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Peripher- a wide range of disorders cheap 240 mg calan mastercard, whereas opponents question its ally cheap 120 mg calan with visa, marijuana produces prominent effects on the cardiovas- efficacy and point to potential deleterious effects of smoked cular system characterized by tachycardia generic calan 80mg with mastercard, and at high doses marijuana. The scientific rationale for deciding the fate of it can produce orthostatic hypotension. There are several marijuana as a therapeutic agent is often ignored. However, THC has provided most of the evidence for can- Billy R. Dewey: Department of Pharmacology nabinoid effects in laboratory animals. As for chronic mari- and Toxicology, Virginia Commonwealth University, Richmond, Virginia. Vincenzo DiMarzo: Istituto per la Chimica di Molecole Di Interesse juana use in humans, concerns arise because of potential Biologico, Consiglio Nazionale delle Ricerche, Naples, Italy. There has been considerable been proposed that chronic marijuana use in adolescents interest in cannabinoid effects on performance, cognition, may result in long-term memory impairment (6). There are and the development of dependence, discussed in the fol- also indications that persons with learning disabilities may lowing sections. Almost all stud- ies have shown that marijuana has no effect on retrieval of already-learned material. THC reliably alters the perception Performance of time, with subjects overestimating elapsed time or experi- Cannabinoids affect sensory, psychomotor, and cognitive encing an increase in the subjective rate of time (2). Evi- function and the ability to perform certain tasks. There dence has emerged from several studies that chronic mari- is little dispute that high doses of marijuana can disrupt juana use after many years produces subtle cognitive performance when the task is difficult. As may be expected, changes, specifically with regard to attention, as well as orga- the effects of marijuana on performance become more vari- nization and integration of complex information (8). In a comprehensive review, Chait binoid-induced deficits in several animal models. The natu- and Pierri concluded that marijuana, at doses that produce rally occurring cannabinoids as well as a wide range of syn- moderate levels of intoxication, can affect a wide range of thetic compounds have been demonstrated to impair learned and unlearned behaviors, including simple motor learning and memory in numerous laboratory animal mem- tasks, and more complex psychomotor and cognitive tasks ory tasks. Cannabinoid-induced impairment of flying and driving cannabinoids impaired spatial memory in rats, as assessed has been documented in numerous studies, although inter- by the eight-arm radial maze, and retarded completion time pretation of the results remains controversial. Direct injection of cannabinoids into the hippocampus quently found in the blood of drivers involved in automo- impaired memory, and this appeared specific to cognition bile accidents, and marijuana use has been associated with because no other pharmacologic effects were produced (10). One study compared the effects of marijuana on equilib- Tolerance and Dependence rium and simulated driving (3). Marijuana smoking that produced a 'high' also increased body sway and increased There is convincing evidence for the development of toler- brake latency to a degree comparable to that found in per- ance to THC in humans (11). Tolerance developed to a sons with breath alcohol concentrations near 0. Although robust acute effects of nomic functions, increases in intraocular pressure, sleep dis- marijuana were found on subjective and physiologic mea- turbances, and mood changes (11). High doses of 9-THC sures, and on smooth-pursuit eye tracking performance, no were required for a sustained period of time to achieve be- 9 effects were evident the day after administration, a finding havioral tolerance. If the doses of -THC were sufficiently indicating that the residual effects of smoking a single mari- small and infrequent, little behavioral tolerance seemed to juana cigarette are minimal. Several early reports came from countries where potent marijuana was used for long periods of time. Cognition On deprivation of marijuana, users experienced auditory 9 There is lack of consensus regarding the effects of -THC and visual hallucinations and irritability. The development on memory and learning in that results are often inconsis- of tolerance and dependence has been studied under rigor- tent and test specific (2,6).

