Headache

Headache

Headache is, without question, one of the most common symptoms that
neurologists evaluate.

Not unexpectedly, the differential diagnosis of this highly prevalent symptom is

vast, with over 300 different headache types and etiologies.

Understanding headache classification and diagnosis is, therefore, a clinical

imperative and a requisite for diagnostic testing and treatment.
Headache in the emergency room

Patients with headache constitute up to 4.5% of the emergency department visits

The differentiation of the small no. of patients with life-threatening headaches

from the overwhelming majority with benign primary headache (ie, migrane,
tension-type, cluster) important!

A careful history and physical examination remain the most important part of the
assessment of the headache patient; they enable the clinician to determine whether the
patient is at significant risk for a dangerous cause of their symptoms and what additional
workup is necessary.
Failure to recognize a serious headache can have potentially fatal consequences!!!
Pain-sensitive cranial structures

There are no pain receptors in the brain parenchyma itself!

Headache is caused by mechanical traction, inflammation or
irritation of other structures that contain pain receptors:
Skin, subcutaneous tissue, extracranial arteries, periostum
Eye, ears, nasal cavities, paranasal sinuses
Intracranial venous sinuses and their large tributtaries
Parts of the dura and the arteries within the dura (wall of blood vessels contain pain
fibers)
Middle meningeal and superficial temporal arteries
Cranial nerves II,III,V,IX,X and first three cervical nerves
Primary headache vs. secondary headache
Characteristics of headache with potential serious underlying pathology

HISTORY
Explosive onset
No similar headaches in the past
Concomitant infection
Altered mental status
Headache with exertion
Age over 50
Immunosuppresion

PHYSICAL EXAMINATION
Neurologic abnormalities

Decreased level of consciousness

Meningismus

Toxic appearance

Papilledema
Patient history
 High risk historical features of headache (red flags)

SUDDEN ONSET
A severe persistent headache that reaches maximal intensity within a few
seconds or minutes after onset of pain warrants aggressive investigation
Subarachnoid hemorrhage (SAH) often presents with abrupt onset,
excruciating pain
Other serious etiologies of sudden-onset headache include: carotid artery and
vertebral artery dissections, venous sinus thrombosis, pituitary apoplexy, acute
angle-closure glaucoma, hypertensive emergencies
In contrast migraine headaches generally begin mild and then gradually increase
to a maximum level over few hours
Cluster headache may be confused with a serious headache since the pain can
reach full intensity in a few minutes BUT it is associated with characteristic
ipsilateral autonomic signs, such as tearing or rhinoreea
 High risk historical features of headache
(red flags)

NO SIMILAR HEADACHES IN THE PAST

The first or worst headache of my life is a description that sometimes accompanies
an intracranial hemorrhage or CNS infection
A new or unusual headache in a patient with AIDS or cancer is worrisome, as it may
suggest an intracranial lesion or infection
In contrast patients suffering from migraine have had similar headaches in the past

CONCOMITANT INFECTION
Infection in a nonintracranial location may serve as a nidus for the development of
meningitis or intracranial abscess
 High risk historical features of headache
(red flags)

ALTERED MENTAL STATUS OR SEIZURES

Any change in mental status, personality or fluctuation in the level of consciousness

suggests a potentially serious problem

Syncope or near syncope may be suggestive of SAH

! Headache + Seizures Intracranial pathology!

AGE OVER 50 YEARS

Patients over 50 with new onset or progressively worsening headache are at significantly

greater risk for a secondary headache: intracranial mass lesion, temporal arteritis, etc

HIV AND IMMUNOSUPPRESSION

Risk for intracranial disease: toxoplasmosis, malignancy, brain abscess, meningitis, stroke
 High risk historical features of headache
(red flags)

MEDICATIONS
Anticoagulants, glucocorticoids, analgesics
Use of anticoagulants and NSAID increases the risk of intracranial bleeding
Analgesics can mask severe symptoms or sometimes exacerbate migraine headache
through a rebound effect

ILLICIT DRUGS
Cocaine, methamphetamine, sympathomimetic agents increase the risk of stroke
and intracranial bleeding
 High risk historical features of headache
(red flags)

ADDITIONAL HISTORY
Toxic exposure (CO)
Malignancy with risk of intracranial metastasis
Polycystic kidney disease or connective tissue disease increase the risk of
aneurysms with resultant SAH
Liver disease or clotting disorders may predispose to intracranial bleeding
Hypercoagulable states may increase the risk of stroke or cerebral venous
thrombosis
 High risk examination findings

Abnormal findings on neurologic exam remain the single-best clinical

predictor of intracranial pathology!

