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withdrawal of prescribed or over the counter
medications or drugs of abuse) or toxins (e.g.,
heavy metal poisoning, carbon monoxide), metabolic/endocrine causes (e.g., hypertension, dialysis, hypothyroidism, fasting, hypo/hyperglycemia)
and resulting from psychiatric disorders.
Classifications of Headache
The most recent classification of headaches by the
International Headache Society is the International
Classification of Headache Disorders-3 (ICHD-3),
published in 2013, which uses numeric codes.
7
Primary headaches are part 1 (groups 1–4). Secondary headaches are part 2 (groups 5–12). Part 3
(groups 13–14) includes the cranial neuralgias, and
central and primary facial pain. The primary headaches are migraines, tension-type, cluster and trigeminal autonomic cephalgias.
The National Institute of Neurological Disordersand Stroke (NINDS)of the National Institute
of Health (NIH) classification of headaches designates four categories of headaches: vascular, muscle
contraction (tension), traction and inflammatory.
15
Pathophysiology of Headaches
There are only a few structures in the cranium
that are capable of generating painful stimuli
including the dura at the base of the skull (basal
dura), vessels (major arteries at the base of the
brain, dural arteries, venous sinuses and their
branches, extracranial blood vessels) and extracranial structures (skin, mucosa, muscles, fascial
planes, blood vessels, nerves). Structures incapable of producing pain are the brain parenchyma,
subarachnoid, pia mater and most of the dura.
2
(Figure 35.1)
Pathophysiologic mechanisms responsible for
headache pain effect are (1) intra- or extra-cranial
arteries undergoing distention, traction, or dilatation; (2) dura or large intracranial veins undergoing traction or displacement, (3) cranial or spinal
nerves undergoing compression, traction or
inflammation; (4) head and neck undergoing
muscle spasm, inflammation or traction; (5) meningeal irritation; (6) increased intracranial pressure; and (7) disturbance of intracerebral
serotonergic projections
2,16
Tension, presumed
to be the key factor causing tension headaches,
pertains to the muscle contraction of the head
and/or neck. Traction results from the stretching
of intracranial structures from a mass effect – as
caused by a hematoma, tumor, abscess or other
intracranial mass – and is typically a constant
pain of variable severity. Inflammation arising
from the basal dura, the head/neck soft tissues
or the nerves is the pathologic process accounting
for the pain from sinusitis, mastoiditis, meningitis
Figure 35.1 Structures Capable of Producing Pain and Non-pain Producing Structures
courtesy of Dr. Sharon E. Mace, Mr. Dave Schumick and the Medical Art and Photography Department at the Cleveland Clinic, Cleveland, Ohio.
Headaches
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21:05:09
(initial pain), and SAH (initial pain). Dilatation or
distention of vessels has been suggested as the
pathophysiologic mechanism behind vascular
headache pain, which characteristica lly causes a
throbbing pain, and is presumed responsible for
the headache from severe hypertension and
migraines,
2
although more recent data suggests
other additional mechanisms. Moreover, any
given headache may involve one or any permutation of these various mechanisms.
Pathophysiology of Migraines
Theories on the Pathogenesis of
Migraine Headaches
The vascular or vasogenic theory, an early hypothesis, ascribed the aura of the migraine to intracranial vasoconstriction, followed by rebound
dilatation of the blood vessels, which activates the
perivascular nocioceptive neurons and causes the
headache.
17
More recently, the central neural or
neurovascular hypothesis is that neural dysfunction occurs first and is followed by the vascular
changes. Neural events triggered by various stimuli
occurring in a genetically susceptible individual
precipitate a migraine.
18
Cortical Spreading Depression
The aberrant firing of neurons with ionic changes
and the release of neurotransmitters cause abnormal activation of the trigeminal/cervical afferents.
This likely involves the phenomenon of cortical
spreading depression, a short-lasting depolarization wave that moves across the cerebral cortex
with a brief excitation phase followed by prolonged depression of the nerve cells that occurs
concurrently with a failure of brain ion homeostasis and release of neurotransmitters and metabolites from the neurons.
