Semantic dementia

Short description: Loss of semantic memory, primarily in the verbal domain

Main articles: Medicine:Aphasia and Primary progressive aphasia

Semantic dementia

Other names| semantic variant primary progressive aphasia
Specialty| Neurology

In neurology, semantic dementia (SD), also known as semantic variant primary progressive aphasia (svPPA), is a progressive neurodegenerative disorder characterized by loss of semantic memory in both the verbal and non-verbal domains. However, the most common presenting symptoms are in the verbal domain (with loss of word meaning).[1][2][3] Semantic dementia is a disorder of semantic memory that causes patients to lose the ability to match words or images to their meanings.[4] However, it is fairly rare for patients with semantic dementia to develop category specific impairments, though there have been documented cases of it occurring.[5] Typically, a more generalized semantic impairment results from dimmed semantic representations in the brain.[6]

SD is one of the three canonical clinical syndromes associated with frontotemporal lobar degeneration (FTLD), with the other two being frontotemporal dementia and progressive nonfluent aphasia. SD is a clinically defined syndrome but is associated with predominantly temporal lobe atrophy (left greater than right) and hence is sometimes called temporal variant FTLD (tvFTLD).[7] SD is one of the three variants of primary progressive aphasia (PPA), which results from neurodegenerative disorders such as FTLD or Alzheimer's disease. The other two variants of primary progressive aphasia (PPA) are logopenic variant PPA (lvPPA) and confluent-agrammatic variant PPA (navPPA). There are distinctions between Alzheimer's disease and semantic dementia with regard to types of memory affected.[citation needed] In general, Alzheimer's disease is referred to as a disorder affecting mainly episodic memory, defined as the memory related to specific, personal events distinct for each individual. Semantic dementia generally affects semantic memory, which refers to long-term memory that deals with common knowledge and facts.

SD was first described by Arnold Pick in 1904 and in modern times was characterized by Professor Elizabeth Warrington in 1975,[8] but it was not given the name semantic dementia until 1989.[9] The clinical and neuropsychological features, and their association with temporal lobe atrophy were described by Professor John Hodges and colleagues in 1992.[10]

## Contents

* 1 Presentation
* 1.1 Hemispheric Lateralization and Modality-Specific Deficits
* 2 Genetics
* 2.1 Alzheimer's Disease and Semantic Dementia
* 3 Diagnosis
* 3.1 Physical changes
* 3.2 Memory in dementia: musical objects, musical concepts, and semantic memory
* 4 Treatment
* 5 Summary
* 6 References
* 7 Further reading
* 8 External links

## Presentation

The defining characteristic of SD is decreased performance on tasks that require semantic memory. This includes difficulty with naming pictures and objects, single word comprehension, categorizing, and knowing uses and features of objects. SD patients also have difficulty with spontaneous speech creation, using words such as "this" or "things" where more specific and meaningful words can be used.[2] At earlier stages, patients may replace words with vague terms; as an example, 'crow' may become 'bird', then 'animal', before ultimately becoming 'thing'.[10] Syntax is spared, and SD patients have the ability to discern syntactic violations and comprehend sentences with minimal lexical demands.[11] SD patients have selectively worse concrete word knowledge and association, but retain knowledge and understanding of abstract words.[12] SD patients are able to retain knowledge of numbers and music, but have more difficulty with concrete concepts with visual associations.[2] Impairments of processing of phonemic structure and prosodic predictability have also been observed.[13]

### Hemispheric Lateralization and Modality-Specific Deficits

Research has shown that the lateralization of temporal lobe atrophy in semantic dementia produces distinct patterns of semantic memory impairment. A study was done on a cohort of 41 patients with semantic dementia, where it was shown that performance deficits occurred in accordance with the predominantly affected hemisphere[14]. Patients with predominantly left temporal lobe damage (31 patients) exhibited poorer naming and comprehension abilities. Conversely, patients with predominantly right temporal lobe damage (10 patients; a smaller subgroup) exhibiting poorer facial recognition, picture interpretation, and comprehension of visual information[14]. This hemispheric dissociation indicates that semantic memory is organized in a modality-specific manner. While semantic dementia affects both the right and left temporal lobe, the incongruence of atrophy will play a role in the clinical symptoms displayed.

