By E. Brontobb. Bemidji State University.
However proven 100 mg pletal, given the cognitive and behavioral degenerative process as- Costs sociated with AD cheap pletal 100 mg amex, the use of alternative respondents may be unavoidable. Additionally, measuring outcomes as 'time First of all, no prospective measurement of resource use spent in less than severe state' does not inform health and associated with the drug or usual care was made. Costs were social care decision makers about the value of quality of life estimated from retrospective analysis of available data sets for people with AD and their family and carers. The range of cost items Effectiveness and the costing methodologies employed in each study were heterogeneous. Some of these Three analyses (37,38,49) directly or indirectly associ- trials have been criticized elsewhere (50) for having enrolled ated the dynamic of treatment costs with the progression a carefully selected subgroup of patients with mild-to-mod- of disease severity, measured with the MMSE. The MMSE erate AD and excluded those with coexisting illness or con- score was shown to be strongly correlated with costs of de- current treatment. In real practice, the eligible population mentia care, but it is unclear to what extent the use of may be considerably different. Consequently, only a limited this instrument is robust in modeling studies. It has been proportion of people may be adequately and safely treated. The cost-effec- tiveness of cholinesterase inhibitors depends on the distribu- Outcome Measures tion of patients across different severity states (38). In this context, the correct assessment of the duration of the treat- One study used QALYs to measure the benefits derived ment effect of anticholinesterase drugs assumes a central from introducing the drug (39). In the other studies, bene- role because it affects the number of people having mild- fits were measured in terms of 'time spent in condition less to-moderate AD at any one time. Modeling However, this instrument has not been validated in patients with AD, and its ability to detect small improvements in Some authors have recently challenged the use of Markov potentially important clinical aspects is doubtful. The models in the evaluation of antidementia drugs (33,48). Given the considerable context largely characterized by uncertainty surrounding the uncertainty surrounding the available data, deterministic value of the key variables, modeling techniques can be used models in which simplistic sensitivity analysis techniques to assess the value for money of new management strategies are used may not be adequate to assess the robustness of for the treatment of AD and compare them with the alterna- the results. The application of stochastic models allows the tive policy options. Further primary and secondary research uncertainty associated with relevant parameters of a model is required to provide robust estimates of the formal and to be incorporated and quantified. CONCLUSION REFERENCES As a direct consequence of changes in the age structure of 1. The epidemiologically based disorder focuses on assisting patients in their daily activities needs assessment reviews. The impact of the symptoms residential or nursing home care. In: Wimo A, Jonsson B, Karlsson trigger the need for long-term institutional care, including G, et al. Chichester: John the age of family carers, the behavioral problems of patients, Wiley and Sons, 1998. Institutionalization has been identified review of the disease, its epidemiology and economic impact. Some clinical evidence indicates that anticholinesterase 8. If the drugs are effective in controlling symp- 167–173. Canadian Study of Health and Aging: toms or slowing progression of the illness, they may delay study methods and prevalence of dementia. Can Med Assoc J the need for intensive support or institutionalization of pa- 1994;150:899–913. The high acquisition cost of the drugs, however, has 10. Prevalence of medically significant number of studies addressing the issue of costs diagnosed dementia in a defined United States population: Roch- and patient benefits. To date, a conclusive analysis has not clarified the most 12. The prevalence of demen- appropriate management strategy for the disorder. In the tia: a quantitative integration of the literature. Acta Psychiatr near future, new drugs for the treatment of AD are expected Scand 1987;76:465–479. Cochrane able to compare them in a clear and well-defined framework. In addition, if economic evaluation is to inform health and 14.
