The aim of this review was to provide an update review of the best quality evidence for the clinical effectiveness and cost-effectiveness of donepezil, rivastigmine, and galantamine for mild to moderately severe AD. It also aimed to provide a review of the best quality evidence for the clinical effectiveness and cost-effectiveness of memantine for moderately severe to severe AD!
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Address correspondence and reprint requests to Dr. Kenneth L. Rock, Chair, Department of Pathology, University of Massachusetts Medical School, S2-109, 55 Lake Avenue North, Worcester, MA 01655. E-mail address: kenneth.rock umassmed.
O The hospitals submit, in the manner required Kaplan-Meier method ; their individual and pooled experience and survival data; and o The hospitals otherwise meet the remaining Medicare criteria for heart transplant facilities; that is, the criteria regarding patient selection, patient management, program commitment, etc. C. Pediatric Hospitals.--Cardiac transplantation is covered for Medicare beneficiaries when performed in a pediatric hospital that performs pediatric heart transplants if the hospital submits an application which HCFA approves as documenting that: o The hospital's pediatric heart transplant program is operated jointly by the hospital and another facility that has been found by HCFA to meet the institutional coverage criteria in HCFA Ruling 87-1; o The unified program shares the same transplant surgeons and quality assurance program including oversight committee, patient protocol, and patient selection criteria and o The hospital is able to provide the specialized facilities, services, and personnel that are required by pediatric heart transplant patients. D. Follow-up Care.--Follow-up care required as a result of a covered heart transplant is covered, provided such services are otherwise reasonable and necessary. Follow-up care is also covered for patients who have been discharged from a hospital after receiving a noncovered heart transplant. Coverage for follow-up care would be for items and services that are reasonable and necessary, as determined by Medicare guidelines. See Intermediary Manual 3101.l4 and Carriers Manual 2300.1. ; E. Immunosuppressive Drugs.-- See Intermediary Manual 3660.8 and Carriers Manual 2050.5, 4471 and 5249. ; F. Artificial Hearts.--Medicare does not cover the use of artificial hearts or ventricular assist devices, either as a permanent replacement for a human heart or as a temporary life-support system until a human heart becomes available for transplant often referred to as a "bridge to transplant" ; . See 65-15. ; 35-88 EXTRACORPOREAL PHOTOPHERESIS Effective for services performed on or after April 8, 1988, for example, fda!
Click here x-rays yield mechanism of new drug alzheimer disease march 19, 2003 a team of weizmann scientists has gained new insight into the effects of a newly approved drug, rivastigmine, in treating alzheimer disease.
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The manufacturers' summaries of product characteristics should be referred to for full prescribing information. INDICATIONS FOR USE Donepezil, Rivatsigmine and Galantamine are licensed for mild to moderate dementia in Alzheimer's disease. Dose Usual maintenance doses are: Donepezil 5-10mg daily, taken as a single dose in the evening, just prior to retiring; Rivastigmine, 3-6mg twice a day with meals, swallowed whole; Galantamine, 8-12mg twice a day with meals. SAFETY ISSUES Contra-indications The summaries of product characteristics includes the following contra-indications: patients with hypersensitivity to Donepezil, Rivastigmine, Galantamine or the excipients; Donepezil is contra-indicated in pregnancy and breast-feeding; Galantamine is contra-indicated in patients with severe renal and or hepatic impairment, and in patients with rare hereditary problems of galactose intolerance, glucose-galactose malabsorption or the Lapp lactase deficiency. It should not be used while breast-feeding and should be used with caution in pregnancy and sertraline.
The Dietary Reference Intakes DRIs ; released by the Food and Nutrition Board of the US Academy of Sciences are intended to be used for planning and assessing the diet for an apparently healthy population in the US and Canada : iom IOM IOMHome.nsf Pages Food + and + Nutrition + Board ; . These values may eventually be used for updating the RDIs Reference Daily Intakes ; . 2.
