Exercise Program for Dementia

Exercise may benefit the Alzheimer’s patient by improving both symptoms and quality of life. For the same level of brain deterioration, physically active people exhibit higher levels of cognitive functioning than sedentary people. It is thought that physically active people have a ‘cognitive reserve’ that is used when other areas of the brain are damaged.

An exercise routine may decrease the severity of symptoms of dementia as well as lead to increased mobility and independence. An exercise routine for the elderly should be composed of four components:

  1. Aerobic exercise
  2. Strength training
  3. Balance training
  4. Flexibility exercises

All training programs should be entered into gradually and only after checking with his/her physician.

An aerobic training program, improves cardiovascular health as well as brain health. It is associated with decreased risk of stroke and the related dementia. Physical activity may also decrease the beta-amyloid proteins leading to decreased amyloid plaque and decreased disruption between neurons. For maximum health benefit, 30-minutes of aerobic activity should be performed most days of the week. This need not be intense and the participant should be able to talk throughout. The 30-minutes can be split into smaller, 10-minutes segments if that is more desirable. When beginning a training program, you can start with intervals as short as 5-minutes and progress.

Strength training programs combat the loss of muscle mass associated with aging. It can improve independence, mobility, and balance. Daily tasks (e.g. getting out of bed, getting out of chairs, climbing stairs) become easier with increased strength. Ideally, 10-15 repetitions of 8-10 exercises should be performed 2 or 3 times per week. The resistance should be great enough that each set of repetitions is difficult to complete. Resistance may be applied with bands or tubing, light weights, or even cans of food. If the sets are completed easily, the resistance should be increased.

Balance exercises can be performed almost anywhere. Balance is position specific so both standing balance and sitting balance should be targeted. With improved standing balance, there is decreased risk of falls and fractures. Standing on one-leg, with or without assistance, will help improve standing balance. Sitting balance can be improved by sitting on a chair, couch, or balance ball, with the lower back straight, and lifting an arm or a leg into a different position. Also, chair stands can be included. The more unstable the sitting surface is, the more difficult the exercise will be. More advanced exercises such as backwards walking and leaning can be gradually added into the program.

Flexibility exercises are best performed with the aid of a personal trainer, training partner, or care giver. Flexibility exercises can improve back pain and shoulder pain and increase range of motion.

There are certainly challenges in starting and keeping a patient in an exercise program. However, older adults are among the most willing to begin exercise programs as they are more aware of health issues. With dementia patients, there may be additional challenges as the disease progresses. However, there are many techniques that may help combat challenges that arise. The improvement in functioning and quality of life should make the challenges worthwhile.

Published research related to this topic:
American College of Sports Medicine Position Stand. Exercise and Physical Activity for Older Adults.
Mazzeo, R., Cavanaugh, P., Evans, W. et al.
Med. Sci. Sports Exerc. 1998: 30(6): 992-1008.

Exercise and activity level in Alzheimer’s disease : A potential treatment focus.
Teri L., McCurry, S., Buchner, D., et al. J.
Rehab. Research and Development. 1998: 35(4): 411-419



UPDATE on Dementia with Lewy Bodies



©Family Caregiver Alliance


Fact Sheet : Dementia with Lewy Bodies




Dementia with Lewy Bodies (DLB) is a progressive degenerative disease or syndrome of the brain. It shares symptoms—and sometimes overlaps—with several diseases, especially Alzheimer’s and Parkinson’s.

People who develop DLB have behavioral and memory symptoms of dementia like those of Alzheimer’s Disease and, to varying extents, the physical, motor system symptoms seen in Parkinson’s Disease. However, the mental symptoms of a person with DLB might fluctuate frequently, motor symptoms are milder than for Parkinson’s, and DLB patients usually have vivid visual hallucinations.



Dementia with Lewy Body (DLB) is also called “Lewy Body Dementia” (LBD), “Diffuse Lewy Body Disease”, “Lewy Body Disease”, “Cortical Lewy Body Disease”, “Lewy Body Variant of Alzheimer’s Disease” or “Parkinson’s Disease Dementia.” It is the second most common dementia, accounting for 20% of those with dementia (Alzheimer’s Disease is first). Dementia is a gradual, progressive decline in mental ability (cognition) that affects memory, thinking processes, behavior and physical activity. In addition to these mental symptoms, persons with DLB experience physical symptoms of parkinsonism, including mild tremor, muscle stiffness and movement problems. Strong visual hallucinations also occur.

