Neurological diseases Flashcards
delirium
definition
acute, confused state that usually occurs in response to a trigger
Typical triggers: alcohol &/or drug intoxication, withdrawal, medication side effect, infection (example: elderly with UTI), electrolyte abnormality, high or low glucose, other metabolic problems, sleep deprivation, neurological disorders (example: seizure, stroke), hypoxemia
Different than dementia BUT dementia patients can have delirium
Think elderly with UTI*
Delerium
S/Sx
Acute, rapid onset
Confusion
Fluctuates between awake, drowsy, agitation
Patient also often has anxiety and irritability, visual hallucinations, restlessness/ insomnia
Poor short-term memory
delirium
Dx and Tx
Dx:
Nothing specific; just need to find cause (start with labs to look for electrolyte problems, metabolic issues, intoxication, etc.)
Treatment
Fix the cause after you find it, delirium will improve
Delerium
sundowning
Sundowning is a type of delirium at night associated with preexisting dementia; usually mild to moderate; often associated with recent hospital stay or change in medication
Pearl
Wernicke Encephalopathy
General
Thiamine deficiency (The biologically active form of** vitamin B1)**
In the US, typically due to alcoholism
May also be caused by dialysis, AIDS, hyperemesis gravidarum, anorexia, and bariatric surgery (malabsorption issues or lack of nutrition)
Wernicke Encephalopathy
S/Sx
Confusion
Ataxia (uncoordinated movement with gait, speech and eyes)
Tingling in fingers and toes
wernicke encephelopathy
PE
Confusion
Ataxia
Nystagmus
Ophthalmoplegia (conjugate gaze palsy- meaning eyes cannot move together in the same direction because of muscle weakness/ paralysis)
Peripheral neuropathy
Wernicke encephelopathy
Dx
Thiamin diphosphate
Must use whole blood, minimal found in plasma/ serum
Some labs will call it TDP, TPP, thiamine, vit B1, liquid chrom/mass spec thiamine
Wernicke Encephelopathy
Tx
- Give thiamine
- Treat with 200-500 mg of thiamine hydrochloride (dissolved in 100 ml of normal saline) infused intravenously over 30 min three times daily for 2 to 3 days.
- DO NOT give IV glucose given BEFORE thiamine can make the symptoms WORSE (thiamine is important in intracellular glucose metabolism, SO giving glucose can deplete what is left of patient’s thiamine if it is already low)
- GIVE THIAMINE FIRST
Wernicke encephalopathy
Pearls
Sometimes the lab takes a long time to come back, so don’t wait for treatment if suspect diagnosis and other things have been ruled out (blood glucose issues, hypoxia,…)
Diagnosis is confirmed by improvement in signs and symptoms after giving thiamine
Eye movement issues are typically related to CN VI palsy
Korsakoff syndrome
- Severe Wernicke encephalopathy for extended period of time
- WE= acute, KS= chronic
- Anterograde and retrograde amnesia; confabulation (honest lying, creating incorrect memory)
- Delirium
- Treat thiamine like you would with Wernicke, but some issues are permanent; often require long-term care type of setting
anteroretrograde amnesia
Decreased ability to create new memories or retain new information following the onset of amnesia.
confabulation
Generation of a false memory without the intention of deceit.
honest lying.
Dementia
general
Chronic deterioration of mental functions
“Progressive intellectual decline”
Age is main risk factor, then family history and vascular disease
Typically starts after age 60 and prevalence increases with age (37+% by age 90 in one study and 50% by mid-80s in another)
New concerns it is related to high glucose
dementia
types
Main types of dementia
#1- Alzheimer
#2- Vascular
#3- Dementia with Lewy bodies
#4- Frontotemporal
Dementia
modifiable risk factors
1/3 of cases might be linked to modifiable risk factors: less education, midlife hypertension, midlife obesity, hearing loss, late-life depression, diabetes, physical inactivity, SMOKING, social isolation
Associated with dementia but not definite causes: a fib, alcoholism, chronic kidney disease (CKD), traumatic brain injury, obstructive sleep apnea, air pollution, gait impairment
Dementia
possible first alert to disease
Functional impairment may be the first alert or warning sign (difficulties in planning meals, managing finances, managing medications, using a telephone, and driving without getting lost)
dementia
*Usually, a gradual and progressive cognitive decline; difficulty in one or more of the following six cognitive domains:
- Complex attention: Staying focused, especially when there are multiple distractions and parallel tasks
- Executive function: Reasoning and planning (difficulty in managing complex tasks such as planning an event, planning a meal, using tools, driving a car)
- Learning and memory: Retaining new information (trouble remembering and recalling events)
- Language: Word finding, comprehension, etc.
