Patch treatment for dementia

A six-month, transdermal nicotine intervention improved cognitive performance across those who received it. Newhouse plans to enroll participants in the MIND study. Men and women at more than 35 study sites will wear a transdermal nicotine or placebo patch daily. The daily nicotine dose will titrate up to 21 mg in the first six weeks, and remain at 21 mg for nearly two years, with a taper in the final month. The researchers will use a battery of tests to assess participant cognition before and after the intervention.

This might allow potential use of evidence based preventive interventions as and when they become available. The recognition of MCI as a diagnostic allows us to have a better understanding of the nature of mild memory loss, which is far more common than dementia among the older segments of the population. Table-4 lists out the main differences between the two clinical conditions.

We need to rule out delirium and mild cognitive disorder before we make a clnical diagnosis of dementia. Then one should apply and see if the person meets the diagnostic criteria for Dementia.

If that is met, then there is a need to make further evaluations. The next part of evaluation is aimed at establishing the cause for the dementia syndrome. Dementia is a syndrome which can be caused by many diseases. After the clinical recognition of dementia syndrome, the evaluations shall focus on identifying the cause of dementia. Thus the evaluation for all potentially reversible conditions which cause dementia syndrome is the first most important step in the assessment of dementia syndrome and this is essential in all cases presenting with features of dmentia.

The type of investigations can be decided based on the clinical features and context of care. Patients who seek help in clinical settings often do not represent cases prevalent in the community. Reversible causes thus may be much more common in clinical settings than in community settings.

CT scan or MRI scan, at times, can be a very useful investigation in the differential diagnosis of dementia. A reliable, detailed history will guide us in identifying the causes of dementia. We have to rule out common reversible causes and the eminently reversible causes first.

See table-5 for the list. Investigations to rule out less common causes may be needed when the clinical features indicate a high index of suspicion of reversible dementia. Dementia syndrome is linked to many underlying causes and diseases of the brain. The most common causes accounting for vast majority of cases are due to Alzheimer's disease, Vascular dementia, Dementia with Lewy Bodies and Fronto-temporal dementia. STEP 3 Evaluation after recognition of the syndrome of dementia look for medical problems.

Cognitive assessment can be made as part of detailed examination of higher functions. Addenbrooke's Cognitive Examination ACE is a more detailed test battery for assessing cognitive functions. Assessment of the activities of daily living is very important.

This information is essential in formulating the individualized plan of intervention. Use of simple instruments like the Clinical Dementia Rating Scale can help in assessing the severity of dementia in routine clinical practice.

Assessment of non-cognitive symptoms like Behavioural and Psychological Symptoms of Dementia BPSD is yet another important part of clinical assessment. ICD- 10 clinical criteria may be used for diagnosis of Dementia and subtyping. Alterantively one could use the DSM-5 criteria too. You may use the consensus clinical diagnostic criteria.

After detailed assessment usually, the clinician would be in a position to judge the cause of the dementing illness. Clinical recognition of the subtypes of dementia is important and is easier during the early part of the illness. Such differentiation is feasible in clinical practice by using clinical criteria for these subtypes. The clinicians might choose any standard criteria for making clinical diagnosis of dementia, especially common sub-types.

See Table 6 for the criteria which may be useful in clinical practice. The impairment applies to both verbal and non-verbal material. The decline should be objectively verified by obtaining a reliable history from an informant, supplemented, if possible, by neuropsychological tests or quantified cognitive assessments.

The severity of the decline, with mild impairment as the threshold for diagnosis, should be assessed as follows:. Mild : a degree of memory loss sufficient to interfere with everyday activities, though not so severe as to be incompatible with independent living. The main function affected is the learning of new material. For example, the individual has difficulty in registering, storing and recalling elements in daily living, such as where belongings have been put, social arrangements, or information recently imparted by family members.

Moderate : A degree of memory loss which represents a serious handicap to independent living. Only highly learned or very familiar material is retained. New information is retained only occasionally and very briefly. The individual is unable to recall basic information about where he lives, what he has recently been doing, or the names of familiar persons.

Severe : a degree of memory loss characterized by the complete inability to retain new information. Only fragments of previously learned information remain. The subject fails to recognize even close relatives. Evidence for this should be obtained when possible from interviewing an informant, supplemented, if possible, by neuropsychological tests or quantified objective assessments. Deterioration from a previously higher level of performance should be established. The decline in cognitive abilities causes impaired performance in daily living, but not to a degree making the individual dependent on others.

More complicated daily tasks or recreational activities cannot be undertaken. The decline in cognitive abilities makes the individual unable to function without the assistance of another in daily living, including shopping and handling money. Within the home, only simple chores are preserved. Activities are increasingly restricted and poorly sustained. The decline is characterized by an absence, or virtual absence, of intelligible ideation.

The overall severity of the dementia is best expressed as the level of decline in memory or other cognitiveabilities, whichever is the more severe e. Preserved awarenenss of the environment i.

When there are superimposed episodes of delirium the diagnosis of dementia should be deferred. A decline in emotional control or motivation, or a change in social behaviour, manifest as at least one of the following:. For a confident clinical diagnosis, G1 should have been present for at least six months; if the period since the manifest onset is shorter, the diagnosis can only be tentative.

Comments: The diagnosis is further supported by evidence of damage to other higher cortical functions, such as aphasia, agnosia, apraxia. Judgment about independent living or the development of dependence upon others need to take account of the cultural expectation and context.

Dementia is specified here as having a minimum duration of six months to avoid confusion with reversible states with identical behavioural syndromes, such as traumatic subdural haemorrhage S There is no evidence from the history, physical examination or special investigations for any other possible cause of dementia e.

