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Many pathologies may cause nystagmus 7daystodie infection 200mg floxin for sale, the most common being demyelina tion antimicrobial gym bag floxin 200 mg cheap, vascular disease antibiotic 300 mg order floxin 200mg with mastercard, tumour antimicrobial usage rate generic floxin 400mg line, neurodegenerative disorders of cerebellum and/or brainstem, metabolic causes. Wernicke–Korsakoff’s syndrome), paraneopla sia, drugs (alcohol, phenytoin, barbiturates, sedative-hypnotic drugs), toxins, and epilepsy. Pendular nystagmus may respond to anticholinesterases, consistent with its being a result of cholinergic dysfunction. Periodic alternating nystagmus responds to baclofen, hence the importance of making this diagnosis. These symp toms are thought to re ect critical compromise of optic nerve head perfusion and are invariably associated with the nding of papilloedema. Obscurations mandate urgent investigation and treatment to prevent permanent visual loss. Cross Reference Papilloedema Obtundation Obtundation is a state of altered consciousness characterized by reduced alert ness and a lessened interest in the environment, sometimes described as psy chomotor retardation or torpor. An increased proportion of time is spent asleep and the patient is drowsy when awake. Cross References Coma; Psychomotor retardation; Stupor Ocular Apraxia Ocular apraxia (ocular motor apraxia) is a disorder of voluntary saccade initia tion; re exive saccades and spontaneous eye movements are preserved. Ocular apraxia may be overcome by using dynamic head thrusting, with or without blinking (to suppress vestibulo-ocular re exes): the desired xation point is achieved through re ex contraversive tonic eye movements to the midposition following the overshoot of the eyes caused by the head thrust. Ocular apraxia may occur as a congenital syndrome (in the horizontal plane only: Cogan’s syndrome), or may be acquired in ataxia telangiectasia (Louis–Bar syndrome), Niemann–Pick disease (mainly vertical plane affected), and Gaucher’s disease (horizontal plane only). Cross References Apraxia; Saccades Ocular Bobbing Ocular bobbing refers to intermittent abnormal vertical eye movements, usu ally conjugate, consisting of a fast downward movement followed by a slow return to the initial horizontal eye position. The sign has no precise localizing value, but is most commonly associated with intrinsic pontine lesions. It has also been described in encephalitis, Creutzfeldt–Jakob disease, and toxic encephalopathies. Its patho physiology is uncertain but may involve mesencephalic and medullary burst neurone centres. Variations on the theme include • Inverse ocular bobbing: slow downward movement, fast return (also known as fast upward ocular bobbing or ocular dipping); • Reverse ocular bobbing: fast upward movement, slow return to midposition; • Converse ocular bobbing: slow upward movement, fast down (also known as slow upward ocular bobbing or reverse ocular dipping). Cross Reference Ocular dipping Ocular Dipping Ocular dipping, or inverse ocular bobbing, consists of a slow spontaneous down ward eye movement with a fast return to the midposition. This may be observed in anoxic coma or following prolonged status epilepticus and is thought to be a marker of diffuse, rather than focal, brain damage. Reverse ocular dipping (slow upward ocular bobbing) consists of a slow upward movement followed by a fast return to the midposition. Cross Reference Ocular bobbing Ocular Flutter Ocular utter is an eye movement disorder characterized by involuntary bursts of back-to-back horizontal saccades without an intersaccadic interval (cf. Ocular utter associated with a localized lesion in the paramedian pontine reticular formation. It has occasionally been reported with cerebellar lesions and may be under inhibitory cerebellar control. Cross References Hypotropia; Lateral medullary syndrome; Skew deviation; Synkinesia, Synkinesis; Tullio phenomenon; Vestibulo-ocular re exes Oculocephalic Response Oculocephalic responses are most commonly elicited in unconscious patients; the head is passively rotated in the horizontal or vertical plane (doll’s head maneou vre) and the eye movements are observed. Conjugate eye movement in a direction opposite to that in which the head is turned is indicative of an intact brain stem (intact vestibulo-ocular re exes). With pontine lesions, the oculocephalic responses may be lost, after roving eye movements but before caloric responses disappear. Cross References Caloric testing; Coma; Doll’s head manoeuvre, Doll’s eye manoeuvre; Head impulse test; Roving eye movements; Supranuclear gaze palsy; Vestibulo-ocular re exes Oculogyric Crisis Oculogyric crisis is an acute dystonia of the ocular muscles, usually causing upward and lateral displacement of the eye. It is often accompanied by a dis order of attention (obsessive, persistent thoughts), with or without dystonic or dyskinetic movements. It occurs particularly with symptomatic (secondary), as opposed to idiopathic (primary), dystonias, for example, postencephalitic and