Varicella is a common, typically self-limiting, viral illness that often occurs in childhood. However, neurological complications, such as encephalitis, vasculopathy and cerebellitis, can occur. Postinfectious cerebellitis is presumed to be immune-mediated, typically presenting within days to weeks of rash onset. Diagnosis is primarily clinical, as early neuroimaging and cerebrospinal fluid (CSF) analysis may be normal. Treatment is usually supportive, though corticosteroids or antivirals may be used in severe or atypical cases.We report a case of postinfectious cerebellitis in a preadolescent male, presenting 1 week after the resolution of varicella rash. Symptoms included ataxia, dysarthria, dysdiadochokinesia and hypertonia. Despite classic cerebellar signs, imaging and CSF analysis were unremarkable. Clinical improvement followed a short course of empirical treatment for suspected meningoencephalitis; however, residual neurological deficits persisted, necessitating physiotherapy.This case highlights the potential for significant neurological involvement in postinfectious cerebellitis despite normal investigations, underscoring the need for clinical vigilance, timely intervention and multidisciplinary follow-up.

Acute ataxia is a pediatric condition associated with a plethora of etiologies. This systematic review with meta-analysis was undertaken to provide a hierarchal approach to the differential diagnosis of acute ataxia in the pediatric population. Eleven studies, consisting of 1167 children, met inclusion criteria of 10 or more patients, multiple etiologies of ataxia, and diagnostic data including number of patients with each condition. Extracted data were summarized and expected values (EVs) and 95% credible intervals for each disease entity were estimated using a Bayesian methodology. Postinfectious cerebellitis (EV, 38.0%; 95% CredI, 35.3-40.8%), drug intoxication/poisoning (EV, 14.1%; 95% CredI, 12.1-16.1%), central nervous system infection or inflammation (EV, 8.1%; 95% CredI, 6.6-9.8%), neoplasm (EV 7.3%; 95% CredI, 5.9-8.8%), and peripheral neuropathies including Guillain-Barré syndrome (EV, 6.6%; 95% CredI, 5.3-8.1) occurred most commonly and accounted for 74.1% of cases.

Immune-mediated cerebellar ataxias (IMCAs) represent a group of disorders in which the immune system targets mainly the cerebellum and related structures. We address fundamental questions on the diagnosis and immunological pathogenesis of IMCAs, as illuminated by recent advances in the field. Various types of IMCAs have been identified, including post-infectious cerebellitis, Miller Fisher syndrome, gluten ataxia, paraneoplastic cerebellar degeneration (PCD), opsoclonus and myoclonus syndrome, and anti-GAD ataxia. In some cases, identification of several well-characterized autoantibodies points to a specific etiology in IMCAs and leads to a firm diagnosis. In other cases, various autoantibodies have been reported, but their interpretation requires a careful consideration. Indeed, some autoantibodies have only been documented in a limited number of cases and the causal relationship is not established. In order to facilitate an early treatment and prevent irreversible lesions, new entities have been defined in recent years, such as primary autoimmune cerebellar ataxia (PACA) and latent autoimmune cerebellar ataxia (LACA). PACA is characterized by autoimmune features which do not align with traditional etiologies, while LACA corresponds to a prodromal stage. LACA does not imply the initiation of an immunotherapy but requires a close follow-up. Concurrently, accumulation of clinical data has led to intriguing hypotheses regarding the mechanisms of autoimmunity, such as a pathogenesis of autoimmunity against synapses (synaptopathies), and the vulnerability of the entire nervous system when the immunity targets ion channels and astrocytes. The development of PCD in patients treated with immune-checkpoint inhibitors suggests that molecular mimicry specifically determines the direction of autoimmunity, and that the strength of this response is modulated by co-signaling molecules that either enhance or dampen signals from the antigen-specific T cell receptor.

Acute cerebellitis is a rare complication of pediatric infections. There are many reports that viral infections lead to neurological manifestations, including acute cerebellitis. A retrospective chart review was conducted for pediatric patients diagnosed with enterovirus cerebellitis between 2000 and 2024. The methods involved reviewing clinical and radiological records and assessing the treatment methods. Case Report We present the case of a 4-year-old immunocompetent child who initially presented with acute encephalopathy followed by truncal ataxia, and eventually received a diagnosis of postinfectious cerebellitis. Enterovirus real-time polymerase chain reaction were positive in the nasopharyngeal swab. Therapeutic plasma exchange (TPE) was started due to neurological deterioration despite IVIG treatment. She improved significantly with TPE, and methylprednisolone treatment and was discharged in good health status. The patient is being followed up as neurologically normal. Acute cerebellitis associated with enterovirus is a rare pediatric disorder. Early diagnosis and treatment with TPE in this severe case is thought to be preventive for the potentially fatal complications.

Malaria is a common parasitic infection with a wide range of clinical presentations. Thus, it should be suspected for any symptomatic patient with a recent travel history to a malaria-endemic area. In this case report, we will present a previously healthy 28-year-old patient who developed cerebellar signs that were attributed to infectious etiology later on proven to be a malaria-related complication that responded well to anti-malarial medications. The classical presentation of malaria with attacks of fever is noticed only in around 60% of the patients. The development of immunity, the increasing resistance to anti-malarial drugs, and the indiscriminate use of anti-malarial drugs have led to malaria presenting unusual characteristics. Cerebellar ataxia, extrapyramidal signs, and various psychiatric manifestations have been described as early presentations of cerebral malaria or as a part of the post-malaria neurological syndrome. Other neurological syndromes like peripheral neuropathies, movement disorders, myelopathies, and stroke-like syndrome have also been described. Malaria should be included as a differential diagnosis in a patient presenting with cerebellar signs as its devastating if left untreated. However, it responds well to anti-malarial regimens if started early during the course.