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ITE '23 > Ch. 15 Neuro > Flashcards

Ch. 15 Neuro Flashcards

1
Q

What percent of strokes are ischemic vs hemorrhagic?

A

85% ischemic
15% hemorrhagic

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2
Q

What is the most common cause of stroke in the US?

A

thrombotic – results from clot formation at the site of an ulcerated atherosclerotic plaque

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3
Q

What are the two types of thrombotic strokes?

A

Lacunar - stroke of a small terminal vessel
Cortical

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4
Q

How is Cerebral Perfusion Pressure calculated?

A

CPP = MAP - ICP

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5
Q

What is the NIH Stroke Scale range?

A

0 to 42

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6
Q

What is amaurosis fugax?

A

transient monocular blindness from embolization of carotid plaque to the ophthalmic artery

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7
Q

How is TIA defined?

A

transient neurologic deficits lasting < 1 hour with no evidence of infarction on brain
imaging studies (MRI)

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8
Q

What is Wernicke aphasia?

A

receptive aphasia – an inability to comprehend language input; speech is fluent but disorganized

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9
Q

Where is Wernicke’s ares?

A

Temporal lobe

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10
Q

What is Broca aphasia?

A

expressive aphasia – inability to communicate verbally. Speech is halting and
produced with great effort

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11
Q

Where is Broca area?

A

frontal lobe

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12
Q

The hallmark of ________ circulation
stroke is crossed deficits (eg, sensory loss
on right side of face vs left side of body).

A

posterior

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13
Q

In hypertensive patient, where you are trying to lower BP to give TPA, which two medications are first line?

A

Labetalol, Nicardipine

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14
Q

What artery is implicated with:
Contralateral weakness of leg > arm and face with minimal sensory findings

A

Anterior cerebral artery

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15
Q

What artery is implicated with:
Contralateral weakness AND numbness of arm and face > leg

A

Middle cerebral artery (most common)

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16
Q

In a middle cerebral artery stroke you may see a gaze preference for which side?

A

Gaze preference toward size of infarct

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17
Q

What artery is implicated in clumsy hand–dysarthria syndrome?

A

Lacunar artery?

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18
Q

What artery is implicated if:
Contralateral visual field and light touch/pinprick deficit with minimal weakness

A

Posterior Cerebral Artery

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19
Q

What artery is implicated if:
Crossed deficits: ipsilateral cranial nerve deficits with contralateral weakness

A

Vertebrobasilar artery

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20
Q

What artery is implicated in “Locked in” syndrome?
(complete paralysis of voluntary muscles except eye movement; normal level of consciousness)

A

Basilar artery

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21
Q

What artery is implicated:
Sudden inability to walk or stand with
headache, vertigo, nausea/vomiting,
abnormal gait, CN abnormalities

A

Cerebellar artery

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22
Q

What glucose level is a contraindication to tPA?

A

> 400

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23
Q

What is the dose for tPA for stroke?

A

0.9 mg/kg with 10% given as bolus, remaining infused over 60 minutes.

Ex: 80 kg person: 72 mg total; 7.2 mg bolus, 64.8 mg infusion over remaining hour

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24
Q

If symptomatic intracranial hemorrhage (SICH) is confirmed with non-contrast CT, which thrombolytic and anti-platelet reversal agents should be considered?

A

FFP, platelets, cryoprecipitate

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25
Q

Aspirin should be given within ___ hours (unless thrombolysis candidate) for secondary stroke prevention.

A

48 hours

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26
Q

In secondary stroke prevention, what medications should be given if ASA allergy?

A

Clopidogrel (or ticlopidine)

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27
Q

Is routine seizure prophylaxis recommended in CVAs?

A

NO

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28
Q

What role does heparin have in CVAs?

A

No proven benefit in acute stroke

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29
Q

What is the ABCD^2 score used for?

A

predict likelihood of subsequent stroke within 2 days

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30
Q

What variables are included in ABCD^2 score to predict subsequent stroke in patients with TIA?

A

age >60y
BP >/= 140/90 mmHg
unilateral weakness (2 points)
speech disturbance without weakness
duration >/= 60 min (2 points)
Duration 10-59 min
Diabetes

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31
Q

What are the two categories of hemorrhagic stroke?

A

intracerebral hemorrhage and subarachnoid hemorrhage

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32
Q

What is the most common cause of ICH?

A

chronic hypertension

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33
Q

What are the 3 “B”s of increased ICP?

A

Bradycardia, BP increasing, bradypnea

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34
Q

What is mannitol dose for increased ICP?

A

0.25-2 g/kg IV of 15-25% solution over 30-60 minutes

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35
Q

If no clinical signs of increased ICP, what should target BP be?

A

160/90

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36
Q

If clinical signs of increased ICP exist, consider ICP monitoring with what goal for CPP?

A

60-80 mmHg

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37
Q

What is the difference between simple partial seizures and complex partial seizures?

A

Simple partial = brief event WITHOUT alteration of consciousness
complex partial = impairment of consciousness and +postictal state

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38
Q

What is a secondary generalized seizure?

A

partial seizure that spreads to both hemispheres
(eg generalized seizure preceded by aura or unilateral motor symptoms)

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38
Q

What is a secondary generalized seizure?

A

partial seizure that spreads to both hemispheres
(eg generalized seizure preceded by aura or unilateral motor symptoms)

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39
Q

What are the two types of nonconvulsive seizures?

A

absence or petit mal

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40
Q

What is seen on EEG during nonconvulsive seizures?

A

brief 3Hz, spike and wave discharges on EEG

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41
Q

what is another name for convulsive seizures?

A

Grand mal

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42
Q

What are the different types of convulsive (grand mal) seizures? List 5

A

clonic
tonic
tonic-clonic
myoclonic
atonic

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43
Q

What is Todd paralysis?

A

Focal paralysis, typically following a generalized seizure usually lasts 1-2 hours but may last 1-2 days

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44
Q

How is status epilepticus defined?

A

Seizure lasting ≥ 5 minutes
or
≥ 2 discrete seizures without a complete recovery in between the events

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45
Q

If seizure due to alcoholism is suspected, which two things should be given (besides benzos)?

A

thiamine and glucose

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46
Q

What are two possible side effects of phenytoin administration?

A

hypotension and cardiac dysrhythmias (due to its propylene glycol diluent)

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47
Q

What is the difference between phenytoin and fosphenytoin?

