Cervical dystonia (CD) is characterized by painful, involuntary twisting of the neck, and sometimes tremor. Unfortunately, treatment options for CD are limited and the underlying pathophysiology is not well understood. Recent evidence implicates cerebellar dysfunction may play a role in the development of CD symptoms. Non-invasive brain stimulation is able to modulate neural excitability of the cerebellum. The present study examined the effect of five consecutive days of anodal transcranial direct current stimulation (tDCS) over the cerebellum of adults with CD (2 mA, 20 min). Patients received five sessions of anodal tDCS and sham tDCS in a randomised, cross-over design that was double-blinded. During tDCS, patients performed a motor imagery task (first 10 min) and a real movement task (last 10 min). We hypothesised that anodal tDCS would improve patient’s clinical features and modulate neural excitability of the cerebellum. Clinical features were examined using the TWSTRS2, CDQ-24, cervical range of motion, and visual analogue scales of pain. Behavioural outcomes were assessed using a motor learning finger tracking task. Neural excitability was inferred using eye-blink conditioning to examine cerebellar excitability and single-pulse transcranial magnetic stimulation (TMS) over the motor cortex to examine corticomotor excitability and intracortical inhibition. Motor evoked potentials (MEP) and cortical silent periods (cSP) were recorded bilaterally from the upper trapezius (UT) and first dorsal interosseous (FDI) muscles. All dependent measures were assessed on day-1 and day-5 of the intervention, and follow up questionnaires were completed one and four weeks later. There was a minimum washout period of 5 weeks between treatment blocks, and patients undergoing Botox were tested 4 weeks post injections. The study is in the late stages of data collection and analysis (n = 14 patients enrolled, 8 males). The outcome of this research may lead to the development of an alternative or adjuvant intervention for the management of CD and improve our understanding of the dysfunctional neurophysiology in this condition.