- Department of Neurosurgery, Saitama Medical Center, Saitama Medical University, 1981 Kamoda, Kawagoe, Saitama 350-8550, Japan
Correspondence Address:
Soichi Oya
Department of Neurosurgery, Saitama Medical Center, Saitama Medical University, 1981 Kamoda, Kawagoe, Saitama 350-8550, Japan
DOI:10.4103/2152-7806.157444
Copyright: © 2015 Oya S. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.How to cite this article: Oya S, Fujisawa N, Matsui T. Hemichorea-hemiballismus caused by postoperative hyperperfusion after clipping of a giant unruptured middle cerebral artery aneurysm. Surg Neurol Int 21-May-2015;6:84
How to cite this URL: Oya S, Fujisawa N, Matsui T. Hemichorea-hemiballismus caused by postoperative hyperperfusion after clipping of a giant unruptured middle cerebral artery aneurysm. Surg Neurol Int 21-May-2015;6:84. Available from: http://surgicalneurologyint.com/surgicalint_articles/hemichorea-hemiballismus-caused-postoperative/
Abstract
Background:Movement disorders after the clipping for an unruptured giant aneurysm are rare. The information on the pathogenesis and treatment options for this condition is largely unknown.
Case Description:An 82-year-old female with no neurological deficits underwent a clipping for a giant middle cerebral artery (MCA) aneurysm. Immediately after surgery, she presented with hemichorea–hemiballismus (HC–HB) on the left side. Postoperative angiograms and single-photon emission computed tomography demonstrated the hyperperfusion in the right frontal cortex and the decreased perfusion in the basal ganglia, indicating that the abrupt hemodynamic changes due to the obliteration of the giant aneurysm caused the dysfunction of the frontal cortical and subcortical pathway and the basal ganglia. Administration of tiapride hydrochloride was dramatically effective in controlling the HC–HB until the hyperperfusion resolved. Single-photon emission computed tomography obtained 8 weeks after surgery revealed that the cerebral blood flow had been normalized in the right frontal cortex. The relative hypoperfusion of the right basal ganglia was also resolved. Then tiapride hydrochloride was discontinued without a relapse of HC–HB.
Conclusion:This case appears consistent with the theory that the connecting fibers responsible for the development of HC–HB are also located in the frontal lobe. The treatment of giant aneurysms involving the M1 portion can cause abrupt hemodynamic changes in both frontal cortex and the basal ganglia, which can potentially induce postoperative movement disorders.
Keywords: Aneurysm, chorea, clipping, giant aneurysm, hyperperfusion, single-photon emission computed tomography
INTRODUCTION
Movement disorders can occur as secondary to a variety of neurological, metabolic, infectious, traumatic, and other systemic diseases.[
Here we report a case of HC–HB on the left side of the body that started immediately after clipping of a right unruptured giant middle cerebral artery (MCA) aneurysm at the M1 portion. This patient had no hemorrhage or infarct appreciable on postoperative magnetic resonance (MR) images. However, SPECT showed some degree of postoperative hyperperfusion in the right frontal lobe as well as the hypoperfusion of the right basal ganglia. These hemodynamic changes resolved 8 weeks after surgery with remission of HC–HB. Our findings indicated that hyperperfusion as well as hypoperfusion can induce contralateral HC–HB and substantiated the previous theory that dysfunction of the frontal cortical subcortical motor pathway is one of the possible mechanisms of HC–HB. The treatment of giant aneurysms involving the M1 portion might be at an increased risk of postoperative movement disorder because it can potentially cause abrupt hemodynamic changes in both frontal cortex and the basal ganglia.
CASE REPORT
An 82-year-old female was referred to our hospital with a 1-month history of pulsatile headache. A head computed tomography (CT) scan taken at the previous hospital showed a 2.5-cm sized mass in the right temporal region. MR imaging demonstrated a round and partially thrombosed aneurysm of the MCA [
Figure 2
(a and b) Axial diffusion-weighted MR images obtained 1 day after surgery revealing no acute ischemia. (c) Axial T2-weighted MR image performed 1 day after surgery showing no new changes other than the preexisting edema around the aneurysm. (d) Preoperative angiogram demonstrating a giant MCA aneurysm. (e) Postoperative angiogram showing the complete obliteration of the aneurysm with preservation of the parent artery. Note the remarkable increase of the arterial flow in the MCA territory (arrowheads). (f) Right lateral carotid angiogram demonstrating that the bypass flow covered only a small area of the frontal lobe distal to the site of anastomosis (arrow)
Figure 3
(a) 99mTc-ECD SPECT performed 3 days after surgery revealing hyperperfusion in the frontal cortex (arrowheads). There was also slight hypoperfusion in the right basal ganglia including the subthalamic nucleus (arrows). (b) 99mTc-ECD SPECT obtained 8 weeks after surgery showed the resolution of hyperperfusion in the right frontal cortex (arrowheads) with the resolved laterality of the perfusion in the subthalamic regions (arrows)
DISCUSSION
HC–HB can occur as a sequela to a variety of strokes.[
In summary, we encountered a case of HC–HB that developed immediately after clipping of a giant unruptured MCA aneurysm. Postoperative angiography and SPECT indicated that hyperperfusion in the frontal cortex and hypoperfusion in the basal ganglia appeared to provoke this hyperkinetic movement disorder. Administration of tiapride hydrochloride was effective in controlling the HC–HB until the hyperperfusion resolved. This study also supports the recent theory that the connecting fibers in the frontal cortical and subcortical motor pathway play a significant role in the development of HC–HB.
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