Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neuro Block 2 > Headache (5) > Flashcards

Headache (5) Flashcards

0
Q

What are the three main types of primary headaches?

A
  1. Migraine
  2. Cluster headache
  3. Tension headache (both episodic and chronic types)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Difference b/n primary and secondary headache

A

Primary has no identifiable underlying cause whereas a secondary has an identifiable structural or metabolic cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What characteristic way do subarachnoid hemorrhages present?

A

Sudden explosive onset of severe headache

*cerebral ischemia may also cause headache, can be seen in the post-ictal period following seizure as well

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are 9 causes of acute onset headache (get as many as you can, gay boy)?

A
  1. Subarachnoid hemmorhage
  2. Parenchymal brain hem.
  3. Subdural/epidural hem.
  4. Pituitary apoplexy
  5. Malignant HTN
  6. Acute closed angle glaucoma
  7. Carotid/ vertebral artery dissection
  8. Acute obstructive hydrocephalus
  9. Low pressure headache (CSF leak)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are 8 causes of headache with subacute onset?

A
  1. Brain tumor/ other mass
  2. Meningitis/ encephalitis
  3. Cerebrovascular ischemia
  4. Cerebral venous sinus thrombosis
  5. Idiopathic intracranial HTN (aka Psuedotumor cerebri)
  6. Giant cell arteritis
  7. Chronic subdural hematoma
  8. Metabolic encephalopathies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is responsible for the pain that causes headaches?

A

inflammation or physical traction of nerves fibers in structure in the head including meninges, vessels, scalp, and periosteum of the skull

*brain parenchyma itself has no pain fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What nerve innervates pain fibers from the supratentorial dura (nost of intracranial cavity)?

A

CN V

*Anterior fossa, middle fossa, and scalp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What nerves are responsible for the pain in the posterior fossa?

A

CN X (primarily); also CN IX and cervical nerve roots C2-3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What two places do pain fibers from the intracranial cavity synapse 1st beffore going to the VPL and VPM of the thalamus?

A
  1. Trigeminal nucleus caudalis

2. Dorsal horn of the upper cervical spine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are 12 RED FLAG signs indicating a headache may be a possible secondary and therefore more dangerous etiology?

A
  1. Abrupt onset
  2. Hx of recent head trauma
  3. Fever
  4. Hx of immunosuppresion
  5. Altered conciousness
  6. Focal neurological symptoms/signs
  7. New onset in patient over 50
  8. Neck pain/ stiffness
  9. Anticoagulant use
  10. Headache progression over days
  11. Recently altered cognition
  12. “Worst headache of life”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are three characteristics of migraine headaches in terms of presentation (including length)?

A
  1. frequently unilateral (may not always be on same side)
  2. pulsating
  3. Duration 4-72 hours
    * relief usually seen after sleeping
    * if always on same side, may merit a CT to look for an underlying cause
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are 3 associated symptoms frequently seen with migraine?

A
  1. Nausea (with or w/o vomiting)
  2. Photphobia and/or phonophobia
  3. May be preceded by a prodromal phase, including aura (in 20%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Is there a genetic component to migraines?

A

Yes; 75% of patients have FHx of migraines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are five symptoms that can be seen in a migraine prodrome?

A
  1. mood swings
  2. odd food cravings
  3. Malaise
  4. fatigue
  5. Muscle aches and stiffness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Other than visual aura, what are some other ways aura may present?

A

Can have transient limb weakness, sensory symptoms, transient aphasia—> therefore may mimic TIAs in some ways

*aura may also lead to fortification scotoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What 3 main categories of triggers that may start migraines?

A
  1. Changes in daily cycles (no breakfast, menses, late hours)
  2. Environment or diet (weather, altitude, light, EtOH)
  3. Emotional (fear, anxiety, depression, anger)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

At what age will most patients with migraines have presented?

A

age 20

may get better with age and many have decreased occurrence by 55

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What sex are migraines more common in?

A

Females (only slightly—> 10-15% of woman, compared to 5-10% of men

*affects 15-25% of population, so fairly common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What nerve serves as the anatomical substrate for all migraines?

A

CN V–> CN V1 innervation of pain receptors in the dura, meninges, and medium/large cerebral arteries and veins that lie on surface of brain and above the tentorium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What anatomically is responsible for the vasodilation and other parasympathetic symptoms associated with migraines?

A

Central connections between pain pathways from CN V and the superior salivatory nucleus

*input from the trigeminal nucleus caudalis to the superior salivatory ganglion mediates parasympathetic signals to vessels via CN VII–>vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What two things initiate the nerve stimulation that leads to neurogenic inflammation of meningial vasculature responsible for pain in migraine?

A
  1. “Central Generator” (in patients that do not experience aura)
  2. Internal/external triggers in those with aura

*Either way, a wave of neural depolarization begins that excites already hypersensitized (via genetics or previous episodes) peripheral and central pain pathways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is a cortical spreading depression? What does it do to blood flow initally, then right after?

A

A wave of brief neuronal excitation, which spreads across certain areas of cortex–> usually is followed by a period of prolonged depolarization (likely due to the sensitazion of the neuronal pathway)
*Blood flow is increased during the excitation, than oligemia (low blood flow) is associated with the phase in which there is prolonged depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How is the scotoma and other transient losses in function associated with aura mediated?

A

The oligemia that accompanies the prolonged depolarization phase usually leads to a period of transient loss of function, regardless of where it occurs (makes sense, low blood flow = poor function)

*the deficit occuring during aura depends on where in the cortex the cortical spreading depression occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What part of cortex is responsible for visual disturbance in aura?

A

Cortical spreading depression in calcarine cortes of occipital lobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What two chemicals are responsible for the pathogenesis of neurogenic inflammation/ pain in migraine?

A
  1. CGRP (especially)
  2. Substance P

*these can sensitize nerves to pain stimuli AND also directly cause vasodilation themselves–> vasodilation is the cause for much of th pain in migraine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Via what two mechanisms does CGRP cause vasodilation?

A
  1. Dural and cerebral vascular SM have CGRP receptors on them
  2. CGRP directly causes mast cells to degranulate (releases histamine and mast cells also responsible for the local inflammatory reaction, the neurogenic inflammatory response)
26
Q

Chronic or repetitive activation of peripheral pain receptors causes release of _______ and other NT peptides in the CNS which sensitize these CNS neurons to fire an antidromic volley back down to peripheral nerve recpetors.

A

Glutamate–> antidromic signals then sensitize the peripheral nerves; self-propagating process leading to both central and peripheral pain pathway sensitization

27
Q

How do the triptans work in general to help with migraine?

A

Are 5HT receptor agonists–> work to block CGRP release at severl sites in the pain pathway

28
Q

Where are 5HT1 receptors found? (3 places)

A

On dural arteries and on peripheral and central trigeminal nerve terminals

29
Q

Where are 5HT1D receptors specifically found?

A

On peripheral trigeminal nerve terminals

30
Q

What 3 serotonin receptor subtypes are found on the central synapse of the trigeminal nerve?

A

5HT1 B, D, F

31
Q

What is the target for the class of drugs in phase 3 trials, the Gepants?

A

These are CGRP antagonists, so should work to block cerebral vessel vasodilation, pain transmission and neurogenic inflammation

FUCKING FANCY, I tell you

32
Q

How does the headache often present in cluster headaches (pattern of pain)? What are three adjectives for the character of the pain?

A

Always unilateral, frontal, or retro-orbital (steady boring sensation behind eye)

  • pain is Constant, Severe, Non-pulsating–> HAs have been so sever some patients have committed suicide
33
Q

How long does a cluster headache usually last?

A

From minutes - ~3 hours ; usually fairly short

34
Q

What is unique about cluster headache recurrence?

A

Patients may have daily attacks for weeks or months, then have remission of symptoms for years
*may have up to 8 attacks in a single day

35
Q

What age and sex are cluster headaches most common in?

A

Mean age of onset is ~25 years; Men affected more than women (4:1)

36
Q

What types of characteristic associated symptoms are often seen with cluster headaches? (General type, three specific)

A

Unilateral autonomic symptoms–>
*Unilateral conjunctival irritation (red eye) and lacrimation
*Rhinorrhea (or stuffy nose, so either)
* Unilateral Horner’s syndrome
may see unilateral flushing, sweating, or swelling of eyelid as well–> all these possible symptoms will be on the same side if present

37
Q

What are two “triggers” often associated with cluster headaches?

A
  1. Smoking
  2. EtOH

*Family history is rare, so likely sporadic issue

38
Q

What are two acute Tx for cluster HA?

A
  1. Nasal O2
  2. Subq Sumatriptan

*Ca Channel blockers (verapamil), Lithum, valproic acid, and prednisone are used for prophylaxis

39
Q

What are 4 defining features of Tension headaches?

A
  1. Pain is BILATERAL and “bandlike”
  2. No auras
  3. No N/V
  4. No photo/phonophobia
40
Q

How long do tension headaches usually last?

A

Few minutes to 3 hours; also very short

41
Q

What is the difference b/n episodic and chronic tension HA?

A

Chronic is when daily attacks occur more than 15 days of the month; episodic is anything less

  • episodic is the most common form; these are the headaches most people have experienced at one time or another
  • Chronic tension HA require careful evaluation and lengthy f/u–> refer to neurologist or headache specialist for Dx and Tx
42
Q

What characteristic does the trigmeinal ganglion have that enable it to cause both central and peripheral issues in migraine?

A

In addition to receiving sensory pain input and sending it to the CNS like all sensory nuclei, it can also send information orthodromically back to the peripheral nerves it receives info from

*Irritation causes CGRP and Substance P release both afferently into central system and back efferently to the periphery–>sensitization occurring at both ends

43
Q

What is psuedotumor cerebri? What age/ sex most common in?

A

Condition of unknown cause characterized by headache and elevated intracranial pressure.

  • Most commonly seen in females (9:1), age 20-45; often the females are overweight
  • aka Idiopathic Intracranial HTN
44
Q

What 3 visual symptoms may be seen in Pseudotumor cerebri?

A
  1. Papilledema
  2. Transient visual obscurations (constrictions of visual fields, blind spots)
  3. Diplopia (secondary to CN VI paresis)
45
Q

What is an auditory symptom seen in pseudotumor cerebri? Why is it important to Dx quickly?

A

Tinnitus–> this condition is a neurologic emergency= failure to dx and treat in timely fashion may lead to loss of vision

46
Q

What is the cause of the majority of pseudotumor cerebri (Idiopathic Intracranial HTN)?

A

Most are idiopathic–>possible due to altered CSF met (either too much produced or decreased reabsorbtion)

47
Q

What are three causes of IIH (pseudotumor cerebri) in Primary symptomatic cases?

A
  1. Hypervitaminosis A
  2. Abx (tetracycline)
  3. Steroid withdrawal
48
Q

What are three causes of secondary IIH?

A
  1. Venous sinus thrombosis
  2. Chronic meningitis
  3. Chiari malformation
49
Q

What are three main symptoms that should increase supsicion of IIH?

A
  1. Headache
  2. Visual symptoms
  3. Papilledema

*esp in overweight younger woman (20-45)

50
Q

What are MRI findings in pt with IIH?

A

Should be negative, but could reval an underlying mass or venous sinus thrombosis

51
Q

What test can confirm a case of IIH?

A

Lumbar puncture–> if opening pressure is over 250 mmHg, this is diagnostic (in background of clean MRI)
200-250 mmHg is elevated and is suggestive, but obese people can have these pressures normally, so not conclusive

52
Q

What additional thing should be done outside of MRI and LP in the workup of a suspected case of idiopathic intracranial HTN (pseudotumor cerebri)?

A

Document visual fields–> establishes a baseline to measure treatment success or disease progression

53
Q

What is the most effective Tx for IIH? What two pharm treatments are used?

A

Weight loss is most effective, but difficult to achieve at times

Acetazolamide and furosemide are given to reduce CSF production/ pressure

54
Q

What type of vasculitis is a Giant Cell (temporal) Arteritis?

A

Autoimmune, GRANULOMATOUS infiltration and occlusion of small arteries

55
Q

What type of arteries does temporal cell arteritis preferentially affect?

A

Medium/ small ELASTIC arteries

56
Q

What is the chief complaint in 70% of Giant cell arteritis cases?

A

Unilateral headache (usually with point scalp tenderness over temporal artery)

57
Q

What 5 symptoms may be seen in the 50% of cases of Giant cell arteritis that have associated Polymyalgia Rheumatica? (if you miss #5, you sux dix)

A
  1. jaw claudication
  2. malaise
  3. fever
  4. weight loss
  5. myalgias
58
Q

What visual symptoms may be seen in patients with Giant Cell arteritis?

A

Monocular obscurations (secondary to opthalmic artery occlusion)

59
Q

What is a possible complication of Giant cell arteritis (not visual)?

A

May have Stroke (particularly in vertebral arteries)

60
Q

In what patient (age, presenting complaint) should temporal arteritis be highly suspected? What two lab tests can support, but not confirm a Dx?

A

Patient over 55, with new onset unilateral headache

  • ESR (elevated in 75% of cases)
  • C-reactive protein (may be elevated as well)
61
Q

What is a confirmatory test for the Dx of Giant Cell arteritis? What would the characteristic finding be if positive?

A

Temporal artery biopsy–> reveal inflammation and Multinucleated Giant cells in the elastic laminae of the artery

  • lesions have a SKIP nature, so biopsy can be false positive, if biopsy happens to take a sample from a nearby unaffected region
62
Q

What Tx should be started IMMEDIATELY after getting a biopsy? Why is this dz a medical/neurological emergency?

A

Corticosterioids! –> can lead to acute onset monocular blindness

*give steroids after biopsy, b/c they can reduce the inflammation quickly and resolve lesions before they can be confirmed by pathology

Neuro Block 2 (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions