Neuro: Change in MS Flashcards
Acute confused state that is likely reversible and fluctuates over hours or days.
Delirium
Encephalopathy, MS change, ICU psychosis are all synonyms for what?
Delirium
What is required for delirium to be diagnosed at bedside?
Has to be acute onset with fluctuating course AND
inattention accompanied by disorganized thinking OR altered level of consciousness
Hallmark of delirium
Deficit in attention
Alcohol withdrawal can produce hallucinations, agitation, ANS changes that are classified as what?
Hyperactive delirium
Opiate intoxication can produce withdrawn patients that are classified as what?
Hypoactive delirium
True or False: We have a screening tool to assess who is at risk for delirium.
False
What surgery increases risk of delirium?
Cardiac bypass
True or false: delirium is caused by a focal brain lesion.
False. It is more likely caused by widespread cerebral dysfunction (cortical and subcortical regions)
What might you find on an EEG in someone with delirium?
systemic slowing
What meds can bring out delirium in susceptible people?
Anticholinergics
What are 3 important things to remember when assessing someone for delirium clinically?
- Baseline mental status
- Timeline of illness
- Current meds or recent changes
How many cases of delirium are a result of meds?
1/3
What labs would you order on someone with delirium?
Glucose
CBC and CMP
Check urine
MRI
True or false: Chemical restraints should be used at the lowest effective dose.
True
Which works better as a chemical restraint, antipsychotics or benzodiapzepines?
Antipsychotics
Acquired, chronic deterioration in cognitive abilities that impairs ADLs.
Dementia
What is the most common symptom in dementia?
Memory loss
Which type of dementia is memory impairment NOT the most common presenting feature? what is?
Frontotemporal dementia.
Disinhibition
What is the most common form of dementia?
Alzheimers
Memory served by which areas is affected in early AD?
hippocampus
Mesial temporal lobes
What are the two primary cardinal lesions associated with AD?
Neurofibrillary tangles (intracellular tau and ubiquitin proteins) and extracellular senile plaques (beta amyloid)
What is needed to diagnose Alzheimers?
Need to look at clinical criteria, lab tests, and imaging to exclude other diagnoses. Most are diagnosed clinically, but a definitive diagnosis requires histopathologic exam (autopsy)
What abnormal findings may you expect to see on PE of an advanced Alzheimer’s patient?
Myoclonus
Seizures
Incontinence
Frontal release signs
What is it called when the pt persistently blinks during the glabellar reflex test?
Myerson’s sign
What lab tests should be drawn on an AD patient?
TSH Vitamin B12 Folate RPR Biomarkers (tau protein, beta amyloid protein, ApoE4)
What imaging studies should be done on an AD patient?
MRI. Can help exclude other dx of vascular dz, NPH, neoplasm, and subdural hematoma. May show generalized atrophy, focal atrophy, or be normal.
What is the imaging study in which IV injection of fluorine is given to measure cerebral metabolic rates of glucose? Tests for hypometabolism
FDG PET
What is the imaging study in which Florbetapir F18 is injected to measure amyloid lesion burden in the brain?
Amyloid PET
When is an Amyloid PET scan indicated?
Progressive AD at an early age or for those who are following atypical course of AD
used to treat mild to moderate dementia
Cholinesterase inhibitors Vitamin E (2000 IU/day)
Used to treat moderate to severe AD
Memantine (Namenda)
Used to treat vascular dementia
Memantine (Namenda)
Used to treat moderate to severe agitation with severe hallucinations
Atypical neuroleptics
Cholinesterase inhibitor that is not used in the US because of hepatotoxicity
Tacrine (Cognex)
Cholinesterase inhibitor that causes bradycardia and syncope
Donepezil (Aricept)
Cholinesterase inhibitor that can be worn as a patch and causes headache and anoreia but not diarrhea.
Rivastagimine (Exelon)
Comes in a tab or oral solution. Cholinesterase inhibitor that comes in extended release or immediate release and causes weight loss.
Galatamine (Razadyne)
Med that blocks receptor sites for glutamate
Memantine (Namenda)
Your pt is on Namenda and says it is not working. You want to up to the dose to see if that will help. When do you change the dose? What if the new dose doesn’t work either?
