ClinicuiNadogy ~tndNamsurguy, 95 ( 1993)159- 162 0 1993Elsevier Science Publishers B.V. All rights reserved ODOR-8~67/9~/$06.00 CLINEU 159 00281 Case report -- _ ----. A case of pontine lacunar infarction with ulcerative colitis Toru Fukuhara”, Shohei Tsuchidab, Kazushi Kinugasa” and Takashi Ohmoto” (Received (Revised, (Accepted Key words 16 November, 1992) received 24 February. 24 February, 1993) 1993) Pontine infarction: Pure motor hemiplegia; Ulcerative colitis Summary We present the case of a young man who experienced a sudden onset of pure motor hemiplegia in association with ulcerative colitis. Based on a review of earlier reports, ulcerative colitis was suspected to be the background disease leading to cerebral infarction. A cerebra1 infarction of the lacunar type in the right ventromedial aspect of the upper pons was seen on magnetic resonance images. These images detected small lesions in the brain stem, and were used to follow-up their transitions. Introduction The causes of cerebral infarction in the young are various [I]_ and ulcerative colitis has been suspected as one of the background diseases leading to cerebral infarction [2]. Thirteen patients with ulcerative colitis have been previously reported to suffer from cerebral infarction (Table 1). We report the case of another patient with ulcerative colitis who experienced the sudden onset of pure motor hemiplegia. Case report An l&year-old boy experienced sudden motor weakness of the left arm and leg but no impairment of consciousness. He came to our hospital the second day after Cwrrsponttewr /(I: Toru Fukuhara, cal Surgery. Okayama Okayama 700, Japan. University MD, Department Medical Tel.: 81-86-223-7151; School, of Neurologi- 2-S-l Shikata-cho, Fax: 81-86-227-0191. onset. The patient had a 5-year history of ulcerative colitis and reported that his diarrhea had recently become more severe. The patient’s neurologic examination revealed left hemiparesis including left lower facial weakness, but his sensory systems were not disturbed and no other neurologic deficits were apparent. His blood pressure and pulse rate were within normal range, and both an electrocardiogram and echocardiog~m showed good function of his heart. Laboratory tests revealed slight microcytic anemia (red blood cell count 5 120 000; hematocrit value 35.6; hemoglobin 9.9). but other data including a platelet count (420 000) were all within normal limits. Partial thromboplastin time, prothrombisl time, fibrinogen content, fibrinogen degradation products. and anti-thrombin III were all normal. All coagulation factors and protein C were measured and found normal. No inflammatory signs were detected. To uncover any background diseases, his ASLO, antibodies to viruses, rheumatic serology, and the concentration of anti-nuclear antibodies were examined. Along with a lupus erythematosus test, these elements were 160 found to be normal. abnormal fluid showed of the brain low-density magnetic high-intensity area resonance revealed in the right (MR) were detected tively. Follow-up infarction Many authors of ing convulsive aspect (Fig. 1B). subtraction the patient and treated recovered figures of ulcerative dramatically and was discharged was di- conserva- the etiologic factors disturbances having an etiologic infarction (Table I). Discussion In the young, background to cerebral of cerebral infarc- tion differ greatly from those in older individuafs [3], and in three includ- fever of unknown [4]. Mayeux ulcerative enema after 2 months. [3], infection but is unclear. of a variety ot were the first to suspect soon followed: colitis. The conditions, the existence head trauma reports stroke before the onset of stroke. episodes origin and minor as ‘idiopathic with the infarction have reported diseases this di- from his left hemiparesis only have abnormal relationship background x-ray taken after a barium showed the characteristic the etiologic a MR images did not contradict An abdominal an unA on a digital Based on these findings, with a pontine agnosis. are described pons. area on the right ventromedial No abnormalities agnosed cases image showed the upper pons that did not cross the midline angiogram. many Some of these patients tomogram abnormal Tz-weighted patient no findings. A computed clear, His cerebrospinal and Fahn [5] colitis as one of the connection of their patients. ours is the fourteenth Other such case Because embolic complications such as pulmonary embolism or thrombophlebitis are well