neuroleptic-induced dystonia, the latter now being the most common cause. This is usually an acute effect but may on occasion be seen as a consequence of chronic therapy (tardive oculogyric crisis). It has also been described with Wilson’s dis ease, neuroleptic malignant syndrome, and organophosphate poisoning. Lesions within the lentiform nuclei have been recorded in cases with oculogyric crisis. Treatment of acute neuroleptic-induced dystonia is either parenteral benzo diazepine or an anticholinergic agent such as procyclidine, benztropine, or trihexyphenidyl. Oculogyric crisis and abnormal magnetic resonance imaging signals in bilateral lentiform nuclei. Fascicular (within substance of midbrain): all muscles or speci c mus cles involved, + other clinical signs expected, such as contralateral ataxia (Claude’s syndrome), hemiparesis (Weber’s syndrome). Orbit: paresis of isolated muscle almost always from orbital lesion or muscle disease. Oculomotor nerve palsies may be distinguished as ‘pupil involving’ or ‘pupil sparing’, the former implying a ‘surgical’, the latter a ‘medical’ cause, but this distinction only holds for complete palsies. Transtentorial (uncal) 250 Onion Peel, Onion Skin O herniation due to raised intracranial pressure may, particularly in its early stages, cause an oculomotor nerve palsy due to stretching of the nerve, a ‘false-localizing sign’. In young patients this is most often due to demyelination, in the elderly to brainstem ischaemia; brainstem arteriovenous malformation or tumour may also be responsible. A vertical one-and-a-half syndrome has also been described, characterized by vertical upgaze palsy and monocular paresis of downgaze, either ipsilateral or contralateral to the lesion. Electro-oculographic analyses of ve patients with deductions about the physiological mechanisms of lateral gaze. A unilateral disorder of the pontine tegmentum: a study of 20 cases and a review of the literature. It re ects the somatotopic sensory representation in the spinal nucleus of the trigeminal nerve: midline face (nose, mouth) represented rostrally, lateral facial sensation represented caudally. A distinction is sometimes drawn between: • External ophthalmoplegia: weakness of the extraocular muscles of central, neuromuscular, or myopathic origin: Supranuclear. The term ‘ophthalmoplegia plus’ has been used to denote the combination of progressive external ophthalmoplegia with additional symptoms and signs, indicative of brainstem, pyramidal, endocrine, cardiac, muscular, hypothalamic, or auditory system involvement, as in mitochondrial disease. Cross References Coma; Decerebrate rigidity; Emposthotonos Oppenheim’s Sign Oppenheim’s sign is a variant method for eliciting the plantar response, by appli cation of heavy pressure to the anterior surface of the tibia, for example, with the thumb, and moving it down from the patella to the ankle. Extension of the hal lux (upgoing plantar response, Babinski’s sign) is pathological. Like Chaddock’s sign, Oppenheim’s sign always postdates the development of Babinski’s sign as a reliable indicator of corticospinal pathway (upper motor neurone) pathology. Although some normal individuals can voluntarily induce opsoclonus, gen erally it re ects mesencephalic or cerebellar disease affecting the omnipause cells which exert tonic inhibition of the burst neurones which generate saccades. Of the paraneo plastic disorders, opsoclonus associated with lung and breast tumours persists and the patients decline from their underlying illness; neuroblastoma associated opsoclonus may be steroid responsive. Clinical outcome in adult onset idiopathic or paraneoplastic opsoclonus–myoclonus. Cross References Ocular utter; Saccadic intrusion, Saccadic pursuit; Square wave jerks Optic Aphasia Optic aphasia is a visual modality-speci c naming disorder. It has sometimes been grouped with associative visual agnosia, but these patients are not agnosic since they can demonstrate recognition of visually presented stimuli by means other than naming. Moreover, these patients are not handicapped by their de cit in everyday life, whereas agnosic patients are often functionally blind. Objects that are semantically related can be appropriately sorted, indicat ing intact semantics. This is not simply anomia, since the de cit is speci c to visual stimuli; objects presented in tactile modality, or by sound, or by spoken de nition, can be named. Naming errors are often semantic, and perseverations (‘conduit d’approche’) are common. Perception is intact, evidenced by the ability to draw accurately objects which cannot be named. Optic aphasia is associated with unilateral lesions of the left occipital cortex and subjacent white matter. Visual agnosia: disorders of object recognition and what they tell us about normal vision. A visual-speech disconnexion syndrome: report of a case with optic aphasia, agnosic alexia and colour agnosia. Cross References Anomia; Conduit d’approche; Visual agnosia 254 Optic Atrophy O Optic Ataxia Optic ataxia is impaired voluntary reaching for a visually presented target, with misdirection and dysmetria.

