Headaches Flashcards
Headache
Overview
A very common reason people seek medical attention.
Globally, the most common cause of neurologic disability.
Headache
Definition
Irritation of pain-sensitive intracranial structures, including dural sinuses; intracranial portions of the trigeminal, glossopharyngeal, vagus, and upper cervical nerves; large arteries; and venous sinuses.
Classification of Headache
3 major categories:
Primary Headache Syndromes
Secondary Headache Syndromes
Cranial Neuralgia Syndromes
Primary Headache Syndromes
Headache in the absence of exogenous cause.
- Tension-type headache (most common)
- Migraine (2nd most common cause of headache)
- Trigeminal autonomic cephalgias – includes cluster headache
- Primary stabbing headache (i.e., “Ice pick headache”)
- Transient and localized stabs of pain in the head which last for a few seconds
- Occur spontaneously in the absence of organic disease of underlying structures or of the cranial nerves
- Primary thunderclap headache
- High-intensity headache of abrupt onset in the absence of any intracranial pathology
- Mimics ruptured cerebral aneurysm
- Primary headache associated with sex or exercise
- Cold-stimulus headache
- Due to external application, ingestion, or inhalation of a cold stimulus (ex. very cold weather or eating ice cream)
Secondary Headache Syndromes
A long list of conditions can lead to secondary headaches:
-
Infection (most common cause of secondary headache)
- Ex. sinusitis, meningitis, or abscess
- Headache associated with systemic infection (accounts for almost ⅔ of secondary causes)
- Post-traumatic (i.e. head injury) – acute or chronic
- Vascular – Subarachnoid hemorrhage; vasculitis; or arterial dissection (carotid or vertebral)
- Non-vascular – Brain tumor; Giant cell arteritis; Glaucoma; Idiopathic (benign) intracranial hypertension (previously called pseudotumor cerebri); low CSF pressure (post-LP or CSF leak)
- Medication – Side effects (ex. nitrates) or withdrawal (ex. caffeine)
- Disordered homeostasis – Hypoxia or hypercapnia (ex. obstructive sleep apnea); dialysis-associated headache; hypoglycemia
Cranial Neuralgia Syndromes
Injury or inflammation of cranial nerves causing headache.
Includes trigeminal neuralgia and post-herpetic neuralgia.
Tension-type Headache
Epidemiology
- Most common cause of headache overall
- Occurs in all age groups
- Anyone can get a tension headache
Tension-type Headache
Characteristics
- Pain is steady and non-pulsatile
- Often described as “pressure” or “band-like”
- Mild to moderate in intensity
- Bilateral - frontal, occipital, or generalized location
- Often associated with neck pain
- Pain can last for days
- Builds slowly and fluctuates
- Can be episodic or chronic (>15 days per month)
- Generally, no associated sx such as aura, nausea/vomiting, photophobia/phonophobia, etc.
Tension-type Headache
Pathophysiology
- Incompletely understood
- Thought to be a disorder of CNS pain modulation
- ? Genetic component
- No definitive evidence that tension is the etiology
Tension-type Headache
Clinical Management
-
Diagnosis
- Based on history and symptoms
-
Treatment
- Behavioral approaches including relaxation
- Physiologic approaches - cervical or dental alignment or correction of vision
- Analgesics – acetaminophen, aspirin, NSAIDs, or muscle relaxants
- Prevention – tricyclic antidepressant amitriptyline is only proven agent
Migraine
Epidemiology
- 2nd most common cause of headache
- Most common cause of neurologic related disability
- Female predominance
- Begins at any age from early childhood and later
- Peak age of onset is adolescence through early adulthood
- Onset after age 50 is rare
Migraine
Factors
Complex neurovascular disorder involving:
- Genetic factors
- Non-genetic components
- Interictal traits (not comparable)
- Peripheral and central CNS involvement
Migraine Definition
ICHD-2
At least 5 attacks fulfilling criteria below:
- Headache lasts 4-72 hours if untreated
- Headache has at least two of the following:
- Unilateral
- Moderate or severe
- Aggravated by routine activity
- Pulsating
- During the headache at least one of the following:
- Nausea and/or vomiting
- Photophobia and phonophobia
- Not attributed to another disorder
Typical Aura w/ Migraine Headache
ICHD-2
At least two attacks fulfilling criteria below:
- Aura consisting of at least one of the following, but NO motor weakness:
- Fully reversible visual sx (May have ⊕ or ⊖ features)
- Fully reversible sensory sx
- Fully reversible dysphasic speech disturbances
- ≥ 2 of the following:
- Homonymous visual sx or unilateral sensory sx
- At least one aura sx develops gradually over ≥ 5 min
- Each sx lasts ≥ 5 min & ≤ 60 min
- Headache fulfilling criteria for Migraine Without Aura begins during the aura or follows aura within 60 minutes
- Not attributed to another disorder
Migraine-Associated Symptoms
- Photophobia: ~75%
- Phonophobia: ~ 70%
- Nausea and vomiting: 50-55%
- Osmophobia: ~ 40%
- Aura: ~ 15-30%
Auras
-
Stems from cortical spreading depression
- Wave of excessive signaling across large areas of the brain ⇒ abnormal silence in the previously overactive areas
- Spreading moves across the cortex at the rate of 2-3 mm/min
- May correlate w/ observed changes in blood flow
- In pts w/o aura, a wave of neuronal hyperexcitability resembling cortical spreading depression might take place in subcortical regions
Migraine Initiation
Cortical Origin
- Cortical spreading depression triggered by neurons prone to hyperexcitability
- Those neurons release substances that activate trigeminal nerves, which send pain signals to the trigeminal nucleus in the brain stem
- The trigeminal nucleus conveys the signals to the thalamus, which relays them to the sensory cortex, involved in the sensation of pain
Migraine Initiation
Brainstem Origin
- Abnormal brainstem activity ⇒ spreading depression in cortex or subcortex ⇒ trigeminal system activation
- Specifically, raphe nucleus, locus coeruleus and periaqueductal gray
- Brain stem misbehavior can also independently activate pain pathways leading to the sensory cortex
Migraines
Source of the Pain Signal
- Early in the attack, vasoactive peptides released from primary sensory nerve terminals
- Calcitonin gene-related peptide (CGRP) and substance P
- Peptides activate perivascular trigeminal nerves
- 1st order neurons terminate in the trigeminal nucleus
- 2nd order in the thalamus
- 3rd order in the cortex
Headache Characteristics
Comparison
