I was first suspected of having a dementing illness in 1998:
On 9 September 1998 Dr. Tom at UCLA wrote as follows to the neurologist who had referred me for evaluation for possible frontotemporal dementia: First, the MRI brain revealed very mild atrophy that appears more diffuse to me than based on frontal regions only. PET scan of brain revealed diffuse hypometabolism but a more severe degree of hypometabolism in parieto-temporal lobes, consistent with Alzheimer's disease. ... Quantitative EEG then further supported a diagnosis of Alzheimer's disease due to increased delta and theta activity in a pattern consistent with AD.... Our current working diagnosis is atypical clinical presentation of early Alzheimer's disease.
A PET scan in Houston in 2002 supported this diagnosis: The findings of decreased activity in the left temporal and parietal regions, although minimal, are suggestive of early Alzheimer's disease, in the absence of any history of trauma to this region.
Here is a discussion of my diagnosis that I wrote in February 2003:
"Part of the difficulty of my situation is the uncertainty of my prognosis. What sort of future challenges should I expect, and when? Alzheimer's cannot be definitively diagnosed except by brain biopsy or autopsy, but PET scans are about 90% accurate. The PET scans I had in 1998 and 2002 indicated Alzheimer's disease. I believe that the absence of the typical qualitative symptoms of AD at this time is due to my rehabilitative efforts. As I wrote 3 years ago in "Potential for Rehabilitation in Alzheimer's Disease," "... a primary feature of [AD] is neuronal hypoactivity, resulting in progressively decreased processing capacity and lowered stress threshold. This suggests ... that the qualitative symptoms of moderate AD, disorientation, gross forgetfulness, and loss of abstraction and judgment, are susceptible to rehabilitative intervention.... Insofar as a person with AD can relearn activities using a greater number of easier steps, he can regain function. And there is evidence that substantial capacities for procedural and implicit learning are retained."
"There is a small probability that I do not have a dementing disease at all, but benign aging combined with decompensation of a longstanding nonverbal learning disorder and/or atypical depression. There is also a small probability that I have a dementing disease which is not Alzheimer's. This might be bad news, since in that case medications for Alzheimer's which are currently under development might be ineffective for me. Another small probability is that I have Alzheimer's pathology but that my current high level of functioning is due to the effect of my rehabilitative efforts on comorbidities (a nonverbal learning disorder and/or depression) rather than on the main disease process. If so, I may quickly lapse into dementia in the not-too-distant future. On the other hand, there is a small probability that I can develop far more effective techniques than I yet have for warding off the dementia usually consequent on Alzheimer's pathology.
"I believe it is highly probable that I have Alzheimer's disease but that my rehabilitative efforts are currently effective. Typically the course of AD is 8 years between diagnosis and death, but one may survive 20 years. The absence of marked progression of hypometabolism between the two PET scans suggests a longer course but is far from definitely predictive."
I wrote the following in August 2004:
"I finally got my mother's brain autopsy report. AD was confirmed. In April I had another round of neuropsychological testing. No change; in particular, no clinical dementia. My neurologist said there's still no test that can tell definitely whether I have brain pathology or not. My own assessment, based primarily on the reported 85% accuracy of PET scans, is that I probably do have AD pathology, but that this is by no means certain. In my efforts to forestall clinical AD I'm encouraged by a recent report from the Nun Study that 8% of participants with the most severe spread of Alzheimer disease pathology ... did not show any symptoms of memory impairments. But compared to my former self or to others my age my memory for details is faint unless I concentrate intensely, and my mind works slowly (particularly in visual processing or in keeping pace with a conversation). Thus I continue to identify with those with mild traumatic brain injury or mild chronic fatigue syndrome. And my clouded future makes me identify with those who have cancer in remission."
Here's what I have learned more recently:
L. S. Prichep (New York University School of Medicine) et. al., "Prediction of longitudinal cognitive decline in normal elderly with subjective complaints using electrophysiological imaging," Neurobiology of Aging 27, (2006) 471-481, concluded: "Using logistic regression an R2 of 0.93 (p<0.001) [44 subjects] was obtained between baseline QEEG features and probability of future decline, with an overall predictive accuracy of 90%. These data indicate high sensitivity and specificity for baseline QEEG as a differential predictor of future cognitive state in normal, subjectively impaired elderly." They found increased theta activity particularly prognostic. The authors note that "a prospective replication with an independent sample is necessary for the demonstration of robustness of this approach."
InThe Wisdom Paradox (Gotham Books, NY: 2005) Dr. Elkhonon Goldberg, a clinical professor of neurology at New York University School of Medicine, declared: A body of evidence now exists (and is growing) that aging individuals may remain functionally and cognitively sound despite the neuropathological signs of Alzheimer's disease and other dementias.
On May 21, 2007 I had another PET scan: "The temporal lobes are hypometabolic.... In the clinical context of cognitive impairment the imaging pattern suggests a vascular etiology. The pattern does not suggest a neurodegenerative process." I continue to think, however, that AD pathology is likely and that my rehabilitative activities may have normalized my frontal and parietal metabolism.