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The symptom in Criterion A must have been present for at least 6 months and must be experienced on almost all or all (approximately 75%-100%) occasions of sexual activ­ ity (in identified situational contexts or antimicrobial on air filters studies about floxin 400 mg on line, if generalized antibiotic kills 99.9 bacterial population order floxin visa, in all contexts) bacteria in space discount floxin 200 mg without a prescription. The symptom in Criterion A causes clinically significant distress in the individual infection wisdom tooth extraction order floxin overnight. Specify whether; Lifelong: the disturbance has been present since the individual became sexually active. Specify whether: Generalized: Not limited to certain types of stimulation, situations, or partners. Specify current severity: iUlild: Ejaculation occurring within approximately 30 seconds to 1 minute of vaginal penetration. Moderate: Ejaculation occurring within approximately 15-30 seconds of vaginal pen­ etration. Severe: Ejaculation occurring prior to sexual activity, at the start of sexual activity, or within approximately 15 seconds of vaginal penetration. Estimated and measured intravaginal ejaculatory latencies are highly correlated as long as the ejaculatory latency is of short duration; therefore, self-reported estimates of ejaculatory latency are sufficient for diagnostic pu oses. A 60-second intravaginal ejaculatory latency time is an appropriate cutoff for the diagnosis of lifelong premature (early) ejaculation in heterosexual men. There are insufficient data to determine if this duration criterion can be applied to ac­ quired premature (early) ejaculation. The durational definition may apply to males of varying sexual orientations, since ejaculatory latencies appear to be similar across men of different sexual orientations and across different sexual activities. Associated Features Supporting Diagnosis Many males with premature (early) ejaculation complain of a sense of lack of control over ejaculation and report apprehension about their anticipated inability to delay ejaculation on future sexual encounters. The following factors may be relevant in the evaluation of any sexual dysfunction: 1) partner factors. Prevaience Estimates of the prevalence of premature (early) ejaculation vary widely depending on the definition utilized. Internationally, more than 20%-30% of men ages 18-70 years report concern about how rapidly they ejaculate. Some men may experience premature (early) ejaculation during their initial sexual encounters but gain ejaculatory control over time. It is the persis­ tence of ejaculatory problems for longer than 6months that determines the diagnosis of pre­ mature (early) ejaculation. In contrast, some men develop the disorder after a period of having a normal ejaculatory latency, known as acquired premature (early) ejaculation. There is far less known about acquired premature (early) ejaculation than about lifelong premahire (early) ejaculation. The acquired form likely has a later onset, usually appearing during or af­ ter the fourth decade of life. Reversal of medical conditions such as hyperthyroidism and prostatitis appears to restore ejaculatory latencies to baseline values. In approximately 20% of men with premature (early) ejacu­ lation, ejaculatory latencies decrease further with age. Age and relationship length have been found to be negatively associated with prevalence of premature (early) ejaculation. Premature (early) ejaculation may be more common in men with anx­ iety disorders, especially social anxiety disorder (social phobia). There is a moderate genetic contribution to lifelong prema­ ture (early) ejaculation. Premature (early) ejaculation may be associated with dopamine transporter gene polymorphism or serotonin transporter gene polymorphism. Thyroid disease, prostatitis, and drug withdrawal are associated with acquired premature (early) ejaculation. Positron emission tomography measures of regional cerebral blood flow dur­ ing ejaculation have shown primary activation in the mesocephalic transition zone, includ­ ing the ventral tegmental area. C uiture-R elated Diagnostic issues Perception of what constitutes a normal ejaculatory latency is different in many cultures. Such differences may be ex­ plained by cultural or religious factors as well as genetic differences between populations. Gender-Reiated Diagnostic Issues Premature (early) ejaculation is a sexual disorder in males. Males and their sexual partners may differ in their perception of what constitutes an acceptable ejaculatory latency. There may be increasing concerns in females about early ejaculation in their sexual partners, which may be a reflection of changing societal attitudes concerning female sexual activity. Diagnostic iViarlcers Ejaculatory latency is usually monitored in research settings by the sexual partner utilizing a timing device. For vaginal intercourse, the time between intravaginal penetration and ejaculation is measured. Functional Consequences of Prem ature (Eariy) Ejaculation A pattern of premature (early) ejaculation may be associated with decreased self-esteem, a sense of lack of control, and adverse consequences for partner relationships. It may also cause