Clinicul 0 Neurology 1993 Elsevier CLINEU und Neurosurger?: Science Publishers 95 (1993) 147 1477149 B.V. All rights reserved 0303-8467/93/S 06.00 265 Case report Central nervous system lymphoma presenting with ataxic hemiparesis: a case report Hiroyuki Depurtments of”Neurology Arai”, Kuniaki Tomiokab und ‘Radiology, Motojima Generul Hospital, Ota, Gunma 373, Jupan, ’ Depurtment of’ Pathology, University School qf Medicine, Muehcrshi, Gunrnu 371. Jupan (Received (Revised version wordx Ataxic hemiparesis; Malignant 31 August, lymphoma; I2 January, Gunma 1992) received 22 December. (Accepted Key and Yoh-ichi Nakazato” 1992) 1993) Stereotactic biopsy; Magnetic resonance imaging Summary An 81-year-old man with central nervous system (CNS) lymphoma presenting with acute, progressive ataxic hemiparesis. Computed tomography and magnetic resonance imaging localized the lesion extending from the right internal capsule to the ventrolateral aspect of rostra1 midbrain tegmentum. A stereotactical biopsy yielded a microscopic diagnosis of medium-sized diffuse B-cell lymphoma. Although the most frequent cause of the syndrome of ataxic hemiparesis is a lacunar type of cerebral infarction, this article emphasizes that CNS lymphoma can produce the syndrome. Introduction Case report Fisher and Cole [l] described an unusual cerebrovascular syndrome in which corticospinal and cerebellar signs occurred on the same side of the body, and subse- A previously healthy, 81 -year-old man was admitted because of a suddenly unsteady gait. He had noticed mild weakness of the left leg two weeks before admission, but quently designated this syndrome ‘ataxic hemiparesis’ [2]. This article describes a patient with ataxic hem- without impairment of walking. There were no other neurologic symptoms, nor were there systemic symptoms on general examination. The patient was alert and ori- iparesis in whom a malignant lymphoma (diffuse B-cell type), that extended from the rostra1 midbrain tegmenturn to the internal capsule, was identified by stereotactic biopsy. ented. On neurological examination, speech and cranial nerves were normal and there was no nystagmus. Muscle strength of proximal muscles of the left leg was graded as 4+ or 5- of British MRC system, and Barre’s leg sign was positive on the left. Muscle strength in other limbs Corr~spond~ncc~ tojima Generdl 10: Dr. Arai. Hospital. Fax: 0276-22-4682. H.. Department Ota. Gunma 373, Japan. of Neurology, Mo- Tel.: 0276-22-7131; was intact. Deep tendon reflexes were diffusely hypoactive. Plantar responses were flexor. The finger-nose and heel-knee-tibia tests revealed an irregular dysmetria on the left. Rapid alternating movements were slow and clumsy on the left. Neither a tremor at rest nor intention tremor were noted. The patient walked with a broad- 14x based gait and had difficulty tempts to walk. Romberg’s was intact his legs on at- test was equivocal. to pin prick, touch, joint-position tion. A clinical made. Brain computed admission in moving revealed sion, isodense diagnosis of ataxic hemiparesis was (CT) on the day of tomography an ill-defined. compared Sensation and vibra- contrast-enhancing with normal le- brain parenchyma in the ventrolateral portion of the midbrain tegmentum. Magnetic resonance image (MRI) obtained on the 10th hospital day demonstrated a slightly hypointense lesion in deep structures of the temporal lobe and the ventrolateral part of the midbrain tegmentum, as well as a slight shift of 4th ventricle to the left on the T,-weighted image (Spin echo, TR 500 msec/ TE 20 msec, Fig. 1A). The lesion was homogeneously hyperintense on the gadolinium-DTPA enhanced T,weighted image (Fig. 1B). A coronal gadolinium-DTPA enhanced T,-weighted image demonstrated the craniocaudal extent of the lesion, involving the internal capsule and the rostra1 midbrain (Fig. 1C). During admission, the left hemiparesis increased. The plantar responses became extensor on the left. The cerebrospinal fluid findings, including cytology, were normal. Carotid and vertebral angiography also were unreon the plain study, localized Fig. 1. MRI appearances of the patient with ataxic hemiparesis. A and B: MRI delineates the extent of the lesion on T,-weighted (A) and gadolinium-DTPA enhanced T,-weighted (B) images. C: a coronal image clearly demonstrates the crania-caudal extent of the lesion on gadolinium-DTPA enhanced T,-weighted image. These MRI images are produced on a 1.5 tesla superconducting magnetic operating system. markable. A possible diagnosis of either primary or metastatic brain tumor was made. The patient became almost totally hemiplegic, and the lesion appeared slightly hyperdense even on plain CT study on the 20th hospital day. The midbrain mass was stereotactically biopsied for histological examination. Microscopically, sections cut from the biopsied specimen revealed diffuse infiltration of medium-sized hyperchromatic neoplastic cells with scant cytoplasm. Immunohistochemical studies showed 149 that the malignant cells were positive but not for T cell markers. phoma of medium-sized tion treatment the radiation piratory Gamma deficit improved therapy, with no contrast the patient A diagnosis of diffuse lym- B-cell type was made and radia- with a Leksell The neurologic for B-cell markers, dramatically following hypodense on CT study. died from an unexpected tract infection. Autopsy lesions, too, should causes of ataxic hemiparesis, rological be considered as possible particularly when the neu- deficit evolves progressively. Unit was begun. and the lesion became enhancement plastic Acknowledgements However, We are grateful of res- complication was not done. Discussion to Dr. H. Yarita for referring the patient. The stereotactic brain was performed by Dr. C. Ohye at Gunma University School of Medicine. The pa- tient was treated with a Leksell Gamma biopsy Hospital. Appreciation also is expressed janowski and Dr. H.I. Hurtig Unit at Hidaka to Dr. J.Q. Tro- for providing a critical re- view of the manuscript. The initial consistent neurological with previously ataxic hemiparesis Cole [l]. However, profile of the present published syndrome our patient descriptions case was of the reported by Fisher and showed progressive neu- rological deterioration following several hospital days. This clinical course is unusual, as in most reported instances neurological deficit eventually improves [ 1,2]. This, together with the bulky appearance of the lesion with intense contrast enhancement in both CT and MRI suggested an underlying neoplasm. The idea that focal encephalitis and demyelinating disorders as well as several other well-documented [336] also were considered causes of ataxic hemiparesis as alternative possibilities led us to perform biopsy a stereotactic of the brain lesion. Central nervous system lymphoma is a rare cause of ataxic hemiparesis, although it presents with a variety of focal neurological signs and symptoms [7]. To our knowledge one case with B-cell lymphoma surrounding the region of red nucleus [3] and another with leukemic infiltration to the rostra1 midbrain to produce the syndrome, [5] have been reported supporting the idea that neo- References Fisher, C.M. and Cole, M. (1965) Homolateral ataxia and crural paresis: a vascular syndrome. J. Neural. Neurosurg. Psychiat., 28: 48-55. Fisher, C.M. (1978) Ataxic hemiparesis. Arch. Neurol.. 35: 126-128. 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