Week 6: Stroke, Sleep Flashcards
What is a Transient Ischemic Attack (TIA)
cerbral ischemic event lasting less than 24 hours (typically only minutes without apparent parmanent neurologic deficit)
What is Completed Stroke-
cerebral ischemic acute event with deficit that persists
Other types of ischemic strokes
a)Hemispheric Infarct
b)Lacunar Infarct
c)Microvascular Ischemic White Matter Lesions
a) stroke, usually caused by occlusions of carotid artery, leading to infarct of entire hemispheres of the brain. can be
b) blockage of arteries that supply deeper portions of the brain
c) occlusion of very small blood vessels in white matter. Pts. often times can be asymptomatic. treatment is controversial
Treatable Risk factors for Stroke
HTN
hypercholesterolemia
heart disease (espatrial fibrillation)
DM
cigarette smoking
excessive alcohol intake
phsyical inactivity
obesity
carotid bruit
Untreatable risk factors for stroke
age
sex
race
prior stroke
stroke pathophysiology
thrombus formation
1. asymptomatic atherosclerotic plaque
- platelet deposition
- occlusive thrombus formation
- plaque fissure-> red thrombus->embolism
a.primary hemostasis-platelet plug
b-coagulation->fibrin clot->thrombus
cardiogenic embolus-blood stasis->thrombus->ejected to brain
Clinical presentation of stroke/TIA
Carotid territory
unilateral weakness
unilateral sensory symptoms
aphasia- difficulty understanding peech or speaking, or both
monocular visual loss
transient global amnesia
Clinical presentation of stroke/TIA
vertebrobasilar territory
bilateral weakness, sensory, and/or visual complaints
- diplopia, ertigo, ataxia w.o weakness, dysphagia (difficulty swallowing)
hard to distinguaish a vertebrobasilar stroke from other differential diagnosis. one distinguishing factor is the rapidity of symptoms for a vertebrovascular stoke.
General SS of stroke
unilateral weakness
unilateral sensory symtpms
dysphasia
dysarthria (slurred speech)
vision disturbances
sudden confusion/mental status changes
facia droop
seizures (rare)
ataxia
loss of balance
verigo
dizziness
dysphagia
headache
vomiting
Phases of stroke care
Primary prevention
acute management of stroke
secondary prevention
primary prevention of stroke
modifiable risk factors
a. HTN, HLD, smoking, DM, a. fib, cad, obesity, post menopausal hormone therapy
nonmodiafiable risk factors:
a.age>55, race (black,hispanic), male gender, family hx of stroke/TIA, personal hx of stroke/tia
Who are at highest risk for having a stroke
patients who have had a previous stroke
General Treatment of an intial cerebrovacular event
ANTIPLATELET THERAPY
*small vessel lacunar
*Large Vessel Embolic
*Large Vessel thrombotic
WARFARIN THERAPY
Cardioembolic
General Platelet cascade in thrombus formation
fissure in lipid plaque recongnized by the body as injury activates platelets, adhere to fissure, followed by platelet aggregation on fissure.
recruit fibrin and RBC, causing a clot
Mechanism of Action of Anti-platelet Agents
a)Ticlopidine/Clopidogrel/ Praugrel: IRREVERSIBLY Block ADP receptors, inhibiting platelet aggregation
b)Aspirin: IRREVERSIBLY inhibits COX enxyme and thromboxane(potent activcator of platelet aggregation), leading to inhibition of platelets
c) Dipyridamole: REVERSIBLY increases plasma adenosine and inhibits platelet phosphodiesterase, causing inhibition of platelet activation and aggregation
Secondary stroke ppx
ASA
Ticlopidine
Clopidogrel
Prasugrel
Ticagrelor
ASA/ER dipyrdamole
Notes on PK of aspirin
~18-25% decreased risk of having another stroke
- inhibition of plt. aggregation require ~97% of COX-1 inhibition
*in ~70% of pts. this is achieved with an aspirin dose of 80-100 mg
*older age and obese patient may require higher doses of aspirin to produce effect
*inhibition of thromboxane occurs pre-systemically in portal circulation
*enteric coated products are erratically absorbed from the GI tract
Ticlopidine vs. Aspirin
additional 21% risk reduction of having another stroke in comparison to aspirin
fatal toxicity risks, including diarrhea, rash, nausea, and gastritis, ulcer, GI bleeding
Clopidogrel vs Aspirin
CAPRIE study shows that clopidogrel has ~7% additional risk reduction of having another stroke, which is not statistically significant.