personal distress in the sexual partner and decreased sexual satisfaction in the sexual partner. Ejaculation prior to penetration may be associated with difficulties in conception. When problems with premature ejaculation are due exclusively to substance use, intoxication, or withdrawal, substance/ medication-induced sexual dysfunction should be diagnosed. It is necessary to identify males with normal ejaculatory latencies who desire longer ejaculatory latencies and males who have episodic premature (early) ejaculation. Neither of these situations would lead to a diagnosis of premature (early) ejaculation, even though these situations may be distressing to some males. Comorbidity Premature (early) ejaculation may be associated with erectile problems. In many cases, it may be difficult to determine which difficulty preceded the other. Lifelong premature (early) ejaculation may be associated with certain anxiety disorders. Acquired premature (early) ejaculation may be associated with prostatitis, thyroid disease, or drug withdrawal. A clinically significant disturbance insexual function is predominant inthe clinical picture. The disturbance is not better explained by a sexual dysfunction that is not substance/ medication-induced. Such evidence of an independent sexual dysfunction could in­ clude the following: the symptoms precede the onset of the substance/medication use; the symptoms persist for a substantial period of time. Note: this diagnosis should be made instead of a diagnosis of substance intoxication or substance withdrawal only when the symptoms in Criterion A predominate in the clinical picture and are sufficiently severe to warrant clinical attention. If a mild substance use disorder is comorbid with the substance induced sexual dysfunction, the 4th position character is “1,”and the clinician should record “mild [substance] use disorder”before the substance-induced sexual dysfunction. With onset during withdrawai: If criteria are met for withdrawal from the substance and the symptoms develop during, or shortly after, withdrawal. With onset after medication use: Symptoms may appear either at initiation of medi­ cation or after a modification or change in use. Specify current severity: Mild: Occurs on 25%-50% of occasions of sexual activity. The name of the substance/medication-induced sexual dysfunction begins with the specific substance. For example, in the case of erectile dysfunction occurring during intoxication in a man with a severe alcohol use disorder, the diagnosis is 291. When more than one substance is judged to play a sig nificant role in the development of the sexual dysfunction, each should be listed separately. When recording the name of the disorder, the comorbid substance use disorder (if any) is listed first, followed by the word "with," followed by the name of the substance-induced sexual dysfunction, followed by the specification of onset. For example, in the case of erectile dysfunction occur­ ring during intoxication in a man with a severe alcohol use disorder, the diagnosis is F10.

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Anemia is present when this value in blood falls below age and gender appro priate normal values safe antibiotics for sinus infection while pregnant generic floxin 200mg on line, which are de ned by values two standard deviations below the mean for normal individuals of similar age and gender antibiotics for canine gastroenteritis discount floxin amex. The volume of red blood cells reported as a percentage of the total volume of blood present is the hematocrit prednisone and antibiotics for sinus infection buy 400mg floxin overnight delivery. In most cases the two values relate to antibiotics walking pneumonia purchase floxin canada one another roughly by a factor of three (hemoglobin 3 hematocrit). During puberty, an increase in hemoglobin occurs in males due to androgenic ster oids. The normal range for hemoglobin in males is therefore higher than for females (Table 4. In particular, over the two decades after 70 years of age, men’s hemoglobin levels drop by about 1g/dL. Acute blood loss Loss of blood acutely may not be associated with an immediate decline in hemoglobin concentration, since this loss consists of an equivalent proportion Concise Guide to Hematology, First Edition. However, after volume repletion a decrease in the hemoglobin concentration or hematocrit proportional to the amount of blood lost may be observed. Inadequate production There are a number of entities commonly associated with an inadequate pro duction of red blood cells. With rare exception iron de ciency anemia in adults results from chronic blood loss. In women, menstrual blood loss may explain its development (and it is present in about 5% of menstruating females in the United States). In men, the identi cation of iron de ciency anemia should always provoke a search for blood loss. Even in younger women, consideration of gastroin testinal blood loss may merit consideration, depending on individual cir cumstance (see Chapter 4). In this condition the iron regulatory protein hepcidin decreases the ability of the reticuloendothelial system to release stored iron. The lack of bioavailable iron essentially mimics the situation with iron de ciency anemia from blood loss. When