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Clinical Medicine Final > Neuro > Flashcards

Neuro Flashcards

1
Q

What can unilateral HA be

A

Migraine, trigeminal neuralgia

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2
Q

What can temporal HA be

A

Temporal arteritis

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3
Q

What can occipital HA be

A

Tension HA

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4
Q

What can HA with eye association be

A

Acute glaucoma, temporal arteritis, sinusitis, migraine

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5
Q

What is the difference between HA with gradual vs sudden onset

A 
Gradual = usually benign
Sudden = may be more serious
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6
Q

HA characterized as pounding/pulsatile =

A

Migraine

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7
Q

HA characterized as sharp/stabbing =

A

Trigeminal neuralgia or cluster HA

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8
Q

HA characterized as pressure/squeezing =

A

Tension HA

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9
Q

HA associated with anxiety =

A

Tension HA

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10
Q

HA associated with auras =

A

Migraine

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11
Q

HA associated with vision change =

A

Temporal arteritis or gluacoma

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12
Q

HA associated with n/v =

A

Increased ICP or Migraine

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13
Q

HA associated with lacrimation/rhinorrhea =

A

Cluster HA

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14
Q

HA associated with photophobia/phonophobia =

A

Migraine or Meningitis

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15
Q

Migraines affect men or women more?

A

Women

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16
Q

At what age do migraines usually start? Disappear?

A

Onset = 10-14 y/o

Disappear in the 50’s

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17
Q

Depolarization theory of migraines =

A

Depressed activity areas lead to platelet and mast cell activation

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18
Q

Seratonin release may cause migraines how?

A

Fluctuations in catecholamine levels cause alternating vasoconstriction/vasodilation which causes wall stretching & pain

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19
Q

What are the types of migraines (the most often seen)

A

Common (w/o aura) or classic (with aura)

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20
Q

What are the indications for imagining in pt presenting with a migraine?

A 
1st/worst migraine
New onset w/ age > 50y/o
Sudden onset HA ("thunderclap")
Abnormal neuro exam
Rapid onset with strenuous activity
HA awakens from sleep
Meningea signs (n/v, altered mental status, personality changes)
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21
Q

What is the 1st line Tx of acute migraine?

A

Excedrin migraine or NSAIDs

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22
Q

What is 2nd line Tx for acute migraine?

A

Triptans or Dihydroergotamine (DHE-45)

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23
Q

What is the best Tx of migraine (not acute)

A

Triptans = Sumatriptan (Imitrex) or Treximet (sumatriptan + naproxen)

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24
Q

What are RFs for migraines

A

Family hx, obesity, sleep apnea, head injury, female,, analgesic overuse, & caffeine

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25
Q

What may cause a rebound HA

A

Overuse of medication for migraine (> 10 days of the month) especially Narcotics!

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26
Q

What is the Tx of rebound HA

A

Go cold turkey from the meds that are causing it, try triptan or steroids

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27
Q

When should you start migraine prophylaxis

A

> 2 HAs/week
Severe HA
Prolonged duration > 2 days

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28
Q

What is the best migraine prophylaxis med?

What else is an option?

A 
Best = Propranolol LA (beta blocker)
Other = tricyclic antidepressants or antiseizure drugs (not in preggos though!)
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29
Q

What is a major side effect of the antiseizure drugs?

A

Unwanted weight gain

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30
Q

What are common features of a Common Migraine

A 
Pulsatile throbbing (50%)
Unilateral HA (50%)
Lasts hrs - days
Associated with n/v
Photophobia/phonophobia
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31
Q

What are common features of a Classic Migraine

A

Aura (20%)
Scintillating scotomas
Fortification spectrum

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32
Q

What is the prodrome phase

A

Increased excitability/irritability, fatigue, depression, appetite changes/cravings

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33
Q

Aura that occurs without a HA is called…

A

Acephalgic migraine

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34
Q

Sensory aura =

A

Numbness, paresthesia, dysphasia

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35
Q

What artery do basilar migraines effect?

What are the SxS?

A 
Artery = basilar artery
SxS = HA, vertigo, slurred speech, impaired coordination (younger pts) NO MOTOR DEFECTS
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36
Q

SxS of hemiplegic migraine =

A

Paralysis on one side of body, may persist x 24hrs w/ or w/o HA

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37
Q

SxS of ophthalmoplegic migraine =

A

HA, eye pain, vomitting, ptosis

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38
Q

Catemenial migraines occur with…

A

Menses
Usually disappear with menopause & pregnancy
Occurs 2-3x a day during menses

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39
Q

If a migraine is VERY refractory what might you try to use?

