Objective & Methods: We presented our experience of managing 10 paediatric WD patients. Data on clinical symptoms, laboratory findings, ultrasound findings, liver biopsies, genetic studies, treatment and outcome were studied. Results: Our patients were between 2 to 18 years of age at diagnosis. 1 patient presented in liver failure. 7 had abnormal liver functions detected incidentally. 2 were diagnosed through sibling screening. The most consistent abnormal liver function was an elevated alanine transaminase ranging from 60 to 419 IU/l (<58). Ceruloplasmin levels were all <0.1 g/l (0.21-0.59). Mean urinary copper excretion was 4 μmol/day (<1.0). 1 patient was treated initially with penicillamine and another trientine. 7 patients were started on zinc therapy. All remained well on follow up. Conclusion: Our patients represented a group of asymptomatic WD patients diagnosed and treated very early. With good treatment compliance, favourable outcome can be anticipated. One way of diagnosing these presymptomatic patients is through following up abnormal liver functions. Cerebral Folate Deficiency Syndrome(CFD) has been adopted for a group of neuro-psychiatric disorders associated with low spinal fluid 5 Nmethyltetrahydrofolate (MTHF) concentrations in the presence of normal folate metabolism outside the CNS. One important mechanism underlying CFD is the presence of serum autoantibodies of the blocking type directed against the folate receptor (FR) attached to membranes at the plasma-side of choroid plexus epithelial cells, which normally mediates the MTHF transport to the CNS. Two clinically recognizable syndromes of FR-antibody mediated CFD have been detected in young children: the infantile-onset CFD syndrome presenting 4 to 6 months after birth and a spastic-ataxic syndrome manifesting after one year. In addition, serum FR autoantibodies and CFD have also been reported in Rett, Aicardi-Goutières syndrome and infantile autism. During late adolescence CFD associated with fluctuating autoantibodies has been identified in intractable schizophrenia. This clinical heterogeneity associated with FR-autoantibody mediated CFD might be explained by differences in the time of onset and period during which these FR autoantibodies are generated leading to folate deficiency during various critical stages of early brain development. More awareness of CFD in association with FR autoimmunity should lead to earlier detection and diagnosis of these potentially treatable neuro-psychiatric disorders.