DLB is named after smooth round protein lumps (alpha-synuclein) called Lewy bodies, that are found in the nerve cells of the affected parts of the brain. These “abnormal protein structures” were first described in 1912 by Frederich Heinrich Lewy, M.D., a contemporary of Alois Alzheimer who first identified the more common form of dementia that bears his name.

Lewy bodies are found throughout the outer layer of the brain (the cerebral cortex) and deep inside the midbrain and brainstem. They are often found in those diagnosed with Alzheimer’s, Parkinson’s, Down syndrome and other disorders.

The cause of DLB is unknown and no specific risk factors are identified. Cases have appeared among families but there does not seem to be a strong tendency for inheriting the disease. Genetic research may reveal more information about causes and risk in the future. It usually occurs in older adults between 50-85 years old and slightly more men than women have the disease.



Initial symptoms of DLB usually are similar to those of Alzheimer’s or Vascular Dementia and are cognitive in nature, such as acute confusion, loss of memory, and poor judgment. Other patients may first show the neuromuscular symptoms of parkinsonism—loss of spontaneous movement, rigidity (muscles feel stiff and resist movement), and shuffling gait, while still others may have visual hallucinations as the first symptom. Patients may also suffer from delusions or depression.

Key symptoms are:

  • Problems with recent memory such as forgetting recent events.
  • Brief episodes of unexplained confusion and other behavioral or cognitive problems. The individual may become disoriented to the time or location where he or she is, have trouble with speech, have difficulty finding words or following a conversation, experience visuospatial difficulty (for example, finding one’s way), and have problems in thinking such as inattention, mental inflexibility, indecisiveness, lack of judgment, lack of initiative and loss of insight.
  • Fluctuation in the occurrence of cognitive symptoms from moment to moment, hour to hour, day to day or week to week. For example, the person may converse normally one day and be mute and unable to speak the next day. There are also fluctuations in attention, alertness and wakefulness.
  • Well defined, vivid, recurrent visual hallucinations. These hallucinations are well formed and detailed. In DLB’s early stage, the person may even acknowledge and describe the hallucinations. They are generally benign and patients are not scared by them. Hallucinations may also be auditory (hearing sounds), olfactory (smelling or tasting something) or tactile (feeling or touching something that is not there).
  • Movement problems of parkinsonism, sometimes referred to as “extrapyramidal” signs. These symptoms often seem to start spontaneously and may include flexed posture, shuffling gait, muscle jerks or twitches, reduced arm swing, loss of dexterity, limb stiffness, a tendency to fall, balance problems, bradykinesia (slowness of movement), tremor, shakiness, and lack of facial expression.
  • Rapid Eye Movement Sleep Behavior Disorder. This is characterized by vivid dreaming, talking in one’s sleep, and excessive movement while asleep, including occasionally hitting a bed partner. The result may be excessive daytime drowsiness and this symptom may appear years before DLB is diagnosed. About 50% of patients have this symptom.

Movement and motor problems occur in later stages for 70% of persons with DLB. But for 30% of DLB patients, and more commonly those that are older, Parkinson’s symptoms occur first, before dementia symptoms. In these individuals, cognitive decline tends to start with depression or mild forgetfulness.


Testing and Diagnosis

Dementia with Lewy bodies is difficult to diagnose. Not only does it resemble other dementias, it overlaps with Alzheimer’s, Parkinson’s and other disorders which may result in it being difficult to rule out or exclude. Because no single test exists to diagnose DLB, a variety of medical, neurological and neuropsychological tests are used to pinpoint it and its possible overlap with other illnesses. A definitive diagnosis can only be made by an autopsy at death. There are no medications currently approved to specifically treat DLB.

Although Lewy bodies are found in brains of patients with other diseases, and because testing will involve several approaches, it is useful to understand what happens to the brain of a person with DLB. Three significant changes or pathological features are seen in brains afflicted by DLB:

  • The brain’s cerebral cortex (outer layers of the brain) degenerates or shrinks. This can affect reasoning and complex thinking, understanding personality, movement, speech and language, sensory input and visual perceptions of space. Degeneration also occurs in the limbic cortex at the center of the brain, which plays a major role in emotions and behavior. Lewy bodies form throughout these degenerating cortical areas.
  • Nerve cells die in the midbrain, especially in an area that also degenerates in Parkinson’s disease, the substantia nigra, located in the brainstem. These cells are involved in making the neurotransmitter (brain messenger) dopamine. Lewy bodies are found in the nerve cells that remain. The midbrain is involved in memory formation and learning, attention, and psychomotor (muscular movement) skills.
  • Lesions called Lewy neuritis that affect nerve cell function are found in DLB brains, especially in the hippocampus, an area of the brain essential for forming new memories.

