Lecture 6 (neuro) -Exam 3

Question 1

Answer 1

Question 2

What is the Stroke Management Timeline?

Answer 2

Question 3

Commonly tested on

Stroke
* What is the minimal initial evaluation prior to giving tPA? (2)

Answer 3

• Blood glucose level
• CT without contrast

Question 4

Stroke
* What is the txt option and when do you give it? Who is it not recommended for? (3)

Answer 4

tPA within 4.5 hours after stroke

Not recommended for
* Nondisabling stroke with NIHSS score 0-5 (not super severe)
* Extensive bleeding risk
* CT evidence of extensive, irreversible injury

Question 5

Time = brain
* What was the outcome with tPA within 3 hours?

Answer 5

32% patients given tPA and 23% of patients given placebo had a good outcome at 3 months (modified Rankin scale score 0 or 1)

Question 6

Time = brain
* What was the outcome when tPA is given within 3-4.5 hr (2)

Answer 6

• 35% patient given tPA and 30% of patients given placebo had a good outcome at 3 months (modified Rankin scale score 0 to 1)
• Large intracerebral hemorrhage occurred in 6.8% of patients given tPA and 1.3% of patients given placebo

Over 4.5 hr= decrease outcome

Question 7

Fill in for the modified rankin scale

Answer 7

Question 8

Wake up trial
* What happened with the patients?
* What was historic recommendation?

Answer 8

• Wake-up stroke-patient goes to sleep normal; wakes up with stroke symptoms
• Historic recommendation – no tPA (bc did not know duration)

Question 9

Wake up trial
* What was the populatoin group?
* What was the criteria for the trial? (3)
* What scoring did they use?
* What class recommendation?
* What is still preferred if available?

Answer 9

RCT 503 patients with unclear stroke onset (94% woke up with stroke)

Randomized to tPA or placebo within 4.5 hours of stroke discovery
* Abnormal diffuse-weighted MRI, not > 1/3 territory of MCA
* NIHSS score ≤ 25
* No planned thrombectomy

90-day modified Rankin score 0 or 1- 53% treatment group and 42% placebo group

Class IIa recommendation for patients who meet criteria

Thrombectomy still preferred if available

For clinical, not testing-> if over 4.5 hours or unknown, no tPA

Question 10

What is the TPA criteria? (3)

Answer 10

• Age 18 years or older
• Clinical dx of ischemic stroke with significant deficit
• Time of symptom onset established to be < 4.5 hours before treatment

Question 11

Low yield but know red and the BP

TPA criteria
* Who cannot get tPA?

Answer 11

Question 12

KNOW RED for sure

TPA criteria
* What are the bleeding diathesis? (6)

Answer 12

Question 13

TPA criteria
* What are the additional exclusion criteria between 3-4.5 hrs? (4)

Answer 13

• Age >80 years
• Severe stroke (NIHSS > 25)
• History of diabetes and prior stroke
• Taking an oral anticoagulant regardless of INR

Question 14

There was a past question in spring about the MOA

Thrombolytics

Answer 14

Question 15

Said FYI

Answer 15

Question 16

tPA monitoring
* Admission to where?
* What do you need to monitor and how often? (3)
* What should the BP be maintained at?

Answer 16

Admission to intensive care unit

Close neurologic and cardiovascular including blood pressure
* Every 15 minutes for 2 hours after tPA administration, then
* Every 30 minutes for 6 hours, then
* Every hour for next 16 hours

Blood pressure should be maintained < 180/105 for at least 24 hours

Question 17

Thrombectomy
* When is it a first line recommended?
* Most studies evaluated what?
* What is the timeframe?

Answer 17

First-line recommendation when performed within 6 hours of stroke onset if not a candidate for tPA
* Most studies evaluated internal carotid artery and first segment of MCA
* > 6-to-24-hour thrombectomy

Question 18

Thrombectomy
* What did the dawn/defuse trials do and show?

Answer 18

• NIHSS ≥ 10 who met specific MRI criteria and stroke onset between 6 and 24 hours earlier
• Large anterior circulation strokes
• Modified Rankin scale score of 0 to 2 at 90 days 49% in treatment group; 13% control group

Question 19

Transient ischemic attack (TIA)
* What is it?
* What can happen after? Who has a higher risk?

