Headaches and Facial Pain (updated 09/06)

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1 Headaches and Facial Pain (updated 09/06) 1. Review the sensory innervation to the ear and discuss pathways of referred pain. Medical Clin North Am 1991;75:677. SW 2. Discuss sinonasal innervation. Medical Clin North Am 1991;75:677. CB 3. Brain parenchyma is pain insensitive. Explain source of pain with migraines AL The parenchyma of the brain is insensitive to direct noxious stimuli. The trigeminal nerve is the largest of all the cranial nerves. It is a mixed nerve situated on the ventrolateral aspect of the pons. The sensory root conveys impulses from the face and scalp, parts of the external ear and acoustic meatus, the nasal and oral cavities, teeth, temporomandibular joint (TMJ), nasopharynx, and most of the meninges of the anterior and middle fossa. It passes outward and forward over the petrous temporal bone near the apex, extending into the trigeminal ganglion. These pseudounipolar cells pass peripherally to become the three major divisions: ophthalmic, maxillary, and mandibular. In the primary head and face pains, abnormal activation of peripheral neurons or central structures results in distinctive pain description, phenomenology, and associations (5). These may then refer to areas of the head, neck, or face at distance from the area of activation, making diagnosis more challenging (Table 18.1). The central connections of second-order sensory neurons of the trigeminal system project to the thalamus and thence to the primary sensory cortex of the parietal lobe. Descending inhibitory projections from periaqueductal gray and paracentral aminergic nuclei modify the pain experience and have become increasingly important in our understanding of the primary headaches. J Vestib Res. 2011;21(6): The science of migraine. Burstein R, Jakubowski M, Rauch SD. Departments of Anesthesia, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA. rburstei@bidmc.harvard.edu Abstract The cardinal symptom of migraine is headache pain. In this paper we review the neurobiology of this pain as it is currently understood. In recent years, we discovered that the network of neurons that sense pain signals from the dura changes rapidly during the course of a single migraine attack and that the treatment of an attack is a moving target. We found that if the pain is not stopped within minutes after it starts, the first set of neurons in the network, those located in the trigeminal ganglion, undergo molecular changes that make them hypersensitive to the changing pressure inside the head, which explains why migraine headache throbs and is worsened by bending over and sneezing. We found that if the pain is not stopped within minutes, the second group of neurons in the network, those located in the spinal trigeminal nucleus, undergoes molecular changes that convert them from being dependent on sensory signals they receive from the dura by the first set of neurons, into an independent state in which they themselves become the pain generator of the headache. When this happens, patients notice that brushing their hair, taking a shower, touching their periorbital skin, shaving, wearing earrings, etc become painful, a condition called cutaneous allodynia. Based on this scenario, we showed recently that the success rate of rendering migraine patients pain-free increased dramatically if medication was given before the establishment of cutaneous allodynia and central sensitization. The molecular shift from activity-dependent to activity-independent central sensitization together with our recent conclusion that triptans have the ability to disrupt communications between peripheral and central trigeminovascular neurons (rather than inhibiting directly peripheral or central neurons) explain their clinical effects. Both our clinical and pre-clinical findings of the last five years point to possible short- and long-term advantages in using an early-treatment approach in the treatment of acute migraine attacks.

