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A thesis submitted in partial fulfilment of - Queen Margaret University

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<strong>in</strong>herently more complex neuronal system, environmental studies reveal the<br />

importance <strong>of</strong> a stimulat<strong>in</strong>g environment for shap<strong>in</strong>g cortical development.<br />

Robertson (1999) suggests that education nurtures a better-connected network<br />

<strong>of</strong> neurones and as a result the patterns <strong>of</strong> skills and memories are less easily<br />

destroyed. He stated that one <strong>of</strong> the great benefits <strong>of</strong> education is that you<br />

actually learn how to learn and this <strong>in</strong>volves skills <strong>of</strong> th<strong>in</strong>k<strong>in</strong>g, remember<strong>in</strong>g,<br />

plann<strong>in</strong>g and problem solv<strong>in</strong>g. Due to this education process a more densely<br />

connected network <strong>of</strong> neurones evolves from the <strong>in</strong>creased number <strong>of</strong> bra<strong>in</strong><br />

cells that have become wired together through fir<strong>in</strong>g together. It is therefore<br />

more likely that skills and memories woven <strong>in</strong>to these wired connections can be<br />

recovered follow<strong>in</strong>g damage. De Riesthal and Wertz (2004) assert that years <strong>of</strong><br />

education as a prognostic factor <strong>in</strong> recovery from aphasia is debatable. Smith<br />

(1971) reports that a person with more years’ education tends to make more<br />

improvement follow<strong>in</strong>g aphasia therapy. Tompk<strong>in</strong>s (1990) however observed<br />

that variables such as education are poor predictors <strong>of</strong> improvement <strong>in</strong> aphasia.<br />

De Riesthal and Wertz (2004) also noted that the number <strong>of</strong> year’s education<br />

was not significantly correlated with recovery.<br />

2.6.1.3 Cognitive Reserve<br />

The variability <strong>in</strong> both the severity and duration <strong>of</strong> aphasia, and the successful<br />

recovery <strong>of</strong> language follow<strong>in</strong>g cortical damage has been discussed (see section<br />

2.4.1). Variation is also observed <strong>in</strong> the severity <strong>of</strong> cognitive function<strong>in</strong>g despite<br />

<strong>in</strong>dividuals present<strong>in</strong>g with similar neurological damage. This phenomenon is<br />

<strong>of</strong>ten expla<strong>in</strong>ed with the hypothetical concept <strong>of</strong> ‘cognitive reserve’ (Staff,<br />

Murray, Deary and Whalley, 2004; Whalley, Deary, Appleton and Starr, 2004;<br />

Kesler, Adams, Blasey and Bigler, 2003). This hypo<strong>thesis</strong> suggests passive and<br />

active factors which are thought to <strong>in</strong>fluence the capacity <strong>of</strong> the bra<strong>in</strong> to<br />

withstand cognitive decl<strong>in</strong>e/ damage to a predeterm<strong>in</strong>ed threshold after which<br />

cognitive deficits appear (Staff et al., 2004). The size <strong>of</strong> a person’s bra<strong>in</strong> is one<br />

such passive factor hypo<strong>thesis</strong>ed to <strong>in</strong>fluence cerebral reserve, suggest<strong>in</strong>g that<br />

35

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