Narrative and procedural discourse in temporal lobe epilepsy

Abstract

It is well established that some individuals with temporal lobe epilepsy (TLE) demonstrate language deficits at the single word level. However, discourse production rarely has been examined quantitatively within this group. This study compared adult TLE patients with an early seizure onset (< or = age 14 years, n = 27) to a control group (n = 28) on narrative and procedural discourse tasks. As a group, the TLE patients performed normally on the procedural discourse task, but differed significantly from the controls on several narrative discourse variables. At the individual level, 30% of the TLE patients versus 4% of the controls demonstrated impaired discourse ability (p and 0.01). Within this early onset TLE group, discourse performance was not associated with demographic or seizure history variables. Considering the cognitive domain, discourse performance correlated significantly with working memory. In summary, mild discourse dysfunction was present in a significant minority of early onset TLE patients, but this deficit was not closely associated with other language measures. Discourse ability and its neuropsychological, neuroanatomical and conversational speech correlates deserve further study in TLE patients.

Functional connectivity networks are disrupted in left temporal lobe epilepsy

“…23 Experimental studies have shown that TLE is associated with subtle language disturbances at a discourse level, including longer and more variable pause durations, 44 failure to produce increasingly compact forms of a narrative with repetition, 43 and reduced speech rate, inadequate descriptive detail, and excessive mistakes and repairs. 47 Macrolinguistic dysfunctions of this type have been linked to capacity limitations affecting the multilevel planning of language output. 48,49 This, in turn, implies poor coordination between the neural apparatus of planning, working memory, and selective attention (such as dorsolateral prefrontal cortex, anterior cingulate region) and classic language structures.…”

Hippocampal amnesia disrupts the flexible use of procedural discourse in social interaction

“…Given the prevalence of procedural discourse in everyday communication, it is not surprising that it has been a frequently examined discourse genre in both clinical assessment and research of discourse-level performance across a variety of populations including healthy older adults , individuals with traumatic brain injury (TBI) (Hartley & Jensen, 1991;Snow, Douglas, & Ponsford, 1997), aphasia (Ulatowska, Doyel, Stern, Haynes, & North, 1983); Alzheimer's disease (AD) (Ripich, Carpenter, & Ziol, 1997), and temporal lobe epilepsy (TLE) (Bell et al, 2003). The underlying assumption supporting such widespread use of clinical and research tasks designed to tap into procedural and other discourse forms (e.g., narrative, picture description) is that each discourse task places unique linguistic and other cognitive (e.g., memory) demands on the communicator (Shadden, Burnette, Eikenberry, & DiBrezzo, 1991;Ulatowska & Chapman, 1989).…”

“…Shadden et al (1991) found that in healthy participants procedural discourse samples were longer and syntactically more complex than narrative or picture description samples. However, attempts to correlate discourse performance post hoc with indices of cognitive ability have yielded modest and variable effects (e.g., Bell et al, 2003;Hartley & Jensen, 1991;Ulatowska et al, 1983) and few attempts have been made to offer a theoretical perspective or description of how various cognitive domains would support distinct aspects of discourse performance across tasks.…”

Interictal language functions in temporal lobe epilepsy

“…Three studies were interested in discourse abilities in TLE and two of them found that the patients performed significantly worse in a narrative discourse task that required description of the sequence of events. [10][11][12] Reasons for linguistic deficits found in patients with TLE are not completely clear, and different hypotheses can be formulated. First, multiple regions of the brain, which may also include the left perisylvian areas critical for language, may be subject to neuronal cell loss and deafferentiation in chronic TLE.…”

“…Furthermore, information about language comprehension, discourse production, repetition, and reading is sparse, and findings are divergent. [11][12][13][14] To our knowledge, to date there are no reports on spontaneous speech or writing abilities in TLE. Thus, studies have very rarely administered tests tapping different language domains in order to provide a linguistic profile of patients with TLE.…”