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Primary word-finding difficulty may occur as an isolated language disturbance or may occur as part of a more extensive cognitive or behavioural syndrome. Secondary word-finding difficulty occurs when a deficit within another cognitive domain interferes with the function of a more or less intact language system. For example, a patient in whom failure to name household objects on bedside testing is accompanied by a failure to locate or correctly use the same items may have a primary visual perceptual problem, patients who participate less in conversations may be deaf, while difficulty remembering the names of acquaintances or in delivering messages may indicate a more general problem with episodic memory.
It is also important to recognize the wide spectrum of normal variation in word-finding ability, and the potential effects of fatigue, anxiety or mood disorders. The evaluation of word-finding ability therefore requires both an objective assessment of performance, and an awareness of the wider context in which the problem has developed and its impact on the patient's daily life. Obtaining an accurate history of word-finding difficulty Table 1 depends on interviewing both the patient and an informant who knows the patient well.
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A complaint of word-finding difficulty must be interpreted in light of a patient's premorbid verbal skills. Information about bilingualism was English the first language, and if not, what level of competence was achieved? The family history may be relevant not only to the diagnosis in general but also to the interpretation of the word-finding problem in particular: Establishing the mode of onset and time course of the word-finding difficulty will assist in distinguishing acute processes for example, stroke, encephalitis, delirium , chronic processes with static or fluctuating deficits for example, head-injury or seizures and chronic processes with progressive deficits for example, a degenerative dementia.
The context in which the problem developed may be crucial. Whereas in acute disease processes, associated disturbances of alertness, perceptual and motor functions are often prominent or may dominate the clinical presentation ; in chronic disease processes, associated features may be subtle. However, the distinction between acute and chronic processes is not always clear. Patients who have sustained an acute event may present later with ongoing word-finding difficulty: Conversely, neurodegenerative disease can occasionally appear to present acutely following a particular event e.
This may be secondary to a superimposed acute confusional state or due to the fact that mild word-finding or cognitive difficulties had previously gone unnoticed: The history often provides clues to the nature of the word-finding difficulty and associated cognitive, behavioural or neurological features which can then be explored systematically during the examination. Systematic analysis of an extended sample of the patient's spontaneous propositional speech Table 2 is the single most valuable aspect of the examination.
Where little spontaneous conversation is offered, the patient can be asked to describe a scene in a photograph or drawing an example is shown in Fig. This is preferable to asking the patient to recount an event in their daily routine, as it allows speech to be evaluated independently of episodic memory and provides a standard with which to compare speech characteristics in different clinical situations. Examples of scene descriptions produced by patients with canonical speech disorders are presented in Table 3. Valuable information is often obtained from observing the patient's general behaviour and approach to the clinical interview.
The inert patient with a frontal dementia, who offers little speech at all and sits passively throughout the interview, makes a very different impression from the patient with PNFA, who is obviously frustrated by their difficulties and struggles to compensate with an excess of non-verbal gestures, and both contrast with the garrulous patient with semantic dementia SD , who produces a steady stream of circumlocutory speech. Materials for assessing speech at the bedside. Reproduced with permission of Professor EK Warrington. A A beach scene, illustrating one means of eliciting conversational speech see examples in Table 3.
B A passage for reading aloud see text. This is true for acute lesions Brust et al. Fluency describes the flow of speech output, but it is multidimensional: As these impairments tend to occur together, an individual patient's speech can often be reliably categorized as fluent or non-fluent; moreover, certain dimensions particular motor aspects such as rate and articulation make a relatively greater contribution to the impression of dysfluency.
However, the component processes are dissociable: In practice, an individual patient's word-finding difficulty is rarely confined to a single one of these categories, although in many cases one category will predominate. Furthermore, deficits in these true word-finding categories may overlap with a difficulty in the motor programming of speech: The ease of initiation of conversational propositional speech provides important information about the generation of verbal thought the ability to express thoughts in words.
This process involves the formulation of a plan for the verbal message Fig. Although patients with word-finding difficulty of all kinds may participate less in conversations as a non-specific result of reduced facility with language, a striking reduction in propositional speech is the hallmark of dynamic aphasia Luria and Tsvetkova, ; Costello and Warrington, ; Robinson et al.
