Test 3: Neurological Disorders Flashcards
(56 cards)
What is dementia?
Loss of cognitive abilities such as memory, perception, verbal ability, and judgement
What are some causes of dementia?
Vascular disorders, degenerative neuro disorders, infections, chronic drug use, types of hydrocephalus
What are mini-mental status exams used for?
Testing mental function over time. Not good for diagnosing.
What are some items that are tested on a mini-mental status exam?
Orientation, language, follow command, write a sentence, copy a picture
What are the types of dementia?
Cortical Dem- Subcortical Dem Progressive Dem Primary Dem Secondary Dem
What are the characteristics of cortical and subcortical dementia?
Cortical dem-primarily affects brain’s cortex. Causes problems with memory, language, thinking, and social behavior
Subcortical dem-affects the brain below the cortex. Causes changes in emotions and movement and problems in memory
What is the difference between primary and secondary dementia?
Primary-does not result from any other disease
Secondary-Resulted from physical disease or injury
Vascular Dementia
2nd most common type of dem after Alzheimer’s
Multiple-Infarct Dementia
- Type of vascular dem
- Caused by multiple strokes
Symptoms:
Confusion or problems with short-term memory; wandering, or
getting lost in familiar places; walking with rapid, shuffling
steps; losing bladder or bowel control; laughing or crying
inappropriately; having difficulty following instructions; and
having problems counting money
Binswanger’s disease
- Type of vascular dem
- Widespread, microscopic damage to myelin
- Causes thickening and narrowing (atherosclerosis) of arteries that feed the subcortical areas of the brain
- Rare
- Also called subcortical vascular dem
Symptoms – disruption of executive cognitive
functioning: short-term memory, organization, mood, the
regulation of attention, the ability to act or make
decisions, and appropriate behavior.
• Psychomotor slowness (e.g. increase time for fingers to turn the thought of a
letter into the shape of a letter on a piece of paper).
• Forgetfulness (but not as severe as Alzheimer’s), changes in speech,
unsteady gait, clumsiness or frequent falls, changes in personality or mood
(apathy, irritability, and depression), and urinary symptoms
Frontotemporal Dem
Originally Pick’s disease
- Type of vascular dem
- Shrinking of frontal and temporal anterior lobes
- Some cases have build up of Pick bodies in neurons (abnormal tau proteins) that cause tangles and kills cells
- 2-10% of dem cases
- about 50% have family history
Symptoms
• Behavior Change
– Impulsive, apathetic, inappropriate social behavior, distractible, change
food preferences, neglect hygiene, compulsive behavior, lack motivation
• Language Problems
– Difficulty making or understanding speech
• Spatial skills and memory remain intact
Dem with Lewy bodies
- Caused by the build up of bits of alpha-synuclein protein (Lewy bodies) inside the nuclei of neurons in neocortex and substantia nirgra
- Common type of progressive dementia (10-20% of dem cases)
- Possible relationship to Alz and Parkinson’s
• Symptoms – cognitive decline
• pronounced “fluctuations” in alertness and attention
• recurrent visual hallucinations
• parkinsonian motor symptoms (e.g. rigidity and loss of
spontaneous movement)
Alzheimer’s Disease
- Type of degenerative dem
- Cause: build up of plaques and tangles
- Includes degeneration of the hippocampus, entorhinal cortex, neocortex, nucleus basaalis, locus coeruleus, and raphe nuclei
-Symptoms– memory loss, language deterioration,
impaired ability to mentally manipulate visual
information, poor judgment, confusion, restlessness,
and mood swings
What are amyloid plaques?
- Extracelluar deposit containing a dense core of B-amyloid (AB) protein surrounding by degenerating axons and dendrites along with activated microglia and reactive astrocytes.
- Phagocytic glial cells destroy the degenerating axons and dendrites
- Caused by defective form of AB from the precursor amyloid precursor protein (APP)
Why is having the long form of B-amyloid bad?
Cells can destroy small numbers of AB42, but cannot keep up with large numbers. (Normal 5-10%, Alz around 40%)
High concentrations of AB42 fold improperly and have toxic effects on cell
Neurofibrillary tangles
Dying neurons containing intracelluar accumulations of twisted filaments of hyperphosphoryated tau protein
Abnormal filaments disrupt transport within the cell
Tangles result from excessive amounts of phosphase ions attaching to strands of tau protein changing the molecular structure
Do AB proteins or tau proteins cause Alz?
Excessive AB (not plaques) cause microglia to release toxic cytokines and trigger excessive release of glutamate from glial cells (excitotoxicity-too much Ca2+ through NMDA receptors)
Mutations of tau only produce tangles
Therefore, AB is more likely to be responsible for Alz.
Mutations of APP can result in both plaques and tangles.
What genes are associated with Alz?
- 21-gene for APP
- 1 & 14-contain presenilin genes
- Mutation of apolipoprotein E (ApoE) increases risk of late-onset Alz
Is Alz generally hereditary? What are non-genetic risk factors?
No, most are sporatic.
Strongest: TBI
Higher education level is associated with lower rates
What are preventative measures that can be taken against Alz?
Cognitive activity
Physical activity
Diet
Lifestyle
-High stress levels associated with higher risk of alz
-Sleep may help decrease AB levels
-Reduced social networks more susceptible to Alz
What treatments are available for Alz?
Acetylcholinesterase inhibitors and NMDA receptor antagonist
NSAIDs may protect from Alz
Vaccines are being tested that sensitize the immune system against AB
What is amyotrophic lateral sclerosis?
ALS/Lou Gehrig’s Disease
Degenerative disorder that attacks the spinal cord and cranial nerve motor neurons
What causes sporadic cases of amyotropic lateral sclerosis?
- Errors in RNA translation of glutamate receptor subunits in motor neurons
- (cells die from excitoxcity)
What are the symptoms of amyotrophic lateral sclerosis?
- Increased tension of muscles, causing stiff and awkward movements
- Exaggerated stretch reflex
- Progressive weakness and muscular atrophy, and finally paralysis
- Death usually occurs 5-10 years after onset due to respiratory muscle failure
- Eye control and cognitive abilities are spared
