All About Estates

Testamentary Capacity and Lewy Body Dementia

Today’s blog was written by guest blogger Dr. Richard Shulman. Dr. Shulman is a Geriatric  Psychiatrist, and is the Service Medical Director for Seniors Mental Health Services at Trillium Health Partners (Mississauga Hospital, Credit Valley Hospital and Queensway Health Centre). He is available for independent medical-legal capacity assessments. He is an assistant professor at the University of Toronto.

It was my pleasure to have participated in the recent 18th annual Estates and Trusts Summit. I’d like to thank co-chairs Paul Dancause, Paul Wollaston, and Archie Rabinowitz for inviting me. During his presentation, Archie described his difficulty in understanding Lewy body dementia (LBD) as described in Walman v. Walman Estate[i] in relation to testamentary capacity. I’d like to explain the medical aspects of this condition and related diagnoses and comment on how this particular cause of dementia can pose challenges in testamentary capacity evaluation.

As I explained during the Summit, dementia is a medical term used to describe various brain disorders characterized by progressive decline in cognition, function and behaviour[ii] such that the person can no longer live independently.[iii] [iv] LBD[v] is an umbrella term for two related diagnoses; dementia with Lewy bodies and Parkinson’s disease dementia.

Dementia with Lewy bodies is characterized by a gradual onset of cognitive decline with these specific diagnostic features:[vi]

  1. fluctuating cognition with pronounced variations in attention and alertness;
  2. recurrent visual hallucinations; and
  3. Parkinsonism, a movement disorder consisting of:
  • tremor at rest (unintentional, rhythmic shaking, particularly of the hands or thumb while not moving);
  • slow initiation of voluntary movement;
  • increased muscle tone causing rigidity; and
  • postural instability, the loss of balance causing a person to feel unsteady.

When Parkinsonism is present without a known cause in the brain (i.e. the symptoms cannot be attributed to strokes), it is referred to as Parkinson’s disease, a neurodegenerative illness that initially affects movement only.[vii] The movement disorder features of Parkinson’s disease are the same as described above with Dementia with Lewy bodies. As the disease progresses, cognitive and behavioural symptoms with functional decline may appear similarly as described in dementia with Lewy bodies.[viii] [ix] In Parkinson’s disease, there is a spectrum of cognitive decline, ranging from mild cognitive impairment to “Parkinson’s disease dementia,” which can occur in up to 80% of seniors with Parkinson’s disease over the course of the illness.[x] In the latter stages of “Parkinson’s disease dementia” and Dementia with Lewy bodies, the two syndromes are clinically indistinguishable and come under the umbrella term LBD.

Fluctuating cognition with pronounced variations in attention and alertness (i.e. swings in lucidity) is a hallmark diagnostic criterion of LBD. Decline in attention and alertness is referred to as clouding of consciousness, which is episodic in LBD despite the illness being a constant affliction. These episodes resemble periods of delirium (acute confusion) superimposed on dementia (chronic confusion). These delirious like episodes are uniquely seen in LBD patients. Patients with other causes of dementia (such as Alzheimer’s disease) do not have clouding of consciousness except when suffering comorbid delirium from additional causes or in the advanced end-stage of dementia. Parkinson’s disease on the other hand, without having progressed into at least the moderate stage of “Parkinson’s disease dementia” (inability to function independently and needing assistance with at least one activity of daily living, such as showering) is typically free of swings in lucidity. It all depends on what degree of dementia the Parkinson’s patient has progressed to.

The fluctuations in lucidity that we see with LBD patients would suggest that in a more lucid period, a testator with LBD would have better alertness and attentiveness in order to pay better attention while giving instructions to a solicitor. However, this does not guarantee that clarity of attentiveness would permit the testator with LBD to demonstrate intact testamentary capacity as per the Banks v Goodfellow[xi] criteria.

References

[i] Walman v. Walman Estate, 2015 ONSC 0185

 

[ii] Ganguli, M., Blacker, D., Blazer, D. G., Grant, I., Jeste, D. V., Paulsen, J. S., … & Sachdev, P. S. (2011). Classification of neurocognitive disorders in DSM-5: a work in progress. The American Journal of Geriatric Psychiatry, 19(3), 205-210.

 

[iii] McKhann, G. M., Knopman, D. S., Chertkow, H., Hyman, B. T., Jack Jr, C. R., Kawas, C. H., … & Phelps, C. H. (2011). The diagnosis of dementia due to Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimer’s & Dementia, 7(3), 263-269.

 

[iv] What is dementia? Retrieved July 2015 from https://www.alzheimer.ca/en/About-dementia/Dementias/What-is-dementia

[v] What Is LBD? Retrieved July 2015 from https://www.lbda.org/category/3437/what-is-lbd.htm

[vi] McKeith, I. G., Dickson, D. W., Lowe, J., Emre, M., O’brien, J. T., Feldman, H., … & Yamada, M. (2005). Diagnosis and management of dementia with Lewy bodies third report of the DLB consortium. Neurology, 65(12), 1863-1872.

[vii] Hughes, A. J., Daniel, S. E., Kilford, L., & Lees, A. J. (1992). Accuracy of clinical diagnosis of idiopathic Parkinson’s disease: a clinico-pathological study of 100 cases. Journal of Neurology, Neurosurgery & Psychiatry, 55(3), 181-184.

 

[viii] Ferreri, F., Agbokou, C., & Gauthier, S. (2006). Recognition and management of neuropsychiatric complications in Parkinson’s disease. Canadian Medical Association Journal, 175(12), 1545-1552.

[ix] Dubois, B., Burn, D., Goetz, C., Aarsland, D., Brown, R. G., Broe, G. A., … & Emre, M. (2007). Diagnostic procedures for Parkinson’s disease dementia: recommendations from the movement disorder society task force. Movement Disorders, 22(16), 2314-2324.

 

[x] Hely, M. A., Reid, W. G., Adena, M. A., Halliday, G. M., & Morris, J. G. (2008). The Sydney multicenter study of Parkinson’s disease: the inevitability of dementia at 20 years. Movement Disorders, 23(6), 837-844.

 

[xi] Banks v Goodfellow (1870) L.R. 5 QB 549

 

Dr. Shulman graduated from the Faculty of Medicine, University of Toronto in 1973 and did postgraduate training in Psychiatry at the University of Toronto. He then went on to do specialty training in Geriatric Psychiatry in London, England. Since 1978, he has been based at Sunnybrook Health Sciences Centre, University of Toronto. He is the inaugural recipient of the Richard Lewar Chair in Geriatric Psychiatry at Sunnybrook Health Sciences Centre, University of Toronto. Currently, he is the Chief of the Brain Sciences Program at Sunnybrook. Dr. Shulman has had a longstanding interest in the issue of testamentary capacity and vulnerability to undue influence and has been qualified as an expert witness in Estate matters in Ontario and Alberta. Together with colleagues he has published several papers in the area of testamentary capacity in international journals and is a frequent presenter at legal continuing education conferences on Estates and Trusts. Email: Ken.Shulman@sunnybrook.ca