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How life imitates Tourette syndrome: reflections aged children eskalith 300mg otc. J Am Acad Child Adolesc Psychiatry 1986;25: of an afflicted neuroscientist buy eskalith 300 mg lowest price. Simple tic disease in children: a analysis of 200 pediatric and adolescent cases 300mg eskalith free shipping. CNS Spectrums drome in Monroe County school children. J Clin Psychiatry 1992;5: syndrome in a mainstream school population. Proc Natl Tourette syndrome and associated disorders. New York: Lippincott Acad Sci USA 1988;85:5733–5737. Caudate glucose meta- and classification of tic disorders. Arch Neurol 1993;50: bolic rate changes with both drug and behavior therapy for 1013–1016. Regional cerebral 1696 Neuropsychopharmacology: The Fifth Generation of Progress blood flow measured during symptom provocation in obsessive- 55. SPECT imaging compulsive disorder using oxygen 15–labeled carbon dioxide of cerebral bloodflow in Tourette syndrome. Basal ganglia/limbic magnetic resonance imaging study of tic suppression in Tourette striatal and thalamocortical involvement in craving and loss of syndrome. Basal ganglia dopamine of the hippocampus in temporal lobe epilepsy. Uber das anatomische Substrat der geralisierten 193–203. Tic-Krankheit (maladie des tics, Gilles de la Tourette): En- 62. PET studies of the twicklungshemmung des Corpus striatum. Archiv Psychiatr presynaptic and postsynaptic dopaminergic systems in Tou- Nervenkr (Berl) 1957;195:531–549. Basal ganglia peptidergic staining in caudate nucleus D2 receptor binding. Science 1996;273: Tourette syndrome: a follow-up study. Obsessive-compulsive ysis of subcortical monoamines and amino acids in Tourette symptom clusters and urinary amine correlates in Tourette syn- syndrome. Mol Chem Neuropathol 1994; sum morphology in children with Tourette syndrome and atten- 21:55–60. Reduced basal ganglia human putamen in children with Tourette syndrome. Abnormalities of the blink reflex in Gilles Chapter 117: Tourette Syndrome and Related Tic Disorders 1697 de la Tourette syndrome. J Am Acad Child comparison with learning disabilities and schizophrenia. Stereotactic surgery in outcomes in low birth-weight children at age 6 years: relation to Gilles de la Tourette syndrome. Zh Nevropatol Psikhiatr Im S S Korsakova 1991;91: toxic hippocampal damage in rats causes post-pubertal changes 100–101. Complex segregation depleted of dopamine as neonates: potential relevance to find- analysis of families ascertained through Gilles de la Tourette ings in schizophrenic patients. J Am Acad Child Adolesc Psychiatry 1996;35: immune response of adult rats. Group A streptococcal infections and rheumatic sive, addictive behaviors: Tourette syndrome, ADHD, patho- fever. Pediatric autoimmune neuropsychiatric disor- linkage disequilibrium between the dopamine D4 receptor locus ders associated with streptococcal infections: clinical description and Tourette syndrome. The Tourette Syndrome Association International Consortium 116. A complete genome screen in sib pairs affected children with pediatric autoimmune neuropsychiatric disorders by Gilles de la Tourette syndrome. Am J Hum Genet 1999;65: associated with streptococcal infections by a marker associated 1428–1436. Arch Gen Psychiatry 1987; antigen D8/17: a peripheral marker for childhood-onset obses- 44:100. A double-blind, Tic Severity Scale: initial testing of a clinician rated scale of tic placebo-controlled, crossover trial of an antiandrogen in the severity. Vocal tics in Gilles activity disorder and chronic multiple tic disorder. Arch Gen de la Tourette syndrome treated with botulinum toxin injec- Psychiatry 1999;56:330–336. Vandewalle V, van der Linden C, Groenewegen HJ, et al. Risperidone as a treatment for Tou- frequency stimulation of thalamus. Ziprasidone treatment patient with a tic and a depression. J Am Acad in cerebral glucose metabolic rate after successful behavior modi- Child Adolesc Psychiatry 1995;34:1140–1146. Paroxetine treatment of episodic rages Psychiatry 1996;53:109–113. J Neurosci 1999;19: improvement with pergolide in a randomized, double-blind, 5044–5053. D1 receptor trafficking and delivery in striatal neurons in dopa- 128. Proc Natl Acad Sci USA 