- Email: [email protected]
Ocular flutter induced only by optokinetic stimulation
Case reports / Journal of Clinical Neuroscience 13 (2006) 479–481 28. Kattner KA, Bailes J, Fukushima T. Direct surgical management of large bulbous and giant aneurysms involving the paraclinoid segment of the internal carotid artery; report of 29 cases. Surg Neurol 1998;49:471–80.
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29. Freuerberg I, Lindquist C, Lindquist M, Steiner L. Natural history of postoperative aneurysm rests. J Neurosurg 1987;66:30–4. 30. Lawton MT, Spetzeler RF. Surgical strategies for giant intracranial aneurysms. Neurosurg Clin N Am 1998;9:725–42.
doi:10.1016/j.jocn.2005.05.022
Ocular flutter induced only by optokinetic stimulation S.H. Koh, S.H. Kim
*
Department of Neurology, College of Medicine, Hanyang University Hospital, Hangdang-dong 17, Seongdong-gu, Seoul 133-792, Korea Received 10 January 2005; accepted 3 May 2005
Abstract Ocular flutter (OF) refers to occasional bursts of involuntary horizontal oscillation around the point of fixation, characterised by rapid horizontal repetitive oscillation without intersaccadic interval in electro-ocular recording. In spite of numerous reports of OF, there has been no previous report describing OF developed by simply looking at moving objects. We report a patient with olivopontocerebellar atrophy (OPCA), with OF induced only by optokinetic stimulation (OKS). A 65-year-old man, with OPCA complained of dizziness and oscillopsia occurring only with a specific type of eye movement. The electro-oculographic recording showed a decreased gain of pursuit, catch-up saccade, and decreased velocity of saccade, and OF was induced only by OKS of more than 40/second. In OPCA, partial loss of omnipause neurons and/or abnormal firing of burst neurons, especially those involved in optokinetic movement, could be the cause of OF occurring only with OKS. 2006 Elsevier Ltd. All rights reserved. Keywords: Ocular flutter; Optokinetic stimulation; Olivopontocerebellar atrophy
1. Introduction Ocular flutter (OF) refers to occasional bursts of involuntary horizontal oscillation around the point of fixation, characterised by rapid, repetitive, horizontal, symmetrical and sinusoidal oscillation without intersaccadic interval.1 OF is probably caused by loss of tonic stimulation of omnipause neurons.2 Nevertheless, the precise mechanism of OF is not understood. In general, OF occurs unrelated to eye movements; and there has been no previous report describing OF occurring only with a specific type of eye movement, although it is well known that OF can be accentuated by eye movements. We report a patient with olivopontocerebellar atrophy (OPCA) with OF occurring only with optokinetic stimulation (OKS). 2. Case report A 65-year-old man was admitted for evaluation of repeated, brief and paroxysmal attacks of dizziness and oscillopsia. These symptoms developed only when he fixed on moving subjects, but instantly disappeared when he changed *
Corresponding author. Tel.: +82 2 2290 8371; fax: +82 2 2296 9370. E-mail address: [email protected] (S.H. Kim).
his gaze. Laboratory tests, including for spinocerebellar atrophy (SCA) type 1, 2, and 6, and for the neurologic paraneoplastic antibodies anti-Ri, anti-Hu and anti-Yo, were negative. On neurologic examination, severe dysarthria, dysmetria on the finger-to-nose test, and unsteadiness of tandem gait were noted. Brain MRI revealed an atrophied cerebellum and brainstem, consitent with OPCA (Fig. 1). Analysis of ocular movement using electro-oculography (EOG) recording showed decreased gain of pursuit (left : right = 0.56 : 0.59 at 0.2 Hz and 0.49 : 0.53 at 0.4 Hz), catch-up saccade and decreased velocity of saccade (Fig. 2A). During optokinetic stimulation, dizziness and involuntary rapid eye movements developed only when the velocity of OKS was more than 40/second (Fig. 2B). Rapid, repetitive, horizontal, symmetrical and sinusoidal movements without intersaccadic interval were detected in EOG, findings compatible with OF. The frequency of OF was 18 Hz, and the amplitude was 40. OF was precipitated only by OKS, not pursuit movements (Fig. 2A, B). 3. Discussion Ocular flutter is a rapid and sinusoidal abnormal ocular movement on a horizontal plane, without intersaccadic interval.1 Although the precise mechanism of OF is not
480
Case reports / Journal of Clinical Neuroscience 13 (2006) 479–481
Fig. 2. Electro-oculographic (EOG) findings. EOG recording for analysis of smooth pursuit shows decreased gain of pursuit (left : right = 0.56 : 0.59 at 0.2 Hz and 0.49 : 0.53 at 0.4 Hz) and catch-up saccade (A). Involuntary, rapid, repetitive, horizontal, symmetrical and sinusoidal eye movements without intersaccadic interval is compatible with ocular flutter, which developed only with OKS speed of more than 40º/second (B). OF was not present velocities of 20º or 30º/second.
Fig. 1. Brain MRI showing olivopontocerebellar atrophy. Axial (A) and sagittal (B) T1-weighted images show marked atrophy of the cerebellum and brainstem.
known, it is thought it may develop due to an abnormality of the saccade control system. Among several mechanisms suggested, loss of tonic inhibition of omnipause neurons in the paramedian pontine reticular formation (PPRF) has been considered to be the most plausible hypothesis.1,2 Under normal conditions, during fixation, omnipause neurons inhibit the burst neurons located in the PPRF, and cease to discharge immediately prior to and during the saccade. However, in some pathologic conditions, omnipause neurons cannot inhibit the burst neurons, resulting in OF.2 Furthermore, OF is sometimes found in neurodegenerative diseases associated with cerebellar atrophy, including OPCA, thalamic haemorrhage, demyelinating disease, hydrocephalus, neuroblastoma, paraneoplastic syndromes, benign encephalitis and lithium toxicity.3–5 In patients with OPCA, OF might be caused by damage to the omnipause neurons in the PPRF during disease pro-
gression.1–5 Differing from previous reports, in this patient OF occurred only with OKS of more than 40/second. A report that the omnipause neurons could be involved in pursuit movements,6 together with the fact that optokinetic nystagmus (OKN) is a part of the pursuit system, led us to suggest that the omnipause cells might be related to optokinetic movement. Therefore, selective loss or partial damage of these neurons could provoke OF only with OKS. In our patient, abnormal firing of burst neurons could also be the mechanism of OF.1,2 As smooth pursuit is mainly mediated by the occipital cortex and cerebellar structures, whereas the velocity storage component of OKN depends almost exclusively on brainstem structures (particularly the nucleus reticularis tegmenti pontis (NRTP)) via the accessory optic tract,2,7,8 OKN probably has input independent of the burst neurons, which is not the case for smooth pursuit. Moreover, OKN is composed of both direct (smooth pursuit) movement and the velocity storage component, and OKN abnormalities are occasionally independent of a disturbance of pursuit.9 Therefore, abnormalities of these burst neurons located in the brainstem, including the NRTP, might be related to the unusual OF in the present patient.
Case reports / Journal of Clinical Neuroscience 13 (2006) 481–485
The mechanisms described above may not fully explain the OF in this patient, but suggest at least plausible mechanisms. OKS at variable speeds could be useful to provoke and detect OF in other patients. Acknowledgements The authors would like to thank Professor Woon Ki Paik at Hanyang University for his careful review of this manuscript. References 1. Gaymard B, Pierrot C. Neurology of saccades and smooth pursuit. Curr Opin Neurol 1999;12:13–9. 2. Leigh RJ, Zee DS. The Neurology of Eye Movements. 3rd ed. New York: Oxford University Press USA; 1999. p. 133–4, 449–56.
