By N. Zapotek. The Sage Colleges.

The mechanism by which the These newer agents are remarkably well tolerated generic 0.25 mg cabergoline with visa, and a anticonvulsants exert their antidepressant effects is poorly majority of patients receiving ECT have had at least one understood and is hypothesized to occur through a number complete trial of an antidepressant without improvement 0.5mg cabergoline otc. The ECT response hancing the effect of inhibitory neurotransmitters and neu­ rate in antidepressant medication-refractory patients is ropeptides. The problem of decreased acute response for the antidepressant properties of ECT. Examining the to ECT in this growing population of medication-refractory relationship of the anticonvulsant effects of ECT to the patients has led to new interest in the technical factors that efficacy of the treatments by blocking or augmenting control the response to acute ECT. Among these factors are the anticonvulsant properties of ECT can test this hypothe­ electrode placement, stimulus dose, and possibly concurrent sis. For example, CSF neuropeptides associated with the medications. These neuropep­ has only recently come to appreciate the relative contribu­ tides could be given in conjunction with ECS to determine tions of stimulus electrode placement and stimulus intensity if the coadministration of these neuropeptides would block to the therapeutic and adverse effects of ECT. As previously discussed, clinical wisdom prior to 1987 taught that as long the therapeutic efficacy of ECS (50). Although ethical con­ as the EEG seizure during ECT was �25 seconds, then the siderations may limit this type of research in humans, stud­ treatment was maximally effective. Further veloping algorithms to determine the relationship of ECT work by this group clarified that the efficacy of right unilat­ treatment variables (e. ANTIDEPRESSANT RESPONSE RATE BY ELECTRODE PLACEMENT AND STIMULUS DOSE OPTIMIZATION OF ACUTE EC Barely 2. More recently, RUL 17% 43% tients achieving remission after an acute BL 65% 63% conservatively estimated at between 50% Chapter 76: Electroconvulsive Therapy 1101 This work demonstrated that, within the stimulus dose patients even a suprathreshold stimulus set at 400 mC may studied, the efficacy for RUL was sensitive to dose, whereas be too low to achieve antidepressant efficacy. Continued support for the efficacy of suprathreshold Also, RUL ECT appeared inferior to BL ECT at any dose. RUL ECT has raised some concern about the fact that ECT Subsequent work confirmed that the efficacy of RUL ECT machines in the United States are restricted in the amount is dose dependent and that RUL ECT administered at six of energy they can deliver per treatment (504 to 576 mC times the initial seizure threshold is as effective as BL ECT maximal output). Abrams argues that the FDA mandated with fewer cognitive side effects than BL ECT (54). McCall maximum output for ECT machines used in this country and colleagues found a dose–response relationship in pa­ often does not allow for the administration of effective su­ tients receiving RUL ECT that extended to 12 times the prathreshold treatments and has called for a reexamination seizure threshold and, as predicted, cognitive side effects of these guidelines (59). The response rate for RUL ECT at or initiate antidepressant medication during a course of eight to 12 times threshold was about 70%, approximately acute ECT is also pertinent to the issue of improving the the rates typically quoted for BL ECT. Clinically, physicians are divided recommend that ECT be delivered with either BL electrode in their practice regarding antidepressant medications dur­ placement at a stimulus dose just above threshold, or with ing ECT, and there are no good data to support any posi­ RUL placement at a stimulus dose markedly above thresh- tion. One of the developments in ECT practice in the 1990s old. Although the virtual lack of TCA trials in these same patients before it is clear that the lower intensity RUL strategies have less coming to ECT. This is especially important because there acute amnesia side effects, this advantage is probably offset are some data to suggest that TCAs (i. Possibly, the addition of an antide­ dictors of QOL in severely depressed patients (56,57). There is a potential risk to stimulating the vagus nerve with subconvul­ PREVENTION OF RELAPSE AFTER ECT sive stimuli without adequate compensatory adrenergic dis­ charge from a seizure and the possibility of prolonged asys­ In general, patients who receive an acute course of ECT are tole. However, a controlled operative setting with cardiac either subsequently resistant or intolerant of antidepressant monitoring decreases the possibility of brief periods of medications. Patients diagnosed with psychotic depression bradycardia causing any significant risk for a majority of are particularly susceptible to relapse after an acute course patients. Two studies found a relapse rare of approximately Second, some would argue that the initial treatment in 70% in 1 year for a total of 53 patients with a diagnosis of a series of titrated seizures is a 'wasted' seizure, adding psychotic depression (61,62). These studies were retrospec­ to costs and potential cognitive side effects without any significant therapeutic benefit to the patient. The unilateral tive and could not examine compliance rates or the ade­ seizure at or near the seizure threshold used during the initial quacy of either the initial (pre-ECT) or continuation medi­ treatment setting to determine seizure threshold probably cation trial. However, the potential advantages of In a prospective study, Sackeim and co-workers (63) fol­ determining the seizure threshold and adjusting the subse­ lowed 58 patients for 1 year after ECT. They examined a quent seizures to the threshold has advantages in maximiz­ number of clinical variables including a retrospective review ing benefit and decreasing the potential for future ineffective of the adequacy of the pre-ECT medication trial. The most treatments (if the energy delivered is too low) and cognitive important factor in determining relapse on maintenance side effects (if the energy is too high). Patients (with and without ment for depression (55,58) and this data could obviate the psychotic features) who were rated as receiving a therapeutic need to determine seizure threshold. Because the majority medication trial(s) prior to their acute course of ECT re- of patients treated with ECT are older and older patients lapsed at a rate that was twice the rate found in patients have very high seizure thresholds, dose titrations at eight to who did not receive an adequate pre-ECT medication trial ten times threshold are generally at or above the 400-mC (64% versus 32%). The maintenance medication was not range used by McCall and associates. In fact, in some older standardized but the results indicated that the adequacy of 1102 Neuropsychopharmacology: The Fifth Generation of Progress the post-ECT medication trial was only marginally related senting for ECT after multiple failed medication trials and to the relapse rate and then primarily in patients who did there may be little benefit from yet another trial of an SSRI.

