1.Prevalence among adults of headache disorder 47%.

More than 10% have reported

migraine
2.headaches have been able to wake the patient up from sleep
meningitis or subarachnoid haemorrhage.
3.Lesions of the paranasal sinuses, teeth, eyes, upper cervical vertebrae usuall
y have a sharply localized pain.
4.Intracranial lesions in the posterior fossa cause pain in the occipitoneuchal
region.
5.Localization of pain may thus be misleading.
6.frontal headache may be a consequence of
glaucoma,
sinusitis,
throbosis of the vertebral artery or the basilar artery,
pressure on the tentorium or
increased intracranial pressure.
7.very gradual progression in meningitis, over several hours and days
8.Most of the understanding of headaches comes from the surgeries on the brain
9.
Cranial structures sensitive to noxious stimuli:
Skin, subcutaneous tissue, muscles, arteries (extra-cranial) and the periosteum
of the skull.
Intracranial venous sinuses and their tributaries
Parts of the dura at the base of the brain,
arteries within the dura (such as
the proximal parts of anterior and middle cerebral arteries and
the intra-cranial segment of the internal carotid artery)
The middle meningial and superficial temporal arteries.
The optic, occulomotor, trigeminal, glossopharyngeal, vagus, first three cervica
l nerves
10.
Pain from the intracranial arteries, is felt in the eye and the orbito-temporal
regions.
11.
Primary Headache Disorders
Migraine/Tension/Cluster/trigeminal autonomic headaches
12.
Ray and Wolff:
intracranial mass lesions cause headaches only if they deform, displace or exert
traction on the vessels and dural structures at the base of the brain.
might start before the increase in the intracranial pressure
dura and blood vessels was important since
simply raising the intracranial tension does not result in headaches
13
Headache due to intracranial or extra-cranial dilatation of blood vessels.
post-seizures, post-alcohol consumption, post-histamine infusion.
Nitroglycerine, nitrates in the food (leading to what is called "hot-dog headach
e"),
monosodium glutamate in Chinese food
14
Headache due to
Rapid increases in blood pressure
Phaeochromocytoma, malignant hypertension, sexual activity, monoamine oxidase in
hibitors
15
extra-cranial temporal and occipital arteries, when involved in giant cell arter
itis, give rise to severe, persistent headache
16

posterior communicating or the distal internal carotid arteries very often cause
pain projected to the eye
17
traction on extra-ocular muscles or the iris will evoke pain.
18
Increased intra-ocular pressure causes steady aching type of pain in the region
of the eye and the forehead, as seen in angle closure glaucoma
19
Younger women, menstrual migraine attacks are called catamenial headaches
20
during PET scanning,
reduction in the blood flow in the occipital cortex and spread forward slowly on
both sides,
similar to the concept of spreading cortical depression of Leao.
21
The sensory sensitivity, characteristic of migraine, is proposed to be caused by
a dysfunction of monoaminergic sensory control systems in the brainstem and the
thalamus.
22
Stimulation of the cells in the trigeminal nucleus causes release of
vasoactive neuropeptides,
particularly CGRP (Calcitonin gene-related peptide), at the vascular termination
s of the trigeminal nerve and the within the trigeminal nucleus.
23
CGRP receptor antagonists effective in the treatment of migraine
24
Sensory input modulatory pathways: The key pathway for the pain in an acute atta
ck of migraine is the trigeminovascular input from the meningeal vessels, which
passes through the trigeminal ganglion and synapses on the second order neurons
in the trigeminocervical complex. These neurons project into the quintothalamic
tract and after decussating in the brainstem, synapse on the neurons in the thal
amus
25
Molecular genetic findings of migraine susceptibility:
Four different mis-sense mutations in 1 subunit of P/Q-type, voltage-gated calci
um channel on chromosome 19 are responsible for Familial Hemiplegic Migraine (FH
M) in some families, specifically FHM-1
The gene ATP1A2, which encodes the 2 subunit of NA+/K+ pump is associated with F
HM-2, linked to chromosome 1q23 Mutations of SCN1A gene cause FHM-3. Dopamine D2
receptor gene may also have some affect on the susceptibility of
26
involvement of the neurotransmitter 5-hydroxytryptamine (= 5-HT = Serotonin) in
migraine
27
Dopamine receptor has been shown to be hypersensitive in migraine patients as de
monstrated by induction of vomiting, hypotension and other migraine symptoms by
administering dopamine agonistic drugs in doses that failed to elicit any respon
se in individuals who have never had a migraine headache (non-migraneurs)
28
The efficacy of the triptans is due to their potency at 1B, 1D receptors
29
Migraine with aura :'classical migraine' or 'neurological migraine'
Migraine without aura:'common migraine'.
The ratio of classic: common is usually 1:5.
30
Basilar migraine:
In young women or children with a family history
They first develop visual symptoms
occupy the whole of both the visual fields
associated vertigo, staggering, in coordination of the limbs,

dysarthria and parasthesias of both hands and feet,

quadriplegia or go into a coma
sometimes in the corner of the mouth.
Symptoms last for 10 to 30 minutes, followed by the headache.
Some patients faint
confused or stuporous,might persist for a few hours.
These symptoms closely resemble the symptoms seen during ischaemia in the area o
f basilar-posterior cerebral arteries, hence the name.
It is benign and transient.
31
Ophthalmoplegic and Retinal Migraine:
These are recurrent unilateral headaches associated with weakness of the extra-o
cular muscles. Transient third nerve palsy, with ptosis,
with or without the involvement of the pupil is the usual picture;
rarely the sixth nerve is affected.
More common in children.
The ocular weakness usually persists beyond the headache, up to days or even wee
ks.
After many attacks, pupil might get involved (causing mydriasis) and rarely opht
halmoparesis may remain permanently.
In a few cases of uniocular visual disturbance with scotoma, the retinal arterie
s have been found to be attenuated and rarely, retinal haemorhages are noted.
32
Migraine following Head injury:
seen in a child or an adolescent, following a trivial head injury.
may lose sight, suffer severe headache,state of confusion with irrational behavi
our, which may last for hours or several days.
abrupt onset of either hemiparasis or aphasia, after every instance of minor hea
d injury
Family history of headaches is seen, but no history of hemiparesis in the family
.
33
Migraine in young child
diagnosis difficult
Vomiting more frequent than in the adults
episodic vertigo and staggering (paroxysmal disequilibrium) followed by headache
(probably a type of basilar headache).
may present with repeated bouts of fever, temporary disturbances in the mood and
abdominal pain (abdominal migraine).
Some patients may present with hemiplegia on one side, complete recovery, and th
en hemiplegia on another side.
34
Familial Hemiplegic migraine (FHM):
FHM-1, FHM-2 and FHM-3
mostly infant and children, rarely adults
episodes of unilateral paralysis which may outlast the headache.
35
Stroke and Transient Ischaemic attacks with Migraine:
Fisher:
transient aphasic, hemianaethetic, or hemiplegic attack of later life that may b
e migranous in origin.
Increased coagualability,
oedema of the arterial wall,
platelet aggregation,
intense prolonged vessel spasm, etc.
has all been implicated in the pathogenesis of arterial occlusion and strokes th
at complicate migraine. In children, MELAS (mitochondrial myopathy, encephalopat

hy, lactic acidosis and stroke-like episodes)

and
in adults with the rare cerebral vasculopathy CADASIL ( cerebral autosomal domin
ant arteriopathy with subcortical infarcts and leukoencephalopathy),
migraine may be a prominent feature.
36
Migraine with CSF pleocytosis:
migraine is found to have a lymphocytic pleocytosis in the spinal tap.
Most of these have turned out to be cases of aseptic meningitis
no clear explanation as to why, white blood cells are found in the spinal fluid
during an acute migraine attack.
37
Status Migrainosus:
for unknown reason,
migraines may increase in frequency for several months.
As many as 3 4 attacks occur per week, leaving the scalp on one side continuousl
y tender.
condition of daily, virtually continuous headache.
This is referred to as status migrainosus.
Initially,unilateral, then generalized,
more or less throbbing but with a constant superimposed ache and
is disabling, vomiting and/or nausea is common at the outset but disappears late
r.
This condition sometimes follows a head injury or a viral infection, although mo
st cases do not have a discernable cause.
38
DIAGNOSTIC CRITERIA FOR MIGRAINE:
Repeated attacks of headaches lasting
4-72 hours
in patients with a normal physical examination,
no other reasonable cause for the headache, and:
At least two of the following:
1.Unilateral pain
2.Throbbing pain
3.Aggravated by movement
4.Moderate or severe intensity
Plus at least one of the following:
1.Nausea/vomiting
2.Photophobia and phonophobia
39
Initial symptoms are usually
'positive symptoms'
(such as paraesthesias) and
they later become
negative symptoms
(scotoma,aphasia or paresis)
40
Ergotamine = a non-selective means of stimulating 5 HT1 receptors.
higher doses = accentuate nausea and worsen the headache.
The average oral dose 2 mg
41
5HT1B/1D are contraindicated in individuals with a history of cardiovascular dis
ease
42
Rizatriptan and eletriptan are the most efficacious
43
nasal formulations efficacy to be ~50-60% when compared to the oral forms.
44

Patients, especially those on oral narcotics, tend to disrupt their migraine tre
atment regime, developing narcotic craving and withdrawal symptoms, which in tur
n can precipitate a migraine attack
45
patients having five or more attacks a month should be considered for preventati
ve management
46
Topiramate = Paraesthesias/Weight loss/Cognitive symptoms/ Glaucoma/nephrolithia
sis
47
Indomethacin-responsive headaches
Orgasmic headaches
Chronic paroxysmal hemicrania
Hypnoeic headache
Brief head pains (jabs, jolts and "ice-pick" headaches)
Prementrual headaches (few cases)
48
Botulinum toxin type A is gaining popularity as a preventative option. This is u
sually an outpatient procedure and is effective in preventing migraine attacks f
or 6 months.
49
Tension-type headache:
most common variety of headache
bilateral with an occipito-nuchal/temporal or frontal/diffuse over the top of th
e cranium
50
Tension-type headache
the head is swollen and might just burst open.
Waves of aching pain are superimposed on this sensation.
If this is interpreted as throbbing or pulsating pain
and
if the pain is slightly more on one side, this could lead to a diagnosis of migr
aine without aura
51
Feature
Migraine
Tension Headache
Persistent throbbing

