Neurology >
Dementia

“An acquired disorder of cognitive function”

Causes

The potential causes of dementia are diverse, but the disorder is mainly due to neurodegenerative and/or vascular disease associated with increased age

  • Alzheimer’s disease (60-80% of dementia cases)
  • Cerebrovascular disease – vascular dementia (~20% of dementia cases)
  • Parkinson’s disease
  • Frontotemporal dementia (younger-onset, 40–60 years, memory generally remains intact)
  • Dementia with Lewy bodies
  • Huntington disease, Wilson disease
Risk Factors
  • Age (>65 years)
  • Family history
  • Genetics (risk gene – apolipoprotein E-E4, deterministic gene – APP, PS-1, PS-2)
  • Down Syndrome
  • Alcohol consumption
  • Smoking
  • Diabetes
  • Obesity
  • Head trauma + repetitive injury (e.g. boxing)
  • Cardiovascular disease
Clinical Presentation
  • Memory impairment
  • Cognitive impairment
    • Speech: aphasia, word-finding difficulties, semantic paraphasia
    • Intellectual capacities, reasoning, planning capabilities, and self-control
    • Spatial-temporal awareness (awareness of oneself remains stable for a long time)
    • Apathy
  • Changes in personality, mood, and behaviour
  • Early-stage – due to gradual onset, this stage is often overlooked
    • forgetfulness, losing track of the time, becoming lost in familiar places.
  • Middle stage – at this stage, signs and symptoms become clearer and more restricting
    • becoming forgetful of recent events and names, becoming lost at home, increased difficulty with communication, needing help with personal care, behaviour changes, wandering and repeated questioning
  • Late-stage – late-stage dementia entails total dependence and inactivity. Memory disturbances and physical signs and symptoms become more pronounced.
    • becoming unaware of the time/place, difficulty recognizing relatives and friends, increased need for assisted self-care, difficulty walking, behaviour changes that may escalate and include aggression
Pathophysiology

The reasons for this pathophysiology are still not fully understood

  • Alzheimer’s disease:
    • Beta-amyloid plaques are derived from fragments of amyloid proteins
      • These fragments aggregate and clump to form plaques. These clumps of plaques interfere with neuron synapses and recruit immune cells → inflammation.
      • It is still not fully understood whether this process causes or is a result of the disease
    • Tau protein tangles (neurofibrillary tangles) are found inside of neurons. They are derived from the tau proteins on microtubules that support the inside of neurons.
      • In Alzheimer’s, these proteins are changed and aggregate to form tangles with the neuron microtubules → neurofibrillary tangles
      • These tangles reduce neuron communication → to cell death + neurodegeneration
    • Affect temporal lobe (learning + memory) → speaking + communication areas, as well as the frontal (thinking + planning) and parietal (sensory integration) lobe
      • ↑ progression through cortex → ­ neurodegeneration → cerebral atrophy/shrink
  • Vascular dementia:
    • Reduced blood flow and oxygen delivery to the brain causes neuronal degeneration and cognitive dysfunction → vascular dementia
  • Dementia with Lewy bodies:
    • Lewy bodies are abnormal protein structures derived from alpha-synuclein proteins found in terminal axons. They also feature in Parkinson’s disease.
    • If not processed correctly by the body → accumulation → harmful Lewy bodies
    • Symptoms include reduced cognitive abilities, problems with movement and trembling, hallucinations and sleepwalking/talking/ kicking
Investigations
  • Patient and family history + physical examination
  • Neurological examination, psychiatric evaluation
  • Neuropsychological test – Mini-mental state examination (MMSE) with grading score, mini-cog test (name 3 objects → draw a clock → name the 3 objects)
  • CT and MRI scans – differential diagnosis (type), rule out co-morbidities, monitor disease
Management

Target actions of acetylcholine + glutamate, manage comorbidities

  • Cholinesterase inhibitors (donepezil, rivastigmine, galantamine)
    • Prevents Ach breakdown by acetylcholinesterase (AChE) → ↑ ­Ach concentration → ↑ improve memory and cognitive function
  • NMDA receptor antagonist (memantine)
    • blocks overstimulation of NMDA by glutamate release as glutamate is released in excessive amounts in neuronal damage
  • Medication may also be required for conditions related to dementia such as stroke, CVD, diabetes, HTN, depression
  • Cognitive stimulation therapy may also be used
Complications
  • Increased frailty → accidents and falls risk
  • Memory loss → reduced nutrition and weight loss
  • Dysphagia → aspiration pneumonia
  • Reduced mobility → pressure sores and skin ulcers
  • Comorbidities → co-existing illness

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