Hence, if the data are to be interpreted as showing pathology of his personality structure, this is secondary to the amnesic syndrome. To these standardized results can be added the clinical observations made about H. It is also noted that his adjustment to all changes in relationships and circumstances has been smooth (Corkin, 1984), although whether this reflects maturity or is a function of his adynamia is a moot point. To date, personality change from the premorbid state has not been examined in people with amnesia. Although the traumatic brain-injured group is one for which changes in personality are commonly reported, very few studies with that group have used standardized measures of personality, including ratings taken of the premorbid state soon after onset of injury. Employing the Eysenck Personality Questionnaire-Revised (Eysenck & Eysenck, 1991), Tate (submitted) found more extensive changes between premorbid and 6 month posttrauma ratings: significant decrease in Extraversion and increases in Neuroticism and Criminality, as well as Psychoticism at 12 months posttrauma. These data are interpreted as being changes in personality structure that are a direct consequence of the injury. One of these pertains to the effect of the memory disorder on the development of personality over time. What is the effect of an individual being unable to incorporate and integrate new information and life experiences into the existing personality structure? They hypothesized that, if individuals with amnesia predominantly draw upon immediate memory as a reference point for their personality structure, then they will likely experience fluctuations in emotional states in response to changes in everyday events. By contrast, if they draw upon remote memories, then a much more stable profile will likely emerge. Their own data point to the latter alternative, but clearly this depends upon the nature of the memory disorder. This left him with the most severe episodic memory impairment reported to date, such that he is described as living in "a moment with no past to anchor it and no future to look ahead to" (Wearing, 1988, cited in Wilson & Wearing, 1995, p. With such devastating losses of personal knowledge, in addition to the inability to retain and build upon new memories, one can only speculate that his memory disorder must cut across his very sense of self. Articulate individuals, such as the psychologist Malcolm Meltzer (1983), who writes about the effect of his own (albeit comparatively less severe) memory disorder on his psyche, had such an experience: I felt to some extent that I had lost some of my identity. This was not total or extreme, but there were some questions in my mind about beliefs, values and purposes in life. In addition, I felt I had lost some of my cultural background when I had difficulty remembering some of the customs, traditions and beliefs of the groups to which I belonged. Emotional Status There is a substantial literature on the emotional distress encountered in other groups with acquired neurological conditions, such as stroke and traumatic brain injury, with anxiety and depression, in particular, commonly reported. The data are generally given a straightforward interpretation as being indirect consequences of the neurological event. Rather, he "maintains a steadfastly optimistic, and sometimes unrealistic, view of his own life and progress" (p. The authors suggest three hypotheses to account for the test scores: first, that S. A second hypothesis pertains to the presence of psychological denial as a protective mechanism to shield himself from the full knowledge of his situation. To these possibilities needs to be added the method by which data are gathered, namely self-report instruments. Hermann (1982, cited in Schacter, 1991) observed that completing a self-report instrument is itself a memory task, and this could be a reason why memory-disordered individuals fail to reliably endorse items on checklists such as the Everyday Memory Questionnaire (Sunderland et al. The hypothesis is not only of theoretical importance but is also clinically relevant because it impacts upon management. Ben-Yishay, 2000; Prigatano, 2000) maintain that awareness and insight are requisites for successful rehabilitation. Those with the so-called "pure amnesias" from circumscribed temporal and diencephalic lesions do not have problems with insight. Although their temporal lobe group rated their memory performances worst of any group, nonetheless the frontal and diencephalic (mostly Korsakoff) groups endorsed significantly more severe responses than the normal control group. This would imply that these people have shallow and superficial emotional responses to many situations, not just to their own altered life circumstances, but also that their close relationships may be lacking in warmth, sensitivity and spontaneity.