Yes
No

Photophobia

Yes
No

Phonophobia

Yes
No
Clear, Distinct lateralization of pain
Yes
No
Interference with daily activities
Yes
No
Onset
Within minutes to hours
Gradual
Age of onset
Childhood, Adolescence
Middle age/Adult life
52
Tension-type headache is the only kind of headache where the pain is present thr
oughout the day, day after day, for long periods of time for which the term 'chr
onic tension-type headache' is used
53
tension headaches more common in women.
54
A common and useful clinical approach is to diagnose tension headaches in patien
ts whose headaches are devoid completely of associated symptoms like

nausea, vomiting, photophobia, osmophobia, throbbing and aggravation of pain wit

h movement of the head
55
nitric oxide has been implicated in the pathogenesis of tension headaches
56
neuro-imaging such as MRI, CT scanning should be considered
in a patient with a normal neurological examination if:
Headaches are rapidly increasing in frequency
Headaches are associated with dizziness or lack of co ordination
History of paraesthesias associated with headaches
Headaches awakens the subject from sleep
57
tension headaches
The daily use of analgesics may have health consequences,
potentiate the occurrence of medication overuse headache,
or lose efficacy over time
58
tension headaches
Preventive measures
anxiolytics
SSRIs
novel antidepressants,
tricyclic anti-depressants
MAO inhibitors.
59
Cluster headache:
same hour at the same spot
unilateral,
short duration,
signs of autonomic dysfunction
a type of trigeminal autonomic cephalgia
divided into episodic and chronic types
a "male" headache disorder
at any age
cluster period lasts for 6 to 12 weeks
cannot last for more than 12 months
Typically starts retro-orbitally, peri-orbitally, supra-orbitally or temporally
May be nocturnally, waking up from sleep with pain,corresponds to the rapid eye
movement phase
Ipsilateral nasal congestion/rhinorrhoea/eye lid oedema/forehead and facial swea
ting
Ipsilateral miosis and/or ptosis A sense of agitation/restlessness
may change character during the attack
Cutaneous allodynia hypersensitivity of the scalp in the affected area
induced by vasodilators = alcohol, nitroglycerin or histamine
some patients may postpone attacks by a few days
Treatment: Acute attack:
100% oxygen via a non-re-breathing mask /Sumatriptan SC
Oral sumatriptan is not useful in an acute attack, but can be used in the preven
tative measures.
Other agents:
Dihydroergotamine/Ketorolac/Chlorpromazine/Lidocaine viscous solution intranasal
solution/Cocaine intranasal/Capsaicin
Short term prevention:Prednisone/Methysergide/Verapamil/Greater occipital nerve
injection
Long term Prevention:Verapamil/Lithium/Methysergide/Topiramate/Gabapentin/Melato
nin
60

The term chronic cluster headache describes attacks occurring for more than 1 ye
ar without remission or with a remission lasting less than 1 month
61
verapamil = 80% reduction in the number of attacks.
Constipation side effect
first-line preventative measure
baseline ECG is taken, and repeated every 6 months.
62
Lithium carbonate is the first choice of treatment of chronic cluster headaches
mechanism of action of unknown
no measurable effect on the cerebral haemodynamics
has a central neurogenic effect influencing the biological clock in the area of
the suprachiasmatic nucleus.
narrow therapeutic window
usually lower than the dose required to treat bipolar disorder
63
Cluster headaches
Methysergide
clonidine
Clomiphene citrate is a synthetic, non-steroidal ovulatory stimulant which alter
s the hypothalamic oestrogen receptors, thus producing an increase in Leuinizing
hormone and follicular stimulating hormone levels with subsequent increase in t
estosterone production
neurostimulation
Deep-brain stimulation in = posterior hypothalamic gray matter
occipital nerve stimulation.
64
Surgical intervention in chronic cluster headache:
Involving sensory trigeminal nerve:
Chemical denervation of the supra-orbital and infra-orbital nerves
Avulsion of the supra-orbital, infra-orbital, supra-trochear nerves
Chemical denervation of the Gasserian ganglion
Retrogasserian glycerol injection
Radiofrequency ganglio-rhizolysis
Trigeminal root section
Gamma knife surgery
Involving the autonomic pathways:
Lesion of the greater superficial petrosal nerve
Lesion of the nervus intermedius
Sphenopalatine ganglion blockade
65
Cluster Variants:
"Trigeminal Autonomic Cephalgia".
Cases of paroxysmal pain behind the eye or nose or in the upper jaw or temple,
associated with the blocking of nostril or lacrimation and
described in the past under the names such as
sphenopalatine, petrosal, vidian or ciliary neuralgia
Chronic paroxysmal hemicrania = unilateral cluster headache
But are of shorter duration (2 to 45 minutes) and usually affect the temporo-or
bital region of one side, accompanied by
conjunctival hyperemia,
rhinorrhoea,
partial Horner's syndrome.
Unlike clusters
paroxysms occur several times in a day,
respond dramatically to indomethacin
66
SUNCT
more frequent, briefer and do not do not usually respond to Indomethacin.

short-lasting
unilateral
neuralgiform attacks with
conjunctival injection and
tearing.
Diagnosis requires at least 20 attacks, lasting for 5-240 seconds,
ipsilateral conjunctival involvement and lacrimation.
If conjuctival component (injection and lacrimation) absent
= SUNA
(Shortlasting
unilateral
neuralgiform attacks with
cranial autonomic symptoms).
Diagnosis: The pain of SUNCT/SUNA is
unilateral
located anywhere in the cranium
may occur as single stabs,
group of stabs or
a longer attack where many stabs occur,
and the pain does not completely resolve between stabs,
thus leading to a "saw tooth" phenomenon.
Diagnosis of SUNCT is easily confused with that of Trigeminal Neuralgia
Minimal presence or
complete absence of autonomic symptoms and
a clear refractory period to triggering indicated a diagnosis of
trigeminal neuralgia.
Secondary SUNCT may be seen with posterior fossa or pituitary lesions.
All with SUNCT or SUNA must be evaluated with pituitary function tests and neuro
imaging:
MRI brain with pituitary views.
Treatment: Therapy of acute attacks in not a useful approach in SUNCT/SUNA since
the attacks are of a very short duration, however,
IV lidocaine arrests the symptoms and are useful in hospitalized patients.
Preventive therapy
anti-convulsants such as lamotrigine 200mg-400mg/day.
Topiramate and
Gabapentin
Surgical approaches
vascular decompression or
destructive trigeminal procedures are not very effective
Nerve stimulations (occipital) useful
Deep brain stimulation useful
Short-term prevention using IV lidocaine may be useful.
67
Hemicrania continua:
moderate, continuous, unilateral with the fluctuations of severe pain,
complete resolution of pain on administration of indomethacin;
exacerbations with autonomic features, including
conjunctival injection, lacrimation, and photophobia on the affected side.
Women are most (female: male 2:1)
between 11 and 58 years.

cause not known.

Treatment:
indomethacin; other NSAIDs little/no benefit
IM injection of 100mg indomethacin is considered a diagnostic tool
oral indomethacin 25mg tid, then 50mg tid, and then 75mg tid.
for at least 2 weeks
Topiramate in some patients
unable to tolerate indomethacin, occipital nerve stimulation may be tried.
68
Primary Stabbing headache: "ice-picks" or "jabs and jolts".
stabbing type of headache,
confined to the head or rarely the face
lasts for 1 to many seconds or minutes occurring as a single 'stab', or a series
of stabs.
no associated cranial autonomic features,
no cutaneous triggers
a pattern of recurrence at regular intervals (hours to days).
Treatment:
indomethacin
after a certain period of control with indomethacin, it can gradually be withdra
wn.
69
Primary Cough headache:
severe,
transient cranial pain on coughing,on sneezing, laughing lifting heavy weights,
straining
in the frontal region and is usually generalized,
bursting
so severe that the patient finds a need to cradle his head in his hands, thus si
mulating subarachnoid haemorrhage.
a benign syndrome
occurring over a period of several months to a year
and then disappears
occasionally be found to have serious intracranial disease,
most often traced to lesions of the posterior fossa and foramen magnum, arteriov
enous malformation, subdural haematoma,
Sometimes this headache starts for the first time and persists after a lumbar pu
ncture.
Treatment: Indomethacin 25-50mg two to three times a day
Some patients with cough headache are relieved with a lumbar puncture, which is
a simpler option compared to a long-term use of indomethacin.
ergot preparations and propranolol are alternatives.
70
Primary exertional headaches:
resemble primary cough headache + migraine
exercise precipitates + pulsatility of a migraine
bilateral, throbbing type
lasting from 5mins to 24 hours
preventive measure avoid severe exertion, hot weather /high altitudes.
mechanism unclear ~ acute venous distention
special variant "weight-lifter's headache"
occurs as a single event or repeatedly over a period of several months
last several hours or days
begins in a matter of minutes after lifting weights

If resolves in an hour = there is no meningismus or signs of bleeding on a CT s

can,
there is no need of a lumbar puncture but rest is advised for a couple of weeks
Rarely pain from cardiac angina may be referred to the head, most probably via t
he central connections of the vagus nerve and may present as exertional headache
.
This is referred as cardiac cephalgia.
Treatment: Exercise routines must begin modestly and gradually progress to highe
r levels of intensity.
Indomethacin
prophylactic measures
Ergotamine
dihydroergotamine (2 mg by nasal spray)
methysergide (given as 1-2 mg PO, 30-45 minutes before exercise)
Propranolol
In some patients, a lumbar puncture may relieve pain for a long time.
71
Headaches related to Sexual activity:
Pain begins as a dull bilateral headache that suddenly becomes more intense at o
rgasm.
Three types of these orgasmic headaches:
Dull, aching pain in the head and neck that increases as the intensity of the se
xual activity increases.
Severe, throbbing, "explosive" headache that occurs at the time of orgasm and pe
rsists for several minutes or hours
Postural headache that develops after coitus that resembles the headache of a lo
w CSF pressure.
a form of low CSF pressure headache.
not always benign,
a hypertensive haemorrhage,
rupture of an aneurysm or
vascular malformation or
myocardial infarction may occur
more common in men
who stop the sexual activity on the onset of headache, the pain may subside in 5
minutes to 2 hours. In many patients, six months.
Treatment:
reassurance,
stop the sexual activity at the onset
Preventive 30 45 minutes prior to sexual activity
propranolol 40 to 200 mg per day.
Diltiazem
Ergotamine 1mg
Indomethacin 25-50mg
72
Primary Thunderclap Headache:
sudden onset of a severe headache in the absence of any noticeable provocation.
"the most severe headache ever experienced".
Differential diagnosis of thunderclap headache:
commonly associated withMigraine variant
Subarachnoid Headache

Cerebral venous thrombosis

Diffuse cerebral vasculopathy (Call-Fleming syndrome)
Subdural haematoma
Accelerated hypertension
Pituitary Apoplexy
Cervical arterial dissection
Cocaine
Serotoninergic drugs
Perimesencephalic haemorrhage
Patients on MAO inhibitors ingesting tyramine-containing foods
Phaeochromocytoma
Neuroimaging and lumbar puncture exclude a subarachnoid haemorrhage
good prognosis with other causes
Neuroimaging:
CT scan and/or MRI with MR angiography and CSF examination
Cerebral angiography is reserved for high suspiscion intracranial aneurysm.
Reversible segmental cerebral vasoconstriction may be seen in primary thundercla
p headache without the intracranial aneurysm.
In presence of
posterior leukoencephalopathy, the differential diagnosis includes
cerebral angitis, drug toxicity (cyclosporine, intrathecal methotrexate, pseudoe
phedrine).
73
Hypnic Headache:
occur after a few hours of sleep.
lasts between 15 and 30 minutes
moderately severe and generalized
In a few cases, unilaterality has been noted and there have been reports of thro
bbing type of headaches too.
awaken from sleep, and usually fall back asleep once the pain has subsided,
only to wake up in a few hours with headache.
Up to 3 repetitions of such pattern can occur in one night's sleep.
mostly seen in women above 60 years.
Photophobia, phonophobia, nausea and or any other neurological alterations are u
sually absent. Poorly controlled hypertension can present like this, so when thi
s diagnosis is being considered in a patient, a 24-hour blood pressure monitorin
g is ideal.
Treatment:
lithium carbonate at a dose of 200 600 mg once at bedtime.
who do not tolerate lithium, verapamil (at 160mg once at bedtime)
or methysegide (1-4mg once at bedtime)
Caffeine /at bedtime
Flunarizine, 5m at bedtime help maintain a normal sleep pattern.
74
Erythrocyanotic headache:
intense, generalized, throbbing headache may occur in conjuction
with flushing of face and hands and numbness of the fingers (erythromelalgia).
Episodes tend to be present onawakening from sound sleep.
associated with:
Mastocytosis ( the infiltration of cells with mast cells which release histamine
, heparin and serotonin) Carcinoid tumours Serotonin-secreting tumours
Tumours of the pancreatic islet
Phaeochromocytoma
believed to be secondary to a cause that is unknown for the present.

75
Medication overuse headache/chronic daily headache:
Near-daily headaches
require medication everyday
occurs for nearly 15 of the 30 days in a month
not a single entity, and it encompasses a number of different headache syndromes
could be primary or secondary
episodic primary headache transformed into a chronic headache
"a pattern of greater than or equal to 15 days of primary headache per month for
at least 3 months applies to the use of simple analgesics and caffeine-containi
ng combination analgesics
For patients on narcotics, this is reduced to 10 days a month
Most patients who stop taking the medication will improve significantly
76
Diagnostic Criteria for Chronic Migraine and Medication Overuse
Headache:
Migraine:
*Migraine headache occurring on 15 or more days per month for more than 3 months
in the absence of medication overuse and not attributable to other causes
*Headache which has at least 2 of the 3 qualities:
Unilateral location
Pulsating quality
Moderate to severe intensity
Aggravated with activity
*During the headache, at least one of the following
Nausea and or vomiting
Photophobia and phonophobia
Medication overuse headache:
Headache greater than 15 days per month that has developed or markedly worsened
during the medication overuse
Headache resolves or reverts to its previous pattern with 2 months of discontinu
ing the overused medication
77
Classification of chronic daily headache:
>4 hours per day
Chronic migraine
Chronic tension-type headache
Hemicrania continua
New daily persistent headache
<4 hours a day
Chronic cluster headache
Chronic paroxysmal hemicrania
SUNCT/SUNA
Hypnic headache
Secondary Post traumatic:
Head injury
Iatrogenic
Post-infection
Inflammatory, such as:Giant cell arteritis Sarcoidosis Behet's syndrome
Chronic CNS infection
Medication overuse headache
78
Proposed mechanisms of Chronic headache, Analgesic rebound headache and Medicati

on overuse headache:
The pathophysiology of migraine
Raskin and Appenzeller proposed a continuum model of migraine with aura at one e
nd of the headache spectrum and chronic tension-type headache at the other and b
etween these two extremes are the different clinical phenotypes of primary heada
ches observed in clinical practice.
migraine becomes more chronic, the threshold for the next migraine is lowered an
d that analgesics and ergotamine expedited this change in threshold.
gastrointestinal and neurovascular symptoms as the chronocity set in,
greater association of myogenic and psychological symptoms.
A 'convergence hypothesis'
primary headaches, at least in the migraine population, evolved from a single pa
thophysiological mechanism.
Treatment:
The first step is to diagnose and rule out any underlying condition. For patient
s with primary headaches, the diagnosis of the headache type will guide the trea
tment choice.
Preventive treatments
such as tricyclic antidepressants (amitriptyline or nortriptyline) at doses up t
o 1mg/klg are very useful in patients with chronic headache arising from migrain
e or tension type headaches. They are started at low doses and given in twice-da
ily doses.
Anticonvulsants like topiramate, valproate and gabapentin are also useful in mig
raineurs. Flunarizine has been found to be especially useful.
Medically intractable chronic daily headache:
Most promising approach thus far seems to be occipital nerve stimulation.
Medication overuse headache:
Outpatients: First step is to reduce and eliminate the analgesic responsible. Th
is can be done by reducing the dose of the analgesic by 10% every 1- 2 weeks.
A small dose of an NSAID such as Naproxen (500mg BiD) will help relieve residual
pain.
NSAID overuse is not usually a problem when taken 1 or 2 times in a day.
Preventive medications usually don't work in the presence of analgesics and usua
lly take about 2 weeks for their action to set in.
Inpatients:
if the patient has been using a narcotic agent. Such patients have typically fai
lure efforts at outpatient withdrawal or have developed a significant addiction.
With medical conditions such as Diabetes Mellitus also require admission, since
the medical condition could complicate on withdrawal of the analgesic.
Anti-emetics and fluids are administered as required.
Clonidine is used for opioid withdrawal.
For acute intolerable pain in the waking hours, IV aspirin (1gram) is used.
IM chlorpromazine can be helpful at nighttime.
After 3 to 5 days, diethylergotamine may be introduced IV, for about 5 days, at
a TiD dose.
This is then stopped and a preventive agent may be introduced.
79
Posttraumatic Headache:
Severe, chronic, continuous or intermittent headaches lasting days or weeks
separable in every way from the headache that immediately follows head injury (s
uch as pain of a scalp laceration or cerebral contusion with blood).
In cases of a chronic subdural haematoma, the pain is deep-seated, dull steady,

usually unilateral and may be accompanied or followed by drowsiness, confusion a

nd fluctuating hemiparesis.
Positional worsening of pain.
Usually, the patient forgets the pain.
Increases in severity over several weeks or months.
Who have received anti-coagulation at any time after the trauma are at risk.
A CT/MRI establishes the diagnosis.
Chronic posttraumatic headache: persistence as headache lasting longer than 3 mo
nths after injury.
feature of the post-concussion syndrome, comprising of giddiness, fatigability,
insomnia, nervousness, irritability and inability to concentrate.
Resembles a tension type headache.
Reassurance
gradually increase the physical activity/drugs that reduce anxiety and depressio
n.
With whiplash injuries of the neck, there may be unilateral or bilateral retroau
ricular or occipital pain, probably as a result of stretching or tearing of liga
ments and muscles at the
occipitonuchal junction or
a worsening of a pre-existing cervical arthropathy.
Less frequently cervical intervertebral and nerve roots are involved.
alert to headache as a sign of carotid artery dissection
CT or MRI usually are unrevealing and the neurological exam is typically normal.
Treatment:
Empirical = Tricyclic antidepressants/Antiepileptic/gabapentin
In most cases, headache usually resolves in 3 to 5 years.
80
Headache secondary to intracranial haemorrhage:
sudden onset, abrupt, severe headache
subarachnoid haemorrhage/ruptured intracranial aneurysm, arteriovenous malformat
ion, or an intraparenchymal heamorrhage
Half of the patients, the sudden onset of the headache follows a period of exert
ion.
Although sudden headache in the absence of focal neurologic symptoms is the hall
mark of aneurysmal rupture, focal neurologic deficits may occur.
Anterior communicating artery or MCA bifurcation aneurysms may rupture into the
adjacent brain or subdural space and form a haematoma large enough to produce ma
ss effect.
deficits:hemiparesis, aphasia, and abulia.
Aneurysms can undergo small ruptures and leaks of blood into the subarachnoid sp
ace and these are referred to as sentinel bleeds.
SAH : CT scan within 72 hours of the onset of headache.
if the heamorrhage is below the foramen magnum, the head CT may appear normal.
Delayed neurological deficits include a re-rupture, hydrocephalus, vasospasm and
hyponatremia. Treatment
Early aneurysm repair prevents rerupture and
allows the safe application of techniques to improve blood flow (e.g., induced h
ypertension and hypervolemia) should symptomatic vasospasm develop.
The aneurysm may be "clipped" or "coiled".
seizures can cause a re-bleeding.
Glucocorticoids may help reduce head and neck ache cause by irritation caused by
the subarachnoid blood.
Vasospasm remains the leading cause of morbidity and mortality following aneurys
mal SAH.
nimodipine (60 mg PO every 4 h) improves outcome, perhaps by preventing ischemic
injury rather than reducing the risk of vasospasm.

81
Headache secondary to meningitis:
Meningitis typically presents with severe headache, with neck stiffness and feve
r. A lumbar puncture is diagnostic of meningitis. Patients also complain of phot
ophobia. There is an undeniable accentuation of pain on eye movement. Meningitis
can be easily mistaken for migraine in that the cardinal symptoms of pounding h
eadache, photophobia, nausea, and vomiting are frequently present. Treatment fol
lows the medications for the underlying meningitis. Gluocorticoids may help in d
ecreasing the intracranial pressure and thus the headache.
82
Headache secondary to a brain tumour:
Approximately 30% of patients with a brain tumour present with headache as the m
ain symptom. The headache is usually non-descript, usually intermittent, dull, d
eep aching of moderate intensity, which usually increases due to exertion or cha
nge in position, and may be associated with vomiting. Symptoms are thus similar
to that of migraine headaches.
Vomiting that precedes the appearance of headache by weeks is highly characteris
tic of posterior fossa brain tumors.
Head pain appearing abruptly after bending, lifting, or coughing can be due to a
posterior fossa mass, a Chiari malformation, or low CSF volume.
The diagnosis is made by neuroimaging such as CT scan and/or MRI with/ without c
ontrast.
stereotactic biopsy may be indicated
83
Headache secondary to temporal arteritis:
Temporal arteritis or giant cell arteritis is an inflammatory disorder, which fr
equently involves the extracranial circulation of the carotid artery.
Common disorder of elderly
average age of onset is 70 years,
women more than half of cases.
half of patients with untreated temporal arteritis develop blindness
due to involvement of the ophthalmic artery
The ischaemic optic neuropathy induced by giant cell arteritis is a major cause
of rapidly developing blindness in patients >60 years of age.
Presenting symptoms include:
Headache
Polymyalgia rheumatica
Jaw claudication
Fever
Weight loss
may be unilateral or bilateral
in most cases is located temporally but may present in any other part of the cra
nium.
Pain usually increases over hours, gradually before peaking.
dull and boring type of pain, with superimposed stabbings.
Most patients can recognize that the origin of their head pain is superficial, e
xternal to the skull, rather
than originating deep within the cranium.
Scalp tenderness may be marked,
so much so that combing the hair or resting the head on a pillow may be too pain
ful.
may be worse at night, and aggravated by exposure to cold.
Patients may also present with red streaking of the skin overlying the temporal
arteries, and tenderness over the temporal or less commonly the occipital arteri
es.

elevated erythrocyte sedimentation rate

temporal artery biopsy is confirmatory.
Immediate treatment involves the administration of oral prednisone 80mg daily fo
r the first 4-6 weeks, and then tapered gradually.
84
There is no single unifying theory so far to explain the clinical findings and i
nvestigational findings see in migraine.
The frequency of migraine attacks varies from once in a lifetime to almost daily
The key pathway for the pain in an acute attack of migraine is the trigeminovasc
ular input from the meningeal vessels Mis-sense mutations in 1 subunit of P/Q-ty
pe, voltage-gated calcium channel on chromosome 19 lead to FHM1, The gene ATP1A2
, which encodes the 2 subunit of NA+/K+ pump is associated with FHM-2, linked to
chromosome 1q23, Mutations of SCN1A gene cause FHM-3 and dopamine D2 receptor g
ene may also have some affect on the susceptibility of migraine.

In its most basic level, migraine is headache with associated features, while te
nsion headache is featureless.
Tension-type headache is the most common variety of headache.
Tension-type headache is the only kind of headache where the pain is present thr
oughout the day, day after day, for long periods of time for which the term 'chr
onic tension-type headache' is used.
Cluster headache
The pain is deep, usually retro-orbital, often excruciating in intensity, non-fl
uctuating and explosive in quality.
A core feature of cluster headache is periodicity.
cluster headache may be preceded by prodromal as a vague discomfort or poorly de
scribable feeling in the region of one eye, temple, forehead, or neck.
Fatigue, euphoria, depression or mood changes, apathy, irritability, and photoph
obia and phonophobia may be experienced.
Treatment of a cluster headache includes administration of oxygen, sumatriptan a
nd other agents such as parenteral ketorolac, chlorpromazine, lidocaine, etc.
Preventative measures include the use of methyl prednisone for short term, verap
amil, methysergide, etc for a longer-term prophylaxis.
When the medical therapies fail, neurostimulation strategies may be employed.
A small percentage of patients with chronic cluster headaches who do not respond
to pharmacological therapy may benefit from surgical intervention.
This is considered only in those patients who are suffering from strictly unilat
eral headaches.
Apart from symptomatic management, the most important part of treatment of secon
dary headache involves the dealing with the underlying condition that is actuall
y causing the headache.
==
Craniofacial Pains
Acute Zoster and Post-herpetic pain:
Neuralgia affect cranial as well as peripheral nerves.
In the Cranial nerve regions, two syndromes :
Herpes zoster auricularis
Herpes zoster ophthalmicus
Both may be exceedingly painful, especially in the acute condition.

Herpes zoster auricularis:"Ramsay-Hunt syndrome"

Herpes of the external auditory meatus and pinna and
sometimes of the palate and the occipital region with or without
deafness, tinnitus and vertigo is combined with facial paralysis.
Herpes zoster ophthalmicus:
Pain and herpetic eruption due to the infection of the gasserian ganglion and th
e central and peripheral pathways of the trigeminal nerve are almost always limi
ted to the ophthalmic division. The eruption usually appears within 4 to 5 days
of onset of pain.
Pain in many cases is localized characteristically to a dermatome.
Treatment:
The acute pain usually subsides after several weeks
Acyclovir at 800 mg orally five times daily for 7 to 10 days for the primary inf
ection
In the elderly becomes chronic and intractable
Local Capsaicin
Amitryptline 75mg once daily at bedtime
Ketamine cream
Trigeminal rhizotomy
Otalgia:
Localized to in and around one ear and is usuall
an incipient symptom of Bell's palsy.
Neurosurgical studies have shown that otalgia is relieved by the section of nerv
us intermedius (sensory part of VII cranial nerve or of nerves IX and X.
Rule out:
Nasopharyngeal tumour
Vertebral artery aneurysm
Outbreak of Herpes zoster
Lateral sinus thrombosis.
Once these are ruled out, the possibilities remain
primary idiopathic,
lower cluster headaches,
glossopharyngeal neuralgia.
Treatment is that of the underlying cause.

Costen Syndrome (Temporo-mandibular joint pain):

dysfunction of one temporomandibular joint
Malocclusion : ill-fitting dentures or loss of molar teeth on one side,
lead to distortion
degenerative changes in the joint
pain in front of the ear, with radiation to the temple and over the face.
diagnosis:
Tenderness over the joint
Crepitus on opening the mouth
Limitation of jaw opening.
diagnostic maneuver
palpating the joint from its posterior aspect by placing a finger in the externa
l auditory meatus and pressing for- ward.
The diagnosis can be made with some confidence only if this entirely reproduces
the patient's pain. CT and plain films are rarely helpful, but effusions have be

en shown in the joints by MRI. Management consists of:

Adjustment by a dentist
may also be
rheumatoid arthritis and other connective tissue diseases.
Occipital Neuralgia:
Paroxysmal pain may occasionally occur in the distribution of the greater or les
ser occipital nerves (suboccipital, occipital, and posterior parietal areas).
Tenderness localized where these nerves cross the superior nuchal line,
there is only questionable evidence of an occipital nerve lesion at this site.
Treatment:
Carbamazepine
Blocking the nerves with lidocaine may abolish the pain and encourage attempts t
o section one or more occipital nerves or the second or third cervical dorsal ro
ot.
Repeated injections of local anesthetic agents and the use of steroids, traction
, local heat, and analgesic and anti-inflammatory drugs
The pain at times may be difficult to distinguish from that arising in the upper
three cervical apophysial joints, one
type of which is discussed below.
Carotidynia and Extracranial artery dissection:
compression of the artery or mild electrical stimulation at or near the bifurcat
ion, produced a dull ache that was referred to the ipsilateral face, ear, jaws,
and teeth or down the neck.
This type of carotid sensitivity occurs rarely as part of cranial (giant-cell) a
rteritis and of the rare condition known as Takaysu arteritis and during attacks
of migraine or cluster headache.
It has also been described with displacement of the carotid artery by tumor
and dissecting aneurysm of its wall;
The idiopathic variety may have to do with a swelling or inflammation surroundin
g
carotid bifurcation,
A variant of carotidynia takes the form of
recurrent,
self-limited attacks in the aforementioned distribution and
tenderness at the carotid bifurcation
lasting a week or two.
During the attack, aggravation of the pain by
head movement,
chewing, and swallowing
Treated with simple analgesics.
Yet another variety of carotidynia appears at any stage of adult life and
recurs in attacks lasting minutes to hours in association with
throbbing headaches
indistinguishable from common migraine
responds to the ergotamine, methysergide, and other drugs that are effective i
n the treatment of migraine.
Facial Pain of Dental or Sinus Origin
Maxillary and mandibular discomfort is common effects of nerve irritation from
deep caries,
dental pulp degeneration,

periodontal abscess.
The pain of dental nerve origin is most severe at night,
slightly pulsating, associated with local tenderness at the root of the tooth
in response to heat, cold, or pressure.
eradicated by infiltrating the base of the tooth with lidocaine.
Trigeminal neuritis may be iatrogenic, following dental extractions or
oral surgery is another vexing problem.
There may be sensory loss in the tongue
or lower lip and weakness of the masseter or pterygoid muscle.
Treatment:
isolation of the affected region by local anesthetic blocks
Curetted the bone, and administered antibiotics
Following the above the pain resolved.
The removed bone fragments showed vascular and inflammatory changes and infectio
n with oral bacterial flora.
Facial Pain of Uncertain Origin ("Atypical" Facial Pain)
most often young women,
who describe the pain as constant and unbearably severe, deep in the face, or at
the angle of cheek and nose and unresponsive to all varieties of analgesic medi
cation.
depression of varying severity is found in nearly half. Many such patients, with
or without depression, respond to tricyclic antidepressants and monoamine oxida
se inhibitors.
requires close observation of the patient,
looking for lesions such as nasopharyngeal carcinoma
The pain should be managed by the conservative and not by destructive surgery.
Antidepressants
==
Trigeminal Neuralgia
prosopalgia,
Suicide disease,
Fothergill disease
tic douloureux
More than one nerve branch can be affected by the disorder.
In most cases (unilateral),/right side.
Rarely,(bilateral).
60 to 70 years of age.
Females are affected up to twice as often as males.
Patients who present with the disease when aged 20-40 years are more likely to s
uffer from a demyelinating lesion in the pons secondary to multiple sclerosis
Another risk factor for this syndrome is hypertension
Types:
Trigeminal neuralgia is mainly classified into 2 main types
Type 1:Episodic
Causes extreme, sporadic, sudden burning or shock-like facial pain that lasts an
ywhere from a few seconds to as long as two minutes per episode.
These attacks can occur in quick succession, in volleys lasting as long as two h
ours.
Type 2:Constant
Characterized by constant aching, burning, stabbing pain of somewhat lower inten
sity than Type 1.

New classification: (Dr. Burchiel's classification system)

Based on information provided in the patient's history and incorporates seven di
agnostic criteria, as follows.
1.
And
2.
Trigeminal neuralgia Types 1 and 2 (TN1 and TN2) refer to idiopathic, sp
ontaneous facial pain that is either predominantly episodic (as in TN1) or const
ant (as in TN2) in nature.
3.
Trigeminal neuropathic pain results from unintentional injury to the tri
geminal nerve from trauma or surgery.
4.
Trigeminal deafferentation pain results from intentional injury to the n
erve by peripheral nerve ablation, gangliolysis, or rhizotomy in an attempt to t
reat either TN or other related facial pain.
5.
Symptomatic TN results from multiple sclerosis.
6.
Post herpetic TN follows a cutaneous herpes zoster outbreak in the trige
minal distribution.
7.
The category of atypical facial pain is reserved for facial pain seconda
ry to a somatoform pain disorder and requires psychological testing for diagnost
ic confirmation (the term atypical facial pain is replaced with Facepain of Obsc
ure Etiology {FOE or POE})
Causes:
Most cases of trigeminal neuralgia are idiopathic, but compression of the trigem
inal roots by tumors or vascular anomalies may cause similar pain.
TN can be caused by a blood vessel pressing on the trigeminal nerve as it exits
the brain stem. This compression causes the wearing away or damage to the protec
tive coating around the nerve (the myelin sheath). In one study, 64% of the comp
ressing vessels were identified as an artery, most commonly the superior cerebel
lar (81%). Venous compression was identified in 36% of cases.
Vascular causes include a pontine infarct and arteriovenous malformation or aneu
rysm in the vicinity.
Inflammatory causes include multiple sclerosis (common), sarcoidosis, and Lyme d
isease neuropathy.
Tumor-related causes of trigeminal neuralgia (most commonly in the cerebello-pon
tine angle) include acoustic neurinoma, chordoma at the level of the clivus, pon
tine glioma or glioblastoma, epidermoid, metastases, and lymphoma. Trigeminal ne
uralgia may result from paraneoplastic etiologies.
Clinical features:
Paroxysms of intense, stabbing pain in the distribution of the mandibular and ma
xillary divisions (rarely the ophthalmic division) of the fifth cranial nerve. T
he number of attacks may vary from less than 1 per day to 12 or more per hour an
d up to hundreds per day. The pain seldom lasts more than a few seconds or a min
ute or two, but it may be so intense that the patient winces involuntarily, henc
e the term tic. The paroxysms recur frequently, both day and night, for several
weeks at a time.
Pain:
Characteristics
Characteristically severe, paroxysmal, and lancinating
Commences with a sensation of electrical shocks in the affected area
Crescendos in less than 20 seconds to an excruciating discomfort felt deep in th
e face, often contorting the patient's expression
Begins to fade within seconds, only to give way to a burning ache lasting second
s to minutes
Pain fully abates between attacks, even when they are severe and frequent
Trigger factors
Attacks may provoke patients to grimace, wince, or make an aversive head movemen
t, as if trying to escape the pain, thus producing an obvious movement, or tic;
hence the term "tic douloureux"
by stimulation of certain areas of the face, lips or gums, as in shaving or brus

hing the teeth,

by movement of these parts in chewing, talking, blowing nose or yawning, or even
by a breeze
Localization
Patients can localize their pain precisely
The pain commonly runs along the line dividing either the mandibular and maxilla
ry nerves or the mandibular and ophthalmic portions of the nerve
In 60% of cases, the pain shoots from the corner of the mouth to the angle of th
e jaw
In 30%, pain jolts from the upper lip or canine teeth to the eye and eyebrow, sp
aring the orbit itself
In less than 5% of cases, pain involves the ophthalmic branch of the facial nerv
e
Diagnosis:
The diagnosis must rest on the strict clinical criteria.
International Headache Society criteria:
A.
Paroxysmal attacks of pain lasting from a fraction of a second to 2 minu
tes, affecting 1 or more divisions of the trigeminal nerve and fulfilling criter
ia B and C
B.
Pain has at least 1 of the following characteristics: (1) intense, sharp
, superficial or stabbing; or (2) precipitated from trigger areas or by trigger
factors
C.
Attacks stereotyped in the individual patient
D.
No clinically evident neurologic deficit
E.
Not attributed to another disorder
(MRI) scan to rule out a tumor or multiple sclerosis/blood vessel compressing th
e nerve
A diagnosis of classic trigeminal neuralgia may be supported by an individual's
positive response to a short course of an antiseizure medication.
Diagnosis of TN2 is more complex and difficult, but response to low doses of tr
icyclic antidepressant medications (such as amitriptyline and nortriptyline)
Differential diagnosis:
Migraine and cluster headaches may produce severe unilateral pain, but unlike tr
igeminal neuralgia, these conditions are not triggered by movement or contact wi
th the face nor do they respond promptly to carbamazepine.
Pains of dental or gingival origin
uralgia. A mandibular or maxillary
ain. It becomes throbbing with the
l exam supported by a dental x-ray

- mimic pains of a maxillary or mandibular ne

tooth, when diseased can produce an intense p
formation of a dental abscess. A good clinica
settles the diagnosis.

Pains from the nose or paranasal sinuses - the pains from sinusitis are usually
preceded by cold, are constant and usually associated with a fever. They become
throbbing when the secretions block the sinus outlets. Clinical examination and
X-ray of the paranasal sinuses (PNS view) or CT scan of paranasal sinuses is hel
pful.
Ocular or orbital pains
mimic pains of ophthalmic or first division neuralgia. T
he most common cause is a glaucoma which produces intense, throbbing pain in and
around the eye. A good clinical examination and tonometry is helpful.
Diabetic cranial neuropathies can involve branches of trigeminal nerve and produ
ce facial pains. Clinical examination and blood sugar level estimations are help
ful.

Management:
carbamazepine(600-1200mg/d),
oxcarbazepine,
gabapentin(300-900mg/d),
pregabalin 150-300mg/d),
clonazepam (2-6mg/day),
phenytoin(300-400mg/d) and
valproic acid (800-1200mg/d).
Carbamazepine is effective in 70-80% of the patients, but half become tolerant o
ver a period of several years.
Tricyclic antidepressants such as amitriptyline or nortriptyline can be used to
treat pain.
Common analgesics and opioids are not usually helpful
if medication fails to relieve pain or produces intolerable side effects such as
cognitive disturbances, memory loss, excess fatigue, bone marrow suppression, o
r allergy, then surgical treatment may be indicated.
Surgery
presence of multiple sclerosis,
upper/ophthalmic branch is involved
facial numbness is expected after many of these procedures
surgical risks
hearing loss, balance problems, leaking of the cerebrospinal fluid (the fluid th
at bathes the brain and spinal cord), infection, anesthesia dolorosa (a combinat
ion of surface numbness and deep burning pain), and stroke, although the latter
is rare.
A rhizotomy nerve fibers are damaged to block pain.
causes some degree of sensory loss and facial numbness.
Balloon compression works by injuring the insulation on nerves that are involved
with the sensation of light touch on the face.
The procedure is performed in an operating room under general anesthesia.
A tube called a cannula is inserted through the cheek and guided to where one br
anch of the trigeminal nerve passes through the base of the skull. A soft cathet
er with a balloon tip is threaded through the cannula and the balloon is inflate
d to squeeze part of the nerve against the hard edge of the brain covering (the
dura) and the skull. After about a minute the balloon is deflated and removed, a
long with the catheter and cannula. Balloon compression is generally an outpatie
nt procedure, although sometimes the patient may be kept in the hospital overnig
ht. Pain relief usually lasts one to two years.
Glycerol injection is also generally an outpatient procedure in which the indivi
dual is sedated with intravenous medication. A thin needle is passed through the
cheek, next to the mouth, and guided through the opening in the base of the sku
ll where the third division of the trigeminal nerve (mandibular) exits. The need
le is moved into the pocket of spinal fluid (cistern) that surrounds the trigemi
nal nerve center (or ganglion, the central part of the nerve from which the nerv
e impulses are transmitted to the brain). The procedure is performed with the pe
rson sitting up, since glycerol is heavier than spinal fluid and will then remai
n in the spinal fluid around the ganglion. The glycerol injection bathes the gan
glion and damages the insulation of trigeminal nerve fibers. This form of rhizot
omy is likely to result in recurrence of pain within a year to two years. Howeve
r, the procedure can be repeated multiple times.
Radiofrequency thermal lesioning (also known as "RF Ablation" or "RF Lesion") is
most often performed on an outpatient basis. The individual is anesthetized and
a hollow needle is passed through the cheek through the same opening at the bas
e of the skull where the balloon compression and glycerol injections are perform
ed. The individual is briefly awakened and a small electrical current is passed
through the needle, causing tingling in the area of the nerve where the needle t

ips rests. When the needle is positioned so that the tingling occurs in the area
of TN pain, the person is then sedated and the nerve area is gradually heated w
ith an electrode, injuring the nerve fibers. The electrode and needle are then r
emoved and the person is awakened. The procedure can be repeated until the desir
ed amount of sensory loss is obtained; usually a blunting of sharp sensation, wi
th preservation of touch. Approximately half of the people have symptoms that re
occur three to four years following RF lesioning. Production of more numbness ca
n extend the pain relief even longer, but the risks of anesthesia dolorosa also
increase.
Stereotactic radiosurgery (Gamma Knife, Cyber Knife) uses computer imaging to di
rect highly focused beams of radiation at the site where the trigeminal nerve ex
its the brain stem. This causes the slow formation of a lesion on the nerve that
disrupts the transmission of sensory signals to the brain. People usually leave
the hospital the same day or the next day following treatment but won't typical
ly experience relief from pain for several weeks (or sometimes several months) f
ollowing the procedure. The International Radio Surgery Association reports that
between 50 and 78 percent of people with TN who are treated with Gamma Knife ra
diosurgery experience "excellent" pain relief within a few weeks following the p
rocedure. For individuals who were treated successfully, almost half have recurr
ence of pain within three years.
Micro-vascular decompression (MVD) is the most invasive of all surgeries for TN,
but also offers the lowest probability that pain will return. About half of ind
ividuals undergoing MVD for TN will experience recurrent pain within 12 to 15 ye
ars. This inpatient procedure, which is performed under general anesthesia, requ
ires that a small opening be made through the mastoid bone behind the ear. While
viewing the trigeminal nerve through a microscope or endoscope, the surgeon mov
es away the vessel (usually an artery) that is compressing the nerve and places
a soft cushion between the nerve and the vessel. Unlike rhizotomies, the goal is
not to produce numbness in the face after this surgery. Individuals generally r
ecuperate for several days in the hospital following the procedure, and will gen
erally need to recover for several weeks after the procedure.
A neurectomy (also called partial nerve section), which involves cutting part of
the nerve, may be performed near the entrance point of the nerve at the brain s
tem during an attempted microvascular decompression if no vessel is found to be
pressing on the trigeminal nerve. Neurectomies also may be performed by cutting
superficial branches of the trigeminal nerve in the face. When done during micro
-vascular decompression, a neurectomy will cause more long-lasting numbness in t
he area of the face that is supplied by the nerve or nerve branch that is cut. H
owever, when the operation is performed in the face, the nerve may grow back and
in time sensation may return. With neurectomy, there is risk of creating anesth
esia dolorosa.
Surgical treatment for TN2 is usually more problematic than for TN1, particularl
y where vascular compression is not detected in brain imaging prior to a propose
d procedure. Many neurosurgeons advise against the use of MVD or rhizotomy in in
dividuals for whom TN2 symptoms predominate over TN1, unless vascular compressio
n has been confirmed. MVD for TN2 is also less successful than for TN1.
Complementary approaches
Some individuals manage trigeminal neuralgia using complementary techniques, usu
ally in combination with drug treatment. These therapies offer varying degrees o
f success. Some people find that low-impact exercise, yoga, creative visualizati
on, aroma therapy, or meditation may be useful in promoting well-being. Other op
tions include acupuncture, upper cervical chiropractic, biofeedback, vitamin the
rapy, and nutritional therapy. Some people report modest pain relief after injec
tions of botulinum toxin to block activity of sensory nerves.
Chronic pain from TN is frequently very isolating and depressing for the individ
ual. Conversely, depression and sleep disturbance may render individuals more vu
lnerable to pain and suffering. Some individuals benefit from supportive counsel
ing or therapy by a psychiatrist or psychologist. However, there is no evidence
that TN is psychogenic in origin or caused by depression, and persons with TN re
quire effective medical or surgical treatment for their pain.

==
Glossopharyngeal Neuralgia
"Glossopharyngeal neuralgia is a rare condition characterized by paroxysms of pa
in in the sensory division of the ninth cranial nerve".
-Waldman's textbook of pain management 2nd Edition.
Glossopharyngeal neuralgia is much less common compared to Trigeminal neuralgia,
but resembles it in many respects. The description of this entity dates back to
the 1910-1920s. In 1910, Weisenburg first described the pain in the distributio
n of the glossopharyngeal nerve in a patient with a cerebellopontine angle tumou
r. In 1921, Harris reported the first case and coined the term "glossopharyngeal
neuralgia"
Clinical presentation:
Population studies have shown that glossopharyngeal neuralgia is 100 times less
common when compared to trigeminal neuralgia. It is more commonly seen in patien
ts older than 50 years. It occurs in episodes, with the pain in each episode las
ting from a few seconds to minutes. Paroxysms of pain are often triggered by act
ivities such as chewing, coughing, laughing, talking or yawning.
Pain is described as shooting/stabbing/needle-like.
It occurs in paroxysms.
Pain is localized in the ear or radiate from the throat to the year, thereby imp
licating the auricular branch of the vagus nerve. Investigators have noted the s
pread of pain beyond the distribution of the glossopharyngeal nerve to areas inn
ervated by the vagus (as mentioned above) and the upper cervical segments. This
is referred to as overflow pain.
Overflow pain has been postulated as occurring due to spillover of the intense i
mpulses from the glossopharyngeal nerve through the tractus solitarius of the me
dulla to the vagus nerve.
Fibres of the glossopharyngeal nerve may also join the decending portion of the
trigeminal nerve, thereby contributing to this phenomenon.
Involvement of the vagus nerve concomitantly has been noted for a long time, wit
h glossopharyngeal neuralgia being the main craniofacial neuralgia that may be a
ccompanied by bradycardia and even syncope, presumably because of the triggering
of the cardio-inhibitory reflexes by the afferent vagal pain impulses.
There is no demonstrable sensory or motor deficit.
In very rare cases, carcinoma or epithelioma of the otopharyngeal-infracranial r
egion or peritonsillar abscess may give rise to a pain that is clinically indist
inguishable from glossopharyngeal neuralgia.
Diagnosis:
As with other headaches, a targeted history and physical examination contributes
significantly in arriving at the diagnosis. Most cases are idiopathic.
Most cases of glossopharyngeal neuralgia are idiopathic; however, care must be t
aken to exclude tumors of the head and neck, especially those that occur at the
cerebellopontine angle that may be the cause of the patient's symptoms
Although the condition is exceedingly rare, a careful cardiac examination is ind
icated to rule out glossopharyngeal neuralgia with associated syncope.
Idiopathic glossopharyngeal neuralgia has four major characteristics that includ
e:
A history of shooting, stabbing, shock-like pain in the neck, throat, or ear tha
t occurs in paroxysms and is triggered by talking, chewing, drinking or coughing
;
The neurologic examination results are normal, and the ear, pharynx, hypopharynx
, piriform sinuses, and larynx are free from objective disease
The patient is relatively pain free between attacks and can carry out normal act
ivities
The pain is markedly improved or relieved by blockade of the glossopharyngeal ne
rve with local anesthetic.12 Dull, aching, poorly localized pain that persists b
etween paroxysms of tic-like pain is strongly suggestive of a space-occupying le
sion and requires a thorough evaluation

Treatment:
In most patients, the pain of glossopharyngeal neuralgia can be controlled. In t
he acute, uncontrolled attack of glossopha- ryngeal neuralgia, hospitalization i
s indicated to facilitate the relief of pain and to monitor for side effects fro
m the treatments chosen.
Pharmacoogical treatment
Carbamazepine:
It is the first line of treatment in the case of glossopharyngeal neuralgia
A rapid response to this drug helps confirm the clinical diagnosis of glossophar
yngeal neuralgia.
Guidelines for the initiation/administration of Carbamazepine:
o
Order baseline complete blood count, blood chemistry, and urinalysis bef
ore initiation of therapy.
o
Start therapy slowly if the pain is not out of control.
o
Begin with a 200-mg bedtime dose for 2 nights.
o
Drug is increased in 200-mg increments in equally divided doses every 2
days, as side effects allow, until pain relief is obtained or a total dose of 12
00 mg daily is reached.
o
Patient is cautioned regarding side effects, including dizziness, sedati
on, confusion, and rash.
o
Carefully monitor laboratory data to avoid life-threatening blood dyscra
sias.
o
Discontinue drug at the first sign of blood count abnormality or rash.
o
After pain relief is obtained, the patient should be left at this dose o
f carbamazepine for at least 6 months before tapering.
o
Patient should be informed that under no circumstances should the dose o
f drug be changed or the prescription refilled or discontinued without consultat
ion with the pain management specialist.
o
Patient should be aware that premature tapering or discontinuation may l
ead to recurrence of pain with subsequent pain control being more difficult.
o
Hospitalize patients for pain emergencies.
Gabapentin:
In the patient in whom carbamazepine does not adequately control the pain of glo
ssopharyngeal neuralgia, gabapentin is the next step
Guidelines for the use of Gabapentin:
o
Order baseline complete blood count, blood chemistry, and urinalysis.
o
Begin treatment with 300-mg bedtime dose for 2 nights.
o
Increase drug in 300-mg increments in equally divided doses every 2 days
, as side effects allow, until pain relief is obtained or a total dose of 300 mg
daily is reached.
o
If patient has experienced partial pain relief, blood level is drawn and
the drug is carefully titrated upward with 100-mg tablets.
o
Rarely is more than 2400 mg needed to control pain.
o
Patient is cautioned regarding side effects, including dizziness, sedati
on, confusion, and rash.
Baclofen:
Baclofen has been reported to be of value in some patients with glossopharyngeal
neuralgia who do not obtain relief from carbamazepine and gabapentin
Guidelines for the use of Baclofen:
o
Order baseline complete blood count, blood chemistry, and urinalysis.
o
Begin treatment with 10 mg at bedtime for 2 nights.
o
Increase drug in 10-mg increments in equally divided doses every 5 days,
as side effects allow, until pain is controlled or a total dose of 80 mg daily
is reached.
o
Patient is cautioned regarding side effects, including dizziness, sedati
on, confusion, and rash.
Other Procedures/Invasive interventions:
Glossopharyngeal Nerve Block
Neurodesrtucive procedures
Microvascular Decompression of the Glossopharyngeal Root

