نام پریشی در وضعیت افسردگی ماژور
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|29947||1998||12 صفحه PDF||سفارش دهید||محاسبه نشده|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Psychiatry Research, Volume 77, Issue 3, 27 February 1998, Pages 197–208
Anomia, or word finding difficulty, is a frequent clinical symptom of the depressive state. This study investigates naming and lexicalization processes (or word production processes) in 11 depressive patients (major depressive state), through a picture naming task of 53 images corresponding to low frequency words. Depressives showed significantly more anomia and made more naming errors (semantically related substitution words) than control subjects. Tip-of-the tongue (TOT) states, which correspond to an impairment at a later stage of phonological encoding with partial activation of phonological shape, remained rare in depressives despite the increase of lexicalization difficulties observed. Anomia observed in depressives could thus be related to an impairment at the early stage of lexicalization or word production processes (pre-phonological item selection and access, or storage of the semantic lexical item in Working Memory for further phonological encoding), without lexical–semantic disorganization. We discuss the relationship between such an elementary speech production disorder and cognitive impairments demonstrated in the depressive state (deficit of effortful and attentional processes, impairment in activation or initiation of cognitive processes and responses). © 1998 Elsevier Science Ireland Ltd.
A number of recent studies have demonstrated impairments in memory, attention, language and information encoding in depression (Willner, 1984 and Austin et al., 1992). This study deals with lexical access impairment, or anomia, in subjects suffering from major depressive state. Anomia, or word finding difficulty, is a frequent complaint in depression, but is often confused with a memory impairment. On the other hand, lexical access difficulty, or anomia, is one of the most frequent speech production disorders, either in neurological pathology or functional impairments of normal subjects (Geschwind, 1967). Anomia is a process in which a speaker is unable to produce specifically sought words either during normal conversation or during naming tasks. More rarely it is an isolated symptom in aphasia (pure anomia or `amnesic aphasia', Benson, 1979); however, it is more often encountered in patients with various forms of aphasia due to different lesions and exhibiting other language difficulties. Isolated anomia is also one of the symptoms of Alzheimer dementia that occurs the earliest and that is the most frequently observed. Normal people, however, also experience anomia with its characteristic, peculiar feeling of having a word on `the tip of the tongue' or TOT state (Rochford and Williams, 1965Brown and McNeill, 1966Rubin, 1975Jones and Langford, 1987Freedman and Landauer, 1987Levelt, 1993). This state was defined by Brown and McNeill (1966), who showed that normal subjects could demonstrate anomia when presented with the definitions of rare words in a word finding test. In TOT state subjects fail to generate target words, but nevertheless `know' the word they are trying to find and show some knowledge of its first or last letter, initial sound, the word's length or number of syllables, its gender. They often produce sound-related errors, phonological paraphasia or `substitution words' which share formal characteristics with the missing word. These different lexicalization impairments in aphasia or normal subjects do not result from a single mechanism, such as a `mnesic' deficit (Kay and Ellis, 1987 and Levelt, 1993). Different forms of anomia have been identified which result from impairments at different stages of a sequential word production process (Kempen and Huijbers, 1983, Seidenberg and McClelland, 1989, Levelt et al., 1991 and Levelt, 1993). After the perceptual stage of object identification (categorization), word production (or `lexicalization') can be decomposed into at least two successive stages of lexical retrieval (Levelt, 1993). The first stage involves semantic activation of a set of lexical candidates in the long-term memory and then the selection of an appropriate `abstract lexical representation' or semantic pre-phonological item (L1 item or `Lemma', Kempen and Huijbers, 1983 and Levelt, 1993) which consists of the word's conceptual specifications. These procedures deposit their results in the Working Memory for further processing. The second stage involves phonological encoding of the selected L1 item and access to the morphological and metrical composition of the word, followed by the word's segmental composition and finally its phonetic or articulatory plan or program, the `phonological shape' (L2 item), which is eventually completed by the real articulation of the