Chronic Neurologic Problems Flashcards
HA
Primary vs sexonday
Primary: not caused by disease
-tension
-migraine
-cluster
Secondary: caused by other medical things
-infection
-tumor
Interventions simmilar across all 3 types of HA
Diary
Avoid triggers
Education on meds and SE
Stress management
Exercise
HA diagnostic test
H&P
Test to r/o other causes:
-neuro
M/S
Infections
Tension HA
Aka
S/s
Stress HA
S/s:
-band-like
-dull, constant pressure
-light and sound sensitivity
Does not have N/V or warning aura
Tension HA
Meds and other tx
Meds:
Tylenol, Nsaids
Others:
Remove stress
Hydration
Migraine HA
S/s
Associated with 5 things
Triggers
Has what
S/s:
Unilaterl
Throbbing pain
Light, sound, smell sensitivity
Associated w/ seizure disorders:
-asthma, depression, anxiety, IBS, raynauds
Triggers: a bunch: food, alcohol, stress, weather
Has an aura (feeling)
Migraine HA
Meds
Nsaids
ASA w/ caffeine
Need provider for:
Sumatriptan (abortive) (causes vasoconstriction systemic)
Topiramate (preventative)
Botulinum toxin A (prophylactic) (last months)
Cluster HA
Involves what and how bad is it
Irregularities in what 2 things
Up to how may times in a day
S/s
Triggers
Most severe HA
Involves hypothalamus
Irregularities in melatonin and cortisol
Occures up to 8 times a day
S/s:
Sharp stabbing pain around eye
Radiating to other parts of face
Triggers: same as others
Cluster HA
Meds
Other tx
Meds:
Sumatriptan: gold standard
-causes vasoconstriction (cant take with CAD)
Other tx:
Oxygen- high flow for 10 mins
-causes vasoconstiction
Epilepsy and seziure disorders
What is happening
Etiology
Epilepsy definition
Uncontrolled electrical activity in the brain
Etiology:
Trauma, tumors
Overdose/withdrawal
Metabolic issues: F&E
Congenital, genetics
Infection
Idiopathic
Epilepsy=reoccurring seizures
Epilepsy and seizure disorders CM
2 classifications
Phases
Generlized: both hemispheres
Partial: one hemisphere
Phases:
Prodromal: sensation or behavior prior to seizure
Aural: sensory warning
Ictal: beginning to end of seizure
Post-ictal: recovery after seizure
Generalized seizures
Name
S/s
Tonic clonic sz (grnad mal)
S/s:
LOC
Stiff body (tonic)
Jerking (clonic)
Cyanosis, salivation, tongue/cheek biting, incontinence
Other generalized seizures
Names and what they look like
If not sure what type what should you do?
Myoclonic:
sudden excessive jerking, twitching
Atonic:
Drop attack, tonic or loss of tone, pt conscious
Tonic:
Increased tone, remains conscious
Clonic:
LOC, loss of tone followed by rhythmic jerking
If not sure: observe and report behaviors, movements, tone to HCP
Partial seizures
Names and what they look like
Simple focal seizure:
Remains conscious, experience unusual sensations:
Ex:joy, happiness, anger, taste, smells, visions
Complex focal seizures:
Unconscious (dream-like state)
Automatisms: lip smacking, chewing, strange behavior
Psychogenic seizures
Not what
Diagnose how
Check what
Non-epileptic although mimic symptoms
Diagnose: video EEG monitoring
HX emotional, physical abuse or traumatic event
Complications
Name of it
Med emergency what to do/what you see
Meds if dont work then give what meds
Status epilepticus:
Continuous sz or rapid succession w/o. Return of LOC lasting longer than 5 mins
Med emergency: brain using more energy than supply
-permanent brain damage
Oxygenations/ventilation impaired
Hyperthermia (increase metabolic rate)
Cardiac dysrhythmias
Med:
IV benzos(ativan, diazepam) if dont work give IV phenytoin or fosphenytoin
SUDEP
Sudden unexplained death in epilepsy
Due to impaired resp and cardiac
Were also worried about these patients falling
Pschogenic seizures/ status epilepticus
Diagnostic test
H&P, presentation, length of time
EEG: GOLD STANDARD
R/o other causes w/:
CT, MRI, CBC, LP, BMP
seizure medications
phenobarbital
phenytoin (Dilantin)
Gabapentin
valporic acid
fospenytoin Na
primodon
levetriacetam (Kappra)
administer during sz:
lorazepam
diazepam
Common side effects of sz meds
Resp despression
dysrhythmias
Sucididal ideations
Gum hypertrophy
Wt gain
Liver damage
Sz meds
Which med should we check therapeutic levels?
