1. Rule out serious underlying pathology (secondary causes) 2. Determine the type of primary headache

Headache Flashcards by Emily Tremblay

What nerve senses head pain

Trigeminal nerve (CN V)
*Brain parenchyma itself has no sensation

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Intracranial pain sensitive structures (4)

-Arteries of the circle of Willis
-Meningeal / dural arteries
-Large veins and dural venous sinuses
-Portions of the dura near blood vessels

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Extracranial pain sensitive structures (6)

-External carotid artery
-Scalp and neck muscles
-Skin and cutaneous nerves
-Cervical nerves and nerve roots
-Mucosa of sinuses
-Teeth

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Primary vs secondary headaches

Primary: headache is the condition itself
Secondary: headache is a symptom of an underlying illness

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Examples of primary headaches (3)

-Migraine
-Tension headache
-Cluster headache

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Issues that can present with “thunderclap” headaches (2)

Stroke + intracranial hemorrhages

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Approach to headache

Rule out serious underlying pathology (secondary causes)
Determine the type of primary headache

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Red flags (SNOOP)

-Systemic: symptoms (fever, night sweats, weight loss) or underlying illness (cancer, pregnancy, immunocompromised, etc.)
-Neurologic signs/symptoms: confusion, impaired alertness/consciousness, focal neurologic signs/symptoms, papilledema, meningismus, seizures
-Onset is new or sudden: first onset >40 y/o or thunderclap onset
-Other associated conditions or features: head trauma, illicit drug use/toxic exposure, headache awakens from sleep, worse with valsalva maneuvers, precipitated by cough, exertion, or sexual activity
-Previous headache hx with change in status: worsening severity, increased frequency, new features

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What to do when there is a red flag

Brain imaging (MRI or CT)

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Symptoms of increased ICP (5)

-Blurring vision w forward bending (more pressure on CNs)
-Headaches in the morning, improve with sitting up (gravity helps clear CFS and releases pressure on brain)
-Double vision - abducen’s nerve (CN VI) becomes stretched, lateral rectal muscle palsy, eyes can’t abduct and become misaligned
-Loss of coordination + balance (compression of the cerebellum)
-Chronic, daily, progressively worsening headaches w nausea

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Symptoms of increased ICP may indicate ?

A tumor or another enlarging lesion

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Cause of intracranial hypotension

Leak of CSF from the meninges (spontaneous tear in dural sheath or after LP)

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Symptoms of intracranial hypotension (1)

Headache worse when standing (gravity pulls CSF down from brain) and relieved by lying down

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MRI findings of intracranial hypotension

“Sagging” of the brain

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Features of temporal arteritis (5)

-Age >50 y/o
-Unilalteral temporal headache
-Jaw claudication (apin/cramping)
-Proximal muscle weakness + pain
-High ESR (inflammatory)

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What could temporal arteritis progress to?

Unilateral vision loss - don’t wait for biopsy to treat

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Subarachnoid headache main feature

Thunderclap headache (0 to 100 in seconds)

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Investigation for subarachnoid hemorrhage

-CT scan (w/o contrast)
-LP: if the CT scan is negative, look for blood cells in the CSF

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Features of pituitary mass

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Visual field deficit - lesion of optic pathway

Features of optic neuritis

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-Acute, severe unilateral vision loss
-Eye pain with movement

Features of pheochromocytoma

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Intermittent headaches with flushing, sweating, and high BP

Pathophysiology of migraine - cortical spreading depression (CSD)

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CSD: a self-propagating wave of neuronal and glial depolarization that spreads across the cortex - responsible for aura symptoms
*Where it spread affects which aura symptoms occur

Pathophysiology of migraine - trigeminovascular system

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Spreading depression activates the trigeminal pain afferents –> results in release of vasoactive neuropeptides –> neurogenic inflammation + vasodilation –> prolonged + intensified pain