Dr S S Ye, Southampton General Hospital. "Molecular genetic and functional analyses of ABCA 1 gene variants" 3 years ; . 117, 549 Professor J M Squire, Imperial College, London. Myosin filament ultrastructure in health and disease" 3 years ; . 144, 715 Professor M R Bennett, University of Cambridge. "Manipulation of cell death in vivo" 3 years ; . 146, 084 Dr G K Dhoot, The Royal Veterinary College, London. "The relationship of slow skeletal muscle troponin T expression with coronary vasculoangiogenesis in normally developing and pathological heart" 3 years ; . 121, 115 Dr D S Steele, University of Leeds. "Atrioventricular differences in sarcoplasmic reticulum Ca2 + regulation" 3 years ; . 151, 535 Fellowships Committee: April 2002 DEFERRED APPLICATIONS AWARDED Junior Research Fellowship Dr K. Chitkara, Glenfield Hospital, Leicester. "Preclinical assessment of antithrombotic and antiproliferative action of stents eluting eptifibatide integrilin ; ". 2 years ; 95, 622. PhD Studentship Dr R Motterlini, Northwick Park Hospital. "Pharmacological activities of cardon monoxidereleasing molecules Co-RMs ; in the cardiovascular system". 3 years ; 63, 432. PhD Studentship Clinical ; Dr C.J. Redpath, University of Glasgow. "The effects of neurohumoral activation on the electrophysiology of human isolated atrial myocytes". 2.5 years ; 101, 127 NEW APPLICATIONS AWARDED Intermediate Research Fellowships Dr M.J. Coffey, University of Wales College of Medicine. "Mechanisms and consequences of platelet 12-lipoxygenase of activation by collagen in the vasculature". 3 years ; 124, 819. Junior Research Fellowship Dr A.M. Ross, University of Aberdeen. "The role of MTHFR genotypes and dietary folate in the development of ventricular septal defects". 2 years ; 84, 944. Dr K.J. Hogg, University of Glasgow. "Characterisation of patients with heart failure despite preserved left ventricular systolic function: a prospective, descriptive, cohort study". 2 years ; 75, 011 and sildenafil, for example, reminyl!
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1.1 APPOINTMENT OF THE TASK FORCE. In September 2002, the Injury and Violence Prevention Branch of the North Carolina Department of Health and Human Services Division of Public Health NC-DHHS DPH ; released preliminary findings documenting an escalation in the number of deaths in North Carolina residents from unintentional drug overdoses. Deaths from fatal unintentional drug overdoses had increased over 100 percent in the five years between 1997 and 2001. In response to this epidemic, NC-DHHS Secretary Carmen Hooker Odom created the Task Force to Prevent Deaths from Unintentional Drug Overdoses hereafter called "the Task Force" ; in November 2002 to study this problem and to develop recommendations to identify, reduce and ultimately prevent unintentional deaths from the use of illicit and licit drugs. The Injury and Violence Prevention Branch provided administrative and technical support to the 25-member Task Force. Diverse and broad representation on the Task Force from public health, mental health, substance abuse services, law enforcement, medical examiners, pharmacists and physicians afforded a collaborative approach. Dr. Jeffrey Engel, the State Epidemiologist, and Larry Smith, Assistant Director for Support Services Division of the State Bureau of Investigation, co-chaired the Task Force. 1.2 CHARGES TO THE TASK FORCE. The specific charges to the Task Force were to 1. 2. describe the scope and magnitude of the increase in unintentional drug-related deaths in North Carolina that began in 1997; identify the procedures and polices of the agencies organizations represented on the Task Force that impact the use of illicit and licit drugs resulting in unintentional deaths; identify the factors that contribute to the abuse and misuse of illicit and licit drugs prior to, during, and after the lethal exposure; identify the prevention strategies applicable to each of the factors as they occur; identify areas of collaboration among the agencies organizations represented on the Task Force; develop recommendations to enhance collaboration of these agencies organizations in reducing and preventing the use of illicit and licit drugs that result in unintended deaths; develop recommendations to enhance the reduction and prevention of unintentional drug-related deaths and simvastatin.
In regards to randomization, the MMA requires a randomized study design. We plan to comply with standard procedures for randomization. CMS has every confidence that this program will succeed and as such, are diligently working no w on how to operationally implement this program nationwide in the most effective and efficient way. Programs such as these that target beneficiaries with chronic conditions are extremely important, and I'm also committed to using the broader demonstration authority under the statute to continue to find ways to get higher quality and lower cost care for these beneficiaries. Question 39: Information Technology Almost a year ago, several different federal agencies, including the Department of Health and Human Services, reached agreement on a set of technical standards for the electronic exchange of health information. HHS requires reporting of health information for quality, public health, research, and drug approval purposes. However, much of this data is not formatted in accordance with the standards agreed upon last year. How will you work with FDA, CDC, NIH and other HHS agencies to ensure that all data electronically reported to HHS uses the agreed health information exchange standards?.
