Mrs JZ lived alone, in her own home. Her four daughters were increasingly concerned about her memory and arranged an initial assessment by her general practitioner, who referred her on for specialist assessment, now 2 years ago.
She had a past history of only hysterectomy. She was taking no medications.
Memory had been deteriorating for 2 years. At the time of initial assessment she was forgetting details of recent events (eg who had come to visit the last weekend), forgetting arrangements frequently and had become much more reliant on her diary. She was repeating information and questions, at intervals as short as 10 minutely, and up to 3 times. She was finding it more difficult to navigate when driving even to familiar destinations.
She remained independent in all activities of daily living, including operating household appliances, doing all banking, bill paying and finances and undertaking other community chores such as shopping. There was no change in her mood or personality but she had become more addicted to gambling- and had been banned from at least one Melbourne club for uncontrolled activity on the poker machines. Later it emerged that she was surreptitiously drinking considerable amounts of alcohol, sometimes pouring it down the sink if her children arrived unexpectedly. She seemed more avoidant and withdrawn in her interactions with her daughters.
She had been widowed 11 years earlier. Her 4 daughters were her only children, and were very supportive. She received no support services.
There was an older brother with dementia, and possibly also an aunt. Her mother died young and her father was cognitively normal when he died in his 80s.
Physical examination revealed a blood pressure of 195/95 but no other abnormalities. There were no extrapyramidal features or focal neurological signs.
Cognitive assessment revealed an MMSE score of 25, including 0/3 for short term memory. On the Montreal Cognitive Assessment she scored 20/30 with deficits across several domains including executive, language and visuospatial. Short term memory was 2/5 with the remaining 3 words recalled when cued. She was however well orientated to time and place.
A diagnosis of likely Alzheimer’s disease was made, but with no functional impairment dementia was not present. The high blood pressure needed review by the GP, and suggested the possibility of a vascular component to her cognitive impairment. Alcohol excess was also considered a possible contributory factor. Neuroimaging was arranged.
The MRI revealed only mild periventricular small vessel ischaemic changes. The hippocampi were not atrophic. SPECT scanning showed mild hypoperfusion in bilateral temporoparietal cortices with some extension into the frontal lobes, but this was not the characteristic picture of changes that reflect accumulating Alzheimer’s pathology. She proceeded to the more accurate FDG-PET scanning and this showed a pattern of hypometabolism that almost certainly is due to Alzheimer’s disease. There was markedly reduced metabolism in parietal, temporal and frontal cortices with clear involvement of the posterior cingulate regions and the precunei, and sparing of the primary sensorimotor cortices.
The diagnosis of Alzheimer’s disease, without dementia, was relayed to her and her daughters. It was explained that alternate terms for this condition are prodromal Alzheimer’s disease and Mild Cognitive Impairment due to Alzheimer’s (and now, under DSM V, the diagnosis is Minor Neurocognitive Disorder due to Alzheimer’s disease). She was advised to reduce alcohol consumption. Repeat blood pressure readings, without treatment, were normal, according to her GP.
Unfortunately she began to decline functionally. She was struggling to operate remote controls (eg for her gate) and finding it more difficult to prepare a meal. The MMSE had dropped to 20, some 6 months after the initial evaluation. The diagnosis was thus changed to Alzheimer’s dementia. As she was living alone and possibly still unreliable with alcohol consumption reduction, it was felt unwise to commence a cholinesterase inhibitor. Souvenaid was begun and based on purchases, it seemed that she was consuming one a day. She enjoyed it, and there were no adverse effects. Her MMSE rose to 21 four months later, and the family noted a range of improvements in her memory, function and demeanour. As an example, she now was aware that she had been repeating herself, and would preface some questions with “I know I probably asked you this before..”. She was however repeating herself much less, and was less reliant on her diary to recall the day’s planned routine. She was also more interactive with her daughters.
An Aged Care Assessment was arranged to access additional supports but it was decided she needed to move to low level residential care, where she settled in well. She was observed there to be drinking very little alcohol. She continued to improve cognitively and functionally. Donepezil was then commenced and she remained on Souvenaid she had begun 8 months earlier. At her most recent specialist assessment three months after commencing donepezil she has made further clinically significant improvements, with an MMSE now up to 23- these changes will allow her to remain on PBS- prescribed donepezil when she reaches the 6 month mark, in a further three months. She will continue the Souvenaid.
A/Professor Michael Woodward,