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Sensory neuropathy of the trigeminal, glossopharyngeal, and vagal nerves in Sjögren's syndrome
Journal of the Neurological Sciences 186 Ž2001. 59–63 www.elsevier.comrlocaterjns
Sensory neuropathy of the trigeminal, glossopharyngeal, and vagal nerves in Sjogren’s syndrome ¨ P.P. Urban a,) , A. Keilmann b, E.M. Teichmann c , H.C. Hopf a a
b
Department of Neurology, UniÕersity Hospital of Mainz, Mainz, Germany Department of Communication Disorders, UniÕersity Hospital of Mainz, Mainz, Germany c Department of Radiology, UniÕersity Hospital of Mainz, Mainz, Germany
Received 28 September 2000; received in revised form 28 February 2001; accepted 28 February 2001
Abstract Isolated cranial nerve involvement in primary Sjogren’s syndrome Žprimary SS. has rarely been described. We report the case of a ¨ patient with sensory neuropathy of the trigeminal and also the glossopharyngeal and vagal nerves, which has not been identified previously. The electrophysiological findings in our patient with primary SS confirmed trigeminal sensory neuropathy with abnormal blink reflexes and abnormal cutaneous masseter inhibitory reflexes. q 2001 Elsevier Science B.V. All rights reserved. Keywords: Sensory neuropathy; Sjogren’s syndrome; Trigeminal nerve; Glossopharyngeal nerve; Vagal nerve ¨
1. Introduction Peripheral neuropathy, most commonly of the distal sensory symmetrical type w1x, is present in 10–20% of cases with primary Sjogren’s syndrome Žprimary SS.. Iso¨ lated cranial nerve lesions in primary SS, affecting the third w2x, fourth w3x, fifth w4–7x, sixth w8x, and seventh w9x nerve have been reported previously. In addition, pure sensory neuropathy ŽPSN. of the limbs with w10x trigeminal nerve involvement w10,11x has been described in patients with Sjogren’s syndrome ŽSS.. ¨ We observed a patient presenting with primary SS and isolated cranial sensory neuropathy involving not only both trigeminal nerves, but also both glossopharyngeal and vagal nerves, which has not been identified thus far.
2. Case report A 53-year-old woman presented with an 8-year history of primary SS with initial recurrent corneal ulcerations of
)
Corresponding author. Department of Neurology, University of Mainz, Langenbeckstrasse 1, D 55101 Mainz, Germany. Tel.: q49-6131175162; fax: q49-6131-173271. E-mail address: [email protected] ŽP.P. Urban..
both eyes. One year after the onset, she noted progressive numbness of the perioral region including the lips, beginning on the right side of the face, followed by numbness of the entire face and mouth without awareness of saliva dribbling and running of the nose. The patient also reported a change in her voice, especially when singing at a high pitch, and further complained of dysphagia. During the past 6 years, she experienced intraoral burning sensations and reduced taste perception. The neurological examination showed a decreased perception of pinprick, light touch, and temperature in all three trigeminal divisions on both sides, including the intraoral area, i.e. the area of the glossopharyngeal nerves Žpharynx, soft palate, posterior third of the tongue, lingual side of the epiglottis. and the vagal nerve innervated area Žlaryngeal side of the epiglottis and