- Perceptual-motor function including spatial ability and orientation (getting lost in familiar places) & ability to recognize objects and manipulate them
- Social cognition or behavior: Maintaining appropriate behavior based on social norms; recognizing social cues; making proper decisions based on safety (behavior out of normal social range, making decisions without regard to safety, inability to recognize social cues, decreased inhibition, decreased empathy, increased introversion or extroversion, inappropriate clothing for weather or social setting, etc.)
Dementia
Hx and PE
History and Physical Exam
Get good family history (family members with dementia, family members with vascular dz, HTN, etc)
Get a good social history (smoking, diet, exercise, living situation, alcohol, etc)
Obviously get a good patient medical history (depression/psych, HTN, vascular dz, etc)
Discuss ability to perform ADLs and make sure there is a family member you can talk to (patient might think things are going well or can’t remember that they left the stove on 3 days ago)
Ask about physical impairments (new onset balance issues, gait problems, vision problems, incontinence, sleep pattern, etc)
Perform mental status exam
Perform memory testing
Alzheimer
Warning signs
1.Memory loss that disrupts daily life
2.Challenges in planning or solving problems
3.Difficulty completing familiar tasks
4.Confusion with time or place
5.Trouble understanding visual images and spatial relationships
6.New problems with words in speaking or writing
7.Misplacing things and losing the ability to retrace steps
8.Decreased or poor judgment
9.Withdrawal from work or social activities
10.Changes in mood and personality
alzheimers
Alarm signs that reflect a severe stage of dementia and possible need of 24-hr assistance, support, or supervision:
1.Inability to perform personal self-care
2.Impaired judgment with potential harm to self or others
3.Concerns about personal safety or ability to seek help in unsafe situations
Alzheimer
Dx
What do you see?
Must rule out all other causes (low glucose, stroke, etc); get CBC, electrolytes, TSH, vitB12
Brain MRI
MRI findings in Alzheimer disease include generalized and focal atrophy, and white matter lesions. The most characteristic findings are reduced hippocampal volume and medial temporal lobe atrophy
Dementia
Tx goals and Non pharm
Goals: slow the progression, reduce mortality, improve quality of life for patient and family
Exercise twice weekly helps with cognition, balance, and overall health
Counsel patient on long-term planning regarding advance directives, driving safety, finances, and estate planning
Alzheimers
Tx for mild-mod Dz
- A cholinesterase inhibitor is recommended; they have been recently shown to slow cognitive decline and improve mortality risk
- Galantamine has been shown to be superior to both rivastigmine and donepezil (in that descending order)
- Treat other issues as needed (hearing loss, vision issues, depression, sleep problems); use caution with meds
- Encourage socialization, puzzles/ brain-engaging activities
alzheimers
Tx
mod to severe dz
For moderate to severe dz
Cholinesterase inhibitors may be effective in patients with moderate to severe Alzheimer disease
Memantine is usually added to cholinesterase inhibitors after patient has progressed to the moderate to severe dementia stage; has a small additional benefit on cognition
For advanced dz
Comfort measures
Dementia - vascular
General
Cause: multifocal ischemic changes (stroke)
3 main causes: large artery atherosclerosis, cardioembolic event, small vessel dz
Stepwise/ progressive cognitive deficits with each stroke
Often co-occurs with Alzheimer dz
Dementia vascular
S/Sx/PE
Physical signs of a stroke
Gait disturbance/ balance issues
Urinary frequency, urgency, incontinence (not explained by urological issues)
Personality and mood changes, most commonly depression, followed by psychosis (delusions, hallucinations, etc)
vascular dementia
imaging Dx
MRI or CT will show evidence of cerebrovascular disease
vascular dementia
Tx
Difficult and often not very successful
