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Bull Am Acad Psychiatry Law Acad Psychiatry Law 1995;23:607–611 generic 5 mg finasteride visa hair loss cure just like heaven. POTENZA ERIC HOLLANDER Impaired regulation of impulse is a central feature in several Theoretic Conceptualizations psychiatric disorders and behaviors 5mg finasteride fast delivery hair loss cure cnn, including drug use dis- PG has been described as sharing features with several orders, cluster B personality disorders such as borderline groups of disorders (Fig. Some authors have hypoth- personality disorder, bipolar disorders, and suicide attempts. Consistent with the classification than other psychiatric conditions. This heterogeneous of PG as an OC-spectrum disorder, individuals with PG group of illnesses includes intermittent explosive disorder, kleptomania, pyromania, pathologic gambling (PG), tri- engage in repetitive (gambling-related) behaviors, often in chotillomania, and ICDs not otherwise specified. We review response to overwhelming thoughts to engage in the behav- the neurobiology and treatment of one of these ICDs, PG, ior (11). Studies of comorbidity between OC disorder and describe the nature and treatments of several other po- (OCD) and PG have yielded mixed results, with some stud- tentially related conditions that have recently received in- ies finding rates of OCD in individuals with PG higher creased attention: (a) compulsive buying (CB); (b) compul- than in the general population (12,13), whereas others have sive sexual behavior (CSB); and (c) compulsive computer not found elevated rates of comorbidity (14–17) or elevated use (CCU). These disorders, linked by a failure to resist rates of positive family histories for PG in patients with urges to engage in ultimately self-destructive behaviors, ap- OCD (18). A direct investigation into OC characteristics pear to be relatively common, frequently go unrecognized of individuals with PG found that those with PG scored for considerable periods, and may constitute greater threats significantly higher than those without on the Padua Inven- to personal health than is often appreciated. The differences clustered within two factors corre- sponding to obsessive qualities of impaired control over mental activity and worries of losing control over motor PATHOLOGIC GAMBLING behavior, respectively (19). Although the findings support the notion that PG lies toward the impulsive end of a com- Descriptions of gambling and gambling disorders are found pulsive-impulsive spectrum, the authors cite a central differ- in some of the earliest human records (2,3). Historically, ence between gambling in PG and repetitive behaviors in gambling has been viewed as a sin and later as a vice (2–5). Namely, gambling and actions in other ICDs More recently, disordered gambling has been seen as an are often related as pleasurable or egosyntonic, whereas per- illness determined by genetic and environmental factors and formance of repetitive activities in OCD is generally de- individual decision making. The most extreme form of dis- scribed as egodystonic. Although one study reported the ordered gambling, PG, was first included in the DSM in possibility of the association of PG and OCD with the Hun- 1980 (1). Since that time, there has been increasing research tington disease mutation in a family with PG, OCD, and into the clinical features and neurobiological causes of PG. Huntington disease (20), the neurobiological similarities and differences between PG and OCD remain to be defined more clearly, to explore their relatedness further. Potenza: Director, Problem Gambling Clinic; Department of Psychiatry, Yale University School of Medicine and Connecticut Mental Researchers and clinicians have also described PG as an Health Center, New Haven, Connecticut. PROPOSED ROLES FOR NEUROTRANSMITTER SYSTEMS IMPLICATED IN THE PATHOPHYSIOLOGY OF PATHOLOGIC GAMBLING Neurotransmitter Proposed Role Norepinephrine Arousal, excitement Serotonin Behavioral initiation and cessation Dopamine Reward, reinforcment Opioids Pleasure, urges the later discussion on pharmacotherapy). Proposed conceptual model for relationships be- are warranted to investigate the precise relationships be- tween pathologic gambling (PG) and other psychiatric conditions. Biochemistry clude aspects of tolerance, withdrawal, and failed attempts Multiple factors, including behavioral initiation, arousal, to control the destructive behavior. High rates of comorbid- reward and reinforcement, and behavioral disinhibition, ity are observed between PG and substance use disorders. Unique roles for specific neuro- ders, with rates of nicotine dependence approaching 70% transmitters have been hypothesized as mediating aspects (24), alcohol abuse or dependence in the range of 45% to of PG and other ICDs (Table 120. Specifically, serotonin 55% (12,25), and other drug use problems nearing 40% (5-HT) has been described as important in behavioral regu- (26). Conversely, individuals with substance use disorders lation (behavioral initiation and inhibition, including con- are four- to tenfold more likely to have PG (27): 9% of trol of aggressive and other impulses) (38–41). Data sup- opiate addicts in methadone maintenance (28), 