Frontotemporal dementia

Short description: Types of dementia involving the frontal or temporal lobes

Frontotemporal dementia

Other names| FTD, Frontotemporal degeneration, Frontal lobe dementia, Pick's disease
FTD primarily affects the frontal and temporal lobes of the brain.
Specialty| Neurology, Psychiatry
Usual onset| Commonly 45–64 years, but can occur earlier
Causes| frontotemporal lobar degeneration
Risk factors| Family history of FTD or ALS; risk-associated mutations of GRN, MAPT, C9orf72 genes, and other less-common genes; ALS diagnosis; environmental risk factors currently unknown
Diagnostic method| Clinical diagnosis of exclusion based on progressive behavioral, cognitive, communication, or movement-based symptoms, with no other explanation. Supportive evidence from neuroimaging or genetic testing. Confirmed diagnosis via brain autopsy.
Differential diagnosis| Alzheimer's disease, Parkinsons' disease, Lewy body dementia, Vascular dementia, Mild cognitive impairment, Depression, Generalized anxiety disorder, other mental disorders
Treatment| As no cures or disease-modifying treatments have been approved, symptom management is the primary focus for FTD. Person-centered care is often used to address heterogeneous symptoms that vary between people.
Medication| No drugs have been approved for the condition, but medications may be prescribed to manage symptoms.
Prognosis| Life expectancy is highly variable but is typically 7–13 years.
Frequency| In 2011 in the United States, 50,000-60,000 [1]

Frontotemporal dementia (FTD), also known as frontotemporal degeneration, and historically as Pick's disease, is a family of neurodegenerative disorders, caused by frontotemporal lobar degeneration that affects the frontal and temporal lobes.[2] The FTD family includes behavioral variant FTD (bvFTD), primary progressive aphasia (PPA) and its semantic and nonfluent/agrammatic variants (svPPA and nfvPPA)[2], primary progressive apraxia of speech (PPAOS),[3][4] progressive supranuclear palsy (PSP), and corticobasal syndrome (CBS).[2] Through a mutual risk gene, FTD and amyotrophic lateral sclerosis (ALS) share a clinical spectrum, where symptoms of both disorders can co-occur.[5] Symptoms of FTD will typically match a specific disorder at first, though symptoms of other disorders will inevitably begin to show as the disease progresses to different areas of the brain.[6] FTD disorders are a common young-onset dementia occurring under the age of 60.[7]

Approximately 60% of people diagnosed with FTD have no known cause and no family history of FTD or related conditions; this is known as sporadic FTD. While environmental causes and unidentified gene variants are suspected causes of sporadic FTD, research in this area is still ongoing. When people have a family history of FTD, other dementias, or conditions like depression and anxiety, it is referred to as familial FTD, and roughly 20% have an underlying genetic basis. Variants in three genes are responsible for most genetic FTD. Notably, in about 10% of people with seemingly sporadic FTD, a genetic variant is identified.[8]

FTD diagnosis currently relies on clinical examination based on the signs and symptoms experienced and imaging of the brain through MRI or FTDG-PET. FTD disorders have heterogeneous symptoms and pathological features, which contribute to a lengthy differential diagnostic process and high rates of misdiagnosis. A neuropathological examination after death usually provides a definitive diagnosis by identifying the specific features of FTD subtypes.[2]

There is no cure for FTD, nor are any disease-modifying treatments approved that could slow disease progression. The aim of treatment is to manage symptoms, which is primarily accomplished through non-pharmacological interventions such as person-centric care strategies or physical and occupational therapy. Medication can be used to address symptoms like depression or anxiety, but some drugs, like sleep or antipsychotic medicines, carry a considerable risk of side effects for people with FTD.[9] Death is usually the result of complications of FTD, such as pneumonia or fall-related injuries. The average life expectancy after symptoms start is 7 to 13 years.[10]

The clinical features of FTD were first described by Czech-German psychiatrist Arnold Pick between 1892 and 1906. Pick's observations were followed by Alois Alzheimer's first description of tau aggregations in neurons (called "Pick bodies") in 1911. The disorder described by Pick, now known as bvFTD, was named "Pick's disease" in 1922.[11] The first research criteria were created in 1994, and the publication was the first to use the term "frontotemporal dementia".[12]

## Contents

* 1 Signs and symptoms
* 2 Subtypes and related disorders
* 2.1 Behavioral variant frontotemporal dementia
* 2.2 Semantic dementia
* 2.3 Progressive nonfluent aphasia
* 2.4 Neuronal intermediate filament inclusion disease
* 2.5 Basophilic inclusion body disease
* 3 Other characteristics
* 4 Genetics
* 5 Pathology
* 6 Diagnosis
* 6.1 Neuropsychological tests
* 7 Management
* 8 Prognosis
* 9 History
* 10 Notable cases
* 11 See also
* 12 References
* 13 Further reading
* 14 External links

## Signs and symptoms

Frontotemporal dementia (FTD) is an early onset disorder that mostly occurs between the ages of 45 and 65,[13] but can begin earlier, and in 20–25% of cases onset is later.[14][15] Men and women appear to be equally affected.[16] It is the most common early presenting dementia.[17] FTD is the second most prevalent type of early onset dementia after Alzheimer's disease.[16][18]

The International Classification of Diseases recognizes the disease as causative to disorders affecting mental and behavioral aspects. Dissociation from family, compulsive buying disorder (oniomania), vulgar speech characteristics, screaming, and inability to control emotions, behavior, personality, or temperament are characteristic social display patterns.[19] The gradual onset and progression of subtle changes in behavior or language deficits commonly leads to a long delay between the onset of symptoms and time of presentation to a neurologist.[16]

## Subtypes and related disorders

The main subtypes of frontotemporal dementia are behavioral variant FTD (bvFTD), two variants of primary progressive aphasia (PPA) – semantic dementia (svPPA) and progressive nonfluent aphasia (nfvPPA)[20][21] – as well as FTD associated with amyotrophic lateral sclerosis (FTD–ALS or FTD-MND).[16] Two distinct rare subtypes are neuronal intermediate filament inclusion disease (NIFID), and basophilic inclusion body disease (BIBD). Related disorders are corticobasal syndrome (CBS), and progressive supranuclear palsy (PSP).[16]

### Behavioral variant frontotemporal dementia

MRI of the brain showing bvFTD. Cortex and white matter atrophy of the frontal lobes is clearly visible.

