Headaches Flashcards
1
Q
Headache
Overview
A
A very common reason people seek medical attention.
Globally, the most common cause of neurologic disability.
2
Q
Headache
Definition
A
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.
3
Q
Classification of Headache
A
3 major categories:
Primary Headache Syndromes
Secondary Headache Syndromes
Cranial Neuralgia Syndromes
4
Q
Primary Headache Syndromes
A
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)
5
Q
Secondary Headache Syndromes
A
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
6
Q
Cranial Neuralgia Syndromes
A
Injury or inflammation of cranial nerves causing headache.
Includes trigeminal neuralgia and post-herpetic neuralgia.
7
Q
Tension-type Headache
Epidemiology
A
- Most common cause of headache overall
- Occurs in all age groups
- Anyone can get a tension headache
8
Q
Tension-type Headache
Characteristics
A
- 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.
9
Q
Tension-type Headache
Pathophysiology
A
- Incompletely understood
- Thought to be a disorder of CNS pain modulation
- ? Genetic component
- No definitive evidence that tension is the etiology
10
Q
Tension-type Headache
Clinical Management
A
-
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
11
Q
Migraine
Epidemiology
A
- 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
12
Q
Migraine
Factors
A
Complex neurovascular disorder involving:
- Genetic factors
- Non-genetic components
- Interictal traits (not comparable)
- Peripheral and central CNS involvement
13
Q
Migraine Definition
ICHD-2
A
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
14
Q
Typical Aura w/ Migraine Headache
ICHD-2
A
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
15
Q
Migraine-Associated Symptoms
A
- Photophobia: ~75%
- Phonophobia: ~ 70%
- Nausea and vomiting: 50-55%
- Osmophobia: ~ 40%
- Aura: ~ 15-30%
16
Q
Auras
A
-
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
17
Q
Trigeminal Neurons
Involvement in Migraine
A
- Neurons carry pain signals from meninges & blood vessels that infuse the membranes
- Pain relayed through trigeminal network → trigeminal nucleus in the brain stem
- Pain messages conveyed from there → thalamus → sensory cortex
18
Q
Migraine Initiation
Cortical Origin
A
- 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
19
Q
Migraine Initiation
Brainstem Origin
A
- 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
20
Q
Migraines
Source of the Pain Signal
A
- 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
21
Q
Migraine
Vascular Theory
A
Now considered an epiphenomenon neither necessary nor sufficient for the sx
Based on 3 observations:
- Extracranial vessels become distended or pulsatile during migraine
- Stimulation of cranial vessels induces an attack
- Vasoconstrictors such triptans/dihydroergotamine improve headache
More recent studies indicate that blood flow ∆’s do not correlate w/ the pain of migraine
22
Q
Cluster Headache
Epidemiology
A
- Relatively uncommon: ~ 0.1% of patients with headache
- Male predominance (3x more in men)
-
Onset usually in adults
- Later in life compared to migraine
- Rarely occurs in childhood
- Family history less common compared to migraine
- Often precipitated by alcohol
23
Q
Cluster Headache
Characteristics
A
-
Pain is intense – stabbing or boring; non-fluctuating
- Strictly unilateral, location is usually retro-orbital
- Explosive in onset and excruciating in severity
- Duration of pain is 15 minutes to a few hours
- Headaches often occur in “clusters”
- Typically 1-2 attacks daily for 8-10 weeks
- Followed by intermittent headache-free periods which can last several months to years
-
Nocturnal onset in 50%
- Occurs 2-3 hours after onset of sleep – “alarm-clock headache”
- Patients may seek activity to distract them – pacing, rocking, or rubbing head
24
Q
Cluster Headache Definition
ICHD-2
A
At least 5 attacks
- Severe unilateral orbital, supraorbital and or temporal pain lasting 15-180 minutes
-
Occurs w/ one of following:
- Ipsilateral conjunctival injection
- Lacrimation
- Nasal congestion
- Rhinorrhea
- Eyelid edema
- Facial sweating
- Miosis
- Ptosis
- Restlessness/agitation
- Attack frequency of 1 every other day to 8 per day
- Not attributed to another cause
25
Cluster Headache
Associated Symptoms
**Ipsilateral sx of cranial parasympathetic autonomic activation:**
* Congestion of nasal mucosa
* Conjunctival injection or lacrimation
* Ipsilateral sweating on the forehead
* Horner syndrome (miosis, ptosis, plus eyelid edema)
26
Cluster Headache
Pathophysiology
Seems to be a disorder of **central pacemaker neurons** and **neurons in posterior hypothalamic region**
27
Cluster Headache
Diagnosis
_Based on description of symptoms:_
* Cyclic pattern and length
* Differential is short-lasting headaches w/o prominent cranial autonomic symptoms (ex. trigeminal neuralgia or primary stabbing headache)
* Patients with TAC should undergo pituitary evaluation due to increase in TAC-type presentations in those with pituitary tumor-related headache
28
Cluster Headache
Treatment
* _Acute treatment_
* **100% oxygen is very effective in many**
* High flow and high oxygen content (Ex. given by mask)
* 60% ♀ vs. 87% ♂ respond to O2 within 15 min
* **Triptan agent nasal sprays** can be used (oral sumatriptan is not effective)
* **Sumatriptan 6 mg SC**
* 74% w/ relief by 15 min vs. 26% placebo
* **DHE-45 IV**
* **Lidocaine 4% Nasal**
* **Noninvasive vagus nerve stimulation** is FDA approved
* _Prevention_
* Multiple medications can be used depending on the length of the individual’s cluster bout
* Shorter bouts may benefit from **glucocorticoids**
* Calcium channel blocker **verapamil** is first-line preventive for those with chronic cluster headaches or prolonged cluster bouts
* **Neuromodulation therapy** is an option for prevention if medications don’t work
29
Headache Characteristics
Comparison
30
Headache Evaluation
History
* **Duration of symptoms**
* Initial symptom description - **intermittent, daily, progressive**?
* Length of time between onset and peak intensity
* **Any warning symptoms (aura)**
* Any significant interference with normal activity
* **Aggravating factors** (light, noise, etc.)
* **Alleviating factors** (rest, medication, etc.)
* **Time of day** headaches are most likely to occur - awaken patient from sleep?
* Specific **triggers** for headache (food, lack of sleep, menstrual cycle)
* **Family history** of headaches
* Need to also consider the **psychological state of the patient**
* There can be a relationship between headache and depression and anxiety
31
Headache Evaluation
“Alarm Findings”
_In new-onset headache suggests structural brain lesion:_
* **Sudden-onset** headache
* **First severe** headache or “**the** **worst headache** **of my life**”
* **Progressively worsening** symptoms over days or weeks
* **Marked exacerbation with straining** (Ex. bending, lifting, coughing)
* Headache that d**isturbs sleep or presents immediately with awakening**
* Known systemic illness
* Onset of headache **over age 55 years**
* **Fever** or other unexplained systemic signs are present
* **Focal neurologic complaints** or **abnormal neurologic examination** are present
* **Vomiting precedes the headache**
* Pain is associated with **local tenderness** (Ex. tender to palpation over the temporal artery)
32
Headache Evaluation
Exam and Tests
* **Careful neurologic examination is crucial**
* **Imaging is required for those with an abnormal exam or concerning symptoms** (ex. alarm findings)
* CT and MRI are both reasonable options
* Lumbar puncture (LP) is required in some cases
