Antidepressants such as amitriptyline and fluoxetine are helpful in some patients, and Bowsher has suggested, on the basis of a small placebo-controlled trial, that treatment with amitriptyline during the acute phase may prevent persistent pain. The use of preemptive measures, such as gabapentin or pregabalin administered at the outset, may be effective but a properly performed clinical trial is lacking. The addition of amitriptyline up to 75 mg at bedtime has proved to be a useful measure. Probably equivalent results are obtained by a combination of valproic acid and an antidepressant, as reported by Raftery. King has reported that two 325-mg aspirin tablets crushed and mixed with cold cream or chloroform (15 mL) and spread over the painful zone on the face or trunk relieved the pain for several hours in most patients with postzoster neuralgia. Ketamine cream has been suggested as an alternative. Extensive trigeminal rhizotomy or other destructive procedures should be avoided, as these surgical measures are not for long successful and may lead to a superimposed diffuse refractory dysesthetic component on the original neuralgia (anesthesia dolorosa).
Under the heading of “primary trochlear headache,” Yanguela and colleagues have described a periorbital pain that emanates from the superomedial orbit in the region of the trochlea (the pulley of the superior oblique muscle). Most of their patients were women. The pain was worsened by adduction and (paradoxically for the superior oblique) upgaze of the globe on the affected side, in the direction of action of the superior oblique muscle. The authors describe a diagnostic method of examination that begins by having the patient look downward so that the trochlea can be palpated and compressed; the patient then looks upward, eliciting or exaggerating the pain, while the examiner continues compression. Injection of the trochlea with corticosteroids relieved the pain in almost all of these patients. The authors made a distinction between primary trochlear headache and “trochleitis,” which seems to us an ambiguous difference. There is no limitation of ocular movement or autonomic change and imaging of the orbit is normal. This syndrome, with which we have no experience, brings to mind the entity of the Brown syndrome of trochlear entrapment with diplopia and pain (Chap. 13). The above authors were also of the opinion that the trochlea may be a trigger point for migraine.
Pain localized in and around one ear is occasionally a primary complaint. It is commonly the incipient symptom of Bell’s palsy or an outbreak of shingles but there are a number of different causes and mechanisms. During neurosurgical operations in awake patients, stimulation of cranial nerves V, VII, IX, and X causes ear pain, yet interruption of these nerves usually causes no or limited demonstrable loss of sensation in the ear canal or the ear itself (superficial sensation in this region is supplied by the great auricular nerve, which is derived from the C2 and C3 roots). The neurosurgical literature cites examples of otalgia that were relieved by section of the nervus intermedius (sensory part of VII) or of nerves IX and X. In otalgic cases, one is also prompted to search for a nasopharyngeal tumor, vertebral artery aneurysm or dissection or to anticipate an outbreak of zoster as mentioned. Formerly, lateral sinus thrombosis was a common cause in children. When these possibilities are eliminated by appropriate studies, there always remain examples of primary idiopathic otalgia, lower cluster headache, and glossopharyngeal neuralgia. Some patients with migraine have pain centered in the ear region and occiput, but we have never observed a trigeminal neuralgia in which the ear was the predominant site of pain. Occasionally, temporomandibular joint disease is the cause (see below).