Case Report Ischemic Stroke of the Pyramidal Decussation Causing Quadriplegia and Anarthria Emilia G. Wilkins, BS, Hooman Kamel, MD, Eric C. B. Johnson, MD, PhD, Sarah M. Shalev, MD, and S. Andrew Josephson, MD A 52-year-old man with a history of hypertension and previously irradiated head and neck cancer presented with quadriplegia and anarthria sparing the face and sensory functions. Brain magnetic resonance imaging (MRI) demonstrated acute infarction of the pyramidal decussation. We describe the clinical and radiological characteristics of infarction at the pyramidal decussation and review the arterial supply to this region in the lower brainstem. Although rare, infarction of the pyramidal decussation should be considered in the differential diagnosis when patients present with atraumatic pure motor quadriplegia. Key Words: Anterior spinal artery—flaccid quadriplegia—pyramidal decussation—stroke. Ó 2012 by National Stroke Association Infarction of the pyramidal decussation is rare and not well described in the literature. The expected clinical syndrome involves quadriplegia with sparing of the face and sensory fibers. Anatomic localization of acute atraumatic quadriplegia is challenging, and a broad differential diagnosis includes disorders affecting the upper motor neurons in the brainstem or, more commonly, cervical spinal cord, as well as disorders of the lower motor neurons, including acute motor neuropathy or neuromuscular junction disease. Case Report A 52-year-old man with a history of hypertension and previously irradiated head and neck cancer awoke with quadriplegia. On examination, the patient was alert. From the Department of Neurology, University of California at San Francisco, San Francisco, California. Received January 20, 2011; revision received January 29, 2011; accepted February 2, 2011. Address correspondence to S. Andrew Josephson, MD, Department of Neurology, University of California at San Francisco, 505 Parnassus Ave, Box 0114, San Francisco, CA 94143-0114. E-mail: ajosephson@memory.ucsf.edu. 1052-3057/$ - see front matter Ó 2012 by National Stroke Association doi:10.1016/j.jstrokecerebrovasdis.2011.02.001 Despite being anarthric, he communicated by mouthing words. Cranial nerves II through VII were normal, but he was unable to move his tongue and had no gag reflex. All 4 limbs were flaccid and plegic. Sensation to all modalities was intact in all 4 limbs. He had hyperreflexia throughout and bilateral Babinski signs. A magnetic resonance imaging scan of the brain revealed an area of restricted diffusion in the pyramidal decussation, just above the cervicomedullary junction (Fig 1). There were also multiple foci of abnormal T2 prolongation in the posterior fossa, likely representing the sequelae of microangiopathy from radiation. The patient was admitted to the intensive care unit and given clopidogrel 75mg daily. He quickly developed respiratory failure requiring intubation because of copious secretions and dysphagia. He remained quadriplegic for 2 months and required tracheostomy and percutaneous endoscopic gastrostomy. Although he was nonverbal, he could communicate using a language board. Examination 1 year poststroke revealed increased spastic tone, hyperreflexia, and moderate to severe weakness in all 4 extremities with bilateral Babinski signs and preserved sensation. Discussion Infarction at the pyramidal decussation can rarely lead to pure motor quadriplegia with sparing of the face.1-3 This has Journal of Stroke and Cerebrovascular Diseases, Vol. 21, No. 7 (October), 2012: pp 620.e1-620.e2 620.e1 E.G. WILKINS ET AL. 620.e2 Figure 1. (A) Axial T2-weighted magnetic resonance imaging scan, (B) coronal diffusion-weighted image, (C) axial diffusion-weighted image, and (D) axial apparent diffusion coefficient (ADC) map showing acute infarction in the corticospinal tract at the level of the pyramidal decussation. not been described in the literature with corresponding radiologic evidence. We speculate that the patient suffered infarction from occlusion of perforators off of the anterior spinal artery, likely caused by radiation-induced microangiopathy. At the level of the pyramidal decussation, the anterior spinal artery does not supply the sensory tracts, which are instead usually fed by the vertebral and posterior spinal arteries, explaining the absence of sensory deficits.4 We hypothesize that his anarthria and dysphagia were caused by involvement of the hypoglossal nucleus and fibers, with perhaps some involvement of cranial nerves IX and X. A similar case was reported in 1889; this patient experienced sudden right-sided hemiplegia, followed by left-sided hemiparesis and dysphagia. A pathologic examination revealed softening of the pyramidal decussation.5 Infarction of the pyramidal decussation must be considered in patients with pure motor quadriplegia. References 1. Meyer JS, Herndon RM. Bilateral infarction of the pyramidal tracts in man. Neurology 1962;12:637-642. 2. Jagiella WM, Sung JH. Bilateral infarction of the medullary pyramids in humans. Neurology 1989;39:21-24. 3. Kobayashi Z, Hino T, Kanazawa T, et al. Bilateral medial medullary infarction presented with monoplegia of the lower limb, followed by paraplegia, and finally by tetraplegia [in Japanese]. Rinsho Shinkeigaku 1993;43:195-198. 4. Stopford JS. The arteries of the pons and medulla oblongata. Part III. J Anat Physiol 1917;51(Pt 3):250-277. 5. Stopford JS. The arteries of the pons and medulla oblongata. Part II. J Anat Physiol 1916;50(Pt 3):255-280.