In essence, the treating clinician should be aware of the severity of pain and n
ot dismiss the suffering endured by the patient, and must target an effective an
algesic protocol.
==
Neck Pain
Overview:
Neck pain is one of the most common pains. It can be due to number of disorders
and diseases of any tissues in the neck. Neck holds various vascular, neural and
extensions of visceral structures. The spinal cord passes from foramen magnum t
o thoracic area through a bony tunnel formed by cervical vertebrae. Cervical spi
ne also permits high mobility compared to other parts of spine probable this may
be the risk factor for neck pain many times. Ligaments and muscles protect vita
l tissue structures in neck from injuries. The annual incidence of neck pain is
reported as being as high as 15%. Reliable sources report that cervical spine de
generative disorders are more common that those affecting the lumbar spine and d
evelops at an earlier age.
Causes:
Various mechanical and non-mechanical factors contribute to the neck pain for ex
ample heavy manual duties involving heavy weight, smoking, driving, operating vi
bration equipment and awkward neck postures during sleep and work.
Muscle sprain / strain (i.e. whiplash) is a common cause of neck pain. Such diso
rders are self-limiting and usually improve in days to a few weeks. Parts of the
cervical spine that may be involved include:
Cervical facet joints or zygapophyseal joints allow the neck to flex, extend, an
d rotate. These small joints are susceptible to arthritis and injury.
Cervical intervertebral discs may bulge, herniate, and prone to other degenerati
ve problems. Cervical disc bulges or herniations may cause nerve irritation or i
mpingement resulting in pain and numbness is course of nerve.
Degenerative disc disease is an often an over-use or age-related condition. Unli
ke whiplash which is an immediate one-time injury, degenerative disorders develo
p over time from over-use and abnormal wear and tear, such as repeated heavy lif
ting. Such abnormal wear and tear may cause micro-traumas that can weaken soft t
issues in the neck.
Spondylosis or spinal osteoarthritis is a common cervical degenerative disorder.
Osteophytes are bony overgrowths. An osteophyte may irritate or impinge a spinal
nerve causing inflammation and pain.
Cervical radiculopathy is pain described as electric or shooting pain. Disc hern
iation and osteophyte formation are common causes.
Signs and symptoms:
Pain: dull aching pain in case of minor whiplash injuries, focal axial neck pain
and occipital headaches is usually originates from the cervical intervertebral
discs. In case with nerve root irritation (cervical radiculopathy) patient compl
aint of pins and needles, burning, shooting lancinating pain in a dermatomal pat
tern.
Radiation: pain may radiate up to the occiput (intervertebral disk problems) and
down to shoulder, arm and even fingers (Cervical radiculopathy). Many of the ti
mes pain is unilateral but some time occurs bilaterally.
Limitation to movement is due to pain (whiplash, facet joints, and intervertebra
l discs dysfunctions) sometime movement decreases due to Stiffness (spondylosis)
. Pain symptoms are usually unilateral sometimes occurs bilaterally. Also moveme
nt away from the affected side relieve the symptoms and movement towards the aff
ected side reproduce the symptoms.
Numbness and weakness: in case of cervical radiculopathy neck pain is associated
with numbness in the course of the affected nerve and weakness in the upper ext
remity function especially hand grip.
Red flag symptoms such as fever, unexplained weight loss, previous history of ca
ncer, immunosuppression or intravenous drug use should warn the clinician to loo
k for tumour or infection. Also look for the symptoms of cervical myelopathy, wh
ich are diffuse hand weakness and clumsiness, difficulty with balance, urinary d

isturbances in the form of urgency and frequency.

Diagnosis:
Obtain an accurate description of the characterization of the pain, including lo
cation, onset, duration, frequency, description, distribution, and aggravating a
nd relieving factors. Identifying specific red flags that are indicators of pote
ntially serious spinal or nonspinal pathology or conditions that may interfere w
ith treatment is extremely important.
Differentiating between referred and radicular pain is important. Referred pain
is more diffuse, whereas radicular pain is more specifically along the course of
a dermatome.
Patients with disc degeneration could have chronic low-grade pain that is period
ically exacerbated for several weeks.
Mechanical pain can be constant or intermittent, whereas chemical pain is more l
ikely to be constant.
Cervicogenic pain is usually worse in positions that involve prolonged sitting,
especially in sitting positions with a protruded head posture or prolonged flexi
on. Pain worse upon awakening is probably related to using an unsuitable pillow
or having adopted an inappropriate posture while sleeping.
Observe for the postural asymmetry (head tilt)
Tenderness on the side along the Paraspinal muscles and some muscle tenderness m
ay be present as triggers in trapezius and rhomboids.
Examination should involve testing sensory, motor and deep tendon reflexes. Pati
ents with cervical myelopathy will have hyperreflexia and hypertonia. Knee, ankl
e and wrist clonus can be present. Babinski, Hoffman signs (flexion and abductio
n of thumb on flexion of the terminal long phalanx).
Special Tests:
Foraminal compression test (spurling test): With extension and head rotated, pre
ssure is applied on the head, if this reproduces nerve root pain, is considered
positive. This is 93% specific, not sensitive (30%). It is not recommended for s
creening, but can help in confirming the diagnosis of cervical radiculopathy.
The Lhermitte test is performed by flexing the neck with the patient in the sitt
ing position. This test may produce an electriclike sensation down the spine and
occasionally the extremities. This electriclike sensation has been reported in
patients with cervical spondylosis, cervical myelopathy, cervical cord involveme
nt secondary to tumor, and multiple sclerosis.
Another helpful clinical sign is pain relief upon arm abduction (shoulder abduct
ion test) in cases of a ruptured cervical disc. No changes in pain occur with ar
m position when the disease process is spondylosis with foraminal stenosis.
Investigations:
Blood tests: CRP, ESR and white cell count can be elevated if there is an underl
ying infection.
Plain X-Ray of cervical spine, which might show evidence of degenerative discs a
long with osteophytes, loss of disc height as well as loss of cervical lardosis.
Magnetic Resonance Imaging: cervical radiculopathy can be rule out clearly using
MRI. Consider an MRI, if the symptoms are not settled in 4 to 6 weeks or if the
re are any red flag. The findings should correlate to the patients signs and sym
ptoms and the clinical findings.
Computerized tomography: CT explores better the bony structures causing foramina
l narrowing. Bone scan can be used in cancer suspicion, but does not help in pat
ients with cervical myelopathy to look at the other structures.
Electromyography: EMG is useful when clinical information and MRI are inconclusi
ve or if there is a suspicion of peripheral entrapment. A normal study, does not
exclude cervical neuropathy, if there are signs and symptoms present.
Selective nerve root block: SNRB, if a particular nerve root is responsible for
the patient's radiculopathy, anesthetizing this should produce resolution of the
radiculopathy might be diagnostic. The down sides to these are the volume of in
jectate and the spread. Even small volumes have shown to spread more than one le
vel making these investigations specificity in question.
Discography is currently used to determine whether the disk is the source of pai
n in patients with predominantly axial back or neck pain. Computed tomography (C

T) is usually performed after discography to assess anatomical changes in the di

sk and to demonstrate intradiscal clefts and radial tears. Pain reproduction dur
ing discography in symptomatic individuals is variable, with a lower incidence o
f pain reproduction in patients with disk degeneration than in those with poster
ior tears of the anulus fibrosus or significant disk bulges.
Differential diagnosis:
Peripheral entrapment syndrome, such as carpal tunnel syndrome
Hypoesthesia and weakness in the nerve distribution. Tinel's sign positive.
Herpes zoster
Neuropathic pain in a nerve root distribution following the typical vesicular ra
sh.
Thorasic outlet syndrome
Pain in shoulder and arm, often aggravated by the use of arm. Paresthesia common
ly in the C8T1 regions with symptoms reproduction on provocation test. Nerve con
duction studies are usually normal with occasional reduction in pulse on the sid
e of the problem.
Brachial pluxes neuralgia
Starts with severe pain in the neck, shoulder and arm followed by neurological w
eakness after few days.
Disorders of rotator cuff and shoulder
Pain in shoulder aggravated by active and passive shoulder movement.
Pancoast tumor
Brachial plexus signs along with ptosis and anhydrosis (Horner's syndrome)
Sympathetic pain
Diffuse pain in arm and hand associated with sympathetic changes, such as sweati
ng, swelling etc.
Referred pain from the neck
Could be a referred pain from cervical facet, disc, atlantoaxail and atlantoocci
pial joints where the pain rarely goes beyond the elbows
Treatment:
Medication:
Standard analgesics, such as paracetamol with or without centrally working analg
esics and physiotherapy are the first line treatment for neck pain. Some have ad
vocated the short-term immobilization to help pain control and also cervical pil
low at night to maintain cervical spine neutrality. However there is not enough
data to support these.
Occasionally opioids have been used to control the pain with not much evidence.
The use of opioids should be reserved due to the complications and possible addi
ctive and long-term effects. Short course of prednisone starting at 70mg and tap
ered over few weeks have been advocated with anecdotal evidence.
Physical therapy:
The aim of physiotherapy is to restore full range of movement and flexibility of
neck and shoulder movements. Therapy includes range of motion exercise, manual
therapy techniques, and aerobic conditioning followed by isometric and progressi
ve resistive exercises after the initial pain has been controlled.
Cervical Epidural Steriod Injection (CESI):
CESI is basically used to treat cervical radiculopathy when patients have not re
sponded to the medications and physiotherapy program. When properly perform by t
rained person under fluoroscopy, a significant number of patients with cervical
radiculopathy improve.
Medial branch block:
This is primarily a diagnostic block but can also be therapeutic. Some patients
do get long term relief from repeated blocks with local anaesthetic alone but ma
ny of these will need a more definitive solution of their problem at some time,
as the pain relief from facet blocks is seldom permanent. It should be noted tha
t there is no additional benefits of adding corticosteroids to the injections.
Radiofrequency neurotomy or denervation:
If the neck pain returns after a period of improvement then a radiofrequency neu
rotomy or denervation of the facet joint will have to be performed. This is a te
chnique for achieving neural ablation of the nerves that supply the facet joints

