Semantic dementia

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Semantic dementia
Other namessemantic variant primary progressive aphasia
Specialty 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]

Contents

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. It is important to note the distinctions between Alzheimer's disease and semantic dementia with regard to types of memory affected. 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]

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] 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]

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. [14] Of all the FTLD syndromes, SD is least likely to run in families and is usually sporadic. [15]

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. [16] 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. [17]

Diagnosis

SD patients generally have difficulty generating familiar words or recognizing familiar objects and faces. [18] Clinical signs include fluent aphasia, anomia, 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. [18]

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, [19] 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. [20]

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]

Due to the variety of symptoms dementia patients present, it becomes more difficult to assess semantic memory capability especially with regard to musical elements. In order to circumvent the explicit verbal learning tests for dementia, semantic melodic matching is a useful technique for detecting the semantic memory of semantic dementia patients. [21] Moreover, it is important to maintain that these tests must be compared to nonmusical domain tests, as music cognition is not often measured in semantic dementia patients (less data available).[ citation needed ]

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 atrophy greater than posterior. This distinguishes it from Alzheimer's disease. [22] 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. [23] 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.[ citation needed ]

Selective hypometabolism of glucose has been observed in the anterior temporal lobe, as well as the medial temporal lobe and limbic areas. [24]

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. [24]

Functional abnormalities have also been observed in hippocampal structures, the ventromedial prefrontal cortex, and the cingulate cortex. [24]

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

Melodies are a key aspect of musical objects that are thought to form the contents of semantic memory for music. [21] Melodies are defined as familiar tunes that become associated with musical or extra musical meaning. Using familiar songs, such as Christmas carols, were used to test whether SD patients were able to recognize the tones and melodies of the songs if the patients were just given the words of the song. In the analysis of semantic memory using melodies as stimuli, the contents of semantic memory can include many other aspects aside from recognition of the melody, such as the general information about the music (composer, genre, year of release). [21] Results have shown that musicians who have semantic dementia are able to identify and recognize certain melodic tones.[ citation needed ]

Further exploring the tests of music and semantic memory, results of a study that centered on the comprehension of emotion in music indicated that Alzheimer's Disease (AD) patients retained the ability to discern emotions from a song while non-AD degenerative disease patients, such as those with semantic dementia (SD), show impaired comprehension of these emotions. [25] Moreover, several dementia patients, all with varied musical experience and knowledge, all demonstrated an understanding of the fundamental governing rules of western music. [26] Essentially, it was found that superordinate knowledge of music, such as the rules of composition, may be more robust than knowledge of specific music.[ citation needed ]

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. [21] 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. [21] 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. [21] 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. The average duration of illness is 8–10 years, and its progression cannot be slowed. [18] 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.[ citation needed ] 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 ]

Related Research Articles

<span class="mw-page-title-main">Aphasia</span> Inability to comprehend or formulate language

In aphasia, a person may be unable to comprehend or unable to formulate language because of damage to specific brain regions. The major causes are stroke and head trauma; prevalence is hard to determine but aphasia due to stroke is estimated to be 0.1–0.4% in the Global North. Aphasia can also be the result of brain tumors, epilepsy, brain damage and brain infections, or neurodegenerative diseases.

<span class="mw-page-title-main">Anomic aphasia</span> Medical condition

Anomic aphasia is a mild, fluent type of aphasia where individuals have word retrieval failures and cannot express the words they want to say. By contrast, anomia is a deficit of expressive language, and a symptom of all forms of aphasia, but patients whose primary deficit is word retrieval are diagnosed with anomic aphasia. Individuals with aphasia who display anomia can often describe an object in detail and maybe even use hand gestures to demonstrate how the object is used, but cannot find the appropriate word to name the object. Patients with anomic aphasia have relatively preserved speech fluency, repetition, comprehension, and grammatical speech.

<span class="mw-page-title-main">Temporal lobe</span> One of the four lobes of the mammalian brain

The temporal lobe is one of the four major lobes of the cerebral cortex in the brain of mammals. The temporal lobe is located beneath the lateral fissure on both cerebral hemispheres of the mammalian brain.

<span class="mw-page-title-main">Brodmann area 38</span>

Brodmann area 38, also BA38 or temporopolar area 38 (H), is part of the temporal cortex in the human brain. BA 38 is at the anterior end of the temporal lobe, known as the temporal pole.

<span class="mw-page-title-main">Frontotemporal dementia</span> Types of dementia involving the frontal or temporal lobes

Frontotemporal dementia (FTD), or frontotemporal degeneration disease, or frontotemporal neurocognitive disorder, encompasses several types of dementia involving the progressive degeneration of frontal and temporal lobes. FTDs broadly present as behavioral or language disorders with gradual onsets. Common signs and symptoms include significant changes in social and personal behavior, apathy, blunting of emotions, and deficits in both expressive and receptive language. Currently, there is no cure for FTD, but there are treatments that help alleviate symptoms.

