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ABIM 2015 > ABIM 2015 - Neuro > Flashcards

ABIM 2015 - Neuro Flashcards

0
Q

What 2 medication types are associated with increased risk of migraine progression causing Medication Overuse Headache?

A
  • Opiates (>8 days/month)

- Barbiturates (>5 days/month)

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1
Q

Episodes of brief, electrical shooting pain to the forehead, cheeks, jaw/chin triggered by talking, chewing, touching, brushing teeth in Pts >40 yo 1. Dx? 2. How do you Dx? 3. Rx?

A
  1. Trigeminal Neuralgia
  2. Must r/o other causes by MRI
  3. Carbamazepine (1st line) or combo (at least 3 drugs or combos before considering surgery
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2
Q

Unilateral throbbing headache uncommon in those >80 yo with +/- photophobia, phonophobia, nausea with visual changes (30%), unilateral numbness, tingling (face, UEs), dizziness, changes in thinking & speech?

A

Migraine headache +/- aura

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3
Q

CSF >250 mm H2O, papilledema, woman of child-bearing age, obese, no obstruction/lesion on brain imaging but c/o headache, visual Sx (diplopia, enlarging blind spot), tinnitus, normal CSF or mildly decreased protein, CN VI palsy (abducens nerve-lateral rectus)1. Dx? 2. Tx?

A
  1. Idiopathic Intracranial Hypertension (IIH) or “Pseudotumor Cerebri)
  2. Preg: serial LPs; Acetazolamide (diuretic - stones, paraesthesias, drowsiness); wt-reduction; surgical shunting or “optic nerve fenestration”
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4
Q

What agents are used to Rx patients with headaches caused by vasoconstriction?

A

Ca - channel blockers (verapamil); steroids (short-term, high-dose); IV-magnesium (eclampsia/pre-eclampsia)

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5
Q

Global, vague headache in older patient associated with malaise and fatigue?

A

Temporal (giant cell) arteritis.

-Check ESR (>80, normal or low); CRP (>2.45)

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6
Q

What study should be done when suspecting either SAH (sub-arachnoid hemorrhage), meningoencephalitis, meningeal carcinomatosis, inteacranial HTN or decreased pressure & CT was normal?

A

LP for CSF evaluation (xanthochromia, cytology, etc.)

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7
Q

Headache seen in elderly (>63 yo), moderate, throbbing, unilateral/bilateral, awake from sleep, can last 15min - 3 hours, associated with REM sleep cycle. 1. Dx? 2. Rx?

A
  1. Hypnic headache.

2. Indomethacin (NSAID); lithium; verapamil; can also try coffee and methylsergides

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8
Q

A persistent, UNILATERAL headache that lasts >3 months, occurs daily with possible lacrimation, ptosis/miosis, rhinorrhea/sinusitis. 1. Dx? 2. Rx?

A
  1. Hemicrania continua

2. Indomethacin (NSAID)

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9
Q
  1. What must you do to diagnose a headache with RED FLAG symptoms with suspected aneurysm? 2. What if there is no SAH (Sub Arachnoid Hemorrhage) but an aneurysm is suspected?
A
  1. CT brain and an LP - if positive for SAH - emergent neurosurgery consult.
  2. If no SAH but positive evidence for aneurysm - CTA or MRA
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10
Q

In what type of headache do neurological Sx last >1 hour?

A

Secondary headache (defined by an underlying disorder rather than by symptoms)

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11
Q

What is the most common headache type seen at a PMD’s office or ER?

A

A migraine headache (primary HA) - 90%

Tension HA (5%)
Cluster HA (5%)
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12
Q

What is required to establish brain death?

A

A POSITIVE apnea test:

  1. Nasal cannula with 100% O2 while vent is disconnected.
  2. Measure PO2, PCO2, pH after 10 minutes of observation (ABG).
  3. If PCO2 >60 mmHg OR >20 mmHg over baseline normal PCO2 (35-45 mmHg), the test is positive.
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13
Q

Would you use Aspirin AND Clopidrogrel vs. Aspirin OR Clopidrogrel for secondary prevention of stroke?

A

Use EITHER Aspirin OR Clopidrogrel as the use of both together shows no added benefit and does show an increased risk of bleeding.

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14
Q

What is the best neuroimaging modality for a secondary HA caused by suspected skull fracture, subarachnoid/intracerebral hemorrhage or paranasal sinus disease?

A

CT Head

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15
Q

Neuroimaging modality sensitive for intracranial pathology

A

MRI brain

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16
Q

What’s the next step for a pt suspected of having SAH with normal CT; suspecting meningoencephalitis; meningeal carcinomatosis; disorders of cranial hypertension or hypotension?

A

LP for CSF

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17
Q

What is a KEY physical examination component in pts with headache?

A

CN assessment

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18
Q

In a case of cervical trauma, a pt presents with Horner syndrome, what should you suspect if you’re not suspecting a hilar lung mass?

A

Dissection of internal carotid or vertebral artery.

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19
Q

Fertile, overweight female with symptoms of headache, visual changes (diplopia, blurring, CN IV palsy), tinnitus.

A

Idiopathic Intracranial Hypertension (IIH) also known as Pseudotumor Cerebri or Benign Inteacranial Hypertension.

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20
Q

What is considered NORMAL CSF opening pressure?

A

60 mmHg to 250 mmHg

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21
Q

How is IIH (Idiopathic Intracranial HTN) treated?

A 
•If pregnant: serial LPs,
Acetazolamide
•If resistant to medical treatment:
-Surgical shunting
-Optic Nerve fenestration
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22
Q
  1. Pt >40 with unilateral brief episodes of shooting pain in 2nd (maxillary) and 3rd (mandibular) divisions of trigeminal nerve?
  2. Required test?
  3. Therapy?
A
  1. Trigeminal neuralgia.
  2. MRI of brain WITH contrast.
  3. Carbamazepine or oxcarbazepine.
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23
Q

When should a pt with trigeminal neuralgia be considered for surgical decompression (rhizotomy or microvascular decompression)?

A

Only after having tried 3 (THREE) drugs or drug combinations. (Carbamazepine or oxcarbazepine with baclofen, gabapentin, clonazepam or lamotrigine).

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24
Q

What is considered first-line therapy for acute migraine?

A

Triptans (subcutaneous sumatriptan is the fastest and most efficacious however contraindicated in pts with vascular disorders, uncontrolled HTN and hemiplegic or basilar migraines.

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25
Q

What is a migraine headache called when it extends beyond 72 hours?

A

Status migranosus

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26
Q

What are the only effective meds for chronic migraine prophylaxis? (5)

A
  1. Propranolol/Timolol (b-blockers)
  2. Amitriptyline
  3. Divalproex Sodium
  4. Topiramate (can cause kidney stones, contraindicated in stones)
  5. Botulinum toxin A
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27
Q

Which are the only oral contraceptives that women with migraines (esp. w/aura) should use?

A

PROGESTIN-ONLY otherwise HIGH risk of stroke!

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28
Q

What are the PREGNANCY-SAFE (Category-B) migraine meds?

A

Acetaminophen, metoclopramide, certain opiates and NSAIDS (but only UNTIL 32 weeks - risk of patent ductus arteriosus “PDA” after that)

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29
Q

In which HA type is caffeine ok to use and in which is it not?

A

Tension HA - caffeine ok.

Migraine HA - caffeine not ok

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30
Q

This HA is B/L, steady and is only mild to moderately painful. It can last from 30 min to 7 days, has no features of photophobia, phonophobia, nausea or vomiting?

A

Tension HA

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31
Q

What is used to Rx tension HA’s!

A

Aspirin + Acetaminophen + Caffeine

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32
Q

How important are MRI and CT in evaluating a chronic headache in a patient?

A

Not important, less than (<1%) diagnostic yield.

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33
Q

What is the best and cheapest treatment of neuropathic pain?

A

TCA’s (amitriptyline, nortriptyline) rather than pregabalin (lyrica).

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34
Q

What is the preferred NSAID for PRIMARY (symptom-defined) headache treatment?

A

INDOMETHACIN

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35
Q

Cerebral aneurysm is suspected, what do you do first?

A

CT/LP

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36
Q

CT/LP positive for SAH, what’s the next step?

A

Consult neurosurgery for intervention (craniotomy, etc.)

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37
Q

CT/LP not diagnostic for SAH but high suspicion remains, what’s the next step?

A

MRA or CTA

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38
Q

Red flags for SECONDARY HA but no SAH suspected, what’s the study of choice?

A

MRI (if neg., try MRA/MRV, LP, check ESR/CRP

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39
Q

Red Flags of SECONDARY HA present but NOT typical for episodic migraine AND occur >15 days/month AND last >4 hours?

A

CHRONIC migraine, CHRONIC tension, hemicrania continua.

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40
Q

Red Flags of SECONDARY HA present but NOT typical for episodic migraine AND occur <15 days/month AND last >4 hours?

A

CHRONIC cluster, CHRONIC paroxysmal hemicrania, SUNCT syndrome, hypnic HA.

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41
Q

Red Flags of SECONDARY HA present but NOT typical for episodic migraine AND occur <15 days/month.

A

EPISODIC cluster, EPISODIC tension.

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42
Q

When is contrast needed on an imaging study such as CT or MRI?

A

When evaluating for malignant or inflammatory disease.

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43
Q

New global and vague headache in older person associated with malaise and fatigue with elevated ESR/CRP.

A

GCA (Giant Cell Arteritis) “temporal arteritis”

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44
Q

HA with ipsilateral Horner syndrome.

A

Internal Carotid Artery or Vertebral Artery dissection.

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45
Q

What is the danger with Reversible Cerebral Vasoconstriction Syndrome (RCVS) “recurrent thunderclap headaches.”

A

Acute Infarction (54%) during episode.

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46
Q

Reversible Cerebral Vasoconstriction Syndrome (RCVS) resolves in how long?

A

12 WEEKS

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47
Q

How is Reversible Cerebral Vasoconstriction Syndrome (RCVS) treated in order to prevent the associated moderate risk of acute infarction?

A

Calcium channel blockers (verapamil or nimodipine), short-term high-dose steroids and IV magnesium (eclampsia and preeclampsia).

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48
Q

PRIMARY HA generally respond to what treatments?

A

Indomethacin (NSAID) and ß-blockers.

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49
Q

Fertile overweight woman with headache, papilledema, visual disturbances (blurring, diplopia) and tinnitus, no mass found on imaging and no obstruction to CSF flow?

A

Idiopathic Intracranial Hypertension (IIH)

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50
Q

What cranial nerve palsy is associated with IIH that causes diplopia, convergence disorder due to the inability to abduct the eye?

A

CN VI (abducens nerve)

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51
Q

Polycystic ovarian syndrome, pregnancy, steroid withdrawal, and hypervitaminosis A can all result in this type of headache.

A

Intracranial hypertension

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52
Q

What is the treatment of choice of IIH on pregnancy?

A

Serial Lumbar Punctures

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53
Q

What medication is routinely used for treating IIH in non-pregnant patients? Why is the pain complication with this drug?

A
  1. Acetazolamide

2. Kidney stones

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54
Q

When trigeminal neuralgia is diagnosed in those >40 (90%) it is caused by? When diagnosed in younger patients?

A
  1. Focal demyelination by vascular compression of the trigeminal root entry zone into the skull at the pons.
  2. Multiple sclerosis.
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55
Q

What test must be done in a patient who presents with signs of trigeminal neuralgia?

A

MRI of the brain with contrast

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56
Q

A headache that is typically UNILATERAL and lasts from 4-72 hours, pulsating and aggravated by walking is what type of headache?

A

Migraine headache

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57
Q

What is present in up to 80% of chronic migraine headache sufferers?

A

Medication overuse headache (opiates and barbiturates)

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58
Q

That are the three (3) types of medications used to treat migraines?

A
  1. NSAIDS
  2. Ergotamines
  3. Triptans
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59
Q

What medication class is contraindicated for migraine treatment in patients with vascular disorders, uncontrolled HTN and hemiplegic migraine subtype?

A

Triptans

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60
Q

What is a migraine attack called that lasts over 72 hours?

A

Status migranosus

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61
Q

How do you treat status migranosus?

A

IV NSAIDS (ketorolac) & valproic acid + dexamethasone or IV ergotamine

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62
Q

Criteria needed for migraine HA prophylaxis

A
  1. HA more than 2 days/week
  2. Impaired lifestyle
  3. Prolonged aura/migraine-induced stroke
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63
Q

What are the general migraine HA prophylaxis agents?

A

ß-blockers, antidepressants, anticonvulsants, ca-channel blockers, NSAIDS

PROPRANOLOL, TIMOLOL, AMITRIPTYLINE, DIVALPROEX SODIUM, TOPIRAMATE (kidney stones)

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64
Q

Why must FIRST be done in pt with migraine HAs prior to starting prophylaxis?

A

Ensure that they have avoided use of ACUTE HA MEDICATIONS FOR MORE THAN 10 DAYS PER MONTH (analgesics, decongestants, stimulants). THIS IS CRITICAL

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65
Q

Should women with migraines use COMBINED (ESTROGEN/progesterone) oral contraceptives?

A

NO!!! 2-4 X risk of STROKE, especially in women with AURA

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66
Q

When can Triptans be used for migraines in PREGNANCY?

A

ONLY when benefit OUTWEIGHS risk (stroke)

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67
Q

Up to what week can NSAIDS be used in PREGNANCY and why?

A

Up to 32 WEEKS ONLY due to risk of PATENT DUCTUS ARTERIOSUS after that.

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68
Q

What are the safe meds to use in migraine HAs during pregnancy?

A

Magnesium, acetaminophen, metoclopramide, opiates, prednisone, [NSAIDS (ONLY UP TO 32 WEEKS!!!)]

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69
Q

In what single way is the treatment of perimenopausal migraine HAs different?

A

Ok to use hormone replacement therapy

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70
Q

What is different about migraine HAs with AURA than those without?

A
  1. They develop within 1 HOUR of AURA onset
  2. Develop over a MINIMUM of 5 MINUTES
  3. They last a MAXIMUM of 60 MINUTES
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71
Q

BILATERAL mild to moderate pain HA like a band, squeezing on the head, with possible scalp tenderness and cervical soreness, can last from 30 MINUTES to 7 DAYS.

A

Tension HA

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72
Q

UNILATERAL HA, with N/V, visual changes, moderate to severe pain.

A

Migraine HA

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73
Q

What are the common triggers of a tension HA (HAs don’t develop nocturnally)?

A

Stress and sleep disruption

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74
Q

When should you do a brain MRI if suspecting a tension HA?

A

If the CHRONIC (>15 days/month) NOT the episodic subtype.

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75
Q

How are TENSION HAs best treated?

A

Tylenol, NSAIDS (caffeine helps both of these)

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76
Q

Which HA types are antidepressants useful for?

A

MIGRAINE HAs

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77
Q

Exquisitely painful temporal or peri-orbital HA with ptosis, lacrimation, conjunctival injection, nasal congestion and rhinorrhea, can occur up to 8 times daily and last from15-180 min, can last weeks to months, is most common in men who are smokers and can be triggered by alcohol.

A

Cluster HA

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78
Q

This headache occurs usually within a few hours of falling asleep.

A

Cluster HA

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79
Q

How are cluster HAs treated acutely? (3 agents)

A

Inhaled oxygen, subcutaneous sumatriptan and intranasal zolmitriptan.

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80
Q

What is the only prophylactic treatment for cluster HAs?

A

Verapamil

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81
Q

Corticosteroids and an occipital nerve block are “transitional prophylactic” (short term use of fast-acting agents) for what HAs?

A

Cluster HAs

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82
Q

Cluster-like HA (episodes of piercing pain associated with conjunctival injection & tearing) however last only 15 minutes and can reoccur 8-40 times per day and responds to NSAIDS (INDOMETHACIN)

A

Chronic Paroxysmal Hemicrania

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83
Q

Cluster-like HA (episodes of piercing pain associated with conjunctival injection & tearing) that last only about 60 seconds and recur 1-30 times per HOUR and may respond to lamotrigine?

A

SUNCT (Short-lasting, Unilateral Neuralgiform headache with Conjunctival injection and Tearing)

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84
Q

What is the study of choice for ACUTE moderate to severe traumatic brain injury?

A

CT with bone windows (looking for skull fracture)

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85
Q

Imaging study of choice for mild traumatic brain injury but with CHRONIC symptoms (no imaging study recommended for mild - 90% of such injuries)?

A

MRI brain

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86
Q

What test MUST be administered to all suspected MODERATE - to - SEVERE traumatic brain injury patients?

A

Glasgow Coma Scale

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87
Q

What are the THREE (3) main categories in the Glasgow Coma Scale?

A
  1. Eye-Opening Response (1-4)
  2. Verbal Response (1-5)
  3. Motor Response (1-6)

≤8 (severe)
9-12 (moderate)
13-15 (mild)

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88
Q

What is DECORTICATE posturing?

A

FLEXION in response to pain (better than decerebrate)

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89
Q

What is DECEREBRATE posturing?

A

EXTENSION in response to pain (worse than decorticate)

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90
Q

Head injury causing transient confusion without amnesia or loss of consciousness and resolves completely within 15 min.

A

Grade 1 CONCUSSION

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91
Q

Head injury causing a transient confusion without loss of consciousness but with a period of AMNESIA and AMS lasting >15 min.

A

Grade 2 CONCUSSION

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92
Q

Head injury associated with a BRIEF (seconds) or PROLONGED (minutes) loss of consciousness.

A

Grade 3 CONCUSSION

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93
Q

When do concussions require CT or MRI imaging!

A

When they are grade 2 or 3 concussions with persistent abnormalities in examination (cognition, vision, coordination) or symptoms lasting >1 week.

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94
Q

When can athletes with a GRADE 1 CONCUSSION return to play?

A
  1. If ALL symptoms clear within 15 min, can return ON THE SAME DAY.
  2. If they suffer a 2nd GRADE 1 CONCUSSION on the same day, then only after asymptomatic for 1 week.
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95
Q

When can athletes with a GRADE 2 CONCUSSION return to play?

A
  1. If asymptomatic for 1 week and normal neuro exam.

2. If they suffer a 2nd GRADE 2 concussion and then only If asymptomatic for 2 weeks and normal neuro exam.

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96
Q

When can athletes with a GRADE 3 CONCUSSION return to play?

A
  1. If BRIEF GRADE 3 CONCUSSION, after asymptomatic for 1 week.
  2. If PROLONGED GRADE 3 CONCUSSION, after asymptomatic and normal neuroimaging after 2 weeks.
  3. If SECOND occurrence, if asymptomatic and normal neuroimaging after 4 weeks.
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97
Q

When does a GRADE 3 CONCUSSION not require neuroimaging?

A

When BRIEF and examination findings are normal WITHOUT persistent symptoms after 1 week or abnormalities on neuro exam.

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98
Q

Pain in the head and neck with possible vertigo or imbalance, cognitive, psychological and sleep disturbances that occurs WITHIN 2 WEEKS of a head injury (closed injury or whiplash)

A

Postconcussion Syndrome (PCS)

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99
Q

How is Posconcussion Syndrome (PCS) treated?

A

SUPPORTIVE measures

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100
Q

Direct head injury causing fracture of the TEMPORAL bone and laceration of the MIDDLE MENINGEAL ARTERY with symptoms of HA, AMS, ipsilateral pupillary dilation and rapid neurological decline is caused by? Tx?

A
  1. Epidural hematoma

2. Immediate surgical evacuation.

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101
Q

Because military personnel have a higher incidence of this condition than civilians, congress has mandated that all military personnel returning from combat be screened for this?

A

Effects of TBI (Traumatic Brain Injury) such as concussion (10% - 20% incidence) and PCS (Postconcussion Syndrome), a syndrome with HA, Neurological and Psychological symptoms.

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102
Q

What is REQUIRED to diagnose Epilepsy?

A

TWO (2) or more UNPROVOKED seizures

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103
Q

Generally, in children and adults over 65, fever, infection, intoxication, drug use or withdrawal, metabolic derangements, sleep deprivation or an acute neurological insult can provoke what?

A

Seizures

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104
Q

What MUST be done for treatment immediately following a seizure?

A

Stabilizing the patient (airway, vitals, offending cause)

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105
Q

In a pt with a seizure, without known seizure history and no available blood glucose level, what must be given?

A

THIAMINE & GLUCOSE

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106
Q

What condition can mimic a seizure?

A

Syncope with convulsions (Convulsive syncope) which can occur in 5% - 10% of pts with cardiogenic or vasovagal syncope.

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107
Q

Family H/O, childhood febrile convulsions, trauma with LOC, CNS infection, brain lesions, prenatal/birth injuries are all RISK factors for?

A

EPILEPSY

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108
Q

What is REQUIRED in ALL pts with a FIRST seizure, abnormal neurologic examination or a partial seizure (affects only one hemisphere with or without LOC)?

A

NEUROIMAGING

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109
Q

What MUST be done in a patient with a seizure in the setting of FEVER, HA, STIFF NECK or AMS (altered mental status)?

A

Lumbar Puncture

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110
Q

What MUST be done in ALL immunocompromised pts with a FIRST seizure?

A

Brain MRI and a LUMBAR PUNCTURE.

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111
Q

How long do epileptic seizures generally last?

A

1-2 min

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112
Q

An aura of lightheadedness and swearing usually indicates what event to come?

A

Syncope

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113
Q

Can you experience incontinence with a TIA, MIGRAINE or VERTIGO?

A

NO

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114
Q

Confusion and Fatigue are usually experienced after which two neurological events?

A

SEIZURES and MIGRAINES (not so after syncope, TIA or vertigo)

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115
Q

Can a person who has had a seizure (single ever, multiple, epilepsy) drive?

A

NO (variable state to state)

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116
Q

What are the three types of partial seizures?

A
  1. Simple
  2. Complex
  3. Secondarily generalized
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117
Q

A focal seizure that DOES NOT IMPAIR AWARENESS?

A

SIMPLE PARTIAL seizure

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118
Q

A seizure that ALTERS CONSCIOUSNESS when spreads to involve one or both temporal lobes?

A

COMPLEX PARTIAL seizure.

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119
Q

What is a seizure called when it spreads to involve BOTH HEMISPHERES diffusely with a generalized convulsion?

A

SECONDARILY GENERALIZED seizure

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120
Q

What is a seizure called when it affects the SENSORY not motor CORTEX with no outward manifestations (no motor involvement)?

A

Epileptic Aura

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121
Q

What part of the brain do most common epileptic auras originate from?

A

Temporal Lobe (epigastric sensations, déjà vu, intense fear)

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122
Q

How long do complex partial seizures last!

A

1-2 minutes with confusion lasting 5-10 min

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123
Q

Blank stare, automatisms (lip smacking, repetitive swallowing, fumbling of the hands) occur in what type of seizures?

A

Complex partial seizures (alteration of consciousness but no tonic-clonic event)

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124
Q

Convulsions that begin as partial seizures, cause impaired awareness, diffuse muscle contraction (tonic) and rhythmic jerking of all limbs (clonic) followed by urinary incontinence and tongue biting and resolve within 1-2 minutes with postictal confusion lasting 10-15 min?

A

Secondarily generalized tonic-clonic seizure

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125
Q

These seizures involve BOTH hemispheres at onset, occur without warning. Example?

A
  1. Primary generalized tonic-clonic seizure.

2. Absence seizure (<5 sec)

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126
Q

What population is generally affected by Absence seizures (a primary generalized seizure)?

A

Children and it typically resolves by puberty

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127
Q

What are the two types of Epilepsy and how do they present? What is seen on MRI?

A
  1. Temporal lobe epilepsy (focal) - complex, partial seizures with epigastric and psychic auras
  2. Idiopathic generalized epilepsy - EEG shows generalized spike-wave activity
  3. Hippocampal atrophy
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128
Q

A type of epilepsy found in adults that is part of idiopathic generalized epilepsy and presents with “jitteriness” where pts drop things and have muscle jerks.

A

Juvenile Myoclonic Epilepsy

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129
Q

How long is medical therapy usually recommended for pts with juvenile Myoclonic epilepsy to prevent future convulsions?

A

LIFE-LONG

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130
Q

What two mood disorders are seen more commonly in pts with epilepsy?

A

MAJOR DEPRESSIVE DISORDER

BIPOLAR DISORDER

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131
Q

Anti-Epilepsy Drugs can put epileptic pts at risk for what two conditions?

A

SUICIDALITY

OSTEOPOROSIS

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132
Q

INITIAL study of choice for pt with new-onset seizure?

A

Head CT

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133
Q

What is most important in diagnosis of epilepsy besides a positive MRI and EEG?

A

Patient’s CLINICAL HISTORY

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134
Q

What must be done in patients with epilepsy who don’t respond to Anti-Epilepsy Drugs (AED) and prior to considering neurosurgery?

A

Inpatient Epilepsy monitoring unit admission (continuous EEG 2-7 days, off meds)

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135
Q

What are pseudoseizures? Who are they most common in?

A

Non-epileptic seizures, common in women with h/o child abuse.

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136
Q

In what patients SHOULD you start Anti-Seizure Drugs after ONY ONE seizure occurrence?

A

Pts >65 yrs old
Pts with SIGNIFICANT h/o heat TRAUMA
Pts with FOCAL SEIZURE

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137
Q

When MUST anti-seizure drugs be started regardless of EEG, MRI, age or other findings?

A

After SECOND UNPROVOKED seizure

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138
Q

BEFORE starting PHENYTOIN, PHENOBARBITAL, CARBAMAZEPINE, OXCARBAZEPINE or LAMOTRIGINE in these pts, what must be considered and why?

