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Neuro-Psych Exam II > Headaches (Ferguson) > Flashcards

Headaches (Ferguson) Flashcards

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1
Q

Cranial structures that are pain sensitive (5)

A
  1. Scalp
  2. Sinuses (periosteum)
  3. Meninges
  4. Pial arteries
  5. Arteries/ Major Veins
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2
Q

Cranial structures NOT sensitive to pain

A
  1. Ventricles
  2. Choroid
  3. Brain parenchyma
  4. Small parenchymal and dural veins
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3
Q

Which part of the brainstem can be activated to induce headache? What happens? What kind of headache is caused?

A

Activation of small area near dorsal raphe nucleus–> ^ 5-HT–> Migraine

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4
Q

What are the three types of headache?

A
  1. primary HA
  2. secondary HA
  3. cranial neuralgia
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5
Q

Which characteristic of migraines must be differentiated from pseudo tumor cerebri?

A

Exacerbation with exertion

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6
Q

Define migraine:
Which primary/secondary/neuralgia?
List associated symptoms (5)

A

Benign, recurring, primary HA

  1. photophobia
  2. phonophobia
  3. N/V
  4. worse with exertion
  5. Aura~
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7
Q

What is the current belief regarding pathophys of migraines? Where does it start? Which system is responsible for HA? Explain asstd. N/V, pallor, flushing, congestion?

A

Begins in brainstem with instability/ activation of cells–> spreads peripherally to stimulate trigenminal system

Involvement of chemoreceptors–> N/V
Involvement of ANS–> pallor, flushing, congestion

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8
Q

What is a migraine without aura (common migraine) and how does it present? How long does the HA last?

A 
Unilateral deep, throbbing sensation
Asstd. photophobia, phonophobia
n/v
worse with exertion 
better with rest

Most 30min-6hrs, possibly up to 72hrs

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9
Q

What is a migraine with aura and how does it present?

A

Common migraine proceeded by aura up to 30 min before HA onset, or 1 hr into HA

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10
Q

List 4 examples of an aura

A
  1. Visual disturbance (scintillating scotoma, central scotoma, monocular vision loss…)
  2. Focal paresthesia
  3. Focal weakness or paralysis
  4. Phonophobia (heightened sensitivity to sound) or other auditory disturbance
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11
Q

What is a complicated migraine and how is it diagnosed?

A

This is a migraine with a dramatic aura that lasts for an extended period of time–mimics stroke

DX by excluding stroke or other path

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12
Q

Describe the onset pattern of a basilar migraine. With which severe pathology might this HA be confused?

A

Vertigo/ Dysarthria/ Ataxia/ Diplopia (brainstem/ posterior cerebral circ. sx.) –> 30 min later throbbing occipital pain

Possible confusion with posterior circ. stroke

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13
Q

Wha tis a Bickerstaff Migraine? How does it present?

A

Most severe basilar migraine

Total blindness–> other postural cerebral circ. sx. –> throbbing occipital pain

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14
Q

List 5 Triggers of migraines

A
  1. Red wine
  2. Food: Chocolate/ Cheese/ MSG/ Nitrates
  3. Hunger
  4. Sleep deprivation/ disturbance
  5. Stress
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15
Q

When should patient take abortive tx for migraine? What are 4 classes of drugs used for abortive therapy?

A

Immediately, keep drugs handy

  1. NSAIDS
  2. 5-HT Agonists (Triptans, ergots)
  3. Dopamine Antagonists
  4. Combinations drugs
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16
Q

When do we generally pursue prophylactic therapy for patients with migraines?

A

> 4-6 migraines per dos, Pt missing work/ school with HA, Recurrent ED visits secondary to sx.

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17
Q

What are 5 classes of drugs used for migraine prophylaxis? How do we decide which to use?

A
  1. Beta blockers
  2. Ca++ channel blockers
  3. TCAs
  4. Anticonvulsants
  5. 5-HT

Decision made based on patient’s comorbidities

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18
Q

Which drug is used to treat skinny kids with migraines so they will gain weight?

A

Cyproheptadine (seritonergic drug)

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19
Q

Define Cluster HAs:
How long do they last?
In what pattern do they occur?

A

Episodic HAs occur in 1s-3s
Last 15min-3hrs
Severe unilateral stabbing pain is periorbital or temporal (facial pain > hemicranial HA) + asstd sx

Occur in clusters for 3-6 weeks at a time
Circadian rhythm (occur at same time every day)
20
Q

What are some associated sx. with cluster HA (4)

A
  1. conjunctival injection/ lacrimation
  2. Miosis/ptosis/eyelid edema
  3. rhinorrhea, nasal congestion
  4. Perspiration
21
Q

Describe pathophys of cluster HAs

A

Derived from hypothalamus–> secondary activation of trigeminal autonomic reflex via trigeminal-hypothalamic pathway

22
Q

What is the most effective abortive agent for cluster HAs?

What is a second agent that may be used for abortive therapy?

A 
#1 = 12L/min O2 (high concentration O2) 
#2= Triptans
23
Q

What are three categories of drugs that can be used for prophylactic treatment of cluster headaches?

A
  1. High dose steroids
  2. Ca++ channel blockers
  3. Lithium
24
Q

What is the most common HA syndrome?

A

Tension HAs

25
Q

How does a Tension HA present?

A

Squeezing pressure around head, possible photophobia or phonophobia

NEVER PRESENTS WITH N/V!

26
Q

What are 4 non-pharm approaches to treating tension HA?

A
  1. Stress reduction
  2. Biofeedback
  3. CBT
  4. sleep hygiene improvement
27
Q

What are 2 abortive pharm treatments for tension HA?

A
  1. Acetaminophen

2. NSAIDS

28
Q

What is analgesic HA syndrome and with what HA syndrome might it be associated?

How is it treated?

A

Patient takes too many OTC analgesics, patient discontinues use and gets rebound HAs

May be associated with self medication for tension HAs

Tx: steroids for about a week

29
Q

What are 2 prophylactic pharm treatments for tension HA? Do we commonly prophylactically treat tension HA?

A
  1. TCAs
  2. Anti-epileptics

Not commonly used because typically if you are doing prophylaxis for tension HA your patient actually has migraines and you’re just and idiot who didn’t take a good enough hx. to figure it out.

30
Q

What is Idiopathic Intracranial Hypertension/ Pseudotumor cerebri? How does it present?

A

^^^ ICP w/o intracranial mass, hydrocephalus, or dural venous stenosis/thrombosis–> Sudden onset continuous, daily HA

WORSE: coughing, sneezing, supine

31
Q

Which population most commonly gets IIH

A

young, obese females

32
Q

What are some drugs that are associated with IIH? (3)

A
  1. Tetracycline
  2. OCPs
  3. Retinoic acid (hypervitaminousis A)
33
Q

What are the three complications associated with IIH?

A
  1. vision loss
  2. diplopia
  3. pulsatile tinnitus
34
Q

Should one do imaging for IIH workup? If so, which modality?

A

YES: MRI with venogram (MRV) to rule out posterior fossa tumor

35
Q

When should you perform an LP to work up IIH? In what position should the patient be? How much fluid should you get to make the diagnosis?

A
  • After MRV
  • Lateral decubitus position for accurate opening pressure
  • Both diagnostic and therapeutic
  • *** > 25cm H2O
36
Q

What is the most concerning complication asstd. with IIH and what should be done to monitor for this?

A

Irreversible vision loss–always get opt consult with formal visual field assessment

37
Q

What is the most important non-pharm treatment for IIH?

A

weight loss

38
Q

What are two pharmacological treatment steps to be taken when treating IIH?

A
  1. Remove offending agents

2. ~Admin drugs to decrease CSF absorption (carbonic anhydrase inhibitors)

39
Q

What are 3 procedural treatments for IIH?

A
  1. Recurrent LP
  2. Optic N fenestration
  3. Shunting (ventriculoperitoneal)
40
Q

What age group typically gets giant cell arteritis?

A

> 50 yrs

41
Q

How does Giant Cell arteritis present? What are some common complaints?

A

Progressive unilateral throbbing HA + tenderness in temporal scalp area

Asstd. Complaints:

  1. jaw claudication
  2. diffuse joint pain
  3. visual disturbance (transient monocular vision loss)
42
Q

What is the most severe complication asstd. with giant cell arteritis

A

*Causes untreated permanent blindness if untreated due to anterior ischemic optic neuropathy

43
Q

How do we definitively diagnose giant cell arteritis?

A

Temporal artery biopsy w/ large segment (disease skips segments)

44
Q

How do we treat giant cell arteritis?

A

Large dose corticosteroids (relief within 3 days)

Maintain on low dosecorticosteroirds for a few years after that

45
Q

What are 9 worrisome symptoms that mandate imaging and further workup with acute onset HA?

A
  1. “worst” HA ever
  2. first severe HA
  3. Subacute, worse with time
  4. abnormal neuro exam
  5. fever/unexplained signs
  6. vomiting prior to HA
  7. Worse with positional change, coughing lifting,
  8. Sleep disturbance, present @ waking
  9. Onset after 55
46
Q

When do we do LP for acute HA?

A

Fever, illness, immunocomp patient

47
Q

Which imaging tests do we do for severe acute HA (2)

A

CT–> MRI

Neuro-Psych Exam II (11 decks)

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