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What is the evidence that specific personality features will tend to influence the form that post-traumatic disability takes Good evidence that a severe head injury will exacerbate prior personality traits or personality disorder is lacking medicine for bronchitis buy loxitane discount. The majority had suffered a severe head injury xerostomia medications side effects loxitane 10mg mastercard, but about 20% of the 74 patients studied had brain injury from other causes treatment goals for ptsd cheap loxitane 10 mg mastercard. No systematic changes were observed; in other words it was not possible to define change in personality based on pre-injury personality treatment 5cm ovarian cyst trusted 10 mg loxitane. There is therefore a dissonance between these empirical findings and common clinical observation and opinion which would have us believe that pre-injury personality has a specific effect on outcome. One explanation for the failure of empirical data to validate clinical wisdom could be that the empirical methods used to identify the personality effects are too weak. They almost invariably rely on post-injury assessment of pre-injury characteristics, a method known to be vulnerable to bias. Alternatively, the measures used are simply not tuned to the personality effects that clinicians observe to have predictive value. Possibly clinical wisdom is based on a few convincing cases, but these good exemplars, being few and far between, are not sufficient to produce statistically significant effects when analysed in large cohorts where the majority show little if any effect. Or perhaps clinical wisdom is at fault, and is based on clinicians and informants incorrectly attributing the consequences of brain injury to the kind of head that was injured. The adverse effects of alcohol abuse before injury are discussed later in this section (see Alcohol and drug abuse and head injury). However, inconsistent effects of educational achievement on likelihood of return to work are found. Of more interest, though not easy to interpret, are the findings from the Vietnam Head Injury Study (Grafman et al. The elderly with moderately severe injuries were more than twice as likely to remain severely disabled or in a vegetative state (35% vs 14%). Russell (1932) found that memory difficulties increased regularly with age and were three times as common among patients over 40 as in younger patients. Adler (1945) found that neurotic symptoms, mainly anxieties and fears, were more frequent as age at time of injury advanced, and attributed this to the increased problems of occupational and financial adjustment which had to be faced by older people. Circumstances of the injury the circumstances of the accident may have important effects on outcome, as when a reckless driver has injured his family or a workman has been forced against his will to use faulty equipment. The setting may have been peculiarly conducive to fear, anger or resentment as in the following case. Age at time of injury Finally, under the heading of constitution it is important to note that many aspects of post-traumatic disability, and especially cognitive impairments, increase with age at the time of injury. This is probably due to the rising incidence of complicating factors such as cerebrovascular disease, the diminishing reserve of neurones, and the general loss of resilience and adaptability among older persons. For 12 months thereafter he showed enduring symptoms of anxiety and depression despite full physical and intellectual recovery. It ultimately emerged that after a series of frustrating setbacks he had come to be employed in a humble capacity by his successful younger brother who ran a flourishing business. Head Injury 195 the concept of cryptotrauma was introduced by Pilowsky (1985) to describe instances in which exploration of the details surrounding the accident can be rewarding in revealing circumstances of special significance. And even ignoring individual determinants of this nature, it is possible to show that disability tends to differ from one broad category of accident to another, whether on the roads, at work or in the home (Brain 1942; Adler 1945; Miller 1966). This may relate to the harmful effects of perception of fault (Rutherford 1989; Wood 2004); those patients who blamed a person or organisation for their injury were more likely to have symptoms. Emotional reaction to the trauma may be one reason why violence-related injury is associated with worse outcome (Wenden et al. However, as noted above, it seems likely that part of this effect is because many of the factors that increase the risk of suffering violence are the same as those that have a negative effect on later outcome, for example alcohol and drug abuse and lower social class (Bogner et al.

