29 HA Flashcards
(42 cards)
Primary headaches?
tension, migraine, and cluster
Primary headaches are typically (acute/subacute)
subacute
All headaches cause:
inflammation or physical traction of pain sensitive structures within or around the cranial vault
Pain sensitive structures:
- 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
Stimulation of cranial pain receptors is transmitted centrally largely through:
CN V, IX, and cervical roots C2-3
~VII, X
Innervates pain sensitive structures of the ant/middle fossa and scalp.
opth branch of V
Innervates pain from posterior fossa, cervical muscles, neck and post scalp.
CN IX, X and cervical roots C2-3
Where do pain sensitive nerve fibers synapse?
trigeminal nucleus caudalis + dorsal horn of the upper cervical spine
Centrally projecting nerve fibers synapse in:
They are then relayed on to:
VPL and VPM nuclei of the thalamus
sensory cortex and other cortical sensory systems.
Red flags suggesting secondary etiology for HA:
abrupt onset recent head trauma fever immunosuppression new onset >50yo progression over days
Migraine prodrome symptoms:
odd food cravings mood swings malaise fatigue muscle aches/stiffness
Location of one known loci for polygenic migraines.
10q23
Dominant migraine condition:
Familial Hemiplegic Migraine
Migraine onset MC =
<20
decr occurrence after 55
Anatomical substrate for all migraines:
Trigeminovascular System (CN V1)
*innervates pain R’s in dura, meninges, and medium/large cerebral arteries/veins on surface of brain + above tentorium
What causes parasymp symptoms associated with migraines?
VII and parasymp innervation of superior salivary nucleus –> central connections between pain pathways from CN V and the superior salivatory nucleus
Migraine pathogenesis?
trigger –> aura –> inflmm –> polygenic predisposition –> hypersensitizes both peripheral (trigeminovascular) and central (nucleus caudalis, thalamus, etc) pathways of HA pain
In auras, the bright, multicolored scintillations represent excitation of:
calcarine cortex (as the initial ‘cortical spreading depression’ wave moves across the cortex)
How does blood blow change when aura appears?
early: increased blood flow at areas of cortical excitation
following excitation: decreased blood flow
What causes scotoma?
depolarized tissue = non-functional –> transient loss of vision until neurons recover
NT that are important in the pathogenesis of neurogenic inflammation/pain and migraine:
calcitonin gene related peptide (CGRP) and substance P (SP)
How does the trigeminal ganglion initiate a migraine, once activated by a “brain stem generator”?
- sends an efferent signal to nerve terminal on a meningeal artery
- CGRP release –> activation CRL = vasodilation and degranulation of mast cells
- Hypersen of synaptic terminal, causing afferent signal sent up trigeminal to brain stem
CGRP mediates:
the initial hypersensitizing signal and a secondary pain signal
Locations of:
5HT1B receptor?
5HT1D receptor?
Combination of 5HT1B,D,F receptors?
vascular terminals
peripheral trigeminal nerves
central synapse of the trigeminal nerve