A

ASIANS with HLA-B*1502 allele (genetic testing)

Because at higher risk for Stevens-Johnson syndrome

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139
Q

What is the danger with TOPIRAMATE?

A

Renal stones, Glaucoma, Metabolic Acidosis, Heat Stroke, Birth Defects

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140
Q

GENERALIZED Epilepsy is treated with what four agents?

A

Lamotrigine, Leviracetam, Valproic Acid, Topiramate

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141
Q

This anticonvulsant exacerbates Polycystic Ovary Syndrome, causes Birth Defects, Weight Gain and Hirsutism?

A

Valproic Acid

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142
Q

Which are the two (2) safest seizure drugs during pregnancy?

A

Lamotrigine, Carbamazepine

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143
Q

These five (5) seizure drugs inactivate OCPs?

A

Carbamazepine, Oxcarbazepine, Lamotrigine, Phenytoin, Topiramate

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144
Q

Cleft Palate is most often seen with this anti-seizure drug?

A

Topiramate

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145
Q

What supplement should ALL women with epilepsy take if planning pregnancy?

A

Folic Acid

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146
Q

When is it appropriate to attempt weaning a pt off anti-seizure drugs?

A

When seizure-free 2-4 years (30%-40% risk of recurrence)

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147
Q

When is epilepsy considered refractory and what can be done?

A

After failing to control seizures with two drugs. Referral to epilepsy center to assess candidacy for surgery

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148
Q

Can hemorrhagic stroke be differentiated from ischemic stroke on clinical exam?

A

NO

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149
Q

Best INITIAl test to assess for hemorrhagic stroke?

A

Head CT WITHOUT contrast

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150
Q

Gold standard for diagnosis of cerebral vasculature?

A

CT angiography (can’t do in pts with renal disease)

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151
Q

A neurologic emergency with high SHORT-TERM risk of subsequent stroke?

A

TIA

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152
Q

When after a TIA is a pt at the HIGHEST risk for stroke?

A

48 hours after TIA

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153
Q

Who should be admitted after a TIA?

A

Pts who score a 3 or higher on ABCD2 (Age Blood pressure, Clinical presentation, Duration of symptoms and presence of Diabetes) or a score less than 3 with visual loss

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154
Q

A TIA causing transient visual loss usually indicates what?

A

Extracranial Internal Carotid Artery (ICA) stenosis

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156
Q

Does absence of a lesion on CT exclude the diagnosis of ischemic stroke?

A

NO!

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157
Q
  1. The greatest risk for stroke in a pt with large artery atherosclerosis is when the stenosis (ICA) is? 2. The risk of recurrent stroke in such a patient is greatest when? 3. Above what BP?
A
  1. > 70%
  2. Within the first 2 weeks.
  3. > 140/80 mmHg
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158
Q

Hypertension causes what type of infarcts most often?

A

Lacunar (pure motor hemiparesis, pure sensory stroke).

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159
Q

What is intra-cranial hemorrhage (ICH) most commonly caused by?

A

HTN

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160
Q

Why must REPEAT imaging be done and when, for patients with hemorrhagic stroke?

A

Because hemorrhage may obscure an underlying tumor, it must be repeated 4-6 weeks after event.

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161
Q

What single lab is CRITICAL to determine in an acute stroke evaluation.

A

Blood Glucose (excludes mimics and hyperglycemia is associated with poor outcome after stroke)

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162
Q

What is the ONLY thing that rtPA does?

A

Improved FUNCTIONAL outcomes at 3 months, NOT with earlier neurological improvement or lower mortality

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163
Q

What should be done with ALL patients after receiving rtPA therapy?

A

Admitted for observation for 24 hours in ICU setting.

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164
Q

When are surgical procedures and anticoagulation therapies ok after pt receives rtPA?

A

AFTER 24 hours of being monitored.

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165
Q

What therapy besides rtPA is specifically recommended for ISCHEMIC stroke involving the Middle Cerebral Artery up to 6 HOURS after event?

A

Intra-Arterial Thrombolysis

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166
Q

In a patient with ischemic stroke, when using rtPA, what should the BP be kept under? What if no rtPA was used?

A
  1. rtPA used: <220/120 mm Hg
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167
Q

In order to achieve a high BP in pts with ischemic stroke and myocardial ischemia or heart failure is it ok to withhold antihypertensive agents?

A

NO

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168
Q

What antithrombotic agent has shown to improve short-term mortality and recurrence of stroke when used within 48 hours of ishchemic stroke onset?

A

ASPIRIN Alone

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169
Q

What agent can ischemic stroke patients benefit from if their stroke was caused by a-fib after cardiac surgery, mechanical heart valve or an arterial dissection?

A

Heparin

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170
Q

Seizure at stroke onset, ANY previous history of hemorrhagic stroke, major surgery within the last 2 weeks, arterial puncture at non-compressible site within past 7 days, recent systemic hemorrhage and coagulopathy are what?

A

ABSOLUTE contraindications to use of rtPA for treatment of ischemic stroke.

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171
Q

What two agent can be used to achieve the desired blood pressure for patients about to undergo rtPA therapy? (<185/110 mmHg)

A

IV labetalol or nicardipine ONLY (DO NOT USE nitroglycerine or nitroprusside)

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172
Q

In what type of stroke do you WANT to lower blood pressure?

A

Hemorrhagic stroke ONLY

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173
Q

What is the ideal blood pressure target for a patient with hemorrhagic stroke?

A

<160/90 mmHg

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174
Q

What is the immediate danger with hemorrhagic stroke?

A

Herniation (hematoma/edema)

175
Q

What immediate steps must be taken for stabilization of a pt with ICH PRIOR to surgical decompression?

A

Intubation AND short-term HYPERventilation AND osmotherapy with MANITO or HYPERtonic Saline

176
Q

What are the FOUR (4) most common risk factors for ICH (subarachnoid and otherwise)?

A

HYPERTENSION, tobacco, cocaine, avm’s.

177
Q

SEVERE HA with change in MS (alertness, consciousness)

A

SAH

178
Q

What agent is used to prevent vasospasm (causing expansion of stroke) post hemorrhagic stroke (ICH)?

A

Nimodipine

179
Q

How is further cerebral ischemia prevented post hemorrhagic stroke?

A

Vasopressors to elevate the Mean Arterial Pressure once no further bleeding is established.

180
Q

HA with ocular engorgement, affecting CN III, IV, V (V1, V2) and sometimes VI?

A

Cavernous sinus thrombosis (venous stroke)

181
Q

What are the risk factors for Cavernous Sinus Thrombosis?

A

Systemic Inflammatory Disease, Malignancy, Trauma, Dehydration/Infection, Pregnancy.

182
Q

What are the two imaging modalities of choice for cavernous sinus thrombosis?

A

CT WITH contrast and MRI Venography

183
Q

Whether in the setting of ICH or not, what are the treatments of choice for cavernous venous thrombosis?

A

Heparin IV followed by WARFARIN for 6 months.

184
Q

Head/neck pain with partial HORNER’s syndrome (no anhidrosis)?

A

Possible carotid or vertebral artery DISSECTION.

185
Q

Best imaging modality for carotid/vertebral artery dissection?

A

MRI of the soft tissues of the neck

186
Q

Treatment of carotid/vertebral artery dissection?

A

IV heparin followed by 3-6 months of po WARFARIN

187
Q

When must an ASYMPTOMATIC cerebral aneurysm be intervened on?

A

If in ANTERIOR circulation, when >12 mm; if in POSTERIOR circulation, when >7 mm. Otherwise, WATCHFUL WAITING

188
Q

What is the ONLY neurosurgical intervention known to REDUCE MORTALITY at 1 year extending to 10 years post stroke?

A

Admission to a STROKE UNIT/CENTER

189
Q

Recurrence of strokes is greatest in patients with BP above?

A

> 140/80 mmHg

190
Q

What are the KEY modifiable risk factors in stroke (3)?

A

HTN, hyperlipidemia and tobacco use.

191
Q

What agents are preferred in stroke patients who have intracranial atherosclerosis? Why?

A
  1. ANTI-PLATELET agents (ASPIRIN, CLOPIDOGREL) 2. Because of mortality associated with WARFARIN in these patients.
192
Q

Best agent to use for stroke prevention in patients with previous stroke (ischemic or ICH, however NOT ICH due to amyloid)?

A

Warfarin/Dabigatran

193
Q

Best agent to use for stroke prevention in patients with previous stroke AND ATRIAL FIBRILLATION who CANNOT tolerate warfarin/dabigatran?

A

ASPIRIN (325 mg) or asa+clopidogrel

194
Q

Best agent to use for stroke prevention in patients with previous stroke WIHOUT a-fib who CANNOT tolerate warfarin/dabigatran?