ventricular folds.. The corneal reflex was diminished bilaterally and the gag reflex was abolished. Taste was slightly impaired for all qualities. Cranial motor functions and masseter reflex were intact. The remaining neurostatus was normal. There was no lung or renal involvement and no history of oral ulcers. Laboratory data included normal sedimentation rate and other routine parameters. ANA, anti-SSA ŽRo., anti-SSB ŽLA., rheumatoid factor, ANCA, AMA, dsDNA, thyroid microsomal antibodies, thyroglobulin, cryoglobulines, and angiotensin-converting enzyme were negative. Immunoelectrophoresis and immunofixation of serum and urine
0022-510Xr01r$ - see front matter q 2001 Elsevier Science B.V. All rights reserved. PII: S 0 0 2 2 - 5 1 0 X Ž 0 1 . 0 0 5 0 1 - 9
60
P.P. Urban et al.r Journal of the Neurological Sciences 186 (2001) 59–63
showed no monoclonal proteins. The CSF was normal. Schirmer’s test showed bilaterally decreased lacrimation Ž2 mm in 5 min. and markedly reduced saliva flow. Salivary gland biopsy revealed chronic fibrosing sialoadenitis with agglomerates of more than 50 mononuclear cells. 2.1. Videofluorography Lateral and anteroposterior views were acquired at 25 imagesrs with the patient swallowing 15 ml of thin liquid
barium in the supine position. Our patient demonstrated oral hypomotility and a considerably prolonged oral phase with repeated to-and-fro movements of the bolus, resulting in delayed triggering of the swallowing reflex. After swallowing reflex initiation, however, the pharyngeal and oesophageal phases showed no abnormalities, and no aspiration occurred. Neurophysiological examinations followed standard procedure described previously w12–14x. Blink reflex R1components were bilaterally absent and the R2-compo-
Fig. 1. Ža. Electrically induced blink reflex with bilaterally absent R1- and delayed R2-components Žstimulation at 0 ms.. Žb. Electrically induced blink reflex in a healthy subject Žstimulation at 0 ms..
P.P. Urban et al.r Journal of the Neurological Sciences 186 (2001) 59–63
61
Fig. 1 Ž continued ..
nents were delayed to 43.4–45.1 ms Žnormal - 40 ms. ŽFig. 1a.. The stimulation threshold of the blink reflex was increased to 45 mA Žnormal - 15 mA.. Cutaneous masseter inhibitory reflexes Žexteroceptive suppression, ES 1 and ES 2. were absent bilaterally up to a stimulation intensity of 50 mA Žnormal - 25 mA. ŽFig. 2a.. The masseter reflex Žjaw reflex. latencies were normal. Magnetic resonance imaging ŽMRI. ŽT1- and T2weighted with gadolinium. and MR-angiography of the brain were normal, and no contrast enhancement was
observed along the course of the trigeminal, glossopharyngeal, and vagal nerves. 3. Discussion European multicenter study w15,16x recently defined and validated diagnostic criteria for the diagnosis of primary SS as follows: Ž1. symptoms of dry eyes Žxerophthalmia. defined by a positive response to one or more of three specifically worded questions; Ž2. dry mouth Žxerostomia.
62
P.P. Urban et al.r Journal of the Neurological Sciences 186 (2001) 59–63
Fig. 2. Ža. Electrically induced masseter inhibitory reflex with bilaterally absent silent-periods Žstimulation at 20 ms.. Žb. Electrically induced masseter inhibitory reflex in a healthy subject Žstimulation at 20 ms..
