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Jugular foramen syndrome caused by varicella zoster virus infection in a patient with ipsilateral hypoplasia of the jugular foramen
Journal of the Neurological Sciences 172 (2000) 70–72 www.elsevier.com / locate / jns
Jugular foramen syndrome caused by varicella zoster virus infection in a patient with ipsilateral hypoplasia of the jugular foramen Toshihiro Hayashi*, Shigeo Murayama, Masaki Sakurai, Ichiro Kanazawa Department of Neurology, Division of Neuroscience, Graduate School of Medicine, The University of Tokyo, Hongo 7 -3 -1, Bunkyo-ku, Tokyo 113 -8655, Japan Received 5 January 1999; received in revised form 14 September 1999; accepted 6 October 1999
Abstract We report a patient with acute cranial polyneuropathy with unilateral involvement of the ninth, tenth, and eleventh cranial nerves. Although this patient lacked a typical cutaneous herpetic manifestation, elevated levels of IgM and IgG antibodies to varicella zoster virus (VZV) in both the serum and cerebrospinal fluid confirmed the clinical diagnosis of VZV infection and zoster sine herpete. Coexisting hypoplasia of the ipsilateral jugular foramen was detected using three-dimensional, surface-rendering displays reconstructed from the cranial helical CT scan. The patient recovered almost completely following treatment with an anti-inflammatory corticosteroid. Anatomical narrowing of the jugular foramen in this patient may have contributed to entrapment of the affected nerves at their passage through the foramen. 2000 Published by Elsevier Science B.V. All rights reserved. Keywords: Jugular foramen syndrome; Hypoplasia of the jugular foramen; Varicella zoster virus infection; Zoster sine herpete; Nerve compression syndromes; Case report
1. Introduction A wide spectrum of neurologic complications have been recorded in association with varicella zoster virus (VZV) infection. Trigeminal and facial nerves are the most common nerves in cranial neuropathies associated with VZV infection. There are, however, only a few case reports of patients with a lower cranial polyneuropathy [1–8]. Here we report a patient with unilateral ninth, tenth, and eleventh cranial nerve palsy, associated with an elevated level of antibodies to VZV and hypoplasia of the ipsilateral jugular foramen. 2. Case report A 60-year-old man presented with acute dysphagia and *Corresponding author. Tel.: 181-3-5800-8672; fax: 181-3-58006548. E-mail address: [email protected] (T. Hayashi)
hoarseness of voice on June 27, 1997. He was admitted to a local hospital 3 days later, at which time, paralysis of the left pharynx and vocal cord was diagnosed. He was fed through a nasogastric tube. A lower pharyngeal tumor was suspected but was not found. Because his condition did not improve, he was transferred to our hospital on August 6, 1997. A neurological examination showed paralysis of the left soft palate and constrictor muscles of the pharynx, hypoesthesia of the left soft palate and pharynx, and weakness of the left sternocleidomastoid and left upper trapezius muscles with muscle atrophy. There was no impairment of taste sensation in the posterior third of the tongue or of muscle function. No meningeal signs, long tract signs, or autonomic dysfunction were observed. Herpetic eruption was neither observed nor recorded. Laryngoscopy showed that the left vocal cord was immobile and remained in the paramedian position. Audiometry was normal. Fluoroscopy showed paralysis of the left pharyngeal constrictor muscles and the pooling of contrast media in the left pyriform sinus
0022-510X / 00 / $ – see front matter 2000 Published by Elsevier Science B.V. All rights reserved. PII: S0022-510X( 99 )00263-4
T. Hayashi et al. / Journal of the Neurological Sciences 172 (2000) 70 – 72
after deglutition. Needle electromyography confirmed active neurogenic changes in the left sternocleidomastoid and left upper trapezius muscles. The left vocal cord was silent electrically. These findings were consistent with acute isolated left ninth, tenth, and eleventh cranial nerve palsy. Cerebrospinal fluid examination showed slight pleocytosis (7 / mm 3 ). Antibody levels to VZV were elevated in both the serum (IgM 3.17, IgG .128; normal value IgM,0.8, IgG,2.0) and cerebrospinal fluid (IgM 0.05, IgG 12.3) as shown by an EIA. This serological finding is consistent with acute VZV infection. Polymerase chain reaction (PCR) did not detect VZV DNA in the cerebrospinal fluid. Skull X-rays showed narrowing of the left jugular foramen. Three-dimensional surface-rendering displays, reconstructed from the cranial helical CT scans showed hypoplasia of the ipsilateral jugular foramen (Fig. 1). Magnetic resonance imaging (MRI) with contrast media did not show any abnormality of the cranial nerves or the brain stem. The patient gradually recovered from the severe dysphagia without medication but on August 15, 1997, suddenly complained of left deafness, tinnitus, and mild pain over the auricle. Audiometry detected moderate sensorineural deafness of the left ear. Vestibular function was intact. No auricular eruption was present. Hydrocortisone sodium succinate was administered intravenously at the average dose of 300 mg for 10 days, alprostadil alfadex (prostaglandin E1) at 60 mg for 10 days, and acyclovir at 750 mg for 7 days. The patient responded dramatically to this treatment and could swallow food on August 25, 1997. The follow-up examination 10 months later showed mild atrophy of the left vocal cord and a
71
decrease in left-side hearing acuity as the only sequelae of the event.
3. Discussion VZV causes cranial polyneuropathies such as trigeminal neuralgia and facial palsy [9], but lower cranial neuropathy is considered uncommon [1–4]. Jugular foramen syndrome with serologically proven VZV infection has been infrequently reported [5–7,10]. Our patient initially presented with unilateral jugular foramen syndrome, which was followed by ipsilateral acoustic neuropathy. The diagnosis of lower cranial neuropathy was based on the elevation of anti-VZV antibody in both his serum and cerebrospinal fluid. Detection of anti-VZV serum IgM is thought to establish the diagnosis of acute VZV infection [11,12]. Furthermore, anti-VZV antibody is not normally found in CSF, and its presence is a finding of essential diagnostic significance [13]. A negative PCR result is not necessarily in conflict with the diagnosis because PCR for VZV DNA does not always provide exquisite sensitivity for the diagnosis of subacute and chronic VZV infection [13]. In addition, diagnosis of herpes simplex encephalitis by PCR is known to be limited up to 4 weeks after the onset of neurological symptoms [14]. The patient’s CSF on which PCR was done was sampled 6 weeks after the onset of his symptoms, which might possibly have missed an optimal phase for PCR examination. Our case confirms the notion that anti-VZV antibody is useful in the diagnoses in patients with subacute and chronic VZV infection with
Fig. 1. A three-dimensional surface-rendering display, reconstructed from cranial helical CT scans with contrast media. Slice 1 mm thick. Hypoplasia of the posterior part of the left jugular foramen (arrow) produces a passage much narrower than the right one.
72
T. Hayashi et al. / Journal of the Neurological Sciences 172 (2000) 70 – 72
negative PCR result [12,13]. Moreover since our patient was considered to have ganglionitis of the ninth, tenth and eleventh cranial nerves, chance of detecting VZV DNA in CSF might be lower than those in patients with VZV encephalitis or myelitis. Hunt proposed that the lower cranial polyneuropathy associated with VZV infection may be caused by inflammation of the nuclei of the affected nerves [15]. This hypothesis is supported by recent MRI findings of gadolinium enhancement in the seventh, ninth, and tenth cranial nerve nuclei of a patient with lower cranial polyneuropathy associated with VZV infection [8]. No such enhancement was found in our patient, probably because the MRI study with enhancement was done after the optimal hyperacute phase. Inflammation of the nuclei associated with epineurial edema in our patient may have caused entrapment of the ninth, tenth, and eleventh cranial nerves where they pass through the hypoplastic jugular foramen. Rapid improvement in nerve function after corticosteroid administration supports this speculation. Entrapment of a peripheral nerve is thought to be a predisposing factor in other inflammatory neuropathies. Bell’s palsy, a common type of cranial neuropathy, also is considered to be caused by acute inflammation and edema of the facial nerve with subsequent entrapment of the nerve in the facial canal [16]. In Guillain-Barre´ syndrome, conduction block in the peripheral nerves frequently is detected at common sites of compression entrapment [17]. This patient initially presented with severe paralytic symptoms but only mild somatic sensory decline. In addition, taste sensation in the left posterior third of the tongue was not impaired. This sensorimotor dissociation suggests that the ninth cranial nerve was relatively unharmed. As they emerge from the jugular foramen, the tenth and eleventh cranial nerves are covered by the same sheath of dura mater and are separated from the ninth cranial nerve by a septum [2]. This anatomical separation may explain the focal sparing of the ninth cranial nerve from epineurial compression and edema, leading to milder damage. A noteworthy feature of this case was the lack of cutaneous herpetic manifestation throughout the course of the disease. A wide spectrum of neurological disorders that include cranial polyneuropathy, aseptic meningitis, encephalitis, acute polyneuropathy, and myelitis, are associated with VZV infection without skin lesions. This condition has been termed zoster sine herpete [18,19]. To our knowledge, jugular foramen syndrome associated with zoster sine herpete, has not previously been reported. VZV infection should be considered in patients with lower
cranial polyneuropathy, because acyclovir ameliorate the symptoms.
corticosteroid
and
References ¨ H, Wohlfart G. Herpes zoster of the seventh, eighth, ninth [1] Engstrom and tenth cranial nerves. Arch Neurol Psychiatry 1949;62:638–52. [2] Font JH. The jugular foramen syndrome. Evidence that transient cases may be of viral origin. Arch Otolaryngol 1952;56:134–41. [3] Sasaki H, Kawamoto S, Masuda N. Herpes of the ear lobe complicated with a mixed laryngeal paralysis. Otolaryngology (Tokyo) 1967;39:815–8, In Japanese. [4] Thomas JE, Howard FM. Segmental zoster paresis — a disease profile. Neurology 1972;22:459–66. [5] Kahane P, De Saint Victor JF, Besson G, Hommel M, Perret J. ´ ´ posterieur ´ Syndrome du trou dechire duˆ au zona. Rev Neurol (Paris) 1993;149:353–4. [6] Kondo M, Hokezu Y, Nagai M, Mori T, Nagamatsu K. A case of herpes zoster meningoencephalitis followed by involvement of cranial nerves IX, X, XI. Rinsho Shinkeigaku Clin Neurol (Tokyo) 1994;34:720–3, In Japanese. [7] Terai T, Kohira I, Shiro Y, Ishizu H, Shohmori T. Vernet syndrome induced by herpes zoster infection. A case report. Neurol Med (Tokyo) 1994;41:71–3, In Japanese. [8] Kikuchi H, Yoshimura T, Hara H, Mihara F, Kobayashi T. A case of multiple cranial neuropathy due to varicella-zoster virus infection: detection of involvement of cranial ganglia with MRI. Rinsho Shinkeigaku Clin Neurol (Tokyo) 1995;35:814–6, In Japanese. [9] Hunt JR. Herpetic inflammations of the geniculate ganglion. A new syndrome and its complications. J Nerv Ment Dis 1907;34:73–96. [10] Muroi M, Kamei T, Yasuoka Y, Ishii H, Watanabe K. Seven cases of cephalic herpes zoster with involvement of the lower cranial nerves. J Jpn Bronchoesophagol Soc 1987;38:434–40, In Japanese. [11] Brunell PA, Gershon AA, Uduman SA, Steinberg S. Varicella-zoster immunoglobulins during varicella, latency, and zoster. J Infect Dis 1975;132:49–54. [12] Gnann Jr. JW, Whitley RJ. Neurologic manifestations of varicella and herpes zoster. In: Scheld WM, Whitley RJ, Durack DT, editors, 2nd ed, Infections of the central nervous system, Philadelphia: Lippincott-Raven, 1997, pp. 91–105. [13] Gilden DH, Bennet JL, Kleinschmidt-DeMasters BK, Song DD, Yee AS, Steiner I. The value of cerebrospinal fluid antiviral antibody in the diagnosis of neurologic disease produced by varicella zoster virus. J Neurol Sci 1998;159:140–4. ˚ Forsgren M. ¨ [14] Aurelius E, Johansson B, Skoldenberg B, Staland A, Rapid diagnosis of herpes simplex encephalitis by nested polymerase chain reaction assay of cerebrospinal fluid. Lancet 1991;337:189–92. [15] Hunt JR. The symptom-complex of the acute posterior poliomyelitis of the geniculate, auditory, glossopharyngeal and pneumogastric ganglia. Arch Intern Med 1910;5:631–75. [16] Chadwick D. The cranial nerves and special senses. In: Walton J, editor, 10th ed, Brain’s disease of the nervous system, Oxford: Oxford University Press, 1993, pp. 76–126. [17] Brown WF, Feasby TE. Conduction block and denervation in Guillain-Barre´ polyneuropathy. Brain 1984;107:219–39. [18] Lewis GW. Zoster sine herpete. Br Med J 1958;2:418–21. [19] Mayo DR, Booss J. Varicella zoster-associated neurologic disease without skin lesions. Arch Neurol 1989;46:313–5.
Jugular foramen syndrome caused by varicella zoster virus infection in a patient with ipsilateral hypoplasia of the jugular foramen Toshihiro Hayashi*, Shigeo Murayama, Masaki Sakurai, Ichiro Kanazawa Department of Neurology, Division of Neuroscience, Graduate School of Medicine, The University of Tokyo, Hongo 7 -3 -1, Bunkyo-ku, Tokyo 113 -8655, Japan Received 5 January 1999; received in revised form 14 September 1999; accepted 6 October 1999
Abstract We report a patient with acute cranial polyneuropathy with unilateral involvement of the ninth, tenth, and eleventh cranial nerves. Although this patient lacked a typical cutaneous herpetic manifestation, elevated levels of IgM and IgG antibodies to varicella zoster virus (VZV) in both the serum and cerebrospinal fluid confirmed the clinical diagnosis of VZV infection and zoster sine herpete. Coexisting hypoplasia of the ipsilateral jugular foramen was detected using three-dimensional, surface-rendering displays reconstructed from the cranial helical CT scan. The patient recovered almost completely following treatment with an anti-inflammatory corticosteroid. Anatomical narrowing of the jugular foramen in this patient may have contributed to entrapment of the affected nerves at their passage through the foramen. 2000 Published by Elsevier Science B.V. All rights reserved. Keywords: Jugular foramen syndrome; Hypoplasia of the jugular foramen; Varicella zoster virus infection; Zoster sine herpete; Nerve compression syndromes; Case report
1. Introduction A wide spectrum of neurologic complications have been recorded in association with varicella zoster virus (VZV) infection. Trigeminal and facial nerves are the most common nerves in cranial neuropathies associated with VZV infection. There are, however, only a few case reports of patients with a lower cranial polyneuropathy [1–8]. Here we report a patient with unilateral ninth, tenth, and eleventh cranial nerve palsy, associated with an elevated level of antibodies to VZV and hypoplasia of the ipsilateral jugular foramen. 2. Case report A 60-year-old man presented with acute dysphagia and *Corresponding author. Tel.: 181-3-5800-8672; fax: 181-3-58006548. E-mail address: [email protected] (T. Hayashi)
hoarseness of voice on June 27, 1997. He was admitted to a local hospital 3 days later, at which time, paralysis of the left pharynx and vocal cord was diagnosed. He was fed through a nasogastric tube. A lower pharyngeal tumor was suspected but was not found. Because his condition did not improve, he was transferred to our hospital on August 6, 1997. A neurological examination showed paralysis of the left soft palate and constrictor muscles of the pharynx, hypoesthesia of the left soft palate and pharynx, and weakness of the left sternocleidomastoid and left upper trapezius muscles with muscle atrophy. There was no impairment of taste sensation in the posterior third of the tongue or of muscle function. No meningeal signs, long tract signs, or autonomic dysfunction were observed. Herpetic eruption was neither observed nor recorded. Laryngoscopy showed that the left vocal cord was immobile and remained in the paramedian position. Audiometry was normal. Fluoroscopy showed paralysis of the left pharyngeal constrictor muscles and the pooling of contrast media in the left pyriform sinus
0022-510X / 00 / $ – see front matter 2000 Published by Elsevier Science B.V. All rights reserved. PII: S0022-510X( 99 )00263-4
T. Hayashi et al. / Journal of the Neurological Sciences 172 (2000) 70 – 72
after deglutition. Needle electromyography confirmed active neurogenic changes in the left sternocleidomastoid and left upper trapezius muscles. The left vocal cord was silent electrically. These findings were consistent with acute isolated left ninth, tenth, and eleventh cranial nerve palsy. Cerebrospinal fluid examination showed slight pleocytosis (7 / mm 3 ). Antibody levels to VZV were elevated in both the serum (IgM 3.17, IgG .128; normal value IgM,0.8, IgG,2.0) and cerebrospinal fluid (IgM 0.05, IgG 12.3) as shown by an EIA. This serological finding is consistent with acute VZV infection. Polymerase chain reaction (PCR) did not detect VZV DNA in the cerebrospinal fluid. Skull X-rays showed narrowing of the left jugular foramen. Three-dimensional surface-rendering displays, reconstructed from the cranial helical CT scans showed hypoplasia of the ipsilateral jugular foramen (Fig. 1). Magnetic resonance imaging (MRI) with contrast media did not show any abnormality of the cranial nerves or the brain stem. The patient gradually recovered from the severe dysphagia without medication but on August 15, 1997, suddenly complained of left deafness, tinnitus, and mild pain over the auricle. Audiometry detected moderate sensorineural deafness of the left ear. Vestibular function was intact. No auricular eruption was present. Hydrocortisone sodium succinate was administered intravenously at the average dose of 300 mg for 10 days, alprostadil alfadex (prostaglandin E1) at 60 mg for 10 days, and acyclovir at 750 mg for 7 days. The patient responded dramatically to this treatment and could swallow food on August 25, 1997. The follow-up examination 10 months later showed mild atrophy of the left vocal cord and a
71
decrease in left-side hearing acuity as the only sequelae of the event.
3. Discussion VZV causes cranial polyneuropathies such as trigeminal neuralgia and facial palsy [9], but lower cranial neuropathy is considered uncommon [1–4]. Jugular foramen syndrome with serologically proven VZV infection has been infrequently reported [5–7,10]. Our patient initially presented with unilateral jugular foramen syndrome, which was followed by ipsilateral acoustic neuropathy. The diagnosis of lower cranial neuropathy was based on the elevation of anti-VZV antibody in both his serum and cerebrospinal fluid. Detection of anti-VZV serum IgM is thought to establish the diagnosis of acute VZV infection [11,12]. Furthermore, anti-VZV antibody is not normally found in CSF, and its presence is a finding of essential diagnostic significance [13]. A negative PCR result is not necessarily in conflict with the diagnosis because PCR for VZV DNA does not always provide exquisite sensitivity for the diagnosis of subacute and chronic VZV infection [13]. In addition, diagnosis of herpes simplex encephalitis by PCR is known to be limited up to 4 weeks after the onset of neurological symptoms [14]. The patient’s CSF on which PCR was done was sampled 6 weeks after the onset of his symptoms, which might possibly have missed an optimal phase for PCR examination. Our case confirms the notion that anti-VZV antibody is useful in the diagnoses in patients with subacute and chronic VZV infection with
Fig. 1. A three-dimensional surface-rendering display, reconstructed from cranial helical CT scans with contrast media. Slice 1 mm thick. Hypoplasia of the posterior part of the left jugular foramen (arrow) produces a passage much narrower than the right one.
72
T. Hayashi et al. / Journal of the Neurological Sciences 172 (2000) 70 – 72
negative PCR result [12,13]. Moreover since our patient was considered to have ganglionitis of the ninth, tenth and eleventh cranial nerves, chance of detecting VZV DNA in CSF might be lower than those in patients with VZV encephalitis or myelitis. Hunt proposed that the lower cranial polyneuropathy associated with VZV infection may be caused by inflammation of the nuclei of the affected nerves [15]. This hypothesis is supported by recent MRI findings of gadolinium enhancement in the seventh, ninth, and tenth cranial nerve nuclei of a patient with lower cranial polyneuropathy associated with VZV infection [8]. No such enhancement was found in our patient, probably because the MRI study with enhancement was done after the optimal hyperacute phase. Inflammation of the nuclei associated with epineurial edema in our patient may have caused entrapment of the ninth, tenth, and eleventh cranial nerves where they pass through the hypoplastic jugular foramen. Rapid improvement in nerve function after corticosteroid administration supports this speculation. Entrapment of a peripheral nerve is thought to be a predisposing factor in other inflammatory neuropathies. Bell’s palsy, a common type of cranial neuropathy, also is considered to be caused by acute inflammation and edema of the facial nerve with subsequent entrapment of the nerve in the facial canal [16]. In Guillain-Barre´ syndrome, conduction block in the peripheral nerves frequently is detected at common sites of compression entrapment [17]. This patient initially presented with severe paralytic symptoms but only mild somatic sensory decline. In addition, taste sensation in the left posterior third of the tongue was not impaired. This sensorimotor dissociation suggests that the ninth cranial nerve was relatively unharmed. As they emerge from the jugular foramen, the tenth and eleventh cranial nerves are covered by the same sheath of dura mater and are separated from the ninth cranial nerve by a septum [2]. This anatomical separation may explain the focal sparing of the ninth cranial nerve from epineurial compression and edema, leading to milder damage. A noteworthy feature of this case was the lack of cutaneous herpetic manifestation throughout the course of the disease. A wide spectrum of neurological disorders that include cranial polyneuropathy, aseptic meningitis, encephalitis, acute polyneuropathy, and myelitis, are associated with VZV infection without skin lesions. This condition has been termed zoster sine herpete [18,19]. To our knowledge, jugular foramen syndrome associated with zoster sine herpete, has not previously been reported. VZV infection should be considered in patients with lower
cranial polyneuropathy, because acyclovir ameliorate the symptoms.
corticosteroid
and
References ¨ H, Wohlfart G. Herpes zoster of the seventh, eighth, ninth [1] Engstrom and tenth cranial nerves. Arch Neurol Psychiatry 1949;62:638–52. [2] Font JH. The jugular foramen syndrome. Evidence that transient cases may be of viral origin. Arch Otolaryngol 1952;56:134–41. [3] Sasaki H, Kawamoto S, Masuda N. Herpes of the ear lobe complicated with a mixed laryngeal paralysis. Otolaryngology (Tokyo) 1967;39:815–8, In Japanese. [4] Thomas JE, Howard FM. Segmental zoster paresis — a disease profile. Neurology 1972;22:459–66. [5] Kahane P, De Saint Victor JF, Besson G, Hommel M, Perret J. ´ ´ posterieur ´ Syndrome du trou dechire duˆ au zona. Rev Neurol (Paris) 1993;149:353–4. [6] Kondo M, Hokezu Y, Nagai M, Mori T, Nagamatsu K. A case of herpes zoster meningoencephalitis followed by involvement of cranial nerves IX, X, XI. Rinsho Shinkeigaku Clin Neurol (Tokyo) 1994;34:720–3, In Japanese. [7] Terai T, Kohira I, Shiro Y, Ishizu H, Shohmori T. Vernet syndrome induced by herpes zoster infection. A case report. Neurol Med (Tokyo) 1994;41:71–3, In Japanese. [8] Kikuchi H, Yoshimura T, Hara H, Mihara F, Kobayashi T. A case of multiple cranial neuropathy due to varicella-zoster virus infection: detection of involvement of cranial ganglia with MRI. Rinsho Shinkeigaku Clin Neurol (Tokyo) 1995;35:814–6, In Japanese. [9] Hunt JR. Herpetic inflammations of the geniculate ganglion. A new syndrome and its complications. J Nerv Ment Dis 1907;34:73–96. [10] Muroi M, Kamei T, Yasuoka Y, Ishii H, Watanabe K. Seven cases of cephalic herpes zoster with involvement of the lower cranial nerves. J Jpn Bronchoesophagol Soc 1987;38:434–40, In Japanese. [11] Brunell PA, Gershon AA, Uduman SA, Steinberg S. Varicella-zoster immunoglobulins during varicella, latency, and zoster. J Infect Dis 1975;132:49–54. [12] Gnann Jr. JW, Whitley RJ. Neurologic manifestations of varicella and herpes zoster. In: Scheld WM, Whitley RJ, Durack DT, editors, 2nd ed, Infections of the central nervous system, Philadelphia: Lippincott-Raven, 1997, pp. 91–105. [13] Gilden DH, Bennet JL, Kleinschmidt-DeMasters BK, Song DD, Yee AS, Steiner I. The value of cerebrospinal fluid antiviral antibody in the diagnosis of neurologic disease produced by varicella zoster virus. J Neurol Sci 1998;159:140–4. ˚ Forsgren M. ¨ [14] Aurelius E, Johansson B, Skoldenberg B, Staland A, Rapid diagnosis of herpes simplex encephalitis by nested polymerase chain reaction assay of cerebrospinal fluid. Lancet 1991;337:189–92. [15] Hunt JR. The symptom-complex of the acute posterior poliomyelitis of the geniculate, auditory, glossopharyngeal and pneumogastric ganglia. Arch Intern Med 1910;5:631–75. [16] Chadwick D. The cranial nerves and special senses. In: Walton J, editor, 10th ed, Brain’s disease of the nervous system, Oxford: Oxford University Press, 1993, pp. 76–126. [17] Brown WF, Feasby TE. Conduction block and denervation in Guillain-Barre´ polyneuropathy. Brain 1984;107:219–39. [18] Lewis GW. Zoster sine herpete. Br Med J 1958;2:418–21. [19] Mayo DR, Booss J. Varicella zoster-associated neurologic disease without skin lesions. Arch Neurol 1989;46:313–5.