Anticholinergics
Antihistamines, including H2 blockers
Overactive bladder treatments
Antispasmodics
Anti-Parkinsonian agents
Antidepressants
Antipsychotics
Benzodiazapines
Nonsteroidal anti-inflammatory drugs (NSAIDs)
Opioids
Sedatives
Steroids
Table 5.2
Causes of non-AD-related cognitive impairment
Type of non-AD-related cognitive impairment | Related symptoms |
|---|---|
Normal pressure hydrocephalus | Wide-based gait, urinary incontinence. Change in gait occurs well in advance of cognitive changes |
Parkinson’s disease | Resting tremor, stooped posture, masked facies |
Dementia with Lewy bodies | Parkinsonian features with visual hallucinations, psychiatric features |
Frontotemporal dementia | Changes in decision making, increased disinhibition, poor control of emotions, problems with language |
Progressive supranuclear palsy | Gait and balance problems, as well as visual disturbances |
Brain neoplasms | Seizures Focal findings on neurological exam |
B12 deficiency | Ataxia, fatigue and easy bruising |
5.1.3 Diagnostic Approach in the Home
Evaluating a patient in the home environment presents a unique opportunity for the clinician to gather information not usually apparent during an office visit.
When evaluating a patient in the home for cognitive decline, the assessment will entail similar evaluation tools as in an office-based setting: a thorough medical history including reviewing all medications, a physical exam, and a formal cognitive assessment. Unique to home-based care, the effects of a person’s cognitive dysfunction can be better assessed by observing how the patient functions in their own environment, the condition of the patient’s home environment and being able to spend time speaking with their family caregivers. In the office setting, patients are often able to present their “best side,” coming in well groomed and nicely dressed. Stepping into someone’s home, you immediately begin to gather information about your patient before even laying eyes on them—clutter, dirty sheets on the bed, papers strewn about, an empty fridge, bare walls – all provide insight into how someone is functioning on a day-to-day basis.
5.2 History
When interviewing the patient, always consider that he or she may not be an adequate informant, and in a nonoffending manner, include family members and caregivers within and outside of the interview to obtain further history. With the patient’s or proxy’s consent, additional relevant history can be obtained from friends, home care workers, housekeepers, neighbors, home care nurses, previous medical providers, doormen, pharmacists, Meals on Wheels representatives, and home/community social workers.
In addition to the usual thorough review, some specific historical elements are particularly important in the evaluation of a patient with dementia:
Cognitive history (worsening short-term memory, word-finding difficulty, behavior changes/emotional lability, difficulty with problem-solving, and complex tasks such as keeping track of appointments, driving or bill paying)
Fall history (any previous history of gait disturbance)
Head trauma (loss of consciousness)
Stroke history (ischemic heart disease, hemiparesis, arrhythmias, hypertension)
Seizure history
Movement disorders history (tremor, parkinsonism)
Work history (toxin exposure)
Recreational habits (alcohol, smoking, drugs)
Eating habits (eating food from garbage)
Sexual history (HIV, hepatitis, syphilis)
Psychosocial history (onset of behavior changes, visual changes, hallucination, depression, paranoia)
Genitourinary history (any new urine/bowel incontinence)
5.3 Medication Review
Being in a patient’s home affords you the opportunity to perform a thorough and accurate medication reconciliation. Seeing how your patients keep and manage their medications provides substantial information about their ability to manage their medical conditions. Ask permission to look in the patient’s medicine cabinets, on the kitchen counter, dining room table, bedroom tables and drawers, etc. Call the patient’s pharmacy to confirm questionable medications. Check dispense dates on prescription bottles, which will provide information regarding adherence to medications. Performing a “pill count”—emptying a bottle’s contents and counting the number of pills inside, looking at the fill date on the bottle, and then calculating the number of pills that should be left – can lead to valuable information regarding your patient’s ability to manage their medications. It is not uncommon to find several types of pills in one bottle, or several unused bottles of the same medication, as the pharmacy may report to you that they dispense the medication every month, not knowing that it is not being taken by the patient. Conduct a thorough review of all prescribed and over-the-counter medications, paying particular attention to medications that can alter cognition. See Table 5.1 for a comprehensive list of medication classes that may affect cognition.