2000; term potentiation of neuroleptics with transdermal nicotine in 15;97:1879–1884. A measure of striatal function predicts 35:1631–1636. Cannabis in sive-compulsive disorder and tic disorders in childhood. Toward a neuroanatomy of obsessive-compulsive dis- drome. YOUNG Over the past several decades, various animal models have (1). Moreover, there is little understanding of the biological been used extensively to characterize the activity of various factors underlying pathologic aggression in humans, so it is drugs and drug classes, and from these results, to anticipate difficult to formulate a rational research program. However, the value of animal sion of the characteristics of pathologic aggression is needed models that purport to predict the potential therapeutic for the development of animal models of this disorder. Thus, two roads are emerging: one studying the a basis for predicting responses in humans are those that fundamental causes of aggression and dysfunctions, the are homologous, that is, those in which both the condition other studying the modification of behavior by pharmaco- being observed and its origin are similar to those in humans.

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Translum bar placem ent of tunneled catheters (arrow) into the inferior vena cava can provide a long-term solution for the patient with no apparent rem aining access sites buy eskalith 300mg low price. Palmer emodialysis is a life-sustaining procedure for the treatment of patients with end-stage renal disease discount eskalith 300 mg with amex. To achieve these goals the dialysis prescription must ensure that an adequate amount of dialysis is delivered to the patient discount eskalith 300mg overnight delivery. Numerous studies have shown a correlation between the delivered dose of hemodialysis and patient morbidity and mortality [1–4]. Therefore, the delivered dose should be measured and monitored routinely to ensure that the patient receives an adequate amount of dialysis. One method of assessing the amount of dialysis delivered is to calculate the Kt/V. The Kt/V is a unitless value that is indicative of the dose of hemodialysis. The Kt/V is best described as the fractional clearance of urea as a func- tion of its distributional volume. The fractional clearance is opera- tionally defined as the product of dialyzer clearance (K) and the treat- ment time (t). Recent guidelines suggest that the Kt/V be determined by either formal urea kinetic modeling using computational software or by use of the Kt/V natural logarithm formula. The delivered dose also may be assessed using the urea reduction ratio (URR). A number of factors contribute to the amount of dialysis delivered as measured by either the Kt/V or URR. Increasing blood flow rates to 400 mL/min or higher and increasing dialysate flow rates to 800 mL/min are effective ways to increase the amount of delivered dialysis. W hen increases in blood and dialysate flow rates are no longer effective, use of a high-efficiency membrane can further increase the dose of C H A P T ER dialysis (KoA >600 mL/min, where KoA is the constant indicating the efficiency of dialyzers in removing urea). Eventually, increases in blood and dialysate flow rates, even when combined with a high-efficiency membrane, result in no further increase in the urea clearance rate. At this point the most important determinant affecting the dose of dialysis is the amount of time the patient is dialyzed. Cellulosic membranes generally tend to be patients can be returned to their dry weight. Dry weight is bioincompatible, whereas noncellulosic or synthetic membranes determined somewhat crudely, being based on clinical findings. The patient should be normotensive patible and bioincompatible membranes is still a matter of debate. The water permeability of a dialysis membrane is a function of Another aspect of the dialysis prescription is the composition membrane thickness and pore size and is indicated by its ultrafil- of the dialysate. The concentrations of sodium, potassium, tration coefficient (KUf). During ultrafiltration additional solute calcium, and bicarbonate in the dialysate can be individualized removal occurs by solvent drag or convection. Because of such that ionic composition