A

Lidocaine, caffeine protocols, or propofol infusions

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40
Q

What sex is cluster HA more common in

A

Men (4X more)

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41
Q

What is the main RF for cluster HA

A

Tobacco use - MUST QUIT

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42
Q

What are possible causes of cluster HA

A

Vascular dilation
Trigeminal nerve stimulation
Circadian rhythms

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43
Q

Pts with cluster HA will often complain they are triggered by…

A

Alcohol ingestion

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44
Q

Cluster HA SxS/description =

A

Excruciating stabbing pain (suicide HA)
Unilateral behind the eye, jaw, or teeth
Last 15min - 3hrs

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45
Q

What are the requirements to Dx cluster HA

A

Must have one of the following:
- Lacrimation, ipsilateral flushing/sweating, ipsilateral nasal DC, conjunctival redness, horner’s syndrome (ipsilaterl ptosis or miosis)

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46
Q

What is the Tx of cluster HA

A

Triptans
OXYGEN (20min) = complete relief in 78% of pts
Prophylaxis = break the cycle

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47
Q

What are the SxS of tension HA

A

Vice-like, gripping HA that forms a band across the forehead bilat
Radiates into posterior neck/trapezius
NO n/v, photo/phonophobia & not worse with activity

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48
Q

What is the Tx of tension HA

A 
Non-pharm = exercise, relaxation therapy/counseling, yoga, PT, acupuncture
Pharm = NSAIDs, Tylenol, myofascial trigger point injections, TCAs or SSRI
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49
Q

What is the origin of tension HA

A

It has a myofascial origin

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50
Q

RFs for tension HA

A

Stress/anxiety, depression, overwork, lack of sleep, posture, conversion syndrome

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51
Q

When does post-traumatic HA occur (be specific not a smart ass)

A

Within the first 7 days of the injury

Acute: < 2mo after injury; Chronic: >2mo after

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52
Q

What type of HA is it characterized as

A

Mix of migraine and tension HA

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53
Q

What do pts with post-traumatic HA often develop

A

Rebound HAs

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54
Q

How do you Tx post-traumatic HA

A

Hard to treat; treat as the HA it presents as and if that doesn’t work adjust Tx

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55
Q

What is idiopathic intracranial HTN (IIH) also called

A

Psuedotumor cerebri or benign intracranial HTN (BIH)

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56
Q

Who is most likely to have IIH

A

Women 15-44 y/o that are obese

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57
Q

What are the SxS of IIH

A 
Retro-orbital pain (worse with movement)
Throbbing (worse in morning)
N/V
Monocular/binocular vision loss
Pulsatile tinnitus (60% of pts)
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58
Q

What is the MC PE finding with IIH

A

Papilledema

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59
Q

What are the diagnostics for IIH

A

LP opening pressure > 200

MRI neg for masses/hydrocephalus

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60
Q

What is the Tx of IIH

A 
Lifestyle changes
Diuretics
NSAIDs/TCAs for HA management
Large volume LP
Sx in extreme cases
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61
Q

Prevelance of trigeminal neuralgia…sex & age =

A 
Sex = women
Age = >40y/o with peak of 60-70 y/o
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62
Q

What is the biggest risk for trigeminal neuralgia

A

Multiple Sclerosis (MS)

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63
Q

Which side is more commonly affected in trigeminal neuralgia

A

Right side

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64
Q

How is trigeminal neuralgia described

A

Stabbing, lancinating, electric shock pain that lasts about 2min and occurs multiple times a day or month but becomes more frequent over time

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65
Q

What causes trigeminal neuralgia

A

Demyelination of trigeminal nerve that causes pain even with light touch

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66
Q

What branches of the trigeminal nerve are MC affected in trigeminal neuralgia

A

Maxillary and mandibular

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67
Q

Temporal arteritis AKA…

A

Giant cell arteritis

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68
Q

What is GCA commonly associate with

A

Polymyalgia rheumatic (50%)

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69
Q

What are the SxS of temporal arteritis

A

Temporal HA
Jaw claudication
+/- diplopia, visual field cuts, and systemic manifestations

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70
Q

What will PE reveal for temporal arteritis

A

Tenderness over temporal arteries

Diminished pulses

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71
Q

How is temporal arteritis Dx

A

Temporal artery biopsy (pos 2 days after starting Tx)

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72
Q

What is the immediate Tx of temporal arteritis

A

Corticosteroids while biopsy results are being processed

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73
Q

What are the causes of a traumatic brain injury (TBI)

A

Penetrating injury or closed head injury

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74
Q

What is primary damage in TBI

A

Skull fx, contusion/bruising, hematomas/blood clots, lacerations, nerve damage (diffuse axonal injury)

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75
Q

What is secondary damage in TBI

A

Edema & infection

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76
Q

What are the main causes of concussion

A

Deceleration injury or coup-countercoup injury

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77
Q

Who is most likely to suffer a concussion

A

Athletes especially in contact sports

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78
Q

What are the main SxS of a concussion

A

Disorientation
Amnesia
Confusion (vacant stare, delayed answers, poor concentration)

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79
Q

What % of concussions result in LOC

A

10% will have LOC

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80
Q

What are the MOST COMMON SxS of concussion

A

HA, dizziness, & impaired executive function

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81
Q

What are the diagnostic tests for consussion

A

CT or MRI (although minor will appear normal)

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82
Q

What is a Grade 1 concussion

A

“Ding” concussion, confusion, no LOC, SxS last for < 15min

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83
Q

What is a Grade 2 concussion

A

No LOC, SxS last > 15min

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84
Q

What is a Grade 3 concussion

A

LOC

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85
Q

What is the gold standard for determining severity of a concussion

A

Gasglow Coma Scale

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86
Q

What constitutes as minor, moderate, and severe on the gasglow scale

A

Minor: 13-15
Moderate: 9-12
Severe: < 8

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87
Q

What is the best Tx of concussion

A

Rest

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88
Q

Who needs a CT with concussion

A

There is a long list. Main one to know is seizure, neruo deficits, and anticoagulation ABSOLUTELY requires CT

