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Journal of

CLINICAL NEUROMUSCULAR DISEASE

Case Review

Volume 15, Number 3 March 2014

Pure T7 Sensory Level as an Isolated Manifestation of Guillain–Barre´ Syndrome Tariq B. Alfahad, MD and John J. Kelly, MD

Abstract Introduction: Truncal sensory level (TSL) is a localizing sign for spinal cord pathology. However, in rare instances, lesions higher up in the spinothalamic tract can cause TSL. Case Report: A 26-year-old woman presented with numbness from waist down with a T7 TSL on examination with negative spine magnetic resonance imaging. Later, the patient developed the full picture of Guillain–Barré syndrome confirmed with electrophysiological testing. Conclusion: TSL can localize to the nerve roots and can be an early manifestation of Guillain–Barré syndrome. Key Words: truncal sensory level, Guillain–Barré syndrome, numbness, spinal roots, ocalization

( J Clin Neuromusc Dis 2014;15:102–104)

INTRODUCTION

From the Department of Neurology, George Washington University, Washington, DC. The authors report no conflicts of interest. Reprints: Tariq B. Alfahad, MD, Building 10, Room 7-4647, 10 Center Drive, Bethesda, MD 20892 (e-mail: [email protected]). Copyright © 2014 by Lippincott Williams & Wilkins

Guillain–Barré syndrome (GBS) encompasses a heterogeneous group of acute immune-mediated polyradiculoneuropathies.1 The cardinal clinical features of GBS are progressive, fairly symmetric muscle weakness accompanied by absent or depressed deep tendon reflexes (DTR). Paresthesias in the hands and feet accompany the weakness in more than 80% of patients. A rare variant of GBS presents with solely sensory symptoms, named sensory Guillain–Barré syndrome.2 Truncal sensory level (TSL) is most commonly associated with spinal cord lesions. Although rare, unilateral TSL has also been described in other levels of the neuroaxis, including medulla, pons, and parietal lobe.3–12 To our

knowledge, an apparent TSL as the initial manifestation of GBS has not been reported before. Here we describe a patient with classical GBS who presented initially with an apparent T7 sensory level.

CASE REPORT A 26-year-old woman presented to the emergency room with a complaint of numbness below her waist. She woke up with numbness in her feet. Two hours later, while taking a shower, she noticed decreased feeling in her body below the waist. She had no other neurological symptoms like weakness, bowel or bladder dysfunction, dysphagia, dysarthria, or back pain. There was no history of trauma or back surgery. She reported having upper respiratory infection 1 week before onset of symptoms. She was previously healthy, nonsmoker, not on medications or recreational drugs. Neurological examination was performed 20 hours after symptom onset. She was alert and oriented. Both pupils were round, symmetrical and reactive to light and accommodation. Other cranial nerves were all normal. Muscle strength was full in the extremities. DTR were normal and symmetric with downgoing plantars. Sensory examination revealed decreased pain and temperature sensations below the T7 level front and back. Unlike on the trunk, on the lower extremities she had patchy sensory loss. Vibration and position sensations, 2-point discrimination, and cortical sensations like graphesthesia were intact. Cerebellar function was intact with normal finger-to-nose, heel-toshin, tandem gait and Romberg test. Rectal tone was normal.

TSL as an Isolated Manifestation of GBS

Complete blood count, erythrocyte sedimentation rate, blood electrolytes, chemistry, and liver enzymes were within normal limits; as well as vitamin B12, angiotensin converting enzyme, and human immunodeficiency virus tests. Computed tomography of the head and magnetic resonance imaging of the cervical and thoracic spine were unremarkable. She opted to go home and follow-up as outpatient. Five days later, she returned to the emergency room with left facial droop and weakness in both legs. Neurological examination revealed left lower motor neuron facial palsy, proximal more than distal bilateral lower extremities weakness, DTR were absent at ankles, minimal at knee, and decreased at upper extremities. No sensory level was detectable this time. Cerebrospinal fluid analysis showed mild lymphocytic pleocytosis (15/mm3) and high protein (114 mg/dL). Tests for oligoclonal bands, herpes simplex virus, West Nile virus, and Lyme disease were negative. Nerve conduction study showed absent F waves, prolonged distal latencies with conduction block, and temporal dispersion that was diagnostic for acute demyelinating polyradiculoneuropathy (GBS). She received intravenous immunoglobulin therapy more than 5 days with good response.

DISCUSSION The initial diagnosis of GBS is based on the clinical presentation. It is important that GBS is diagnosed early as the prognosis is dramatically better with early treatment.13 TSL is considered by physicians, and even many neurologists, to be pathognomonic for spinal cord pathology. There are, however, many reports in the literature of TSL in other neurological localizations. Breuer et al3 reported T6 TSL because of right parietal lobe arteriovenous malformation. Song et al4 reported right-sided TSL because of brain abscess in left parietal lobe. Several case reports published about TSL with pontine and medullary infarcts,5–7 and in patients who have undergone surgical spinothalamic tractotomy at the level of the pons8 and

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medulla for relief of intractable pain. Phan and Wijdicks10 and Song et al11 described TSL in patients with lateral medullary infarct. Leifer et al12 described a man with posttraumatic pontine TSL. A partial lesion of the lateral spinothalamic tract involving only the far lateral fibers may explain selective involvement of the trunk and lower limb. Another localization that can, in rare instances, give a pseudo-TSL is the peripheral nerves as in diabetic truncal polyneuropathy,14 where sensory loss involves a number of thoracic intercostal nerves in a relatively symmetric distribution. Symmetric sensory loss over the trunk does not occur with diabetic polyneuropathy until sensory loss in the limbs has progressed to the thighs and elbows.15 So, when diabetic truncal polyneuropathy involving the lower thoracic intercostal nerves is combined with a symmetric distal peripheral neuropathy involving the limbs in a stocking–glove distribution, the chance of diagnosing a TSL is high leading to a false (pseudo-)TSL. The pathology of GBS is that of multifocal inflammatory demyelination starting at the level of the nerve roots.1 We hypothesize that the reason for having TSL in our patient was because of initial disease process starting at the root level. Since the root supplied dermatomes are horizontally oriented in the thoracic and upper lumbar regions, then a pseudo-TSL was found on neurological examination. So our patient, probably, had disease affecting the nerve roots up to the T7 level giving a symmetric T7 TSL. Furthermore, the patchy sensory loss in the lower extremities is probably because of incomplete involvement of some roots. To our knowledge, this is the first report of GBS presenting with TSL as an early manifestation. REFERENCES 1. Yuki N, Hartung HP. Guillain-Barré syndrome. N Engl J Med. 2012;366:2294. 2. Oh SJ, LaGanke C, Claussen GC. Sensory GuillainBarré syndrome. Neurology. 2001;56:82–86. 3. Breuer AC, Cuervo H, DSelkoe DJ. Hyperpathia and sensory level due to parietal lobe arteriovenous malformation. Arch Neurol. 1981;38:722–724. www.jcnmd.com

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4. Song YM, Kim JI, Lee GH, et al. Teaching neuroimage: sensory level in parietal lobe lesion. Neurology. 2007;68:E38. 5. Amyot R. Syndrome de l’artère cérébelleuse supérieure: observation clinique. Union Med Can. 1939; 68:1067–1073. 6. Matsumoto S, Okuda B, Imai T, et al. A sensory level on the trunk in lower lateral brainstem lesions. Neurology. 1988;38:1515–1519. 7. Izquierdo G, Viguera J, Martinez-Parra C. Sensory levels with brainstem lesions. Neurology. 1989;39:877–878. 8. Hitchcock ER. Stereotaxic pontine spinothalamic tractotomy. J Neurosurg. 1973;39:746–752. 9. Schwartz HG, O’Leary JL. Section of the spinothalamic tract at the level of the inferior olive. Arch Neurol Psychiatr. 1942;47:293–304. 10. Phan TG, Wijdicks EF. A sensory level on the trunk and sparing the face from vertebral artery dissection:

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how much more subtle can we get? J Neurol Neurosurg Psychiatry. 1999;66:691–692. 11. Song IU, Kim JS, Lee DG, et al. Pure sensory deficit at the t4 sensory level as an isolated manifestation of lateral medullary infarction. J Clin Neurol. 2007;3: 112–115. 12. Leifer D, Hochberg FH. Posttraumatic pontine truncal sensory level. Arch Neurol. 1991;48:1216. 13. Visser LH, Schmitz PI, Meulstee J, et al. Prognostic factors of Guillain-Barré syndrome after intravenous immunoglobulin or plasma exchange. Dutch Guillain-Barré Study Group. Neurology. 1999;53:598–604. 14. Waxman SG, Sabin TD. Diabetic truncal polyneuropathy. Arch Neurol. 1981;38:46–47. 15. Sabin TD, Geschwind N, Waxman SG. Patterns of clinical deficits in peripheral nerve disease. In: Physiology and Pathobiology of Axons. New York, NY: Raven Press; 1978:431–438.

Pure T7 sensory level as an isolated manifestation of Guillain-Barré syndrome.

Truncal sensory level (TSL) is a localizing sign for spinal cord pathology. However, in rare instances, lesions higher up in the spinothalamic tract c...
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