Behavioral variant frontotemporal dementia (BvFTD) was previously known as Pick's disease, and is the most common of the FTD types.[22][21] BvFTD is diagnosed four times as often as the PPA variants.[23] Behavior can change in BvFTD in either of two ways—it can change to being impulsive and disinhibited, acting in socially unacceptable ways; or it can change to being listless and apathetic.[24][25] About 12–13% of people with bvFTD develop motor neuron disease.[26]

The Pick bodies which are present in behavioral variant FTD are spherical inclusion bodies found in the cytoplasm of affected cells. They consist of tau fibrils as a major component together with a number of other protein products including ubiquitin and tubulin.[27]

### Semantic dementia

Semantic dementia (SD) is characterized by the loss of semantic understanding, resulting in impaired word comprehension. However, speech remains fluent and grammatical.[25]

### Progressive nonfluent aphasia

Progressive nonfluent aphasia (PNFA) is characterized by progressive difficulties in speech production.[25]

### Neuronal intermediate filament inclusion disease

Neuronal intermediate filament inclusion disease (NIFID) is a rare distinct variant. The inclusion bodies that are present in NIFID are cytoplasmic and made up of type IV intermediate filaments.[28][29] NIFID has an early age of onset between 23 and 56. Symptoms can include behavioral and personality changes, memory and cognitive impairments, language difficulties, motor weakness, and extrapyramidal symptoms.[28] NIFID is one of the frontotemporal lobar degeneration (FTLD)–FUS proteopathies.[29] Imaging commonly shows atrophy in the frontotemporal region, and in part of the striatum in the basal ganglia. Post-mortem studies show a marked reduction in the caudate nucleus of the striatum; frontotemporal gyri are narrowed, with widened intervening sulci, and the lateral ventricles are enlarged.[28]

### Basophilic inclusion body disease

Another rare FTD variant, also a FTLD-FUS proteopathy, is basophilic inclusion body disease (BIBD).[30][31]

## Other characteristics

In later stages of FTD, the clinical phenotypes may overlap.[25] People with FTD tend to struggle with binge eating and compulsive behaviors.[32] Binge eating habits are often associated with changes in food preferences (cravings for more sweets, carbohydrates), eating inedible objects and snatching food from others. Recent findings from structural MRI research have indicated that eating changes in FTD are associated with atrophy (wasting) in the right ventral insula, striatum, and orbitofrontal cortex.[32]

People with FTD show marked deficiencies in executive functioning and working memory.[33] Most become unable to perform skills that require complex planning or sequencing.[34] In addition to the characteristic cognitive dysfunction, a number of primitive reflexes known as frontal release signs are often able to be elicited. Usually the first of these frontal release signs to appear is the palmomental reflex which appears relatively early in the disease course whereas the palmar grasp reflex and rooting reflex appear late in the disease course.[35] Importantly, the presence of primitive reflexes in FTD is not highly sensitive or specific for the disease process, but their presence is helpful when considered within a broader neurological assessment, particularly with other suggestive features like behavioral and personality changes, disinhibition, executive dysfunction, and memory impairment.[36]

In rare cases, FTD can occur in people with amyotrophic lateral sclerosis (ALS), a motor neuron disease. As of 2005[update], the prognosis for people with ALS was worse when combined with FTD, shortening survival by about a year.[37] Up to 50% of patients with ALS go on to develop cognitive and behavioral symptoms, with around 10–15% meeting criteria for FTD, most commonly the behavioral variant.[38] Some FTD patients conversely also go on to develop features of motor neuron disease similar to those of ALS.[39] The two disease entities are thought to have interrelated clinical and genetic factors and are considered part of a disease spectrum rather than two completely separate processes.[38]

Cerebrospinal fluid leaks are a known cause of reversible frontotemporal dementia.[40] This is due to a spontaneous intracranial hypertension which may present with neuropsychiatric symptoms that mimic FTD, particularly the behavioral type.[41] Treatment of the leak results in partial or complete resolution of symptoms in the majority of cases, in contrast with neurodegenerative FTD, which is a primary and mostly irreversible process.[41]

## Genetics

A higher proportion of frontotemporal dementias seem to have a familial component than other neurodegenerative diseases such as Alzheimer's disease. More and more mutations and genetic variants are being identified all the time, needing constant updating of genetic influences.

* Tau-positive frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) is caused by mutations in the MAPT gene on chromosome 17 that encodes the tau protein.[42] It has been determined that there is a direct relationship between the type of tau mutation and the neuropathology of gene mutations. The mutations at the splice junction of exon 10 of tau lead to the selective deposition of the repetitive tau in neurons and glia. The pathological phenotype associated with mutations elsewhere in tau is less predictable, with both typical neurofibrillary tangles (consisting of both 3-repeat and 4-repeat tau) and Pick bodies (consisting of 3-repeat tau) having been described. The presence of tau deposits within glia is also variable in families with mutations outside of exon 10. This disease is now informally designated FTDP-17T. FTD shows a linkage to the region of the tau locus on chromosome 17, but it is believed that there are two loci leading to FTD within megabases of each other on chromosome 17.[43] The only other known autosomal dominant genetic cause of FTLD-tau is a hypomorphic mutation in VCP which is associated with a unique neuropathology called vacuolar tauopathy.[44]
* FTD caused by FTLD-TDP43 has numerous genetic causes. Some cases are due to mutations in the GRN gene, also located on chromosome 17. Others are caused by hypomorphic VCP mutations, although these patients present with a complex picture of multisystem proteinopathy that can include amyotrophic lateral sclerosis, inclusion body myopathy, Paget's disease of bone, and FTD. The most recent addition to the list (as of 2019[update]) was a hexanucleotide repeat expansion in intron 1 of C9ORF72.[45][46][47] Only one or two cases have been reported describing TARDBP (the TDP-43 gene) mutations in a clinically pure FTD (FTD without ALS). * Several other genes have been linked to this condition. These include CYLD, OPTN, SQSTM1 and TBK1.[48] These genes have been implicated in the autophagy pathway.
* Major alleles of TMEM106B SNPs have been found to be associated with risk of FTLD.[49]

## Pathology

Main article: Medicine:Frontotemporal lobar degeneration

There are three main histological subtypes found at post-mortem: FTLD-tau, FTLD-TDP, and FTLD-FUS. In rare cases, patients with clinical FTD were found to have changes consistent with Alzheimer's disease on autopsy.[50] The most severe brain atrophy appears to be associated with behavioral variant FTD, and corticobasal degeneration.[51]

With regard to the genetic defects that have been found, repeat expansion in the C9orf72 gene is considered a major contribution to FTLD, although defects in the GRN and MAPT genes are also associated with it.[52]

DNA damage and the defective repair of such damages have been etiologically linked to various neurodegenerative diseases including FTD.[53]

## Diagnosis

FTD is traditionally difficult to diagnose owing to the diverse nature of the associated symptoms. Signs and symptoms are classified into three groups based on the affected functions of the frontal and temporal lobes:[54] These are behavioral variant frontotemporal dementia, semantic dementia, and progressive nonfluent aphasia. An overlap between symptoms can occur as the disease progresses and spreads through the brain regions.[15]

Structural MRI scans often reveal frontal lobe and/or anterior temporal lobe atrophy, but in early cases the scan may seem normal. Atrophy can be either bilateral or asymmetric.[13] Registration of images at different points of time (e.g., one year apart) can show evidence of atrophy that otherwise at individual time points may be reported as normal. Many research groups have begun using techniques such as magnetic resonance spectroscopy, functional imaging, and cortical thickness measurements in an attempt to offer an earlier diagnosis to the FTD patient. Fluorine-18-fluorodeoxyglucose positron emission tomography scans classically show frontal and/or anterior temporal hypometabolism, which helps differentiate the disease from Alzheimer's disease, as the PET scan in Alzheimer's disease classically shows biparietal hypometabolism.

