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These findings showed significantly greater impairment in orientation discount 0.15mg levlen with amex, lan- would suggest that all depressed patients with coronary ar- guage purchase 0.15 mg levlen, visual–spatial skills, and executive motor and frontal tery disease should be treated, but data indicating the effi- lobe tasks than did nondepressed patients with lesions in cacy and safety of treatments for depression associated with similar locations (59). These findings indicate that major heart disease are very limited. Furthermore, this adverse effect of major depression of depression on physical recovery from stroke (55–57). In on cognitive function lasts for the first year following stroke a study of 25 patients with major or minor depression after (63). Psychoso- cantly greater in the nondepressed than in the depressed cial interventions in post-MI patients with depression or a patients at 2-year follow-up (p. Results tervention, specialized stroke and rehabilitation care, nature should be available by the end of 2001 and should provide and size of the lesion) were controlled (57). This delayed recovery was evident as early as 3 to 6 months following stroke (57,58) (Fig. In addition to the adverse effects of depression on activi- ties of daily living, numerous studies have demonstrated the adverse effects of major depression after stroke on cognitive function (59–62). In a study of 275 patients with acute stroke, the mean Mini-Mental State Examination (MMSE) score for patients with major depression (n 56) was 20. To control for the possibility that the location of lesions, which has been correlated with affect during acute stroke, might have influenced these findings, patients with and without major depression were matched for size and location of stroke le- FIGURE 81. Mini-Mental State Examination scores in patients sion (64). Patients with major depression had significantly with major and minor depression and patients without depres- lower MMSE scores than did their lesion-matched counter- sion. Chapter 81: Depression and the Medically Ill 1183 answers to the question of whether psychosocial treatments should be initiated in patients with post-MI depression. TREATMENT WITH ANTIDEPRESSANTS The evidence for antidepressant use is also limited. Tricyclic antidepressants are known to cause adverse cardiovascular effects, including orthostatic hypotension and slowed intra- ventricular conduction (66,67); therefore, it would not be prudent to use these agents in a population at risk. Pilot studies suggest that the selective serotonin reuptake inhibitors are safe and effective in persons with ischemic heart disease and depression (68,69). The only study of an antidepressant in post-MI patients is that of Shapiro et al. Change in Hamilton Depression Scale (28 items) scores during 12 weeks of treatment for all patients entered in (70). In this study, sertraline (Zoloft) was well tolerated, the study (i. A multicenter study of sertraline is under way in post-MI patients with major depression (SADHART). Currently, at least four double-blinded, placebo-con- tion of 50% in the HAM-D score and no longer meeting trolled studies have examined the efficacy of antidepressant criteria for depression) of patients treated with nortriptyline medication in the treatment of post-stroke depression who completed the trial was significantly greater (77%) than (71–74). In the first study, reported in 1984, 11 patients the response rate of the patients treated with placebo (31%) given nortriptyline showed a significantly greater improve- or fluoxetine (14%). The HAM-D scores of nortriptyline- ment on the Hamilton Depression Scale (HAM-D), the treated patients were significantly lower after 12 weeks of Zung Self-Rating Depression Scale, and the profile of de- treatment than the scores of the patients treated with fluoxe- pressive symptoms assessed by the Present State Examina- tine or placebo, which were not significantly different from tion than did 14 placebo-treated controls (71). The dropout rate of the patients noting that three of the original 14 patients treated with treated with fluoxetine in doses that were increased from nortriptyline dropped out of the study. Two patients be- 10to 40mg during 12 weeks (10-mg increase every 3 weeks) came delirious, and one had a sudden syncopal episode of was significantly higher (9 of 23) than those of the other unknown cause. Often, the symptoms that are used to identify depres- tients with positive Problem Solving Therapies (PSTs) who sion are confused with the underlying symptoms of the were treated with placebo. Another of the selective serotonin reuptake inhibitor citalopram in approach is to replace some of the vegetative symptoms, and a controlled study of 66 patients with stroke. HAM-D and a third approach is to include all symptoms. The inclusive Melancholia Scale scores were significantly better after 3 approach is favored because of its ease of use and practical and 6 weeks of treatment in the 33 patients given citalopram applicability, and it appears to be sufficient.
