UPDATE on Dementia with Lewy Bodies



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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.



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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.



How I find a Word in my head? Oops! Pam fell down!

Thought I’d try to catch up a little bit today.

Overall, Pam has been doing a little bit better. The pain specialist has been working for over a year to find the right combination of meds for her. Finally, I think we have something. He’s managed to narrow it down to two meds. She has several conditions which we’ve managed to get a grip on over the last 4-6 months of evaluation. Each condition seems to have its own type of pain. Some of the types of pain she suffers from is neuropathic pain, radiculopathy and fibromyalgia all of which are relieved with Topiramate (brand name Topamax). He also needs to use a narcotic agent (unfortunately) to manage some of the other types of pain.

So, overall, we see some mild improvement. But, low and behold! After much protesting from me, last week she decided to go outside to get the mail. Yep, she slipped on the snow and ice in the driveway and fell on her knee! Gosh! How could I turn around and say, "I told you so." Well, I did, but only several days later when the time was right. Smile, smile.

Because of her osteoporosis, she has a 5-6X risk of bone fractures. I saw her go down and immediately pictured in my head of having to call an ambulance. Fortunately, she was able to get up. Needless to say, she is sore and bruised all over with a big ‘egg’ on her knee! I did take her for evaluation and no fractures!! But it sure doesn’t help deal with Mr. Arthur in her knee which many of us also have.

Some of my latest thoughts and insights have to do with language difficulty — expression and word finding.

  • difficulty finding the right words. I can remember a long medical terminology word but can’t always retrieve a simple word such as sofa, fork, etc.
  • I tend to use descriptions in place of words “that thing behind the house you sit on" instead of “patio or back porch”). Recently I couldn’t remember the word "fork" so I resorted to saying, "You know, that thing you stab into food."
  • occasionally have difficulty with some pronunciation; familiar words don’t sound right
  • sentences don’t sound right or are phrased incorrectly (don’t make sense)
  • have difficulty explaining a thought or idea
  • I rely on Pam and Chad to guess at the meaning of what I am trying to say
  • very frustrating when I have trouble say what I mean
  • Now I have a lot of trouble talking on the telephone unless it’s someone I know very well or from many years ago. I think part of it is that there are visual cues over the telephone.

One of the descriptions I was able to use with Pam recently was this. At times, whenever a word won’t come, it’s as though I can picture a long tunnel starting at the front of my head progressing to the back of my head. The tunnel gets more narrow and blacker as it goes to the back. At the back, sometimes there is nothing there, thus no word.

At other times, there is a vague dot or small object or small word which is incomprehensible. Sometimes I can visualize it slowly coming to the front of the tunnel. How far it comes up seems to determine whether I get the ‘word.’ Sometimes, I literally pause and wait for "it" to come forth. Sometimes, it will only come half way and then stops. This is actually more frustrating than if it is just totally blocked. Other times, it all comes forward with the right word but in "slow motion." That’s when I find myself talking and literally saying, "wait a minute." I just need some time for it to crawl up.

It seems very hard to describe all this. If someone can’t follow what I just said, I totally understand.

Enough for today. Just thought I’d share my perspective on word finding.


Wandering VS. Getting Lost in Individuals with Dementia

The Alzheimer’s Association reports that of the estimated 5.3 million Americans living with the AD, six out of 10 will wander from their homes or care giving facilities at some point during their illness.

Read more…



Family Caregiver U.S. Postage Stamp Campaign Initiated by Volunteers of the National Family Caregivers Association — Please Sign the Petition

2000 more signatures are needed. Please show your support for family caregivers by completing this petition letter at the bottom of this page.    Thank you for your support of the U.S. Postage Stamp Family Caregiver Campaign!

My response to: Anyone have experience with Psychiatrists being used for LBD patient?

I received this email this morning from LBDcaregivers@yahoogroups.com. My response follows this copy of the email.

