Headache disorder Flashcards

1
Q

Background

A
  1. 65-85% of the population has >1 headache annually
  2. 5-7% of the population seeks medical attention for headache
  3. Headache is the reason for 2% of doctor’s visits and 3% of ER visits
  4. 15% of women, 6% of men and 4% of children have migraine
  5. Annual lost productivity attributed to migraine is $5.5-17 billion
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2
Q

Headache Anatomy: Cranial pain producing structures: structures which are sensitive to pain

A

a. Pain is a normal response from a healthy nervous system
b. Cranial structures which are pain sensitive
i. Scalp
ii. Sinuses (periosteum)
iii. Meninges
iv. Pial arteries
v. Arteries and major veins

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3
Q

Headache Anatomy: Cranial pain producing structures: structures which are not sensitive to pain

A

. Cranial structures which are not sensitive to pain

i. Ventricles
ii. Choroid
iii. Brain Parenchyma (exception is small part of the midbrain)
iv. Small parenchymal and dural veins

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4
Q

Headache Anatomy:Anatomic etiologies for pain

A

a. Vascular
i. Distension/Traction/Dilation of intracranial arteries or major veins
ii. Traction or displacement of a larger caliber vein
b. Nerve
i. Traction or compression of a nerve
c. Meninges
i. Traction, displacement, irritation, or inflammation of the dura
d. Muscles
i. Abnormal contraction, spasm, irritation or inflammation of cranial or
cervical musculature
e. Brainstem
i. Activation of a small area near the dorsal raphe nucleus (high
concentration of serotonin) in the midbrain has been proven to induce
migraine type pain

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5
Q

Migraine: Defined

A

Migraine is defined as a benign reoccurring primary headache disorder that has
associated symptoms which can include any of the following: photophobia,
phonophobia, nausea, vomiting, worsening with exertion, and/or neurologic
symptoms (including but not limited to vision change, focal weakness or
parasthesia, dizziness/vertigo).
i. Migraine is very common with 15% of women and 6% of men affected

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6
Q

Migraine: Pathophysiology

A

Migraines were once believed to be caused by constriction
and subsequent dilation of cerebral blood vessels-but this is now believed to not
be the case. The current thought is that migraines begin in the brainstem with
an abnormal instability or activation of certain cells which spread peripherally
and stimulate the trigeminal system (cranial nerve responsible for sensory to
the head and face). This eruption of abnormal activity in the brainstem may
affect other local systems including chemoreceptors (resulting in nausea and
vomiting) and the autonomic nervous system (resulting in pallor, flushing, and
congestion

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7
Q

Migraine without aura

A
  1. This is a typically unilateral headache which is often described
    as a deep ache or throbbing sensation. Patients often complain
    of associated symptoms of phonophobia, photophobia, and/or
    nausea vomiting. Symptoms often worsened by exertion and
    relieved by rest.
  2. Symptoms will often last between 30 minutes and 6 hours, but
    can last longer (as much as 72 hours)
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8
Q

Migraine with aura

A

Same as migraine without aura but is preceded by an aura up to
30 minutes before headache onset or occurring up to one hour
into the headache. Aura occurs in 60-70% of migraines.
a. Aura is perceptual disturbance experienced prior to
headache onset which can manifest as:
i. Visual disturbance- scintillating scotoma, zig-zag
lines, kaleidoscope, tunnel vision or even
monocular vision loss.
ii. Sensory disturbance - often focal parasthesia
described as pins-and-needles sensation
iii. Motor disturbance - often focal weakness or
even paralysis
iv. Auditory Disturbance- Modification of voices or
sounds in the environment: buzzing, amplitude
modulation. Could manifest as heightened
sensitivity to sound.

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9
Q

Complicated Migraine

A

Same as migraine with aura but the aura is quite dramatic and
can last for an extended period of time. These can often mimic
the appearance of stroke. Diagnosis is made by exclusion of
other more serious underlying pathology.

