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Gerontology > 4 Vascular and Frontotemporal dementia > Flashcards

4 Vascular and Frontotemporal dementia Flashcards

1
Q 
Art 8 
Frontotemporal dementia (FTD)
A

3 Forms of FTD=

  1. Behavioral Variant (bv-FTD) = Early changes in personality and behavior.
  2. Semantic Variant (sv-FTD) = Loss of word knowledge.
  3. Non-fluent Variant (nf-FTD) = Loss of syntax- and motor speech output.
  • FTD is under the age of 65 equally common as AD
  • 3th most common form of dementia (after AD and Dementia Lewy Bodies)
  • duration of the disease is 8-11 years.
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2
Q

Art 8

Earliest signs of bvFTD

A
  • Subtle personality and behavioral changes: apathy, disinhibition, reduced emotional response, poor judgement, impairments in personal and social awareness
  • Partners and family members don’t recognize their loved one anymore
  • The cognitive ability remains relatively intact for some time.
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3
Q

Art 8
Diagnostic Criteria
Possible VS probable bvFTD

A

Possible bvFTD=
-Based solely on the clinical presentation
-3 out of 6 of the following:
Early apathy; Early loss of sympathy and empathy; Early behavioral disinhibition; Hyperorality or dietary changes; A neuropsychological profile of worse executive functioning and a relatively spared memory and visuo-spatial skills.

Probable bvFTD=

  • Possible bvFTD;
  • Significant functional decline;
  • MRI: evidence of frontal and/or temporal atrophy.
  • PET: evidence of hypo-metabolism.
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4
Q

Art 8

Neuroanatomy and Pathology

A

With bvFTD, the neurodegeneration pattern shows initial degeneration primarily in the paralimbic structures.
These structures are important for=
- Human social functioning;
- Awareness of the self;
- Decoding the emotional salience of a stimuli in order to facilitate appropriate action.
Progressing neurodegeneration is seen in frontal and temporal lobes.

The 2 most common pathologies seen are=

  1. Frontotemportal Lobar Degeneration (FTLD) with tau-positive inclusions.
  2. FTLD with TDP-43 positive inclusions.
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5
Q

Art 8

FTD Genetics

A

30-40 % of the cases of bvFTD seems to be genetic (due to genetic manipulations of the chromosomes 3, 9 and 17).

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6
Q

Art 8

Differential Diagnosis

A

Early onset AD
Overlap: executive dysfunctions, neuropsychiatric disturbances.

  • Neurodegenerative or motor syndromes like PSP or ALS
  • Huntington’s Disease
  • Late onset psychiatric disturbance.
    51 % of bvFTD receives prior a diagnose of a psychiatric disorder (compared to 23% in AD)
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7
Q

Art 8

Neuropsychological profile

A

There is not a neuropsychological profile specific for bcFTD. This is the consequence of the fact that there is a lot of variance in the available data about bvFTD, and tests that measure motivation or performance instead of the actual construct that the test is designed for.

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8
Q

Art 8

FTD and Memory

A
  • Relatively spared in episodic memory, compared to AD (severe verbal and visuospatial episodic memory deficits), most reliable differences between AD and bvFTD!
  • Learning with a disorganized and inefficient approach
  • Able to retain info over delays, compared to AD showing a more rapid forgetting over a delay
  • Visual memory: also, relatively spared, when both visual and verbal memory are intact it is probably not AD.
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9
Q

Art 8

FTD and Language

A
  • Not the decline that is seen in the other variant of FTD.
  • But some decline is seen in spontaneous speech, which can potentially progress to complete mutism
  • Syntactic and semantic knowledge: remain relatively spared.
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10
Q

Art 8

FTD and Visuospatial

A
  • Visuoconstruction and visual-perceptual skill are better in bvFTD than in AD
  • Difficult for bvFTD patients: tasks with heavy top-down control of spatial processing
  • Overall: visuospatial skills remain stable in bvFTD, but progresses in AD.
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11
Q