In a prospective study of over 2000 people coming to post-mortem medicine zolpidem cheap loxitane 10mg on-line, sensitivity was 93% and specificity 55% (Mayeux et al symptoms 2 months pregnant buy cheapest loxitane and loxitane. In more elderly groups the survival was on average shorter medications jfk was on proven loxitane 10mg, presumably due to deaths from competing causes symptoms lead poisoning order loxitane with american express, but even so the span could sometimes exceed 20 years. Rare cases are described in which the disorder becomes arrested for a time, but these must be regarded as exceptional. Aphasia and apraxia have been found by others to be predictors of rapid decline and mortality (Burns et al. Loss of function is a predictor of mortality, and behavioural disturbance, perhaps unsurprisingly, a predictor of entry into nursing homes (Bianchetti et al. Once in a nursing home increased age, male sex, limitation in physical function, evidence of malnutrition, pressure sores, diabetes mellitus and cardiovascular disease predicts a more rapid decline to death (Gambassi et al. Neuropathology In a paper in 1907, Alzheimer described the clinical features and neuropathology of one of his patients, Auguste D. The lesions he described were subsequently shown by Corsellis and the Newcastle group to also occur in the brains of older people with dementia, thus suggesting that the two conditions were essentially the same, although there may be differences in aetiology and possibly in pathogenesis. The two key lesions are the amyloid or neuritic (previously senile) plaque and the neurofibrillary tangle. All amyloid deposits share this biochemical property but the parent molecules from which they are derived are different. The neuritic plaque has a dense amyloid core surrounded by neuritic change and is visible on various silver staining techniques as pioneered by Nissl and utilised by Alzheimer, in addition to being readily visible with Congo red staining. When the amyloid peptide and its parent molecule were discovered, antibodies were developed that allowed the more subtle techniques of immunocytochemistry to be used on brain material. This revealed that the amyloid peptide was also depositied in diffuse aggregates that were not Congo-red positive. Strictly speaking these are therefore not amyloid deposits but this distinction is often lost. It is likely though that these diffuse plaques are precursors of the mature, neuritic plaque as seen by Alzheimer. The plaque is found in all cortical areas of brain and also occurs in striatum and the cerebellum (Braak et al. It is important to distinguish neuritic plaques from diffuse or non-neuritic plaques as the latter do correlate reasonably well with cognitive state (Dickson 1997). However, it is true that both plaques and tangles occur in people not known to have dementia (Davis et al. They are readily visible with silver staining techniques such as Bielschowsky: initially they appear as aggregates in the cell body, and then as they increasingly fill the cell body, particularly in pyramidal neurones, they appear as flame-shaped accumulations extending into the axonal hillock. Also seen with Bielschowsky staining are fine hair-like structures in the brain substance known as neuropil threads. Most probably these are tangles accumulating in the axons and dendrites of affected neurones. Under the electron microscope neurofibrillary tangles can be shown to be composed of many separate filaments, most appearing to be paired structures with a periodicity suggesting two twisted ropes. These are paired helical filaments and are abnormal and not to be confused with other normal filamentous structures in neurones such as neurofilaments and microtubules, of which more details will be given later. Paired helical filaments (and also straight filaments) occur not only in tangles but also in neuropil threads and in the neuritis surrounding neuritic plaques. Tangles occur first in the entorhinal cortex and spread in a systematic fashion through hippocampus to wider cortical structures but always sparing the cerebellum (Braak et al. In fact the important studies of Braak have shown that the earliest changes in neurones are an increase in tau phosphorylation and a redistribution of tau from the axon to the cell body. This appears to occur some years, possibly decades, before the clinical onset of dementia and both changes in tau phosphorylation and changes in tau expression and/or redistribution may be necessary precursors of the tau aggregation that results in tangle formation. It is not known, but is the subject of much interest and speculation, why some areas of brain are exquisitely sensitive and others apparently completely resistant to tangle formation.

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It is facilitated by fatigue or the consumption of alcohol or hypnotics before retiring medicine 93 3109 order loxitane with mastercard. It has also been described in persons of irritable disposition and in people subject to frequent terrifying dreams medicine with codeine buy generic loxitane pills. Sleep apnoea syndromes the importance of hypersomnias accompanied by alveolar hypoventilation has been increasingly recognised medicine man movie cheap loxitane 10 mg amex. A division is traditionally made into apnoeas of obstructive or central origin premonitory symptoms proven 10 mg loxitane, but this is now regarded as being to some extent artificial. The great majority, over 90%, are associated with airway obstruction and it is this that must be detected if treatment is to be successful. Rare familial forms are probably due to inherited insensitivity of the respiratory centres to hypercapnia. An element of obstructive apnoea usually accompanies these central cases because the pharyngeal and diaphragmatic muscles are responsive to chemical respiratory stimuli. Obstructive sleep apnoea is usually due to occlusion or narrowing of the upper airway behind the tongue or palate. Fibreoptic endoscopy shows that the lateral walls of the oropharynx oppose during episodes of apnoea, commencing with constriction in the upper oropharynx (Parkes 1985). During inspiration the pressure within the upper airway is always subatmospheric, and the patency of the airway depends on the bracing effect of the surrounding musculature. Since muscle tone drops during sleep, there is an enhanced tendency towards narrowing at this time, being greatest when lung volume is minimal at the