17% of al- port a central role for norepinephrine (NE) in the control cohol abusers (29), and 15% of cocaine addicts (30) have of levels of arousal and detection of novel or aversive stimuli PG. The high rates of comorbidity have implications with (42). Multiple lines of evidence from studies of human and regard not only to potential similarities in the underlying other organisms cite dopamine (DA) function, particularly neurobiological bases of PG and substance use disorders, within the mesocorticolimbic (MCL) pathways, as critical but also to the clinical needs of individuals with PG. Specifi- in processing and modulating rewarding and reinforcing cally, individuals dually diagnosed with a substance use dis- stimuli and behaviors (43–45). Abnormalities in these neu- order and PG were found to require more psychiatric admis- rotransmitter systems as they relate to PG are explored in sions and detoxifications than individuals with a substance the following sections. A separate study found that individuals with comorbid substance use disorders and PG Serotonin were at greater risk for contemplated and attempted suicide than individuals with either diagnosis alone (32). These and A role for 5-HT system dysfunction in the neurobiology of other findings (33,34) indicate that dually diagnosed indi- PG has come from results of pharmacologic challenge stud- viduals with PG appear to be more severely ill than those ies (38,46). The 5-HT and NE reuptake inhibitor clomi- with either illness alone. Taken together with emerging data pramine (CMI) has been used to investigate neurochemical suggesting neurobiological similarities between substance responses in individuals with PG as compared with those use disorders and PG (see the later discussions of genetics without PG (46). Eight men and women with PG and eight and neuroimaging), there is mounting evidence supporting age- and gender-matched controls received a relatively low the notion of substance use disorders and PG lying along intravenous dose of clomipramine (12.

Almost all the in male to female ratios of bipolar disorder were found inter- studies found a strong association between depression and nationally (1) generic finasteride 1 mg visa hair loss dogs. Mean age of onset for bipolar depression was subsequent cardiovascular morbidity and mortality buy finasteride 5 mg otc hair loss itchy scalp. Several generally younger than for MD, ranging from 18 to 27 important physiologic aspects of depression may account years of age in different countries (1). They include HPA dysregulation, sym- age of onset at 21. LIFETIME PREVALENCE OF BIPOLAR DISORDERa Lifetime Rates/100 Overall Females Males F/M Ratio Mean Age at Onset United States (ECA 1980) 0. Chapter 70: Risk Factors for Major Depression andBipolar Disorder 1023 Other Sociodemographic Variables recurrence. It is unlikely that psychosocial factors play a major role in the risk of first onset of bipolar disorder, but Historically bipolar disorder was thought to be more fre- they may have an important role in increasing the risk of quent among higher socioeconomic classes, and there were recurrence. However, popula- Chrono-biological disturbances have long been associ- tion-based studies over the last two decades have not repli- ated with bipolar disorder (44). In the ECA, occupation, income, and dian rhythm disturbances are core symptoms of bipolar epi- education were not found to influence prevalence (42). Some have theo- have annual incomes less than $20,000. The notion of rized that disruption in social zeitgebers (i. Malkoff-Schwartz In the ECA, bipolar disorder was much less frequent and colleagues (46) found than severe social rhythm disrup- among married people, as contrasted with divorced or tions (e. Bipolar disorder was more prevalent ing a job) were associated with onsets of mania, but not among those with multiple divorces (42). DISCUSSION Genetic and Familial Factors Beliefs and hypotheses about risk factors for depression In a review of the eight family studies of bipolar I disorder (such as undue interpersonal dependency) emerged from that included a control group, a metaanalysis (43) showed clinicians treating individual patients and from studies done that bipolar I disorder was seven times more likely among in psychiatric settings. Both suffer from sampling bias: those relatives of bipolar I probands than of controls. These stud- presenting for treatment are evaluated, but many factors in ies also demonstrate an increased risk of MD in relatives of addition to the illness itself affect treatment seeking (e. Jones (43) calculated an estimate of proband-wise concor- For MD there is strong evidence that women have two- dance of 50%, although the authors believe this to be an fold the prevalence of men, an age of onset between 25 and underestimate. There are signifi- Craddock and Jones conclude that there is a substantial cant differences in lifetime rates around the world. Personality factors are non- determining the actual genes involved in bipolar illness. Early life trauma, particularly sexual abuse, is asso- tempts to demonstrate linkage to the X-chromosome, to ciated with early-onset depression in women. Increased rates color blindness, to chromosomes 4, 11, 18, and others