The presence of a percentage of OCDpatients cheap pletal 100 mg line, impairment in function and tic disorder predicted more severe symptoms of OCDat quality of life is severe (45) purchase pletal 100 mg fast delivery. It is the only major psychiatric follow-up in children (47). The predictive power of a per- disorder for which neurosurgery continues to be a treatment sonal or family history of multiple tics in regard to remission option. It will be important in future studies to gather pro- and relapse rates should be investigated. In the National Collab- been investigated in a number of acute treatment studies orative Study of Depression, even subsyndromal symptoms with inconsistent findings. In a study by Baer et suggest that psychosocial functioning continues to be im- al. A subsequent single-site study of the effect of a personality disorder on the response to fluoxetine failed to confirm that a cluster PREDICTORS OF LONG-TERM COURSE OF A diagnosis is a negative predictor of outcome (55). ILLNESS The DSM-IV field trial of OCD established that a signif- icant percentage of patients with OCDhave poor insight Although a number of studies have examined predictors of (56). The validity of this new diagnostic category is still in outcome in OCD, the results have been inconsistent. Data pertaining to the effect of poor insight or have focused on identifying predictors of short-term out- overvalued ideation on behavioral treatment response have come following pharmacologic or behavioral treatment. Eisen and Rasmussen (59) retro- None of the existing studies has examined predictors of spectively assessed the course of illness in four subgroups remission or relapse rates. These studies have been methodo- of OCD: OCDand schizophrenia, OCDand schizotypal logically compromised by small sample size, inclusion or personality disorder, OCDwith poor insight, and OCD exclusion criteria that led to sample bias, and inadequate without psychotic features. A deteriorative course was noted duration of follow-up. Characteristics such as age at onset in 82% of the patients with coexisting schizophrenia, 69% of OCD, duration of illness, severity of illness at baseline, of those with coexisting schizotypal personality disorder, and phenomenologic subtype have not been associated with 17% of those with poor insight, and only 8% of those with- Chapter 111: Obsessive-Compulsive Disorder 1601 out psychotic features. This study was hampered by the lack tomography (PET) have shown that regional activation of of a valid and reliable scale to measure poor insight and by the prefrontal cortex varies according to factor (69), and the retrospective assessment of the course. We have recently emerging genetic data suggest that familial loading varies published data on the reliability and validity of a new scale, according to factor (70). Symmetry and certain obsessions, the Brown Assessment of Beliefs Scale (BABS), that has such as aggressive and sexual obsessions, are more frequent demonstrated excellent sensitivity to change with short-term in patients with OCDand chronic tics (71). The phase of a double-blinded relapse study of sertraline in analytic technique used to identify factors from the Y-BOC OCD. They found no significant correlation between de- Symptom Checklist may be fruitful in predicting the course gree of insight as measured by the BABS and outcome after of OCD. Evidence is increasing that patients in whom 16 weeks of sertraline. The role of insight in remission and hoarding is a primary obsessive-compulsive symptom are relapse deserves further scrutiny. In addition, hoarding was the only com- tions in neurologic function involving the basal ganglia after pulsion associated with a lower probability of remission in head trauma, encephalitis, and birth events (62). In a number of studies, an earlier age psychological abnormalities in comparison with a control at onset of OCDwas associated with a worse prognosis. Thomsen (36) reported that attainment ceiver operating characteristic analysis found that a cutoff of puberty by the time of referral predicted a better prog- of three or more signs yielded the minimum number of nosis than a prepubertal onset. In a reanalysis of the multi- combined errors of sensitivity and specificity in blindly dis- center efficacy and safety data for clomipramine, Ackerman tinguishing OCDsubjects from controls. A second study of OCDadolescents for confounds, found a later age at onset to be a strong found a high frequency of age-inappropriate synkinesias and predictor of response. Skoog and Skoog (42) reported that lateralization of deficits to the left side of the body (64). In onset of OCDbefore age 20 was related to a poorer out- a nonblinded study in which a clinical neurologic examina- come, especially in men. In other studies, age at onset did tion was performed in childhood and adolescent OCDsub- not predict severity of illness at follow-up. Adolescents in jects, most of the patients had abnormal neurologic find- the study of Berg et al. It seems likely sided signs that were suggestive of right-sided dysfunction. However, in the only study we could locate that type in OCD. Thus far, specific obsessions and compulsions have not predicted outcome in the vast majority of follow- examined level of functioning in OCD, pretreatment func- up studies. In a preliminary analysis of 544 patients from tioning did not predict follow-up outcome (73). Duration a multicenter trial of acute clomipramine, the authors failed of symptoms was not predictive in any study (78,79,81, to find any significant correlation between symptom sub- 82), although it is possible that chronicity accompanied by type, identified by the Y-BOC Symptom Checklist, and comorbidity may worsen prognosis. However, STABILITY OVER TIME few systematic clinical psychopathologic studies had been completed before 1985.
