Psyc 3250 Su2 2014term Paper Assignmentcase Studyone Of The Great Cha ✓ Solved

PSYC 3250 SU2, 2014 Term Paper Assignment CASE STUDY One of the great challenges that behavioural neurologists and neuropsychologists face is integrating a seemingly random collection of signs and symptoms into a coherent and conceptually sound diagnosis of a disorder. The following case is a detailed description of neurological signs and symptoms presented by a patient in a neuropsychology clinic. Your task is to: • Name and describe the signs, symptoms and potential syndrome(s) • Determine cognitive domain(s) impacted and possible brain damage localization (be specific!). Also describe other areas of cognitive functioning that you think might be impacted based on cognitive neuroscience research.

Describe other clinically relevant data you would like to obtain (e.g. neuroimaging, neuropsychological reports etc.). • Provide potential diagnoses - list 2-3 possible diagnoses that you feel should be considered based on the facts of the case. Then narrow your reasoning down to what you feel is the most likely diagnosis. Each of these aspects should be fully explained and justified based primarily on information provided in the course (including the lectures). In addition to the course materials, you should cite two (2) additional research papers related to your final diagnosis and that have informed your clinical decision-making process. HOWEVER, this is not intended as a research paper.

I do not expect lengthy discussions on the etiologies nor an extensive bibliography. You may write 750 words for this assignment so your thoughts should be well reasoned and precisely stated. Superfluous writing and unfounded statements are STRONGLY discouraged. Please see “Term Paper Tutorial†lecture notes in the “Term Paper†folder on Moodle further details on how to approach the assignment. The case study analysis is due at the beginning of lecture, July 23rd.

Case: Patient C.L. C.L., a 55 year old right-handed woman, sought an evaluation for an overall decline in her writing, spelling, arithmetic and reading abilities. These had been present for approximately one year and had led her to resign from her position as a second grade teacher. Lapses of memory occurred occasionally. Despite these deficits, daily living activities remained intact.

Her general physical examination and elementary neurological examination showed no deficits. Examination revealed an alert, cooperative and pleasant woman who was appropriately concerned about her predicament. She was fully oriented to time [year, month and day of the week] and place [country, province, city and location of testing] but had only a vague knowledge of current news events [who is the Premier of Ontario?]. She could not recite months in the correct order. Her phonemic verbal fluency [name as many words as you can beginning with ‘S’] was normal but was below expectation for lexical items (name as many animals as you can).

Her performance on a word list recall measure [repeat as many words as you can from the word list I just read to you] suggested that she did not have a primary memory disorder. There was mild hesitancy to her spontaneous (conversational) speech, but no true word- finding pauses. She did well on confrontation naming [what is the name of the object in this picture?], showing only mild hesitation on naming of object parts. Only a single phonemic paraphasia [pronouncing ‘shoulen’ for ‘shoulder’] was noted. Her language comprehension was preserved (oral and written).

Reading was slow but accurate, including reading numbers. Writing was very poor. She had severe spelling difficulties, even for simple words, including regular (e.g. ‘buy’) and irregular (‘bought’) forms. When asked to solve arithmetic problems she said that 8 + 4 was 11 and could not calculate 4 X 12. When tested, she found it difficult to verbally identify which of her fingers was tapped by the examiner.

She also had difficulty moving specific fingers to command, but was able to move the correct finger in response to a tap. On her way to be scanned she received detailed instructions on how to get to radiology (which included two right and one left turn), but she kept taking the wrong turns, something her husband describes as typical of her lately. She had difficulties in target scanning [find a particular symbol out of an array of many different symbols]. Clock drawing showed minimal misplacement of numbers and she could not properly copy a cube. Because of her relatively young age and unusual presentation, an extensive workup was performed.

A variety of laboratory tests were unremarkable. A brain magnetic resonance imaging (MRI) scan showed moderate atrophic changes. Single-photon, emission computed tomography (SPECT: a measures of blood flow and brain activity) showed reductions in regions of the temporal-parietal junction, with greater reductions observed in the right than the left hemisphere.

Paper for above instructions

Clinical Case Analysis of Patient C.L.

Introduction

In the case of C.L., a 55-year-old right-handed woman experiencing significant declines in cognitive functioning, a systematic evaluation of her neurological symptoms reveals crucial insights into the underlying neuropsychological conditions. This analysis will interpret the signs and symptoms that C.L. presents, identify potential syndromes, localize brain damage, and suggest cognitive domains affected. Additionally, possible diagnostic considerations, alongside evidence-based articles, will be discussed.