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10
Q

Basilar Migraine

A
  1. The migraines have associated brainstem and posterior cerebral
    circulation symptoms including vertigo, dysathria, ataxia, and
    diplopia. Headache onset follows in 20-30 minutes following
    neurologic symptom onset as is described as an occipital
    throbbing pain.
  2. Bickerstaff’s Migraine is the most severe and dramatic form of a
    basilar migraine. It begins with total blindness and is followed
    by admixtures of vertigo, ataxia, dysarthria, and/or tinnitus.
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11
Q

Migraine Treatment: Non-Pharmacologic Approach

A
  1. Avoid triggers:

a. Red Wine, certain foods (chocolate, some cheeses,
MSG, heavy nitrite containing foods-i.e. highly
processed meats), hunger from missing meals, sleep
deprivation and irregular sleeping patterns, and stress

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12
Q

Migraine Treatment: Pharmacologic Abortive or Rescue Therapy

A
  1. Abortive or Rescue Therapy (to be taken with headache onset)
    a. NSAIDS
    i. Ibuprofen, Naprosyn, Ketorolac
    b. 5HT1 agonists (Triptans and Ergots)available in oral,
    inhaled and subcutaneous forms (examples below)
  2. Sumatriptan (short onset and duration)
  3. Zolmitriptan (intermediate onset and
    duration)
  4. Frovatriptan (long onset and duration)
    ii. Contraindicated in those with history of CAD or
    ischemic stroke
    c. Dopamine antagonists available in oral and
    subcutaneous forms
  5. Metoclopramide (Reglan)
  6. Prochlorperazine (Compazine)
    d. Combinations
  7. Acetaminophen, ASA, and caffeine
    (Excedrin Migraine)
  8. Acetaminophen, butalbital, and caffeine
    (Fioricet)
  9. Acetaminophen, Isometheptene and
    Dichloralphenazone (Midrin)
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13
Q

Migraine Treatment: Pharmacologic: Prophylactic Therapies

A
Daily medications should be used to
prevent migraines when they are severe enough to cause
functional impairment and are occurring at least three times
per month. None of the drugs is particularly more effective than
another. Drug choice is often based on comorbidities (i.e.
depression and other psychiatric disease) and/or hypertension)
a. β-Adrenergic Blockers
1. Propranolol
2. Atenolol
ii. Calcium Channel Blockers
1. Verapamil
iii. Tricyclic Antidepressants
1. Amitriptyline
2. Nortriptyline
iv. Anticonvulsants (AED’s)
1. Gabapentin (Neurontin)
2. Valproic Acid (Depakote)
3. Topiramate (Topamax)
4. Levetiracetam (Keppra)-not FDA
approved)
v. Serotonergic Drugs
1. Cyproheptadine (Periactin)
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14
Q

Cluster Headaches

A

a. Cluster headaches are one of the most painful headache conditions. They are
defined as an episodic headache condition characterized by 1-3 short duration
(15 minutes to 3 hours in length) attacks of severe unilateral stabbing periorbital
or temporal pain. They tend to occur in clusters for approximately 3-6 weeks.
They are typically associated with at least one of the following associated
symptoms: conjunctival injection/lacrimation, miosis, ptosis, eyelid edema,
rhinorrhea/nasal congestion and/or perspiration. They have a remarkable
circadian rhythm as reflected by the tendency to occur at the exact same time
every day during a cluster period. The attack frequency can be from one every
other day up to eight times per day

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15
Q

Cluster Headaches: Pathophysiology

A

Cluster headaches are believed to be derived in part by the
hypothalamus, especially so in those with prominent autonomic symptoms.
There is then a secondary activation of the trigeminal-autonomic reflex,
probably via a trigeminal-hypothalamic pathway.

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16
Q

Cluster Headaches: TX

A

Acute Treatments
1. Treating cluster headaches can be difficult given the short
duration of the individual attack. The treatment should begin
with immediate use of oxygen and if pain is still present at 20
minutes one should use intranasal or subcutaneous sumatriptan
(preferred over oral due to improved onset time).
a. Oxygen
i. Administration of high concentration O2
(12L/min) for 15 minutes will decrease the
headache duration-this is the most effective
abortive agent
b. Triptans- effective in about 75 percent of patients (painfree
at 20 minutes after administration)
i. Should use a short onset, short duration drug
(i.e. Sumatriptan)
ii. Prophylactic (should only be started at onset of cluster):
1. High Dose Steroids
a. Use of high dose prednisone during the patient’s cluster
of events (typically dosed for 2-4 weeks) will
dramatically lessen the frequency of attacks in the
cluster. Is often combine with additional prophylactic
agents (see below)
2. Calcium Channel Blockers (i.e. Verapamil) –adjuvant agent of
choice