combined with the suppressive effect of certain cytokines on red blood cell production, this circumstance leads to a mild to moderate anemia that may share some morphologic features with iron de ciency. The syn thesis of this hormone is regulated by the oxygen tension in the peri glomerular cells of the kidney. Hypoxia drives the synthesis of erythropoietin and its release into the bloodstream, which stimulates the maturation and development of erythrocyte precursors in the bone marrow. These activities 26 Concise Guide to Hematology result in an increase in red blood cell mass, bringing additional oxygen to the kidney, and ultimately completing the feedback loop by down regulating production of erythropoietin. A reduction in renal function is generally accompanied by a reduction of erythropoietin production. To provide a few examples, hypothy roidism may be associated with a mild to moderate anemia sometimes associated with macrocytosis; adrenal cortical insuf ciency may be accom panied by a normocytic anemia; and decreased levels of serum testosterone may lead to a mild anemia in males. In contrast to aplastic anemia, in which two or more cell lineages are affected, pure red cell aplasia is characterized by preservation of the white blood cell count and platelet count. In this case, the blood forming bone marrow space is taken over by cells or material that should not be there. Causes of bone marrow replacement include hematologic malignancies such as leukemia or lymphoma, meta static cancer (most commonly breast or prostate), infection with fungi or other microorganisms, and brosis such as that which may occur in con junction with primary myelo brosis. Folate de ciency is generally related to inadequate dietary intake or to increased requirements due to red blood cell hemolysis. Vitamin-B12 is released from food in the acidic environment of the stomach and binds to the intrin sic factor that is secreted by the parietal cells in the stomach. The intrinsic factor vitamin B 12 complex then travels to the terminal ileum where it is absorbed. The deposition of iron in mitochondria leads to the mor phologic entity of ringed sideroblasts in the bone marrow when it is stained for iron. Exactly as the name implies, ringed sideroblasts are cells in which Anemia: Clinical Approach 27 iron-laden mitochondria encircle at least one-third of the circumference of the erythroblast nucleus. Usually at least ve iron laden mitochrondria need to be seen encircling the nucleus to make diagnostic criteria. Heredi tary forms of sideroblastic anemia are rare and may be X-linked, autosomal dominant or recessive. Destruction Normally red blood cells circulate for about 100 to 120 days before they are cleared by the reticuloendothelial system. Premature red blood cell destruc tion may result from intrinsic defects within hemoglobin, cytoskeletal pro teins, or enzymes. It may also result from defects extrinsic to the erythrocyte, including mechanical forces and antibody or complement-mediated red cell breakdown. Alpha or beta thalassemia traits (loss of two alpha genes, or one beta gene) are common causes of microcytosis associated with little or no anemia. Microcytosis occurs in thalassemia because the de ciency in hemoglobin stimulates additional cell divisions of erythrocyte precursors in order to try to preserve the hemoglobin concentration. Tha lassemia trait is particularly common in individuals from Africa, Asia, and the Mediterranean Basin. Among the most commonly encountered struc tural mutations is a glutamine to valine substitution at position 6 of the beta globin gene. This change results in the production of hemoglobin S, which tends to polymerize in its deoxygenated state. Heterozygotes with one copy of hemoglobin S (sickle cell trait) are relatively protected against infection with the malaria parasite. This structural mutation provides a survival advantage; it is the selective pressure leading to persistence of this mutation. Homozygotes with two copies of hemoglobin S have sickle cell anemia, a serious life-de ning hematologic disorder. Many other structural mutations exist and can result in changes in the properties of hemoglobin, such as reducing its solubility. Mainte nance of the normal biconcave shape requires intact cytoskeletal architec ture. Defects in any of the proteins involved, including ankyrin, spectrin, and band 3, among others, can lead to changes that reduce the resiliency of red blood cells as they pass through the narrow passageways in the spleen and other portions of the circulation. This initially leads to the for mation of spherocytes, and ultimately results in hemolysis. The resulting disorder, hereditary spherocytosis, is most common in individuals of north ern European descent. Abnormalities in the lipid composition 28 Concise Guide to Hematology of the red blood cell membrane result in cells that are abnormally stiff and unable to rebound from deformities arising from transit of the circulation. The lack of one such erythrocyte phosphatidylinositolglyan linked membrane protein, decay accelerating factor, is associated with the hemolysis of red blood cells through the unopposed constitutive activation of components of the complement cascade (see Chapter 7). This pathway provides the red blood