In my journeys after diagnosis of dementia and then Alzheimer’s, I have met Michael Ellenbogen, and he shared his book with me. It read like a diary me and he detail his numerous neurological exams, PET Scans, and most importantly, his neuropsychs…which might have some informational value those waiting get their neuropsych results see what they look like. While I commend Michael for his honest reporting of his evaluations, I find myself a bit confused as I read his book because his scans are essentially normal and unchanging through the years, he report levels of dysfunction in his book that he does not report or show evidence of in person, and his neuropsyhcs don’t show the appropriate pattern of dysfunction essential for a dementia diagnosis. Although, quite a few people DO, in fact, experience trouble with getting a diagnosis…I admit I am perplexed by a 10 year effort that showed little decline. It certainly is an interesting read.
Some Quotes from his book:
“In August, I had a Brain ScanW/Spect. Here is the report: The interhemispheric fissure appears slightly widened for age. The distance between the caudate nuclei appears slightly widened for age. The activity in the pons was moderately increased when compared to the results in most other patients and health volunteers. There was minimally decreased activity in the medial aspect of both temporal lobes. The impression included the following: The study fails to detect a cause for the cognitive impairment. The minimally decreased perfusion in the medial aspect of both temporal lobes is not a specific finding. It is frequently seen in healthy human volunteers as well as patients with true hippocampal dysfunction.”
“Another EEG was requested by Dr. Grossman, which I had in August of 1999. The impression said: This is a minimally abnormal EEG because of slowing of the alpha rhythm to 8-8.5Hz in frequency. This minimal slowing of the alpha rhythm is nonspecific abnormality that can be seen in a setting of any toxic or multifocal structural encephalopathy. In September, I met back with Dr. Grossman. He looked over all the results and he was not sure what was causing my problems. One thing that was interesting, when he looked at my MRI he made the following comments. “The MRI scan demonstrated some minimal superior parietal atrophy that can be seen in a setting of normal aging.” He wanted to see me back in six months and to repeat the Neuropsychological testing.”
“Her summary and recommendations were: Current level of overall intellectual functioning is in the average range, with no significant discrepancy between verbal cognitive skills and nonverbal reasoning abilities, There is no significant change in overall intellectual ability in comparison with the evaluation in June of 1999. On neuropsychological testing, Mr. Ellenbogen displays generalized psychomotor slowing and inconsistent impairments in attention, concentration, and memory. In comparison with the previous evaluation, a variable, inconsistent pattern of change was demonstrated, with improvements on some measures and declines on others. This pattern of performance is not suggestive of focal or lateralized organic cerebral dysfunction, and is not consistent with the presence of a progressive cognitive disorder. Rather, Mr. Ellenbogen’s neuropsychological test performance suggestive of fluctuating levels of attention, concentration, and performance speed. Objective psychological screening suggest the presence of mild to moderate symptoms of depression and anxiety, and an introspective, perfectionistic personality style. These psychological symptoms are most likely playing a significant role in Mr. Ellenbogen’s subjective cognitive dysfunction.”
“I went back for counseling from May through June of 2001. Talking made me feel better, but it did not help with my issues. I was amazed by the ways I kept finding to deal with my memory issues. I kept finding new tricks to simplify my life. It was my way of trying to survive. It was a good thing I was accustomed to change. The counselor’s impressions were: Client and wife reject the physician’s notion of depression as a cause and, although many of his symptoms could be seen in a depressed individual, in terms of affect, mood, motivation, energy, etc., he does not fit the usual picture of depression. It seems that stress, anxiety and difficulty relaxing may be underlying factors.”
“After about 10 years since my symptoms began, my frustration level was very high. It was becoming too hard for me to hide this from others. I had to work so much more than my colleagues did. While I always enjoyed the opportunity to work, it was just too overwhelming trying to keep up. I lost many years of my life, without knowing why I was becoming this way. I have to tell you this is very scary. Sometimes you think that you may be losing your mind. In January 2006, I met with my family doctor and informed him that I wanted to start a new work-up. I wanted all new doctors to look at my memory and processing issues. I did not want the new doctors to see the old records, because I did not want their opinion to be influenced in any way. I was sent to Dr. Roy A. Jackel, a Neurologist. I told him that I had seen other doctors but no longer had the records. I wanted him to start as if I were a new patient. He ordered new lab work, EEG, MRI and some neuropsychological testing. The good news was that my new insurance did not require going back to my primary doctor. The EEG report found nothing abnormal. I had two different brain MRI’s. One MRI with, and one without, contrast. Both tests of the brain came back normal.
I went back to Dr. Lindsey J. Robinson, the Clinical Neuropsychologist, in January. She was going to redo the neuropsychological testing. I thought it would be best to use this doctor again because she had a baseline for me and could compare my new results with the old. It would take months for the results. The other issue was that there were not many doctors, who performed this test, that were covered under my health insurance policy.