2
Increased interstitial potassium and increased
glutamate levels with activation of the NMDA
receptor leading to an influx of calcium ions
and triggering nitrogen oxide synthetase (NOS)
activity is believed to precipitate the abnormal
neuronal excitability that results in the cortical
spreading depression with depressed electrical
activity extending to adjacent areas of the cerebral
cortex.
19
Both sodium and calcium enter the
cells, while potassium and hydrogen ions enter
the extracellular space. (Figure 35.2) The initial
increasing interstitial potassium decreases the
resting membrane potential and could eliminate
the voltage-sensitive Mg2+ block of the NMDA
receptor, thus, sensitizing it to glutamate.
19
Cortical spreading depression, thought to be
the basis for the aura of migraine headaches, may
lead to activation of the trigeminal nerve afferents
(trigeminal nocioception) and changes the
permeability of the blood -brain barrier via upregulation and activation of matrix metalloproteinases (MMPs).
16
Anatomy
The hallmark of migraines is the activation of the
trigeminocervical pain system. Migraine pain is
mediated by the trigeminal nerve (cranial nerve
V), especially the ophthalmic (V1) branch, and by
the upper cervical spinal cord levels (C1 and C2)
via the greater occipital nerve.
20
(Figure 35.3)
Activation of the sensory afferents from the
trigeminal nerve and the upper cervical spinal
cord roots that innervate the dura and facial
structures occurs. This input is sent via the trigeminal ganglion to the trigeminocervical complex (TCC) in the dorsal horn of the spinal cord.
The first-order sensory afferents of the trigeminal
nerve and the upper cervical spinal nerves synapse
on second -order neurons within the TCC in the
spinal cord, then these second-order neurons
ascend to the third-order neurons within the thalamus and other nuclei. (Figure 35.4)
Figure 35.2 Ion channels in the neural membrane may be
involved. Blocking sodium channels, for example, inhibits nerve
impulse propagation
courtesy of Dr. Sharon E. Mace, Mr. Dave Schumick and the Medical
Art and Photography Department at the Cleveland Clinic,
Cleveland, Ohio.
Sharon E. Mace
039
21:05:09
Figure 35.3 Trigeminal Nerve (Cranial Nerve V)
courtesy of Dr. Sharon E. Mace, Mr. Dave Schumick and the Medical Art and Photography Department at the Cleveland Clinic, Cleveland, Ohio.
Figure 35.4 Anatomy of CNS and Dorsal Horn of the Spinal Cord
courtesy of Dr. Sharon E. Mace, Mr. Dave Schumick and the Medical Art and Photography Department at the Cleveland Clinic, Cleveland, Ohio.
Headaches
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The TCC serves as the critical relay center
for the transmission of nocioceptive input to the
higher cortical centers where pain is perceived.
The TCC extends from the tr igeminal nucleus
caudalis in the rostral pons to the upper cervical
spinal cord leve ls (C1 and C2). The trigeminothalamic tract consists of second-order neurons from
the TCC projecting to the thalamus. The ventral
posteromedial thalamic nucleus (VPM) is the key
thalamic relay sending nocioceptive information
to the cortical pain matrix. Transmission from
the spinal cord goes to the thalamus, at the upper
end of the brainstem, via the spinothalamic tract,
and from the spinal cord to the sensory cortex
via the spinoreticular tract. (Figure 35.4 and
Figure 35.5)
The CNS can alter or even abolish pain. Both
inhibitory and facilitatory mechanisms can occur
with upward and downward modulation.
21
Modulation of this nocioceptive information occurs by
projections from the periaqueductal grey (PAG),
dorsal raphe nucleus (DRG), nucleus raphe
magnus (NRM), locus coeruleus (LC) and the
hypothalamus. Indeed, lesions in the periaqueductal grey (PAG) or the diencephalic nuclei in the
rostral brainstem can precipitate a migraine headache. Multiple other second-order neurons from
the TCC project to various subcortical sites suggesting that this nocioceptive information is transmitted to other regions of the brain.
20
(Figure 35.4
and Figure 35.5)
Cellular and Biochemical Basis
It has been proposed that a sterile neurogenically
initiated inflammation of the dura mater, characterized by vasodilatation and plasma protein
extravasation, could be the cause of migraine
pain. (Figure 35.6) Neurogenic plasma extravasation does occur with electrical stimulation of
the trigeminal ganglion and can be blocked by
various drugs, such as sumatriptan, the ergot
alkaloids and indomethacin.