Cholinesterase inhibitors andN-methyl-d-aspartate (NMDA) antagonists have only limited evidence for use, although some of this may represent underrecognition of mixed dementia in AD trials
Prevention is key (manage HTN, hyperlipidemia, etc)
Dementia
Lewy Bodies
Cause: Same as Parkinson dz
Lewy bodies in brainstem, midbrain, olfactory bulb, and neocortex
Can coexist with Alzheimer
Cognitive dysfunction, visuospatial & executive deficits (disrupts a person’s ability to manage their own thoughts, emotions and actions)
Psychiatric disturbance, hallucinations (visual), occasional delirium
Tx like parkinsons
Frontotemporal (FTD) Dementia
general
Abnormal proteins found in the brain are most likely the cause, exact pathophysiology is unknown, sometimes linked to family/ gene mutations
Somewhat uncommon compared to other types
FTD
behavioral issues
Right frontal atrophy
Behavioral issues: lack of empathy, social norms, abstract thought and executive fxn; very impulsive and apathetic; okay memory; focal right frontal atrophy
FTD
Semantic variant
Temporal pole atrophy
Semantic variant primary progressive aphasia: can’t find words, doesn’t recognize faces, object and category knowledge loss; similar behavioral issues as above; asymmetrical temporal pole atrophy
FTD
non fluent variant
Nonfluent variant primary progressive aphasia: poor grammar, difficulty with the act of speaking (sound distortion, poor jaw movement); abnormal movement (loss of learned motor skills) with right arm and leg; left front atrophy
dementia
don’t forget!
Pseudodementia can happen with severely depressed people, memory loss and confusion, but improves with treating depression
Be careful with elderly people and depression; they might be depressed because of memory problems rather than having memory problems related to depression (you have to find out which came first, chicken/egg)
Do not do memory drills- causes frustration and does not help regain lost skills
Use trazodone for sleep- NOT antihistamines or benzos- can cause delirium
Creutzfeldt- Jakob Disease
Dementia
general
Rapidly progressing dementia and movement disorder
Rare, incurable, caused by misfolded proteins, genetic; sometimes random, sometimes familial/inherited, sometimes acquired or infectious
Definitive diagnosis is usually post-mortem and requires brain biopsy, but you can see cortical ribboning pattern on MRI and sharp wave complexes on EEG to help with clinical diagnosis
Treatment is symptomatic; no cure
Due to potential transmission, exposure to bodily fluids and brain matter from infected patients should be avoided (also should avoid eating cow and pig brain- “Mad Cow dz”)
cerebral edema
general
Fluid builds in the brain and increases intracranial pressure
categorizes into either vasogenic, cellular, osmotic, and interstitial causes
cerebral edema
Causes
variety of more common causes: head trauma, hepatitis/ liver disease, vascular ischemia, intracranial lesions, obstructive hydrocephalus, hypoxia, infection, metabolic derangements, acute hypertension
Other less common causes: Reye syndrome, carbon monoxide poisoning, lead poisoning, and high-altitude cerebral edema (HACE). A rare cause of cerebral edema is pseudotumor cerebri.
cerebral edema
S/Sx
vary widely depending on the location and extent of the cerebral edema
Focal edema: weakness, visual disturbances, seizures, sensory changes, diplopia, and other neurologic disturbances
Diffuse edema: headaches, nausea, vomiting, seizure, lethargy, altered mental status, confusion, coma
cerebral edema
PE
- Varies depending on severity and local vs diffuse
- Severe: altered mental status and development of fixed and dilated pupil
- Some patients may appear agitated and others lethargic.
- Delusions (fixed false beliefs) and hallucinations are common.
- Asterixis (negative myoclonus) is common.
- Other physical findings, such as fever, ascites, jaundice, or tachycardia, may vary depending on the underlying cause of encephalopathy.
S/Sx of an expanding intracranial lesion
Tuberous sclerosis
Brain related Sx
Tuberous sclerosis
Skin related Sx
Neurocutaneous disorders
Bulbar palsy
S/Sx
pseudobulbar palsy
S/Sx