of the body is restored toward increased pore size, high-flux membranes (KUf >20 mL/h/mm Hg) normal during the dialytic procedure. This topic is discussed in are associated with much higher clearances of average to high mol- detail in chapter 2. Because blood Although hemodialysis is effective in removing uremic toxins flow rates over 50 to 100 mL/min result in little or no further and provides adequate control of fluid and electrolyte abnor- increase in the clearance of these molecules, clearance is primarily malities, the procedure does not provide for the endocrine or membrane-limited. In contrast, clearance values for urea are not metabolic functions of the normal kidney. Therefore, the dialy- significantly greater with a high-flux membrane compared with a sis prescription often includes medications such as erythropoi- high-efficiency membrane because the blood flow rate, and not the etin and 1,25(OH)2 vitamin D. The dose of erythropoietin membrane, is the principal determinant of small solute clearance. Vitamin D therapy is often used in patients undergoing membrane is one in which minimal reaction occurs between the dialysis to help limit the severity of secondary hyperparathy- humoral and cellular components of blood as they come into roidism. Dosages usually range from 1 to 2 µg given intra- contact with the surface of the dialyzer. Trea t m e n t FIGURE 6-1 Diffusion Diffusional and convective flux in hem odialysis. Dialysis is a Blood Dialysate process whereby the composition of blood is altered by exposing it to dialysate through a semipermeable membrane. Solutes are transported Urea, 100 mg/dL Urea, 0 mg/dL across this membrane by either diffusional or convective flux. A, In diffusive solute transport, solutes cross the dialysis m em brane in a direction dictated by the concentration gradient established across the m em brane of the hem odialyzer. At a given tem perature, diffusive transport is directly proportional to both the solute concentration gradient across the membrane and the membrane surface area and inversely proportional to m em brane thickness. Bicarbonate, 20 mEq/L Bicarbonate, 35 mEq/L (Continued on next page) A Dialysis membrane The Dialysis Prescription and Urea M odeling 6. Experimental (eg,caffeine, midodrine, ephedrine, phenylephrine, carnitine) The rate of ultrafiltration is determ ined by the m agnitude of this pressure gradient. M ovem ent of water tends to drag solute across the m em brane, a process referred to as convective transport or sol- vent drag. The contribution of convective transport to total solute FIGURE 6-2 transport is only significant for average-to-high m olecular weight The com m on treatm ents for hem odynam ic instability of patients solutes because they tend to have a sm aller diffusive flux. It is im portant to begin by excluding reversible causes associated with hypotension because failure to recognize these abnorm alities can be lethal. Perhaps the m ost com m on rea- son for hem odynam ic instability is an inaccurate setting of the dry weight. O nce these conditions have been dealt with, the use of a high sodium dialysate, sodium m odeling, cool tem perature dialysis, and perhaps the adm inistration of m idodrine m ay be attem pted. All of these m aneuvers are effective in stabilizing blood pressure in dialysis patients. FIGURE 6-3 ACCEPTABLE M ETHODS TO M EASURE Acceptable m ethods to m easure hem odialysis adequacy as recom - HEM ODIALYSIS ADEQUACY* m ended in the Dialysis O utcom es Q uality Initiative (DO Q I) Clinical Practice Guidelines. These guidelines m ay change as new inform ation on the benefit of increasing the dialysis prescription becom es available. For the present, however, they should be con- •Formal urea kinetic modeling (Kt/V) using computational software sidered the m inim um targets. W hen prescribing the blood flow KoA 900 High-efficiency rate for a hem odialysis procedure the following m ust be considered: 300 dialyzer KoA 650 the relationship between the type of dialysis m em brane used, blood flow rate, and clearance rate of a given solute. For a sm all solute KoA 300 Conventional such as urea (m olecular weight, 60) initially a linear relationship 200 dialyzer exists between clearance and blood flow rates.