19
Structural alterations in the dura occur after stimulation of
the trigeminal ganglion including mast cell
degranulation and platelet aggregation in postcapillary v enules.
22
Neurons contain a variety of neuropeptides
and neurotransmitters. Calcitonin gene-related
peptide (CGRP), substance P and neurokinin
A are among the substances released when trigeminal neurons are stimulated.
18,21
Release of
these neuropeptides has been linked with sterile
neurogenic induced inflammation. (Figure 35.6)
Elevated levels of CGRP have been found in
migraine patients and a CGRP antagonist has
been mentioned as a treatment for migraines.
18
Nitric oxide (NO) has been shown to trigger
headaches and blockade of NO synthetase (NOS)
has been suggested as an abortive treatment
for migraine headaches.
21
Drugs that affect the
various ion channels, thereby, blocking neuronal
transmission may be effective in treating
headache pain.
Nocioceptive fibers consist of A-δ fiber
neurons and C-fiber neurons. A-δ fibers conduct
sharp pain, while C-fiber neurons take longer to
respond and are responsible for the dull, aching
or throbbing pain.
21,22
Sodium channels are
responsible for the neural transmission of most
alpha-beta fibers. Sodium channel blockers, for
example, the tricyclic antidepressan ts, are used
to treat pain. Calcium channels regulate C-fiber
and spinal cord neural transmission. Calcium
Figure 35.5 Anatomy of CNS and
Trigeminocervical Complex
courtesy of Dr. Sharon E. Mace, Mr. Dave
Schumick and the Medical Art and
Photography Department at the Cleveland
Clinic, Cleveland, Ohio.
Sharon E. Mace
039
21:05:09
channel blockers, for example, gabapentin, may
be used for pain therapy.
21
Sensitization
Sensitization is the painful perception of an otherwise non-noxious stimuli. Multiple changes are
present when sensitization occurs including a
decreased response threshold, an increased size
or magnitude of response, an expansion of receptive fields, and the development of spontaneous
neural activity.
23
Migraine symptoms attributed
to sensitization include the throbbing quality of
the pain; the worsening of the pain with bending,
coughing, or sudden movements of the head;
hyperalgesia and allodynia. Hyperalgesia is the
increased sensitivity to painful stimuli, while allodynia refers to the condition in which pain is
produced by stimuli that are normally not painful
or not noxious. Sensitization may be peripheral
or central.
Peripheral sensitization refers to the increased
excitability of primary afferent neurons to stimulation (usually mechanical). There is the release
of proinflammatory vasoactive substances from
the peripheral neurons. These proinflammatory
substances – such as substance P, neurokinin A,
nitric oxide (NO) and CGRP – interact with the
blood vessel wall to cause vasodilatation, protein
extravasation and sterile inflammation with
mast cell activation and membrane disruption.
21
Stimulation of the trigeminal ganglion leads to
release of CGRP, a substance found in increased
amounts in patients with acute migraines. Secondorder neurons are then barraged with an increased
number of stronger impulses form the primary
afferent neurons. Peripheral sensitization may
involve changes in ion channels, release of neuropeptides and neurotransmitters, and increased peripheral nocioceptor receptivity.
22,23
Central sensitization refers to the increased
sensitivity or responsiveness of second order
neurons in the TCC and higher order neurons
in the CNS to mild stimuli that previously did
not activate them. This may occur by increased
sensitivity of higher order neurons or via disinhibition of descending modulatory pathways.
There is evidence that windup or sensitization is
present with migraines and that therapy may
affect this hypersensitivity as with the ß adrenergic antagonists or beta blockers, propanolol and
atenolol, which inhibit the firing of third-order
thalmocortical neurons to dural stimulation and
to glutamate injection.
17,21
Central sensitization
may be related to abnormal neuronal activity in
specific aminergic brainstem nuclei with prostaglandin and proinflammatory cytokines (such as
interleukins [IL] and tumor necrosis factor [TNF]
and cyc looxygenase enzymes) initiating and
maintaining the central stimulation or a form of
disinhibitory sensitization with dysfunction of
descending modulatory pathways.