Such patients have a selective deficit at the level of the generation of verbal thought: Sentence generation is dependent on context: Compared to this decreased spontaneous output, speech can be produced relatively normally in specific contexts, such as naming tasks, repetition or reading. A similar decrease in speech output occurs in many patients with frontal and subcortical deficits who exhibit a generalized inertia and slowing of thought. However in pure dynamic aphasia there is retained ability to generate novel non-verbal material such as song, suggesting that dynamic aphasia is a true language disorder and not simply a consequence of abulia Warren et al.
Some patients with impaired generation of verbal messages have defective rather than simply absent verbal output. Once a plan for a verbal message is generated, the message must be elaborated with specific content and function words. The sense of a spoken thought or message depends on its conceptual content. It is possible to convey the constituent concepts of a message even where the structure is disorganized or degraded, and the converse is also true.
The content of speech can be assessed at the level of individual words themselves, and the way they are combined to convey a more extended message in a sentence Fig. Impaired content at the level of individual words is evident as a deficient vocabulary—the patient may use approximate or imprecise expressions circumlocutions that substitute for a single word e. Such fluent but ultimately empty speech is characteristic of conditions in which there is damage to the verbal knowledge store, the paradigm for which is SD with focal degeneration of the left temporal lobe Warrington, , Snowden et al.
In this situation there is often evidence from the history and on further specific language tasks for impaired comprehension of single-word meaning. A more common scenario is difficulty retrieving words from storage despite evidence that comprehension of the meaning of words at least initially is well preserved: In this situation there may be prolonged word-finding pauses affecting both spontaneous discourse and naming.
Impairments of sentence-level content manifest as a lack of coherence in conveying the message—sentences may trail off unfinished, or tangential and context-inappropriate words or fragmentary phrases may be inserted, so that it is difficult to follow the patient's line of thought. Disordered speech of this kind is observed in acute brain syndromes, in which attentional and executive deficits may make organized or sustained verbal expression impossible Chedru and Geschwind, , and also in the intermediate and later stages of AD.
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Disorganized verbal output at the level of more complex narrative or discourse is a feature of the behavioural variant of frontotemporal lobar degeneration bvFTLD , in which executive dysfunction is typically prominent Ash et al. The structure of a verbal message can be considered at two levels: Such errors often first appear and remain more evident with polysyllabic words.
Agrammatism and phonological breakdown commonly occur together but relatively pure dissociations have been described in degenerative disease Caramazza et al. Agrammatism may be partly masked by other speech-production impairments, unless more detailed testing of the receptive aspects of sentence comprehension or written output is undertaken Bak et al. Disorders of the motor programming of speech Fig. Nevertheless such deficits frequently co-occur, and this assists in anatomical localization and diagnosis.
Here we consider these deficits at some length, because they are difficult to characterize with precision and because they entail several concepts which continue to stimulate controversy in the literature on progressive aphasias. One example is apraxia of speech AOS. AOS is probably therefore synonymous with phonetic breakdown or disintegration. The characteristic features of AOS are slow speech rate with hesitancy difficulty initiating utterances , effortfulness with articulatory groping, i.
Patients may describe the problem as a stutter or stammer and there may be re-emergence of a childhood stutter. In principle, phonetic errors errors in the execution of a programmed speech sound are distinct from phonemic errors errors in the selection of speech sounds to be executed: However, in practice this is a difficult distinction to make at the bedside, and the two types of error frequently coexist. Clues to phonetic errors include the presence of distortions commonly either distorted substitutions e.
This is in contrast to patients with pure phonological or phonemic breakdown: Speech features such as volume, rate, rhythm and intonation relate principally to the motor programming of speech output. These non-verbal aspects of speech output are most commonly affected in extrapyramidal disease [for example, the disorder of speech timing in Huntington's disease Darvesh and Freedman, ], and with cerebellar and subcortical pseudobulbar or bulbar pathologies. Dysarthric and phonetic speech errors are generally difficult to distinguish.
However, patients with phonetic impairment AOS make variable, inconsistent sound errors, and may articulate a word correctly on one occasion but not another, whereas the patient with dysarthria tends to make consistent errors. Indeed, it is likely that all three disorders have frequently been conflated in the literature Duffy, , due both to the overlap and difficulty in distinguishing them and still unresolved problems of definition.
This is underlined by the plethora of terms for motor speech disorders in the literature: Patients with progressive AOS or cortical dysarthria classically have well-preserved writing, indicating that these are disorders of speech output and that language processing per se is spared Broussolle et al.