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Patients usually have 1988 1989 1990 1991 1992 1993 1994 1995 type I diabetes mellitus and must have the Year physical stamina to undergo a major abdomi- nal operation discount 300 mg eskalith with mastercard. FIGURE 15-4 In some transplantation centers order 300mg eskalith overnight delivery, the cutoff Relative proportion of simultaneous pancreas-kidney (SPK) transplantations versus cadaveric age is 50 years buy generic eskalith 300mg. The patient should demon- kidney transplantations in the United States. Despite an increasing number of SPK transplan- strate emotional and psychological stability, tations over the past 7 years, pancreas transplantation is a less com m on procedure than is and significant secondary complications of cadaveric kidney transplantation alone. Because M edicare does not pay for pancreas transplantations, recipients must use either private insurance or personal funds. EXCLUSION CRITERIA FOR 1000 PANCREAS TRANSPLANTATION SPK PTA 800 PAK Significant cardiac disease Substance abuse Psychiatric illness 600 History of noncompliance Extreme obesity Active infection or malignancy 400 No secondary complications of diabetes 200 FIGURE 15-6 The exclusion criteria for pancreas trans- 0 plantation include significant cardiac disease, 1988 1989 1990 1991 1992 1993 1994 1995 1996 substance abuse, psychiatric illness, and a history of noncom pliance. Extrem e obesity, Year active infection, and m alignancy are relative contraindications to transplantation. Patients with few or very m ild secondary com plica- FIGURE 15-7 tions of diabetes may be candidates for kidney Types of pancreas transplantation procedures and relative frequency per year (January 1988 transplantation alone. Three different indications for pancreas transplantation exist. Patients with type I insulin-dependent diabetes who require kidney transplantation m ay undergo a simultaneous pancreas-kidney (SPK) transplantation or receive a kidney transplan- tation followed by a pancreas transplantation during a separate operation (called pancreas after kidney [PAK] transplantation). Patients without significant renal disease may undergo pancreas transplantation alone (PTA). The relative proportion of the types of transplantations is shown. M ost pancreas transplantations performed in the United States are of the SPK type, followed by PAK transplantations. The portal vein of the allograft is anastomosed to the common iliac vein or distal inferior vena cava. Likewise, on the left side the renal artery and vein are anastom osed to the com m on iliac artery and vein, respectively. To restore the continuity of the urinary tract, a standard ureteroneocystostomy is constructed to the dom e of the bladder. Because the pancreas has dual endocrine and exocrine functions, it is necessary to perform another anastom osis to handle exocrine secretions. A variety of techniques to m anage pancreatic exocrine secretions have been proffered over the years with less than satisfac- tory results. These include duct occlusion, open drainage into the peritoneal cavity, and creation of a button of duodenum and anasto- mosing this or the pancreatic duct directly to the bladder. Currently, the m ost com m only perform ed technique in the United States is drainage of pancreatic exocrine secretions into the bladder (bladder drainage, BD), as depicted. The BD technique involves fashioning a short segm ent of donor duodenum , which is transplanted along with the pancreas. Then the donor duodenum is anastom osed to the dom e of the recipient bladder in a side-to-side m anner. In this way exocrine secretions, including enzym es, proenzym es, water, and sodium bicarbonate, are diverted into the urinary tract. This technique is safe, reliable, and well tolerated; however, it is associated with a num ber of specific urinary tract com plications. As a consequence of implantation into the iliac fossa, the pancreatic allograft is drained into the system ic venous circulation, as depicted. This results in systemic venous, rather than portal venous, insulin release and peripheral hyperinsulinem ia. An alternative approach practiced by som e surgeons is portal venous drainage. In this approach the portal vein of the allograft is anastomosed to the