defined by a positive response to one or more of three specifically worded questions; Ž3. ocular signs including a positive Schirmer’s test or rose Bengal dye test for keratoconjunctivitis; Ž4. diagnostic histopathologic features in salivary gland biopsy; Ž5. one or more of three other
specific salivary gland abnormalities Žsaliva scintigraphy, parotid scintigraphy, unstimulated saliva flow.; and Ž6. present RorSS-A or LarSS-B antibodies. In patients without any possibly associated disease, the presence of any four of the six items is regarded as indicative of primary
P.P. Urban et al.r Journal of the Neurological Sciences 186 (2001) 59–63
SS. In our patient, five out of the six listed diagnostic criteria were positive, thus, allowing the definite diagnosis of primary SS. Other diagnoses were excluded. Trigeminal sensory neuropathy characterized by slowly progressing unilateral or bilateral facial numbness or paresthesia and occasionally associated with pain has been reported in association with many of the connective tissue diseases, including PSS, systemic sclerosis, mixed connective tissue disease, systemic lupus erythematosus, dermatomyositis, and amyloidosis w4,7,17x. The sensory deficits in our patient also involved the pharyngeal and laryngeal region with abolished gag reflex, an indication of additional bilateral sensory involvement of the glossopharyngeal and vagal nerves. We could find no previously reported cases with this combination in primary SS. The electrophysiological findings in our patient confirmed trigeminal sensory neuropathy with abnormal blink reflexes and abnormal cutaneous masseter inhibitory reflexes. The masseter reflex was normal, indicating normal function of the thick myelinated proprioceptive trigeminal afferents. This electrophysiological pattern is consistent with previously reported findings Žabnormal blink reflexes and cutaneous masseter inhibitory reflex, normal masseter reflex. in patients with primary SS and sensory neuropathy w9x. Dysphagia as a sequelae of delayed initiation of the swallowing function shown by videofluorography is most likely due to a combination of xerostomia and sensory neuropathy w18,19x. Saliva production is required for normal bolus formation and lubrication and provides an important sensory cue in triggering of the pharyngeal swallow response w20x. However, after triggering the swallowing reflex, the pharyngeal and esophageal stages of deglutition showed no abnormalities, thus, supporting the concept of a preprogrammed motor swallowing sequence, independent of sensory afferents w21x. The minimal pathological data available on primary SS-associated sensory neuropathy demonstrates ganglionitis with lymphocytic T-cell infiltration in patients with sensory neuropathy of the limbs w22x, although the target antigen responsible for sensory neuropathy is not yet identified. These findings support the assumption of peripheral myelinated axon degeneration due to an inflammatory lesion of the gasserian ganglion w7x. The cause of trigeminal sensory neuropathy in SS is suspected to be due to either vasculitis or fibrosis w7,23x.
References w1x Olney RK. Neuropathies associated with connective tissue disease. Semin Neurol 1998;18:63–72.
63
w2x Pou-Serradell A, Vinas-Gaya J. Trois cas de neuropathies periphe´ ´ riques rares associees primitif. ´ au syndrome de Gougerot–Sjogren ¨ Rev Neurol 1993;149:481–4. w3x Kuhl V, Urban PP, Mayet WJ, Hopf HC. Isolated trochlear nerve palsy and repetitive Raynaud’s phenomenon of the tongue in primary Sjogren’s syndrome. J Neurol 1999;246:974–5. ¨ w4x Ashworth B, Tait GBW. Trigeminal neuropathy in connective tissue disease. Neurology 1971;21:609–14. w5x Graus F, Pou A, Kanterewicz E, Anderson NE. Sensory neuronopathy and Sjogren’s syndrome: clinical and immunological study of ¨ two patients. Neurology 1988;38:1637–9. w6x Kaltreider HB, Talal N. The neuropathy of Sjogren’s syndrome: ¨ trigeminal nerve involvement. Ann Int Med 1969;70:751–62. w7x Lecky BRF, Hughes RAC, Murray NMF. Trigeminal sensory neuropathy. Brain 1987;110:1463–85. w8x Matsukawa Y, Nishinarita S, Morie T. Abducent and trochlear palsies in a patient with Sjogren’s syndrome. Br