2 4. What is Eagle s syndrome? Trotter s syndrome? SW 5. Differentiate temporamandibular joint disorder from myofascial pain-dysfunction syndrome. AL The TMJ and the muscles of mastication can be a source of pain that radiates to the head and the ear. The TMJ and its articulations are innervated by the auriculotemporal nerve as it passes behind the condyle and then upward in front of the ear. Pain can be reported as a diffuse temporal headache or as ipsilateral ear pain The temporomandibular disorders (TMDs) can occur as diffuse temporal headache, earache, and facial pain. True TMJ pain is characterized by tenderness to palpation over the condyle and by pain on jaw movement. Internal derangements are characterized by anterior and medial displacement of the articular disk when the teeth are interdigitated in occlusion. About 25 mm of space between the anterior teeth is the limit of rotational opening because further opening requires translation of the condyle. Degenerative joint disease (DJD) is characterized by crepitus and pain on jaw movement. It is usually selflimited and can be managed with NSAIDs. Most patients have combined muscle and joint pain with tenderness of the masticatory muscles and worsening with joint movement. A click on movement may be present. Mouth opening is limited. Management is similar to that for tension headache. NSAIDs and physical therapy form the mainstay of treatment. Other methods for muscle pain management such as biofeedback, trigger-point injection, and physical therapy are useful. Dental splints may be useful, and referral to dentistry is indicated. MPD syndrome is a muscular disease that is believed to be multifactorial in origin.43 It is generally accepted that centrally induced muscle tension from stress and anxiety combined with parafunctional habits such as clenching or grinding of the teeth results in abnormal muscle function and hyperactivity. This leads to fatigue and spasm of the muscles that ultimately produces pain and dysfunction. The pain stimulates muscle fibers to react, leading to further muscular dysfunction and spasm. Thus one can appreciate the cyclic nature of this disorder. Similar symptoms can also occasionally result from muscular overextension, muscle overcontraction, or trauma (Fig. 94-3). MPD syndrome most frequently affects females in the 20- to 40-year age group. Men are much less affected, with a ratio of approximately 1 : 4. Children are rarely affected. MPD syndrome is characterized by diffuse, poorly localized pain that ranges from complaint of preauricular pain to generalized pain throughout the muscles of mastication. The pain is often described as dull, aching, radiating pain that may be more severe in the morning. Patients also complain of pain and limitation of opening during function. The condition generally involves only one side of the face, and on examination, tenderness can usually be elicited in one or more of the muscles of mastication or their tendinous attachments.44 Headache is frequently mentioned as a symptom. Ciancaglini and Radaelli45 report a significant increase in headache in patients with TMD symptoms (27.4% vs. 15.2%). The only type of headache that is functionally related to MPD syndrome, however, is the tension-type headache, with other types being coincidental findings. The same is true for multiple complaints noted by MPD patients such as decreased hearing, tinnitus, burning tongue, and neuralgic pains. MPD syndrome that is left untreated can ultimately lead to organic changes in the TMJ and the masticatory muscles and may even cause alterations in the dentition. The cardinal signs and symptoms of MPD syndrome are similar to those produced by intracapsular disorders, as well as by a variety nonarticular conditions (Tables 94-2 and 94-3). A careful history and thorough clinical evaluation should be performed to rule out these other clinical entities. Screening radiographs, particularly intraoral periapical films and a panoramic film delineating the structures of the jaws and the TMJ, can be helpful. If the screening views of the TMJ show some abnormality, tomographic views or CT scans are useful in further evaluating bony abnormalities. Magnetic resonance imaging is valuable in evaluating soft tissue structures particularly

3 when an internal derangement of the TMJ is suspected. In addition, certain laboratory tests may be helpful in some patients. These tests include a complete blood cell count if an infection is suspected; serum calcium, phosphorus, and alkaline phosphatase measurements for possible bone disease; serum uric acid determination for gout; serum creatinine and creatine phosphokinase levels as indicators of muscle disease; and erythrocyte sedimentation rate, rheumatoid factor, latex fixation, and antinuclear antibody tests for suspected rheumatoid arthritis. In patients suspected primarily of MPD syndrome, muscular function may be evaluated through electromyography. Many clinicians recommend psychologic evaluation, primarily to help determine patient compliance and to predict anticipated treatment outcomes. 6. Characterize migraines. Discuss the treatment to include drugs, behavior modification, etc. How do migraines differ from cluster headaches? Otolaryngol Head Neck Surg 2000;123:66. AL Migraine with and without aura 1.1 Migraine without aura A. Headache attacks lasting 4 72 h (untreated or successfully treated) B. Headache has at least two of the following characteristics 1. Unilateral location

4 2. Pulsating quality 3. Moderate or severe intensity 4. Aggravation by or causing avoidance of routine physical activity (e.g., walking or climbing stairs) C. During headache, at least one of the following: 1. Nausea or vomiting 2. Photophobia and phonophobia D. Not attributed to another disorder C. At least two of the following: 1. Homonymous visual symptoms and/or unilateral sensory symptoms 2. At least one aura symptom develops gradually over Ñ 5 min, and/or different aura symptoms occur in succession over Ñ 5 min D. Headache fulfilling criteria B D for 1.1 Migraine without aura begins during the aura or follows within 60 min E. Not attributed to another disorder 1.2 Migraine with typical aura A. At least two attacks B. Aura consisting of at least one of the following but no motor weakness: 1. Fully reversible visual symptoms including positive features (e.g., flickering lights, spots, or lines) and/or negative features (i.e., loss of vision) 2. Fully reversible sensory symptoms including positive features (i.e., pins-and-needles) and/or negative features (i.e., numbness) 3. Fully reversible dysphasic speech disturbance Treatment: ACUTE Therapies: Triptans/5-HT1B/D agonists CGRP antagonists (calcitonin gene related peptide receptor) or Gepants onset of action is slower than triptans but no adverse effects Telcagepant Newer Promising Drugs: Lasmiditan highly selective 5-HT1F agonists, but lacks vasoconstricting effect. Side effects: dizziness, paresthesias, sensation of limb heaviness NXN-188: inhibition of neuronal nitric oxide synthase AND bidning to 5HT1B/D receptors, mild side effects (dizziness) Neuromodulation: Transcranial magnetic stimulation Nonspecific: butorphanol, ibuprofen, naproxen, prochlorperazine, ASA, APAP/ASA/Caffeine, APAP, isometheptine, opioids Triptans: almotriptan, eletriptan, frovatriptan, naratriptan, rizatriptan, sumatriptan, zolmitriptan, dihydroergotamine Comment: There is a triptan class effect for side effects, the majority of which are minor and not dangerous. Chest tightness, throat or head pressure, tingling, nausea, and flushing usually improve with patient education and repeated use. Daily maximums vary, although no more than two doses in 24 hours is the rule. They are contraindicated in patients with uncontrolled hypertension or a history of cerebral or coronary artery disease but are generally extremely safe and effective. Preventive Therapy: Anticonvulsants: Divalproex, topiramate, gabapentin Antidepressants: Tricyclics, SSRI, B blockers Calcium Channel Blockers: verapamil NSAIDS: naproxen Other: Riboflavin, magnesium, feverfew Alternative Nonpharmacological Procedures; Biofeedback and basic relaxation techniques did not significantly increase the outcome of relaxation alone Combination of B blocker and behavioural migraine management is significantly superior to either treatment alone Endovascular patent forament ovale closure: reported improvement in migraine Chronic Migraine Management: most disabling form of migraine, highly drug resistant

