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Neuro II > 29 HA > Flashcards

29 HA Flashcards

1
Q

Primary headaches?

A

tension, migraine, and cluster

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2
Q

Primary headaches are typically (acute/subacute)

A

subacute

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3
Q

All headaches cause:

A

inflammation or physical traction of pain sensitive structures within or around the cranial vault

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4
Q

Pain sensitive structures:

A
  • dura and meninges at base of brain
  • large arteries at base of brain and meningeal arteries
  • venous sinuses
  • scalp muscles + upper cerv muscles
  • periosteum of skull
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5
Q

Stimulation of cranial pain receptors is transmitted centrally largely through:

A

CN V, IX, and cervical roots C2-3

~VII, X

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6
Q

Innervates pain sensitive structures of the ant/middle fossa and scalp.

A

opth branch of V

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7
Q

Innervates pain from posterior fossa, cervical muscles, neck and post scalp.

A

CN IX, X and cervical roots C2-3

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8
Q

Where do pain sensitive nerve fibers synapse?

A

trigeminal nucleus caudalis + dorsal horn of the upper cervical spine

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9
Q

Centrally projecting nerve fibers synapse in:

They are then relayed on to:

A

VPL and VPM nuclei of the thalamus

sensory cortex and other cortical sensory systems. 


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10
Q

Red flags suggesting secondary etiology for HA:

A 
abrupt onset
recent head trauma
fever
immunosuppression
new onset >50yo
progression over days
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11
Q

Migraine prodrome symptoms:

A 
odd food cravings
mood swings
malaise
fatigue
muscle aches/stiffness
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12
Q

Location of one known loci for polygenic migraines.

A

10q23

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13
Q

Dominant migraine condition:

A

Familial Hemiplegic Migraine

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14
Q

Migraine onset MC =

A

<20

decr occurrence after 55

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15
Q

Anatomical substrate for all migraines:

A

Trigeminovascular System (CN V1)

*innervates pain R’s in dura, meninges, and medium/large cerebral arteries/veins on surface of brain + above tentorium

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16
Q

What causes parasymp symptoms associated with migraines?

A

VII and parasymp innervation of superior salivary nucleus –> central connections between pain pathways from CN V and the superior salivatory nucleus

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17
Q

Migraine pathogenesis?

A

trigger –> aura –> inflmm –> polygenic predisposition –> hypersensitizes both peripheral (trigeminovascular) and central (nucleus caudalis, thalamus, etc) pathways of HA pain 


18
Q

In auras, the bright, multicolored scintillations represent excitation of:

A

calcarine cortex (as the initial ‘cortical spreading depression’ wave moves across the cortex)

19
Q

How does blood blow change when aura appears?

A

early: increased blood flow at areas of cortical excitation

following excitation: decreased blood flow

20
Q

What causes scotoma?

A

depolarized tissue = non-functional –> transient loss of vision until neurons recover

21
Q

NT that are important in the pathogenesis of neurogenic inflammation/pain and migraine:

A

calcitonin gene related peptide (CGRP) and substance P (SP)

22
Q

How does the trigeminal ganglion initiate a migraine, once activated by a “brain stem generator”?

A
  1. sends an efferent signal to nerve terminal on a meningeal artery
  2. CGRP release –> activation CRL = vasodilation and degranulation of mast cells
  3. Hypersen of synaptic terminal, causing afferent signal sent up trigeminal to brain stem
23
Q

CGRP mediates:

A

the initial hypersensitizing signal and a secondary pain signal

24
Q

Locations of:
5HT1B receptor?
5HT1D receptor?
Combination of 5HT1B,D,F receptors?

A

vascular terminals

peripheral trigeminal nerves

central synapse of the trigeminal nerve

25
Q

Function of triptans?

A

5HT1 agonists, inh release of GCRP

26
Q

Features of cluster HA’s?

A

Unilateral, frontal, retro-orbital pain

Unilateral conjunctival inf and rhinorrhea

Unilateral Horner’s and lacrimation

Ct, severe non-pulsating pain lasting min-3hrs

Daily attacks for weeks/months, then yrs of remission

27
Q

Triggers of cluster HA’s?

A

ETOH, tobacco

28
Q

Epidemiology of cluster HA’s?

A

M>F (4:1), ~25 y/o

29
Q

Features of tension headaches?

A

band-like, bil headaches

lasts min-3hrs

can be episodic (15d/mo)

30
Q

Why is Idiopathic Intracranial Hypertension an emergency?

A

no rapid trx = vision loss

31
Q

Features of Idiopathic Intracranial Hypertension?

A
  • headache
  • papilledema
  • transient visual obscurations
  • diplopia 2’ to CNVI paresis
  • tinnitus
  • constriction of visual fields, enlarged blind spot
32
Q

Epidemiology of Idiopathic Intracranial Hypertension?

A

F > M (9:1)
20-45 yo
overweight by 20%

33
Q

Cause of primary Idiopathic Intracranial Hypertension?

A

unk

but prob incr CSF prod and decr CSF reabs

34
Q

Cause of primary symptomatic Intracranial Hypertension?

A

d/o that alters CSF production/reabs

incr Vit A
abx
steroid withdrawal

35
Q

Cause of secondary Idiopathic Intracranial Hypertension?

A

condition that blocks CSF circulation or reabs

venous sinus thrombosis
chronic meningitis
chiari malformation

36
Q

Trx of Idiopathic Intracranial Hypertension?

A
  1. wt loss **
  2. reduce CSF production
  3. repeat LPs
  4. surgical
37
Q

Clinical features of giant cell (temporal) arteritis?

A
  • unilateral HA
  • point scalp tenderness over temporal a
  • vision problems –> blindness 2’ to opthalmic artery occlusion
38
Q

Conditions associated with giant cell (temporal) arteritis?

A

stroke (vertebral arteries esp)

polymyalgia rheumatica

39
Q

Tests for giant cell (temporal) arteritis?

A

incr CSP and ESR

+/- temporal artery biopsy (skip lesions)

40
Q

Pathology of giant cell (temporal) arteritis?

A

inflmm and multinucleated giants cell in elastic laminae of medium/small arteries

41
Q

Why is giant cell (temporal) arteritis a medical emergency?

A

potential to cause monocular blindness

42
Q

Trx of giant cell (temporal) arteritis?

Neuro II (18 decks)

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