CJ's Neuropsychological Evaluation

History

Currently, CJ is a 67-year-old right-handed man who has visited the hospital for neuropsychological testing due to difficulties in handling different aspects of his work such as calculations, computing net commissions and deducting personal credit card spending. CJ also reports that this writing has become scruffy, finds difficulty in reading and struggles reading both digital and analogue clocks. His inability to perform various activities of daily living has fairly exacerbated his condition. For a more comprehensive understanding and support, seeking psychology dissertation help could provide valuable insights into his neuropsychological challenges.

Because CJ’s speech abilities were okay, he undertook a reading test to deduce his pre-morbid functioning, which emerged to be average when combined with his demographic factors. His literacy and numeracy skills have also emerged to be above average. Ultimately, CJ’s pre-morbid functioning level can therefore be concluded as an average.

CJ has been diagnosed with posterior cortical atrophy (PCA), which corroborates with the neuropsychological findings despite his difficulties being a bit wider, also involving the left and temporal areas. Meanwhile, there is no history of any cognitive difficulties among his immediate family members, a phenomenon that does not contradict the diagnosis because in most cases, posterior cortical atrophy is sporadic. No other pertinent medical history about CJ though.

PCA is often characterised by a progressive decline in visuoperceptual, praxis, literacy, and visuospatial skills (Hardy et al. 2020). The patient undergoes progressive neurodegeneration, which affects their parietal, occipitotemporal and occipital cortices, making PCA attributable to Alzheimer's disease. However, according to Schott & Crunch (2019), PCA has alternative underlying causes such as dementia with Lewy bodies, prion disease, and corticobasal degeneration.

Results

CJ’s visual perceptual capability tests emerged to be averagely weak, which corroborates with evidence-based neuropsychological features associated with PCA. According to Ahmed et al. (2020), some of the most features include alexia, Bálint's syndrome features such as environmental agnosia, optic ataxia, oculomotor apraxia and simultanagnosia; and feature of Gerstmann's syndrome such as left-right disorientation, finger agnosia, agraphia and acalculia (Harding et al. 2018). this is characterised by various forms of visual dysfunction, whereby they only initially fixate prominent features but later fixate on uninformative aspects of the scene, missing out on important contextual details of the image (Miller et al. 2018).

Existing research evidence (Wong et al. 2019) indicate that PCA patients are more likely to report visual symptoms such as difficulties in reading texts, and challenges in judging distances (leading to difficulties in parking or repeating minor car accidents). This explains why CJ reported difficulties in reading large fonts as well as why he tends to bump the curb. According to Ahmed et al. (2020), the visual sensitivity in PCA patients also presents in the form of light sensitivity, explaining why, despite living in one house for a long time, he sometimes walks past his home when it is dark.

CJ’s tests also revealed difficulties slow attention or processing speed and compromised executive functioning. This was manifested in his inability to accurately calculate his net commission, figure out his credit card spending. He also mentioned not being able to sometimes arrange coffee cups in dispensers. According to Wong et al (2019), individuals with PCA often report difficulties in using common objects, as well as difficulties in spelling or calculations, indicating the presence of dyspraxia.

Further examination may also reveal signs of occipital or parietal dysfunction, which includes but is not limited to ideomotor or ideational dyspraxia or both (Ahmed et al. 2018), problems with spelling and dyscalculia. However, according to Hodges (2007), the physical examination for PCA is always unremarkable. Nonetheless, if the patient displays signs of cortical visual impairment, then it may be difficult to interpret their visual fields or visual acuity. This often leads to the misdiagnosis of hemianopia due to the presence of higher-order visual attentional impairments (Larner, 2008).

CJs history and symptomatic presentation fit the evidence-based diagnostic criteria. According to Ahmed et al. (2020), there are two sets of diagnostic criteria for PCA, including insidious onset and gradual progression, visual deficits with no ocular diseases; episodic memory, personal insight, and verbal fluency; availability of symptoms such as dyspraxia and environmental disorientation, ocular apraxia, optic ataxia, simultanagnosia visual agnosia, and absence of tumour or stroke. Wong et al. (2019) suggested that other supportive features include hypoperfusion, acalculia, agraphia, ideomotor apraxia, and alexia.

Even though these criteria are useful in various clinical contexts, they are largely dependent on various clinical experiences during research and have not been widely validated. In this regard, Schott & Crunch (2019) argued that without any objective evidence linking the underlying pathology to the clinical phenotype, there is a continuous inconsistency, with the PCA term being used both as a diagnostic label and as a syndromic term.

The asymmetric atrophy of visual cortex areas also reveals CJ’s visuoperceptual and visuospatial deficits with hemianopsia to the contralateral side, as well as the right-handed optic ataxia. The argraphia, alexia as well as ideomotor apraxia hint at parietal deficits while the higher cognitive dysfunctions with difficulty with the strategic elements of memory encoding signified the underlying Alzheimer pathology. As per Schott & Crunch (2019), this might be accompanied by the additional affection of mid-temporal areas at a later stage of CPA. Nonetheless, the disentanglement of all these symptoms, as well as putting together all these pieces of the puzzle revealed PCA as the most probable diagnosis.

Against that backdrop, it would be interesting to examine the approach that would be taken if the visuospatial deficits have occurred later in the course of the disease long after the PCA diagnosis, or if the visuospatial deficits are overseen during the diagnosis. As such, a review of medical reports and literature points to the latter scenario, as the parieto-occipital dysfunctions have been anamnestically among the first clinical symptoms in some cases (Wong et al. 2019).

Conclusion

PCA is a neurodegenerative condition that presents in heterogenous neuropsychological sequelae, with pathophysiology like Alzheimer’s disease. This case report revealed that PCA is a complex disorder that presents many challenges to both the care provider and the patient. The case report focused on a 67-year-old right-handed man. The man underwent a neuropsychology test, which revealed various results. Regarding his intellectual state, the neuropsychology test revealed that the patient’s verbal intellectual functioning was within the expected levels, while his verbal memory was broadly intact. However, he showed some weaknesses with specific elements of his memory encoding. He also showed difficulty with word retrieval, to a lesser extent with naming and to a notable extent, semantic verbal fluency. The patent also showed signs of mild dyscalculia, dysgraphia as well as difficulty with spelling. More worryingly, the patient showed significant difficulty with certain aspects of executive ability. These results are generally consistent with existing diagnosis, with no evidence of any aspect of the results that complicate the PCA diagnosis. Furthermore, none of the found neuropsychological deficits indicated any known areas of brain damage. The lack of consistency in the classification of PCA is likely to continue until a standardized terminology and diagnostic criteria is developed. Meanwhile, a better awareness and understanding of PCA among the lay and medical community is required to enhance diagnosis, treatment and support services provided to PCA patients and their families.

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References

• Ahmed, S., Culley, S., Blanco-Duque, C., Hodges, J.R., Butler, C. and Mioshi, E., 2020. Pronounced impairment of activities of daily living in posterior cortical atrophy. Dementia and geriatric cognitive disorders, 49(1), pp.48-55.
• Ahmed, S., Loane, C., Bartels, S., Zamboni, G., Mackay, C., Baker, I., Husain, M., Thompson, S., Hornberger, M. and Butler, C., 2018. Lateral parietal contributions to memory impairment in posterior cortical atrophy. NeuroImage: Clinical, 20, pp.252-259.
• Harding, E., Sullivan, M.P., Woodbridge, R., Yong, K.X., McIntyre, A., Gilhooly, M.L., Gilhooly, K.J. and Crutch, S.J., 2018. ‘Because my brain isn’t as active as it should be, my eyes don’t always see’: a qualitative exploration of the stress process for those living with posterior cortical atrophy. BMJ open, 8(2), p.e018663.
• Hardy, C.J., Yong, K.X., Goll, J.C., Crutch, S.J. and Warren, J.D., 2020. Impairments of auditory scene analysis in posterior cortical atrophy. Brain, 143(9), pp.2689-2695.
• Hodges, J. R. 2007. Cognitive assessment for clinicians, 2nd ed. Oxford University Press.
• Larner, A. J. 2008. Neuropsychological neurology: The neurocognitive impairments of neurological disorders. Cambridge University Press.
• Miller, Z.A., Rosenberg, L., Santos-Santos, M.A., Stephens, M., Allen, I.E., Hubbard, H.I., Cantwell, A., Mandelli, M.L., Grinberg, L.T., Seeley, W.W. and Miller, B.L., 2018. Prevalence of mathematical and visuospatial learning disabilities in patients with posterior cortical atrophy. JAMA neurology, 75(6), pp.728-737.
• Schott, J.M. and Crutch, S.J., 2019. Posterior cortical atrophy. CONTINUUM: Lifelong Learning in Neurology, 25(1), p.52.
• Wong, B., Lucente, D.E., MacLean, J., Padmanabhan, J., Quimby, M., Brandt, K.D., Putcha, D., Sherman, J., Frosch, M.P., McGinnis, S. and Dickerson, B.C., 2019. Diagnostic evaluation and monitoring of patients with posterior cortical atrophy. Neurodegenerative disease management, 9(4), pp.217-239.