## Genetics

The majority of SD patients have ubiquitin-positive, TDP-43 positive, tau-negative inclusions, although other pathologies have been described more infrequently, namely tau-positive Pick's disease and Alzheimer's pathology.[15] Of all the FTLD syndromes, SD is least likely to run in families and is usually sporadic.[16]

### Alzheimer's Disease and Semantic Dementia

Alzheimer's disease is related to semantic dementia, which both have similar symptoms. The main difference between the two being that Alzheimer's is categorized by atrophy to both sides of the brain while semantic dementia is categorized by loss of brain tissue in the front portion of the left temporal lobe.[17] With Alzheimer's disease in particular, interactions with semantic memory produce different patterns in deficits between patients and categories over time which is caused by distorted representations in the brain. For example, in the initial onset of Alzheimer's disease, patients have mild difficulty with the artifacts category. As the disease progresses, the category specific semantic deficits progress as well, and patients see a more concrete deficit with natural categories. In other words, the deficit tends to be worse with living things as opposed to non-living things.[18]

## Diagnosis

SD patients generally have difficulty generating familiar words or recognizing familiar objects and faces.[19] Clinical signs include fluent aphasia, anomia (inability to recall names of persons or things), impaired comprehension of word meaning, and associative visual agnosia (inability to match semantically related pictures or objects). As the disease progresses, behavioral and personality changes are often seen similar to those seen in frontotemporal dementia.[19]

SD patients perform poorly on tests of semantic knowledge. Published tests include both verbal and non-verbal tasks, e.g., The Warrington Concrete and Abstract Word Synonym Test,[20] and The Pyramids and Palm Trees task.[10] Testing also reveals deficits in picture naming (e.g. "dog" for a picture of a hippopotamus) and decreased category fluency. The question "What is a Stapler?" has been used as a primary diagnostic technique for discerning how SD patients understand word meaning.[2]

Speech of SD patients is marked by word-finding pauses, reduced frequency of content words, semantic paraphasias, circumlocutions, increased ratios of verbs to nouns, increased numbers of adverbs, and multiple repeats.[21]

SD patients sometimes show symptoms of surface dyslexia, a relatively selective impairment in reading low-frequency words with exceptional or atypical spelling-to-sound correspondences.[2]

It is currently unknown why semantic memory is impaired and semantic knowledge deteriorates in SD patients, though the cause may be due to damage to an amodal semantic system. This theory is supported by the atrophy of the anterior temporal lobe, which is believed to contain a component of the semantic system that integrates conceptual information. Others hypothesize that the damage is predominantly to the ventral temporal cortex, since SD patients remember numbers and music, but have trouble associating visual cues to concrete words.[2]

### Physical changes

Structural and functional MRI imaging show a characteristic pattern of atrophy in the temporal lobes (predominantly on the left), with inferior greater than superior involvement and anterior temporal lobe (including hippocampal formation and amygdala) atrophy greater than posterior. As the disease progresses, this atrophy spreads to the ventromedial prefrontal cortical regions[22]. This distinguishes it from Alzheimer's disease.[23] Meta-analyses on MRI and FDG-PET studies confirmed these findings by identifying alterations in the inferior temporal poles and amygdalae as the hotspots of disease - brain regions that have been discussed in the context of conceptual knowledge, semantic information processing, and social cognition.[24] Based on these imaging methods, semantic dementia can be regionally dissociated from the other subtypes of frontotemporal lobar degeneration, frontotemporal dementia, and progressive nonfluent aphasia. Selective hypometabolism of glucose has been observed in the anterior temporal lobe, as well as the medial temporal lobe and limbic areas.[25]

Damage to white matter tracts connecting the anterior temporal cortex to the inferior longitudinal, arcuate, and uncinate fasciculi, which are regions of the language network, is also seen using diffusion tensor imaging.[2] Imaging also shows the integrity of the axonal connections from the anterior temporal cortex to frontal and posterior associative areas to be altered.[25]

Functional abnormalities have also been observed in hippocampal structures, the ventromedial prefrontal cortex, and the cingulate cortex.[25]

### Memory in dementia: musical objects, musical concepts, and semantic memory

Regarding the neurobiological correlates for this study, it was determined, via lesion studies, that bilateral (but especially the left-side of the brain) fronto-temporoparietal areas are significant in the associative processing of melodies.[26] Based on the data of imaging studies that looked at the localization of processing melodies, it can be inferred that the anatomical location of the processes in consistent with the findings that some SD patients have intact melody recognition.[26] Additionally, the neurobiological basis for musical emotion identification implicated the limbic and paralimbic structures in this process. Overall, the results of these studies suggest that the neurobiological basis of musical semantic memory is bilaterally located in the cerebral hemispheres, likely around the fronto-temporal areas of the brain.[26] Unfortunately, due to the lack of studies studying musical semantic memory, conclusions cannot be more specific.

## Treatment

There is currently no known curative treatment for SD, and no pharmacological interventions have been shown to slow disease progression. The average duration of illness is 8–10 years.[19] Progression of SD can lead to behavioral and social difficulties, thus supportive care is essential for improving quality of life in SD patients as they grow more incomprehensible. Continuous practice in lexical learning has been shown to improve semantic memory in SD patients.[27] No preventative measures for SD are recognized.{{citation needed|date=December 2019} While no pharmacological interventions have been introduced, there have been behavioral interventions that have shown success in experimental settings. These experimental approaches focus on vocabulary retraining in order to improve word retrieval. [28] Studies also show that semantic dementia patients can improve their ability to name objects through targeted cognitive intervention[29]. Notably, these improvements do have a tendency to fade overtime if the intervention practice is not maintained, and longevity of treatment is variable among patients depending on the progression of the disease.[30]

## Summary

Semantic dementia (SD), or semantic variant primary progressive aphasia (svPPA), is aprogressive neurodegenerative disease that is characterized by gradual loss of semantic memory (knowledge of word meaning, objects, and general facts).[1][2]

SD is the progressive deterioration of conceptual knowledge while other cognitive abilities, including syntax, phonology, and episodic memory, remain relatively preserved in early stages.[1] Usually the condition is considered an anomia, because it causes the inability for patients to recall the names of persons or things. Patients can typically describe the object in detail, or even use hand gestures to show what the object does, but are unable to name it instead using vaguer terms like "thing". Over time, patients lose their knowledge of the meaning of words, and may begin to struggle with understanding the use of everyday objects.

Neuroimaging reveals a characteristic pattern of asymmetric temporal lobe atrophy, predominantly affecting the left hemisphere, with the anterior temporal lobes and temporal pole showing the greatest degeneration. Research has demonstrated that the lateralization of atrophy produces distinct clinical profiles: left-predominant damage results in verbal semantic deficits, while right-predominant damage causes greater impairment in face and picture recognition.[14] The disease typically progresses over 8–10 years, with atrophy spreading from anterior to posterior temporal regions, eventually affecting ventromedial prefrontal areas.[22]

Currently, there is no curative treatment or pharmacological intervention for SD. Treatment plans focus on behavioral interventions, specifically vocabulary retraining programs. Experimental trials have shown success in improving word retrieval for trained items in experimental settings, though ongoing maintenance practice is necessary[28][31]. Supportive care addressing communication difficulties and behavioral changes remains essential for maintaining quality of life as the disease progresses.[17]

## References

1. ↑ 1.0 1.1 1.2 Gorno-Tempini, M.L. et al. (March 2011). "Classification of primary progressive aphasia and its variants". Neurology 76 (11): 1006–14. doi:10.1212/WNL.0b013e31821103e6. PMID 21325651.
2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 Bonner, M.F.; Ash, S.; Grossman, M. (November 2010). "The new classification of primary progressive aphasia into semantic, logopenic, or nonfluent/agrammatic variants". Curr Neurol Neurosci Rep 10 (6): 484–90. doi:10.1007/s11910-010-0140-4. PMID 20809401.
3. ↑ Harciarek, M.; Kertesz, A. (September 2011). "Primary progressive aphasias and their contribution to the contemporary knowledge about the brain-language relationship". Neuropsychol Rev 21 (3): 271–87. doi:10.1007/s11065-011-9175-9. PMID 21809067.
4. ↑ "Alzheimer Europe - Dementia - Other forms of dementia - Neurodegenerative diseases - Fronto-Temporal Degeneration - Semantic Dementia (SD)" (in en). https://www.alzheimer-europe.org/Dementia/Other-forms-of-dementia/Neurodegenerative-diseases/Fronto-Temporal-Degeneration/Semantic-Dementia-SD.
5. ↑ "Encephalitis, Herpes Simplex" (in en-US). https://rarediseases.org/rare-diseases/encephalitis-herpes-simplex/.
6. ↑ Lambon Ralph, M. A.; Lowe, C.; Rogers, T. T. (2006-11-21). "Neural basis of category-specific semantic deficits for living things: evidence from semantic dementia, HSVE and a neural network model". Brain 130 (4): 1127–1137. doi:10.1093/brain/awm025. ISSN 0006-8950. PMID 17438021.
7. ↑ "Frontotemporal dementias: a review". Ann Gen Psychiatry 6. 2007. doi:10.1186/1744-859X-6-15. PMID 17565679.
8. ↑ Warrington, E.K. (November 1975). "The selective impairment of semantic memory". Q J Exp Psychol 27 (4): 635–57. doi:10.1080/14640747508400525. PMID 1197619.
9. ↑ Snowden, J.S.; Goulding, P.J.; Neary, D. (1989). "Semantic dementia: a form of circumscribed cerebral atrophy". Behav Neurol 2 (3): 167–82. doi:10.1155/1989/124043.
10. ↑ 10.0 10.1 10.2 Hodges, J.R.; Patterson, K.; Oxbury, S.; Funnell, E. (December 1992). "Semantic dementia. Progressive fluent aphasia with temporal lobe atrophy". Brain 115 (Pt 6): 1783–806. doi:10.1093/brain/115.6.1783. PMID 1486461.
11. ↑ Wilson, Stephen M.; DeMarco, Andrew T.; Henry, Maya L.; Gesierich, Benno; Babiak, Miranda; Mandelli, Maria Luisa; Miller, Bruce L.; Gorno-Tempini, Maria Luisa (May 2014). "What role does the anterior temporal lobe play in sentence-level processing? Neural correlates of syntactic processing in semantic PPA". Journal of Cognitive Neuroscience 26 (5): 970–985. doi:10.1162/jocn_a_00550. ISSN 0898-929X. PMID 24345172.
12. ↑ Cousins, Katheryn AQ; York, Collin; Bauer, Laura; Grossman, Murray (April 2016). "Cognitive and anatomic double dissociation in the representation of concrete and abstract words in semantic variant and behavioral variant frontotemporal degeneration". Neuropsychologia 84: 244–251. doi:10.1016/j.neuropsychologia.2016.02.025. ISSN 0028-3932. PMID 26944874.
13. ↑ Hardy, Chris J. D.; Agustus, Jennifer L.; Marshall, Charles R.; Clark, Camilla N.; Russell, Lucy L.; Bond, Rebecca L.; Brotherhood, Emilie V.; Thomas, David L. et al. (2017-07-27). "Behavioural and neuroanatomical correlates of auditory speech analysis in primary progressive aphasias". Alzheimer's Research & Therapy 9 (1): 53. doi:10.1186/s13195-017-0278-2. ISSN 1758-9193. PMID 28750682.
14. ↑ 14.0 14.1 14.2 Snowden, Julie S.; Harris, Jennifer M.; Thompson, Jennifer C.; Kobylecki, Christopher; Jones, Matthew; Richardson, Anna M.; Neary, David (Oct 2018). "Semantic dementia and the left and right temporal lobes" (in en). Cortex 107: 188–203. doi:10.1016/j.cortex.2017.08.024. https://linkinghub.elsevier.com/retrieve/pii/S0010945217302812.
15. ↑ Davies, R.R.; Hodges, J.R.; Kril, J.J.; Patterson, K.; Halliday, G.M.; Xuereb, J.H. (September 2005). "The pathological basis of semantic dementia". Brain 128 (Pt 9): 1984–95. doi:10.1093/brain/awh582. PMID 16000337.
16. ↑ Goldman, J.S. et al. (December 2005). "Comparison of family histories in FTLD subtypes and related tauopathies". Neurology 65 (11): 1817–9. doi:10.1212/01.wnl.0000187068.92184.63. PMID 16344531.
17. ↑ 17.0 17.1 "Alzheimer Europe - Dementia - Other forms of dementia - Neurodegenerative diseases - Fronto-Temporal Degeneration - Semantic Dementia (SD)" (in en). https://www.alzheimer-europe.org/Dementia/Other-forms-of-dementia/Neurodegenerative-diseases/Fronto-Temporal-Degeneration/Semantic-Dementia-SD.
18. ↑ Devlin, Joseph T.; Gonnerman, Laura M.; Andersen, Elaine S.; Seidenberg, Mark S. (January 1998). "Category-Specific Semantic Deficits in Focal and Widespread Brain Damage: A Computational Account". Journal of Cognitive Neuroscience 10 (1): 77–94. doi:10.1162/089892998563798. ISSN 0898-929X. PMID 9526084.
19. ↑ 19.0 19.1 19.2 "Semantic variant Primary Progressive Aphasia". Association for Frontotemporal Degeneration. https://www.theaftd.org/understandingftd/disorders/semantic-dementia.
20. ↑ Warrington, E.K.; McKenna, P.; Orpwood, L. (April 1998). "Single word comprehension: a concrete and abstract word synonym test". Neuropsychological Rehabilitation 8 (2): 143–54. doi:10.1080/713755564.
21. ↑ Marcotte, Karine; Graham, Naida L.; Fraser, Kathleen C.; Meltzer, Jed A.; Tang-Wai, David F.; Chow, Tiffany W.; Freedman, Morris; Leonard, Carol et al. (2017-03-02). "White Matter Disruption and Connected Speech in Non-Fluent and Semantic Variants of Primary Progressive Aphasia". Dementia and Geriatric Cognitive Disorders Extra 7 (1): 52–73. doi:10.1159/000456710. ISSN 1664-5464. PMID 28611820.
22. ↑ 22.0 22.1 Irish, Muireann; Addis, Donna Rose; Hodges, John R.; Piguet, Olivier (2012-05-22). "Considering the role of semantic memory in episodic future thinking: evidence from semantic dementia". Brain 135 (7): 2178–2191. doi:10.1093/brain/aws119. ISSN 1460-2156. https://doi.org/10.1093/brain/aws119.
23. ↑ Chan, D. et al. (April 2001). "Patterns of temporal lobe atrophy in semantic dementia and Alzheimer's disease". Annals of Neurology 49 (4): 433–42. doi:10.1002/ana.92. PMID 11310620.
24. ↑ Schroeter, M.L.; Raczka, K.K.; Neumann, J.; von Cramon, D.Y. (2007). "Towards a nosology for frontotemporal lobar degenerations – A meta-analysis involving 267 subjects". NeuroImage 36 (3): 497–510. doi:10.1016/j.neuroimage.2007.03.024. PMID 17478101.
25. ↑ 25.0 25.1 25.2 Iaccarino, Leonardo; Crespi, Chiara; Della Rosa, Pasquale Anthony; Catricalà, Eleonora; Guidi, Lucia; Marcone, Alessandra; Tagliavini, Fabrizio; Magnani, Giuseppe et al. (2015-03-10). "The Semantic Variant of Primary Progressive Aphasia: Clinical and Neuroimaging Evidence in Single Subjects". PLOS ONE 10 (3). doi:10.1371/journal.pone.0120197. ISSN 1932-6203. PMID 25756991. Bibcode: 2015PLoSO..1020197I.
26. ↑ 26.0 26.1 26.2 Cite error: Invalid `<ref>` tag; no text was provided for refs named `ReferenceA`
27. ↑ Henry, Maya; Beeson, Pélagie; Rapcsak, Steven (February 2008). "Treatment for Anomia in Semantic Dementia". Seminars in Speech and Language 29 (1): 060–070. doi:10.1055/s-2008-1061625. ISSN 0734-0478. PMID 18348092.
28. ↑ 28.0 28.1 Carthery-Goulart, Maria Teresa; Silveira, Amanda da Costa da; Machado, Thais Helena; Mansur, Leticia Lessa; Parente, Maria Alice de Mattos Pimenta; Senaha, Mirna Lie Hosogi; Brucki, Sonia Maria Dozzi; Nitrini, Ricardo (March 2013). "Nonpharmacological interventions for cognitive impairments following primary progressive aphasia: A systematic review of the literature". Dementia & Neuropsychologia 7 (1): 122–131. doi:10.1590/S1980-57642013DN70100018. ISSN 1980-5764. PMC 5619554. http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1980-57642013000100122&lng=en&tlng=en.
29. ↑ Duffy, Joseph R.; Strand, Edythe A.; Josephs, Keith A. (2014-09-02). "Motor speech disorders associated with primary progressive aphasia" (in en). Aphasiology 28 (8-9): 1004–1017. doi:10.1080/02687038.2013.869307. ISSN 0268-7038. PMID 25309017. PMC 4191906. https://www.tandfonline.com/doi/full/10.1080/02687038.2013.869307.
30. ↑ Duffy, Joseph R.; Strand, Edythe A.; Josephs, Keith A. (2014-09-02). "Motor speech disorders associated with primary progressive aphasia" (in en). Aphasiology 28 (8-9): 1004–1017. doi:10.1080/02687038.2013.869307. ISSN 0268-7038. PMID 25309017. PMC 4191906. https://www.tandfonline.com/doi/full/10.1080/02687038.2013.869307.
31. ↑ Duffy, Joseph R.; Strand, Edythe A.; Josephs, Keith A. (2014-09-02). "Motor speech disorders associated with primary progressive aphasia" (in en). Aphasiology 28 (8-9): 1004–1017. doi:10.1080/02687038.2013.869307. ISSN 0268-7038. PMID 25309017. PMC 4191906. https://www.tandfonline.com/doi/full/10.1080/02687038.2013.869307.

