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Medicine year 2 semester 2 > Case 22- Dementia > Flashcards

Case 22- Dementia Flashcards

1
Q

Dementia

A

A syndrome in which there is deterioration in memory, thinking, behaviour and the ability to perform everyday activities

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2
Q

Diagnosing dementia

A

At least two cognitive domains (memory, language, behaviour and visuospatial or executive function) leading to significant functional decline (enough to affect ADLs) that cannot be explained by another disorder or adverse effects of medication.
Not a normal part of ageing

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3
Q

Signs and symptoms of dementia

A
  • Cognitive- memory, language, executive function
  • Physical- weight loss, anorexia, gait disturbance
  • Behavioural and psychological- withdrawal, disinhibition, depression, psychosis, sleep disturbance
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4
Q

Risk factors for dementia

A
  • Age
  • Cardiovascular (diabetes, hypertension, smoking)
  • Genetics
  • Lifestyle (smoking, alcohol)
  • South Asian ethnicity
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5
Q

Causes of acute confusional states which arent dementia

A
  • Psychiatric and neurological- depression, delirium, normal pressure hydrocephalus
  • Neoplastic- primary and secondary brain tumours, paraneoplastic syndromes
  • Endocrine- vitamin deficiency, thyroid disorders, Crushings
  • Trauma- traumatic brain injury, subdural haematoma
  • Inflammatory- demyelination, lupus, limbic encephalitis
  • Drugs- opiates, anticholinergics, lead poisoning
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6
Q

Alzheimer’s

A

The most common type, 60-70% of dementia cases. It involves early loss of episodic memory followed by a slow decline in function and cognition

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7
Q

Vascular dementia

A

Associated with cerebrovascular disease, second most common cause (15-20%). Cerebral ischaemia impairs neurological function. There may be obvious stroke syndromes in the past or a step wise decline in cognition with each vascular event.

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8
Q

Dementia with Lewy bodies (DLB)

A

Lewy bodies are abnormal clumps of protein which develop within the brain, affects 10-15% of people with dementia. Symptoms can include parkinsonian movement features, visual hallucinations and REM sleep disturbances

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9
Q

Fronto-temporal dementia

A

Less then 5% but second most common cause in under 65’s (after early onset Alzheimers). Can present with personality change, social inhibition and loss of language. Memory disturbance is a later symptom. Selective neurodegeneration of the frontal and temporal lobes, which may be visible as focal atrophy on imaging.

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10
Q

Other types of dementia

A

One in ten people will have a mixed dementia. This is where more than one disease is occurring at the same time, such as a person with Alzheimer’s who also has significant cerebrovascular disease, leading to a mixed Alzheimer’s/vascular dementia. Other forms of dementia are CJD, Parkinsons dementia and Korsakoffs.

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11
Q

Screening for dementia

A

Confusion screen- history and cognitive assessment, bloods, imaging. Involves excluding differentials. Looking for patterns of specific types of dementia

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12
Q

Dementia- History

A
  • Cognitive, behavioural and psychological symptoms
  • Functional state- can they perform activities of daily living
  • Physical symptoms
  • Collateral- from relative or carer
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13
Q

Dementia- Bloods

A
  • FBC- anaemia/infection
  • Calcium- Hypercalcaemia
  • Thyroid function (TFT’s)- Hypo/hyperthyroidism
  • Liver function- Cirrhosis
  • U+E’s- uraemia, dehydration, hyponatraemia
  • B12 and folate- vitamin deficiency, neurological impairment
  • HbA1C and random glucose- Hyper/hypoglycaemia
  • ESR- Vaculitis and autoimmune disease
  • Other tests- HIV, Syphillis, Bloods/urine culture (sepsis)
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14
Q

Dementia- Radiology and nuclear medicine

A
  • CT/MRI
  • SPECT/PET if diagnostic uncertainty
  • Cannot diagnose dementia purely based on imaging, clinical picture must be there
  • Helps for detecting other conditions that mimic dementia like hydrocephalus or stroke
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15
Q

Alzheimer’s disease- Presentation

A

Irreversible, global and progressive impairment of cognitive function. Visuo-spatial skills, memory, verbal abilities and executive function are all affected. Tends to be insidious with a progressive decline over the years called the Alzheimer’s continuum, time period varies between patients

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16
Q

Alzheimer’s continuum

A
  • Preclinical AD- no symptoms
  • MCI (mild cognitive impairment) due to AD- very mild symptoms that do not interfere with everyday activities
  • Mild (Dementia due to AD)- symptoms interfere with some everyday activities
  • Moderate (dementia due to AD)- symptoms interfere with many everyday activities
  • Severe (dementia due to AD)- symptoms interfere with most everyday activities
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17
Q

Symptoms of Alzheimers

A
  • Memory- especially recent events and new information, memory for past information is not affected
  • Dysphasia- may be receptive or expressive
  • Apraxia- difficulties in co-ordinated motor tasks, causes problems with dressing/eating
  • Disorientation- get lost in familiar settings or lose track of the day/date
  • Impairment of executive function- such as difficulties in planning and problem solving
  • Behavioural and psychological symptoms- agitation and emotional lability, depression and anxiety, withdrawal, disinhibition, psychosis, sleep cycle disturbances, motor disturbances i.e. wandering, restlessness.
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18
Q

Mixed dementia

A

1 in 10 people with dementia hve mixed dementia, the most common is Alzheimer’s disease with vascular dementia

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19
Q

Atypical Alzheimers

A

Memory issues are not the first symptom; a different part of the brain is affected first. Atypical is most commonly seen in those with early onset.

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20
Q

Probable AD

A
  • Meets criteria for dementia
  • Insidious onset (months-years)
  • Clear cut history of worsening cognition
  • Deficits in one or more of the following categories: Amnestic presentation (learning and recall), Language presentation, Visuospatial presentation, Executive dysfunction
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21
Q

Possible AD

A

• Dementia with an atypical onset or course i.e. sudden onset or insufficient documentation of progressive decline
OR
• Aetiologically mixed presentation i.e. other criteria fit the diagnosis but the features of other brain disorders or alternative causes of dementia are also present

22
Q

Investigations AD

A

Specialist diagnostic services give a diagnosis of AD where there is a cognitive decline in the absence of a reversible cause. If unclear further neuropsychological testing and structural imaging can be undertaken.

23
Q

Alzheimer’s disease- Cognitive testing

A

Includes a test of episodic memory about recent or part events/experiences. For example asking a person to remember a list of words both immediately and after a short delay

24
Q

Alzheimer’s disease- Structural brain imaging (CT/MRI)

A

May show patterns of cortical atrophy associated with Alzheimers disease. For example, medial temporal lobe atrophy (including the hippocampus, entorhinal cortex and perirhinal cortex) and temporoparietal atrophy. Medical temporal lobe atrophy can be assessed on imaging using the MTA score. A high MTA score is very sensitive for the diagnosis of Alzheimer’s disease, however its not specific. Can be used to exclude other causes of dementia i.e. multi-infarct. MRI is more sensitive then CT.

25
Q

Alzheimers- Functional imaging (PET) and CSF

A

Less widely used then structural imaging but can be used when diagnosis is still unclear. Is used when diagnosis is still unclear and helps determine the exact position of certain types of dementia. The PET scan of someone with AD can show bilateral tempoparietal hypometabolism, which may help to differentiate AD from frontotemporal dementia (which would instead show frontal hypometabolism).
CSF- Some patients may undergo CSF analysis, its examined for the precense of tau and amyloid beta.

26
Q

Lewy body dementia

A

An age associated neurodegenerative disorder with features of progressive cognitive decline, Parkinsonism and visuospatial impairment. Third most common type of dementia, more common in men and incidence increases with age. DLB is progressive and reduces life expectancy, the average survival from onset is 5-8 years

27
Q

Presentation of DLB

A

Presenting feature is normally dementia which mainly affects attention and executive function (planning/organising). Memory impairment appears later

28
Q

DLB- Core clinical features

A
  • Fluctuating cognition- normally delirium like (spontaneous alterations in cognition, attention and arousal). Ask questions about excessive daytime drowsiness, lethargy, staring into space. Can occur in advanced stages of dementia so more indicative of DLB when early
  • Visual hallucinations-recurrent, detailed and well formed. Featuring people (including children and family members) or animals i.e. little people walking around the house
  • Parkinsonism- spontaneous features with one or more of bradykinesia, resting tremor and muscle rigidity
  • REM sleep behaviour disorder- a parasomnia characterised by dream enactment behaviours that occur during a loss of normal REM sleep atonia. Can range from benign hand gestures to violent thrashing/kicking. Important to rule out other conditions which mimic this i.e. severe obstructive sleep apnoea.
29
Q

Supportive clinical features of DLB

A
  • Autonomic nervous system dysfunction i.e. orthostatic hypotension, syncope, urinary incontinence, constipation
  • Recurrent falls and postural instability
  • Hypersomnia- excessive daytime sleepiness
  • Hyposmia- reduced ability
  • Hallucinations in other modalities i.e. gustatory (taste), olfactory (smell)
  • Depression and apathy
  • Sensitivity and antipsychotic medication- can worsen motor symptoms and cause life threatening reactions
30
Q

Probable dementia with Lewy bodies- 2 or more clinical features

A
  • Fluctuating cognition
  • Recurrent visual hallucination
  • REM sleep behaviour disorder
  • 1+ of the 3 cardinal features of parkinsonism (bradykinesia, rest tremor, rigidity)
  • Either with or without indicative biomarkers
31
Q

Probable dementia with Lewy bodies- only 1 core clinical feature present but with 1 or more indicative biomarkers

A
  • Decreased dopamine transporter uptake in the basal ganglia- on SPECT/PET scanning
  • Abnormal low uptake of 123iodine-MIBG myocardial scintigraphy
  • Polysomnographic confirmation of REM sleep without atonia
32
Q

Possible dementia with Lewy bodies

A
  • Only 1 core clinical feature is present with no indicative biomarkers present
  • No clinical features present but one or more indicative biomarkers are present
33
Q

Differentiating between Dementia with Lewy bodies and Parkinson’s disease

A

• Patients who develop cognitive symptoms and motor features of Parkinson’s disease within 1 year - should be classified as Dementia with Lewy Bodies
• Patients with a diagnosis of Parkinson’s disease who develops dementia more than 1 year after the diagnosis - should be classified as having Parkinson’s Disease Dementia
The only way to definitively diagnose Alzheimer’s and DLB in a post partum autopsy

34
Q

Dementia investigations- Cognitive testing

A

Dementia screens such as the Mini-Mental State Examination (MMSE) can help to identify the global impairment. For DLB, cognitive tests should cover the cognitive domains that may be affected. This is typically: attentional & executive function and visuospatial / visual perception difficulties (e.g. drawing 2 intersecting pentagons).

35
Q

Dementia investigations- Structural imaging, SPECT/PET

A

Structural imaging- Neuroimaging (CT or MRI scan). The absence of features helps differentiate DLB from other dementia subtype. Normally low/no atrophy.
Single-photon emission CT (SPECT) / Positron Emission Tomography (PET) scan- these scans monitor biological activity in an a anatomical area. In DLB the scans show reduced dopamine transporter uptake in the basal ganglia

36
Q

Dementia investigations- 123iodine-metaiodobenzylguanidine (MIBG) myocardial scintigraphy

A

A nuclear medicine imagine test. In DLB there will be reduced cardiac uptake of 123iodine-MIBG. This test has high sensitivity and specificity for DLB, especially when compared to Alzheimer’s dementia

37
Q

Dementia investigations- Polysomnography

A

Measures electroencephalography (EEG) i.e. brain activity, eye movements and muscle movements during sleep. In DLB, polysomnography can demonstrate REM sleep without atonia which identifies REM sleep behaviour disorder - this predicts Lewy Body related disease with high specificity.

38
Q

Characteristics of Alzheimer’s- structuraly

A
  • Pronounced loss of cortical volume- neuronal apoptosis
  • Cortex shrivels up, damaging areas involved in thinking, planning, remembering
  • Ventricles (filled with CSF) enlarge, the hippocampus shrinks severely
39
Q

Hypothesis for Alzheimer’s disease: Cholinergic defecit

A
  • The earliest mechanistic hypothesis
  • There is a specific cholinergic deficit, involving the cholinergic projection from a basal forebrain neuronal population, to the cortex and hippocampus. The cholinergic projection was shown to die early in AD patients. Acetyl choline signalling is particularly badly affected in AD.
  • This serves a modulatory function in cognition, by optimizing cortical information processing and influencing attention.
  • The activity of choline acetyltransferase, was found to be remarkably decreased, in pathological samples from the cortex and hippocampus of Alzheimer’s patients
  • This led to the first generation of anti-AD medications.
40
Q

MoA of AD treatment- AcH summary

A

AD treatments mostly try to increase effective concentration of acetyl choline by inhibiting Acetylcholinesterase. Difficult to treat as acetylcholine is used throughout the parasympathetic nervous system. Have to be able to cross the blood brain barrier

41
Q

The different types of AD treatment- ACh inhibitors

A
  • Mechanism of Donepezil; selective & reversible AChE (Acetylcholinesterase) inhibitor, long half life (70-80h) -> once a day dosing
  • Mechanism of Rivastigmine: pseudo-irreversible (forms a carbamyl bond with the allosteric site of AchE preventing it from binding with acetylcholine, reverses itself over hours) nonselective cholinesterase inhibitor – 8-10 hour action despite ~3-4 hour plasma availability -> twice daily dosing
  • Rivastigmine patch is useful for AD population as they may forget to take their meds and GI upset is an appreciable source of medicine nonadherance for AChE inhibitors.
  • Treatment tends to slow the rate of decline but does not prevent it
42
Q

Glutamate

A
  • Glutamate receptors- AMPA and Kainate sensitive receptors mediate ‘normal’ neurotransmission. Causes Na+ ions to enter to cause a signal to fire
  • Glutamate receptors are present at 90% of excitatory receptors in the CNS
  • NMDA receptors mediate synaptic plasticity as co-incidence detectors. In a non-depolarised membrane, the channel will be blocked by Mg+ so it doesn’t matter if Glutamate binds as the channel is blocked. In order For Na+ and Ca+ to enter, Glutamate has to bind whilst the membrane is depolarised. The entry of Ca+2 then causes the signalling changes which results in synaptic plasticity causing learning and memory
43
Q

Neurodegenerative diseases

A

Neurodegenerative diseases are characterised by progressive neuronal dysfunction with consecutive neuronal loss of specific populations of neurones. Diseases with known vascular, toxic, metabolic, infectious or immunologic determined causes are NOT classified as neurodegenerative diseases.

44
Q

Neurodegenerative diseases- the accumulation and aggregation of misfolded proteins:

A
  • Hyperphosphorylated tau (HPτ)
  • Amyloid-beta (Aβ)- Alzheimer’s disease
  • α-synuclein (α-syn)- Parkinsons and dementia with Lewys bodies
  • Huntingtin protein- Huntingtons disease
45
Q

Testing for misfolded proteins

A

Standard neuropathological assessment uses immunohistochemistry: antibodies specific to protein aggregates, histological staining- H&E (aren’t specific to the proteins themselves but allow us to see clumps of proteins in the brain).

46
Q

Types of Lewy body diseases

A

Parkinson’s disease, Parkinson’s disease dementia and dementia with Lewy bodies.

47
Q

Vascular dementia

A

Stepwise deterioration in cognition rather than gradual decline. Memory impairment and confusion. Visualised in MRI as hyperintensities (lots of white)- distinguishes it from AD. You can see vascular lesions and vascular insults
Not classified as a proteinopathy as it doesn’t involve misfolding proteins, its due to cerebral vascular disease. Caused by cerebral vascular pathologies which can include atherosclerosis which effects larger vessels and small vessel disease which affects the small vessels in the brain and cerebral amyloid angiopathy.

47
Q

Causes of vascular dementia

A

Amyloid pathology can be deposited in the blood vessels as seen in Alzheimer’s disease this can lead to vascular insults and all three of these pathologies lead to cerebrovascular lesions. Cerebral vascular disease can cause a cerebral vascular lesion which can be classified as an Infarction, Haemorrhage or White matter lesion

48
Q

The three causes of vascular dementia

A
  • Infarction- Ischaemic or Haemorrhagic= Large infarct (15-20mm), Lacunar infarct (5-15mm), Microinfarct (<5mm)
  • Haemorrhage- Cerebral haemorrhage (>10mm), Microbleed (<10mm)
  • White matter lesion- Deep WML (white matter lesion), PVWML (Peri-ventricular white matter lesion), Lacunes
49
Q

Microscopic changes in vascular dementia

A
  • Atherosclerosis- affects large vessels, causes narrowing of the lumen. Most commonly affects the circle of Willis
  • Small vessel disease- affects smaller intracerebral vessels and leptomeningeal arteries, mainly in the basal ganglia and brainstem
  • Cerebral amyloid angiopathy- deposition of amyloid-beta proteins in the vessel walls. Decreases permeability of vessels making them less elastic and brittle
50
Q

Vascular cognitive impairment neuropathology guidelines (VCING)

A

Records the likelihood that vascular insults have contributed to a cognitive decline. Takes into account infarcts, the amount of cerebral amyloid angiopathy, the amount of small vessel disease and white matter pathology and lesions we see in the brain and determine whether this could have contributed to a cognitive decline (determined as low, moderate or high likelihood).

51
Q

Vascular pathologies and Cerebrovascular lesions

A

Vascular pathologies:
• Atherosclerosis
• Small vessel disease
• Cerebral amyloid angiopathy

Cerebrovascular lesions:
• Infarcts
• Hemorrhages
• White matter lesions

Medicine year 2 semester 2 (47 decks)

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