CLINICS 2011;66(9):1655-1657 CASE REPORT DOI:10.1590/S1807-59322011000900026 Choreoathetosis after subarachnoid hemorrhage related to an aneurysm of the posterior fossa Ju´ lio Leonardo Barbosa Pereira,I Lucas Alverne Freitas de Albuquerque,I Mauro Cruz Machado Borgo,I Gerival Vieira Junior,I Paulo Pereira Christo,II Gerva´ sio Teles C. de CarvalhoIII I Neurosurgery, Santa Casa de Belo Horizonte, Belo Horizonte/MG, Brazil. II Research Program of the Santa Casa, Belo Horizonte/MG, Brazil. III Neurosurgery, Santa Casa de Belo Horizonte and Faculdade de Cieˆ ncias Medicas de Minais Gerais, Belo Horizonte/MG, Brazil. Email: lucasalverne@yahoo.com.br Tel.: 31 3238-8100 INTRODUCTION Non-traumatic subarachnoid hemorrhage (NSAH) is a neurological emergency with a high rate of death and complications.1,2 A ruptured intracranial aneurysm accounts for approximately 80% of NSAH cases. The classic clinical manifestations of NSAH are headache, nausea and vomiting, focal neurological signs, meningeal irritation, and a reduction in the level of consciousness. In the present work, we describe a case of choreoathetosis that developed in a young patient who presented with a subarachnoid hemorrhage (SAH) related to an aneurysm of the posterior fossa. We also review the corresponding literature. CASE REPORT A 17-year-old boy, with no previous co-morbidity or neurological disability, reported the sudden onset of a severe headache associated with an alteration of his level of consciousness and meningeal signs. Upon admission to our department, three days after the acute event, he was confused, dysarthric, exhibited choreoatetoid movements of the distal upper limbs, exhibited postural instability, and exhibited the inability to walk, stand up, or sit up without help. The choreoathetosis began just after the onset of the SAH. The results of the motor, sensitivity , and reflex examinations were normal. The patient’s hyperkinesia ceased with sleep. In addition, there was no family history of movement disorders. A computed tomography (CT) scan revealed a hemor- rhage in the fourth ventricle but no evidence of a parenchyma lesion. A cerebral angiography (Figure 1A) revealed a small saccular aneurysm of the basilar artery, which was located close to the emergence of the anterior inferior cerebellar artery (AICA). No evidence of vasospasm was observed. On the fourth day after the ictus, the patient was administered haloperidol, and a progressive reduction in the frequency of choreoatetoid movements was observed. However, the dysarthria and postural instability remained. The patient was administered phenytoin for seven days Copyright 2011 CLINICS – This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http:// creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non- commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. 1655 prior to the endovascular aneurysm repair, which was completed uneventfully. A control CT scan did not reveal hydrocephalus. At the one-year follow-up visit, the patient did not exhibit any choreoatetoid movements; however, the cerebellar alterations remained, with an important static and dynamic imbalance and significant dysmetria. Magnetic Resonance Imaging (MRI) at the one year follow-up revealed cerebellar atrophy (Figure 1B). DISCUSSION Stroke-related movement disorders are uncommon (3.6%) and are very rare in SAH cases . Chorea, tremor, dystonia, Parkinsonism, and myoclonus have all been associated with cerebral infarcts and hemorrhaging.3 Movement disorders, which represent a portion of the clinical spectrum of acute stroke, may be delayed or progressive. The first case of a movement disorder (chorea) after a SAH was reported by Sakai et al.4 and occurred eight days after the SAH onset. The CT scans revealed a SAH with ventricular dilation and periventricular lucency involving the bilateral caudate nuclei. The chorea was attributed to the vasospasm and hydrocephalus.4 In another case, reported by Morigaki et al.,5 the involuntary movements began shortly after the SAH onset. There was no acute hydrocephalus, and the authors attributed the symptoms to a hematoma on the corpus callosum that resulted from a rupture of an aneurysm of the distal accessory anterior cerebral artery. The hyperkinetic involuntary movements were suggested to have occurred due to the interruption of the cortico-striato-pallido-tha- lamo-cortical feedback loop. Alarco´n et al. analyzed 1,500 consecutive stroke patients over a period of ten years to identify patients with a movement disorder, which was observed in only 56 patients (3.6%). Chorea was the most common movement disorder (35.7%). Thirty-nine (69.6%) patients experienced an ischemic stroke, 14 (25%) experienced a parenchymal hemorrhage, and only three (5.3%) experienced a SAH. All of the patients with a movement disorder that was secondary to a SAH in the Alarco´n et al. series presented with a tremor (Table 1) as their principal involuntary movement.3 The time that elapses between a stroke onset and the development of a movement disorder is variable. Alarco´ n et al. observed involuntary movements that began on the first day of the stroke in 12.5% of their patients but reported