have of depression are found in several general medical illnesses. The most likely explanation for The association between depression and cardiovascular ill- lack of success is that these strategies assume a single genetic ness is strong, with depression predicting increased rates of mode of inheritance for a complex multiple-gene interaction morbidity and mortality among cardiovascular patients. Analytic studies (such as twin studies) have suggested some interaction among genetic and environmental factors. The incidence of depression was increased when several life Environmental Factors events (such as death of a close relative) occurred in the Although biological and genetic factors have long been prior month in individuals with high genetic liability. The known to play a major role in the etiology of bipolar disor- ongoing NIMH sib-pair study of early-onset depression will der, psychosocial factors are gaining attention. In particular, shed light on the possible genetic etiology of early-onset many studies have identified the association between stress- recurrent MD. There is little variation in chronicity and recurrence. J Affective Disord 1993;29(2–3): lifetime rates around the world (about 1%), and nearly equal 85–96. Bipolar spectrum is much rates of major depressive disorder among relatives of patients with more frequent, in the range of 3% to 6%. Age, period range of studies strongly support a genetic predisposition and cohort effects on the risk of major depression: results from to bipolar disorder, but specific replicable genetic factors five United States communities. The prevalence action with environmental factors is most likely, a situation and distribution of major depression in a national community that is challenging to research and to isolate. Life events, sample: the National Comorbidity Survey. Am J Psychiatry 1994; especially disruptions in social zeitgebers, increase the likeli- 151(7):979–986. Demographic and clinical risk factors for first onset. An intriguing new area of interest is emerging in risk 8.

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In Western countries discount finasteride 5mg hair loss women vitamin deficiency, the pat- is emerging regarding the nature of cannabinoid effects both tern of use among age groups has not deviated significantly in vivo and in vitro and the endogenous system through since the mid-1970s discount finasteride 1 mg without prescription hair loss 45 women. The most prevalent use occurs in per- which marijuana acts. The emphasis of this chapter is to sons who are in their late teens and early twenties. Despite summarize recent discoveries of the endogenous system as modest declines from the pinnacle of its use in the mid- they relate to both putative adverse effects and therapeutic 1970s, there was an upsurge in use during the 1990s. Mari- uses of marijuana and its psychoactive constituent, 9-tetra- juana smoking is prevalent regardless of age, ethnicity, and hydrocannabinol (THC). Epidemiologic data reveal that the rates of use during breakthroughs occurred that greatly increased our under- the year 2000 by United States students in grades 8, 10, standing of the cannabinoids. It is now evident that an and 12 were 17%, 32%, and 38%, respectively (1). A receptor has been was a steady increase in daily marijuana use (defined as use characterized and cloned, second messenger systems identi- on at least 20 occasions in the past 30 days) in all three fied, a putative endogenous ligand isolated and synthesized, age groups. For example, 2% of high school seniors used and biochemical pathways for both synthesis and degrada- marijuana daily in 1991, with this figure rising to 6% in tion of endogenous ligands described. Two factors that undoubtedly contribute to the prev- alence of marijuana use are the declining perception that marijuana produces harmful effects and the relative ease of PHARMACOLOGY acquiring marijuana. Although marijuana has long been a subject of folklore Marijuana has prominent effects on the central nervous sys- medicine, interest as a potential therapeutic agent has inten- tem as well as numerous peripheral effects in humans that sified in recent times, likely as a result of numerous factors. Acutely, cannabis produces an altered state riod in our history marked by increased interest in nontradi- of consciousness characterized by mild euphoria, relaxation, tional medications, increased awareness of several disease perceptual alterations including time distortion, and the en- states not readily treated by current medications, and in- hancement of ordinary sensory experiences. Cognitive ef- creased discourse about the public policy concerning recrea- fects are also marked, such as impaired short-term memory. Proponents cite a plethora of self- Motor skills and reaction time are also altered, so skilled reports regarding the effectiveness of medical marijuana for activity of various kinds is frequently disrupted. Peripher- a wide range of disorders, whereas opponents question its ally, marijuana produces prominent effects on the cardiovas- efficacy and point to potential deleterious effects of smoked cular system characterized by tachycardia, 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.