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89
Q

What is the problem with multiple concussion

A

It will take longer to heal each time, will result in more easily being concussed again, may lead to more severe issues (like post-concussion syndrome)

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90
Q

The typical course for an athlete to be cleared to resume play takes 5 days. What happens if the symptoms return at any point in that time

A

Player MUST STOP and rest until they are asymptomatic for 24hrs then they return to the level that they were at before

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91
Q

What is a basal skull fx

A

Fx at the base of the skull; accounts for % of Fx

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92
Q

What are the most prevalent SxS

A

Hemotympanum
Battles sign = mastoid process ecchymosis
Raccon eyes = periorbital ecchymosis
CSF leakage from nose/ears

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93
Q

Bleeding between the dura mater and arachnoid layer is called…

A

Subdural hematoma

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94
Q

Subdural hematoma is caused by…

A

Tearing of the “bridging veins” during a shearing injury (acceleration-deceleration injury)

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95
Q

What are major RFs for subdural hematoma

A

Age (elderly) and anticoagulation are major

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96
Q

SxS of subdural hematoma are…

A 
Confusion
Slurred speech
HA
Lethargy
LOC
N/V
Weakness
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97
Q

What is the main diagnostic test? What is its classic result

A

CT scan

Crescent shape with midline shift of ventricle

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98
Q

What is the Tx of subdural hematoma

A

Small one = burr holes

Larger one = craniotomy to evacuate clots

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99
Q

Bleeding between the dura mater and skull is called

A

Epidural hematoma

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100
Q

Epidural hematoma is due to…

A

Trauma/skull fx

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101
Q

Epidural hematoma is caused by…

A

Tearing of the middle meningeal artery

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102
Q

What is the classic presentation of epidural hematoma

A

Initial LOC followed by lucid state

“Talk and die”

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103
Q

What is the diagnostic test of choice? What is the finding/result

A

CT

Shows biconcave lens (looks like lens with part outside and part inside skull)

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104
Q

What is the Tx for epidural hematoma

A

Surgical evacuation & ligation of bleeding vessels

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105
Q

Bleeding into the subarachnoid space is…

A

Subarachnoid hemorrhage

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106
Q

Subarachnoid hemorrhage is usually due to…

A

Rupture of a cerebral aneurysm (but can also be due to trauma)

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107
Q

What is the classic presentation of subarachnoid hemorrhage

A

Thunderclap HA or HA of a lifetime

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108
Q

What are other SxS of subarachnoid hemorrhage

A 
HA
N/V
Stiff neck
Confusion
Seizure
May report popping/snapping prior to HA
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109
Q

What is the diagnostic of choice for subarachnoid hemorrhage?

A

CT without contrast (best within 12hrs then sensitivity decreases)

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110
Q

What is the diagnostic test to do if CT is inconclusive for suspected subarachnoid hemorrhage

A

Lumbar puncture (LP); presence of blood is positive result

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111
Q

What is the Tx of subarachnoid hemorrhage

A

Depends on size, location, etc.

Tx includes clipping or coiling procedures

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112
Q

Which type of stroke is more common; hemorrhagic or ischemic?

A

Ischemic (87% of all strokes)

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113
Q

Which causes more hemorrhagic strokes…intracerebral hematoma (ICH) or subarachnoid hematoma (SAH)

A

Intracerebral hematoma

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114
Q

What is the main cause for hemorrhagic stroke

A

Ruptured berry aneurysm (80%)

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115
Q

AV malformations also cause hemorrhagic stroke; what are the SxS of this

A

Pulsatile tinnitus, HA, & seizures

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116
Q

Where do most aneursyms occur/develop

A

Develop at the branching points of arteries

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117
Q

Where is the most common location for an aneurysm to occur

A

Anterior communicating artery

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118
Q

Why is hemorrhagic stroke so important (think prognosis)

A

B/c 10-15% die before reaching the hospital and 25% within the 1st 24hrs
1/3 of survivors will have neuro deficits

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119
Q

What are the management goals for hemorrhagic stroke

A

SBP < 140-160 w/o fluctuations
Monitor cardiac dysrythmias
ICP monitoring (< 20mmHg)
Normothermia

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120
Q

What is a sentinel bleed

A

A small bleed or warning leak at the site several days before the larger event; accompanied by milder HA, neck stiffness, and nausea

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121
Q

What are complications of hemorrhagic stroke

A

Rebleeding
Hydrocephalus
Cerebral ischemia (d/t vasospasm)

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122
Q

What are the two causes/types of ischemic stroke

A

Thrombotic or embolic

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123
Q

Which is more common…thrombotic or embolic ischemic stroke

A

Thrombotic

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124
Q

What causes thrombotic ischemic stroke

A

Atherosclerosis (injured endothelial lining allows platelets to adhere -> plaque formation)

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125
Q

What is the origin of most embolic ischemic strokes

A

Carotid arteries & heart (a-fib vegetation)

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126
Q

What is the least common cause of ischemic stroke

A

Lucunar infarcts

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127
Q

What is a TIA

A

Transient ischemic attack; sudden onset of neurological deficit including speech, hemiparesis, and monocular blindness

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128
Q

What is amaurosis fugax

A

Sudden, monocular blindness described as a shade/curtain being pulled over the affected eye

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129
Q

What diagnostic test do you do for ischemic stroke

A

Head CT (or MRI)
TEE for uspected cardiac source
Carotid US for carotid artery stenosis

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130
Q

What is the main way to differentiate TIA vs CVA

A

TIA = symptoms resolve within 24hrs (most within 10 minutes)

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131
Q

Why is TIA cause for concern

A

Stroke follows TIA within 90 days in 20-25% of cases

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132
Q

If ischemia occurs at the anterior circulation what artery is commonly invovled

A

Anterior cerebral artery

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133
Q

What are the SxS of anterior circulation ischemia

A

Confusion, amnesia, personality change, cognitive change, contralateral hemiparesis & sensory impairment, if left there is expressive aphasia, & eyes deviate TOWARD affected side

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134
Q

If ischemia occurs at the anterior circulation what artery is MOST commonly invovled

A

Middle cerebral artery

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135
Q

What is a common SxS of middle cerebral artery infarct

A

Neglect of the affected side

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136
Q

If ischemia occurs in the posterior circulation what arteries are commonly affected

A

Posterior inferior cerebellar artery
Vertebrobasilar artery
Posterior cerebral artery

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137
Q

What are SxS of posterior ischemic stroke

A

Nystagmus, ataxia, vertigo, dysphagia, dysarthria

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138
Q

What is TPA

A

Tissue plasminogen activator = clot buster

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139
Q

What are the indications for TPA

A

Age > 18
NIH stroke scale of 5+
< 3hrs since onset of SxS

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140
Q

How quickly should TPA Alteplase be given

A

10% of dose as immediate bolus and remainder given within 60min

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141
Q

Are there risks with TPA? If so why use it?

A

Yes there are risk; increases risk for ICH but we still use it since it prevents 11-13 deaths and disability for every 100 pts (benefit > risk)

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142
Q

What is the most common complication in stroke pts

A

Depression (30%)

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143
Q

What are the scores for the NIH stroke scale

A 
0 = no stroke
1-4 = minor stroke
5-15 = moderate stroke
16-20 = moderate-severe stroke
21-42 = severe stroke
144
Q

Major TPA contraindications include

A

Score < 5 on scale, seizure, glucose abnormalities, previous head injury/CVA (90 days), Hx of ICH, recent major trauma/Sx, GI or GU hemorrhage, bleeding condition

145
Q

What causes carotid artery stenosis

A

Plaque formation/build up in the carotids

146
Q

Where does carotid artery stenosis typically occur

A

The bifurcation and flow into the internal carotids

147
Q

What diagnostic tests are used to determine carotid artery stenosis

A

Can use carotid US or MRA ($$$) however; current GOLD STANDARD = angiography (invasive)

148
Q

When does carotid artery stenosis Tx require Sx

A

Asymptomatic pt with > 80% stenosis

Symptomatic pt with > 50% stenosis

149
Q

When does carotid artery stenosis Tx require medical management

A

Asymptomatic pts with > 60% stenosis

Symptomatic pts with < 80% stenosis

150
Q

What drugs are used in carotid artery stenosis Tx

A

Plavix or Dipyridamole + ASA = 37% RR reduction which is the best

151
Q

Occlusion of a single deep penetrating artery is…

A

Lacunar infarct

152
Q

Lacunar infarcts typically affect…

A

Deep nuclei (caudate, thalamus, putamen)

153
Q

What is the most commonly affected area for bacterial meningitis

A

Subarachnoid space

154
Q

What is the typical cause of bacterial meningitis

A

Hematogenous spread from OM, sinusitis, PNA, or immmunocompromised

155
Q

What are the causative organisms of bacterial meningitis in neonates

A

Group B beta hemolytic strep and enteric gram neg bacilli

156
Q

What are the causative organisms of bacterial meningitis in children

A 
MC = H influenzae
Others = Neisseria meningitidis & S pneumoniae
157
Q

What are the causative organisms of bacterial meningitis in adults

A 
MC = S pneumoniae & N meningitidis
Others = Staph, H influenzae, Gram neg bacilli, Listeria
158
Q

What are the causative organisms of bacterial meningitis in elderly

A

S pneumoniae, E coli, Klebsiella, Listeria

159
Q

What are the classic SxS of bacterial meningitis

A

HA
Stiff neck
Fever
Photophobia

160
Q

What are other SxS of bacterial meningitis

A

Mental status change, n/v, seizures, lethargy, and confusion

Infants = high pitched crying, refusal to eat, bulging fontanelles

161
Q

What are the classic PE findings for bacterial meningitis

A

Nucchal rigidity, kerning’s sign, brudzinski’s sign, and maybe skin rash (65%)

162
Q

What is the diagnostic choice for bacterial meningitis

A

LP

Cloudy is poor result

163
Q

What is the 1st line Tx of bacterial meningitis

A

Pt under 50 y/o = vancomycin + ceftriaxone

Over 50 y/o = add ampicillin

164
Q

What are some preventions of bacterial meningitis

A

Vaccines (pneumococcal & meningococcal)

165
Q

When is bacterial meningitis contagious

A

7 days before illness and 24 hrs after Abx started

166
Q

Which is more common…viral or bacterial meningitis

167
Q

What are common causitive agents for viral meningitis

A

Enterovirus, HSV

168
Q

Pt with viral meningitis may present with…

A

Flu like symptoms, HA, fever, malaise, photophobia, & meningeal irritation

169
Q

How do you differentiate viral and bacterial meningitis

A

Impossible to determine from H&P so treat as bacterial until proven otherwise

170
Q

Inflammation of the brain =

A

Encephalitis

171
Q

What is the most common type of encephalitis

A

Herpes simplex encephalitis

172
Q

Common SxS of encephalitis are

A

HA
Fever
Mental status change

173
Q

What is the MC causative agent of herpes simplex encephalitis and where is it found

A

HSV1; primarily in trigeminal ganglion

174
Q

Presence of the HSV1 causes severe…

A

Inflammation, edema, necrosis, and hemorrhage

175
Q

What is the diagnostic of choice for herpes encephalitis? What other test is commonly done?

A

Gold standard = PCR PCE for HSV

Other test = LP to check CSF leukocytes, protein, and glucose

176
Q

What is the imaging of choice for herpes encephalitis

A

MRI preferred over CT

177
Q

What is the Tx of herpes encephalitis

A

Acyclovir +/- steroids

178
Q

What is the leading cause of epidemic encephalitis

179
Q

West nile virus has an abrupt onset of SxS what are they

A

Fever, malaise, profound fatigue, weakness

+/- HA, eye pain, and n/v

180
Q

What is the classic finding for west nile on PE

A

Occipital LAN

Other = conjunctivitis and flushing

181
Q

What is the diagnostic of choice for west nile

A

IgM ELISA (positive 8-21 days post onset)

182
Q

What type of encephalitis is common in HIV pts

A

CMV encephalitis

183
Q

What commonly presents in conjuction with CMV encephalitis

184
Q

What is the Tx of CMV encephalitis

A

Ganciclovir & foscarnet

185
Q

What pathogen is in cat bite infections

A

Pasteurella multocida

186
Q

What are the stages of syphilis

A 
Primary = chancre, 21-90 days
Secondary = macular rash, 2-8 weeks
Latent = 1-20 years
Tertiary = 1-20 years
187
Q

A common neuro complication of syphilis is tabes dorsalis…what is it and what are its SxS

A

It is peripheral neuropathy, an inflammatory process involving the dorsal root ganglion
SxS = lightening pains (abs & legs), decreased proprioception, vibratory sense, & DTRs, Argyll-Robertson pupil, and syphilitic paresis (dementia paralytica)

188
Q

How do you Dx neurosyphilis

A

LP for CSF with FTA-ABS test

189
Q

How do you Tx neurosyphilis

A

PCN and monitor CSF

190
Q

What is the MCC of cerebral mass lesions in HIV pts with CD4 < 100

A

Toxoplasmosis (parasitic infection)

191
Q

What is the diagnosic of choice and result for toxoplasmosis

A

CT scan = ring enhancing lesions

192
Q

What sex is more likely to develop brain CA? What is the peak age

A

Men > women

Peak age = 65-79 y/o

193
Q

What is the only truly proven risk factor for brain CA

A

High dose ionizing radiation

194
Q

What is the most common type of brain CA

A

Meningioma

195
Q

Who is more likely to develop a meningioma

A

Women 3X more

196
Q

Where do meningiomas arise from

A

The meninges in the subarachnoid space

197
Q

What are the 2 locations for meningiomas? What are the associated SxS of each

A

Intraventricular: SxS = ICP

Posterior fossa: SxS = CN abnormalities

198
Q

What are the distinct radiological characteristics of meningiomas

A

Dura tail & indentation of the brain

199
Q

What are the grades of meningiomas

A

Grade 1 = meningioma; bening
Grade 2 = atypical meningioma; not benign or malignant
Grade 3 = anaplastic meningioma; malignant & invasive

200
Q

What is the Tx for meningioma

A

Watchful waiting
Craniotomy
Radiation (sterotactic radiation/radiosurgery, gamma knife)

201
Q

What is the familial link of pituitary adenoma

A

Multiple endocrine neoplasia 1 (MEN1)

202
Q

What is the most common type of pituitary adenoma

A

Prolactinoma

203
Q

What cells are involved in prolactinomas? What are the SxS

A 
Cells = lactotrophs
SxS = gallactorrhea & gynecomastia
204
Q

What is the size classification for pituitary adenomas

A

Macroadenoma: 10+ mm
Microadenoma: <10 mm

205
Q

This type of brain CA is not common, occurs near the pituitary gland, and is classified as a pituitary tumor even though it differs from a pituitary adenoma. What is it?

A

Craniopharyngioma

206
Q

Where do pituitary adenomas arise from?

Where do craniopharyngiomas arise from?

A 
Adenoma = cells in anterior lobe
Craniopharyngioma = cells in Rathke's duct
207
Q

What are the SxS of craniopharyngioma

A

May disrupt pituitary fxn, may result in optic nerve compression, may have increased ICP

208
Q

Where are schwannomas (accoustic neuromas) found?

