Clinical Anatomy 10:409–415 (1997)

REVIEW

Trigeminal Neuralgia: An Anatomically Oriented Review

DAVID BOWSHER*
Pain Research Institute, Walton Hospital, Liverpool, United Kingdom

Trigeminal neuralgia (TGN) is a peculiarly painful paroxysmic disorder with an annual

incidence of 4.3 per 100,000, which undergoes spontaneous remissions and recurrences. The
pain, which is subserved by large, not small, fibers, can in some cases be triggered from outside
the trigeminal territory and by other than mechanical stimuli. There are strong autonomic
influences on the pain, and there is cutaneous vasoconstriction in the trigeminal territory in
which it occurs. There are also sensory perception deficits for temperature in the affected
region and for touch in the whole trigeminal territory. There is now increasing evidence that the
majority of cases are caused by vascular compression of the fifth nerve at its point of entry into
the pons, for the pain can be relieved (with restoration of the sensory deficit) by surgical
decompression. No anatomical abnormalities of the (peripheral) trigeminal nerve have ever
been satisfactorily demonstrated. Arguments are examined for the hypothesis that TGN is
essentially a disorder of central processing, the term being taken to include the oligodendroglial-
sheathed proximal segment of the nerve. Clin. Anat. 10:409–415, 1997. r 1997 Wiley-Liss, Inc.

Key words: trigeminal nerve; trigeminal neuralgia; autonomic nervous system;

sensory deficit; vascular compression

INTRODUCTION Donald (1957) reported that one-half of TGN patients

Attacks of trigeminal neuralgia (TGN) are among
the most painful experiences known. In a series of 126
successive cases investigated by the author, mean pain
score was rated as 94.32 6 10.85 and median as 100 out
of 100 on the Visual Analogue Scale. The incidence of
new cases (in Rochester, Minnesota) is 4.3 per 100,000
per year (Yoshimasu et al., 1972), with a female:male
ratio of 1.17:1 (Rothman and Monson, 1973), a predomi-
nance of onset in the sixth and seventh decades, and
right-left ratio of 3:2 (White and Sweet, 1969). In 70%
of our cases, only one division was affected, the second
division being the most frequently affected (52%),
followed by the third (39%); two divisions were
affected in 25% of our patients.
The essential features of idiopathic trigeminal neu-
ralgia are defined by the International Association for
the Study of Pain (IASP) as sudden, transient, intense
bouts of superficially located pain, strictly confined to
the distribution of one or more divisions of the tri-
geminal nerve usually precipitated by light mechani-
cal activation of a trigger point or area. No sensory or
reflex deficit is detectable by routine neurologic testing.
To this ‘‘official’’ description should be added the
interesting, inexplicable, and no doubt important fact
that spontaneous remissions occur. Rushton and Mc-
have remissions lasting for 6 months or more, and
one-quarter for 1 year or more.
For the history of this unique disease, one cannot do
better than read Terrence (1987). He quotes the first
recognizable description as having been given by the
Persian physician Jurjani (1066–1136); and the first
Western description in the obituary of J.L. Bausch,
written by J. Fehr and E. Schmidt in 1688, prior to the
famous description by N. André in 1756.
What it is perhaps more salutary to recall, turning to
the era of modern medicine, is that it was in 1853 that
Trousseau described trigeminal neuralgia as a form of
sensory epilepsy, but another 89 years elapsed before
its treatment by an anticonvulsant (phenytoin) was
recommended (Bergouignan, 1942).
WHAT KIND OF FIBERS SUBSERVE
THE PAIN?
Implicit in the preceding paragraph is the fact that
the pain of trigeminal neuralgia is not susceptible to
*Correspondence to: David Bowsher, M.D., Ph.D., F.R.C.P.Ed.,
F.R.C.Path., Pain Research Institute, Walton Hospital, Liverpool
L9 1AE, U.K. E-mail: pri@liv.ac.uk.
Received 6 January 1997; Revised 31 January 1997

r 1997 Wiley-Liss, Inc.

410 Bowsher
relief by morphine, used (in the form of laudanum) as a
panacea for all painful conditions in the late 18th and
19th centuries. This has important anatomical implica-
tions, for it is known that, at spinal cord and brainstem
level, morphine acts principally in the substantia
gelatinosa (presumably imitating the action of enkepha-
linergic stalked cells [Bennett et al., 1982] which are
found in human substantia gelatinosa [Abdel-Maguid
and Bowsher, 1985]), where small primary afferent
fibers terminate, and has no effect on large (Ab)
primary afferent fibers.
The pain of trigeminal neuralgia is essentially
allodynia—i.e., a pain set off by a non-noxious stimu-
lus. The vast majority of TGN attacks are provoked by
gentle mechanical stimuli, such as a breeze blowing on
the face, attempting to wash the face with a flannel,
touching the gums with a toothbrush, or moving food
into contact with the oral mucosa. Kugelberg and
Lindblom (1959) suggested that the pain is subserved
by Ab fibers. This was proven in the case of touch-
evoked allodynia in ophthalmic post-herpetic neural-
gia by Nurmikko et al. (1991), who showed that when
Ad and C fibers, but not Ab, are inactivated by local
anesthetic, allodynia still occurs; but it is abolished by
anesthesia of Ab fibers. In the present author’s series,
three patients were found in whom attacks were set off
by bright lights and/or loud noises (large fibers) and
three others in whom sugar (but no other substance) in
the mouth caused pain; taste buds are innervated by
small fibers.
A personal observation of the present author sup-
ports this: careful questioning of TGN sufferers elicits
the information that while the pain shoots into the
gums, it is never felt within the teeth themselves—
from which latter Ab fibers are absent. This did not
prevent 27% of these patients from consulting a
dentist in the first instance.
WHAT ABOUT AUTONOMIC INFLUENCES?
Orthodox anatomical teaching takes great care to
emphasize that although autonomic fibers (mostly
from the sphenopalatine ganglion and to a lesser
extent from the otic and submandibular ganglia) are
distributed with the trigeminal nerve, the trigeminal
nerve itself does not have any autonomic component
in the sense that such fibers emanate from, or end in,
the motor and sensory trigeminal nuclei respectively.
White and Sweet (1969) reported facial flushing and
eye-watering during attacks. It has been noted that
when an electrode is inserted into the trigeminal
ganglion through the cheek and foramen ovale, in-
tense vasodilation occurs, often involving the whole
side of the face (Bowsher et al., 1988); this is a much
larger area than would be involved by a simple axon
reflex. Brodal (1965) states that there is a visceral
afferent component in the distribution of the trigemi-
nal nerve; and taste fibers, of course, end in the
nucleus of the solitary tract. There are no well-
documented reports of intrinsic brainstem connections
between visceral afferent and sensory trigeminal nu-
clei. However, two of the six neuron types found in the
human solitary nucleus are also represented in the
descending trigeminal nucleus; one of these is also
found in the interpolar nucleus, and two others in the
principal sensory nucleus (Abdel-Maguid and Bow-
sher, 1985), i.e., four out of six solitary neuron types are
represented in the trigeminal sensory complex.
Yet out of 126 successive TGN patients, 55.5% had
their attacks exacerbated by cold and 38% by emo-
tional stress; 19% were alleviated by a warm environ-
ment, although two-thirds of patients said they knew
of no alleviating factors. However it should be noted
that TGN sufferers generally have no difficulty in
falling asleep, thereby demonstrating that relaxation
effectively alleviates. It thus appears that the fre-
quency and/or intensity of TGN attacks may in some
instances be influenced by factors associated with
visceral afferent input.
IS THE PAIN IN THE DISTRIBUTION
OF THE NERVE?
All clinical textbooks and articles (and patients!)
describe and/or illustrate the pain as spreading out-
wards from the trigger point to cover an area which
roughly approximates to the territory of distribution of
one (or more) of the trigeminal divisions. Pain never
appears to be distributed proximo-distally and rarely
disto-proximally along the anatomically defined
branches of the ophthalmic, maxillary, or mandibular
nerves. Trigger zones may be located in the distribu-
tion of trigeminal divisions other than that in which
the pain is felt (White and Sweet, 1969), or even in a
limb (Crue et al., 1956; White and Sweet, 1969).
Reference to triggers in the distribution of the chorda
tympani, eighth and second cranial nerves has already
been made. On the other hand, it must be borne in
mind that pain does not occur outside the distribution
of the fifth cranial nerve.
IS ANYTHING WRONG WITH THE NERVE?
Young (1977), examining a single case, reported that
there are 124,000 fibers in the normal human trigemi-
nal sensory root, half of which are unmyelinated. He
pointed out that this proportion of myelinated fibers,
also found in the cat and baboon, is considerably

higher than that found in mammalian dorsal spinal
roots, in which the figure is about 25% (Williams et al.,
1989). It is therefore interesting to compare TGN with
the ‘‘lightning pains’’ of anticonvulsant-relieved tabes
dorsalis (Bowsher et al., 1987), in which loss of deep
pain sensation suggests loss of C fiber function, and in
which reaction time to intense stimuli is also greatly
delayed (see below). Taken together, these facts may
suggest that an increase in the myelinated:unmyelin-
ated ratio in the root entry zone predisposes towards
the initiation of paroxysmal pains.
Much painstaking work has been performed by
light microscopists on peripheral portions of the tri-
geminal nerve in the vain attempt to find abnormali-
ties, including that ultimate chimera, the ephapse.
Exception must be made for the not inconsiderable
proportions of cases of TGN associated with multiple
sclerosis (MS), when plaques (and sometimes com-
pressing vessels as well) are usually found at the
attachment of the nerve to the pons. From 2 to 10% of
TGN cases are due to MS (authors vary in their
estimates) and TGN is 100 times commoner in the MS
population than in the population at large. There is
also a powerful but completely unexplained associa-
tion of TGN with peroneal muscular atrophy (Charcot-
Marie-Tooth disease). It is also reported that about
10% of cases are due to cerebellopontine angle tumors
(Cheng et al., 1993) compressing the nerve; but such
cases are not, of course, idiopathic.
FUNCTIONAL ASPECTS
Using liquid crystal contact thermography, Hardy
and Bowsher (1989) observed that there is cutaneous
vasoconstriction in the painful region, even in the
absence of attacks. This was subsequently verified by
skin thermometry by Hampf et al. (1990), who found a
median temperature difference of 0.5–0.75°C between
the affected region and the mirror-image area on the
unaffected side. Interestingly, these authors found
that the vasoconstriction disappeared when the pain
was relieved by radiofrequency thermocoagulation,
but re-appeared if and when the pain recurred.
The majority of authors concur in stating that there
are no clinically evident sensory deficits, although
Lewey and Grant (1938) claimed to have found some
rather inconsistent changes. However, quantitative
instrumental evaluation of sensory perception thresh-
olds has altered the situation. Nurmikko (1991) exam-
ined 26 patients and found deficits for tactile and
warm sensations in the affected area. More recently,
Bowsher et al. (1997) have investigated 50 affected
divisions in 28 patients and compared them with
unaffected divisions on the same and opposite sides.
Trigeminal Neuralgia and Anatomy 411
They found deficits for touch (using von Frey fila-
ments), warmth, and cold sensations (using the Mar-
stock thermode [Fruhstorfer et al., 1976]) in the
affected divisions. In agreement with Nurmikko (1991),
they found no deficit for heat pain or for pinprick
(sharpness) sensation (Chan et al., 1992).
While a significant deficit for heat pain1 is not
found in any neurogenic pain condition (Bowsher,
1991), pinprick deficit is a marked feature of all other
neurogenic pains—post-herpetic neuralgia (Nurmikko
and Bowsher, 1990), central post-stroke pain (Bow-
sher, 1996), painful diabetic neuropathy (Benbow et
al., 1994) and reflex sympathetic dystrophy (McGlone
and Dhar, 1996)—as are critical deficits for warm and
cold. Touch may or may not be affected, and is not
essential. Thus the pattern of sensory deficit in TGN,
apart from being quantitatively very small, differs from
that in all other neurogenic pains in not involving
pinprick (sharpness).
The most striking feature in the investigation of
TGN patients by Bowsher et al. (1997), however, was
the finding that there was a deficit for touch (but not
for thermal modalities) in the unaffected divisions on
the affected side.
Recording from the juxtapontine proximal root of
the trigeminal nerve following stimulation of affected
supra-orbital, infra-orbital or mental nerves in cases of
trigeminal neuralgia due to vascular compression (see
below), Leandri et al. (1996) have shown that there are
either changes in conduction velocity or a reduction in
evoked potential amplitude.
Kugelberg and Lindblom (1959) had noted that
there is a measurable delay of 15 sec or more between
stimulation of a trigger point and the onset of a painful
paroxysm, when in fact the conduction time from
periphery to consciousness would be of the order of 20
msec. There is also an absolute, followed by a relative,
refractory period following an attack, during which
further paroxysms cannot be elicited by trigger-point
stimulation. Some patients exploit this by deliberately
triggering a paroxysm before putting a bolus of food
into the mouth and masticating it.
WHAT CAN WE LEARN FROM
THERAPEUTIC PROCEDURES?
Medical
Trousseau (1853) likened TGN to sensory epilepsy.
Although Bergouignan (1942) obtained some success
1Although coolness, warmth, and heat pain are all conveyed by small primary
afferent fibers in the periphery, an interesting difference in anatomical
organization can be demonstrated by using thermodes of different sizes:
there is summation (convergence on central neurones) for warmth and
coolness, but not for heat pain.
412 Bowsher
with phenytoin, it was not until the introduction of
carbamazepine, a tricyclic anticonvulsant, by Blom in
1962, that medical control of TGN became a real
possibility. It turns out that some other anticonvulsants
(e.g., Na valproate, lamotrigine) can also be (less)
effective; but so can some other tricyclics (e.g., amitrip-
tyline). So is TGN a form of sensory epilepsy, or is it a
neurogenic pain like post-herpetic neuralgia? Ba-
clofen, an antispastic drug, has also been found to be
effective in controlled trials (Fromm et al., 1984); and
baclofen shares with carbamazepine and phenytoin
the ability to depress the response of mechanoceptive
neurons in the cat’s trigeminal nucleus oralis (Fromm
et al., 1981).
Very recently, some success has been claimed for
gabapentin, a GABA-aminobutyric acid facilitator li-
censed for use as an anticonvulsant (Ranieri et al.,
1996). Since mechanical allodynia (of which TGN
almost exclusively consists) is mediated peripherally
by rapidly adapting Ab low-threshold mechanorecep-
tors (Nurmikko et al., 1991) (and suppressed by the
activation of slowly adapting Ab low-threshold mecha-
noreceptors), one would expect there to be a tendency
for the suppression of this input by the activation of
GABA-ergic islet cells in the substantia gelatinosa
(Todd and McKenzie, 1989). The fact that gabapentin
sometimes does so would appear to confirm the
hypothesis about the manner in which mechanical
allodynia is mediated in TGN. However, the fact that
carbamazepine is the most effective anticonvulsant in
the relief of TGN may to some extent militate against
this: carbamazepine binds to a large number of recep-
tors on neurones, not all of which are known; but
GABA receptors do not appear to be among them.
Carbamazepine is by far the most widely used and
(currently) effective drug in TGN. It has, however, a
wide range of undesirable side-effects, some of which
(particularly wooziness) are dose-dependent. A minor-
ity of patients are unable to use it from the word go.
Others find that, as increasing doses are required due
to habituation/adaptation, side-effects become intoler-
able. For those to whom neither of the foregoing apply,
it is eventually found that the drug ceases adequately
to control the painful paroxysms. When drug therapy
cannot be used, some kind of invasive procedure is
usually called for.
Surgical
The number and type of interventions that have
been undertaken in the hope of relieving TGN are
legion. The earliest was peripheral neurectomy/
neurotomy and avulsion of peripheral nerve branches—
the latter is still practiced, particularly by maxillo-
facial surgeons. This was followed by various methods
of destroying the trigeminal ganglion, in whole or in
part. This was done at first by the injection of alcohol
(Harris, 1912) or phenol-with-glycerine. Partial section
of the proximal root of the trigeminal nerve had
already been introduced by Spiller and Frazier in 1901,
though it did not come into general use until the 1930s
and later. A great advance was made when Sweet and
Wepsic (1974) introduced radiofrequency thermocoagu-
lation of the trigeminal ganglion and retroganglionic
root, a procedure which brings about a preferential
destruction of small fibers, as could be shown by
comparing pre- and post-operative threshold testing
(Hampf et al., 1990). Håkanson (1981) introduced the
gentle technique of glycerol injection into the trigemi-
nal cave, which caused some damage to small ganglion
cells by sucking water out of them.
Surgical compression of the trigeminal nerve was
introduced in the middle 1950s. It has enjoyed great
popularity in Italy in recent decades (see Lobato et al.,
1990). Again, this procedure theoretically inactivates
the most susceptible nerve cells and fibers as a result
of relative ischemia.
What all these methods have in common is that
they totally or partially destroy the nerve (or part
thereof), producing greater or lesser degrees of sensory
loss or impairment. In addition to this disadvantage, all
of them can be followed by recurrence of the trigemi-
nal neuralgia. Worst of all, a proportion of patients
subsequently develop anesthesia dolorosa, such that
their last state is worse than their first.
The notion that the proximal trigeminal root might
be compressed by an aberrant blood vessel has been
around for some time (see Dandy, 1934). The introduc-
tion of the operating microscope led to increasing use
of microvascular decompression as a treatment for
TGN (Janetta, 1976). The ability to visualize and
localize aberrant blood vessels by means of advances
in radiographical techniques (Meaney et al., 1994)
(Fig. 1) has led to a much more widespread and
effective use of microvascular decompression (Barker
et al., 1996). Although it involves posterior fossa
craniotomy, microvascular decompression is a surpris-
ingly untraumatic operation which can safely be per-
formed on otherwise fit patients well into their 80s.
Intraoperative monitoring of eighth cranial nerve func-
tion by the elicitation and recording of auditory
evoked potentials avoids the commonest operative
complication.
Is neurovascular contact the cause of TGN? Barker
et al. (1996) found such contacts in 96% of cases,
Meaney et al. (1995a) in 93%. In their earlier report on
38 TGN patients with positive findings, Meaney et al.
(1994) stated that in 30 instances (79%) the offending
vessel was the superior cerebellar artery; in four

Fig. 1. Axial (A) and parasagittal (B) views of the pons and
attachment of the fifth nerve in a case of right second division
trigeminal neuralgia. Magnetic resonance tomographic angiography,
without contrast. A: On the right (viewer’s left), the nerve root (white
arrow) can be seen running apparently dorsalwards as it leaves the
pons. The transversely cut superior cerebellar artery (black arrow) is
seen as a white dot clearly compressing the nerve at its entry into the
pons. On the left, the nerve root can again be seen (white arrow), with
the superior cerebellar artery (black arrow) well dorsal to it. B: This
oblique parasagittal cut illustrates the right side of the pons only. The
nerve root (white arrow) can be clearly seen coursing forwards (to the
left of the picture) from the pons. The superior cerebellar artery (black
arrow) can be seen as a white thread looping down onto the nerve root
from above, and reappearing as a white dot below the nerve, which is
constricted at its point of entry into the pons. Illustration kindly
provided by Mr. J.B. Miles, Consultant Neurosurgeon, and Dr. T.E.
Nixon, Consultant Neuroradiologist.
instances (10.5%) two arteries, the superior and ante-
rior inferior cerebellar, were implicated, while in the
other four (10.5%) the petrosal vein was found to be
compressing the nerve.
A post-mortem anatomical study by Hamlyn and
King (1992) suggested that vessels may be found in
contact with the fifth nerve root in 3% of subjects who
did not have TGN, while Meaney et al. (1994), using
Trigeminal Neuralgia and Anatomy 413
magnetic resonance tomographic angiography, re-
ported that 8% of subjects without TGN had a vessel
compressing the root of the fifth nerve. Follow-up has
not yet been long enough to determine whether or not
any of these subjects subsequently develop TGN.
It is particularly interesting that the majority of
suitably investigated patients with trigeminal neural-
gia associated with multiple sclerosis have vascular
compression, with or without concomitant demyelinat-
ing plaques at the root entry zone; this has been
demonstrated both radiologically (Meaney et al., 1995b)
and anatomically at autopsy (Crooks and Miles, 1996).
In view of this, it is tempting to suggest that the
concomitant presence of a compressing vessel and
increased susceptibility of the nerve will inevitably
lead to TGN—though such a theory does not explain
spontaneous remissions.
When TGN is relieved by surgical decompression,
pain relief is immediate. Evoked potential latency and
amplitude, measured at the proximal root, recover
within minutes (Leandri et al., 1996), as does the
median nerve following decompression for carpal tun-
nel syndrome (Gilliat, 1980). Within 72 hr of operation,
the deficit for warmth has disappeared (i.e., there is no
difference in threshold between the affected region
and its mirror-image on the contralateral side). Those
for the other affected modalities (touch and cold) have
greatly diminished, and have disappeared by the next
examination, carried out at 6 months. However, a rise
in pinprick threshold appears post-operatively, and
gradually lessens, being completely absent within 12
months of operation in patients who are pain-free
(Miles et al., 1997). Doubtless the pinprick deficit is
due to reversible functional damage to the nerve at the
time of operation, since it is not present pre-
operatively. But the fact that there is no discernible
sensory deficit in TGN patients who are painfree 12
months (and more) after microvascular decompression
appears to dispose of Adams’s (1989) hypothesis that
TGN is only relieved when the nerve is damaged and
sensation impaired.
IS THE FUNCTIONAL ABNORMALITY
IN TGN CENTRAL OR PERIPHERAL?
In favor of a peripheral abnormality is the fact of
(temporary) relief by avulsion or section of peripheral
nerve branches. However, it will be recalled that
headache (as well as TGN) can be relieved by decapi-
tation. More powerful arguments in favor of a periph-
eral origin are the immediate relief of pain and
restitution of other sensory functions following proce-
dures such as radiofrequency thermocoagulation and
microvascular decompression, and the immediate re-
414 Bowsher
turn of measurable electrophysiological nerve function
in the decompressed proximal nerve root.
The fact that TGN is confined to the distribution of
trigeminal divisions, but fails to respect the distribu-
tion of individual nerve branches, may be thought to
implicate the sensory trigeminal nuclei. Which? Sjö-
qvist’s (1938) trigeminal tractotomy at the level of the
obex was aimed at the descending intramedullary root
of the nerve supplying the spinal (descending) nucleus,
while Fromm’s (Fromm et al., 1981, 1984) drug hypoth-
esis concerns the more rostral nucleus oralis.
Clinical and therapeutic evidence point to the
epileptiform nature of the paroxysmal discharge which
occurs in TGN. The seat of epilepsy is generally
regarded to be the cerebral cortex (including the
hippocampal formation). The reaction time between
stimulus and response (Kugelberg and Lindblom,
1959) is certainly long enough to allow for the involve-
ment of a cortical loop.
The dissociated nature of the sensory deficit indi-
cates a disorder of central processing of afferent
information; and the fact that the tactile deficit spreads
to the distribution of uninvolved trigeminal divisions
also militates in favor of a central dysfunction. The
rare but verified instances in which afferent informa-
tion in nerves other than the trigeminal can trigger
attacks of TGN point in the same direction.
If, then, on balance, the abnormality is more likely
to be central than peripheral, the question arises: how
far central? Most of the evidence presented in this
review would appear to point to the root entry zone.
One vital piece of anatomical information is too
frequently overlooked. It is that axons in the proximal
root of a nerve, and in this instance particularly the
juxtapontine portion of the trigeminal nerve, have an
oligodendroglial and not a Schwann cell sheath. We
may thus expect them to behave as in the central
rather than as in the peripheral nervous system.
A few years ago, there was emphasis on the active
transport and transfer of electrolytes and other metabo-
lites by glial cells. Why should not glia also actively
transport (perhaps secrete) and transfer substances of
‘‘second messenger’’ type? Since the answer to this
question is not currently known, the hypothesis must
for the time being remain in the care of Aunt Sally; but
it is worth considering.
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