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Efficacy of biphasic waveform cardioversion for atrial fibrillation and atrial flutter compared with conventional monophasic waveforms discount 120 mg calan fast delivery. Initial energy for external electrical cardioversion of atrial fibrillation cheap calan 80mg with visa. Efficacy and safety of ibutilide for cardioversion of atrial flutter and fibrillation in patients receiving amiodarone or propafenone cheap calan 120 mg line. Design and rationale of a randomized study to compare amiodarone and Class IC anti-arrhythmic drugs in terms of atrial fibrillation treatment efficacy in patients paced for sinus node disease: the PITAGORA trial. Intravenous amiodarone bolus immediately controls heart rate in patients with atrial fibrillation accompanied by severe congestive heart failure. Towards evidence based emergency medicine: best BETs from the Manchester Royal Infirmary. Beta-blockers or digoxin for rate control of acute atrial fibrillation in the emergency department. Specific linear left atrial lesions in atrial fibrillation: intraoperative radiofrequency ablation using minimally invasive surgical techniques. Time courses and quantitative analysis of atrial fibrillation episode number and duration after circular plus linear left atrial lesions: trigger elimination or substrate modification: early or delayed cure? Mid-term results of endoscopic mitral valve repair in combination with endocardial or epicardial ablation. Low risk of major complications associated with pulmonary vein antral isolation for atrial fibrillation: results of 500 consecutive ablation procedures in patients with low prevalence of structural heart disease from a single center. Early recurrences after atrial fibrillation ablation: prognostic value and effect of early reablation. Comparison of recurrence rates after direct-current cardioversion for new-onset atrial fibrillation in patients receiving versus those not receiving rhythm-control drug therapy. The effect of different treatment strategies on left atrial size in patients with lone paroxysmal atrial fibrillation-a prospective cohort study. Detection and quantification of left atrial structural remodeling with delayed-enhancement magnetic resonance imaging in patients with atrial fibrillation. Ablate and pace revisited: long term survival and predictors of permanent atrial fibrillation. Improved outcome following restoration of sinus rhythm prior to catheter ablation of persistent atrial fibrillation: A comparative multicenter study. Journal of Interventional Cardiac Electrophysiology 2012;33(3):297. Efficacy of adjuvant anterior left atrial ablation during intracardiac echocardiography-guided pulmonary vein antrum isolation for atrial fibrillation. Key to Included Primary and Companion Articles Appendix Table E-1. Included primary and companion articles Study Designation Primary Abstracted Article Companion Articles* 1 2 5A Study (Antiarrhythmics Roux, 2009 Leong-Sit, 2011 After Ablation of Atrial Fibrillation) 3 A4 Study (Catheter ablation Jais, 2008 None versus antiarrhythmic drugs for atrial fibrillation) 4 5 AF-CHF (Atrial Fibrillation Talajic, 2010 Roy, 2008 and Congestive Heart Failure) 6 AFFIRM (Atrial Fibrillation Anonymous, 2003 None Follow-up Investigation of 7 8 Rhythm Management) Wyse, 2002 Guglin, 2010 9 Jenkins, 2005 10 Sherman, 2005 11 Steinberg, 2004 12 Bush, 2006 13 Chung, 2005 14 Curtis, 2005 15 Anonymous, 2002 * 16 7 AFFIRM (Atrial Fibrillation Van Gelder, 2006 Wyse, 2002 17 Follow-up Investigation of Van Gelder, 2002 Rhythm Management) RACE (RAte Control vs. Electrical cardioversion) 18 19 AIRCRAFT (Australian Weerasooriya, 2003 Lim, 2007 Intervention Randomized Control of Rate in Atrial Fibrillation Trial) 20 21 APAF (Ablation for Pappone, 2006 Pappone, 2011 