onset of respiration (Bradley et al. Snoring can result from the turbulent flows engendered, or periods of apnoea when occlusion is complete. Once apnoea has occurred, normal breathing is only restored following arousal for a few seconds, resulting chiefly from the negative intrapleural pressure as the patient struggles to breathe (Douglas 1994). The cycle of recurrent apnoeas and arousals may occur up to 100 times per hour, leading to great disruption of normal sleep patterns. Fat deposition in the submucous tissues around the nasopharynx then contributes to the obstruction. Others may have grossly enlarged tonsils or small mandibular size, the latter often being associated with palatal, tongue or pharyngeal deformity. Most cases of obstructive sleep apnoea commence over the age of 40, with a steady increase in prevalence thereafter. In contrast, the rare central forms can affect all age groups and without definite sex distribution. The usual presentation is with excessive daytime sleepiness occasioned by the disrupted nocturnal sleep. A hallmark of the condition is loud snoring or honking at night as reported by sleeping partners, but the absence of snoring does not exclude the condition. Obesity is common, being found in perhaps 50% of subjects, often with a characteristic facial appearance caused by a short thick neck and heavy jowls. The phases of daytime sleepiness are usually profound and often compelling, leading to a significant increase in accidents including road traffic accidents (George et al. The daytime naps are typically of brief duration and are frequent throughout the day. During sleep, by day and by night, respiratory disturbances give a characteristic stamp to the picture. Nocturnal sleep is characterised by restlessness, frequent changes of posture, flailing arm movements and repeated awakenings. While awake, respiratory function studies typically show normal results or there may be persistent alveolar hypoventilation. Reported complications include pulmonary hypertension resulting from the increase in pulmonary blood pressure during apnoeic periods, and cor pulmonale with right heart failure. The classic Pickwickian syndrome consists of somnolence with obesity, cor pulmonale and secondary polycythaemia, coupled with daytime hypoxia and carbon dioxide retention. Cardiac dysrhythmias, myocardial infarction and cerebrovascular accidents may contribute further to mortality in marked examples of the syndrome. Not surprisingly, a high incidence of unexpected deaths has been reported (MacGregor et al.

Immunosuppressive drugs (cyclophosphamide 86 treatment ideas practical strategies 10mg loxitane fast delivery, azathioprine medications journal effective 10mg loxitane, chlorambucil) may also be of benefit medicine valley high school purchase loxitane 10mg on-line, though side effects limit their usefulness medicine just for cough order loxitane 10mg with visa. Sarcoidosis Sarcoidosis is characterised by the development of chronic granulomatous lesions in various parts of the body. The aetiology is unknown, though an immunologically determined alteration in tissue reactivity appears to be fundamental to the disease. It is assumed, but not proven, that this is induced by exposure to some environmental, perhaps infectious, agent. A familial aggregation has long been noted, although this does not appear to fall into any recognised pattern of inheritance (Buck & McKusick 1961). The characteristic lesion is the epithelioid cell granuloma or follicle, consisting of a well-demarcated collection of epithelioid cells with occasional giant cells. The centres may show necrosis but the caseation seen with tubercular infection is lacking. The commonest site is the respiratory system, presenting with hilar lymphadenopathy or reticular shadowing in the lungs. The mildness of symptoms often contrasts with the extent of the lesions, cases sometimes being discovered on routine chest radiography. Other parts of the body commonly involved are the superficial lymph nodes, spleen, liver and phalanges of the hands and feet. In general sarcoidosis runs an indolent course with relapses and remissions, showing a tendency to subside spontaneously after several years. Individual lesions gradually resolve while others make an appearance, the cycle sometimes being narrowly confined and sometimes widespread in different organs. A minority of patients are left disabled by pulmonary fibrosis or ocular complications. Treatment with steroids is often effective in inducing remission and promoting the healing of lesions, although maintenance therapy must sometimes continue for many years. Immunosuppressive therapy plays a role and newer treatments are emerging (Baughman et al. During active phases of the disease there may be a normochromic anaemia, raised erythrocyte sedimentation rate and eosinophilia. The serum immunoglobulins, especially IgG, are usually elevated and hypercalcaemia of moderate degree is not infrequent. In uncertain cases and with unusual presentations chest radiography may reveal the characteristic picture, likewise radiograph of the phalanges. The Kveim test consists of an intradermal injection of sarcoid tissue extract; this has fair reliability, yielding a nodule with the histological features of sarcoidosis. Involvement of the nervous system is estimated to occur in 5% of patients (Vinas & Rengachary 2001; Stern 2004; Joseph & Scolding 2007). Neurological dysfunction may be the presenting feature or indeed the sole clinical manifestation, although cases with lesions entirely confined to the nervous system are very rare (Allen et al. There are no clear demarcations between the various forms of nervous system involvement but certain broad categories can be discerned. The parts most frequently involved are the cranial nerves, meninges, hypothalamus and pituitary. Lesions of the cranial and peripheral nerves are the commonest neurological feature. The seventh cranial nerve is particularly vulnerable, leading to unilateral or bilateral facial palsies. Involvement of the optic nerves results in blurring of vision, papilloedema, optic atrophy or field defects. Basal meningitis or brainstem involvement can lead to multiple fluctuating cranial nerve palsies. Chronic headache is accompanied by focal signs as the adjacent chiasm and hypothalamus become infiltrated. An adhesive arachnoiditis can lead to raised intracranial pressure and hydrocephalus.

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