Art 8

FTD and Attention and Executive functioning

A
  • Data shows discrepancies in these areas, because of two reasons:
    o Stage of disease as long as the DL-PFC isn’t affected, the patient won’t show executive deficits.
    o Executive functioning is a poorly defined construct.
  • Conclusion: bvFTD patients will perform faster but make more mistakes on executive/attention tasks than AD patients. This is because of their imbalance in the ability to make accurate speed/error trade-offs.
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12
Q

Art 8

FTD and Social behavior and personality

A

Dl-PFC degeneration is seen in both AD and bvFTD. But the difference between the two that they show this degeneration at different point during their disease:

  • bvFTD
    1. Behavior: flat affect, reduced initiative, deficits in social pragmatics, poor social judgements.
    2. Personality: decreased agreeableness, less self-awareness regarding their current behavioral and personality changes.
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13
Q

Art 8

FTD and Learning and decision making

A

bvFTD patients take more risks and show bad reward-punishing learning.

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14
Q

Art 8

Clinical assessment in bvFTD

A

Clinical interview=
Preferable with a collateral source, because the patient often lacks insight in their own social functioning. Ask about the onset, progression of symptoms (slow/abrupt?). Abrupt symptom onset is less likely to point to the direction of bvFTD.

Ask about the nature of change, using the next 6 symptom areas=
1. Early behavioral disinhibition;
For instance: gambling, inappropriate behavior.
2. Early apathy / inertia (a loss of interest, drive or initiation);
3. Early loss of empathy or sympathy;
For instance: not noticing pain in others, showing no warmth.
4. New onset of compulsive or stereotyped behavior; For example: counting, checking, hoarding.
5. Hyper orality or dietary changes; Showing by weight gain, binge eating.
6. Neuropsychological profile;
Executive deficits, with preservation of memory and visuospatial functioning

  • Family history
  • Neuroimaging
  • Cognitive Assessment
  • Behavioral observation
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15
Q

Art 8

Informant based measures

A
  • Neuropsychiatric inventory (NPI) bvFTD will show higher overall scores, compared to AD.
  • Revised self-monitoring scale.
  • Interpersonal reactivity index.
  • Dynamic affect recognition test.
  • Social norms questionnaire bvFTD will see many behaviors as normal, compared to AD.
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16
Q

Art 9

Vascular Cognitive Impairment (VCI)

A

Vascular Cognitive Impairment (VCI) are all the forms of cognitive impairment caused by cerebrovascular disease.

The type of impairment depends on=
- The location of the damaged tissue; - The amount of damaged tissue.
The extent of the cognitive impairment is not necessarily correlated with the size of a lesion or burden.

70% of people over 70 exhibit evidence of vascular lesions on MRI. Because many risk factors for VCI are modifiable, early detection of VCI is necessary.

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17
Q

Art 9

2 Stages of VCI

A
  1. The mildest stage: vascular cognitive impairment, no dementia (VCIND).
  2. The more severe stage: Vascular Dementia (VaD).

1/3 of people will develop dementia within 1 year after a stroke. The clinical symptoms that are associated with the stroke vary: it depends on the area of impact.

Impairment due to large vessel stroke or strategic areas (like Broca) are most commonly tied to the development of VaD. However, this is not the most common expression of VaD. VaD shows more often=

  • An insidious onset
  • A slow and gradual decline.

Less likely=
A sudden onset and a stepwise decline. The form of a mixed form of dementia: VCI + AD is common.

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18
Q

Art 9
Vascular Cognitive Impairment NO Dementia
(VCIND)

A

The vascular lesions in VCIND are too mild to impact daily living. The most common types of lesions associated with VCIND are:

  • Lacunes (small cerebrospinal filled cavities in the white matter)
  • Subcortical hyper intensities (areas of bright white matter on neuroimaging)

Often an individual will have ‘silent infarcts’, which represent damage that can be considered as age related cognitive decline. Nevertheless, VCIND can be a prodromal stage for VaD, so it is important to reduce the progression of the disease. 1⁄2 of the VCIND cases progress in dementia over the course of 5 years. When an individual shows frontal white matter hyper intensities, they will be less likely to revert to normal cognitive functioning within one year. There is no predictive neuropsychological profile for the progression from VCIND to VaD.

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19
Q 
Art 9 
Vascular Dementia (vaD)
A

The result of:

  • Extensive white matter lesions and lacunar infarcts due to small vessels disease; - One or more strokes to the main cerebral activities;
  • A combination of the above.

Most consistently impaired domains are=
1. Executive functioning;
Typically found on test of verbal fluency, mental flexibility and response inhibition.
2. Learning;
3. Delayed memory (still intact: recognition memory). The recognition memory remains intact when the median temporal lobe is spared.

The behavioral feature that is most commonly associated with stroke is depression (20%). A predictor of depression is a reduction in the ability to carry out tasks of daily living.

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20
Q

Art 9

The 3 most commonly used criteria for VaD

A
  1. DSM-IV=
    These criteria is used most, but the downside of the DSM is that it uses memory deficits as the most prominent feature of the disease, while it seems that the episodic memory can remain intact in VaD. Another downside is that the diagnosis in the DSM doesn’t require neuroimaging evidence of the disease, which increases the chance of a misdiagnosis.
  2. ADDTC=
    These criteria are mostly used in research settings. It requires neuroimaging evidence. It is a
    more flexible diagnosis because memory impairment doesn’t have to be prominent.
  3. NINDS-AIREN=
    These criteria are used in research settings. It requires memory impairment and neuroimaging evidence.
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21
Q

Art 9

VCI Risk factors

A
  • Age (greatest risk factor)
  • Male sex
  • Low birth weight
  • Race (African American)
  • Ethnicity (Latino)
  • Atrial fibrillation

Genetic risk factors=
- CADASIL deterministic factor= CADASIL is a rare autosomal disease, associated with a Notch3 defect. Notch3 defects cause infarcts in the deep white matter, basal ganglia and brain stem. Individuals with CADASIL will experience migraines around the age of 30, and often experience a stroke, with an average onset aroundthe age of 45. They will typically develop dementia in the 6th decade of their lives, with death in the 7th decade. The cognitive deficits that are seen in CADASIL are executive dysfunctioning, attention deficits and impairment in organizing abilities.
- Angiotensinogen susceptibility factor=
May be involved in abnormal vascular responsivity and the development of subcortical ischemic disease.

22
Q

Art 9

Differential Diagnosis of VCI

A

Considerations during the differential diagnosis of VCi are:
- Lewy Body Dementia - Alzheimer’s Disease=
AD and vascular neuropathology often coexist. It is still unclear if both conditions develop independently or not.
- Frontotemporal Dementia=
FTD shows more unique symptoms (significant aphasia and personality abnormalities). The age of onset differs too, FTD: age of onset before 65, in VCI: the age of onset is older.
- Normal Pressure Hydrocephalus (NPH) =
Both NPH and VCI share frontal symptoms. In NPH, urinary urgency and gait disturbance is seen more often compared to VCI

23
Q

Art 9

Clinical evaluation

A
  1. Clinical interview and history
  2. Neuropsycholoical assessment
  3. Neuroimaging corroboration
24
Q

Art 9

1. Clinical interview and history

A

Some patients may have very good insight into their cognitive difficulties, but it is incorrect to presume that this insight is fully intact for all patients. The interview can also provide information about:
- Language skills (evidence of aphasic abnormalities?);
- Memory impairments (showing the Tip of The Tongue Phenomenon); - Mood and apathy (seen in large vessel strokes).
One difficulty clinicians face during the interview is differentiating between a progressive or a stepwise decline.

A stepwise decline shows a repetitive pattern of sharp decline, followed by a period of stabilization.

This pattern is seen in large vessel infarcts and very strategic small vessel strokes.This pattern is not seen in small vessel disease, which shows a progressive

25
Q

Art 9

2. Neuropsychological assessment

A
  • The Mini Mental State Exam (MMSE)= Lacks sensitivity.
  • The Montreal Cognitive Assesment (MoCa)=
    Shows a greater coverage of the executive processes, is more sensitive to subtle cognitive impairments and early AD but it is unclear if it captures mild or moderate cognitive impairments.

These brief screening measures don’t offer sufficient neuropsychological coverage for detecting milder forms of VCI. Solution= o 30-minute battery, that measures verbal memory, psychomotor speed and verbal fluency;

Vascular pathology will result in poorer performance on lexical than semantic tasks, while AD will show the opposite pattern.

26
Q

Art 9

3. Neuroimaging corroboration

A

It is critical that neuroimaging results are integrated in the case conceptualization. The neuroimaging technique that is often used is the high-powered MRI (3T), using fluidattenuated inversion recovery (FLAIR) scans.

Vascular disease is characterized by a pattern of=

  • Lacunes in subcortical grey- and white matter;
  • White matter hyper intensities;
  • Periventricular capping along the perimeter of the lateral ventricles.

The degree of vascular burden must be gleaned from a radiologist report.

27
Q

Art 9

Conclusive points

A
  1. The presence of an insidious course shouldn’t be used to differentiate between VCI or another primary dementia disorder;
  2. Executive functioning impairment may be dominant but not universal and are not necessary for the diagnosis of VCI.
28
Q

Art 9

How does a neuropsychologist incorporate neuroimaging data into the clinical evaluation?

A

Diagnosis of VCI can only be described as a possibility, when there is no MRI data available;

  • When there is no mention of vascular disease on the MRI, it is unlikely that the person’s cognitive impairment is driven by vascular mechanisms;
  • When there is some degree of vascular disease on the MRI, the possibility of vascular etiology is present, but not necessarily confirmed.
29
Q

Lec
Vascular dementia
Diagnostic labels

A

First described by in 1894 by Otto Binswanger (An association between atherosclerosis, reduction in
cerebral perfusion and cognitive decline in older adults).

Different diagnostic labels=
- Old labes
o Senile dementia (Term for various forms of dementia)
o Multi-infarct dementia (Muliple and diffuse strokes)

  1. Vascular dementia
    a. Vascular pathologies aside from stroke, such as subcortical microvascular disease are
    realted to dementia
  2. Vascular cognitive impairment
    a. The spectrum of mild to sever cognitive deficits presumed to be caused by
    cerebrovascular disease

=> Currently used diagnostic labels

30
Q

Lec
Vascular dementia
DSM5

A
  1. Criteria met for major or mild neurocognitive disorder
  2. Evidence of significant cognitive decline from previous level in 1+ domains
    a. Concern of individual or clinician/informant
    b. Au substantial impairment in cognitive performance
  3. Cognitive deficits interfere with everyday activities
  4. Cognitive deficits do not occur exclusively in context of delirium
  5. Cognitive deficits are not better explained by another mental disorder
  6. Clinical feature consistent with a vascular etiology as suggested by either of the following
    a. Onset of cognitive deficits is temporally related to one or more cerebrovascular
    events
    b. Evidence for decline Is prominent in complex attention (including processing speed)
    and frontal-executive function.
  7. There is evidence of the presence of cerebrovascular disease from history, physical
    examination and/or neuroimaging
  8. Symptoms are not better explained by another brain disease or systemic disorder
31
Q

Lec

Vascular dementia prevelance

A
  • 2nd or 3rd most common type of dementia
  • Prevelance:
    o 50% in China and Japan of alle dementia
    o North America: 2:1 AD:VD
    o Europe: 10-30% of all dementia cases
32
Q

Lec

Vascular dementia and Neuropathology

A
  • There is no definitive set of pathological criteria for vascular dementia (unlike AD)
  • The underlying verebrovascular pathology of VD is expansive -> result: a diffuse patter of brain injury
  • Difficult to define a gold standard for the neuropathological diagnosis of vascular dementia
There are some key neuropathological feature:
The presence of
- Small or large vessel disease
- White matter lesions
- Infarcts
- Lacunes
The absence of
- Confounding pathologies
(Neurofibrillary tangles and amyloid plaques and Lewy Bodies)
33
Q

Lec

White matter lesions

A

White matter lesions are varied and diffuse

  • White matter hyperintensities (leukoariosis)
    o Frequently present in older individuals
  • Diffuse demyelination
  • Stroke and Lacunes are not confined to white matter!!
34
Q

Lec

Stroke

A

Ischaemic stroke =
- Occlusion (einschluss) of major cerebral blood vessel or a series of small cerebral blood
vessels
- Due to: Acute blockage due to embolism, Thickening of the vascular wall

Hemmorrhagic stroke =
- Rupture (Bruch) of large or small cerebral blood vessel

Large vessel stroke or large vessel disease =

  • One or more arteries supplying blood to the brain rupture or experience blockage
  • Effects are relatively focal

Small vessel stroke/disease or lacunar stroke =
- Blockage of the cerebral microvessels
o Strongly associated with hypertension
- Effects are relatively diffuse
- MORE OFTEN ASSOCIATED WITH VASCULAR DEMENTIA

35
Q

Lec

Vascular dementia origin

A

The result of:

  1. Extensive white matter lesions and lacunar infarcts due to small vessel disease
    a. Slow onset and gradual decline
  2. One or more strokes to main cerebral arteries (large vessel disease)
    a. Abrupt onset and stepwise decline, related to one or more strokes
  3. The combination of 1 and 2
36
Q

Lec
Vascular dementia and
Clinical manifestation

A
  • Heterogeneity is the rule
  • The neuropsychological manifestation is driven by the extend of focal and diffuse vascular lesions
  1. Middle cerebral artery
    - Hemiplegia, Aphasia, Hemianesthesia
  2. Anterior cerebral artery
    - Paraplegia, Abulia, Executive dysfunctions, Personality changes
  3. Posterior cerebral artery
    - Homonyous hemianopia
    - Alexia with or without agraphia
    - Visual agnosia, Balint syndrome, prospagnosia
  4. Patients with a vascular dementia can have an impairment in:
    - Learning and memory, executive functions, attention, language, visuoperceptual functions,
    psychomotor skills
  5. There is no consistent pattern that is present in most patients:
    - Impairments in attention and executive functions are most salient
    o Impaired performance on tests of
     Planning, set-shifting, inhibition, selective attention, info-processing
  6. Comparison AD patients and VD patients:
    - Patient with VD and AD have a comparable performance across most cognitive domains
    - Differences are found regarding attention and executive functions
  7. Other typical features of VD:
    - Language
    o Naming difficulties (worsen as VD progresses)
    - Visuoperceptual skills
    o Impaired performance on visual organization tasks
    - Psychomotor function
    o Impaired performance on tests of psychomotor speed
  8. Neuropsychiatric disturbances
    - Depression, anxiety and apathy
    - Patients with VD are more often depressed than AD patients due to preserved disease insight
    o Pathological changes also play a role
37
Q

Lec

AD and VD

A

Post mortem: Pathology of AD is relatively common in patients with VD = mixed dementia

  • Also clinically “pure” AD is postmortem associated with VD
  • Do AD an VD co-occur or interactive?
    o Different ypotheses:
    Independent pathologies co-occur, Vascular changes stimulate the formation of AD etc etc
38
Q