None of the symptoms of Dementia with Lewy Bodies is specific only to DLB. To address this problem, an international group of researchers and clinicians developed a set of diagnostic criteria in 1995, called the Consensus Guidelines that can reliably point to DLB:

Must be present:

  • Progressive cognitive decline (decrease in thinking ability) that interferes with normal social or occupational activities. Memory problems do not necessarily occur in the early period but will occur as DLB progresses. Attention, language, understanding and reasoning, ability to do arithmetic, logical thinking and perceptions of space and time will be impaired.

Two of the following are present (one also indicates possibility of DLB):

  • Fluctuating cognition and mental problems, vary during the day, especially attention and alertness.
  • Visual hallucinations, detailed and well-formed visions occur and recur.
  • Parkinsonism: motor related and movement problems appear.

A DLB diagnosis is even more likely if the patient also experiences repeated falls, fainting, brief loss of consciousness, delusions, or is sensitive to neuroleptic medications that are given to control hallucinations and other psychiatric symptoms.

Finally, the timing of symptoms is a reliable clue: if both mental and motor symptoms appear within one year of each other, DLB is more likely the cause. Signs of stroke or vascular dementia usually negate the likelihood of DLB.

Testing is usually done to rule out other possible causes of dementia. Brain imaging (CT scan or MR imaging) can detect brain shrinkage and help rule out stroke, fluid on the brain (normal pressure hydrocephalus), or subdural hematoma. Blood and other tests might show vitamin B 12 deficiency, thyroid problems, syphilis, HIV, or vascular disease. Depression is also a common cause of dementia-like symptoms. Additional tests can include an electroencephalogram (EEG) or spinal tap. Scans using SPECT or PET technology have shown promise in detecting differences between DLB and Alzheimer’s disease.


Alzheimer’s and Parkinson’s: Differences and Overlap with DLB

DLB’s similarity to Alzheimer’s and Parkinson’s diseases and the fact that Lewy bodies are often found in the brains of patients with these diseases means that clinicians must pay close attention to the factors that distinguish DLB:

  • Memory and other cognitive problems occur in both DLB and Alzheimer’s. However, in DLB they fluctuate frequently.
  • DLB patients experience more depression than do Alzheimer’s patients.
  • Hallucinations are experienced by Alzheimer’s patients in late stages, and by Parkinson’s patients who take medications to improve movement and tremor. In DLB, hallucinations occur in early stages, and they are frequent, vivid and detailed.
  • Neuroleptic drugs (sometimes called psychotropic drugs) prescribed to lessen the so-called psychiatric symptoms of dementia, such as hallucinations, agitation or restlessness will induce Parkinson’s in some DLB patients.
  • Life expectancy is slightly shorter for DLB than for Alzheimer’s patients.
  • At autopsy the brains of DLB patients have senile plaques, a hallmark of Alzheimer’s. Another Alzheimer’s feature, neurofibrillary tangles, are absent or found in fewer numbers and are concentrated in the neocortex. Other Alzheimer’s features—regional neuronal loss, spongiform change and synapse loss, neurochemical abnormalities and neurotransmitter deficits—are also seen. However, DLB-afflicted brains are less damaged than are Alzheimer’s brains.
  • In DLB movement problems are spontaneous; the symptoms begin suddenly.
  • Tremor is less pronounced in DLB than in Parkinson’s. Also, DLB patients respond less dramatically to drugs such as Levodopa that are used to treat Parkinson’s. Nerve cell loss in the subtantia nigra is not as severe in DLB. Both DLB and Parkinson’s patients may sometimes experience fainting and wide alterations in blood pressure. Some Parkinson’s patients develop dementia in later stages. Dementia is usually the presenting symptom in DLB.
  • Parkinson’s patients lose the neurotransmitter dopamine; Alzheimer’s patients lose the neurotransmitter acetylcholine. DLB patients lose both.
  • In DLB, Alzheimer-like and Parkinson-like symptoms appear within one year of each other.

Despite these differences, a diagnosis of Dementia with Lewy Bodies does not preclude a positive diagnosis of Alzheimer’s, Parkinson’s or other diseases common in older age.


Duration and Treatment

With an average lifespan after onset of 5 to 7 years, the progress of Dementia with Lewy Bodies is relentless; however, the rate of decline varies with each person. DLB does not follow a pattern of stages as is seen in some other dementias. Death usually occurs from pneumonia or other illness. There is neither cure nor specific treatment to arrest the course of the disease.

