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primary headaches vs secondary headaches
primary - no identifiable organic cause
secondary - caused by underlying organic pathology
headache diagnostic assessment
diagnostic tests are generally absent in primary
health history - old carts
onset, location, duration, characteristics, aggravating/alleviating factors, radiation, timing, severity
tension-type headache
most common type of headache in both men and women
tension-type headache: pain location
bilateral
frontal-occipital region
“hatband” distribution
tension-type headache: pain quality
constant, dull, non-throbbing pressure
tension-type headache: associated symptoms
photophobia + phonophobia
you do not feel nausea/vomiting or prodrome
tension-type headache: triggers
stress
forward-head posture
muscle tenderness
tension-type headache: medications
aspirin, acetaminophen, or nsaids
tension-type headache: preventative medications
tricyclic antidepressants
anti-seizure medications
migraine headache
onset typically 25-55 years old
20% females and 8% males affected
linked to estrogen/menstrual cycle
migraine headaches - pathophysiology
trigeminal nerve (V) = causes intracranial vasodilation and neurogenic inflammation → pain nerves
migraine headache: pain location
unilateral, retro-orbital, or temporal
migraine headache: pain quality
severe, throbbing, pulsatile
migraine headache: associated symptoms
photophobia + phonophobia
nausea + vomiting
migraine headaches with aura symptoms
25% of migraines
visual: sparkles, flashing lights, scotomata (partial vision loss), halos
sensory motor: paresthesia, dysphasia
migraine headache: triggers
stress, seasonal changes, sleep disturbance
missed meals + menstruation
food + bright lights
migraine headache: meds
mild-to-moderate: aspirin, acetaminophen, nsaids, or caffeine
moderate-to-severe: triptans
causes vasoconstriction, therefore, contraindicated for heart diseases
migraine headache: preventative meds
tricyclic antidepressants
anti-seizure medications
ssris + botox
cluster headache
rare <1% prevalence
male-to-female ratio is 4:1
onset between 20s-40s
cluster headache: pain location
unilateral, orbital, retro-orbital, or temporal
cluster headache: pain quality
excruciating
stabbing, sharp, “suicide headache”
can last 15 mins-3 hours
cluster headache: associated symptoms
related to autonomic nervous system
includes: miosis (pupil constriction), ptosis, lacrimation, rhinorrhea
cluster headache: triggers
alcohol + volatile smells
napping
weather/seasonal changes
cluster headache: meds
100% high-flow oxygen: 12 L/min via non-rebreather for 15 mins sitting upright
second line: subcutaneous or intranasal triptans
cluster headache: preventative meds
high-dose verapamil (calcium channel blockers)
steroid injections
seizure
uncontrolled electrical discharges in brain neurons
provoked causes: bg <79, hyponatremia <135, meningitis, drug and alcohol withdrawal
epilepsy
chronic neurological disorder defined by recurrent, unprovoked seizures occurring more than 24 hours apart
seizures: infancy/childhood etiology
birth injury and acute trauma
congenital defects
high fevers
seizures: young adults (20s-30s) etiology
brain lesions, tbi, substance use
seizures: older adults (>50s) etiology
cerebrovascular disease (stroke)
brain tumors
dementia and systemic illness
which antiepileptic drugs should older adults not take and why?
phenytoin (Dilantin), carbamazepine (Tegretol), phenobarbital (Luminal)
because it can cause cognitive issues, ataxia, nystagmus
which antiepileptic drugs should older adults take?
levetiracetam (Keppra)
lamotrigine (Lamictal)
oxcarbazepine (Trileptal)
gabapentin (Neurontin)
stages of seizures
prodromal: changes in mood hours or days before seizure
aural phase: sensory warning occurring immediately before seizure (eyesight change or strange smell)
ictal phase: actual seizure
postictal phase: recovery period
tonic-clonic seizure: phase 1
tonic phase (10-20 secs)
muscle contraction, loss of consciousness, jaw clenching, salivation, cyanosis
tonic-clonic seizure: phase 2
clonic phase (30-40 secs)
rapid, rhythmic, symmetric jerking and contraction of extremities
tonic-clonic seizure: phase 3
postictal phase
muscle soreness, tired (sleep for hours), confusion and amnesia of event
absence seizures
typical in children and brief (few seconds)
staring spells resembling daydreaming
immediate recovery without postictal phase
atonic seizures
loss of postural muscle tone → pt collapses to ground → high risk for head trauma
myclonic seizures
brief shock-like muscle contraction of extremity or trunk
focal seizures
localized area of one cerebral hemisphere
commonly temporal or frontal
focal seizures - focal aware
simple partial
pt fully conscious, paresthesia, or sensory hallucinations
focal seizures - focal impaired awareness
complex partial
pt experiences altered consciousness, behavioral automatisms (lip smacking or repetitive hand movements), and postictal confusion
focal seizures - focal to bilateral tonic-clonic
starts as focal seizure with aura → goes to both hemispheres → postictally pt may exhibit todd's paralysis (temp weakness or paralysis in one part of the body)
status epilepticus
seizure lasting more than 5 minutes or repeated seizures without the person regaining consciousness between them
status epilepticus - what happens?