. When correctly performed in the right patients the results are excellent. When
performed badly, at best it will not work and at worst the consequences can be
disastrous. After this technique, there is usually a period of increased pain th
at can be sever and may last a few days to few weeks and may require strong anal
gesics, including opioids. It is important that the patient is aware of this. Th
ey also need to be aware that there will be sensory loss in the skin from the ne
ck down towards the trapezius which usually lasts for three to six months.
Nucleoplasty:
It is a percutaneous disc decompression using coblation technology. This involve
s passing a wand to the cervical disc, which evaporates the nucleus pulposus wit
hout producing much heat damage to the surrounding tissues. On healing, the disc
shrinks and takes the pressure away from the nerve root. This is ideal for smal
l disc bulge with corresponding nerve root symptoms not responding to all conser
vative treatments.
Surgery:
In appropriate selected patients surgery may relieve symptoms. Procedures, such
as discectomy, laminectomy, and fusion, including disc replacements have been ad
vocated in managing radiculopathy. Future treatments will be more biological wit
h gene therapy so that disc can regenerate.
==
Costosternal Syndrome
Introduction:
Clinical condition characterized by pain and tenderness at costochondral or chon
drosternal joints of the anterior chest wall without swelling or induration, usu
ally at multiple levels.
Also known as:
Anterior chest wall syndrome
Chest wall pain syndrome
Costochondritis
Parasternal chondrodynia
approximately 28% of undifferentiated noncardiac chest pain patients
more common in women
age greater than 40yrs.
Cause:
arthritis, including osteoarthritis, rheumatoid arthritis, ankylosing spondyliti
s, Reiter's syndrome, and psoriatic arthritis.
Trauma
Overuse or misuse
inflammation
invasion by tumor from primary malignant diseases, including thymoma, and metast
atic disease.
Clinical features:
aggravated by coughing, sneezing, deep inspiration, or any chest-wall movement.
patient attempts to splint the joints by keeping the shoulders stiffly in neutra
l position.
Pain is reproduced with active protraction or retraction of the shoulder, deep i
nspiration, and full elevation of the arm. Shrugging of the shoulder may also re
produce the pain.
Coughing may be difficult, and this may lead to inadequate pulmonary toilet in p
atients who have sustained trauma to the anterior chest wall.
tender
clicking sensation with movement of the joint.
Diagnosis:
Plain radiographs
If trauma = radionuclide bone scanning may be useful to exclude occult fracture
s
complete blood count,

prostate-specific antigen level,

erythrocyte sedimentation rate,
antinuclear antibody testing
evaluation for collagen vascular disease
Differential diagnosis:
Cardiac pain: primary concern; ischemic chest pain, acute pericarditis, aortic d
issection
Gastrointestinal: gastroesophogeal reflux disease
Pulmonary embolism, pneumonia, pneumothorax
Musculoskeletal : Tietze's syndrome, cervical or thoracic spine disease, fibromy
algia, arthritis
Involvement of ribs by trauma, infections (Candida albicans) or neoplasms (breas
t cancer, prostate cancer, sarcoma, plasma cell cytoma)
Psychiatric: panic attack
Neuropathic pain involving the chest wall may also be confused or coexist with c
ostosternal syndrome. Examples of such neuropathic pain include diabetic polyneu
ropathies and acute herpes zoster involving the thoracic nerves.
Treatment:
(NSAIDs)
Local heat and cold
elastic rib belt
For conditions that do not respond to these treatment modalities, the following
injection technique with local anesthetic and steroid may be a reasonable next s
tep.
For intra-articular injection of the costosternal joint, the patient is placed i
n the supine position. Proper preparation with antiseptic solution of the skin o
verlying the affected costosternal joints is carried out. A sterile syringe cont
aining 1 ML of 0.25% preservative-free bupivacaine for each joint to be injected
and 40 mg of methylprednisolone is attached to a 1.5-inch 25-gauge needle with
strict aseptic technique.
With use of strict aseptic technique, the costosternal joints are identified. Th
e costosternal joints should be easily palpable as a slight bulging at the point
where the rib attaches to the sternum. The needle is advanced carefully through
the skin and subcutaneous tissues medially with a slight cephalad trajectory in
to proximity with the joint . If bone is encountered, the needle is withdrawn ou
t of the periosteum. After the needle is in proximity to the joint, 1 mL of solu
tion is gently injected. Limited resistance to injection should be found. If sig
nificant resistance is encountered, the needleshould be withdrawn slightly until
the injection proceeds with only limited resistance. This procedure is repeated
for each affected joint. The needle is removed, and a sterile pressure dressing
and ice pack are placed at the injection site.

Intercostal Neuralgia
Iintercostal neuralgia is neuropathic
If the subcostal nerve is involved, patients may believe they are suffering from
gallbladder disease.
Causes:
Occurs commonly after thoracotomy. It can also be seen in elderly debilitated pa
tients without a known precipitating event. Other causes include rib trauma, ben
ign periosteal lipoma and pregnancy.
Clinical features:
The pain is constant and burning in nature and may involve any of the intercosta
l nerves as well as the subcostal nerve of the twelfth rib.
The pain usually begins at the posterior axillary line and radiates anteriorly i
nto the distribution of the affected intercostal or subcostal nerves, or both.
Deep inspiration or movement of the chest wall may slightly increase the pain of

intercostal neuralgia, but to a much lesser extent compared with the pain assoc
iated with the musculoskeletal causes of chest wall pain, such as costosternal j
oint pain, Tietze's syndrome, and broken ribs.
Pain is unilateral
Has typical features of neuropathic pain
dysesthesias, paroxysmal pain and allod
ynia
o
Dysesthetic pain is an abnormal sensation described as unpleasant. Patie
nts commonly use the terms such as aching, cramping, pressure and heat to descri
be a dysesthetic pain.
o
Paroxysmal pain is pain that comes in waves and is often described as la
ncinating or electric.
o
Allodynia is abnormal perception of pain after a normally non-painful me
chanical or thermal stimulus. Patients with allodynia respond to light touch wit
h an exaggerated pain response or report a sensation of heat when a cold stimulu
s is applied.
Physical examination generally reveals minimal findings unless the patient has a
history of previous thoracic or subcostal surgery or cutaneous evidence of herp
es zoster involving the thoracic dermatomes.
Unlike patients with musculoskeletal causes of chest wall and subcostal pain, th
ose with intercostal neuralgia do not attempt to splint or protect the affected
area.
Careful sensory examination of the affected dermatomes may reveal decreased sens
ation or allodynia.
When motor involvement of the subcostal nerve is significant, the patient may co
mplain that his or her abdomen bulges outward.
Diagnosis:
Plain radiographs
If trauma radionuclide bone scanning
complete blood count,
prostate-specific antigen level,
erythrocyte sedimentation rate,
antinuclear antibody testing.
Computed tomography of the thoracic contents is indicated if an occult mass is s
uspected.
Differential diagnosis:
Cardiac or gallbladder origin
Trauma
Tietze's syndrome
diabetic polyneuropathies
acute herpes zoster
Treatment:
Initial
non-steroidal anti-inflammatory
Ifdo not control
tricyclic antidepressant /gabepentin should be added.
heat and cold
The use of an elastic rib belt
The patient is placed in the prone position with the patient's arm hanging loose
ly off the side of the cart. Alternatively, this block can be done with the pati
ent in the sitting or lateral position. The rib to be blocked is identified by p
alpating its path at the posterior axillary line. Subsequent daily nerve blocks
are carried out in a similar manner, substituting 40 mg methylprednisolone for t
he initial 80-mg dose. Because of the overlapping innervation of the chest and u
pper abdominal wall, the intercostal nerves above and below the nerve suspected
of subserving the painful condition will have to be blocked.

Post-Thoracotomy, Post-Cardiac Surgery Post-Mastectomy Pain Syndromes

Introduction:
Chronic post-surgical pain after thoracotomy, cardiac surgery and mastectomy can
last for several months to years.
Post- thoracotomy pain syndrome describes chronic pain conditions that last beyo
nd the expected recovery after thoracotomy
Persistent anterior chest wall and sternal pain are common after cardiac surgery
Post mastectomy pain is common after radical mastectomy, lumpectomy or any other
surgical procedures involving the breast.
Causes:
Post-thoracotomy pain:
The common causes are surgical exploration and damage to ribs, retractor compres
sion or stretch of intercostal nerves and consequent formation of neuroma. It ma
y be nociceptive pain related to injury of musculoskeletal structures or neuropa
thic pain of intercostal nerves.
Post- cardiac surgery pain:
The potential causes are sternal wires, sternal or costosternal instability and
intercostal neuralgia due to dissection of internal mammary artery from the ches
t wall.
Post-mastectomy pain:
Commonly associated with axillary dissection and surgical injury of an intercost
obrachial nerve. Neuropathic mechanism plays a major role.
Clinical Features:
Post-thoracotomy pain:
Presents with severe chest wall pain aggravated by deep respiratory movement.
Physical examination general y reveals tenderness along the healed thoracotomy i
ncision.
Occasionally, palpation of the scar elicits paresthesias, a finding suggestive o
f neuroma formation.
Patients suffering from post-thoracotomy syndrome may attempt to splint or prote
ct the affected area.
Careful sensory examination of the affected dermatomes may reveal decrease sensa
tion or allodynia.
Post- cardiac surgery pain:
Post-cardiac surgery pain may consist of pain and tenderness over the costostern
al region in addition to other findings similar to those of post-thoracotomy pai
n syndrome.
Post-mastectomy pain:
Post-mastectomy pain syndrome involves the breast, anterior chest wall, axilla a
nd the medial aspect of the arm.
Patients complain of numbness and tingling, burning and stabbing pain.
Diagnosis:
There is no specific test for confirmation of these pain syndromes.
Plain radiographs are ordered as a first step to rule out bone pathology, includ
ing unsuspected fracture or tumor.
Radionuclide bone scanning may be useful to exclude occult fractures of the ribs
or sternum
Computed tomography scanning of the thoracic contents is indicated if an occult
mass or pleural disease is suspected
Based on the patient's clinical presentation, additional testing may be warrante
d, including a complete blood count, prostate-specific antigen level, erythrocyt
e sedimentation rate, and antinuclear antibody testing.
Treatment:
Pharmacotherapy:
Acetaminophen, non-steroid anti-inflammatory drugs (NSAIDS)
skeletal muscle relaxants
Anticonvulsants,
tricyclic antidepressants (TCA's), serotonin or epinephrine reuptake inhibitors

(SNRI's), and sodium channel blocking

opioids
Non-Pharmacological approaches:
Physical and occupational therapy are essential components of comprehensive mana
gement after thoracotomy and mastectomy. Common hands-on and physical modalities
including manipulation, adjustments, massage, ultrasound, and transcutaneous el
ectric nerve stimulation (TENS)
Interventional procedures:
A thoracic epidural catheter
pre-emptive and perioperative analgesia should be considered to minimize the inc
idence of phantom breast.
Thoracic paravertebral nerve blocks
Intercostal nerve or brachial plexus block with local anesthetic and corticoster
oid are indicated as both for diagnostic and therapeutic approaches for post tho
racotomy or post mastectomy pain. Cervicothoracic sympathetic block for alleviat
ion of sympathetic overlay,
whether brachial plexopathy or complex regional pain syndrome (CRPS) as a workin
g diagnosis after thoracotomy, cardiac surgery, mastectomy.
Cryoanalgesia offers a useful technique that does not cause any long term histol
ogical damage to intercostal nerves and is thus without serious side effects.
Neuromodulation therapy, such as a trial of peripheral nerve stimulation or deep
brain stimulation,