B12 or folic acid deficiency, hypercalcaemia , or alcohol- or drug-abuse. Comments: The diagnosis is confirmed by post mortem evidence of neurofibrillary tangles and neuritic plaques in excess of those found in normal ageing of the brain. The following features support the diagnosis, but are not necessary elements: Involvement of cortical functions as evidenced by aphasia, agnosia or apraxia; decrease of motivation and drive, leading to apathy and lack of spontaneity; irritability and disinhibition of social behaviour; evidence from special investigations that there is cerebral atrophy, particularly if this can be shown to be increasing over time.

In severe cases there may be Parkinson-like extrapyramidal changes, logoclonia, and epileptic fits. Specification of features for possible subtypes. Because of the possibility that subtypes exist, it is recommended that the following characteristics be ascertained as a basis for a further classification: age at onset; rate of progression; the configuration of the clinical features, particularly the relative prominence or lack of temporal, parietal or frontal lobe signs; any neuropathological or neurochemical abnormalities, and their pattern.

The division of AD into subtypes can at present be accomplished in two ways: first by taking only the age of onset and labeling AD as either early or late, with an approximate cut-off point at 65 years. Unequal distribution of deficits in higher cognitive functions, with some affected and others relatively spared.

Thus memory may be quite markedly affected while thinking, reasoning and information processing may show only mild decline.

There is clinical evidence of focal brain damage, manifest as at least one of the following:. There is evidence from the history, examination, or tests, of a significant cerebrovascular disease, which may reasonably be judged to be etiologically related to the dementia e.

Neuropsychology: impairment on frontal lobe tests without severe amnesia, aphasia, or perceptuospatial disorder. Electroencephalography: normal on conventional EEG despite clinically evident dementia. Revised criteria for the clinical diagnosis of probable and possible dementia with Lewy bodies DLB. Essential for a diagnosis of DLB is dementia, defined as a progressive cognitive decline of sufficient magnitude to interfere with normal social or occupational functions, or with usual daily activities.

Prominent or persistent memory impairment may not necessarily occur in the early stages but is usually evident with progression. Deficits on tests of attention, executive function, and visuoperceptual ability may be especially prominent and occur early. Core clinical features The first 3 typically occur early and may persist throughout the course.

One or more spontaneous cardinal features of parkinsonism: these are bradykinesia defined as slowness of movement and decrement in amplitude or speed , rest tremor, or rigidity. Severe sensitivity to antipsychotic agents postural instability; repeated falls; syncope or other transient episodes of unresponsiveness; severe autonomic dysfunction, e. Abnormal low uptake iodine-MIBG myocardial scintigraphy. Polysomnographic confirmation of REM sleep without atonia. Two or more core clinical features of DLB are present, with or without the presence of indicative biomarkers.

Only one core clinical feature is present, but with one or more indicative biomarkers. Only one core clinical feature of DLB is present, with no indicative biomarker evidence. One or more indicative biomarkers is present but there are no core clinical features. In the presence of any other physical illness or brain disorder including cerebrovascular disease, sufficient to account in part or in total for the clinical picture, although these do not exclude a DLB diagnosis and may serve to indicate mixed or multiple pathologies contributing to the clinical presentation.

I parkinsonian features are the only core clinical feature and appear for the first time at a stage of severe dementia. DLB should be diagnosed when dementia occurs before or concurrently with parkinsonism. The term Parkinson disease dementia PDD should be used to describe dementia that occurs in the context of well-established Parkinson disease.

In a practice setting the term that is most appropriate to the clinical situation should be used and generic terms such as Lewy body disease are often helpful. In research studies in which distinction needs to be made between DLB and PDD, the existing 1-year rule between the onset of dementia and parkinsonism continues to be recommended.

This is essentiality about the the ablity for feeding, bathing, dressing, mobility, toileting, continence and also the ability to manage finances and medications. Assess the Cognitive Status using a reliable and valid instrument e.

Identify the Primary Caregiver: Assess the adequacy of family and other support systems. Assess the patient's decision-making capacity and whether a surrogate has been identified.

Multimorbidity is common in latelife. A clear understanding of physical aand mental health is important for planning dementia care. Assess for. Nutritional Status. Poor nutritional status can be a consequence of poor self care and poor dietary intake.

Identify the Primary caregiver. Novartis is proud to offer Patient Assistance Now , an easy-to-use, comprehensive resource that allows you to access programs that may help you pay for your Novartis medicines. Use of website is governed by the Terms of Use and Privacy Statement. All rights reserved. Getting the Right Exelon Patch Dose. Follow-Up Visits. Using the Exelon Patch to Treat Alzheimer's.

Monthly Tracker. Daily Routines. But these symptoms may progress at a rate that's slower than expected. That's why it makes sense to continue treating with Exelon Patch as the doctor instructs. Most mistakes have involved not removing the old patch when putting on a new one and the use of multiple patches at one time. Dehydration may result from prolonged vomiting or diarrhea and can be associated with serious outcomes.

The incidence and severity of these reactions are dose related. Stop using EXELON PATCH and call your health care provider right away if you experience reactions that spread beyond the patch size, are intense in nature, and do not improve within 48 hours after the patch is removed. Symptoms of ACD may be intense and include itching, redness, swelling, warmth or tenderness of the skin, or peeling or blistering of the skin, which may ooze, drain, or crust over. Extrapyramidal symptoms e.

EXELON PATCH should not be taken at the same time as metoclopramide used to treat heartburn, nausea, and vomiting and with medicines that have a similar effect on the body and the brain cholinomimetic agents or with anticholinergic medicines.