481
3. Bergenius J. Saccade abnormalities in patients with ocular flutter. Acta Otolaryngol 1986;102:228. p. 228–33. 4. Furman JMR, Eidelman BH, Fromm GH. Spontaneous remission of paraneoplastic ocular flutter and saccadic intrusions. Neurology 1988;38:499–501. 5. Kuban KC, Ephros MA, Freeman RL, et al. Syndrome of opsoclonusmyoclonus caused by Coxsackie B3 infection. Ann Neurol 1983;13:69–71. 6. Missal M, Keller EL. Common inhibitory mechanism for saccades and smooth-pursuit eye movements. J Neurophysiol 2002;88:1880–92. 7. Precht W. Anatomical and functional organization of optokinetic pathways. In: Lennerstrand G, Zee DS, Keller EL, editors. Functional Basis of Ocular Motility Disorders. Oxford: Pergamon; 1982. p. 291–302. 8. Crandall WF, Keller EL. Visual and oculomotor signals in nucleus reticularis tegmenti pontis in alert monkey. J Neurophysiol 1982;54:1326–45. 9. Daroff RB, Hoyt WF. Supranuclear disorders of ocular control systems in man: clinical, anatomical, and physiological correlations. In: Bach-yRita P, Collins CC, Hyde JE, editors. The Control of Eye Movements. New York: Academic Press; 1971. p. 175–236.
doi:10.1016/j.jocn.2005.05.023
Nocardial brain abscess: Review of clinical management Cumhur Kilincer a,*, M. Kemal Hamamcioglu a, Osman Simsek a, Tufan Hicdonmez a, Bayram Aydoslu b, Ozlem Tansel b, Mehmet Tiryaki a, Mehmet Soy c, Mu¨serref Tatman-Otkun d, Sebahattin Cobanoglu a a
Department of Neurosurgery, Trakya Universitesi Medical Faculty, Tip Fakultesi Norosirurji Anabilim Dali, Beyin Cerrahisi, 22030 Edirne, Turkey b Department of Clinical Bacteriology and Infectious Diseases, Trakya University Medical Faculty, Edirne, Turkey c Department of Internal Medicine, Section of Rheumatology, Trakya University Medical Faculty, Edirne, Turkey d Department of Microbiology and Clinical Microbiology, Trakya University Medical Faculty, Edirne, Turkey Received 16 December 2004; accepted 15 April 2005
Abstract Nocardiosis has become a significant opportunistic infection over the last two decades as the number of immunocompromised individuals has grown worldwide. We present two patients with nocardial brain abscess. The first patient was a 39-year-old woman with systemic lupus erythematosus. A left temporoparietal abscess was detected and aspirated through a burr-hole. Nocardia farcinica infection was diagnosed. The patient had an accompanying pulmonary infection and was thus treated with imipenem and amikacine for 3 weeks. She received oral minocycline for 1 year. The second patient was a 43-year-old man who was being treated with corticosteroids for glomerulonephritis. He was diagnosed with a ring-enhancing multiloculated abscess in the left cerebellar hemisphere, with an additional two small supratentorial lesions and triventricular hydrocephalus. Gross total excision of the cerebellar abscess was performed via a left suboccipital craniectomy. Culture revealed Nocardia asteroides, and the patient was successfully treated with intravenous ceftriaxone, then oral trimethoprime-sulfamethoxazole for 1 year. The clinical course, radiological findings, and management of nocardial brain abscess are discussed in light of the relevant literature, and current clinical management is reviewed through examination of the cases presented here. 2006 Elsevier Ltd. All rights reserved. Keywords: Brain abscess; Immunosuppression; Nocardia infection; Opportunistic infection; Trimethoprim-sulfamethoxazole combination; Minocycline
q *
This article was presented at the 18th Scientific Congress of the Turkish Neurosurgical Society, 2004, Kemer-Antalya, Turkey. Corresponding author. Tel.: +90 284 2355798. E-mail addresses: [email protected], [email protected]. (C. Kilincer). E-mail address: .