Cerebral atrophy is a common feature of many of the diseases that affect the brain. Atrophy of any tissue means a decrement in the size of the cell, which can be due to progressive loss of cytoplasmic proteins. In brain tissue, atrophy describes a loss of neurons and the connections between them. Brain atrophy can be classified into two main categories: generalized and focal atrophy. Generalized atrophy occurs across the entire brain whereas focal atrophy affects cells in a specific location. If the cerebral hemispheres are affected, conscious thought and voluntary processes may be impaired.

<span class="mw-page-title-main">Frontotemporal lobar degeneration</span> Medical condition

Frontotemporal lobar degeneration (FTLD) is a pathological process that occurs in frontotemporal dementia. It is characterized by atrophy in the frontal lobe and temporal lobe of the brain, with sparing of the parietal and occipital lobes.

Progressive nonfluent aphasia (PNFA) is one of three clinical syndromes associated with frontotemporal lobar degeneration. PNFA has an insidious onset of language deficits over time as opposed to other stroke-based aphasias, which occur acutely following trauma to the brain. The specific degeneration of the frontal and temporal lobes in PNFA creates hallmark language deficits differentiating this disorder from other Alzheimer-type disorders by the initial absence of other cognitive and memory deficits. This disorder commonly has a primary effect on the left hemisphere, causing the symptomatic display of expressive language deficits and sometimes may disrupt receptive abilities in comprehending grammatically complex language.

<span class="mw-page-title-main">Primary progressive aphasia</span> Medical condition

Primary progressive aphasia (PPA) is a type of neurological syndrome in which language capabilities slowly and progressively become impaired. As with other types of aphasia, the symptoms that accompany PPA depend on what parts of the left hemisphere are significantly damaged. However, unlike most other aphasias, PPA results from continuous deterioration in brain tissue, which leads to early symptoms being far less detrimental than later symptoms.

<span class="mw-page-title-main">Hippocampal sclerosis</span> Medical condition

Hippocampal sclerosis (HS) or mesial temporal sclerosis (MTS) is a neuropathological condition with severe neuronal cell loss and gliosis in the hippocampus. Neuroimaging tests such as magnetic resonance imaging (MRI) and positron emission tomography (PET) may identify individuals with hippocampal sclerosis. Hippocampal sclerosis occurs in 3 distinct settings: mesial temporal lobe epilepsy, adult neurodegenerative disease and acute brain injury.

Semantic dyslexia is, as the name suggests, a subtype of the group of cognitive disorders known as alexia. Those who have semantic dyslexia are unable to properly attach words to their meanings in reading or speech. When confronted with the word "diamond", they may understand it as "sapphire", "shiny" or "diamonds"; when asking for a bus ticket, they may ask for some paper or simply "a thing".

Logopenic progressive aphasia (LPA) is a variant of primary progressive aphasia. It is defined clinically by impairments in naming and sentence repetition. It is similar to conduction aphasia and is associated with atrophy to the left posterior temporal cortex and inferior parietal lobule. It is suspected that an atypical form of Alzheimer's disease is the most common cause of logopenic progressive aphasia.

<span class="mw-page-title-main">Corticobasal degeneration</span> Rare neurodegenerative disease

Corticobasal degeneration (CBD) is a rare neurodegenerative disease involving the cerebral cortex and the basal ganglia. CBD symptoms typically begin in people from 50 to 70 years of age, and the average disease duration is six years. It is characterized by marked disorders in movement and cognition, and is classified as one of the Parkinson plus syndromes. Diagnosis is difficult, as symptoms are often similar to those of other disorders, such as Parkinson's disease, progressive supranuclear palsy, and dementia with Lewy bodies, and a definitive diagnosis of CBD can only be made upon neuropathologic examination.

<span class="mw-page-title-main">Frontal lobe disorder</span> Brain disorder

Frontal lobe disorder, also frontal lobe syndrome, is an impairment of the frontal lobe of the brain due to disease or frontal lobe injury. The frontal lobe plays a key role in executive functions such as motivation, planning, social behaviour, and speech production. Frontal lobe syndrome can be caused by a range of conditions including head trauma, tumours, neurodegenerative diseases, neurodevelopmental disorders, neurosurgery and cerebrovascular disease. Frontal lobe impairment can be detected by recognition of typical signs and symptoms, use of simple screening tests, and specialist neurological testing.

<span class="mw-page-title-main">Posterior cortical atrophy</span> Medical condition

Posterior cortical atrophy (PCA), also called Benson's syndrome, is a rare form of dementia which is considered a visual variant or an atypical variant of Alzheimer's disease (AD). The disease causes atrophy of the posterior part of the cerebral cortex, resulting in the progressive disruption of complex visual processing. PCA was first described by D. Frank Benson in 1988.

The neuroanatomy of memory encompasses a wide variety of anatomical structures in the brain.

Phonagnosia is a type of agnosia, or loss of knowledge, that involves a disturbance in the recognition of familiar voices and the impairment of voice discrimination abilities in which the affected individual does not suffer from comprehension deficits. Phonagnosia is an auditory agnosia, an acquired auditory processing disorder resulting from brain damage, other auditory agnosias include cortical deafness and auditory verbal agnosia also known as pure word deafness.

Corticobasal syndrome (CBS) is a rare, progressive atypical Parkinsonism syndrome and is a tauopathy related to frontotemporal dementia. CBS is typically caused by the deposit of tau proteins forming in different areas of the brain.

Semantic amnesia is a type of amnesia that affects semantic memory and is primarily manifested through difficulties with language use and acquisition, recall of facts and general knowledge. A patient with semantic amnesia would have damage to the temporal lobe.

<span class="mw-page-title-main">Limbic-predominant age-related TDP-43 encephalopathy</span> (LATE) -- a form of dementia

LATE is a term that describes a prevalent condition with impaired memory and thinking in advanced age, often culminating in the dementia clinical syndrome. In other words, the symptoms of LATE are similar to those of Alzheimer's disease. 

References

  1. ↑ Gorno-Tempini, M.L.; Hillis, A.E.; Weintraub, S.; et al. (March 2011). "Classification of primary progressive aphasia and its variants". Neurology. 76 (11): 1006–14. doi:10.1212/WNL.0b013e31821103e6. PMC   3059138 . PMID   21325651.
  2. 1 2 3 4 5 6 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. PMC   2963791 . 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. PMC   3158975 . PMID   21809067.
  4. ↑ "Alzheimer Europe - Dementia - Other forms of dementia - Neurodegenerative diseases - Fronto-Temporal Degeneration - Semantic Dementia (SD)". www.alzheimer-europe.org. Retrieved 2020-07-18.
  5. ↑ "Encephalitis, Herpes Simplex". NORD (National Organization for Rare Disorders). Retrieved 2020-07-19.
  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.
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  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. 1 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. PMC   4006153 . 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. PMC   4808428 . 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.; Crutch, Sebastian J. (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. PMC   5531024 . PMID   28750682.
  14. ↑ 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.
  15. ↑ Goldman, J.S.; Farmer, J.M.; Wood, E.M.; 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. S2CID   37191580.
  16. ↑ "Alzheimer Europe - Dementia - Other forms of dementia - Neurodegenerative diseases - Fronto-Temporal Degeneration - Semantic Dementia (SD)". www.alzheimer-europe.org. Retrieved 2020-07-19.
  17. ↑ 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. S2CID   8838693.
  18. 1 2 3 "Semantic variant Primary Progressive Aphasia". Association for Frontotemporal Degeneration. Retrieved 2017-12-18.
  19. ↑ 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.
  20. ↑ Marcotte, Karine; Graham, Naida L.; Fraser, Kathleen C.; Meltzer, Jed A.; Tang-Wai, David F.; Chow, Tiffany W.; Freedman, Morris; Leonard, Carol; Black, Sandra E. (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. PMC   5465709 . PMID   28611820.
  21. 1 2 3 4 5 6 20
  22. ↑ Chan, D.; Fox, N.C.; Scahill, R.I.; et al. (April 2001). "Patterns of temporal lobe atrophy in semantic dementia and Alzheimer's disease". Annals of Neurology. 49 (4): 433–42. CiteSeerX   10.1.1.569.8292 . doi:10.1002/ana.92. PMID   11310620. S2CID   41627534.
  23. ↑ 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. S2CID   130161.
  24. 1 2 3 Iaccarino, Leonardo; Crespi, Chiara; Della Rosa, Pasquale Anthony; Catricalà, Eleonora; Guidi, Lucia; Marcone, Alessandra; Tagliavini, Fabrizio; Magnani, Giuseppe; Cappa, Stefano F. (2015-03-10). "The Semantic Variant of Primary Progressive Aphasia: Clinical and Neuroimaging Evidence in Single Subjects". PLOS ONE. 10 (3): e0120197. Bibcode:2015PLoSO..1020197I. doi: 10.1371/journal.pone.0120197 . ISSN   1932-6203. PMC   4354903 . PMID   25756991.
  25. ↑ 21
  26. ↑ 22
  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. PMC   2699352 . PMID   18348092.
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.

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