Thus cheap levlen 0.15mg without prescription, Summary as in the earlier study of Breiter et al purchase levlen 0.15 mg visa. Although several brain regions were commonly ac- tion suggest that a simple DA hypothesis of stimulant effects tivated by both craving and rush, rush-associated ventral (including craving) may be insufficient. One study com- tegmental area/basal forebrain signals rapidly declined while pared the subjective and brain DA response of cocaine users the craving-associated signals in the nucleus accumbens/ (3 to 6 weeks post cocaine) with that of controls after an subcallosal cortex persisted. This partial dissociation sug- injection of methylphenidate, which (like cocaine) blocks gests at least some independence of substrates for these two DA reuptake (51). The early onset of brain activation in cocaine-induced methylphenidate per kilogram was followed by an injection craving is consistent with the priming hypothesis; the partial of 11C-raclopride, a dopamine D2 ligand sensitive to com- dissociation with rush/euphoria is not. Regions of interest were the 'offset' activations correlated with craving is inconsistent striatum, thalamus, and cerebellum (as a comparison region with a simple opponent process view, but conditioned op- devoid of D2 receptors). Subjective measures were taken ponent effects could occur very early in highly experienced 5 minutes before and 27 minutes after methylphenidate. This dual time course of effects may account for lation may have been compromised by taking the subjective some of the variability or inconsistency in effects reported. Interest- With regard to which dopaminergic neuronal elements 1580 Neuropsychopharmacology: The Fifth Generation of Progress are involved in the craving response, the results are mixed. Is cue-elicited cocaine craving more 'druglike' or 'drug- Cocaine-induced craving was unrelated to DAT occupancy. Do the multiple cues surrounding the cocaine However, methylphenidate-induced cocaine craving was experience become linked predominantly to the brief, in- correlated with right striatal and right orbitofrontal in- tense, orgasmic euphoria... These findings could support a postulated predictions for neuroimaging and pharmacotherapies. If DA dysfunction in the striatal–thalamic–orbitofrontal cir- craving to common external (paraphernalia, other users, cuit in cocaine addiction (33,67). One similarity between drug-buying locations, drug talk) or internal (e. As mesolimbic–mesocortical DA system activated by cocaine discussed in the final section, the orbitofrontal cortex is thus itself are also activated during cue-induced craving. In ani- far the only region linked to craving in all three paradigms: mals, cues for cocaine can indeed trigger mesolimbic DA (early) cessation, stimulant administration, and exposure to overflow in nucleus accumbens and amygdala (70) and can drug-related cues. Patients ministration, a role of transmitters other than DA in meth- often describe cocaine-like effects in response to cues, in- ylphenidate-induced effects (both high and craving) seems cluding heart pounding, ear ringing, head buzzing, stomach likely. Methylphenidate alone was insufficient to increase 'flipping,' mild euphoria, a 'taste' of cocaine in the back frontal metabolism, and in other studies by the Brookhaven of the throat, even the 'smell' of cocaine in the room... But what do the brains of methylphenidate did not always result in a subjective high in cocaine users say about the nature of cue-induced cocaine healthy controls (craving was not probed) (68). It tested whether video-induced cocaine IMAGING OF CRAVING DURING COCAINE craving might increase endogenous DA, as indexed by com- CUES 123I-iodobenzamide, in SPECT. After this initial effort, imaging studies ad- (5,6). According to this view, cocaine cues trigger cocaine- dressed the neuroanatomic rather than the neurochemical related subjective and physiologic responses, including crav- substrates of cue-induced craving. Drug-related conditioning can result cocaine cues since 1992. These studies cover a range of 15 18 in both responses similar to those produced by the drug imaging technologies (PET with O bolus, PET with F- itself ('druglike') and responses opposite to those of the fluorodeoxyglucose, fMRI) and include several variations drug ('drug-opposite') (69), likely reflecting a conditioned on the method of presenting drug cues to induce craving. Both kinds of The variations are useful because results obtained in only responses may be of motivational significance. Druglike re- one laboratory, or with one method of cue presentation, sponses to cues reminiscent of the drug ('Wow... Conversely, any replication and ing the user back to the drug. If drug-opposite responses convergence of findings across multiple laboratories and to the cues are uncomfortable (in opiate users, these include methods are very encouraging. BRAIN IMAGING OF CUE-INDUCED COCAINE CRAVING Imaging Cocaine Days of Laboratory Technology Population Cessation Cue Description Resultsa U. Nac/SCC +,^(–) each, same order) OFC 0 DLPFC 0 Cerebellum 0 Medical College of Wisconsin Garavan et al. When controls were studied, the summary reflects significant difference between groups for the drug cue vs.
