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By Y. Nafalem. Greensboro College.

Recent work order aceon 4mg line, for physiology of mental disorders may guide theoretical models example generic aceon 2mg on line, suggests that the amygdala has significant ana- of behavioral state regulation in diverse mental disorders tomic connections and recently established modulatory ef- (see Chapters 128 to 133) order aceon 2 mg without prescription. This pattern of activation is super- play in cortical arousal order 8mg aceon mastercard. Several studies have discovered that sleep deprivation is asso- ciated with a global reduction in metabolism with some Mechanisms Underlying Behavioral State preference for the prefrontal cortex. This reduction is mag- Changes: Evidence from Human Sleep nified with successive nights of sleep deprivation. These Imaging Studies changes have recently been shown to play a role in the cognitive alterations associated with sleep deprivation (31). The advent of brain imaging methods that can be used to study the functional neuroanatomy of human sleep has recently created a venue for linking preclinical work with human sleep electrophysiology. Several models of sleep/wake regulation attempt to define parameters that may influence the probability at any point Global Changes in Brain Function across in the day that sleep may occur. One such model is the two-process model described by Borbely (32). One process, Behavioral States called process S, describes a homeostatic sleep process. As sleep deprivation in- blood flow or metabolism ranges from 10% below to 41% creases, for example, process S increases and amplifies sleep above levels obtained during wakefulness (23,24). The second process, process C, varies through- report cited a positive correlation between waking global out the day in relation to a sinusoidal circadian phase across and regional cerebral blood flow and slow wave sleep mea- a 24-hour day. The intensity of this sleep propensity is unre- sures from the subsequent night of sleep (25). The authors lated to the amount of prior wakefulness. The sleep parame- interpreted these findings as reflecting an energy conserva- ter most affected by this process is process C; nonsleep corre- tion or restorative role for slow wave sleep. These changes garding forebrain function in information processing. Buz- are consistent with preclinical studies showing reductions saki (33) emphasized a two-stage model of waking hippo- in brainstem, basal forebrain, and hypothalamus sources of campal memory trace formation and suggested parallels for ascending activation. Karni and associates and Wilson and McNaughton in ascending activating structures. Llinas and Pare (34) suggest that wakefulness and asleep at night. In one study, subjective sleep differing only in the degree to which external stimuli are quality was rated worse by patients with major depression capable of modulating the global brain state. They suggest than by patients presenting with a chief complaint of insom- that these oscillations serve the purpose of generating an nia or other sleep disorder patients. Whereas insomnia char- internal representation of the world guided by innate predis- acterizes the melancholia of middle age and elderly unipolar positions of the brain to categorize and integrate the sensory depression, younger patients and bipolar depressed patients world in certain ways. During wakefulness, these tem- hypersomnia, however, does not translate into an increased plates are modulated by sensory events. These include increases in sleep to ensure the efficacy of circuits that otherwise may suffer latency and decreases in sleep continuity. Depressed women appear to have relative preserva- from functional brain imaging studies are also reviewed. For tinal polypeptide, and nerve growth factor in the sleep dis- instance, individuals who have severe stressful events pre- turbances in depression remain to be defined. A tryptophan-free diet, secretion rates, a flattening of the circadian rhythms in corti- which depletes central serotonin activity, is noted to de- sol, and elevated cortisol nadir. Given the activating qual- cortical paralimbic structures. Ho and Gillin and colleagues and paralimbic function related to the pathophysiology of (53) demonstrated that whole brain and regional cerebral depression. In contrast to meostatic mechanisms in mood disorders patients, perhaps healthy controls, depressed subjects show large activations secondary to cortical hyperarousal. These areas include anteriorly located paralimbic structures such as the ventral striatum, anterior cingulate cortex, and medial prefrontal cortex. The lower two images show the same comparisons,butindepressed patients. Clark and colleagues (56) found that alcoholism played to clarify this notion. Further, the in order to generate hypotheses about specific brain struc- presence of sleep disruption at 5 months was shown to pre- tures that show a relationship between increased beta power dict relapse by 14 months. Regions that demon- pothesis that schizophrenia is a spillover of the dream state strated significant correlations between beta power and rela- into wakefulness. Finally, in the depressed conflicting with increases, decreases, as well as no change being found (58,59). This study demonstrated a similar treated subjects may reflect effects of medication withdrawal relationship between electrophysiologic arousal and glucose and/or changes related to the acute psychotic state (61). They found that depressed patients who remitted states; and in never-medicated, neuroleptic- demonstrated high pretreatment relative glucose metabolic treated, as well as unmedicated patients (58); however, not rates in the medial prefrontal cortex were more likely to all studies show these deficits. Studies that fail to find differ- respond to sleep deprivation. Other groups have described similar reduc- stable when polysomnographic studies were repeated at 1 tions in delta counts. Consistent with this view, delta sleep abnormalities have been found to correlate with negative symptoms (60) and with impaired outcome at 1 Sleep Deprivation Studies and at 2 years (71). The help clarify the primary nature of sleep abnormalities. A defect in this structure could explain in remitted schizophrenic patients (58). There is evidence (65) that following total sleep dep- context of a neurodevelopmental framework for schizophre- rivation, recovery of Stage 4 sleep is diminished in schizo- nia. Converging evidence suggests a substantial reorganiza- phrenia. Pronounced reductions dysfunction and schizophrenia (66). Thus, the maturational pro- physiology of psychiatric disorders. Tandon and associates tional parameters discussed in the preceding. No association has been seen be- tion of cortical and subcortical brain regions have been ob- tween sleep abnormalities and depressive symptoms (61), served in schizophrenia. Activation of the cholinergic sys- pointing to a thalamocortical dysfunction (64). Studies that have system alterations, are reversed following sleep in schizo- phrenia (80). Disturbances in catecholaminergic mecha- zapine following acute administration (87). Neylan and associates delta sleep has also received some attention. Adenosine, an relapse has larger impairments in sleep. The effects of neuro- amino acid neuromodulator has drawn increasing interest leptic discontinuation continued to worsen from 2 to 4 in recent years as a possible endogenous sleep-promoting weeks of a neuroleptic-free condition, and did not correlate agent, as it tends to accumulate during waking hours (83). These findings highlight the im- Adenosine agonists have been proposed as possible thera- portance of controlling for medication state in investigation peutic agents in schizophrenia (84). Chapter 134: Sleep Disturbances and Neuropsychiatric Disease 1955 Future Directions significant losses or in acute depressive episodes. First, functional brain imaging studies sug- velop an episode of major depression. Second, sleep architecture changes dramati- pressed bereaved volunteers. These findings are similar to cally during development; sleep studies during development those of elderly patients with recurrent unipolar depression. These findings are similar to those of Cartwright for schizophrenia are likely to be fruitful (92).

A role for somatosensory tions of the MRI analysis pipeline environment at the Brain cortices in the visual recognition of emotion as revealed by three- Imaging Centre (BIC) of the Montreal Neurological Insti- dimensional lesion mapping purchase aceon mastercard. The key conceptual elements of this environment are 17 and 18 brought into stereotaxic space-where and how variable? The use of stereotaxic space for consolidation of large 4 cheap aceon 8 mg. High-dimensional image registration using symmetric priors buy generic aceon on-line. Neuroimage 1999;9(6 pt 1): ensembles of MRI data into a common spatial frame for 619–628 aceon 2mg for sale. Fully automated 3D image preprocessing and segmenta- ods. Identifying global 312 Neuropsychopharmacology: The Fifth Generation of Progress anatomical differences: deformation-based morphometry. Automatic 3D model- based neuroanatomical segmentation. Cortical con- classification in MRI: a three-dimensional multispectral discrimi- straints for non-linear cortical registration. In: Proceedings of 4th nant analysis method with automated training class selection. J International Conference on Visualization in Biomedical Comput- Comput Assist Tomogr 1999;23(1):144–154. Automatic 3D registra- and temporal lobe epilepsy: MR imaging deformation-based seg- tion of MR volumetric data in standardized Talairach space. Radiology 2000; Comput Assist Tomogr 1994;18(2):192–205. Enhancement of MR in fully automated non-linear spatial normalization of 3d brain images using registration for signal averaging. Brain segmentation and the struction of a realistic digital brain