A

ASPIRIN (81 mg)

195
Q

What is the preferred agent for subsequent stroke prevention in patients with PERIPHERAL ARTERY DISEASE?

A

CLOPIDOGREL (plavix)

196
Q

What do you treat a pt with for whom aspirin and optimal risk factor management did not prevent recurrent stroke?

A

Clopidogrel OR ASPIRIN + DIPYRIDAMOLE

197
Q

When is ASPIRIN + CLOPIDOGREL used together in stroke prevention?

A

In patients who had cardioEMBOLIC stroke (not a-fib), have vascular stents or previous h/o MI.

198
Q

What are the two interventions of choice (equivalent) for pt’s with SYMPTOMATIC ICA stenosis >70% and why?

A

Internal Carotid Endarterectomy or Angioplasty with Stenting, because risk of 2-year recurrent stroke with SYMPTOMATIC ICA stenosis >70% is >26%

199
Q

What is the preferred intervention for MCA (middle cerebral artery infarction) affecting >50% of its territory?

A

Hemicraniectomy within 48 HOURS

200
Q

What is the current recommendation for Patent Foramen Ovale as it is a risk for Ischemic Stroke in young people?

A

Aspirin OR Warfarin, NOT CLOSURE.

201
Q

Best chance for optimal functional recovery after stroke?

A

INTENSIVE REHABILITATION

202
Q

What is the STRONGEST predictor of long-term disability after stroke?

A

SEVERITY of INITIAL neurologic deficit.

203
Q

What is the major risk factor for dementia?

A

Aging

204
Q

What can be a precursor to dementia, presenting as a loss of cognitive ability that exceeds the age-related memory loss but does not interfere significantly with daily activities?

A

Mild Cognitive Impairment (MCI) - progresses to probable Alzheimer’s disease at the rate of 10%-15% per year. DOES NOT interfere with occupational or social functioning.

205
Q

What score on a Mini Mental State Examination constitutes dementia?

A

A score of 22 or less.

206
Q

Besides PASSIVITY (sitting quietly while spouse speaks) what reflexes can be abnormal in dementia?

A

Grasp, rooting and snout reflex.

207
Q

What are the three most common types of dementia?

A

Alzheimer’s, Parkinson’s and Vascular

208
Q

A rapidly progressive dementia (weeks to months) is suggestive of what type of dementia?

A

Paraneoplastic or Crutzfeldt-Jakob disease.

209
Q

What lab not tested for routinely in the evaluation of dementia should be tested for when the dementia is rapidly progressive, age of onset is less than 60, there is systemic cancer, infection or inflammatory, autoimmune disease, immunosuppressed states or syphilis?

A

CSF

210
Q

What is the KEY pathologic agent in Alzheimer’s disease?

A

B-amyloid protein (its pathologic cleavage

211
Q

What chromosome is affected in Alzheimer’s dementia?

A

Chromosome 21

212
Q

In the setting of an acute ischemic stroke, what is the BEST medication to use?

A

Aspirin 160 mg

213
Q

In the setting of acute ischemic stroke due to post-cardiac surgery a-fib, prosthetic valve or dissection, what is the BEST medication to use?

A

Anticoagulant such as heparin

214
Q

What do lamotrigine, (lamotigine + valproic acid), carbamazepine, oxcarbazepine and phenytoin have in common?

A

They can all cause RASH, Steven Johnson’s Syndrome and Toxic Epidermal Necrolysis (TEN)

215
Q

What patients are must susceptible to the adverse effects (Steven Johnson’s and TEN rashes) from using phenytoin, carbamazepine, oxcarbazepine and lamotrigine?

A

ASIANS

216
Q

What do valproic acid, gapapentin and pregabalin all have in common?

A

Cause weight gain

217
Q

How does topiramate affect weight?

A

Causes anorexia

218
Q

What is the lifespan of a patient diagnosed with Alzheimer’s disease?

A

5-15 years

219
Q

Diffuse brain atrophy, widening of sulci, enlargement of ventricles?

A

Alzheimer’s disease

220
Q

Neurofibrillary tangles, amyloid-containing neuritic plaques and granulovacuolar degeneration of neurons?

A

Alzheimer’s disease

221
Q

What medications slow down the disease progression of Alzheimer’s disease?

A

NONE

222
Q

What are the effects of medications such as CHOLINESTERASE inhibitors DONEPEZIL, RIVASTIGMINE, TACRINE and GALANTAMINE?

A

Improve cognitive function

223
Q

What adjunct meds are there for Alzheimer’s disease (added to the cholinesterase inhibitors (donepezil, rivastigmine, tacrine and galantamine)?

A

Memantine, Vitamin E, Selegiline

224
Q

What meds are optimal for treating depression in Alzheimer’s patients?

A

SSRI’s

225
Q

PSychosis, paranoia, agitation and violent behavior in Alzheimer’s patients are treated with what?

A

Tranquilizers and sedatives

226
Q

What meds should be AVOIDED in Alzheimer’s disease?

A

Dopamine antagonists, anticholinergic drugs

227
Q

What is the second most common cause of dementia?

A

Lewy Body Dementia

228
Q

What dementia affects >80% of patients with Parkinson’s?

A

Lewy Body Dementia

229
Q

Cognitive impairment with psychiatric features, hallucinations and abnormal dream enactment behavior?

A

Lewy Body Dementia

230
Q

Eosinophilic Intracytplasmic Accumulations of Alpha-synuclein

A

Lewy Body Dementia

231
Q

How do you treat ewy Body Dementia?

A

As with Alzheimer’s Dementia - cholinesterase inhibitors

232
Q

What must you be careful of when prescribing the cholinesterase inhibitor TACRINE to an Alzheimer’s patient?

A

Monitor for HEPATIC TOXICITY

233
Q

Although all anti-epileptic drugs (AEDs) are teratogenic, which is most and which two are least?

A

MOST teratogenic: valproic acid (6-17%)

LEAST teratogenic: lamotrigine & carbamazepine

234
Q

What drugs and in what progression are used to treat status epilepticus?

A

Lorazepam, Phophenytoin (phenytoin can cause necrosis), Phenobarbital, Valproate, Propofol.

235
Q

What anti-epileptic drugs affect oral conreaceptive pills?

A

ALL of them

236
Q

Which anti-epileptic drugs are safe for breastfeeding?

A

ALL of them

237
Q

Dementia associated with significant behavioral deterioration such as disinhibition, impulsivity, obsession and loss of verbal fluency?

A

Frontotemporal Dementia (Pick’s Disease)

238
Q

Abnormal accumulation of TAU proteins in neurons or glia due to a mutation in the TAU protein on chromosome 17?

A

Frontotemporal Dementia (Pick’s Disease)

239
Q

What is typically seen on a head CT of a patient with Vascular Dementia?

A

Cerebral Ischemia (from previous stokes, etc.)

240
Q

The TRIAD of COGNITIVE DECLINE, GAIT IMPAIRMENT and URINARY INCONTINENCE in the setting of NORMAL CSF pressure is seen in?

A

Normal Pressure Hydrocephallus

241
Q

How do you treat Normal Pressure Hydrocephalus (NPH)?

A

Ventricular Shunt placement.

242
Q

Movement disorders involve the “ExtraPyramidal” motor control system at the center of which is a group of nuclei: substantial nigra, putamen, caudate, globes plaids, thalamus and the sub thalamic nucleus, all of which comprise the?

A

Basal Ganglia

243
Q

What is the MAJOR risk factor for Parkinson’s disease and what is the defect?

A

Aging, loss of dopamine.

244
Q

Brain trauma, use of well water, exposure to herbicides and pesticides as well as manganese toxicity as well as genetic inheritance (small) are associated with which movement disorder?

A

Parkinson’s disease

245
Q

LRRK2 gene mutation

A

Parkinson’s disease

246
Q

Tremor at REST, rigidity (cogwheel), bradykinesia, loss of postural reflexes, gait FREEZING?

A

Parkinson’s disease

247
Q

What is seen histologically in Parkinson’s disease?

A

Lewy Bodies

248
Q

Facial masking (expressionless) is seen in?

A

Parkinson’s disease

249
Q

What is the symmetry of Parkinson’s disease at onset?

A

Typically ASYMMETRIC

250
Q

What is the most dangerous motor impairment of Parkinson’s disease?

A

Loss of postural reflexes (postural instability) - causing falls, fractures, etc.

251
Q

What movement disorder can present early on with loss of olfactory function?

A

Parkinson’s disease

252
Q

What testing modality is indicated in diagnosing Parkinson’s disease?

A

Brain MRI

253
Q

Most effective drug to suppress motor effects of Parkinson’s disease?

A

Levodopa-Carbidopa (dopamine AGONIST)

254
Q

How long on average do levodopa (dopamine precursor) and dopamine agonists last before “wearing-off” episodes begin to occur? What is used then?