In contrast, impairment at the level of phonological structure will manifest as phonemic errors in both speech and writing. Comparison of the patient's speech and writing is therefore generally a useful means of distinguishing primary phonological and phonetic disorders at the bedside. The severity of the speech deficit also provides a clue: However, mutism is an end-stage of a number of disease processes Kertesz and Orange, and can occur as an early feature in PNFA Gorno-Tempini et al.
Other components of the motor programme that are functionally separate from phonetic encoding can also be disrupted by degenerative disease: Many patients with speech-production difficulties lose the normal rhythms of conversational speech and the ability to regulate fine pitch and accent shifts. If severe, dysprosody may disrupt the intelligibility of the utterance as a whole and could be misinterpreted as a primary verbal problem. Commonly, dysprosody is secondary to poor articulation but rare cases of primary progressive dysprosodia have been described Confavreux et al.
The patient's word-finding difficulty can be further analysed using specific speech and language tasks Table 4 , which both corroborate the information obtained so far and may also expose additional deficits. As a result of these tasks, it should be possible to categorize the word-finding difficulty in terms of a core defect summarized in Fig. Each of the suggested bedside tasks can be refined and amplified by more specialized and detailed neuropsychological tests. This is particularly useful in detecting and tracking disease progression.
The information obtained at neuropsychometry, however, is most useful if the neuropsychologist is guided by information provided by the neurologist based on an initial bedside characterization of the problem and differential diagnosis. Word-finding depends fundamentally on a capacity to retrieve words from the verbal knowledge store in the appropriate context. This is most conveniently assessed as the ability to name. However, this ability is not related simply to word retrieval: Impaired naming, or anomia, is frequent in patients who complain of word-finding difficulties indeed, patients and their carers frequently characterize the language deficit as a problem with names , and it is a feature of many different disorders.
The diversity of clinical situations that lead to anomia underlines the need to evaluate other cognitive functions in order to arrive at a diagnosis. Although pure anomia is uncommon in degenerative settings, both primary verbal storage and word retrieval disorders typically present with anomia. Anomia is the most salient linguistic feature of early AD Mendez et al.
Early striking anomia is a characteristic feature of SD: Because of its importance as a presenting symptom, the broad spectrum of clinical associations and the fundamental role of word retrieval in the language output pathway, we consider the problem of anomia and its practical evaluation in detail.
The evaluation of naming begins with the analysis of the patient's spontaneous speech see previous section and Tables 2 and 3. Clues to anomia include a dearth of content words especially low frequency or proper nouns , abundant circumlocutions or frequent word-finding pauses. The nature of the defect is established using a structured series of subtests designed to assess different aspects of naming. Poor performance on these naming tasks may lead to the characterization of a word-finding problem even in patients who do not present with a primary complaint of word-finding difficulty.
Conversely, particular patterns of performance on naming tasks may help to establish that the basis for the word-finding impairment lies beyond or is not confined to the language system. Naming of objects in the environment depends on intact perceptual processing and activation of the appropriate semantic associations by the percept; only if these operations are successfully accomplished can verbal processing proceed.
Naming should be tested directly both in response to pictured items confrontational naming and from verbal description e. Primary deficits of visual perception or visual knowledge manifest as a better performance in naming to verbal description than naming pictures. Having established a primary verbal deficit, naming performance should be assessed for words of both high and low frequency e. It should be established whether there is improvement with phonological first letter or semantic associated item cueing.
Different categories of items should be presented animals, inanimate objects, familiar faces, colours, nouns versus actions, etc. Striking category effects are more commonly observed in acute brain damage such as herpes simplex encephalitis than in degenerative disease Warrington and Shallice, ; Silveri et al. Naming deficits may be relatively specific for a particular grammatical class for example, naming of verbs may be more impaired than naming of nouns in PNFA Hillis et al. Any errors made on naming tasks should be recorded: With primary involvement of the verbal knowledge store, there are typically highly consistent deficits that affect naming both to confrontation and from description, but which affect unusual low frequency items e.
Naming errors take the form of semantic paraphasias: There may also be circumlocutory responses e. Such errors are characteristically made by patients with SD, however similar errors are also observed not uncommonly in other dementias, including AD and vascular dementia VaD Lukatela et al.
Deficits involving the process of word retrieval proper common in early AD lead to a relatively pure anomia: The selective nature of the anomia can be established from the overall pattern of performance on naming versus other speech and language tasks. On confrontational naming tasks, such patients may offer no response at all or they may produce circumlocutions or semantically or phonologically related alternatives to the target item, either due to aberrant activation of alternative stored word codes or in an attempt to compensate for their naming difficulty.