479
29. Freuerberg I, Lindquist C, Lindquist M, Steiner L. Natural history of postoperative aneurysm rests. J Neurosurg 1987;66:30–4. 30. Lawton MT, Spetzeler RF. Surgical strategies for giant intracranial aneurysms. Neurosurg Clin N Am 1998;9:725–42.
doi:10.1016/j.jocn.2005.05.022
Ocular flutter induced only by optokinetic stimulation S.H. Koh, S.H. Kim
*
Department of Neurology, College of Medicine, Hanyang University Hospital, Hangdang-dong 17, Seongdong-gu, Seoul 133-792, Korea Received 10 January 2005; accepted 3 May 2005
Abstract Ocular flutter (OF) refers to occasional bursts of involuntary horizontal oscillation around the point of fixation, characterised by rapid horizontal repetitive oscillation without intersaccadic interval in electro-ocular recording. In spite of numerous reports of OF, there has been no previous report describing OF developed by simply looking at moving objects. We report a patient with olivopontocerebellar atrophy (OPCA), with OF induced only by optokinetic stimulation (OKS). A 65-year-old man, with OPCA complained of dizziness and oscillopsia occurring only with a specific type of eye movement. The electro-oculographic recording showed a decreased gain of pursuit, catch-up saccade, and decreased velocity of saccade, and OF was induced only by OKS of more than 40/second. In OPCA, partial loss of omnipause neurons and/or abnormal firing of burst neurons, especially those involved in optokinetic movement, could be the cause of OF occurring only with OKS. 2006 Elsevier Ltd. All rights reserved. Keywords: Ocular flutter; Optokinetic stimulation; Olivopontocerebellar atrophy
1. Introduction Ocular flutter (OF) refers to occasional bursts of involuntary horizontal oscillation around the point of fixation, characterised by rapid, repetitive, horizontal, symmetrical and sinusoidal oscillation without intersaccadic interval.1 OF is probably caused by loss of tonic stimulation of omnipause neurons.2 Nevertheless, the precise mechanism of OF is not understood. In general, OF occurs unrelated to eye movements; and there has been no previous report describing OF occurring only with a specific type of eye movement, although it is well known that OF can be accentuated by eye movements. We report a patient with olivopontocerebellar atrophy (OPCA) with OF occurring only with optokinetic stimulation (OKS). 2. Case report A 65-year-old man was admitted for evaluation of repeated, brief and paroxysmal attacks of dizziness and oscillopsia. These symptoms developed only when he fixed on moving subjects, but instantly disappeared when he changed *
Corresponding author. Tel.: +82 2 2290 8371; fax: +82 2 2296 9370. E-mail address: [email protected] (S.H. Kim).
his gaze. Laboratory tests, including for spinocerebellar atrophy (SCA) type 1, 2, and 6, and for the neurologic paraneoplastic antibodies anti-Ri, anti-Hu and anti-Yo, were negative. On neurologic examination, severe dysarthria, dysmetria on the finger-to-nose test, and unsteadiness of tandem gait were noted. Brain MRI revealed an atrophied cerebellum and brainstem, consitent with OPCA (Fig. 1). Analysis of ocular movement using electro-oculography (EOG) recording showed decreased gain of pursuit (left : right = 0.56 : 0.59 at 0.2 Hz and 0.49 : 0.53 at 0.4 Hz), catch-up saccade and decreased velocity of saccade (Fig. 2A). During optokinetic stimulation, dizziness and involuntary rapid eye movements developed only when the velocity of OKS was more than 40/second (Fig. 2B). Rapid, repetitive, horizontal, symmetrical and sinusoidal movements without intersaccadic interval were detected in EOG, findings compatible with OF. The frequency of OF was 18 Hz, and the amplitude was 40. OF was precipitated only by OKS, not pursuit movements (Fig. 2A, B). 3. Discussion Ocular flutter is a rapid and sinusoidal abnormal ocular movement on a horizontal plane, without intersaccadic interval.1 Although the precise mechanism of OF is not
480
Case reports / Journal of Clinical Neuroscience 13 (2006) 479–481
Fig. 2. Electro-oculographic (EOG) findings. EOG recording for analysis of smooth pursuit shows decreased gain of pursuit (left : right = 0.56 : 0.59 at 0.2 Hz and 0.49 : 0.53 at 0.4 Hz) and catch-up saccade (A). Involuntary, rapid, repetitive, horizontal, symmetrical and sinusoidal eye movements without intersaccadic interval is compatible with ocular flutter, which developed only with OKS speed of more than 40º/second (B). OF was not present velocities of 20º or 30º/second.
