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Multiple sclerosis presenting with a Brown–Séquard syndrome
Journal of Neurological Sciences 156 (1998) 112–113
´ Multiple sclerosis presenting with a Brown–Sequard syndrome ¨ ¨ Jurgen A. Kraus, Bettina K. Stuper, Peter Berlit* Department of Neurology, Alfried-Krupp Hospital, Alfried-Krupp-Strasse 21, 45117 Essen, Germany Received 29 September 1997; accepted 28 October 1997
Abstract ´ The Brown–Sequard syndrome as spinal hemiplegia with contralateral sensory deficits has been related to a variety of underlying ´ diseases. We describe the case of a 35-year-old right-handed white female presenting with a Brown–Sequard syndrome as the first and ´ sole symptom of multiple sclerosis, underscoring the importance of multiple sclerosis as a rare condition for the Brown–Sequard syndrome. 1998 Elsevier Science B.V. ´ syndrome; Oligoclonal bands Keywords: Multiple sclerosis; Brown–Sequard
1. Case report A 35-year-old right-handed white female was admitted to our hospital in June 1997 when, for the first time, she noticed hypersensitivity and a subsequent disorder of temperature sensation of her right leg ascending to the C7 level on the right within three days. She mentioned a slight weakness of her left leg, too. She could not remember having been bitten by a tick, nor had there been a history of recent viral infection. On physical examination, the patient presented with a slight hemiparesis on the left with her leg being more affected than her arm and the muscle monosynaptic reflexes more pronounced on the left. There was a positive Babinski sign on the left. On the right side, there was absence of pain and temperature sensation from C7. Motor evoked potentials showed prolongation of central motor conduction time and a reduced amplitude of the compound muscle action potential on the left, while visual, auditory and somatosensory evoked potentials were normal. The patient was HIV negative. The antibodies against Borrelia burgdorferi were within the normal range.
*Corresponding author. Tel.: 149 201 4342527; fax: 149 201 4342377.
0022-510X / 98 / $19.00 1998 Elsevier Science B.V. All rights reserved. PII S0022-510X( 98 )00016-1
VDRL tests were negative. There was a normal erythrocyte sedimentation rate. Laboratory data gave no evidence for a collagenosis. Vitamins B 12 and folic acid were within the normal range. Spinal magnetic resonance imaging (MRI) was performed with T2-weighted images as well as T1-weighted images after administration of contrast media delineating a high signal intensity area within the left posterolateral aspect of the spinal cord at the level of the sixth cervical vertebra; there was no evidence for a spinal mass (Fig. 1). The cerebral MRI was normal. A lumbar puncture revealed pleocytosis with 22 cells / mm 3 , consisting predominantly of lymphocytes (75%) and monocytes (25%), a normal protein content of 45.2 mg / dl with glucose being within the normal range. Positive oligoclonal bands gave evidence for authochtone IgG antibody synthesis in the cerebrospinal fluid. No neurotropic viruses were detected. Based on these findings, the diagnosis of the first manifestation of ´ multiple sclerosis presenting with a Brown–Sequard syndrome was made. For three days the patient was treated with 1000 mg methyl-prednisolone, intravenously. There was complete recovery from the left-sided hemiparesis and contralateral hypersensitivity and the disorder of temperature sensation within ten days.
J. A. Kraus et al. / Journal of Neurological Sciences 156 (1998) 112 – 113
113
variety of underlying diseases like tumors, trauma, degenerative disease, subdural or epidural hemorrhage (Koehler and Endtz, 1986). Only a few cases of infectious or inflammatory genesis have been described like syphilis, tuberculosis (Koehler and Endtz, 1986) or infection with Borrelia burgdorferi (Berlit et al., 1991). Less often, the ´ Brown–Sequard syndrome presented as a spinal complication of an already known multiple sclerosis (Koehler and Endtz, 1986). There are even fewer reports of a spinal manifestation of multiple sclerosis as the first and sole presenting symptom of this disease (Meurice et al., 1994). Our case report presents a patient with a Brown– ´ Sequard syndrome as the first and sole manifestation of multiple sclerosis, thus underscoring the importance of keeping in mind multiple sclerosis as a rare condition in the broad spectrum of diseases presenting with a Brown– ´ Sequard syndrome.
References Fig. 1. Axial T2-weighted MRI (TE 22.0; TR 650.0) delineates a high signal intensity area (arrows) within the left posterolateral aspect of the spinal cord at the level of the sixth cervical vertebra.
2. Discussion ´ In 1846, Brown–Sequard reported on patients suffering from spinal hemiplegia with contralateral sensory deficits ´ ´ (Brown–Sequard, 1846). Since then, the Brown–Sequard syndrome has been diagnosed many times and related to a
´ Berlit, P., Pohlmann-Eden, B., Henningsen, H., 1991. Brown–Sequard syndrome caused by Borrelia burgdorferi. Eur. Neurol. 31, 18–20. ´ ´ Brown–Sequard, C.E., 1846. Recherches et experiences sur la physiologie ´ ` These ` de Paris. de la moelle epiniere. ´ Koehler, P.H., Endtz, L.J., 1986. The Brown–Sequard syndrome. Arch. Neurol. 43, 921–924. Meurice, A., Flandroy, P., Dondelinger, R.F., Reznik, M., 1994. A single focus of probable multiple sclerosis in the cervical spinal cord mimicking a tumour. Neuroradiology 36, 234–235.
´ Multiple sclerosis presenting with a Brown–Sequard syndrome ¨ ¨ Jurgen A. Kraus, Bettina K. Stuper, Peter Berlit* Department of Neurology, Alfried-Krupp Hospital, Alfried-Krupp-Strasse 21, 45117 Essen, Germany Received 29 September 1997; accepted 28 October 1997
Abstract ´ The Brown–Sequard syndrome as spinal hemiplegia with contralateral sensory deficits has been related to a variety of underlying ´ diseases. We describe the case of a 35-year-old right-handed white female presenting with a Brown–Sequard syndrome as the first and ´ sole symptom of multiple sclerosis, underscoring the importance of multiple sclerosis as a rare condition for the Brown–Sequard syndrome. 1998 Elsevier Science B.V. ´ syndrome; Oligoclonal bands Keywords: Multiple sclerosis; Brown–Sequard
1. Case report A 35-year-old right-handed white female was admitted to our hospital in June 1997 when, for the first time, she noticed hypersensitivity and a subsequent disorder of temperature sensation of her right leg ascending to the C7 level on the right within three days. She mentioned a slight weakness of her left leg, too. She could not remember having been bitten by a tick, nor had there been a history of recent viral infection. On physical examination, the patient presented with a slight hemiparesis on the left with her leg being more affected than her arm and the muscle monosynaptic reflexes more pronounced on the left. There was a positive Babinski sign on the left. On the right side, there was absence of pain and temperature sensation from C7. Motor evoked potentials showed prolongation of central motor conduction time and a reduced amplitude of the compound muscle action potential on the left, while visual, auditory and somatosensory evoked potentials were normal. The patient was HIV negative. The antibodies against Borrelia burgdorferi were within the normal range.
*Corresponding author. Tel.: 149 201 4342527; fax: 149 201 4342377.
0022-510X / 98 / $19.00 1998 Elsevier Science B.V. All rights reserved. PII S0022-510X( 98 )00016-1
VDRL tests were negative. There was a normal erythrocyte sedimentation rate. Laboratory data gave no evidence for a collagenosis. Vitamins B 12 and folic acid were within the normal range. Spinal magnetic resonance imaging (MRI) was performed with T2-weighted images as well as T1-weighted images after administration of contrast media delineating a high signal intensity area within the left posterolateral aspect of the spinal cord at the level of the sixth cervical vertebra; there was no evidence for a spinal mass (Fig. 1). The cerebral MRI was normal. A lumbar puncture revealed pleocytosis with 22 cells / mm 3 , consisting predominantly of lymphocytes (75%) and monocytes (25%), a normal protein content of 45.2 mg / dl with glucose being within the normal range. Positive oligoclonal bands gave evidence for authochtone IgG antibody synthesis in the cerebrospinal fluid. No neurotropic viruses were detected. Based on these findings, the diagnosis of the first manifestation of ´ multiple sclerosis presenting with a Brown–Sequard syndrome was made. For three days the patient was treated with 1000 mg methyl-prednisolone, intravenously. There was complete recovery from the left-sided hemiparesis and contralateral hypersensitivity and the disorder of temperature sensation within ten days.
J. A. Kraus et al. / Journal of Neurological Sciences 156 (1998) 112 – 113
113
variety of underlying diseases like tumors, trauma, degenerative disease, subdural or epidural hemorrhage (Koehler and Endtz, 1986). Only a few cases of infectious or inflammatory genesis have been described like syphilis, tuberculosis (Koehler and Endtz, 1986) or infection with Borrelia burgdorferi (Berlit et al., 1991). Less often, the ´ Brown–Sequard syndrome presented as a spinal complication of an already known multiple sclerosis (Koehler and Endtz, 1986). There are even fewer reports of a spinal manifestation of multiple sclerosis as the first and sole presenting symptom of this disease (Meurice et al., 1994). Our case report presents a patient with a Brown– ´ Sequard syndrome as the first and sole manifestation of multiple sclerosis, thus underscoring the importance of keeping in mind multiple sclerosis as a rare condition in the broad spectrum of diseases presenting with a Brown– ´ Sequard syndrome.
References Fig. 1. Axial T2-weighted MRI (TE 22.0; TR 650.0) delineates a high signal intensity area (arrows) within the left posterolateral aspect of the spinal cord at the level of the sixth cervical vertebra.
2. Discussion ´ In 1846, Brown–Sequard reported on patients suffering from spinal hemiplegia with contralateral sensory deficits ´ ´ (Brown–Sequard, 1846). Since then, the Brown–Sequard syndrome has been diagnosed many times and related to a
´ Berlit, P., Pohlmann-Eden, B., Henningsen, H., 1991. Brown–Sequard syndrome caused by Borrelia burgdorferi. Eur. Neurol. 31, 18–20. ´ ´ Brown–Sequard, C.E., 1846. Recherches et experiences sur la physiologie ´ ` These ` de Paris. de la moelle epiniere. ´ Koehler, P.H., Endtz, L.J., 1986. The Brown–Sequard syndrome. Arch. Neurol. 43, 921–924. Meurice, A., Flandroy, P., Dondelinger, R.F., Reznik, M., 1994. A single focus of probable multiple sclerosis in the cervical spinal cord mimicking a tumour. Neuroradiology 36, 234–235.