Although the nature of circumlocutions and semantic paraphasias in nominal aphasia has been recognized for many years Luria, , these are frequently misinterpreted as evidence for a primary semantic verbal knowledge store defect. More conclusively, single word comprehension is intact see later , whereas this is impaired from an early stage of the illness in diseases particularly SD with primary verbal semantic impairment.
Naming errors in patients with a primary breakdown in the phonological encoding of verbal concepts into speech sounds as in PNFA generally take the form of literal phonemic paraphasias e. Primary deficits of both word retrieval and phonological encoding in contrast to primary verbal store defects may benefit from cueing with the initial letter of the target word. Personal names may present particular difficulties: Neologisms on confrontational naming tasks are comparatively rare in degenerative disease, however the presence of jargon should be noted as it may be of localising value Fig.
Speech-comprehension difficulties commonly coexist with word-finding and language output problems in both acute settings such as left hemisphere stroke and degenerative disease. Speech comprehension can be assessed at the level of single words, which depends both on intact perceptual mechanisms and the verbal knowledge store vocabulary , and sentences, which depends on the ability to hold verbal information on line and to process grammatical relations between words. Impaired single-word perception manifesting as progressive word deafness has been described rarely in degenerative disease Serieux, ; Mesulam, ; Ikeda et al.
The perceptual deficit is likely to lie with auditory temporal acuity and discrimination of speech sounds Otsuki et al. The auditory deficit can be demonstrated at the bedside by testing discrimination of phoneme pairs e. Impaired comprehension of single words in the setting of intact acoustic analysis results from a breakdown in verbal knowledge systems. The most striking and selective deficits of single-word comprehension are associated with SD, however semantic impairment is also well documented in AD Hodges et al.
Primary deficits of the verbal knowledge store lead to reduced vocabulary and also impair comprehension of both spoken and written material at single-word level. The comprehension of nouns can be assessed by asking the patient to point to items named or otherwise described by the examiner, to generate a definition or provide other information about a target word e. This can be finessed according to the examiner's assessment of the patient's premorbid level of competence for example, a highly competent patient with excellent premorbid verbal skills could be asked the difference between laziness and idleness.
Degradation of word knowledge typically progresses from more specific to superordinate categories for example, loss of knowledge about dogs might evolve in the sequence: Typically, meaning is retained for broad categories of nouns when more fine-grained classifications are impossible. The organization of brain knowledge systems, in particular the extent to which different modalities and categories of knowledge are dissociable, remains a core theoretical issue in contemporary cognitive neuropsychology. Category-specific deficits of verbal knowledge have been documented in degenerative disease, but category effects are unusual and occur much less frequently than with acute pathologies.
There may be selective impairment of the ability to comprehend the names of living things McCarthy and Warrington, ; Lambon Ralph et al. Conversely, there may be relatively preserved comprehension of the names of body parts Coslett et al. Though rare, category-specific deficits are of theoretical importance: One well-established category effect in degenerative disease is the dissociation between noun and verb knowledge. Impairments of noun retrieval and comprehension are well documented Silveri et al. Conversely, selective impairments of verb retrieval and comprehension have been demonstrated in patients with frontal dementia syndromes including frontotemporal dementia associated with motor neuron disease FTD-MND Bak et al.
Under most circumstances in daily life, words must be processed not in isolation but combined into sentences. Difficulty with sentence comprehension may occur despite normal single-word comprehension. This pattern suggests that the processing of grammatical relations is deficient, and it may also be associated with particular difficulty understanding verbs rather than nouns Price and Grossman, Having established that the comprehension of single words nouns is normal, the sentence level of comprehension can be assessed by asking the patient to perform a short sequence of actions according to different syntactic rules e.
Alternatively, the patient can be asked to identify a picture based on a syntactical sentence description e. The comprehension of grammar involves a number of different procedures including determination of tense and number, interpretation of pronouns and prepositions, analysis of word order and subject-object relations and parsing of clauses. These procedures can be broadly classified as syntactical relations between words and morphological word modifications according to grammatical context and may have distinct neural bases.
Some aspects of grammar processing may be dissociable from sentence comprehension Cotelli et al. Patients with progressive aphasias may exhibit different types of deficits on sentence comprehension tasks, and these may assist in differential diagnosis. An early selective deficit in comprehending grammatical relations may be found in PNFA Grossman, ; Grossman and Moore, ; Price and Grossman, , whereas in SD, comprehension of syntactical constructions is typically intact within the limitations of reduced vocabulary. More subtle impairment of sentence comprehension has been documented in patients with AD: Repetition of heard speech depends on intact input and output pathways and the ability to transfer information between these pathways.
