Headache Flashcards
Primary Headache?
Headaches without identifiable structural cause
Secondary Headache?
Headaches with underlying structural/metabolic cause
Acute Headaches?
abrupt-sudden onset, rapid worsening
Subacute Headaches?
Gradual onset, progressive buildup
Is the brain parechyma has how many sensory receptors? Is it sensitive to pain?
None
No
Underlying cause of headaches?
Inflammation or physical traction of pain sensitive nerve fibers
Through what nerves is headache pain transmitted?
CN V, VII, IX, X
Upper Cervical roots C 2-3
What innervates pain sensitive structures of the anterior/inferior fossa and scalp?
Ophthalmic branch of CN V
What innervates the posterior fossa, the cervical muscles and posterior scalp?
CN IX, X, C 2-3
Where do the pain sensitive nerve fibers synapse? Where do they go from there?
Trigeminal nucleus caudalis & Dorsal Horn of the upper cervical spine –>
VPL & VPM –> Sensory cortex
What is a migraine?
Chronic neurological disorder causing recurrent headaches
Features of migraines?
Freq. unilateral Pulsating Moderate to severe intensity Duratation of 4 - 72 hrs Photophobia and/or phonophobia May be preceded by a prodromal phase May be preceded by an aura "Triggers" are frequent Frequent FHx
Prodrome symptoms for migraines?
Mood swings Odd food cravings Malaise or vague feeling of un-wellness Fatigue Muscle aches and stiffness
Scotoma?
Blind spot
Most common location for aura to occur?
Occipital (Visual) Cortex
Cause of an aura?
A spreading depression wave
When does the occurrence of migraines begin to decline?
55
In what population are migraines seen more often?
Women
Is there a correlation between genetics and migraines? If so, what?
Yes
Polygenic - one loci at 10q23
Familial hemiplegic migraine (dominant gene)
What is the anatomical substrate for migraines?
Trigeminovascular System
What does the trigeminovascular system involve?
CN V1 innervation of pain receptors located in the dura, meninges, and medium/large cerebral arterys and veins that lie on the surface of the brain and above the tentorium
What mediates the vascular changes associated with migraines?
Trigeminovascular System
Pathogenesis of migraines?
In hypersensitized pain pathways, migraines may be triggered by either a so-called “Central Generator” located in the brainstem or by internal or external triggers that initiate an aura that stimulates neurogenic inflammation of meningeal vasculature that then excites already hypersensitive peripheral and central pain pathways
Where are auras typically located?
Cortex
Which NTs are important in the pathogenesis of neurogenic inflammatory pain and migraine?
Calcitonin gene related peptide (CRGP) Substance P (SP)
One big function of CGRP and Sub P?
Potent vasodilator properties
What does CGRP activate? Producing what? Causing what?
CRL receptors
To relax vascular smooth muscle (vasodilate) and to cause degranulation of mast cells.
Process causes sensitize this synaptic terminal to become hypersensitive and thereby fire off an antidromic signal (afferent) back through the trigeminal nerve to the brain stem
What mediates the local inflammatory reaction in migraines?
Mast Cells
What else is mediated by CGRP?
Mediate the synaptic juncture between the trigeminal nerve and the central brain stem neuron
What is MoA of triptans?
5-HT1 receptor agonist leading to inhibition of the release of CGRP
Where are trigger mechanisms found for migraines?
Both peripherally (trigeminovascular) and/or centrally (brain stem)
What is a cluster headache?
Chronic neurological disorder causing recurrent headaches
Characteristics of cluster headaches?
Pain always unilateral, frontal, retro-orbital
Unilateral Horner’s Syndrome and lacrimation
Unilateral conjuctival injection and rhinorrhea
Constant, severe, non-pulsating pain
Duration of minutes - 3 hrs
Daily attacks for weeks/months; remit for yrs
Men to women ration 4:1
Triggers are alcohol and tobacco
Rare FHx
Cluster Rx?
Acute Rx - Nasal oxygen at 8 -10 l/min
SubQ Sumatriptan
Prophylaxis - CCBs (Verapamil)
Lithium
Valproic Acid
PrednisoneCharacteristics of Episodic/chronic tension headaches?
Pain usually bilateral and bandlike Not associated with auras Not associated with nausea/vomiting Not associated with photo- or phonophobia Duration of minutes - 3 hrs Daily attacks < 15 days/month = Episodic Daily attacks > 15 days/month = Chronic
Daily headaches > 15 days/month
Chronic tension headaches
Daily headaches < 15 days/month
Episodic tension headaches
Clinical features of idiopathic intracranial hypertension (Pseudotumor cerebri)?
Headache of varying character Pailledema Transient visual obscurations Diplopia secondary to CN VI paresis Tinnitus Constriction of visual fields, enlarged blind spots Female to male ratio ~ 9:1 Age 20 - 45 yrs Overweight (20% over normal body weight)
What is special about pseudotumor cerebri?
Is a neurologic emergancy and must be treated as soon as possible to prevent loss of vision
Causes of pseudotumor cerebri?
Primary idiopathic - cause unknown
Primary symptomatic - cause related to underlying metabolic abnormality that alters CSF production or reabsorption
Secondary - cause related to underlying process that physically blocks CSF circulation and/or absorption.
Clinical features of Giant Cell (Temporal) Arteritis?
Autoimmune, systemic vasculitis causing granulomatous infiltration and occlusion of medium/small elastic arteries.
Headache - usually unilateral
Point scalp tenderness over temporal artery
Monocular obscurations leading to blindness secondary opthalmic artery occlusion
Associated polymyalgia rheumatica
Stroke - particularly involving the vertebral arteries