5.4 Physical Exam
When conducting a thorough head-to-toe physical examination , be sure to gather the following information, which may also help determine if there is a modifiable cause for the memory loss:
Vital signs: orthostatic blood pressures (especially if patient has a history of syncope/dizziness)
Skin: assess for infected decubitus/abscess, shunts
Eyes: cataracts, poor vision, double vision
Ears: cerumen impaction, hearing loss
Cardiac: murmurs, irregular rhythm, pacemaker/automated implantable cardioverter defibrillator (AICD)
Neuro: cranial nerves, deep tendon reflexes, tremor, rigidity, bradykinesia, myoclonic twitching, agnosia, apraxia, aphasia, gait
5.5 Cognitive and Functional Assessment Tools
You should conduct cognitive and functional assessment tests without family or caregivers present, to avoid distractions or potential patient embarrassment. It is important to put the patient at ease and emphasize that there are no repercussions or consequences for wrong answers. Explain the findings and recommendations to the patient. Obtain consent to share findings with family members/caregivers. Choose the appropriate cognitive assessment tool based on your clinical findings and the amount of time you have available. Table 5.3 lists the most commonly used cognitive assessment tools available [10] and the amount of time they take to administer. These cognitive tools may be influenced by patient’s age, educational level, language, attention, visuospatial ability, and reduced attention. Referral for neuropsychological testing, an extensive evaluation of multiple cognitive domains done over several hours by a licensed clinical psychologist, is not essential but may prove helpful in making the diagnosis in certain difficult cases, such as in the very early stages of the disease, when the patient or caregiver senses something is wrong but the usual cognitive assessment tools do not pick up any abnormalities.
Test | Description | Scoring | Limitations | Time to administer |
|---|---|---|---|---|
Clock drawing | Patient asked to draw a clock face with all the numbers and place a number and place hands at a stated time | 12 must appear on top (3 points) 12 numbers must be present (1 point) Two distinguishable hands (1 point) Time must be correctly identified for full credit Score of <4/6 implies impairment | Quick screening test, not diagnostic | 3 min |
Mini-Cog | Consists of recall of three unrelated words and clock drawing test | If no words recalled, diagnosis is dementia If one or two out of three words recalled, look at the clock draw test. If abnormal, diagnosis is dementia If all numbers on the clock are presented in the correct sequence and the hands display the correct time, no dementia | Quick screening test, not diagnostic | 5 min |
Mini-mental state examination (MMSE) | Tests a broad range of cognitive functions including orientation, recall, attention, calculation, language manipulation, and constructional praxis | Maximum score is 30, score must be adjusted based on education, language, and age; <24 implies dementia | Limited by education level, literacy, and language. The patient should have at least an eighth-grade education and be fluent in English Test is copyrighted | 10 min |
Montreal cognitive assessment (MoCA) | Tests a broad range of cognitive functions including orientation, memory recall, visuospatial relations, sustained attention, verbal fluency and executive function | Maximum score is 30; <26 implies mild cognitive impairment or dementia (dementia diagnosis dependent on presence of associated functional impairment) | 10 min | |
Verbal fluency test | The test consists of giving the person 60 s to list out loud as many words as possible from a category, such as animals, vegetables or fruits; or words beginning with a certain letter | Fewer than 12 correct words in a minute is considered abnormal | Not diagnostic Schizophrenics do poorly at this test | 2 min |
Geriatric depression screening—15 | It is a series of 15 yes/no questions | 0–4 considered normal 5–8 indicates mild depression 9–11 indicates moderate depression 12–15 indicates severe depression | Successful in differentiating depressed from nondepressed | 10 min |
Bristol activities of daily living scale (BADLS) | This scale is a 20-item questionnaire designed to measure the ability of someone with dementia to carry out daily activities | 5 min |
5.5.1 Tests
The home-based medical provider should obtain appropriate lab work to diagnose modifiable causes of cognitive changes. Table 5.4 lists the labs to consider ordering and what each test evaluates.
Table 5.4
Laboratory tests for evaluating modifiable causes of cognitive changes
Laboratory test | Evaluating for |
|---|---|
Complete blood count (CBC) | Possible infection, immune disorders, anemia, blood disorder |
Comprehensive blood chemistry | Metabolic, kidney, liver disorders |
Calcium level | Parathyroid problem |
TSH level | Thyroid, endocrine disorders |
Vitamin B12, folate, iron level | Nutritional, vitamin deficiency |
Erythrocyte sedimentation level | Signs of inflammation |
Syphilis | Brain infection |
HIV, Hepatitis | Viral infections |
Lyme | Affecting central nervous system |
Urine analysis and urine toxin screening | Infection, drugs that can be affecting cognition |
Drug levels: dilantin (phenytoin), digoxin | Drug toxicity affecting cognition |
Obtain consent to obtain medical records for any previous CT/MRI/angiograms/EKG/EEG and lab results for comparison. Neuroimaging can be helpful in the exclusion of secondary causes of dementia, such as masses or normal pressure hydrocephalus [10], and a finding of medial temporal lobe atrophy on MRI supports a clinical diagnosis of AD [11] but a normal head CT or MRI does not rule out dementia. In cases where you cannot obtain past records or the patient has not had any past imaging, it is important to use your clinical judgment as to whether you think it is of value to obtain a head CT. In a patient with a history of high blood pressure and strokes, with a step-wise decline in cognition, imaging is highly unlikely to reveal anything other than vascular changes. NPH will present with clinical exam findings; you do not need a head CT to rule it out. Did you find a focal deficit on the neurologic exam? Is there something about the patient’s presentation or history that points you away from thinking their cognitive changes are due to AD or vascular dementia? Are getting them out of the home to obtain imaging and keeping them calm or still enough for a study insurmountable challenges? Will the results change your management based on the goals of care? These are all issues you need to consider before deciding to recommend imaging. In patients with a history consistent with AD and nonfocal neurological examination, our practice is to forego head imaging if it would be difficult to obtain.