Accordingly, difficulties with speech repetition occur in patients with impaired processing of incoming speech signals such as word deafness and in those with impaired speech output. Like speech comprehension, repetition can be assessed at the level of words and sentences. Patients with word deafness or primary speech production problems may have difficulties even with single word repetition especially for polysyllabic words Westbury and Bub, Repetition is hesitant and effortful and there are typically many phonemic errors.
Single-word repetition is generally preserved in SD, though sentence repetition is influenced by the level of comprehension.
Although overt speech repetition is seldom called upon outside the clinical setting, the cognitive operations that support speech repetition may be involved in processes such as monitoring of one's own spoken output, which is likely to improve the accuracy of communication.
Reduced phonological working memory Nestor et al. Reading, writing and spelling deficits often accompany word-finding problems in speech, and the assessment of these other language channels is helpful in characterizing word-finding difficulty. Literacy skills are learned rather than innate capacities, and the neural mechanisms that sustain them are likely to have been at least partly adapted from brain systems that support more elementary functions. Deficits of literacy skills are often accompanied by, or secondary to, deficits of visual perceptual or knowledge systems, in addition to any speech disorder.
Conversely, performance on literacy tests must take into account any specific longstanding limitation, such as developmental dyslexia. These classifications have both neuroanatomical and clinical implications. However, mixed forms of dyslexia and dysgraphia are common in degenerative disease, and the extent to which alternative sound- and meaning-based routes to reading and spelling are functionally separate has not been finally resolved.
The patient should be asked to read aloud a passage that includes both irregular words and non-words e. The types of error made when reading a passage aloud provides information about the core reading defect. Patients who exhibit letter-by-letter reading have a defect in processing visual word forms: Mild forms of peripheral dyslexia are not uncommon in AD Glosser et al. Regularization errors are more prominent for lower-frequency words. Analogous deficits occur in languages besides English: Patients with motor programming deficits tend to stumble reading polysyllabic words.
Analogous errors occur in written spelling of irregular and non-words, respectively. Loss of spelling vocabulary is characteristic of the SD syndrome Graham et al. Involvement of another language channel writing indicates a disturbance of language rather than speech production per se , and may be helpful in distinguishing a true word-finding difficulty from a motor speech disorder.
It should be noted however that written expression is often relatively better preserved with fewer errors than speech in patients with primary disturbances of speech production for, example, early in the course of PNFA. In patients with a disorder of written spelling, the capacity to spell aloud is in general comparably affected. However, relatively selective impairment of oral spelling has been described in patients with AD Croisile et al.
Although the generation of a verbal thought or message is the earliest operational stage in the verbal output pathway Fig. If dynamic aphasia is suspected based on the constellation of very impoverished propositional speech despite normal or nearly normal comprehension, repetition and reading Luria, ; Costello and Warrington, ; Warren et al. Although they are not strictly part of the assessment of word-finding difficulty, it is useful to characterize deficits of motor programming at the bedside, in order to disambiguate these from any language deficit and more broadly, to advance the clinical diagnosis.
The patient can be asked rapidly to repeat a single syllable e. Performance will be inaccurate in dysarthric patients with changes in either rate or rhythm, whereas performance is usually relatively normal in AOS. The analysis of spontaneous speech and specific speech and language tasks together allow the patient's speech syndrome to be defined Fig. While it is usually possible to align the individual case with one of these syndromes predominantly, syndromes commonly overlap and fragmentary syndromes are common. Moreover, each of the syndromes can occur in isolation albeit with widely varying frequency or as part of a more widespread disorder.
Considered as a group, however, the taxonomy of the progressive aphasias remains among the most problematic confronting clinical neurology. Despite these caveats, an appreciation of the relations between the progressive aphasia syndromes and their disease associations helps guide the assessment of the individual patient and the formulation of a differential diagnosis.
Here we consider each of the syndromes as they are schematized in Fig. Dynamic aphasia generally occurs in the context of an executive syndrome such as progressive supranuclear palsy PSP Esmonde et al. In contrast, PNFA frequently occurs without cognitive features beyond the domains of speech and language output or other neurological features.
