- Email: [email protected]
Central positioning upbeat nystagmus and vertigo due to pontine stroke
977
Case Reports / Journal of Clinical Neuroscience 18 (2011) 977–978 3. Danesh-Meyer HV, Savino PJ, Bilyk JR, et al. Aggressive glioma of adulthood simulating ischemic optic neuropathy. Arch Ophthalmol 2005;123:694–700. 4. Van Tassel P, Lee YY, Bruner JM. Synchronous and metachronous malignant gliomas: CT findings. Am J Neuroradiol 1988;9:725–32. 5. Tumialan LM, Dhall SS, Biousse V, et al. Optic nerve glioma and optic neuritis mimicking one another: case report. Neurosurgery 2005;57:E190.
6. Rothfus WE, Curtin HD, Slamovits TL, et al. Optic nerve/sheath enlargement. A differential approach based on high-resolution CT morphology. Radiology 1984;150:409–15. 7. Dinh TT, Wang YY, Rosenfeld JV, et al. Glioblastoma of the optic chiasm. J Clin Neurosci 2007;14:502–5. 8. Albers GW, Hoyt WF, Forno LS, et al. Treatment response in malignant optic glioma of adulthood. Neurology 1988;38:1071–4.
doi:10.1016/j.jocn.2010.12.010
Central positioning upbeat nystagmus and vertigo due to pontine stroke Mario Habek a,⇑, Tereza Gabelic´ a, Goran Pavliša b, Vesna V. Brinar a a b
Department of Neurology, Zagreb Medical School and University Hospital Center, Kišpatic´eva 12, Zagreb HR 10000, Croatia Department of Radiology, Zagreb University Hospital Center, Zagreb, Croatia
a r t i c l e
i n f o
Article history: Received 11 February 2010 Accepted 9 November 2010
a b s t r a c t We present a female patient with central positioning nystagmus and vertigo (c-PPV) due to a pontine stroke. To our knowledge this is the first report of central upbeat positioning nystagmus caused by pontine lacunar stroke. This report, together with those published previously, supports the existence of a crossing ventral tegmental tract in humans.
keywords: Nystagmus Pontine stroke Upbeat Ventral tegmental tract Vertigo
Ó 2011 Elsevier Ltd. All rights reserved.
1. Introduction
3. Discussion
We report a patient with central positioning nystagmus and vertigo (c-PPV) due to pontine stroke.
Central positioning nystagmus and vertigo is caused by a central lesion, usually in the posterior fossa either dorsolateral to the fourth ventricle or in the dorsal vermis.1 This is usually due
2. Case report A 60-year old female presented with a 3-week history of vertigo. Her symptoms were most prominent when getting up from bed and turning in bed, and vertigo was not accompanied with nausea or vomitting. At the time of symptom onset she was on holiday and was examined in a local emergency department. Her neurological examination was normal and she was discharged home. As her symptoms persisted, she presented to our emergency room when she returned home. Neurological examination was again normal, there was no ophthalmoplegia, saccadic pursuit, spontaneous or gaze-evoked nystagmus, weakness, or cerebellar ataxia. Her medical history was unremarkable. Because her symptoms were consistent with benign paroxysmal positional vertigo (BPPV), a Dix–Halpike test was performed. In the right position pure up-beat nystagmus was noted without latency lasting for 15 s (Supplementary Video 1). On repeated test there was no attenuation of the nystagmus. In addition, there was no improvement after repeated Eppley maneuvers. A brain MRI revealed a lacunar post-ischemic lesion visible in the pons (Fig. 1). MRI angiography was normal. Laboratory examination revealed hypercholesterolemia. Holter electrocardiography and heart ultrasound were normal. Blood pressure and glucose levels were normal. She was prescribed aspirin (100 mg daily) and atorvastatin (20 mg daily). ⇑ Corresponding author. Tel.: +38598883323; fax: +38512388045. E-mail address: [email protected] (M. Habek).
Fig. 1. (A) Axial T2-weighted MRI, (B) axial fluid-attenuated inversion recovery MRI, and (C) coronal T2-weighted MRI showing a lacunar ischemic lesion visible in the pons; and (D) an axial apparent diffusion coefficient map showing elevated diffusion in the lesion.
978
Case Reports / Journal of Clinical Neuroscience 18 (2011) 978–980
to a tumor or hemorrhage, and rarely infarction.1 The direction of the nystagmus in c-PPV can be downbeat in the head-hanging position, counterclockwise in the right-hanging position, downbeat and left beating in the left-hanging position, upbeat in the supine position, or torsional with positioning.1 Isolated upbeat nystagmus in c-PPV is extremely rare. There are several reports of upbeat nystagmus due to pontine lesions. One of the most interesting, pertinent to our case, is a patient with a lacunar infarction located in the paramedian and posterior part of the basis pontis, at the upper pons level, who presented with spontaneous upbeat nystagmus.2 It was suggested that lesions in this region could damage the ventral tegmental tract (VTT). The VTT connects the superior vestibular nucleus, which receives the excitatory anterior canal inputs, thus generating the upward slow phases, to the superior rectus and inferior oblique motor neurons in the third nerve nucleus.2,3 The course of this tract could explain how a relatively small unilateral paramedian lesion involving the VTT decussation may result in upbeat nystagmus.3 Differentiation between BPPV and c-PPV can be difficult, but careful examination of the nystagmus is usually sufficient in making the right diagnosis. The isolated upbeat nystagmus (without rotatory component), no latency, no attenuation or resistance to
the Eppley maneuver are ‘‘red flags’’ that should prompt the clinician to order an MRI. This is the first report of a patient with central upbeat positioning nystagmus caused by a pontine lacunar stroke. This report, together with those published previously, supports the existence of the VVT in humans. Appendix A. Supplementary material Supplementary video (the patient in a Dix–Halpike test showing pure upbeat nystagmus without latency) associated with this article can be found, in the online version, at doi:10.1016/ j.jocn.2010.11.021. References 1. Büttner U, Helmchen C, Brandt T. Diagnostic criteria for central versus peripheral positioning nystagmus and vertigo: a review. Acta Otolaryngol 1999;119:1–5. 2. Pierrot-Deseilligny C, Milea D, Sirmai J, et al. Upbeat nystagmus due to a small pontine lesion: evidence for the existence of a crossing ventral tegmental tract. Eur Neurol 2005;54:186–90. 3. Pierrot-Deseilligny C, Milea D. Vertical nystagmus: clinical facts and hypotheses. Brain 2005;128:1237–46.
doi:10.1016/j.jocn.2010.11.021
B-cell lymphoma infiltration of cerebrospinal fluid with minimal symptoms and benign course Thomas Skripuletz a,⇑, Refik Pul a, Ulrich Wurster a, Dietrich Peest b, Reinhard Dengler a, Martin Stangel a a b
Department of Neurology, Hannover Medical School, Carl-Neuberg-Strasse 1, Hannover 30625, Germany Department of Haematology, Haemostaseology, Oncology and Stem Cell Transplantation, Hannover Medical School, Hannover, Germany
a r t i c l e
i n f o
Article history: Received 22 June 2010 Accepted 15 November 2010 keywords: Cerebrospinal fluid Marginal zone B-cell lymphoma Monoclonal cells Flow cytometry
a b s t r a c t We report a patient diagnosed with a B-cell lymphoma after detecting monoclonal B-cells in the cerebrospinal fluid (CSF) and who had only minimal symptoms and a benign course. A 46-year-old man experienced three transitory episodes with neurological symptoms. On examination papilledema in both eyes was found. Flow cytometry (FACS)-analysis detected monoclonal B-cells in the CSF as well as in the peripheral blood and the bone marrow. Results were consistent with a low-risk lymphoma, most probably a marginal zone B-cell lymphoma. Interestingly, our patient had no progressive clinical symptoms and remained without specific therapy during 36 months of follow-up. Nevertheless, CSF-analysis led to the diagnosis of the B-cell lymphoma. Ó 2011 Elsevier Ltd. All rights reserved.
1. Introduction
2. Case report
Infiltration of the central nervous system (CNS) with a low-risk lymphoma resulting in neurological symptoms is rare,1,2 and owing to the few reports published, the clinical course and outcome are still unclear. Furthermore, infiltration of the CNS with lymphoma cells presenting as the first clinical manifestation, is not only rare but an unusual complication.3 Here, we describe a patient diagnosed with a B-cell lymphoma after detection of monoclonal B-cells in the cerebrospinal fluid (CSF) and who had only minimal symptoms and a benign course. To our knowledge, diagnosis of a Bcell lymphoma after detection of monoclonal B-cells in the CSF as the first clinical manifestation and a stable clinical course during 36 months of follow-up has not been reported to date.
A 46-year-old man experienced three transitory episodes of impaired vision, speech disorder with amnestic aphasia, headaches, and numbness and weakness of his right arm, over 3 weeks. He reported dermatomyositis, which had been treated with steroids more than 20 years ago (1982–1988), and splenomegaly had been noted since that time. There was no history of any neurological disease or symptoms. He suffered from hypertension and took an angiotensin-converting enzyme inhibitor combined with hydrochlorothiazide, a beta-1-receptor blocker, and 100 mg of acetylsalicylic acid daily. He had stopped smoking 10 years prior. On examination, in the patient had papilledema in both eyes and hypertensive changes of the fundus. The remaining physical examination, including vision, was unremarkable. A brain CT scan followed by an MRI showed no abnormalities, including infarction
⇑ Corresponding author. Fax: +49 511 532 3115. E-mail address: [email protected] (T. Skripuletz).
Case Reports / Journal of Clinical Neuroscience 18 (2011) 977–978 3. Danesh-Meyer HV, Savino PJ, Bilyk JR, et al. Aggressive glioma of adulthood simulating ischemic optic neuropathy. Arch Ophthalmol 2005;123:694–700. 4. Van Tassel P, Lee YY, Bruner JM. Synchronous and metachronous malignant gliomas: CT findings. Am J Neuroradiol 1988;9:725–32. 5. Tumialan LM, Dhall SS, Biousse V, et al. Optic nerve glioma and optic neuritis mimicking one another: case report. Neurosurgery 2005;57:E190.
6. Rothfus WE, Curtin HD, Slamovits TL, et al. Optic nerve/sheath enlargement. A differential approach based on high-resolution CT morphology. Radiology 1984;150:409–15. 7. Dinh TT, Wang YY, Rosenfeld JV, et al. Glioblastoma of the optic chiasm. J Clin Neurosci 2007;14:502–5. 8. Albers GW, Hoyt WF, Forno LS, et al. Treatment response in malignant optic glioma of adulthood. Neurology 1988;38:1071–4.
doi:10.1016/j.jocn.2010.12.010
Central positioning upbeat nystagmus and vertigo due to pontine stroke Mario Habek a,⇑, Tereza Gabelic´ a, Goran Pavliša b, Vesna V. Brinar a a b
Department of Neurology, Zagreb Medical School and University Hospital Center, Kišpatic´eva 12, Zagreb HR 10000, Croatia Department of Radiology, Zagreb University Hospital Center, Zagreb, Croatia
a r t i c l e
i n f o
Article history: Received 11 February 2010 Accepted 9 November 2010
a b s t r a c t We present a female patient with central positioning nystagmus and vertigo (c-PPV) due to a pontine stroke. To our knowledge this is the first report of central upbeat positioning nystagmus caused by pontine lacunar stroke. This report, together with those published previously, supports the existence of a crossing ventral tegmental tract in humans.
keywords: Nystagmus Pontine stroke Upbeat Ventral tegmental tract Vertigo
Ó 2011 Elsevier Ltd. All rights reserved.
1. Introduction
3. Discussion
We report a patient with central positioning nystagmus and vertigo (c-PPV) due to pontine stroke.
Central positioning nystagmus and vertigo is caused by a central lesion, usually in the posterior fossa either dorsolateral to the fourth ventricle or in the dorsal vermis.1 This is usually due
2. Case report A 60-year old female presented with a 3-week history of vertigo. Her symptoms were most prominent when getting up from bed and turning in bed, and vertigo was not accompanied with nausea or vomitting. At the time of symptom onset she was on holiday and was examined in a local emergency department. Her neurological examination was normal and she was discharged home. As her symptoms persisted, she presented to our emergency room when she returned home. Neurological examination was again normal, there was no ophthalmoplegia, saccadic pursuit, spontaneous or gaze-evoked nystagmus, weakness, or cerebellar ataxia. Her medical history was unremarkable. Because her symptoms were consistent with benign paroxysmal positional vertigo (BPPV), a Dix–Halpike test was performed. In the right position pure up-beat nystagmus was noted without latency lasting for 15 s (Supplementary Video 1). On repeated test there was no attenuation of the nystagmus. In addition, there was no improvement after repeated Eppley maneuvers. A brain MRI revealed a lacunar post-ischemic lesion visible in the pons (Fig. 1). MRI angiography was normal. Laboratory examination revealed hypercholesterolemia. Holter electrocardiography and heart ultrasound were normal. Blood pressure and glucose levels were normal. She was prescribed aspirin (100 mg daily) and atorvastatin (20 mg daily). ⇑ Corresponding author. Tel.: +38598883323; fax: +38512388045. E-mail address: [email protected] (M. Habek).
Fig. 1. (A) Axial T2-weighted MRI, (B) axial fluid-attenuated inversion recovery MRI, and (C) coronal T2-weighted MRI showing a lacunar ischemic lesion visible in the pons; and (D) an axial apparent diffusion coefficient map showing elevated diffusion in the lesion.
