Acta Anaesthesiol Scand 1998; 42: 133-135 Printed in Denmark. All rights resewed Copyright 0 Acta Anaesthesiol Scand 1998 ACTA ANAESTHESIOLOGICASCANDINAVICA ISSN OOO1-5172 Case Report Hemiballism-hemichorea from marked hypotension during spinal anesthesia H. IT OH^, K. SHIBATA', E. NITTA~ and M. TAKAMOR? 'Department of Anesthesiology and Intensive Care Medicine, and 2Department of Neurology, Kanazawa University School of Medicine, Kanazawa, lapan Hemiballism and hemichorea following anesthesia-induced hypotension has rarely been described, but a recent case suggests an association. After experiencing marked hypotension during spinal anesthesia, a 70-year-old woman developed hemiballism and hemichorea. Involuntary ballistic movements with writhing, consisting of repetitive rotation and flexion-extensionwithout apparent muscle weakness, affected her left limbs proximally. Low-amplitude, involuntary, choreiform movements involved the distal portions of these limbs. Magnetic resonance imaging demonstrated an area of high signal intensity in the contralateral subthalamic nucleus, suggestive of a focal ischemic lesion. Although such Occurrences are rare, anesthesiologists should be aware of the risk of subthalamic nucleus ischemia following marked hypotension. H more than 120 mm Hg before the start of surgery. Oxygen saturation ranged from 95 to 97%. About 30 min after anesthesia induction, systolic blood pressure and heart rate suddenly decreased to 50 mm Hg and to 50/min, respectively. Oxygen saturation could no longer be measured by pulse oximetry, probably due to poor peripheral perfusion. Two hundred mL of lactated Ringer's solution and 15 mg of ephedrine were given, with improvement of hemodynamic status within 3 min. Rostra1 extension of spinal anesthesia was diagnosed and, because of breathing problems, the trachea was intubated for mechanical ventilation. The operation was completed without additional problems. Systolic blood pressure and oxygen saturation remained over 100 mm Hg and 97%, respectively, during general anesthesia. Her recovery from anesthesia was uneventful. Ten hours after completion of surgery, involuntary movements of the patient's left arm were observed which, 10 h later, were followed by similar symptoms in her left leg. Her symptoms were involuntary writhing and ballistic movements consisting of repetitive rotation and flexion-extension without apparent muscle weakness (hemiballism). In addition, low-amplitude, involuntary choreiform movements involved the distal portions of these limbs (hemichorea). The YPOTENSION is a widely known, relatively frequent complication of spinal anesthesia. The basal ganglia reportedly may be even more sensitive than cortical regions to reductions of cerebral blood flow (1).However, reports of basal ganglia dysfunction related to hypotension induced by spinal anesthesia are rare. We present a case of hemiballism and hemichorea caused by focal ischemia of the subthalamic nucleus, most likely resulting from hypotension occurring during spinal anesthesia. Case report A 70-year-old woman weighing 62 kg was scheduled for resection of a cystocele by anterior colporrhaphy. Her state of health was excellent except for a history of untreated hypertension. Her preoperative concentration of blood glucose was 4.9 mmol/L. After premedication with 25 mg of hydroxyzine and 0.5 mg of atropine, 2 mL of 0.5% tetracaine was injected intrathecally via the L&L5 interspace. When the patient was turned supine 15 min after the injection, the level of sensory block was at Th7 bilaterally. Arterial blood pressure was measured noninvasively at 2.5-min intervals, and pulse oximetry was continuously monitored. Systolic blood pressure remained at Received 3 March, acceptedfor publication 28 May 1997 Key words: Anesthesia: spinal; complications: hemiballism, hemichorea, hypotension. 