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Parkinson's disease in a neurodegenerative disorder that affects as many as 1-2 % of persons aged 60 years and older. Parkinson's disease occurs infrequently under 40 years of age, with major genetic implication. Alpha-synuclein plays significant pathogenic role in Parkinson's disease. Therapeutic advances based on a synucleinrelated mechanism are now developed : immunotherapy against alpha-synuclein for example. The diagnosis of Parkinson's disease remains mostly clinical. DatScan® may be helpful to distinguish parkinsonian syndrome and essential tremor. Current therapy is mainly based on a dopamine replacement strategy using the precursor levodopa (L-Dopa) and dopamine receptor agonists. Parkinson's is also associated with non-motor symptoms like sleep disorders, autonomic symptoms, neuropsychiatric symptoms. Advanced disease is associated with emergence of feature such as freezing, falling and neuropsychological dysfunction. Nonpharmacologic treatments like exercise are fundamental elements of patients' management. Motor complications and dyskinesia are common in advanced Parkinson's disease. Continuous administration of L-Dopa/carbidopa infusion in the jejunum provides more continuous dopaminergic drug delivery and stimulation and reduce motor complications. Further other approach are developped like surgical procedures: ex : high frequency stimulation of subthalamic nucleus, the more rational target for stimulation in Parkinson's disease.

The diagnosis of idiopathic Parkinson's disease (IPD) remains mostly clinical. Nevertheless, differentiating IPD from essential tremor or other parkinsonian syndromes solely by clinical examination can be challenging in some cases, especially in the early stage of the disease. The introduction of new isotopic functional imaging techniques, and more specifically the labelling of dopamine transporter derivatives, has improved the understanding and early detection of some diseases affecting the basal ganglia. Iodine-123-FP-CIT (DaTSCAN), a (presynaptic) dopamine transporter analogue for nuclear medicine imaging, has recently been introduced for the non-invasive differential diagnosis between IPD and essential tremor or secondary (e.g. drug-related) parkinsonian syndromes. DaTSCAN scintigraphy has also demonstrated some usefulness in the evaluation of other neurodegenerative parkinsonian syndromes such as Lewy-body dementia or multiple system atrophy. For this latter however, the DaTSCAN has to be combined with a second scintigraphy, imaging the post-synaptic dopaminergic receptors, such as the D2-ligand 123I-iodobenzamide. Combining DaTSCAN scintigraphy to a functional study of the brain cortical activity using a brain perfusion scintigraphy or to the evaluation of the cardiac adrenergic system by means of a myocardial MIBG scintigraphy (a norepinephrine storage analogue) can also be helpful to refine the diagnosis. Our experience shows that a good collaboration between the neurologist specialized in movement disorders and the nuclear medicine physician is useful, if not mandatory, to optimize the diagnostic performances of DaTSCAN scintigraphy.

We describe a 52-year-old woman presenting a 2-year history of limb clumsiness and gait difficulties, characterized by progressive worsening. Neurological examination revealed cerebellar intention tremor, cerebellar dysmetria of all 4 limbs and ataxic gait. However, brain MRI was normal. Analysis of fast wrist flexion movements demonstrated hypometric movements, with decreased intensities of agonist EMG activities and increased durations of antagonist EMG activities. Such EMG abnormalities have been demonstrated in patients presenting lesions of the middle cerebellar peduncle, affecting the crossed cerebellopontine projections. Moreover, adaptation motor learning during a pinch task (isometric force) showed a severe inability to adapt motor programming, indicating a disruption of cerebellolivary and cerebellopontine afferent systems. We suggest that our patient presented an exceptional brainstem syndrome involving the function of cerebellar inflow tracts. Such electrophysiological findings are not encountered in patients presenting a cerebellar cortical degeneration or cerebellovlivopontine atrophy, and might have important implications in the treatment of cerebellar ataxia in the future.