Meta-analyses based on imaging methods have shown that frontotemporal dementia mainly affects a frontomedial network discussed in the context of social cognition or "theory of mind".[55] This is entirely in keeping with the notion that on the basis of cognitive neuropsychological evidence, the ventromedial prefrontal cortex is a major locus of dysfunction early on in the course of the behavioral variant of frontotemporal degeneration.[56] The language subtypes of FTLD (semantic dementia and progressive nonfluent aphasia) can be regionally dissociated by imaging approaches in vivo.[57]

The confusion between Alzheimer's and FTD is justifiable due to the similarities between their initial symptoms. Patients do not have difficulty with movement and other motor tasks.[58] As FTD symptoms appear, it is difficult to differentiate between a diagnosis of Alzheimer's disease and FTD. There are distinct differences in the behavioral and emotional symptoms of the two dementias, notably, the blunting of affect seen in FTD patients.[13] In the early stages of FTD, anxiety and depression are common, which may result in an ambiguous diagnosis. However, over time, these ambiguities fade away as this dementia progresses and defining symptoms of apathy, which are highly prevalent in FTD, start to appear.[59][60]

Recent studies over several years have developed new criteria for the diagnosis of behavioral variant frontotemporal dementia (bvFTD). The confirmatory diagnosis is made by brain biopsy, but other tests can be used to help, such as MRI, EEG, CT, and physical examination and history.[61] As of 2011[update], six distinct clinical features have been identified as symptoms of bvFTD.[62]

1. Disinhibition
2. Apathy / inertia
3. Loss of sympathy / empathy
4. Perseverative / compulsive behaviors
5. Hyperorality
6. Dysexecutive neuropsychological profile

Of the six features, three must be present in a patient to diagnose one with possible bvFTD. Similar to standard FTD, the primary diagnosis stems from clinical trials that identify the associated symptoms, instead of imaging studies.[62] The above criteria are used to distinguish bvFTD from disorders such as Alzheimer's and other causes of dementia. In addition, the criteria allow for a diagnostic hierarchy distinguished possible, probable, and definite bvFTD based on the number of symptoms present.[62]

A 2021 study, determined that using cerebrospinal fluid (CSF) biomarkers of pathologic amyloid plaques, tangles, and neurodegeneration, collectively called ATN, can be useful in diagnosing FTD.[63]

### Neuropsychological tests

The progression of the degeneration caused by bvFTD may follow a predictable course. The degeneration begins in the orbitofrontal cortex and medial aspects such as ventromedial prefrontal cortex. In later stages, it gradually expands its area to the dorsolateral prefrontal cortex and the temporal lobe.[64] Thus, the detection of dysfunction of the orbitofrontal cortex and ventromedial cortex is important in the detection of early stage bvFTD. As stated above, a behavioral change may occur before the appearance of any atrophy in the brain in the course of the disease. Because of that, image scanning such as MRI can be insensitive to the early degeneration and it is difficult to detect early-stage bvFTD. In neuropsychology, there is an increasing interest in using neuropsychological tests such as the Iowa gambling task or Faux Pas Recognition test as an alternative to imaging for the diagnosis of bvFTD.[65] Both the Iowa gambling task and the Faux Pas test are known to be sensitive to dysfunction of the orbitofrontal cortex. The Faux Pas Recognition test is intended to measure one's ability to detect faux pas types of social blunders (accidentally making a statement or an action that offends others). It is suggested that people with orbitofrontal cortex dysfunction show a tendency to make social blunders due to a deficit in self-monitoring.[66] Self-monitoring is the ability of individuals to evaluate their own behavior to make sure that their behavior is appropriate in particular situations. The impairment in self-monitoring leads to a lack of social emotion signals. The social emotions such as embarrassment are important in the way that they alert the individual to adapt social behavior in an appropriate manner to maintain relationships with others. Though patients with damage to the OFC retain intact knowledge of social norms, they fail to apply it to actual behavior, because they fail to generate social emotions that promote adaptive social behavior.[66]

The other test, the Iowa gambling task, is a psychological test intended to simulate real-life decision making. The underlying concept of this test is the somatic marker hypothesis. This hypothesis argues that when people have to make complex uncertain decisions, they employ both cognitive and emotional processes to assess the values of the choices available to them. Each time a person makes a decision, both physiological signals and evoked emotion (somatic markers) are associated with their outcomes, and this accumulates as experience. People tend to choose the choice which might produce the outcome reinforced with positive stimuli; thus it biases decision-making towards certain behaviors while avoiding others.[67] It is thought that somatic markers are processed in the orbitofrontal cortex.

In order to solve this problem, some researchers have combined neuropsychological tests which detect the dysfunction of orbitofrontal cortex into one grouping, so that it increases its specificity to the degeneration of the frontal lobe, in order to detect early-stage bvFTD. They invented the Executive and Social Cognition Battery which comprises five neuropsychological tests:[65]

* Faux Pas test
* Hotel task
* Iowa gambling task
* Mind in the Eyes
* Multiple Errands task

The result has shown that this combined test is more sensitive in detecting the deficits in early bvFTD.[65]

## Management

Currently, there is no cure for FTD. Treatments are available to manage the behavioral symptoms. Rehabilitation services supporting every day functioning have demonstrated some positive results, in particular the Tailored Activity Programme, which is occupational therapy based. Positive behavior support (PBS) has also been identified as potentially beneficial for people with bvFTD.[68] Pharmacologic therapy is primarily aimed towards managing neuropsychiatric symptoms associated with FTD. Disinhibition, hyperorality, and compulsive behaviors can be controlled by selective serotonin reuptake inhibitors (SSRIs).[69][70] Agitation or aggression can be controlled with small doses of atypical antipsychotics.[71] Although Alzheimer's and FTD share certain symptoms, they cannot be treated with the same pharmacological agents because the cholinergic systems are not affected in FTD.[13]In fact, cholinesterase inhibitors and memantine, used frequently in the treatment of Alzheimer’s disease, have not shown benefit and may even worsen behavioral symptoms in FTD.[72]

## Prognosis

Symptoms of frontotemporal dementia progress at a rapid, steady rate. Patients with the disease can survive for 2–20 years. Eventually patients will need 24-hour care for daily function.[73]

## History

Features of FTD were first described by the Czech psychiatrist Arnold Pick between 1892 and 1906.[74][75] The name Pick's disease was coined in 1922.[76] This term is now reserved only for behavioral variant FTD which shows the presence of the characteristic Pick bodies and Pick cells,[77][54] which were first described by Alois Alzheimer in 1911.[76]

In 1989, Snowden suggested the term semantic dementia to describe the patient with predominant left temporal atrophy and aphasia that Pick described. The first research criteria for FTD, "Clinical and neuropathological criteria for frontotemporal dementia. The Lund and Manchester Groups", was developed in 1994. The clinical diagnostic criteria were revised in the late 1990s, when the FTD spectrum was divided into a behavioral variant, a nonfluent aphasia variant, and a semantic dementia variant.[23] A nonprofit organization, the Association for Frontotemporal Degeneration (AFTD) was founded in 2002 and convenes a number of scientific conferences, a global FTD registry, and provides investment in research to slow and potentially treat the disease.[78] The most recent revision of the clinical research criteria was by the International Behavioural Variant FTD Criteria Consortium in 2011.[62]

## Notable cases

People who have been diagnosed as having FTD (often referred to as Pick's disease in cases of the behavioral variant) include:

* John Berry (1963–2016), American hardcore punk musician and founding member of the Beastie Boys[79]
* Clancy Blair (1960–2024), American developmental psychologist and professor[80]
* Don Cardwell (1935–2008), Major League Baseball pitcher[81]
* Charmian Carr (1942–2016), who played Liesl, from the Sound of Music, born Charmian Anne Farnon
* Jerry Corbetta (1947–2016), frontman, organist and keyboardist of American psychedelic rock band Sugarloaf[82]
* Ted Darling (1935–1996), Buffalo Sabres television announcer
* Robert W. Floyd (1936–2001), computer scientist[83]
* Curtis Hanson (1945–2016), American film director, screenwriter, and producer[84]
* Lee Holloway (born 1982), computer scientist, co-founder of Cloudflare[85]
* Colleen Howe (1933–2009), sports agent and ice hockey team manager, known as "Mrs. Hockey"[86]
* Kazi Nazrul Islam (1899–1976) national poet of Bangladesh[87]
* Terry Jones (1942–2020), Welsh comedian (Monty Python) and director
* Ralph Klein (1942–2013), former premier of Alberta, Canada
* Kevin Moore (1958–2013), English footballer[88]
* Ernie Moss (1949–2021), English footballer[89]
* Nic Potter (1951–2013), British bassist for Van der Graaf Generator[90]
* Christina Ramberg (1946–1995), American painter associated with the Chicago Imagists[91]
* Björn Skifs (born 1947), Swedish musician and songwriter[92]
* Sir Nicholas Wall (1945–2017), English judge[93]
* Bruce Willis (born 1955), American actor[94]
* Mark Wirtz (1943–2020), French pop musician, composer and producer[95]
* Bobby Kimball (born 1947), American singer[96]

## See also

* Alcoholic dementia
* Lewy body dementia
* Logopenic progressive aphasia
* Mini-SEA
* Proteopathy
* Transportin 1
* Vascular dementia