The findings may be subtle, such as slight pupillary asymmetry,

unilateral pronator drift or extensor plantar response or pronounced,
such as unilateral vision loss, ataxia, seizure

Focal neurologic findings and alterations in mental status usually

accompany secondary headaches
 High risk examination findings

Decreased level of consciousness (Obtundation, Confusion)

Meningitis, Encephalitis, SAH, Space occupying lesion
Meningismus
Meningitis, Encephalitis
SAH
Abnormal vital signs
Fever CNS infection
Severe hypertension
Toxic appearance
CNS infection or systemic illness
Ophthalmologic findings
Papilledema indicative of increased intracranial pressure
Traumatic findings
Nausea and vomiting
Can accompany increased intracranial pressure
 Evaluation of high risk patients

Neuroimaging
A meta-analysis on the utilization of CT and MR scanning in patients with headache
revealed abnormalities in only 2.4% of patients with normal neurologic
examination!
Noncontrast CT scan helpful for identifying intracranial lesions or bleeding
Use Contrast CT scan or MRI in selected cases

CSF evaluation
Lumbar puncture is most helpful for diagnosing infection and SAH
Primary Headaches
 MIGRAINE

Migrane is a primary headache and may occur with or without aura

Very common disorder
More prevalent in women
Is often hereditary, the inheritance is polygenic
Has characteristic triggers: exertion, emotional stress, not eating,
sleep disturbances, alcohol, odors, smoke, heat, hormonal influences
and medications
It is usually unilateral but in about 40% of adults can be bilateral
MIGRAINE

Migraine is a disorder of recurrent attacks.

The attacks unfold through a cascade of events that occur over the course of several
hours to days.
A typical migraine attack progresses through four phases: the prodrome, the
aura, the headache, and the postdrome.

Migraine prodrome
occurs in up to 60 percent of people
consists of affective or vegetative symptoms that appear 24 to 48 hours prior to the
onset of headache
Frequently reported prodromal symptoms: euphoria, depression, irritability, food
cravings, constipation, increased yawning
MIGRAINE

Migraine aura
occurs in only 20% of patients with migraines
the most common manifestation is visual (enlarging scotoma, dots, waving lines,
shapes, complex patterns)
less common are sensory auras (paresthesias that begin in the hand and slowly, over
minutes ascend to the shoulder, ipsilateral face, mouth)
still less common are auras causing hemiparesis or hemiplegia or speech disturbance
usually develops gradually over more than five minutes
some patients may experience aura without an associated headache. Migraine aura
without headache (also known as migraine equivalent or acephalgic migraine)
manifests as isolated aura unaccompanied by headache.
MIGRAINE

Migraine headache
the headache of migraine is often but not always unilateral and tends to have a throbbing or pulsatile

quality, especially as the intensity increases.

as the attack severity increases over the course of one to several hours, patients frequently

experience nausea and sometimes vomiting.

many individuals report photophobia or phonophobia during attacks, leading such migraine

sufferers to seek relief by lying down in a darkened, quiet room.

additional features such as cutaneous allodynia may occur during attacks

headache can last as little as some hours and as long as several days.

Migraine postdrome
once the headache resolves, the patient may experience a postdromal phase, during which sudden

head movement transiently causes pain in the location of the antecedent headache.
during the postdrome, patients often feel drained or exhausted, although some report a feeling of

mild elation or euphoria

 Pathophysiology of migraine (1)

The current state of knowledge suggests that a primary neuronal dysfunction

leads to a sequence of changes intracranially and extracranially that account for
migraine

Cortical spreading depression (CSD)

a self propagating wave of neuronal and glial depolarization that spreads across the
cerebral cortex.
is hypothesized to: Cause the aura of migraine, Activate trigeminal nerve afferents,
Alter blood-brain barrier permeability by matrix metalloproteinase activation
The activation of trigeminal afferents by CSD in turn causes inflammatory changes in
the pain-sensitive meninges that generate the headache of migraine through central
and peripheral reflex mechanisms
 Pathophysiology of migraine (2)

Activation of the trigeminovascular system , which consists of sensory neurons that originate
from the trigeminal ganglion and upper cervical dorsal roots and innervate large cerebral vessels, pial
vessels, dura mater, and large venous sinuses. Most of the innervation of the anterior structures is via the
ophthalmic division of the trigeminal nerve with a greater contribution of upper cervical roots to posterior
structures.