A

fosphenytoin is the water soluble prodrug of phenytoin (with better side effect profile)

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48
Q

what is the onset of action of phenytoin and fosphenytoin?

A

10-30 minutes

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49
Q

What are possible side effects of phenobarbibtal?

A

sedation, respiratory depression, and hypotension

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50
Q

What is the onset of action of phenobarbital?

A

15-30 minutes

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51
Q

What should be given for seizures in pregnancy?

A

Magnesium sulfate, if eclamptic
Otherwise, discuss with neuro and OB – risk of seizures is likely much worse than risk of teratogenicity

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52
Q

What should be given if seizure is suspected to be due to isoniazid overdose or gyromitrin toxin (mushroom)?

A

Pyridoxine (Vitamin B6)

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53
Q

What is the most common bacteria implicated in meningitis?

A

streptococcus pneumoniae
(gram positive diplococci)

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54
Q

In meningitis in ages >60 years old, what organism should be considered and covered with antibiotics?

A

Listeria monocytogenes
(gram-POSITIVE rod)
cover with Ampicillin

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55
Q

What are the three most common organisms implicated in meningitis in those <1 month old?

A

Group B strep
E coli
L monocytogenes

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56
Q

What are the three most common causes of meningitis following neurosurgical procedure or head trauma?

A

S pneumoniae
Staph aureus
Pseudomonas aeruginosa

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57
Q

What is the most common viral cause of meningitis and what season is it most common?

A

Enterovirus
summer months

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58
Q

Which 2 organisms should always be considered as cause for meningitis in immunocompromised?

A

Fungal (eg cryptococcus)
Parasitic (eg Toxoplasma gondii)

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59
Q

What are some noninfectious causes of meningitis?

A

SLE
Drug induced
Carcinomatosis
Sarcoidosis
Behcet disease

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60
Q

What does bacterial meningitis typically start?

A

nasopharyngeal colonization –> hematogenous spread –> CNS infection

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61
Q

Meningitis due to fungi typically spread from what source?

A

Pulmonary

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62
Q

What do you call the following physical exam finding?
Position the patient with hips and knees flexed. Extend the knees. Flexion of neck or pain in neck is positive sign.

A

Kernig sign

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63
Q

What do you call the following sign?
Neck flexion results in flexion at hips (neck sign) or passive flexion of hip on one side results in contralateral hip flexion (contralateral sign).

A

Brudzinski sign

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64
Q

What three concomitant infections should you look out for in suspected meningitis?

A

Sinusitis, otitis, pneumonia

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65
Q

When is a Head CT recommended BEFORE LP in suspected meningitis?

A
  1. patients >60 years old
  2. immunocompromised (eg HIV)
  3. History of CNS disease (stroke, mass lesions, or head trauma)
  4. New onset seizures within 1 week
  5. Marked CNS depression, papilledema, or focal neuro deficits
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66
Q

What are the 3 contraindications to LP?

A
  1. Coagulopathy (relative): INR > 1.5, Platelets <50k (<20k = absolute)
  2. infection at skin puncture site (absolute)
  3. Increased ICP or trauma to lumbar vertebrae
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67
Q

What is normal opening pressure for LP?

A

5-20 cm H2O

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68
Q

What are normal leukocyte levels for CSF?

A

</=5

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69
Q

What is a normal CSF protein level?

A

20-45

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70
Q

What is normal glucose for CSF?

A

50-80% or 60-70% of serum level

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71
Q

How does the LP opening pressure change in bacterial meningitis?

A

elevated

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72
Q

How does the LP opening pressure change in viral meningitis?

A

normal or slightly elevated

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73
Q

What is the typical CSF leukocyte count in bacterial meningitis?

A

> /= 500 leuks/mm3

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74
Q

What is the typical CSF leukocyte count in bacterial meningitis?

A

100-500 leuks/mm3

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75
Q

What is the CSF %neutrophil count in bacterial meningitis?

A

> 80%

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76
Q

What is the CSF %neutrophil count in bacterial meningitis?

A

<50%

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77
Q

What is the CSF protein level in bacterial meningitis?

A

> 200

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78
Q

What is the CSF protein level in bacterial meningitis?

A

<200

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79
Q

What is the CSF glucose level in bacterial meningitis?

A

</=40% or <50% of serum

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80
Q

What is the CSF glucose level in viral meningitis?

A

usually normal

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81
Q

What is the CSF glucose level in fungal meningitis?

A

<50%

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82
Q

What is the CSF protein level in fungal meningitis?

A

> 200

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83
Q

What is the CSF %neutrophil level in fungal meningitis?

A

<50%

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84
Q

What is the CSF leukocyte count in fungal meningitis?

A

10-500

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85
Q

What is the LP opening pressure in fungal meningitis?

A

elevated

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86
Q

CSF gram stain with gram positive diplococci suggests what organism?

A

pneumonoccocus

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87
Q

CSF gram stain with gram negative diplococci suggests what organism?

A

meningococcus

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88
Q

CSF gram stain with small pleomorphic gram negative coccobacilli suggests what organism?

A

H influenzae

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89
Q

CSF gram stain with gram positive rods and coccobacilli suggests what organism?

A

listeria

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90
Q

What immediate empiric antibiotics should be given if meningitis suspected?

A

Vancomycin 1gIV
Ceftriaxone or Cefotaxime 2g IV
+/- Ampicillin if neonate, >60 yrs old, debilitated, or alcoholic
+/- Metronidazole if concern for extension from sinusitis or otitis

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91
Q

Giving antibiotics before LP will not decrease ability to detect organism in CSF fluid if LP performed
within ___ hours and antigen assays are utilized

A

2

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92
Q

Should steroids be given for meningitis?

A

YES– Appears to decrease morbidity and mortality in adults with bacterial meningitis (especially S pneumoniae) and children with H influenzae
meningitis.

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93
Q

What is the dose for steroids for meningitis?

A

Dexamethasone 0.15 mg/kg IV 15 minutes before or concurrent with the first dose of antibiotics, repeat every 4-6 hours (max 10 mg in adults).

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94
Q

What is the treatment for viral meningitis?

A

no specific treatment unless herpes simplex meningitis – then acyclovir

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95
Q

If neisseria meningitidis or H influenzae type b is identified as cause for meningitis, what should close contacts be treated with?

A

rifampin (4 doses 10 mg/kg q12h) is recommended
once bacterial organism is identified.
Alternatively, ciprofloxacin can be used (500 mg PO single dose).

