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Bell (1992) gives detailed advice about the evidence to be gathered and the preparation of the report. Time should be spent in obtaining the fullest possible information about details of the injury itself, from which to judge the likely severity and distribution of brain damage. Drugs, particularly analgesic and sedative, administered in the early days after injury should be documented; they may prolong the period of reduced conscious level so that if their effects are ignored the severity of injury may be overestimated. It is rarely possible to compare the results of psychological testing with results obtained before the injury occurred, but valuable interpretations can often be made when results are judged against previous educational and occupational attainments. The results of psychological testing should not be given unbacked by the general clinical impression of severity of impairment, since dementia may be manifest in behaviour and personality deterioration as well as in cognitive dysfunction. Some understanding of the psychological test methods used to detect poor effort or malingering may be required. The report should embody the date and place of examination and specify the length of contact with the patient and his illness. Additional sources of information that have contributed to the material in the report should be listed: reports from informants, general practitioners and other hospitals, and the results of special investigations performed. In other words, full descriptive evidence should always be presented before matters of interpretation. The question of prognosis should be handled with caution, and expressed in probabilities rather than certainties. Finally, the formulation of aetiology will embrace the likely role of trauma in relation to the picture presented by the patient, together with such constitutional and other antecedent circumstances that may have conferred special vulnerability. In cases where there is evidence of antecedent vulnerability it may be useful to consider the likely natural history of the patient had the injury not occurred. Where causal chains of circumstances have followed in the wake of injury and added to the disability, these should also be clearly and simply explained. Full supporting data must always be given to help define the contribution due to injury and that due to other additional factors. The report should be as concise as possible and should avoid technical jargon, or where this is inevitable a simple explanation may need to be included. It is sometimes necessary to bear in mind that the patient may himself have access to the report, although this should not be allowed to dictate any alteration in material content. Finally, it is perhaps worth mentioning that in the interests of justice it behoves doctors to re-read their reports with scrupulous attention to the overall impression that it makes. Their evidence will have a powerful influence, even though the final decision regarding compensation will be made by others. Conversely, when the patient has been importunate, dilatory or difficult to treat, a careful re-reading of the report may indicate that the writer has come to be unfairly biased against him. Nevertheless, it should be noted that clinicians are well placed to inform the public and government about the consequences of head injury and the value of measures aimed at reducing the risk of head injury. Depending on the severity of the injury, strategies for return to work or for more intensive rehabilitation, possibly in a residential unit, will need to be considered. The first step must always be the systematic evaluation of residual disabilities and assessment of the causes operating in the individual case. Early management Prevention of post-concussion syndrome Guidelines for management of head injuries in the accident and emergency room of a severity that may or may not require admission tend to focus on early detection of neurosurgical complications. What is often lacking is guidance for the patient with less severe injury on how to manage over the days and weeks that follow, back at home and trying to get back to work. The majority of patients with mild head injury are going to do well without any intervention and, for example, early enforced bed rest of a few days is probably not helpful (De Kruijk et al. However, for those whose injury was severe enough to require admission to hospital this intervention did reduce postconcussional symptoms and social disability at 6 months (Wade et al. Others, using similar strategies aimed at providing guidance on how to manage symptoms, have found similar effects (Mittenberg et al. It seems that a single session of assessment and advice may be sufficient (Paniak et al. Early rehabilitation for severe injury Rehabilitation should be planned and supervised with care from the early stages of recovery. The initial convalescent period is usually undertaken in hospital, and ideally in an atmosphere as free from stress as possible. Physical activity should be encouraged, provided certain limits are imposed, and the value of early mobilisation has come to be generally recognised (Lewin 1968). It is essential that the patient and family know that a full assessment has been made of any possible damage to his brain, and feel confident that the advice given is soundly based. However, early estimates of prognosis should be given cautiously, offering a broad window of possible outcomes. Neurological sequelae the main areas that require evaluation are locomotion, upper extremity function and impairment of communication. Hemiparesis requires physiotherapy when more than mild and transient, similarly paraparesis or ataxia of gait. Occupational therapy has a special place in restoring useful function to the upper limbs, and speech therapy in assessing that food and drink can be safely swallowed and in helping the resolution of dysphasia or dysarthria. When treatment is undertaken in hospital or in rehabilitation units the nursing staff can contribute usefully in these areas, likewise the relatives when patients are treated on an outpatient basis. Cognitive impairment Full psychometric assessment is a first essential, and serves to highlight both areas of deficit and areas of preserved function on which to capitalise. Memory functions are of crucial importance and should be comprehensively evaluated from the outset. Some general principles should underlie the planning of the therapeutic programme. First, the confidence, and where possible the full cooperation, of the patient must be secured. The relatives also must be kept informed of aims, progress and necessary limitations. Second, an optimistic and positive approach is required in order to instil enthusiasm, with ready allowance for fatigue and tolerance of shortcomings. Third, the programme must be graded, with goals at any stage that are realisable, rational and acceptable to the patient (Wilson et al. Self-esteem is bolstered by the setting of tasks that can be mastered, however simple these may need to be at first. Finally, throughout the course of rehabilitation careful attention must be paid to basic matters such as the maintenance of optimal physical health. It is vital to detect depression, and to make due allowance for matters of personality change as well as intellectual impairment. Reviews of the efficacy of cognitive rehabilitation suggest that some treatments may be effective (Cicerone et al. However, there has been a tendency to concentrate on outcomes that are closely linked to the intervention, for example Head Injury 247 a measure of speed of information processing in a study aimed at improving attention, rather than outcomes that patients themselves will be aware of, for example in terms of improved quality of life or reduced handicap (Carney et al. It is important to use outcome measures that as well as being reliable are relevant to the patient or carer (Fleminger & Powell 1999). Whereas impairment refers to the direct effects of the disease on physiological or psychological performance, disability refers to the consequences of impairments on the ability of the person to undertake activities. An example of this latter effect is the dramatic differences in handicap experienced by a professional violinist compared with a right-handed painter, when both suffer the same disability due to a left hemiplegia. Cognitive rehabilitation can be broadly categorised into those strategies that attempt to reduce the impairment and those that attempt to reduce the disability and handicap through compensatory techniques (Ylvisaker et al. For example, in patients with amnesia, rehabilitation might aim to reduce the degree of memory impairment by the use of memory exercises or drills aimed at improving memory, or it might look at compensatory strategies to help them cope with memory impairment and enable them to remain independent at home. Compensatory strategies could include electronic memory aids, errorless learning strategies, mnemonics, and cooking with an electric cooker with a timer rather than gas. A good example is Neuropage, an electronic paging device that is programmed according to the needs of the individual patient to bleep several times during the course of the day to remind the patient to undertake various activities. This was found not only to reduce memory failures but to improve planning (Wilson et al. Such compensatory techniques are readily aligned with goal planning, which almost invariably forms the basis for planning and implementing rehabilitation. The research evidence suggests that rehabilitation aimed at reducing cognitive impairments may not be as effective as techniques aimed at improving disability and handicap (Wilson 2002). It is sometimes argued that rehabilitation does not necessarily require a full theoretical understanding of the psychological processes underpinning the cognitive function that is impaired; and that a simple functional analysis of the consequences of the impairment is adequate to guide the rehabilitation strategy to be used. Evidence in support of this was presented in a meta-analysis examining studies aimed at improving attention (Park & Ingles 2001). Attention retraining techniques typically involve repetitive exercises or drills requiring a response to visual or auditory stimuli and are often informed by the theoretical ideas of cognitive neuroscience.


