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Dementia

Dementia is the progressive impairment of multiple higher cortical functions, such as memory, thinking, orientation, comprehension and language, which impairs activities of daily living. It affects 7-10% of those aged 65+ years, with the rate doubling every 5 years between 60-90 years. There are many types of it, including:

  • Alzheimer’s disease (50-60%)

  • Vascular (15-20%)

  • Dementia with Lewy bodies (10-15%)

  • Frontotemporal dementia (4-6%)


The general features of Dementia are:

  • Memory loss

  • Cognitive impairment

  • Decline in social behaviour

  • Symptoms present for 6+ months

  • Awareness of environment is preserved (not delirium)


Alzheimer’s Disease (50-60%)

This is due to:

  • Build up of amyloid protein plaques around brain cells and tau protein tangles within brain cells

  • Cholinergic neuronal cell death

“An illustration of the neuropathology of Alzheimer's disease.” © BruceBlaus CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0/)

It presents with:

  • Memory loss

  • Aphasia - word-finding problems, muddled and disjointed speech

  • Agitation

  • Wandering

  • Personality change


CT Head will show Hippocampal Atrophy (Temporal lobe).


Management:

  • Acetylcholinesterase Inhibitors (1st line) - Donepezil, Rivastigmine

  • NMDA receptor antagonist (2nd line) - Memantine


Vascular Dementia (15-20%)

It presents with a sudden onset cognitive decline and stepwise deterioration in those with CVS disease or CVE, as a result of the developing infarcts. The 2 types of it are:

  • Large vessel - Single infarct, Multiple cortical grey matter infarcts

  • Small vessel - Multiple lacunar white matter infarcts, Occlusion of single deep penetrating artery

“Brain atrophy from vascular dementia” © James Heilman, MD CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0/)

Investigations include:

  • Detailed hx and examination

  • Cognition screen

  • Medication review

  • Rule out reversible organic causes

  • MRI


Parkinson’s Disease Dementia/PDD and Lewy Body Dementia/LBD (10-15%)

PDD is diagnosed when there are Parkinsonian symptoms that develop 12+ months before cognitive decline.

  • 60-75% of PD patients develop Dementia


LBD is diagnosed when there are Parkinsonian symptoms that develop 12+ months after cognitive decline. This is due to the formation of Lewy Bodies (alpha-synuclein cytoplasmic inclusions) leading to cognitive decline associated with parkinsonism (bradykinesia, rigidity, tremor).

“Photomicrograph of regions of substantia nigra in a Parkinson's patient showing Lewy bodies and Lewy neurites in various magnifications. Top panels show a 60-times magnification of the alpha synuclein intraneuronal inclusions aggregated to form Lewy bodies. The bottom panels are 20 × magnification images that show strand-like Lewy neurites and rounded Lewy bodies of various sizes. Neuromelanin laden cells of the substantia nigra are visible in the background. Stains used: mouse monoclonal alpha-synuclein antibody; counterstained with Mayer's haematoxylin.” © Suraj Rajan CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0/)

It presents with 3 core features:

  • Fluctuating cognition

  • Parkinsonism

  • Visual hallucinations


Management:

  • Acetylcholinesterase Inhibitors (1st line) - Donepezil, Rivastigmine

  • NMDA receptor antagonist (2nd line) - Memantine


N.B. Avoid Antipsychotics as they work to reduce dopamine, which is already low in those with PD.


Frontotemporal Dementia (4-6%)

It typically occurs at a younger age than other types of dementia, presenting with:

  • Early personality change and frequently become disinhibited

  • Poor verbal fluency


One of its causes is Pick’s Disease, which involves the formation of Pick bodies (Tau inclusions) and Pick cells (Ballooned cells).


Imaging shows atrophy of Frontal and Anterior Temporal lobes.

“Brain MRI of a female 65 y.o. white patient with Pick's disease. Cortex and white matter atrophy of the frontal lobes is clearly visible. The MRI was done without contrast enhancement utilizing Magnetom Vision 1.5 Tesla with superconductive magnet.” © Mikhail Kalinin CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0/)

Alcoholism

Wernicke’s Encephalopathy occurs due to a Thiamine (vit B1) deficiency, and presents with Ataxia, ophthalmoplegia, nystagmus, and an acute confusional state. The mammillary bodies (involved in memory function, specifically in its formation and retrieval) in the brain tend to be affected.


Korsakov’s Syndrome is a complication of untreated Thiamine deficiency, and presents with:

  • Antegrade and Retrograde amnesia

  • Confabulation (creation of false memories w/o the intent to deceive)



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