore, few treatments in psychiatry that was theoretically based would be more effective in treating depression. Although the original hypothesis that epilepsy and Both of these assumptions have been questioned recently. Although the acute release of One of the most confusing aspects of accepting ECT as neuroendocrine markers did correlate with the type of sei­ a treatment for depression in the lay public and patients is zure administered and seizure duration, the expected corre­ the inability of clinicians to clearly explain how ECT is lation between the acute surge in plasma oxytocin, vasopres­ effective in relieving symptoms of depression. Patients have sin (19), or prolactin (20), and clinical response to ECT difficulty understanding how a treatment that is so seem­ was not shown in studies of depressed patients receiving a ingly toxic to the brain (i. ECT have focused less on the quantitative analysis of seizure However, the antidepressant medications have a number of duration and more on the relationship between a qualitative other effects on a variety of neurotransmitters, regulatory analysis of the ictal and postictal seizure morphology to hormones, and cellular mechanisms. ECT-induced seizures have a The mechanism by which a convulsive stimulus acts as characteristic pattern of hypersynchronous neuronal dis­ one of the most powerful antidepressants is equally complex charge with excitation of cortical neurons during the initial but the explanation may be as simplistic: ECT works by tonic phase, followed by alternating excitatory and inhibi­ increasing natural brain substances that decrease the excita­ tory effects in the clonic phase, and finally postictal suppres­ bility of the brain. The unique therapeutic action of ECT sion owing to inhibition and neuronal hypoexcitability. Seizure termination is an tered, and the stimulus waveform (23). A number of features active process that underlies the therapeutic mechanism of of the ictal EEG seizure that demonstrate a more intense the treatment. This idea is elaborated on in the following seizure predict clinical response to ECT. The initial finding was that an ECT seizure had to characteristics have been used to predict the efficacy of an continue for at least 25 seconds to be therapeutic (13) and ECT course (22,25–27), or more precisely these variables the patient had to accumulate a minimal number of seconds can be used to predict when a seizure is not adequate. Inade­ of EEG seizure time during a course of ECT (14). Chapter 76: Electroconvulsive Therapy 1099 Analysis of the EEG morphology has been used to deter- 1 minute and there is an active inhibitory process in the mine seizure intensity (26). Clinicians can be trained to interictal and postictal states evident by the development of visually inspect the EEG strips during ECT and determine slow or delta waves and decreases in the CBF and metabolic the adequacy of the seizure by evaluating the amplitude of uptake of glucose. The anticonvulsant properties of ECT the ictal EEG relative to baseline, symmetry of right and are hypothesized to occur because of enhanced transmission left hemispheric EEGs, distinct spike and wave pattern, and of inhibitory neurotransmitters and neuropeptides (e. Both the Thymatron GABA and endogenous opioid concentrations) and are an DGx ECT device (Somatics Inc. The magnitude of the seizure threshold increase is greater Although further testing of the clinical use of the computer- in more effective methods of administering ECT (i. Clinically, Sackeim in patients administered UL ECT, in determining if a sei­ cites unpublished data that the patients who return to an zure is adequate (24,27,29). However, nism of ECT is research correlating functional brain imag­ it is unclear whether the return of the seizure threshold to ing with response to ECT. Studies have shown an increase baseline occurs after an acute course of ECT in all patients in cerebral blood flow (CBF) up to 300% of baseline values or only in patients who relapse. The duration of the seizure with an accompanying increased permeability of the is also decreased over a series of treatments and is another blood–brain barrier and increased cerebral metabolic rate indication of the anticonvulsant effect of ECT. However, (CMR) up to 200% during the ictal period (30). In contrast, seizure duration is not related to efficacy unlike seizure CBF decreased to levels below baseline (31) or returned to threshold (43). Inhibitory processes include the early onset with clinical response, Nobler and colleagues (34) found a of high amplitude slow-wave activity after the tonic phase correlation between decreased CBF in the immediate postic­ of the seizure and bioelectric postictal suppression processes tal period and clinical response. The efficacy of ECT has been correlated included 54 depressed patients imaged using the Xenon with the early onset of these inhibitory processes, a fact that inhalation technique. Patients showed a low baseline CBF supports the anticonvulsant hypothesis. Two elements of compared to matched controls, and their response to ECT seizure expression, seizure strength and peak amplitude of was correlated with the further decrease in CBF from base- slow-wave activity, were inversely correlated with seizure line. These changes were greatest in the anterior cortical threshold and the third element, postictal bioelectric regions and the degree of change was correlated with clinical suppression, was not related to seizure threshold (40). Be- improvement on the Hamilton Depression Rating Scale. This finding provides the rationale Nobler and Sackeim (35) point out that decreased CBF in for developing EEG algorithms (see the preceding), increas­ the anterior cortex supports earlier findings by Max Fink ing the stimulus dosing or retitrating the seizure threshold (36,37) and their own group (38) of a relationship between during a course of ECT in patients who are not responding. There During a course of ECT, as in epilepsy, CBF/ CMR are additional data suggesting that the reductions in cerebral increase dramatically during the seizure and decrease below blood flow that occur immediately after ECT may persist baseline in the interictal and postictal states (35).

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