Reference 29: Snowden, J.S., Harris, J.M., Thompson, J.C., Kobylecki, C., Jones, M., Richardson, A.M., & Neary, D. (2018). Semantic dementia and the left and right temporal lobes. Cortex, 107, 188-203. https://doi.org/10.1016/j.cortex.2017.08.024

Reference 33/24: Irish, M., Addis, D.R., Hodges, J.R., & Piguet, O. (2012). Considering the role of semantic memory in episodic future thinking: evidence from semantic dementia. Brain, 135(7), 2178-2191.

Reference 32/33: Jokel, R., Graham, N.L., Rochon, E., & Leonard, C. (2014). Word retrieval therapies in primary progressive aphasia. Aphasiology, 28(8-9), 1038-1068. https://doi.org/10.1080/02687038.2013.869307

Reference 32: Carthery-Goulart, M.T., Silveira, A. da C., Machado, T.H., Mansur, L.L., Parente, M.A.M.P., Senaha, M.L.H., Brucki, S.M.D., & Nitrini, R. (2013). Nonpharmacological interventions for cognitive impairments following primary progressive aphasia: A systematic review of the literature. Dementia & Neuropsychologia, 7(1), 122-131. https://doi.org/10.1590/S1980-57642013DN70100018

Reference 20: Rohani Omar, Julia C. Halistone, and Jason D. Warren, "Semantic Memory for Music in Dementia," Music Perception 29, no. 5 (June 2012):, doi:10.1525/mp.2012.29.5.467.

Reference 21:Lise Gagnon, Isabelle Peretz, and Tamàs Fülöp, "Musical structural determinants of emotional judgments in dementia of the Alzheimer type.," Neuropsychology 23, no. 1 (2009): doi:10.1037/a0013790.

Reference 22: J. C. Hailstone, R. Omar, and J. D. Warren, "Relatively preserved knowledge of music in semantic dementia," Journal of Neurology, Neurosurgery & Psychiatry 80, no. 7 (2009): doi:10.1136/jnnp.2008.153130.

## Further reading

* Gliebus, G. (March 2010). "Primary progressive aphasia: clinical, imaging, and neuropathological findings". Am J Alzheimers Dis Other Demen 25 (2): 125–7. doi:10.1177/1533317509356691. PMID 20124255.
* Henry, M.L.; Beeson, P.M.; Rapcsak, S.Z. (February 2008). "Treatment for anomia in semantic dementia". Semin Speech Lang 29 (1): 60–70. doi:10.1055/s-2008-1061625. PMID 18348092.
* Henry, M.L.; Gorno-Tempini, M.L. (December 2010). "The logopenic variant of primary progressive aphasia". Current Opinion in Neurology 23 (6): 633–7. doi:10.1097/WCO.0b013e32833fb93e. PMID 20852419.
* Reilly, J.; Rodriguez, A.D.; Lamy, M.; Neils-Strunjas, J. (2010). "Cognition, language, and clinical pathological features of non-Alzheimer's dementias: an overview". J Commun Disord 43 (5): 438–52. doi:10.1016/j.jcomdis.2010.04.011. PMID 20493496.
* Rohrer, J.D.; Knight, W.D.; Warren, J.E.; Fox, N.C.; Rossor, M.N.; Warren, J.D. (January 2008). "Word-finding difficulty: a clinical analysis of the progressive aphasias". Brain 131 (Pt 1): 8–38. doi:10.1093/brain/awm251. PMID 17947337.

## External links

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* MeSH: D003704

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