Paroxysmal Atrial Fibrillation) 22 BEST AF (Biphasic energy Glover, 2008 None selection for transthoracic cardioversion of atrial fibrillation) 23 CACAF (Catheter Ablation Stabile, 2006 None For The Cure Of Atrial Fibrillation Study) 24 CAFE-II (chronic atrial Shelton, 2009 None fibrillation and heart failure) E-1 Study Designation Primary Abstracted Article Companion Articles* 25 26 CTAF (Canadian Trial of Roy, 2000 Dorian, 2002 Atrial Fibrillation) 27 Dorian, 2003 28 Lumer, 2002 29 30 CRRAFT (Control of Rate Vora, 2004 Vora, 2004 versus Rhythm in rheumatic Atrial Fibrillation Trial) 31 DIONYSOS (Randomized, Le Heuzey, 2010 None Double-Blind TrIal to Evaluate the Efficacy and Safety of DrOnedarone [400 mg bid] Versus AmiodaroNe [600 mg qd for 28 daYS, then 200 mg qd Thereafter] for at Least 6 mOnths for the Maintenance of Sinus Rhythm in Patients with AF) 32 FAST (Atrial Fibrillation Boersma, 2011 None Catheter Ablation Versus Surgical Ablation Treatment) 33 34 HOT CAFÉ (How to Treat Opolski, 2004 Opolski, 2003 35 Chronic Atrial Fibrillation) Pietrasik, 2007 36 Szulc, 2006 37 MOBIPAPA Kirchhof, 2005 None 38 PABA-CHF (Pulmonary Vein Khan, 2008 None Antrum Isolation versus AV Node Ablation with Bi- Ventricular Pacing for Treatment of Atrial Fibrillation in Patients with Congestive Heart Failure) 39 PAF 2 (paroxysmal atrial Brignole, 2002 None Fibrillation) 40 PAVE (Post AV Nodal Doshi, 2005 None Ablation Evaluation) 41 42 PIAF (Pharmacological Hohnloser, 2000 Gronefeld, 2003 Intervention in Atrial Fibrillation) 43 QOLAF (Quality of Life and Tsuneda, 2006 None Atrial Fibrillation) E-2 Study Designation Primary Abstracted Article Companion Articles* 44 17 RACE (RAte Control Groenveld, 2009 Van Gelder, 2002 vs. Electrical cardioversion) 17 45 Van Gelder, 2002 Hagens, 2004 46 Hagens, 2006 47 Rienstra, 2007 48 Rienstra, 2005 49 Hagens, 2005 50 51 RACE II (Rate Control Van Gelder, 2010 Groenveld, 2011 52 Efficacy in Permanent Atrial Smit, 2011 53 Fibrillation: a Comparison Van Gelder, 2006 * between Lenient versus Strict Rate Control II) 54 RASTA (Randomized Dixit, 2012 None Ablation Strategies for the Treatment of Persistent Atrial Fibrillation) 55 56 SAFE-T (Sotalol Amiodarone Singh, 2005 Atwood, 2007 57 Atrial Batcher, 2007 58 Fibrillation Efficacy Trial) Singh, 2009 59 Singh, 2003 * 60 SAFIR (Surgery for atrial Chevalier, 2009 None fibrillation) 61 62 STAF (Strategies of Carlsson, 2003 Carlsson, 2003 Treatment of Atrial Fibrillation) 63 STAR AF (Substrate and Verma, 2010 None Trigger Ablation for Reduction of Atrial Fibrillation) 64 SWEDMAF (SWEDish Blomstrom-Lundqvist, 2007 None Multicentre Atrial Fibrillation study) 65 66 ThermoCool AF (ThermoCool Wilber, 2010 Reynolds, 2010 Atrial Fibrillation) 67 VEPARAF (VErapamil Plus De Simone, 2003 None Antiarrhythmic drugs Reduce Atrial Fibrillation recurrences after an electrical Cardioversion) 68 VERDICT (The Verapamil Van Noord, 2001 None versus Digoxin Cardioversion Trial) 69 VERDICT (Verapamil Versus Hemels, 2006 None Digoxin and Acute Versus Routine Serial Cardioversion Trial) 70 None Abreu Filho, 2005 None E-3 Study Designation Primary Abstracted Article Companion Articles* 71 None Akpinar, 2003 None 72 None Alatawi, 2005 None 73 None Albrecht, 2009 None 74 None Alp, 2000 None 75 None Ambler, 2006 None 76 None Arentz, 2007 None 77 None Balla, 2011 None 78 None Bellandi, 2001 None 79 None Bertaglia, 2002 None 80 None Bittner, 2011 None 81 None Boodhoo, 2007 None 82 None Boos, 2003 None 83 None Brazdzionyte, 2006 None 84 None Bulava, 2010 None 85 None Calo, 2006 None 86 None Capucci, 2000 None 87 None Chen, 2011 None 88 None Corrado, 2010 None 89 None de Lima, 2004 None 90 None De Simone, 2002 None 91 None Deisenhofer, 2009 None 92 None Delle Karth, 2001 None 93 None Demircan, 2005 None 94 95 None Deneke, 2002 Khargi, 