In June, just a few weeks after my 48th birthday, Dr. Lindsey J. Robinson finally got back with the results of my testing. Her results for neuropsychological testing were as follows: Background – Previous neuropsychological evaluation in 1999 and 2001 revealed fluctuating, inconsistent impairments in attention, concentration, and performance speed, and symptoms consistent with anxiety and depression. Summary and recommendations – Multiple aspects of Mr. Ellenbogen’s behavior and test performance suggestive of inconsistent /incomplete effort during the evaluation. Thus, this test results described are not regarded as a valid representation of his optimal cognitive functioning. Mr. Ellenbogen’s clinical presentation and test are unchanged in comparison with prior neuropsychological evaluation in 1999 and 2001. There is no evidence of progression of cognitive impairments, and Mr. Ellenbogen’s developmental history and current test performance are not consistent with a diagnosis of attention deficit/hyperactivity disorder or any other organically-based cognitive disorder. Mr. Ellenbogen demonstrated an anxious/ obsessive personality style and some symptoms of depression. His cognitive can be most parsimoniously attributed to affective disorder and/or other motivational or psychological factors. Diagnostic Impression; R/O Dementia (not in evidence) R/O Anxiety Disorder, NOS R/O Personality Disorder, NOS
Her recommendations – Mr. Ellenbogen should be reassured that thorough medical/neurological evaluation on multiple occasions has revealed no evidence of neurological cause for his cognitive symptoms. A trial of psychotropic medication could be considered to address Mr. Ellenbogen’s apparent effective symptoms. He is unlikely to benefit from psychotherapy due to his reluctance to accept a non-medical explanation for his symptoms.”
“October 1, 2007. Her summary states: Mr. Ellenbogen’s performances on the various test of memory were, at times, consistent with recognized neurobehavioral correlates to temporal and parietal lobe dysfunction, but not consistently so. Mr. Ellenbogen’s demonstrated significant impairments in the domains of learning and memory, primarily for verbal information. Current results indicating possible worsening of his verbal memory provide a basis for considering of a neurological disorder, i.e. mild cognitive impairment. Conversely, visuospatial, visual motor, and constructional abilities remained intact, and generally improved which would not be expected.
- Mild Cognitive Impairment
- Emotional Disturbace
- R/O Anexity Disorder
- R/O Dysthymic v. Depressive Disorder
- R/O Obsessive-Compulsive Personality Disorder
- R/O Remote Effects of Prior Head Injury (unlikely)“
“Dr. David J. Libon’s neuropsychological evaluation results were available in June. His Summary and diagnosis are as follows: Michael Ellenbogen is a middle-aged man who was referred for a neuropsychological evaluation because of suspected dementing illness. The patient gives a 10-year history of cognitive decline including difficulty maintaining employment. On the basis of the patient’s self description a primary progressive aphasia appears to be present. Mr. Ellenbogen described increasing word finding, comprehension, writing and spelling difficulty. Today’s evaluation verifies the patient’s self-report. Performance on all language related tests was quite impaired. Conversational speech was positive for mild word finding difficulty. Word finding difficulty was also seen on formal tests requiring the patient to name pictures and define words etc. Performance on tests that assess comprehension was quite impaired considering the patient premorbid occupational history. Spelling and writing problems were also noted. Mr. Ellenbogen also displayed problems on selected tests that assess executive control and working memory. The verbal nature of these test contributed to his difficulty. Problems were also seen on verbal memory test were a primary amnesia is present. By contrast, the patient performed very well on visuospatial test such as when asked to produce clock drawings and copy the Rey Complex Figure. Visual memory, as assess with immediate and delayed recall of the Rey Complex Figure, was intact. In sum, the profile obtained today suggests the presence of an emerging semantic dementia. Diagnosis – semantic dementia”
NOTE: This would be FTD….but I find this remarkable, and strange, since Michael Ellenbogen speaks and writes quite well now, 10 years later. I have Aphasia, and not only did Michael NOT recognize it when it happened me, he did not endorse ANY of the symptoms of Aphasia.
“Treatment Plan/ Recommendations
Present & Future Living Situation
1.) A mild to moderate level of supervision is recommended to monitor the patient’s compliance with the patient’s medication regime and everyday activities.
1.) A driving evaluation should be considered.
1.) Mr. Ellenbogen is fully able to make very routine decisions. However, the assistance of a family member is necessary in order for the patient to make complex decision regarding financial matters. In this regard the patient and family should consider consulting an attorney to discuss drawing up a living will, power of attorney, and related issues.
Activities of Daily Living
1.) In order to facilitate the patient’s independence, everyday tasks should be made routine. Also, wherever possible, Mr. Ellenbougen should rely on past knowledge. For example, the patient might have comparatively little difficulty preparing a meal with familiar utensils and ingredients in a familiar environment. However, tasks requiring the use of newly learned information, or in situations that are not familiar will be more problematic.
2.) The patient should be encouraged to perform only one task at a time, and the patient should not be interrupted while performing activities. It will be more difficult for the patient to perform activities of daily living if engaged in conversation. In addition, environmental distractions (e.g., television, radio, etc.) should be kept at a minimum to allow the proper focus to complete the task at hand.
Language and Communication
1.) The family must not assume that the patient comprehends what is being said. Just as one can repeat a phrase in a foreign language, but not know the meaning of the words, dementia patients may be capable of repeating verbal information even when the meaning of words is lost. It is important that the family does not assume that the patient comprehends information just because a phrase or sentence can be repeated.
2.) In an attempt to facilitate the comprehension of everyday conversation, caretakers should speak in simple sentences. Gestures and exaggerated prosody may also increase the patient’s comprehension.
Further Diagnostic and Treatment Services
1.) A trial of medication designed to treat the patient’s memory disorder should be considered.
2.) The patient’s depression should be monitored.”
NOTE: That by stating that Michael was not competent handle his financial affairs, this neuropsychologist was essentially stating that Michael Ellenbogen was not-competent any longer. Again, this is not the Michael Ellenbogen that I have met 10 years later.
“In August I met with Dr. Libon to obtain his recommendations on what type of work I can do going forward. Below is a copy of his letter of our conversation: I recently met with Mr. and Mrs. Ellenbogen to review the findings of my recent neuropsychological examination. In the time I spent with the family I reviewed my recent evaluation, the prior neuropsychological evaluations, the results of the PET scan, the results of other medical studies I explained to the family that we are dealing with a primary progressive neurodegenerative disorder. My current diagnosis is Semantic Dementia which is one of the Frontotemporal Dementia Syndromes. The family asked me about future work. I responded that Mr. Ellenbogen is not able to return to work because of his dementia. I do not believe he is able to manage any type of job. At the time of my evaluation I urged Mr. Ellenbogen to apply for disability.
In September 2008….”
NOTE: So it would appear that Michael finally was able get a diagnosis of FTD dementia.
“Cognitive Neuroscience Section
Summary of Research Results
Patient Name: Michael Ellenbogen
Testing Dates: September 15th – 23rd, 2008
Introduction Mr. Ellenbogen was examined in the Cognitive Neuroscience Section of the National Institute of Neurological Disorders and Stroke as a participant in our Frontotemporal Dementia (FTD) and Corticobasal Syndrome (CBS) research protocol. Mr. Ellenbogen is a 50 year-old right-handed male with 14 years of education. He was most recently employed as Data Transmission Analyst – his retirement was related to his current symptoms. Mr. Ellenbogen has symptoms reportedly compatible with a diagnosis of FTD – semantic dementia subtype, but at the beginning of our evaluation it was uncertain what his final diagnosis would be. He was accompanied to our evaluation by his wife Sheri and an extensive family and medical history is available from the family. This report is a summary of research data and is not a clinical neuropsychological report. No clinical implications should be made about diagnosis or therapy. Test Behavior Mr. Ellenbogen demonstrated excellent effort during the testing and had an excellent grasp of test instructions. During the testing, he demonstrated very mild conceptual disorganization, anxiety, memory impairment, depressed affect, and language deficits.”
“The patient’s performance on a Driving Simulator was mildly impaired and included one collision, one hit pedestrian, and a speeding ticket. His memory for billboards contained in the simulator drive was severely impaired. At the time of this evaluation, the patient was still driving.”
“Summary Mr. Ellenbogen’s overall performance on our experimental neuropsychological evaluation is incompatible with his reported 11-year history of behavioral symptoms suggesting that his diagnosis is currently uncertain. The visual inspection of Mr. Ellenbogen’s MRI scan by a neuroradiologist revealed a normal brain with no obvious atrophy. A visual inspection of Mr. Ellenbogen’s PET scan indicated that he had mild reductions of glucose metabolism in some areas of the temporal and parietal lobes in both hemispheres. Primary visual cortex, cerebellum, and subcortical structure glucose metabolism was viewed as within normal limits. These findings are not compatible with the typical course of a FTD. Mr. Ellenbogen’s cognitive abnormalities are compatible with the mild severity and pattern of abnormalities noted on his PET scan. His MRI scan was read as normal. These research findings would not support a clinical diagnosis of FTD – semantic dementia variant given the length of time of symptoms, the minimal findings on MRI and PET scanning, and the pattern of deficits noted on his neuropsychological evaluation. While his history, neuropsychological testing and PET Scan point to a very slowly progressive dementia, at this time, we are unable to provide any more specific a diagnosis.”