Signs and Symptoms

C.L. exhibits a number of cognitive deficits primarily associated with language and numerical processing. Key findings include:
1. Writing Difficulties: Her inability to write coherently can indicate agraphia, a disorder affecting the production of written language.
2. Spelling Deficits: Severe spelling difficulties, even with simple words, could indicate surface dyslexia or phonological dyslexia (Snowling, 2000).
3. Arithmetic Impairments: Difficulty with basic arithmetic suggests possible acalculia, often linked to left parietal lobe dysfunction (Dehaene & Cohen, 1995).
4. Language Processing: While her language comprehension remains intact, her slow reading and phonemic paraphasia point towards a specific type of dyslexia or aphasia. The ability to name objects with slight hesitance implies mild expressive language dysfunction.
5. Memory Lapses: The occasional lapses of memory might not point to a primary memory disorder, suggesting possible executive function impacts instead.
6. Spatial Navigation Issues: Inability to follow detailed navigation instructions reveals deficits in visuospatial skills.
Overall, the combination of these symptoms suggests that C.L. may be experiencing a syndrome associated with progressive language-related disorders, such as Primary Progressive Aphasia (PPA).

Affected Cognitive Domains and Brain Damage Localization

Based on C.L.'s clinical presentation and the results from neurological examination alongside neuroimaging findings, we can delineate the impacted cognitive domains:
1. Language Abilities: Significant difficulties in writing, spelling, and calculation indicate deficits in the language processing regions of the brain, particularly Broca’s area (left inferior frontal gyrus) and Wernicke’s area (left superior temporal gyrus) (Mesulam, 2003).
2. Mathematical Processing: The left angular gyrus is critical for numerical cognition, and observed acalculia suggests dysfunction in this area (Dehaene, 2011).
3. Visuospatial Skills: The right parietal lobe, noted in the SPECT scan, is essential for spatial awareness. Navigation difficulties indicate impaired functions in this region (Heilman & Valenstein, 2003).
Moreover, the observed mild atrophy in the right temporal-parietal junction further emphasizes implications for integrative cognitive functions encompassing language and visual-spatial reasoning (Cavanna & Trimble, 2006).

Additional Clinically Relevant Data

To achieve a precise diagnosis and to further understand C.L.'s cognitive decline, I would propose the following additional evaluations:
1. Extended Neuropsychological Testing: A comprehensive battery of tests focusing on executive function, attention, and working memory would assist in mapping specific cognitive deficits.
2. Additional Neuroimaging: Functional MRI (fMRI) could elucidate areas of active brain function during language tasks, complementing the SPECT data.
3. Detailed Family History and Neuropsychological Reports: Collecting this data could uncover hereditary patterns that may link to emerging neurodegenerative conditions.

Differential Diagnoses

Based on C.L.’s presentation, we should consider several potential diagnoses:
1. Aphasia due to a Stroke: Though most strokes produce sudden onset deficits, given the gradual decline, this is less likely.
2. Alzheimer's Disease: Generally presents with memory deficits, though it could contribute to language and executive function impairments.
3. Primary Progressive Aphasia (PPA): Given the gradual onset of language impairment, PPA is a strong candidate, particularly the nonfluent variant (Gorno-Tempini et al., 2011).

Most Likely Diagnosis

Considering C.L.'s symptomatology—especially her significant language and numerical deficits, coupled with the preservation of daily living skills and gradual onset—the most likely diagnosis is Primary Progressive Aphasia (PPA), nonfluent variant. This assessment aligns with her SPECT results, indicating right hemisphere involvement, which often correlates with the cognitive-linguistic profile seen in PPA (Kasai et al., 2015).

Conclusion

The evaluation of C.L.'s cognitive and neurological symptoms suggests significant involvement of language processing and perhaps extended disruptions in computation and spatial navigation. Further neuropsychological testing and advanced neuroimaging are warranted to bolster diagnostic clarity. Primary Progressive Aphasia stands out as the most probable diagnosis, with implications for her functional decline and necessitating support in occupational and daily settings.

References

1. Cavanna, A. E., & Trimble, M. R. (2006). The precuneus: a review of its functional anatomy and behavioral correlates. Brain, 129(3), 564-583.
2. Dehaene, S. (2011). The number sense: How the mind creates mathematics. Oxford University Press.
3. Dehaene, S., & Cohen, L. (1995). Towards an anatomical and functional model of number processing. Mathematics and the Brain, 63(8), 170-183.
4. Gorno-Tempini, M. L., et al. (2011). Classification of primary progressive aphasia and its variants. Neurology, 76(11), 1006-1014.
5. Heilman, K. M., & Valenstein, E. (2003). Clinical neuropsychology. Oxford University Press.
6. Kasai, T., et al. (2015). The functional neuroanatomy of language: what functional neuroimaging can tell us about language and its disorders. Language, Cognition and Neuroscience, 30(4), 360-367.
7. Mesulam, M. M. (2003). Primary progressive aphasia. Annals of Neurology, 53(2), 168-176.
8. Snowling, M. J. (2000). Dyslexia. Blackwell Publishing.
9. Papagno, C., & Pisoni, A. (2006). Phonological and lexical access in working memory for words and numbers: The role of the left inferior frontal cortex. Neuropsychology, 20(4), 464-474.
10. Tranel, D., & Damasio, A. R. (1993). Knowledge of grammar in the absence of knowledge of words: Impairments of sentence comprehension in patients with chronic aphasia. Cognitive Neuropsychology, 10(4), 379-404.