There is convergence of the projections from the upper cervical nerve roots and the trigeminal nerve at the
trigeminal nucleus. From the trigeminal nucleus fibers ascend to the thalamus and the sensory cortex and to
numerous subcortical sites including the reticular formation of the brain stem, cerebellum, midbrain and
pontine nuclei.
Stimulation of the trigeminal ganglion results in release of vasoactive neuropeptides, including substance P,
calcitonin gene-related peptide, and neurokinin A . Release of these peptides is associated with the process
of neurogenic inflammation. The two main components of this sterile inflammatory response are
vasodilation (calcitonin gene-related peptide is a potent vasodilator) and plasma protein extravasation.
Neurogenic inflammation is thought to be important in the prolongation and intensification of the pain of
migraine. Neurogenic inflammation may lead to the process of sensitization
 Pathophysiology of migraine (3)

Sensitization
refers to the process in which neurons become increasingly responsive to nociceptive
and non-nociceptive stimulation: response thresholds decrease, response magnitude
increases, receptive fields expand, and spontaneous neuronal activity develops

is likely responsible for many of the clinical symptoms of migraine, including the
throbbing quality of the pain, the worsening of pain with coughing, bending, or
sudden head movements, hyperalgesia (increased sensitivity to painful stimuli), and
allodynia (pain produced by normally non-noxious stimulation).
 Migraine without aura - diagnostic criteria

A. At least 5 attacks fulfilling criteria B through D

B. Headache attacks lasting 4 to 72 h (untreated or successfully treated)
C. Headache has at least two of the following characteristics
1. Unilateral location
2. Pulsating quality
3. Moderate or severe pain intensity
4. Aggravation by or causing avoidance of routine physical activity
D. During headache at least one of the following
1. Nasusea and/or vomiting
2. Photophobia and phonophobia
E. Not attributed to another disorder
 Typical aura with migraine headache - diagnostic criteria

A. At least 2 attacks fulfilling criteria B through D

B. Aura consisting of at least one of the following, but no motor weakness
1. Fully reversible visual symptoms including positive features (flickering, lights, spots, lines) and/or
negative features (loss of vision)
2. Fully reversible sensory symptoms including positive features (eg, pins and needles) and/or negative
features (eg, numbness)
3. Fully reversible dysphasic speech disturbance
C. At least two of the following
1. Homonymous visual symptoms and/or unilateral sensory symptoms
2. At least one aura symptom develops gradually over > 5 minutes and/or different aura symptoms
occur in succesion over > 5 minutes
3. Each symptom lasts > 5 minutes and < 60 minutes
D. Headache fulfilling criteria B through D for migraine without aura begins during
the aura or follows aura within 60 minutes
E. Not attributed to another disorder
Migraine - acute treatment
(Abortive, symptomatic therapy)

The abortive therapy of migraine ranges from the use of simple

analgesics such as nonsteroidal antiinflammatory drugs (NSAIDs) or
acetaminophen to triptans, antiemetics, or the less commonly used
dihydroergotamine
Abortive treatments are usually more effective if they are given early in
the course of the headache!!
The pharmacologic approach to migraine is directed by:
the severity of the attacks
the presence of associated nausea and vomiting
patient-specific factors, such as the presence of vascular risk factors and drug
preference
 Migraine - acute treatment
(Abortive, symptomatic therapy)

