| Quality of Life After Stroke: Clinical, functional, psychosocial and cognitive correlates | ||
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Aphasia is a common consequence of stroke, the reported prevalence ranging up to one third of the patients in the acute phase (Kotila et al. 1984, Reinvang et al. 1984, Wade et al. 1986). Spontaneous recovery of aphasia is at its greatest during the first 3 months, but some improvement may take place even later on (Demeurisse et al. 1980, Kotila et al. 1984, Wade et al. 1986). The frequency of complete recovery varies from 21% to 50% (Kertesz & McCabe 1977, Pashek & Holland 1988, Pedersen et al. 1995). The initial severity of aphasia has been shown to be highly predictive of ultimate language function (Kertesz & McCabe1977, Pedersen et al. 1995), and a valid prognosis of aphasia can usually be made within the first month after stroke (Pedersen et al. 1995).
According to Western Aphasia Battery (Kertesz 1982) aphasia is classified as non-fluent aphasias, including global, Broca’s, isolation and transcortical motor aphasias, and as fluent aphasias, including Wernicke’s, transcortical sensory, conduction and anomic aphasias. It has been shown that different types of aphasia have distinctive recovery patterns (Kertesz 1984, Pashek & Holland 1988), but some contrary evidence is also available (Demeurisse et al. 1980, Lendrem & Lincoln 1985). Among the aphasia types global aphasia has the poorest prognosis, Broca’s aphasics often recovering towards anomic aphasia, and Wernicke’s aphasics tending to recover towards anomic or conduction aphasias. Anomic aphasia is a common endstage in the evolutionary process of both fluent and non-fluent aphasias. Both anomic aphasia and conduction aphasia have a favorable spontaneous recovery pattern (Kertesz 1984, Pashek & Holland 1988).
Although clinical experience has shown that communicative disorders may markedly contribute to the severity and persistence of depression, psychiatric evaluations of aphasic patients are scarce. Herrmann et al. (1993) concluded that “moderately and severely aphasic patients are an important subpopulation in investigations of PSD that must not be disregarded by exclusion for methodological reasons”.
In their prospective study of PSD Åström et al. (1993) found that aphasia was an important predictor of depression in the acute phase. The correlation between aphasia and depression lasted for 3 months, but no longer. In another study (Robinson & Benson 1981) almost half of the hospitalized aphasic patients were depressive, but the sample was highly selective. Among long-term survivors of stroke no relationship between aphasia and depression could be found (Oder et al. 1991, Sharpe et al. 1994).
The non-fluency of aphasia has been shown to be related to frequency and severity of PSD by some investigators (Robinson & Benson 1981, Herrmann et al. 1993), but not all (Starkstein & Robinson 1988). This relationship is thought to be caused by the better awareness of their impairments of patients with non-fluent aphasia.
The etiology of depression in post-stroke aphasic patients seems to be multi-factorial. Psychosocial and coping factors associated with aphasia are relevant for the development of reactive depression (Herrmann et al. 1993, Åström et al. 1993). On the other hand, aphasia and depression can be viewed as coincident consequences of stroke resulting from an underlying brain lesion (Starkstein & Robinson 1988, Herrmann et al. 1993).
Most studies have found no evidence of an association between prevalence and recovery of aphasia and age (Reinvang 1984, Lendren & Lincoln 1985, Pedersen et al. 1995). In one study old age appeared to predict a poor prognosis for change in global aphasia (Pashek & Holland 1988). Sex has not been found to be a determinant of aphasia in stroke (Kertesz & McCabe 1977, Kertesz 1984, Pedersen et al. 1995).
Aphasia has been shown to be related to the severity of motor deficits and impairment in ADL during the first post-stroke months (Wade et al. 1986). The association may be due to the fact that patients with aphasia may have larger lesions, causing both more severe impairment in ADL and more language disturbance (Wade et al. 1986). In the presence of motor deficits the severity of aphasia in the subacute stage does not, however, influence the long-term outcome after cerebral infarction (Oder et al. 1988).
The difficulty of defining intelligence in aphasic patients hampers research design and the interpretation of results. Verbal tests of intelligence are clearly inappropriate in aphasia but the verbalization used to perform the nonverbal tests remains undetermined. (Kertesz 1977) The findings of the correlations between non-verbal cognitive impairment and type and severity of aphasia have been contradictory. In the study of Basso et al. (1981) the presence and severity of aphasia was definitely associated with low non-verbal test scores, but the type of aphasia was not. In another study, using the same test for measuring logical reasoning and visuospatial ability, the type of aphasia was a significant determinant of poor performance in the non-verbal test, but the severity of aphasia was not (Kertesz & McCabe 1975).