5 Occipital nerve stimulation: prelim data is encouraging Botox: failed in chronic tension HA, episodic MA, or chronic daily HA. Only small studies so far Cluster Headache CH is an uncommon disorder. Abrupt onset of strictly unilateral, blinding, and shortduration attacks raise questions about potentially devastating consequences including subarachnoid hemorrhage. Among the primary headaches, CH pain is assumed to be the most severe pain, and the accompanying autonomic features may confuse the diagnosis with pathology in orbital or periorbital areas or sinuses. Awakening the patient from sleep at a time when dreaming is presumed to occur leads to sleep evaluations, and CH's seasonal or circannual occurrence implies botanical allergy. Secondary causes of CH can include cranial, cervical, or vascular disorders. The carotid artery, cavernous sinus, and various brain structures, including the periaqueductal gray matter, appear to participate in pain generation and modulation associated with this disease (21). CH occurs in 0.2% to 0.6% of the population, with a male-to -female ratio of 4:1 to 12:1. Recent studies have suggested that although the gender ratio of CH may be changing, the overall prevalence has remained stable for the last 2 to 3 decades. Genetic studies suggest autosomal dominant transmission with a low frequency of the susceptibility allele. CH has been recognized as a distinctive clinical entity since as early as the 1700s. During active periods, most commonly in the spring and autumn, clusters of individual headaches lasting between 30 and 180 minutes occur daily, with episodes lasting weeks or months. The majority of patients have episodic, recurrent attacks of unilateral, temporal, or periorbital pain associated with autonomic features including ptosis, miosis, lacrimation, rhinorrhea, and ipsilateral stuffiness. In a chronic form of this disorder, unrelenting and daily attacks of typical CHs persist without interruption. Episodic cluster is defined by gaps in time between painful periods. Chronic cluster is unremitting. Episodes occur once or twice per year in 75% of patients, with a typical episode lasting approximately 2 months. Attacks typically last between 72 and 159 minutes, with attack frequency between two per week and five per day (Table 18.8), and 73% of patients have a predictable onset of attacks at night. Of episodic patients, 43% describe a seasonal onset, and chronic sufferers also describe seasonal exacerbations. CH is a strictly unilateral headache in 100% of attacks occurring during a symptomatic cluster episode. Autonomic features including ipsilateral facial flushing, lacrimation, nasal stuffiness, ptosis, or miosis occur in 70% to 90% of patients. Previous head trauma appears to be associated with CH, although duration from time of trauma is extremely variable. Differentiating CH from migraine is not clinically difficult. CH is of shorter duration and male preponderant. Photophobia, nausea, or other features classically associated with migraine may occur. The defining clinical feature is the tendency for patients to describe attack-associated behavioral agitation. During attacks, up to 93% of patients experience restlessness (22) during which they rock, pace, and rub or beat their heads. 3.1 Cluster headache A. At least five attacks fulfilling criteria B D B. Severe or very severe unilateral orbital, supraorbital, and/or temporal pain lasting min if untreated C. Headache accompanied by at least one of the following: 1. Ipsilateral conjunctival injection and/or lacrimation 2. Ipsilateral nasal congestion and/or rhinorrhea 3. Ipsilateral eyelid edema 4. Ipsilateral forehead and facial sweating 5. Ipsilateral miosis and/or ptosis 6. A sense of restlessness or agitation D. Attacks have a frequency of from one every other day to eight per day E. Not attributed to another disorder 7. Discuss the classic presentation of temporal arteritis? Why is this a headache emergency? SW 8. Differentiate trigemenal neuralgia from atypical facial pain. How would you treat each? CB

6 9. Is sinus surgery effective in the management of patients with headaches? Laryngoscope 1998;108:696 and Arch Otolaryngol Head Neck Surg 2000;126:1274. TT 10. What is the anterior ethmoid nerve syndrome? TT