REVIEW
relief by morphine, used (in the form of laudanum) as a larger area than would be involved by a simple axon
panacea for all painful conditions in the late 18th and reflex. Brodal (1965) states that there is a visceral
19th centuries. This has important anatomical implica- afferent component in the distribution of the trigemi-
tions, for it is known that, at spinal cord and brainstem nal nerve; and taste fibers, of course, end in the
level, morphine acts principally in the substantia nucleus of the solitary tract. There are no well-
gelatinosa (presumably imitating the action of enkepha- documented reports of intrinsic brainstem connections
linergic stalked cells [Bennett et al., 1982] which are between visceral afferent and sensory trigeminal nu-
found in human substantia gelatinosa [Abdel-Maguid clei. However, two of the six neuron types found in the
and Bowsher, 1985]), where small primary afferent human solitary nucleus are also represented in the
fibers terminate, and has no effect on large (Ab) descending trigeminal nucleus; one of these is also
primary afferent fibers. found in the interpolar nucleus, and two others in the
The pain of trigeminal neuralgia is essentially principal sensory nucleus (Abdel-Maguid and Bow-
allodynia—i.e., a pain set off by a non-noxious stimu- sher, 1985), i.e., four out of six solitary neuron types are
lus. The vast majority of TGN attacks are provoked by represented in the trigeminal sensory complex.
gentle mechanical stimuli, such as a breeze blowing on Yet out of 126 successive TGN patients, 55.5% had
the face, attempting to wash the face with a flannel, their attacks exacerbated by cold and 38% by emo-
touching the gums with a toothbrush, or moving food tional stress; 19% were alleviated by a warm environ-
into contact with the oral mucosa. Kugelberg and ment, although two-thirds of patients said they knew
Lindblom (1959) suggested that the pain is subserved of no alleviating factors. However it should be noted
by Ab fibers. This was proven in the case of touch- that TGN sufferers generally have no difficulty in
evoked allodynia in ophthalmic post-herpetic neural- falling asleep, thereby demonstrating that relaxation
gia by Nurmikko et al. (1991), who showed that when effectively alleviates. It thus appears that the fre-
Ad and C fibers, but not Ab, are inactivated by local quency and/or intensity of TGN attacks may in some
anesthetic, allodynia still occurs; but it is abolished by instances be influenced by factors associated with
anesthesia of Ab fibers. In the present author’s series, visceral afferent input.
three patients were found in whom attacks were set off
by bright lights and/or loud noises (large fibers) and
IS THE PAIN IN THE DISTRIBUTION
three others in whom sugar (but no other substance) in
the mouth caused pain; taste buds are innervated by
OF THE NERVE?
small fibers. All clinical textbooks and articles (and patients!)
A personal observation of the present author sup- describe and/or illustrate the pain as spreading out-
ports this: careful questioning of TGN sufferers elicits wards from the trigger point to cover an area which
the information that while the pain shoots into the roughly approximates to the territory of distribution of
gums, it is never felt within the teeth themselves— one (or more) of the trigeminal divisions. Pain never
from which latter Ab fibers are absent. This did not appears to be distributed proximo-distally and rarely
prevent 27% of these patients from consulting a disto-proximally along the anatomically defined
dentist in the first instance. 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
WHAT ABOUT AUTONOMIC INFLUENCES?
the pain is felt (White and Sweet, 1969), or even in a
Orthodox anatomical teaching takes great care to limb (Crue et al., 1956; White and Sweet, 1969).
emphasize that although autonomic fibers (mostly Reference to triggers in the distribution of the chorda
from the sphenopalatine ganglion and to a lesser tympani, eighth and second cranial nerves has already
extent from the otic and submandibular ganglia) are been made. On the other hand, it must be borne in
distributed with the trigeminal nerve, the trigeminal mind that pain does not occur outside the distribution
nerve itself does not have any autonomic component of the fifth cranial nerve.
in the sense that such fibers emanate from, or end in,
the motor and sensory trigeminal nuclei respectively.
IS ANYTHING WRONG WITH THE NERVE?
White and Sweet (1969) reported facial flushing and
eye-watering during attacks. It has been noted that Young (1977), examining a single case, reported that
when an electrode is inserted into the trigeminal there are 124,000 fibers in the normal human trigemi-
ganglion through the cheek and foramen ovale, in- nal sensory root, half of which are unmyelinated. He
tense vasodilation occurs, often involving the whole pointed out that this proportion of myelinated fibers,
side of the face (Bowsher et al., 1988); this is a much also found in the cat and baboon, is considerably
Trigeminal Neuralgia and Anatomy 411
higher than that found in mammalian dorsal spinal They found deficits for touch (using von Frey fila-
roots, in which the figure is about 25% (Williams et al., ments), warmth, and cold sensations (using the Mar-
1989). It is therefore interesting to compare TGN with stock thermode [Fruhstorfer et al., 1976]) in the
the ‘‘lightning pains’’ of anticonvulsant-relieved tabes affected divisions. In agreement with Nurmikko (1991),
dorsalis (Bowsher et al., 1987), in which loss of deep they found no deficit for heat pain or for pinprick
pain sensation suggests loss of C fiber function, and in (sharpness) sensation (Chan et al., 1992).
which reaction time to intense stimuli is also greatly While a significant deficit for heat pain1 is not
delayed (see below). Taken together, these facts may found in any neurogenic pain condition (Bowsher,
suggest that an increase in the myelinated:unmyelin- 1991), pinprick deficit is a marked feature of all other
ated ratio in the root entry zone predisposes towards neurogenic pains—post-herpetic neuralgia (Nurmikko
the initiation of paroxysmal pains. and Bowsher, 1990), central post-stroke pain (Bow-
Much painstaking work has been performed by sher, 1996), painful diabetic neuropathy (Benbow et
light microscopists on peripheral portions of the tri- al., 1994) and reflex sympathetic dystrophy (McGlone
geminal nerve in the vain attempt to find abnormali- and Dhar, 1996)—as are critical deficits for warm and
ties, including that ultimate chimera, the ephapse. cold. Touch may or may not be affected, and is not
Exception must be made for the not inconsiderable essential. Thus the pattern of sensory deficit in TGN,
proportions of cases of TGN associated with multiple apart from being quantitatively very small, differs from
sclerosis (MS), when plaques (and sometimes com- that in all other neurogenic pains in not involving
pressing vessels as well) are usually found at the pinprick (sharpness).
attachment of the nerve to the pons. From 2 to 10% of The most striking feature in the investigation of
TGN cases are due to MS (authors vary in their TGN patients by Bowsher et al. (1997), however, was
estimates) and TGN is 100 times commoner in the MS the finding that there was a deficit for touch (but not
population than in the population at large. There is for thermal modalities) in the unaffected divisions on
also a powerful but completely unexplained associa- the affected side.
tion of TGN with peroneal muscular atrophy (Charcot- Recording from the juxtapontine proximal root of
Marie-Tooth disease). It is also reported that about the trigeminal nerve following stimulation of affected
10% of cases are due to cerebellopontine angle tumors supra-orbital, infra-orbital or mental nerves in cases of
(Cheng et al., 1993) compressing the nerve; but such trigeminal neuralgia due to vascular compression (see
cases are not, of course, idiopathic. below), Leandri et al. (1996) have shown that there are
either changes in conduction velocity or a reduction in
evoked potential amplitude.
FUNCTIONAL ASPECTS Kugelberg and Lindblom (1959) had noted that
Using liquid crystal contact thermography, Hardy there is a measurable delay of 15 sec or more between
and Bowsher (1989) observed that there is cutaneous stimulation of a trigger point and the onset of a painful
vasoconstriction in the painful region, even in the paroxysm, when in fact the conduction time from
absence of attacks. This was subsequently verified by periphery to consciousness would be of the order of 20
skin thermometry by Hampf et al. (1990), who found a msec. There is also an absolute, followed by a relative,
median temperature difference of 0.5–0.75°C between refractory period following an attack, during which
the affected region and the mirror-image area on the further paroxysms cannot be elicited by trigger-point
unaffected side. Interestingly, these authors found stimulation. Some patients exploit this by deliberately
that the vasoconstriction disappeared when the pain triggering a paroxysm before putting a bolus of food
was relieved by radiofrequency thermocoagulation, into the mouth and masticating it.
but re-appeared if and when the pain recurred.
The majority of authors concur in stating that there WHAT CAN WE LEARN FROM
are no clinically evident sensory deficits, although THERAPEUTIC PROCEDURES?
Lewey and Grant (1938) claimed to have found some
Medical
rather inconsistent changes. However, quantitative
instrumental evaluation of sensory perception thresh- Trousseau (1853) likened TGN to sensory epilepsy.
olds has altered the situation. Nurmikko (1991) exam- Although Bergouignan (1942) obtained some success
ined 26 patients and found deficits for tactile and
warm sensations in the affected area. More recently, 1Although coolness, warmth, and heat pain are all conveyed by small primary
Bowsher et al. (1997) have investigated 50 affected afferent fibers in the periphery, an interesting difference in anatomical
organization can be demonstrated by using thermodes of different sizes:
divisions in 28 patients and compared them with there is summation (convergence on central neurones) for warmth and
unaffected divisions on the same and opposite sides. coolness, but not for heat pain.
412 Bowsher
with phenytoin, it was not until the introduction of of destroying the trigeminal ganglion, in whole or in
carbamazepine, a tricyclic anticonvulsant, by Blom in part. This was done at first by the injection of alcohol
1962, that medical control of TGN became a real (Harris, 1912) or phenol-with-glycerine. Partial section
possibility. It turns out that some other anticonvulsants of the proximal root of the trigeminal nerve had
(e.g., Na valproate, lamotrigine) can also be (less) already been introduced by Spiller and Frazier in 1901,
effective; but so can some other tricyclics (e.g., amitrip- though it did not come into general use until the 1930s
tyline). So is TGN a form of sensory epilepsy, or is it a and later. A great advance was made when Sweet and
neurogenic pain like post-herpetic neuralgia? Ba- Wepsic (1974) introduced radiofrequency thermocoagu-
clofen, an antispastic drug, has also been found to be lation of the trigeminal ganglion and retroganglionic
effective in controlled trials (Fromm et al., 1984); and root, a procedure which brings about a preferential
baclofen shares with carbamazepine and phenytoin destruction of small fibers, as could be shown by
the ability to depress the response of mechanoceptive comparing pre- and post-operative threshold testing
neurons in the cat’s trigeminal nucleus oralis (Fromm (Hampf et al., 1990). Håkanson (1981) introduced the
et al., 1981). gentle technique of glycerol injection into the trigemi-
Very recently, some success has been claimed for nal cave, which caused some damage to small ganglion
gabapentin, a GABA-aminobutyric acid facilitator li- cells by sucking water out of them.
censed for use as an anticonvulsant (Ranieri et al., Surgical compression of the trigeminal nerve was
1996). Since mechanical allodynia (of which TGN introduced in the middle 1950s. It has enjoyed great
almost exclusively consists) is mediated peripherally popularity in Italy in recent decades (see Lobato et al.,
by rapidly adapting Ab low-threshold mechanorecep- 1990). Again, this procedure theoretically inactivates
tors (Nurmikko et al., 1991) (and suppressed by the the most susceptible nerve cells and fibers as a result
activation of slowly adapting Ab low-threshold mecha- of relative ischemia.
noreceptors), one would expect there to be a tendency What all these methods have in common is that
for the suppression of this input by the activation of they totally or partially destroy the nerve (or part
GABA-ergic islet cells in the substantia gelatinosa thereof), producing greater or lesser degrees of sensory
(Todd and McKenzie, 1989). The fact that gabapentin loss or impairment. In addition to this disadvantage, all
sometimes does so would appear to confirm the of them can be followed by recurrence of the trigemi-
hypothesis about the manner in which mechanical nal neuralgia. Worst of all, a proportion of patients
allodynia is mediated in TGN. However, the fact that subsequently develop anesthesia dolorosa, such that
carbamazepine is the most effective anticonvulsant in their last state is worse than their first.
the relief of TGN may to some extent militate against The notion that the proximal trigeminal root might
this: carbamazepine binds to a large number of recep- be compressed by an aberrant blood vessel has been
tors on neurones, not all of which are known; but around for some time (see Dandy, 1934). The introduc-
GABA receptors do not appear to be among them. tion of the operating microscope led to increasing use
Carbamazepine is by far the most widely used and of microvascular decompression as a treatment for
(currently) effective drug in TGN. It has, however, a TGN (Janetta, 1976). The ability to visualize and
wide range of undesirable side-effects, some of which localize aberrant blood vessels by means of advances
(particularly wooziness) are dose-dependent. A minor- in radiographical techniques (Meaney et al., 1994)
ity of patients are unable to use it from the word go. (Fig. 1) has led to a much more widespread and
Others find that, as increasing doses are required due effective use of microvascular decompression (Barker
to habituation/adaptation, side-effects become intoler- et al., 1996). Although it involves posterior fossa
able. For those to whom neither of the foregoing apply, craniotomy, microvascular decompression is a surpris-
it is eventually found that the drug ceases adequately ingly untraumatic operation which can safely be per-
to control the painful paroxysms. When drug therapy formed on otherwise fit patients well into their 80s.
cannot be used, some kind of invasive procedure is Intraoperative monitoring of eighth cranial nerve func-
usually called for. tion by the elicitation and recording of auditory
evoked potentials avoids the commonest operative
Surgical complication.
The number and type of interventions that have Is neurovascular contact the cause of TGN? Barker
been undertaken in the hope of relieving TGN are et al. (1996) found such contacts in 96% of cases,
legion. The earliest was peripheral neurectomy/ Meaney et al. (1995a) in 93%. In their earlier report on
neurotomy and avulsion of peripheral nerve branches— 38 TGN patients with positive findings, Meaney et al.
the latter is still practiced, particularly by maxillo- (1994) stated that in 30 instances (79%) the offending
facial surgeons. This was followed by various methods vessel was the superior cerebellar artery; in four
Trigeminal Neuralgia and Anatomy 413
turn of measurable electrophysiological nerve function Barker, F.G., P.J. Janetta, D. Bissonette, M.V. Larkins and H.H.
in the decompressed proximal nerve root. Jho 1996 The long-term outcome of microvascular decom-
The fact that TGN is confined to the distribution of pression for trigeminal neuralgia. New Engl. J. Med. 334:
1077–1083.
trigeminal divisions, but fails to respect the distribu-
Benbow, S.J., A.W. Chan, D. Bowsher, I.A. MacFarlane and G.
tion of individual nerve branches, may be thought to Williams 1994 A prospective study of painful symptoms,
implicate the sensory trigeminal nuclei. Which? Sjö- small-fibre function and peripheral vascular disease in chronic
qvist’s (1938) trigeminal tractotomy at the level of the painful diabetic neuropathy. Diabetic Med. 11:17–21.
obex was aimed at the descending intramedullary root Bennett, G.J., M.A. Ruda, S. Gobel and R. Dubner 1982
of the nerve supplying the spinal (descending) nucleus, Enkephalin-immunoreactive stalked cells and lamina IIb islet
while Fromm’s (Fromm et al., 1981, 1984) drug hypoth- cells in cat substantia gelatinosa. Brain Res. 240:162–166.
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