word. Phonological encoding involves working memory. These successive stages have also been defined as positional and functional levels of retrieval, respectively (Garret, 1982). Dysfunctions at either of these two levels of retrieval have consequences which can be distinguished by the type of error made by subjects in the `substitution words' or paraphasia produced (Fromkin, 1973, Butterworth, 1981, Garret, 1982 and Howard and Orchard-Lisle, 1984). In some cases of aphasia or neurological anomia, errors or substitute words are semantically related to the target word (Rinnert and Whitaker, 1973 and Howard and Orchard-Lisle, 1984). This impairment is sometimes associated with low or severe comprehension disorders (Kay and Ellis, 1987). In the most severe cases of aphasia (with comprehension disorders), anomia is qualitatively similar to that of demented patients (Gainotti et al., 1988). Semantic errors are less related to the target words and reveal a disorganisation of the underlying semantic lexicon in the long-term memory. This suggests an impairment of the first semantic stage of retrieval, accessing and selecting the abstract pre-phonological L1 item. There is no evidence of TOT state in these cases. On the other hand, in most aphasic patients as well as in normal subjects, often with TOT, errors (substitution words) show mostly phonological or formal relationships with the target word (phonological paraphasias) (Kohn and Goodglass, 1985, Gainotti et al., 1988 and Miceli et al., 1991). There are no associated comprehension disorders. Such lexicalization difficulties are often characterized by a TOT state, qualitatively similar in either normal or aphasic subjects (Goodglass et al., 1976 and Le Dorze and Nespoulous, 1989). Thus, although unable to utter the target word, the subject demonstrates a partial knowledge of the structure of the word. The lexicalization disorder is therefore clearly related to the second stage of lexicalization: the phonological encoding of the previously selected L1 item (Levelt, 1993). Errors or substitution of one word for the sought-after target word accompanying the failure of the lexicalization or naming processes is accounted for by an erroneous selection at the first or second stage of lexicalization. Two clinical forms of anomia can thus be distinguished as being either semantically or phonologically based forms of anomia (Kempen and Huijbers, 1983 and Kay and Ellis, 1987). Semantically based anomia is due to an impairment in accessing the abstract pre-phonological L1 item in the semantic lexicon. It is observed in aphasia and dementia and gives rise to semantically based word exchanges (such as `toe' for `finger'), or unclassifiable errors. There is no TOT in these cases because there is no access to syntaxic or phonological shape (Levelt, 1993). Relationships between the target and substitution words can often be even weaker in demented patients. On the other hand, phonologically based anomia (in aphasic or normal subjects) are due to an impairment of phonological encoding (L2 level) of the selected L1 item in the working memory and give rise to sound related or phonological errors (e.g. `mushroom' for `mustache'). In these cases a typical TOT state with knowledge of the missing word (length, number of syllables, first and last letters) and production of phonologically similar substitution words (also including some meaning-related errors) can occur. There is a partial activation of the word-form representation (at the L2 level). Such phonologically based examples of anomia represent an elementary perturbation of speech production and appear qualitatively similar in moderate aphasia (without comprehension disorders) and in normal subjects with functional TOT (Geschwind, 1967, Jones and Langford, 1987, Kay and Ellis, 1987 and Le Dorze and Nespoulous, 1989). Cognitive deficits in depression are various and correlated to the severity of the clinical state (Braff and Beck, 1974, Weingartner et al., 1981, Willner, 1984, Clark et al., 1985, Roy Byrne et al., 1986, Watts et al., 1988, Golinkof and Sweeney, 1989 and Austin et al., 1992). Depressives demonstrate deficits in attention and concentration (Cohen et al., 1982 and Roy Byrne et al., 1986), explicit long-term and short-term memory (Working Memory) (Sternberg and Jarvik, 1976, Dannenbaum et al., 1988, Watts et al., 1990 and Hertel and Rude, 1991), and semantic encoding (Weingartner et al., 1981). They also show a general retardation of responses (Widlöcher, 1983 and Austin et al., 1992). The cognitive performances are more altered when the severity of the depression is greater, when the tasks require sustained effort or attention and when the information is more complex. These cognitive impairments are sometimes difficult to distinguish from those of sub-cortical dementia (depressive pseudo-dementia, Caine, 1981 and Lachner and Engel, 1994). These cognitive deficits have