2001 96 None Di Biase, 2009 None 97 None Dixit, 2006 None 98 None Dixit, 2008 None 99 None Doukas, 2005 None 100 None Elayi, 2008 None 101 None Fassini, 2005 None 102 None Fiala, 2008 None 103 None Forleo, 2009 None E-4 Study Designation Primary Abstracted Article Companion Articles* 104 None Fragakis, 2009 None 105 None Gaita, 2008 None 106 None Gavin, 2011 None 107 None Hassan, 2007 None 108 None Haissaguerre, 2004 None 109 None Hocini, 2005 None 110 None Hofmann, 2006 None 111 None Holming, 2001 None 112 None Jessurun, 2003 None 113 None Joglar, 2000 None 114 None Joseph, 2000 None 115 None Kafkas, 2007 None 116 None Kanoupakis, 2004 None 117 None Katritsis, 2004 None 118 None Katritsis, 2003 None 119 None Kawabata, 2007 None 120 None Khand, 2003 None 121 None Khaykin, 2003 None 122 None Khaykin, 2009 None 123 None Kim, 2010 None 124 None Kirchhof, 2002 None 125 None Kirkutis, 2004 None 126 None Kochiadakis, 2004 None 127 None Kochiadakis, 2004 None 128 None Kochiadakis, 2000 None 129 None Kochiadakis, 2001 None 130 None Kochiadakis, 2000 None 131 None Korantzopoulos, 2006 None 132 None Krittayaphong, 2003 None 133 None Lee, 2000 None 134 None Levy, 2001 None 135 None Lindholm, 2004 None E-5 Study Designation Primary Abstracted Article Companion Articles* 136 None Liu, 2010 None 137 None Liu, 2006 None 138 None MacDonald, 2011 None 139 None Manios, 2003 None 140 None Marinsek, 2003 None 141 None Mazzocca, 2006 None 142 None Mortensen, 2008 None 143 None Mun, 2012 None 144 None Nergardh, 2007 None 145 None Nilsson, 2006 None 146 None Okcun, 2004 None 147 None Oral, 2004 None 148 None Oral, 2005 None 149 None Oral, 2006 None 150 None Oral, 2008 None 151 None Oral, 2009 None 152 None Page, 2002 None 153 None Petrac, 2005 None 154 None Pires, 2010 None 155 None Plewan, 2001 None 156 None Pontoppidan, 2009 None 157 None Rashba, 2002 None 158 None Rashba, 2004 None 159 None Redfearn, 2006 None 160 None Ricard, 2001 None 161 None Sawhney, 2010 None 162 None Scholten, 2003 None 163 None Schuetz, 2003 None 164 None Sheikh, 2006 None 165 None Siaplaouras, 2005 None 166 None Siaplaouras, 2004 None 167 None Simpson, 2001 None E-6 Study Designation Primary Abstracted Article Companion Articles* 168 None Siu, 2009 None 169 None Srivastava, 2008 None 170 None Tamborero, 2009 None 171 None Thomas, 2004 None 172 None Turco, 2007 None 173 None Van Breugel, 2010 None 174 None Vijayalakshmi, 2006 None 175 None Villani, 2000 None 176 None von Oppell, 2009 None 177 None Wang, 2008 None 178 None Wang, 2009 None 179 None Wattanasuwan, 2001 None 180 None Wazni, 2003 None 181 None Wazni, 2005 None 182 None Willems, 2006 None 183 None Yildiz, 2008 None 184 None Knaut, 2010 None 185 None Karch, 2005 None *The three companion articles marked with an asterisk did not individually meet criteria for inclusion but were considered for supplemental information (e. Antiarrhythmics After Ablation of Atrial Maintenance of sinus rhythm and survival in Fibrillation (5A Study). Rhythm fibrillation (5A Study): six-month follow-up control versus rate control for atrial study. Maintenance of sinus rhythm Catheter ablation versus antiarrhythmic in patients with atrial fibrillation: an drugs for atrial fibrillation: the A4 study. Baseline characteristics of comparison of rate control and rhythm patients with atrial fibrillation: the AFFIRM control in patients with atrial fibrillation. Does intensity of rate-control influence is associated with fewer heart failure outcome in atrial fibrillation? An analysis of symptoms: insights from the AFFIRM trial. Van Gelder IC, Hagens VE, Bosker HA, et Quality of life in atrial fibrillation: the Atrial al. A comparison of rate control and rhythm Fibrillation Follow-up Investigation of control in patients with recurrent persistent Rhythm Management (AFFIRM) study.

