Lecture 67-69: Headaches Flashcards
Two kinds of migraine
With and without aura
Migraine without aura criteria
5 attacks at least 4 - 72 hours
Migraine with aura criteria
Migraine w/out aura symptoms + aura (visual, sensory, dysphasic…)
Migraine w/ aura symptom progression
Prodrome (cold hands/feet, odd feeling, food craving) –> aura –> headache
Cortical spreading depression theory of migraine; related to what brain state?
Wave of neuronal depolarization followed by a suppression of neuronal activity with corresponding blood flow changes moved across cerebral cortex at about 3 mm/minute; “hyperexcitable brain”
Describe meningeal involvement in migraine
Meninges innervated by V1; activation causes neural-related inflammation in meninges, which may be related to incredible pain
What brainstem centers are activated in migraine? Describe.
PAG and TNC (trigeminal nucleus caudalis); PAG connecs to the TNC and is known to exert inhibitory influences on that structure. This region of the midbrain is activated during a migraine attack and this activity persists even after the pain has been relieved.
Pathway of head pain
- Cortical spreading depression; 2. Inflammatory release in blood vessels of meninges; 3. Pain information travels through trigeminal nerve into brainstem nuclei
Describe the numbness pattern of migraine and the formal name
Cheiro oral numbness: face/hand numbness
Glial cells and migraine. Why and relation to vulnerable cortex?
Glial cells may propagate cortical depression wave; glial cells redistribute ions, etc and primary occipital cortex has lowest glial-neronal ratio, so if there is an ion imbalance, this region would be extra vulnerable
Describe astrocyte waves in more detail (ion, and what is released)
Astrocyte calcium waves could mediate propagated cortical phenomena of migraine via release of neuroactive and vasoactive messengers
Vascular issues with migraine might not be due to blood flow, but due to…
Intercellular communication with astrocytes
Most common headache? Describe
Tension headache; pressing, bilateral, steady mild-moderate pain, not aggravated by activity
What does a tension headache not have?
Nausea, photophobia, phonophobia
ANS migraine involvement
TNC can irritate superior salvitory nucleus –> ANS symptoms (sinus symptoms)
Childhood migraine: 7 unique symptoms
Benign paroxysmal vertigo, alternating hemiplegia, cyclic vomiting, recurring ab pain, benign torticollis (head turns to one direction), confusion, car sickness
Four associations with migraines being bad…
- Progression (get worse over time, so you should TREAT early); 2. Migrainous stroke (risk factor for stroke, especially for women); 3. Persistant aura without infarction (aura that never goes away); 4. Epilepsy (more miraines, increased risk for epilepsy)
Two neurological changes associated with migraine
- Iron deposition in PAG; 2. White matter changes on MRI
3 Primary head aches
F
Red flags (6)
New/different headache; abrupt onset; cancer/HIV/preg; abnormal physical; neuro symptoms; headache onset with syncope/exertion
Comfort signs (5)
Stable; family/personal hx; normal physical; triggers; variable locations
Is it common for brain tumors to present with just headaches?
No: N/V, abnormal neurological exam, etc…
Idiopathic intracranial hypertension common in…What’s happening? Presents like…
Obese women w/ menstrual abnormalities; brain swelling; brain tumor w/out local symptoms
Idiopathic increased intracranial pressure most commonly effects which nerve? What is this like?
VI nerve; causes VI nerve palsy = double vision in distance
Describe headaches with idiopathic intracranial hypertension
“Brain tumor headache,” visual complaints (double vision), cranial bruits, N/V, radiculopathies
What does increased idiopathic intracranial pressure look like in a lab? (MRI and spinal tap)
Flattened post globes and normal CSF w/ increased pressure
Treatment…watch for?
Correct predisposing factors, diuretics, shunt; watch eyes (blindness can occur)
Headache and stroke: which circulation most frequently presents with headache?