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Clouding of consciousness denotes the mildest stage of impairment of consciousness which is detectable clinically, on the continuum from full alertness and awareness to coma. As such it is manifest as slight impairment of thinking, attending, perceiving and remembering, in other words as mild global impairment of cognitive processes in association with reduced awareness of the environment. The patient will frequently, though not always, appear to be drowsy but this is not to be confused with the normal transition to sleep. The essential features appear to include abrupt onset and ending, variable duration from hours to weeks, and the interruption of quiet periods of behaviour by unexpected and sometimes violent acts or outbursts of rage or fear. Clearly, therefore, the term is used to cover a variety of syndromes and can now have little useful meaning. It is, moreover, widely employed to describe hysterical manifestations in addition to acute organic reactions (particularly some types of complex partial seizure). Coma represents the extreme of a graded continuum of impairment of consciousness, at the opposite pole of the spectrum from full alertness and awareness of the environment. The patient is incapable of sensing or responding adequately to external stimuli or inner needs, shows little or no spontaneous movement apart from respiration, and no evidence whatever of mental activity. At its deepest there is no reaction to stimuli of any intensity, and corneal, pupillary, pharyngeal, tendon and plantar reflexes are absent. Lighter degrees of coma (semicoma) allow partial response to stimulation, though this is incomplete, mostly non-purposive and usually consists of ineffectual movements or rubbing and scratching of the stimulated area. Bladder distension may call forth groaning or ill-coordinated motor stirring but the patient is still incontinent. Tendon reflexes may or may not be obtainable, and the plantars may be either flexor or extensor. The Glasgow Coma Scale, which has proved its usefulness for the grading of depth of coma, is described in Chapter 4, Measuring head injury severity. In deep sleep and in coma the pictures may be closely similar on superficial observation, but the sleeper can be roused again to normal consciousness by the efforts of the examiner. He may wake spontaneously to unaccustomed stimuli, or in response to inner sensations such as hunger or bladder distension. In sleep there is sporadic continuing mental activity in the form of dreams which leave traces in memory. The distinguishing features usually accepted are that in coma the eyes remain shut even in response to strong arousal stimuli, do not resist passive opening, and do not appear to be watchful or follow moving objects; movements in response to stimulation are never purposeful, and there is no subsequent recall of events or inner fantasies from the time in question (see also persistent vegetative state, Chapter 4). Stupor is an exceedingly difficult term to define, principally because it has been used widely in neurological and psychiatric practice to refer to conditions with markedly different causation. Sometimes it is used loosely and wrongly to refer to an intermediate stage on the continuum of impairment of consciousness that leads ultimately to coma; sometimes to refer to a syndrome characteristic of lesions in the neighbourhood of the diencephalon and upper brainstem and called akinetic mutism; and sometimes to clinical states superficially similar to this but due to hysterical, depressive or schizophrenic illness. Stupor is thus a term without definite nosological status, but valuable when properly used in referring, in essence, to a clinical syndrome of akinesis and mutism but with evidence of relative preservation of conscious awareness. There is a profound lack of responsiveness, and evidence of impairment, or at least putative or apparent impairment, of consciousness. Speech and spontaneous movement are absent or reduced to a minimum, and the patient is inaccessible to the great majority of external stimuli. Unlike coma and semicoma, however, the patient may at first sight appear to be conscious, since the eyes may be open and seem to be watchful. The patient may direct his gaze towards the examiner and the eyes may follow moving visual stimuli in a manner which appears to be purposeful rather than random. Relative preservation of consciousness is also betrayed by the response to stimulation: strong painful stimuli may induce blinking or purposeful coordinated efforts to dislodge the noxious agent. Moreover, in some cases there is subsequent recall of events or delusional fantasies occurring in the stuporose state. Typically, spontaneous movements are absent but there may be tremors, coarse twitching or, in light stupor, restless stereotyped motor activity. The latter may seem to occur in response to hallucinatory experiences, or to display special meaning in stupors due to psychotic illness. Complete mutism is the rule, but again there may sometimes be partially coherent muttering, or arousal may be possible to the extent of brief stereotyped exclamations. In light stupor there may be no sphincter disturbance, and even feeding may be possible with coaxing. Simple responses to commands may then be obtained, though these are slow, inaccurate and often ill-coordinated. The least severe examples may merge indefinably with severe psychomotor retardation in psychotic depression, or with severe blocking of thought and volition in catatonic schizophrenia. The causes of stupor and their differential diagnoses are considered later in this chapter. Brain damage often results in changes of temperament, or changed patterns of reaction to events and to other people. As a result, behavioural tendencies that have previously been enduring characteristics of the individual are found to be altered. Areas typically affected include the control of emotions and impulses and aspects of motivation and social judgement (Lipowski 1980). But sometimes brain damage may operate more directly by disruption of regional cerebral systems upon which the synthesis of the personality depends. This situation is compatible with excellent preservation of intellect to formal testing, yet the personality change is nonetheless organic in origin. Most examples occur with strictly focal brain damage, the best known being with lesions of the frontal lobes of the brain. A clear discontinuity between the current and premorbid personality is essential if this term is to retain its meaning. Disorder of memory, especially for recent events, is an integral part of dementia, but can also exist without global impairment of intellect. Such memory disturbance may emerge as the sole defect, as after bilateral hippocampal lesions, or more commonly may stand out as the obtrusive defect while other cognitive processes are but little affected. It may be defined as an organic impairment of memory out of all proportion to other cognitive changes. A focal rather than a diffuse brain pathology can be confidently predicted as described. Organic hallucinosis refers to a syndrome of recurrent or persistent hallucinations, occurring in a setting of full preservation of consciousness and awareness of the environment yet attributable to organic factors. The patient is not disorientated and proves capable of thinking with normal clarity throughout. The hallucinations occur mostly in the auditory or visual modalities but any sensory modality can be affected. Insight into the unreal nature of the phenomena may vary markedly in degree, but any delusions that occur are secondary to the hallucinatory experiences. Such a syndrome may be occasioned by circumscribed brain lesions, strategically placed to irritate cortical or subcortical areas, but is more commonly seen as a result of toxic processes. The hallucinations occurring during the early phase of alcohol withdrawal or after ingestion of hallucinogenic drugs are typical examples. The prototypical acute and chronic organic reactions are delirium and dementia respectively. There are many meanings and definitions of this term, sometimes embracing all varieties of acute organic reaction, sometimes referring to the degree of overt disturbance, and sometimes confining its use to clinical pictures with certain specific features. Special characteristics have included wakefulness with ability to respond verbally, increased psychomotor activity, pronounced disturbance of affect, defective reality testing, or the appearance of productive symptoms in the form of illusions and hallucinations. B A change in cognition (such as memory deficit, disorientation, language disturbance) or the development of a perceptual disturbance. C the disturbance develops over a short period of time (usually hours to days) and tends to fluctuate during the course of the day. D There is evidence from the history, physical examination or laboratory findings that the disturbance is caused by the direct physiological consequences of a general medical condition/ substance intoxication/withdrawal/multiple aetiologies. It is clear, however, that not all patients who meet current criteria for delirium present like this, some showing predominant listlessness, inertia and dulling of the senses. It is important to appreciate that consciousness is not merely quantitatively reduced in delirium, but also qualitatively changed. Typically the patient becomes preoccupied with his own inner world which is distorted by illusions, hallucinations and delusions, and sometimes by powerful 8 Chapter 1 Box 1. Deterioration from a previously higher level of performance should be established. For a confident diagnosis both 1 and 2 must have been present for at least 6 months.