Immunocompromised hosts lack factors required to control infection; the consequences are progressive focal destruction and organ failure. Clinical disease usually resolves within several weeks, although lymphadenopathy may persist for several months. Toxoplasma pneumonia is often confused with Pneumocystis pneumonia because of an overlapping pt population and similar clinical presentations (i. Diagnosis Culture of the parasite is difficult and can be done only at specialized laboratories. Radiologic studies demonstrate bilateral contrast-enhancing lesions, typically in the basal ganglia and corticomedullary junction. Personal Protection Measures Toxoplasma infection can be prevented by the avoidance of undercooked meats and oocyst-contaminated materials. Tissue Nematode Infections With the exception of trichinellosis, these infections are due to invasive larval stages that do not reach maturity in humans. Trichinellosis Microbiology and Epidemiology Eight species of Trichinella cause human infection; two-T. Visceral and Ocular Larva Migrans Microbiology and Epidemiology Humans are an incidental host for nematodes that cause visceral larva migrans. Infection results when humans-most often preschool children-ingest soil contaminated by puppy feces that contain infective T. Ocular disease usually develops in older children or young adults and includes an eosinophilic mass that mimics retinoblastoma, endophthalmitis, uveitis, and/or chorioretinitis. Stool examination for eggs is ineffective because larvae do not develop into adult worms in humans. Cutaneous Larva Migrans this disease is caused by larvae of animal hook- worms, usually the dog and cat hookworm Ancylostoma braziliense. Larvae in contaminated soil penetrate human skin; intensely pruritic, erythematous lesions form along the tracks of larval migration and advance several centimeters each day. Intestinal Nematode Infections Intestinal nematodes infect >1 billion persons worldwide, most commonly in regions with poor sanitation and particularly in developing countries in the tropics or subtropics. Because most helminthic parasites do not selfreplicate, clinical disease (as opposed to asymptomatic infection) generally develops only with prolonged residence in an endemic area and is typically related to infection intensity. Ascariasis Microbiology Ascariasis is caused by Ascaris lumbricoides, the largest intestinal nematode, which reaches lengths up to 40 cm. Clinical Manifestations Most infections have a low worm burden and are asymptomatic. Pyrantel pamoate (a single dose of 11 mg/kg; maximal dose, 1 g) is safe in pregnancy. Hookworm Microbiology Two hookworm species, Ancylostoma duodenale and Necator americanus, cause human infections. Infectious larvae present in soil penetrate the skin, reach the lungs via the bloodstream, invade the alveoli, ascend the airways, are swallowed, reach the small intestine, mature into adult worms, attach to the mucosa, and suck blood (0. Chronic infection causes iron deficiency and-in marginally nourished persons- progressive anemia and hypoproteinemia, weakness, and shortness of breath. Larvae may cause pruritic rash ("ground itch") at the site of skin penetration as well as serpiginous tracks of subcutaneous migration (similar to those of cutaneous larva migrans). Strongyloidiasis Microbiology and Epidemiology Unlike other helminths, Strongyloides stercoralis can replicate in the human host, permitting ongoing cycles of autoinfection from endogenously produced larvae. Clinical Features Uncomplicated disease is associated with mild cutaneous and/or abdominal manifestations such as recurrent urticaria, larva currens (a pathognomonic serpiginous, pruritic, erythematous eruption along the course of larval migration that may advance up to 10 cm/h), abdominal pain, nausea, diarrhea, bleeding, and weight loss.
One recently developed and successful memory aid that has been helping people with widespread cognitive deficits is NeuroPage r (Hersh & Treadgold, 1994). NeuroPage r is a simple and portable paging system with a screen that can be attached to a belt. Larry Treadgold, the engineer father of a head-injured son, and Neil Hersh, a neuropsychologist, combined their skills to produce a programmable messaging system that utilizes an arrangement of microcomputers linked to a conventional computer memory and, by telephone, to a paging company. The scheduling of reminders or cues for each individual is entered into the computer and from then on no further human interfacing is necessary. The user is alerted to an incoming reminder by a flashing, light-emitting diode and an audible "chirp". Once the message appears, users are requested to telephone a person or an answer service to confirm the message. Users of NeuroPage r can control everything with one rather large button, easy to press even for those having motor difficulties. It has an audible alarm that can be adapted to vibrate if required, together with an accompanying explanatory message, unlike many watch alarms. Perhaps the biggest advantage of the NeuroPage r is that once it has been programmed it is easy to use. Most other systems require considerable time for memory-impaired people to learn how to handle them. We found a statistically significant improvement between the baseline and treatment phases for each of the 15 clients. During the second (posttreatment) baseline phase, the overall percentage of targets achieved was 74%. In fact, some clients learned their routines during the baseline while others did not. This suggests that for some clients, the pager may only be needed for a short while in order to establish certain behaviours. Others, particularly those with executive deficits, may need the reminding service on a longer-term