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12.7:
Central causes of head and facial pain other than tic douloureux
Resistent
atypical or unusual facial pain may come from central disease such as
thalamic infarction.
The IHS
lists two classifications of central causes of head and facial pain
other than trigeminal neuralgia, namely 12.7.1, anaesthesia dolorosa,
and 12.7.2, thalamic pain. The description of anaesthesia dolorosa is as
follows: Painful anaesthesia or dysaesthesia, often related to surgical
trauma or the trigeminal ganglion, evoked most frequently after
rhizotomy or thermocoagulation has been performed for treatment of
idiopathic trigeminal neuralgia. Anaesthesia dolorosa may also follow
upon trauma to the trigeminal complex, and, rarely, after vascular
lesions of the central trigeminal pathways.
The IHS
diagnostic criteria are:
 |
A.
Pain or dysaesthesia is limited to the distribution of one or more
division of the trigeminal nerve. |
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B.
Sensation to pinprick is diminished over the affected area. |
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C.
Symptoms follow a lesion of the trigeminal nerve or its central
projections. |
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Thalamic
pain is described as unilateral facial pain and dysaesthesiae attributed
to a lesion of the quintothalamic pathway or thalamus. Symptoms may also
involve the trunk and limbs of the affected side.
The IHS
diagnostic criteria for thalamic pain are:
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A.
Pain and dysaesthesiae of one half of the face, associated with
impaired sensation to pinprick, not explicable by a lesion of the
trigeminal nerve. |
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B.
One or more of the following: |
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1.
A history of sudden onset suggesting a vascular lesion. |
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2.
A remitting and relapsing history of symptoms in the face or
elsewhere suggesting multiple sclerosis. |
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3.
The demonstration of a lesion in an appropriate site by
computerized tomography or magnetic resonance imaging. |
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The IHS
comments that thalamic facial pain is usually part of a hemisyndrome,
but may occur in isolation.
Facial
Pain From Brainstem and Thalamic Lesions
We
referred earlier to facial neuralgia with multiple sclerosis. The facial
pain in this disease closely resembles, or is identical with idiopathic
trigeminal neuralgia (McDonald, 1980). The responsible lesion in the few
cases in which necropsy has been performed was found to be at the
junction of the trigeminal root with the pons (see the section on ``Trigeminal
Neuralgia'' above). In addition, we have seen several patients who
complained of severe, paroxysmal, hemifacial pain several weeks or
months prior to the development of other signs of an intrinsic pontine
tumor.
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Other
Signs of Intrinsic Pontine Tumor |
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Another
patient with paroxysmal burning facial pain has been described with
bilateral horizontal gaze palsy and central facial pain due to brainstem
encephalitis (Fukutake, 1992).
Facial
pain on the side of fifth nerve involvement is a common feature of
Wallenberg's syndrome, but is one that has received little emphasis. Of
39 patients with the lateral medullary syndrome studied by Currier et
al. (1961), 18 had definite persisting ipsilateral facial pain, while 9
others had transitory head or face pain, lasting less than 2 or 3 hours.
The 18 patients who complained of lasting ipsilateral facial pain noted
that it was most often in or around the eye. Several patients with
incomplete lesions had pain only in the area of sensory loss that was
often limited to the first and second divisions of the trigeminal nerve.
No patient complained of pain in the mandibular division alone. The pain
was usually described as "burning," "stinging,"
"unbearable," or "sore." It usually began with the
onset of the syndrome, and sometimes was the first symptom noted. In
some patients, the onset of pain was delayed for at least 2 weeks. In 8
of the 39 patients, pain was the prominent complaint after the acute
phase of the disease had subsided. Several patients had pain for years,
but it tended to become milder with time.
Pain in
the head and face was also an initial complaint in 5 of 14 patients with
Wallenberg's syndrome examined by Hörnsten (1974). In two of them,
headache appeared as a prodromal symptom, while in the other three
patients, it appeared concurrently with other symptoms and signs of the
syndrome. In three patients, the headache was localized to the
suboccipital region. In addition, three patients noted severe orbital
and supraorbital pain on the side of the infarction. In one patient, the
pain was so severe that she was initially admitted to the hospital with
a preliminary diagnosis of acute glaucoma.
The
cause of facial pain in patients with medullary lesions is open to
conjecture. The work of Bishop (1959) may shed some light on this
problem. He demonstrated the presence of a slowly conducting, probably
phylogenetically old, multisynaptic pathway through the medial areas of
the medulla and higher brainstem that ends in part in the medial
thalamic nuclei. It is believed to transmit slow, burning, delayed pain
such as that conducted through the C or unmyelinated fibers in
the peripheral nerves. This pathway lies in the reticular substance of
the medulla medial to the descending root of the trigeminal nerve and
the spinothalamic tract, and evidently receives fibers from these two
tracts. Currier et al. (1961) postulated that complete involvement of
both the descending root and the reticular pain pathway produces
spontaneous pain, while a more superficial lesion incompletely involving
the descending trigeminal tract produces pain by irritation of the
reticular pain pathway alone.
We have
previously discussed the thalamic syndrome of Déjerine and Roussy
(1906) that occurs primarily from thrombosis of the thalamogeniculate
artery. In this syndrome, there is complete contralateral hemianalgesia
(and homonymous hemianopia) that is usually transient, giving way to
painful sensations of a peculiarly disagreeable quality upon stimulation
of the opposite side of the body. These sensations are usually most
pronounced in the face. Coulter et al. (1970) have reported a case of
thalamic ocular pain that was successfully treated with carbamazepine
(see also the section in this chapter on ``Photophobia'').
12.8:
Facial pain not fulfilling criteria in groups 11 or 12
Occasionally,
facial parathesias are interpreted as painful or quite uncomfortable to
patients. Parathesias also may be associated with many of the
anesthestic or painful facial syndromes discussed earlier.
The IHS
description of this condition is persistent facial pain that does not
have the characteristics of the cranial neuralgias classified previously
and is not associated with physical signs or a demonstrable organic
cause. The diagnostic criteria are:
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A.
Is present daily and persists for most or all of the day. |
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B.
Is confined at onset to a limited area on one side of the face.
May spread to the upper or lower jaws or a wider area of the face
or neck. Is deep and poorly localized. |
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C.
Is not associated with sensory loss or other physical signs. |
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D.
Laboratory investigations including X-ray or face and jaws do not
demonstrate relevant abnormality. |
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The IHS
comments that pain may be initiated by operation or injury to face,
teeth or gums but persists without any demonstrable local cause.
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