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A study of chronic facial pain

Chronic facial pain may be indicative of any of a number of underlying diseases. The facial pain syndromes may be due to any eye, ENT, dental or neurological problems. The facial pain syndromes are often misdiagnosed. It is not uncommon for patients suffering form trigeminal neuralgia to have been to many dentists and doctors and being misdiagnosed several times before finally being correctly diagnosed. Trigeminal neuralgia should always be suspected in a patient reporting facial pain and unresponsiveness to pain killers. It should be diagnosed as early as possible to save the patient from the severe and resistant pain that is characteristic of trigeminal neuralgia. If the clinical signs are carefully examined and analyzed, the diagnosis of trigeminal neuralgia can be made quickly and correctly and it can easily be differentiated from other facial pain pathologies.

A 46- year old female patient started experiencing severe pain in her lower right third molar (wisdom tooth) after a series of dental surgeries including root canals, extractions and implants. The pain was not relieved with the use of Paracetamol, Aspirin or Diclofenac. She consulted a dentist for this problem, the dentist after examining the tooth reached the conclusion that the best possible treatment for this patient would be to have this tooth extracted. After extraction of this tooth, the patient’s pain increased in severity. The dentist diagnosed her as a case of alveolar osteitis, a complication which is common after the extraction of wisdom teeth. In this condition, the cavity formed after extraction undergoes delayed healing, becomes severely painful and may become infected. She was put on Metronidazole and Diclofenac. A week after the extraction, the dentist informed the patient that her alveolar osteitis had been healed. Even after the complete healing of her extraction cavity, her pain kept on increasing. The pain started radiating to her throat, ear, upper jaw and forehead. The dentist referred her to an ENT specialist who examined her and did not find any disease related to his specialty. He referred the patient to a neurologist.

Chronic facial pain may indicate any of a wide variety of disorders: Glaucoma, Heterotropia, Sinusitis, Odontalgia, Pulpitis, Periodontitis, abscess, Alveolar osteitis , Gingival disease, Cluster syndrome, SUNCT (Short-lasting, Unilateral, Neuralgiform headache attacks with Conjunctival injection and Tearing), Trigeminal neuralgia (typical and atypical), Glossopharyngeal neuralgia, Nervus intermedius neuralgia, Postherpetic neuralgia, TMJ syndrome, Raeder syndrome, Neuralgia-Inducing Cavitational Osteonecrosis, Thalamic pain syndrome, Hemicrania continua, Persistent Idiopathic Facial Pain or Migraine. At this point of time, history of the patient may prove to be the best diagnostic tool. The character, duration and severity of the pain may provide a hint to the problem.

The patient experienced pain in episodes which had a sudden onset, usually at night. The patient could not sleep because of the pain. The pain was severe, heavy and stabbing pain which had now diffused all over the face and she could not identify where the pain originated from. There were no identifiable relieving or aggravating factors. The pain lasted for several hours and was resistant to almost all pain killers. Her face was non-tender on palpation.

Although, the characteristics of the pain in this patient match closely the characteristics of pain in Atypical Trigeminal Neuralgia (ATN), but ATN is rare in patients less than 50 years old. The pain in typical trigeminal neuralgia is described as shock-like, pressing or shooting pain which lasts from a few seconds to several minutes. The pain in atypical trigeminal neuralgia usually lasts longer and is described as heavy, stabbing pain radiating across the jaws, ear and throat. A point of significance in this patient is that she has had many dental surgeries. Dental surgeries may lead to Trigeminal Neuralgias. Facial pain after dental surgeries especially extraction may be indicative of Neuralgia-Inducing Cavitational Osteonecrosis (NICO). A simple examination by a dentist can exclude the possibility of NICO.

An examination by the dentist excluded the possibility of Neuralgia-Inducing Cavitational Osteonecrosis. The neurologist ordered MRI of brain with contrast to confirm the diagnosis of Trigeminal Neuralgia and started the patient on Carbamazepine (Tegretol).

Trigeminal neuralgia may be caused by an aneurysm of a vessel, a tumor, a cyst, dental procedures, infections or trauma. Any of these causes may injure the myelin sheath of the nerve thus causing hyperactivity of the nerve. This hyperactivity causes the nerve to sense pain on even the slightest of stimuli. The pain was relieved with Carbamazepine. Carbamazepine makes the neurons less excitable and this reduces the spontaneous firing of the trigrminal nerve thus reducing the pain. MRI with contrast is needed to confirm the diagnosis of trigeminal neuralgia and to highlight the vessels so any vessel engorging on the trigeminal nerve would be clearly visible.

The MRI did not show any aneurysm, cyst or tumor. It was then assumed that the neuralgia was caused by the dental procedures.

Many times trigeminal neuralgia is idiopathic and is not caused by any identifiable causes. In such a situation, it is advised to start the patient on Carbamazepine, which is an anti-convulsant, to relieve the patient of the severe pain. In such cases, trigeminal neuralgias must be distinguished from Persistent Idiopathic Facial Pain (PIFP). They can be distinguished on the basis of patient history. The pain in PIFP is usually continuous, while in trigeminal neuralgias there are periods of remission. The pain of PIFP is usually unilateral while the pain of trigeminal neuralgias is mostly, but not always, bilateral. Initially, the pain of trigeminal neuralgia may also present as unilateral but later, as the disease process progresses, the pain usually becomes bilateral. Some patients with Multiple Sclerosis experience trigeminal neuralgia as a symptom. The patients diagnosed with trigeminal neuralgia should also be tested for multiple sclerosis.