basis. Health and Social Services saved considerable amounts of money on these clients following the implementation of the pager (Wilson & Evans, in press). Some were referred by other therapists who were feeling some desperation because all else had failed. We employed a randomized control trial in the larger study whereby, following a 2 week baseline, clients were allocated to either the treatment group (pager) or to a waiting list control group. After a further 7 weeks, those on the waiting list were given a pager and those who had been using the pager were taken off the paging service. Group A then went on to receive the pager while group B members were on the waiting list. At time 2 (weeks 6 and 7), following the end of baseline, there was a significant difference in favour of group A. At time 3 (weeks 6 and 7 following the changeover), there was a significant difference in the number of target behaviours achieved in favour of group B. One big advantage of a system like NeuroPage r is that it is adaptable and suitable for a wide range of people and problems, from different diagnostic groups and at different times postinsult. The main disadvantage is that people cannot programme the system themselves and have to telephone or otherwise contact a centre so that the messages can be entered on to a computer and, on the right date and time, be transmitted to the individual pager. A study comparing two different keyboards of microcomputers found some people preferred one system while others preferred the other. The use of pagers, computers and other technological aids in memory rehabilitation is likely to expand in the future, given the current growth in information technology. One of the first studies to use an electronic aid with a brain-injured person was that of Gouvier (1982). A small portable timer was used to remind a memory-impaired man to check his memory book. Although computers have been used in cognitive rehabilitation since the 1970s, these were used, on the whole, to provide exercises, in the belief that exercising an impaired function such as memory would lead to an improvement in that function (Gianutsos, 1980; see also Wilson, 1997, for a critique of this approach). Another series of studies using computers is that of Glisky and colleagues (Glisky, 1995; Glisky & Schacter, 1986, 1987, 1989).
Recognition of the Lambert-Eaton syndrome should lead to a search for an occult tumor, particularly of the lung. If found, it should of course be treated; this alone may result in improvement in the neurologic syndrome. If none is found, the search should be repeated at regular intervals, since the tumors at first are small and may be inapparent even at autopsy. The drug is given as 20 mg, up to 5 times a day either alone or in conjunction with pyridostigmine (Lundh et al). This has largely replaced the use of guanidine hydrochloride (20 to 30 mg/kg/day in divided doses), which had proved to be more effective in increasing strength than neostigmine or pyridostigmine but had significant hematologic and renal toxicity with long-term use. With regard to more long-term relief, numerous regimens have been tried and favored by different groups. Dau and Denys have claimed the best results in nontumor cases with repeated courses of plasmapheresis in combination with prednisone and azathioprine. Bain and coworkers indicate that the benefit is due to reduction in calcium channel autoantibodies, but the precise mechanism whereby intravenous immune globulin produces this effect could not be established. Because of the unpredictable side effects of these drugs, many clinicians prefer alternate-day administration of prednisone and azathioprine- prednisone 25 to 60 mg/day, and azathioprine 2 to 3 mg/kg body weight daily- supplemented intermittently as needed by intravenous immune globulin. The response to treatment tends to be slow, over a period of months and sometimes up to a year. Diagnosis A syndrome of symmetrical weakness and fatigability of proximal muscles- coupled with dry mouth, sphincter distur- bances, aching muscles, and diminished reflexes- should be diagnostic. The illnesses with which it might be confused are myasthenia gravis, inclusion body myopathy, and polymyositis. There is a superficial resemblance to hysterical paralysis, where the patient may do better with encouragement on making a succession of voluntary contractions, and arthritis, where pain hampers the first movements more than the successive ones. Neonatal Myasthenia Gravis An estimated 12 to 20 percent of babies born to mothers with myasthenia show transient signs of myasthenia (hypotonia, weak cry and suck). This transitory phenomenon is apparent at birth and has a mean duration of about 2 to 5 weeks; recovery is usually complete within 2 months of birth (rarely longer), without later relapse. Uncommonly, the mother with myasthenia reports reduced intrauterine movements, suggesting a dangerous degree of myasthenia in the fetus. A few of these children will be born with arthrogryposis, the result of a sustained period of intrauterine immobility, and this complication then tends to recur in subsequent births. Administration of plasma exchange and anticholinesterase drugs to the infant may be useful in hastening recovery from neonatal myasthenia. Congenital Myasthenic Syndromes (See Table 53-2) Sporadically in the medical literature, there have appeared reports of a benign congenital myopathy in which myasthenic features could be recognized in the neonatal period or soon thereafter. The affected infants had been born to mothers who did not have myasthenia and were in the past described under headings such as "Myasthenia Gravis in the Newborn" and "Familial Infantile Myasthenia" (Greer and Schotland; Robertson et