Caution must be used in treating a person with DLB. Medications must be monitored closely for proper balance because some patients are adversely affected by some drugs. Neuroleptic (tranquilizing) anti-psychotic medications such as haloperidol (Haldol) or thioridazine (Mellaril), as well as benzodiazepines (Valium, Ativan) and anti-histamines can cause extreme adverse reactions in DLB patients. Side effects include motor related symptoms, catatonia (non-responsiveness), loss of cognitive function and/or development of muscle rigidity. These medications are sometimes used in Alzheimer’s patients to help with hallucinations and behavioral symptoms, but should not be used in patients with DLB. Levodopa may be given to treat the parkinsonism, however, it may increase the hallucinations of DLB patients and aggravate other symptoms, such as cognitive functioning. It is less effective in treating tremor in DLB patients than in Parkinson’s patients. Aricept or other cholinesterase inhibitors are given to treat the hallucinations. Some anti-depressants have shown positive results, while others are counter indicated.

When considering surgery, families should meet with the anesthesiologist to discuss possible side effects of anesthesia, as DLB patients are prone to delusions and a decline in motor functioning after anesthesia.


Caregiving and DLB

DLB patients can live at home with frequent reassessment and careful monitoring and supervision. Caregivers must watch the patient closely because of the tendency for them to fall or lose consciousness. Particular care should be taken when a patient is standing up from a chair or getting out of bed, as blood pressure can drop, causing the patient to lose his or her balance. Dementia prevents patients from learning new actions that might help them overcome movement problems, such as learning to use a walker. They may need more assistance some days than others, and can be reassured by a caregiver’s help in turning attention away from the hallucinations.

Caregivers must learn to navigate both skills in dealing with cognitive, behavioral and motor disabilities. Attending support groups and learning skills in how to communicate with someone with dementia as well as learning skills in helping someone with a motor disorder will reduce caregiver stress and frustration.

Caregivers can turn to a California Caregiver Resource Center for assistance and to a qualified diagnostic center for initial diagnosis and follow up. In other states, resources can be found through local and state offices on aging and health such as your Area Agency on Aging or the Alzheimer’s Association in your area.


Credits and References

Lewy Body Dementia Association. P.O. Box 451429. Atlanta, GA 31145. (404) 422-5434. www.lbda.org

Riding the Roller Coaster with Lewy Body Dementia by Helen Whitworth, available at lbd@whitworth2.com, or (480) 981-1117.

LewyNet, The University of Nottingham, Division of Pathology, University Park, Nottingham, England NG7 2RD. Telephone +44 115 9515151. Web site: http://www.ccc.nottingham.ac.uk/~mpzjlowe/lewy/lewyhome.html.

“Dementia with Lewy Bodies: A Distinct Non-Alzheimer Dementia Syndrome?” by Paul G. Ince, Elaine K. Perry, and Chris M. Morris, Brain Pathology, April, 1998. (Available with extensive bibliographies at LewyNet web site.)

“Similarities to Alzheimer’s and Parkinson’s Make Lewy Body Dementia Difficult to Recognize and Challenging to Treat,” John Douglas French Center for Alzheimer’s Disease Journal, 1998/1999.

Parkinson’s Disease UPDATE, a monthly newsletter, Medical Publishing Company, P. O. Box 450, Huntingdon Valley, PA 19006. Issue #10, 2000.

“Dementia with Lewy Bodies” by Ian G. McKeith, M.D., FRCPsych., High Notes, News from the John Douglas French Alzheimer’s Foundation, Fall, 1996.

“Consensus guidelines for the clinical and pathological diagnosis of dementia with Lewy bodies (DLB): report of the consortium on DLB International Workshop,” by I. G. McKeith, D. Galasko, K. Kosaka, E. K. Perry, et al, 1996. Neurology, 47:1113-24.

Dementia with Lewy Bodies by Robert H. Perry, Ian G. McKeith, and Elaine K. Perry (editors), Forward by Jeffrey L. Cummings, 1996. Cambridge University Press, Cambridge.


Other References

Ala, T. A., Yang, K. H., Sung, J. H., Frey, W. H., 1997. Hallucinations and signs of parkinsonism help distinguish patients with dementia and cortical Lewy bodies from patients with Alzheimer’s disease at presentation: a clinicopathological study. Journal of Neurology, Neurosurgery and Psychiatry, 62:16-21.

Dickson, D. W., Ruan, D., Crystal, H., Mark, M. H., et al, 1991. Hippocampal degeneration differentiates diffuse Lewy body disease (DLBD) from Alzheimer’s disease. Neurology, 41:1402-9.

Galasko, D., Katzman, R., Salmon, D. P., Hansen, L., 1996. Clinical features and neuropathological findings in Lewy body dementias. Brain Cognition, 31:166-75.