0 Acta Anaesthesiologica Scandinavica 42 (1998) 133 H.Itoh et al. Fig. 1. T2-weighted magnetic resonance imaging showing an area of high signal intensity in the right subthalamic nucleus (arrow) and bilaterally in subcortical periventricular white matter. patient was fully wake and oriented. Her muscle tone was normal on the right side but reduced on the left. Deep tendon reflexes were symmetric, with no Babinski sign. Results of sensory examination were normal. The patient was severely disabled by the continuous hemiballism-hemichorea (HH) which, however, could be volitionally suppressed momentarily and disappeared during sleep. T2-weighted magnetic resonance imaging (MRI) demonstrated areas of high signal intensity in the right subthalamic nucleus and bilaterally in the subcortical periventricular white matter (Fig. 1).Singlephoton emission computed tomography (SPECT) using 99mTc-ethylcysteinate dimer showed no apparent asymmetry in cerebral blood flow (CBF). Haloperidol at dosages up to 9 mg per day was administered orally, which gradually decreased frequency of the movements. A month later, HH at rest disappeared. Three months later, all involuntary movements of the upper limb disappeared. However, the choreiform movements in the distal left lower limb remained, causing impairment in her activities of daily living. underlying causes, one of the most frequent being focal cerebral ischemia (2). About a quarter of the patients with HH have involvement of the contralateral subthalamic nucleus (3), like our patient. Such a lesion results in decreased excitation of the internal segment of the globus pallidus and disinhibition of the thalamus, leading to excessive excitation of cortical neurons (4).Lesions in the basal ganglia, thalamus, pons, midbrain, or subcortical white matter may also be associated with the development of HH (2). Although some patients with HH have reduced CBF on the ipsilateral side demonstrated by SPECT (5), perfusion was normal in our patient. HH is rarely mentioned in the anesthesiological literature. Despite the fact that the period of hypotension was brief, focal cerebral ischemia was observed in our patient, as suggested by MRI. Leblhuber et al. (6) described a diabetic patient who showed hemichorea immediately after general anesthesia, possibly due to intraoperative cerebral hypoperfusion. Thus, our and their cases suggest that the two major cases for HH are cerebrovascular and metabolic disturbances, such as diabetes mellitus. Our patient showed no symptom of glucose intolerance (small vessels in cerebral lesion may possibly be injured). Because of her history of hypertension, her CBF autoregulation curve most likely had shifted to the right. Additionally, the white matter lesions on MRI suggest significant atherosclerotic changes in small intracranial vessels. Both factors may have predisposed to an ischemic subthalamic lesion during hypotension. The prognosis of HH is considered to be good (2, 3). Our patient was treated with haloperidol up to 9 mg per day. We believe that this therapy was effective, because discontinuation of haloperidol reportedly worsens HH in some patients (3), although spontaneous remission remains a consideration, possibly involving resolution of edema surrounding the subthalamic lesion (2). Our patient developed a permanent neurological condition, suggesting some degree of irreversible damage. In conclusion, given this patient with subthalamic ischemia and incompletely resolved choreiform movements, we emphasize that intraoperative hypotension particularly in patients with small-vessel disease may result in focal cerebral ischemia. References Discussion This patient’s clinical presentation was consistent with a diagnosis of HH. This condition has diverse 134 1. Zawadzki BM, Pereira B, Weinstein P, Moore S, Kucharczyk W, Berry I et al. MR imaging of acute experimental ischemia in cats. Am J Neuroradiol 1986:7 7-11. 2. Dewey Jr RB, JankovicJ. Hemiballism-hemichorea:Clinical Hemiballism after spinal anesthesia and pharmacological findings in 21 patients. Arch Neurol 1989:46 862-867. 3. Vidakovic A,Dragasevic N, Kostic VS. Hemiballism: Report of 25 cases. J Neurol Neurosurg Psychiatry 1994 5 7 945-949. 4. DeLong MR. Primate models of movement disorders of basal ganglia origin. Trends Neurosci 1990:13:281-285. 5. Mochizuki H, Miwa H, Imai H, Muzuno Y. Hemiballismhemichorea caused by a putaminal hemorrhage with worsening after smoking: A case report. Clin Neurol (Tokyo) 1993:33: 562-564. 6. Leblhuber F, Koltringer P, Reisecker F. Treatment of acute hemichorea with aspirin. Acta Med Austriacu 1991: 18: 105106. Address: Hironori Itoh, MD Department of Anesthesiology and Intensive Care Medicine Kanazawa University School of Medicine 13-1Takara-machi, Kanazawa 920 Japan 135