al) to distinguish the condition from passively transmitted neonatal myasthenia. In the 1970s and 1980s, after the autoimmune basis of myasthenia gravis was established and its morphologic and physiologic features defined, the differences between this disease and the familial infantile forms became evident. Since then, at least eight distinct and rare congenital myasthenic syndromes have been delineated on the basis of their electrophysiologic and ultrastructural features, and a number of others have been partially characterized. As indicated in Table 53-2, the congenital myasthenic syndromes are inherited defects in components of the presynaptic, synaptic, or postsynaptic junctional apparatus. It has been estimated that in three-fourths of the cases the defect is postsynaptic. Moreover, heritability (typically autosomal recessively) is suggested by familial occurrence of the disorders among siblings. In the neonate, the most important clue to the disease is an increase in ptosis and in bulbar and respiratory weakness with crying. Later in infancy these symptoms, as well as fluctuating ocular palsies and abnormal fatigability, are brought out by other types of sustained activity. In some cases, the myasthenic weakness and fatigability do not become evident until the second and third decades of life. The intravenous edrophonium test is inconsistently positive in a few forms of congenital myasthenia, but it usually is negative.
In contrast, detection of early brain deterioration requires imaging techniques too scarce and costly for routine use in general practice. The challenge is to detect asymptomatic brain lesions early with cost-effective techniques for mass population screening. In particular, blood-based biomarkers were explored due to their potential for providing a more accessible, rapid and less expensive solution, requiring minimal expertise to interpret. References in retrieved articles were also reviewed to search for additional pertinent sources. This silent and progressive damage over decades subsequently leads to peripheral artery disease and/or damage to heart, kidneys and brain. Chronic ischemia or acute disruption of blood supply to brain tissue can further trigger mild cognitive impairment, dementia, transient ischemic attacks or stroke. That is, the vast majority of the population had degenerative changes, which were associated with impaired cognitive and lower extremity function. They concluded that subtle vascular brain injury caused by raised blood pressure develops gradually, with noticeable effects even in young adults. Other more accessible and less expensive techniques to assess risk of subclinical brain damage have been proposed, such as ambulatory blood pressure monitoring,[16,24] quantitative retinal microvascular assessment,[30,31] quantitative electroencephalography,[17,32] carotid ultrasonography[19] and neurocognitive studies. Milder degrees of retinopathy appear to be largely nonspecific arteriolar alterations (grades 1 and 2) and their usefulness for prognosis has been questioned. This approach provided interesting data on quantitative and qualitative assessment of retinal microvascular abnormalities in a general population and their relationships with blood pressure values. Blood-based biomarkers Blood withdrawal is a very simple and common procedure for assessing numerous cellular and biochemical parameters in medical conditions. Some of these have been explored in connection with subclinical brain damage in asymptomatic individuals. These chronically affected brain regions-mainly involving white matter-could be leaking brainspecific molecules into the blood stream at a rate much lower than in acute brain injuries (stroke, brain trauma, global ischemia due to cardiac arrest). Nevertheless, the possibility of detecting these brain-specific proteins in blood is undoubtedly increasing with the greater availability and sensitivity of current commercial kits. Differences were not statistically significant,[71] possibly because of small sample size. They found that serum concentrations of these molecular factors varied significantly by blood pressure level, even between those with optimal blood pressure and those whose blood pressure was merely "normal. To date, none of these has been introduced in general medical practice due mainly to prohibitive cost, and the need for specific technologies and highly specialized expertise. Although still infrequently assessed, blood-based biomarkers, especially brain-specific proteins, show promise as more accessible and less expensive tools to help stem the increased disease burden of stroke, cognitive decline and dementia. Effects of systolic blood pressure on white-matter integrity in young adults in the Framingham Heart Study: a cross-sectional study. Reappraisal of European guidelines on hypertension management: a European Society of Hypertension Task Force document. Detection of silent cerebrovascular disease refines risk stratification of hypertensive patients. Cerebral small vessel disease: from pathogenesis and clinical characteristics to therapeutic challenges. Microvascular brain damage with aging and hypertension: pathophysiological consideration and clinical implications. Silent brain infarcts and white matter lesions increase stroke risk in the general population: the Rotterdam Scan Study. Presence and severity of cerebral white matter lesions and hypertension, its treatment, and its control. Ambulatory blood pressure, asymptomatic cerebrovascular damage and cognitive function in essential hypertension. Multimodal quantitative neuroimaging databases and methods: the Cuban Brain Mapping Project. Resistive cerebral blood flow as a potential marker of subclinical brain damage in essential hypertension.