Graham, C., Ballard, C., Saad, K., 1997. Variables which distinguish patients fulfilling clinical criteria for dementia with Lewy bodies from those with dementia, Alzheimer’s disease. International Journal of Geriatric Psychiatry, 12:314-8.

Hansen, L. A., Samuel, W. 1997. Criteria for Alzheimer’s disease and the nosology of dementia with Lewy bodies. Neurology, 48:126-32.

Ince, P., Irving, D., MacArther, F., Perry, R.H., 1991. Quantitative neuropathology of the hippocampus: comparison of senile dementia of Alzheimer type, senile dementia of Lewy body type, Parkinson’s disease and non-demented elderly control patients. J Neurol Sci, 106:142-52.

Ince, P. G., McArthur, F. K., Bjertness, E., Torvik, A., et al, 1995. Neuropathological diagnoses in elderly patients in Oslo: Alzheimer’s disease, Lewy body disease and vascular lesions. Dementia, 6:162-8.

Klatka, L. A., Louis, E. D., Schiffer, R. B., 1996. Psychiatric features in diffuse Lewy body disease: a clinicopathological study using Alzheimer’s disease and Parkinson’s disease. Neurology, 47:1148-52.

Kosaka, K., Iseki, E., Odawara, T., et al, 1996. Cerebral type of Lewy body disease. Neuropathology, 16:32-5.

Louis, E. D., Klatka, L. A., Lui, Y., Fahn, S., 1997. Comparison of extrapyramidal features in 31 pathologically confirmed cases of diffuse Lewy body disease and 34 pathologically confirmed cases of Parkinson’s disease. Neurology, 48:376-80.

McKeith, I. G., Fairbairn, A., Perry, R. H., Thompson, P., Perry, E. K., 1992. Neuroleptic sensitivity in patients with senile dementia of Lewy body type. British Medical Journal, 305:673-8.

Mega, M. S., Masterman, D. L., Benson, D. F., Vinters, H. V., et al, 1996. Dementia with Lewy bodies: reliability and validity of clinical and pathological criteria. Neurology, 47:1403-9.

Perry, E. K., Haroutunian, V., Davis, K. L., Levy, R., et al, 1994. Neocortical cholinergic activities differentiate Lewy body dementia from classical Alzheimer’s disease. Neuroreport, 5:747-9.

Salmon, D. P., Glasko, D., Hansen, L. A., Masliah, E. et al, 1996. Neuropsychological deficits associated with diffuse Lewy body disease. Brain Cognition, 31:148-65.

Samuel, W., Alford, M., Hofstter, C. R., Hansen, L., 1997. Dementia with Lewy bodies versus pure Alzheimer’s disease: differences in cognition, neuropathology, cholinergic dysfunction, and synaptic density. Journal of Neuropathology and Experimental Neurology, 56:499-508.



Family Caregiver Alliance
180 Montgomery Street, Suite 900
San Francisco, CA 94104
(415) 434-3388 or
(800) 445-8106
(415) 434-3408 (Fax)
E-mail: info@caregiver.org
Web Site: www.caregiver.org
Family Care Navigator: http://caregiver.org/caregiver/jsp/fcn_content_node.jsp?nodeid=2083

Family Caregiver Alliance (FCA) seeks to improve the quality of life for caregivers through education, services, research and advocacy.

FCA’s National Center on Caregiving offers information on current social, public policy and caregiving issues; provides assistance in the development of public and private programs for caregivers; publishes timely reports, newsletters and fact sheets; and assists caregivers nationwide in locating resources in their communities.

For residents of the greater San Francisco Bay Area, FCA provides direct family support services for caregivers of those with Alzheimer’s disease, stroke, ALS, head injury, Parkinson’s and other debilitating health conditions that occurs most often in adults.


Reviewed by William Jagust, MD and prepared by Family Caregiver Alliance. February 2001. Updated June, 2010. Funded by the Alameda County Area Agency on Aging and the California Department of Mental Health. ©2010 All rights reserved.


Drug overuse threatens nursing home residents. Routine prescribing of powerful medications occurs too often, our investigation finds

Last reviewed: December 2010

More than five years after the Food and Drug Administration warned that drugs routinely prescribed to nursing-home residents posed serious threats, including an increased risk of death, inappropriate use remains high, according to a recent analysis by the American Society of Health-System Pharmacists (ASHP). The project is part of a CRH Best Buy Drugs ongoing investigation of medication prescribed “off-label.”

