Invasive treatment of TN

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Transcript Invasive treatment of TN

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The majority of CH patients will achieve
satisfactory results with pharmacologic treatment.
For those who remain refractory to medical
treatment, a number of invasive procedures are
available. These include peripheral nerve blocks,
peripheral or central neurostimulation and ablative
surgery. Peripheral nerve block, mostly targeting
the greater occipital nerve (GON), may also be used
in less refractory patients, as an adjunct to
pharmacologic therapy.
If all drug treatment procedures are ineffective
and a secondary cluster headache has been excluded,
surgical treatment can be discussed with the
patient. Surgical procedures should be considered with
great caution because no reliable long-term data are
available and because they can induce trigeminal
neuralgia or anaesthesia dolorosa :
1-application of glycerol or local anaesthetics into the
cisterna trigeminalis of the Gasserian ganglion
2-radiofrequency rhizotomy of the Gasserian ganglion
3-microvascular decompression
4-resection or blockade of the N petrosus superficialis
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Hypothalamic deep-brain stimulation (hDBS)
acts rapidly and has lasting efficacy, but is
not without risk
Patient
Duration
of chronic
phase
(years
Outcome
45, M
2
Unstable for 7months Pain-free
for 5 months Recent relapse
34, M
5
Relief for 8 months,
Pain-free for the last 5 months
53, M
5
Panic and vegetativedysfunction
during
procedure
2
Pain-free for 9 months Relapse
51, M
4
Pain-free for the last 3 months
51, F
9
Died from ic haemorrhage
46, M
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1- Patients received lidocaine 2% (0.5 mL)
with either betamethasone or saline. CH
attacks disappeared within 72 hours for 4
weeks in 61% of the lidocaine +
betamethasone group compared with none of
those in the lidocaine + saline group.
Injections were well tolerated
2- Nerve blockade was achieved using 3 mL
of lidocaine 1% with triamcinolone 40 mg.
64% of the patients had a good or moderate
response
In general, it has to be said that
any surgical procedure on peripheral trigeminal
structures
in episodic cluster headache has to be judged with
great caution, as the natural course of the disease
includes remission.
On the other hand, in chronic cluster
headache, there is strong evidence that even a
complete
trigeminal denervation is not effective in
preventing
headache attacks or autonomic symptoms .
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The cisternal segment of the nerve was
targeted with a single 4 mm collimator (80–
85 Gy max
Robert G Ford in 1988
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Surgery may be recommended, either to
relieve the pressure on the nerve or to
selectively damage it in such a way as to
disrupt pain signals from getting through to
the brain. In trained hands, surgery has been
reported to have an initial success rate
approaching 90 percent
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Microvascular decompression, also known as the
Jannetta procedure,is the only one aimed at fixing
the presumed cause of the pain. In this
procedure, the surgeon enters the skull through a
25-millimetre (1 in) hole behind the ear. The
nerve is then explored for an offending blood
vessel, and when one is found, the vessel and
nerve are separated or "decompressed" with a
small pad, usually made from an inert surgical
material such as Teflon. When successful, MVD
procedures can give permanent pain relief with
little to no facial numbness.
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Other procedures use needles or catheters that
enter through the face into the opening where
the nerve first splits into its three divisions. Some
have excellent success rates using a costeffective percutaneous surgical procedure known
as balloon compression have been
reported.This technique has been helpful in
treating the elderly for whom surgery may not be
an option due to coexisting health conditions.
Balloon compression is also the best choice for
patients who have ophthalmic nerve pain or have
experienced recurrent pain after microvascular
decompression.
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The trigeminal ganglion is located
intracranially and measures approximately 1
× 2 cm. In its intracranial location, it lies
lateral to the internal carotid artery and
cavernous sinus and slightly posterior and
superior to the foramen ovale, through which
the mandibular nerve leaves the cranium
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Patients are placed in a supine position and
asked to fix their gaze straight ahead, as if they
were looking off into the distance. The
anesthesiologist should be positioned at the
patient’s side, slightly below the level of the
shoulder, so that by looking toward the patient’s
face . A skin wheal is raised immediately medial
to the masseter muscle, which can be located by
asking the patient to clench the teeth . (It most
often occurs approximately 3 cm lateral to the
corner of the mouth.
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A 22-gauge, 10-cm needle is inserted through
this site. The plane of insertion should be in line
with the pupil. This allows the needle tip to
contact the infratemporal surface of the greater
wing of the sphenoid bone, immediately anterior
to the foramen ovale. This occurs at a depth of
4.5 to 6 cm. Once the needle is firmly positioned
against this infratemporal region, it is withdrawn
and redirected in a stepwise manner until it
enters the foramen ovale at a depth of
approximately 6 to 7 cm, or 1 to 1.5 cm past the
needle length required to contact the bone
initially
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The nerve can also be damaged to prevent
pain signal transmission using Gamma Knife
or a linear accelerator-based radiation
therapy
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No incisions are involved in this procedure. It uses very
precisely targeted radiation to bombard the nerve. This
option is used especially for those people who are
medically unfit for a long general anaesthetic, or who are
taking medications for prevention of blood clotting (e.g.,
warfarin, heparin, aspirin). It also may be used for those
who may need to have a less invasive procedure.
