Acute Cerebellitis in Identical Twins
Fang Xu, MM, Shi Qing Ren, MD, and Jun Yan Liu, MD
Acute cerebellitis is an inflammatory syndrome characterized by cerebellar dysfunction, which often develops
in children after certain viral infections.We present for the first time, to the best of our knowledge, a case of河北医科大学第三医院神经内科任士卿
identical twin brothers who developed acute cerebellitis 8 days apart. The presence of the same magnetic resonance imaging lesions in both twins suggests viral transmission from one to the other.

Pediatr Neurol 2008;39:432-434.
Introduction
Acute cerebellitis is one of the main causes of acute cerebellar dysfunction in children. Typically, the clinical presentation includes limb or gait ataxia, wide-based gait,nystagmus, dysarthria, tremor associated with headache,somnolence, stiff neck, and vomiting [1]. Many cases of acute cerebellitis have been reported, but to date, to the best of our knowledge, no cases were reported in twins [2,3]. We report on identical twin brothers who developed acute cerebellitis 8 days apart.
Case Reports
Case 1
A previously healthy 15-year-old boy was admitted to the Third Hospital of HeBei Medical University with a 4-day history of dizziness, vomiting, unsteadiness, and inability to walk. During the 6 days before admission
to the hospital, an upper respiratory-tract infection with clear rhinorrhea,cough, and no evidence of fever was reported. No recent history of vaccination or drug intoxication was reported.Upon admission, a neurologic examination revealed the patient to be somewhat lethargic, with severe trunk and gait ataxia. His vital signs
were stable; his speech was dysarthric and slurred. Meningeal signs were absent. The cranial nerve and sensory examination was unremarkable.Muscle tone, muscle strength, and deep-tendon reflexes of the extremities were normal. Bilateral finger-nose-finger and heel-knee-shin tests produced normal results. Plantar responses were flexor. Routine hematology and blood chemistry revealed no abnormalities. Cerebrospinal fluid examination revealed a cell count of 100/mm3 (80% lymphocytes), a protein content of 19 mg/dL, a glucose level of 7.1 mmol/L, an immunoglobulin G index of 0.03, and the absence of an oligoclonal band. The next day,T2-weighted, proton density-weighted, and fluid-attenuation inversion recovery(FLAIR) magnetic resonance imaging brain scans demonstrated increased signal intensity in the bilateral dentate nucleus (Fig 1). The patient was treated with dexamethasone and acyclovir for 2 weeks, which gradually alleviated his signs. After 16 days of treatment, the patient was discharged with complete recovery.
Case 2
Ten days after the admission of patient 1, his identical twin brother was referred to the Third Hospital of HeBei Medical University after a 6-day history of dizziness, unsteadiness, and emotional disturbance.A neurologic examination revealed the patient to be conscious, alert, and awake, but agitated,with severe dysarthria. A mildly stiff neck was reported. Motor examination revealed mild muscular hypotonia and trunk titubation, such that upright posture could not be maintained. A lumbar puncture revealed normal glucose and protein levels. The white blood cell count was 56 cells/mL, with 79% lymphocytes. The T2-weighted and FLAIR magnetic resonance imaging scans performed on day 3 after admission revealed increased
signal of the bilateral dentate nucleus (Fig 2). The patient was treated with intravenous acyclovir and dexamethasone for 28 days, after which his neurologic signs completely resolved.

Discussion
Acute cerebellitis, i.e., childhood encephalitis largely restricted to the cerebellum, is an inflammatory syndrome that causes acute cerebellar dysfunction. The etiology of acute cerebellitis is usually viral. Varicella zoster, mumps, mycoplasma, and Epstein-Barr virus are among the most frequently involved agents [4]. Although acute cerebellitis is typically viral, it may be infectious, or may occur postinfection or after vaccination. Acute cerebellitis typically presents with acute cerebellar ataxia signs, abnormal cerebrospinal fluid results, and abnormal magnetic resonance imaging features. Moreover, clinical signs generally improve after acyclovir and steroid therapy. Although patient 1 had a history of upper respiratory-tract infection, the twins most likely manifested postinfectious viral cerebellitis, as described previously [5,6]. The differential diagnosis of
our patients included acute disseminated encephalomyelitis and rhombencephalitis. Although central nervous system white-matter lesions are usually evident in acute disseminated encephalomyelitis and rhombencephalitis, they were not evident in the present cases.In both patients, no virus was identified that could have caused the cerebellitis. However, the patients developed acute cerebellitis 8 days apart while sharing a common bedroom,so we think that a virus infected both patients at the same time, or else was transmitted from one patient to the other. The identical genetic susceptibility of twins may also have played a role in the pathogenesis of acute cerebellitis in these patients. Although no data are available in the
literature about a potential genetic etiology, there are reports of genetic factors associated with the occurrence of the same disease in twins. Examples include human leukocyte antigen-B35 for subacute thyroiditis, and the allele DRB1 0803 for focal myosotis [7,8]. Similar magnetic resonance imaging findings in both twins cannot rule out a genetic predisposition that ultimately triggered the acute cerebellitis.Abnormal magnetic resonance imaging findings in cerebellitis were reported, including hyperintense signals of cerebellar gray and white matter in T2-weighted sequences,diffuse cortical swelling, and secondary obstructive hydrocephalus
[1,3]. Follow-up magnetic resonance imaging studies indicated that abnormal signals disappeared, or
that cerebellar atrophy occurred in some cases [1,2,9]. In the twins presented here, magnetic resonance imaging examinations revealed that the hyperintensities on T2-weighted sequences only involved the isolated corpus dentatum cerebelli diffusely and symmetrically. We think that this is the first report of such magnetic resonance imaging findings in acute cerebellitis.

In conclusion, the occurrence of acute cerebellitis in identical twins is rare. The identical twins described here
revealed similar magnetic resonance imaging lesions,allowing us to hypothesize that the same viral infection
may have been responsible for the codevelopment of their condition, although we cannot exclude the possible contribution of genetic factors. Future studies would benefit from a genetic study of patients diagnosed with acute cerebellitis.