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Lind50 reported similar events: "They are apt, upon being moved, or exposed to fresh air, suddenly to expire. The mechanisms for these cardiovascular and respiratory events are somewhat unclear. The decreased blood pressure seems to arise from a defect in the ability of resistance vessels to constrict in response to adrenergic stimuli, as demonstrated in experimental scurvy. Another factor possibly responsible for low blood pressure, chest pain, dyspnea, and sudden death is myocardial hemorrhage, which, although not described in humans, occurs in scorbutic guinea pigs. Hemopericardium as a complication of scurvy was later recognized and treated with pericardiocentesis in outbreaks in Russia both in 1847 and during the Crimean War of 1854-1856. In most patients who die of this disease, however, autopsies reveal no anatomic abnormalities in the heart,67 and impaired vasoconstriction to adrenergic stimuli, as discussed above, seems the most plausible explanation. Gastrointestinal symptoms Anorexia is common in scurvy, and some patients have gastrointestinal bleeding. On upper endoscopy submucosal hemorrhages have been present anywhere from the distal esophagus to the duodenum. In naturally occurring disease, however, anemia is common,69-71 and its degree apparently correlates with the severity and duration of the scurvy. Recent hemorrhage into tissue or loss into the gastrointestinal tract is probably responsible for the anemia in some cases. In these, the red cells are normochromic-normocytic, the reticulocyte count is elevated, and bone marrow samples reveal erythrocyte hyperplasia. Such findings, however, are also consistent with hemolysis, and, indeed, the red cell life span may be decreased, as demonstrated by a diminished survival of erythrocytes from normal patients transfused into patients with scurvy. The hemolysis is reflected by an increased indirect bilirubin in many patients,69,71 and repletion with ascorbic acid alone may correct the anemia. In addition, because ascorbic acid prevents oxidation of folate to forms that are excreted in the urine, vitamin C deficiency may deplete folate stores by increasing urinary excretion. The combination of follicular hyperkeratosis and perifollicular hemorrhage is pathognomonic and occurs early in the disease. Supporting findings, which usually occur later, are ecchymoses, hairs with corkscrew or swan-neck deformities, and swollen, red or purplish gums in patients who have teeth. These manifestations of scurvy occur when the body pool of ascorbic acid, normally about 1500 mg, falls below 300 mg. Plasma values are affected by recent dietary intake, while leukocyte levels, which change more slowly, better indicate tissue and total body content. Alternatively, disappearance of the clinical abnormalities with vitamin C repletion establishes the diagnosis without laboratory studies. The gums change from purple to red in 1 to 2 weeks, with more gradual resolution of the gingival edema, complete recovery being apparent by 3 months. Human experimental scurvy and the relation of vitamin C deficiency to postoperative pneumonia and to wound healing. Scurvy, osteoporosis and megaloblastic anaemia due to alleged food intolerance [letter]. Hemarthrosis and femoral head destruction in an adult diet faddist with scurvy [letter]. Scurvy presenting with cutaneous and articular signs and decrease in red and white blood cells. Capillary hemorrhage in ascorbic-acid-deficient guinea pigs: ultrastructural basis. Rapid reversion of electrocardiographic abnormalities after treatment in two cases of scurvy. In a diet totally deficient in vitamin C, the earliest clinical findings occur after a minimum of a. The most important reason for the emergence of descriptions of scurvy in the late 15th century and early 16th century was a. The clinician who did a controlled trial of citrus fruits compared with other treatments of scurvy in 1747 was a. The animal lacking the capacity to derive ascorbic acid from glucose metabolism in which experimental scurvy was first demonstrated is the a. The first symptom most commonly noted in experimental and naturally occurring scurvy is a. The musculoskeletal manifestations of scurvy include each of the following except a. The ophthalmologic manifestations of scurvy include each of the following except a. Plausible explanations of syncope from scurvy include each of the following except a. Plausible explanations for the anemia associated with scurvy include each of the following except a. In patients whose anemia is from scurvy alone, the hematocrit returns to normal in a. Which of these laboratory tests most accurately reflects the tissue and total body content of ascorbic acid? Ascorbic acid is necessary for the formation of mature collagen, which exists in the following structure: a. The first person to prove conclusively that vitamin C deficiency causes impaired wound healing in humans was a. Each bound volume contains a subject and author index and all advertising is removed. Copies are shipped within 60 days after publication of the last issue in the volume. The binding is durable buckram with the journal name, volume number, and year stamped in gold on the spine. Leave the subject line blank and type the following as the body of your message: subscribe jaad toc You will receive an e-mail to confirm that you have been added to the mailing list. Note that table of contents e-mails will be sent out when a new issue is posted to the Web site. Avoid use in patients with substantial alcohol use or evidence of chronic liver disease (5. Concomitant use of antiplatelet drugs and anticoagulants may increase this risk (5. These studies did not show an increase in the risk of suicidal thoughts and behavior with antidepressant use in patients over age 24; there was a reduction in risk with antidepressant use in patients aged 65 and older [see Warnings and Precautions (5. In patients of all ages who are started on antidepressant therapy, monitor closely for worsening, and for emergence of suicidal thoughts and behaviors. Advise families and caregivers of the need for close observation and communication with the prescriber [see Warnings and Precautions (5. Do not chew or crush, and do not open the delayed-release capsule and sprinkle its contents on food or mix with liquids because these actions might affect the enteric coating. If it is almost time for the next dose, skip the missed dose and take the next dose at the regular time. While a 120 mg/day dose was shown to be effective, there is no evidence that doses greater than 60 mg/day confer any additional benefits. Periodically reassess to determine the need for maintenance treatment and the appropriate dosage for such treatment. While a 120 mg once daily dosage was shown to be effective, there is no evidence that doses greater than 60 mg/day confer additional benefit. Nevertheless, if a decision is made to increase the dosage beyond 60 mg once daily, increase dosage in increments of 30 mg once daily. Periodically reassess to determine the continued need for maintenance treatment and the appropriate dosage for such treatment. If a decision is made to increase the dose beyond 60 mg once daily, increase dose in increments of 30 mg once daily. If a decision is made to increase the dose beyond 60 mg once daily, increase dosage in increments of 30 mg once daily. There is no evidence that doses higher than 60 mg once daily confer additional significant benefit and the higher dosage is clearly less well tolerated. For patients for whom tolerability is a concern, a lower starting dose may be considered. Since diabetes is frequently complicated by renal disease, consider a lower starting dosage and gradual increase in dosage for patients with renal impairment [see Dosage and Administration (2. There is no evidence that dosages greater than 60 mg/day confer additional benefit, even in patients who do not respond to a 60 mg/day dosage, and higher dosages were associated with a higher rate of adverse reactions.

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Pathogenesis of enterotropic mouse hepatitis virus in immunocompetent and immunodeficient mice. Pathogenesis of mouse hepatitis virus infection in gamma interferon-deficient mice is modulated by coinfection with Helicobacter hepaticus. Confirmed persistent mouse hepatitis virus infection and transmission by mice with a targeted null mutation of tumor necrosis factor to sentinel mice, using short term exposure. History: Tissues are from three rats that were part of a group of 60 rats receiving a trial diet that contained a single protein source. Gross Pathology: Rats were in a poor state of nutrition and weighed less than would be predicted for their age. Examination of the urinary system revealed pitted kidneys with white streaks within the cortex. Laboratory Results: A pure growth of Escherichia coli was cultured from a sample of kidney from one of the rats. This inflammation consists predominantly of lymphocytes and plasma cells with some sections also containing significant numbers of neutrophils. The transitional epithelium within the renal pelvis has undergone squamous metaplasia. Inflammation and necrosis is visible extending from the renal pelvis into the cortex. Pyelonephritis, moderate, subacute, neutrophilic, with marked squamous metaplasia of the transitional epithelium. In addition to the renal pelvis, squamous metaplasia of the transitional epithelium was also visible within the ureters and bladder suggesting vitamin A deficiency. Subsequent analysis revealed that the experimental diet that these rats were receiving contained an inadequate concentration of vitamin A. Bilateral pyelonephritis was detected histologically in 43% of rats and unilateral pyelonephritis in 25%. Vitamin A regulates epithelial cell growth and differentiation, enables production of visual pigment, is necessary for normal function of the immune system, and influences skeletal development. Photograph courtesy of Institute of Veterinary, Animal, and Biomedical Sciences, Massey University, The restriction of the lesions to the transitional epithelium in these rats suggests that the transitional epithelium is the most susceptible to squamous metaplasia due to moderate vitamin deficiency. While squamous metaplasia of the transitional epithelium lining the renal pelvis can occur secondary to bacterial infection, the metaplasia visible within the present case was considered an excessive reaction to an ascending bacterial pyelonephritis. Conference Comment: Vitamin A is one of four fat soluble vitamins, along with vitamins D, E and K, and has multiple functions. Vitamin A as retinoic acid functions in morphogenesis during embryonic development, maintenance of epithelial cells, bone growth, reproduction, immunostimulation, and may also have antioxidant effects. Nephroliths and uroliths were present in 5 and 27%, respectively, of examined rats. Photographs courtesy of Institute of Veterinary, Animal, and Biomedical Sciences, Massey University, Urothelium is hyperplastic, piling up several layers deep, and the superficial layers are composed of flattened squamous epithelium (squamous metaplasia). Hypovitaminosis A affects immune function, as vitamin A is thought to stimulate T-cells directly through 14-hydroxyretinol. During infection, synthesis of the negative acute phase protein, retinol-binding protein, is down-regulated, decreasing availability of vitamin A. Squamous metaplasia of the parotid gland is a pathognomonic lesion of hypovitaminosis A in cattle. Cellular adaptations, injury, and death: morphologic, biochemical, and genetic bases. Anomalous growth of rat incisor teeth during chronic intermittent vitamin A deficiency. Cystitis, pyelonephritis, and urolithiasis in rats accidentally fed a diet deficient in vitamin A. History: the mouse was infected by intracerebral inoculation with a lethal dose of rabies virus (genotype 1). Some affected neurons are surrounded by lymphocytes and glial cells (neuronophagia). Focally distributed throughout the neuropil, aggregates of glial cells and lymphocytes are present (glial nodules). Perivascularly, there is a slight lymphocytic and histiocytic infiltration (perivascular cuffing) and few lymphocytes and histiocytes are found in submeningeal regions. The characterization of the rabies virus isolates based on monoclonal antibodies grouped the rabies-associated viruses into four serogroups, with classical rabies forming serogroup 1, the African lyssaviruses forming serogroup 2 (Lagos bat virus), serogroup 3 (Mokola virus), and serogroup 4 (Duvenhage virus). Many neurons contain 2-7 micron bright eosinophilic intracytoplasmic inclusion bodies (Negri bodies). Dogs are the source of infection in all of the estimated 55,000 human rabies deaths annually in Asia and Africa. Bats are the source of most human rabies deaths in the United States of America and Canada. Bat rabies has also recently emerged as a public health threat in Australia, Latin America and Western Europe. Infections due to contact to rabid foxes, raccoons, skunks, jackals, mongooses and other wild carnivore are very rare. The transmission occurs via the bite of rabid animals shedding virus within their saliva, or direct contact of infectious material (i. The anterograde transport of virus to secretory tissues of salivary glands leads to viral shedding via saliva. Potentially, the prodromal stage is followed by the excitative phase with severe agitation and aggressiveness. Further, in the paralytic phase, the infected animals are unable to swallow, leading to a typical sign of foaming saliva around the mouth. Topographic dissociation between location of inflammatory reactions and of Negri body has been reported in an autopsy study of 49 cases. Inflammatory changes were most frequently found in medulla, pons and spinal cord followed by thalamus and less frequently in cerebellum and hippocampus. A recent study showed that the whole virion is transported to the cell body in an endosomal vesicle, although the exact mechanism by which this occurs remains unclear. However, as the rabies virus glycoprotein is inside the vesicle, it should not be able to interact directly with a specific transporter complex. Based on these observations, it is speculated that entry into the vesicle determines the direction and provides the driving force of rabies virus transport. This indicates that the nature of the vesicle formed dictates the transport method that follows. The patient had detectable antibody and the treatment applied was aimed to allow the humoral immune response to develop. High IgG titres developed and might have contributed to the survival of this patient. Several other factors are discussed, as for example that the infectious dose transmitted with a bite is too small to trigger immune responses and further enable the virus to infect sensory nerves. A final explanation for the lack of antibody could result from immunosuppression induced by the virus. It is speculated that interferon inhibition is transitory and provides a short delay in the host response. It occurs in various species of flying foxes and occasionally in other Geographical distribution Worldwide Africa Africa Southern Africa Europe Western Europe Australia Kyrgistan Kyrgistan Eastern Siberia Species from which the virus is predominantly isolated. Lesions are similar to rabies and consist of nonsuppurative meningoencephalomyelitis and ganglioneuritis with Negri bodies.