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The mitochondrial theory of aging suggests that aging is a result of accumulating genetic mutations that, over time, erode the body s natural defenses and adversely affect cellular processes. This theory of aging provides for the utilization of nutrition as an intervention, specifically in order to enhance mitochondrial function and thereby deter a number of adverse age-related cellular processes. Today, our understanding of disease etiology warrants the study of molecular determinants of disease risk. Genetics and genomics now have an important place in an integrated approach to nutrition. Yet, it may be argued that the health and resilience of humans and animals remains, in large part, determined by the quality and quantity of the diet. This, in turn, may influence an individual s capability to deal with stressors that may precipitate disease. As a result, scientists taking advantage of the knowledge gleaned through the Human Genome Project and sporanox.
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A Qualified Medical Child Support Order is a medical child support order which creates or recognizes an Alternate Recipient's right to, or assigns to an Alternate Recipient the right to, receive benefits for which a Covered Person is eligible, and which the Plan Administrator has determined meets the requirements of this Section. A Medical Child Support Order to be qualified must clearly: 1. Specify the name and last known mailing address if any ; of the Covered Employee and the name and mailing address of each Alternate Recipient covered by the order; and 2. Include a reasonable description of the type of coverage to be provided by the Plan to each Alternate Recipient, or the manner in which such type of coverage is to be determined; and 3. Specify each period to which such order applies; and 4. Specify each plan to which such order applies; and 5. Not require the Plan to provide any type or form of benefits or any option not otherwise provided under the Plan except to the extent necessary to meet the requirements described in Section 1908 of the Social Security Act relating to the enforcement of state laws regarding child support and reimbursement of Medicaid ; . Upon receipt of a Medical Child Support Order, the Plan Administrator shall: a. Promptly notify in writing the Covered Employee, each Alternate Recipient covered by the order, and each representative for these parties of the receipt of the Medical Child Support Order. Such notice shall include a copy of the order and these QMCSO procedures. b. Permit the Alternate Recipient to designate a representative to receive copies of notices sent the Alternate Recipient regarding the Medical Child Support Order. c. Within a reasonable period after receiving a Medical Child Support Order, determine whether it is a qualified order and notify the parties indicated in subsection a ; above of such determination. d. Ensure the Alternate Recipient is treated by the Plan as a beneficiary for reporting and disclosure purposes, such as by distributing to the Alternate Recipient a copy of the Summary Plan Description and any subsequent Summaries of Material Modifications generated by a Plan Amendment and sumatriptan.
Finally, the GDS-15 has certain limitations. It is questionable whether a demented patient can answer the 15 questions accurately, since these patients can be disoriented and anosognostic. But since this questionnaire is evaluated as a reliable and valid screening instrument for both cognitively normal and cognitively impaired elderly31, 32, we judged it acceptable to use the GDS-15. Future study is needed to replicate in a larger sample and with less heterogeneity in follow-up period, the predictive value of brain atrophy and the presence of depressive symptoms on cognitive decline in MCI and AD. It would also be interesting to investigate if other factors, such as the genetic risk factor for AD the apolipoprotein E APOE ; epsilon4 allele or the presence of other psychiatric disturbances such as delusions or hallucinations can predict cognitive decline in MCI and AD. There are several clinical implications of this study. First of all, we were not able to predict which MCI and AD patients will show more cognitive decline than others. This means that, once patients have been diagnosed as MCI or AD we cannot predict the course the disease may take. Secondly, we have found no effect of 4ivastigmine on the longer term. The use of describing rivastigmne to AD patients for more than one year therefor, is highly questionable. In conclusion, cognitive decline in AD and MCI, nor crossover from AD to MCI, can be predicted by mediotemporal volume, whole brain volume or the presence of depressive symptoms. The only factor which showed some predictive value on cognitive decline was the cognitive test-score at baseline. Second, no effect of rivastigmie on the longer term was found.