been linked by several authors to a reversible overall alteration of the depressive subject's performances requiring effort and allocation of attention (controlled or effortful processes, Weingartner et al., 1981, Cohen et al., 1982, Roy Byrne et al., 1986 and Watts et al., 1988), like controlled attentional processes and working memory. In contrast, tasks relying on automatic processes without cost (which do not involve limited attention capacity), like implicit memory and repetition priming, are preserved (Danion et al., 1991). This distinguishes cognitive depressive deficits from demential disorders (Tancer et al., 1990 and Lachner and Engel, 1994). Semantic encoding of verbal information and organization of information by effortful processes involving attention, use of attentional strategies and cognitive cost are the most impaired in depression (Weingartner et al., 1981 and Watts et al., 1990). Some authors do, however, report that complex tasks are sometimes less impaired than simple and less effortful tasks (Hart and Kwentus, 1987 and Golinkof and Sweeney, 1989). The results thus seem to be task-dependent. According to another hypothesis, cognitive deficits in depression rely on depressive retardation, an elementary cognitive impairment of action which involves motor action, thought, memory and language and which affects all activities (Widlöcher, 1983). Psychomotor retardation may be an alteration of the early stages of response: preparation, initiation and activation of action and decision making. Retardation consists of longer pauses between actions (Greden and Carroll, 1981 and Widlöcher, 1983). This may explain why the performances of depressed subjects are the most altered, as the tasks are complex: slower information processing may cause an overload. The function of attention in the preparation of action makes it possible to relate the hypothesis of depressive psychomotor retardation to impairments of attention and effortful processes. With regard to language, there is an overall retardation of speech flow. This retardation consists only of longer speech pauses than in control subjects (Szabadi et al., 1976, Greden and Carroll, 1981 and Hoffman et al., 1985). On the other hand, structural linguistic analysis shows that there is no alteration at the lexical or syntactic levels (Andreasen and Pfohl, 1976). Depressives often complain of difficulties in `finding their words'. Most commonly, however, it has been suggested that these difficulties may be related to explicit memory disorders. Cognitive psycholinguistic data about word production help us to define this impairment more precisely. In depression, anomia may be an early cognitive deficit, correlated to the severity of the general depressive cognitive impairment, allowing for an evaluation of this impairment. Lexicalization or word production is a fragile process that requires the automatic activation of an intact lexical–semantic network in the long-term memory and then attentional resources for each level of further semantic (L1) and formal (L2) processing. Anomia is easily the first sign of an aphasia through lesions to language zones, as well as being one of the first signs of dementia. Anomia with or without TOT is induced in normal subjects by attentional impairment (Rochford and Williams, 1965), definition of rare words, or with `blocking words' phonologically related to the target word (causing phonological interferences) (Brown and McNeill, 1966, Rubin, 1975 and Jones and Langford, 1987). Selection of an L1 prephonological item and then its phonological encoding (L2 level) relies on attentional or controlled processing, in a Working Memory, of information stored in the long-term memory and automatically accessed. These successive attentional stages of processing (selection of an L1 item and its phonological encoding) occur in Working Memory, which contains all the information accessible to the speaker at each stage of speech production (Levelt, 1993). Impairments in Working Memory in depressives could then be correlated to word production deficits at the first or second level. Our aim was to demonstrate anomia (or lexicalization impairment) in depressed patients with major depressive state and to determine whether word production difficulties occurred mostly at the semantic (L1, first stage of semantic pre-phonological item selection, with TOT state) or phonological (L2, second stage of phonological encoding, without TOT state) level. We compared 11 major depressives and normal control subjects in a naming task, specifically designed in order to induce anomia in non-aphasic control subjects. Identification of the mechanism of anomia relied on the analysis of errors (semantically or phonologically based) and evidence of TOT states, which reflect a partial activation of the word-form representation in Working Memory and suggest an impairment of phonological encoding (L2 level).