Answer 19

Transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia without radiographic evidence of infarction

Incidence of subsequent stroke in 48 hours is high (4 to 10%)
* Higher ABCD2 score = higher risk (USE THIS SCORE TO SEE WHO IS HIGHER RISK OF STROKE)

Question 20

I believe low yield

Transient ischemic attack (TIA)
* What is the risk stratification instrument?

Answer 20

Question 21

Transient ischemic attack (TIA)
* What is the initial txt? (2)

Answer 21

• Evaluation for carotid artery versus cerebral artery
• Carotid – endarterectomy vs stenting (if candiates for)

Question 22

Transient ischemic attack (TIA)
* What is the txt for patients without cardioembolic source depending on ABCD2 score?

Answer 22

Question 23

AIS or TIA - Antiplatelet therapy (non cardioembolic)
* When do you start seconday preventation? (2)

Answer 23

Therapy at presentation
* Start immediately in patients not candidates for tPA
* Start 24 hours after tPA administration

Question 24

AIS or TIA - Antiplatelet therapy (non cardioembolic)
* Who is it recommended for? What is the medication/dose?

Answer 24

Recommended for patients with
* ABCD2 score < 4 (TIA)
* NIHSS score > 5 (ischemic stroke)

Dose = 162 to 325mg of ASPIRIN daily

Question 25

AIS or TIA - **Antiplatelet therapy** **(non-cardioembolic)** * Duel antiplatelet therapy is recommended for who? (3)

Answer 25

* NIHSS ≤ 5 who are not candidates for tPA * ABCD2 score ≥ 4 * Intracranial large artery stenosis of > 70 %

Question 26

AIS or TIA - **Antiplatelet therapy** **(non-cardioembolic**)-> Dual Antiplatelet Therapy * What are the short term benefit? * What is the long term benfit? * What is recommended in high risk patients?

Answer 26

* Aspirin + clopidogrel x 21 days lowered 90-day stroke risk * Long-term DAPT offered no outcome benefits / increased bleeding risk * 90-day therapy recommended in select high-risk patients (see guidelines)

Question 27

AIS or TIA - **Antiplatelet therapy** **(non-cardioembolic)** * What is the dosage for dual treatment? When do you switch to single treatment?

Answer 27

* Aspirin 325 mg x 1, then 81mg daily plus * Clopidogrel 300mg x1, then 75 mg daily * Single agent therapy after 21 days

Question 28

AIS or TIA - **Antiplatelet therapy** **(non-cardioembolic)** * What is the long term single agent therapy? (3)

Answer 28

* **Aspirin 81mg PO daily** or * Clopidogrel 75mg PO daily or * Aspirin plus dipyridamole 25mg/200mg PO BID

Question 29

AIS or TIA – **Anticoagulation** (**cardioembolic**) * TIA: May consider early initation if what?

Answer 29

May consider early initiation if clear indication for anticoagulation * **Atrial fibrillation** * Venous thromboembolism * Mechanical heart valve ## Footnote Anticoagulation has a limited role for acute therapy

Question 30

AIS or TIA – **Anticoagulation (cardioembolic)** * What is the recommendation for AIS

Answer 30

Anticoagulation generally not recommended as acute therapy ## Footnote Anticoagulation has a limited role for acute therapy-> TPA is antithromblytic

Question 31

AIS or TIA – **Anticoagulation** (**cardioembolic**) * What is the long term therapy? (2)

Answer 31

Oral anticoagulants * Warfarin if mechanical valve * DOACs if no mechanical valve

Question 32

AIS or TIA – Secondary prevention * What are the risk factor management? (6)

Answer 32

* Weight control * Exercise * Smoking cessation * Limit ETOH * **Cholesterol control - statin** (add on after) * Blood pressure control

Question 33

Blood Pressure Management * What shows no benefit? * What is reasonable with BP?

Answer 33

* f BP is < 220/120 mmHg, treatment of HTN within the first 48 to 72 hours after acute ischemic stroke (AIS) is of no benefit * If BP is ≥ 220/120 mmHg, the benefit of lowering BP is unknown, but lowering by 15% in the first 48 to 72 hours after AIS is reasonable

Question 34

Blood Pressure Management * What is the tPA BP goal ? * What is the BP goal for mechanical thrombectomy?

Answer 34

* tPA goal: BP should be maintained below 180/105 mmHg and for 24 hours after administration * If mechanical thrombectomy: It is reasonable to maintain BP below 180/105 mmHg during and for 24 hours after the procedure

Question 35

Subarachnoid hemorrhage (SAH) * What is the MC SXS? * What is the MCC?

Answer 35

Sudden onset of severe headache * Thunderclap * “worst headache of my life” MCC (85%) – ruptured aneurysm

Question 36

Subarachnoid hemorrhage (SAH) * Treatment is aimed at what? What are the examples (4)

Answer 36

Treatment primarily supportive aimed at decreasing re-rupture * Surgical coiling (non-invas) or clipping (invas) * Reverse anticoagulation * Decrease blood pressure (SBP < 160, MAP < 110mm Hg) * ± antiepileptics – seizure prophylaxis (all patients-keppra is an example)

Question 37

Subarachnoid hemorrhage (SAH) * What is definitive treatment? (2)

Answer 37

Definitive coaling or clipping

Question 38

SAH * High incidence of what? When?

Answer 38

High incidence of vasospasm and delayed cerebral ischemia (DCI) within 2 weeks * 30% of patients with SAH (4 to 14 days after initial event)

Question 39

SAH * What will the patients develop with vasospasms? (6)

Answer 39

Patients develop new focal neurologic impairment * Hemiparesis * Aphasia * Apraxia * Hemianopia * Decrease of GCS by 2 points for 1 hour * Not attributed to other causes

Question 40

SAH - DCI * What are the treatment goals? (2) * What is first line+ dose? For who? What does it improve?

Answer 40

Treatment goals * Maintain euvolemia – MC fluid recommendation 0.9% sodium chloride * Prevent vasospasm Nimodipine * All patients with SAH within 48 hours * 60mg PO/NG Q4H x 21 days * Improved odds of good outcome, reduced odds of deficit, mortality or both

Question 41

SAH-DCI * What is the MOA of CCB? * What is an unique characteristic of Nimodipine that is good for cerebral BVs?

Answer 41

* Block voltage-gated L-type calcium channels in their inactive conformation * Avoid Ca influx; prevents vasoconstriction * **Lipophilic**; preference for cerebral blood vessels

Question 42

SAH - DCI * What are the SE of CCB? (5)

Answer 42

* Blood pressure fluctuations * Monitor to prevent decrease in cerebral perfusion pressure * Headache, * Flushing * Edema

Question 43

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Question 44

What do you need to rule out with seizures

Answer 44

Need to rule out things that can cause seizures

Question 45

Generalized (change in consciousness)->**MOTOR** * What are the different types (3) Example some of them

Answer 45

Tonic (total stiffness) and/or clonic Myoclonic (think about the girl eating the cereal) * Small muscle contractions * MC with stress, sleep deprivation Atonic – loss of muscle tone * Drop attacks

Question 46

Generalized (change in consciousness)->**NON- MOTOR-ABSENCE** * MC in who? * What are the sxs? (4) * Often midiagnosed as what?

Answer 46

MC children / adolescents Altered consciousness without change in muscle tone * Starring in space * Day dreaming * Inattentive Often misdiagnosed as ADHD

Question 47

Focal * What happens to consciousness? * What can happen with motor? * What can happen with sensory?

Answer 47

* ± Change in consciousness (most not) * Motor – motor cortex; tonic-clonic of contralateral extremity * Sensory – occipital; see flashing lights or smells ## Footnote Based on my research, they usually have one of the components- motor, sensory, autonomic

Question 48

Focal * What are the sxs when autonomic system is involved? * Can progress to what?

Answer 48

Autonomic * Involve automatisms – chewing, lip smacking, rapid eye movements, weird smells, or feeling of fear (increase anxiety) Can progress to generalized ## Footnote Based on my research, they usually have one of the components- motor, sensory, autonomic

Question 49

# It is long lol Seizure pathophysiology * What is the pathway during excitation?

Answer 49

Voltage-gated Na channels open sending Na into cell – depolarization Depolarization causes voltage activated Ca channels to open allowing Ca influx (opens them) Ca influx results in **glutamate** release from presynaptic vesicles (stimulator NT) Glutamate binds to * AMPA – opens to permit Na ion entry * NMDA –opens to permit Ca ion entry * Ca influx can also occur through low voltage (T-type) calcium channels * Depolarization and propagation of action potential

Question 50

What does overactivation of the excitation pathway lead to?

Answer 50

Overactivation – leads to seizure

Question 51

Seizure pathophysiology * What does GABA regulate?

Answer 51

GABA - Regulates excitatory neurons to help prevent seizures

Question 52

Seizure pathophysiology * What is the inhibitory pathway? What helps get rid of GABA (2)

Answer 52

GABA is released from inhibitory neurons and binds to GABAA receptors * **GABA binding causes influx of Cl- ions counter acting cell depolarization** (decrease excitation) GABA transporter-1 responsible for GABA reuptake into presynaptic neuron GABA-aminotransferase (AT) breaks down GABA

Question 53

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Question 54

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Question 55

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Question 56

Currently available AEDs * What is the difference between older and newer AEDs?

Answer 56

Older AEDs * Narrow therapeutic index * Drug interactions * Serious toxicities Newer AEDs * Wide therapeutic index * Less drug interactions * More moderate toxicities * Less side effects

Question 57

Seizure management * What are the goals? (4)

Answer 57

* Control seizures * Prevent/restore brain development * Avoid adverse effects * Maximize quality of life

Question 58

Seizure management: Treatment modalities * What are the different ways? (4)

Answer 58

Medications * 63% controlled with medications * Likelihood of response declines with subsequent mediations Surgery (need focal onset-> ablat via radiofreq or remove connection) Vagal nerve stimulators (changing excitation and inhibition) Ketogenic diet

Question 59

Seizure treatment – General approach * First Unprovoked Seizure: Individualized based on what? Risk of reoccurence is what?

Answer 59

* Individualized based on risk of seizure reoccurrence vs AED adverse effects * Risk of seizure reoccurrence in first 2 years (40 to 50%)

Question 60

Seizure treatment – General approach * What are the factors that increase risk? (3)

Answer 60

* Epileptiform activity on electroencephalogram (EEG) * Abnormal neuroevaluation * First seizure occurs during sleep

Question 61

Seizure treatment – General approach * How many people get AED adverse effects ? * What are the consequences? * When do you start treatment?

Answer 61

* Risk of AED adverse effects 7 to 31% (mostly mild, reversible) * Consequences of recurrent seizure (employment / driving) * **Second unprovoked seizure – start treatment**

Question 62

Seizure treatment – general approach: **provoked seizures** * Treatment depends on what? Give examples

Answer 62

Treatment dependent on etiology * Drug withdrawal/intoxication, electrolyte imbalance – immediate treatment, treat underlying cause * Trauma, tumor – treatment generally recommended [levetiracetam (Keppra)]

Question 63

Seizure treatment – general approach * Antiepileptic medication selection based on what several factors? (6)

Answer 63

Specific seizure type (generalized vs focal vs specific (infantile spasm, Lennox Gastaut) * Side effect profile * Dosing frequency * Concomitant comorbidities and medications * Age * Pregnancy status

Question 64

Seizure treatment – general approach * What is recommended at first? * All patients should be treated by who?

Answer 64

* Initial monotherapy is recommended * ALL patients should be treated by a neurologist

Question 65

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Question 68

Answer 68

## Footnote (*) Also includes fosphenytoin (^) warfarin, hormonal contraception, chemotherapy interactions (#) Drug rash with eosinophilia and systemic symptoms (fever, lymphadenopathy)

Question 69

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Question 70

Antiepileptic Adverse effects by class * What are the SE of valproic acid and phenytonin?(4)

Answer 70

Question 71

Antiepileptic Adverse effects by class * What are the SE of topiramate and carbamazepine?

Answer 71

Question 72

Antiepileptic Adverse effects by class * What are the SE of levetiracetam?

Answer 72

Question 73

What are the SE of ethosuximide and gabapentin/pregabalin?

Answer 73

Question 74

What are the SE of vigabatrin and ketamine?

Answer 74

Question 75

barbiturates * What does it bind to? What does it increase and decrease?

Answer 75

Bind GABAA receptor at site different from BDZ and GABA * Increased duration of GABA channel opening Increasing Cl- influx; hyperpolarizing neuron * Decreasing ability to create action potential * Decrease activity of Ach and glutamate

Question 76

barbiturates * Mimic what at high doses? * What is its therapeutic index? What are the SE? (3)

Answer 76

Mimic GABA at high doses and directly activate GABA receptors **Narrow therapeutic index** * CNS depression * Hypotension * Cardiovascular / respiratory depression

Question 77

Infantile spasms (West Syndrome) * Onset when? * Generally underlaying what? * Spasms include what? (aka sxs) * What is the duration?