Approximately 10 days after the patient started taking Carbamazepine, the pain started returning. The neurologist increased the dose of Carbamazepine. The increased dose caused nausea and vomiting in the patient so the neurologist advised the patient to take the medicine in halves at different times of the day.

As the patient continues to take Carbamazepine, the clearance rate of her kidneys for Carbamazepine increases and thus a higher dose is required to maintain the same blood plasma concentration of Carbamazepine. This is the reason why the dose was increased after 10 days.

The patient continued on the same treatment regime and after several months, her pain disappeared.

The patient should continue to take the medications as long as the pain returns. It may take up to a couple of months for the pain to completely disappear.

COMMENTARY:

Chronic facial pain may be caused by a wide variety of problems which may include eye, ENT, dental or neurological disorders. For effective treatment, it is important to differentiate them clinically. As with all diseases, in accurately diagnosing a facial pain syndrome, detailed history of the patient is the most important diagnostic tool. Facial pain syndromes should always be diagnosed after multi-disciplinary consultations to avoid missing any disease. Although many of the facial pain syndromes may easily be misdiagnosed, they have individual characteristic pain pattern and character. Before suspecting any facial pain syndrome, local problems of eye, ENT and dentistry should be excluded.

If eye, ENT and dental problems have been excluded, the nature of the pain can give very useful hints. If the pain is explosive, stabbing, shock-like or burning, then it may indicate neuralgias. If the pain is mild, continuous and dull, then it may indicate temporo-mandibular dysfunctions. The pain from dental infections is usually brief but severe. If the pain is brief and boring, it may indicate SUNCT (Short-lasting, Unilateral, Neuralgiform headache attacks with Conjunctival injection and Tearing). As in the case of this patient, the nature of the pain can give us an important clue regarding the etiology of the pain. The patient described the pain as heavy, stabbing pain. This pain is characteristic of atypical trigeminal neuralgia. Typical and atypical trigeminal neuralgias can also be differentiated on the basis of patient history. Pain from typical trigeminal neuralgia lasts from a few seconds to a few minutes or hours with longer periods of remission, the pain is burning, shock-like or exploding. While the pain from atypical trigeminal neuralgia is stabbing and is of longer duration with shorter periods of remission. Both typical and atypical neuralgias generally have the same causes and are treated with the same medications.

The high risk people for trigeminal neuralgia are women who are above 50, have multiple sclerosis, have had many dental procedures or tongue piercings. It is common for people with trigeminal neuralgia to have been to many dentists and doctors before being properly diagnosed. As in this case, the patient had been to the dentist multiple times, who referred her to an ENT specialist, who referred her to a neurologist. Patients with trigeminal neuralgia do not find relief with the regular pain killers. It is common for patients with trigeminal neuralgia to have tried many medications for pain but found them ineffective.

This patient could neither identify any trigger points nor any relieving or aggravating factors, but many patients are able to point out a region on their face which triggers the pain. Even small stimuli, like air, to that region are able to start the pain. Similarly, many patients point out that smiling, laughing, chewing, talking and other movements with the face aggravate the pain. These trigger points and aggravating factors are not present in all the patients. It is important to note here that although the disease process in some patients starts out as atypical trigeminal neuralgia, but as the disease progresses, atypical trigeminal neuralgia may convert to typical trigeminal neuralgia. This may lead to a change in the nature of pain. This possibility should always be kept in mind when dealing with long, untreated atypical trigeminal neuralgia.

The psychological health of the patient should also be monitored. Depression is common among patients of trigeminal neuralgia. In addition to the depression caused by all chronic diseases, patients suffering from trigeminal neuralgia are especially prone to suffer from depression because of the severe pain which is unresponsive to most pain killers.

When the trigeminal nerve is being compressed due to an engorged vessel, a cyst or a tumor, the myelinated sheath of the nerve is damaged and the nerve becomes demyelinated. As the myelination prevents the nerve from spontaneous firing of impulses, after the demyelination the nerve starts firing pain signals spontaneously or on minor stimuli. MRI is the most important diagnostic tool. The presence of an aneurysm or a tumor is ruled out on the basis of MRI. With contrast, there is an 80% chance that any vessel that is compressing the nerve will be shown. It is important to remember that some cases of trigeminal neuralgia are idiopathic like the one of this patient. MRI should always be carried out to rule out tumors and aneurysms but even if the MRI does not show anything, this does not rule out trigeminal neuralgia. If Carbamazepine is effective against the pain, then this is a positive sign that the patient is suffering from trigeminal neuralgia. Although MRI of the patient did not show any abnormality, still we diagnosed the patient as trigeminal neuralgia because of the responsiveness of her pain to Carbamazepine.

The first line of treatment for trigeminal neuralgia is Carbamazepine but if it does not sufficiently reduce the pain then other drugs like Baclofen, Clonazepam or Gabapentin may be given individually or in combination. When medicines fail, surgical treatment may be availed. There are many surgical treatments available including nerve blocks, microvascular decompression, balloon compression, glycerol injections, radiofrequency rhizotomy and stereotactic radiosurgery. [1]

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