Ulnar nerve ganglion cyst at the elbow 543 Table 1 1 2 3 Motor nerve conduction for right ulnar nerve Site Latency Amplitude Duration Distance mm CV m/s Wrist Below elbow Above elbow 4.6 ms 11.3 ms 18.2 ms 0.426 mv 0.373 mv 0.251 mv 6.2 ms 5.6 ms 6.4 ms 200 100 30 14 Impression: Motor nerve conduction study shows ulnar nerve compression in the cubital fossa. MS; + milliseconds; MV, + millivolts; CV, + conduction velocity. DISCUSSION Involvement of a peripheral nerve by a ganglion cyst is uncommon.1 The most frequent location is the common peroneal nerve at the head of fibula, which comprise 75% of the total reported cases in the literature.1–3 Suprascapular nerve involvement is the next most common.4 Involvement of the ulnar nerve at the elbow in the cubital tunnel is extremely rare.4–6 In the largest series, comprising 27 cases of ganglion cyst involving peripheral nerve, not a single case was observed at the cubital tunnel.2 In the majority of the cases, the diagnosis was not made until the time of surgical exploration,2 as happened in our case. Cystic degeneration of neurilemmomas, progressive enlargement of synovial rests displaced during embryological development, herniation of joint synovium and traumatic intraneural haemorrhage are some of the theories of pathogenesis.1–5 Ganglion cysts may or may not be associated with an obvious connection with the neighboring joint. Our case had no connection with the elbow joint and the cyst was entirely in the cubital tunnel, flattening and compressing the ulnar nerve. Motor weakness and pain in the distribution of the involved peripheral nerve are the most common presenting symptoms, which were also observed in the present case. Detailed history, physical examination and electrophysiological studies are important in the initial evaluation of cases. Except in isolated instances of cyst recurrence, imaging studies by and large are not performed before operative exploration, although ultrasonography, CT and MRI have been performed for diagnosis in isolated cases. MRI4 is able to provide detailed morphology of the cyst and the nerve and other adjacent structures. Ganglion cysts are usually multilocular and nonenhancing lesions, usually hypointense to muscle on T1 weighted MRI and hyperintense on T2 weighted MRI. Ganglion cysts are well differentiated from nerve sheath tumours, glomus tumours and lipomas on MRI morphology.5 Complete excision is possible in the majority of cases2 of epineural ganglion cyst, as in our case. However, in cases of intraneural cyst a complete excision may not be possible and the chance of recurrence exists.1 The majority of patients benefit from microsurgical excision of a ganglion cyst of a peripheral nerve; however, motor recovery may not be complete if the ganglion cyst extensively involves the nerve and symptoms have been present for more than one year. In our case, symptoms were present for 3 years but fortunately the patient recovered completely following the microsurgical excision. CONCLUSION An epineural ganglion cyst of the ulnar nerve in the cubital tunnel is extremely rare. Progressive sensory and/or motor deficits and pain are the chief presenting symptoms. MRI is diagnostic. Microsurgical excision may be curative even in the presence of advanced neural compression and severe neurological deficits. ACKNOWLEDGEMENT We sincerely thank Dr Veersinge, ISS, Muscat for referring this case, Dr S.D. Lad, Senior Consultant Neurosurgeon, for his kind © 2000 Harcourt Publishers Ltd help and guidance and Dr Mrugesh Doctor, Al Afaq centre for MRI of the cervical region. REFERENCES 1. 2. 3. 4. 5. 