我们研究的目的是确定最常见的病因,临床表现,以及急性共济失调(AA)儿童预后的预测因素,并确定AA儿童的诊断方法中的“危险信号”。回顾性研究包括2015年至2021年在该研究所接受治疗的AA患者。纳入标准为1-18岁儿童,共济失调的演变时间在72小时内,和医生的诊断。排除标准是关于共济失调的记忆数据,未经任何医生确认,慢性/持续性共济失调,和心理性或后期共济失调。临床表现分为两类:(1)孤立的小脑体征(CS):共济失调步态,dysmetria,运动障碍,意图震颤,构音障碍,和眼球震颤;(2)CS-plus症状,包括与任何其他症状相关的CS,如脑病(GCS<15),意识障碍,呕吐,头痛,新出现的肢体或面部麻痹,斜颈,低张力,和Opsoclonus.结果在住院结束时进行评估,并定义为完全或不完全康复。这项研究包括76名儿童,平均年龄5.7岁(IQR2.1-8.3)。AA的最常见原因是27例(35.5%)的免疫介导/感染性小脑共济失调,和中毒24例(31.6%),其次是前庭共济失调,眼阵风-肌阵风-共济失调综合征,和颅内扩张过程。42例(56%)出现孤立性CS,35例(46%)有CS-plus。62例(81.6%)患者完全恢复。对一些危险因素的分析(性别,年龄,以前感染的存在,“小脑加上症状,“和结构异常/神经影像学异常)及其与结果的关系。分析表明,共济失调的其他症状,所谓的“小脑加症状”(p=0.002)和结构异常(p<0.001),具有统计学上较高的不良结果频率。单变量分析中仍有统计学意义。多变量逻辑回归分析中包含了重要数据,该数据还表明存在“小脑加症状”(p=0.021)和结构异常(p=0.002)与不良预后有关。大多数AA患儿具有“良性”病因,例如中毒和小脑后/副性共济失调,结果良好。另一方面,AA可能是中枢神经系统肿瘤或副肿瘤现象的首发表现。与小脑体征相关的“危险信号”是四肢或面部麻痹,低张力,GCS<15,呕吐,视阵风,头痛,肌阵鸣,视力障碍,斜颈,和眩晕.这些体征和/或大脑结构异常的存在与AA儿童的不良预后有关。
The aim of our study is to define the most frequent etiology, clinical presentation, and predictive factors of outcome in children with acute ataxia (AA) and to determine \"the red flags\" in the diagnostic approach to children with AA. The retrospective study included the patients with AA treated in the institute from 2015 to 2021. The inclusion criteria were children aged 1-18 years, evolution time of ataxia within 72 h, and diagnosis made by a physician. The exclusion criteria were anamnestic data about ataxia without confirmation by any physician, chronic/persistent ataxia, and psychogenic or postictal ataxia. Clinical presentation was divided into two categories: (1) isolated cerebellar signs (CS): ataxic gait, dysmetria, dysdiadochokinesia, intention tremor, dysarthria, and nystagmus; (2) CS-plus symptoms which included CS associated with any of other symptoms such as encephalopathy (GCS < 15), awareness disturbances, vomiting, headache, a new onset limb or facial paresis, torticollis, hypotonia, and
opsoclonus. The outcome was assessed at the end of hospitalization and was defined as complete or incomplete recovery. The study included 76 children, with a mean age of 5.7 years (IQR 2.1-8.3). The most frequent causes of AA were immune-mediated/infective cerebellar ataxia in 27 (35.5%), and intoxication in 24 (31.6%) cases, followed by vestibular ataxia,
opsoclonus-myoclonus-ataxia syndrome, and intracranial expansive process. Forty-two (56%) cases experienced isolated CS, and 35 (46%) cases had CS-plus. Complete recovery was experienced by 62 (81.6%) patients. Analysis of some risk factors (sex, age, presence of previous infection, \"cerebellar plus symptoms,\" and structural abnormalities/neuroimaging abnormalities) and their relation to outcome was performed. Analysis showed that presence of additional symptoms to ataxia, so called \"cerebellar plus symptoms\" (p = 0.002) and structural abnormalities (p < 0.001), had statistically higher frequency of poor outcome. Statistical significance remained in the univariate analysis. Significant data was included in multivariate logistic regression analysis which also showed that presence of \"cerebellar plus symptoms\" (p = 0.021) and structural abnormalities (p = 0.002) is related to a poor outcome. Most of the children with AA have \"benign\" etiology such as intoxication and post/parainfectious cerebellar ataxia with favorable outcomes. On the other hand, AA might be the first manifestation of CNS neoplasm or paraneoplastic phenomena. \"The red flags\" associated with cerebellar signs are limbs or facial palsy, hypotonia, GCS < 15, vomiting,
opsoclonus, headache, myoclonus, visual impairment, torticollis, and vertigo. The presence of those signs and/or structural brain abnormalities was related to poor outcomes in children with AA.