The drugs in question, atypical antipsychotics, are approved by the FDA to treat bipolar disorder and schizophrenia. But they’re frequently used off-label to control agitation, aggression, hallucinations, and other behavioral symptoms in elderly patients with Alzheimer’s disease or other forms of dementia. There are no FDA-approved drugs to treat these behavioral symptoms, but doctors can legally prescribe any drug for any reason they deem appropriate.

But those medications—such as aripiprazole (Abilify); olanzapine (Zyprexa); quetiapine (Seroquel); and risperidone (Risperdal and generic)—pose substantial risks, especially to older people, that include diabetes, movement disorders (some permanent), pneumonia, stroke, weight gain, and even sudden cardiac death.

“There is limited evidence for the efficacy of these medications and evidence of significant safety risks,” says E. Ray Dorsey, M.D., an associate professor of neurology at the Johns Hopkins University School of Medicine. “In addition, many of the people receiving them have limited capacity to weigh the risks and benefits of taking them.”

According to FDA estimates, the rate of death among elderly dementia patients with behavioral problems who received antipsychotics was about 4.5 percent over the course of a typical 10-week controlled trial, compared with about 2.6 percent for a placebo group. This prompted the FDA to require black-box warnings—the strongest type—to be added to the labeling of atypical antipsychotic medications in 2005. The FDA broadened the warning in 2008 to include the labels on “typical” or older antipsychotics, including chlorpromazine (only available as a generic now) and haloperidol (Haldol and generic).

What measures should you try first?

In a study published in the 2010 Archives of Internal Medicine, researchers found that the use of antipsychotics often began during a patient’s first week in a nursing home. That suggests that behavioral interventions—the treatment of choice—are used minimally, if at all.

“The patient is scared and upset in a strange environment, and the caregiver may lack training in how to respond,” explains Kenneth Brubaker, M.D., a geriatrician and board member of the American Medical Directors Association (AMDA), a group of health professionals who work in nursing homes and assisted living facilities.

“I would advocate that a family member be present as much as possible during the adjustment period, because that’s the patient’s only contact with reality,” says Brubaker. “Having frequent phone conversations between patient and family help, as do looking through family photo albums together or compiling a DVD of the patient’s life story to remind them of the past.”

Frontline caregivers—who deal directly with residents with dementia-related behavioral problems—often have limited skills in using such approaches, Brubaker says. At those nursing homes, according to Brubaker, agitated new residents are likely to be quieted with antipsychotic drugs in lieu of family photos.

This off-label drug use report is made possible through a collaboration between Consumer Reports Best Buy Drugs and the American Society of Health-System Pharmacists. This is the18th and 19th in a series based on professional reports prepared by ASHP.

These materials were made possible by a grant from the state Attorney General Consumer and Prescriber Education Grant Program, which is funded by a multistate settlement of consumer fraud claims regarding the marketing of the prescription drug Neurontin (gabapentin).


Now I Have 2 Types of Dementia

No, I’m not bragging. I had my 6-month visit with the neurologist on Friday down in Pittsburgh. Even though it was only 20 degrees, it was a nice 2-hr sunny drive. On the way back, we stopped at Pam’s sister’s for a late lunch.

It was quite an interesting visit. Since I was the last patient for the morning, he was more relaxed than usual. And, of course, friendly, as usual. He spent more time than usual discussing and explaining about dementia.

Since I’ve been feeling quite well recently (I told him about the bad 6-8 week spell I had in August), I’ve found myself going into denial again. Thinking that I have been misdiagnosed and that I really don’t have any type of dementia and that its all psychological.

He once again showed me the results of the SPECT scan which I had a little over 1 year ago. He reviewed it and explained it to me. I’ve looked all over the web for SPECT scan pictures. I was not able to find one that looked exactly like mine. But I did find some which show relatively normal and abnormal results.


Spect Normal Spect Abnormal

                             Relatively Normal                          Abnormal

On SPECT scans, the colors which are pink, red, orange, yellow are the normal areas. Those which are blue and green are abnormal. The above scans are taken from a different cross section from mine, so they do not represent the same pathology as mine. I posted these just to show the contrast in colors.  

Very baffling to me. How can I be functioning at a relatively high level and have such highly abnormal scans? The majority of my pics were green and blue with a scattering of red, orange and yellow, consistent with frontotemporal dementia (FTD) and Lewy Body Dementia (LBD). He explained to me that individuals with FTD are highly intelligent with a high cognitive reserve which allow them to function in a relatively normal way and not always noticed by others as having anything wrong. He also said that I have the "slow" type which will allow me to go much further in life before becoming totally impaired. (Funny. I’ve never seen myself as all that intelligent. I was what I was and just took it for granted.)