Most frequent in posterior circulation
Is headache severity related to stroke severity (infarct size)?
No
% headache w/ intra parenchymal hematoma
50%
Sudden onset sever headache, think…
Aneurysm (subarachnoid)
How to diagnose SAH and how to diagnose aneurysm…
CT scan; catheter angiography
Cluster headaches
Intense, boring, unilateral pain with ANS effects (Horner’s syndrome; eye watering); male predominance
Cluster headaches can be either…(2)
Episodic (bouts of headaches lasting 1-4 months w/ circadian patterns); chronic (no circadian patterns)
T/F: Cluster headaches can wake people out of sleep?
True
What is Giant Cell Artertis? Describe headache and location. Lab tests and what can it lead to?
Inflammation of arterial lining; generalized, throbbing, temporal; sedimentation rate; blindness due to ischemic optic neuropathy (stroke)
Did ya know, angina pain can refer to…
The head!
Describe headaches associated with sexual activity
Come on with orgasm, explosive onset
Describe headaches associated with carotid artery dissection
Headache w/ neck pain, facial pain, Horner’s syndrome
Meningeal enhancement is typical with a…What else is associated with these?
Low pressure headache; positional (worse upon standing)
What procedure can bring about a LP-headache? Treatment?
An LP! caffeine, epidural blood patch if it persists
Describe trigeminal neuralgia headaches. Which V roots are typically affected?
Brief paroxysms of electric-like, intense pains; V2 and V3
Trigeminal neuralgia headaches caused (by age, treatment option for one)?
In young: MS; in old: looping SCA abutting trigeminal nerve
Treatment for SCA abutting trigeminal nerve?
Surgery: microvascular decompression
If you have >6 migraines/month, what kind of therapies (2)?
Preventative and acute
What is pulsating in migraines?
Spinal fluid
How is inflammation generated in migraine?
Release of neurochemicals from the nerve terminals leads to vasodilation and inflammation of vessels in meninges
T/F: Central sensitization plays a role in migraine.
True! TNC sensitization
Are opioids good for treating headache? Why (4)?
No. Pro-inflammatory, increases N/V, increases CSD via glutamate, sedating
What responds to triptans? Importance?
Headaches; does not diagnose type of headache
NSAID advantages for headache (4)
Does not induce headache, safe if you have vascular disease, non-sedating, no increase in nausea
What are prodromal symptoms due to? What drug class can be used to treat migraines? Advantages/disadvantages
DA activation; neuroleptics (D2 receptor blockers); effective, reduce N/V; cause sedation, prolonged QT, orthostatic hypotension
Dihydroergotamine: derived from and concerns
Ergot; vascular disease
What larger 5-HT families are were interested in migraine? Mechanism. What drug family?
5-HT1s (B: targets blood vessels and D: neural inhibition); agonists –> stimulating decreases neurogenic inflammation; triptans
Describe triptans
Reduce all aspects of migraine disability, minimal/no sedation, does not increase nauseau
Triptans we need to know (2)
Sumatriptan, eletriptan
Describe “triptan effect” and contraindications
Chest/back of the neck pressure; heart disease/HT
Serotonin syndrome (def and triad) and triptan
Life threatening condition associated with increased serotonin in CNS; mental status changes, autonomic hyperactivity, neuromuscular abnormalities; triptan + SSRIs might increase risk of serotonin syndrome
Theory of treating acute migraine
Treat early!
Model: drugs that are useful in the prophylaxis of migraine suppress…what’s a lab test demonstrating this?
Cortical spreading depression; plasma glutamate increased with migraine and reduced with prophylaxis
Some SEs for migraine prophylactic drugs?
Weight gain, memory loss, depression, tremor
Classes and examples for prophylactic migraine treatment (4)
Beta-blockers (propranolol), tricyclic antidepressants (amitriptyline), antiepileptic (valproate, topiramate), anticholinergic (botox)
What is the one drug approved for chronic migraine?
Botox