phantom. Human frontal neocortex: an MRI-based analysis of volume and variance. Hippocampal morphome- functional brain asymmetries in human situs inversus totalis. Improved localization of cortical activity post-processing evaluation. In: Proceedings of the 4th International by combining EEG and MEG with MRI cortical surface recon- Conference on Visualization in Biomedical Computing, VBC 1996. MRI simulation-based evalua- decades and the challenges ahead. IEEE Trans Pattern Analysis tion of image processing and classification methods. Statistical sulcal atlas of normal human neuroanatomy. Proceedings of the 3rd shape comparisons: application to the detection of genetic en- International Conference on Functional Mapping of Human Brain, 1997. Automated extraction Record, Nuclear Science Symposium and Medical Imaging Confer- and variability analysis of sulcal neuroanatomy. Sulcal variability trials of multiple sclerosis: comparison of image processing tech- of twins. Lesion segmentation and and matching in magnetic resonance imaging. Visualization in manual warping to a reference brain: intra- and interobserver Biomedical Computing 1994. Neuroim- II: Inflation, flattening, and a surface-based coordinate system. Quantitative 24: Automated 3D Analysis of Large Brain MRI Databases 313 in vivo measurement of gyrification in the human brain: changes intensity nonuniformity correction methods for MRI. A non-parametric method parcellation of human cerebral white matter and nuclei ii. A probabilistic built 3d morphometric brain atlas: study of cerebral ventricle ribbon model for shape analysis of the cerebral sulci: application shape. J Comput Assist Tomogr 1998;22(6): tional Conference, VBC 1996 Proceedings. Digital brain atlases brain: 3-dimensional proportional system: an approach to cerebral [letter]. Stat Methods Med Res 1997;6(3): correcting for variable cortical morphology in functional imaging 267–299. IEEE International Conference on Ro- mesh algorithms for creating a probabilistic 3d surface atlas of botics and Automation Symposia Proceedings (Cat. A voxel-based mor- ing three-dimensional images of the brain. IEEE Trans Med Imag- phometry study of semantic dementia: relationship between tem- ing 1996;15(4):402–417. Corpus callosum shape and and surface anatomy using magnetic resonance imaging. Psychia- size in male patients with schizophrenia [see comments]. Finding parametric representations of gray matter in patients with schizophrenia and healthy control the cortical sulci using an active contour model. J Neuropsychiatry Clin Neurosci 1998; 1997;1(4):295–315. Stutt- of human cerebral cortex using a surface-based atlas. Functional and struc- paracingulate sulci: pattern, variability, asymmetry, and probabi- tural mapping of human cerebral cortex: solutions are in the listic map. Cerebellar mor- neural pathway in children and adolescents. Science 1999;283: phology as a predictor of symptom and psychosocial outcome in 1908–1911. Quantifying variability in anatomical differences in human primary auditory cortex: proba- the planum temporale: a probability map. Cerebral Cortex 1999; bilistic mapping and volume measurement from MR scans. Volumetry of hippocampus statistical analysis for CBF activation studies in human brain. J and amygdala with high-resolution MRI and three-dimensional Cereb Blood Flow Metab 1992;12:900–918. A voxel-based method longitudinal magnetic resonance imaging study. Arch Gen Psy- for the statistical analysis of gray and white matter density applied chiatry 1999;56(7):649–654. Automatic quantification struction of the human central sulcus reveals a morphological of multiple sclerosis lesion volume using stereotaxic space. Proceedings of the 4th International Conference on Visualization in 66. A comparison of retrospective Biomedical Computing, VBC 1996. SHULMAN In the last 5 years there has been a renewed interest in the tory and excitatory neuronal function requiring energy. Ob- role of metabolism in supporting brain function. Much of servation of a regional increase or decrease of the functional this interest is based on the development of functional posi- imaging signal is not sufficient to distinguish these possibili- tron emission tomography (PET) and magnetic resonance ties. Glia also requires energy, and the relationship between imaging (MRI). Although often incorrectly described as di- its energy demands and neuronal activity remains to be es- rectly mapping neuronal activity, both functional PET and tablished. Given these uncertainties about the meaning of MRI actually measure changes in either glucose metabolism the signal at a neuronal level, the validity of functional imag- or physiologic parameters coupled to glucose metabolism ing as a tool for studying mental processes has been largely such as blood flow and volume (1). A major limitation in established based on agreement with prior expectation from interpreting functional imaging is that the relationship be- psychological paradigms (3,5).