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Gross Pathology: A post mortem examination was conducted on one of the affected animals in the field by the local veterinarian, who subsequently submitted both fresh liver and formalin fixed tissues to the Western Australian Department of Agriculture and Food for examination. The veterinarian reported extremely dry ruminal contents (suggesting dehydration) and the presence of peritoneal and pleural "proteinaceous" effusions. The liver was reportedly small with a yellow tinge and the kidneys appeared very dark. Laboratory Results: Aerobic and anaerobic culture performed on the samples of fresh liver yielded no growth. Numerous hepatocytes appear swollen with moderate to marked anisocytosis and there are numerous mitotic figures, many of which appear abnormal, often arrested in metaphase. There are occasional scattered shrunken hypereosinophilic hepatocytes with condensed nuclei, consistent with apoptosis. Low numbers of lymphocytes, macrophages and neutrophils are present, particularly periportally. Marked disruption of hepatocellular architecture with nodulear regeneration, bile plugs, necrotic, rounded up hepatocytes (arrowhead), and mitotic figure (arrow), changes consistent with phomopsin toxicosis in the small ruminant. Photograph courtesy of the Department of Anatomic Pathology, Murdoch University School of Veterinary and Biomedical Sciences, Faculty of Health Sciences. Lupinosis is a mycotoxicosis seen in animals ingesting lupin stubble or seed (Lupinus spp. Diaporthe woodii (anamorph Phomopsis leptostromiformis) was originally (and incorrectly) thought to be the source of the causative toxins. This in turn disrupts mitosis, resulting in mitotic arrest in metaphase and commonly fatty infiltration. Most animals within a flock are affected and deaths occur within three or four days. Variable numbers of sheep within a flock are affected and animals are typically weak and in poor body condition. Jaundice may or may not be apparent, and those sheep that are jaundiced are commonly anemic. The disease course may also be subacute and intermediate in severity, and it is this form of the disease that is most commonly observed in Australia. The degree of fatty change is variable and depends largely on the nutritional status of the animal. As the disease course progresses, increased, but ineffective mitotic activity becomes evident with the presence of numerous arrested mitoses. Progressive hepatic fibrosis occurs and there is accumulation of complex granular pigment within macrophages in the affected tissue, and may include any combination of copper, ferric iron, ceroid or lipofuscin. In Australia, sheep grazing lupin stubble may also be concurrently exposed to plants containing pyrrolizidine alkaloids such as heliotrope (Heliotropium europaeum), which may result in additive or synergistic hepatotoxity. Conference Comment: A few other noteworthy histologic features in this case include a decrease in the lobule size and a decrease in the distance separating central and portal areas, reflecting hepatocyte necrosis and atrophy. Other potential toxic causes for this lesion would include aflatoxin, which may present with more hepatic regeneration, bridging portal fibrosis, biliary hyperplasia and hemorrhagic necrosis, with maintenance of hepatic trabeculae; sporidesmin, a mycotoxin which targets biliary epithelium and causes necrosis; microcystin, a toxin of blue-green algae, which causes disassociation of centrilobular hepatocytes and submassive hepatic necrosis and hemorrhage; and pyrrolizidine alkaloids, which also cause bridging fibrosis, biliary hyperplasia, and megalocytosis. The contributor mentioned the possibility of photosensitization in acute phomopsin toxicosis. Photosensitization appears as erythema, dermal edema, vesicle or bullae formation, exudation and extensive epidermal necrosis. Ty p e I, o r p r i m a r y photosensitization, occurs from ingestion of a plant or drug containing photoreactive substances, which are deposited in the skin. Diseases associated with toxins in plants, fungi, cyanobacteria, plant-associated bacteria, and venoms in ticks and vertebrate animals. History: Gross lesions were identified during the postmortem inspection of the carcass at slaughter. Due to the gross lesions, the carcass was condemned (not used for human consumption). The left parotid lymph node, and to a lesser degree the adjacent lymph nodes of the head, contained irregularly shaped areas which were discolored green. The facial musculature adjacent to the parotid lymph node, the tracheobronchial lymph nodes, and mediastinal lymph nodes were also multifocally green. Numerous algal cells with low numbers of eosinophils, multinucleate giant cells, lymphocytes and plasma cells are intermixed with the macrophages. The algal cells are round, 7 to 15 microns in diameter, have a thin refractile cell wall, single basophilic round nucleus and amphophilic to eosinophilic granular cytoplasm. Low numbers of larger algal cells (sporangia) are filled with 2 to 6 daughter cells (sporangiospores or endospores). Intact algal cells and empty cell walls with no internal structures (degenerate algal cells) are both free in the sinuses and within macrophages. The left parotid lymph node, and to a lesser degree the adjacent lymph nodes of the head contained irregularly shaped areas which were discolored green. The normal nodal architecture is effaced by multifocal to coalescing areas of granulomatous inflammation. Epithelioid macrophages and multinucleate giant cell macrophages contain numerous Chlorella algal cells, as well as multinucleated endosporulating sporangia (small arrows), and degenerate forms consisting primarily of a collapsed cell wall (large arrow). The large silver-positive granules are helpful in differentiating Chlorella from Prototheca, according to Chandler. Protothecosis occurs more commonly than disease by green algae and Prototheca spp. Conference Comment: the contributor provided an excellent discussion of Chlorella spp. Conference participants discussed the differences between Chlorella and Prototheca, and the difficulties in differentiating the two entities by standard histologic methods. In addition to Chlorella and Prototheca, other pathogens that reproduce asexually by endosporulation include Rhinosporidium seeberi and Coccidioides immitis. Chlorella infection in a sheep in Mexico and minireview of published reports from humans and domestic animals. History: Abnormal growth noted in both eyes over a period of several months; left eye enucleated 2 months prior to enucleation of the right eye. Gross Pathology: A 1cm diameter homogenous, soft white-tan mass occupies the vitreous, posterior and part of the anterior chamber in both globes, obscuring the lenticular and iridial structures. There is a densely cellular, poorly circumscribed population of neoplastic cells filling the anterior and posterior chambers and vitreous. Neoplastic cells are dimorphic: the first population is spindloid with a small amount of fibrillar eosinophilic cytoplasm, a large oval nucleus with finely stippled chromatin and infrequent visible nucleoli. The second neoplastic cell population is composed of well differentiated neurons, and this population is scattered throughout the fibroblastic 1-1. Globe, silver carp: the anterior chamber and vitreous, sclera, uvea, choroid, and even the cornea is infiltrated by a densely cellular neoplasm composed of broad streams and bundles. Globe, silver carp: Bland spindle cells are the primary cell population; mitoses are rare. Globe, silver carp: A second neoplastic cell type are large polygonal cells resembling neurons. Globe, silver carp: Small triangular cells with apical nuclei form prominent rosettes (neuroblasts). Neoplastic cells arranged in thick interlacing fascicles and infiltrated by a diffuse population of heterophils macrophages. The architecture of the iris, ciliary body and lens is diffusely effaced by a poorly circumscribed population of neoplastic cells that fills the vitreous body and protrudes into the anterior chamber. Neoplastic cells are dimorphic: the first population is spindloid with tapered cell borders, a moderate amount of fibrillar eosinophilic cytoplasm and a large elongate nucleus with stippled chromatin. Interspersed within this population of neoplastic spindle cells, there is a subpopulation of polyhedral to stellate neoplastic cells with abundant eosinophilic cytoplasm, a large eccentric nucleus with a fine chromatin pattern and prominent eosinophilic nucleolus. Mitotic figures average three per ten high power fields for all neoplastic cell types. Neoplastic cells invade the lens capsule and disrupt the lens, and there is moderate histiocytic and lymphoplasmacytic inflammation surrounding the lens fragments. The histologic features of this tumor include a classic single or grouped neoplastic ganglion cell with prominent vesicular chromatin and eosinophilic nucleoli, separated by interlacing fascicles of spindle neoplastic cells. Unlike retinoblastomas, ganglioneuromas do not exhibit rosette formation, and unlike schwannomas, they contain neuronally differentiated cells. Neoplasms of the retina in fish have been reported in association with exposure to methylazoxymethanol experimentally. The bilateral origin of the tumor in this case suggests an underlying genetic predisposition, which may be analogous to that of retinoblastomas.