6. Tindall S C. Ganglion cysts of peripheral nerves. In: Wilkins R H, Rengachary S S (Eds) Neurosurgery. New York: Mc Graw-Hill, 2nd ed. 1996;3225. Harbaugh K S, Tiel R L, Kline D G. Ganglion cyst involvement of peripheral nerves. J Neurosurg 1997;87:403–408. Gurdjian E S, Larsen R D, Lindren D W. Intraneural cyst of the peroneal and ulnar nerves. Report of two cases. J. Neurosurg 1965;23:76–78. Gross T P, Aronow M S, Coumas J M. The use of MRI to diagnose suprascapular nerve entrapment caused by a ganglion. Orthopedics 1994;17:359–362. Seddon H. Carpal ganglion as a cause of paralysis of the deep branch of the ulnar nerve. J Bone Joint Surg (Br) 1952;34:386–390. Ferlic D C, Ries M D. Epineural ganglion cyst of the ulnar nerve at the elbow J Hand Surg (Am) 1990;15:996–998. Bilateral medial medullary infarction Masahito Katoh MD, Takashi Kawamoto MD Department of Neurosurgery, Tomakomai City General Hospital, Honkocho1, Tomakomai, Hokkaido, 053–8567, Japan Summary We present a case of bilateral medial medullary infarction demonstrated by magnetic resonance imaging (MRI) and review 12 previously reported cases. We classify these 13 cases (including the present case) into two groups according to the extent of the ischemic region: type 1, the ischemic lesion developed from the medullary pyramid to the medial longitudinal fasciculus; type 2, the lesion was confined to the medullary pyramid. A 71 year old man presented with slight disturbance of consciousness, dysarthria, disturbance of leftward gaze, no gag reflex and tetraparesis. He developed nearly complete horizontal ophthalmoplegia. MRI revealed upper medial medullary infarction bilaterally that extended to the pontomedullary junction. We propose that the prognosis of type 2 bilateral medial medullary infarction is better than that of type 1. Furthermore, the prognosis of bilateral medial medullary infarction itself may be better than previously indicated. © 2000 Harcourt Publishers Ltd Journal of Clinical Neuroscience (2000) 7(6), 543–545 © 2000 Harcourt Publishers Ltd doi: 10.1054/ jocn.1999.0675, available online at http://www.idealibrary.com on Keywords: bilateral, medial medullary syndrome, infarction, stroke Received 26 July 1999 Accepted 25 October 1999 Correspondence to: Masahito Katoh MD, Department of Neurosurgery, Hokkaido University School of Medicine North-15, West-7, Kita-ku, Sapporo 060, Japan. Tel. +81 11 716 2111, ex. 5987; Fax: +81 11 706 7878; E-mail: masasama@coral.ocn.ne.jp Journal of Clinical Neuroscience (2000) 7(6), 542–560 544 Katoh and Kawamoto INTRODUCTION Bilateral medial medullary infarction is a rare condition. Only 12 anatomically confirmed cases1,2,4–13 have been reported. We report a patient with slightly impaired conscious state, dysarthria, disturbance of horizontal ocular movement, left hypoglossal nerve palsy and a left dominant tetraparesis. CASE REPORT A 71 year old man with a history of hypertension awoke with dizziness on 2 June 1998. A depressed conscious state and tetraparesis were noted at an out-patient office of a local hospital and he was transferred to our hospital by ambulance. On admission he had a blood pressure of 130/100 mm Hg, a pulse rate of 96 beats per min and a respiratory rate of 32 per min. He was drowsy and his speech was dysarthric. The visual fields were intact and pupils were equal, with a normal light reflex. He could neither direct his gaze voluntarily nor follow a target for leftward gaze. Corneal reflexes were intact, and there was no loss of sensation to pin, temperature or light touch on either side of his face. Facial movements were symmetric and active and hearing appeared intact. No gag reflexes were observed. His left side was flaccid, while the right side exhibited decreased muscle tone. There were no sensory deficits to touch, pain, temperature, vibration or position sense. On 3 June the disturbance of extraocular movement had deteriorated in both