نتیجه گیری انگلیسی
The only disorder observed in depressive subjects in this task was one of word production, and no recognition or identification disorder (agnosia) or impairment due to lack of vocabulary was observed in either group. Control subjects had 17 occurrences of anomia (namely impairment, with or without TOT) (mean rate=1.54; S.D.=1.75) (Table 3Table 4) and produced eight errors (mean rate=0.72; S.D.=0.9). Table 3. Naming impairments, tip-of-the-tongue (TOT) state, and errors in depressive and control subjects Subject 1 2 3 4 5 6 7 8 9 10 11 Mean S.D. Control subjects Naming impairments 3 0 1 4 0 2 5 0 1 0 1 1.54 1.75 Semantic errors 1 0 0 1 0 0 1 0 1 0 0 0.36 0.5 Phonological errors 1 0 0 1 0 0 1 0 0 0 0 0.27 0.46 TOT state 1 0 0 2 0 1 2 0 0 0 1 0.63 0.80 Depressives Naming impairments 3 5 5 9 7 6 6 5 7 6 6 5.90 1.51 Semantic errors 2 2 3 4 3 2 3 2 4 2 2 2.63 0.80 Phonological errors 0 0 0 1 0 1 0 0 1 0 0 0.27 0.46 TOT state 0 1 0 2 0 1 0 0 2 0 0 0.54 0.82 Table options Table 4. Naming impairments, TOTa and errors in depressive and control groups Anomia Phonologial Semantic Mixed TOTa errors errors errors Depressives 65 3 29 5 6 Controls 17 3 4 1 7 a Tip of the tongue state. Table options Only four control subjects found no difficulty in naming all the objects. The 11 words that provoked retrieval failure were least frequently occurring words. Eight errors (lexical substitution) were produced. Four of these had a semantic relationship with the target word (e.g. staple for paper-clip); three words had a phonological relationship [e.g. plumeau (duster)/blaireau (shaving brush)]; and one word had both a phonological and a semantic relationship [`mixed' error: boulier (abacus)/sablier (hourglass)]. Furthermore, in the 17 cases of anomia, seven cases of anomia with associated TOT state were demonstrated. In four cases of TOT, subjects knew the number of syllables of the target word, and in three other cases, they knew only the first letter. No other information was available concerning word structure. Depressives showed 65 occurrences of anomia (naming impairment) (mean rate=5.9; S.D.=1.51) (Table 3 and Table 4) and produced 41 errors (mean rate=3.72; S.D.=0.78). None of the subjects displayed fewer than three naming impairments. Depressed patients demonstrated significantly more anomia than control subjects. One-way ANOVA on group (control/depressive) revealed a significant group effect (F1,20=39.1, P<0.0001). Twenty-seven words induced anomia. These included the 11 words that caused anomia among the control subjects and 16 others (low or medium frequency words). Forty-one errors or substitution words occurred: 29 bore only a semantic relationship, e.g. fossile (fossil/sediment), three had only a phonological relationship [rapporteur (protractor)/répertoire (address book)] and five demonstrated both phonological and semantic relationships with the missing word [e.g. fossile (fossil)/fosse (pit)]. Four errors were unclassifiable. On the 65 anomia cases, six cases of anomia with associated TOT were demonstrated. Subjects knew the first letter of the missing word in five cases and the number of syllables in six cases. These observations were confirmed in a Group×Error Type ANOVA. Increase of total naming errors in the depressive group was confirmed by a significant group effect (F1,80=58.64, P<0.0001). The effect for error type was also reliable (F3,80=53.22, P<0.0001) as was the Group×Type interaction (F3,80=24.64, P<0.0001). Post-hoc analysis (Scheffé test) revealed that the depressed group demonstrated significantly more naming impairments and made significantly more semantic errors than the control group (P<0.05). Within the depressed group, the number of semantic errors was significantly greater than phonological errors and than TOT states (P<0.05). We finally compared the two groups with respect to the number of naming impairments vs. TOT states in a two-way ANOVA on Group×Type (naming, TOT state). The significant interaction (F1,40=32.6, P<0.0001) corresponds to the observation that while the depressed group made approximately four times more naming errors than the control group, the two groups were almost equivalent in the number of TOT state errors.