It does, however, overlap with other degenerative syndromes, such as the corticobasal degeneration CBD syndrome Graham et al. Pure progressive dysarthria is rare Soliveri et al. Discrepancies in the classification of cases between published series precludes a resolution at present, however more accurate differentiation will be important in refinement of clinico-pathological correlations Josephs et al.
Pure progressive anomia is probably rare and there are few cases on record Graham et al. All patients who have been followed for a substantial period of time have subsequently developed more typical features of SD, suggesting that such cases represent an atypical slowly progressive SD rather than a separate syndrome Knibb and Hodges, Logopenic aphasia has been described as an isolated phenomenon in a small number of cases to date Kertesz et al. In the only detailed study Gorno-Tempini et al.
Detailed neuropsychological evaluation in this group showed that as well as the speech output characteristics of slow rate with word-finding pauses, patients had sentence comprehension difficulties, impaired repetition, dyslexia with errors on both irregular and nonwords and anomia but with relatively preserved semantics and phonology. There was also evidence of impaired verbal memory. This clinical picture would be compatible with an atypical variant of AD, and indeed, prominent word-finding pauses are commonly observed in cases of AD with more typical amnestic presentations.
The classical SD syndrome rarely forms part of a more widespread disorder Hodges et al. In contrast to logopenic aphasia, word-finding pauses are not salient, and evidence for an association with progranulin mutations Rohrer et al. The nosological status of this progressive mixed aphasia syndrome and its relationship to the other canonical progressive aphasia syndromes remain to be defined. Speech and language syndromes in degenerative disease are rarely isolated, and in general it is necessary and often helpful to consider associated cognitive and neurological features in localizing the disease process and arriving at a differential diagnosis Figs.
Clinical judgement is required, first, in deciding whether word-finding difficulty is in fact likely to be secondary to deficits in one of these other domains. In many cases the clue to this lies with the history, and examination can then be directed toward an initial evaluation of other deficits before embarking on a detailed and potentially misleading analysis of word-finding proper for example, significant visual perceptual impairment may preclude any meaningful assessment of word retrieval based on picture naming tasks.
A second key objective is to determine whether the patient has a focal language-based dementia, or whether word-finding difficulty is a leading feature of a more generalized process. Impairment of episodic memory, the record of events and episodes from the individual's daily life, is a hallmark of AD and is also seen in many other dementias. Pauses in conversation while the patient struggles to recall a name or other detail are commonly described as difficulty in finding words or names. The evaluation of memory is particularly important in deciding whether the patient's word-finding difficulty is a manifestation of a progressive aphasia in which case episodic memory is typically well preserved or an alternative diagnosis with more widespread cognitive impairment, in particular AD.
An impression of this is usually formed from the history: Available evidence suggests that, while working memory may be deficient in the context of an associated dysexecutive syndrome, episodic memory is generally well preserved in PNFA Libon et al. The situation in SD is more complex: Where appropriate indices are used, episodic memory can be shown to be comparable to that of healthy subjects in only a proportion of cases Nestor et al. The clinical message is that episodic memory impairment should not be equated uncritically with AD just as semantic deficits do not equate to SD: In addition to verbal knowledge, which is probed by tests of single-word comprehension, the non-verbal domains of semantic memory collectively comprise the individual's stored fund of conceptual knowledge about the world.
While deficits of semantic memory are well described in AD Rogers et al. Recognition of familiar faces a privileged category of visual knowledge can be assessed by having the patient provide information about public figures from their pictures and comparing this with recognition from verbal description and ability to match faces based on perceptual rather than semantic criteria. More general aspects of visual object knowledge can be assessed by having the patient draw or colour objects from memory, classify pictures based on semantic criteria e. Egyptian pyramid with a palm rather than a fir tree.
There remains controversy over the relationship between so-called fluent PPA Mesulam et al. The most prominent features in patients with early SD are anomia, single-word comprehension difficulties and fluent, empty, circumlocutory speech.
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As verbal deficits generally predominate without obvious non-verbal deficits, it has been argued that these patients should be considered to have a fluent form of PPA Mesulam, , ; Mesulam et al. While this distinction has theoretical support, in practice patients with progressive fluent aphasia and seemingly isolated verbal deficits later develop prominent non-verbal deficits e.
Furthermore, recent studies have suggested that when tested on a series of more demanding tasks, patients who would fit proposed diagnostic criteria for fluent PPA do have associated deficits in non-verbal domains Adlam et al. Patients with frontal lobe and fronto-subcortical disease may have prominent behavioural disturbances disinhibition, environmental dependency or apathy , however these are not invariable; conversely, they may occur despite well preserved language skills.