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Genuine physical symptoms such as vertigo, headache and paraesthesiae are likewise often reported in distorted fashion. Depersonalisation and derealisation are common, though usually incompletely expressed. Dissolution of the perceptual boundaries between the self and the environment may give rise to terrifying feelings of imminent dissolution or loss of bodily and personal integrity. Perceptual abnormalities readily lead to misinterpretations and illusions which are typically fleeting and changeable. Difficulty with visual recognition combines with faulty thinking and memory to produce false recognitions and faulty orientation in place. The unfamiliar tends to be mistaken for the familiar, or may be interpreted as hostile or persecutory. Thus the patient may misidentify a nurse as a relative, or the doctor as an old friend or enemy. Chance noises may similarly be misinterpreted, contributing to delusion formation. Hallucinations are also commonest in the visual modality, though tactile and auditory hallucinations occur as well. They probably derive partly from failure to distinguish inner images from outer percepts, and partly from vivid dreams carried over into the waking state as consciousness waxes and wanes. Simple visual hallucinations consist of flashes of light, geometrical patterns or colours. More complex phenomena, sometimes kaleidoscopic in nature, may occur, with fully formed hallucinations of scenes, people and animals. The hallucinated Basic Concepts in Neuropsychiatry 13 material may be grossly distorted, as with Lilliputian hallucinations where objects and people appear to be minute in size. The reality of the phenomena is fully accepted by the patient, who may react with fear and alarm but sometimes with interest or even amusement. Hallucinations appear to be particularly characteristic of the acute organic reactions occasioned by certain pathological processes. Delirium tremens remains the classic example, with extremely florid hallucinations as described in Chapter 11. Along with hallucinogenic drugs, prescribed drugs with potent anticholinergic properties are also notorious for the wealth of formed and unformed hallucinations they may provoke. In the setting of delirium, sensory impairments appear to predispose to hallucinations in the corresponding modality and hence are common in the elderly. Other features In the milder stages in particular, the definitive organic features may be less in evidence than those which depend on individual traits and characteristics. Psychological reactions to early cognitive impairment, or to the stress of the underlying physical disease, may dominate the picture and emerge in the form of neurotic symptoms. Similarly, vulnerable aspects of personality may be exaggerated, with the appearance of depressive, hypochondriacal or phobic features. Hysterical conversion symptoms, usually transient but sometimes persistent, may lead to mistakes in diagnosis. Paranoid developments occur frequently, and can become the overriding feature at an early stage in susceptible individuals. A distinct schizophrenic colouring to the total clinical picture is likewise not uncommon. With progression of cognitive disorganisation the true situation usually becomes apparent, but mild self-limiting acute organic reactions can be misdiagnosed for some time as non-organic psychiatric illness. Emotion In early stages, mild depression, anxiety and irritability may be expected, though typically the affect is shallow. With deeper impairment, and further impoverishment of mental processes, apathy usually becomes the striking feature, and the whole course of the illness may pass with indifference and emotional withdrawal. More lively affects are seen in conjunction with increased psychomotor activity when affective disturbance may become intense. A state of wondering perplexity forms a common background to other affective states. The affective reactions are often fleeting and changeable with changing delusional ideas. Sudden displays of primitive and highly charged emotion are often called forth by hallucinatory experiences. In part the emotional state is likely to be determined by the stress of the physical illness, and in part by a vague awareness of cognitive impairments. The extent of such influences has not been determined, nor the degree to which the picture is shaped by different pathogenic agents. There are strong clinical impressions that delirium tremens tends to be accompanied by intense fear, hepatic encephalopathy by euphoria or depression, and uraemia by apathy, but reliable and systematic comparisons have not been made. It is clear, moreover, that several factors are often operative together in leading to delirium in the individual patient, particularly in the elderly (Francis et al. A focal emphasis of pathology may produce special patterns of impairment, but the purpose in what follows is to describe the general clinical picture and to emphasise the shared and common forms of reaction that occur. While the majority of chronic organic reactions are due to diffuse and widespread affections of the brain, some owe their origins to focal pathology, so careful examination for signs of localising value must always be undertaken. Most of the illnesses concerned are slowly progressive with increasing disablement, but static pictures may be seen as with arrested general paresis, or gradual improvement may occur as after head injury. In a small but extremely important group, therapeutic intervention can decisively reverse the process, for example with myxoedema or normal-pressure hydrocephalus, or when a frontal meningioma is discovered to be the cause. Mode of presentation Some chronic organic reactions follow acute episodes such as trauma or anoxia, and are then revealed in full when the patient recovers consciousness, or else emerge by a process of transition from an acute organic reaction. Failures of memory are usually noted earlier by relatives and workmates than by the patient himself. They show in missed appointments, apparent unawareness of recent happenings, a tendency to mix up times or to lose things. More general cognitive failure emerges in slipshod work and loss of overall efficiency. The patient may be noticed to think and speak less coherently than usual, to muddle money or to fail to grasp essentials. Change in personality as the first manifestation is much less common, but when it occurs the patient is especially likely to come before the psychiatrist. Here intellectual deficits are mild or absent in the early stages, or pass unnoticed because of curtailment of activities and the use of props and evasions. Deterioration of manners may be the earliest sign, or diminished awareness of the needs and feelings of others. Some social blunder may disclose the problem, such as stealing or disinhibited behaviour out of character for the individual. Sometimes the earliest change is merely the exaggeration of long-standing personality traits such as suspiciousness or egocentricity. Neurotic traits may be elaborated with the production of depressive, obsessional, hysterical or hypochondriacal symptoms. More rarely the illness presents with the picture of a psychotic illness of depressive, paranoid or schizophrenic type in especially predisposed individuals. It is then only by careful examination that the onset of cognitive impairment is revealed. Whatever the form of presentation, the illness may declare itself abruptly even though its evolution has been insidious. Or relatives may have adjusted to the Basic Concepts in Neuropsychiatry 15 slow decline until some dramatic instance forces their attention to the true situation. Not infrequently a tenuous adjustment is concealed until new demands must be met, for example on the death of a partner or a move to a new environment. Admission to hospital may be the step which reveals the disorder, and only careful retrospective enquiry then establishes that the onset has been gradual. Intercurrent illness may bring the situation to light by pushing the patient below the threshold at which the brain was previously coping, especially infection, anoxia or postoperative metabolic derangements. The content of thought is impoverished, with fewer associations, inability to produce new ideas, and a tendency to dwell on set topics and memories from the past. The ability to reason logically and to manipulate concepts is impaired, likewise the ability to keep in mind various aspects of a situation simultaneously. Intellectual flexibility is lost, leading to difficulty in shifting from one frame of reference to another.