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We need to be alert to the danger of classifying all forms of human experience (such as normal disappointment) as mental disorders buy 5 mg finasteride mastercard hair loss zantac. Last modified: November purchase 1 mg finasteride with mastercard hair loss in men taking prednisone, 2017 2 Classification systems Currently, there are two main classification systems. They are composed by large teams of informed professionals using extensive resources. These separate teams also work together, so that their documents are very similar or the same, in most respects. The American Psychiatric Association produces the DSM (mentioned above). The World Health Organisation produces the International Classification of Diseases. However, in many parts of the world (including Australia) it is predominantly used for administrative purposes (for example, as a tool for the counting of the number of cases of particular disorders presenting at clinics, etc. Basis of Classification th Psychiatry is currently where internal medicine was in the 19 century – that is, psychiatry is classifying disorders according to the appearance and statements made by the patient (signs and symptoms), rather than etiology (McHugh, 2005). However, the current systems of classification do have good reliability, which is a good start. The aetiology, anatomy, physiology and pathology underpinning psychiatric disorders is not clear; work is continuing. This is where you come in – I will tell you all I know, but it is your responsibility to extend our knowledge. Neuroimaging, immunology genetics and epigenetics will be among the useful stepping stones. Symptoms and signs These terms are used in all branches of clinical medicine. If you wake up one morning with a severe pain in your big toe, that is a symptom – a symptom is something the patient notices and usually complains about. If your toe is swollen, red and tender to touch, these are signs – that is, observations which are made during an examination. Recognising a particular pattern (thereby identifying the disorder which the patient is suffering) is called making a diagnosis. The most likely disorder in the case of the painful, swollen, red, tender big toe, would be gout. For most medical disorders special tests, such as blood studies and imaging confirm the diagnosis. Unfortunately, at this time, there are no special tests which confirm the presence of particular mental disorders. However, special tests may be used to exclude certain conditions. For example, imaging excludes brain tumours, which may present with signs and symptoms suggestive of major depression or schizophrenia. Last modified: November, 2017 3 No single symptom is found in only one disorder. A pain in the toe may be the result of a broken bone, an infection, a form of arthritis other than gout, pressure on a nerve in the back, leg or foot, or a brain disease. A pain in the toe may commence after the toe and the entire leg have been amputated. A bent leg following a motorbike accident strongly suggests a fractured bone. But other possibilities include dislocation of the knee, or the individual may have escaped injury altogether, and be carrying a congenital deformity of the lower limb. To diagnose a disorder, even with relatively straightforward medical conditions, we collect all the available symptoms and signs, and match them with patterns which have been previously noted and named by individual experts, or panels of experts. There is a wide range of psychiatric signs and symptoms. Examples of symptoms include disturbances of mood (sadness/depression, elation/mania, fear/anxiety), delusions (incorrect beliefs which are held in the absence of evidence, such as, that the individual is being watched by aliens) and hallucinations (perceptions in the absence of stimuli, such as hearing voices when no one else is present). Examples of psychiatric signs include disturbances in behaviour (slowed, rapid or bizarre movement, or inappropriate crying or laughing) and disturbances in thought processes (distractibility or inability to think in a logical manner). Different mental disorders have different patterns of symptoms and signs. As no symptom or sign occurs exclusively in any single disorder, making a diagnosis in a particular case depends on balancing possibilities and probabilities. For example, schizophrenia, mania, drug induced psychosis, and major depressive disorder, may all present with delusions. The nature of the symptom may give some clue (but this should not be given too much weight): the person with schizophrenia is more likely to believe he is being followed by spies, the person with mania is more likely to believe he is the most talented person in the world, the person with drug induced psychosis is more likely to believe he is being watched by the police, and the person with major depressive disorder is more likely to believe he is guilty of neglecting his responsibilities. The combination of the signs and symptoms gives the answer. While the deluded person with schizophrenia is more likely to be also hearing voices, the deluded person with mania is more likely to be also unable to stop talking, and the deluded person with major depression is more likely to be moving slowly or attempting to hang himself. Faking it The topic of faking mental disorder will be discussed in later chapters, but it is worth briefly mentioning the topic at this stage.