medical emergency!!
brain consumes energy → neuronal exhaustion → permanent brain hypoxia → systemic lactic acidosis → hyperthermia → cardiac dysrhythmias → death
status epilepticus - first-line emergency drug
IV benzodiazepines
ex. lorazepam (Ativan) or diazepam (Valium)
if IV is not available = rectal diazepam (DiaStat)
status epilepticus - second emergency drug
first drug is followed by IV long-acting anti-seizure
levetiracetam (Keppra), phenytoin (Dilantin), or phenobarbital
status epilepticus - diagnostic eeg
pinpoints epileptogenic focus and helps classify seizure type
pt prep: wash hair thoroughly so electrodes can stick to scalp, avoid coffee 12-24 hrs, does not need to be npo
status epilepticus - diagnostic ct/mri
performed to rule out structural lesions, tumors, or hemorrhage
status epilepticus - laboratory studies
serum sodium and calcium
bg + urinalysis
liver/renal function + tox screens
pre-seizure set-up
suction equipment and oxygen ready
maintain patent IV - saline lock
bed positioned to lowest height
padded side rails
active seizure interventions
turn pt to lateral (side-lying) side + do this postictal
cushion pt head + loosen clothing around neck
note exact start time and duration of seizure
active seizure interventions: what not to do?
never insert any object into pt’s mouth
never attempt to force open a clenched jaw
never restraint pt’s extremities
ketogenic diet
high fat and low-carb diet
decreases seizures in drug resistant epilepsy:
ketone bodies cross blood-brain → replace glucose as energy source for neurons → reduces hyperexcitability → stabilizes neurons firing
parkinson’s disease
chronic, progressive, neurodegenerative disorder
onset >50 years of age + males>females
parkinson’s disease - pathophysiology
progressive and degenerative loss of dopamine neurons in substantia nigra of basal ganglia
dopamine levels decline = unchecked overactive acetylcholine activity bc dopamine inhibits ACh
parkinson’s disease - cardinal motor manifestations
t - tremor
rest tremor, described as “pill-rolling” motion of hand
r - rigidity
higher muscle tone → jerky, ratchet-like “cogwheel” motion
a - ankiesnia/bradykinesia
p - postural instability
parkinson’s disease - ankiesnia/bradykinesia
akinesia - loss of voluntary movement + bradykinesia - slowness of movement
freezing spells + mask-like facial expression bc low blinking
hypokinetic dysarthria (soft, slurred, monotone speech)
parkinson’s disease - postural instability
shuffling, gait imbalances with flexed arms and loss of arm swings
parkinson’s disease - non-motor manifestations
autonomic dysfunction - excessive sweating, orthostatic hypotension, constipation, urinary retention
sensory dysfunction - depression, anxiety, dementia
parkinson’s disease - diagnosis
based strictly on patient history and physical motor assessment (presence of cardinal trap symptoms)
no specific lab or imaging unless to rule out secondary causes
parkinson’s disease - diagnostic confirmation
drastic clinical improvement in motor symptoms in response to initial trial of levodopa
parkinson’s disease - gold standard med
levodopa: crosses the bbb and converts into dopamine
carbidopa: does not cross bbb and prevents levodopa from breaking in bloodstream → allowing more to brain + prevents peripheral side effects (nausea + hypotension)
parkinson’s disease - complications of chronic therapy
“wearing off” phenomenon: medication wears off sooner, so symptoms return before the next dose
“on-off” fluctuations: periods of good mobility and sudden severe ankinesia
drug toxicity/dyskinesia: can cause involuntary movements, hence, provider may adjust the dose
which antiviral drug helps with parkinson’s as an adjunctive medications?
amantadine (Symmetrel) - stimulates dopamine release from surviving presynaptic terminals
blocks dopamine reuptake + helpful in managing levodopa-induced dyskinesias
which mao-B inhibitor helps with parkinson’s as an adjunctive medications?
selegiline
inhibits breakdown of dopamine in brain
prolonging half-life + effectiveness of levodopa
which anticholinergic helps with parkinson’s as an adjunctive medications?
benztropine
blocks overactive cholinergic receptors to balance neurotransmission and decrease tremors
parkinson’s disease - deep brain stimulation surgery
electrodes are surgically implanted into thalamus and connected to pulse generator in chest
electrical impulses disrupt abnormal firing patterns
reserved for severe cases + drug-resistant pt
parkinson’s disease - ablative surgery
destruction of specific thalamic or globus pallidus tissue to reduce severe tremors or dyskinesis
parkinson’s disease - aspiration + nutrition
position pt upright at 90 degrees during all meals and 30 mins post-meal
provide soft, pureed, or bite-sized meals
avoid high-protein meals during levodopa + consume small high-carb meals
parkinson’s disease - vitamin b6
needs to be managed according to provider instructions to prevent altered drug metabolism
parkinson’s disease - safe mobility
teach conscious gait technique: step over imaginary lines with heel-toe walking, lift feet high, actively force arm swings
encourage yoga and dance therapy
parkinson’s disease - bowel management
need to manage constipation due to anticholinergic meds