Before the introduction of highly active impairment generic 0.25mg cabergoline visa. It has an insidious onset 0.25mg cabergoline with amex, and patients often exhibit apathy, cognitive and motor slow- although persons with HADmay experience an acceleration ing, and impaired memory, abstract reasoning, and judg- 1284 Neuropsychopharmacology: The Fifth Generation of Progress TABLE 90. DIAGNOSTIC CRITERIA FOR concentration, forgetfulness, mental slowing). In some pa- DEMENTIA DUE TO HIV DISEASE tients, HADprogresses rapidly after the diagnosis has been made (within weeks to months), whereas other patients A. The development of multiple cognitive deficits manifested by both show cognitive stability for months or years or very slow 1. Per- information or to recall previously learned information) and sons in the early stages of HADoften complain of poor 2. They typically present with significantly less impair- b. The cognitive deficits in criteria A1 and A2 each cause significant impairment in social or occupational functioning The later stage of HADcorresponds to ADC as originally and represent a significant decline from a previous level of functioning. Evidence from the history and physical examination or laboratory findings indicate that the disturbance is the direct TABLE 90. AIDS DEMENTIA COMPLEX STAGING physiologic consequence of HIV infection affecting the central SCHEME nervous system. Deficits do not occur exclusively during the course of a delirium. ADC Stage Characteristics Stage 0 (normal) Normal mental and motor function. HADrepresents the more severe end of a continuum characteristic of ADC, or mild signs of HIV-related cognitive deficits; the milder end is repre- (snout response, slowed extremity sented by the presence of a single cognitive impairment, movements), but without impairment of such as psychomotor slowing. The deficits observed in this work or capacity to perform ADL; gait disorder result in impaired social and occupational func- and strength are normal. Stage 1 (mild) Unequivocal evidence (symptoms, signs, tioning. Stage 2 (moderate) Cannot work or maintain the more Other causes, such as depression and delirium, which can demanding aspects of daily life, but manifest as cognitive impairment, must also be ruled out. Stage 3 (severe) Major intellectual incapacity (cannot be the direct pathophysiologic consequence of HIV disease follow news or personal events, and has outlined its own diagnostic criteria (Table 90. Price and Brew (66) argued that it is not enough simply Stage 4 (end stage) Nearly vegetative; intellectual and social to characterize HIV-infected persons as demented or not. J Infect Dis 1988;158:1079–1083, and Sidtis JJ, Gatsonis C, Price RW, et al. HADbegins with Zidovudine treatment of the AIDS dementia complex: results of a subtle deficits in cognitive processes (e. Chapter 90: Neuropsychiatric Manifestations of HIV-1 Infection and AIDS 1285 TABLE 90. CRITERIA FOR A CLINICAL DIAGNOSIS defined, and survival expectancy at this stage may be 6 OF HIV-1-ASSOCIATED COGNITIVE/MOTOR months or less. Features includes global cognitive dysfunc- COMPLEXa tion, significant functional impairment, and psychotic symptoms. Not sufficient for diagnosis of AIDS confusion, disorientation, delusions, hallucinations, sei- A. HIV-1-associated minor cognitive/motor disorder Probable (must have each of the following): zures, and muscular weakness and paralysis (particularly in 1. Cognitive/motor behavioral abnormalities (must have the lower limbs). Advanced dementia may result in disinhi- each of the following): bition, mutism, catatonia, and incontinence (5,60). At least two of the following acquired cognitive, ropsychiatric complications of late-stage HAD include motor, or behavioral symptoms (present for at least 1 depression, mania, and psychosis. Acquired cognitive/motor abnormality verified by An early prospective study of HIV infection in the United clinical neurologic examination or neuropsychological States revealed that HADdevelops in approximately 15% testing (e. The WHO cross-cultural study perceptual motor skills, attention/concentration, speed of processing of information, abstraction/ examining the neuropsychiatric consequences of HIV infec- reasoning, visuospatial skills, memory/learning, or tion represents the best study of the prevalence of HAD speech/ language) based on a diverse clinical sample. Disturbance from cognitive/motor/behavioral abnormal- persons at five sites around the world (Bangkok, Thailand; ities (see #1) causes mild impairment of work or activities Kinshasa, Zaire; Munich, Germany; Nairobi, Kenya; and of daily living (objectively verifiable or by report of a key informant). Does not meet criteria for HIV-1-associated dementia patients with AIDS ranged from 4. No evidence of another etiology, including active central Bangkok, no cases of HADwere recorded). In addition, no nervous system opportunistic infection or malignancy, or patients met the criteria for HADwhile in the asymptomatic severe systemic illness determined by appropriate history, physical examination, and laboratory and radiologic stage (11). In 1997, the CDC reported that 5% of adults investigation (e. The with an AIDS-defining opportunistic illness had HIV en- above features should not be attributable solely to the cephalopathy (dementia) (67). Criteria for minor cognitive motor disorder include Impairment at least two of the following acquired cognitive, motor, or behavioral symptoms, generally assessed with To classify appropriately HIV-1-seropositive persons who neuropsychological evaluation: do not meet the criteria for dementia, the American Acad- a.

