Headache Flashcards
Int’l hadache society classification
Primary- headaches without identifiable structural cause
Secondary- headaches with underlying cause
Pathophys of headaches, general
Inflammation or physical traction of pain sensitive nerve fibers
Pain sensitive structures in the head:
- Dura and meninges
- Large Arteries at the base of the brain, meningeal arteries
- Venous sinuses
- Scalp muscles
- Upper Cervical muscles
- Periosteum of the skull
- Facial and head structures/organs, skin, eyes, teeth, sinuses, muscles etc…
Brain parenchyma has sensory receptors T or F?
False. Brain parenchyma has no receptors and is insensitive to pain.
Most of the pain sensitive structures lie in the dura/meninges and/or are large to medium sized arteries that lie in the back of the brain
Stimulation of cranial pain receptors carried by what nerve troots?
V. VII, IX, X and the upper cervical nerve roots C2-3
mostly 5,9, c2-3
The opthalmic branch of V innervates pain sensitive structures where
Anterior and Middle Fossa and the anterior half of the skull. Includes the tentorium
POsterior scalp and neck
C2-3
CN IX and X
Posterior fossa
Some common migraine features
frequently unilateral
- Pulsating
- 4-72 hours
- nausea with or without vomitting
- May be preceded by a prodromal phase
- May be preceded by an aura
- Triggers or precipitating factors are frequent
- Frequent family history
Migraine Prodrome
Experienced by approximately 40% or migraineurs
- a vague constellation of symptoms that include mood swings
odd food cravings
malaise or vague feeling of unwellness
fatigue
muscle aches and stiffness
Migraine aura
Usually a visual disturbance that precedes the headache by no more than 60 minutes. Begins near the center of the visual field as a small gray area with indefinite boundaries. During the next few minutes, the gray area slowly expands into a horseshoe with zigzag lines and expands out toward the periphery of the visual field
What percentage of migraineurs have clearly defined auras?
only 20%
Women affected 2-3 times more frequently than men by migraines
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Migraine carries strong family hx
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Familial hemiplegic migraine?
inherited genetic abnormalities at several different loci… dominant gene
Trigeminovascular system?
anatomical substrate for migraines
- Involves CN V1 innervation of pain receptors located in the dura, meninges, and medium/large cerebral arteries and veins that lie on the surface of the brain and above the tentorium.
Know Dermatomes of the faceo
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Slide 21
Nuclues caudalis of trigeminal system projects afferent pain sensation from the face to the VPM of the Thalamus which is then sent to sensory cortex
What is responsible for mediating the vascular changes associated with migraines?
Trigeminovascular system- AFFERENTS come from the vasculature running through the Dura Mater which comes back to the Trigeminal nucleus. EFFERENTS then come from the superior salivatory nucleus then cause vascular changes (vasodilation)
The vasodilation associated with migraine headaches is mediated by:
Superior salivatory nucleus which carries parasympathetics along CN VII
What is the current thinking on Migraine pathogenesis
It is due to polygenic predisposition that hypersensitizes both the peripheral (trigeminovascular- afferent and efferent) and central (nucleus caudalis, etc..) pathways of heahache.
- May be triggered by central causes or external causes.
- Neurogenic inflammation of meningeal vasculature
What is the most common aura
visual scintillations followed by scotoma or blind spot.
Where do aura’s usually arise from in the brain?
Cortex- triggered either remotely from a central brain stem genearator or locally by a variety of external stimuli
Clinical manifestations of an aura depend on…
What part of the brain is being excited
Visual auroa due to excitation of which part of the brain?
calcarine cortex
What happens to bloodflow during an aura?
Blood flow in the area of excitation briefly increases in concert with the excitation, then decreases which gives way to the transient loss of vision in this area.
What are the two neurotransmitters that are important in the pathogenesis of neurogenic inflammation/pain and migraine
Calcitonin gene related peptide and substance p.
CGRP and SP
Know that sensory (afferent) systems can also sometimes function as an efferent system sending action potentials to the nerve terminals where Neurotransmitters are released. CGRP and SP have potent vasodilator properties among other functions
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SLIDE 28
KNOW
What do triptans do
They are 5-HT1 receptor agonists. Remember 5-HT is serotonin. As 5-HT1b-d receptor agonists, they inhibit the release of CGRP
How do Geptans work?
They are CGRP antagonists, that is, they block the CRL receptor.
Cluster headache features
- Pain always unilateral, frontal, retro-orbital
- Unilateral conjunctival infection and rhinorrhea
- unilateral horner’s syndrome
- constant severe non-pulsating pain
- duration of minutes…3 hrs
- daily attacks for weeks/mths; remission for years
- triggers are alcohol and tobacco
- onset usually around age 25
acute tx of cluster headaches?
nasal oxygen
subcutaneous sumatriptan
Episodic/chronic/tension headaches
pain usually bilateral and bandlike no auras no phono/photophobia duration 3 hours more than 15 a month = chronic
slide 39
KNOW
Idiopathic intracranial hypertension features:
- headache of varying character
- papilledema
- transient visual obscurations
- diplopia secondary to CN VI paresis
- tinnitus
- Female: Male 9:1
- Overwt generally by 20% over normal
Failure to treat in a timely manner may lead to loss of vision.
Typical presentation is a young woman who is over wt by at least 20% of her normal body wt.
Is IIH an emergency?
Yes. Failure to treat in a timely manner can lead to permanent vision looss
Classification of IIH
- Primary Idiopathic: cause unknown
- Primary symptomatic: cause related to underlying METABOLIC ABNORMALITY that alters CSF production and/or reabsorption
- Secondary: Cause relatued to underlying proocess that physically blocks CSF circulation and or absorption.
So remember that Idiopathic intracranial hypertension is generally related to CSF
Pathogenesis of Primary symptomatic IIH
Hypervitaminosis A
Antibiotics
Steroid Withdrawal
Others
Secondary IIH causes
venous sinus thrombosis
chronic meningitis
chiari malformation
Giant Cell Arteririts
Systemic vasculitis causing granulomatous infiltration and occlusion of small/medium sized elastic arteries
The most common primary headaches (migraine, cluster, tension) generally have what kind of temporal onset?
subacute
Know that electrical stimulation of the thalamus or trigeminal nucleus caudalis will trigger…
pain response
Remember that pain sensitive fibers synapse in the trigeminal nucleus caudalis and dorsal horn of upper cervical spine.
Central pain fibers then synapse in the VPL and VPM nucleus of the Thalamus and onto the sensory cortex
Diagnosis of IIH (pseudomotor cerebri)
- Imaging should be normal
- Lumbar punctures showing a CSF pressure over 250 is diagnostic.
Note that obese ppl may have pressures between 200 and 250 normally
Treatment of IIH (Pseudotumor cerebri
wt loss
- Reduce CSF with acetazolamide and furosemide
- repeated lumbar punctures
Giant Cell Arteritis
vasculitis causing granulomatous infiltration and occlusion of small to medium elastic arteries.
- headache unilateral overtemporal artery
- visual symptoms…can lead to blindness due to opthalmic artery occlusion
- Associated with polymyalgia rheumatica in about 50% .. jaw claudication, malaise, fever, wt. loss, myalgia
- Stroke involving cerebral arteries
Dx of Gint Cell
ESR over 75, C-reactive protein high
Biopsy but remember its a skip lesion
Look for inflammation and MNGCs in the elastic lamina