2,17, 22–25
Figure 35.6 Migraine Pathophysiology with Sterile Inflammation, Vasodilatation and Release of Various Substances
courtesy of Dr. Sharon E. Mace, Mr. Dave Schumick and the Medical Art and Photography Department at the Cleveland Clinic, Cleveland, Ohio.
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Pathophysiology of Pain
Periphery
When nocioceptive nerve fibers in the periphery
(with migraines: the trigeminal nerve, C1 and/or
C2) are stimulated, local tissue damage occurs,
which includes the release of chemical mediators
(histamine, bradykinan, and prostaglandins) and
activation of mast cells, which produces an
“inflammatory soup.”
21
This causes capillary leakage with plasma protein extravasation, platelet
aggregation and the release of serotonin. Mast cell
leukotrienes produce superoxides, which stimulate
additional inflammatory cells. This inflammatory
milieu initiates neuronal activity. In addition to
these mediators, the cells release ions (e.g., potassium and hydrogen), cytokines and growth factors.
The cations and adenosine triphosphate (ATP) are
direct stimulants of the nerve. These substances
(e.g., bradykinin, prostaglandin E
2
, nerve growth
factor) sensitize the neuron so that lower levels of
input, previously subthreshold, now cause activation of the peripheral neuron with the result
being peripheral sensitization. Activation of
the nocioceptive fibers releases neuropeptides
(e.g., CGRP) that foster additional vasodilatation,
edema, and inflammation (see also pathohysiology
section in seizure chapter on ion channels and on
action potentials).
21–25
(Figure 35.6)
Spinal Cord and Dorsal Root Ganglion
When depolarization and conduction along the
pain fibers occurs, excitatory amino acids (e.g.,
glutamate and aspartate) and neuropeptides (e.g.,
substance P) are released at the synaptic junction
in the dorsal root ganglion (DRG). When the
action potential reaches the DRG, glutatmate (an
excitatory neurotransmitter) and substance P
(a neuropeptide) are released. Glutamate stimulates the AMPA receptors. Activation of the Nmethyl-D-aspartate (NMDA) receptor occurs via
removal of the magnesium from the NMDA receptor by glutamate and substance P. Intracellular
calcium release occurs as a result of NMDA activation, which in turn, stimulates nitric oxide (NO)
and protein kinase C. The inhibitory neurotransmitters, gamma-aminobutyric acid (GABA) and
glycine, block the excitatory neurotransmitters,
glutamate and AMPA. NMDA antagonists, such
as ketamine, may decrease the pain response by
blocking the NMDA receptor. NMDA receptors
are widespread throughout the CNS. (Figure 35.7)
Figure 35.7 Neurotransmitters, neuropeptides, ions and receptors involved in the response to pain
courtesy of Dr. Sharon E. Mace, Mr. Dave Schumick and the Medical Art and Photography Department at the Cleveland Clinic, Cleveland, Ohio.
Sharon E. Mace
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Central Nervous System
Facilitation of pain sensation is induced by glutamate, serotonin and norepinephrine; inhibitionofpainoccurswithGABA,glycine,and
endorphins. There are mu receptors throughout
the CNS: in the cortex, thalamus, spinal cord,
and in the DRG. Mu receptors are generally
quiescent until stimulated by painful input.
21
It
may be that th ese mu rece ptors are involved in
headache pain. The maladaptive pain of
migraine and other primary headache disorders
may be due to an imbalance between the facilitory and inhibitory systems, whereby the facilitory system dominates the inhibitory system,
thereby, allowing normally nonpainful stimuli
from the trigeminal nerve , C1 and/or C2 to cause
pain.
21
(Figure 35.5)
Other Research
Decreased GABA levels in the brain may be
a factor in the neuronal hyperexcitability or lack
of inhibitory control.
24
Increased levels of
CGRP, a potent vasodilator released from trigeminal ganglia neurons, are found in migrainers and are normalized when sumatriptan is
administered, which may be a mechanism of
action of this drug.
The tricyclic antidepressants, which block
serotonin (5-hydroxytryptamine or 5-HT) reuptake, are efficacious prophylactic drugs for
migraines. Serotonin is released from brainstem
serotonergic nuclei. This suggests that serotonin
may be involved.
