Cortical Dementias Flashcards
Dementia
A deterioration of cognitive function. Can be progressive, static, reversible or due to some other cause.
Cortical Dementia
Preferential neuron loss in the cortical and subcortical grey matter (cortex and hippocampus).
Dementia of the Alzheimer’s Type
Irreversible, progressive dementia with average onset of 70+ years.
Neuropathology of DAT
Disease targets grey matter of the temporal, frontal and parietal lobes, the hippocampus, amygdala, subthalamic nuclei and olfactory area.
Markers of DAT
Neurofibrillary tangles within the neuron and senile plaques between the cells. Tangles cause the neuron to die and plaques fill the empty space. High concentration of these in the frontal, temporal and parietal areas indicates DAT.
Neurotransmitters and DAT
ACh is synthesised in the BFCC. Damage to the BFCC results in loss of ACh in the frontal, parietal and temporal lobes and the hippocampus.
Neuropsychology of DAT
Progresses through a series of deficits to memory, attention, information processing, reasoning and language (like a reversal of infant development).
Behavioural Changes of DAT
Clinging to caregiver, distractible, disinterested, poor self-care, restlessness, wandering, lack of impulse control, paranoia and depression.
Frontal Lobe Dementia
Preferentially targets neurons in the frontal and temporal lobes, leaving subcortical structures intact. Average age of onset around 50 to 60 years.
Neuropsychology of DFT
Silliness, poor judgement, inappropriate behaviour (early stage). Blunt affect and apathy (mid stage). Motor rigidity and muteness (late stage).
Cognitive Ability in DFT
Lack of self-awareness and executive functions, hyperorality, language difficulty, impulsivity, inappropriateness.
BFCC
Synthesizes ACh. Cell bodies lie I. Sub cortical frontal structures and project to hippocampus. Loss of BFCC results in loss of ACh in frontal temporal and parietal regions and explains memory loss (connection between frontal and Limbic areas destroyed)