Pathophysiology of migraine - sensitization

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Neurons (central and peripheral) become more sensitize (responsive) to painful and non-painful stimuli –> hypersensitization to pain

Phases of migraine

1. Prodrome 2. Aura 3. Headache 4. Postdrome *Not each phase is experienced by everyone

Migraine prodrome

-Occurs 24-48hrs before a migraine -Increased yawning, depression, irritability, food cravings, constipation, and neck stiffness

Overview of migraine aura

Gradual development (over 5-20mins) of transient symptoms (<1hr) -Positive symptoms caused by discharges in the CNS -Negative symptoms caused by depression of the CNS

Hemiplegic migraine

When the cortical spreading depression affects the motor cortex, causing transient neuronal dysfunction and weakness or paralysis on one side of the body

Features of migraine (4)

-Pounding / pulsating -Photophobia / phonophobia -Lasts **4-72hrs** -Unilateral

Migraine postdrome

-Feeling drained/exhausted -Head movement can increase pain where the migraine was

Advanced pharmacological treatment of migraines

**Triptans:** serotonin agonists -Inhibit the release of vasoactive peptides -Promote vasoconstriction -Block pain pathways

Triptans are contraindicated in? (4)

-Migraines with focal motor symptoms (hemiplegic or basilar) -History of ischemic stroke or heart disease -Uncontrolled hypertension -Pregnancy *Due to vasoconstrictive effects

Indications for prophylactic treatment in migraines

-Frequent / long-lasting migraines -Migraines that cause significant disability / diminished QOL -Contraindicated for or failure of acute therapies (NSAIDs, acetominophen)

Classes of migraine prophylactives

-**Beta blockers:** best for htn and <60 y/o -**Antidepressants:** good for concomitant mood disorder -**Anticonvulsants** -**Calcitonin gene-related peptide monoclonal Abs:** since CGRP is one of the neuropeptides that causes pain in headaches

Most common headache in the population

Tension headache

Tension headache features (5)

Basically just not migraine features -Bilateral -Non-pulsating -Lasts **30 mins to 7 days** -No nausea, vomiting, photophobia, or phonophobia -Not disabling

Cluster headache features

-Severe or very severe -Unilateral -Attacks last **15-180 mins** -Attacks can come in clusters -Associated with ipsilateral autonomic features (tearing, congestion, rhinorrhea, facial sweating, ptosis, etc.)

Treatment of cluster headaches - acute (2) and preventative (2)

**Acute:** -Subcutaneous sumatriptan -High flow O2 inhalation **Preventative:** -Verapamil -Lithium, topiramate (anti-epileptic)

Trigeminal neuralgia is more frequent in what population?

Elderly

What is trigeminal neuralgia?

Recurrent, brief (~1s) episodes of unilateral shock-like pains in the distribution of one or more divisions of the trigeminal nerve

Treatment of trigeminal neuralgia

Analgesics: -Carbamazepine -Gabapentin

Idiopathic intracranial hypertension (IIH)

Elevated intracranial pressure with no identifiable cause

Risk factors for IIH

-Obesity -Medications (GH, tetracyclines for acne, corticosteroids, lithium, hypervitaminosis A) -Systemic illnesses

Symptoms of increased ICP

-Headache -Transient visual obstructions (esp with bending over, valsalva) -Pulsatile tinnitus -Diplopia (compression of CN VI) -Vision loss (pressure over optic nerve)

Papilledema

Swelling of the optic disc

Evaluation of IIH

1. **Neuroimaging:** MRI, CT, MR venogram - rule out tumor or thrombosis 2. **LP for CSF pressure:** perform if the neuroimaging was normal - normal CSF pressure is 10-18 mmHg 3. **Ophthalmologic evaluation:** essential - shows severity of optic nerve involvement

Treatment of IIH

-Lifestyle: weight loss -Medical: **carbonic anhydrase inhibitors** (reduces CSF production) -Surgical: lumbar shunt, optic nerve fenestration

Headache Flashcards

(47 cards)