Combining stimulants with monoamine oxidase inhibitors: a review of uses and one possible additional indication buy finasteride 1mg otc hair loss in pregnancy. A systematic review of agomelatine-induced liver injury effective 5 mg finasteride hair loss in men and diet. Comparative benefits and harms of second- generation antidepressants: background paper for the American College of Physicians. Effectiveness and safety of adjunctive antidepressants in the treatment of boipolar depression: a review. Anti-inflammatory treatments for mood disorders: systematic review and meta-analysis. Minocycline as an adjunct for treatment-resistant depressive symptoms. National trends in antidepressant medication treatment among publicly insured women. The effects of maternal depression and use of antidepressants during pregnancy on risk of a child small for gestational age. The effects of cognitive behavioural therapy as an anti- depressant is falling. Pecent Pat Endocr Metab Immune Drug Discov 2014; 8: 38-41. Kirsch I, Deacon B, Huedo-Medina T, Moore T, Johnson B. Initial severity and antidepressant benefits: a meta-analysis of data submitted to the Food and Drug Administration. The treatment of depressive stats with G22355 (imipramine hydrochloride). Journal of the American Medical Association 2005; 293:2526-2528. The role of new antidepressants in clinical practice in Canada. Neuropsychiatric Disease and Treatment 2017; 13: 2913-2919. The creation of the concept of an antidepressant: An historical analysis. Antidepressant actions of ketamine: from molecular mechanisms to clinical practice. The mothers, omega-3, and mental health study: a double- blind, randomized controlled trial. Efficacy and long-term tuning parameters of vagus nerve stimulation in long-term treated depressive patients. Antidepressants on trial: how valid is the evidence? Treating depression with the evidence-based psychotherapies: a critique of the current evidence. Australian and New Zealand Journal of Psychiatry 2003; 37:774-775. The psychoimmunological role of omega-3 polyunsaturated fatty acids in major depression. Antipsychotic augmentation for major depressive disorder. The association between C-reactive protein, Interleukin-6 and depression among older adults in the community: a systematic review and meta- analysis. Lamotrigine compared to placebo and other agenst with antidepressant activity in patients with unipolar and bipolar depression. Antidepressant drugs and cardiovascular pathology: a clinical overview of effectiveness and safety. Remission rates during treatment with venlafaxine or selective serotonin reuptake inhibitors. Omega-3 supplementation from pregnancy to postpartum to prevent depressive symptoms. DELIRIUM Introduction Delirium is from Latin and literally means the individual is not at the top of his/her form and travelling at a lower level than normal [de – (off, away from) + lira (a ridge between ploughed furrows)]. Delirium can be an outcome of a general medical conditions, head injury and drug intoxication or withdrawal. It may be the result of the dysfunction of various bodily organs such as kidneys and liver, but it may also be the result of primary pathological processes in the brain. Hospitalized patients > 65 years who experience delirium (compared to those who do not) are at greater risk of mortality (p<.

