Levodopa is the most effective drug for treating Parkinson's disease. However, long-term use of levodopa is often complicated by significantly disabling fluctuations and dyskinesias negating its beneficial effects. Younger age of Parkinson's disease onset, disease severity, and high levodopa dose increase the risk of development of levodopa-induced dyskinesias (LID). The underlying mechanisms for LID are unclear though recent studies indicate the importance of pulsatile stimulation of striatal postsynaptic receptors in their pathogenesis. The non-human primates with MPTP-induced parkinsonism serve as a useful model to study dyskinesia. Once established, LID are difficult to treat and therefore efforts should be made to prevent them. The therapeutic and preventative strategies for LID include using a lower dosage of levodopa, employing dopamine agonists as initial therapy in Parkinson's disease, amantadine, atypical neuroleptics, and neurosurgery. LID can adversely affect the quality of life and increase the cost of healthcare.

Essential tremor (ET) affects approximately 4% of the population above 65 years of age. The traditional view that ET is a familial monosymptomatic disorder with a benign prognosis has recently been challenged, as it is now known to be a progressive and clinically heterogeneous condition with sporadic and familial forms. The pathogenesis of ET is not fully understood, though a disordered central mechanism is the most likely site of origin with possible modulation by muscle adrenoreceptors. The limited post-mortem studies have not shown consistent abnormalities in the brains of ET patients. ET is often misdiagnosed as Parkinson's disease, particularly in the older population. Tremor amplitude increases with age, accounting for substantial disability in older people. Current therapy (drugs and neurosurgery) has significant limitations in older people. A better understanding of its pathophysiology in the future will help in developing more effective therapy, including neuroprotective strategies.

Parkinsonism due to cerebrovascular disease (vascular parkinsonism, VP) is a distinct clinicopathological entity. It accounts for 4.4-12% of all cases of parkinsonism. Since there are no specific diagnostic criteria, true incidence and prevalence rates of VP are not known. Typically, parkinsonism in slow-onset VP tends to be bilaterally symmetrical, affecting the lower limbs more than the upper limbs ('lower-body parkinsonism'), and resting tremor is usually absent. Commonly noted lesions on brain imaging in VP are lacunes, white matter changes and, rarely, territorial infarcts. As coincidental vascular lesions in idiopathic Parkinson's disease (PD) are common, the mere presence of these lesions on brain imaging is not diagnostic of VP. Pathological evidence of a vascular disease in the absence of typical PD lesions (e.g. Lewy bodies) is the diagnostic 'gold standard'. VP is generally considered to be poorly or non-responsive to L-dopa therapy. However, recent studies have shown a beneficial effect of L-dopa in a subset of patients. Despite great advances in overall understanding of the disease, there are several gaps in our knowledge.

The UK's population is ageing and an adequately staffed geriatric medicine workforce is essential for high quality care. We evaluated the current and future geriatric medicine workforce, drawing on data relating to the UK population, current geriatric medicine consultants and trainees, recruitment into the specialty and trainee career progression.

this study shows that the two depression screening questions can be used as an initial screen for depression in patients with PD who have no significant cognitive impairment. A positive response to either of the questions would indicate that further diagnostic assessment may be warranted.