Answer 77

Onset early infancy (peak 6 months) * Generally underlying brain abnormality (genetic, metabolic, structural) * Spasms include stiffening of extremities, neck flexion (single extremity to generalized) * Duration – 10 to 20 seconds, subtle, occur several times a day

Question 78

Infantile spasms (West Syndrome) * What are the ways dx it? (3)

Answer 78

* **Electroencephalogram (24-video EEG); hypsarrhythmia is classic pattern** * MRI * Blood tests

Question 79

Infantile spasms (West Syndrome) * What is the prognosis? * What is the txt? (3)

Answer 79

Prognosis generally poor with mild to moderate intellectual delay Treatment – early intervention key * Adrenocorticotrophic hormone (ACTH)-> too expensive * Prednisolone-> first line * Vigabatrin-> next line if no response to Prednisolone

Question 80

Status epilepticus * What is the definition? * What was the old time from? * What increases likelihood of seizure control?

Answer 80

* Unremitting generalized convulsive seizure lasting > 5 minutes or >1 convulsive seizure without return to baseline level of consciousness * Old time frame was > 30 minutes * Time to first dose of benzodiazepine increases likelihood of seizure control

Question 81

Status Epilepticus * What is the supportive care? (4)

Answer 81

Supportive care – airway, breathing, circulation * POC fingerstick glucose (possible hypoglycemia) * Establish IV / IO * Initial antiseizure treatment

Question 82

Status Epilepticus * What is first line? * What is IV and not IV? * Repeat how often?

Answer 82

First-line = benzodiazepines * IV – Lorazepam, diazepam * Not IV - Midazolam (IM, IN, buccal), diazepam (rectal, IN) * Repeat x 2 if no response

Question 83

status epilepticus * When do you go to a second line? * What is the DOC ? (3)

Answer 83

Second-line therapy * Seizures refractory to BDZ * Seizures responding to BDZ to prevent reoccurrence DOC depends on patient history * **Levetiracetam** * Phenytoin/Fosphenytoin * Valproic acid

Question 84

Refractory Status Epilepticus * What is the definition?

Answer 84

Seizure refractory to at least two doses of BDZ and at least two doses of non-BDZ antiepileptic

Question 85

Refractory Status Epilepticus * Consult who? * What is necessary? * What should be monitored? * What medication can you use? (4)

Answer 85

Stat neurology consult Mechanical ventilation necessary (if not already intubated) Continuous EEG monitoring * Midazolam (if you given two doses of benzo, might not be next in line) * Pentobarbital * Propofol * Ketamine

Question 86

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Question 87

Dementia * What is it? * What happens with cognitive? * What happens with psychologic?

Answer 87

* Chronic, acquired loss of 2 or more cognitive abilities caused by brain disease or injury * Cognitive – memory * Psychologic - apathy, depressive symptoms

Question 88

Dementia * What happens with behavioral? * What happens with sleep? * What happens physically? * What are the MC types?

Answer 88

* Behavioral – withdrawal, disinhibition * Sleep – Altered sleep-wake cycle * Physical – gait, stability * Alzheimer disease and mixed dementia MC

Question 89

Dementia pathophysiology * What is the cholinergic hypotheses? * What is the amyloid hypothesis?

Answer 89

Cholinergic * Loss of central cholinergic neurons – ACh deficiency which impairs memory and learning Amyloid hypothesis * Accumulation of beta amyloid proteins outside the cell * Beta amyloid plaques – neuroinflammation, disruption of communication between cells, and weakened blood vessels

Question 90

Dementia pathophysiology * What is the tau hypotheses?

Answer 90

Abnormal aggregation of tau proteins which normally support neuron structure * Thought to be stimulated by amyloid plaques Tangles inside nerve cells – decrease biochemical communication within neurons

Question 91

Dementia treatment * What are the goals? (2)

Answer 91

* Reduce symptoms caused by cognitive decline and accompanying symptoms * Delay progressive cognitive decline

Question 92

# said fyi

Answer 92

Question 93

Dementia pharmacotherapy: Anticholinesterase inhibitor * Promotes what?

Answer 93

Promote relative increases in Ach at the synaptic cleft for cholinergic neurotransmission

Question 94

Dementia pharmacotherapy: Anticholinesterase inhibitor * What has modest improvement? * What has minimal improvement? * All agents in class with what?

Answer 94

Modest improvements * Six-month advantage in cognitive decline * Prevent 2 months per year of cognitive decline * NNT = 12 patients Minimal improvements in activities of daily living All agents in class with similar efficacy and side effect profiles

Question 95

Dementia Pharmacotherapy * Amyloid accumulation thought to cause what?

Answer 95

Amyloid accumulation thought to cause abnormal rise in extra synaptic glutamate levels (too much NT= decrease cognition)

Question 96

Dementia Pharmacotherapy * What is the MOA of NMDA receptor antagnoist?

Answer 96

Inhibit glutamate from stimulating post-synaptic NMDA receptors Decrease calcium influx and overstimulation of neuron caused by amyloid * Calcium influx causes membrane excitability and stimulation * Excess Ca influx causes cell apoptosis ## Footnote Block receptor to uptake glutmate and excitation

Question 97

What are the anticholinesterase inhibitors examples? (3) When are they used?

Answer 97

Question 98

What are the SE of anticholinesterase inhibitors (donepexil, rivastigmine and galantamine)? What are the advantages?

Answer 98

Question 99

What is the NMDA receptor antagonist? When do you use it?

Answer 99

## Footnote Add as disease gets worst

Question 100

What are the NMDA receptor antagonist SE? What is the advantage?

Answer 100

SE: * Headache * Constipation * Confusion * Dizziness Advantages: * Can be used with acetylcholinesterase inhibitor or as monotherapy

Question 101

New dementia therapies: Immuniotherapy * Targets what? * Appears to work better when? * What does it clear?

Answer 101

* Targets amyloid plaques -> causes plaque breakdown and slows the progression of disease * Appears to work better when used earlier in the disease process * Current amyloid plaque clearance rates up to 70% ## Footnote need clear cut amyloid plaque

Question 102

New dementia therapies: immunotherapy * Improves what? What are the examples (4)

Answer 102

Improves time to decline 20 to 40% * Donanemab * Lecanemab * Remternetug * Aducanumab

Question 103

Multiple Sclerosis Types * What is relasping remitting MS * What is clinically isolated syndrome?

Answer 103

* Relapsing-remitting MS: The most common type, characterized by clearly defined relapses (also known as attacks or exacerbations) with partial or full recovery. Have to exhibit at least 2 or more attacks for diagnosis * Clinically isolated syndrome - Patient with a first clinical attack (Optic Neuritis, Transverse Myelitis, etc…)

Question 104

Multiple Sclerosis Types * What is secondary progressive syndrome? * What is primary progressive MS?

Answer 104

* Secondary Progressive Syndrome - Gradual worsening of an initially remitting relapsing syndrome * Primary progressive MS -Insidious neurological progression of neurological disabilities suggestive of primary progressive MS (no acute relapses) ## Footnote Relapsing remitting MS can go into secondary progressive syndrom

Question 105

MS – Acute Exacerbations * What are the sxs? (4)

Answer 105

Symptoms variable * Optic neuritis (unilateral painful vision loss) * Painless diplopia * Brainstem or cerebellar syndrome * Partial transverse myelitis

Question 106

MS – Acute Exacerbations * What are the treatments? (4)

Answer 106

**Methylprednisolone (Solu-Medrol): High dose 1000mg IV daily for 5 days** * Oral Prednisone 625-1250 mg daily for 3-7 days with or without short taper * ACTH Adrenocorticotropic Hormone IM or SQ 80-120 units daily for 1 week * Plasma exchange daily 3-7 treatments for patients with severe neurological deficit; steroid refractory

Question 107

Treatment of MS * What are the goals of relapsing remitting MS? (3)

Answer 107

Disease modifying therapies * Relapse reduction * Reduced accumulation of MRI lesions * Stabilize, delay, modestly improve disability

Question 108

# She skipped this slide Treatment of MS * Who should start disease modifying therapies? * What are the 3 examples?

Answer 108

Everyone with relapsing remitting MS should begin DMT: * Infusion Therapies: Natalizumab, Ocrelizumab, Rituximab, Alemtuzumab * Oral therapies: Dimethyl Fumarate, , Diroximel Fumera5e, Teriflunomide, Fingolimod, Siponimod, Ozanimod. * Injection therapies: (IM, SQ) Human Interferon beta-1b, human interferon beta-1a, Glatiramer Acetate and Ofatumumab.

Question 109

# She skipped this slide MS – maintenance treatments for highly effective

Answer 109

Question 110

# She skipped this slide MS – Maintenance treatments for moderately effective

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Question 111

# She skipped this slide MS – Maintenance treatments for moderately effective

Answer 111

Question 112

# She skipped this slide MS – Maintenance treatments

Answer 112

Question 113

Myasthenia Gravis (MG) * What is it? What is the patho?

Answer 113

Myasthenia gravis is an autoimmune disease involving the skeletal muscle * T-and B-cells produce antibodies which block and destroy acetylcholine (ACh) receptors faster than new ACh receptors can be synthesized

Question 114

Myasthenia Gravis (MG) * Characterized by what? (2)

Answer 114

Characterized by weakness and fatigability ## Footnote fatigued easily-> rested and feels better (feels better in morning)

Question 115

Myasthenia Gravis (MG) * What is the early symptom? * What are the bulbar symptoms? * What are the generalized myasthenia?

Answer 115

* Ocular Myasthenia – More than 50% of patients present with ocular myasthenia or ptosis, with or without diplopia. Most often only early symptom. * Bulbar Symptoms – 15% of patients develop dysarthria, dysphasia and fatigable chewing and swallowing difficulty, while 5% present with proximal muscle weakness. * Generalized Myasthenia – Neck and limb muscle weakness, respiratory muscle weakness and facial muscle weakness.

Question 116

* What are the clinical manifestations of MG? * What is a myasthenic crisis? * How do you dx it?

Answer 116

Question 117

MG

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Question 118

pyridostigmine (Mestinon) * What is the MOA? * What is the usual dose?

Answer 118

MOA: Acetylcholinesterase inhibitor; decreased breakdown of acetylcholine (cholinomimetic) Usual dose: * Immediate release: 60 to 600mg/day PO divided into 5 to 6 doses * Sustained release:180 to 540 mg/day PO once or twice daily

Question 119

pyridostigmine (Mestinon) * Titrate dose to what? * CI in who?

Answer 119

* Titrate dose to balance symptoms and adverse effects * CI: bowel or urinary obstruction

Question 120

pyridostigmine (Mestinon) * What are the SE? (6)

Answer 120

* GI upset * Increased salivation and bronchial secretions * Miosis * Diaphoresis * Muscle cramps * Fasciculation and weakness

Question 121

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Question 122

Encephalopathies with specific treatments

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Question 124

Bell’s Palsy * What are the sxs? (4)

Answer 124

* Facial weakness * Decreased lacrimation and salivation * Loss of taste (anterior 2/3) * Dysacusis

Question 125

Bell’s Palsy * Rule out what? (2) * What is the prognosis?

Answer 125

Rule out: * Ramsey hunt * Lyme’s disease Prognosis: * 71% full recovery * Starts within 3 weeks; takes 6 to 12 months for full recovery

Question 126

Bell’s palsy vs stroke * What is the patho and sxs difference between bells and stroke?

Answer 126

Bell’s Palsy: * lower motor neuron lesion of cranial nerve VII; upper and lower face affected Stroke and other upper motor neuron lesions: * upper face is spared due to input from both sides of the brain

Question 127

Bell Palsy treatment * What is the House-Brackmann Classification of facial nerve dysfunction

Answer 127

* Above the line, give only steriods * Below the line, give steriods and antivirals ## Footnote Cannot close eye= need eye protection

Question 128

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Question 129

Bell Palsy specific treatments * What do you give to all patients?

Answer 129

Glucocorticoids – all patients * Prednisone 60 mg PO daily x 5 to 7 days (no taper needed) * Reduced relative risk of incomplete recovery by 37% * NNT to avoid one incomplete recovery 10

Question 130

Bell Palsy specific treatments * What is the antiviral therapy?

Answer 130

* Acyclovir 400 mg PO 5 times daily x 10 days * Valacyclovir 1000 mg PO TID x 10 days * **Not effective as monotherapy; minimal improvements overall**

Question 131

Carpal tunnel syndrome (CTS) * Mild to moderate CTS - What are the first and second line nonsurgical options?

Answer 131

First-line: * Nocturnal wrist splinting in neutral position Second-line * Local glucocorticoid injection * Methylprednisolone 40 to 80 mg; symptom improvement up to 1 year (10 weeks MC)

Question 132

Carpal tunnel syndrome (CTS) * What do you give for patients who fail or decline injection therapy and fail wrist splinting?

Answer 132

* Prednisone 20 mg daily for 10 to 14 days (mean duration of action 8 weeks) * Not as effective as local glucocorticoid injections

Question 133

Carpal tunnel syndrome (CTS) * What is not recommended? * Surgical decompression should be offered to patients with what?

Answer 133

* NSAIDS not recommended * Surgical decompression should be offered to patients with severe CTS with nerve damage

Question 134

Guillain-Barre syndrome (GBS) * What is it? * What is the sxs? * What is the MCC?

Answer 134

* Autoimmune destruction of peripheral nervous system * Symmetric ascending paralysis ± dysautonomia * MCC – infections ## Footnote Usually sick a few weeks before

Question 135

Guillain-Barre syndrome (GBS) * What is the course?

Answer 135

* Worsen over 2 weeks * Plateau 2 to 4 weeks * Gradual recovery

Question 136

Answer 136

Question 137

Guillain-Barré syndrome (GBS) * What is the supportive care? (2) * What type of support?

Answer 137

Supportive care * Close respiratory monitoring – hospitalization * Monitor for bowel and bladder dysfunction ± Ventilatory support

Question 138

Guillain-Barré syndrome (GBS) * What do you need to monitor? (2) * What is the pain control?(2)

Answer 138

Autonomic dysfunction (20%) * Monitor BP and HR Pain control * Nociceptive and neuropathic pain common * Agents used for neuropathic pain highest efficacy

Question 139

Answer 139

Question 140

GBS treatment * What is the goal?

Answer 140

Disease Modifying Treatments * Decreases recovery time and ameliorate symptoms

Question 141

GBS treatment * What do you give? When do you start?

Answer 141

Intravenous Immune Globulin (IVIG) * Best if started within 2 weeks of symptom onset * 400mg/kg/day x 5 days or 2gm/kg/day x 2 days * Easier to administer with less complications than plasma exchange

Question 142

GBS treatment * What can you give besides IVIG? Best when? * What is not recommended?

Answer 142

Plasma exchange * Removes circulating immune complexes * Best when initiated within 7 days of symptom onset Corticosteroids not recommended

Question 143

Intravenous immune globulin * What is it? * Important to what? * What is it made out of?

Answer 143

Concentrate of pooled immunoglobulins obtained from healthy volunteers * Important to humoral immunity * 90% IgG

Question 144

Intravenous immune globulin * What are the indications? (3)

Answer 144

* Immunodeficiencies * Immunomodulation / anti-inflammatory therapy * Hyperimmune therapy against specific infectious agents

Question 145

Intravenous immune globulin * What is the MOA? * How is it administered? * What are the SE? What can help?

Answer 145

MOA: Various effects on the inflammatory cascade and mediation of the immune system Administration: IV or subcutaneously Adverse effects: * Infusion reactions * Slow titration recommend * Premedication helpful (acetaminophen, diphenhydramine) * Aseptic meningitis (HA after IVIG-> give dethamethasome)

Question 146

distal symmetric polyneuropathy (DSPN) * Synonymous with the term what? * What loss? * What experience?

Answer 146

Synonymous with the term “diabetic neuropathy” * Sensory loss * 15 to 20% of patients experience pain

Question 147

distal symmetric polyneuropathy (DSPN) * What is the prevention/progession control? (3)

Answer 147

* Glycemic control * Metabolic syndrome control * Foot care – daily inspection

Question 148

Diabetic neuropathy treatments * What should you control? * What are the initial therapies? (4)

Answer 148

Question 149

Diabetic neuropathy treatments * Guideline recommneds what? * Specific agent used determined by what? * What is second line?

Answer 149

* Guideline recommendations support either gabapentinoids, SNRIs, or TCAs(not first line) as first line * Specific agent used determined by comorbidities, costs, drug interactions, side effect profile * **TCAs generally second-line in most patients due to worse side effect profile**

Question 150

Answer 150