Mild to moderate attacks

not associated with vomiting or severe nausea : simple analgesics (NSAIDs,
acetaminophen) or combination analgesics are first choice agents because they are
effective, less expensive, and less likely to cause adverse effects than migraine-specific
agents such as triptans or ergots.
associated with severe nausea or vomiting: an oral antiemetic drug can be used in
conjunction with simple or combination analgesics.
Moderate to severe attacks
not associated with vomiting or severe nausea: oral migraine-specific agents are
first-line, including oral triptans and the combination of sumatriptan-naproxen
when complicated by vomiting or severe nausea: nonoral migraine-specific
medications including subcutaneous sumatriptan, nasal sumatriptan and zolmitriptan,
nonoral antiemetic agents, and parenteral dihydroergotamine.
 Migraine abortive therapy
ANTIEMET
TRIPTAN
NSAIDs ICS
S
Sumatriptan Prochlorperazi
(tablets, intranasal, Ibuprofen 400-
sc) 800 mg ne
Naproxen 125- Metoclopramid
Rizatriptan
550 mg e
Eletriptan Chlorpromazin
Diclofenac 50 mg
Zolmitriptan e
Ketoprofen 50-75
Fravatriptan EGOT
Ondansetron
mg
Naratriptan Aspirin 650-1000 ALKALOIDS
mg
! Ischemic Dihydroergota
complications
(contraindicated in
mine
coronary artery
disease)
Migraine preventive therapy

Is indicated if the headaches are frequent, long lasting, or account for a significant
amount of total disability
The goals of preventive therapy are to :
Reduce attack frequency, severity and duration
Improve responsiveness to treatment of acute attacks
Improve function and reduce disability
The following factors indicate the need for prophylactic therapy
Recurring migraines that significantly interfere with daily routine in the patient's opinion, despite
acute treatment
Contraindication to or failure or overuse of acute therapies
Adverse events with acute therapies
Patient preference
Prophylactic therapy also should be considered to prevent neurologic damage in the
presence of uncommon migraine conditions including hemiplegic migraine, basilar
type migraine, migraine with prolonged aura
 Migraine preventive therapy
Calcium
channel
Beta- antagonists
adrenergic Antidepressa
Blockers nts Diltiazem 80-240 mg
Verapamil 180-480
mg
Propranolol 80-240 Amitriptyline 25-150 Antiepileptic
Amlodipine 10mg
mg mg drugs
Metoprolol 50-150 Venlafaxine 37-150
mg mg Valproate/ Divalproex
Atenolol 50-100 Sertraline 50-150 mg sodium 250-1500mg
mg Fluoxetine 20-60 mg Gabapentin 300-1800
Timolol 10-20 mg Duloxetine 30-90 mg mg
Pregabalin 50-200
mg
Topiramate 25-150
mg
CLUSTER HEADACHE

Cluster headache belongs to a group of idiopathic headache entities, the

trigeminal autonomic cephalalgias (TACs), all of which involve
unilateral, often severe headache attacks and typical accompanying
autonomic symptoms.

The prevalence of cluster headache is <1% and mostly affects men

(male to female ratio 4:1).
Cluster headache - pathophysiology

The pathogenesis of cluster headache is complex and remains incompletely

understood.

The most widely accepted theory is that primary cluster headache is

characterized by hypothalamic activation with secondary activation of the
trigeminal-autonomic reflex, probably via a trigeminal-hypothalamic
pathway.

Another theory holds that neurogenic inflammation of the walls of the

cavernous sinus obliterates venous outflow and thus injures the traversing
sympathetic fibers of the intracranial internal carotid artery and its branches.
Cluster headache clinical features

Cluster headache is characterized by attacks of severe orbital, supraorbital, or temporal pain, accompanied by
autonomic phenomena and/or restless or agitation.

The stereotypical attacks may strike up to eight times a day and are relatively short-lived.

Cluster headache is strictly unilateral, and the symptoms remain on the same side of the head during a single
cluster attack.

However, the symptoms can switch to the other side during a different cluster attack (so-called side shift) in
approximately 15 percent of cases.

In contrast to migraineurs, patients with cluster are restless and prefer to pace about or sit and rock back and
forth.

The attacks of cluster headache can be so vicious that patients may commit suicide if the disease is not
diagnosed or treated.
Cluster headache clinical features

Autonomic symptoms associated

unilateral and ipsilateral to the pain
ptosis, miosis, lacrimation, conjunctival injection, rhinorrhea, and nasal congestion,
occur only during the pain attack
These symptoms are indicative of both parasympathetic hyperactivity and
sympathetic impairment.
In some patients, the signs of sympathetic paralysis (miosis and ptosis) persist
indefinitely, but intensify during attacks.
Sweating and cutaneous blood flow also increase on the painful side
About 3% of patients lack autonomic symptoms.
Cluster headache clinical features

Circadian periodicity of the painful attacks

In the episodic form of cluster headache, attacks occur daily for some weeks
followed by a period of remission.
On average, a cluster period lasts 6 to 12 weeks while remissions can last up to 12
months or longer.
In a cluster period, patients may experience one to eight attacks per day
When not in a cluster, patients are usually asymptomatic.
The episodic form is the most common, affecting 80 to 90 percent of patients with
cluster headache.
The chronic form of cluster headache lacks remissions and is diagnosed after a
year without remission, or if remission has lasted less than one month.
Cluster headache diagnostic criteria
Cluster headache acute treatment

Oxygen
Oxygen (100 percent) is administered via a facial mask with a flow rate of at least 12
L/min with the patient in a sitting, upright position.
The inhalation should continue for 15 minutes to prevent the attack from returning,
although the pain may subside as soon as five minutes after starting oxygen.
Triptans
Subcutaneous sumatriptan
Intranasal sumatriptan
Intranasal rizatriptan
Oral rizatriptan
Cluster headache preventive treatment

Should be started as soon as possible at the onset of a cluster episode.

The goal is to suppress attacks over the expected duration of the cluster period.

An effective preventive regimen is of utmost importance because patients typically have 1 to 8

cluster attacks/day, and repeated use of abortive medications may result in toxicity and/or
rebound.

Verapamil (240-360 mg/day) is the agent of choice for the preventive therapy of cluster
headache.

Other agents that may be effective include glucocorticoids, lithium, topiramate, and
methysergide.
TENSION TYPE HEADACHE

Tension-type headache (TTH) is the most ubiquitous headache in the

general population, and is one of the most common reasons why over-
the-counter analgesics are purchased.

Women have a slightly higher prevalence of TTH than men.

Tension type headache (TTH) - pathogenesis

The pathogenesis of TTH is multifactorial.

Given the wide variation in frequency and intensity in TTH, not only between individuals, but
within individuals over time, it is likely that the underlying pain mechanisms in TTH are dynamic
and vary from one individual to another

The current pathophysiologic model of TTH posits that peripheral activation or sensitization of
myofascial nociceptors are most likely of major importance in episodic TTH, while sensitization of
pain pathways in the central nervous system due to prolonged nociceptive stimuli from pericranial
myofascial tissues seems to be responsible for the conversion of episodic to chronic TTH.
Thus, stimuli that are normally innocuous are misinterpreted as pain in chronic TTH. Continuous
nociceptive input from peripheral myofascial structures may induce central sensitization. The
increased nociceptive stimulation of supraspinal structures results in increased facilitation and
decreased inhibition of pain transmission at the level of the trigeminal nucleus and in increased
pericranial muscle activity.
Tension-type headache clinical features

The typical presentation of a TTH attack is that of a mild to moderate intensity,

bilateral, nonthrobbing headache without other associated features.

Descriptions of TTH pain are characteristically nondescript: "dull," "pressure,"

"head fullness", "head feels large," or, more descriptively, "like a tight cap",
"band-like," or a "heavy weight on my head or shoulders.

Pericranial muscle tenderness

The tenderness of pericranial myofascial tissues is considerably increased in patients with TTH.
Muscle tenderness in the head, neck, or shoulders (ie, pericranial tenderness) is associated with
both the intensity and the frequency of TTH attacks and is typically exacerbated during the
headache experience. The presence or absence of pericranial muscle tenderness should be elicited
from the history and confirmed on examination by manual palpation (of the frontal, temporal,
masseter, pterygoid, sternocleidomastoid, splenius, and trapezius muscles)
Acute therapies for tension type headache

Acetaminophen 500-1000 mg/daily

Aspirin 500 1000 mg
Ibuprofen 200 800 mg
Ketoprofen 25 50 mg
Naproxen 375 550 mg
Diclofenac 12.5 100 mg
Caffeine 65 200 mg

Guidelines from the European Federation of Neurological Societies

Preventive therapies for tension type headache

Amitriptyline 30 75 mg/ daily

Mirtazapine 30mg
Venlafaxine 150mg
Clomipramine 75 150 mg

Cognitive-behavioral therapy
Relaxation training
Physical therapy

Guidelines from the European Federation of Neurological Societies

TRIGEMINAL NEURALGIA

Trigeminal neuralgia (TN) is one of the most common causes of facial pain.