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Studies looking at different ethnic and cultural groups have found that AD AD is a progressive disease with insidious onset in which is common in elderly persons from all ethnic and socioeco- the underlying neurodegenerative changes probably begin nomic backgrounds cheap calan 120mg with amex, but there may be some Asian ethnic years before clinical symptoms are obvious 80mg calan with visa. Studies of popu- groups who are less vulnerable to AD (78) buy calan 240 mg line. Environmental lations at risk of developing AD have been conducted to risk factors for AD have been difficult to identify, but there determine whether there are changes in cognitive function is some evidence that persons with higher educational at- that can be detected with neuropsychological tests before tainment are less likely to develop AD in old age (79). Neu- patients meet clinical criteria for the diagnosis of AD. For robiological mechanisms that may account for the protec- these studies, persons who are cognitively normal but who tive effect of education have not been elucidated, but it is are at increased risk of developing AD, usually because of possible that persons with more education have a greater old age, are followed longitudinally with a structured battery reserve of brain capacity that enables those persons to re- of neuropsychological tests. After a period of 1 to 5 years, main cognitively intact for longer periods of time during the baseline performance of patients who have subsequently the early stages of AD. Specific genetic mutations studies using this model have demonstrated consistently that cause AD have been identified in the gene coding for that impairment in memory is significantly worse at baseline the amyloid precursor protein, in the presenilin 1 gene, and in those persons who subsequently are diagnosed with AD in the presenilin 2 gene (24,80). In most instances, the memory tests most im- of these mutations develop AD when they are quite young, paired before diagnosis are those measuring delayed recall, often as early as age 40 to 50 years. In families carrying one that is, recall of newly learned information but after a delay of these mutations, the inheritance of AD follows the classic of several minutes during which the subject must perform pattern of autosomal dominant inheritance, with 50% of other cognitive tasks. A deficit in the rate of new learning each generation developing the disease. Language tion they provide about possible pathophysiologic mecha- function, particularly difficulty with naming, has also been nisms leading to the development of plaques, tangles, cell found to differentiate those persons who subsequently de- loss, and dementia. From a population standpoint, however, velop dementia from others who remain free of dementia these genetically determined cases of AD are of less interest (83). Occasionally, other cognitive tasks such as those plac- because they constitute a small fraction of all cases observed ing great demands on executive function and working mem- clinically. Most estimates are that less than 2% of all AD ory show deficits before the onset of dementia, but memory cases result from specific genetic mutations (80). Family (81) and population (82) studies have demon- Evidence indicates that some of the predictive power of strated that persons who carry the 4 form of the apolipo- poor performance on neuropsychological tests results from protein E (Apo E) gene (APOE) have a greater likelihood the fact that memory deficits are, in part, a subclinical surro- of developing AD than do persons who carry only the 3 gate identifying those at increased risk because of old age and the 2 forms. Apo E is a cholesterol-transporting pro- or presence of an APOE 4 genotype. Because studies have 1194 Neuropsychopharmacology: The Fifth Generation of Progress clarified that APOE genotype may confer additional risk of has important implications for clinical trials of agents that AD primarily within a certain age range (86), it is likely are expected to slow the rate of cognitive deterioration (88, that APOE genotype and neuropsychological test perfor- 94). Analyses of data from these data on neuropsycho- rate of cognitive deterioration have been investigated exten- logical antecedents of dementia have consistently shown sively. Apart from the relationship of rate with stage of dis- that the memory and other deficits cannot be accounted ease described earlier, no other factors have been found to for simply by considering age as a predictor. Rather, it ap- affect the rate of deterioration consistently. Age, age of dis- pears that deficits in memory and, to a lesser extent, lan- ease onset, gender, ethnicity, and APOE genotype have all guage and executive function are predictors of subsequent been examined as possible predictors, and none has consis- dementia across a broad range of ages and for all APOE tently been shown to affect the rate of decline. Longitudinal Studies Behavioral disturbances have also been investigated lon- Numerous longitudinal studies have documented the pro- gitudinally, and it is clear that symptoms such as psychosis, gression of cognitive, behavioral, and functional changes agitation, and depressed mood can be very disturbing both throughout the course of illness. As expected, given the stud- to the patient and to caregivers. Because of the importance ies of populations at risk for AD described earlier, studies of of these symptoms in patient management, new tools have very mild AD have documented that memory impairment is been developed in an effort to provide reliable and valid the earliest and most prominent feature of the illness (87). In contrast to the cognitive defi- earliest stages of AD or who may be at high risk of develop- cits of AD, however, these behavioral disturbances are quite ing AD. As the disease progresses, deficits in both expressive variable from one patient to another and over time in indi- and receptive language and deficits in praxis and visuospatial vidual patients (95,97). These disturbances are episodic ability become quite pronounced. Longitudinal studies have phenomena that wax and wane over the course of AD, with also documented that cognitive deterioration in AD is re- little evidence of progression. Most trials of potential new lentlessly progressive, with little evidence of improvement treatments for AD now include some assessment of these (88). Among the most commonly used assessment tools By definition, all patients with AD have some impair- are the Mini-Mental State Examination (89) , the Blessed ment in their ability to perform daily activities (98).