Verbal fluency depends on an efficient mechanism for searching the verbal knowledge store and is properly considered a frontal-executive rather than a primary language function. It requires generation of a strategy for producing verbal output de novo according to some rule or criterion nominated by the examiner.
Impaired verbal fluency is often accompanied by other evidence of executive dysfunction, notably in patients with frontal lobe damage Perret, ; Alvarez and Emory, However, it is worth noting that patients with deficits of the verbal knowledge store itself e. Reductions in fluency may be useful in distinguishing progressive aphasias from other degenerative conditions Marczinski and Kertesz, , and in particular, reduced letter fluency is a pointer to PNFA Clark et al. Performance on such tasks can be scored as the number of words produced in one minute; a useful bedside rule of thumb is that patients should be able to produce words as quickly as the examiner can write them down.
Poor performance on these tasks should be explored with further tests to identify the nature of the difficulty more precisely. PNFA is rarely associated with a behavioural syndrome early in the illness Rosen et al. Symptoms include irritability, apathy, disinhibition and altered eating behaviour. Orofacial apraxia refers to an impairment of volitional coughing, yawning or other complex orofacial actions despite intact reflex movements. Orofacial apraxia is also described in atypical PSP syndromes Josephs et al. Posterior cerebral functions including visual perceptual and spatial processing, calculation and limb praxis should be assessed both to ensure that apparent word-finding difficulties are interpreted correctly and to provide a complete picture of the cognitive syndrome, which may in turn suggest a particular diagnosis [such as corticobasal degeneration, CBD Graham et al.
Significant early posterior cortical dysfunction is unusual in PNFA, SD and the FTLD spectrum in general, though emerging evidence suggests that apraxia and other posterior hemispheric deficits may be relatively more common in patients with mutations in the progranulin gene Rohrer et al. The general neurological examination is frequently normal in many of the degenerative speech and language disorders.
However, associated neurological features, if present, can be diagnostically helpful in certain situations. Orofacial apraxia is a special instance, due to the intimate relation between the control of speech and other orofacial movements, however certain other features should also be sought specifically. Particularly relevant to the complaint of word-finding difficulty are associated behavioural abnormalities bvFTLD or PSP , dysphagia fronto-subcortical processes , primitive reflexes frontal lobe disorders , upper motor neuron signs VaD , fasciculations and amyotrophy MND or extrapyramidal features parkinsonian syndromes.
Some conditions have signature neurological abnormalities for example, gaze palsy and postural instability in PSP, an asymmetric akinetic-rigid syndrome and alien limb in the CBD syndrome. Asymmetric predominantly right-sided extrapyramidal signs are not uncommon in patients with PNFA Mesulam and Weintraub, ; Mesulam et al. Traditionally in clinical neurology, the history of the mode of onset and development of the complaint suggests the type of disease process responsible, while the findings on examination allow anatomical localization.
Applied to word-finding difficulty in degenerative disease, the bedside assessment Fig. This reflects both the distributed nature of the language system Hillis, and the nature of the underlying disease processes. While for some syndromes notably, SD clinico-anatomical correlation is relatively precise, in other syndromes brain atrophy is often subtle or equivocal in the early stages, many patients have mixed phenotypes that cannot be simply correlated with structural damage seen on the scan, and a number of degenerative diseases in which word-finding difficulty may be prominent for example, CBD lack diagnostic atrophy profiles.
From the perspective of anatomical localization in progressive aphasia, group and longitudinal cohort studies therefore have a particularly important role to play, and are in general more informative than information derived from individual patients or detailed single case studies. Unbiased techniques for the analysis of group data such as voxel-based morphometry VBM can establish consistent neuroanatomical correlations at a population level that would be difficult to detect from visual inspection alone. A corollary of this is that clinical interpretation is essential to avoid misinterpreting potentially spurious correlations.
In principle, the problem of anatomical correlation can be considered at the level of deficits in particular cognitive operations and at the level of syndromes, though these levels are frequently difficult to distinguish in practice. Here we consider available information concerning each of these levels of anatomical correlation, based on structural and functional imaging and pathological studies in patients with degenerative disease.
Propositional speech production in normal subjects involves the left superior frontal gyrus, left frontal operculum and rostral left temporal cortex Blank et al. In patients with dynamic aphasia and focal lesions, brain imaging has implicated the anterior left frontal lobe Luria, ; Costello and Warrington, ; Snowden et al. While it is not possible to draw firm conclusions regarding the macro-anatomical correlates of propositional speech failure in dynamic aphasia, it is likely that the syndrome results from damage involving a distributed left fronto-subcortical network Warren et al.