TN is characterized by recurrent brief episodes of unilateral electric shock-like pains,

abrupt in onset and termination, in the distribution of one or more divisions of the
fifth cranial (trigeminal) nerve that are triggered by innocuous stimuli

TN is one of the most frequently seen neuralgias in the elderly. The incidence
increases gradually with age; most idiopathic cases begin after age 50, although
onset may occur in the second and third decades.

The male to female ratio of TN is about 1:1.7

Trigeminal nerve is the sensory
supply of the face and the
motor supply of the muscles of
mastication

It has three major divisions:

Ophthalmic (V1)
Maxillary (V2)
Mandibular (V3)

The nerve starts at the

midlateral surface of the pons,
and its sensory ganglion
(gasserian gg.) resides in
Meckel's cave in the floor of the
middle cranial fossa.
TRIGEMINAL NEURALGIA - Etiology and pathogenesis

Most cases of TN are caused by compression of the trigeminal nerve root, usually within a few millimeters of
entry into the pons. Compression by an aberrant loop of an artery or vein is thought to account for 80 to 90
percent of cases. Idiopathic TN or TN caused by a vascular compression is considered classic TN.
Other causes of TN via nerve compression include vestibular schwannoma (acoustic neuroma), meningioma,
epidermoid or other cyst, or rarely a saccular aneurysm or arteriovenous malformation. TN caused by
conditions other than vascular compression is classified as painful trigeminal neuropathy.
The mechanism by which compression of the nerve leads to symptoms appears to be related to demyelination
in a circumscribed area around the compression. Precisely how demyelination results in the symptoms of TN
is not entirely clear. Demyelinated lesions may set up ectopic impulse generation, possibly causing ephaptic
transmission. Ephaptic cross-talk between fibers mediating light touch and those involved in pain generation
could account for the precipitation of painful attacks by light tactile stimulation of facial trigger zones.
Furthermore, alteration of afferent input may disinhibit pain pathways in the spinal trigeminal nucleus.
Demyelination of one or more of the trigeminal nerve nuclei may also be caused by multiple sclerosis or other
structural lesions of the brainstem. In multiple sclerosis, a plaque of demyelination typically occurs in the
root entry zone of the trigeminal nerve.
 TRIGEMINAL NEURALGIA - Classification

The International Classification of Headache Disorders classifies TN into:

Classical trigeminal neuralgia caused by neurovascular compression and
Painful trigeminal neuropathy caused by a number of other conditions

Classic TN encompasses both idiopathic TN cases and those related to vascular compression.

Painful trigeminal neuropathy is caused by lesions other than vascular compression and
encompasses the following:
Painful trigeminal neuropathy attributed to acute herpes zoster
Postherpetic trigeminal neuropathy
Painful posttraumatic trigeminal neuropathy
Painful trigeminal neuropathy attributed to multiple sclerosis plaque
Painful trigeminal neuropathy attributed to space-occupying lesion
Painful trigeminal neuropathy attributed to other disorders
TRIGEMINAL NEURALGIA Clinical features