978
Case Reports / Journal of Clinical Neuroscience 18 (2011) 978–980
to a tumor or hemorrhage, and rarely infarction.1 The direction of the nystagmus in c-PPV can be downbeat in the head-hanging position, counterclockwise in the right-hanging position, downbeat and left beating in the left-hanging position, upbeat in the supine position, or torsional with positioning.1 Isolated upbeat nystagmus in c-PPV is extremely rare. There are several reports of upbeat nystagmus due to pontine lesions. One of the most interesting, pertinent to our case, is a patient with a lacunar infarction located in the paramedian and posterior part of the basis pontis, at the upper pons level, who presented with spontaneous upbeat nystagmus.2 It was suggested that lesions in this region could damage the ventral tegmental tract (VTT). The VTT connects the superior vestibular nucleus, which receives the excitatory anterior canal inputs, thus generating the upward slow phases, to the superior rectus and inferior oblique motor neurons in the third nerve nucleus.2,3 The course of this tract could explain how a relatively small unilateral paramedian lesion involving the VTT decussation may result in upbeat nystagmus.3 Differentiation between BPPV and c-PPV can be difficult, but careful examination of the nystagmus is usually sufficient in making the right diagnosis. The isolated upbeat nystagmus (without rotatory component), no latency, no attenuation or resistance to
the Eppley maneuver are ‘‘red flags’’ that should prompt the clinician to order an MRI. This is the first report of a patient with central upbeat positioning nystagmus caused by a pontine lacunar stroke. This report, together with those published previously, supports the existence of the VVT in humans. Appendix A. Supplementary material Supplementary video (the patient in a Dix–Halpike test showing pure upbeat nystagmus without latency) associated with this article can be found, in the online version, at doi:10.1016/ j.jocn.2010.11.021. References 1. Büttner U, Helmchen C, Brandt T. Diagnostic criteria for central versus peripheral positioning nystagmus and vertigo: a review. Acta Otolaryngol 1999;119:1–5. 2. Pierrot-Deseilligny C, Milea D, Sirmai J, et al. Upbeat nystagmus due to a small pontine lesion: evidence for the existence of a crossing ventral tegmental tract. Eur Neurol 2005;54:186–90. 3. Pierrot-Deseilligny C, Milea D. Vertical nystagmus: clinical facts and hypotheses. Brain 2005;128:1237–46.
doi:10.1016/j.jocn.2010.11.021
B-cell lymphoma infiltration of cerebrospinal fluid with minimal symptoms and benign course Thomas Skripuletz a,⇑, Refik Pul a, Ulrich Wurster a, Dietrich Peest b, Reinhard Dengler a, Martin Stangel a a b
Department of Neurology, Hannover Medical School, Carl-Neuberg-Strasse 1, Hannover 30625, Germany Department of Haematology, Haemostaseology, Oncology and Stem Cell Transplantation, Hannover Medical School, Hannover, Germany
a r t i c l e
i n f o
Article history: Received 22 June 2010 Accepted 15 November 2010 keywords: Cerebrospinal fluid Marginal zone B-cell lymphoma Monoclonal cells Flow cytometry
a b s t r a c t We report a patient diagnosed with a B-cell lymphoma after detecting monoclonal B-cells in the cerebrospinal fluid (CSF) and who had only minimal symptoms and a benign course. A 46-year-old man experienced three transitory episodes with neurological symptoms. On examination papilledema in both eyes was found. Flow cytometry (FACS)-analysis detected monoclonal B-cells in the CSF as well as in the peripheral blood and the bone marrow. Results were consistent with a low-risk lymphoma, most probably a marginal zone B-cell lymphoma. Interestingly, our patient had no progressive clinical symptoms and remained without specific therapy during 36 months of follow-up. Nevertheless, CSF-analysis led to the diagnosis of the B-cell lymphoma. Ó 2011 Elsevier Ltd. All rights reserved.
1. Introduction
2. Case report
Infiltration of the central nervous system (CNS) with a low-risk lymphoma resulting in neurological symptoms is rare,1,2 and owing to the few reports published, the clinical course and outcome are still unclear. Furthermore, infiltration of the CNS with lymphoma cells presenting as the first clinical manifestation, is not only rare but an unusual complication.3 Here, we describe a patient diagnosed with a B-cell lymphoma after detection of monoclonal B-cells in the cerebrospinal fluid (CSF) and who had only minimal symptoms and a benign course. To our knowledge, diagnosis of a Bcell lymphoma after detection of monoclonal B-cells in the CSF as the first clinical manifestation and a stable clinical course during 36 months of follow-up has not been reported to date.
A 46-year-old man experienced three transitory episodes of impaired vision, speech disorder with amnestic aphasia, headaches, and numbness and weakness of his right arm, over 3 weeks. He reported dermatomyositis, which had been treated with steroids more than 20 years ago (1982–1988), and splenomegaly had been noted since that time. There was no history of any neurological disease or symptoms. He suffered from hypertension and took an angiotensin-converting enzyme inhibitor combined with hydrochlorothiazide, a beta-1-receptor blocker, and 100 mg of acetylsalicylic acid daily. He had stopped smoking 10 years prior. On examination, in the patient had papilledema in both eyes and hypertensive changes of the fundus. The remaining physical examination, including vision, was unremarkable. A brain CT scan followed by an MRI showed no abnormalities, including infarction
⇑ Corresponding author. Fax: +49 511 532 3115. E-mail address: [email protected] (T. Skripuletz).