Headache Pathophysiology Flashcards
(35 cards)
what’s difference between primary and secondary headache?
Primary: a disorder unto itself like migraine
Secondary: a symptom of another disorder - after trauma for example
what are examples of primary headaches?
cluster, tension-type and migraine
what is the definition of migraine?
Headache + > or equal 2 of these characteristics - Unilateral (can be bilateral in kids) - Pulsating quality - Moderate-Severe - Aggravated by movement
1 or more of these associated features
-Nausea or vomiting- Photo and phonophobia
what is aura?
Fully reversible visual, sensory, speech disturbance
Aura has 2 or more of the following
- Unilateral
- Develops over _5 minutes
- Lasts between 5-60 min
preceeds 20% of migraines
what is a tension-type headache?
Headache lasts 30min _ 7 days with 2 or more of these characteristics - Bilateral - Non-pulsatile/tightening quality - Mild-Moderate - Not aggravated by movement - Does not have associated features of migraine
what were the other examples of primary headaches? (4 - I don’t think we need to know these)
Side-locked and/or autonomic features
- Hemicrania Continua
- Cluster Headache
- Paroxysmal Hemicrania
- Short-lasting Unilateral Neuralgiform Headache with Conjunctival Injection and Tearing (SUNCT)
-vary in the amount of time headaches lasts
how common are headache disorders?
one year prevalance of migraine - 18% women, 6 % men (different due to hormones)
episodic tension-type - 40% both men & women
frequent headaches - 5% women, 3% men
what nerve is responsible for relaying sensory and pain information from the face?
trigeminal
what nerve is responsible for Sensation and pain from the back of the head
C2 via occipital nerve
what other areas on the head are sensitive to pain?
the scalp, the dura, the arteries and the venous sinuses.
what nerve is responsible for pain from scalp, dura, and others?
ophthalmic branch of the Trigeminal Nerve.
This overlap is important when we consider why patients often report pain in their forehead and behind their eyes, when in fact that pain is referred from an intracranial process
how are painful messages transmitted in headaches?
Painful messages are relayed through the trigeminal ganglion, down the spinal trigeminal tract to the nucleus caudalis, which is a subdivision of the spinal trigeminal nucleus.
why can headache pain be felt on the back of the head?
The spinal nucleus is a hub of communication with other cranial nerves and with messages from the occipital area innervated by C2.
where do fibers go from nucleus caudalis?
Fibers from the nucleus caudalis then cross and ascend in the trigeminothalamic tract to the ventral posteromedial (VPM) nucleus of the thalamus, and then the messages are relayed to the somatosensory cortex.
what other nuclei does spinal trigeminal nuclei make connections with?
1) the superior salivatory nucleus, is involved in the parasympathetic system, and it plays a role in blood vessel dilatation as well as autonomic symptoms that can accompany headache.
2) The spinal nucleus also makes ascending connections with the hypothalamus, which explains why there are changes in appetite and sleep during the headache.
3) the spinal nucleus projects to the posterior nucleus of the thalamus, which in turn projects to multiple association areas of the cortex. These contribute to disturbances in neurological functions involved in vision, hearing, memory, motor, and cognitive performance during the headache.
*noted in slide we don’t need to know these details - just that anatomy explains symptoms of migraine
what is the vascular theory?
vasoconstriction of the cerebral vessels led to
decreased cerebral bloodflow –> symptoms of aura and simultaneous compensatory vasodilation of blood vessels –> perivascular inflammation which causes headache.
what is the evidence for & against vascular theory?
Evidence supporting this:
_ Vasodilators in migraineurs trigger migraine HA
_ Vasoconstrictors relieve migraine HA
_ Migraine is associated with some vasculopathies
Evidence against this:
_ Functional imaging has shown that regional blood flow decreases during aura, but headache often starts before normalization of blood flow
_ Vasodilation of meningeal and/or extracranial arteries is neither necessary nor sufficient for migraine pain
what are five steps in pathophys of migraine ?
1) abnormal cortical activity
2) corical spreading depression
3) activation/sensitization of trigeminovascular system
4) abnormal brainstem activity
5) central sensitization
what is abnormal cortical activity?
people with migraines have hyperexcitable brains - heightened reactivity to sensory stimuli. (stress, sleep, diet changes, sensory stimuli trigger migraine)
Simple things like disrupted sleep or alcohol can trigger the cascade of events that will lead to a migraine in someone who is susceptible, but similar triggers will not cause headache in someone without this predisposition.
are migraines genetic?
yes- high rate of concordance in mono vs dizygotic twins, relatives have 3x higher risk
what is familial hemiplegic migraine?
uncommon type with unilateral headache, aura, and motor weakness.
-associated with three genes - all for ion channels –> increased gluatamate
what is cortical depressing spreading?
is a wave of electrophysiological hyperactivity followed by a wave of inhibition, usually in the visual cortex
rate of propagation of CSD and aura are the same
what is the mechanism of CSD?
unclear but the following is known:
- efflux of K+ ions
- glial glutamate transmission at sites other than synapses -> synchronization of neurons (like in seizures)
- Several medications used to prevent migraines have been shown to inhibit glutamate-induced CSD
how does CSD sensitize/activate the trigeminal nerve? (details from notes)
1)CSD is accompanied by large increase in the concentration of extracellular potassium ions and protons as well as neuropeptides 2) This triggers vasodilatation of blood vessels. The perivascular axons also release neuropeptides such as substance P and calcitonin gene-related peptide, which contribute to an inflammatory soup.
3) This in turn causes mast cells to release histamine, serotonin, bradykinin, TNF-alpha, and nitric oxide, again leading to more inflammation. These inflammatory substances activate receptors that are coupled to second-messenger cascades which, in turn, modulate voltage-gated ion channels.
4) Through this mechanism, the meningeal nociceptors become hypersensitive (hence, the term sensitized), and normal fluctuations like pulsation of the blood vessels are perceived as painful.
5) The meningeal nociceptors
send these messages of pain through the trigeminal ganglion to the trigeminal nucleus caudalis.