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96
Q

What is the most common cause of encephalitis?

A

viruses - majority of cases
Arbovirus and HSV = most common

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97
Q

What is the diagnostic imaging of choice for encephalitis?

A

MRI with contrast
(CT with contrast is alternative but is less sensitive)

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98
Q

What is the empiric treatment for encephalitis where HSV or HZV are suspected?

A

Acyclovir 10mg/kg IV q8h

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99
Q

What is the empiric treatment for encephalitis where cytomegalovirus is suspected?

A

Ganciclovir

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100
Q

What are the 3 mechanisms of spread that cause brain abscesses?

A
  1. Contiguous infection of middle ear, sinus, or teeth
  2. Neurosurgery or penetrating trauma
  3. Hematogenous spread
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101
Q

How does a brain abscess appear of MRI/CT with contrast?

A

ring-enhancing lesions

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102
Q

What is the empiric treatment for brain abscesses with no obvious source?

A

Vancomycin + ceftriaxone or cefotaxime +
metronidazole

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103
Q

What is the most common cause of secondary seizures in the developing world?

A

Neurocysticercosis (CNS T solium larvae
infection – from eating undercooked pork)

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104
Q

What is the treatment for Neurocysticercosis (CNS T solium larvae infection)?

A

Antiparasitic agents (praziquantel and albendazole).

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105
Q

The majority of shunt infections present within _______ (time period) of placement).

A

within 6 months
(50% within 2 weeks).

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106
Q

Which two organisms are most commonly implicated in intracranial shunt infections?

A

■ Staphylococcus epidermidis (50%)
■ S aureus

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107
Q

What percentage of SAH have a completely normal neuro exam?

A

50%

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108
Q

What is the Hunt and Hess classification?

A

The Hunt and Hess scale is a grading system used to classify the severity of a subarachnoid hemorrhage based on the patient’s clinical condition. The scale ranges from a score of 1 to 5. It is used as a predictor of prognosis/outcome with a higher grade correlating to a lower survival rate.

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109
Q

How sensitive is a noncon Head CT for identifying SAH?

A

Symptoms < 24 hours = sensitivity > 90%-95% (controversial, some sources cite 98% within 12 hours). Increasing evidence that the sensitivity
of CT within the first 6 hours after a minor SAH approaches 100%.

Symptoms for 1 week = sensitivity < 50%.

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110
Q

What is the gold standard for diagnosing SAH if CT negative?

A

Xanthochromia (via spectrophotometry, NOT naked eye) ≥ 12 hours after onset of headache

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111
Q

In SAH, what should BP goal be?

A

Control BP (MAP < 130).

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112
Q

What medication has been shown to prevent vasospasm and ischemic stroke?
(initiate within 4 days of symptom onset)

A

Nimodipine PO

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113
Q

What is a subdural hygroma?

A

Collection of blood-tinged fluid in dural space of uncertain etiology; tends to follow trauma; on CT fluid density is same as CSF; surgical evaluation is needed, if symptomatic

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114
Q

What is the most common cause of brain tumor?

A

metastases from lung or breast carcinoma

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115
Q

What should steroids be considered for brain mets?

A

if edema is present on imaging or if severe symptoms

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116
Q

What is the diagnosis criteria for Temporal arteritis?

A

3 of 5 criteria:
■ Age > 50
■ New onset localized headache
■ Temporal artery tenderness or decreased pulse
■ Erythrocyte sedimentation rate > 50 mm/h
■ Refer urgently for temporal artery biopsy to confirm diagnosis if highly suspicious

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117
Q

What is the treatment for Temporal Arteritis?

A

Immediate high dose steroids: Prednisone 40-80 mg/d
NSAIDs for pain relief

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118
Q

What is a complication of temporal arteritis?

A

loss of vision due to ischemic optic neuritis

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119
Q

What is idiopathic intracranial hypertension also known as?

A

Pseudotumor cerebri

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120
Q

What are risk factors for idiopathic intracranial hypertension (aka pesudotumor cerebri)?

A

young obese female
oral contraceptives
vitamin A
chronic steroid use
tetracyclines
and thyroid disorders

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121
Q

What are signs/symptoms of idiopathic intracranial hypertension (aka pesudotumor cerebri)?

A

■ Long-standing headache ± visual disturbances and nausea/vomiting.
■ Visual loss may occur.
■ Eye findings may include papilledema, loss of peripheral vision, and CN VI palsy.

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122
Q

How is idiopathic intracranial hypertension (aka pesudotumor cerebri) diagnosed?

A

increased intracranial pressure (> 25 cm H2O) with
normal CSF evaluation
(Head CT may show small ventricles and an enlarged cisterna magna)

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123
Q

When diagnosing idiopathic intracranial hypertension (aka pesudotumor cerebri), what test should be done/what should be excluded?

A

Consider magnetic resonance venography (MRV) for evaluation of cerebral venous thrombosis

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124
Q

What is the treatment for idiopathic intracranial hypertension (aka pesudotumor cerebri)?

A

Acetazolamide (decreases CSF formation) +/- furosemid

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125
Q

When are steroids and/or therapeutic LP indicated for idiopathic intracranial hypertension (aka pesudotumor cerebri)?

A

In the setting of acute vision loss at temporizing measure until surgical intervention

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126
Q

What is the treatment for refractory idiopathic intracranial hypertension (aka pesudotumor cerebri)?

A

Optic nerve sheath fenestration or shunt placement

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127
Q

What are the most common causes of stroke in patients <45 years old?

A

internal carotid and vertebral artery dissection
(usually due to trauma or injury)

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128
Q

What are symptoms of internal carotid dissection?

A

Unilateral anterior neck pain or headache around the eye or frontal area, classically abrupt in onset.
■ ipsilateral Horner syndrome, contralateral stroke, or TIA symptoms.

Horner syndrome:
partial ptosis (drooping or falling of the upper eyelid), miosis (constricted pupil), and facial anhidrosis (absence of sweating) due to a disruption in the sympathetic nerve supply

129
Q

What are signs/symptoms of vertebral artery dissection?

A

Marked occipital or posterior neck pain with signs of brainstem TIA or stroke

130
Q

How are internal carotid and vertebral artery dissection diagnosed?

A

CTA and/or MRI/MRA to confirm diagnosis
(noncon CT is NOT diagnostic study of choice)

131
Q

What is the treatment for internal carotid and
vertebral artery dissection?