A prospective Phase I trial performed at Marseille, France,
showed that 83% of patients were pain-free at 12 months,
with 58% pain-free and off all medications. Side effects
were mild, with 6% experiencing mild tingling and 4%
experiencing mild numbness.
However, there is no guarantee for a permanent success
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This surgery has only recently been initiated
in the US and involves removing the
corrugator muscle found above the eyebrows.
The theory is that the surgery eliminates
migraines by eliminating the muscle,
responsible for negative interaction with
nerves around the area creating the
migraines.
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The surgery targets the trigger point where
migraine headaches usually begin. On
eliminating the muscle, the point at which it
interacts with surrounding nerves, which creates
the debilitating pain and pressure is removed.
This procedure does not help all migraines. It will
only work for corrugator muscle triggered
migraines and the specific nerve group in the
head. A screening test must be done to
determine if this trigger is the cause and if the
patient is a suitable candidate for the surgery.
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Occipital nerve block is a procedure where
anesthetic agents (lidocaine and bupivacaine) are
injected near the occipital nerve on the back of
the head near the base of the skull on the side of
the migraine headache. Within five minutes after
the nerve block, 60% of patients had mild or no
headache and 75% of patients had mild or no
light sensitivity (photophobia). The investigators
of the study concluded that greater occipital
nerve blocks are safe and easy procedures that
can be performed in the office and show results
more quickly than oral triptan medications.
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a recent study presented at the American
Academy of Neurology suggested that up to
60% of patients with an acute migraine may
respond without return of the
headache. Adding steroid medication to the
local anesthetic does not seem to improve
outcome. However, occipital nerve block with
steroid medication (Depo-Medrol, Celestone,
and other) is effective in aborting cluster
headaches.
The greater occipital artery, which serves as the most
reliable landmark, is palpated. TCD ultrasonography
can be used to easily and precisely detect pulsation
of the greater occipital artery. The patient was placed
in the prone position, and the 8-MHz probe was
manipulated along the superior nuchal ridge until the
blood flow in the occipital artery was audible and
visible.
After the pulsating vessel was identified, a 25gauge 1.5-inch needle was inserted just medial to the
point of pulsation, and a local anesthetic was injected
around the artery.
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The mechanism of Botox is complex. When
botulinum neurotoxin is injected into a target
tissue, a series of events occur, blocking the
release of acetylcholine which result in flaccid
paralysis .
Botulinum toxin has been found to have no direct
effects on the central nervous system .
On the spinal level, botulinum toxin is capable
of producing reflex inhibition of the muscle
spindle organ.
On the supraspinal level, studies have shown that
botulinum toxin can normalize altered
intracortical inhibition and altered
somatosensory evoked potentials
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Botox treatment for painful conditions such
as headaches: Chronic daily headaches
pertain to a group of headache disorders that
are defined by the presence of headaches
greater than 15 days per month for more
than three months . These can include both
tension-type headaches, cervicogenic
headaches and migraine headaches,
Head/Neck Area
Recommended Dose (Number of
Sitesa
Frontalis
20 Units divided in 4 sites
Corrugator
10 Units divided in 2 sites
Procerus
5 Units in 1 site
Occipitalis
30 Units divided in 6 sites
Temporalis
40 Units divided in 8 sites
Trapezius
30 Units divided in 6 sites
Cervical Paraspinal
Muscle Groupb
20 Units divided in 4 sites
Total Dose:
155 Units divided in 31 sites
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Anesthetic blockade of the occipital nerves and
supraorbital nerve have not provided significant
relief. Occipital nerve blockade helps in
distinguishing CPH and HC from cervicogenic
headache. Supraorbital nerve blockade may help
in distinguishing HC and supraorbital nerve
neuralgia (in which nerve block is markedly
effective).
Reliable evidence of efficacy of chiropractic
manipulation, acupuncture, or surgical
management in the treatment of CPH does not
exist.
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Neck pain and cervical muscle tenderness are
common and prominent symptoms of
primary headache disorders. Conversely, it is
plausible that head pain can be referred from
bony structures or soft tissues of the neck, a
condition called cervicogenic headache
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The anatomic locus for cervicogenic headache
is the trigeminocervical nucleus in the upper
cervical spinal cord, where sensory nerve
fibers in the descending tract of the
trigeminal nerve (trigeminal nucleus caudalis)
are believed to interact with sensory fibers
from the upper cervical roots.
The first three cervical spinal nerves and their
rami are the primary peripheral nerve
structures that can refer pain to the head
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Panel 1: Clinical criteria for the diagnosis of cervicogenic
headache
1 Unilateral headache without side-shift
2 Symptoms and signs of neck involvement: pain triggered
by neck movement or sustained awkward posture and/or
external pressure of the posterior neck or occipital region;
ipsilateral neck, shoulder, and arm pain; reduced range of
motion
3 Pain episodes of varying duration or flactuating
continuous pain
4 Moderate, non-excruciating pain, usually of a
non-throbbing nature
5 Pain starting in the neck, spreading to
oculo-fronto-temporal areas
6 Anaesthetic blockades abolish the pain transiently
provided complete anaesthesia is obtained, or occurrence
of sustained neck trauma shortly before onset
7 Various attack-related events: autonomic symptoms and
signs, nausea, vomiting, ipsilateral oedema and fl ushing
in the peri-ocular area, dizziness, photophobia,
phonophobia, or blurred vision in the ipsilateral eye