Congenital Congenital Autosomal-dominant X-linked Autosomal-recessive Autosomal-recessive Acquired Acquired Post-traumatic Renal diseases (medullary cystic disease 50mg pletal with amex, Iatrogenic polycystic disease pletal 100mg with amex, analgesic nephropathy, Tumors (metastatic from breast, sickle cell nephropathy, obstructive uro- craniopharyngioma, pinealoma) pathy, chronic pyelonephritis, multiple myeloma, amyloidosis, sarcoidosis) Cysts Hypercalcemia Histiocytosis Hypokalemia Granuloma (tuberculosis, sarcoid) Drugs (lithium compounds, demeclocycline, Aneurysms methoxyflurane, amphotericin, foscarnet) Meningitis Encephalitis Guillain-Barré syndrome Idiopathic FIGURE 1-35 Congenital central diabetes insipidus (DI), autosom al-dom inant form. This condition has been described in m any fam ilies in Europe and N orth Am erica. It is an autoso- m al dom inant inherited disease associated SP VP NP NP NP CP with m arked loss of cells in the supraoptic nuclei. M olecular biology techniques have Exon 1 Exon 2 Exon 3 revealed m ultiple point m utations in the vasopressin-neurophysin II gene. This con- 83 dition usually presents early in life. This has been linked 17 to a defect in chrom osom e-4 and involves 57 abnorm alities in m itochondrial DN A. Central DI m ay be treated with horm one replacem ent or drugs. In acute settings when renal water losses are extensive, aqueous vasopressin (pitressin) is Condition Drug Dose useful. It has a short duration of action that allows for careful m on- itoring and avoiding com plications like water intoxication. This Complete central DI dDAVP 10–20 (g intranasally q 12–24 h drug should be used with caution in patients with underlying coro- Partial central DI Vasopressin tannate 2–5 U IM q 24–48 h nary artery disease and peripheral vascular disease, as it can cause Aqueous vasopressin 5–10 U SC q 4–6 h vascular spasm and prolonged vasoconstriction. For the patient Chlorpropamide 250–500 mg/d with established central DI, desm opressin acetate (dDAVP) is the Clofibrate 500 mg tid–qid agent of choice. It has a long half-life and does not have significant Carbamazepine 400–600 mg/d vasoconstrictive effects like those of aqueous vasopressin. It can be conveniently adm inistered intranasally every 12 to 24 hours. It is safe to use in pregnancy and resists degradation by circulating vasopressinase. In patients with partial DI, agents that potentiate release of antidiuretic horm one can be used. These include chlorpropam ide, clofibrate, and carbam azepine. They work effectively only if com bined with horm one therapy, decreased solute intake, or diuretic adm inistration. FIGURE 1-37 T T S A M Extracellular P * S L M –NH2 Congenital nephrogenic diabetes insipidus, P S H V A 1 S L L G P X-linked–recessive form. This is a rare dis- N S P S ease of m ale patients who do not concen- S F trate their urine after adm inistration of Q R E D R antidiuretic horm one. The pedigrees of R T G P A P A E P affected fam ilies have been linked to a L P L F W G L D D K D C R group of Ulster Scots who em igrated to R T W A A S G G P E A P A L W G E R H alifax, N ova Scotia in 1761 aboard the R A V T D L A L C C V Y * W E ship called “H opewell. Recent studies, howev- A L H V M T A L V V L I T L Y A * * L I L V F M S er, disproved this hypothesis. The A P R D P E R R S S F L C C R A H R I V S A gene defect has now been traced to 87 dif- R H V L R R W A N A T S S G ferent m utations in the gene for the vaso- G H W S K S E L R R R R G I H S A pressin receptor (AVP-R2) in 106 presum - C L V T R A V H A V P G * A A ably unrelated fam ilies. In the autosom al recessive form of N DI, m utations D N A T G A 8 P G have been found in the gene for the antiiuretic horm one (ADH )– R L N K sensitive water channel, AQ P-2. This form of N DI is exceedingly I S M F D N S D rare as com pared with the X-linked form of N DI. Thus far, a A S 13 C D total of 15 AQ P-2 m utations have been described in total of 13 P T G H T 6 T T W fam ilies. The acquired form of N DI occurs in various kidney I A Y V Q A L P E G H F diseases and in association with various drugs, such as lithium S V H L Q I W P W L L A T V G L L I G and am photericin B. Hypernatremia always Causes and mechanisms of acquired nephrogenic diabetes insidpidus. It usually diabetes insipidus occurs in chronic renal failure, electrolyte imbalances, with certain drugs, occurs in a hospital setting (reported inci- in sickle cell disease and pregnancy. The exact mechanism involved has been the subject of dence 0. The prim ary goal in the treatm ent Muscle twitching of hypernatrem ia is restoration of serum tonicity. H ypovolem ic hypernatrem ia in the con- Spasticity text of low total body sodium and orthostatic blood pressure changes should be m anaged Hyperreflexia with isotonic saline until blood pressure norm alizes. Thereafter, fluid m anagem ent general- ly involves adm inistration of 0. The goal of therapy for hypervolem ic hypernatrem ias is to rem ove the excess sodium , which is achieved with diuretics plus 5% dextrose. Patients who have renal im pairm ent m ay need FIGURE 1-41 dialysis. In euvolem ic hypernatrem ic patients, water losses far exceed solute losses, and the Signs and sym ptom s of hypernatrem ia. To correct the hypernatrem ia, the total body water H ypernatrem ia always reflects a hyperosm o- deficit m ust be estim ated. This is based on the serum sodium concentration and on the lar state; thus, central nervous system sym p- assum ption that 60% of the body weight is water.
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