## References

1. ↑ Knopman, David (2011-05-17). "Estimating the Number of Persons with Frontotemporal Lobar Degeneration in the US Population". Journal of Molecular Neuroscience 45 (3): 330–335. doi:10.1007/s12031-011-9538-y. PMID 21584654.
2. ↑ 2.0 2.1 2.2 2.3 Ljubenkov, P. A.; Miller, B. L. (2016). "Psychiatry Online" (in en). Focus (American Psychiatric Publishing) 14 (4): 448–464. doi:10.1176/appi.focus.20160018. PMID 31975825. PMC 6519586. https://psychiatryonline.org/action/cookieAbsent. Retrieved 2026-03-06.
3. ↑ Croot, Karen; Wauters, Lisa; Staiger, Anja (2025). "Apraxia of speech in primary progressive aphasia and primary progressive apraxia of speech". The Oxford Handbook of Communication Disorders in Neurodegenerative Diseases. pp. 110–128. doi:10.1093/oxfordhb/9780198888482.013.0007. ISBN 978-0-19-888848-2.
4. ↑ Ljubenkov, Peter A.; Miller, Bruce L. (2016). "A Clinical Guide to Frontotemporal Dementias". Focus 14 (4): 448–464. doi:10.1176/appi.focus.20160018. PMID 31975825.
5. ↑ Strong, Michael J.; Abrahams, Sharon; Goldstein, Laura H.; Woolley, Susan; Mclaughlin, Paula; Snowden, Julie; Mioshi, Eneida; Roberts-South, Angie et al. (May 2017). "Amyotrophic lateral sclerosis - frontotemporal spectrum disorder (ALS-FTSD): Revised diagnostic criteria". Amyotrophic Lateral Sclerosis & Frontotemporal Degeneration 18 (3–4): 153–174. doi:10.1080/21678421.2016.1267768. PMID 28054827.
6. ↑ Zhang, Xin; Irish, Muireann; Piguet, Olivier; Ahmed, Rebekah M. (2025-03-21). "Behavioural and cognitive profiles in frontotemporal dementia and Alzheimer's disease: a longitudinal study" (in en). Journal of Neurology 272 (4): 279. doi:10.1007/s00415-025-13025-z. ISSN 1432-1459. PMID 40116949. PMC 11928428. https://doi.org/10.1007/s00415-025-13025-z.
7. ↑ Urso, Daniele; Giannoni-Luza, Stefano; Brayne, Carol; Ray, Nicolas; Logroscino, Giancarlo (1 November 2025). "Incidence and Prevalence of Frontotemporal Dementia: A Systematic Review and Meta-Analysis". JAMA Neurology 82 (11): 1144–1152. doi:10.1001/jamaneurol.2025.3307. PMID 40920400.
8. ↑ Greaves, Caroline V.; Rohrer, Jonathan D. (August 2019). "An update on genetic frontotemporal dementia". Journal of Neurology 266 (8): 2075–2086. doi:10.1007/s00415-019-09363-4. ISSN 1432-1459. PMID 31119452.
9. ↑ Magrath Guimet, Nahuel; Zapata-Restrepo, Lina M.; Miller, Bruce L. (October 2022). "Advances in Treatment of Frontotemporal Dementia" (in en). The Journal of Neuropsychiatry and Clinical Neurosciences 34 (4): 316–327. doi:10.1176/appi.neuropsych.21060166. ISSN 0895-0172. PMID 35578801. https://psychiatryonline.org/doi/10.1176/appi.neuropsych.21060166.
10. ↑ Onyike, Chiadi U. (2011). "What Is the Life Expectancy in Frontotemporal Lobar Degeneration?" (in en). Neuroepidemiology 37 (3–4): 166–167. doi:10.1159/000333347. ISSN 0251-5350. PMID 22056969.
11. ↑ Ulugut, Hulya; Pijnenburg, Yolande A. L. (November 2023). "Frontotemporal dementia: Past, present, and future" (in en). Alzheimer's & Dementia 19 (11): 5253–5263. doi:10.1002/alz.13363. ISSN 1552-5260. PMID 37379561. https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.13363.
12. ↑ "Clinical and neuropathological criteria for frontotemporal dementia. The Lund and Manchester Groups." (in en). Journal of Neurology, Neurosurgery & Psychiatry 57 (4): 416–418. 1994-04-01. doi:10.1136/jnnp.57.4.416. ISSN 0022-3050. PMID 8163988.
13. ↑ 13.0 13.1 13.2 13.3 "Frontotemporal dementia". The British Journal of Psychiatry 180 (2): 140–143. February 2002. doi:10.1192/bjp.180.2.140. PMID 11823324.
14. ↑ "RNA Binding Proteins and the Pathogenesis of Frontotemporal Lobar Degeneration". Annual Review of Pathology 14: 469–495. January 2019. doi:10.1146/annurev-pathmechdis-012418-012955. PMID 30355151.
15. ↑ 15.0 15.1 "Frontotemporal lobar degeneration: epidemiology, pathophysiology, diagnosis and management". CNS Drugs 24 (5): 375–398. May 2010. doi:10.2165/11533100-000000000-00000. PMID 20369906.
16. ↑ 16.0 16.1 16.2 16.3 16.4 "Frontotemporal Dementias". Continuum 22 (2 Dementia): 464–489. April 2016. doi:10.1212/CON.0000000000000300. PMID 27042904.
17. ↑ "Focus on Frontotemporal Dementia (FTD)". National Institute of Neurological Disorders and Stroke. U.S. National Institutes of Health. https://www.ninds.nih.gov/Current-Research/Focus-Disorders/Alzheimers-Related-Dementias/Focus-Frontotemporal-Dementia-FTD.
18. ↑ "FRONTotemporal dementia Incidence European Research Study-FRONTIERS: Rationale and design". Alzheimer's & Dementia 18 (3): 498–506. March 2022. doi:10.1002/alz.12414. PMID 34338439.
19. ↑ The ICD-10 Classification of Mental and Behavioural Disorders Clinical descriptions and diagnostic guidelines. World Health Organization. 1992. p. 51. ISBN 92-4-154422-8. https://cdn.who.int/media/docs/default-source/classification/other-classifications/9241544228_eng.pdf.
20. ↑ Sivasathiaseelan, Harri; Marshall, Charles; Agustus, Jennifer; Benhamou, Elia; Bond, Rebecca; van Leeuwen, Janneke; Hardy, Chris; Rohrer, Jonathan et al. (April 2019). "Frontotemporal Dementia: A Clinical Review". Seminars in Neurology 39 (2): 251–263. doi:10.1055/s-0039-1683379. PMID 30925617.
21. ↑ 21.0 21.1 "What is frontotemporal dementia". https://www.dementiauk.org/understanding-dementia/types-and-symptoms/frontotemporal-dementia/.
22. ↑ "What are the Different Types of Frontotemporal Disorders?" (in en). https://www.nia.nih.gov/health/types-frontotemporal-disorders.
23. ↑ 23.0 23.1 "Frontotemporal Dementia". Neurologic Clinics 35 (2): 339–374. May 2017. doi:10.1016/j.ncl.2017.01.008. PMID 28410663.
24. ↑ "Frontotemporal Dementia Information Page". National Institute of Neurological Disorders and Stroke. U.S. National Institutes of Health. https://www.ninds.nih.gov/health-information/disorders/frontotemporal-dementia-and-other-frontotemporal-disorders.
25. ↑ 25.0 25.1 25.2 25.3 "Molecular pathways of frontotemporal lobar degeneration". Annual Review of Neuroscience 33 (1): 71–88. 2010. doi:10.1146/annurev-neuro-060909-153144. PMID 20415586.
26. ↑ "Frontotemporal dementia". Lancet 386 (10004): 1672–1682. October 2015. doi:10.1016/S0140-6736(15)00461-4. PMID 26595641.
27. ↑ "Pick bodies". Radiology Reference Article. Radiopaedia. https://radiopaedia.org/articles/pick-bodies?lang=gb.
28. ↑ 28.0 28.1 28.2 "Clinical and neuropathologic variation in neuronal intermediate filament inclusion disease". Neurology 63 (8): 1376–1384. October 2004. doi:10.1212/01.wnl.0000139809.16817.dd. PMID 15505152.
29. ↑ 29.0 29.1 "Spatial patterns of FUS-immunoreactive neuronal cytoplasmic inclusions (NCI) in neuronal intermediate filament inclusion disease (NIFID)". Journal of Neural Transmission 118 (11): 1651–1657. November 2011. doi:10.1007/s00702-011-0690-x. PMID 21792670.
30. ↑ "Basophilic inclusions and neuronal intermediate filament inclusions in amyotrophic lateral sclerosis and frontotemporal lobar degeneration". Neuropathology 34 (6): 589–595. December 2014. doi:10.1111/neup.12119. PMID 24673472.
31. ↑ "FUS pathology in basophilic inclusion body disease". Acta Neuropathologica 118 (5): 617–627. November 2009. doi:10.1007/s00401-009-0598-9. PMID 19830439.
32. ↑ 32.0 32.1 "Eating disturbance in behavioural-variant frontotemporal dementia". Journal of Molecular Neuroscience 45 (3): 589–593. November 2011. doi:10.1007/s12031-011-9547-x. PMID 21584651.
33. ↑ "Frontotemporal dementia". The Lancet. Neurology 4 (11): 771–780. November 2005. doi:10.1016/S1474-4422(05)70223-4. PMID 16239184.
34. ↑ "Distinctive neuropsychological patterns in frontotemporal dementia, semantic dementia, and Alzheimer disease". Cognitive and Behavioral Neurology 16 (4): 211–218. December 2003. doi:10.1097/00146965-200312000-00002. PMID 14665820.
35. ↑ Hogan, David B.; Ebly, Erika M. (1995). "Primitive Reflexes and Dementia: Results from the Canadian Study of Health and Aging". Age and Ageing 24 (5): 375–381. doi:10.1093/ageing/24.5.375. PMID 8669338.
36. ↑ Bang, Jee; Spina, Salvatore; Miller, Bruce L (October 2015). "Frontotemporal dementia" (in en). The Lancet 386 (10004): 1672–1682. doi:10.1016/S0140-6736(15)00461-4. PMID 26595641.
37. ↑ "The effects of executive and behavioral dysfunction on the course of ALS". Neurology 65 (11): 1774–1777. December 2005. doi:10.1212/01.wnl.0000188759.87240.8b. PMID 16344521.
38. ↑ 38.0 38.1 Carbayo, Álvaro; Borrego-Écija, Sergi; Turon-Sans, Janina; Cortés-Vicente, Elena; Molina-Porcel, Laura; Gascón-Bayarri, Jordi; Rubio, Miguel Ángel; Povedano, Mónica et al. (5 July 2024). "Clinicopathological correlates in the frontotemporal lobar degeneration–motor neuron disease spectrum". Brain 147 (7): 2357–2367. doi:10.1093/brain/awae011. PMID 38227807.
39. ↑ Gijselinck, Ilse; Van Langenhove, Tim; van der Zee, Julie; Sleegers, Kristel; Philtjens, Stéphanie; Kleinberger, Gernot; Janssens, Jonathan; Bettens, Karolien et al. (January 2012). "A C9orf72 promoter repeat expansion in a Flanders-Belgian cohort with disorders of the frontotemporal lobar degeneration-amyotrophic lateral sclerosis spectrum: a gene identification study". The Lancet Neurology 11 (1): 54–65. doi:10.1016/S1474-4422(11)70261-7. PMID 22154785.
40. ↑ "Hypotension May Cause Frontotemporal Dementia". Neurology Today 2 (9): 35–36. 2002. doi:10.1097/00132985-200209000-00013.
41. ↑ 41.0 41.1 Lashkarivand, Aslan; Eide, Per Kristian (10 May 2022). "Brain Sagging Dementia—Diagnosis, Treatment, and Outcome: A Review". Neurology 98 (19): 798–805. doi:10.1212/WNL.0000000000200511. PMID 35338080.
42. ↑ "Comparative biochemistry of tau in progressive supranuclear palsy, corticobasal degeneration, FTDP-17 and Pick's disease". Brain Pathology 9 (4): 681–693. October 1999. doi:10.1111/j.1750-3639.1999.tb00550.x. PMID 10517507.
43. ↑ "Frontal temporal dementia: dissecting the aetiology and pathogenesis". Brain 129 (Pt 4): 830–831. April 2006. doi:10.1093/brain/awl035. PMID 16543401.
44. ↑ "Autosomal dominant VCP hypomorph mutation impairs disaggregation of PHF-tau". Science 370 (6519). November 2020. doi:10.1126/science.aay8826. PMID 33004675.
45. ↑ "Review: Clinical, genetic and neuroimaging features of frontotemporal dementia". Neuropathology and Applied Neurobiology 45 (1): 6–18. February 2019. doi:10.1111/nan.12535. PMID 30582889. https://discovery.ucl.ac.uk/id/eprint/10068269/.
46. ↑ "How do C9ORF72 repeat expansions cause amyotrophic lateral sclerosis and frontotemporal dementia: can we learn from other noncoding repeat expansion disorders?". Current Opinion in Neurology 25 (6): 689–700. December 2012. doi:10.1097/WCO.0b013e32835a3efb. PMID 23160421.
47. ↑ "DNA repair and neurological disease: From molecular understanding to the development of diagnostics and model organisms". DNA Repair 81. September 2019. doi:10.1016/j.dnarep.2019.102669. PMID 31331820.
48. ↑ "CYLD is a causative gene for frontotemporal dementia – amyotrophic lateral sclerosis". Brain 143 (3): 783–799. March 2020. doi:10.1093/brain/awaa039. PMID 32185393.
49. ↑ "Physiological and pathological functions of TMEM106B: a gene associated with brain aging and multiple brain disorders". Acta Neuropathologica 141 (3): 327–339. March 2021. doi:10.1007/s00401-020-02246-3. PMID 33386471.
50. ↑ "Clinical and psychometric distinction of frontotemporal and Alzheimer dementias". Archives of Neurology 64 (4): 535–540. April 2007. doi:10.1001/archneur.64.4.535. PMID 17420315.
51. ↑ "Clinical and neuroanatomical signatures of tissue pathology in frontotemporal lobar degeneration". Brain 134 (Pt 9): 2565–2581. September 2011. doi:10.1093/brain/awr198. PMID 21908872.
52. ↑ "Dementia in 2013: frontotemporal lobar degeneration-building on breakthroughs". Nature Reviews. Neurology 10 (2): 70–72. February 2014. doi:10.1038/nrneurol.2013.270. PMID 24394289.
53. ↑ "DNA Damage and Repair Deficiency in ALS/FTD-Associated Neurodegeneration: From Molecular Mechanisms to Therapeutic Implication". Frontiers in Molecular Neuroscience 14. 2021. doi:10.3389/fnmol.2021.784361. PMID 34975400.
54. ↑ 54.0 54.1 "Frontotemporal dementia: a review for primary care physicians". American Family Physician 82 (11): 1372–1377. December 2010. PMID 21121521. http://www.aafp.org/afp/2010/1201/p1372.html.
55. ↑ "Neural networks in frontotemporal dementia – a meta-analysis". Neurobiology of Aging 29 (3): 418–426. March 2008. doi:10.1016/j.neurobiolaging.2006.10.023. PMID 17140704.
56. ↑ "Specific cognitive deficits in mild frontal variant frontotemporal dementia". Brain 122 (8): 1469–1493. August 1999. doi:10.1093/brain/122.8.1469. PMID 10430832.
57. ↑ "Towards a nosology for frontotemporal lobar degenerations-a meta-analysis involving 267 subjects". NeuroImage 36 (3): 497–510. July 2007. doi:10.1016/j.neuroimage.2007.03.024. PMID 17478101.
58. ↑ "Impact of DNA testing for early-onset familial Alzheimer disease and frontotemporal dementia". Archives of Neurology 58 (11): 1828–1831. November 2001. doi:10.1001/archneur.58.11.1828. PMID 11708991.
59. ↑ Cardarelli, Roberto; Kertesz, Andrew; Knebl, Janice A. (Dec 1, 2010). "Frontotemporal Dementia: A Review for Primary Care Physicians". American Family Physician 82 (11): 1372–1377. PMID 21121521. https://www.aafp.org/pubs/afp/issues/2010/1201/p1372.html.
60. ↑ Collins, Jessica D.; Henley, Susie M.D.; Suárez-González, Aida (September 2023). "A systematic review of the prevalence of depression, anxiety, and apathy in frontotemporal dementia, atypical and young-onset Alzheimer's disease, and inherited dementia". International Psychogeriatrics 35 (9): 457–476. doi:10.1017/S1041610220001118. PMID 32684177.
61. ↑ MedlinePlus Encyclopedia Frontotemporal dementia
62. ↑ 62.0 62.1 62.2 62.3 "Sensitivity of revised diagnostic criteria for the behavioural variant of frontotemporal dementia". Brain 134 (Pt 9): 2456–2477. September 2011. doi:10.1093/brain/awr179. PMID 21810890.
63. ↑ "ATN incorporating cerebrospinal fluid neurofilament light chain detects frontotemporal lobar degeneration". Alzheimer's & Dementia 17 (5): 822–830. May 2021. doi:10.1002/alz.12233. PMID 33226735.
64. ↑ "Conflict monitoring in early frontotemporal dementia". Neurology 73 (5): 349–355. August 2009. doi:10.1212/wnl.0b013e3181b04b24. PMID 19652138.
65. ↑ 65.0 65.1 65.2 "A neuropsychological battery to detect specific executive and social cognitive impairments in early frontotemporal dementia". Brain 132 (Pt 5): 1299–1309. May 2009. doi:10.1093/brain/awp041. PMID 19336463.
66. ↑ 66.0 66.1 "Orbitofrontal cortex and social behavior: integrating self-monitoring and emotion-cognition interactions". Journal of Cognitive Neuroscience 18 (6): 871–879. June 2006. doi:10.1162/jocn.2006.18.6.871. PMID 16839295.
67. ↑ "The somatic marker hypothesis and the possible functions of the prefrontal cortex". Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences 351 (1346): 1413–1420. October 1996. doi:10.1098/rstb.1996.0125. PMID 8941953.
68. ↑ "Rehabilitation Services for Young-Onset Dementia: Examples from High- and Low-Middle-Income Countries". International Journal of Environmental Research and Public Health 21 (6): 790. June 2024. doi:10.3390/ijerph21060790. PMID 38929036.
69. ↑ "Frontotemporal dementia: treatment response to serotonin selective reuptake inhibitors". The Journal of Clinical Psychiatry 58 (5): 212–216. May 1997. doi:10.4088/jcp.v58n0506. PMID 9184615.
70. ↑ "Medications for behavioral symptoms". Weill Institute for Neurosciences. University of California San Francisco. http://memory.ucsf.edu/ftd/overview/ftd/treatment/multiple/behavioral.
71. ↑ "Diagnosis and management of behavioral issues in frontotemporal dementia". Current Neurology and Neuroscience Reports 12 (5): 528–536. October 2012. doi:10.1007/s11910-012-0302-7. PMID 22847063.
72. ↑ Neylan, Kyra D.; Miller, Bruce L. (July 2023). "New Approaches to the Treatment of Frontotemporal Dementia" (in en). Neurotherapeutics 20 (4): 1055–1065. doi:10.1007/s13311-023-01380-6. PMID 37157041.
73. ↑ "Frontotemporal dementia/Pick's disease". Archives of Neurology 61 (6): 969–971. June 2004. doi:10.1001/archneur.61.6.969. PMID 15210543.
74. ↑ "History of Pick's disease". Revue Neurologique 174 (10): 740–741. 2018. doi:10.1016/j.neurol.2018.09.009.
75. ↑ "Uber die Beziehungen der senilen Hirnatrophie zur Aphasie" (in de). Prag Med Wochenschr 17: 165–167. 1892. NAID 10010657196.
76. ↑ 76.0 76.1 "Pick's disease". Journal of Neurology, Neurosurgery, and Psychiatry 74 (2): 169. February 2003. doi:10.1136/jnnp.74.2.169. PMID 12531941.
77. ↑ Adams and Victor's Principles of Neurology (11th ed.). McGraw Hill. 2019. p. 1096. ISBN 978-0-07-184262-4.
78. ↑ "A Vision for Hope: The Early History of The Association for Frontotemporal Degeneration (AFTD)". 17 September 2025. https://www.theaftd.org/wp-content/uploads/2019/09/AFTD_Early_HIstory.pdf.
79. ↑ "Beastie Boy John Berry Died of Frontal Lobe Dementia – But What Is It?". 31 May 2016. https://scitechconnect.elsevier.com/beastie-boy-died-frontal-lobe-dementia/.
80. ↑ "Honoring Dr. Clarence “Clancy” Blair Jr. | CAS News". https://www.uab.edu/cas/news/arts-sciences-magazine/honoring-dr-clarence-clancy-blair-jr.
81. ↑ "Don Cardwell, 72, Pitcher for 1969 Mets, Is Dead". The New York Times. 16 January 2008. https://www.nytimes.com/2008/01/16/sports/baseball/16cardwell.html.
82. ↑ "Sugarloaf frontman Jerry Corbetta dead at 68". The Denver Post. 2016-09-20. http://www.denverpost.com/2016/09/20/colorado-hitmaker-jerry-corbetta-dead-at-68/.
83. ↑ Knuth, Donald E. (December 2003). "Robert W Floyd, In Memoriam". ACM SIGACT News 34 (4): 3–13. doi:10.1145/954092.954488.
84. ↑ Kenneally, Tim (September 21, 2016). "Curtis Hanson Suffered From Rare Illness, His Partner Reveals". https://www.thewrap.com/curtis-hanson-cause-of-death/.
85. ↑ "The Devastating Decline of a Brilliant Young Coder". Wired. 15 April 2020. https://www.wired.com/story/lee-holloway-devastating-decline-brilliant-young-coder/.
86. ↑ "Fans mourn loss of "Mrs. Hockey," Colleen Howe". March 6, 2009. http://www.freep.com/article/20090306/SPORTS05/90306069?imw=Y.
87. ↑ "Kazi Nazrul Islam: Illness and Treatment". http://www.nazrul.org/nazrul_life/illness.htm.
88. ↑ Sportsteam. "Grimsby Town legend Kevin Moore passes away". http://www.thisisgrimsby.co.uk/Grimsby-Town-legend-Kevin-Moore-passes-away/story-18838049-detail/story.html#axzz2RsGaeCI7.
89. ↑ "Support for Valiants hero Ernie Moss after he is diagnosed with Pick's Disease". The Sentinel. 11 October 2014. http://www.stokesentinel.co.uk/Port-Vale-Support-Valiants-hero-Ernie-Moss/story-23091273-detail/story.html.
90. ↑ "Nic Potter obituary | Music | guardian.co.uk". London: Guardian. 22 January 2013. https://www.theguardian.com/music/2013/jan/22/nic-potter.
91. ↑ "The Sexy, Proto-Feminist Art Of Christina Ramberg's Tragically Short Life". 27 February 2014. https://www.wbur.org/artery/2014/02/27/the-sexy-proto-feminist-art-of-christina-rambergs-tragically-short-life.
92. ↑ Hjetland, Geir Bjarte (2025-07-17). "Björn Skifs har fått demens – sluttar som artist" (in nn-NO). https://www.nrk.no/norge/bjorn-skifs-har-fatt-demens-_-sluttar-som-artist-1.17495226.
93. ↑ "Sir Nicholas Wall, once Britain's top family law judge, commits suicide after dementia diagnosis". The Daily Telegraph. 23 February 2017. https://www.telegraph.co.uk/news/2017/02/23/sir-nicholas-wall-britains-top-family-law-judge-commits-suicide/.
94. ↑ "Bruce Willis Diagnosed With Dementia After Retiring Due to Aphasia". 2023-02-16. https://variety.com/2023/film/news/bruce-willis-dementia-aphasia-retire-1235525599/.
95. ↑ "Mark Wirtz, musician and producer who had a global hit with Excerpt from a Teenage Opera – obituary". The Daily Telegraph. 13 August 2020. https://www.telegraph.co.uk/obituaries/2020/08/12/mark-wirtz-musician-producer-had-global-hit-excerpt-teenage.
96. ↑ Staff, T. M. Z. (2025-09-04). "Toto's Bobby Kimball Documentary Delves Into His Dementia, Life After Diagnosis" (in en). https://www.tmz.com/2025/09/04/totos-bobby-kimball-diagnosed-with-frontotemporal-dementia/.