cell with reduction capacity against oxidant stress. The two most common mutations cause a reduction in cell enzyme activity in the aging erythrocyte (A-variant) or result in absent function throughout the red cell life span (Mediterranean variant). Common causes of oxidant stress include medications such as antimalarials, dapsone, and sulfamethoxazole (see Chapter 7). In these conditions abnor malities in the microvasculature result in shearing of the red blood cell and the formation of red cell fragments called schistocytes. Certain uncom mon infections, such as those with clostridia or bartonella species can also be associated with the production of toxins that lead to red blood cell destruction through what is essentially mechanical disruption of the mem brane. Accelerated or malignant hypertension and vasculities are addi tional etiologies producing mechanical destructional of red blood cells. Malfunctioning mechanical valves, perivalvular leaks, as well as long dis tance running can all result in the mechanical destruction of red blood cells by trauma. Warm autoantibodies are often idiopathic, but may be associated with hematologic malignancies such as chronic lymphoid leukemia or rheumatologic disorders such as systemic lupus erythematosus. Similarly, Anemia: Clinical Approach 29 cold autoantibodies may be idiopathic or associated with lymphoprolifera tive or rheumatologic disorders. Transient cold agglutinins may be associ ated with infectious mononucleosis and infection with mycoplasma (see Chapter 8).

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Thus functional imaging has led to antibiotics for uti webmd purchase floxin 400mg visa an even greater explosion of data in this area than in the other domains of neuropsychology discussed in this book antibiotic resistance netherlands discount floxin 200mg on line. In addition to antibiotic 3 pack purchase floxin 200 mg free shipping the amygdala prescribed antibiotics for sinus infection purchase floxin us, fearful expressions have also been reported to activate the thalamus, anterior cingulate, and anterior insula (Morris et al. Facial expressions of anger activate regions of the temporal and pre frontal cortices, including anterior cingulate (Blair et al. Sadness, in contrast, activates right-sided tem poral lobe regions and the amygdala (Blair et al. Enhanced activity correlating with increasing intensity of neural response in the amygdala associated with viewing aversive disgust (Phillips et al. Data obtained at the Neuroscience and been shown to activate areas of the basal ganglia Psychiatry Unit, Manchester. Happiness is the only positive emotion of the six and, interestingly, increasing happiness in stimuli has been associated with decreasing amygdala response (Morris et al. Of the six basic emotions, surprise is the least investigated and has some distinct qualities. Speci cally, surprise can be described as a “transitory emotion”, in that it is brie y experienced and can change into other expressions depending on the nature of the surprise (Posamentier & Abdi, 2003). You may be surprised to see a long-lost friend and the surprise gives way to happiness. By contrast, you may be surprised to nd your car windscreen smashed and the surprise gives way to anger. Kim and colleagues (2003) investigated brain responses to surprised facial expressions in relation to how they were rated (positive–negative) by partici pants. Negative ratings of surprised facial expressions elicited enhanced activation in the right amygdala, while positive ratings were associated with larger signal changes in ventral prefrontal regions. Neuroimaging thus reveals a common network of regions involved in process ing face emotion information, with some variation depending on the emotion involved. More recent studies have looked at face emotion processing in various patient groups as well as how social factors may in uence normal face processing. This study reported di erential amygdala activity depending on the race of people depicted in the stimulus materials (photographs) and that of participants. Meanwhile Kaplan, Freedman, and Iacoboni (2007) have reported di erences in responses to politicians’ faces depending on the political a liation of participants. These studies hint at the wide range of cultural and social factors that may in uence how we process face emotion. Neuroimaging of emotion and motivation 275 Imaging studies of other emotional stimuli Face stimuli have been more widely used in imaging studies than other emotional stimuli. Pleasant and unpleasant emotions were both associated with enhanced blood ow in regions including medial prefrontal cortex and thalamus. Unpleasant emotion addition ally activated regions including parahippocampal gyrus, hippocampus, and amygdala. A similar nding has been observed in a study using an emotional go–no-go task with verbal stimuli (Elliott et al. The evaluation of unpleasant words additionally activated subcortical regions, including the thalamus, caudate, and amygdala (Maddock, Garrett, & Buonocore, 2003). By contrast, pleasant music evoked responses in regions including inferior frontal gyrus and ventral striatum. Imaging emotion generation the studies described above have considered how the brain responds to external