W ith the enor- mous expansion of travel and immigration purchase aceon online pills, the world has become Ta global village order 8 mg aceon free shipping. Today 2mg aceon with mastercard, a health problem in a particular region has worldwide repercussions discount aceon 4mg without prescription. Typical examples are the acquisition of malaria in European airports, renal disease associated with herbal medications, and increasing encounters of parasitic infections in immunocompromised persons [1–3]. Lessons learned from the study of tropical diseases have considerably enriched worldwide medical knowledge of the basic and clinical aspects of nontropical diseases. Examples include better understanding of macrophage function in vitro, the role of cytokines in acute renal failure, and the importance of immunoglobulin A deposits in the progression of glomerular disease [4–7]. The so-called typical tropical nephropathies are broadly classified as infective or toxic. Infective nephropathies include renal diseases associat- ed with endemic bacterial, viral, fungal, and parasitic infections. Toxic tropical nephropathies include exposure to poisons of animal origin, such as snake bites, scorpion stings, and intake of raw carp bile, and plant ori- gin, such as certain mushrooms and the djenkol bean. Tropical bacterial infections often are associated with renal complica- tions that vary according to the causative organism, severity of infection, and individual susceptibility. The principal acute infections reported to affect the kidneys are salmonellosis, shigellosis, leptospirosis, melioidosis, C H A P T ER cholera, tetanus, scrub typhus, and diphtheria [8–16]. Renal involvement in mycobacterial infections such as tuberculosis and leprosy usually pur- sues a subacute or chronic course [17–19]. The respective renal pathologies include cosis, which occurs in underdeveloped tropical regions, partic- glomerular, microvascular, and tubulointerstitial lesions. Also described is The pathogenesis of renal complications in tropical bacterial ochratoxin, a fungal toxin often incriminated in the pathogen- infections is multifactorial. The principal factors are direct tis- esis of Balkan nephropathy. Ochratoxin also contributes to pro- sue invasion by the causative organisms and remote cellular and gressive interstitial nephropathy in Africa. The rela- Three ways exist by which parasitic infections cause renal tive significance of the different pathogenetic mechanisms disease: 1) direct physical invasion of the kidneys or urinary varies with the causative organism. Infective Tropical Nephropathies Bacterial Infections CLINICAL M ANIFESTATIONS OF TROPICAL BACTERIAL NEPHROPATHIES Disease Abnormal sediment Proteinuria ARF CRF HUS Hemolysis DIC Jaundice Commonly associated features Salmonellosis +++ ++++ + - + + + + Gastrointestinal Shigellosis + - ++* + + + Neurologic† Leptospirosis ++++ ++++ ++++ - + + + ++++ Hemorrhagic tendency Polyuria‡ Melioidosis +++++ + ++ - Hyponatremia§ Cholera + - Hypokalemia, acidosis Tetanus + ++++ +++ - Sympathetic overflow Scrub typhus + ++ + - + + Diphtheria + + + - Myocarditis, polyneuritis Tuberculosis ++ +/+++ + Retroperitoneal nodes Leprosy ++ +++ + + Lepromas *Associated with Shigella serotype I endotoxin. ARF— acute renal failure; CRF— chronic renal failure; DIC— disseminated intravascular coagulation; HUS— hemolytic uremic syndrome; +— <10%; ++— 10%–24%; +++— 25%–49%; ++++— 50%–80%; +++++— >80%. FIGURE 6-1 Clinical m anifestations of tropical bacterial nephropathies. N ote the wide spectrum of clinical m anifestations that m ay ultim ately reflect on the kidneys [33–35]. AIN— acute interstitial nephritis; ATN— acute tubular necrosis; CGN— crescentic glomerulonephritis; EXGN— exudative glomeru- lonephritis; MCGN— mesangiocapillary glomerulonephritis; MN— membranous glomerulopathy; NG— necrotizing glomerulitis; +— <10%; ++— 10%–24%; +++— 25%–50%. FIGURE 6-2 Spectrum of renal pathology in tropical bacterial infections [36–38]. A B FIGURE 6-3 Glom erular lesions associated with tropical bacterial patient with shigellosis. A, Sim ple proliferative glom erulonephritis in a patient with salm onellosis. D, M em branous nephropathy associated with leprosy. A, Acute tubular necrosis with erythrocyte aggregates in the tubular lum ina in a patient with