Anyone have experience with Psychiatrists being used for LBD patient   Posted by: "drh488" Wed Nov 18, 2009 3:17 pm (PST)

Today we had a Psychiatric nurse visit Mom. By the time she left, she had my mother so emotionally upset that she is ready to go back to a nursing home and die. She brought up things to my mother that happened 30 years ago and hasn’t been discussed in 20 years. Our battle with the outside caregivers has turned into a social worker telling us that WE have become Lewy body dementia. Our extreme efforts to make people understand the disease has taken the place of taking care our mother. Our mother does best when she has structured days. Up at 6, breakfast at 8, regis at 9, lunch at noon….etc. Anything out of that structure causes problems with her. This company sends occ. therapy, phys therapy, and a nurse. We have explained time and time again that our Mom needs structure. To no avail we wont here from them for 3-4 days then they call saying "We are on our way". Next thing you know, 3 people in one day unexpected. My sister is so frustrated. Psych nurse told my Mom that she has LBD, what it is and everything. Brought up old memories of my sister dying, my dad dying. Then she leaves with my mom all upset and my sister to deal with it. Psych nurse wont be back for 2 weeks. I’m calling my Mom’s neurologist tomorrow to see if she should be talking to this psycho nurse…no pun intended….It seems to me that it is more destructive than constructive.  Interested if anyone has had similar experiences Thank You

I felt appalled as I read this post. It goes to show that not all educated individuals use good old fashioned common sense. Even a small child realizes something isn’t right when they see someone being hurt and being in distress.

As an aside, I should mention that dementia is not only a neurological diagnosis but is also an official psychiatric diagnosis.

Unfortunately, in spite of being taught to first DO NO HARM to a patient, medical professionals don’t always have good common sense either. One doesn’t always learn certain things from medical, psychology and nursing books.

Having said this, there is not excuse for someone to get someone upset like this. Psychiatrists, psychologists and psychiatric nurses are taught that certain mental health diagnoses should not be treated with traditional psychotherapy such as schizophrenia and dementia. These disorders are treated with supportive psychotherapy, not with insight-oriented psychotherapy as described in the email.

What good does it do to dredge up the past with someone who has dementia? How can it be helpful? I certainly don’t know. However, if an individual unsolicitedly brings up past memories, that is fine. They can be dealt with in a supportive way whether positive or negative. And reminding someone of past positive memories can be therapeutic as well. But to stir up past memories in any of us against our will is certainly cruel in my opinion.

So, yes, this behavior is undoubtedly more destructive than constructive. Definitely confront the involved providers and request them to discontinue this type of communication and involvement. If it doesn’t stop, go to the next level, etc. If it continues, and if it is possible, go somewhere else! If it smells like a duck, quacks like a duck and walks like a duck then it is a duck………….

This makes me wonder. How many of all caregivers, professional and non-professional unwittingly aggravate and/or cause some of the argumentativeness, irritability and combativeness seen in the dementia population?

I’d be interested to hear of others’ thoughts and opinions.


Brain tumor, MRI and Computer Crash

Crying  GGGRRRWWWW!!! So much has happened. I just gained my computer and Internet access today. It crashed big time over 1 week ago. Fortunately I’ve liked computers and am a geek when it comes to tweaking and ‘suping up’ Vista and browsing speeds. Fortunately, I had my document files backed up including passwords and product keys. I worked at it a little bit day by day………and now…….Voila!

In addition to Pam having her chronic back and neck pain, she has been suffering from headaches more than usual. They now last 24-7 which she describes as a pounding throbbing headache. Two weeks ago she had her usual monthly visit with the pain specialist. He noticed muscle weakness in her upper shoulders and arms. So, he ordered an MRI of the neck. This past Friday, he called her saying that the MRI showed a mass on the back of her brain on the cerebellum. We both felt shock! She immediately thought of her mother’s brain tumor to which she succumbed. I immediately thought of the time when the Dr. told me my first wife and cancer. “Not 2 wives,” I thought.

She now has an MRI of the head scheduled for this Friday and will see a neurosurgeon on December 3.

We’re kind of reeling with the news but are remaining optimistic. Perhaps it’s just an arachnoid cyst which may need fenestration and a shunt. We will see.

Erik, Dr. Char and Dr. Howard………….I’ve been wanting to write you all an email but you can blame the computer crash on my not doing it.

We’re preparing for Pam’s brother, sister-in-law and their 2 children this weekend for the Thanksgiving holiday.

I need to start blogging more. But enough for today. Am still processing all my thoughts which I’ll be able to share later.


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