horizontal directions. Brain magnetic resonance imaging (MRI) with a 0.5-T superconducting magnet performed on 4 June revealed a high intensity area on fluid attenuated inversion recovery (FLAIR) imaging, which was noted in the medulla oblongata extending to the lower pons (Fig. 1). The lesion involved the medial medulla oblongata bilaterally, mainly the ventral half with partial extension dorsally. The disturbance of ocular movement gradually improved, and only mild leftward gaze limitation was detected. Moreover, improvement of tetraparesis was observed, and only a mild left hemiparesis was detected a year after the onset. DISCUSSION The medial medullary syndrome is characterised by contralateral hemiparesis and hemisensory disturbance of posterior column function with ipsilateral paralysis of the tongue.3 It results from infarction of the paramedian region of the medulla oblongata due to occlusion of the vertebral or anterior spinal artery or their small branches. Bilateral medial medullary infarction is a rare condition and only 12 anatomically confirmed cases1,2,4–13 have been reported. The clinical findings of these 12 cases are summarised in Table 1. Including our case, there were 9 male and 4 female patients, ranging in age from 23 to 71 years, and the mean age was 53.7 years. The first 8 cases were diagnosed by autopsy, but in vivo diagnosis by MRI became possible in the 1990s. In addition, the treatment improved with advances in diagnostic technology and this condition is not necessarily associated with a poor prognosis. Motor pareses were recognised in all cases, and tetrapareses were noted in 10 of 12 cases in which precise neurological findings were available. Caudal/cranial nerve palsy was detected in 6 of 13 cases, including those described as dysarthria or dysphagia, and may result in respiratory infection. Three studies on this lesion described the presence of oculomotor disturbance. Upward extension of the lesion, especially to the pontine medial longitudinal fasciculi (MLF) and caudal paramedian pontine reticular formations (PPRFs), may be responsible for horizontal gaze palsy. However, some previous studies12,13 indicated that a vertical gaze Journal of Clinical Neuroscience (2000) 7(6), 542–560 Fig. 1 FLAIR image showing axial sections. Infarction is clearly demonstrated in the medial medulla oblongata bilaterally (arrows). palsy was present. The mechanisms for these symptoms remain unclear. We classified the 13 cases into 2 groups according to the extent of the ischaemic region (Fig. 2): type 1, the ischaemic lesion developed from the medullary pyramid to MLF; type 2, the lesion was confined to the medullary pyramid. Type 1 infarction may be caused by occlusion of the main artery to the medial medulla oblongata. Type 2 infarction might be caused by occlusion of the arterial branch to the medullary pyramid. The main cause of death was respiratory infection. Two cases of type 2 did not die of respiratory infection. The prognosis of type 2 might be better than that of type 1. © 2000 Harcourt Publishers Ltd pneumonia aspiration pneumonitis bronchopneumonia, renal failure pneumonia pulmonary infection subarachnoid haemorrhage urosepsis bronchopneumonia attack of coronary occlusion Cause of Death Medullary infarction 545 MRI 71 1998 13 Present case M I alive, 81 days able to walk alive, 5 months able to walk I MRI M 69 1996 12 Wada et al. MRI 59 11 Kim et al. 1995 M II died, 2 weeks MRI 59 1993 © 2000 Harcourt Publishers Ltd 10 Kleinert et al. M I died, 7 weeks died, 6 days died, 261 days died, 24 hours died, 7 years died, 13 months alive, 60 days, I I I I II II I autopsy autopsy autopsy autopsy autopsy autopsy MRI M M F F F M M 45 57 28 23 60 71 71 1962 1977 1980 1983 1986 1989 1992 3 4 5 6 7 8 9 Meyer