A

5 years, Amantadine (flu antiviral)

255
Q

Pts with rapidly progressing Parkinson’s disease WITHOUT tremor at rest, SYMMETRIC presentation and that do NOT respond to levodopa and with EARLY falling in their course indicates what?

A

Atypical Parkinson’s or “Parkinson’s-PLUS” syndrome

256
Q

How long do Parkinson’s-PLUS pts typically live?

A

8-12 years

257
Q

When is the “Pull Test” for Parkinson’s considered positive?

A

When the patient takes more than ONE step backward

258
Q

Most adult CHRONIC ataxia syndromes are caused by? Subacute? Acute?

A

Chronic: cerebellar degeneration (check B12 and Vit E)
Subacute: Prion disease, paraneoplastic syndrome
Acute: substance intoxication, stroke

259
Q

Most common INTENTION tremor, 50% familial?

A

Essential tremor

260
Q

What are the symmetries of Essential & Parkinson’s tremors?

A

Essential: bilateral; Parkinson’s unilateral

261
Q

What is used to treat Essential tremor?

A

Propranolol, primidone and Deep Brain Stimulator

262
Q

Adult with TREMOR & DEMENTIA with family history of mental retardation?

A

Fragile X syndrome

263
Q

Focal or generalized torsional, twisting movement disorder caused by stroke, tumor, infection, Parkinson’s, drugs, anoxic insult, birth injury or Wilson’s disease?

A

Dystonia

264
Q

Why must ALL persons with generalized dystonia be trialed on levodopa?

A

Because (rarely) they may have Dopamine-Responsive Dystonia

265
Q

How is Non Dopamine-Responsive Dystonia treated if Focal? Generalized?

A

Focal: Botulinum Toxin; Generalized: Baclofen or dopamine depleting drugs (reserpine)

266
Q

What part of the brain is affected in Dystonia?

A

Basal Ganglia

267
Q

Fatal progressive choreiform disorder affecting the caudate nucleus?

A

Huntington’s Chorea

268
Q

What type of meds are used in Huntington’s Chorea?

A

Dopamine-Depleting drugs (reserpine)

269
Q

What are most dopamine-blocking agents called and what can they cause?

A

Neuroleptics (tranquillizers); Tardive Dyskinesia

270
Q

What is the term for single, rapid, shock-like muscle jerks (like hiccups) which can be physiologic or caused focally by tumors or stroke? How do you treat?

A

Myoclonus; anti-convulsants (valproic acid, clonazepam)

271
Q

What is the best agent to use for acute dystonia?

A

Diphenhydramine

272
Q

What psychiatric diseases are Tourette’s syndrome associated with?

A

OCD and ADHD

273
Q

What meds are used to treat Tourette’s?

A

Alpha-agonists (Clonidine, Guanfacine); Clonazepam; Neuroleptics: Haldol, Risperidone, Olanzepine (can cause TD)

274
Q

Whom does Tourette’s syndrome affect mostly?

A

Males 3:1

275
Q

What is the ONLY reversible (non-iatrogenic) movement disorder that affects the Basal Ganglia if treated early?

A

Wilson’s Disease

276
Q

Young adult presenting with Parkinsonism?

A

Wilson’s Disease

277
Q

How is Wilson’s disease treated?

A

Copper-restricted diet, Copper chelators (penicillamine)

278
Q

How is Wilson’s disease cured?

A

Liver transplant

279
Q

Life threatening disorder manifesting as hyperthermia (>38ºC/>100.4ºF), tachycardia, diaphoresis, labile blood pressure, muscle rigidity or dystonia, elevated muscle enzyme levels (rhabdo w/renal injury) and delirium caused by neuroleptics/antipsychotics?

A

Neuroleptic Malignant Syndrome

280
Q

How is Neuroleptic Malignant Syndrome treated?

A

Discontinuation of offending drug and administration of Bromocriptine (dopamine agonist) & Dantrolene (muscle relaxant)

281
Q

Confusion, myoclonus, shivering, diaphoresis after administration of these drugs?

A

Serotonin Syndrome; OD on serotonergic meds or SSRI+MAOI

282
Q

Iron deficiency, uremia, peripheral neuropathy, DM, RA, pregnancy and fibromyalgia are associated with this dopamine-related, hereditary movement disorder?

A

Restless Leg Syndrome

283
Q

What are the first-line agents used in Restless Leg Syndrome?

A

Bromocriptine and Pramipexole (dopamine agonists)

284
Q

Most important test in diagnosing MS?

A

MRI WITH GADOLINIUM (to differentiate inflammatory MS lesions from non-MS lesions)

285
Q

CNS demyelinating disease involving brain, spinal cord and optic nerves with focal demyelinating white matter plaques associated with inflammation?

A

MS

286
Q

In MS, acute neurologic symptoms may arise from what? Chronic symptoms?

A

Disruption of white matter PATHWAYS; Subsequent degenerative changes in BOTH white & gray matter

287
Q

What are the risk factors for MS?

A

Northern latitudes (BEFORE ADOLESCENCE), low vitamin D levels, EBV exposure in childhood, women

288
Q

What is Neuromyelitis Optica?

A

“Devic disease” demyelination of optic nerve and spinal cord but unlike MS, it spares the brain, common in non-white women

289
Q

This myelitis occurs typically in childhood, its subacute and often follows an infection

A

Acute Disseminated Encephalomyelitis

290
Q

What is typically found in CSF of acute disseminated encephalomyelitis?

A

Significant leukocytosis

291
Q

What is considered an MS flare or relapse?

A

A newly developed focal demyelinating plaque due to focal inflammation

292
Q

Acute loss of vision and pain with eye movement showing inflammation of the optic nerve is called what and a common presenting syndrome of what?

A

Optic Neuritis; MS

293
Q

How does myelitis (inflammation of the spinal cord) present in MS?

A

Sensory or motor symptoms BELOW involved spinal level INCLUDING bladder and bowel function abnormalities

294
Q

How does paralysis present in MS?

A

Flaccid at first, progressive to spastic

295
Q

What is L’hermitte sign in MS?

A

Electric shock sensations provided by head and neck movement

296
Q

Eye movement abnormalities such as diplopia, nystagmus and vertigo are seen when MS involves what part of the CNS?

A

The Brainstem

297
Q

Cortical involvement in MS causes only subtle, chronic symptoms such as?

A

Cognitive dysfunction and fatigue

298
Q

What is the Uhthoff phenomenon in MS?

A

A TEMPORARY worsening of any MS symptom with elevation in body temperature

299
Q

Where are the white matter lesions (plaques) seen in MS?

A

Periventricular and around corpus callosum

300
Q

Elevated CSF OLIGOCLONAL BANDS not present in the serum and elevated IgG?

A

MS

301
Q

What are the three possible courses of MS?

A

Primary Progressive, Secondary Progressive and Relapsing-Remitting

302
Q

What is the 10-year risk of MS in a pt with a FIRST replacing demyelinating event, with brain lesions on MRI and in a pt without?

A

90% vs 20%

303
Q

What is the median time for conversion from relapsing-remitting MS to secondarily progressive MS?

A

10-15 years

304
Q

Progressive MS from initial symptom, 25% of pts undergo rapid progression (7-years) to requiring gait-assisting devices and 25% very slow progression (not requiring gait-assisting devices > 25 years after)

A

Primary Progressive MS

305
Q

How many patients with relapsing-remitting MS convert to secondary-progressive MS? over what time period?

A

2/3 of pts; 10-15 years average

306
Q

What lifestyle modifications are recommended in MS?

A

Active lifesyle, physical therapy, occupational therapy, calcium+vit D supplementation, immunizations, intermittent urinary catheterization +/- prophylactic antibiotics for UTIs

307
Q

What happens in MS and pregnancy?

A

Significantly reduced relapse risk in 3rd trimester but significant risk of relapse un the first 3 months after delivery

308
Q

What habit causes a 3x risk in secondary progression of MS?

A

Smoking

309
Q

What can happen in MS patients who have infections, fever, etc.?

A

PSEUDO-relapses

310
Q

How are acute relapses treated in MS?

A

IV steroids for 3-5 days followed by 10-14 day oral taper

311
Q

What can be done for MS pts who do not respond to steroid treatment for acute relapses?

A

PLASMAPHARESIS

312
Q

What are the 2 first-line DISEASE-MODIFYING agents in treating chronic MS?

A

Interferon and Glatiramer (equivalent agents)

313
Q

What do the disease modifying agents do in modifying MS?

A

Direct the immune response AWAY from autoimmunity and protect the blood-brain barrier

314
Q

Why is use of Natalizumab in MS limited?

A

Because of potential for PML by JC-virus reactivation

315
Q

What is the only ORAL disease-modifying agent for MS?

A

Fingolimod

316
Q

What is the ONLY disease modifying drug for MS that has shown benefit in Secondary-Progressive MS?

A

Mitoxantrone

317
Q

What disease-modifying therapy is there for Primary-Progressive MS?

A

NONE

318
Q

What are BOTOX, Baclofen, Cyclobenzaprine, Tizanidine as well as stretching exercises recommended for in MS?

A

Symptoms of muscle spasms and painful cramping

319
Q

What is neuropathy pain treated with in MS pts?

A

TCA (amitriptyline, nortriptyline), gabapentin and pregabalin

320
Q

Which is the ONLY pregnancy SAFE disease-modifying agent for MS?

A

Glatiramer

321
Q

What two meds can be used to treat fatigue in MS patients? (One is a drug used in Narcolepsy, the other an anti-viral)

A

Modafinil; Amantadine

322
Q

What is the ONLY drug available for improved mobility in MS patients which acts by increasing conductance through demyelinated axons?

A

Dalfampridine

323
Q

When is oxybutynin a good choice and when is it a bad choice for bladder dysfunction in pts with MS?

A

Good: urinary frequency/urgency Bad: urinary retention

324
Q

Presenting symptoms and signs of spinal cord injury usually occur where?

A

At or Below the level of injury

325
Q

Where does sensation of pain occur with spinal injury?

A

At site of injury

326
Q

What type of motor deficit does one notice BELOW the level of spinal injury?

A

Spastic, paralysis, hyperreflexia and extensor plantar responses

327
Q

Involvement of the spinal sensory pathways results in loss of what sensation?

A

Vibration, pain, temperature, position sense

328
Q

What is the best test to pinpoint the level of injury?

A

ASCENDING pin-prick evaluation

329
Q

Spinal compression (fracture, neoplasm, abscess, hematoma) is a NEUROSURGICAL EMERGENCY and best diagnosed?

A

MRI/CT myelography (if MRI is contraindicated)

330
Q

Neck or back pain, followed by weakness, sensory changes and bladder or bowel dysfunction?

A

Compressive myelopathy (spinal cord compression)

331
Q

How should TRAUMATIC spinal cord compression be treated acutely?

A

High-dose steroids and spinal stabilization

332
Q

What affords the BEST chance for future ambulation in newly-diagnosed metastatic spinal cord tumors?

A

EARLY DECOMPRESSIVE SURGERY

333
Q

What are spondylosis and spinal canal stenosis?

A

CHRONIC compressive myelopathies (spinal cord injury)

334
Q

What is the level of MOST spinal stenosis and disk herniations resulting in groin, thigh, leg and buttock pain, that is increased with activity and improved with rest?

A

LUMBAR spine

335
Q

What is the treatment for spinal stenosis and disk herniation?

A

Physical therapy and surgical decompression

336
Q

What are some disease processes that can cause inflammatory myelopathies?

A

MS, Sarcoidosis, Rheumatologic disease

337
Q

A post-infectious (viral gastroenteritis or URI) syndrome resulting in inflammation of a segment of the spinal cord resulting in back pain, weakness, sensory changes and bowel/bladder dysfunction?

A

Idiopathic Transverse Myelitis

338
Q

What are the two tests necessary in Idiopathic Transverse Myelitis?

A

MRI with contrast of the spine and CSF (leukocytosis)

339
Q

How is Idiopathic Transverse Myelitis treated?

A

IV steroids (plasmapharesis/cyclophosphamide if refractory)

340
Q

What happens if symptoms of Idiopathic Transverse Myelitis linger BEYOND 30 days or recur?

A

Consider MS

341
Q

Vitamin B12 deficiency, Zinc TOXICITY and Copper deficiency can result in what neurological pathology?

A

Degeneration of Corticospinal Tracts (vibration, position)

342
Q

How do you test for low vitamin B12 levels?

A

Low Vit B12 (cobalamin) in serum, low methylmalonic acid level, MACROcytic anemia (MCV >110)

343
Q

Infarction of the Anterior Spinal Artery results in what?

A

Acute onset of B/L weakness, loss of pain/temp but not vibration/position

344
Q

Best imaging modality to test for spinal vascular disorders?

A

Angiography

345
Q

Vascular infarcts of the spinal arteries are usually caused by?

A

Cardiogenic, prolonged hypotension (cardiovascular/aortic surgeries)

346
Q

Congenital genetic myelopathy with finding of VERY LONG CHAIN FATTY ACIDS in the serum?

A

X-linked adrenoleukodystrophy (adrenomyeloneuropathy)

347
Q

Peripheral neuropathies can affect what types of nerves?

A

Motor, Sensory, Autonomic

348
Q

What is the symmetry of peripheral neuropathies?

A

Symmetric with a distal-to-proximal gradient

349
Q

What portion of the peripheral nervous system is affected when there are directly-associated symptoms of orthostatic hypotension, cardiac arrhythmias and sweating?

A

Autonomic nervous system

350
Q

Most common cause of peripheral neuropathy?

A

DM

351
Q

Besides conventional laboratory studies such as SPEP, CBC, ESR, fasting glucose, HbA1c, Vit B12 for peripheral neuropathy work-up, what must also be tested if the neuropathy is RAPIDLY progressing?

A

CSF

352
Q

Large nerve fiber neuropathies can be evaluated additional by what test?

A

EMG

353
Q

What diagnostic test is best for small-fiber neuropathies (DM)?

A

Sensory testing for pressure and thermal function

354
Q

Are cramps or fasciculations found in CNS nerve injury?

A

NO

355
Q

Can atrophy be seen in CNS nerve injury?

A

NO

356
Q

What are pre-surgical recommendations for carpal tunnel syndrome?

A

Wrist splints, occupational therapy, steroid injections

357
Q

When is surgery recommended for carpal tunnel syndrome?

A

When symptoms are progressive ins spite of pre-surgical treatments

358
Q

How can you differentiate a CNS lesion (tumor) from a peripheral lesion (Bell’s Palsy) when the face is involved?

A

CNS: affects LOWER face; Peripheral: UPPER and LOWER

359
Q

Upper and Lower facial muscle paralysis with inability to close eyes tightly, raise eyebrows with hyperacusis, dry mouth and impaired taste?

A

Bell’s Palsy

360
Q

What should be done within the first 72 hours of diagnosing Bell’s Palsy?

A

Prednisone

361
Q

Synkinesis?

A

Aberrant re-innervation after Bell’s Palsy (voluntary smiling causes involuntary eyelid closure)

362
Q

Generalized polyneuropathies beginning at the feet and ascending up the limbs, affecting the hands in a stocking-glove distribution with pain can bee seen in these two common diseases?

A

DM, alcoholism

363
Q

Which neuropathy becomes more prevalent in poorly-controlled long-standing DM?

A

Autonomic neuropathy

364
Q

Pt with previously undiagnosed DM or even mild DM with significant weight loss followed by acute severe unilateral leg pain with numbness followed by proximal weakness and atrophy?

A

Diabetic AMYOTROPHY (L2 to L4 radiculopathy)

365
Q

A hereditary neuropathy with mutation in genes encoding for myelin formation with palpable peripheral nerves, very high foot arches, hammer toes and atrophy of distal extremity muscles (stork legs)?

A

Charcot-Marie-Tooth (CMT) disease

366
Q

What are the two immune-mediated peripheral neuropathies that attack the nerve roots and peripheral nerves distinguished only by symptom duration?

A

Gullain-Barré syndrome (GBS) and Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)

367
Q

Recent diarrheal infection with Campylobacter jejuni followed by lower back pain then, rapid-onset symmetric weakness of the upper and lower limbs over days to weeks with only mild sensory loss?

A

Guillain-Barré syndrome (GBS)

368
Q

Why should Guillain-Barré patients be hospitalized?

A

Because of high-risk of respiratory failure and dysautonomia (labile blood pressure, constipation, arrhythmias)

369
Q

What is seen in the CSF of Guillain-Barré patients?

A

Elevated protein count

370
Q

What treatment has absolutely NO effect in Guillain-Barré syndrome?

A

Steroids

371
Q

How is Guillain-Barré treated?

A

Either IV IgG or Plasma Exchange 7-14 days from symptom onset

372
Q

How is Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) different than Guillain-Barré?

A

Evolves more slowly (MONTHS) with progressive but also relapsing-remitting symptoms with PAIN and responds to PREDNISONE as well as IV IgG and Plasmapharesis

373
Q

What is the CSF of patients with Critical Illness Polyneuropathy different than that of Guillain-Barré?

A

It is NORMAL

374
Q

What are the agents used in treating neuropathic pain such as in DM?

A

Pregabalin, gabapentin, TCA’s (amitriptyline), venlafaxine, duloxetine, capsaicin

375
Q

When is it considered a therapeutic failure for a neuropathic pain medication?

A

> 4 weeks without efficacy

376
Q

Dysfunction in BOTH UPPER and LOWER motoneurons in one or more areas of the body with death within 3-5 years of diagnosis?

A

Amyotrophic Lateral Sclerosis (ALS)

377
Q

Spasticity, hyperreflexia, flaccid paralysis, extensor plantar responses?

A

UPPER motoneurons

378
Q

Fasciculations, muscle weakness, atrophy, cramps?

A

LOWER motoneurons

379
Q

What is the ONLY drug that slows down ALS progression (by 3 months)?

A

RILUZOLE

380
Q

Autoimmune disease which results from an autoantibody blocking postsynaptic acetylcholine receptor OR the muscle-specific tyrosine kinase (MuSK) receptor at the neuromuscular junctions?

A

Myesthenia Gravis (MG)

381
Q

Fatigable muscle weakness worsening with activity and improves with rest, especially affecting ocular and bulbar muscles?

A

Myesthenia Gravis (MG)

382
Q

What is the general presenting symptom of patients with Myesthenia Gravis?

A

Diplopia or Ptosis (bilateral)

383
Q

30% of patients with Myesthenia Gravis (MG) also have a diagnosis of what? 75% have what else?

A

Thyroid disease; Thymic hyperplasia or Thymoma (CT chest)

384
Q

What cancers are associated with Myesthenia Gravis besides Thymoma?

A

Breast cancer, Small Cell Lung Cancer and Hodgkin Lymphoma

385
Q

What is the first line therapy for MILD Myesthenia Gravis but does not work well with MG caused by autoantibodies against MuSK receptors?

A

Pyridostigmine

386
Q

How do you treat SEVERE Myesthenia Gravis (MG)?

A

Immunosuppression with Prednisone, Mycophenolate Mofetil, Azathioprine, Cyclosporine, Rituximab

387
Q

What is a rescue treatment for patients with refractory Myesthenia Gravis and severe limb weakness or respiratory/bulbar dysfunction?

A

IV IgG or Plasma Exchange/Plasmapharesis

388
Q

A rare, usually paraneoplastic syndrome caused by autoantibodies against P/Q-type calcium channels at the PRESYNAPTIC neuromuscular junction associated with Small Cell Lung Cancer?

A

Lambert-Eaton Myasthenic Syndrome

389
Q

How is Lambert-Eaton Myaesthenic Syndrome DIFFERENT than Myasthenia Gravis (MG)?

A

Activity and exercise IMPROVE (opposite) reflexes and strength

390
Q

Which is the only myopathy in which onset is asymmetric?

A

Inclusion Body Myositis

391
Q

Very slow progression (years) of a myositis suggests one of two types?

A

Congenital (dystrophy) or Inclusion Body Myositis

392
Q

Subacute progression (months) of myositis suggests what type of myositis?

A

Endocrine

393
Q

Acute progression (weeks) of myositis suggests what two types of myositis?

A

Inflammatory or Toxic

394
Q

What myositis is associated with Frontal Balding, Cataracts and Mental Retardation?

A

Myotonic Dystrophy

395
Q

What lab should be tested for in myopathy and when will this be normal?

A

CK level; normal if slowly-progressing myopathy

396
Q

Slowly progressive myopathy with PROXIMAL muscle weakness and cushinoid-appearance?

A

Steroid-induced myopathy

397
Q

What other endocrinological disorder can cause myopathy?

A

Thyroid disease

398
Q

What vitamin deficiency can cause a myopathy with myalgia, bone pain, diffuse fatigue and proximal limb weakness?

A

Vitamin D deficiency

399
Q

What do you look for if suspecting an inherited myopathy (Duchenne or Emery-Dreifuss)?

A

Family history, genetic testing, muscle biopsy

400
Q

What is found in myotonic dystrophy that is different than other myopathies?

A

Myotonia (can’t release handshake)

401
Q

What type of myopathy mimics Myesthenia Gravis?

A

Mitochondrial myopathy

402
Q

What types of myopathies are associated with dysmorphic facial and skeletal features with neuropathy and cardiomyopathy?

A

Congenital (hereditary) myopathies

403
Q

What is the strongest risk factor for Critical Illness Myopathy (which presents exactly like but is more common than Critical Illness Neuropathy)?

A

IV steroids

404
Q

What is the most common TOXIC myopathy caused by?

A

Statins or concomitant use of statins with Macrolides (-mycin’s), Cyclosporine (anti-rejection, immunosuppressant), Itraconazole and Protease Inhibitors (HIV, Hep C)

405
Q

Pravastatin, Rosuvastatin, Fluvastatin?

A

Less myopathy risk

406
Q

Most common presentation of intracranial tumors?

A

Seizures

407
Q

Most common symptom of Frontal Lobe Tumors?

A

Personality/Behavioral changes

408
Q

Best study for intracranial tumor?

A

MRI with contrast

409
Q

What is the most common type of brain tumor and where from?

A

Metastatic (breast, lung, melanoma)

410
Q

What is the most common PRIMARY brain (CNS) tumor?

A

Glioblastoma Multiforme

411
Q

What is REQUIRED for diagnosis of Glioblastoma Multiforme?

A

Brain Biopsy

412
Q

Primary CNS tumor that presents without seizures, also needs biopsy for diagnosis like Glioblastoma Multiforme and can also be diagnosed by slit lamp evaluation of the eye and CSF?

A

Primary CNS Lymphoma (non-Hodgkin lymphoma)

413
Q

How do you manage brain edema in patients with a brain tumor? EXCEPT!?

A

Steroids; Except if a Primary CNS Lymphoma is suspected

414
Q

What is the first step in the treatment of MOST brain tumors? Except?

A

Maximal surgical resection; Except in Primary CNS Lymphoma

415
Q

What are common NON-neurological complications of brain tumors?

A

DVTs and PEs

416
Q

What can occur 6-12 months after radiation therapy for brain tumors and what does it present like?

A

Delayed Radiation Necrosis - presents like the initial brain tumor (seizures, etc.)

417
Q

Tumor-Associated Immune-Mediated Injury?

A

Paraneoplastic Syndromes (immune reaction to a primary tumor)

418
Q

ANNA, NMDA, CRMP-5, MA, PCA-1, VGCC?

A

Paraneoplastic antibodies found in serum and CSF

419
Q

Unexplained, subacute progressive neurologic disorder should raise the suspicion for what?

A

Paraneoplastic syndrome

420
Q

How early can a paraneoplasic syndrome present PRIOR to the neoplasm being found?

A

YEARS

421
Q

Suspicion for a paraneoplastic syndrome should prompt what kind of work-up?

A

PET, CT-chest/abd/pelvis, antibody testing

422
Q

How are paraneoplastic syndromes treated besides addressing the neoplasm?

A

IV IgG, Plasmapharesis, Steroids

423
Q

Locked-In state is caused by a lesion where?

A

Brainstem (usually pons)

424
Q

Absence of corneal reflexes indicates damage to what?

A

Pons (also no response to caloric manuvers) and midbrain

425
Q

Absence of gag reflex, cough, respiration indicated damage to?

A

Medulla

426
Q

Describe Apnea test for confirmation of brain death

A
  1. Remove from vent, put on 100% NC
  2. Baseline ABG with Pco2 40-60 mmHg
  3. Repeat ABG at 1 & 5 minutes, watch for spontaneous respirations
  4. If Pco2 increased by >20 mmHg AND no spontaneous respirations, test is POSITIVE
  5. Need an additional POSITIVE test AT LEAST 6 hours after the first positive test for confirmation of BRAIN DEATH
427
Q

What is the BEST prophylactic agent to use for a woman who experiences migraines in the perimenstrual period?

A

Mefenamic Acid

428
Q

Should women with migraines use combined oral contraceptive pills?

A

NO - STROKE!! (x2) (migraine with aura + combined oral contraceptive pills = stroke x8)

429
Q

Should you perform a Lumbar Puncture in a patient with papilledema?

A

Fuck the Fuck NO!! (herniation)

430
Q

Factor V leiden

A

Hypercoagulation anomaly resulting in CLOTS

431
Q

What should MOST patients with atrial fibrillation be treated with?

A

Warfarin

432
Q

What atrial fibrillation patients can be started on ASPIRIN rather than warfarin?

A

Non-valvular AF,

433
Q

What do ALL patients with stroke or TIA require emergently and why?

A

Non-contrast head CT to r/o intracranial hemorrhage

434
Q

Patients with TIA have an elevated risk of what in the next 48 HOURS?

A

STROKE

ABIM 2015 (11 decks)

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