Lec
Vascular dementia
Risk factors

A
  1. Age:
    - as people get older the prevalence of risk factors for VD increases (Diabetes, Hypertension,
    cerebrovascularture fragility
  2. Genetics:
    - One rare hereditary form of micro vessel disease: Cerebral autosomal dominant arteriopathy
    with subcortical infarct and Leukocephalopathy
    o CADASIL
    o Deep and periventricular white matter changes
    o Transient Ischmeic Attack and stroke
     Vascular dementia (other forms of VD not related to a specific gene)
  3. Other risk factors:
    - Hypertension and Diabetes = strongest risk factors for vascular dementia
    - Obesity and smoking
  4. Cardiovascular disease
    - Cardiac arrhythmia and mycordial infarcts = Reduced cerebral blood flow
    - Heart failure: systolic and diastolic heart failure = Reduced blood flow to body and brain
39
Q

Lec

Summary VD

A

Result of:
1. Extensive white matter lesions and lacunar infarcts due to small vessel disease
2. One or more strokes to the main cerebral arteries (large vessel disease)
3. The combination of 1 and 2
- Vascular dementia has a slow onset and gradual decline or an abrupt onset and a stepwise
decline, related one or more strokes

  • The clinical manifestation is heterogeneous
  • Impairments in attention and executive functions are, however, most salient
  • Many patients with a dementia have a mixed pathology (AD and VD)
40
Q 
Lec 
Frontotemporal dementia (Frontoremporal lobar degeneration)
A
  • Formally Pick’s Disease (Arnold Pick 1982)
  • Progressive neurodegenerative disease
    o Selectively affects the frontal and/or temporal lobes
  • Common cause of dementia in patients 65-
    o Mean 52-56 years
    o More common than AD in patients 60-
  • Atrophy in the frontal and temporal lobes
  • Hypometabolism in the media and lateral prefrontal cortex
  • Inclusion of Pick bodies
  • 29-54% of patients with FTD have a positive family history
  • Family member with FTD: 3,5 times higher risk of developing FTD
41
Q

Lec

FTD DSM5 Criteria

A

A. Criteria met for major or mild neurocognitive disorder

B. Disturbance has insidious onset and gradual progression

C. Either
a. Behavioral variant
i. 3 or more of following behavioral symptoms
1. Disinhibition
2. Apathy or inertia
3. Loss of sympathy or empathy
4. Perservative, stereotyped or compulsive/ritualistic behavior
5. Hyperorality and dietry changes
ii. Prominent decline in social cognition and/or exevutive abilities
b. Language variant
i. Prominent decline in language ability, in the form of speech production, word
finding, object naming, grammar, or word comprehension

D. Relative sparing of learning and memory and perceptual-motor function

E. Not better explained by cerebrovascular disease, etc.

42
Q

Lec

Behavioral variant of FTD (BFTD)

A
  • 50% of all patients
  • Progress to death relatively fast
    o Median survival: 8,7 +- 1,2 years
    o AD: 11,8+-0,6 years
    o Semantic dementia: 11,9+-02 years

Initially most prominent feature:
- Insidious onset of personality changes and behavioral abnormalities
o Poor insight (deny existens of illness, lack of concern)
o Loss of personal awareness
o Loss of social awareness
o Blunting of affect
- Frontal lobe is initially specifically affected

Other behavioral changes that can be present in daily life:
- Increased submissiveness
- Lack of empathy, self-centeredness, emotional coldness
- Decreased concern about family and friends
- Inappropriate sexual comments and gestures, theft an assault
- Inappropriate or offensive speech
- Features of obsessive-compulsive disorder
o Repetitive cleaning, pacing, organizing objects into groups, hoarding, counting
 Some patients initially receive this diagnosis of OCD

43
Q

Lec

Orbifrontal lobe dysfunction

A
  • Disinhibition or distractibility and poor impulsive control
    o Restlessness, irritability, aggressiveness, violent outburst, etc
  • Antisocial beavrio
  • Stereotyped behavior
  • Decreased agreeableness
44
Q