only statisticlaly significant finding from CAPRIE study was that clopidogrel had 23.8% relative risk reduction of PAD over aspirin
Dipyridamole ER vs. Aspirin
Dipyridamole ER (which has ~ same RRR as aspirin) not available in the US, only IR
ESPS2 study showed that inorder to achieve same time conc. of Dipyridamole ER with IR, pt must take IR 100 mg QID for the rest of their life, which would drastically increase risk of pt noncompliance.
Aggrenox vs. Aspirin
Aggrenox is Dipyridamole ER+ASA combo
ESPS 2 study showed 36.8% RRR vs placebo and 23% RRR vs ASA.
HOWEVER, PROFESS study showed there is no difference btw. aggrenox and clopidogrel
Overall, how to pick an antiplatelet agent best for the patient
Since there are no significant differences btw. anti-plt. choices, anti-plt agents used is based on whats best for individual patient.
A)base it on pt specific needs
consider..
side effect profile relative to your pts hx
(ex. Aggrenox can cause vascular headache, can cause GI problems->caution in GI problems..etc.)
the agent that produces an inhibition of aggregation in your specific patients (ex: some pts can be aspirin reisstant due to genetics)
can be used in lowest effective dose to reduce risk of bleeds
b) will aparticular agent be less than optimal for a particulr pt
*ex: ASA allergy
*pts on clopidogrel may have DDI w. agents that inhbit CYP2C19 such as CCBs, PPI’s etc.
*aggrenox therapy andmigraine hx
*aggrenox therapy and spastic colon or IBS
c)does your patient warrent dual anti-plt therapy
*Clopidogrel + ASA only has increased anti-plt effects in firt 30-90 days, then risk of bleeding outweighs beenfit
*coronary artery stenrs and new cerbral ischemia
*a. fib not able to take coumadin
d) are your pt plt. responding to their anti-plt agent
*ex: ASA or Plavix resistance
Individualized pharmacotherapy for anti-plt. choice
urgency of needing full antiplt. therapy
agent least likely o produce adverse effects
*headache hx
*spastic coloitis or ulcerative colitis/chrons
*gastric ulcer hx
*true aspirin alergy
agent least likely for drug interactions
*need for chronic NSAID, PPI, or CCB use
dual anti-plt therapy
*failure of monotherpay
*first 3-6 mo post troke w. high risk factors
*a. fib w. CI for anticoagulation
approach to ASA resistance
assurance compliance
*urinary salicyates
remove drugs that compromise ASA effects
*NSAIDS other than celecoxib(celebrex)
*some herbal supplements
change from EC to chewable ASA or alka seltzer
*particularly in older women
*change ASA dose where appropriate
approach to plavix resistace
minimize use of other drugs that inhibit cyp3a4 AND CYP2C19
SUBSTITUTE DRUGS THAT HAVE LESSOR EFFECT ON THESE p450 is iso enzymes
add meds that can induce CYP enzyme activity
common meds that influence CYP3A4 or CYP2C19
statins other than Rosuvastatin (crestor)
CCBs, not BB, ACE, or ARBS
*NOTE: IF CCB + clopidogrel is an issue in a pt, before switching the CCB, be sure pt is on CCB for htn and not rate control. if ccb used for rate control is changed, might do more harm in pt.
Ambien, Lunesto (Sonata least likely)
Gliburide, not glipizide or metformin
Enablex, Ditropan, not detrol or sanctura
PPI’s
what to do if pt is truly resistant to both aspirin and clopidogrel
- ticagrelor
*prasugrel
BOTH OF THESE NOT FDA approved.
*max ASA dose 100 mg daily w. ticagrelor
Signs and symptoms of sleep disorders
excessive daytime sleepiness (EDS)
impaired daytime funcitoning
irregular breathing
increased movement during sleep
irregular sleep and wake cycle
difficulty falling asleep
common types of sleep disorders
insomnia
sleepapnea
narcolepsy
circadian rhythm disorders
parasomnia
restless leg syndrome
What is insomnia
most common reported sleep disorder
difficulty falling asleep, maintaining sleep, or non restorative sleep
categories of insomnia
transient insomnia: several days
<3 months: short-term insomnia
atleast 3 nights per week for >/=3 mo.: chronic insmonia
causes of transient insomnia
stress
jet ag or shift work
schedule change
medical (chornic pain0
psychiatric (eg. anxiety, PTSD)
pregnancy
pharm. induced
causes of short term (<3 mo.) insomnia
untreated or undertreated transient insomnia
acquired exacerbating behavior
common drrugs that can cause or worsen insomnia
alcohol, caffeine, nicotine
anticholinergics
SSRISNRIs
alpha blockers
beta blockers
ACE and ARBS
cholinesterase inhibitors
bronchodilators
CNS stimulants
corticosterois
decongestants
diuretics
H2RAs
statins
opioids
treatment goals for transient insomnia
orrect ynderlying sleep complaint, avoid AE of meds
treatment: adequate bedtime doses of benzos for 2-3 weeks
selection of specific med is patient dependent:
*desirability for daytime anxiolytics
*need fo rnext day early morningcognitive sharpness
*interactions with other medications
*d/c of problematic meds
*pk profile of the BZDRA and specific insomnia complaints
tratment of short term insomnia goal
a treatment plan that will result in the pt sleeping normally w. no medications
non pharm treatment of insomnia
maintaine a regula sleep schedule
establish a calm bedroom setting (quiet room, no bright lights, comfortable temp/)
do not spend time in bed if awake
imit intake of nicotine, caffeine, and alcohol
exercise regulalrly but not close to bedtime
have a light snack or warm bevarage befor ebedtime
avoid watching the clock, remove bedroom clock if necessary
treatment oflongterm insomnia
proper dx of root/psychiatric cause of insomnia
CBT for insomnia
*preffered 1st line therapy for chronic insomnia in mos patients
*CBT-I+/- meds> meds alone
if rapid improvement is necessary, can use CBT-I_ meds initially w. plan to taper medication over time
Treatment options for insomnia
BZDRAs
most commonly used trt. for insomnia
fda approved for insomnia
labels include a cuation for anaphylaxis, facial angioedema, and complex sleep behaviors
agonist effects on gaba receptors
includes newer non-benzo GABA agonists and traditional benzos
always ake before bedtime
use w. caution in elderly
drowsiness, dizziness, confusion, risk of falls
avoid w.alcohol
withdrawal symptoms upon abrupt d/c i.e termors, muscle cramps, seizures
considerations for BZDRAs
benzo hypnotics
CHOICE OF A PARTICULAR BZDRA IS BASED ON PK PROFILE AND PT. PRESENTATION
reduce sleep larency
increased stage 2 sleep and decrease delta sleep
anxiolytic effect
so not use in pts w. sleep apnea or substance abuse
avoid alcohol and cns depressants
side effects are dose dependent
BBW: concaminant use with opioids can cause resp. depression,sedation, coma, and death
*increased risk of abuse, misuse, and addiction
*continued use can lead to clinically significant physical dependence
considerations for BZDRAs
Non benzo GABA agonists
CHOICE OF A PARTICULAR BZDRA IS BASED ON PK PROFILE AND PT. PRESENTATION
“Z” drugs
more selective
increase total sleep time
less disruptive of sleep stages
geenrally have less withdrawls. tolerance, and rebound insomnia
associated w. parasomnic episodes w. amnesia
BBW: can cause complex sleep behaviors(i.e sleep walking, sleep driving, and engaging in other activities while now fully awake. d/c immediately if develops.
Estazolam
Schedule:
Benzo vs Z drug:
Indication:
PK(t1/2 &tmax):
AE:
considerations:
Schedule: CIV
Benzo vs Z drug: Benzo
Indication: sleep onset or maintenance. short term mgt of insomnia characterized by difficuly in falling asleep, frequent nocturnal awakenings, or/or early morning awakenings
PK(t1/2 &tmax):
*tmax:2
t1/2: 10-24 hrs
AE: hypokinesia
considerations:
CI in pregnancy or w. itroconazole or ketoconazole
Eszopiclone (Lunesta)
Schedule:
Benzo vs Z drug:
Indication:
PK(t1/2 &tmax):
AE:
considerations:
Schedule: CIV
Benzo vs Z drug: Z drug
Indication: sleep maintenance or early morning awakenings
PK(t1/2 &tmax):
t1/2: 1 hr
tmax: 6 hr (up to 9 in elderly
AE: headaches, dysgeusia, nervousness/anxiety, xerostomia, infection, upset stomach
considerations:
*rapid absorption tat can be delyed w. food
*can be used long term fo rup to 6 months
*major cyp3a4 substrate
*monitor w. concurrent use of cyp3a4 inhibitors (keto, itraconazole)
Zaleplon (Sonata)
Schedule:
Benzo vs Z drug:
Indication:
PK(t1/2 &tmax):
AE:
considerations:
Schedule: cIV
Benzo vs Z drug: Z drug
Indication: short term trt of insomnia. does not reduce nighttime awakening
PK(t1/2 &tmax):
t1/2: 1 hr: could be delayed w. absorption
tmax: 1 hr
AE: headache, nausea, abdominal pain
considerations:
*cyp3a4 substrate
ultra short acting, rapid onset
avoid taking after a highfat meal delays absorption
short term treatment
Zolpidem
Schedule:
Benzo vs Z drug:
Indication:
PK(t1/2 &tmax):
AE:
considerations:
Schedule:CIV
Benzo vs Z drug: Z drug
Indication: depends on formulation
IR tablet or spray: sleep onset. off label for sleep maintenance
ER tablet: sleep onset or maintenance
SL tablet: dif. dose based on sex: take if more than 4 hours remain before waking and pt has trouble returning to sleep
PK(t1/2 &tmax):
t1/2: 0.6-4hrs
tmax:1.4-8.4 hrs
AE:headache and nausea, increased hypotension and falls in elderly
considerations:
avoid use in severe hepatic impairment
minimal tolerance and rebound at recommended doses
diff formulations have diff indications
Trazadone
Schedule:
Benzo vs Z drug:
Indication:
PK(t1/2 &tmax):
AE:
considerations:
Schedule:–
Benzo vs Z drug:–
Indication: offlabel use for sleep continuity
PK(t1/2 &tmax):
AE: caryover sedation, alpha adrenergic blockade(orthostasis) priapism is a rare side effect
considerations:
usefel in pts. w. hx of substance abuse and or depression
when d/c taper dose over 2-4 weeks
BBW: suicidal thoughts and behaviors, same risks as antidepressants
first gen antihistamines
Schedule:
Benzo vs Z drug:
Indication:
PK(t1/2 &tmax):
AE:
considerations:
Schedule:–
Benzo vs Z drug:–
Indication: OTC option for mild insomnia
PK(t1/2 &tmax):–
AE: anticholinergics
considerations:
avoid in elderly
tolerance to sedative effects develop quickly
Suvorexant (Belsmora)
Schedule:
MOA:
Indication:
PK(t1/2 &tmax):
AE:
considerations:
Schedule:CIV
Benzo vs Z drug:–
*dual orexin A and orexin B antagonist (DORA)
Indication:sleep onset and maintening sleep by wurning off wake signaling
PK(t1/2 &tmax):
t1/2: 12 hrs
onset: <30 min
AE: DROWSINESS, dizziness, headache, sleep paralysis, abnormal dreams, URTI
considerations:
interactions w. cym3a4 inhibitors
decrease dose w. mod. cyp3a4 inhibitors, CI w. strong 3a4 inhibitors
CI in narcolepsy
Lemborexant (Dayvigo)
Schedule:
MOA:
Indication:
PK(t1/2 &tmax):
AE:
considerations:
Schedule:CIV
MOA: Dual Orexin A and Orexin B receptor antagonist (DORA)
Indication: assists in getting to and maintainning sleep, turns off wake signaling
PK(t1/2 &tmax):
Onset:<30 min
t1/2: 17-19 hours
AE: drowsiness, dizziness, headache, complex sleep behaviors, abnormal dreams (nightmares)
considerations:
*decrease dose w. weak CYP3A4 inhibitors
8not recommend w. strong cyp3a4 inhibitors
CI in narcolepsy
*take at bedtime w. atleast 7 hrs beforeplanned time of awakening
Ramelteon (Rozeram)
Schedule:
MOA:
Indication:
PK(t1/2 &tmax):
AE:
considerations:
Schedule:– not controled
MOA:meletonin receptor agonis selective for MT1(induces sleep) MT2 (regulates circadian rhythm) (MT1>MT2)
Indication: isleep onset insomnia and for long term use
PK(t1/2 &tmax):
onset: 30 min
t1/2: 1-2.6 hrs
AE: headahce, dizziness, somnelance
considerations:
do not use in pts w. liver disease
not controlled
not as effective in pts who have beent reated already with a BZDRA
CI: w. fluvoxamine
Melatonin
Schedule:
MOA:
Indication:
PK(t1/2 &tmax):
AE:
considerations:
Schedule:– Dietary supplement not fda approved
MOA:
Indication: beneficial effects on sleep latency, shift workers, and jet lags
PK(t1/2 &tmax):–
AE:-
considerations:
should not be used in pts w. autoimmune conditions on immune modulators and has been shown to alleviate some autoimmune conditions but exacerbate others
less effectin pts whove used bzdraS
Doxepin
Schedule:
MOA:
Indication:
PK(t1/2 &tmax):
AE:
considerations:
Schedule:–
MOA: INHIBITS REUPTAKE OF SERETONIN AND NOREPINEPHRINE ANTAGONIZES h1 HISTAMINE RECEPTOR
Indication: sleep maintenance insomnia
PK(t1/2 &tmax):
AE:
considerations:
lower than dose used for depression is used for sleep
BBW for suicidality in pts <24 years
do not tak w. in 3 hrs of a meal due to slower absoprtion
Considerations for pharmacotherapy for elderly and pregnant women
non pharm preffered initially, if oharm therapy is needed…
Elderly
*CBT-I
*Ramelteon
*Eszopiclone
*Zolpidem
*low dose doxepin
Pregnancy
*diphenhydramine
*Doxylamine
*low dose doxepin
Sleep apnea
what is it
repeated episodes of cessation of breathing during sleep, followed by blood oxygen desaturation and arousal from sleep to restart breathing
fragmented sleep and poor sleep architecture w.periodsof apnea and hypopnea
TYpes of sleep apnea
Dx w. polysomnography
*Central (csa): impairment of resp. drive
Obstructive(OSA): upper airway collapse and obstruction
Mixed: CSA and OSA
CHaracteristics of Obstructive slepe apnea
multiple episodes of airway closure and cessation of breathing per hour
can be caused by obesity, narrow airway, or other anatomical factors
multiple awakenings and arousals perr hour w. apneas, gasping or both throughout the night
significant o2 desaturations per hour
associated w. MVA, depresison, increased cancer risk, stroke, and cva
linked to CV AND cerebrovascular morbidity
increased risk for drug resistant htn
treatment of sleep apnea
first line: standard of trt is nasal positive airway pressure during sleep through a cpap