Accident in medical care Causation table (Table D) Combination code Conflict in linkage Contributory cause Direct cause of death Direct sequel "Due to" position Entity Error in medical care Further linkage a misadventure or poisoning occurring during surgery or other medical care. The originating antecedent cause is, from a medical point of view, the starting point of the train of events that eventually caused the death. Intervening cause Late maternal death Maternal death Modification table (Table E) Multiple one-term entity One-term entity Originating antecedent cause Preference code Perinatal period the period which commences at 22 completed weeks (154 days) of gestation (the time when birth weight is normally 500 g), and ends seven (7) completed days after birth. Properly positioned Selected underlying cause of death a condition which is chosen either temporarily or finally by the application of an international selection rule. Sequence two or more conditions entered on successive lines of Part I, each condition being an acceptable cause of the one entered on the line above it. Special five-character subcategories are for use in coding and processing the multiple cause data; however, they will not appear in official tabulations. Some examples have been omitted and additional examples and explanations presented. When more than one cause of death is recorded, the first step in selecting the underlying cause is to determine the originating antecedent cause by application of the General Principle or of Selection Rules 1, 2 and 3. For example, there are some categories for combinations of conditions, or there may be overriding epidemiological reasons for giving precedence to other conditions on the certificate. The next step, therefore, is to determine whether one or more of the Modification Rules A to F, which deal with the above situations, apply. Rules for selection of the originating antecedent cause Sequence the term "sequence" refers to two or more conditions entered on successive lines of Part I, each condition being an acceptable cause of the one entered on the line above it. I (a) Bleeding of esophageal varices (b) Portal hypertension (c) Liver cirrhosis (d) Hepatitis B If there is more than one cause of death on a line of the certificate, it is possible to have more than one reported sequence. In the following example, four sequences are reported: I (a) Coma (b) Myocardial infarction and cerebrovascular accident (c) Atherosclerosis hypertension the sequences are: coma due to coma due to coma due to coma due to myocardial infarction due to atherosclerosis cerebrovascular accident due to atherosclerosis myocardial infarction due to hypertension cerebrovascular accident due to hypertension General Principle the General Principle states that when more than one condition is entered on the certificate, the condition entered alone on the lowest used line of Part I should be selected only if it could have given rise to all the conditions entered above it. If the General Principle does not apply and there is a reported sequence terminating in the condition first entered on the certificate, select the originating cause of this sequence. If there is no reported sequence terminating in the condition first entered on the certificate, select this first-mentioned condition. Some considerations on selection rules: In a properly completed certificate, the originating antecedent cause will have been entered alone on the lowest used line of Part I and the conditions, if any, that arose as a consequence of this initial cause will have been entered above it, one condition to a line in ascending causal order. However, even if the certificate has not been properly completed, the General Principle may still apply provided that the condition entered alone on the lowest used line of Part I could have given rise to all the conditions above it, even though the conditions entered above it have not been entered in the correct causal order. I (a) Generalized metastases (b) Bronchopneumonia (c) Lung cancer 5 weeks 3 days 11 months the General Principle does not apply when more than one condition has been entered on the lowest used line of Part I, or if the single condition entered could not have given rise to all the conditions entered above it. Where the General Principle cannot be applied, clarification of the certificate should be sought from the certifier whenever possible, since the selection rules are somewhat arbitrary and may not always lead to a satisfactory selection of the underlying cause. Where further clarification cannot be obtained, however, the selection rules must be applied. Rule l is applicable only if there is a reported sequence, terminating in the condition first entered on the certificate. If such a sequence is not found, Rule 2 applies and the first-entered condition is selected. The condition selected by the above rules may, however, be an obvious consequence of another condition that