In Material to Human Material this lateral preparation of Ludwig and Klingler (53) buy levlen 0.15mg otc, the sample tract is the human superior longitudinal fasciculus levlen 0.15 mg discount, which is a In the monkey, it is known how different pathways correlate long, associational, corticocortical connection. Its three compo- with radioactively labeled material, so that their origin and nents are (a) the stem, where axons run compactly and in a bidi- termination can be delineated. Because the stems of the rectional fashion;(b) thesplays or sprays,where theaxons diverge or converge; and (c) the extreme peripheries, the cortical regions major pathways are similar in the monkey and the human, within which the axons originate or terminate. Arrows denote one can extrapolate the origins and terminations of the ob- the bidirectionality of axons within the stem and the splays of served pathways in the human to correlate specific fiber the fiber tract as they run from origin to termination. Drawing these inferences, we can formulate for each individual fiber bun- dle a specific map that characterizes the tract in terms of its connections. Al- though this is currently the case for the nonhuman primate, the status of research in human brain anatomic connectivity Maps of Anatomic Connectivity is very different. A map of anatomic connectivity (MAC) is a set of neuroana- tomic regions interconnected by a particular white matter fiber Studies in Human Postmortem Material pathway, and we can symbolize it as PATHWAYMAC. For instance, the MAC for cingulum bundle (CB) would be In human postmortem material, traditional techniques such CB (Fig. Whereas in the human we have precise MAC as myelin stain, bichromate fixation, and gross anatomic knowledge only of the stem of this bundle, the architectonic dissection allowvisualization of the stems of these fiber bun- connections in the nonhuman primate are well docu- dles (10). With very fewexceptions, in which dyes such as mented. A comprehensive description of maps for anatomic the carbocyanine dye (DiI) were used for very short connec- cerebral connectivity has been formulated, derived from an- tions (13), histologic description of human fiber pathways atomic studies in the human and by extrapolation from is incomplete because it does not provide a detailed under- experimental material, and has been integrated in the con- standing of their origins and terminations, and no technique text of a methodology for topographic characterization and is available that can identify with certainty the origin and quantification of human forebrain white matter (16,17). The closest inferences at this level of description formulation of more sophisticated tractographic experi- are obtained from white matter degeneration studies of ments and in interpreting neurofunctional data. Most of these stud- the neuroanatomic knowledge of fiber tracts within an ies deal with cortico-subcortical connections and are not fMRI experiment is an additional challenge, but at the same specific because the cortical lesions that cause the remote time it seems to be key if we are to study behavior in normal degeneration are very large (10,14). Studies in the Experimental Nonhuman Primate In Vivo Analysis of Fiber Pathways Experimental approaches with available techniques have ad- The capability of studying tracts in the living human brain dressed the problem of origin and termination of fiber path- opens up a newwindowin structural–functional and ana- ways in the monkey. The injection of radioactively labeled tomic–clinical relationships. Currently, the detection of 360 Neuropsychopharmacology: The Fifth Generation of Progress fiber tracts in vivo has been addressed by MRI techniques such as DTI. DTI analysis enables us to characterize a white matter fiber pathway in terms of its orientation, location, and size. To date, tractography has been performed in two different ways. Using manual or model-independent methods, we can derive the trajectory of the fiber bundle and approxi- mate its extreme peripheries (12). Using mathematically driven model-based methods, we can also trace a fiber path- way (18–20). In the section on applications, we give exam- ples in which both methods are used and different tracts A are visualized in two and three dimensions. Although the field of DTI-based brain tractography is expanding rapidly with impressive results, it has to be pointed out that certain basic conceptual obstacles still need to be overcome. For instance, in this stage, it has not been demonstrated that we are able to delineate completely and precisely a fiber tract in the brain by means of any DTI analysis technique. At the most, we can identify and characterize the stems of the major fiber tracts (12,21); however, the problem of elucidating the splays and extreme peripheries of the bun- dles remains to be solved reliably. Therefore, when we use the term pathway, tract, or bundle, we currently refer to its B stem. Map of cortical anatomic connectivity (MAC) for the cingulum bundle (CB), or CBMAC. The connections of the CB Self-diffusion of molecules has been studied with magnetic are represented in the mesial (A), lateral (B), and ventral (C) views of the human brain on a cortical parcellation system (46). The resonance methodologies for several decades (22,23). For shaded area in blue within the frontal pole in the ventral view comprehensive reviews of the use of diffusion in nuclear corresponds approximately to the rostralpart of the frontoorbital cortexthat is anterior to the transverse orbital sulcus. AG, angular magnetic resonance, we refer the reader to other sources gyrus; CALC, intracalcarine cortex; CGa, cingulate gyrus, anterior; (24–26). With respect to the physical principles underlying CGp, cingulate gyrus, posterior; CN, cuneiform cortex; CO, central diffusion (also known as brownian motion), water in tissues operculum; F1, superior frontal gyrus; F2, middle frontal gyrus; F3o, inferior frontal gyrus, pars opercularis; F3t, inferior frontal with an oriented structure tends to diffuse more along the gyrus, pars triangularis; FMC, frontal medial cortex; FO, frontal orientation of the tissue structure (Fig.