A
  1. Surgical
  2. Anticoagulation with IV heparin –> warfarin with target INR 2-3

thrombolysis with IV alteplase for eligible patients with acute ischemic stroke

132
Q

In what population is cerebral venous thrombosis most common?

A

neonates and children
in adults, more common in women

133
Q

What are some causes of cerebral venous thrombosis?

A
  1. adjacent local infection (meningitis or ear, nose, and throat [ENT] infections),
  2. direct injury (eg, trauma) or
  3. hypercoagulable state (eg, pregnancy, Factor V Leiden, lupus anticoagulant, nephrotic syndrome, cancer).
134
Q

Cerebral venous thrombosis must be considered in any patient with new diagnosis of ____________.

A

idiopathic intracranial hypertension

135
Q

How is Cerebral Venous Thrombosis diagnosed?

A

MRV combined with MRI is imaging modality of choice
CT and standard MRI are useful only if positive and CANNOT exclude the diagnosis

CT venography is a rapid, readily available, and accurate technique for detecting cerebral venous thrombosis; use may be limited because of low resolution of the deep venous system and cortical veins

136
Q

What is the treatment for Cerebral Venous thrombosis?

A

Heparin
If severe –> catheter-based thrombolysis

137
Q

What causes a post-LP headache

A

persistent CSF leak from the LP puncture site

138
Q

What are the characteristics of post-LP headache?

A

headache that is worse with upright posture and improved with laying flat

139
Q

What is the treatment for a post-LP headache

A

simple analgesics
IV fluids
Caffeine IV

if no relief with above –> blood patch (epidural injection of autologous blood)

140
Q

What precautions can be taken to prevent post-LP headache?

A
  1. Use small-bore needle with noncutting tip, angle needle parallel to longitudinal fibers of the dura and reinsert stylet prior to needle removal.

Bed rest after LP and patient positioning have not been shown to reduce incidence

141
Q

When does a post LP headache typically occur relative to LP?

A

within 24-48 hours of LP

142
Q

What is the suspected pathophysiology of a migraine headache?

A

Hypothesis is related to a slowly spreading wave of neuronal depolarization across the brain → ion dysfunction and vasoconstriction → prodrome and
aura (seen in 20%)

Trigeminovascular activation and release of peptides → inflammation of the pain-sensitive areas and vasodilation.

143
Q

What are some factors thought to trigger migraine headaches?

A

■ Menstruation, contraceptive estrogens, pregnancy
■ Certain foods or drinks, such as chocolate, caffeine, hard cheese, alcoholic beverages (especially red wine), monosodium glutamate (MSG), nitrites
■ Alterations in circadian rhythm

144
Q

What is the difference between a “common migraine” and a “classic migraine”?

A

common migraine = migraine without aura
classic migraine = migraine WITH aura

145
Q

What is the most common type of aura associated with a classic migraine?

A

visual = most common
- scintillating scotomata or visual field deficit

146
Q

How is an ophthalmoplegic migraine defined?

A

Headache + CN 3, 4, 6 deficits

147
Q

How is a retinal migraine defined?

A

headache + sudden monocular blindness

148
Q

What is the mechanism of action of triptans in the treatment of migraines?

A

Selective 5-HT (Serotonin) agonists
- cause vasoconstriction and blocks peptide release = decreased inflammation and pain

149
Q

When are Triptans contraindicated?

A

Patients with hypertension or other cardiovascular disease (because they are potent vasoconstrictors)
(do not use within 24 hours of other ergotamine-containing medications)

150
Q

What is the mechanism of action of dihydroergotamine (DHE, aka Migranal) in the treatment of migraines?

A

Nonselective 5-HT agonist

151
Q

When is dihydroergotamine (DHE, aka Migranal) contrainidicated?

A

Those with cardiovascular disease or within 24 hours of triptan use
or if you are taking any of the following medications: antifungals such as itraconazole, ketoconazole; HIV protease inhibitors such as indinavir (Crixivan), nelfinavir (Viracept), and ritonavir (Norvir); or macrolide antibiotics such as clarithromycin (Biaxin), erythromycin (E.E.S., E-Mycin, Erythrocin), and troleandomycin (TAO).

152
Q

What are common side effects of dihydroergotamine (DHE, aka Migranal)?

A

Nausea and vomiting

153
Q

What anti-emetics are best in migraines?

A

prochlorperazine, metoclopramide

154
Q

What population is prochlorperazine contraindicated?

A

older adults with dementia taking antipsychotics

155
Q

Nausea and vomiting are proposed to arise from peripheral or central stimulation of serotonin type 3 (5-HT3) and dopamine type 2 receptors, the predominant receptors expressed at the ___________ (part of the brain).

A

chemoreceptor trigger zone (CTZ)

156
Q

chemoreceptor trigger zone (CTZ) is also commonly known as what?

A

Area postrema

157
Q

Where is the chemoreceptor trigger zone (CTZ) (aka Area Postrema) located?

A

located within the dorsal surface of the medulla oblongata, on the floor of the fourth ventricle of the brain

158
Q

What is the utility of steroids in migraine headaches?

A

parenteral dexamethasone (10-24mg IV) is effective for reducing the rate of migraine recurrence (but not immediate relief)

159
Q

What is a common side effect of metoclopramide?

A

Tardive dyskinesia

160
Q

What medications are used for migraine prevention?

A

initial treatment with amitriptyline, venlafaxine, one of the beta blockers (metoprolol or propranolol), or topiramate.

161
Q

Describe characteristics of tension-type headaches.

A

bilateral, non-pulsating, not worsened by exertion
usually not associated with nausea and vomiting

162
Q

What is the treatment for tension-type headaches?

A

NSAIDs
for severe headache –> treat same as migraine

163
Q

In what population are cluster headaches most common?

A

young to middle aged men

164
Q

What are common precipitates of cluster headaches?

A

alcohol and stress

165
Q

Cluster headaches result from dysfunction of the ____ nerve.

A

trigeminal

166
Q

What are characteristics of Cluster headaches?

A

severe, unilateral orbital, supraorbital, or temporal pain;
episodes last 15-180 minutes, but recur in clusters (daily on same side for weeks)

167
Q

What are some symptoms associated with headache in cluster headaches?

A

Associated ipsilateral findings:
■ Conjunctival injection, lacrimation, nasal congestion, rhinorrhea, facial swelling, miosis, or ptosis

168
Q

What is the most effective treatment of cluster headaches?

A

High flow O2 is effective in 70% of patients
(7-12L via NRB)

169
Q

Besides O2, what are some other treatments for cluster headaches?

A

■ IV dihydroergotamine or sumatriptan; oral preparations take too long to
be effective.
■ Prophylaxis with oral steroid burst, verapamil, or antiepileptic agents (carbamazepine,
phenytoin).

170
Q

What are the three categories of confusional states (AMS)?

A
  1. delirium
  2. dementia
  3. psychosis
171
Q

What are the signs/symptoms of delirium?

A

■ Acute confusional state
■ Transient attention and cognition impairment
■ Waxing and waning symptoms
■ Hallucinations, if present, are visual and/or auditory

172
Q

What is the treatment for delirium?

A

treat underlying cause & be attentive to needs, sleep patterns, reorientation and redirection

Sedate with Haloperidol or benzos if severe agitation as a last resort as these meds can worsen delirium

173
Q

What is the most common cause of dementia?

A

Alzheimer disease

174
Q

What is the pathophysiology of Alzheimer disease?

A

Reduction of neurons in the cerebral cortex and increased amyloid deposition → neurofibrillary tangles and plaques

175
Q

What are examples of treatable causes of dementia?

A

■ Depression (most common treatable cause)
■ Vitamin B12 deficiency
■ Neurosyphilis
■ Hypothyroidism
■ Normal pressure hydrocephalus
■ Intracranial mass (eg, brain tumor)
■ Chronic drug use

176
Q

How is dementia diagnosed?

A

Diagnosis is primarily based on history of slow, progressive change in behavior.

All patients warrant neuroimaging, thyroid-stimulating hormone (TSH), and vitamin B12 level at minimum.

177
Q

What examination can be used test cognitive impairment and screen for dementia?

A

Mini-mental state examination

178
Q

Which six categories does the mini-mental state exam test?

A
  1. orientation
  2. memory
  3. attention
  4. calculation
  5. recall
  6. Language
179
Q

What score on the MMSE identifies cognitive impairment?

A

Cutoffs of < 24 or < 25 out of 30 are used to identify cognitive impairment

180
Q

What are two medications used in the treatment of Alzheimer disease?

A

donepezil (Aricept) and tacrine (Cognex)
reduce the metabolism of acetylcholine

181
Q

How is vascular dementia treated?

A

treat risk factors (hypertension)

182
Q

What causes normal pressure hydrocephalus (NPH)?

A

results from defective CSF uptake
(either a primary process or secondary to prior infection/injury/bleed)
leading to increased CSF volume

183
Q

What is the triad of signs/symptoms seen in NPH?

A
  1. dementia
  2. ataxia
  3. Urinary frequency or incontinence
    (wacky wobbly wet)
184
Q

How is NPH diagnosed?

A

Based on CT showing ventricular enlargement (without other pathology) and LP with normal intracranial pressure and fluid studies.

185
Q

What is the treatment for NPH?

A

Neurosurgical consultation for shunt placement.

186
Q

What are signs and symptoms of psychiatric psychosis?

A

■ Loss of contact with reality.
■ Hallucinations, if present, are auditory.
■ Usually not waxing and waning.
■ Consciousness not clouded.

187
Q

Consciousness can be divided into ____ and ___ functions.

A

arousal and content

188
Q

Arousal functions reside in the ___________ in the midbrain, pons, and medulla.

A

reticular activating system (RAS)

189
Q

Content functions reside in the ______ .

A

cerebrum

190
Q

_____ represents a failure in both arousal and content functions of the brain

A

Coma

191
Q

What is the mnemonic for causes of coma?

A

TIPS AEIOU

Trauma, temperature
Infection
Psychiatric, poisonings
Space occupying lesion, subarachnoid
Alcohol
Epilepsy, electrolytes, encephalopathy
Insulin
Opioids/overdose, oxygen (hypoxia, CO2 narcosis)
Uremia (metabolic)

192
Q

What is the oculovestibular reflex?

A

(Also known as caloric stimulation)

Direction of FAST component of nystagmus,
with irrigation of cold versus warm water
in patient with intact brainstem:

COWS
Cold
Opposite
Warm
Same

With ICED WATER – as consciousness is lost, the FAST component (towards the non-irrigated ear) is lost and the slow component deviates the eye in the direction of the irrigated ear.

193
Q

What is the oculocephalic reflex?

A

Oculocephalic reflex:

ensure the C-spine is cleared.
With patient’s eyes open, the head is briskly turned from side to side with the head held briefly at the end of each turn.
a POSITIVE response occurs when the eyes rotate to the opposite side to the direction of head rotation, thus indicating that the brainstem (CN3,6,8) is intact.
a similar result is seen when the head is flexed and extended — a positive result is downward deviation of the eyes during extension, and upward deviation during flexion (the eyelids, if closed, may also open as part of the ‘doll’s head phenomenon’).
These vertical responses indicates that the brainstem (CN3,4,8) is INTACT.

The eyes should gradually return to the mid-position in a smooth, conjugate movement if the brainstem is intact.

Patients with metabolic coma (e.g. hepatic failure) may have exaggerated, brisk oculocephalic reflexes.

194
Q

How is ataxia defined?

A

failure to make smooth, intentional movements

195
Q

What are the two types of ataxia?

A

MOTOR (CEREBELLAR) ATAXIA
SENSORY ATAXIA

196
Q

How does location of lesion within cerebellum affect incoordination?

A

lateral cerebellar lesion –> limb incoordination
midline cerebellar lesion (vermis) –> axial incoordination

197
Q

Describe a cerebellar ataxic gait.

A

wide based with unsteady and irregular steps

198
Q

Describe a sensory ataxic gait.

A

abrupt movement of legs and slapping of feet with each step

199
Q

What is dysmetria?

A

inaccurate fine movements

200
Q

What is dysdiadochokinesia?

A

clumsy rapid movements

201
Q

What is dyssynergia?

A

breakdown of movements into parts

202
Q

What is Romberg test?

A

Worsened unsteadiness with eyes closed (loss of visual input) is suggestive of SENSORY ataxia. If unsteadiness present with patient’s
eyes open, consider cerebellar pathology.

203
Q

How is nystagmus named directionally?

A

The direction of nystagmus is named by
the fast (cortical) component.

204
Q

How is vertigo defined?

A

the perception of movement where no movement exists

205
Q

Describe nystagmus that would suggest a central cause of vertigo.

A

Vertical and bi-directional (direction changing) nystagmus

206
Q

What are some other symptoms associated with vertigo that may suggest posterior fossa pathology?

A

diplopia, dysarthria, visual changes

207
Q

What is the imaging study of choice to visualize the posterior fossa (cerebellum, medulla, and pons)?

A

MRI
(CT may miss up to 80% of posterior cerebrovascular accidents (CVAs))

208
Q

What are some characteristics that more commonly suggest peripheral causes for vertigo?

A
  1. dramatic and sudden onset
  2. +n/v
  3. positional
  4. rotatory-vertical or HORIZONTAL nystagmus
  5. hearing loss
  6. no central findings
209
Q

What test, if positive, confirms posterior canal BPPV?

A

Dix-Hallpike test

210
Q

Describe the Dix Hallpike test.

A
  1. The patient begins sitting up, head oriented 45 degrees toward the ear to be tested.
  2. Lay patient down quickly with head past the end of the bed and extends their neck 20 degrees below the horizontal, maintaining the initial rotation of the head.
  3. Watch the patient’s eyes for torsional and up-beating nystagmus, which should start after a brief delay and persist for no more than one minute.

This would indicate a positive test.

211
Q

What are some characteristics of central vertigo?

A

classically ill defined and constant
vertical nystagmus

212
Q

What are some characteristics of central vertigo?

A

classically ill defined onset (rather than sudden onset) and constant
VERTICAL nystagmus

213
Q

What is the pathophysiology of BPPV?

A

Otoconia in the semicircular canals

214
Q

What is the pathophysiology of Meniere disease?

A

Increased endolymph within the chochlea and labyrinth

215
Q

What is the pathophysiology of Labyrinthisis?

A

viral or bacterial infection

216
Q

What is the pathophysiology of Ramsay-Hunt Syndrome (vestibular ganglionitis)?

A

viral infection of vestibular ganglion

217
Q

What are the signs/symptoms of Ramsay Hunt syndrome?

A

Hearing loss, vertigo, facial nerve palsy, grouped vesicles

218
Q

What is the pathophysiology of perilymph fistula?

A

trauma, sudden pressure change

219
Q

What are common causes of CN VIII lesions?

A

schwannomas, meningioma

220
Q

What are characteristics of CN VIII lesions?

A

gradual onset of vertigo, preceded by hearing loss

221
Q

Which five muscles does the Oculomotor Nerve (CN III) supply?

A
  1. levator muscle of the eyelid
  2. medial rectus muscle
  3. superior rectus muscle
  4. inferior rectus muscle
  5. inferior oblique muscle

also constricts the pupil through its parasympathetic fibers

222
Q

What physical exam findings suggest an oculomotor nerve palsy?

A

lid ptosis
mydriasis (a “blown” pupil)
then “down and out” eye

223
Q

What muscle is innervated by the Trochlear Nerve (CN IV)?

A

Superior Oblique muscles
– deficit results in vertical diplopia

224
Q

What are the three anatomic divisions of the trigeminal nerve (CN V)?

A

V1 - ophthalmic
V2 - maxillary
V3 - mandibular

225
Q

What are signs/symptoms of trigeminal neuralgia?

A
  1. brief, recurrent episodes of excruciating, unilateral facial pain lasting only seconds
  2. Right more than left side predominance
  3. May be able to elicit pain by tapping the side of the face, otherwise there should be no demonstrable physical findings
226
Q

What is the treatment for trigeminal neuralgia?

A

Carbamazepine and analgesics
(will need outpatient follow up to monitor carbamazepine levels, CB, and LFTs)

227
Q

Which muscle is innervated by the Abducens Nerve (CN VI)?

A

Lateral rectus muscle

228
Q

Describe an Abducens nerve (CN VI) palsy.

A

diplopia due to unopposed action of the medial rectus muscle; affected eye is pulled medially
diplopia is worse with lateral gaze towards the affected eye

229
Q

What is the most common cause of CN VI impairment?

A

diabetic neuropathy

230
Q

What is the most common cause of Bell Palsy?

A

Herpes virus infection
(pregnant women are at greater risk)

231
Q

In addition to facial paralysis, what other findings are seen in Bell palsy?

A

loss of taste of anterior 2/3s of tongue
hyperacusis (sound distortion or tinnitus)
bell phenomenon: eye appears to roll back in head when patient attempts to close the lid

232
Q

What is the treatment for ramsay hunt syndrome?

A

prednisone;
controversial – acyclovir for severe cases

233
Q

What organism is implicated in malignant otitis externa?

A

pseudomonas (especially if diabetic or immunocompromised)

234
Q

What are symptoms of an acoustic neuroma?

A

hearing loss accompanying facial weakness
(Schwannoma of CN VIII)
Classic triad:
1. hearing loss
2. tinnitus
3. disequilibrium

235
Q

What is the test of choice for diagnosing an acoustic neuroma?

A

MRI

236
Q

What is the treatment for Bell Palsy?

A

if within 1 week of symptoms:
- corticosteroids
- antiviral therapy
Eye protection, artificial tears

237
Q

Which tract contains motor pathways and has its fibers cross in medulla then descend in the spinal cord?

A

Corticospinal tract

238
Q

Which tract contains pain and temperature pathways and has its fibers first cross then ascend in the spinal cord?

A

Spinothalamic tract

239
Q

Which part of the spinal cord contains vibration and proprioceptive pathways and has its fibers ascend in ipsilateral spinal cord to medulla, then crosses?

A

Posterior (dorsal) columns

240
Q

What part of the spinal cord contains lumbar and sacral nerve roots?

A

Cauda equina

241
Q

How does damage to upper motor neurons affect reflexes?

A

decreased reflexes initially, then hyperreflexia after several days

242
Q

How does damage to lower motor neurons affect reflexes?

A

decreased reflexes

243
Q

What are classic findings of Central Cord Syndrome?

A

Bilateral motor weakness of upper extremities > lower extremities
&
distal > proximal extremities

244
Q

What is the likely mechanism of injury Central Cord Syndrome?

A

Hyperextension injury of narrowed cervical spinal
canal

245
Q

What are classic findings of Brown-Sequard injury?

A

Ipsilateral motor weakness and vibration/
position loss
Contralateral pain and temperature loss

246
Q

What is the likely mechanism of injury Brown-Sequard Syndrome?

A

Pentrating trauma

247
Q

What are classic findings of Anterior Cord Syndrome?

A

Motor weakness,
Loss of pinprick and light touch.

Preserved vibration and position sense

248
Q

What is the likely mechanism of injury Anterior Cord Syndrome?

A

Infarction of Anterior Spinal Artery

249
Q

What are classic findings of Cauda Equina Syndrome?

A

Urinary retention (overflow incontinence),
decreased rectal tone, saddle anesthesia,
motor weakness

250
Q

What is the likely mechanism of injury Cauda Equina Syndrome?

A

Ruptured L4-5 disc

251
Q

What are the signs/symptoms of discitis?

A

Back pain, fever, and refusal to walk in child < 10 y

252
Q

What is the likely etiology of discitis?

A

Inflammatory process in disc (viral or
Staphylococcus aureus)

253
Q

What are the signs/symptoms of Dorsal column disorders?

A

Loss of position sense, vibration, and light touch

254
Q

What is the likely etiology of Dorsal column disorders?

A

Syphilis or vitamin B12 deficiency

255
Q

What are the signs/symptoms of HIV myelopathy?

A

Weakness, gait problems, spasticity, sphincter dysfunction

256
Q

What is the likely etiology of HIV myelopathy?

A

Advanced HIV

257
Q

What are the signs/symptoms of spinal epidural abscess?

A

Severe pain with radiation down spine, signs of cord
compression, fever
ESR elevated
Get MRI (or if unavailable, CT myelogram)

258
Q

What is the likely etiology of Spinal epidural abscess?

A

Expanding abscess (IDU or
immunocompromise)

259
Q

What are the signs/symptoms of Spinal epidural hematoma?

A

Severe pain with radiation down spine, signs of cord
compression

260
Q

What is the likely etiology of Spinal epidural hematoma?

A

Expanding hemorrhage (trauma/procedures or
coagulopathy)

261
Q

What are the signs/symptoms of syringomyelia?

A

Dissociative anesthesia (loss of pain and temperature sensation with preservation of proprioception and light touch),
weakness, spasticity, interosseous wasting of hands

262
Q

What is the likely etiology of syringomyelia?

A

Syrinx formation in central spinal cord
(usually seen in cervical spine in association with Arnold-Chiari malformation)

263
Q

What are the signs/symptoms of transverse myelitis?

A

Transverse level of sensory loss, paresis,
sphincter dysfunction

264
Q

What is the likely etiology of transverse myelitis?

A

Post-viral or toxic inflammation

265
Q

What is the pathophysiology of Guillain-Barre Syndrome (GBS)?

A

an acute demyelinating disorder of the peripheral nerve
Antecedent illness (viral or Campylobacter jejuni gastroenteritis, upper respiratory infection [URI]) → autoimmune response → damage to myelin sheath → symptoms

266
Q

hat are signs and symptoms of Guillain Barre Syndrome?

A

antecedent illness –> latent period
ascending symmetric paresthesias and motor weakness (peaks within 3 weeks of onset)

decreased DTRs
normal rectal tone
may progress to ventilatory failure

267
Q

What is the Miller Fisher Variant of Guillain Barre Syndrome?

A

Ophthalmoplegia, ataxia, ↓ or absent reflexes.
Around 25% will have limb weakness in addition to cranial nerve/cerebellar findings.

268
Q

How is Guillain Barre Syndrome diagnosed?

A

Electrodiagnostic testing – nerve conduction studies (NCS) and electromyography (EMG)

CSF = markedly elevated protein (>45 ug/dL) with up to 100 lymphocytes/uL

269
Q

What is the treatment for Guillain Barre Syndrome?

A

Supportive therapy
IVIG or plasmapheresis
Respiratory, FEV1, NIF monitoring

270
Q

What organism causes diptheria?

A

Corynebacterium diptheriae

271
Q

What is the pathophysiology of diptheria?

A

Respiratory or skin (tropical climates or poor hygiene) infection with
C diphtheriae → exotoxin release →
■ Local membrane formation
■ Peripheral neuropathy → neurologic symptoms

272
Q

What disease classically causes Exudative pharyngitis with progressive weakness?

A

Diptheria

273
Q

How is diptheria treated?

A

Diptheria antitoxin
+abx (penicillin or erythromycin)

274
Q

What causes diabetic distal symmetric polyneuropathy?

A

microvascular injury to the nerve

275
Q

What is the treatment for diabetic polyneuropathy?

A

duloxetine, pregabalin, and the capsaicin patch [8%]

276
Q

What is the treatment for radial mononeuropathy?

A

Splint wrist in 60° of dorsiflexion

277
Q

What is the treatment for ulnar mononeuropathy?

A

Corticosteroid injection may help.
May require surgical intervention if persistent.

278
Q

What is the treatment for median mononeuropathy?

A

■ Wrist splinting in neutral position
■ Corticosteroid injection into carpel tunnel
■ Oral corticosteroid burst
■ Release of flexor retinaculum for severe symptoms

279
Q

What is the treatment for sciatic and common fibular mononeuropathy?

A

Splint ankle at 90° with posterior splint

280
Q

How is mononeuropathy multiplex defined?

A

characterized by the presence of multiple
mononeuropathies
asymmetric

281
Q

What is the most common cause of mononeuritis multiplex?

A

diabetes mellitus

282
Q

How is mononeuropathy multiplex diagnosed?

A

■ Electrodiagnostic studies
■ Sural nerve biopsy if diagnosis in question

283
Q

_________________________ is a disorder characterized by upper motor neuron disease in addition to lower motor neuron pathology.

A

Amyotrophic lateral sclerosis (ALS)

284
Q

What is the pathophysiology of Amyotrophic lateral sclerosis (ALS)?

A

■ Anterior horn cell neuronopathy → peripheral nerve findings
■ Loss of Betz cells in the CNS motor cortex → upper motor neuron findings

285
Q

What are the signs and symptoms of Amyotrophic lateral sclerosis (ALS)?

A

LMN involvement:
- muscle fasciculations and atrophy
- muscle cramps
- asymmetric distal weakness
UMN involvement:
- hyperreflexia and clonus
- spasticity
- positive babinski

286
Q

How do people with Amyotrophic lateral sclerosis (ALS) typically die?

A

progressive respiratory muscle weakness (→ respiratory failure) or dysphagia (→ aspiration). ↑ risk with forced vital capacity < 25 mL/kg

287
Q

How is ALS diagnosed?

A

electrodiagnostic testing

288
Q

What is the treatment for ALS?

A

supportive
Riluzole – modulates glutamate metabolism

289
Q

What is the pathophysiology of myasthenia gravis?

A

Antibodies against acetylcholine receptors at the neuromuscular junction → destruction of receptors → decrease in available receptors

290
Q

How does the muscle fatigue of MG compare to that of Lambert Eaton syndrome?

A

Repeated muscle use increases weakness (vs Lambert-Eaton myasthenic syndrome where repeated muscle use improves strength).

291
Q

What is acute myasthenic crisis?

A

respiratory failure requiring mechanical
ventilation

triggers include infection, medications

292
Q

What 3 things should be on your differential for ptosis?

A

myasthenia gravis
CN3 palsy
Horner Syndrome

293
Q

What is the Edrophonium (Tensilon) test?

A

■ Edrophonium is a short-acting acetylcholinesterase blocking agent
→ increased acetylcholine available at neuromuscular junction
→ improvement in measured ptosis (and other symptoms).
■ Test dose must be administered first to ensure that cholinergic crisis will not be induced. Cholinergic crisis from excess anticholinesterase
inhibitors can present with flaccid paralysis and is difficult to distinguish from myasthenic crisis.
■ Have atropine ready in case of excessive cholinergic symptoms.

294
Q

What is the treatment of MG?

A

Cholinesterase inhibitors
■ Pyridostigmine, neostigmine.
■ Should NOT be used during myasthenic crisis!
■ Excessive administration → cholinergic crisis with weakness, tachycardia, excessive secretions, etc.

295
Q

What is Lambert Eaton Myasthenic Syndrome commonly associated with?

A

About half the time it is associated with cancer (small cell carcinoma of the lung, lymphoma).

296
Q

What is the pathophysiology of Lambert-Eaton Myasthenic Syndrome?

A

Antibodies → inadequate release of acetylcholine at neuromuscular junctions → symptoms

297
Q

What are the signs and symptoms of Lambert Eaton Myasthenic Syndrome?

A

■ Proximal (primarily leg) muscle weakness that improves with repeated stimulation
■ Autonomic symptoms (dry mouth, impotence)

298
Q

What is the treatment for Lambert Eaton Myasthenic Syndrome?

A

■ Treat underlying malignancy, when present.
■ Immunosuppressive agents.
■ Plasmapheresis and IVIG, if severe.

299
Q

What is the pathophysiology of botulism?

A

Toxin produced by Clostridium botulinum → presynaptic inhibition of acetylcholine release at the neuromuscular junction.

300
Q

How is botulism diagnosed?

A

■ Clinical suspicion
■ Electrodiagnostic testing
■ Botulinum toxin testing of serum and stool

301
Q

What is the pathophysiology of Tick Paralysis?

A

Tick toxin → decreased release of acetylcholine at neuromuscular junction → symptoms

302
Q

What are symptoms of Tick Paralysis?

A

Symmetric ascending paralysis
Tx: remove tick

303
Q

What are the two types of inflammatory myopathies?

A

Polymyositis and dermatomyositis

304
Q

What is the difference between polymyositis and dermatomyositis?

A

Both cause:
■Chronic symmetric proximal muscle weakness.
■ Muscle pain and tenderness.
But, Dermatomyositis has additional skin findings, including photosensitivity and extensor rashes.

305
Q

How are polymyositis and dermatomyositis diagnosed?

A

Electromyography and muscle biopsy confirm diagnosis.

306
Q

How are polymyositis and dermatomyositis treated?

A

Oral prednisone or cytotoxic drugs

307
Q

What disease is caused by regions of CNS demyelination with sparing of axons?

A

Multiple Sclerosis

308
Q

What are risk factors for MS?

A

females are 3x more likely
Caucasians are 2x more likely than AAs

309
Q

What is internuclear ophthalmoplegia? (as seen in MS)

A

Abnormalities in eye adduction bilaterally
associated with horizontal nystagmus

310
Q

What is Uhthoff phenomenon (associated with MS)?

A

Small increases in body temperature (eg, exercise,
fever) → worsened symptoms (visual symptoms often most affected).

311
Q

What is Lhermitte phenomenon?

A

Electric shock sensation down spine with flexion
of neck (common with all cervical myelopathies (disc bulge, spinal stenosis, etc)

312
Q

Describe CSF findings of MS?

A

CSF cell counts, protein, and glucose are typically normal;
CSF may show oligoclonal bands of IgG and/or myelin-based proteins

313
Q

What is the treatment for MS?

A

■ High-dose methylprednisolone burst with taper for acute exacerbations
■ β-Interferon, azathioprine

314
Q

What do you call the chronic neurodegenerative disease of the elderly resulting from damage to dopaminergic neurons in the substantia nigra?

A

Parkinson Disease

315
Q

What are the 4 characteristic findings of Parkinson Disease?

A

■ Resting tremor (“pill-rolling”)
■ Cogwheel rigidity
■ Bradykinesia or akinesia
■ Postural instability

“TRAP”
Tremor
Rigidity
Akinesia
Postural instability

316
Q

How is Parkinson Disease diagnosed?

A

Based on clinical findings
CT/MRI is not definitive

317
Q

What is the treatment for Parkinson Disease?

A

Agents to increase CNS dopamine and anticholinergics to decrease central
muscarinic activity
(Drug “holidays” of 1 week may be used as effectiveness diminishes over time.)

318
Q

Which medications are used for acute migraine treatment?

A
  1. triptans
  2. dihidryergotamines
  3. NSAIDs
  4. Acetaminophen
  5. Antiemetics
319
Q

What medications are used for migraine prevention prophylaxis?

A
  1. Beta blockers (propanolol)
  2. Calcium channel blockers (verapamil)
  3. Tricyclic antidepressants (amitriptyline)
  4. Anticonvulsants (valproic acid, topiramate)
  5. Calcitonin gene-related peptide receptor antagonists
  6. Botulinum toxin A
320
Q

How is degree of cerebral edema evaluated on a noncontrast head CT?

A

estimating the density ratio of gray to white matter

This density is measured in Hounsfield units. Normally, the gray to white matter density ratio is 1:3.
In cerebral edema (the result of hypoxic-ischemic injury), this ratio is decreased

ITE '23 (20 decks)

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