21
Possible mechanisms include
low serotonin levels causing a lessening of the
serotonin descending pain inhibitory system, an
effect on cranial vessels or on central pain pathways or by an effect on the brainstem nuclei.
Nitric oxide as a proinflammatory mediator
could lead to sensitization. cGMP, a second messenger of NO, is increased in the platelets of
migrainers.
24
Abnormal iron homeostasis with
increased iron deposits in the PAG has been
found in migrainers and those with chronic daily
headaches.
24
Investigations into the genetics of
migraine headaches suggests that some migraine
headaches, or at least the aura, may be secondary
to a channelopathy with a mutation in a voltage
gated calcium channel causing an abnormal electrochemical gradient for Na+ with a build-up of
the excitatory transmitter glutamate or a mutation in the sodium chan nel gene.
18
(Figure 35.2)
Pathophysiology Summary
Some of the possible pathophysiologic mechanisms responsible for migraine headaches are
the activation of the trigeminovascular system,
whether by cortical spreading depression or other
mechanisms; brain stem (particularly, thalamus)
activation, windup or sensitization (whether central or peripheral, or both); the electrophysiological and ion changes in the brain; and the
neurogenic inflammation leading to neuronal
hyperexcitability or a dyshabituation.
Patient Selection
Patients who need further diagnostic evaluation
with the goal of ruling out a serious or lifethreatening basis for their headache are appropriate candidates for an observation stay. Individuals
who need additional pain management of their
headache can be successfully treated in an observation unit (OU). Since most headache patients
have tried oral and/or subcutaneous medications
prior to their arrival in the ED, parenteral medications are generally warranted.
2
Additionally, if
the headache diagnosis is known, the specific
drugs or therapy of choice may be administered,
such as oxygen for cluster headaches.
Patients inappropriate for an observation stay
include those with a serious or dangerous cause of
their headache. Thus, patient exclusion criteria
include: increased intracranial pressure from any
cause (tumor, hydrocephalus, etc.), intracranial
bleed (e.g., subdural hematoma, epidural hematoma, intracerebral bleed, subarachnoid hemorrhage), acute/subacute stroke and acute CNS
infection (e.g., acute encephalitis, brain abscess,
epidural abscess). Bacterial meningitis is not
appropriate for an OU. However, some observation protocols might allow inclusion of a patient
with an uncomplicated viral meningitis patient,
who has no acute focal neurologic deficits, a
normal mental status and stable vital signs.
Exclusion criteria include an abnormal CT
scan with a lesion needing immediate surgical
intervention, hypertensive crisis (although hypertensive urgency is acceptable for observation) and
patients w ith characteristics of high-risk headaches. Attributes of a high-risk headache include
an acute alteration in mental status, co-existing
seizures and headache (in a patient without a
history of epilepsy), nuchal rigidity, acute visual
loss (may be acute glaucoma or a stroke), new
Headaches
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focal neurologic deficit, abnormal pupils (unequal
[if not congenital] and/or sluggishly reactive),
apnea or abnormal respiratory pattern, significantly abnormal vital signs (bradycardia and
hypertension suggestive of Cushing’s reflex), and
other significant comorbidity, such as AIDS.
Patients with unstable vital signs, an altered
mental status or acute psychiatric issues also
should not be placed into observation. Patients
unlikely to improve and be ready for discharge
within < 24 hours should be considered for inpatient admission.
Observation Unit Management
The history is the most critical part of the assessment of a patient with a headache. Important data
to obtain include the onset (acute “thunderclap”
or gradual), duration, location, type or quality
(dull throbbing, sharp lancina ting, band-like,
etc.) of the pain; precipitating and/or relieving
factors; headache pattern; associated symptoms
(nausea, vomiting, cough, myalgias, rashes, fever,
chills, altered mental status, photophobia) and
any history of trauma. Medications (whether
prescribed, over-the-counter or illicit) and the
pattern of use (initiation, discontinuation/withdrawal, tapering) should be noted since drugrelated headaches are common. Allergies should
be asked in view of medications for treatment and
possible allergic reactions. Social history should
include drug, alcohol and tobacco use, and diet
(caffeine use, fasting).
