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Neuropsychology

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1. Do neuropsychological dissociations support stronger theoretical inferences than neuropsychological associations? 2. Is the study of single patients more informative than the study of patient groups? 3. What is a stroke and what are the main risk factors? 4. What do brain lesion studies te...

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  • 18 januari 2021
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SP611 Short Answer Questions

1. Do neuropsychological dissociations support stronger theoretical inferences than
neuropsychological associations?
In neuropsychology, there are various methods in which inferences can be drawn about how
cognition is structured. Fundamentally, dissociations support stronger theoretical inferences than
associations due to the nature of allowing a direct method to draw infer valid inferences regarding the
structure of cognitive systems. Through examining the performance of brain-damaged patients
compared to healthy-brain patients, inferences can be made about the ways in which the brain-
damaged patient has been affected by the brain lesion. For example, through dissociations, the
relationship between perceptual categories and explicit categorisation can be considered in order to
explain specific domains in language impairment [1], whereas associations lack such a breadth of
specificity. However, through the utilisation of neuroimaging techniques, associations can be
inferred, despite the failure to capture direct evidence for brain areas associated with cognitive
functions. In light of dissociations, a double dissociation can be indicated in brain-lesion patients,
leading to a conclusive demonstration of two separate functions and the localisation of these
functions in different areas of the brain. As a case in point, separate systems have been established in
face recognition [2], as well as the various stages involved in object recognition [3], due to the
contribution of dissociations. Overall, it can be gathered that dissociations have stronger theoretical
support than associations, as ultimately, associations can be misleading within neuropsychological
research.

2. Is the study of single patients more informative than the study of patient groups?
The widespread utilisation of single-patient studies (studying individual patients) has contributed
towards our understanding of structure and functions of the human brain. The intensive analysis of
the individual facilitates knowledge on the development of the phenomena i.e. rare disorders, as well
as effective treatment [4]. Fundamentally, single-patient studies have the capacity to confirm a
prediction from cognitive theory that may not have been advocated before [5], thus various hypotheses
can be derived; however, it can be disputed that only the general hypothesis can infer a valid
explanation and that the rest is uncontrollable, therefore disreputable. Other common issues in
regards to single-patient studies derive from researcher subjectivity, construct validity, and
specifically, external validity or generalisability [4], due to the imperceptible abnormalities of the
individual. Another approach used in scientific research is the study of groups (studying a group of
patients). Studies show that group studies are a valid and informative methodology [6][7], and as
opposed to single-patient studies, establish prominent generalisability; therefore the results are more
representative. In group studies, pooled data from various patients are analysed resulting in high
statistical power, however, group studies fail to capture the representative performance of the patient,
e.g. lesions responsible for cognitive deficits, as individuals’ cognitive systems differ. Both single
and group studies contribute significantly towards scientific research; however, it is entirely
dependent on the nature of the investigation being considered. Ultimately, the multiple single-case
approach is appropriate in scientific research as it yields more robust results, obtains high statistical
power and replicability.

3. What is a stroke and what are the main risk factors?
Stroke, also identified as cerebrovascular disease, is a heterogeneous condition and a global
health problem in which the flow of oxygen-rich blood to an area of the brain is blocked; profoundly,

, it is the fourth single leading cause of death in the UK, accounting for over an estimated 5.7 million
deaths worldwide [8], which could reach 23 million by 2030 [9]. Broadly, strokes are classified as
either haemorrhagic or ischemic: haemorrhagic strokes, accounting for 15% of strokes [10], occur as a
result of a rupture to a blood vessel inside or around the brain flooding the surrounding tissue with
blood. Alternatively, ischaemic stroke, accounting for 85% of cases [8], occurs when blood vessels to
the brain become obstructed, due to the process of atherosclerosis (an accumulation of fatty deposits
inside the vessels); this initiates a blood clot which disrupts the blood supply to the brain. Both forms
of stroke deprive the brain tissue of oxygen, leading to cellular death. Recently, the World Health
Organization (WHO) [11] reported that an estimated 6.7 million people died from stroke in 2015, with
80% of deaths occurring in low and middle-income countries. While there are unmodifiable risk
factors associated with strokes such as genetics, gender, age, race, and ethnicity, there are several risk
factors that can be modified including diabetes, smoking, alcohol abuse, atrial fibrillation (AFib),
hypertension and cardiovascular disease[12]. More recently, however, it has been shown that pollution,
infection, inflammatory disorders and cardiac atrial disorders identify as risk factors for stroke [13].

4. What do brain lesion studies tell us about cognition that functional brain imaging studies do
not?
Brain lesion studies have made major contributions towards our knowledge and understanding of
the anatomical organization of the human brain. They are the removal of part of the brain and thus a
comparison is made between performance before and after the lesion and consequent deficits are
noted. In essence, lesions illustrate “dissociations in cognition we could have never hypothesized” [14].
By removing a part/parts of the brain, one can see what roles those play in the creation and control of
thought. For example, early research indicates that removal of the amygdala bilaterally can cause
Klüver-Bucy syndrome, eliciting neuro-behavioral disturbances which can dramatically change
cognition in the afflicted individuals. First described in 1937, Klüver & Bucy conducted a study
where they removed rhesus monkeys’ temporal lobes. The monkeys showed various permanent
impairments such as the inability to recognize objects (“psychic blindness”), hypersexuality,
hypermetamorphosis, hyperorality and emotional changes [15]. An additional contribution of brain
lesion studies includes the discovery of Chronic Traumatic Encephalopathy (CTE) through autopsy;
symptoms of CTE include behavioural and mood problems, associated with cognition. Functional
imaging techniques measure blood flow and metabolism [16] to identify brain areas responsible for
distinct functions. For example, fMRI, a powerful tool used to show levels of oxygenation to
different areas of a brain during different activities, can show what areas are used in different
functions, but not the before and after of cognitive abnormalities; whereas a lesion study can indicate
functions of the area, and what its loss caused, through its removal.

5. What problems stand in the way of inferring normal function from the study of brain-
damaged patients?
Studies on brain-damaged patients have informed our understanding of the regions of the brain
correlated with certain functions, however, there are several limitations associated with this method.
For example, when attempting to inferring normal function from brain-damaged patients, it is
difficult to prevent damage to other areas of the brain; this is problematic as the brain is a complex
system mediated by signals and various interconnected cerebral and mental processes e.g. cognitive
functions [17], therefore, brain damage can influence neighbouring regions with distinct functions.
Specifically, when attempting to infer normal function from brain-damaged patients, this is a major
limitation as the established impairment cannot be explained if there is secondary damage elicited

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