Dementia Flashcards
Define compression fracture in TBI
a depressed skull fracture in which the broken bone exerts pressure on the brain
Define concussion
bow to head or sudden deceleration usu causing an AMS, either temporary or prolonged. “brief loss of consciousness”
Define countrecoup
bruising or damage to brain tissue on the side opposite where the blow was struck
Define diffuse brain injury
injury to cells in many areas of the brain rather than in one specific location
Define epidural, subdural, intracerebral and subarachnoid hematomas
Epidural -outside the brain and its fibrous dura but under the skull; rupture of middle meningeal arteries (“lucid period”)
subdural - btw brain and dura; rupture of bridging veins
intracerebral -in the brain tissue (often basal ganglia)
subarachnoid -around the surfaces of the brain, btw dura and arachnoid membranes; usu due to rupture of saccular/berry aneurysm
Define focal injury in TBI
confined to a specific area of the brain
Define penetrating injury in TBI
when an object, such as a bullet or hay hook, breaks thru the skull, enters the brain and rips the soft brain tissue in its path
Define skull fracture
breaking the bones surrounding the brain. A depressed skull fracture is one in which the broken bone exerts pressure on the brain
T/F Memory is the slowest part of the conscious mind to recover from a TBI. It can be weeks or months before your survivor is able to routinely store new memories.
True
Post-traumatic amnesia can occur for longer than the coma itself and causes the patients to act in an almost child-like state. The best environment is little or no stimulation. What are some guidelines to follow when interacting with someone suffering from post-traumatic amnesia?
- always identify yourself when entering the room
- tell her that it is morning, afternoon or evening to help her orient to time
- warn her when you are going to touch her
- show photos of familiar ppl
- surround her with familiar objects
- repeat that she has been injured and is in hospital
- dont’ ask her to recall injury
- be patient
What are the three stages to your family member’s rehabilitation?
- Acute inpatient rehabilitation in a specialized facility offering a full range of therapies
- An outpatient day program in a structured group setting with a full range of therapies
- Individual outpatient therapy to treat more troublesome impairments
What are the 2 primary components of rehabilitation after TBI?
- relearning forgotten skills
2. compensating for more enduring impairments
What’s the first goal in rehab after TBI?
relearn ADLs
If your survivor is not yet ready for rehabilitation, but no longer requires the special care of an acute hospital, your health insurer will no longer pay the hospital bill. In this situation, you have three options:
- You can pay the bill yourself, if a bed is available.
- You can care for your patient at home, but this is a demanding job that requires medical skills.
- You can place your loved one in a long-term care facility, such as a nursing home, until she’s ready for rehabilitation.
What is chronic traumatic encephalopathy?
a progressive neurodegenerative disease in the category of tauopathies
multiple mild TBIs –> late-life dementia
symptoms: tremors, unsteadiness, masked faces, mental deterioration (parkinsonism)
About how many ppl a year in the US suffer TBI? What are the 2 top likely causes? Which age group and gender is at most risk?
1.7 million
1) falls and 2) MVAs
males; 0-4 and 15-19
TBI to the pituitary glands can affect?
- growth in children
- BP
- fatigue
- depression
- sex drive
- body temp
- pain
TBI to the amydala can affect?
- memory formation
- emotional sensitivity
- learning & retention
- depression
- anxiety
TBI to the frontal lobes can affect?
- emotions
- impulse control
- language
- memory
- social & sexual behavior
TBI to the parietal lobes can affect?
-ability to locate parts of your body & recognize parts of your body
TBI to the temporal lobes can affect?
hearing, language, ability to recognize a familiar person’s face, processing sensory info
TBI to the occipital lobes can affect?
distortion of visual field, perception of size, color & shape
TBI to the cerebellum can affect?
movement, muscle tone and gait
TBI to the brainstem can affect?
HR, breathing, swallowing
TBI to the hypothalamus can affect?
sex drive, sleep, hunger, thirst, emotions
TBI to the hippocampus can affect?
new memory creation, new memory retention, mood, confusion, disorientation
What are age-associated cognitive changes?
- difficulty retrieving words and names (names are hardest to remember)
- slower processing speed
- difficulty sustaining attn when faced with competing environmental stimuli
- learning something new takes a bigger effort
- no functional impairment (function is key!)
What is mild cognitive impairment (MCI)?
- memory complaint confirmed by others
- objective memory impairment for age and education
- preserved general cognition
- normal activities of daily living
- not demented
- **no functional impairment; may or may not progress to Alzheimers
Early onset Alzheimer’s disease is rare. It occurs btw 30-60, familial in most cases. What are some genes involved and on what chromosomes?
- abnormal presenilin 2 on chromosome 1
- abnormal presenilin 1 on chromosome 14
- abnormal amyloid precursor protein (APP) on chromosome 21
The late onset Alzheimer disease is the most common form and develops after age 60. Which apolipoprotein gene increases risk? Which one is protective?
E4 = increases risk E2 = protective
List gross and microscopic findings in someone with Alzheimer’s disease
Gross –> cerebral atrophy (occipital lobe is spared) with ventricular enlargement
Microscopic
1) amyloid plaques of extracellular deposits of beta-amlyoid with neuritic plaques
2) beta amyloid deposits near vessels –> cerebral amyloid angiopathy
3) filamentous intracellular inclusions of tau protein called neurofibrillary tangles and neuropil threads
4) granulovacuolar degeneration
5) hirano bodies
Comment on the activity of a, b, and y-secretase on Alzheimer’s disease
a-secretase cleaves APP into normal protein that won’t aggregate
b-secretase and y-secretase (catalytic subunit is presenilin) cleave APP to form beta amyloids, and more Ab42 vs Ab40.
In AD, more total Ab and more Ab42
What are two biggest risk factors for developing late onset AD? Briefly list other symptoms
1) age!!!
2) ApoE e4
female, family h/o of dementia, lower income, fewer yrsof education, lower occupational status, depression, head injury, low folate and B12, high homocysteine, postop delirium, alcohol abuse
What are the 3 key features of AD
- impaired cognition
- impaired function
- behavioral disturbances
List some early symptoms w/in the 3 key features of AD.
1) impaired cognition: trouble keeping appts, difficulty finding words, misplacing objects
2) impaired function: difficulty driving, difficulty selecting clothes, missing appts, probs at work
3) behavioral disturbances: subtle changes in personality, social withdrawal, depression
What is pseudodementia?
When elderly are actually depressed, but are diagnosed with dementia. Treat with anti-depressants (SSRIs)
AD is usually sporadic and late-onset. Frontotemporal Dementia aka Pick’s Disease has an insidious onset with gradual progression. How is pick’s disease distinct from AD clinically?
A person with Pick’s disease will show behavioral disturbances, often inappropriate ones before having memory loss. So 1st thing to go is social interpersonal conduct, emotional blunting, loss of insight with memory loss occurring much later. Therefore, it’s characterized by behavioral abnormalities (lose filter!)
What are pick bodies found in Pick’s disease?
circular bodies made of tau proteins
AD is assoc with degeneration of the basal nucleus of meynert due to ach deficiency, which contributes to the memory deficits. List the 3 achase inhibitors in our notes that can be used to slow down memory loss.
donepezil
rivastigmine
galantamine
excitotoxicity may cause neuronal damage in AD so there are drugs used in AD that are glutamate NMDA receptor blocker. List one.
Memantine -a partial agonist of NMDA receptor (not first-line unlike donepezil; but often given with donepezil)
List the 3 categories of drugs that can be used to treat neuropsych disturbances in AD patients
- antipsychotics (risperidone, haloperidol)
- antidepressants (sertraline -ssri, venlafaxin -snri)
- anxiolytics (buspirone and lorazepam)
After AD, vascular dementia is the 2nd leading cause of dementia. What is involved?
- hypertension related small vessel disease
- multi-infarcts (lacunar infarcts)
- cerebral amyloid angiopathy (so not unique to AD)
- can have subcortical leukoencephalopathy –> affecting deep white matter; subcortical dementia
How does vascular dementia progress? Whats most likely in someone’s PMH?
Vascular dementia progresses in a step-wise fashion and usually seen with cardiovascular risk factors
You can use achase inhibitors in AD and vascular dementia, but is of no use in?
pick’s disease/frontal temporal dementia
What is parkinson’s disease? Most cases are?
PD cases due to low dopamine seen on pallor of substantia nigra are sporadic and usu affect ppl over 65. Symptoms are resting tremor, akinesia, bradykinesia, shuffling gait, rigidity, postural instability, and at times dementia. Will contain lewy bodies which have eosinophilic inclusions of a-synuclein
Lewy body dementia is primarily sporadic and late onset. HOw is this clinical course different from the dementia present in AD/Pick’s?
In lewy body dementia, memory is less affected compared to AD. Huge deficits in attention and alertness with vivid hallucinations, delusions. REM sleep problems, autonomic dysfunction as well as frequent falls. Basically, when you see someone with parkinson’s symptoms + dementia that will have the onset of dementia w/in 12 months of parkinsonism.
T/F: avoid antipsychotics in lewy body dementia
true due to increased sensitivity