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Cognition and work after closed and penetrating head injury: a report of the Vietnam head injury study. Predicting course of recovery and outcome for patients admitted to rehabilitation. Cerebral blood flow and its regulation after closed head injury with emphasis on clinical correlations. The possible contribution of alterations in the genetic material to tumour formation has been reviewed by Hill et al. There is evidence for the presence of tumour-suppressor genes on chromosome 10 (Ichimura et al. It is truncated when mutated, resulting in structural abnormalities that presumably lend themselves to tumour formation. Deletion of loci on chromosome 22q occurs in approximately 30% of sporadic meningiomas. Other mechanisms that may be involved in the development of oncogenicity include abnormalities in signal transduction pathways. However, brain metastases, predominantly originating in the lung and breast, are commoner than primary cerebral tumours by a ratio of 10; 1 (Culine et al. Over twothirds (70%) of all tumours are supratentorial and their distribution by lobe and age of onset are influenced to some extent by histology (Price et al. For example, medulloblastomas are most common in the posterior fossa and in children, whereas gliomas predominate in the middle-aged population and meningiomas and metastatic disease are more frequent in the elderly (Price et al. There is little good evidence for the role of electromagnetic fields, cell phones producing non-ionising radiation, diet, alcohol, tobacco, exposure to industrial chemicals, or medications as aetiological factors in the pathogenesis of brain tumours. There could be a negative association between varicella-zoster herpesvirus and the development of glioma in adults; those with gliomas have been found to have higher levels of anti-varicella-zoster IgG (Wrensch et al. Genetic susceptibility the association of hereditary syndromes with cerebral malignancies is well known. In low-grade gliomas, the allelic loss of chromosomes 1p and 19q renders them chemosensitive (Rees 2002). Corpus callosum Optic chiasm and nerve Lateral ventricle General characteristics of neuropsychiatric symptoms Patients with brain tumours typically present with headaches, papilloedema, seizures, focal neurological deficits, or non-specific cognitive or personality changes. The clinical constellation of symptoms varies depending on the location, histology and tumoral rate of growth (Wen et al. When mental disturbance is the most prominent feature, the patient may come first to the attention of the psychiatrist. It is, of course, comparatively rare for the psychiatrist to find a cerebral tumour in a patient with mental disorder. However, the converse is extremely common and many patients with cerebral tumours show pronounced mental symptoms at some time in their course. The frequency has been reported variously as 10% to virtually 100% of cases, depending on the care with which psychological symptoms are sought. Two of the larger series of tumour patients studied personally by the authors, and with psychological symptoms in mind, were those of Keschner et al. From the clinical point of view, mental symptoms are generally of little use as a guide to the location or nature of the tumour. Neurological signs are greatly superior in this regard, and neuroimaging has diminished the importance Third ventricle Pituitary region Fourth ventricle Pineal region Cerebellum/posterior fossa Cerebellopontine angle Cerebral Tumours Table 5. Tumour material has also proved disappointing for the study of the cerebral basis of mental phenomena. It is often hard to disentangle the effects of the lesion itself from remote pressure effects, circulatory disturbances or the generalised effects of raised intracranial pressure. Nevertheless, the psychological effects of cerebral tumours show many features of interest, and can occasionally be of crucial clinical importance, affecting the quality of life of the patient. Although fatigue, emotional and existential issues are common in all cancer patients, the presence of depressive symptoms was the single most important predictor of quality of life in a cohort of 73 brain tumour patients (Pelletier et al. Changes may be seen in any aspect of psychological function, and may be localised to one aspect or quite widespread. Complex psychological symptoms such as hallucinations and delusions may also appear, and the picture can be complicated by paroxysmal disorders consequent on an epileptogenic focus. Occasionally, frank psychotic illnesses are seen or more frequently stress-related disturbances occasioned by the constitution of the individual. In the exceptional case the tumour will present with psychiatric symptoms, but more usually the psychiatric symptoms accompany a tumour that is already known to be present. Fourteen patients displayed severe depression, seven excitements, and one each showed schizophrenia, an anxiety state, an obsessional disorder and hysteria. In very general terms it may be said that slow-growing tumours tend to produce changes of personality, and allow premorbid tendencies to manifest themselves; more fastgrowing tumours lead to cognitive defects, whereas the most rapid lead to acute organic reactions with obvious impairment of consciousness. Cognitive changes Disturbance of cognitive function is the most commonly noted psychological change. In minor degree it shows as diminished capacity to attend and concentrate, faulty memory and easy fatiguability. These rather subtle changes may be the first manifestation of the lesion, and sometimes provide the sole indication of disease for long periods of time. The cognitive changes may encompass changes in memory, attention, problem-solving, psychomotor speed and visuospatial functioning, among other deficits (Garofalo & Baum 2001). More severe cognitive impairment may present in the form of dementia, with slowed and concrete thinking, impoverished associations, defective judgement and obvious difficulty with memory. Speech may be slowed and incoherent, even in the absence of dysphasia and even with tumours of the nondominant hemisphere. Such changes can be steadily progressive, but more characteristically tend to fluctuate in severity from one occasion to another. Focal cognitive changes are commoner than generalised dementia as befits the focal nature of the lesion. A circumscribed amnesic syndrome may appear while other functions remain well preserved, with markedly defective memory for recent events, disorientation and even confabulation. All varieties of dysphasia can be seen, also apraxia, visuospatial defects and topographical disorder, and serve as a guide to location. Certain cognitive disturbances characteristic of tumours are considered in the following text. Later, drowsiness and somnolence appear, and as the lesion extends the level of consciousness declines progressively, ending, if untreated, in coma. In patients with glioma those with poor cognitive function have a worse prognosis (Meyers et al. This is probably partly explained by the observation that tumour regrowth (local or diffuse) or leptomeningeal metastases may induce cognitive deficits (Taphoorn & Klein 2004). The effects on cognition of the treatment of cerebral tumours may have important repercussions for quality of life in both children and adults. This is particularly relevant given the improvements in survival time that are now being seen. Whereas the cognitive dysfunction following surgery appears to be less significant in adults (Tucha et al. In addition radiationinduced neurotoxicity in the brain is a well-known phenomenon and a cause for concern (see also section on Management of the tumour; Radiotherapy). Its complications may be acute and reversible or delayed and permanent (New 2001). Neurological complications have been described with the use of chemotherapy and biological therapies (Hildebrand 2006), ranging from headache to cognitive slowing and even encephalopathy. Lower non-verbal memory scores have been found in patients with low-grade glioma treated with chemotherapy and radiotherapy compared with those receiving no treatment (40 patients, 24 receiving no treatment) (Correa et al. Therefore it has been suggested that a comprehensive assessment of cognitive functions, activities of daily living and quality of life can provide insights into the degree of impairment due to the tumour and neurotoxicity following its treatment (Weitzner & Meyers 1997). Affective and anxiety disorders Anxiety, sleep difficulties and depressive illness are common in patients with brain tumours (Stark et al. Other significant stressors include the disability caused by the tumour, and being diagnosed with a lifethreatening illness. The majority of those at more advanced stages of the disease or with severe disability and/or pain are likely to have significant depressive symptoms.

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In these multiply affected families, 16 of 67 who suffered schizophrenia reported having had a head injury before age 11 compared with 12 of 102 unaffected controls. However, in almost all cases the head injury was mild, of whom probably a good proportion suffered no loss of consciousness. Subjects from families in whom at least two members had schizophrenia or two members had bipolar disorder were asked whether they had ever had a head injury. Those who came from a schizophrenia pedigree and suffered a head injury were more likely to develop schizophrenia than bipolar disorder, whereas this was not the case with bipolar disorder; there may be a pathoplastic effect of familial predisposition to schizophrenia on the outcome of head injury. Of particular interest was the finding that those at risk of developing schizophrenia have a greater risk of suffering a head injury. More recent studies have used large databases of health records to enable direct comparison between those recorded, at the time, as being admitted with a head injury and subsequently recorded as suffering a psychotic illness. The psychiatric health of the subjects during the year before the head injury was also assessed. For each person, three age- and sexmatched controls without head injury were likewise followed up. It seems that merely being prescribed an antipsychotic was sufficient for a person to be labelled as suffering a psychotic illness. And as David and Prince (2005) point out, those subjects with apparent new-onset psychosis in the 3 years post injury may well have had a history of psychosis in the more distant past. In fact the most striking finding from analysis of this database is that having a mental illness makes a person at increased risk of suffering a head injury within 1 year (Fann et al. In this study the cases studied were 8288 patients having their first admission for schizophrenia. They were compared with 82 880 age- and sex-matched controls without schizophrenia. The register of all admissions to Danish general hospitals was then searched to see if these cases and controls had suffered a head injury requiring admission to hospital in the 15 years before the admission for schizophrenia (or in the case of controls an equivalent risk period). To try to control for accident proneness, the database was also searched to see if the subjects had been admitted for a fracture but without head injury. Compared with controls, patients with schizophrenia were not at increased risk of head injury. Closer analysis of the data did suggest that in men there was a relative excess of head injury compared with fractures, but it is difficult to interpret exactly what this finding means. The effect was greatest in the year before diagnosis of schizophrenia; this was the time the patients seemed to be at greatest risk, over and above controls, of suffering a head injury. This is compatible with reverse causality; during the prodrome of the schizophrenia the risk of head injury is increased. However, this explanation does not sit comfortably with the observation that risk of fractures was not increased in the year before schizophrenia. Nevertheless, it can be argued that a patient who is significantly disabled after a head injury, compared with a previously fit person, is likely to take a different pathway to care when becoming psychotic for the first time. These patients might also be expected to be diagnosed with an organic psychosis rather than schizophrenia. Both effects could result in underreporting of the number of patients who develop a non-affective psychosis after a head injury. And these effects would be most evident in those with the severest injuries, perhaps those most at risk of developing a psychotic illness. This finding is combatible with the argument that there is a slight increased risk of non-affective psychoses after head injury. From this review of the evidence it can be seen that it is not possible to come to any definite conclusion about whether head injury can cause a chronic psychotic illness, a schizophrenia or schizophreniform psychosis, not secondary to hypomania or depression. Nevertheless, across a range of study designs there is a fairly consistent message that there may be an increased risk of schizophrenia-like illness after head injury. However, in many of these studies the head injury was mild, probably making the studies more vulnerable to spurious reporting and ascertainment effects, and also hinting that the head injury was acting as a non-specific psychological