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Others state that dieting counteracts feeling of worthlessness (Herpertz-Dahlmann et al safe 1mg finasteride hair loss cure 2013 loreal, 2011) 1 mg finasteride mastercard hair loss 7 months postpartum. Socio-cultural factors have shaped “the modern cult of thinness” in Western societies. Evidence suggests a culture bound syndrome, as AN is rare in Asia and developing countries - although this pattern is probably changing (Jennings et al, 2006). Earlier reports found that the prevalence of AN was higher in higher socio-economic schools, but the evidence is now equivocal. Recent studies, however, indicate the risk for hospitalization for NA is related to mothers level of education (higher risk is associated with higher maternal education; Ahren et al, 2011). Perhaps such mothers are more demanding of their daughters. Maintaining factors Mentioned under etiology, the relief of anxiety by dieting and dysphoric mood caused by eating, may also serve as a maintaining factor. Starvation is another maintaining factor, inducing complex physiological and psychological reactions involving central and peripheral mechanisms. Such mechanism may have had evolutionary value, allowing animals to survive periods of food shortage, but in the current setting they serve only to perpetuate a vicious cycle of weight loss. Neuropsychological testing Neuropsychological testing reveals cognitive deficits (Weider et al, 2013) which are related to severity of the disorder, and may play a role in cause and outcome (Zakzanis et al, 2009). Executive control is impaired with problems in set-shifting, attention and decision-making (Treasure & Russell, 2011). A link has been demonstrated between amenorrhoea, brain structure and deficits in cognition, including recall, verbal fluency, working memory, visual reproduction, reading, maths and oral language (Chui et al, 2008). Neuroimaging Neuroimaging studies demonstrate structural and functional abnormalities. There is global reduction of grey (GM) and white matter (WM) during the acute stage. GM is reduced by 5-20%, and WM is reduced to a lesser extent. GM loss is found in the anterior cingulate, hippocampi and the temporal, parietal and prefrontal regions. With recovery GM is restored, but most studies find small residual deficits remain. In one study, there was 60% restoration after 15 weeks of successful treatment. A recent diffusion tensor imaging study (DTI; Kazlouski et al, 2011) revealed WM abnormalities in the fornix, fronto-occipital fasciculus and the posterior cingulum. Magnetic resonance spectroscopy (MRS), which gives information on nerve cell damage by assessing brain metabolites, indicates altered cell membrane turnover which is reversible with recovery. Functional magnetic resonance imaging (fMRI) using visual stimuli of food or body image has been reviewed (Garcia-Garcia et al, 2013). Differences between those with eating disorders and healthy controls located differences in two circuits, 1) limbic and paralimbic areas (associated with reward), and 2) prefrontal regions associated with cognitive functions and control. The insula may be of particular importance (Kaye et al, 2009), as it integrates interoceptive information – confirmation is awaited. The hippocampal volume of women with AN who are food restricting and exercising is larger than that of normal controls. Interestingly hippocampal volume of healthy individuals who engage in food restriction and exercise is also enlarged and is considered to have a protective function (Beadle et al, 2014). Neurotransmitters and cells The pathogenic involvement of the serotonergic system in eating disorders is an established finding (Sigurth et al, 2013). Dopamine (DA) dysfunction, particularly in striatal circuits, may contribute to altered reward centre responses (Kontis and Theochari et al, 2012). The clinical picture The clinical picture is embodied in the DSM-5 diagnostic criteria listed above. The patient is usually a teenage female, brought in by her parents. There has been weight loss, cessation of the menses, fine hair growth on the face and limbs, refusal to eat in the manner expected for her age and family circumstances, particular avoidance of carbohydrate and fatty foods, frequent weighing, often vomiting and excessive laxative use, insomnia, irritability, sensitivity to cold, and withdrawal from friends. The hands and feet are cold, the skin is dry, the pulse is slow (50-60/min) and the blood pressure is low (e. There may be calluses on the dorsum of the second and third digits through frequent contact with the front teeth and erosion of Pridmore S. There may be disorder of hormones, including cortisol, gonadal and thyroid hormones.