J Rheumatol ¨ 1995;34:484–5. w9x Valls-Sole J, Graus F, Font J, Pou A, Tolosa ES. Normal proprioceptive trigeminal afferents in patients with Sjogren’s syndrome and ¨ sensory neuronopathy. Ann Neurol 1990;28:786–90. w10x Vincent D, Loron P, Awada A, Gautier JC. Paralysies multiples et recidivantes des nerfs craniens. Syndrome de Gougerot–Sjogren. ´ ¨ Rev Neurol 1984;4:318–21. w11x Malinow K, Yannakakis GD, Glusman SM, et al. Subacute sensory neuronopathy secondary to dorsal root ganglionitis in primary Sjogren’s syndrome. Ann Neurol 1986;27:304–15. ¨ w12x Hopf HC. Topodiagnostic value of brain stem reflexes. Muscle Nerve 1994;17:475–84. w13x Connemann BJ, Urban PP, Luttkopf V, Hopf HC. A fully automated ¨ system for the evaluation of masseter silent periods. Electroencephalogr Clin Neurophysiol 1997;105:53–7. w14x Urban PP, Forst T, Lenfers M, Koehler J, Connemann BJ, Beyer J. Incidence of subclinical trigeminal and facial nerve involvement in diabetes mellitus. Electroencephalogr Clin Neurophysiol 1999;39: 267–72. w15x Vitali C, Bombardieri S, Moutsopoulos HM, et al. Preliminary criteria for the classification of Sjogren’s syndrome. Arthritis Rheum ¨ 1993;36:340–7. w16x Vitali C, Bombardieri S, Moutsopoulos HM, et al. Assessment of the European classification criteria for Sjogren’s syndrome in a series of ¨ clinically defined cases: results of a prospective multicentre study. Ann Rheum Dis 1996;55:116–21. w17x Traynor AE, Gertz MA, Kyle RA. Cranial neuropathy associated with primary amyloidosis. Ann Neurol 1991;29:451–4. w18x Bastian RW, Riggs LC. Role of sensation in swallowing function. Laryngoscope 1999;109:1974–7. w19x Mansson J, Sandberg N. Effects of surface anesthesia on deglutition in man. Laryngoscope 1974;84:427–37. w20x Cook IJS. Normal and disordered swallowing: new insights. Bailliere’s Clin Gastroenterol 1991;5:245–67. ` w21x Dodds WJ, Stewart ET, Logemann JA. Physiology and radiology of the normal oral and pharyngeal phase of swallowing. Am J Radiol 1990;154:953–63. w22x Griffin JW, Cornblath DR, Alexander E, Campbell J, Low PA, Bird S, et al. Ataxic sensory neuropathy and dorsal root ganglionitis associated with Sjogren’s syndrome. Ann Neurol 1990;27:304–15. ¨ w23x Fox RI, Robinson CA, Curd JG, Kozin F, Howell FV. Sjogren’s ¨ syndrome: proposed criteria for classification. Arthritis Rheum 1986;29:577–85.
Sensory neuropathy of the trigeminal, glossopharyngeal, and vagal nerves in Sjogren’s syndrome ¨ P.P. Urban a,) , A. Keilmann b, E.M. Teichmann c , H.C. Hopf a a
b
Department of Neurology, UniÕersity Hospital of Mainz, Mainz, Germany Department of Communication Disorders, UniÕersity Hospital of Mainz, Mainz, Germany c Department of Radiology, UniÕersity Hospital of Mainz, Mainz, Germany
Received 28 September 2000; received in revised form 28 February 2001; accepted 28 February 2001
Abstract Isolated cranial nerve involvement in primary Sjogren’s syndrome Žprimary SS. has rarely been described. We report the case of a ¨ patient with sensory neuropathy of the trigeminal and also the glossopharyngeal and vagal nerves, which has not been identified previously. The electrophysiological findings in our patient with primary SS confirmed trigeminal sensory neuropathy with abnormal blink reflexes and abnormal cutaneous masseter inhibitory reflexes. q 2001 Elsevier Science B.V. All rights reserved. Keywords: Sensory neuropathy; Sjogren’s syndrome; Trigeminal nerve; Glossopharyngeal nerve; Vagal nerve ¨
1. Introduction Peripheral neuropathy, most commonly of the distal sensory symmetrical type w1x, is present in 10–20% of cases with primary Sjogren’s syndrome Žprimary SS.. Iso¨ lated cranial nerve lesions in primary SS, affecting the third w2x, fourth w3x, fifth w4–7x, sixth w8x, and seventh w9x nerve have been reported previously. In addition, pure sensory neuropathy ŽPSN. of the limbs with w10x trigeminal nerve involvement w10,11x has been described in patients with Sjogren’s syndrome ŽSS.. ¨ We observed a patient presenting with primary SS and isolated cranial sensory neuropathy involving not only both trigeminal nerves, but also both glossopharyngeal and vagal nerves, which has not been identified thus far.