Fig. 1. Brain MRI showing olivopontocerebellar atrophy. Axial (A) and sagittal (B) T1-weighted images show marked atrophy of the cerebellum and brainstem.
known, it is thought it may develop due to an abnormality of the saccade control system. Among several mechanisms suggested, loss of tonic inhibition of omnipause neurons in the paramedian pontine reticular formation (PPRF) has been considered to be the most plausible hypothesis.1,2 Under normal conditions, during fixation, omnipause neurons inhibit the burst neurons located in the PPRF, and cease to discharge immediately prior to and during the saccade. However, in some pathologic conditions, omnipause neurons cannot inhibit the burst neurons, resulting in OF.2 Furthermore, OF is sometimes found in neurodegenerative diseases associated with cerebellar atrophy, including OPCA, thalamic haemorrhage, demyelinating disease, hydrocephalus, neuroblastoma, paraneoplastic syndromes, benign encephalitis and lithium toxicity.3–5 In patients with OPCA, OF might be caused by damage to the omnipause neurons in the PPRF during disease pro-
gression.1–5 Differing from previous reports, in this patient OF occurred only with OKS of more than 40/second. A report that the omnipause neurons could be involved in pursuit movements,6 together with the fact that optokinetic nystagmus (OKN) is a part of the pursuit system, led us to suggest that the omnipause cells might be related to optokinetic movement. Therefore, selective loss or partial damage of these neurons could provoke OF only with OKS. In our patient, abnormal firing of burst neurons could also be the mechanism of OF.1,2 As smooth pursuit is mainly mediated by the occipital cortex and cerebellar structures, whereas the velocity storage component of OKN depends almost exclusively on brainstem structures (particularly the nucleus reticularis tegmenti pontis (NRTP)) via the accessory optic tract,2,7,8 OKN probably has input independent of the burst neurons, which is not the case for smooth pursuit. Moreover, OKN is composed of both direct (smooth pursuit) movement and the velocity storage component, and OKN abnormalities are occasionally independent of a disturbance of pursuit.9 Therefore, abnormalities of these burst neurons located in the brainstem, including the NRTP, might be related to the unusual OF in the present patient.
Case reports / Journal of Clinical Neuroscience 13 (2006) 481–485
The mechanisms described above may not fully explain the OF in this patient, but suggest at least plausible mechanisms. OKS at variable speeds could be useful to provoke and detect OF in other patients. Acknowledgements The authors would like to thank Professor Woon Ki Paik at Hanyang University for his careful review of this manuscript. References 1. Gaymard B, Pierrot C. Neurology of saccades and smooth pursuit. Curr Opin Neurol 1999;12:13–9. 2. Leigh RJ, Zee DS. The Neurology of Eye Movements. 3rd ed. New York: Oxford University Press USA; 1999. p. 133–4, 449–56.
