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MRS211 > Dementia > Flashcards

Dementia Flashcards

1
Q

What is dementia?

A
  • Is not a specific disease.
  • It is the broad term for a group of diseases causing a progressive decline of neurological function.
  • Presents with symptoms severe enough to interfere with normal daily life.
  • Symptoms include memory loss, confusion, and personality and behavioural changes.
  • More common in elderly but not part of normal aging
  • Famous dementia sufferers include Ronald Regan, Margaret Thatcher, Robin Williams, Sugar Ray Robinson, and Malcolm Young.
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2
Q

Signs and symptoms for dementia

A
  1. Subtle short-term memory changes. Trouble with memory can be an early symptom of dementia.
  2. Difficulty finding the right words.
  3. Changes in mood.
  4. Apathy.
  5. Difficulty completing normal tasks.
  6. Confusion.
  7. Difficulty following storylines.
  8. A failing sense of direction.
  9. Being repetitive.
  10. Struggling to adapt to change.
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3
Q

Types of dementia

A
  • Alzheimer’s disease (most common 60-80%) • Vascular dementia
  • Dementia with Lewy bodies (DLB)
  • Mixed dementia
  • Parkinson’s disease
  • Frontotemporal dementia
  • Creutzfeldt-Jakob disease
  • Normal pressure hydrocephalus • Huntington’s disease
  • Wernicke-Korsakoff Syndrome
  • Others
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4
Q

Alzheimers disease

A
  • 1906, Alois Alzheimer documented first case Auguste Deter • Most common progressive, neurodegenerative disease
  • Most common form of dementia in the elderly
  • Complex aetiology > genetics, environment & lifestyle
  • Classification based on heritability & age of onset:
  • Late-onset AD; >65 YOA onset, classical disease
  • Early-onset AD; <65 YOA onset, often inherited, rare, faster progression • High socioeconomic burden
  • Need for early diagnosis
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5
Q

Alzheimers risk factors

A
  • Age
  • Sex
  • Family history and genetics
  • Down syndrome
  • Mild cognitive impairment (MCI) • Head trauma
  • Chronic stress
  • Depression
  • Diabetes
  • Hypertension
  • Vascular disease • Oxidative stress
  • Vitamin D deficiency
  • Obesity & inflammation
  • Smoking or exposure to second-hand smoke
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6
Q

Plaques in alzheimers disease

A

• “Amyloid hypothesis”
• Amyloid precursor protein (AAP) severed beta & gamma secretase
(enzymes) > resultant beta-amyloid (sticky protein)
• A𝛽 accumulation = initial pathological event
• A𝛽 folds into insoluble clumps or fibrils that form plaques (surface of neuron) > may block signalling at synapses
• A𝛽 accumulation > A𝛽-induced neuroinflammation (activation/dysfunction of microglia - main brain immune cell) > neuronal death

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7
Q

Tangles in alzheimers disease

A

• Form inside the neuron
• Health neurons connect via branches called neurites that contain
microtubules (support, carry nutrients & neurotransmitters)
• Microtubules are reinforced by tau proteins (ladder rungs)
• Tau proteins loosen and form neurofibrillary tangles > microtubules breakdown > neuronal death

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8
Q

Loss of neutrons and synapse causes:

A 
neurofibrillary tangles
• Cognitive Symptoms:
• Attention deficit
• Language impairment
• Short term memory loss
• Impaired activities of daily living (apraxia)
• Loss of orientation (time, space)
• Behavioural Symptoms:
• Apathy
• Depression
• Anxiety
• Aggressive behaviour
• Hallucinations
• Social withdrawal
  neuritic plaques
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9
Q

Morphological changes in Alzheimers disease include?

A

Narrowed gyro
Increased sylvan fissure
global shrinkage
widened sulcal margins

These effect the patients language and memory

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10
Q

Imaging Alzheimers disease

A 
Structural:
• MRI > CT
• Exclude differentials
• Not typically used to diagnose
• Determine degree of atrophy – Hippocampus
– Entorhinal cortex
– Temporal parietal cortical
• Diffusion Tensor Imaging
Functional:
•MRI
• BOLD
• Hippocampal BBB breakdown •SPECT
•PET
• F-18 FDG; demonstrates hypometabolism
• Amyloid; range of radiotracers that bind to A𝛽 fibrils demonstrating increased activity
• Tau; range of agents that bind to tau proteins demonstrating increased activity in atrophic regions
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11
Q

CT for Alzheimers disease

A
  • Similar appearance to normal aging brain in early stages • Atrophy
  • Enlarged ventricles
  • Prominent sulci
  • Correlate with clinical symptoms
  • Rule out other brain causes for symptoms • Impacts allocation for care funding
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12
Q

MRI for Alzheimers disease

A
  • Similar appearance to normal aging brain in early stages • Atrophy
  • Enlarged ventricles
  • Prominent sulci
  • High intensity periventricular region T2 / FLAIR • Correlate with clinical symptoms
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13
Q

NM for Alzheimers disease

A
  • FDG-PET – decreased glucose metabolism in Alzheimer’s regions
  • Measures synaptic activity
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14
Q

Treatment for Alzheimers disease

A
  • No cure
  • Can slow progression
  • Diet
  • Exercise
  • Education
  • Memory aids
  • Medication
  • Acetylcholinesterase inhibitors (Prevent destruction of neurotransmitter acetylcholine)
  • Memantine (Prevents calcium moving into brain cells causing damage
  • Other drugs that treat symptoms (Sleep and psychological issues)
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15
Q

What is Parkinson’s disease

A
  • Complex
  • Chronic, progressive, neurological degenerative movement disorder:
  • Degeneration/death of dopaminergic neurons, resultant dopamine deficiency within basal ganglia > movement disorders
  • Also involves other neurotransmitters and other regions • Manifests with a broad range of symptoms
  • Complex cause; genetics & environment
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16
Q

Clinical signs and symptoms

A
  • Bradykinesia (slowness of movement)
  • Rest temor (Involuntary rhythmic tremor when limbs are relaxed)
  • Muscular rigidity (Inability of the muscles to relax normally)
  • Postural and hair impairment (small shuffling steps)
17
Q

Classification of Parkinson’s disease

A 
• No consensus on subtypes
• Distinct aetiologies &amp; pathogenesis (hypothosised)
• Empirical clinical observations:
1. Tremor-dominant PD
2. Non-tremor dominant PD
3. Mixed or indeterminate
• Tremor-dominant:
– Relative absence of other motor symptoms – Slower progression
– Less functional disability
18
Q

Motor features of Parkinson’s disease

A
  • Tremor (usually occurring at rest - the classic slow, rhythmic tremor of Parkinson’s disease typically starts in one hand, foot, or leg and can eventually affect both sides of the body)
  • Bradykinesia (slowness of movement)
  • Muscle Rigidity (may feel like a cogwheel or ratchet when the limb is moved passively through its range of motion or it may be consistent like bending a lead pipe)
  • Postural Instability (falls- usually a late symptom in Parkinson’s)
  • To be diagnosed generally you need to have bradykinesia plus rigidity and tremor or both. Postural Instability is usually a late symptom of Parkinson’s.
19
Q

Non-motor features of Parkinson’s disease

A
  • Sensory dysfunction including loss of the sense of smell and visual disturbances.
  • Mood disorders including anxiety, apathy and depression
  • Constipation and gastrointestinal issues
  • Fatigue, pain and cramping
  • Speech problems including changes in verbal fluency similar to stuttering and decreased volume of speech
  • Sexual issues including impotence
  • Changes in hand writing (it often becomes smaller in height and the written words may be unclear by the end of the sentence).
  • Postural hypotension (drop in blood pressure on rising from a lying or sitting position)
  • Excessive salivation
  • Sleep disorders including REM sleep disorder (where a person acts out their dreams), intense or vivid dreams and excessive daytime sleepiness
  • Swallowing difficulties
  • Sweating and increased sensitivity to temperatures.
  • Cognitive changes - changes in the ability to think and reason, memory difficulties, personality changes and dementia
  • Urinary urgency, frequency and incontinence
  • Mental health issues including hallucinations and delusions. Impulsive control disorders (binge eating, excessive shopping or gambling) may be an issue and this is usually a side effect of some Parkinson’s medications
20
Q

Risk factors for Parkinson’s disease

A
  • Pesticides
  • Toxins
  • Chemicals
  • Genetic factors • Head trauma
21
Q

Pathophysiology for Parkinson’s disease

A
  • No standard criteria exist
  • 2 major neuropathological findings
  • Loss of pigmented dopaminergic neurons of the substantia nigra pars compacta
  • The presence of Lewy bodies and Lewy neurites
  • Approximately 60-80% of dopaminergic neurons are lost before the motor signs of Parkinson disease emerge
22
Q

Diagnosis of Parkinson’s disease

A
  • Currently there is no definitive laboratory test or radiological procedure which diagnoses Parkinson’s and autopsy - based studies have shown that even among neurologists, diagnostic accuracy results in up to 25% of cases proven incorrect at time of death.
  • Provisional medical diagnosis continues to be based on the clinical picture of four cardinal symptoms
  • The diagnostic check list is composed of: • Bradykinesia
  • Musclerigidity
  • Tremor
  • PosturalInstability
  • Positive response to levodopa. (Drug creates Dopamine in the body)
  • Improvement in patient symptoms
23
Q

Imaging for Parkinson’s disease

A
  • CT – Similar appearance to normal aging brain
  • Rule out structural abnormalities which may result in Parkinson’s–like symptoms.
  • MRI – Rule out other neurological conditions which may resemble Parkinson’s. • Research - fMRI and spectroscopy
  • PET / SPECT – Confirmation of diagnosis / research
24
Q

CT for parkinsons disease

A
  • Similar appearance to normal aging brain
  • Performed routinely to rule out other causes
  • Many brain pathologies exhibit similar symptoms
  • Rule out
  • Tumours
  • Infective/inflammatory process • Other degenerative disorder
25
Q

SPECT/PET for parkinsons disease

A
  • Functional imaging of dopamine transporter
  • Both SPECT and PET tracers have a high sensitivity for assessment of presynaptic dopaminergic deficits
  • SPECT (123 I) ioflupane (DaTscan) established
  • Demonstrates binding of 123I-fluoropropyl to DaT protein in the nigrostriatal nerve endings of the striatum
  • DaTscan can differentiate from essential tremor only
  • PET imaging using 6-fluorodopa (FDOPA) demonstrates decreased uptake in posterior striatum, particularly in the putamen
  • 18F Fluorodeoxyglucose (FDG) demonstrates diffuse cortical hypometabolism (marked in parietotemporal cortex)
  • Novel PET tracers β-amyloid, tau protein, or α-synuclein aggregates
26
Q

PET/CT for parkinsons disease

A
  • Gives exact anatomical reference for increased activity

* Important for PD diagnosis as it effects particular areas of the brain

27
Q

MRI for parkinsons disease

A
  • Recommended by NICE for PD differential & patients with atypical features
  • Structural & functional
  • 3-7T MR scanning can detect structural nigral abnormalities
  • Ultra high field MRI with diffusion-tensor (tractography) & diffusion-weighted imaging are being explored for early disease diagnosis
  • Other areas of research: • Spectroscopy
  • resting-statefMRI
  • arterialspinlabeling
28
Q

Soft signs in MRI for Parkinson’s

A
  • Hummingbird or penguin sign (mid brain atrophy)
  • Mickey mouse sign
  • Swallow tail sign
29
Q

Treatment for parkinson’s disease

A
  • Exercise
  • Oral medications
  • Advanced therapy medications given by injection or by a tube directly into the small intestine
  • Surgical treatments including deep brain stimulation (Electrical impulses to stimulate areas of the Basal Ganglia)
  • Advice and support from a Parkinson’s Specialist Nurse
  • Physical and Supportive therapies including Physiotherapy, Occupational Therapy, Speech Pathology, Nutrition and Dietetics, Psychology and Social Work
30
Q

Follow up imaging post placement of deep brain stimulation electrodes

MRS211 (18 decks)

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