2. Case report A 53-year-old woman presented with an 8-year history of primary SS with initial recurrent corneal ulcerations of
)
Corresponding author. Department of Neurology, University of Mainz, Langenbeckstrasse 1, D 55101 Mainz, Germany. Tel.: q49-6131175162; fax: q49-6131-173271. E-mail address: [email protected] ŽP.P. Urban..
both eyes. One year after the onset, she noted progressive numbness of the perioral region including the lips, beginning on the right side of the face, followed by numbness of the entire face and mouth without awareness of saliva dribbling and running of the nose. The patient also reported a change in her voice, especially when singing at a high pitch, and further complained of dysphagia. During the past 6 years, she experienced intraoral burning sensations and reduced taste perception. The neurological examination showed a decreased perception of pinprick, light touch, and temperature in all three trigeminal divisions on both sides, including the intraoral area, i.e. the area of the glossopharyngeal nerves Žpharynx, soft palate, posterior third of the tongue, lingual side of the epiglottis. and the vagal nerve innervated area Žlaryngeal side of the epiglottis and ventricular folds.. The corneal reflex was diminished bilaterally and the gag reflex was abolished. Taste was slightly impaired for all qualities. Cranial motor functions and masseter reflex were intact. The remaining neurostatus was normal. There was no lung or renal involvement and no history of oral ulcers. Laboratory data included normal sedimentation rate and other routine parameters. ANA, anti-SSA ŽRo., anti-SSB ŽLA., rheumatoid factor, ANCA, AMA, dsDNA, thyroid microsomal antibodies, thyroglobulin, cryoglobulines, and angiotensin-converting enzyme were negative. Immunoelectrophoresis and immunofixation of serum and urine
0022-510Xr01r$ - see front matter q 2001 Elsevier Science B.V. All rights reserved. PII: S 0 0 2 2 - 5 1 0 X Ž 0 1 . 0 0 5 0 1 - 9
60
P.P. Urban et al.r Journal of the Neurological Sciences 186 (2001) 59–63
showed no monoclonal proteins. The CSF was normal. Schirmer’s test showed bilaterally decreased lacrimation Ž2 mm in 5 min. and markedly reduced saliva flow. Salivary gland biopsy revealed chronic fibrosing sialoadenitis with agglomerates of more than 50 mononuclear cells. 2.1. Videofluorography Lateral and anteroposterior views were acquired at 25 imagesrs with the patient swallowing 15 ml of thin liquid
barium in the supine position. Our patient demonstrated oral hypomotility and a considerably prolonged oral phase with repeated to-and-fro movements of the bolus, resulting in delayed triggering of the swallowing reflex. After swallowing reflex initiation, however, the pharyngeal and oesophageal phases showed no abnormalities, and no aspiration occurred. Neurophysiological examinations followed standard procedure described previously w12–14x. Blink reflex R1components were bilaterally absent and the R2-compo-
Fig. 1. Ža. Electrically induced blink reflex with bilaterally absent R1- and delayed R2-components Žstimulation at 0 ms.. Žb. Electrically induced blink reflex in a healthy subject Žstimulation at 0 ms..
P.P. Urban et al.r Journal of the Neurological Sciences 186 (2001) 59–63
61
Fig. 1 Ž continued ..
nents were delayed to 43.4–45.1 ms Žnormal - 40 ms. ŽFig. 1a.. The stimulation threshold of the blink reflex was increased to 45 mA Žnormal - 15 mA.. Cutaneous masseter inhibitory reflexes Žexteroceptive suppression, ES 1 and ES 2. were absent bilaterally up to a stimulation intensity of 50 mA Žnormal - 25 mA. ŽFig. 2a.. The masseter reflex Žjaw reflex. latencies were normal. Magnetic resonance imaging ŽMRI. ŽT1- and T2weighted with gadolinium. and MR-angiography of the brain were normal, and no contrast enhancement was
observed along the course of the trigeminal, glossopharyngeal, and vagal nerves. 3. Discussion European multicenter study w15,16x recently defined and validated diagnostic criteria for the diagnosis of primary SS as follows: Ž1. symptoms of dry eyes Žxerophthalmia. defined by a positive response to one or more of three specifically worded questions; Ž2. dry mouth Žxerostomia.
62
P.P. Urban et al.r Journal of the Neurological Sciences 186 (2001) 59–63
Fig. 2. Ža. Electrically induced masseter inhibitory reflex with bilaterally absent silent-periods Žstimulation at 20 ms.. Žb. Electrically induced masseter inhibitory reflex in a healthy subject Žstimulation at 20 ms..
defined by a positive response to one or more of three specifically worded questions; Ž3. ocular signs including a positive Schirmer’s test or rose Bengal dye test for keratoconjunctivitis; Ž4. diagnostic histopathologic features in salivary gland biopsy; Ž5. one or more of three other
specific salivary gland abnormalities Žsaliva scintigraphy, parotid scintigraphy, unstimulated saliva flow.; and Ž6. present RorSS-A or LarSS-B antibodies. In patients without any possibly associated disease, the presence of any four of the six items is regarded as indicative of primary
P.P. Urban et al.r Journal of the Neurological Sciences 186 (2001) 59–63
SS. In our patient, five out of the six listed diagnostic criteria were positive, thus, allowing the definite diagnosis of primary SS. Other diagnoses were excluded. Trigeminal sensory neuropathy characterized by slowly progressing unilateral or bilateral facial numbness or paresthesia and occasionally associated with pain has been reported in association with many of the connective tissue diseases, including PSS, systemic sclerosis, mixed connective tissue disease, systemic lupus erythematosus, dermatomyositis, and amyloidosis w4,7,17x. The sensory deficits in our patient also involved the pharyngeal and laryngeal region with abolished gag reflex, an indication of additional bilateral sensory involvement of the glossopharyngeal and vagal nerves. We could find no previously reported cases with this combination in primary SS. The electrophysiological findings in our patient confirmed trigeminal sensory neuropathy with abnormal blink reflexes and abnormal cutaneous masseter inhibitory reflexes. The masseter reflex was normal, indicating normal function of the thick myelinated proprioceptive trigeminal afferents. This electrophysiological pattern is consistent with previously reported findings Žabnormal blink reflexes and cutaneous masseter inhibitory reflex, normal masseter reflex. in patients with primary SS and sensory neuropathy w9x. Dysphagia as a sequelae of delayed initiation of the swallowing function shown by videofluorography is most likely due to a combination of xerostomia and sensory neuropathy w18,19x. Saliva production is required for normal bolus formation and lubrication and provides an important sensory cue in triggering of the pharyngeal swallow response w20x. However, after triggering the swallowing reflex, the pharyngeal and esophageal stages of deglutition showed no abnormalities, thus, supporting the concept of a preprogrammed motor swallowing sequence, independent of sensory afferents w21x. The minimal pathological data available on primary SS-associated sensory neuropathy demonstrates ganglionitis with lymphocytic T-cell infiltration in patients with sensory neuropathy of the limbs w22x, although the target antigen responsible for sensory neuropathy is not yet identified. These findings support the assumption of peripheral myelinated axon degeneration due to an inflammatory lesion of the gasserian ganglion w7x. The cause of trigeminal sensory neuropathy in SS is suspected to be due to either vasculitis or fibrosis w7,23x.
References w1x Olney RK. Neuropathies associated with connective tissue disease. Semin Neurol 1998;18:63–72.
63
w2x Pou-Serradell A, Vinas-Gaya J. Trois cas de neuropathies periphe´ ´ riques rares associees primitif. ´ au syndrome de Gougerot–Sjogren ¨ Rev Neurol 1993;149:481–4. w3x Kuhl V, Urban PP, Mayet WJ, Hopf HC. Isolated trochlear nerve palsy and repetitive Raynaud’s phenomenon of the tongue in primary Sjogren’s syndrome. J Neurol 1999;246:974–5. ¨ w4x Ashworth B, Tait GBW. Trigeminal neuropathy in connective tissue disease. Neurology 1971;21:609–14. w5x Graus F, Pou A, Kanterewicz E, Anderson NE. Sensory neuronopathy and Sjogren’s syndrome: clinical and immunological study of ¨ two patients. Neurology 1988;38:1637–9. w6x Kaltreider HB, Talal N. The neuropathy of Sjogren’s syndrome: ¨ trigeminal nerve involvement. Ann Int Med 1969;70:751–62. w7x Lecky BRF, Hughes RAC, Murray NMF. Trigeminal sensory neuropathy. Brain 1987;110:1463–85. w8x Matsukawa Y, Nishinarita S, Morie T. Abducent and trochlear palsies in a patient with Sjogren’s syndrome. Br J Rheumatol ¨ 1995;34:484–5. w9x Valls-Sole J, Graus F, Font J, Pou A, Tolosa ES. Normal proprioceptive trigeminal afferents in patients with Sjogren’s syndrome and ¨ sensory neuronopathy. Ann Neurol 1990;28:786–90. w10x Vincent D, Loron P, Awada A, Gautier JC. Paralysies multiples et recidivantes des nerfs craniens. Syndrome de Gougerot–Sjogren. ´ ¨ Rev Neurol 1984;4:318–21. w11x Malinow K, Yannakakis GD, Glusman SM, et al. Subacute sensory neuronopathy secondary to dorsal root ganglionitis in primary Sjogren’s syndrome. Ann Neurol 1986;27:304–15. ¨ w12x Hopf HC. Topodiagnostic value of brain stem reflexes. Muscle Nerve 1994;17:475–84. w13x Connemann BJ, Urban PP, Luttkopf V, Hopf HC. A fully automated ¨ system for the evaluation of masseter silent periods. Electroencephalogr Clin Neurophysiol 1997;105:53–7. w14x Urban PP, Forst T, Lenfers M, Koehler J, Connemann BJ, Beyer J. Incidence of subclinical trigeminal and facial nerve involvement in diabetes mellitus. Electroencephalogr Clin Neurophysiol 1999;39: 267–72. w15x Vitali C, Bombardieri S, Moutsopoulos HM, et al. Preliminary criteria for the classification of Sjogren’s syndrome. Arthritis Rheum ¨ 1993;36:340–7. w16x Vitali C, Bombardieri S, Moutsopoulos HM, et al. Assessment of the European classification criteria for Sjogren’s syndrome in a series of ¨ clinically defined cases: results of a prospective multicentre study. Ann Rheum Dis 1996;55:116–21. w17x Traynor AE, Gertz MA, Kyle RA. Cranial neuropathy associated with primary amyloidosis. Ann Neurol 1991;29:451–4. w18x Bastian RW, Riggs LC. Role of sensation in swallowing function. Laryngoscope 1999;109:1974–7. w19x Mansson J, Sandberg N. Effects of surface anesthesia on deglutition in man. Laryngoscope 1974;84:427–37. w20x Cook IJS. Normal and disordered swallowing: new insights. Bailliere’s Clin Gastroenterol 1991;5:245–67. ` w21x Dodds WJ, Stewart ET, Logemann JA. Physiology and radiology of the normal oral and pharyngeal phase of swallowing. Am J Radiol 1990;154:953–63. w22x Griffin JW, Cornblath DR, Alexander E, Campbell J, Low PA, Bird S, et al. Ataxic sensory neuropathy and dorsal root ganglionitis associated with Sjogren’s syndrome. Ann Neurol 1990;27:304–15. ¨ w23x Fox RI, Robinson CA, Curd JG, Kozin F, Howell FV. Sjogren’s ¨ syndrome: proposed criteria for classification. Arthritis Rheum 1986;29:577–85.