The relative onsets were determined byfinding the latencywith B which the correlation coefficient was maximized with each of three reference functions representing three parts of the response curve: the entire curve purchase cabergoline 0.5 mg without prescription, the rising section purchase cabergoline 0.5mg without prescription, and the falling section. The standard deviations of the whole curve, rising phase, and falling phase were found to be 650, 1,250, and 450 ms, respectively. Across-region differences in the onset and return to base- C line of the BOLD signal during cognitive tasks have been FIGURE 26. Comparison of activation-induced signal changes observed. For example, during a visuallypresented event- in perfusion and BOLD (blood oxygenation-dependent) measure- ments. Perfusion mea- related word stem completion task, Buckner et al. BOLD (bloodoxygenation-dependent) measure- ments were obtained by using gradient-echo EPI with an echo One might argue that this observation makes sense from a time of 30 ms. Others would argue that the neuronal onset latencies should not be more than about 200 ms. When brain activation inferences of the cascade of brain activation be made on is observed on a scale of centimeters, this has not been a this time scale from fMRI data? Nevertheless, this issue is discussed in detail strain or work around the intrinsic variabilityof the onset later in the chapter. These latencies changes is that after activation, the BOLD signal takes about were also shown to correlate with the underlying vascular 2 to 3 s to begin to deviate from baseline (16,38). The earliest onset of the signal change appeared the BOLD signal is highlyweighted toward venous oxygen- to be in graymatter, and the latest onset appeared to occur ation changes, with a flow increase, the time for venous in the largest draining veins. Similar latencydispersions in oxygenation to begin to increase is about the time that it motor cortex have been observed. In one study, latency dif- takes blood to travel from arteries to capillaries and draining ferences, detected in visual cortex with the Hilbert trans- veins, which is 2 to 3 s. In addition, it can be de- course from the motor cortex as a result of 2-second finger rived bydeconvolving the neuronal input from the mea- tapping. As mentioned, the first source of variabilityis the sured hemodynamic response (42,43). This type of analysis intrinsic noise in the time series signal. The standard devia- assumes that the BOLD response behaves in a manner that tion of the signal is on the order of 1%. The second source can be completelydescribed bylinear systems analysis, of variabilityis that of the hemodynamic response. Regardless, observed hemody- tioned, this ranges from 450 to 1,250 ms, depending on namic response to anyneuronal activation can be predicted whether one is observing the rising phase of the signal or 26: Spatial, Temporal, and Interpretive Limits of Functional MRI 347 A B FIGURE 26. Demonstration of several of the limits of functional magnetic resonance imagingtemporal resolution. Echo-planar imag- ing was performed at3Tbyusing a Bruker Biospec 3T/60 equipped with a local head gradient coil. A time course series of axial images (matrix size 96 96, field of view 20 cm, echo time 40 ms, repetition time 500 ms, flip angle 80 degrees) through the motor cortex was obtained. Bilateral finger tapping was performed for 2 s, followed by 18 s of rest. These figures demonstrate that the upper temporal resolution is determined by the variability of the signal change in time and space. A: Time course of the signal elicited by tapping fingers for 2 s. The standard deviation at each point is in the range of 1% to 2%. The standard deviation of the hemodynamic change, in time, is in the range of 450 to 650 ms. B: Map of the dot product (a measure of the activation-induced signal change magni- tude) and the relative latencies or delays of the reference function (the plot in A was used as the reference function) at which the corre- lation coefficient was maximized. The spatial distribution of hemo- dynamicdelayshasastandarddeviation ofabout900ms. Thelongest delays approximately match the regions that show the highest dot product and the area where veins are shown as dark lines in the T2*- weighted anatomic image. The third source of variabilityis the la- maybe almost fullydiluted back to resting state oxygena- tencyspread over space. Again, work is ongoing to characterize this correlation analysis and allowed to shift 2 s. The spread in As previouslydiscussed, the magnitude of the fMRI signal latencies is more than 4 s.

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