emotional stimuli, whether faces, pictures, words, or music. In general these studies have shown that both positive and negative emotional stimuli are medi ated by neural responses in temporal and prefrontal cortices and limbic struc tures. Negative emotions tend to be more associated with amygdala responses while positive emotions may elicit di erential prefrontal and striatal responses. Some of the stimuli used in these experiments may also have a ected the emo tional state of participants. Emotional lm clips and music, in particular, can be used as part of mood-induction procedures as they can evoke a transient state of emotional experience. Happy music can lift our mood for example, while a frightening lm clip may cause us to feel genuine fear. Neuroimaging studies have also looked more explicitly at the experience of emotion. In a more direct attempt to separate perception of emotional content from subjective experience of emo tion it was found that amygdala response was speci c to perceiving emotion, while hippocampal and prefrontal responses were associated with subjective feelings of emotion (Garrett & Maddock, 2006). These studies are beginning to 276 Chapter 10 Emotion and motivation explore the subtleties of emotional experience in a way that is inaccessible to classic neuropsychology. As we shall see in the last section of this chapter, under standing how emotion is perceived and generated has enormous implications for psychiatry. Imaging studies of people eating or drinking are problematic because they involve large amounts of head movements, and an important prerequisite of good imaging data is that partici pants keep their heads still! So, rather than studying people actually eating, an alternative approach has been to use tastes and smells strongly associated with food. Even if you do not recognise the term, you will be familiar with an e ect known as “sensory-speci c satiety”. If you have just eaten a large amount of a particular food, the reward value of that food rapidly diminishes; after one chocolate biscuit you may be very keen to have another but after ve or six, your desire to eat more is substantially reduced. Participants were fed large amounts of chocolate and asked to rate how pleasant it was at regular intervals. Imaging studies of nancial reward and loss In the neuroimaging context, most studies of reinforcement have used nancial rewards. As we discussed earlier, money is not a primary reinforcer in the classic sense; it has no intrinsic physiological value, but it does have enormous social value, and is a strong behavioural motivator in most modern societies. From an empirical viewpoint, money is a very useful reinforcer, as various parameters (size of reward, probability of reward, etc. Participants were presented with a series of computerised cards on which they knew a number from 1 to 9 would appear, and had to guess whether the number would be greater or less than 5. Increased responses were seen in the dorsal and ventral striatum after a reward, while decreased responses were seen after a punishment. A similar study (Elliott, Friston, & Dolan, 2000) also assessed responses to winning and losing money and reported striatal responses to winning. These studies are predicated on the fact that reinforcement is critically dependent on the extent to which outcomes match expectations. If you fully expect to receive a reward, your response to it may be more muted than if it was at least partly unexpected. In fact if you do not receive an expected reward, the experience feels more like a punishment. Similarly, if you don’t receive an expected punishment, you may feel almost as though you had received a reward (the positive experience of “getting away with it”). Thus reward and punishment responses in the brain are extensively modulated by expectations, and new modelling and analysis techniques in functional imaging are allowing these relationships to be explored. Imaging gambling tasks Neuropsychologically, the Iowa gambling task has been an important tool for studying how people translate knowledge of reinforcement contingencies into appropriate behavioural choices. The Iowa task is extremely complicated and hard to use in an imaging context because there are so many variables to control. The size of the segments re ected the probability of winning on that colour and boxes below the spinner showed how large a win would be associated with each colour. Neural responses in the orbitofrontal cortex associated with varying the value of nancial reward in a cognitive task. By contrast, once the decision had been made, anticipa tion of reinforcement was associated with activity in the ventral striatum. Studies have also allowed di erences in individual behaviour on gambling tasks to be studied. Among normal people there is considerable variation in how willing someone is to take a risk. Some people are characterised as “loss averse” which means that they are less likely to make risky choices that could lead to a sub stantial loss. In studies of emotion, imaging has con rmed the importance of the amygdala and ventromedial prefrontal cortex, highlighting a particular role for the amygdala in the recognition and experience of negative emotions.

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