Flashcards in Neuro AD done Deck (38):
A condition of progressive dementia resulting in:
• Impaired memory•
AD really stands for ___________, but we can say __________ to remeber it.
Aggressive dimentia, because this is what it is, dimentia.
AD is NOT
What kind of dimentia is the most common for the elderly?
Is AD a natural part of aging?
Is AD fatal?
Does exposure to aluminum cause AD.
Only the elderly get AD?
Does aspartame cause AD?
Are there any therapies to stop the progression of AD?
• Family History
• Gender: Women > Men
• Level of education (a protective factor)• Higher education less incidence, because they stimulate their brains more.
• History of head injury/trauma, so there is damage there.
• Exposure to heavy metals & toxins, same as in heavy metal concerts that they shake their heads alot.
Converging studies reveal that risk factors for CVA &cardiovascular disease
overlap with AD
• High cholesterol & LDL, HTN, DM
• inc levels of homocysteine, a risk factor for heart
disease, is associated w/ risk of AD
• Suppression of cholesterol by statin drugs reducesformation of plaques & lowers risk of AD
• Smoking triples the risk of AD
• # of β-amyloid neuritic plaques w/ amount of smoking
So there are tarry blackness on one's lungs, so there are tarry blackness in one's brain.
• Social Risk Factors: Loneliness linked to AD
• Environmental Risk Factors:
• Exposure to second-hand smoke• Environmental pollutants
• Hormone Therapy in any form before age 65• Lowers the risk by half
What are some suggested causes for AD?
Cause is unkown.
But genetics is a strong indicator.
An improper processing of amyloid.
What are four areas of the brain that are affected by AD and the associated dysfunctions that we would expect?
• Limbic system,emotions.
• Hippocampus, STM to LTM
• Thalamus, sensory deficit
• Hypothalamus, Monitors body temp & appetite, and the body’s in-ternal clock
What is the firsts tructure to see damage from AD.
The cerebral cortex
What are two seposits that are found in the brain?
Amyloid and neurofibrillary tangles
Other Neuropathic Findings are?
• Widespread cortical depletion of ACh, its like Ach, my head hurt and it now all ADs up.
• Areas of brain involved initially include hippocampus, neocortex, amygdala, & basal nucleus of Meynert
• Eventually spread to cerebral cortex
• Cerebral atrophy
How many types of dimentia do we have? And whata ee these types?
Acute and chronic.
Explain acute dimentia.
sudden, reversible• 10% of all dementias are transient
Its like a cold, it comes on quickly and it goes away.
Explain chronic dimentia.
• Chronic dementia – gradual, irreversible
• Degenerative diseases (AD, PD, Huntington’s, NPH, etc)
• Multi-infarct dementia / vascular dementia
• Infections (AIDS, Neurosyphilis)
• Head Trauma
• Alcoholic dementia
Characteristics of Reversible Dementia
Use the anacronym, DIEMENTIA
• Drug use (meds S/E)
• Emotional disorders (depression)
• Metabolic disorders (electrolyte imbalance)
• Endocrine disorders (hyper/hyposecretions)
• Nutritional disorders (Vitamin B12 deficiency)• Trauma or tumor
• Infection (UTI, acute bronchitis)
Ten Warning Signs of AD are?
1. Recent memory loss affecting job skills hipposcampus
2.Difficulty performing familiar tasks hipoocampus
3. Problems with speech & language,
4. Disorientation of time & place, hipoocampus,
5. Poor or decreased judgment
6. Problems with abstract thinking
7. Misplacing things, hippocampus
8. Changes in personality hippocampus
9. Mood & behavior changes, hippocampus
10.Loss of initiative
There seems to be alot of problems with the issue of the memeory.
Cahnges between satge I and stage II and stage III AD?
They are basicaly the progression of each other.
That I is the start of the memory loss but we cannot really fnd any imaging problems. II there mild • Moderately Enlarged Ventricles• Cortical Shrinkage
• Hippocampal Shrinkage.