5.5.2 Pharmacologic Treatment
5.5.2.1 Alzheimer’s Disease
Medications indicated for Alzheimer’s dementia have been shown to have a minimal effect on slowing the progression of disease, so the mainstay of treatment is not pharmacological. Medications should be used cautiously under close monitoring [12]. The mantra “start low, go slow” should be considered when it comes to dosing of these medications. Medications for Alzheimer’s dementia have shown to minimally improve scores on cognitive function tests but still have not shown improvement in the ability of patients to perform activities of daily living (ADL) or instrumental activities of daily living (IADL), which would be more likely to translate into improvement in the quality of life of these patients. Cholinesterase inhibitors (AChEI) and noncompetitive N-methyl-d-aspartate (NMDA) receptor antagonist are currently the medications approved for Alzheimer’s dementia. There is no difference in the efficacies of the three cholinesterase inhibitors [13].
Medications approved for the treatment of dementia are described in Table 5.5 [14 ]. Often patients’ family members will ask to start their loved one on one of the medications they have seen advertised to help people with dementia. We take this as an opportunity to educate them on the limited efficacy of these medications seen in our practice, not to “burst anyone’s bubble” but to set realistic expectations. If it is the family’s wish to try one of the medications, we review the potential major side effects of the medications (data in Table 5.5) and offer a 2-month trial, making it clear that they can stop the medication at any time if they are concerned about side effects. After 2 months, we review together whether any beneficial changes have been observed, and if not, we do not write a new prescription. The pharmacologic treatment of vascular dementia focuses on management of risk factors for hypertension and hyperlipidemia to avoid further deterioration of the vascular system in the brain.
Medications | Dosing | Major side effects |
|---|---|---|
Cholinesterase inhibitors | ||
Donepezil (Aricept) | Mild to moderate dementia | Neuro: seizures, syncope, altered sleep with vivid dreams |
5 mg PO QHS for 4–6 weeks, then increased to target dose of 10 mg PO QHS | Cardiac: bradycardia | |
MSK: muscle cramps | ||
Moderate to severe dementia | GI: nausea, diarrhea, cramping | |
5 mg PO QHS for 4–6 weeks, increased to 10 mg PO QHS for 3 months, and then increased to target dose of 23 mg PO QHS | GU: urinary frequency, urinary obstruction | |
Rivastigmine (Exelon, Exelon patch) | Mild to moderate AD | Neuro: seizures, syncope, depression, hallucinations |
1.5 mg PO BID, increased by 1.5 mg PO BID Q2 weeks as tolerated to target dose of 6 mg PO BID | Cardiac: bradycardia, hypotension | |
GI: vomiting, diarrhea, peptic ulcer, GI bleeding | ||
Transdermal Patch: | ||
4.6 mg patch daily for 4 weeks, increased to 9.5 mg patch daily for 4 weeks, and then increased to target dose of 13.3 mg patch daily | ||
Mild to moderate PDD | ||
1.5 mg PO BID, increased by 1.5 mg PO BID Q4 weeks as tolerated to target dose of 6 mg PO BID | ||
Transdermal Patch: | ||
4.6 mg patch daily for 4 weeks, increased to 9.5 mg patch daily for 4 weeks, and then increased to target dose of 13.3 mg patch daily | ||
Galantamine (Razadyne and Razadyne ER) | Mild to moderate AD | Neuro: syncope, dizziness |
Regular: | Cardiac: bradycardia | |
Start 4 mg PO BID, increased to 4 mg PO BID Q4 weeks as tolerated to maximum of 12 mg PO BID | GI: vomiting, nausea, anorexia | |
Renal: renal impairment or failure | ||
Liver: hepatotoxicity | ||
ER: | ||
Start 8 mg PO QAM, increased by 8 mg PO QAM Q4 weeks to maximum of 24 mg PO QAM | ||
If either form is stopped for more than 3 days, medication must be restarted at 8 mg and retitrated up | ||
Medication needs to be renally dosed, not advised for patients with liver problems | ||
Noncompetititve N-methyl-d-aspartate (NMDA) receptor antagonist | ||
Memantine (Namenda) | Moderate to severe AD | Neuro: dizziness, headache, somnolence, anxiety |
Start 5 mg PO daily, increased to 5 mg PO BID at 1 week as tolerated, and then increased by 5 mg weekly to a maximum of 10 mg PO BID | Pulm: dyspnea | |
GI: vomiting, constipation | ||
GU: urinary incontinence | ||
MSK: back pain | ||
AD Alzheimer’s dementia, BID twice a day, ER extended release, GI gastrointestinal, GU genitourinary, MSK musculoskeletal, PO by mouth, PDD Parkinson’s Disease with Dementia, QAM every morning, QHS at bedtime
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