## Further reading

* Hughes, Virginia (2024-12-22). "Fighting to Avoid Her Mother's Fate, for Her Daughters' Sake". The New York Times. https://www.nytimes.com/2024/12/22/health/frontotemporal-dementia-genetic-mutation-linde-jacobs.html.
* "Behavioral disorders in the frontal and temporal variants of frontotemporal dementia". Neurology. 5 62 (5): 742–748. March 2004. doi:10.1212/01.WNL.0000113729.77161.C9. PMID 15007124.
* "A study of stereotypic behaviours in Alzheimer's disease and frontal and temporal variant frontotemporal dementia". Journal of Neurology, Neurosurgery, and Psychiatry 74 (10): 1398–1402. October 2003. doi:10.1136/jnnp.74.10.1398. PMID 14570833.
* "'Til Death or Dementia Do us Part, a memoir". River Rock Books. https://www.riverrockbooks.com/prints/til-death-or-dementia-do-us-part-a-memoir-by-marilyn-reynolds.
* "The Devastating Decline of a Brilliant Young Coder". Wired. 15 April 2020. https://www.wired.com/story/lee-holloway-devastating-decline-brilliant-young-coder/. Retrieved 17 September 2020.

## External links

* "AFTD – The Association for Frontotemporal Degeneration" (in en-US). https://www.theaftd.org/. Patient group

Classification|

* ICD-11: 6D83
* ICD-10: G31.0
* ICD-9-CM: 331.19
* OMIM: 600274 Online Mendelian Inheritance in Man (OMIM) 105550 Online Mendelian Inheritance in Man (OMIM) 614260
* MeSH: D003704
* DiseasesDB: 10034

|

External resources|

* GeneReviews: MAPT-Related Disorders

* v
* t
* e

Mental and behavioral disorders (F00–F99 & 290–319)

Adult personality and behavior

| Gender dysphoria|

* Ego-dystonic sexual orientation
* Paraphilia
* Fetishism
* Voyeurism
* Sexual maturation disorder
* Sexual relationship disorder

|

Other|

* Factitious disorder
* Munchausen syndrome
* Impulse control disorder
* Dermatillomania
* Kleptomania
* Pyromania
* Trichotillomania
* Personality disorder

Childhood and learning

| Emotional and behavioral|

* ADHD
* Conduct disorder
* ODD
* Emotional and behavioral disorders
* Separation anxiety disorder
* Movement disorders
* Stereotypic
* Social functioning
* DAD
* RAD
* Selective mutism
* Speech
* Stuttering
* Cluttering
* Tic disorder
* Tourette syndrome

|

Intellectual disability|

* X-linked intellectual disability
* Lujan–Fryns syndrome

Psychological development
(developmental disabilities)|

* Pervasive
* Specific

Mood (affective)

* Bipolar
* Bipolar I
* Bipolar II
* Bipolar NOS
* Cyclothymia
* Depression
* Atypical depression
* Dysthymia
* Major depressive disorder
* Melancholic depression
* Seasonal affective disorder
* Mania

Neurological and symptomatic

| Autism spectrum|

* Autism
* Asperger syndrome
* High-functioning autism
* PDD-NOS
* Savant syndrome

|

Dementia|

* AIDS dementia complex
* Alzheimer's disease
* Creutzfeldt–Jakob disease
* Frontotemporal dementia
* Huntington's disease
* Mild cognitive impairment
* Parkinson's disease
* Pick's disease
* Sundowning
* Vascular dementia
* Wandering

Other|

* Delirium
* Organic brain syndrome
* Post-concussion syndrome

Neurotic, stress-related and somatoform

| Adjustment|

* Adjustment disorder with depressed mood

|

Anxiety|

| Phobia|

* Agoraphobia
* Social anxiety
* Social phobia
* Anthropophobia
* Specific social phobia
* Specific phobia
* Claustrophobia

|

Other|

* Generalized anxiety disorder
* OCD
* Panic attack
* Panic disorder
* Stress
* Acute stress reaction
* PTSD

Dissociative|

* Depersonalization disorder
* Dissociative identity disorder
* Fugue state
* Psychogenic amnesia

Somatic symptom|

* Body dysmorphic disorder
* Conversion disorder
* Ganser syndrome
* Globus pharyngis
* Da Costa's syndrome
* Hypochondriasis
* Mass psychogenic illness
* Neurasthenia
* Nosophobia
* Psychalgia
* Somatization disorder

Physiological and physical behavior

| Eating|

* Anorexia nervosa
* Bulimia nervosa
* Rumination syndrome
* Other specified feeding or eating disorder

|

Nonorganic
sleep|

* Hypersomnia
* Insomnia
* Parasomnia
* Night terror
* Nightmare
* REM sleep behavior disorder

Postnatal|

* Postpartum depression
* Postpartum psychosis

Sexual dysfunction|

| Arousal|

* Erectile dysfunction
* Female sexual arousal disorder

|

Desire|

* Hypersexuality
* Hypoactive sexual desire disorder

Orgasm|

* Anorgasmia
* Delayed ejaculation
* Premature ejaculation
* Sexual anhedonia

Pain|

* Nonorganic dyspareunia
* Nonorganic vaginismus

Psychoactive substances, substance abuse and substance-related

* Drug overdose
* Intoxication
* Physical dependence
* Rebound effect
* Stimulant psychosis
* Substance dependence
* Withdrawal

Schizophrenia, schizotypal and delusional

| Delusional|

* Delusional disorder
* Folie à deux

|

Psychosis and
schizophrenia-like|

* Brief reactive psychosis
* Schizoaffective disorder
* Schizophreniform disorder

Schizophrenia|

* Childhood schizophrenia
* Disorganized (hebephrenic) schizophrenia
* Paranoid schizophrenia
* Pseudoneurotic schizophrenia
* Simple-type schizophrenia

Symptoms and uncategorized

* Catatonia
* False pregnancy
* Intermittent explosive disorder
* Klüver–Bucy syndrome
* Psychogenic non-epileptic seizures
* Psychomotor agitation
* Stereotypy

* v
* t
* e

Diseases of the nervous system, primarily CNS (G04–G47, 323–349)

Inflammation|

| Brain|

* Encephalitis
* Viral encephalitis
* Herpesviral encephalitis
* Limbic encephalitis
* Encephalitis lethargica
* Cavernous sinus thrombosis
* Brain abscess
* Amoebic

|

Spinal cord|

* Myelitis: Poliomyelitis
* Demyelinating disease
* Transverse myelitis
* Tropical spastic paraparesis
* Epidural abscess

Both/either|

* Encephalomyelitis
* Acute disseminated
* Myalgic
* Meningoencephalitis

Brain/
encephalopathy|

| Degenerative|

| Extrapyramidal and
movement disorders|

* Basal ganglia disease
* Parkinsonism
* PD
* Postencephalitic
* NMS
* PKAN
* Tauopathy
* PSP
* Striatonigral degeneration
* Hemiballismus
* HD
* OA

* Dyskinesia
* Dystonia
* Status dystonicus
* Spasmodic torticollis
* Meige's
* Blepharospasm
* Athetosis
* Chorea
* Choreoathetosis
* Myoclonus
* Myoclonic epilepsy
* Akathisia

* Tremor
* Essential tremor
* Intention tremor
* Restless legs
* Stiff-person

|

Dementia|

* Tauopathy
* Alzheimer's
* Early-onset
* Primary progressive aphasia
* Frontotemporal dementia/Frontotemporal lobar degeneration
* Pick's
* Dementia with Lewy bodies
* Posterior cortical atrophy

* Vascular dementia

Mitochondrial disease|

* Leigh syndrome

Demyelinating|

* autoimmune
* Multiple sclerosis
* Neuromyelitis optica
* Schilder's disease
* hereditary
* Adrenoleukodystrophy
* Alexander
* Canavan
* Krabbe
* ML
* PMD
* VWM
* MFC
* CAMFAK syndrome
* Central pontine myelinolysis
* Marchiafava–Bignami disease
* Alpers' disease

Episodic/
paroxysmal|

| Seizure/epilepsy|

* Focal
* Generalised
* Status epilepticus
* Myoclonic epilepsy

|

Headache|

* Migraine
* Familial hemiplegic
* Cluster
* Tension

Cerebrovascular|

* TIA
* Amaurosis fugax
* Transient global amnesia
* Acute aphasia

* Stroke
* MCA
* ACA
* PCA
* Foville's
* Millard–Gubler
* Lateral medullary
* Medial medullary
* Weber's
* Lacunar stroke

Sleep disorders|

* Insomnia
* Hypersomnia
* Sleep apnea
* Obstructive
* Congenital central hypoventilation syndrome
* Narcolepsy
* Cataplexy
* Kleine–Levin
* Circadian rhythm sleep disorder
* Advanced sleep phase disorder
* Delayed sleep phase disorder
* Non-24-hour sleep–wake disorder
* Jet lag

CSF|

* Intracranial hypertension
* Hydrocephalus/NPH
* Choroid plexus papilloma
* Idiopathic intracranial hypertension
* Cerebral edema
* Intracranial hypotension

Other|

* Brain herniation
* Reye's
* Hepatic encephalopathy
* Toxic encephalopathy
* Hashimoto's encephalopathy

Spinal cord/
myelopathy|

* Syringomyelia
* Syringobulbia
* Morvan's syndrome
* Vascular myelopathy
* Foix–Alajouanine syndrome
* Spinal cord compression

Both/either|

| Degenerative|

| SA|

* Friedreich's ataxia
* Ataxia–telangiectasia

|

MND|

* UMN only:
* Primary lateral sclerosis
* Pseudobulbar palsy
* Hereditary spastic paraplegia

* LMN only:
* Distal hereditary motor neuronopathies
* Spinal muscular atrophies
* SMA
* SMAX1
* SMAX2
* DSMA1
* Congenital DSMA
* SMA-PCH
* SMA-LED
* SMA-PME
* Progressive muscular atrophy
* Progressive bulbar palsy
* Fazio–Londe
* Infantile progressive bulbar palsy

* both:
* Amyotrophic lateral sclerosis

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