And III is severe • Severely Enlarged Ventricles
• Extreme Cortical Shrinkage
• Extreme Hippocampal Shrink-age
Stage I: Early Stage (1-3 years)
• Forgetfulness & mild memory deficit
• Difficulty w/ novel or complex tasks, new tasks
• Apathy & social withdrawal, lack of spontaneity
• Repeating same thing over & over again, maybe because the person forgot that they had done it.
• Emotional lability, moodiness, hypochondriasis
• Time disorientation
• judgment, problem solving, abstract thinking
• May display catastrophic reactions to stressful events
Stage II: Moderate Stage (3-10 yrs)
• Moderate to severe objective memory deficit, a more severe progression of stage I
• Disorientation to time & place, more of stage I
• Restless & wanders aimlessly, sundowning, paranoia, hallucinations, sleep pattern disturbances, impulse
• Personality & behavioral changes, mpre of stage I
• Language disturbance, visuoconstructive difficulty & apraxia
• Inability to learn new things, very similar to stage I
• Requires supervision, major
A big change is that they wonder and they hallucinate and now require supervision
Stage III: Late Stage (8-10 yrs)
• Intellectual functions virtually untestable
• Verbal communication severely limited
• Incapable of self-care
• Physical impairment
• Difficulty swallowing
• Weight loss
• Incontinence of B/B
• Inability to recognize family members
• Return of primitive reflexes:
• Reversal of encephalization process of childhood,
whereby primitive reflexes fade as higher cortical ar-eas take control over lower subcortical centers
• In AD, positive release from higher control re-
emergence of primitive reflexes
• “Once a man, twice a child”
That a person is a child a man and now a child again.
Stage IV: Terminal Stage
• Loss of all abilities – speech, motor, perceptual• Unaware of environment
• Joint contractures
• Pathological reflexes
• Loss of “self”
Stage III was reverting back to a child, but now he is like reverting back to even before birth, not living.
• Definitive diagnosis of AD can only be made on
• Current tools for diagnosing AD:
• Detailed patient history – symptoms
• Detailed history of illness from family/friends
• R/O other non-AD causes thru physical &
neurological exams and lab tests
• CT or MRI to r/o strokes, tumors
• Conduct neuropsychological testing to assessmemory, language, & other cognitive domains
So see if they have had a history of this, and see if they are exhibiting any of the signs and symptoms of this disease.
Criteria for “Probable” AD (accuracy of 85%)
• Dementia confirmed by clinical & neuropsych
• Problems in at least 2 areas of cognition
• Progressive worsening of memory & other
• No disturbances of consciousness (no “blacking
• Sx beginning btw ages 40 to 90, usually after 65
• No other d/o that can account for the dementia
Some aging older adults develop memory deficits
greater than their expected age norm, but w/o personal-ity changes or cognitive problems that characterize AD
• Not considered to have AD, but are said to have MildCognitive Impairment (MCI).
• 40% of MCI will develop AD w/in ~3 years.
• Anticholinesterase therapy (Cognex, Aricept,
• Used to block the enzyme that normally degradesthe neurotransmitter ACh
• Memantine (Namenda)
• Regulates excess glutamate activity
• Glutamate also involved in memory functions
• Used for treatment of moderate to severe AD
• Amphetamines (Ritalin or Dexedrine)
• Given for abulia or inattention
• Benzodiazepines (Ativan)
• Given for behavior control related to agitation and confusion
• Anti-Inflammatories (NSAIDS, glucocorticoids)
• Limit neurodegeneration
• Neuroprotective & Neurotrophic factors
• Nerve Growth Factors (NGF)
• Enhances survival of cholinergic neurons• Antioxidants – also neuroprotective
• Vitamins E & C
• Co-enzyme Q10
Which med is the one that is approved for all stages?
Has side effects of?
Headache, constipation, confusion and dizziness.
Possible liver damage, nausea, and vomiting