TN is defined clinically by paroxysmal, stereotyped attacks of usually intense, sharp, superficial or stabbing pain in
the distribution of one or more branches of the fifth cranial (trigeminal) nerve
The pain of TN tends to occur in paroxysms and is maximal at or near onset. Facial muscle spasms can be seen
with severe pain. This finding gave rise to the older term for this disorder, tic douloureux. The pain is often
described as electric, shock-like or stabbing. It usually lasts from one to several seconds, but may occur
repetitively. A refractory period of several minutes during which a paroxysm cannot be provoked is common.
Unlike some other facial pain syndromes, TN typically does not awaken patients at night.
TN is typically unilateral. Occasionally the pain is bilateral, though rarely on both sides simultaneously. The
distribution of pain most often involves the V2 and/or V3 subdivisions of the trigeminal nerve. The V1 subdivision
is involved in <5 percent of patients. Of note, V1 is most commonly affected by postherpetic neuralgia.
Trigger zones in the distribution of the affected nerve may be present and are often located near the midline.
Lightly touching these zones often triggers an attack, leading patients to protect these areas. Trigger zones can
sometimes be demonstrated on physical examination. Other triggers of TN paroxysms include chewing, talking,
brushing teeth, cold air, smiling, and/or grimacing. TN can be precipitated by dental procedures (eg, dental
extraction).
The course of TN is variable. Episodes may last weeks or months, followed by pain-free intervals. Most often, the
condition tends to wax and wane in severity and frequency of pain exacerbations.
TRIGEMINAL NEURALGIA -Diagnosis

The diagnosis of TN is based upon the characteristic clinical features described, primarily paroxysms of pain in the
distribution of the trigeminal nerve.

Once the diagnosis of TN is suspected or confirmed on clinical grounds, a search for secondary causes should be
undertaken. Patients with trigeminal sensory loss or bilateral involvement are probably at higher risk of secondary TN
. Younger age is also probably associated with a higher risk of secondary TN. However, age is not a clinically useful
predictor for distinguishing classic from secondary TN because there is considerable age overlap. In addition, absence
of any of these clinical features (sensory loss, bilateral involvement, younger age) does not rule out secondary TN.

Neuroimaging and trigeminal reflex testing are considered useful for distinguishing patients with classic TN (ie,
idiopathic or caused by vascular compression) from those with secondary TN (ie, caused by structural brain lesion
other than vascular compression).

The finding of hypoesthesia or hypoalgesia in the affected trigeminal region always indicates axonal damage and
therefore a trigeminal neuropathy. In such cases, an extensive diagnostic work-up may be necessary to identify the
cause.
TRIGEMINAL NEURALGIA -Diagnosis

Diagnostic criteria for classic TN:

A) At least three attacks of unilateral facial pain fulfilling criteria B and C
B) Occurring in one or more divisions of the trigeminal nerve, with no radiation
beyond the trigeminal distribution
C) Pain has at least three of the following four characteristics:
Recurring in paroxysmal attacks lasting from a fraction of a second to two minutes
Severe intensity
Electric shock-like, shooting, stabbing or sharp in quality
At least three attacks precipitated by innocuous stimuli to the affected side of the face (some
attacks may be, or appear to be, spontaneous)
D) No clinically evident neurologic deficit
E) Not better accounted for by another diagnosis
TRIGEMINAL NEURALGIA - Neuroimaging

Neuroimaging with head CT or MRI is useful for identifying the small proportion of patients who have a structural lesion (eg,
tumor in the cerebellopontine angle, demyelinating lesions including multiple sclerosis) as the cause of painful trigeminal
neuropathy. In addition, high resolution MRI and magnetic resonance angiography (MRA) may be useful for identifying
vascular compression as the etiology of classic TN.

Brain MRI to rule out a causative structural brain lesion is suggested for the following groups:
Patients with trigeminal sensory loss
Patients with bilateral symptoms
Young patients (under the age of 40)

Some clinicians obtain an imaging study in all patients who present with TN.

Electrophysiologic tests
Electrophysiologic trigeminal reflex testing is probably useful for distinguishing classic TN from painful trigeminal neuropathy
Trigeminal reflex tests include the blink reflex (obtained by recording from the orbicularis oculi muscles after electrical stimulation of the supraorbital
nerve [V1]) and the masseter inhibitory reflex (obtained after electrical stimulation of the infraorbital [V2] and mental [V3] nerves). The responses are
recorded by surface electrodes using standard electromyography equipment [32]. These tests are usually normal in patients with classic TN.
TRIGEMINAL NEURALGIA Medical Treatment
TRIGEMINAL NEURALGIA Surgical treatment

Is recommended for patients with trigeminal neuralgia who become

refractory to pharmacological treatment or cannot tolerate its adverse
effects
Surgical techinques are:
Glycerol injection
Ballon Compression
Radio Rhizotomy
Partial Rhizotomy
Gamma knife
Microvascular decompression