Dementia Flashcards
IMC606
Give an example of
Working memory
remembering a phone number through rehearsal; doing mental arithmetic
Give an example of
Episodic memory
remembering what I ate for dinner last night
Give an example of
Semantic memory
knowing what a library is; knowing what a computer is
Give an example of
Procedural memory
knowing how to dance, swim, ride a bike
The function of
Amygdala
recognizing threatening stimuli and responding to them; attaching emotional responses to life events
The function of
Hippocampus
memory consolidation; transferring episodic memories to cortical areas for long term storage.
Cause of Kluver-Bucy
bilateral damage to the amygdala
Deficits that occur in Kluver-Bucy
loss of aggression/fear, hypo-emotionality, hyperorality, hypersexuality
What is the role of nucleus accumbens in behavior?
Nuc Accumbens influences our response to rewarding stimuli. It is involved in our motivation/drive to participate in behaviors that are rewarding/positive/pleasurable.
What transmitter is significant in the nucleus accumbens activation, and how is it related to addiction?
It is activated by dopamine. Highly rewarding activities release larger amounts of dopamine in Nuc Accumbens and facilitate reinforcing those activities/behaviors.
Name the structures involved in the Papez circuit and link the structures to show how activity progresses through the circuit.
hippocampus -> fornix -> mammillary body -> anterior nucleus of thalamus -> cingulate gyrus -> entorhinal cortex (area around olfactory cortex ) -> hippocampus
Pathological features and proteins in
Alzheimers Disease
Senile plaques – b amyloid aggregate, neurofibrillary tangles – hyperphosphorylated t, gliosis, hydrocephalus ex vacuo, brain atrophy
Pathological features and proteins in
Lewy Body dementia
Lewy Bodies – a synuclein, neuromelanin inclusions
Pathological features and proteins in
Frontotemporal Lobe Degeneration
hyperphosphorylated t inclusions, TDP-43, frontal lobe atrophy
Pathological features and proteins in
Creutzfeldt Jacob Disease
prions – misfolded, transmissible proteins, spongiform encephalopathy, amyloid aggregates, MRI: cortical ribbonning, BG/Thalamus intensity; 14-3-3 protein in CSF, sharp waves EEG
Pathological featues and proteins in
Vascular Dementia
multiple cortical infarcts
Affected areas in
Alzheimers Disease
Cortex, hippocampus, amygdala
Affected areas
Lewy Body Dementia
Diffuse cortex
Affected areas in
Frontotemporal Lobe Degeneration
Frontal and temporal lobes
Areas affected in
Creutzfeldt Jacob Disease
Diffuse Brain
Areas affected in
Vascular Dementia
Multiple cortical infarcts
Symptoms of
Alzheimers Disease
amnesia (anterograde early, retrograde late)
executive dysfunction
loss of insight
aphasia
visuo-spatial impairment
Symptoms of
Lewy Body Dementia
visual hallucinations
fluctuating cognition
PD symptoms
(memory good initially)
Symptoms of
Creutzfeldt Jacob Disease
myoclonus
ataxia
rapid progression
cognitive decline
Symtpoms of
Frontotemporal Lobe Degeneration
Disinhibited behavior
apathy
loss of empathy
overeating sweets
compulsive
aphasia subtypes
(<65 yo, memory good initially)
Symptoms of
Vascular Dementia
Focal neurological deficits
loss of cognitive abilities
Onset of dementia vs delirium
Dementia- abrupt onset
Delirium- ongoing condition
Reversibility of dementia vs delirium
Dementia- irreversible
Delirium- reversible
Chronicness of dementia vs delirium
Dementia- chronic
Delirium- acute
Changing in delirium and dementia
Dementia- unchanging mental status
Delirium- waxing and waning mental status
Ability to focus in dementia vs delirium
Dementia- maintains focus
Delirium- distractible, loss of attention
Consciousness in dementia vs delirium
Dementia- stable consciousness
Delirium- fluctuating consciousness
What is the cause and symptomatic triad of Wernicke Encephalopathy?
Thiamine deficiency, a condition often associated with chronic alcohol use, results in hemorrhage of the mammillary bodies.
Symptomatic Triad: confusion, ophthalmoplegias, ataxia.
In Wernicke’s Encephalitis What pathological changes occur? How does this disorder fit the definition of encephalopathy?
This is a metabolic/nutritional disorder that results in an acute state of confusion. A patient with WE presenting to the ED in a state of confusion would be exhibiting delirium or the effects of an encephalopathy.
How is the memory deficit in Korsakoff Syndrome related to the memory structures in Papez’s circuit?
Korsakoff syndrome is associated with late stages of Wernicke encephalopathy. KS causes anterograde amnesia and confabulation (fabricating stories to explain unremembered events). It is a consequence of damage to the mammillary bodies, which are connected to the hippocampus via the fornix as part of Papez’s circuit.
How are focal neurological deficits associated with vascular dementia? What about Alzheimer D, LBD, FTLD?
These are deficits that can be attributed to a lesion at a specific location in the central nervous system. Vascular dementia results from strokes that affect specific locations of the cerebral cortex. Damage to specific areas will result in specific deficits associated with those functional areas. In contrast, AD, LBD, FTLD result in diffuse damage to cortical areas that cause a more general loss of cognitive function. However, the restricted areas of frontal and temporal damage and their related symptoms in FTLD could be considered focal deficits.
What score on the MMSE indicates mild cognitive impairment?
26-21
Which disorders (AlzheimerD, LewyBodyD, FTLD) are associated with anterograde amnesia?
Anterograde amnesia is a feature of Alzheimer D due to atrophy of the hippocampus. LBD and FTLD do not affect the hippocampus.
Formation of protein aggregates is one of the mechanisms underlying neurodegenerative diseases. Describe how amyloid and tau proteins are involved in this process: what leads to aggregate formation, where are the aggregates deposited.
Improper cleavage of APP by secretase molecules results in longer b-amyloid fragments that aggregate as they accumulate. These aggregates form insoluble, extracellular deposits in the cortex. They appear either as separate deposits (b-amyloid plaques) or they become surrounded by degenerating neurites (neuritic plaques). (neurite=unidentified axon or dendrite)
In AD, the microtubule associated protein, tau, becomes hyperphosphorylated. This causes it to form insoluble, intracellular aggregates that accumulate as twisted filaments (neurofibrillary tangles) in the cell body, axons, and dendrites.
Disorder associated with image A
Lewy Body Dementia
Disorder associated with image B
Neuritic Plaques
Disorder associated with image c
Creutzfeldt Jacob Disease
Disorder associated with image D
Neurofibrillary tangles
Disorder associated with image E
Frontotemporal Lobe Degeneration
How can Down’s syndrome provide insight into the role of b-amyloid in AD?
In Down’s syndrome there are 3 copies of chromosome 21. This chromosome contains the gene for APP, increasing the expression of amyloid compared to normal. Most individuals with Down’s syndrome develop b-amyloid plaques and AD by their 50s.
Is hydrocephalus ex vacuo a feature of Alzheimer Disease? Explain your answer.
YES! Cortical atrophy that occurs in AD is accompanied by expansion of the lateral ventricles. The volume of CSF in the lateral ventricles expands to fill the space in the cranial cavity vacated by cortical tissue.
How do the areas of degeneration in FTLD correlate with the clinical subtypes of FTLD?
Frontal lobe -
impaired executive functions (judgment, impulse control, social behavior, personality) correlates with bv-FTLD and damage to Broca area correlates with PPA type where speech is affected.
How do the areas of degeneration in FTLD correlate with the clinical subtypes of FTLD?
Temporal lobe
Wernicke language area correlates with PPA type where language comprehension is impaired.
Which cholinesterase inhibitors are used to treat AD and what is the rationale for their use?
Donepezil, rivastigmine, galantamine. Circuits involved in memory function depend on acetylcholine as an important transmitter. As neurodegeneration progresses and neurons become impaired, transmitter levels decrease, which can be compensated by inhibiting breakdown of acetylcholine in the brain.
Disorders that affect the Loop of Meyer
HSV1
Stroke
Deficits that affect the Loop of Meyer
Contralateral superior quadrantanopia
Disorders that affect the Olfactory Cortex Uncus
Uncinate seizures
HSV1
Deficits that occur in the Hippocampus
Inability to remember recent events
Disorders that affect the hippocampus
HSV1
Seizure
Alzheimers Disorder
Kluver-Bucy
Deficits in the Olfactory Cortex Uncus
Olfactory hallucination
Anosmia
Disorders that affect the amygdala
HSV1
Seizure
Kluver-Bucy
Disorders that affect Wernickes Area
HSV1
Stroke
Tumor
Seizure
FTLD
Alzheimer Disease
Deficits in the Amygdala
Loss of fear and awareness of threat to self
Deficits in Wernickes Area
Impaired ability to comprehend language
