Logigian E L, Kaplan R F, Steere A C
Department of Neurology, Tufts University School of Medicine, Boston, MA 02111.
N Engl J Med. 1990 Nov 22;323(21):1438-44. doi: 10.1056/NEJM199011223232102.
Lyme disease, caused by the tick-borne spirochete Borrelia burgdorferi, is associated with a wide variety of neurologic manifestations. To define further the chronic neurologic abnormalities of Lyme disease, we studied 27 patients (age range, 25 to 72 years) with previous signs of Lyme disease, current evidence of immunity to B. burgdorferi, and chronic neurologic symptoms with no other identifiable cause. Eight of the patients had been followed prospectively for 8 to 12 years after the onset of infection.
Of the 27 patients, 24 (89 percent) had a mild encephalopathy that began 1 month to 14 years after the onset of the disease and was characterized by memory loss, mood changes, or sleep disturbance. Of the 24 patients, 14 had memory impairment on neuropsychological tests, and 18 had increased cerebrospinal fluid protein levels, evidence of intrathecal production of antibody to B. burgdorferi, or both. Nineteen of the 27 patients (70 percent) had polyneuropathy with radicular pain or distal paresthesias; all but two of these patients also had encephalopathy. In 16 patients electrophysiologic testing showed an axonal polyneuropathy. One patient had leukoencephalitis with asymmetric spastic diplegia, periventricular white-matter lesions, and intrathecal production of antibody to B. burgdorferi. Among the 27 patients, associated symptoms included fatigue (74 percent), headache (48 percent), arthritis (37 percent), and hearing loss (15 percent). At the time of examination, chronic neurologic abnormalities had been present from 3 months to 14 years, usually with little progression. Six months after a two-week course of intravenous ceftriaxone (2 g daily), 17 patients (63 percent) had improvement, 6 (22 percent) had improvement but then relapsed, and 4 (15 percent) had no change in their condition.
Months to years after the initial infection with B. burgdorferi, patients with Lyme disease may have chronic encephalopathy, polyneuropathy, or less commonly, leukoencephalitis. These chronic neurologic abnormalities usually improve with antibiotic therapy.
莱姆病由蜱传播的螺旋体伯氏疏螺旋体引起，与多种神经系统表现相关。为进一步明确莱姆病的慢性神经异常，我们研究了27例患者（年龄范围25至72岁），这些患者既往有莱姆病体征，目前有对伯氏疏螺旋体免疫的证据，且有慢性神经症状但无其他可识别病因。其中8例患者在感染发病后接受了8至12年的前瞻性随访。
27例患者中，24例（89%）出现轻度脑病，在疾病发病后1个月至14年开始，表现为记忆力减退、情绪改变或睡眠障碍。24例患者中，14例神经心理测试有记忆损害，18例脑脊液蛋白水平升高，有鞘内产生抗伯氏疏螺旋体抗体的证据，或两者皆有。27例患者中有19例（70%）有神经根性疼痛或远端感觉异常的多发性神经病；除2例患者外，其余患者均有脑病。16例患者电生理检查显示轴索性多发性神经病。1例患者有白质脑炎，伴有不对称性痉挛性双侧瘫、脑室周围白质病变及鞘内产生抗伯氏疏螺旋体抗体。27例患者中，相关症状包括疲劳（74%）、头痛（48%）、关节炎（37%）和听力丧失（15%）。在检查时，慢性神经异常已存在3个月至14年，通常进展甚微。在接受为期两周的静脉注射头孢曲松（每日2 g）治疗6个月后，17例患者（63%）病情改善，6例（22%）改善后复发，4例（15%）病情无变化。
在初次感染伯氏疏螺旋体数月至数年之后，莱姆病患者可能出现慢性脑病、多发性神经病，或较少见的白质脑炎。这些慢性神经异常通常经抗生素治疗后会改善。