Lec

Anterior cingulated cortex and medial frontal lobe dysfunction

A
  • Apathy
    o May be mistaken for depression, nut depression is uncommon in patients with the
    behavioral variant of FTD
  • Predominately right hemisphere dysfunction
    o Dramatic changes in beliefs, attitude and/or religious sentiment
45
Q

Lec

Behavioral variant of FTD PT.2

A

Dietry changes: craving for sweets and decreased satiety (weight gain)
As disease progresses:
- Feature of Kluver-Bucy syndrome: Hyperorality and oral exploratory behavior
More advanced disease:
- Many patients develop a language dysfunction
o Involvement of left frontal cortex
 Progressive non-fluent aphasia
o Involvement of medial frontal and anterior cingulated cortex
 Akinetic mutism

46
Q

Lec

BFTD Neuropsychological assessment

A
  • Impairments in executive functions and social cognition are most often present in patients
    with the behavioral variant of FTD
  • Memory and visuospatial functions are relatively spared
  • Language impairments may be evident in later stages
47
Q

Lec

Summary BFTD

A
  • Characterized by behavioral symptoms
    o Disinhibition, apathy, loss of sympathy or empathy, obsessive compulsive behavior,
    hyperorality and dietry changes
  • Decline in social cognition and/or executive abilities
  • Related to progressive neurodegeneration of the frontal cortex
48
Q 
Lec 
Semantic Dementia (SD)
A
  • Progressive loss of semantic knowledge or knowledge about people, facts and words
    o Result associative agnosia
     Daily life: misuse or inability to recognize household items
  • Presenting complaint involves language
    o Loss of memory for words, loss of word meaning
    o Result: progressive fluent aphasia
    o Speech is fluent, semantic paraphasias are frequently present
    o Substitute phrases (thing, stuff) are often used
  • Patients with semantic dementia are aware of their expressive deficits
  • Patients are often unaware of their comprehension difficulties
  • Repetition, prosody, syntax and verb generation are preserved
  • Temporal lobe is initially specifically affected
49
Q

Lec

SD Assessment

A

Patients are most impaired on:
- Category fluency tests
o Name as many animals as possible in one minute
- Naming tasks
- Generation of verbal definitions of words and pictures
o Early stages: loss of subordinate knowledge (misidentify an orange as an apple)
o Moderate to severe stages: loss of more superordinate knowledge (both are
identified as fruit and eventually as food)
Patients eventually also show behaviors as seen in the behavioral variant of FTD:
- Disinhibited, compulsive behavior, emotion comprehension
These behaviors are more often present in patients with a right temporal lobe semantic dementia

Early stages:
- Recent memory is relatively spared
- Many autobiographical events are los
 In contrast to AD!!

50
Q

Lec

Progressive non-fluent aphasia

A

Patients present with changes in

  • Fluency, pronounciation, word finding difficulties (more significant for verbs than nouns)
  • Pathology in Brodman’s areas 44 and 45
Language difficulties:
- Agrammatism
o Omission or incorrent use of
 Articles: “cow jumped over moon”
 Preposition: “dog walk bridge”
 Verbs: “cat eated mouse”
o Phonemic paraphasias
 “Head” instead of “bed
 “Efelant” instead of “Elephant
- Stuttering, Impaired repetition, Alexia, Agraphia
  • > Behavioral changes are not present until later in the disease
  • > Executive functions including working memory are often impaired
  • > Episodic memory, semantic memory and visuopatial function are preserved
51
Q

Lec

Differentiation from AD

A

AD is also characterized by
- Language impairments and neuropsychiatric disturbances
Impairment in executive functions can also be present. Historically, many cases of FTD were
diagnosed with AD!

52
Q

Lec

FTD Summary

A

-Most common dementia in individuals under 65
-Associated with progressive
neurodegeneration of the frontal and temporal cortex
-Often misdiagnosed as a neuropsychiatric
disorder or Alzehimer’s Disease!

Gerontology (7 decks)

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