Weight management
avoid all cns depressants (such as benzos or opioids) and drugs that can cuase weight gain. use extreme caution in apioid medications
if cpap doesnt work, can use medication for excessive daytime sleepiness
Narcolepsy
what is it
severly debiliating neurologic disease, oftenundiagnosed
impairment of both oncet and offset of rem AND NREM
narcolepsy tetrad
excessive daytime sleepiness, cataplexy, hallucinations, sleep paralysis
patho: loss of normal funciton of hypocretin orexin neurotransmitter system possibly due to autoimmune process
Narcolepsy treatment
nonpharm
pharm
non pharm: good sleep hygeine and scheduled daytime naps
avoid drugs that can worsen daytime sleepiness (benzos, opiates, aps, ALCOHOL)
pharm: focus on treatment of excessive daytime sleepiness (EDS)
*modafanil or armodanil trt for eds
*tca’s, snris, ssris
Medications EDS in narcolepsy
Modafinil
Schedule:
MOA:
Indication:
PK(t1/2 &tmax):
AE:
considerations:
Medications EDS in narcolepsy
Schedule: C-IV
MOA: unclear, effects on dopamine, GABA, 5HT
Indication: EDS in narcolepsy
PK(t1/2 &tmax):
AE: headache, nausea, anxiety/nervousness, dizziness, dyspepsia, xerostomia, back pain, rhinitis
considerations:
Avoid use in regnancy
may decrease effectiveness of contraceptives (cyp3a4 INDUCERS)
use caution in pts. w. CV disease, esp not recommended in pts. w. left ventricular hypotrophy
Medications EDS in narcolepsy
Amodafinil (Nuvigil)
Schedule:
MOA:
Indication:
PK(t1/2 &tmax):
AE:
considerations:
Medications EDS in narcolepsy
Schedule: c-iv
MOA: r-enantiomer of modafinil, moa unclear
Indication: EDS in narcolepsy
PK(t1/2 &tmax):
AE: headache, insomnia, dizziness, nausea, xerostomia
considerations:
avoid use in pregnancy
may decrease effectiveness of contraceptives (CYP3A4 inducers)
use in caution in pts. w. cv diease, esp not recommended in pts w. a history of left ventricular hypertrophy
Medications EDS in narcolepsy
Solriamfetol (Sunosi)
Schedule:
MOA:
Indication:
PK(t1/2 &tmax):
AE:
considerations:
Medications EDS in narcolepsy
Schedule: C-IV
MOA: dopamine and norepinehrine reuptake inhibitor
Indication: EDS in narcolepsy
PK(t1/2 &tmax):
AE: headache, anxiety, insomnia, decreased appeptite nausea
considerations:
CI w. MAOI, do not use concurrently or w.i 14 days of MAOi
Medications EDS in narcolepsy
Pitolisant ( Wakix)
Schedule:
MOA:
Indication:
PK(t1/2 &tmax):
AE:
considerations:
Medications EDS in narcolepsy
Schedule:–
MOA:antagonist/ inverse agonist at histmaine 3 rceptors
Indication: EDS in narcolepsy
PK(t1/2 &tmax):
AE:headahce, anxiety, musculoskeletal pain, uri
considerations:LOWER MDD FOR KNOWN CYP2D6 METABOLIZERS
MAJOR CYP2D AND CYP3A4 INTERACTIONS
CI IN SEVERE HEPATIC IMPAIRMENT
Medications EDS in narcolepsy
Sodium Oxylate (Xyrem)
Schedule:
MOA:
Indication:
PK(t1/2 &tmax):
AE:
considerations:
Medications EDS in narcolepsy
Schedule: C-III
MOA: cns DEPRESSANT. GABAb receptor activity at noradrenergic and dopaminergic neurons
Indication:
PK(t1/2 &tmax):
AE: ocnfusion, headache, dizzeness, weightloss/decreased appetite, urinary incontinance, drowsiness, depression, somnambulism, anxiety
considerations:
BBW: cns depression, abuse/misuse, restricted access.