He’s very pleased with the Aricept—Namenda combination and doesn’t want to change the dosages or combination. He also smiled and said that if I wanted to I could now go out and work.

"You’ll never be able to go back and function as a physician, but you could get a factory job or any other type of job which doesn’t involve the complexities of thinking required by a physician."

Now then. I couldn’t believe what I was hearing. Able to work again? That has to be some kind of a miracle, I told myself! But I’ll gladly accept it.

Needless to say, my mind has been racing with all kinds of things I’d like to do vs. what I could actually do given our residential location and driving conditions.

I did check online with the CA disability retirement plan which says that I can work as long as the salary + retirement benefits don’t exceed the amount which I made when I worked full time. Another unbelievable moment. I’m actually going to call them and discuss it on the telephone to make sure I’m not just seeing things.

Needless to say, I am excited. I’ve already started to look online for local job possibilities.

I just wish Pam could feel better and get the same kind of good news from her Docs as well. She’s been done with the pain, dizziness and trouble moving her arm and shoulder. She sees the "brain" neurosurgeon this Friday in Pittsburgh. Then we’ll also follow through with seeing the orthopedic surgeon, the physiatrist and physical therapy.

Some sad news though. I just spoke with a dear family-like friend whose husband suffers from Alzheimer’s Disease. He has now progressed to the point where he literally doesn’t know what "up" and "down" are. She’s finally worn down to the point of anxiety and depression. I gave her some recommendations to take to her PCP which I hope will help. Gil has the same neurologist that I do. He feels that Gil will need to be placed in a facility by this summer. Dorie doesn’t feel that they’ll be able to make it that long. I feel very sad about it. Life is just not fair.

Enough rambling for today. Going to watch some football…



Insulin levels in the brain may be the key to understanding how some types of dementia progress

Now this concept sounds very plausible to me. Think of how you feel when your blood sugar drops. I’ll be eager to see if anything more comes of it. More…..


NPH and Dementia

I’m glad many have enjoyed the pics of the flowers and afghans.

I came across some information this morning on normal pressure hydrocephalus. It reminded me of my neurology rotations. Although it is fairly rare, I was able to see several cases of it. And, yes, it truly did manifest itself as dementia in all of the 5 cases which I saw. And it was one of the questions on my medical licensing exam. Fortunately I won’t forget the symptoms after seeing them in real life. But I feel badly that many physicians frequently misdiagnose this disorder. Hopefully, the Dr. will order a consultation from a neurologist to appropriately diagnose it.

Normal pressure hydrocephalus (NPH) is an abnormal increase of cerebrospinal fluid (CSF) in the brain’s ventricles, or cavities. It occurs if the normal flow of CSF throughout the brain and spinal cord is blocked in some way. This causes the ventricles to enlarge, putting pressure on the brain. Normal pressure hydrocephalus can occur in people of any age, but it is most common in the elderly population. It may result from a subarachnoid hemorrhage, head trauma, infection, tumor, or complications of surgery. However, many people develop NPH even when none of these factors are present. In these cases the cause of the disorder is unknown.

Symptoms of NPH include progressive mental impairment and dementia, problems with walking, and impaired bladder control leading to urinary frequency and/or incontinence. The person also may have a general slowing of movements or may complain that his or her feet feel "stuck." Because these symptoms are similar to those of other disorders such as Alzheimer’s disease, Parkinson’s disease, and Creutzfeldt-Jakob disease, the disorder is often misdiagnosed. Many cases go unrecognized and are never properly treated.


Raquel says …"But I had never seen that entrelac type. How do you knit it as not to show the yarn overlapping on the wrong side? Can you tell me the secret?"

Some people like the texture of the overlap on the wrong side. However, if you want to eliminate it, when picking up the stitches on each rectangle just pick up only the outer loop—not both loops. Or, don’t slip each stitch on every row. There are some other technique variations which can make the front and the back of entrelac lay flat.


Imogene says…1. "David, a warm hello this morning! I love your Afghans. I would certainly ask you to make one for me if I felt it wasn’t too much. But, everyone else would ask for one also, and so, that would be too much." 2. "The Androderm Patch sounds like a winner to me. I have often thought my husband was low in testosterone. I am going to ask his Doctor if he can try the patch. How long did you use it before you saw results?"

The patch releases testosterone into the blood system immediately. However, it make take some time for it to actually see visible results.