stressor, rather than brain injury explaining the link. First, those with a predisposition to psychosis are at greatest risk of developing psychosis after head injury. This suggests that those who develop psychosis after head injury might well have become psychotic even if they had not been injured. Second, those at risk of developing a psychotic illness are probably also at greater risk of suffering a head injury, an Head Injury 215 example of reverse causality. Others will suggest that though large and apparently robust, even this study is open to question, and that a reasonable conclusion to draw is that head injury does increase the risk of psychosis, perhaps doubling it. Nevertheless, probably the majority of those who become psychotic after head injury, particularly if it is a mild head injury, would have developed a chronic psychosis anyway. Furthermore, it is quite likely that in fact these patients only had a head injury in the first place because their predisposition to psychosis was associated with being accident prone. Given this tentative conclusion that head injury causes chronic psychosis, more specific conclusions, for example that psychosis is especially linked to temporal lobe damage (Davison & Bagley 1969), must be regarded as somewhat speculative. Another question of interest is the effect of head injury on the course of schizophrenia. It is not uncommon for patients with schizophrenia to suffer a head injury, either accidental or due to deliberate self-injury. Of interest is the case report of Pang and Lewis (1996) suggesting that damage to the left prefrontal and temporal cortex following a head injury changed the pattern of symptoms in an individual with past history of bipolar affective disorder, such that the patient developed typical schizophrenia 9 months later. This is particularly the case if information is collected by self-report in response to standard questions, rather than by interview with somebody familiar with psychiatric diagnosis. Rating scales, like the Hamilton Rating Scale or the Beck Depression Inventory or Hospital Anxiety and Depression Scale, are even less reliable ways to identify clinical syndromes. Such methods will fail to distinguish symptoms like concentration impairment that may be a direct consequence of brain injury from bona fide symptoms of a depressive illness. The typical emotional sequelae of head injury overlap with changes of personality, including moodiness and dysthymia, and normal reactions to life events. Symptoms such as feeling miserable, powerless, frustrated and dissatisfied, being irritable and moody do not sit happily in any nosology. The propensity for individual clinicians to rate such symptoms as evidence of a mental illness probably varies markedly, and this may partly explain the large differences in reported rates of depression following head injury. Symonds proposed that as the patients could not appreciate the effects of the injury at the time, this was evidence favouring the view that the illness was the direct result of organic brain disturbance. Occasional case reports of psychosis associated with mood disorder are to be found (McLay et al. This was based on a survey of 100 community-dwelling patients at least 1 year, and on average 7 years, after a head injury; 61% were identified, using a structured interview by a psychologist, to have major depression. Given this very high rate of depression, the finding that about 12 of the 100 patients had psychotic features should be interpreted with caution. However, two important questions about the nosological status of these disorders in somebody with a brain injury emerge (Eames 2001). First, to what extent should emotional reactions that are easily understandable in terms of the adverse effects of the injury on the person be diagnosed as depression? Second, what is one to make of symptoms of mood disorders, for example anhedonia and apathy, when these symptoms may also be a direct consequence of brain injury? Frontal lobe injury may produce states where fatuous jocularity is prominent, not dissimilar to changes sometimes seen in hypomania. Bilateral high brainstem or internal capsule lesions may produce the syndrome of pseudobulbar palsy, with dramatic brief-lived pathological laughter and crying. Is this a disorder of the affect such that the patient feels like laughing or feels sad, or a disorder of the expression of emotion but in the absence of any subjective change in affect? On the other hand, it is quite possible, particularly in those with severe injury, that any subjective mood state is masked because the patient lacks the ability to express feelings. An example of this diagnostic dilemma is to be found in the case report of Mustafa et al. Mania developing later after injury is relatively uncommon and point prevalence studies, for example at 1 year (Deb et al.

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The tiny portion of the axon that contacts the dendrite becomes specialized for the release of neurotransmitters, and the tiny portion of the dendrite that receives the contact becomes specialized to receive and respond to the signal. These processes ensure that the synapse can transmit signals quickly and effectively. Finally, still other molecules coordinate the maturation of the synapse after it has formed, so that it can accommodate the changes that occur as our bodies mature and our behavior changes. Defects in some of these molecules are now thought to confer susceptibility to disorders such as autism, and the loss of others may underlie the degradation of synapses that occurs during aging. Many axons in the brain require a sheath of myelin to enhance the speed of conduction. The process of wrapping axons in myelin occurs last and can take years to complete in some areas of the brain. Peripheral nerves in the cervical region serve the neck and arms; those in the thoracic region serve the trunk; those in the lumbar region serve the legs; and those in the sacral region serve the bowels and bladder. Recently, it has become clear that apoptosis is maintained into adulthood and constantly held in check. This discovery - and its implication that death need not follow insult - have led to new avenues for therapy. For example, in primates, the projections from the two eyes to the brain initially overlap and then sort out to separate territories devoted to one eye or the other. Communica- Paring back After growth, the neural network is pared back to create a more efficient system. Entire populations of neurons are removed through apoptosis, programmed cell death initiated in the cells. In one recent study, scientists found that enriched environments resulted in more neurons in a brain area involved in memory. Interestingly, compared with adults, children have an increased incidence of certain disorders that involve excessive brain activity, such as epilepsy. This process starts around birth and moves from the back of the brain to the front: the frontal lobes are the last to become "connected" with fastconducting myelinated axons. Major functions of the frontal lobes are judgment, insight, and impulse control, and so the acquisition of these attributes becomes the last step in the creation of an adult human brain. About one-fourth of the human brain is involved in visual processing, more than for any other sense. More is known about vision than any other vertebrate sensory system, with most of the information derived from studies of monkeys and cats. Photoreceptors absorb light and send electrical signals to nearby neurons lining the back of the eye. As in a camera, the image on the retina is reversed: Objects to the right of center project images to the left part of the retina and vice versa; objects above the center project to the lower part and vice versa. The size of the pupil, which regulates how much light enters the eye, is controlled by the iris. Photoreceptors, about 125 million in each human eye, are neurons specialized to turn light into electrical signals. The human eye contains three types of cones, each sensitive to a different range of colors. You might be surprised to know that we can see thousands of colors using only three types of cones, but computer monitors use a similar process to generate a spectrum of scene registers in your left hemisphere. Scientists know much about the way cells encode visual information in the retina, the lateral geniculate nucleus - an intermediate way station between the retina and visual cortex - and the visual cortex. Each cell in the middle and third layer typically receives input from many cells in the previous layer, but the number of inputs varies widely across the retina. Whether large or small, the region of visual space providing input to a visual neuron is called its receptive field. In its middle layer, which receives messages from the lateral geniculate nucleus, scientists have found responses similar to those observed in the retina and in lateral geniculate cells. Further studies have shown that different cells prefer edges at different angles or edges moving in a particular direction. Research results indicate the need to understand processes related to normal function of the brain at each of its major stages and suggest that this information might lead to better age-specific therapies for brain disorders. Visual signals pass from each eye along the million or so fibers of the optic nerve to the optic chiasm, where some nerve fibers cross over, so both sides of the brain receive signals from both eyes. Consequently, the left halves of both retinas project to the left visual cortex and the right halves project to the right visual cortex. The result is that the left half of the scene you are watching registers in your right hemisphere. These findings of separate processing systems come from anatomical and physiological studies in monkeys. Perception requires various elements to be organized so that related ones are grouped together. How do all these systems combine to produce the vivid images of solid objects that we perceive? This involves extracting biologically relevant information at each stage and associating firing patterns of neuronal populations with past experience. Information from research in cats and monkeys has improved the therapy for strabismus, or squint, a term for cross-eye or walleye. But because they cannot fuse the images in the two eyes, they tend to favor one eye and often lose useful vision in the other. Hearing Often considered the most important sense for humans, hearing allows us to communicate with each other by receiving sounds and interpreting speech. The stapes pushes on the oval window, which separates the air-filled middle ear from the fluid-filled inner ear, to produce pressure waves in the snail-shaped cochlea of the inner ear. As in a camera, the image on the retina is reversed: Objects to the right of the center project images to the left part of the retina and vice versa. Rods are most sensitive to dim light and do not convey the sense of color; cones work in bright light and are responsible for acute detail, black-and-white vision, and color vision. The human eye contains three types of cones that are sensitive to red, green, and blue but, in combination, convey information about all visible colors. Attached to the tympanic membrane, the malleus (hammer) transmits the vibration to the incus (anvil), which passes vibration on to the stapes (stirrup). Auditory information is analyzed by multiple brain centers as it flows to the temporal gyrus or auditory cortex, the part of the brain involved in perceiving sound. In the auditory cortex, adjacent neurons tend to respond to tones of similar frequency. However the left side in most people is specialized for perceiving and producing speech. Damage to the left auditory cortex, such as from a stroke, can leave someone able to hear but unable to understand language. Taste is detected within taste buds, special structures embedded within papillae, or protuberances, located mainly on the tongue. Specialized receptors for smell are located in a patch of mucous membrane lining the roof of the nose. Each cell has several fine hairlike cilia containing receptor proteins, which are stimulated by odor molecules in the air, and a long fiber (axon), which passes through perforations in the overlying bone to enter the olfactory bulb. Stimulated cells give rise to impulses in the fibers, which set up patterns in the olfactory bulb that are Although different, the two sensory experiences of taste and smell are intimately entwined. However, these two senses act together to allow us to distinguish thousands of different flavors. Tastes are detected by special structures, taste buds, of which every human has some 5,000 to 10,000. Taste buds are embedded within papillae (protuberances) mainly on the tongue, with a few located in the back of the mouth and on the palate. Each taste bud consists of about 100 receptors that respond to stimuli - sweet, salty, "image" of the odor. Impulses created by this stimulation pass to the primary olfactory cortex at the back person has between 5,000 and 10,000 taste buds. Taste signals in the sensory cells are transferred to the ends of nerve fibers, which send impulses along cranial nerves to taste regions in the brainstem. From here, the impulses are relayed to the thalamus and on to the cerebral cortex for conscious perception of taste. Specialized olfactory receptor cells are located in a small patch of mucous membrane lining the roof of the nose.