A

Tumor of CN8

209
Q

What/where do schwannomas arise from

A

Schwann cells

210
Q

What is a major complication of a schwannoma

A

Involvement/impingement of CN7 which runs along CN8

211
Q

Are schwannomas usually uni or bilateral

A

Unilateral except with neurofibromatosis

212
Q

What is the main SxS of schwannomas

A

Unilateral hearing loss

213
Q

What will the results be of the Rhine and Weber test with schwannoma

A

Rinne: AC > BC
Weber: lateralize to the unaffected side

214
Q

What is the imaging study of choice for schwannoma

A

MRI

Will see growth in internal acoustic canal

215
Q

What is the Tx of schwannoma

A

Keyhole Sx or retromastoid/retrosigmoid craniotomy

216
Q

Where do gliomas arise from

A

Glial cells

217
Q

What is the most common type of malignancy (glioma)

A

Astrocytoma

218
Q

What are the grades for astrocytomas

A

Grade 1 = pilocytic; benign
Grade 2 = low grade; benign
Grade 3 = anaplastic; malignant
Grade 4 = gliobalstoma multiforme; very malignant

219
Q

Who are brainstem gliomas MC in

A

MC in children

220
Q

What is the most devestating pediatric malignancy

A

Diffuse Intrinsic Pontine Glioma (DIPG)

221
Q

What is the Tx of brainstem glioma

A

Sx if possible but often resort to XRT

222
Q

Where do ependyomas arise from

A

Ependymal cells

223
Q

What is the problem with ependyomas

A

They block the CSF flow and cause hydrocephalus

224
Q

What are the common locations of ependyomas

A

4th ventricle for kids (more common)

Spine for adults

225
Q

What is the diagnostic test of choice for ependyoma

226
Q

What is the Tx for ependyoma

A

Sx if possible

May or may not use XRT or chemo

227
Q

Where do oligodendrogliomas arise from

A

Oligodendrocytes

228
Q

What is the key characteristic of oligodendrogliomas

A

They are slow growing

229
Q

What is the Tx for oligodendrogliomas

A

Watchful waiting or Sx if possible
XRT
Chemo = temozolamide

230
Q

What is often involved in optic nerve gliomas

A

Optic chiasm

231
Q

What condition are optic nerve gliomas associated with

A

Neurofibromatosis

232
Q

What are the SxS of optic nerve gliomas

A

Vision changes & maybe hormonal disturbances

233
Q

What is the imaging of choice for optic nerve gliomas

234
Q

What are the 2 grades of pineal tumors

A

Low grade = pineocytoma (benin)

High grade = peneoblastoma (malignant)

235
Q

What is the MC pediatric tumor

A

Medulloblastoma

236
Q

Where are medulloblastomas found

A

ALWAYS in cerebellum

237
Q

What are characteristics of medulloblastomas

A

Fast growing, high grade tumors

238
Q

What is the Tx of medulloblastomas

A

Sx, radiation, +/- chemo

239
Q

What are the most common primary CAs to met to the brain

A

Lung and breast CA

240
Q

What are the types of neurofibromatosis

A

Type 1 = von Recklinghausen disease; 1/3,000

Type 2 = 1/25,000; autosomal dominant

241
Q

What are the main SxS of type 1 neurofibromatosis

A

All the skin manifestations (pretty obvious)

15% will develop malignant gliomas

242
Q

What is the most common cause of dementia

A

Alzheimer’s

243
Q

What are the 3 types of dementia

A

Cortical (AD, metabolic)
Subcortical (vascular dementia)
Mixed (Parkinson’s, lewy body)

244
Q

What are the main findings with AD

A

Amyloid plaques

Neurofibrilliary tangles

245
Q

Which neurotransmitter is the problem with AD

A

Decreased ACh due to death of cholinergic neurons

246
Q

How do you Dx AD

A

Dx of exclusion

247
Q

What is the Tx of AD

A 
Cholinesterase inhibitors (Aricept, Exelon, Reminyl)
NMDA receptors (Namenda)
248
Q

What are RFs for multi infarct dementia

A

DM, CAD, HTN, CVA, smoking, men

249
Q

What is the Tx of multi-infarct dementia

A

Manage RFs

250
Q

Who is affected more by dementia with lewey bodies

251
Q

What are lewy bodies

A

protein deposits in nerve cells that can develop into plaques & tangles

252
Q

What is the most prevalent SxS of lewy body dementia

A

Visual hallucinations

253
Q

What is the Tx of lewy body dementia

A 
Same meds as AD, may use Parkinson's meds too
Poor prognosis (dead 5-7years)
254
Q

Picks disease is also known as

A

Frontotemporal lobar degeneration (FTD)

255
Q

Why is FTD called picks disease

A

B/c of the abnormal protein-filled structures found in the pathology

256
Q

What is the classic triad for normal pressure hydrocephalus

A

Gait instability
Urinary incontinence
Dementia
“Wobbly, wet, wacky”

257
Q

What is the diagnostic study of choice for normal pressure hydrocephalus? What is the result

A 
MRI
Shows ventriculomegaly (enlargement of ventricles)
258
Q

What is the Tx of normal pressure hydrocephalus

A

Shunting may be best if responsive to LP

259
Q

_________ is lacking in EtOH dementia

A

Thiamine (B1)

260
Q

What are the tell tale SxS of wernicke’s encephalopathy

A

Opthalmoplegia and verticle & horizontal nystagmus

261
Q

The key finding in progressive supranuclear palsy is…

A

Paralysis of verticle gaze

262
Q

What is the diagnostic test of choice for evaluation of new onset seizures

A

MRI unless suspected bleed

263
Q

When can a pt stop taking seizure meds

A

When they are seizure free for 2 years and have a normal EEG

264
Q

What are the SxS of absence seizures

A

NO AURA
Vacant, dazed expression
Staring
Pallor
Timing (10 seconds max, many times during day)
Post-ictal (picking clothes, pursing lips)

265
Q

What is Tx for absence seizures

A

Zarontin
Depakote
Tx for 2 years then if seizure free wean off

266
Q

What is generalized tonic clonic called

A

Grand mal seizure

267
Q

What often precedes a grand mal

A

Aura with irritability, apathy, HA, scintillating scotoma, nausea, choking sensation, paresthesias

268
Q

What are the SxS of grand mal

A

Sudden LOC, tonic, clonic, incontinence, tongue biting

269
Q

What is the 1st line Tx of grand mal

A

Valproic acid (depakote)

270
Q

What is the 2nd line Tx of grand mal

A

Dilantin or Tegretol

271
Q

What seizure is characterized by sudden single or multiple jerks AKA infantile spasms

A

Myoclonic seizures

272
Q

What are the SxS of atonic seizures

A

LOC, head drop w/ loss of posture, “drop attack” & falls

273
Q

Simple partial seizures have _______ areas but may spread

274
Q

Sensory SxS of simple partial seizures

A

Visual, auditory, olfactory, gustatory

275
Q

Autonomic SxS of simple partial seizures

A

GI SxS, flushing

276
Q

Motor SxS of simple partial seizures

A

Jerking limbs & paresthesias

277
Q

Other SxS of simple partial seizures

A

Hallucinations, deja vu, jamais vu

278
Q

Are simple partial seizures unilateral or bilateral

A

Unilateral

279
Q

What is the Tx of simple partial seizures

A

Dilantin, Tegretol, Depakote

280
Q

What is the most common type of seizure

A

Complex partial

281
Q

Where do complex partials start? Where might they travel

A

Start = temporal

Travel to frontal

282
Q

What may complex partials progress to

283
Q

What are the SxS of complex partial

A

LOC
Aura (GI symptoms, sense of fear)
Stare, automatisms, facial movements

284
Q

How long do complex partial seizures last

A

Lasts 30 sec - 2 min

285
Q

What is the Tx of complex partial seizures

A

Tegretol, Dilantin, temporal lobe resection if meds fail for 2 years

286
Q

Who gets rolandic epilepsy

A

ONLY children

287
Q

What are the SxS of rolandic epilepsy

A

Face/cheek twitch
Drooling
Difficulty speaking
Often only occur during sleep

288
Q

What is the Tx of rolandic epilepsy

A

Tegretol, Trileptal, Neurontin

289
Q

Gelastic seizure is characterized by

A

Laughing outburst

290
Q

Dacrystic seizure is characterized by

A

Crying outburst

291
Q

Postictal period typically lasts_______ and has what SxS

A

Last 5-30 minutes

SxS = HA, exhaustion, confusion, drowsiness

292
Q

What are the RFs for status epilepticus

A 
MEDICATION WITHDRAWL
Alcohol withdrawl
Drug overdose
Intracranial infections
Neoplasms
293
Q

What are the SxS of status epilepticus

A

Seizure lasting > 30min and/or 2+ seizures w/o recovery period

294
Q

What is the 1st line Tx of status epilepticus

A

Lorazepam or daizepam

295
Q

What seizure drugs should NOT be used in pregnant pts

A

Depicote & tegretol

296
Q

What are cateminal seizures

A

Seizure in women with epilepsy due to progesterone withdrawl or mid-cycle estrogen surge

297
Q

What drug is polycystic ovary disease related to

A

Valproate (Depakote)

298
Q

Psychogenic nonepileptic seizure is AKA

A

“pseudoseizures”

299
Q

Causes of pseudoseizures are…

A

Anxiety attacks/PTSD

Conversion disorder

300
Q

What is atypical seizure activity

A 
Nonfocal (opposite arm/leg)
Pelvic thrusting
Head turning side to side
Eyes closed (tight)
Tongue biting limited to tip
Postictal crying
Memory of event
May be triggered by emotional/stressful situation
301
Q

Who is more likely to get MS

A

White > black
Female > male
Age 15-60

302
Q

MS is an __________ disease resulting in…..

A

Autosomal disease results in demyelination of white matter

303
Q

What are the types of MS

A

Relapsing remitting
Secondary progressive (Most Common!)
Primary progressive
Progressive relapsing

304
Q

What is the presentation of MS

A

Sensory loss
Optic neuritis
Weakness
Paresthesias

305
Q

What are other SxS of MS

A 
Ataxia
Diplopia
Lhermitte sign
Telegrapghic speech
Dementia
Facial palsies
Impotence
306
Q

What is the diagnostic of choice for MS

A

MRI shows spotty irregular demyelination

307
Q

What is the 2nd diagnostic test for MS. What does it show

A

LP shows oligoclonal bands (bands of Ig)

308
Q

What is the Tx of MS acute exacerbation

A

Methylprednisone IV x3days then switch to oral prednisone

309
Q

What is the 1st line management of MS

A

Betaseron
Avonex
Rebif
Glatiramer

310
Q

What is 2nd line management of MS

A

Mitoxantrone (Novantrone)

311
Q

What is 3rd line management of MS

A

Natalizumab

312
Q

What other things need to be managed in MS

A 
Spasticity (Baclofen)
Pain (Amitriptyline)
Urinary (Ditropan or Detrol)
Constipation
Fatigue (Provigil)
Depression (SSRI)
313
Q

What is the benign course of MS

A

1-2 relapses then recovery

314
Q

What is commonly lost in pts with MS

A

Independent walking

315
Q

What condition is a common development/association of MS

A

Optic neuritis

316
Q

Is optic neuritis usually uni or bilateral?

What visual acuity constitutes

A

Usually unilateral with acuity of 20/100

317
Q

What is the onset of optic neuritis

A

Usually hours to days

318
Q

What are the PE results for optic neuritis

A

Optic nerve pallor

NORMAL pupillary reflex

319
Q

This is an idiopathic, inflammatory neuropathy that affects men more than women and usually follows infection

A

Gullain barre

320
Q

What neurons are affected by guillain barre

A

Sensory and motor

321
Q

Gullain barre is an example of….

A

Antigen mimicry

322
Q

What is the typical presentation of Guillain barre

A 
Proximal muscle weakness
Legs affected more than arms
Myalgias (shoulder, back, thighs)
Paresthesias
Decreased DTRs
323
Q

What are the types of Gullain barre

A

Acute inflammatory demyelinating polyadiculoneuropathy (AIDP) = 90%
Acute motor axonal neuropathy (AMAN)

324
Q

What are the Txs for Gullain barre

A

Supportive or IVIg or plasmapheresis

Vaccinations (H1N1, tetanus, hepatitis)

325
Q

What are long term effects of Gullain barre

A

Long term foot drop and hand weakness

326
Q

What is the chronic form of Gullain Barre

A

Chronic idiopathic demyelinating polyneuropathy (CIDP)

327
Q

Neuromuscular autoimmune disease with antibody formation to nicotinic ACh receptors

A

Myasthenia gravis

328
Q

Drug induced myasthenia gravis

A

Tetracycline, aminoglycosides, propranolol, lithium

329
Q

What are the main SxS of myasthenia gravis

A 
Asymmetric proximal limb weakness
CN weakness (lid lag, ptosis, diplopia, facial weakness, slurred speech, fatigability)
330
Q

What is the Tx of myasthenia gravis

A 
Anticholinesterase inhibitors (Mestinon)
Immunosuppression (prednisone)
331
Q

Bad complication of myasthenia gravis

A

Paralysis of respiratory muscles

332
Q

Disorder characterized as persistent pain in dermatomal distribution

A

Postherpetic neuralgia

333
Q

Degeneration of dopaminergic neurons in substantia nigra

A

Parkinson’s

334
Q

What are the SxS of Parkinson’s

A

Rest tremor
Bradykinesia
Rigidity

335
Q

What are common aspects of Parkinson’s tremor

A

Rest tremor & pill rolling

336
Q

What are common features of Parkinson’s rigidity

A

Cogwheeling & lead pipe resistance

337
Q

What are common features of Parkinson’s bradykinesia

A

Micrographia & slow, shuffling gait

338
Q

What is the diagnostic test of choice for Parkinson’s

A

Spect imaging to see dopaminergic pathways

339
Q

What is the primary Tx of choice for Parkinson’s

A

Levodopa

Levodopa/carbidopa (Sinemet)

340
Q

What are side effects of levodopa

A

Dyskinesias/choreiform movements

341
Q

What is important to remember regarding Parkinson’s Tx

A

After 5-10 years effectiveness wears off, pt experiences “on-off” stages

342
Q

How do you get benign essential tremor

A

Autosomal dominant inheritance

343
Q

What are exacerbating factors of benign essential tremor

A

Stress, fatigue, stimulants

344
Q

What are alleviating factors of benign essential tremor

A

Alcohol & rest

345
Q

Is benign essential tremor a rest or action tremor

A

Action tremor

346
Q

What areas are commonly affected in benign essential tremor

A

Hands and head

347
Q

What is the Tx of benign essential tremor

A 
Beta blockers (propranolol, metoprolol)
Anticonvulsants (Primidone)
348
Q

Autosomal dominant disease with mid-life onset

A

Huntington’s chorea

349
Q

What are classic SxS of huntington’s chorea

A

Choreiform movements, mental decline/dementia

350
Q

Which type of diabetes is more likely to develop diabetic polyneuropathy

351
Q

What is diabetic polyneuropathy associated with

A

Elevated HgbA1c

352
Q

PE results of diabetic polyneuropathy

A

Decreased monofilament sensation, sharp/dull sensation, vibratory & proprioception sense, DTRs

353
Q

What is the Tx of diabetic polyneuropathy

A 
Optimize glucose control
TCA
Anticonvulsants
SNRI
Opiods (last resort)
354
Q

Inflammation at the geniculate ganglion facial nerve linked with OM & herpes zoster

A

Bell’s palsy

355
Q

Red flags of bell’s

A

Gradual onset > 2wks, no forehead involvement, bilateral involvement

356
Q

What are the PE results of Bell’s

A 
Loss of nasolabial fold
Corner of mouth droops
Inability to close eye
Decreased lacrimation
INTACT SENSATION
357
Q

What is the Tx of Bell’s

A

Steroids and antivirals within 72hrs (acyclovir)

Clinical Medicine Final (2 decks)

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