Jack Kaufman, a tall, slim fifty-three-year-old bespectacled man living alone, came to see me in a state of considerable agitation. The previous week, he had lost the keys to his house and was forced to retrieve the duplicate keys from a neighbor, who luckily still had the extra set that Jack had entrusted to her. A few days later, Jack discovered that he had made a major error in his calculations for an office budget. He worked as an accountant and couldn't recall ever having made such a mistake. He said that his fear about losing his memory was disrupting his sleep, and that he could no longer concentrate on his work or his personal life.
I was a little surprised to see someone like Jack in our Memory Disorders Center. The episodes that he described could have happened to anyone, and most people wouldn't have rushed to seek help from a specialist. When I probed further, the source of his anxiety became clearer. His father had died of stroke, his mother from complications of Alzheimer's disease, and both conditions were present in the extended family on both sides. Jack's fears now made a little more sense.
Based on my interview, I determined that he had a very mild level of anxiety that did not meet diagnostic criteria for any psychiatric disorder. On neurologic examination, he had a generalized increase in deep tendon reflexes that could have been due to the presence of multiple small strokes in the brain. The MRI scan suggested the possibility of a very small stroke in the depths of the left frontal lobe, but the finding was so unclear that the radiologist hedged his bets and refused to call it a small stroke in his written report. I dredged up the scan from an obstinate medical records clerk and couldn't see any abnormality either (the radiologist was obviously much better at this than I, but it's a good idea for the patient's physician to also take a look). It seemed more likely that these abnormal reflexes, because they were widespread and not localized, were caused by heightened anxiety.
Neuropsychological testing produced a profile of no memory loss with mild deficits in attention and in the ability to change between "sets," which means that the rules of the test are changed in midstream and the subject is forced to readjust quickly and answer correctly according to the new rules. These deficits in "executive function" can be caused by a disease of the frontal lobe, that huge part of the brain sitting directly behind the forehead that is vital for intelligence and decision making, as well as storage of long-term memories. Sometimes, these frontal deficits are associated with specific neurological signs on physical examination, but these were totally absent in Jack's case. His performance could also have been caused by a lack of focus while doing the tests.
I wondered if his symptoms were all due to anxiety or if he had early signs of frontal lobe dementia, of which Pick's disease (microscopic structures called Pick's bodies are seen on brain autopsy) is one of the more common types. Or was he having ministrokes, which could give rise to a similar clinical picture, even though the MRI results did not clearly confirm this?
When in doubt, I usually do a few things. First, I talk to my neurologist and psychiatrist colleagues to see if they can give me some interesting leads, come up with a new idea, maybe dig up the files of another patient who presented similar symptoms. This approach didn't help me very much in Jack Kaufman's case. Second, I read the latest books and medical literature to see if they might shed light on the matter. This strategy didn't help me very much either. So I was beginning to consider my fallback position: recognize that I don't have the answer, discuss the situation with the patient, and explain that longer term follow-up with a trial -and-error treatment approach might be necessary.
But my curious diagnostic mind wasn't yet ready to accept defeat. Earlier, Jack had downplayed the impact of migraine headaches that occurred at a frequency of once or twice a month. On further investigation, he divulged the truth. Although the migraine attacks were not frequent, he often took painkillers as soon as he felt that an attack might be coming on. These included not only acetaminophen (regular Tylenol), but also Tylenol 3, which contains a small dose of codeine in addition to acetaminophen. Codeine is a narcotic that belongs to the same chemical class of substances as morphine and heroin, though it is much weaker in its effects. For most people, the codeine dose in Tylenol 3 is too small to have any impact on memory, but Jack sometimes took up to four tablets in a single day when he sensed the "aura" of an impending migraine attack. On days when the attacks did occur, he sometimes exceeded this dose.
Jack was unable to identify a clear time relationship between taking Tylenol 3 and his loss of memory, because his medication intake was erratic and unpredictable, which is why he hadn't reported it to me during the initial evaluation. I explained to him that there was a distinct possibility that the codeine in Tylenol 3 was having a subtle impact on his memory. Jack had obtained the prescription with multiple refills from an internist whom he saw barely once a year. Jack agreed with my recommendation to get an opinion from a headache specialist. The headache specialist stopped Tylenol 3 and switched him to sumatriptan (Imitrex), a powerful antimigraine medication that should be taken only just before or during a migraine attack, because frequent use is potentially risky. Jack had to adjust his approach to this new reality, but the great advantage was that when he took sumatriptan at the start of an attack, the migraine literally disappeared. Over the next few months, his cognitive abilities steadily improved, and he had no further incidents or episodes of memory failure. On repeat neuropsychological testing conducted a year later, he performed significantly better than he had when he first came to see me. We were both delighted with the result, and Jack expressed his heartfelt gratitude to me. He was now confident that he wasn't developing Alzheimer's disease or at risk for a stroke, but being a realist, he also knew that there was no guarantee he would be shielded from these conditions for the rest of his life.
Jack's story shows that it is often difficult to determine the exact cause of memory loss, but that persistence sometimes pays off. A few guidelines can help pigeonhole the symptom of mild memory loss into one of the following broad categories:
1. Memory loss due to the aging process itself.
2. Potentially reversible memory loss caused by a specific abnormality (Jack Kaufman).
3. Dementia, where Alzheimer's disease is the most common type.
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