481
3. Bergenius J. Saccade abnormalities in patients with ocular flutter. Acta Otolaryngol 1986;102:228. p. 228–33. 4. Furman JMR, Eidelman BH, Fromm GH. Spontaneous remission of paraneoplastic ocular flutter and saccadic intrusions. Neurology 1988;38:499–501. 5. Kuban KC, Ephros MA, Freeman RL, et al. Syndrome of opsoclonusmyoclonus caused by Coxsackie B3 infection. Ann Neurol 1983;13:69–71. 6. Missal M, Keller EL. Common inhibitory mechanism for saccades and smooth-pursuit eye movements. J Neurophysiol 2002;88:1880–92. 7. Precht W. Anatomical and functional organization of optokinetic pathways. In: Lennerstrand G, Zee DS, Keller EL, editors. Functional Basis of Ocular Motility Disorders. Oxford: Pergamon; 1982. p. 291–302. 8. Crandall WF, Keller EL. Visual and oculomotor signals in nucleus reticularis tegmenti pontis in alert monkey. J Neurophysiol 1982;54:1326–45. 9. Daroff RB, Hoyt WF. Supranuclear disorders of ocular control systems in man: clinical, anatomical, and physiological correlations. In: Bach-yRita P, Collins CC, Hyde JE, editors. The Control of Eye Movements. New York: Academic Press; 1971. p. 175–236.
doi:10.1016/j.jocn.2005.05.023
Nocardial brain abscess: Review of clinical management Cumhur Kilincer a,*, M. Kemal Hamamcioglu a, Osman Simsek a, Tufan Hicdonmez a, Bayram Aydoslu b, Ozlem Tansel b, Mehmet Tiryaki a, Mehmet Soy c, Mu¨serref Tatman-Otkun d, Sebahattin Cobanoglu a a
Department of Neurosurgery, Trakya Universitesi Medical Faculty, Tip Fakultesi Norosirurji Anabilim Dali, Beyin Cerrahisi, 22030 Edirne, Turkey b Department of Clinical Bacteriology and Infectious Diseases, Trakya University Medical Faculty, Edirne, Turkey c Department of Internal Medicine, Section of Rheumatology, Trakya University Medical Faculty, Edirne, Turkey d Department of Microbiology and Clinical Microbiology, Trakya University Medical Faculty, Edirne, Turkey Received 16 December 2004; accepted 15 April 2005
Abstract Nocardiosis has become a significant opportunistic infection over the last two decades as the number of immunocompromised individuals has grown worldwide. We present two patients with nocardial brain abscess. The first patient was a 39-year-old woman with systemic lupus erythematosus. A left temporoparietal abscess was detected and aspirated through a burr-hole. Nocardia farcinica infection was diagnosed. The patient had an accompanying pulmonary infection and was thus treated with imipenem and amikacine for 3 weeks. She received oral minocycline for 1 year. The second patient was a 43-year-old man who was being treated with corticosteroids for glomerulonephritis. He was diagnosed with a ring-enhancing multiloculated abscess in the left cerebellar hemisphere, with an additional two small supratentorial lesions and triventricular hydrocephalus. Gross total excision of the cerebellar abscess was performed via a left suboccipital craniectomy. Culture revealed Nocardia asteroides, and the patient was successfully treated with intravenous ceftriaxone, then oral trimethoprime-sulfamethoxazole for 1 year. The clinical course, radiological findings, and management of nocardial brain abscess are discussed in light of the relevant literature, and current clinical management is reviewed through examination of the cases presented here. 2006 Elsevier Ltd. All rights reserved. Keywords: Brain abscess; Immunosuppression; Nocardia infection; Opportunistic infection; Trimethoprim-sulfamethoxazole combination; Minocycline
q *
This article was presented at the 18th Scientific Congress of the Turkish Neurosurgical Society, 2004, Kemer-Antalya, Turkey. Corresponding author. Tel.: +90 284 2355798. E-mail addresses: [email protected], [email protected]. (C. Kilincer). E-mail address: .