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Treatment the aim of treatment is to achieve seizure control with a minimum of adverse effects. Complete remission is a realistic target for most patients who can then expect a quality of life comparable to that of the general population. When this is not possible, a secondary aim is reduction in seizure 366 Chapter 6 frequency or severity. Continuing seizures, no matter how infrequent, have a significant impact on overall quality of life, social functioning and psychiatric status (Leidy et al. In addition, epilepsy is associated with significant mortality and a risk of accidental injury. Patients whose seizures are not fully controlled therefore constitute a special clinical group requiring careful reappraisal and a clearly defined, active management plan. Treatment will always represent a compromise between reducing seizure frequency or severity and keeping side effects to an acceptable minimum. The higher mortality rate and risk of injury associated with epilepsy are important factors underlying the rationale for treatment. Causes of this excess mortality include death due to the underlying cause of epilepsy, accidental injury, suicide, status epilepticus and sudden unexplained death. Most accidental injuries in people with epilepsy are seizure related (Wirrell 2006). Retrospective studies have suggested a threefold to sixfold increased risk of submersion injury, with incidents during bathing being more common than those related to swimming. There has been only one prospective controlled study of accidental injury in epilepsy (Beghi & Cornaggia 2002). Over 12 months, accidental injuries occurred in 17% of 952 people with epilepsy and 12% of 909 controls. Most injuries were minor but patients with epilepsy reported a higher rate of injuries requiring hospitalisation (3% vs 1%) or medical treatment (16% vs 10%). At each stage in treatment, these risks, together with the psychosocial burden of ongoing seizures, must be weighed against the likelihood that a proposed treatment will be successful and without significant side effects. As previously mentioned, the risks of untreated epilepsy in the early stages are probably insignificant compared with the dire consequences of a mistaken diagnosis of epilepsy. When to start treatment Treatment is indicated if a patient has had two or more unprovoked seizures occurring within a relatively short interval. Most would consider recurrence within 6 months or 1 year as falling into this category. In practice, seizures usually occur at shorter intervals and the decision to begin treatment is straightforward. The question of whether delaying treatment has an adverse effect on long-term prognosis then arises: do seizures beget seizures? Other evidence, however, suggests that epilepsy is generally a non-progressive disorder and there is little if any harm in delaying treatment. For example, studies of untreated epilepsy have found that it may run a relatively benign course with spontaneous seizure-free periods of a year or more occurring in nearly 50% of patients (Placencia et al. There is also evidence that treatment begun many years after the onset of epilepsy achieves similar results to that initiated soon after seizure onset (Feksi et al. Prophylactic treatment after brain injury or supratentorial neurosurgery should be avoided. Such treatment may decrease the incidence of acute symptomatic seizures in the first week, but confers no protection against seizures in the longer term (Schierhout & Roberts 1998). The needless prescription of antiepileptic drugs undoubtedly contributes to the cognitive and behavioural difficulties in many such patients. One of the most rewarding medical interventions in a neurorehabilitation setting is the withdrawal of unnecessary antiepileptic drugs, an action that is often followed by remarkable improvements in alertness, communication and overall neurological function. Choice of treatment the choice of initial drug treatment is dictated by type of seizure and syndrome, patient characteristics, side effects and practical considerations such as availability and cost. Epilepsy 367 Seizure type/syndrome Carbamazepine has long been regarded as the drug of first choice for localisation-related epilepsy. In terms of efficacy, carbamazepine showed an advantage in relation to time to 12-months seizure remission, but this was statistically significant only in comparison with gabapentin. However, time to treatment failure (failure to control seizures or the advent of intolerable side effects) was longer for lamotrigine, and this difference was statistically significant in relation to all drugs except oxcarbazepine. The authors concluded that lamotrigine was a cost-effective and welltolerated alternative to carbamazepine. As valproate is associated with adverse cosmetic and teratogenic effects (see below), young women with generalised epilepsy present a particularly difficult treatment dilemma. Felbamate and vigabatrin have been omitted from the table as their use is now restricted because of toxicity. Efficacy has been established for a number of the newer drugs as add-on treatment only. Drug toxicity Antiepileptic drugs are associated with four categories of adverse effects (Smith & Chadwick 2001): (i) acute doserelated toxicity; (ii) acute idiosyncratic reactions; (iii) chronic toxicity; and (iv) teratogenicity. They improve as tolerance to the drug develops, usually within a week or two at any given dose, and can be relieved by lowering the dose and subsequently slowing the rate of dose titration. Acute idiosyncratic reactions are rare but potentially lifethreatening and require immediate drug withdrawal. These reactions typically occur in the first 4 weeks of treatment and may be accompanied by symptoms of systemic illness. Severe haematological complications are reported with felbamate, acetazolamide, carbamazepine, phenytoin, lamotrigine and zonisamide. Such reactions are rare with the exception of felbamate, use of which is now restricted because of its association with aplastic anaemia and liver toxicity. Acute hepatotoxicity is a rare complication of valproate and occurs almost exclusively in children with complex Table 6. Important examples include cosmetic effects with phenytoin (hirsutism, coarsening of facial appearance, gum hyperplasia) and valproate (weight gain, alopecia and tremor), hyponatraemia with carbamazepine and oxcarbazepine, folate deficiency with phenytoin, phenobarbital, valproate and carbamazepine, weight loss and renal calculi with topiramate, visual field defects with vigabatrin (which severely restrict its use), and endocrine and bone effects with many drugs, particularly those that induce hepatic enzymes (phenytoin, carbamazepine and phenobarbital). The most commonly reported malformations include neural tube defects, cardiac malformations and skeletal abnormalities. Minor anomalies, including certain dysmophic facial characteristics, have also been described but their prevalence is less certain. Patients taking more than one antiepileptic drug are at greatest risk and there is evidence that the risk is related to higher doses for some drugs. Overall, the risk of major malformations is highest with valproate, especially at doses above 1000 mg daily, but phenytoin, phenobarbital, lamotrigine and carbamazepine are all implicated. They have not been in use long enough to allow even preliminary judgements to be made. Registers of pregnancies in women with epilepsy have been established in a number of centres and are the subject of ongoing investigation. The analysis focused on outcome for women taking carbamazepine (900 women), valproate (715) or lamotrigine (647), as well as a small group (239) of women with epilepsy who had not taken medication during pregnancy. The highest risk (9%) was seen in patients receiving polytherapy combinations that included valproate. Interestingly, a significant relationship between dose and risk was observed for lamotrigine, but was discernible as a trend only for valproate. These results confirm previous impressions that valproate is associated with the highest risk of major congenital malformations but also suggest that lamotrigine is not as safe as had previously been hoped. Finally, there is emerging evidence that children exposed to antiepileptic drugs in utero are at increased risk of developmental delay, learning and behavioural difficulties, and possibly autistic spectrum disorder (Eriksson et al.