supe- FIGURE 15-8 rior mesenteric vein of the recipient in an end-to-side fashion. This Sim ultaneous pancreas-kidney allograft procedure. M ost pancreas technique establishes drainage of insulin into the portal venous transplantations perform ed in the United States are whole organ blood flow, perhaps a m ore physiologic situation (procedure not pancreaticoduodenal allografts from cadaveric donors transplanted shown). The results of the two techniques are largely com parable. Because Fortunately, patients have suffered no adverse effects of system ic the pancreas from a patient with diabetes still subserves digestive venous drainage and hyperinsulinem ia. Therefore, the pancreaticoduodenal Solitary pancreaticoduodenal allografts are im planted into either allograft is transplanted to an ectopic location, usually the right iliac fossa, at whichever point the iliac vessels perm it vascular anas- iliac fossa. Sim ilarly, the kidney allograft is transplanted ectopically tom oses. This procedure is done, usually and preferentially, on the to the contralateral iliac fossa. O therwise, the operative sequence duplicates that of the the pancreas, as shown in Figure 15-9, is anastomosed to the common com bined procedure. The donor pancreas, duodenum, and spleen are perfused in situ with cold University of W isconsin solution and harvested en bloc with the liver. The pancreaticoduodenal graft is separated from the liver graft and prepared on the surgical back table at 4oC. The spleen is first removed by ligating the splenic artery and vein. The duodenal segment is shortened to approximately 10 cm, and the suture lines are reinforced. The common bile duct (CBD) and the superior mesenteric FIGURE 15-10 artery and vein (SM A and SM V) have been ligated previously in the Enteric drainage (ED) technique. A variety of techniques exist to reconstruct the dual arterial drainage, ED is, perhaps, a m ore physiologic m ethod of handling blood supply to the pancreas. In our experience, the most favorable pancreatic exocrine secretions. ED is the preferred method in Europe approach entails using an iliac artery bifurcation graft harvested from and is rapidly gaining popularity in the United States. As shown, the external iliac arterial limb of the graft com m only, it is perform ed as depicted without a Roux-en-Y is anastomosed to the SM A, and the hypogastric arterial limb is anas- anastom osis. The donor duodenal segm ent is anastom osed in a tomosed to the splenic artery. This technique is reliable and associated side-to-side fashion to the ileum or distal jejunum. The venous anastomosis (portal vein survival, throm bosis rates, and prim ary nonfunction rates are no to iliac vein or inferior vena cava) can be performed without tension different when com paring the two techniques [1–3]. Perform ed by complete mobilization of both the donor portal vein and the recip- with expertise, both techniques should yield excellent results.

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This compound is only available intravenously best 300mg eskalith, but this offers promise for related compounds such as the D3 partial ago- Nonspecific Anticraving Agents nist recently reported in the animal laboratory (19) buy 300 mg eskalith. A number of other agents have been tested to reduce the Amantadine increases dopaminergic transmission generic 300 mg eskalith with mastercard, but desire or craving for cocaine. The rationales have broadly whether the mechanism is DA release, direct effects on DA involved mechanisms such as sensitization and kindling as receptors, or DA reuptake blockade is unclear. One study well as neurotransmitter systems that are indirectly affected examined the effects of acute amantadine (200 or 400 mg) by cocaine such as the opioid, excitatory amino acid/gluta- and chronic amantadine (100 mg twice daily for 4 days) mate, and GABAergic systems. For most of these ap- followed by insufflation of cocaine 0. Al- proaches, outpatient clinical trials have been quite limited. Finally, stress responses and the associ- The effectiveness of amantadine was evaluated in a double- ated elevation of cortisol have been considered as potentially blind, placebo-controlled trial in which 42 patients in a day important in cocaine craving induction and as a therapeutic