Nardelli et al. Mizutani et al. Kase et al. Paulson et al. Jagiella et al. Toyoda et al. autopsy 45 1944 2 Davison F I died, 7 weeks died, 13 months left dominant tetraparesis, lt. Gag reflex (–), sensory disturbance, urinary & faecal incontinence lt. Flaccid hemiplegia, bilateral hyperreflexia, posterior column signs dysarthria, tetraparesis dysarthria, respiratory failure, flaccid quadriplegia caudal nerve palsy, tetraparesis respiration arrest, quadriplegia, nystagmus dysarthria, tetraparesis pure motor quadriplegia quadriplegia, disturbance of ocular movement bed rest flaccid tetraplegia, rt. hypoglossal nerve palsy, bilateral disturbance of deep sensation dysphagia, facial palsy, nystagmus, severe motor deficit bilateral facial palsy, lt. Hemiparesis, horizontal & upward gaze limitation dysarthria, disturbance of horizontal gaze, lt. Dominant tetraparesis autopsy 40 1 Davison 1937 M I Prognosis Symptoms Type Diagnosis Sex Age Year Report No. Table 1 Reported cases of bilateral medial medullary infarction (M: male, F: female, rt.: right, lt.: left) Fig. 2 Type 1: the ischaemic lesion develops from the medullary pyramid to MLF; type 2: the lesion is confined to the medullary pyramid. The survival rate of medial medullary syndrome may increase with improvements in diagnostic technology. Bilateral medial medullary infarction, which was previously considered to be fatal, can be effectively treated if respiratory management is performed during the acute period. REFERENCES 1. Davison C. Syndrome of the anterior spinal artery of the medulla oblongata. Arch Neurol Psychiatry 1937;37:91–107. 2. Davison C. Syndrome of the anterior spinal artery of the medulla oblongata. J Neuropatol Exp Neurol 1944;3:73–80. 3. Meyer JS, Herndon RM. Bilateral infarction of the pyramidal tracts in man. Neurology 1962;12:637–42. 4. Nardelli E, Iannucci A, Rizzuto N. Bilateral infarction of pyramidal tracts. Acta Neurol 1978;33:130–6. 5. Mizutani T, Lewis R A, Gonatas N K. Medial medullary syndrome in a drug abuser. Arch Neurol 1980;37:425–8. 6. Kase C S, Varakis J N, Stafford J R, Mohr J P. Medial medullary infarction from fibrocartilaginous embolism to the anterior spinal artery. Stroke 1983;14:413–8. 7. Paulson G W, Yates A J, Paltan-Ortiz J D. Does infarction of the medullary pyramid lead to spasticity? Arch Neurol 1986;43:93–5. 8. Jagiella W M, Sung J H. Bilateral infarction of the medullary pyramids in humans. Neurology 1989;39:21–4. 9. Toyoda K, Hasegawa Y, Yonehara T, Oita J, Yamaguchi T. Bilateral medial medullary infarction with oculomotor disorders. Stroke 1992;23:1657–9. 10. Kleinert G, Fazegas F, Kleinert R, Schmidt R, Payer F, Offenbacher H, Lechner H. Bilateral medial medullary infarction: magnetic resonance imaging and correlative histopathologic findings. Eur Neurol 1993;33:74–6. 11. Kim J S, Kim H G, Chung C S. Medial medullary syndrome. Report of 18 new patients and a review of the literature. Stroke 1995;26:1548–52. 12. Wada K, Gotoh T, Hashimoto Y, Kimura K, Uchino M. A case of bilateral infarction of medial pontomedullary junction. Clin Neurol 1996;36:1186–9. (in Japanese) 13. Ho K-L, Meyer K R. The medial medullary syndrome. Arch Neurol 1981;38:385–7. Delayed presentation of transorbital intracranial pen Gavin A. Davis MBBS FRACS, Anthony D. Holmes MBBS FRACS, Geoffrey L. Klug MBBS FRACS Departments of Neurosurgery and Plastic/Craniofacial Surgery, Royal Children’s Hospital, Melbourne, Victoria, Australia Summary A 13 year old Fijian boy sustained a stab wound to the left orbit 3 years ago. It was not appreciated by the treating physicians in Fiji that the plastic pen had crossed from the left orbit, through the nose, right orbit and right optic nerve, into the right Journal of Clinical Neuroscience (2000) 7(6), 542–560