was not reported in a correct causal relationship with it;. It applies, however, only when there is no doubt about the causal relationship between the two conditions; it is not sufficient that a causal relationship between them would have been accepted if the certifier had reported it. Examples of the General Principle and Selection Rules General Principle When more than one condition is entered on the certificate, select the condition entered alone on the lowest used line of Part I only if it could have given rise to all the conditions entered above it. One condition is entered on the lowest used line and all the conditions entered above it must be entered in a "reported sequence" and there must be only one condition per line. Codes for Record I (a) Cerebral hemorrhage 1 mo I619 (b) Nephritis 6 mos N059 (c) Cirrhosis of liver 2 yrs K746 Select cirrhosis of liver. Each condition on the successive lines in Part I is an acceptable cause of the one entered on the line above it. Or it must be probable that the condition reported alone on the lowest used line could have given rise to all the conditions entered above it. It is not necessary for the conditions on (a) and (b) to be causally related since the condition entered alone on (c) can give rise to both conditions. Congestive heart failure is due to chronic alcoholism and cerebral hemorrhage is due to chronic alcoholism. Reported sequence terminating in the condition first entered on the certificate If the General Principle does not apply and there is a reported sequence terminating in the condition first entered on the certificate, select the originating cause of this sequence.
While the disease model has produced valuable advances in understanding and treatment, it has been criticized for a number of reasons (Kitwood, 1997). Furthermore, there are considerable difficulties associated with diagnosis and classification (see. Differential diagnosis of dementia and depression is also problematic (Small et al. Most importantly, the disease model fails to account for "excess disability", whereby functioning is worse than the degree of impairment would predict (Reifler & Larson, 1990) for periods of "rementing", where functioning improves or stabilizes (Kitwood, 1996; Sixsmith et al. For these reasons, it is suggested that a broader model, which incorporates the role of psychological and social variables, is required (Kitwood, 1997). The term "dialectical" reflects the emphasis on interactions between variables operating at the biological and psychosocial levels. The aim of this "alternative paradigm" is to present an account of the process of dementia that bridges these two levels (Kitwood, 1996, 1997). Where the social psychology is "malignant", the result is an involutional spiral of deterioration. Social interactions and care processes that are undermining and discouraging, and fail to take account of personality and life history, lead to a reduction in self-efficacy which in turn attracts further damaging interactions (Sabat, 1994). It indicates that the primary aim should be to maximize well-being and optimize functioning 714 L. To be effective, care should be person-centred, based on an individualized formulation that takes into account all the relevant biological, psychological and social factors, and delivered in a way that promotes a benign rather than malignant social psychology. Other information required to complete the picture includes a full history, an assessment of mood and well-being, an evaluation of functional ability, and a consideration of the social and environmental context, including the needs of close family members. While neuropsychological tests form an essential component of the assessment, the results should be interpreted with caution, bearing in mind the range of factors that may affect performance. Neuropsychological assessment can often be an aversive experience for the older person, and care should be taken to create a situation that provides a positive and worthwhile experience. The amount of testing should be limited to the minimum necessary to answer the relevant questions satisfactorily, and practical, constructive feedback should be offered to the individual and family. Assessment Measures It is necessary to distinguish screening tests (sometimes described as "cognitive" tests) from neuropsychological tests. Screening tests are often used to provide an indication of whether there is cognitive impairment, and can be valuable provided their limitations are clearly understood. Administration procedures can vary considerably, although a standardized version is available (Molloy et al. Therefore, although a low score (24/30 or below) strongly suggests the presence of impairment, results should always be treated with caution. It is useful to consider memory functions (learning, forgetting), modalities (visual, verbal, sensory), time periods (recent, remote), relation to onset of problems (anterograde, retrograde) and