17
Q

Tension Headaches

A

Tension headaches are the most prevalent headache syndrome. Whether
these are infact mild migraine headaches or rather a unique condition is
continually debated. Patients who suffer from tension type headaches
described a sensation of squeezing or pressure around the head. They may also
complain of being light and sound sensitive. They are never associated with
nausea or vomiting- if this is a complaint then you are most likely dealing with
migraine. These symptoms can last minutes or even days and are constant.

18
Q

Tension Headaches: TX

A

i. Non-Pharmacologic Approach
1. Stress reduction
2. Biofeedback
3. Cognitive Behavioral Therapy
4. Improved sleep hygiene
ii. Pharmacologic
1. Abortive
a. Acetaminophen
b. NSAIDS
2. Prophylaxis
a. Tricyclic Antidepressants
i. Amitriptyline
ii. Nortriptyline
b. Antiepileptic
i. Gabapentin

19
Q

Idiopathic Intracranial Hypertension (IIH)

A

IIH is a disturbance which causes increased intracranial pressure without
evidence of an intracranial mass, hydrocephalus, or dural venous
stenosis/thrombosis. The exact cause of the disease is unclear, hence the term
idiopathic, but is thought to be due to decreased CSF absorption. The disorder
occurs most frequently in obese young females and has a clear correlation with
being caused by certain medications (tetracycline containing prescriptions, oral
contraceptive pills, and hypervitaminosis A are the most well recognized)
Symptoms are typically described as new onset continuous daily headache that
worsen with coughing, sneezing, and moving into the supine position.
Symptoms can progress to include vision loss, diplopia, and pulsatile tinnitus

20
Q

Idiopathic Intracranial Hypertension (IIH): Diagnosis

A

Initial work-up should always include MRI brain with a magnetic
resonance venogram (MRV) to rule out a structural cause for the new headache
symptoms. When this study returns normal, one would the move forward to
obtain a lumbar puncture to test the opening pressure. LP’s must be done in the
lateral decubitus position in order to obtain an accurate opening pressure. The
LP will not only be diagnostic due to the increase opening pressure but will also
be therapeutic at relieving the patient’s headache symptoms.
Patients should always have an ophthalmologic exam with formal visual fields
performed by Ophthalmology to document exam findings. This condition, if left
untreated, will cause patients to have irreversible vision loss which could
ultimately lead to blindness.

21
Q

Idiopathic Intracranial Hypertension (IIH): TX

A

i. Non-pharmacologic
1. Weight loss
ii. Medical
1. Removal of offending drugs if present
2. Treatment with drugs that decrease CSF production (carbonic
anhydrase inhibitors):
a. Acetazolamide
b. Topiramate
iii. Procedural
1. Recurrent LP’s
2. Optic Nerve Fenestration
3. Ventriculoperitoneal shunt placement

22
Q

Giant Cell Arteritis

A

Giant Cell (temporal) Arteritis is a vasculitis that is almost exclusively found in
patients>50 y/o. The condition typically presents clinically with progressive
unilateral throbbing headache with tenderness of the temporal scalp area.
Patients will often complain of concomitant jaw claudication, diffuse joint pains,
visual disturbance, and transient monocular vision loss. Physicians must have a
high index of suspicion for this disease, because if missed it could lead to
permanent blindness due to anterior ischemic optic neuropathy (essentially a
stroke to the eye)

23
Q

Giant Cell Arteritis: Diagnosis

A

Diagnosis is typically made when patient is older than 50, has elevated
inflammatory markers (ESR and CRP) and a compatible history. Temporal artery
biopsy is the gold standard for making the diagnosis. One must obtain a large
section of artery as this vasculitis is notorious for skipping segments.

24
Q

Giant Cell Arteritis: TX

A

Treatment is with high doses steroids which typically relieve the headache
symptoms within three days. Given the chronic nature of this condition, most
patients remain on a constant low dose steroid regimen for a couple of years.