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Thought to manifest themselves more in terms of neuropsychiatric than cognitive symptoms. Evidence In 2000, McKeith et al 1 ; published the results of double-blind, placebo-controlled international study which looked at the efficacy of rivastigmine in DLB. The study showed that patients taking rivastigmine were significantly less apathetic and anxious, and had fewer delusions and hallucinations while on treatment than controls. The conclusion was that rivastigmine 6-12mg daily produces statistically and clinically significant behavioural effects in DLB. There is also some independent evidence. A letter to the Canadian Journal of Psychiatry reports on the case of a 74-year old man with DLB treated with some success with donepezil and risperidone. 2 ; . Shea et al 3 ; reported on nine patients with DLB treated with donepezil; cognition improved in seven, hallucinations improved in eight, but parkinsonian symptoms worsened in three patients. Lanctot and Herrman 4 ; conducted a study in seven patients diagnosed with DLB and treated with donepezil to determine its effect on treating behavioural symptoms. Three of the seven showed marked improvement in behaviour with Neuropsychiatric Inventory scores dropping significantly over time. Sanders et al 5 ; investigated the treatment of patients with DLB using donepezil. They concluded that there were marked improvements in behavioural symptoms. To conclude, there is evidence to suggest that cholinesterase inhibitors may be beneficial in both cognitive and behavioural symptoms associated with the condition.
Good asthma care is a team effort, both in primary and secondary care. Following diagnosis by a doctor, members of the team provide education, inhaler device training and day-to-day clinical management. Whether they work in community pharmacies, hospitals, or GP clinics, pharmacists are in a pivotal position to contribute to the overall management of asthma.The management of all medicines is a specific role for pharmacists and they can help to drive the improvements in asthma patient outcome. Pharmacists can also be a valuable source of important information for other members of the health care team and tagamet.
General information: if you have any questions about rivastigmine , please talk with your doctor, pharmacist, or other health care provider.
NICE has stated that donepezil, rivastigmine and galantamine should be made available in the NHS for the treatment of Alzheimer's disease when used in accordance with the conditions detailed in Technology Appraisal Guidance No. 19 and temovate and rivastigmine.
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The upcoming flu season. In addition to inactive influenza vaccine, MedImmune Vaccines, Inc. anticipates the production of approximately three million doses of live attenuated influenza vaccine FluMist ; . The exact number of vaccine doses and the timing of their availability are unknown. Because of this, the CDC is recommending only the following priority groups receive inactive flu vaccine before October 24, 2005: 1 ; persons at least 65 years of age with or without comorbid conditions; 2 ; residents of long-term care facilities; 3 ; persons aged 2 to 64 years with comorbid conditions; 4 ; children aged 6 to 23 months; 5 ; pregnant women; 6 ; healthcare personnel who provide direct patient care; and 7 ; household contacts and out-of-home caregivers of children less than six months of age. Inactive flu vaccine should be made available to all persons beginning October 24, 2005. Healthy persons aged 5 to 49 years who are not pregnant, including healthcare workers who are not caring for severely immunocompromised patients in special-care units, can receive live attenuated flu vaccine at any time.
Haplotype frequencies in patients with a mean age of 81.7 years are comparable to earlier described younger populations. Amyloid peptide is a substrate for the efflux pump Pglycoprotein. Frequencies of ABCB1 genotypes en haplotypes were not significantly different between patients with dementia and age-matched control patients and between patients with different types of dementia. Chapter 4.2.1 provides an overview of the recent literature into amyloid protein and tau as biomarkers for dementia. Measuring both proteins in cerebrospinal fluid may assist in distinguishing between patients with a stable or a progressive type of mild cognitive impairment with a reasonable sensitivity and specificity. In addition, progress has been made in the use of both proteins in the differential diagnosis of Alzheimer's disease. A lumbar puncture is not regularly performed in clinical practice and therefore amyloid has also been investigated in plasma as a biomarker for dementia. Chapter 4.2.2 describes investigations into fragments of amyloid in cerebrospinal fluid as possible biomarkers for dementia by using a new technique Surface-Enhanced Laser Desorption Ionisation Time of Flight Mass Spectrometry ; . Cerebrospinal fluid of groups of Alzheimer's disease patients, patients with vascular dementia and neurological ; control patients has been investigated. New peaks, corresponding to amyloid fragments, were found and some of these intensities were different between patients with Alzheimer's disease and vascular dementia. Fragments corresponding to those peaks may serve as future biomarkers. Additional research and validation are necessary. Chapter 4.2.3 describes prospective research into patients with Alzheimer's disease, vascular dementia and non-demented agematched control patients. Using the same method as described in chapter 4.2.2, several fragments of amyloid in serum were investigated as biomarker. The amyloid profile in serum was partly comparable to the profile obtained in cerebrospinal fluid. No significant differences in peak intensities between different types of dementia were shown in serum. A significant relation was shown, between presence of polymorphism of the ABCB1 gene, encoding for the efflux pump P-glycoprotein, and the intensities of certain peaks, corresponding to fragments of amyloid . Hopefully, this thesis has contributed to insights into the balance of reducing polypharmacy and prevention of undertreatment, and into clinical pharmacological investigations in geriatric patients. Research into dementia constitutes a primary part of research in geriatric patients. This thesis provides further insights into rivastigmine effectiveness in clinical practice and in patients that respond to this symptomatic therapy. Future research into disease-modifying therapy stays necessary. Studies into biomarkers, genetics or proteomics based, described in this thesis may add to current knowledge in the field of early diagnostics of dementia and terbinafine.