can only be obtained thruogh a REMS program
*even tho a cns depressant, improves pt sleep so they are more well rested the next day
dosed at bedtime after pt is in bed w. second dose 2.5-4 hrs later
List of meds used in cataplexy in narcolepsy
cataplexy (sudden loss of muscle tone)
REM SUPRESSING DRUGS
*Fluoxetine (SSRI)
Venlafaxine (SNRI)
Atomoxetine (SNRI)
Clopiramine (TCA)
Imipiramine (TCA)
Nortriptaline (TCA)
PITOLISANT
SODIUM OXYBATE
Circadian Rhythm Disorders presentation
presents as either insomnia or hypersomnia
commonly manifest as jet lag or shift work disorder
Jet lag treatment
non pharm
pharm
non pharm
*napping (<30 min in length atleast 8 hrs before bedtime)
times light exposure
pharm :
Meletonin
ramelteon
short acting BXDRA- risk for next day drowsiness
takrdrug at target destination bedtimes to reduce jetlag and shorten sleep latency
Shift work disorder
difficulty . sleep or wakefuleness at times that are imposed by shifts running counter to the light dark schedule
non pharm:
sleep scheduling
sleep hygeine
naps before or during shift if possible
esposure to bright lights at night and darkness during the day
pharm:
meletonin (0.5-5)
ramelteon
short acting bzdra. BE CAREFUL for risk of next day drowsiness
modafinil and armodafinil to improve wakefulness
Parasomnias
abnormal behavior or physiological events that occur during sleep such as
sleep walking, sleep driving, sleep terrors, sleep talking, nightmares, etc.
sleep walking terrors and talking during NREM sleep
may be due to a z drug w. alcohol or antidepressants
treatment of parasomniaas
protect the individual fromharm: safety latches on doors/ windows
BZ, ssri, OR TCAs may be beneficial
reduce stress, anxiety, and sleep deprivation to reduce nightmares
Restless leg syndrome
parasthesias felt deep in the calf muscles, thighs, and arms w. an urge to keep limbs in motion; often bilateral
associated w. ckd, iron defiicnecy, vit. b or folate defiiciency, pregnancy, peripheral neuropathies
Rule out/ Treat Possible Causes of RLS
nutrition: iron supplementatino with Fe deficiency
vit. B or folate deficiency
reduce caffeine and alcohol use
wieghtloss
smoking cessation
regular moderate exercise
sleep
withdraeal of meds which may cause RLA
*centrally acting antihistamines (diphenhydramine, doxylamine, hydroxyzine, meclizine)
AD(TCA’S SSRI, SNRI)(NOT buproprion)
APS
antinausea drugs that block dopamine (metoclopramide, promethazine)
non pharm treatment of RLS
treatment factors:
age of pt
severity, duration, and frequency of SS
comorbidities
SS releif: walking, biking, soaking limbs, leg massage
activities to improve mental alertness at time of rest/boredom
yoga or acupuncture?
pharm trt for RLS
intermittent symptoms; carbidopa-levadopa
BZDRA: clonazepam most well studied
chronic and persistent symptoms:
Alpha-2delt calcium ligands
*pregablin
*gabapentin
dopamine agonists
*immediate-release pramipexole
Ropinirole
*rotigotine
considerations for specific classes of drugs for rls TREATMENT
dop. agonists
*use lower doses compared to PD treatment
augmentation is problematic, can cause increase in rls
BZDRAS
cautin: caryover sedation
Alpha-2delt calcium ligands
good choice for painful RLS
gabapentin enacaribl 9Horizant) is FDA approved for RLS