treatment program were randomized to amantadine 100 mg agent. However, a cocaine administration study showed no twice daily (n 21) to be taken over 10 days or placebo reduction in cocaine effects or self-administration with the (n 21). Urine toxicology screens showed that those who cortisol synthesis inhibitor ketoconazole in spite of signifi- had received amantadine were significantly more likely to cant reductions in cortisol levels (59). A double-blind, placebo- human volunteers examined the effects of 10 mg L-deprenyl controlled, crossover study of the interaction of 400 mg of alone and in combination with cocaine, but found no atten- CBZ daily for 5 days with cocaine found no effects on uation of cocaine effects (54). More recently, it was found subjective response to cocaine (60). A double-blind, pla- to attenuate some subjective effects of cocaine, and an out- cebo-controlled study in outpatients included a 20-day, patient trial showed reduced cocaine use reported in com- controlled, fixed-dose (CBZ 200 mg or 400 mg or placebo) Chapter 102: Pathophysiology and Treatment of Cocaine Dependence 1467 trial in 30 volunteers and found that cocaine use was un- caine 'high,' it decreased craving for cocaine. Another study in 183 cocaine abusers ran- cocaine concentration following cocaine administration was domized to CBZ 400 or 800 mg daily or placebo showed significantly greater while on disulfiram, and this may have that CBZ at 400 mg was associated with a significant de- contributed to the decreased craving and increased dys- crease in cocaine-positive urines and a reduction in cocaine phoria observed in some subjects. However, three other double-blind, placebo- that cocaine use was significantly reduced in the disulfiram controlled studies with CBZ treatment in over 150 subjects group compared to psychotherapy alone, with patients who found no significant difference in cocaine use, cocaine-posi- abused both alcohol and cocaine. The patients reported a tive urine samples, or depressive symptoms measured by the significantly lower percentage of cocaine use days and fewer Beck Depression Inventory (63–65). Plasma CBZ levels of days of cocaine use, and fewer positive urine screens for 5. In surveys of cocaine abusers, 65% have reported signifi- Naltrexone is an opioid antagonist that has been exam- cant problems in concentration and 57% reported memory ined as a treatment agent for cocaine abuse. One study ex- problems, and formal testing suggests some sustained abnor- amined the effects of cocaine after 10 days of treatment with malities in memory and concentration among abusers (3, naltrexone 50 mg or placebo in a double-blind, randomized, 16). Initial studies of recovering cocaine-dependent patients within-subjects design (66). Some cocaine-induced subjec- have revealed impairments of short-term memory, atten- tive effects were less during naltrexone than placebo admin- tion, and complex psychomotor and simple motor abilities, istration. A placebo-controlled outpatient study of naltrex- but the data are limited (16,77). The calcium channel antago- functional brain damage caused by cocaine including strokes nist nifedipine has been studied and shows some promise (16). Structural imaging using computed tomographic scan- (68). Nimodipine showed a reduction in the effects of intra- ning and magnetic resonance imaging (MRI) have shown venous cocaine as well as reductions in acute cocaine-related enlarged ventricles and sulci in cocaine abusers (79). Func- cardiovascular toxicity, but lamotrigine did not reduce co- tional neuroimaging studies have shown focal reductions in caine effects in a similar placebo-controlled crossover study regional cerebral blood flow(rCBF) among chronic cocaine (69,70). Memantine, a glutamate inhibitor, showed no effi- abusers (15–17). These defects also appear to be persistent cacy in reducing cocaine effects acutely (71). Outpatient for several weeks of abstinence at least, and can be associated placebo-controlled studies have not been done with these with neuropsychological deficits (15–17,80). Unfortu- normally high levels of phosphomonoesters and lowlevels nately, this agent is not available in the United States, and of nucleotide triphosphates compared to normals (81). However, baclofen, which is a involve