What diagnostic test should be done
Check therapeutic levels: phenytoin
CBC: risk of blood dyscrasias
Give sz meds IV with what fluid, not what fluid
how to give it and monitor what
PH of phenytoin
What to do with valium
Issues with valporic acid (so get what test)
Phenobarbital & phenytoin cause what
Dilantin causes what
Tell pt to take what if on sz meds
What decreases sz threshold
What do many sz meds cause in pregnancy
Give in NS only, no D5W
Give slowly and monitor for phlebitis
Phenytoin PH 12 same as bleach
Valium adheres to plastic so flush well
Valporic acid: bleeding/bruising (get CBC)
Phenobarbital/phenytoin: vit D, folic acid deficiency
Phenytoin: hypertrophy of gums
Tell pt to take birth control
Drugs and alcohol decrease sz threshold
Sz meds are tertogenic
Sz management
Sx
Others
Sx: remove the epileptic focus:
Only if failure to respond to meds
Vagal nerve stimulator:
Disrupt excessive neron firing
Ketogenic diet:
High fat, low carbs
Sz assessment and what to take note of
-Event leading to it
-When it occured
-Length of phases (aural, ictal, postictal)
-Body reaction
-Eye reaction
-What pt does after
-Long does it take until next one
-Autonomic signs: pupil dilate, salivation, alterted breathing, cyanosis, flushing, diaphoresis
-describe it (tonic, clinic, staring, blinking)
At home instructions for sz
Adhere to what
Wear what
When to call ambulance
Adhere to drug regimen
Alert bracelet
Call ambulance if:
-1st sz ever
-prolonged or recurrent sz
-injury with seizure
multiple sclerosis (MS)
What type of disorder
Possible causes (really dont know)
Degenerative disorder (demyelenation in brain/spinal cord)
Autoimmune
Genetic link
Environment exposure
MS patho
Happens, causes what
1st then possibly
Effects what usually
Inflammation, edema, scarring (damages myelin)
Slowed nerve conduction 1st
Then
Possible permanent loss of nerve function
Effects usually: optic, cerebrum, cervical
MS CM
Blurred/double vision
Red/green color distortion
Muscle weakness, coordination/balance
Paresthesia
Speech/cognitive diffculties
Bowel/bladder problems
Depression/sexual dysfunction
MS diagnostic test
LP (elevated protein and WBCs)
MRI (brain and SC for plaques)
Auditory and visual pathway evoked potentials
MS meds
Is there a cure?