You bring up a good topic about making projects for people. Pam and I have made handmade projects over the years as gifts, etc. Later, we’d find that the projects made of wool were tossed in a corner or had not been laundered correctly resulting in severe shrinkage. Some afghans made of good material were discovered on the floor for the pets, etc. We’ve also discovered that it’s difficult to phathom the cost of handmade items. And rightly so. Just walk into Walmart, Kohl’s, Sears, etc. The mass produced sweaters, throws, hats, socks are quite cheap. The yarn can get pricey especially if you make sweaters and scarves with yarn other than the brands which are sold in Walmart. Some handmade scarves are worth $75.00-$100.00 just in the yarn alone. Not to mention the time and work involved it making them. We’ve learned to use only the Red Heart and similar brands to use for regular afghans, kid’s blankets, sweaters and whatnot. They can easily be laundered and last for years even if they end up being a pet’s blanket. We’ve also tailored down our gifts using expensive yarns to only friends and family members who really appreciate the work involved and are willing to properly care for them.

The yarns used for the afghans I posted here cost almost $35.00 for each one and they were inexpensive yarns. I see some of their equivalents going for $50.00+ on Ebay. Actually I’m going to put these 2 scarves up for sale…….probably on Ebay or to someone with the best offer………I can always make more if I need something for a gift.


Johns Hopkins Health Alert — When Is It Time To Stop Driving?

I have great news! I had my 6-month checkup with my neurologist this past Friday. Quite a good visit. My mini-mental status exam improved by 3 points from earlier this year. Obviously, he is pleased as is Pam and I. After much discussion, he feels the gardening has helped a lot but more importantly, he emphasized the combination of Namenda and Aricept as being the main factor in my improvement. "Your underlying problem is still there but you are improving slightly from the plateau you’ve been on. I still have cogwheeling (The ‘pullback,’ jerky or ratcheting effect in an arm or leg that the doctor perceives when moving a patient’s rigid limb, thought to be related to tremor superimposed on limb rigidity), tremors, etc. He asked if I wanted to be placed on anti-Parkinsonian drugs to which I responded no. If I can avoid any extra drugs at this time the better it is. He agreed and decided to wait until it’s absolutely necessary to take them. So, gardening it will be along with watching food intake and increasing exercise!

Johns Hopkins Health Alert     When Is It Time To Stop Driving?

For most of us, driving is not only a symbol of our independence, but a practical tool of everyday living. So it’s no surprise that taking away a patient’s driving privileges is among the most difficult and potentially divisive decisions for the Alzheimer’s caregiver. In this Health Alert, Dr. Peter V. Rabins, Medical Editor of The Johns Hopkins Memory Bulletin, answers questions about driving and the Alzheimer’s patient.

Q. What signs should an Alzheimer’s caregiver watch for when determining a loved one’s driving competence?

A. While there are no set criteria for determining when a person with Alzheimer’s disease should be prevented from driving, there are warning signs. Keep in mind that in some states, driving privileges are based on the stage of the Alzheimer’s disease assigned by the physician.

The following are some common indicators that a person’s Alzheimer’s is making it difficult for them to respond safely while driving. Whenever you notice such problems, record the date and time when these behaviors occur, and discuss them with the person and his or her doctor:

  • Not signaling for turns or signaling incorrectly
  • Confusion at exits
  • Hitting curbs when trying to park
  • Parking inappropriately
  • Driving at inappropriate speeds
  • Delayed responses to typical and atypical situations
  • Getting lost along a familiar route
  • Getting unexplained dents on the car
  • Confusing the brake and gas pedals
  • Stopping at a green or flashing yellow light
  • Having near misses with pedestrians and other cars
  • Getting citations for poor driving
  • Having accident(s)

Q. When should a driving evaluation be sought?

A. If any of the above has occurred and the person will not voluntarily give up driving, then a formal evaluation by the motor vehicle bureau or private driving instructor should be sought. Most caregivers will restrict driving after a loved one has accumulated one or more of the warning signs listed above but many people with Alzheimer’s disease will deny any problems and, when asked to limit their driving or stop driving altogether, will be highly resistant. Some people who have the early stages of Alzheimer’s recognize that they are having changes and go in for testing on their own initiative. I always encourage and support this.

An evaluation by a driver rehabilitation specialist can be of great value in helping to make the difficult decision of taking away the car keys. A driver evaluation will assess the components of driving that may be compromised by this progressive condition. Areas assessed should include: attention, processing speed, visuospatial functioning, decision making, judgment, planning, memory, and behavior.

To find a certified driving rehabilitation specialist in your area who can perform such an evaluation, contact Driver Rehabilitation Specialists, ADED, 2425 N. Center Street #369, Hickory, NC 28601; Tel: 828-855-1623, or toll-free in the U.S. and Canada: 866-672-9466. Email: http://www.driver-ed.org


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