vasoconstriction (82) and platelet abnormalities. Abnormal platelets may produce thrombosis No other controlled trials have been published with this or in cerebral vessels and produce blood flowalterations (18). One study in six cocaine-dependent nary test of 4 weeks of aspirin therapy led to a 50% improve- volunteers examined the effect of disulfiram 250 mg on ment in cerebral perfusion (16). In a placebo-controlled responses to intranasal cocaine (2 mg/kg) using a random- study that has just been completed, aspirin significantly re- ized double-blind, placebo-controlled design (75). Al- duced perfusion defects on single photon emission com- though disulfiram induced no significant differences in co- puted tomography (SPECT) imaging (84,85). It was a large, multisite psychother- apy clinical trial for outpatients who met the DSM-IV crite- Although the simplest peripheral blocking approach of pas- ria for cocaine dependence. For 480 randomized patients, sively injecting polyclonal antibodies to cocaine into a four treatments were compared over an 18-month period. One treat- ies would not last very long and might be of limited use as ment also added cognitive therapy, one added supportive- a sustained treatment. For any type of relapse prevention, expressive psychodynamic therapy, and one added individ- the immune response elements must remain at relatively ual drug counseling. The final group had drug counseling high levels for periods of several weeks or months, which alone. Two specific interaction hypotheses, one involving is best done by active immunization (86). However, three psychiatric severity and the other involving degree of antiso- other approaches using catalytic antibodies, monoclonal cial personality characteristics, were examined, but no major passive antibodies, or injections of butrylcholinesterase have findings related to these hypotheses have been found (88, some promise (87). Either of these was intensive, including 36 possible individual sessions and effects can cause a very significant reduction in the high or 24 group sessions for 6 months. All four of these approaches can also be monthly during active treatment and at 9 and 12 months combined and used together with the pharmacotherapies after baseline. Primary outcome measures were the Addic- described above. The only approach that has been tested tion Severity Index–Drug Use Composite score and the in humans is active immunization (86). The initial animal number of days of cocaine use in the past month. Compared studies showed excellent production of a highly specific an- with the two psychotherapies and with group drug counsel- tibody to cocaine. With active immunization the amount ing (GDC) alone, individual drug counseling plus GDC of inhibition of cocaine entering the brain ranged from 30% showed the greatest improvement on the Addiction Severity to 63% at 30 seconds after cocaine injection in rats. Individual group coun- amount of inhibition was sufficient to extinguish cocaine seling plus GDC was also superior to the two psychothera- self-administration in the rat model. In the initial human study of this vaccine, it was well Hypotheses regarding the superiority of psychotherapy to tolerated with virtually no side effects using a dose of 1,000 GDC for patients with greater psychiatric severity and the g given with two booster injections over a 3-month period superiority of cognitive therapy plus GDC compared with (88).

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The concentration of the metabolic pool of brain GABA 3 discount 300mg eskalith with amex. Behind the scenes of functional brain imaging: a historical and physiological perspective 300mg eskalith for sale. Proc Natl Acad Sci USA may play a critical role in inhibitory GABAergic func- 1998;95:576–772 cheap 300mg eskalith with visa. Measuring cerebral cortex GABA level provides a useful Oxford University Press, 1994. Interpreting functional imaging studies in terms of neurotransmitter cycling. Reduction in the activity of GAD67 by elevation of 6. Homonuclear GABA leads to a major reduction in the rate of GABA 1H-double resonance difference spectroscopy of the rat brain in vivo. GAD67 is the major enzyme controlling nonstimulated Proc Natl Acad Sci USA 1992;89:9603–9606. Through regulation