Acute relapse(3)
Vs
Disease modifying meds (4)
Nd
Pt teaching (3)
No cure
Relapse:
Steroids
Plasmapheresis
Iv immunoglobulin
Disease modifiers:
Interferon beta 1a Avonex (IM), Rebif (SQ)
Interferon beta 1b Betaseron (SQ)
Copaxone (SQ) (helps inflammation/protects myelin)
Teach pt:
Rotate injection site
Protect skin from sun
May get flu-like s/s with meds that okay
MS management
Mobility
Bladder control
Constipation
Mobility:
Goal to decrease spasticity, increase coordination
-pt
-excercise
-muscle relaxants
Bladder control:
-meds for bladder spasms
-self catheterization
Constipation:
-Increase fiber
-bowel regimen
Parkinsons disease
Type of disorder
Characterized by:
Patho: lack of what
Neurogenerative disorder
Characterized by slowed movements:
TRAP
Patho: lack of dopamine
Parkinsons CM
main one
Other s/s
Complications
TRAP:
Tremors: 1st symptoms
Rigidity: jerky (muscle contractions)
Akinesia: loss of control of voluntary muscle movement
-stooped posute, masked face, drooling, shuffling gait
Postural instability: difficulty stopping
Other s/s: depression, anxiety, sleep disturbances
Complications:
-frozen, psychosis, dementia
-dysphagia
Parkinsons tx
MEDS: main ones then others
Sx (use only if)
Meds:
Levodopa: precursor of dopamine
Sinemet: L/C (prevent breakdown of l-dop)
*effects decline with use
Others:
Pramipexole (receptor agonist)
Amatadine (agonist)
Anticholinergic meds: limit use (increases confusion)
Sx:
Deep brain stimulator (decreases neuronal activity
*use only when meds dont work
Parkinsons diagnostic test
S/s of TRAP
HX
Positive response to meds confirm diagnosis
Parkinsons management
Risk of what
Deficit of what
Who else can help
Nurtition
Risk of falls
Self care deficit
PT/OT/ST
Nutrition:
-Increase fiber
-Easy to chew and swallow
-6 small meals
-Decrease protein and Vit B6 (impairs absorption of levodopa)
Myasthenia gravis (MG)
Type of disease
Antibodies affect what receptors
Muscle weakness/fatigue worse when
Autoimmune disease
Affect acetylcholine recptors (decrease muscle contraction)
Worse with activity
MG CM
Primarily
What unefffected
What happens as the day goes on
What improves it
Primarily facial muscle early AM
Diplopia
Ptosis
Impaired swallowing/chewing
Speech impaired
Trunk/limb/sensation/reflexes remain normal
Morexhausted as day goes on
Improves with rest
MG complications
Cause of exacerbation:
Myasthenia crisis (what does that mean with medication)
Acute exacerbation affects water putting you at risk of?
Causes:
-stress, pregnancy, temperature
Meds causes:
-Anesthesia, opioids, neuromuscular blockade
-betablockers, phenytoin
-benzodiasepines, muscle relaxers
MG crisis:under medicated
Acute exacerbation may affect swallowing and breathing:
Risk of aspiration,
Risk of Ineffective breathing patterns
Risk of imparied airway clearance
MG diagnostic test
H&P
EMG
Tensilon test (admin Edrophonium(Tensilon):
-injected, expect muscle contractility to improve)
-imporvement rapidly
MG meds
Mestinon (pyridostigmine)
Steroids
Immunosuppressants
Plasmapheresis
MG sx
Sx removal of thymus gland
-(CT to confirm thymus is an issue)
Distinguishing between MG crisi or cholinergic crisis
MG crisis: s/s, triggers, cause
Cholinergic crisis: cause, s/s, TX
How to distinguish
MG crisis: exacerbation of muscle weakness
Triggered by: stress, illness, meds
Under medicated anticholinesterase meds
Cholinergic crisis: over medicated anticholinesterase meds
-muscle stop reacting to acetylcholine
S/s: SLUD (salivation, lacrimation, urination, defecation)
Tx:
support ventilation until symptoms subside
Atropine help w/ secretions
Distinguish by giving Edrophonium:
MG crisis will get better, Cholinergic crisis worse
Amyotrophic lateral sclerosis: ALS
What happens
What is still intact
Loss of both upper & lower motor neuron
Sensory and cognitive function intact
ALS CM
What is effected, what does to muscle
Classic sign
What is effected 1st then later
Early CM
Dead neurons
No signal to muscles
Classic sign: progressive muscle weakness
Upper body weakness affected 1st, lower later
EARLY:
Dropping things
Tripping
Slurred speech
Muscle fatigue, cramps, twitching
ALS other CM
Sleep disorders
Pain
Drooling
Consitpation
GERD
Muscle wasting
COGNITIVE FUNCTION IS INTACT
ALS management
Is there a cure?
Med
Supportive care
Risk of
Control what
No cure
Med: Riluzole: slows progression
Supportive care
Risk of aspiration, injury, falls
Control pain
