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neuro Flashcards

1
Q

what morphology do each of the following have? s. pneumo, h. flu, n. meningitides, ecoli/kleb/pseudo, listeria

A

s. pneumo (gm+ cocci), h. flu (gm - coccobacilli), n. meningitides (gm - cocci), ecoli/kleb/pseudo (gm - bacilli), listeria (gm + bacilli)

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2
Q

what is important to know about he CSF regarding meds you want to get there?

A

it flows unidirectionally–so injection into lumbar area isn’t best way to go–try to inject into ventricles

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3
Q

what increases penetration of meds into blood brain barrier?

A

low molecular weight, non ionized, meningineal inflammation, non protein bound, lipid soluble

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4
Q

which drugs have therapeutic levels in CSF, even without meningeal inflammation?

A

Sulfonamides/Trimethoprim  Chloramphenicol  Rifampin  Metronidazole  Isoniazid, Pyrazinamide, Ethionamide

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5
Q

which drugs have therapeutic levels in CSF with inflammation?

A

Penicillin G  Nafcillin  Cefotaxime  Ceftriaxone  Ceftazidime  Imipenem  Meropenem  Vancomycin  Linezolid  Aztreonam  Ciprofloxacin  Fluconazole  Ganciclovir  Acyclovir

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6
Q

which drugs don’t have therapeutic levels even with inflamed meninges?

A

Aminoglycosides  First generation cephalosporins  Second generation cephalosporins  Clindamycin  Amphotericin o (except cefuroxime)

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7
Q

what are normal findings in CSF and what is found in bacterial meningitis?

A

(lab test, normal, csf) WBC (per mm3)

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8
Q

what are the likely meningitis pathogens in each of the following groups and empiric tx if gram stain not available? (hint: it needs to cover all those pathogens

A
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9
Q

tx goals of meningitis tx

A

Eradicate infection  Improve signs and symptoms  Prevent development of neurologic sequelae

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10
Q

what are the likely meningitis pathogens in each of the following groups and empiric tx if gram stain not available? (hint: it needs to cover all those pathogens 1-23 mo

A

1-23 months S. pneumoniae, N. meningitidis, Group B Strep, H. influenzae, E coli Vancomycin + third generation cephalosporin a

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11
Q

what are the likely meningitis pathogens in each of the following groups and empiric tx if gram stain not available? (hint: it needs to cover all those pathogens 2-50 yo

A

2-50 years N. meningitidis, S. pneumoniae Vancomycin + third generation cephalosporin a

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12
Q

what are the likely meningitis pathogens in each of the following groups and empiric tx if gram stain not available? (hint: it needs to cover all those pathogens >50

A

> 50 years S. pneumoniae, N. meningitidis, L. monocytogenes, gram-negative bacilli Vancomycin + ampicillin + third generation cephalosporin a

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13
Q

empiric tx of g+ diplococci

A

S. pneumoniae Ceftriaxone or Cefotaxime + Vanco + Dexamethasone

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14
Q

empiric tx of g- diplococci

A

N. meningitidis Ceftriaxone or Cefotaxime

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15
Q

empiric tx of g+ bacilli

A

L. monocytogenes Ampicillin +/- Gentamicin

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16
Q

empiric tx of g- bacilli

A

H. Influenzae, coliforms, P. aeruginosa  Ceftazidime or Cefepime +/- Gentamicin

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17
Q

targeted tx of group B strep and duration

A

Penicillin G or ampicillin for 14-21 days

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18
Q

targeted tx of H. Influenzae (G- bacilli)

A

ceftriaxone 7 days

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19
Q

targeted tx of n. meningitides and duration

A

ceftriaxone 7 days

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20
Q

targeted tx of group listeria and duration

A

Ampicillin +/- Gentamicin >21 days

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21
Q

targeted tx of s. pneomo and duration

A

depends on MIC, but Penicillin G or ampicillin for 10-14 days (add vanco or ceftriaxone if greater mIC)

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22
Q

indications for adding dexamethasone to abx tx for meningitis

A

Infants and children with Haemophilus influenzae type b meningitis (only if started before abx)  Adults with pneumococcal meningitis (only if started before abx)  Administer at 0.15 mg/kg q6 hours for 2-4 days 15 minutes before or with first antimicrobial dose

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23
Q

meningitis prophylaxis of close contacts

A

Haemophilus influenza type b Rifampin 600 mg po q24h x 4 days Neisseria meningitidis Ceftriaxone 250 mg IM x 1 or Rifampin 600 mg po q12h x 4 doses or Ciprofloxacin 500 mg po x 1 (if not resistant)

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24
Q

supportive care of viral enceaphalitis

A

Fluids  Antipyretics/analgesics

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25
Q

what other med can be given to those with west nile or HSV encephalitis in addition to supportive cares?

A

anti seizures meds, tx for intracranial pressure and acyclovir

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26
Q

1 tx for seizure disorders

A

AED

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27
Q

what is the MOA of AED?

A

Effect sodium and calcium channels → stabilization of neuronal membranes  Enhance inhibitory neurotransmission (GABA)  Decrease excitatory neurotransmission (glutamate and aspartate) → Increased seizure threshold → Inhibition of the spread of abnormal (seizure) discharges

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28
Q

define concentration related and idiosyncratic adverse effects of AEDs and ways to manage them

A

Concentration-Related  Most common  Increased drug levels results in increased side effects  Not permanent  See at “peak” concentration or throughout day  Management Lower dose/level Change schedule or formulation of medication Discontinue medication Idiosyncratic  More rare  Not related to dose/level  May be permanent  Seen throughout the day  Management Discontinue the medication Treat adverse reaction as needed

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29
Q

what are some common chronic side effects of AEDs?

A

weight gain or loss, kidney stones, menstrual cycle irregularity, behavior changes, hirsutism, connective tissue changes, skin thickening

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30
Q

which drug has these chronic side effects? Behavior Δs Cerebellar syndrome Connective tissue Δs Skin thickening Folate deficiency Gingival hyperplasia Hirsutism Coarsening of facial features Acne Cognitive impairment Metabolic bone dz Sedation

A

phenytoin

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31
Q

what are common concentration dependent side effects of AEDs?

A

dizziness, drowsiness, lethargy, unsteadiness, sedation, GI distress, N/V, anorexia, somnolence, nervousness, weakness, blurred vision

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32
Q

the risk of suicide is _____ times higher in those on AEDs, esp if taking for seizures

A

two

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33
Q

what 3 possible drug intx are there with AEDs? how do you manage them?

A

antacids may decrease its absorption (take 2 hours before hand), highly protein bound drugs may compete and cause elevated free drug, CYP450 inducers or inhibitors (change dose accordingly)

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34
Q

what intx can cause the total serum concentration to increase?

A

removing an inducer, removing a competitor, adding an inhibitor,

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35
Q

what drugs are common inducers of cytochrome P450? (thus decreasing serum concentrations)

A

carbamezepine, phenytoin, phenobarbital, rifampin

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36
Q

what drugs are common inhibitors of CP450 (thus increasing serum drug concentrations)

A

cimetidine, cipro, erythromycin, clari, amiodarone, fluconazole, valproate, felbamate, ticlpidine, topiramate, zonisamide, propxyphene, ketoconazole

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37
Q

what drugs are rec’d for chronic tx of generalized tonic clonic seizures?

A

carbamazepine, lamotrigne, levetiracetam, oxycarbazepine, phenobarbital, phenytoin, valproate, topiramate, zonisamide

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38
Q

what drugs can be used to tx all kinds of seizures?

A

valproate, lamotrigine

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39
Q

what drugs are rec’d for all partial seizures?

A

same as generalized tonic clonic except not zonisamide and add gabapentin: carbamazepine, lamotrigne, levetiracetam, oxycarbazepine, phenobarbital, phenytoin, valproate, topiramate, zonisamide

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40
Q

how should # of seizures be monitored?

A

have them keep a seizure diary

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41
Q

what criteria must be met before d/cing a AED? how should d/cing be done?

A

All of the five following criteria must be met before considering discontinuation Seizure free for 2 to 5 years Normal neurologic exam Normal intelligence quotient Single type of partial or generalized seizure Normal EEG with treatment  Slowly decrease polytherapy to monotherapy  With monotherapy, slowly decrease AED over at least 1-3 months  Decrease dose by no more than one-third each time

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42
Q

what tx is indicated 1st line (pre hospital) for status epileptics? 2nd line? 3rd line?

A

1st line: pR diazepam or iM midazolam. 2nd line: if not already given can give lorazepam and can repeat. 3rd line: phenytoin or fosphenytoin. if none of those work can give phenobarbital

43
Q

carbamazepine: brand name MOA AE therapeutic range CYP450 inducer or inhibitor?

A

carbamazepine: brand name: tegretol MOA: na channel AE: diplopia, hyponatremia, leukopenia; Pg D therapeutic range: 4-12 mcg/ml inducer

44
Q

gabapentin brand name MOA AE CYP450 intx?

A

gabapentin brand name: neurontin MOA: increase gabaingeric inhibition, decrease glutamate? not fully understood AE: Sedation, dizziness, ataxia, weight gain; behavior changes in children; potential for misuse & abuse CYP50: no

45
Q

lamotrigne brand name MOA AE CYP459 intx?

A

lamotrigne brand name: lamictal MOA: na channel, decrease glutamate AE RASH, ataxia, tremor, sedation, nausea/vomiting, weight gain CYP450 inducer and inhibitor

46
Q

phenobarbital brand name MOA AE therapeutic range CYP450 intx?

A

phenobarbital brand name: N/A MOA: increase GABA inhibition AE: SEDATION, Sedation, irritability, confusion,  cognition and motor skills, aggression, hyperactivity therapeutic range CYP450: INDUCER

47
Q

phenytoin brand name: MOA AE therapeutic range CYP450 intx?

A

phenobarbital brand name: dilantin MOA: na channel AE: Ataxia (cerebellar atrophy), nystagmus, osteoporosis, sedation, dizziness, gingival hyperplasia, hirsutism; Pg D therapeutic range: 10-20 mcg/ml free 1-2 mcg/ml CYP450 intx? inducer

48
Q

felbamate brand name: MOA AE therapeutic range CYP450 intx?

A

felbamate brand name: felbatol MOA: excitatory AA inhibition AE: Anorexia, N/V, insomnia, HA, APLASTIC ANEMIA, HEPATIC FAILURE therapeutic range not defined CYP450 intx? complex

49
Q

pregabalin brand name: MOA AE therapeutic range CYP450 intx?

A

pregabalin brand name:lyrica MOA: calcium channel AE: DIZZINESS somnolence, ataxia, blurred vision, WEIGHT GAIN, ABNORMAL THINKING therapeutic range; not defined CYP450 intx? none

50
Q

topiramate brand name: MOA AE therapeutic range CYP450 intx?

A

topiramate brand name: topamax MOA: sodium channel, NMDA untag AE: lowed thinking, speech difficulties, DECREASED APPETITE AND COGNITION, HA, diplopia; Pg D therapeutic range CYP450 intx?

51
Q

VALPROIC ACID brand name: MOA AE therapeutic range CYP450 intx?

A

VALPROIC ACID brand name: depakote MOA: chloride channel, gaba AE: Nausea/vomiting, TREMOR, ataxia, sedation, WEIGHT GAIN, HEPATIC FAILURE, THROMBOCYTOPENIA; Pg D therapeutic range 50-150 mcg/ml CYP450 intx? inhibitor

52
Q

lorazepam brand name: MOA AE therapeutic range CYP450 intx?

A

lorazepam brand name: ativan MOA: increase GABA inhibition AE: SEDATION, ATAXIA, confusion therapeutic range CYP450 intx? none

53
Q

fosphenytoin brand name: MOA AE therapeutic range CYP450 intx?

A

fosphenytoin brand name: cerebyx MOA: sodium channel AE NYSTAGMUS, DIZZINESS, ATAXIA; ECG or blood changes lower than with PHT therapeutic range CYP450 intx?

54
Q

• Bleeding between inner skull table and dura • Appears “lenticular” on CT (football shaped) • Usually due to skull fx which tears middle meningeal artery (NOT VEIN) • Often little or no injury to underlying brain • May rapidly expand (b/c artery), causing herniation/death • Patient may “talk and deteriorate”- initially alert/talking then decompensates/herniates • If rapid surgical intervention (burr hole), prognosis is often excellent

A

epidural hematoma

55
Q

• Focal hemorrhagic area on brain, often surrounded by edema • May occur on the side of skull impact or on the contralateral side of skull (contrecoup lesion) – brain hits the opposite side of the skull during impact

A

cerebral contusion

56
Q

• a.k.a., parenchymal hemorrhage- bleeding within the brain • Due to torn blood vessels • May be delayed for days • Can produce expanding mass lesion

A

intracerebral hemorrhage

57
Q

when you see battles sign behind the ear, raccoons eyes, and hemotympanum, or CSF out of nose what do you think of?

A

basilar skull fracture

58
Q

when intracranial pressure rises what has to be displaced?

A

CSF, blood, brain

59
Q

what is often calcified on CT in brain and can look like blood?

A

choroid plexus and pineal gland (central)

60
Q

signs of tentorium herniation

A
  1. Ipsilateral fixed, dilated pupil 2. Contralateral weakness of arm/leg- corticospinal tract crosses at the lower brain stem 3. Deteriorating LOC
61
Q

• Bleeding between dura and arachnoid/brain • Appears “sickle-shaped” on CT • Due to tears of bridging veins between cerebral cortex and dura • Greater frequency in elderly/alcoholics − Brain atrophy − Bridging veins span a greater distance, more easily torn • Often with severe underlying brain injury

A

subdural hematoma

62
Q

signs of concussion

A

“mild traumatic brain injury”

Altered mental status, following blunt head trauma with or without LOC

May see LOC, confusion, memory loss, altered personality, focal neuro deficits

Duration usually short (seconds-minutes), but may last hours

Recovery usually complete

We take it a lot more seriously than we used to!

Initial impact of concussion called “coup” secondary impact called “contrecoup”

63
Q

tx of concussion

A

Treatment of concussion

Cognitive and physical rest (no video games, TV, may have to take time off school—tx it like a sprained ankle that you try to avoid using for a while)

Ongoing neuropsych testing for persistent sx

Return to sports guidelines require

Complete clearing of all sx

Complete return of memory and concentration

No sx after provocative testing (jogging, situps, pushups)

64
Q

Tearing/shearing of nerve fibers at time of impact

CT may be normal despite profound neurological deficit- can’t image on a cellular level

Results in prolonged, possibly permanent coma

Mortality 33%, usually due to cerebral edema

Death usually not right away, but with time and cerebal edema it can happen

A

diffuse axonal injury

65
Q

post concussive syndrome

A

Persistent symptoms after head injury

May last weeks to months:

Persistent, recurrent Headache

Memory impairment

Concentration/attention problems

Anxiety, depression

Insomnia

Dizziness/ataxia

66
Q

which head injury is associated with a Greater frequency in elderly/alcoholics b/c they have brain atrophy

may required very little trauma to cause it

A

subdural hematoma

67
Q

what color is blood on CT?

A

bright white

68
Q

indications for CT scan in head injuries

A

Shows hemorrhage, cerebral edema, skull fractures

Indications vary, generally include:

Prolonged LOC (>few seconds)

Persistent decreased mental status

Clinical suspicion of skull fracture

Persistent vomiting

Seizure

Focal neuro deficit (slurred speech, etc)

On Blood thinners

69
Q

what imaging should also be done in someone with head injury?

A

c-spine

70
Q

management of severe head injury

A

Severe Head Injury (if unresponsive, confused, etc)

ABC’s, C-spine immobilized (collar)

Intubate/hyperventilate to decrease pCO2 to 30-35 (if show signs of ^ ICP)

Elevate head of bed to 30 degrees

Correct hypotension if present

If focal deficits, suspect impending herniation

IV mannitol: an osmotic diuretic, decreases ICP

Emergent head CT

Significant mass lesion (EDH, SDH) need rapid neurosurgical evacuation

71
Q

management of mild to moderate head injury

A

Observation (small chance could herniate)

Admit if:

Persistent decreased LOC

Focal neuro deficit,

Seizures

Unreliable pt. with hx of LOC

May discharge if:

Minor injury

Neurologically intact

Reliable family members to observe

72
Q

most effective tx for PD

A

carbidopa/levodopa

73
Q

carbidopa/levodopa

trade name

MOA

ae

A 
MOA: increases DA in CNS
o Levodopa (immediate precursor to DA) crosses BBB, DA doesn’t
o Carbidopa inhibits peripheral conversion of levodopa  DA (although not c

trade name: sinemet

titrate slowly to avoid N/V, hypotension

ae: Agitation, Confusion Insomnia, Psychosis Headache, Dizziness Orthostasis, Dyskinesias Nausea, Vomiting

74
Q

Amantadine

trade name

MOA

AE

A

NMDA receptor antagonist; blocks glutamate transmission, promotes DA release, and blocks acetylcholine

 Antiviral with mild therapeutic effects in PD

 Sedation and confusion common; rebound PD if abrupt discontinuation

trade name: symmetrel

ae: Agitation, Confusion Insomnia, Psychosis Headache, Dizziness Orthostasis, Dyskinesias Nausea, Vomiting

75
Q

MAO-B inhibitors: selegiline and rasagiline

trade names

MOA

AE

A

MOA: Prevent breakdown of DA (and othe neurotransmitters) via MAO-B; rasagiline may be neuroprotective and neurorestorative (2009 trial; needs verification)

trade names: selegiline: eldepryl; rasagiline: azilect

 Drug/food interactions (rasagiline > selegiline):

o TCA, SSRI, SNRI, meperidine →CNS toxicity, autonomic instability, HTN,  temp, death o MAOI → hypertensive crisis
o Tyramine-containing foods (dried, aged, fermented) → risk of hypertensive crisis

ae: Agitation, Confusion Insomnia, Psychosis Headache, Dizziness Orthostasis, Dyskinesias Nausea, Vomiting

76
Q

catechol-o-methyltransferase (COMT inhibitors) entacapone and tolcapone

MOA

trade name

ae

A

MOA: Inhibit breakdown of levodopa
 Increase half life of levodopa by 50% → more continuous stimulation of DA receptors

ae: Agitation, Confusion Insomnia, Psychosis Headache, Dizziness Orthostasis, Dyskinesias Nausea, Vomiting

trade name: entacapone: comtan; tolcapone: tasmar

77
Q

which parkinsons med has dietary restrictions?

A

rasagiline: avoid tyramine containing foods like cheeses, wines, etc

78
Q

what drug can delay need for use of levodopa in early disease or decrease the dose of levodopa in advanced d?

A

dopamine agonists like bromocriptine, pramipexole (mirapex)

79
Q

dopamine agonists: pramipexole

trade name

AE

A

mirapex

AE:

Confusion, Dizziness Hallucinations, Orthostasis Nausea, Asthenia Syncope

Peripheral edema

80
Q

signs of excess dopamine:

A

confusion, hallucinations, GI complaints, orthostatic hypotension, impulse control disorders d/t overstimulation of mesocorticolimbic DA pathways

81
Q

anticholinergics: older tx of parkinsons

MOA

AE

example

A

MOA; Relative increase  in striatal cholinergic activity  tremor

ae: Confusion*, Memory loss* Anti-SLUD effects Sedation, Depression Orthostasis, Drowsiness
example: benztropine (cogentin)

82
Q

how would you adjust dosing for someone whose dose seems to be “wearing off”

A

 Decrease levodopa dosing interval by 30 to 60 minutes
 Add COMT inhibitor if on levodopa (may require levodopa dose )  Add dopamine agonist to levodopa or vice versa
 Add MAO-B inhibitor to levodopa

83
Q

how would you help someone who has delayed on or “no on” response with parkinsons meds?

A

Give levodopa on empty stomach  Use levodopa ODT
 Avoid levodopa CR
 Use apomorphine subcutaneous

84
Q

how would you help someone who has start hesitation (“freezing”)

A

Increase levodopa dose
 Add a dopamine agonist or MAO-B inhibitor
 Utilize physical therapy along with assistive walking devices or

sensory cues (e.g., rhythmic commands, stepping over objects)

85
Q

how would you help someone who is having peak-dose dyskinesia?

A

 Decrease levodopa dose and add/increase DA agonist
 Add amantadine
 If COMPT inhibitor recently added, consider levodopa dose 

86
Q

drug used to tx hypomobility in parkinsons

A

apomorphine (apokyne)

87
Q

T or F: there is no difference in the rate of motor complications between the levodopa formulations (CR and immediate release)

A

T

88
Q

what are the only 2 drugs that are indicated for tx of PD psychosis and why? what is used to tx dementia?

A

only quetiapine rec’d, or maybe clozapine others may worsen it. to tx the dementia; consider donepizil or rivastigmine

89
Q

tx for acute flares of MS

A

coticosteroids and plasmaphoresis

90
Q

first line tx for MS?

A

interferons or glatiramer

91
Q

B interferons

mOa

EXAMPLES

monitoring

ae

A

Interferon -1a: Avonex, Rebif; Peginterferon -1a: Plegridy Interferon -1b: Betaseron & Extavia

 MOA: alter the expression and response to surface antigens, can augment suppressor cell function, suppress T-cell proliferation, may ↓ BBB permeability

 Decrease frequency of exacerbations and delay disability

 First line DMT based on tolerability and efficacy

monitoring:

EDSS (Kurtzke Expanded Disability Status Scale; 0-10) + neuro exam every 3 mo during 1st yr then every 6 mo

 Baseline CBC, plt, LFT, then @ 1 month, then q3 months x 1 yr, then q6 months thereafter

(some can cause leukopenia and anemia, LFtS)

ae: HA, flu-like sx, myalgia, ISR

92
Q

glatiramer:

trade name

indication:

MOA

AE

A

glatiramer:

trade name copaxone

indication: RR MS

MOA: inhibits t cells

AE: with injection: ISR, chest pain, flushing, difficilty breathing, anxiety

93
Q

fingolimod

indications

MOA

AE

A

MOA: prevents some WBCs from migrating to CNS and subsequent damage

 Indication: RR, PR

 Efficacy: modestly better than Avonex at preventing relapses (Pharmacist’s Letter, 2010)

 Adverse Effects: HA, LFTs, HR,  block (ECG with 1st dose), macular edema, bronchitis,

pneumonia, rare PML; avoid in pts with recent MI, angina, stroke, TIA, or severe HF

 Dose:0.5mgpoqd

 Cost: $5000/month ($60,000/yr) (Pharmacist’s Letter, 5/13)

 Comparable in efficacy to first-line drugs

94
Q

which drugs for MS are not first line (interferon and glatiramer) but have comparable effiacy to first line?

A

fingolimod, teriflunimide, dimethyl fumarate

95
Q

teriflunomide (aubagio)

indication

moa

ae

A

Teriflunomide (Aubagio) Note: Leflunomide (Arava) is a prodrug of teriflunomide

MOA: may involve a reduction in the number of activated lymphocytes in the CNS

Indication: approved to treat the relapsing forms of MS

Adverse Effects: nausea, diarrhea, hair loss, hepatotoxicity (black box warning),  infection risk

o Teratogenic: reliable contraception needed for women of child bearing potential

Monitoring: LFTs baseline, qmonth x 6 months, then periodically

Dose: 7 mg or 14 mg po once daily

Cost: $3750/month ($45,000/yr) (Pharmacist’s Letter, 5/13)

96
Q

dimethyyl fumarate (tecfidera)

moa

indication

ae

monitoring

A

Dimethyl fumarate (Tecfidera)

MOA: appears to protect neurons and myelin and have anti-inflammatory effects

Indication: approved to treat the relapsing forms of MS

Adverse Effects: flushing, nausea, diarrhea most common; decreased WBC; rare PML in RA tx

Monitoring: WBC baseline, q3-6 months initially, then periodically

Dose:120mgpobidx7days,then240mgpobid

Cost: $4575/month ($54,900/yr) (Pharmacist’s Letter, 5/13)

Comparable in efficacy to first-line drugs

97
Q

mitoxantrone

A

MOA: suppression of immune cells that attack the body

Indication: approved to ↓ the frequency of relapses and/or neurologic disability in adults with

SPMS, PRMS, or worsening RRMS

• Not considered a replacement for Interferons or glatiramer but often used in conjunction

Adverse Effects: ↓ WBC & plts, anemia, ↑ LFTs, ↓ LVEF, HF (max lifetime dose of 140 mg/m2), UTIs, N/V, mucositis (Black box warning: cardiotoxicity, acute myelogenous leukemia)

Monitoring: LVEF evaluation baseline, before each subsequent dose, after a cumulative dose of 100 mg/m2 has been reached, and if signs or sx of HF develop

 Dose: 12 mg/m2 by IV infusion over 5-15 minutes every 3 months

 Cost:~$1500/dose($6,000/yr)(Pharmacist’sLetter,11/12)

 Reservedforpatientswithworseningdiseasebecauseofcardiactoxicity,riskofAML

98
Q

natalizumab

A

Natalizumab (Tysabri)

 MOA: partially humanized monoclonal antibody directed at α4β-integrin (aka VLA-1); prevents

activated lymphocytes from passing across BBB

 Indication:monotherapyforrelapsingformsofMStodelayphysicaldisabilityandrelapsesin

patients who have a documented inadequate response or intolerance to traditional MS therapies

 AdverseEffects:rarePML(progressivemultifocalleukoencephalopathy);risk~1/1000pts

treated x 18 months (Neurology, 2008;71:766–773); patients followed in an ongoing safety

registry (TOUCH), hepatotoxicity

 Dose:300mgIV(asinfusion)every4weeks

 Cost: $3,800/dose ($45,600/yr) (Pharmacist’s Letter, 11/12)

 Reservedforpatientswhocan’ttolerateordon’trespondtoothertherapiesduetoriskofPML

and hepatotoxicity

99
Q

alemtuzumab

A

Alemtuzumab (Lemtrada) (Pharmacist’s Letter, 5/15)

 MOA: may alter the number, proportions, and properties of some lymphocyte subsets

 Indication:optionforrelapsing-remittingformsofMS;maybemoreeffectivethaninterferon

 AdverseEffects:Autoimmuneorthyroiddisorders,infections,hypersensitivityreactions,

nausea, infusion-associated reactions, potential for PML; requires special registration for health

care facility and patient to ensure adequate follow-up

 Dose:IVinfusionyearly

 Cost:notavailable

 Used for patients who don’t respond adequately to interferon beta or other disease-modifying

therapies

100
Q

drugs for spasticity in MS

A

Baclofen
Dantrolene
Diazepam
Tizanidine
Tiagabine
Gabapentin Pregabalin
Botulinum toxin type A Dalfampridine

101
Q

tx of fatigue in mS

A

Amantadine (Symmetrel) 100 mg BID

Can cause nausea, insomnia, hallucinations, and livedo reticularis, a purplish discoloration of the skin.

Modafinil (Provigil) 100-200 mg BID

Can cause headache, nausea, and insomnia.

Methylphenidate (Ritalin) 10-20 mg early am and noon

Second-line therapy. Can cause weight loss, anorexia, irritability, and insomnia. Caution with heart disease.

Fluoxetine (Prozac) 20-40 mg QD

Can be useful when patients also have depression.

SSRIs (Celexa, Luvox, Paxil, Prozac, Zoloft)

Can also help with fatigue.

102
Q

tx of vertigo in mS

A

Meclizine (Antivert) 25 mg Q6H

Can cause sedation.

Scopolamine patch (Transderm Scop) Q3 days

Can cause dizziness and dry mouth.

Ondansetron (Zofran) 4-8 mg TID

103
Q

TX OF TREMOR IN MS

A

Propranolol (Inderal) LA 80-320 mg daily

Greatest effect for limb and hand tremor.

Primidone (Mysoline) 100-250 mg TID to QID

Can cause sedation.

Gabapentin (Neurontin) 300-600 mg TID

Can cause fatigue & ataxia. Titrate slowly to  sedation.

104
Q
A

Pharmacotherapy (9 decks)

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