Neurol Sci DOI 10.1007/s10072-015-2286-y
LETTER TO THE EDITOR
Lateral medullary infarction masquerading as involvement of spinal cord Tomoya Kon1 • Haruo Nishijima1 • Rie Haga1 • Yukihisa Funamizu1 • Tatsuya Ueno1 • Akira Arai1 • Chieko Suzuki1 • Jin-ichi Nunomura1 • Masayuki Baba1 • Masahiko Tomiyama1
Received: 3 March 2015 / Accepted: 9 June 2015 Ó Springer-Verlag Italia 2015
Dear Editor, Unilateral sensory impairment below the dermatome usually suggests involvement of the spinal cord. Here, we describe a patient presenting with impaired pain and temperature sensation below the right-side Th8 dermatome due to left lateral medullary infarction. An 86-year-old woman visited our clinic presenting with numbness in her right lower leg. Her past medical history included hypertension, diabetes mellitus, dyslipidemia, hyperthyroidism, and postoperative state after the removal of a hemangioblastoma on the right cerebellum. Her consciousness was clear. Vital signs and general physical examination were normal. Neurological examination revealed deficits in pain and temperature sensation below the Th8 dermatome on the right trunk and leg (Fig. 1a). She showed dysmetria of the right arm and a wide-based gait, but both had been present for years since cerebellar tumor surgery. Motor paralysis or Horner’s syndrome was not seen. We initially suspected that she had involvement of the thoracic spinal cord. However, spinal MRI demonstrated no abnormality in the spine or spinal cord. Brain MRI revealed a small infarction in the left lateral medulla
oblongata by diffusion-weighted image (Fig. 1b) and fluid attenuation inversion recovery (Fig. 1c). Magnetic resonance angiography showed an atherosclerotic stenosis at left vertebral artery (Fig. 1d), and high-echoic plaques were found in the bilateral common- and internal-carotid arteries by carotid ultrasonography. Echocardiography and 24-h EEG were normal. The patient was clinically diagnosed with atherothrombotic infarction on the basis of NINDS III classification [1]. Antiplatelet therapy was started subsequently, and the sensory impairment gradually resolved. The lateral spinothalamic tract conveys pain and temperature sensation in the contralateral body and is arranged topographically in the medulla oblongata. Afferents from caudal areas are located in the lateral portions of the tract [2] (Fig. 1e). In our case, the lesion was mostly restricted to the left lateral portion of the spinothalamic tract, affecting sensory fibers conveying superficial sensory information from the sacral, lumbar, and thoracic (to Th8) dermatomes on the right side. Accordingly, the sensory impairment was seen below the right Th8 dermatome. Reports of such patients presenting with sensory deficits in a dermatomal
& Tomoya Kon [email protected]; [email protected] 1
Department of Neurology, Aomori Prefectural Central Hospital, 2-1-1 Higashi-Tsukurimichi, Aomori, Aomori 030-8553, Japan
123
Neurol Sci Fig. 1 a Schematic of pain and temperature sensation deficit. b– d Brain MRI. Diffusionweighted image (b) and fluid attenuation inversion recovery (c) showing a small infarction at the left-side lateral medulla (arrows). Magnetic resonance angiography showed a stenosis at left vertebral artery (arrow head) (d). e Topography of afferent fibers in lateral spinothalamic tract. The gray area indicates lesions in the present case. Revised by authors, reproduced from Haymaker [2], Copyright Elsevier, with permission of Elsevier. S sacral, L lumbar, T thoracic, C cervical, V trigeminal
distribution are rare [3–7]. The lesson from the present case study is that lateral medullary infarction should be considered in the differential diagnosis of dermatomal sensory impairment.
3.
4. Conflict of interest The authors declare that they have no conflicts of interest. 5.
References 6. 1. National Institute of Neurological Disorders and Stroke Committee (1990) Special report from the National Institute of Neurological Disorders and Stroke. Classification of cerebrovascular diseases III. Stroke 21:637–676 2. Haymaker W (1969) Localization of lesions involving the brainstem and emergent nerves, In: Haymaker W (ed) Bing’s
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7.