FIGURE 3-34 (see Color Plate) “Purple toe” syndrom e reflecting peripheral atheroem bolic disease in the patient in Figure 3-33 (ragged aorta) order levlen 0.15mg fast delivery, following an abdom inal aortogram discount levlen 0.15mg on-line. M icroem boli of atherom atous m aterial are readily identified by the characteristic appearance of cholesterol crystal inclusions that appear in a biconvex needle-shaped form. In routine paraffin-em bedded histologic sections, the cholesterol is not seen because the m ethods used in preparing sections dissolve the crystals; the characteristic biconvex clefts in the glom eruli (or blood vessels) persist, allowing easy identification. Several patterns of renal failure in patients with AERD are recognized: 1) insult (eg, abdom inal aortogram ) leads to end-stage renal disease (ESRD) over weeks to m onths; 2) insult leads to chronic stable renal insufficiency; 3) m ultiple insults (repeated angiographic procedures) lead to a step-wise rise in serum creatinine eventuating in end-stage renal failure; and 4) insult leading to ESRD over several weeks to m onths with recovery of som e renal function allowing for discontinuance of dialysis. FIGURE 3-36 Renal biopsy dem onstrating severe arteriolar nephrosclerosis. Arteriolar nephrosclerosis is intimately associated with hypertension. The histology of the kidney in arteriolar nephrosclerosis shows considerable variation in intensity and extent of the arteriolar lesions. Thickening of the vessel wall, edem a of the sm ooth m uscle cells, hypertrophy of the sm ooth m uscle cells, and hyaline degenera- tion of the vessel wall m ay be apparent depending on the severity of the nephrosclerosis. In addition to the vascular lesions of arteriolar nephrosclerosis there are abnorm alities of glom eruli, tubules, and interstitial areas that are believed to be secondary to the ischem ia that results from arteriolar insufficiency. Arteriolar nephrosclerosis is observed in patients with longstanding hypertension; the m ore severe the hypertension, the more severe the arteriolar nephrosclerosis. Arteriolar nephrosclerosis m ay also be seen in elderly norm otensive individuals and is frequently observed in elderly patients with gener- alized atherosclerosis or essential hypertension. FIGURE 3-37 Schematic representation of ischemic nephropathy. Patients with atherosclerotic renal artery Atherosclerosis Nephrosclerosis disease (ASO-RAD) often have coexisting renal parenchymal disease with varying degrees of nephrosclerosis (small vessel disease) or atheroembolic renal disease. W hether or not the renal insufficiency is solely attributable to renal artery stenosis, nephrosclerosis, or atheroembolic renal disease is difficult to determine. The term “ischemic nephropathy” is more complex than being simply due to atherosclerotic renal artery stenosis. In addition, in the azotemic patient with ASO- Atheroembolism RAD, one should exclude other potential or contributing causes of renal insufficiency such as obstructive uropathy, primary glomerular disease (suggested by heavy proteinuria), drug-related renal insufficiency (eg, nonsteroidal anti-inflammatory drugs), and uncontrolled blood pressure. Renovascular Hypertension and Ischemic Nephropathy 3. Atherosclerotic renal artery disease (ASO- 11% Other RAD) has been claimed to contribute to the ESRD population. This diagram from the US Renal Data System Coordinating Center 1994 report indicates that 29% of calendar year 12% 1991 incident patients entered ESRD programs because of “hypertension (HBP). Crude estimates of the percentage of patients entering DM ESRD programs because of ASO-RAD range from 1. Precise bases for making 5% these estimates are both unclear and confounded by the high likelihood of coexisting arterio- Urology 29% lar nephrosclerosis, type II diabetic nephropathy, and atheroembolic renal disease. ASO-RAD High blood as a major contributor to the ESRD population is probably small on a percentage basis, occu- 3% pressure Cyst pying some portion of the ESRD diagnosis “hypertension (HBP). Treatment of Renovascular Hypertension and Ischemic Nephropathy FIGURE 3-39 TREATM ENT OPTIONS FOR RENOVASCULAR Treatment options for renovascular hypertension and ischemic HYPERTENSION AND ISCHEM IC NEPHROPATHY nephropathy. The main goals in the treatment of renovascular hyper- tension or ischemic nephropathy are to control the blood pressure, to prevent target organ complications, and to avoid the loss of renal Pharmacologic antihypertensive therapy function. Although the issue of renal function may be viewed as PTRA mutually exclusive from the issue of blood pressure control, uncon- trolled hypertension may hasten a decline in renal function, and Renal artery stents renal insufficiency may produce worsening hypertension. Even in the Surgical renal revascularization presence of excellent blood pressure control, progressive arterial stenosis might worsen renal ischemia and promote renal atrophy and fibrosis. Therapeutic options include pharmacologic antihypertensive therapy, percutaneous transluminal renal angioplasty (PTRA), renal artery stents, and surgical renal revascularization. Pharmacologic anti- hypertensive therapy is covered in more detail separately in this Atlas. FIGURE 3-40 INCREASING COM ORBIDITY IN PATIENTS Com orbidity in patients undergoing renovascular surgery.