testing methods (recall vs. As well as tests suitable for use in general neuropsychological assessment, the list includes some tests that can be used to explore further and more specific hypotheses within a cognitive neuropsychological framework. For reviews of specific neuropsychological tests and information on the availability of additional age-specific norms, see Spreen & Strauss (1998) and Lezak (1995). The assessment of memory functioning is discussed in detail by Wilson (Chapter 28, this volume). Non-cognitive Measures It is useful to consider including some non-cognitive measures in the assessment; for example mood might be assessed using the Geriatric Depression Scale (Yesavage et al. Measures of functional ability are reviewed by Carswell & Spiegel (1999) and Little & Doherty (1996). Most people who present with concerns about memory problems do not in fact have dementia, and it is also important to note that in specialist clinical practice professionals see an atypical group of patients. It has been demonstrated that memory clinics can provide an effective focus for early intervention and for the development of integrated psychosocial approaches (Moniz-Cook & Woods, 1997; Moniz-Cook et al. Distinguishing Dementia from "Normal" Ageing the boundaries between dementia and normal forgetfulness appear somewhat fluid, and it remains unclear how the difference between dementia and normal ageing should be conceptualized. Although many older people and their families expect to observe a decline in memory functioning, there is a great deal of variation in the general population as regards the kinds of memory changes seen as part of "normal" ageing, and the issue is compounded by cohort effects.
In the hyperendemic regions of northern and subSaharan Africa, the Middle East, and parts of Asia, the prevalence of trachoma is ~100% by the third year of life. Treatment of sexual partners is needed to prevent ocular reinfection and chlamydial genital disease. Clinical Manifestations Psittacosis in humans can range in severity from asymptomatic or mild infections to acute primary atypical pneumonia (which can be fatal in 10% of untreated cases) to severe chronic pneumonia. Seropositivity is first detected at school age and then increases by ~10% per decade. Pts have antecedent upper respiratory tract symptoms, fever, nonproductive cough, minimal findings on auscultation, small segmental infiltrates on chest x-ray, and no leukocytosis. Pain, itching, dysuria, vaginal and urethral discharge, and tender inguinal lymphadenopathy are the predominant local symptoms. In general, these isolates are also resistant to valacyclovir and famciclovir, which have similar mechanisms of action. The virus replicates and causes viremia, which is reflected by the diffuse and scattered skin lesions in varicella; it then establishes latency in the dorsal root ganglia and can reactivate through unknown mechanisms at a later time. Chickenpox Pts present with fever, malaise, and rash characterized by maculopapules, vesicles, and scabs in various stages of evolution. Symptomatic recurrent genital herpes: Short-course (1- to 3-day) regimens are preferred because of low cost, likelihood of adherence, and convenience. Other options include oral acyclovir (200 mg 5 times per day), valacyclovir (500 mg bid), and famciclovir (125 mg bid for 5 days). Pts with >9 episodes per year should take oral valacyclovir (1 g daily or 500 mg bid) or famciclovir (250 mg bid or 500 mg bid). Recurrent episodes: If initiated at prodrome onset, single-dose or 1-day therapy effectively reduces pain and speeds healing. The optimal duration of therapy and the usefulness of its continuation to suppress lesions are unclear. In contrast, immunocompromised pts have numerous slower-healing lesions (often with a hemorrhagic base) and are more likely to develop visceral complications that, if not treated, are fatal in 15% of cases. Cutaneous dissemination occurs in 40% of these pts and increases the risk for other complications (pneumonitis, meningoencephalitis, hepatitis). Prednisone (given along with antiviral therapy at a dosage of 60 mg/d for the first week of zoster, with the dose then tapered by 50% weekly over the next 2 weeks) can accelerate quality-of-life improvements, including a return to usual activity; prednisone treatment is indicated only for healthy elderly persons with moderate or severe pain at presentation. Irrespective of serologic status, pts >60 years old should receive a vaccine with 18 times the viral content of varicella vaccine; zoster vaccine reduces the incidence of zoster and postherpetic neuralgia. The primary adverse events include electrolyte disturbances and renal dysfunction. Influenza A and B viruses are major human pathogens and are morphologically similar; influenza B infection is associated with less severe disease than influenza A infection, and influenza C virus causes subclinical disease.
References:
