Flashcards in dementia Deck (56):
dementia and age?q
it is a disease of aging. 50% chance of having dementia by 85
normal aging decline > mild cognitive impairment > dementia
what are some normal age associated changes
difficulty retrieving words. slower processing speed. difficulty sustaining attention with distractions. learning something new takes more effort. there should be no functional impairment.
mild cognitive impairment
memory complaint corroborated. objective memory impairment for age and education. preserved general cognition. normal activities of daily living. not demented, although some do progress to dementia
memory loss, but not enough to meet dementia criteria. progresses to AD in 10-15%. maybe the earliest phase of AD>
what are the criteria for dementia
memory decline and impairment. at least one of the following: aphasia, apraxia. decline in memory, cognition, complex attention, executive function, learning/memory, language, perceptual/motor or social cognition.
this is an impairment.
early onset AD
between 30-60. rare. familial in most.
what genes/chromosomes associated with early onset AD.
1 - presinilin 2
14 - presinilin 1
21 - amyloid precursor.
late onset AD
most common form. develops after age 60. chromosome 19 seems to be involved. this is E4 gene.
most common cause of dementia. deficits in recent memory that progresses to global impairment of cognition. usually sporadic and late onset. neuronal and synaptic loss effects the cortical and subcortical areas.
gross affects of AD
cerebral atrophy, especially affecting the temporal, parietal, and frontal areas. this is found with ventricular enlargement. flattening of gyri enlarging sulci. the hippocampus is greatly atrophied.
microscopic affects of AD
amyloid plaques, neurofibrillary tangles, granulovacular degeneration. hirano bodies.
where are the A-beta plaques?
they are extracellular and often associated with dystrophic neurites.
where are the neurofibrilary tangles and what are they?
they are intracellular, in the cytoplasm. they are composed of hyperphosphorylated Tau. for AD they are in the shape of the neuron.
what is characteristic about the plaques?
they have apple-green birefringence this confirms the presence of amyloid. perivascualr causes bleeding.
what is Pick's disease?
this is a tauopathy. it is frontal-temporal lobe dementia. the occipital and parietal lobes are spared. typical knife-edge gyri
what are the risk factors for AD?
increasing age, females, family history, fewer years of education, lowr income, depression or emotional illnesses, head injury, low seri, folate/b12, elevated homocysteine, postop delirium, alcohol abuse.
what are three spheres of dementia
impairments in cognition, function, and behavior.
insidious onset, gradual progression, early decline in social interpersonal conduct, loss of regulation of interpersonal conduct with loss of insight. early emotional blunting. behavioral abnormalities. memory loss may occur later but is not as pronounce as AD
treatments for FTLD
NO ACH -DOESNT WORK. use divalproex for behavior. SSRI for irritability.
ACH inhbitors, NMDA antagonists.
why does acetylchoine work?
nucleus basal is of maynert degeneration in AD causes widespread loss of ACH. replenishing that seems to resolve some symptoms.
why use NMDA antagonists?
remember blandens paper. this may be excitotoxicity issue.
what is a common NMDA antagonist used?
why do we not use antipsychotics?
because there are major risks involved. cardiovascular events
multiinfarct dementia. cerebral amyloid angiopathy. HTN related small vessel disease. most common after AD. step-wise progression. can be abrupt after cerebrovascular event. emotional lability.
which arteries are affect the most by HTN in the brain?
how to treat vascular?
focus on reducing the risks. BP, smoking, blood sugar, diet and exercise.
treatment for vascular
donepezil. and other cholinesterase inhibitors.
lewy body dementia
intracellular fibrillary deposits of presynaptic protein alpha-syn. primarily sporadic. parkinsons and LBD. everyone that has one develops the other, if they live long enough.
cardinal symptoms of parkinsons
TRAP. tremor, rigidity, akinesia, postural instability. shuffling gait. dementia also occurs. this is caused by dopaminergic deficit. responds to L-dopa. substantia nigra pars compacta pallor.
characteristics of lewy body
they are intracellular inclusions of alpha-syn/
dementia with lewy bodies LBD.
sporadic, late onset, memory less affected than AD. frontal and subcortical features such as deficits in alertness and attention are common. there are also pronounced fluctuations in symptoms. common with vivid hallucinations and delusions. motor symptoms of PD are variably present. there is nigral pallor, with less cortical atrophy.
clinical aspects of LBD
short term memory loss with gradual onset. visual hallucinations, cognitive fluctuations, REM sleep disorder. frequent falls, autonomic dysfunction.
what to treat
Ach works here for support. dopa for movement. AVOID ANTIs for increased sensitivity. REM sleep can use clonazepam
traumatic brain injury incidence
1.7 million in the US.
causes of TBI
falls, MVA, assaults
what is TBI
efined as a blow or jolt to the head or a penetrating head injury that disrupts the function of the brain. Not all blows or jolts to the head result in a TBI. The severity of such an injury may range from "mild," i.e., a brief change in mental status or consciousness to "severe," i.e., an extended period of unconsciousness or amnesia after the injury. A TBI can result in short or long-term problems with independent function.
A depressed skull fracture in which the broken bone exerts pressure on the brain.
The common result of a blow to the head or sudden deceleration usually causing an altered mental state, either temporary or prolonged. Physiologic or anatomic disruption of connections between some nerve cells in the brain may occur. Often used by the public to refer to a brief loss of consciousness.
Bruising or damage to brain tissue on the side opposite where the blow was struck.
Diffuse Brain Injury
Injury to cells in many areas of the brain rather than in one specific location.
Rupture of a blood vessel leading to the collection of blood in brain tissues or empty spaces. There are several types of hematoma:
– Outside the brain and its fibrous covering, the dura, but under the skull.
– Between the brain and its fibrous covering (dura).
– In the brain tissue.
– Around the surfaces of the brain, between the dura and arachnoid membranes.
how does the brain heal?
some parts of the brain adapt to take over other functions.
rehabilitation is focused on what?
relearning and adapting
mild dysfunction MMSE
what is the acronym for activities of daily living and what does it stand for?
dressing, eating, ambulating, toileting, hygiene.