local diagnosis in neurological disease, 15th edn. Mosby, Saint Louis, p 148 Phan TG, Wijdicks EF (1999) A sensory level on the trunk and sparing the face from vertebral artery dissection: how much more subtle can we get? J Neurol Neurosurg Psychiatry 66:691–692 Song IU, Kim JS, Lee DG, An JY, Ryu SY, Lee SB et al (2007) Pure sensory deficit at the T4 sensory level as an isolated manifestation of lateral medullary infarction. J Clin Neurol 3:112–115 Chang WL, Ke DS, Cheng TJ (2010) Lateral medullary infarction presenting as Brown-Sequard syndrome-like manifestation: a case report and literature review. Acta Neurol Taiwan 19:204–207 Xia C, Wang Q, Chen HS (2013) Pure sensory deficit at the T3 sensory level as an isolated manifestation of lateral medullary infarction. Neurol India 61:327–328 Hongo H, Tanaka Y, Shimada Y, Tanaka R, Hattori N, Urabe T (2014) Dermatomal sensory manifestations in lateral medullary infarction. J Stroke Cerebrovasc Dis 23:182–183
LETTER TO THE EDITOR
Lateral medullary infarction masquerading as involvement of spinal cord Tomoya Kon1 • Haruo Nishijima1 • Rie Haga1 • Yukihisa Funamizu1 • Tatsuya Ueno1 • Akira Arai1 • Chieko Suzuki1 • Jin-ichi Nunomura1 • Masayuki Baba1 • Masahiko Tomiyama1
Received: 3 March 2015 / Accepted: 9 June 2015 Ó Springer-Verlag Italia 2015
Dear Editor, Unilateral sensory impairment below the dermatome usually suggests involvement of the spinal cord. Here, we describe a patient presenting with impaired pain and temperature sensation below the right-side Th8 dermatome due to left lateral medullary infarction. An 86-year-old woman visited our clinic presenting with numbness in her right lower leg. Her past medical history included hypertension, diabetes mellitus, dyslipidemia, hyperthyroidism, and postoperative state after the removal of a hemangioblastoma on the right cerebellum. Her consciousness was clear. Vital signs and general physical examination were normal. Neurological examination revealed deficits in pain and temperature sensation below the Th8 dermatome on the right trunk and leg (Fig. 1a). She showed dysmetria of the right arm and a wide-based gait, but both had been present for years since cerebellar tumor surgery. Motor paralysis or Horner’s syndrome was not seen. We initially suspected that she had involvement of the thoracic spinal cord. However, spinal MRI demonstrated no abnormality in the spine or spinal cord. Brain MRI revealed a small infarction in the left lateral medulla
oblongata by diffusion-weighted image (Fig. 1b) and fluid attenuation inversion recovery (Fig. 1c). Magnetic resonance angiography showed an atherosclerotic stenosis at left vertebral artery (Fig. 1d), and high-echoic plaques were found in the bilateral common- and internal-carotid arteries by carotid ultrasonography. Echocardiography and 24-h EEG were normal. The patient was clinically diagnosed with atherothrombotic infarction on the basis of NINDS III classification [1]. Antiplatelet therapy was started subsequently, and the sensory impairment gradually resolved. The lateral spinothalamic tract conveys pain and temperature sensation in the contralateral body and is arranged topographically in the medulla oblongata. Afferents from caudal areas are located in the lateral portions of the tract [2] (Fig. 1e). In our case, the lesion was mostly restricted to the left lateral portion of the spinothalamic tract, affecting sensory fibers conveying superficial sensory information from the sacral, lumbar, and thoracic (to Th8) dermatomes on the right side. Accordingly, the sensory impairment was seen below the right Th8 dermatome. Reports of such patients presenting with sensory deficits in a dermatomal
& Tomoya Kon [email protected]; [email protected] 1
Department of Neurology, Aomori Prefectural Central Hospital, 2-1-1 Higashi-Tsukurimichi, Aomori, Aomori 030-8553, Japan
123
Neurol Sci Fig. 1 a Schematic of pain and temperature sensation deficit. b– d Brain MRI. Diffusionweighted image (b) and fluid attenuation inversion recovery (c) showing a small infarction at the left-side lateral medulla (arrows). Magnetic resonance angiography showed a stenosis at left vertebral artery (arrow head) (d). e Topography of afferent fibers in lateral spinothalamic tract. The gray area indicates lesions in the present case. Revised by authors, reproduced from Haymaker [2], Copyright Elsevier, with permission of Elsevier. S sacral, L lumbar, T thoracic, C cervical, V trigeminal
distribution are rare [3–7]. The lesson from the present case study is that lateral medullary infarction should be considered in the differential diagnosis of dermatomal sensory impairment.
3.
4. Conflict of interest The authors declare that they have no conflicts of interest. 5.
References 6. 1. National Institute of Neurological Disorders and Stroke Committee (1990) Special report from the National Institute of Neurological Disorders and Stroke. Classification of cerebrovascular diseases III. Stroke 21:637–676 2. Haymaker W (1969) Localization of lesions involving the brainstem and emergent nerves, In: Haymaker W (ed) Bing’s
123
7.
local diagnosis in neurological disease, 15th edn. Mosby, Saint Louis, p 148 Phan TG, Wijdicks EF (1999) A sensory level on the trunk and sparing the face from vertebral artery dissection: how much more subtle can we get? J Neurol Neurosurg Psychiatry 66:691–692 Song IU, Kim JS, Lee DG, An JY, Ryu SY, Lee SB et al (2007) Pure sensory deficit at the T4 sensory level as an isolated manifestation of lateral medullary infarction. J Clin Neurol 3:112–115 Chang WL, Ke DS, Cheng TJ (2010) Lateral medullary infarction presenting as Brown-Sequard syndrome-like manifestation: a case report and literature review. Acta Neurol Taiwan 19:204–207 Xia C, Wang Q, Chen HS (2013) Pure sensory deficit at the T3 sensory level as an isolated manifestation of lateral medullary infarction. Neurol India 61:327–328 Hongo H, Tanaka Y, Shimada Y, Tanaka R, Hattori N, Urabe T (2014) Dermatomal sensory manifestations in lateral medullary infarction. J Stroke Cerebrovasc Dis 23:182–183