of GABA concentration GAD67 metabolites in rabbit brain by 13C NMRspectroscopy following may play a key role in the etiology and pharmacology of administration of [1-13C]glucose. Magn Reson Med 1986;3: epilepsy and other neurologic and psychiatric disorders. The ability of 13C MRS to measure the rate of GABA 9. The flux from glucose to glutamate in the rat brain in vivo as determined synthesis in combination with GABA/glutamine neuro- by 1H-observed, 13C-edited NMRspectroscopy. J Cereb Blood transmitter cycling (39) may allow the functional roles Flow Metab 1990;10:170–179. Cerebral metabolism of [1,2-¨ 13C ] acetate as detected by in vivo and in vitro 13C NMR. The glycogen shunt model provides a mechanistic expla- 11. Direct measure- ment of brain glucose concentrations in humans by 13C NMR nation for the apparent uncoupling of glucose consumption and oxidation during sensory stimulation (151). The majority of energy to support incremental and total Neurochem NMRspectroscopy in the human brain of amino neuronal activity during sensory stimulation is provided by acid labeling from 13C glucose. J Neurochem 1994;63: neuronal oxidative glucose metabolism (14,131,156): 1377–1385. Localized in vivo 13C- [1-13C] glycogen content and metabolism in rat brain in vivo. NMRof glutamate metabolism in the human brain: initial re- J Neurochem 1999;73:1300. Increased tri-carboxylic metabolic rate in human brain by spectroscopic imaging. Magn acid cycle flux in rat brain during forepaw stimulation detected Reson Med 2000;44:673–679. Oxidative glucose for an astrocyte to neuron metabolic shuttle. J Neurochem 1984; metabolism in rat brain during single forepaw stimulation: a 42:1153–1161. In vivo carbon-edited detec- Dev Neurosci 1993;15:359–366. Utilization of glutamine and TCA cycle con- PEPSI): [3,4-13CH ]glutamate/glutamine tomography in rat stituents as precursors for transmitter glutamate and GABA. Magn Reson Med 1999;42:997–1003 Dev Neurosci 1998;15:367–377. In vivo studies of neuro- of the TCA cycle rate and alpha-ketoglutarate/glutamate ex- transmitter and amino acid metabolism in human brain. J Cereb Blood Flow Metab 1992;12: rochem 2000;74(suppl):S44. Simultaneous De- studies of ammonia transport and glutamine synthesis in the termination of the rates of the TCA cycle, glucose utilization, hyperammonemic rat brain. Functional energy metabo- lism: in vivo 13C NMRevidence for coupling of cerebral glucose sis in human brain by NMR. Measurement of total by 1H-13C magnetic resonance spectroscopy at 4. J Cereb neuronal/astroglial glutamate-glutamine trafficking and astro- glial TCA cycle flux in human cerebral cortex using 13C NMR Blood Flow Metab 1999;19:1179–1188. Cerebral metabolism of [1,2- spectroscopy during the infusion of [2- C] acetate. J Neurochem 13C] glucose and [U-13C] 3 hydroxybutyrate in rat brain as 2001;in press. In vivo proton Int Soc Magn Reson Med 2001;in press. Metabolism of glutamate and related substances in mouse brain. Metabolic compartmenta- of cerebral glucose transport and metabolic kinetics by dynamic tion of glutamate and glutamine: morphological evidence ob- MRspectroscopy. Estimation of glucose flux via pyruvate carboxylase/pyruvate 13 13 42. Glutamate immunoreactivity in rat cerebral dehydrogenase by C NMRisotopomer analysis of D-[U- C] cortex is reversibly abolished by 6-diazo-5-oxo-L-norleurcine glucose metabolites. The rate of turnover 13 tochem Cytochem 1994;42:717–726. Quantitative mea- with the GABA-transaminase inhibitor vigabtrin ( -vinyl surements of regional TCA cycle flux in visual cortex of human GABA). Study of oxygen utiliza- glutamate-glutamine cycling, Proc Natl Acad Sci USA 1997;94: tion changes in human visual cortex during hemifield stimula- 2699–2704. Proc Natl Acad Sci USA 1998;95:316–321 low and high frequency inputs on spike timing in visual cortical 27. Failure of GABAergic inhibition: a key to local and TCA cycle flux in rat brain during [2-13C]glucose infusion. Determination of the rate D-[1-13C]glucose metabolism. Noninvasive measurements of and glial glutamate transporters. Metabolic coupling between tic pathway and amino acid metabolism in the brain: an ex vivo glia and neurons. Glutamine 13C]glucose with or without ammonium acetate.

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