Similar changes have been reported in patients with first- episode mood related psychosis (Hirayasu et al order 120 mg calan amex, 1999) discount 240 mg calan mastercard, indicating that early changes occur purchase calan 80mg fast delivery. This is consistent with post-mortem studies which describe reduced glial (Ongur et al, 1998) and neuronal (Bouras et al, 2001) density in the subgenual cingulate cortex of people with bipolar disorder. Koo et al (2008) conducted a longitudinal study of bipolar disorder, scanning patients at the first episode psychosis, and again, 2-3 years later. They found progressive reduction in the volume of the anterior cingulate cortex. A study of chronic bipolar patients found progressive grey matter reduction in the hippocampal, fusiform, and cerebellar cortex, over a 4 year follow-up period (Moorhead et al, 2007). Savits et al (2010) found that compared to healthy controls, un-medicated individuals with bipolar disorder had significantly smaller amygdalae, while medicated individuals with bipolar had larger (trending to significance) amygdalae. The difference between these two disordered samples was attributed to the effects of psychotropic medication. White matter hyperintensities are extensive and are thought to be more pronounced in bipolar disorder than schizophrenia (Altschuler et al, 1995). Heng et al (2010) reviewed 18 diffusion tensor imaging (DTI) studies of the white matter of people with bipolar disorder, and described loss of white matter connectivity, involving prefrontal and frontal regions, projection, associative and commissural fibres. Abnormalities of white matter tracts continue to be demonstrated in patients with bipolar disorder (Barysheva et al, 2013) and their unaffected siblings (Sprooten et al, 2013). A study using resting state functional magnetic resonance imaging reported significant hyperconnectivity between the right amygdala and the right vetrolateral prefrontal cortex (Torrisi et al 2013) in bipolar patients in remission. These authors also remarked on activity in the anterior cingulate cortex. A recent DTI study demonstrated altered axonal structure in the posterior internal capsule, corona radiate and the corpus callosum (Bauer et al, 2015). A huge study (>7000 patients) compared the MRI scans of patients suffering the main psychiatric diagnoses (psychotic and non-psychotic). Grey matter loss in the dorsal anterior cingulate cortex and the anterior insula. Thus this interconnected network appears to underpin all psychiatric disorders (Goodkind et al, 2015). This is a region involved in executive function, which is disrupted in some disorders. If this is supported it will be one of the greatest breakthroughs in the history of psychiatry. Pathophysiology of bipolar disorder Bipolar disorder is believed to result from dysfunction of neural networks (rather than dysfunction at a particular site). A prominent contender is the anterior limbic network (ALN), which includes the prefrontal regions, subcortical structures (such as the thalamus, striatum and amygdala) and the midline cerebellum (Strakowski et al, 2005). The work of Goodkind et al (2015) mentioned two paragraphs above suggests a network connecting the anterior cingulate and the anterior insula. Some pathological changes may be developmental while others may be acquired (possibly through failure of inhibitory feedback between structures). Traditionally, interest has focused on monoamine neurotransmitter pathways (serotonin, acetylcholine, nor/adrenalin, dopamine). Recently, glutamatergic function has also been suggested as underpinning bipolar disorder (Kugaya and Sanacora, 2005). There is interest in intracellular signalling cascades/pathways and neuroplasticity (Manji et al, 2003). They allow the cell to receive, process, and respond to information. They are involved in regulating diverse vegetative functions such as mood, appetite and wakefulness, and are therefore likely to be involved in the pathophysiology of bipolar disorder.

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