PRAMOD : CHRONIC SYNDROMES Indian J. Anaesth. 2006;PAIN 50 (5) : 391 - 396
CHRONIC PAIN SYNDROMES (NON TERMINAL ILLNESS) Dr. Pramod Kumar Keywords : Chronic, Pain syndromes. Introduction The regional analgesia was popular since Second World War but it ignored the complex, multidimensional nature of chronic pain syndromes. There is an obvious ongoing pathology in the peripheral nerve but pain is experienced in some patients even after healing of any peripheral damage is complete. A multimodal approach with combination of medications, stimulation induced analgesia, physical therapy and psychological1 approaches with neural blockade seems to be more appropriate. The regional analgesia has been used during anaesthesia for surgical patients. In the last few decades it has been used in the management of chronic non malignant pain. The greater understanding of neuro physiology of chronic pain indicated that peripheral nerve blocks ignored the complex multidimentional nature of chronic pain. There is an obvious ongoing pathology in the peripheral nerves but pain is experienced in some patients even after healing of any peripheral damage is complete. This is due to initiated central changes in the dorsal horn and higher centers after peripheral nerve damage. Some patients feel pain in the absence of any identifiable pathology.1 The nerve block appears illogical in such patients. A multimodal approach with combination of medications, stimulation induced analgesia, physical therapy and psychological approaches with neural blockade seems to be more appropriate. This article deals with these multidimentional approaches in various chronic non malignant painful conditions. eg. complex regional pain syndromes, cranial neuralgia, herpes zoster and pancreatic pain. The emphasis is on describing pain mechanisms and a relief of pain based on these. Basis for use of peripheral nerve blocks It is to interrupt the nociceptive input at its very source or blocking the nociceptive impulses coursing in the peripheral nerves. This also interrupts abnormal reflex mechanisms contributing towards pathophysiology of some pain syndromes and blocking sympathetic hyperactivity. 1. M.D., D.A. Sr. Prof. And Head Dept. of Anaesthesiology M.P. Shah Medical College, Jamnagar (Guj) E-mail : [email protected]
Low concentrations of local analgesics block unmyelinated C and B fibers and small unmyelinated delta C fibers with only a minor interruption of somatic motor functions.2 The neurolytics also acts in the same way on unmyelinated fibers sparing the other sensations3 e.g. touch, temperature and motor functions for a prolonged period.1 Indications for nerve blocks (1) Diagnostic Blocks : Ascertain specific nociceptive pathways, help determine mechanism of chronic pain syndromes, aid differential diagnosis of the site and cause of pain, determine patients’ reaction to the pain relief (2) Prognostic Block : Predict the effects of neurolytic block/surgery, afford the patient to experience the numbness and other side effects and help patient to decide whether or not to have it done (3) Therapeutic Blocks : Control acute post operative and traumatic pain, breaking of vicious circle involved in the pain syndrome, provide temporary relief to permit other therapies or development of accessory muscle functions providing mobility. Complex regional pain syndromes Reflex Sympathetic Dystrophy (RSD) is a disorder having similar clinical manifestations which arise from injuries like minor strain, sprain and fracture following minor surgery of the extremities. It is characterized by pain, abnormal regulation of blood flow and sweating, oedema of skin and subcutaneous tissues, tropic changes of skin and subcutaneous tissue and active and passive movement disorder. The term causalgia is a condition in which an obvious either complete or partial injury to major nerve trunk is found. The pain is thought to be mediated by sympathetic over-activity.1 RSD has two components, RSD major and RSD minor. RSD major includes causalgia, phantom limb pain, central pain like thalamic syndrome, central lesions, brain stem lesions and spinal cord lesions. RSD minor can occur following trauma or diseases. The traumatic condition includes Sudeck’s atrophy, traumatic arthritis, post-traumatic neuralgia, shoulder-hand syndrome and post-traumatic angiospasm. International Association for Study of Pain has coined the term CRPS (Complex Regional Pain Syndrome) instead of old terminology RSD and Causalgia, to better reflect possible nature of this painful condition.
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Complex Regional is defined as a syndrome of diffuse limb pain and injury of noxious stimuli with variable sensory, motor, autonomic and trophic changes.1 There are some suggestions for reclassification and redefinition of CRPS4 CRPS has two components. Sympathetically mediated (SMP) and sympathetically independent pain. Sympathetically maintained pain (SMP) The sympathetically maintained pain is defined as “pain that is maintained by sympathetic efferent innervation or by circulating catecholamine.4 This term is often used to describe patients who have CRPS. SMP is a pain mechanism while CRPS is a clinical diagnosis which may or may not have SMP. Clinical features SMP occurs in the extremities or the face, which have dense sympathetic Innervation of skin. The limb may be warmer, cooler or of the same temperature while SIP has a striking sensitivity to pain. Some of the clinical features may be due to other conditions, eg.CRPS or neuropathic conditions. Pathophysiology Efferent rather than afferent sensory fibers that may travel with the sympathetic fibers account for SMP.2 The response to nor adrenaline at the sympathetic terminals is a critical factor in SMP. The latter may be due to up regulation α adrenergic receptors or increased receptor sensitivity. Sympathetically independent pain (SIP) The term describes that the subgroup of patients who do not respond well to sympathetic blockade. The pain characteristic in this group suggests possibly neuropathic mechanism for their pain. There may be overlapping contributions from sympathetic and other nerves in the same patient. CRPS incidence : It can affect adults and children. The prognosis in children is favorable. Approximately 10% population referred to pain centers in USA is referred for the CRPS 1. CRPS is more common in women than men (3:1). Incidence of CRPS is between 2-14% after peripheral nerve injury. In adolescent girls, lower limb is more affected. Clinical characteristics : CRPS I : Usually after a trivial or initial injury. Burning pain, allodynia, cold and / or mechanical pressure, occasional hypoesthesia. Not limited to distribution of a single peripheral nerve and involves more than the original injury site. Abnormal pseudo motor activity. Abnormal blood flow, coldness of skin, oedema, skin discoloration and hyperhydrosis. Motor dysfunction like weakness, tremors and joint stiffness. Trophic changes like muscular atropy,
INDIAN JOURNAL OF ANAESTHESIA, OCTOBER 2006
osteopenia, arthropathy, glossy skin, brittle nails and altered hair growth. Most likely normal peripheral pulsations CRPS II : Initial history of peripheral nerve injury or post surgical cases. Burning numbness is the presenting symptom. Allodynia and hyperalgesia beyond the normal distribution of injured nerve. Oedema and abnormal blood flow. Abnormal sudo motor activities in the area. Mechanism of action : The sympathetic nervous system plays an important central role in CRPS. It is not clear if this is due to over activity of the sympathetic efferent directly or if the sympathetic efferent overactivity is accompanying events. Initial pain is associated with over activity of A- delta and C fibers. Injury to some peripheral nerves will activate WDR (wide dynamic range neurons) neurons in dorsal horns. When sensitization persists, WDR neurons will respond to large diameter-A- beta mechanoreceptive afferents which are activated by light touch of brushing. This state will produce allodynia.5 These sensitized WDR neurons respond to mechanoreceptor activity initiated by sympathetic action on sensory receptors in the absence of cutaneous stimulation, and thus produce spontaneous pain or SMP. Following peripheral nerve injury, large diameter myelinated axons sprout from their site of termination in lamina three, region normally innervated by smaller diameter fibers, high threshold efferents. Thus low threshold efferents gain access to a pool of dorsal horn neurons involved in nociceptive processing that were originally accessed only by high threshold afferent input. Devor and Janig have demonstrated the afferent fibers from a neuroma are activated by sympathetic stimulation or by intravenous nor epinephrine and the activation can be blocked by phentolamine. These findings have led to the hypothesis that nociceptors develop sensitivity to nor epinephrine through expression of α 1 receptors on their terminals. Indirect mechanism may include activation of alpha adrenergic receptors on mast cells, leukocytes and platelets by norepinephrine, which then release chemical mediators (histamine, bradykinin, prostaglandins) which in turn activate nociceptor afferents.6 Prolongation of sympathetic response, Peripheral vasoconstriction and vasodilatation7 also plays a role in the aetiology. Peripheral nerve fibers : The efferent fibers in the sympathetic chain if stimulated cause some quality of pain as in CRPS. Nerve damage and cross connection between sympathetic and peripheral nerve play a role. Abnormal sprout of nerve fibers, like in neuromas is present.
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Central mechanism : Janig et al suggested that CRPS I, is a complex neurological disorder involving various levels of integration in brain.4 At spinal cord, plasticity, wind up phenomena is known. Several neuro chemicals like NMDA, GABA, calcium, glycine, glutamate have been suggested to contribute to chronic pain status
Raynaud’s disease produces vasospasm, cold and pale extremities and burning pain. It is usually bilateral. Sympathetic block can relieve vasospasm but does not help in the disease condition. Raynaud’s phenomenon is a vasospastic condition secondary to underlying clinical condition like scleroderma. Sympathetic blocks help in only percentage of patients.
Clinical presentation: Most patients with CRPS have a history of trauma to soft tissues, bone, and nervous tissue. Accidental injury, sprain, fractures, dislocations or post surgical like carpal tunnel, peripheral nerve surgery or even a vaccination have been reported to be a factor in the development of CRPS. Other medical conditions may have associated SMP such as diabetic neuropathy, stroke, post herpetic neuralgia and disc herniation. It is not known why identical injury in different patients develops CRPS. Why in one arm following carpal tunnel surgery a patient may develop CRPS while a similar surgery on the other arm does not. Genetic factors may possibly explain the individual variation.
Diagnostic tests 1. Thermography: Infrared thermo graphic imaging employing quantitative temperature difference has been used to confirm the diagnosis of CRPS I. The inherited problem with this test is that condition such as neuropathic abnormalities, focal inflammation and vasculopathy may alter skin temperature too. 2.
Triple phase bone scan: It has some role in the earlier phase of CRPS I. the sensitivity is about 50%. It shows hypervascularity in the affected extremity in the earlier images followed by delayed uptake in the affected area in later images
Electromyogram : This is useful in some of the unresolved nerve compression at time of CRPS. This may be primary or contributory to the overall condition or secondary to the edema caused by the disease process.
Sensory changes : A persistent spontaneous burning pain and light touch sensitivity are prominent signs. Some patients show abnormal hemi sensory changes on the corresponding side of CRPS suggesting some central mechanism.
Quantitative sensory testing : In patients with CRPS the threshold for pain has decreased significantly in the affected area. With vibrating fork or camel brush a person will feel profound pain. Acetone drop cooling hyperalgesia is produced in SMP.
Autonomic dysfunction : In CRPS there is altered skin temperature in the affected areas. Typically the limb is colder than the opposite side. There are abnormal changes of cold sensitivity, abnormal nail and hair growth, focal loss of calcium in bones and altered micro circulation.
Sympathetic blocks : This is still an important intervention for the physician to diagnose and treat CRPS. In patients with SMP, the patient will have a longer of pain relief than actual duration of local anaesthetic. There may be some placebo effect with this test.
Physical examination : The symptoms and signs of CRPS are visible and vary on duration severity of the condition. Associated SMP or SIP can make a difference in the patient’s findings.
Motor dysfunction : Dystonia focal or multimodal in the affected limb, with or without associated weakness of muscles. This may be related to most likely disuse atrophy or partial use secondary to pain. Joint stiffness occurs in CRPS, I and CRPS II. Differential diagnosis : Several post-operative or post-traumatic conditions have symptoms in common with CRPS I and II. Differential diagnosis includes post traumatic vasoconstriction from thrombophlebitis, arthritis, infection, soft tissue damage, tenosynovitis, fascitis, fractures and radioculopathy. Peripheral nerve injury can cause burning dysthesias type of pain without sympathetic over activity. Positive Tinel’s sign is often present at the site of nerve injury or entrapment. Inflammatory tenosynovitis or bursitis can cause burning type of pain. Myofascial pain can cause burning pain beyond original area of trigger point in muscle.8
Management : (1) Physical therapy and rehabilitation9 (2) Sympathetic blockade (3) Chemical sympathectomy (4) Radiofrequency ablation (5) Surgical sympathectomy (6) Repeated axillary plexus block (7) I.V phentolamine (8) I.V.Biers block (9) Bretyllium (10) I.V.Toradol (11) Epidural local anaesthetic (12) Peripheral nerve stimulation1 (13) Spinal cord stimulation. Adjuvant medication : For acute case of CRPS a trial of oral steroid can be helpful. Also Tricyclic antidepressants, anti epileptic drugs like carbamazepine, phenytoin, gabapentin, alpha adrenergic blockers like prazocin and alpha 2 agonists like clonidine can be used. Psychological factors: severe pain and emotional suffering has major implications in cases of CRPS. Hence it is important to address these issues.
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Herpetic neuralgia The incidence of herpes zoster in the community is about one case per thousand population, and most of these are concentrated on the over sixty age group, where the incidence is about one per hundred.10 The pattern of incidence of the pain syndrome is similar to that of the disease, with the main incidence being in the older age groups, where over 50% may go on to suffer persistent pain. Herpes zoster presents as a pain, which is succeeded by a vesicular rash along the cutaneous distribution of a nerve. It is almost invariably one nerve root that is involved, apart from the trigeminal nerve where often only the ophthalmic division is affected. The infection is caused by the Varicella virus which has lain dormant in a posterior root ganglion since a previous chicken pox infection, and has been reactivated by some immune-suppressing life event. Precise descriptions of the pathology are rare because most patients die at home and are not subject to post mortem examination, but some studies do exist and it has been shown that the infection starts in the dorsal root ganglion cell, spreads to the adjacent dorsal horn cells and along the ascending columns for one or two spinal segments. The main spread of the infection is along the peripheral nerve, with demyelination and Wallerian degeneration right out to the cutaneous nerve endings, and the skin eruption appearing at that site.1 This is a total neuritis from the posterior horn cell to the skin with varying degrees of destruction, and possibly some spread of the inflammation into the spinal cord. The balance of the neuronal destruction is of the large-diameter sensory fibers causing deafferentiation of the control systems in the posterior horn cells. All this is accompanied by severe pain which requires management with strong analgesics in full doses.
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to reduce the incidence of the post-herpetic pain syndrome. Anti-convulsant medication for control of bursts is started with sodium valproate 200 mg at night, increasing to 200 mg until control is achieved. Amitriptyline 25 mg at night is started at the same time. This helps to achieve good sleep pattern and an improvement in the autonomic control. If necessary increase to 50 mg after one week. If burning is very troublesome and the disease is relatively recent, sympathetic ganglion blockade combined with a desensitizing programme is indicated, and repeat block after three days if necessary. If the scarred area is very sensitive despite the above procedures subcutaneous infiltration with local anesthetic and dilute Triamcinolone solution with further desensitizing is indicated. As with any patient who has had a long-standing chronic pain, psychological changes may have taken place. Cranial neuralgias The pain in the distribution of cranial nerves this is Cranial Neuralgia. The various forms of cranial neuralgias have been outlined under the following headings: 1. Tic like pain of cranial nerve origin or the classical cranial neuralgia Trigeminal Neuralgia : With an annual incidence of approx. 4.5 per 1 lac,11 the disorder usually occurs in middle and late age but even young adults and children can be affected. The male to female ratio of occurrence is 1: 1.6.
Nature of pain : (1) Spontaneous posterior horn cell activity leading to bursts of pain and to a vibrating jaggy pain referred to the stigmatized area. (2) Reflex sympathetic dystrophy with burning pain in the segment due to over activity of the sympathetic control systems. (3) Hypersensitivity in the scarred area due to continuing inflammatory changes in the nerve endings and continued release of histamine and bradykinin. With complete nerve destruction, these symptoms may become quiescent and the area may become numb. (4) The whole syndrome goes dormant during sleep is another common feature and an important management ploy.
The symptoms include paroxysm of pain in the distribution of the second and third divisions of the trigeminal nerve. The first division can be involved in about 5 % of cases. The pain is described as lancinating, shooting or electric shock like. It typically lasts for several seconds to two minutes but can occur repetitively many times an hour through out the day and night and might last for weeks at a time. After attacks that occur over several hours the facial pain might linger continuously. The severe paroxysm causes the patient to wince, giving rise to term Tic. The pain can be triggered by stimulation within any area of the affected nerve(s) in the form of light touch, eating, talking, and shaving, yawning, or brushing of teeth. The disorder is episodic with relapses and remissions over many years. The periods of remissions might last for months to years. The reason for the relapses and remissions is unknown. The large majority of trigeminal neuralgia is unilateral but bilateral neuralgia is present in 3-5% cases.1 It is classified as being primary (idiopathic) or secondary to structural intracranial lesions.
Management : The active treatment of the acute infection should reduce the incidence of long-term pain, and application of idoxuridine solution to the vesicles and systemic anti-viral medications such as amantadine appear
Glossopharyngeal Neuralgia : This pain syndrome has similar pain characteristic to trigeminal neuralgia, but the distribution of pain is localized to the glossopharyngeal nerve. The pain is paroxysmal, has a lancinating / sharp
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quality, and is localized to the throat, posterior third of tongue, tonsillar region, nasopharynx, larynx and ear. The pain can be triggered by swallowing, chewing, laughing, yawning, and talking. Rarely the pain may be bilateral. Bradycardia and syncope can be associated with a paroxysm of pain.
of the head, upper respiratory tract infection, tonsillectomy, and carotid end arterectomy. Structural lesions must be excluded through appropriate investigations. Treatment typically consists of local nerve block or ablation of the superior laryngeal nerve.1
For most cases, the neuralgia is primary with no specific aetiology, although there is evidence of micro vascular compression of the auriculo pharyngeal branch of 9th and 10th cranial nerves to be the underlying lesion. The clinical examination in that case demonstrates sensory or motor neurological deficit in the 9th and 10th cranial distribution.1
Other neuralgias : Neuralgias involving the naso cilliary and supra orbital nerves have been described and are rare. They differ only in location in that the symptoms occur in the distribution of each respective nerve. The pain is again paroxysmal and lancinating in nature. Structural lesions must be eliminated through thorough investigations before making a diagnosis. Treatment typically consists of local nerve block or ablation of the appropriate nerve as the last resort.1
Treatment : Includes carbamazepine, phenytoin, gabapentin, clonazepam or baclofen individually or in combination. If these treatments do not adequately control the patient’s symptoms, consideration should be given to nerve block and section of Glossopharyngeal nerve and the upper rootlets of the vagus nerve, which relieves the pain in the majority of patients. Micro vascular decompression of the root entry zone of the Glossopharyngeal nerve has also been reported to alleviate the pain.12 Nervus intermedius neuralgia of Hunt (Geniculate neuralgia) : This exceedingly rare pain syndrome, which tends to affect patients of middle age, involves the pinna of the ear and the auditory canal and has been related to neuralgia of the geniculate ganglion and nervus intermedius. The clinical features of this disorder are paroxysms of pain lasting for seconds to minutes. Longer, more persistent burning / sharp pain has also been described and occassionally abnormalities of lacrimation, salivation and taste can be associated. The pain is triggered by light touch within the posterior aspect of the auditory canal. Though some patients with this disorder respond to treatment with carbamazepine, Lovely and Jannetta report favorable pain relief with nerve block excision of nervus intermedius and geniculate ganglion.13 Occipital neuralgia : A paroxysmal pain disorder in the distribution of the greater, lesser or third occipital nerves can occur unilaterally or sometimes bilaterally, and is associated occassionally with sensory loss in the distribution of the affected nerve(s). The pain in occipital neuralgia is sharp shooting / lancinating in quality, although a more constant dull ache may be present in the appropriate distribution. Treatment :- Carbamazepine can eliminate or reduce the pain in some patients. Effective but often only temporary treatment may be accomplished with local anesthetic injections alone or in combination with a corticosteroid injection. Sectioning of the nerve is futile and this can promote the development of a neuroma or anesthesia dolorosa.1 Superior laryngeal neuralgia : The neuralgic pain occurs in the throat, sub Mandibular region and below ear. The precipitating factors are swallowing, shouting, turning
2. Persistent pain of cranial nerve origin Various pathological lesions of cranial nerves such as demyelination of optic nerve, inflammation of dorsal root ganglion, infarction or compression of occulomotor nerve may lead to persistent pain. Compression/ distortion of cranial nerves and C2, C3 nerve roots : It includes conditions like Tolosa-Hunt Syndrome, Neck-Tongue syndrome, Gradenigo Syndrome, Raeder Para trigeminal syndrome. 3. Headache and facial pain of central origin (A) Anesthesia dolorosa : This is pain in the region of numbness. Over the 5th cranial nerve distribution on the face this type of pain, allodynia and sensory deficit some times occurs after radio frequency thermo coagulation or after Gamma-knife stereo tactic radio surgery of trigeminal neuralgia, if the posterior nerve roots are damaged. This is deafferentiation pain secondary to posterior rhizotomy (B) Thalamic pain : In central nervous system lesion, such pain may occur due to damage of the second order trigeminal neurons, spinothalamic tract or ventrobasal nucleus of thalamus. 4. Atypical facial pain Atypical facial pain is terms given to patients who do not fall in to the diagnostic categories of the other possible aetiologies of facial pain and where investigations have failed to yield a root cause for the patient’s symptoms. The patients tend to be female. Pain is intense, burning or aching in nature and is poorly localized. There is a high incidence of depression and anxiety. Treatment typically consists of Tricyclic antidepressants, mono amine oxidase inhibitors (MAOIs), or benzodiazepines.14 Chronic pancreatitis It is an inflammatory disorder of pancreas which includes recurrent or persistent abdominal pain in the epigastrium, worsened by eating, associated with exocrine and endocrine insufficiency. In 70% patients it is caused by alcoholism while in rest of patients malnutrition, pancreatic
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duct obstruction, cystic fibrosis and trauma are the possible causes. The serum amylase levels are infrequently elevated while insulin deficiency and abnormal glucose tolerance tests are indicative of the diagnosis. An ultrasound, CT scan, endoscopic pancreatography differentiate between chronic pancreatitis and malignancy.1 Treatment : It involves abstinence from alcohol, support for endocrine and exocrine insuffiency (insulin and pancreatic enzymes) and palliation of painful symptoms. Cimetidine for reducing pancreatic secretion and octreotide for relief of pain has limited success. Narcotics are used for pain relief mostly. The left celiac ganglionic block or splanchnic nerve block may relieve pain. The use of local analgesics or alcohol for these blocks can provide pain relief. The resection of celiac ganglion through a surgical operation has been done. Surgical therapy includes endoscopic retrograde cannulation of pancreas, partial pancreatic resection, pancreatico jejenostomy. The overall relief of pain from above procedures varies from 50% to 80% since the pain is related to secretary capacity of pancreas. References 1. Kumar P. A text book of pain, 1st edition, New Delhi, Modern Publishers 2005: 9-15. 2. Kumar Pramod. A guide to peripheral nerve blocks. 1 st edition, New Delhi, Modern Publishers 2005: 2-4. 3. Kumar P. Terminal Cancer Care, 1st edition, New Delhi, Modern Publishers 2005: 10-20.
4. Janig W, Baron R. Complex regional pain syndrome is a disease of central nervous system. Clin Auton Res 2002; 12: 150-164. 5. Roberts WJ. Hypothesis on the physiological basis for causalgia and related pain. Pain 1986; 24: 297-311. 6. Campbell, JN, Meyer RA, Raja SN. Is nociceptors activation by alpha-1 adrenoreceptors, the culprit in sympathetically mediated pain? APS journal 1992; 1: 43-47. 7. 2, Bonica JJ. casualties and other sympathetic dystrophies. Post Grad med 1973; 53: 143. 8. Price DD, Mao J, Meyer DJ. Neural mechanism of normal and abnormal painstates in Raj PP.(Ed), current review of pain, Philadelphia, Saunders 1984; 25-41. 9. Kumar P. A Text Book Of Pain, 1st edition, New Delhi , Modern Publishers 2005; 251. 10. Loeser JD. Treatment of herpes zoster in elderly patients, pain 1986; 25: 149-164. 11. Katusic S, Williams D, Beard C, Bergstralh E, Kurland L. Epidemiology and clinical features of idiopathic trigeminal neuralgia. Similarities and differences, Rochester, Minnesota, 1945-1984. Neuro Epidemiology 1991; 10: 276-81. 12. Fraioli B, Esposito V, Ferrante L, Trubiani L, Lunardi P. Micro surgical treatment of Glossopharyngeal neuralgia: case reports.Neuro surgery 1989; 25: 630-32. 13. Lovely T, Janetta P. Surgical Management of geniculate neuralgia. Am J Otol 1997; 18: 512-17. 14. Paulson GW. Atypical facial pain. Oral surg oral med oral pathol 1977; 43: 338-41.
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