Change up: Painting, Dementia, and FTLD

There are over 50 causes of dementia that affect either cortical or subcortical (or as in Alzheimer’s Disease - AD, traditionally considered a cortical dementia) and mixed types (see also Zillmer, Spiers, & Culbertson, 2008, pp. 406-7). The most common causes are vascular, infectious, and toxic. Generally, dementias are also divided into three types: progressive (cortical dementias like AD, Picks, Wilson’s; subcortical: Huntington’s Disease - HD, Parkinson’s Disease - PD, AIDS dementia, and Creutzfeldt-Jakob Disease - CJD), static (toxic: Alcoholic dementia, heavy metal poisoning; infectious: herpes encephalitis; and others like trauma, tumor, etc.), and reversible dementias (like systemic: anemia and uremia; B12 deficiency as in Korsakov’s Syndrome; endocrine as in Addison’s Disorder and thyroid disorders; and drug toxicity: from antipsychotics and anticholinergics) (p. 406).

Frontotemporal lobar degeneration (FTLD) is a cluster of diseases that have characteristics of primary dementia, warranting a DSM-IV TR diagnosis as a behavioral syndrome, that shows prominent and disproportionate atrophy of the anterior frontal and temporal lobes (Midorikawa, Fukutake, Kawamura, 2008, p. 224). By the DSM-IV TR, required for a dementia diagnosis are: memory impairment and in an additional area of cognition (language, praxis, executive function, etc.), impaired/decline in social/occupational functioning, clouded consciousness, and an organic contributor to etiology or absence of other conditions except an organic mental syndrome (see also American Psychiatric Association, 2000; Zillmer, et al., 2008, p. 407).

Primary dementia is significant for a loss of cognitive ability – memory, perception, verbal, and judgment – often seen in stroke patients and those suffering from AD (Carlson, 2010, p. 543). Additionally, aphasia is present in FTLD, with 2 subtypes, nonfluent aphasia and semantic aphasia. The 2 patients in the study I reviewed had semantic aphasia. Most interesting, however, was that these Japanese patients had no education in painting, did not paint prior to FTLD onset, and painted realistically. While the 2 patients studied did not show creativity in their paintings (that is, they were strictly painting what they saw) creativity does occurs with patients suffering from the nonfluent aphasia subtype (Midorikawa, et al., 2008, p. 228).


People with FTLD and primary dementia suffer from various problems in their day-to-day lives: difficulty recalling the names of certain objects (verbal deficit that worsens over time); difficulty recalling the meanings of words; abnormal behaviors such as intrusiveness and repetitive actions (that worsens); deficits in general verbal functioning (i.e., WAIS VIQ, etc.); frontal lobe function deterioration; preserved speech and comprehension ability, but with severe naming deficits; reading disturbances; other naming deteriorations (i.e. Western Aphasia Battery); sometimes apraxia (trouble following directions due to semantic deficit, with intact imitation and use) (p. 226); possible global deficits in visualizing and understanding objects (p. 228); visual semantic ability described as ‘a central semantic impairment’ (p. 229); marked atrophy in the left temporal lobe; and enlargement of the ventricle with possibilities for lacunar infarctions in the white matter. [important to note that these signs and symptoms are taken quasi-anecdotally, as the N=2] (p. 226). Additional symptoms not unlike those found in PD (including the typical muscular rigidity, slowness, resting tremor, and instability) are also possible in this kind of frontotemporal dementia (Carlson, 2010, pp. 537 & 546).

Interestingly, the patients in the study helped to show that “the assumption that the appearance of painting skills during FTLD does not reflect learning or cultural background, but rather is the expression of innate functions of the brain. In addition, our patients’ paintings were realistic in style, which might be an inherent phenomenon in humans, and not an advanced skill” (Midorikawa, 2008, p. 228).

The authors presented a couple of different theories for this finding: paradoxical functional facilitation (PFF) effects initiated by a disruption of inhibitory mechanisms and/or compensatory plasticity alongside a “decreased inhibition of ‘the right-sided and posteriorly located visual and musical systems’” (p. 228). The authors drew parallels to similar results by studies on children with autism in that “impoverished conceptual representation of the world may actually help rendering what we see’, and may arise from a common functional deficit. With these parallels, they concluded that it was perhaps more parsimoniously accounted for by a regression to childlike, quasi-autistic states. (2008).

Finally, while there are not any FDA approved treatments for FTLD, there are off-label treatments, garnered from experience treating AD, which can be used in addition to behavioral management (Caselli, & Yaari, 2008, p. 489). Currently, there are “six areas of pharmacotherapeutic consideration [which] are prevention (primary and secondary), intellectual decline, behavioral disorders (such as depression, anxiety, and psychosis), sleep disorders, frequently associated disorders (including motor neuron disease), and abrupt decline (pp. 489 & 497). While there are no curative treatments for this disorder, maintenance treatments and even treatments based on traditional Japanese medicine (Kampo - called Yokukansan), show promising results in symptom management (Kimura, Hayashida, Furukawa, Miyauchi, & Takamatsu, 2009, p. 38). Further important non-medical interventions concerning behavior are necessary: care for the care giver, maintenance of quality of life, containing weapons access, and limiting or eliminating driving privileges (Caselli & Yaari, 2008). Additionally, there are things that can be done behaviorally and for the caregivers to ensure that remaining/intact functions are used to a) slow degeneration (use it or lose it), b) increase agency and thereby quality of life (especially for caregivers who may be more reality oriented than patients), and c) treat co-morbid diseases and disorders and d) to take advantage of what intact functioning remains in order to provide reassurance, (acceptance stance) and emotional support to both the patients and those with whom they interact) (see also Midorikawa, et al., 2008, p. 229; Caselli & Yaari, 2008).



References

Carlson, N. (2010). Physiology of behavior, (10th ed.). Boston: Allyn & Bacon.

Caselli, R. & Yaari, R. (2008). Medical management of frontotemporal dementia. American Journal of Alzheimer's Disease and Other Dementias, 22(6), 489-498. doi:10.1177/1533317507306654

Kimura, T., Hayashida, H., Furukawa, H., Miyauchi, D., & Takamatsu, J. (2009). Five cases of frontotemporal dementia with behavioral symptoms improved by yokukansan. Psychogeriatrics, 9(1), 38-43. doi:10.1111/j.1479-8301.2008.00261.x

Midorikawa, A., Fukutake, T., & Kawamura, M. (2008). Dementia and painting in patients from different cultural backgrounds. European Neurology, 60, 224-9. doi:10.1159/000151697

Zillmer, E., Spiers, M., & Culbertson, W. (2008). Principles of neuropsychology, (2nd ed.). Belmont, CA: Thomson Wadsworth.