Features of the physical examination that
should be assessed are: vital signs; mental status;
neurologic examination; head/neck/ENT examination including whether a supple or stiff neck;
presence of tenderness over the temporal artery,
sinuses, mastoid or temporomandibular joint; the
skin for rashes or petechiae; the lungs, cardiovascular and abdominal examination.
Laboratory and radiologic studies depend on
the results of the focused history and physical
examination. If temporal arteritis is suspected,
an erythrocyte sedimentation rate (ESR) should
be drawn. A complete blood count may be useful
if infection is a possibility. In women of childbearing age, a pregnancy test is generally indicated, and may be useful when deciding on
drug therapy. Moreover, the differential of headache in the pregnant and peripartum woman
includes additional unusual etiologies including
pre-eclampsia/eclampsia and cavernous sinus
thrombosis. A lumbar puncture (LP) may be
diagnostic if SAH, meningitis or pseudotumor
cerebri is present. Cerebrospinal fluid (CSF)
analysis is warranted in order to diagnosis meningitis and perhaps, SAH. Radiology studies are
based on the history and physical examination
and may include CT scan, CT angiography, ultrasound and MRI/MRA.
Specific Therapy
Specific treatment for the underlying cause may
begin in the OU. For hypertensive urgency, control of the blood pressure should lessen or even
eliminate the headache. Steroids, specifically oral
prednisone, along with scheduling a temporal
artery biopsy are the treatment of choice for temporal arteritis. A LP is both diagnostic and therapeutic with removal of cerebrospinal fluid (CSF)
for pseudo tumor cerebri. Intravenous (IV) caffeine and, sometimes, a blood patch are the suggested therapy for a spinal headache. Headache
secondary to ophthalmologic disorders, such as
acute angle glaucoma or iritis, need appropriate
urgent treatment. Headache due to a non-lifethreatening infection should improve with treatment of the underlying infection. The most
common cause of headaches is reported to be
systemic infection.
3
According to one study, systemic infection was the etiology of headache in up
to 40% of patients presenting to the ED.
25
For
trigeminal neuralgia, carbamazepine is the drug
of choice. Oxygen is effective in about 70% of
patients with a cluster headache. One medication,
meperidine, should probably be avoided since it is
less effective with a higher incidence of side effects
than other drugs.
2
A decision on the need for
preventive treatment of migraines and if so, what
medications, often in conjunction with the
neurologist or primary care physician, can be
made while the patient is in the OU.
Pharmacologic Management
Given the myriad etiologies of headache, there is
no one panacea or approach. However, several
drugs have efficacy for the common primary
headaches: tension-type and migraines. Since
patients with migraines frequently have nausea
and/or vomiting and poor po intake prior to their
arrival in the ED, management generally includes
IV anti-emetics to treat the nausea/vomiting and
Sharon E. Mace
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21:05:09
IV rehydration for treatment of dehydration and
for maintenance fluids.
Opioids are still used occasionally to treat
acute episodic headaches in the ED and apprehension regarding addiction has not proven to be a
valid concern in those with an acute headache.
2
However, because of their minimal success rate
and the high headache reoccurrence rate, the indications for their use have declined and experts are
now recommending that they be used for acute
therapy of headaches only when other medications have failed or are contraindicated.
2
Indeed,
in conjunction with the headache/neurology specialists, some OU protocols have eliminated
opioids as standard therapy in their headache
protocols (as we have in our headache treatment
protocol for primary headaches). (See Headache,
in the clinical protocol Chapter 82.) Similarly, for
chronic headache pain, opioids are not warranted
because daily opioid use can cause rebound headaches and there is a risk of narcotic abuse in this
patient population.
2
(Specific drugs are discussed
in the headache protocol in the protocol
Chapter 82.)
Summary
Headaches represent the most common neurologic disorder. Headaches are usually benign, but
may have a serious, life-threatening etiology.
Patients with headaches often seek care in EDs
and outpatient facilities. Their management may
involve a diagnostic workup to exclude lifethreatening disorders and multiple drug therapies. The OU can provide cost-effective care with
an opportunity for both evaluation and treatment.
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