Wait at least 1 week between dosage changes.
Even if no improvement, keep the pt on Namenda.
What are the side effects of Namenda?
Dizziness (Most common)
hallucinations
increase agitation, delusional behavior
Can you combine memantine with cholinesterase inhibitors?
Yes
What is first line treatment for AD patients with agitation and aggression?
Try behavioral interventions like avoiding triggers, distract pt, keep structured routines
What important information must be given with atypical neuroleptics?
May increase mortality
What SSRI is the most useful in management of agitation and paranoia?
Citalopram
Olanzapine (Zyprexa), Quetiapine (Seroquel), and Risperidone (Risperdal) are all examples of what?
Atypical neuroleptics
Early alteration in personality, behavior, and executive function. Autosomal dominant inheritance in 10-25%.
Frontotemporal dementia
Most common presenting symptom in frontotemporal dementia
DIsinhibition
Early appearance of visual hallucinations. May also have parkinsonism, ANS dysfunction, neuroleptic sensitivity
Dementia with Lewy Bodies
Suspect this in someone with very rapid onset of dementia
Creutzfeldt Jakob Disease
The presence of what protein in CSF is tested for in this transmissible spongiform encephalopathy?
14-3-3
Prion protein disease
What is the second most common cause of dementia?
Vascular dementia
What is the most common form of vascular dementia from?
Small vessel cerebrovascular disease
Risk factors of vascular dementia
HTN, DM, tobacco use, obesity
What are examples of “treatable” dementias that are reversible to a point?
- Side effects from meds
- B12 deficiency
- Heavy metal poisoning
- Infection
- Hepatic/renal failure
- Hypothyroidism
- Chronic subdural hematoma
- NPH
What are the three causes of hydrocephalus?
Obstruction of CSF circulation Inadequate absorption (communicating hydrocephalus) Overproduction of CSF (rare)
Classic triad of normal pressure hydrocephalus
Dementia, gait disturbance, urinary incontinence (wet, wacky, wobbly)
Most common presenting symptom in NPH
Magnetic gait
Gold standard to diagnose NPH
Improved exam/symptoms after large volume of CSF is drained via LP
Treatment of NPH
Shunting of CSF. Diuretics have NOT been shown to work
Which type of hydrocephalus is third ventriculostomy NOT effective for?
Communicating hydrocephalus
Medical therapy for hydrocephalus
Diuretics
Fibrinolytics (newborns with posthemorrhagic hydrocephalus)
Serial LP
Medical therapy INCREASES complications and are NOT as safe as surgical therapy
Where is CSF produced?
Choroid plexus in lateral ventricles
What would you expect to see on physical exam in someone with suspected hydrocephalus?
Cushing’s Reflex (Triad): Bradycardia, Ataxic breathing, HTN
What would you expect to see when examining the eyes of someone with suspected hydrocephalus?
EOM paralysis (diplopia) or impaired upward gaze. Papilledema
Severe HA with signs of increased ICP
Diagnosis of hydrocephalus in adult
Large head circumference at birth, malformed spine
Diagnosis of hydrocephalus in infants
Which is safer treatment of hydrocephalus? Medical or surgical treatment?
Surgical
Where is the catheter placed in a shunt to treat hydrocephalus?
Right lateral ventricle
Connected to right atrium or peritoneal cavity
In a third ventriculostomy, what is the third ventricle connected to?
Subarachnoid space
Who normally gets Wernicke encephalopathy and what is the cause?
Chronic alcoholics
Thiamine (B1) deficiency
What is the classic triad of Wernicke Encephalopathy?
Global confusion
Opthalmoplegia
Gait ataxia
(80% also have polyneuropathy)
Treatment of Wernicke Encephalopathy
IV thiamine
A patient with Wernicke Encephalopathy comes to the hospital and also has low blood sugar. He is a diabetic. The nurse gives him glucose. What did she do wrong?
She also should have given him thiamine with the glucose–the glucose will use up all the thiamine reserves left over, making his WE worse.
Residual amnesic state that follows resolved Wernicke encephalopathy
Korsakoff syndrome
Symptoms of Korsakoff syndrome
Classic triad (opthalmoplegia, gait ataxia, global confusion) PLUS confabulation and amnesia