known with ulcerative colitis, the cerebrovascular occlusion associated with ulcerative colitis was usually believed to be a thromboembolus resulting from thrombocytosis or a disturbance in coagulation [6]. Other than anemia, which may result from bloody diarrhea, or the usual inflammatory signs of colitis, the hematologic findings in these patients concentrated on the platelet or coagulation test (Tabie 1). TABLE I REPORTS OF CEREBRAL INFARCTION IN PATIENTS WITH ULCERATIVE COLITIS Author Age (yrs) sex Location of infarction Hematologic findings Clinical stage OfUC Mayeux and Fahn [5] 12, M 17, F 26, F 34, M 52, F _~ active active 50 hrs after colectomy active remission 12, F brain stem 20, M 12. F 45. M 33, F basal ganglia left hemisphere PLT 1,2 million normal ESR 20 mm/h, Hct 35% PLT 545,000, ESR 16-20 mm/h PLT 950,000, fibrinogen 440 (ZOO-400),ESR 34-76 mm/h Factor VIII 290% (50-200), PTT 26s (29-40), ESR 9-38 mm/h normal PTT 23.2s (36.8), WBC 14,000 Nelson et al. [7] Jorens et al. [21] 18, M 31, M bilateral hemispheres left internal capsule Karacostas et al. [8] Present case 32, F 18, M right frontal lobe right upper pons Schneiderman et al. [ 181 Hilton-Jones and Warlow [19] Paradis et al. [20] Talbot et al. [9] right fronto-parietal lobe (not detected on CT) left ICA occlusion brain stem PLT 662,000 WBC 10,900, ESR 27 mm/h PLT 520,000, prothrombin 49% (70-130), protein C 46% (70-130), protein S 55% (70-130) ESR 60 mm/h Hb 10.5 WBC 12,200, Hb 9.75 Hct 35.6, Hb 9.9 active active active active 3 months after colectomy active activr active active -__-________ -: not stated in reference, UC: ulcerative colitis, ICA: internal carotid artery, PLT: platelet, PTT: partial thromboplastin time, WBC: white blood cell, ESR: erythrocyte sedimentation rate, Hct: hematocrit, Hb: hemoglobin. The number in parentheses indicates normal values in each examination. 161 Fig. 1. Magnetic resonance images taken at admission (A-C), 2 weeks (D-F) and 3 months (G-I) after onset. The left side of the body appears at the right side of the figure. At the time of admission (2 days after onset) a slight low-intensity area was seen on the Tl-weighted image (A) and a high-intensity area was seen on the T2-weighted image (B). Enhancement with contrast was not observed (C). Two weeks after onset, the lesion seemed to be small on both the T,- (D) and Tz-weighted (E) images. Enhancement was observed (F), however, and the lesion was believed to be in the subacute stage of infarction. Three months after onset, the lesion was clearly of low intensity on the T,-weighted image (G) and of high intensity on the Tz (H). The lesion did not cross the midline on any axial views and the coronal section of the T,-weighted image (I) showed the lesion to be localized in the upper pons. Two groups of investigators, however, believed cerebral vasculitis to be an important mechanism [7,8]; this has also been found to be a vascular complication of ulcerative after a small infarction located in the internal capsule or the pons: consequently. diagnosis using a CT scan is sometimes difficult [14,15]. In patients with multiple le- colitis [9,10]. Thus, steroids may be more effective than anticoagulants in treating patients with vasculitis [l 11. The lesion in our patient appeared to be caused by the occlusion of the right paramedian branch of the basilar artery [12]. Pure motor hemiplegia [13] usually occurs sions, CT scans were not always able to confirm the lesion responsible for the symptoms [ 161. On the other hand, MR images are useful not only for detecting a small lesion, but also for delineating the acute cerebral infarction responsible for symptoms. Using MR images, we could detect the lesion in the right upper pons clearly. and depict the transition of the lesion (Fig. 1). At the time of the patient’s admission, the low-intensity re- gion on the T,-weighted image was not clear (Fig. 1A). After :! weeks, however, the area of infarction was seen after enhancement 1F). After 3 months, the low- intensity (Fig. area was well-demarcated that the infarction The mean (Fig. was in the chronic age of patients years. In all but one patient, I(;). showing stage. in the case reports the clinical is 25.9 stage of ulcera- tive colitis was active or in the postlaparotomy phase at the time of stroke. These factors lead us to believe that adequate of ulcerative colitis may be necessary treatment to prevent the onset of stroke. 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