Affected. These are known as symptoms of the disease. These symptoms are common and may not mean that the person experiencing them has Alzheimer's disease. Also the development of Alzheimer's is slow and this makes it difficult to confirm that the person has the condition. To find out if someone is suffering from Alzheimer's disease, a health professional observes and records the pattern of symptoms, and uses tests to see what the person can remember. These tests are then repeated a few months later and any change can be measured. This process is called an assessment. One of these assessments is called the mini mental state examination MMSE ; . Following this examination a score is given to the person's disease: Mild Alzheimer's is usually linked to an MMSE score of 21 to Moderate Alzheimer's is usually linked to an MMSE score of 10 to Severe Alzheimer's is usually linked to an MMSE score of less than 10 What are donepezil, rivastigmine and galantamine?.
We investigated rivastigmine effectiveness in 84 Alzheimer outpatients, with a special focus on behavioural problems. Cognition, activities in daily living ADL ; and behaviour were assessed during 30 months. Changes in test results between 6 months and baseline were compared with a historical control cohort of Alzheimer patients n 69 ; by performing t-tests and calculation of Cohen's d and standardised response mean SRM ; . During 6 months rivastigmine showed effect on cognition p 0.001, Cohen's d 0.33, SRM 0.78 ; , ADL p 0.001, Cohen's d -0.43, SRM -0.54 ; and memory related behaviour p 0.006, Cohen's d -0.28, SRM -0.28 ; . Depressive behaviour worsened p 0.001, Cohen's d 0.30, SRM 0.37 ; and disruptive behaviour p 0.369, Cohen's d -0.07, SRM -0.09 ; was not effected by rivastigmine. During 30 months, a gradual decline was shown in most domains. Most RMBPC items showed stabilisation during 30 months. Improvement on disruptive behaviour items and depression items was shown after 6 months of treatment in a large proportion of patients in whom behavioural problems were present at baseline. In conclusion, a huge discontinuation rate is experienced within the first half year of treatment. In the subpopulation of patients who continued rivastigmine for 6 months, it shows modest effectiveness on cognition, functionality and memory associated behaviour compared with historical control patients. Unfortunately, disruptive behaviour is not altered by rivastigmine therapy, and depressive behaviour worsened slightly after initial treatment. During 30 months, rivastigmine showed stabilisation on numerous behaviour items as measured by the RMBPC.
STANLEY H. APPEL, M.D. Kim SH, Henkel JS, Beers DR, Sengun IS, Simpson EP, Goodman JC, Engelhardt JI, Siklos L, and Appel SH. PARP Expression Is Increased in Astrocytes but Decreased in Motor Neurons in the Spinal Cord of Sporadic ALS Patients. J Neuropath Exp Neurol, 62 1 ; : 88-103, 2003. Le WD, Xu P, Jankovic J, Jiang H, Appel SH, Smith RG, and Vassilatis DK. Mutations in NR4A2 Associated With Familial Parkinson Disease. Nat Genet, 33 1 ; : 85-9, 2003. He Y, Imam SZ, Dong Z, Jankovic J, Ali SF, Appel SH, and Le W-D. Role of nitric oxide in rotenone-induced nigro-striatal injury. J Neurochem, Sep; 86 6 ; : 1338-45, 2003. Sengun IS and Appel SH. Serum anti-Fas antibody levels in amyotrophic lateral sclerosis. J Neuroimmunol, Sep; 142 1-2 ; : 137-40, 2003. Simpson EP, Yen AA, and Appel SH. Oxidative Stress: A Common Denominator in the Pathogenesis of Amyotrophic Lateral Sclerosis. Curr Opin Rheumatol, Nov; 15 6 ; : 730-6, 2003. Henkel JS, Englelhardt JI, Siklos L, Simpson EP, Kim SH, Pan T, Goodman J Clay, Siddique T, Beers DR, and Appel SH. Presence of Dendritic Cells, MCP-1, and