leptospiro- sis. H ere leptospires (arrow) in the Renal tuberculosis. The subsequent evolution of these pathways m ay lead to different form s of renal injury. The asterisk indicates that the role of hem olysis is augm ented in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency. ATN — acute tubular necrosis; DIC— dissem inated intravascular coagulation; IL— interleukin; N O — nitric oxide; RO M — reactive oxygen m olecules; TN F- — tum or necrosis factor-. FIGURE 6-11 Pathogenetic m echanism s in acute tubular necrosis associated with bacterial infections. N ote the m ultiplicity of factors depending on the bacterial species and their host targets. Viral Infections FIGURE 6-12 90 Clinical m anifestations of renal involvem ent in dengue hem orrhag- 80 ic fever. N ote that proteinuria and abnorm al urinary sedim ent are 70 the m ost com m on m anifestations. Also note the high incidence of 60 hyponatrem ia, like with m any other tropical infections [40,41]. A, M esangial proliferative glom erulonephritis, which usually is associ- ated with deposits of im m unoglobulins G and M and com plem ent 3. N ote the high prevalence of schistosom al, m alarial, filarial, and echinococcal renal com plications in Africa; Echinococcosis S. A, A sheet of Schistosom a haem atobium ova in tissues. Shown is a delayed hypersensi- tivity reaction of the host to soluble oval antigens released from the ova through m icropores in their shells. The granulom a is com posed of m ononuclear cells, a few neutrophils, eosinophils, and fibroblasts, surrounding a distorted egg. B, Bilharzial subm ucous m ass covered by pseudotubercles. The ureters are dilat- ed, with a clear stric- ture at the lower end of the right ureter. Also seen in this patient are bilateral hydroureters with submucous cystic lesions (bilharzial ureteritis cystica). The kidneys show consid- erable scarring, with the right kidney also showing chronic back pressure changes. These erythrocyte necrosis knobs contain novel proteins, m ainly Plasm odium falciparum erythrocyte m em - brane protein (PfEM P), histidine-rich pro- FIGURE 6-21 tein 1, and histidine-rich protein 2, that are The pathogenesis of falciparum m alarial renal com plications. N ote the infection triggers synthesized under the influence of the DN A two initially independent pathways: red cell parasitization and m onocyte activation. These proteins con- subsequently interact, as the infected red cells express abnorm al proteins that induce an stitute the sticky points (arrows) by which im m une reaction by their own right, in addition to providing sticky points (knobs) for parasitized erythrocytes aggregate and clum ping and adherence to platelets and capillary endothelium. TN F- released from the adhere to blood platelets and endothelial activated m onocytes shares in the endothelial activation. EN — electron m icrophoto- interact, a variety of renal com plications develop, including acute tubular necrosis, acute graph. B— B-lym phocyte; CD8— cytotoxic T cell; CIC— circulating im m une com plexes; TH — T-helper cells (1 and 2); TN F- — tum or necrosis factor-. B FIGURE 6-23 Renal lesions in a patient with falciparum m alaria. A, Proliferative and exudative glom erulonephritis, an im m une-com plex–m ediated lesion that m ay lead to an acute nephritic syndrom e, which usually is reversible by antim alarial treatm ent. ATN is seen in 1% to 4% of patients with falciparum m alaria and in up to 60% of those with m alignant m alaria. Often, complement 3, immunoglobulins M and G, and fibrinogen also are seen. Note the pivotal role of + ACDC the monocyte, activated by exposure to para- ADCC – sitic antigens, in stimulating both T-helper 1 Parasite (TH1) and T-helper 2 (TH2) cells. The differ- Eosinophil – + ent cytokine mediators and parasite elimina- + + + + Neutrophil tion mechanisms are shown. B— B-lympho- cyte; -IFN— -interferon; CIC— circulating Complement Antigen immune complexes; GM -CSF— granulocyte- CIC + macrophage colony-stimulating factor; IL-5,13 IL-2 IgM ,E,G,A Ig— immunoglobulin; IL— interleukin. IL-1,6,12 GM -CSF + B TH2 TH1 + + γ-IFN IL-2 IL-4,5,10 FIGURE 6-25 The T-helper1–T-helper 2 (TH 1-TH 2) cell balance that determ ines the clinical expression of different parasitic nephropathies.

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