Left lateral temporal cortex was involved in all disease groups and the volume of this region correlated with naming accuracy. Additional correlations were observed specifically in left inferior and lateral frontal areas in PNFA, anterior cingulate in AD and right inferior frontal and temporal areas in CBD. This evidence is consistent with partially distinct substrates for naming deficits in different diseases, arising from the disruption of component processes such as semantic memory and visual perceptual functions.
Further evidence suggests distinct anatomical substrates for naming specific categories of objects Brambati et al. Functional imaging evidence in healthy subjects has demonstrated that the mesial temporal lobe is engaged during word retrieval verbal fluency tasks Pihlajamaki et al. The consistent and relatively focal involvement of the left temporal pole, anterolateral and inferior left temporal lobe in SD Galton et al.
The degree of atrophy of anterolateral left temporal neocortical areas correlates with VBM measures of semantic impairment Mummery et al. However anterolateral temporal neocortical regions are not affected in isolation: Disconnection between temporal lobe areas Harasty et al. Although it is difficult to establish precise anatomical correlates for particular categories of word knowledge in degenerative diseases, knowledge of verbs has been specifically associated with pathological involvement of inferior frontal areas, perhaps implicating dorsal motor pathways concerned with action processing Bak et al.
Deficits in both the comprehension and production of grammar are associated with atrophy involving the inferior frontal gyrus and insula Harasty et al. Impaired syntactic comprehension has been correlated with involvement of the left posterior temporal-inferior parietal lobe Gorno-Tempini et al. Little evidence is available concerning the substrate of phonological encoding per se , however this is likely to involve a distributed left peri-Sylvian network involving the inferior frontal lobe, anterior and posterior superior temporal areas overlapping that implicated in grammatical processing Harasty et al.
The region of metabolic abnormality extends widely beyond the relatively circumscribed tissue destruction detected on structural imaging Tyrrell et al. The insula may play a crucial role in linking grammatical, phonological and articulatory networks Harasty et al. Early mutism has been associated with atrophy involving the pars opercularis and its subcortical connections Gorno-Tempini et al.
The anatomical basis of progressive dysprosody is poorly defined, but predominantly right-sided peri-Sylvian and frontal atrophy has been demonstrated in individual cases Confavreux et al. The anatomical and pathophysiological substrates of the component operations of the speech output pathway are peculiarly difficult to isolate, and there is a pressing need for detailed neuroanatomical and neurophysiological correlation of specific functions and deficits for example, to help resolve the difficult distinction between phonetic and phonemic deficits.
Whereas correlations between brain anatomy and particular cognitive deficits can be established by applying appropriate neuropsychological measures across syndromes and diseases, to establish the anatomical basis of a syndrome depends on how that syndrome is defined. The different syndromes within the progressive aphasia spectrum lack detailed, universally accepted consensus criteria, and interpretation of anatomical data derived from brain imaging and pathological studies remains difficult.
Despite this caveat, a recent meta-analysis of subjects with FTLD based on both VBM and metabolic imaging data concluded that alterations in specific brain networks could be identified in each of the canonical FTLD clinical subtypes, as defined using available consensus criteria Schroeter et al.
In general, dementias that produce selective impairments of speech and language processing are associated with asymmetric atrophy predominantly involving the left peri-Sylvian cortices and anterior temporal lobe, and certain broad patterns consistently emerge from both single-case and group studies in patients with focal dementia syndromes.
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However, involvement of the left peri-Sylvian cortex typically occurs in the context of more widespread involvement of other cortical and subcortical regions in both cerebral hemispheres Ikeda et al. The functional derangement extends beyond the zone of tissue loss, and there may be abnormal possibly compensatory activation beyond the classical language areas Mesulam, ; Sonty et al. Speech-production impairment associated with PNFA is likely to be attributable to involvement of the left anterior insula Nestor et al.
These patterns correlate with neuropsychological profiles and clinical evolution Tyrell et al. Partial cerebral reorganization has been documented both in PPA Vandenbulcke et al. Proton magnetic resonance spectroscopy has documented asymmetric axonal injury within the arcuate fasciculus in PPA Catani et al. Toggle navigation All Scrabble Words.
- Word-finding difficulty: a clinical analysis of the progressive aphasias | Brain | Oxford Academic!
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