Activated Microglia Macrophages in Amyotrophic Lateral Sclerosis Spinal Cord Tissue. Annals of Neurology, 55: 221-235, 2004. Kim SH, Engelhardt J, Henkel JS, Siklos L, Soos J, Goodman J Clay, and Appel SH. Widespread Increased Expression of the DNA repair enzyme PARP in brain in ALS. Neurology, 62: 319-322, 2004. Le W-D and Appel SH. Mutant genes responsible for Parkinson's disease. Current Opinion in Pharmacology, 4: 79-84, 2004. Simpson EP, Henry YK, Henkel JS, Smith RG, and Appel SH. Increased lipid peroxidation in sera of ALS patients: A potential biomarker of disease burden. Neurology, 62: 1758-1765, 2004. Zhao W, Xie W, Le W, Beers DR, He Y, Henkel JS, Simpson EP, Yen AA, Xiao Q, and Appel SH. Activated microglia initiate motor neuron injury by a nitric oxide and glutamate-mediated mechanism. J Neuropath Exp Neurol, 63 9 ; : 964-77, 2004. Das A, Sribnick EA, Wingrave JM, Del Re AM, Woodward JJ, Appel SH, Banik NL, and Ray SK. Calpain activation in apoptosis of ventral spinal cord 4.1 VSC4.1 ; motoneurons exposed to glutamate: Calpain inhibition provides functional neuroprotection. J Neurosci Res, 81 4 ; : 551-562, 2005. Ringholz G, Appel SH, Bradshaw B, Cooke NA, Mosnik DM, and Schulz PE. Prevalence and Patterns of Cognitive Impairment in Sporadic ALS. Neurology, 65: 586-590, 2005. Henkel JS, Beers DR, Siklos L, and Appel SH. The Chemokine MCP-1 and the Dendritic and Myeloid Cells it attracts are increased in the mSOD1 Mouse Model of ALS. Mol Cell Neurosci, 31: 427-437, 2006. Appel SH. Is ALS a Systemic Disorder? Evidence from Muscle Mitochondria. Experimental Neurology, 198: 1-3, 2006. Goldknopf IL, Sheta EA, Bryson J, Folsom B, Wilson C, Duty J, Yen AA, and Appel SH. Complement C3c and related protein biomarkers in amyo.
24 ; Knopman DS, DeKosky ST, Cummings JL, Chui H, Corey-Bloom J, Relkin N, Small GW, Miller B, Stevens JC.Practice parameter: diagnosis of dementia an evidence-based review ; . Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2001; 56: 11431153. ; Bonte FJ, Weiner MF, Bigio EH, White CL: III. SPECT imaging in dementias. J Nucl Med 2001; 42: 1131 ; Silverman DH, Small GW, Chang CY et al.: Positron emission tomography in evaluation of dementia: Regional brain metabolism and long-term outcome. JAMA 2001; 286: 21202127. ; Petersen RC, Stevens JC, Ganguli M, Tangalos EG, Cummings JL, DeKosky ST: Practice parameter: early detection of dementia: mild cognitive impairment an evidence-based review ; . Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2001; 56: 11331142. ; Seshadri S. Apolipoprotein E4 allele and the lifetimerisk of Alzheimers disease. Arch Neurol 1995; 52: 1074-1079. ; Gutzmann H, Zank S. Demenzen. Medizinische und psychosoziale Interventi onsmglichkeiten. Grundriss der Gerontologie, Band 17, Stuttgart 2004 ; : Kohl hammer. 30 ; Frstl H, Maelicke A, Weichel C. Demenz. Taschenatlas spezial. 2005. 31 ; Del-Ser T, Munoz DG, Hachinski V . Temporal pattern of cognitive decline and incontinence is diffrent in Alzheimers disease and diffuse Lewy body disease. Neurology.1996; 46: 682-686. 32 ; McKeith I, Del Ser T, Spano P, Emre M, Wesnes K, Anand R, Cicin-Sain A, Ferrara R, Spiegel R. Efficacy of rivastigmine in dementia with Lewy bodies: a randomised, double-blind, placebo-controlled international study. Lancet, 2000. 356 9247 ; : 2031-6. 33 ; McKeith I, Fairbairn A, Perry R, Thompson P, Perry E. Neuroleptic sensitivity in patients with senile dementia of Lewy body type. Bmj 1992; 305 6855 ; : 673-8. 34 ; Birks J, Grimley Evans J, Van Dongen M. Ginkgo biloba for dementia and cognitive impairment Cochrane Review ; . In: The Cochrane Library, Issue 3, 2003. Oxford. 86.
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