Depression, the most common psychiatric complication in Parkinson's disease (PD), affects 40-50 % of PD patients [1]. However, exact epidemiological data are missing. Rates of depression in PD vary between 4 % and 70 % depending on diagnostic criteria and selection of the study population. Application of structured diagnostic interviews (e. g. SCID, MINI, NPI) in non-selected populations would be desirable. Severity of depression and anxiety appears to correlate with disability and reduced quality of life in PD patients. Depression and anxiety appear to be underdiagnosed and undertreated in PD [7], even though adequate diagnosis and treatment affect the course of the disease.The profile of depressive symptoms observed in PD is not identical to that reported in patients with primary depression. Distinctive features of depression in PD include elevated levels of dysphoria, irritability, little guilt or feelings of failure, and a low suicide rate despite a high frequency of suicidal ideation. Diagnosis of depression in PD is complicated by overlapping symptoms of the two disorders. Symptoms of depression including psychomotor slowing and retardation; reduced mimics and apathy may be indistinguishable from neurological motor deficits in PD. Diagnosis of depression in PD is almost exclusively based on subjectively experienced depressive symptoms including: (1) feeling of emptiness and hopelessness, (2) reduced reactivity to emotional stimuli, (3) loss of the ability to enjoy and feel pleasure (anhedonia).Observer-and self-rating depression scales (HAMD, BDI) have been validated in order to assess severity and its course in depressed patients with PD. However, because of overlapping clinical symptoms, available rating scales may not reliably measure severity of depression.Quality of life is rather reduced by subjectively expe-■ Abstract Depression occurs in approximately 45 % of all patients with Parkinson's disease (PD), reduces quality of life independent of motor symptoms and seems to be underrated and undertreated.

The combined assessment of motor asymmetry, hyposmia and SN hyperechogenicity improves diagnostic specificity and allows early diagnosis of PD.

Cutaneous symptoms (seborrhoea and hyperhidrosis) in Parkinson's disease were investigated. In 70 treated patients with Parkinson's disease and 22 control subjects, non-invasive bioengineering methods (sebumetry, corneometry, pH) were carried out on the forehead, sternum and forearm. In addition, concomitant dermatoses and medication were recorded. 18.6% of the patients had seborrhoea on the forehead (>220 microg/cm2), 51.4% showed normal sebum values (100-220 microg/cm2) and 30% a sebostasis (<100 microg/cm2). Males has significantly higher sebum values than females. No relationship between the seborrhoea and the therapy for Morbus Parkinson was found. Patients with hyperhidrosis (n = 36) had significantly lower pH values (p < 0.05) on the forehead than those without hyperhidrosis. 22 patients (31.9%) reported a cold/hot flush and a further 13 (18.8%) had clinical rosacea. Seborrhoea is rare in treated Parkinsonian patients but hyperhidrosis is frequently found. Furthermore, a particular lack of vasostability (flush) appears to be an autonomic dysregulation in the skin related to Morbus Parkinson, which has not been studied to any extent to date.

The detection of Parkinson's disease (PD) at stages earlier than current diagnostic criteria allow for may increase the efficacy of disease-modifying therapies. Here we studied the relationship between retrospectively reported prodromal non-motor and motor features of PD, their pre-diagnostic presentation to physicians, and the extrapolated potential of an earlier diagnosis of PD considering early diagnostic markers detected at presence. One hundred and fifteen PD patients (41 women; age 63.2 ± 8.6 years) underwent a structured face-to-face interview on 22 prediagnostic symptoms. Present olfactory function, motor symptoms, and substantia nigra hyperechogenicity (SN-h) were assessed using standardized tools. Most frequently self-perceived symptoms in the early and very early prediagnostic phase (>2, >7 years prior to diagnosis) were hyposmia (23, 10 %), musculoskeletal pain (21, 9 %), and depression/anxiety (14, 11 %). In the late prediagnostic phase (≤ 2 years) mild motor signs, especially asymmetric bradykinesia and rest tremor, increasingly dominated the self-perception. In the prediagnostic phase, 99 % of patients consulted a physician because of motor symptoms but only 36 % with non-motor symptoms, mostly pain (20 %), depression/anxiety (9 %), constipation, bladder urgency, insomnia, REM sleep behaviour disorder, sexual dysfunction, and malignant melanoma (each, <6 %). Assuming the potential detectability of present hyposmia, asymmetric motor slowing and SN-h, a triad highly specific for PD, as early as 5 years prior to diagnosis, up to 84 (73 %) patients could have been identified in the prediagnostic phase using their or their physicians' awareness of early symptoms. We conclude that educating the general population and physicians on the importance of distinct prodromal features and applying symptom-specific diagnostic programs can improve the early detection of PD.

Dementia in idiopathicParkinson's syndrome JON 1607 Jean Marie Charcot first described cognitive deficits in Parkinson patients in 1875: ". . . psychic faculties are definitely impaired . . . at a given point the mind becomes clouded and memory is lost." Modern research has shown some degree of loss in the level of cognitive functioning to be an integral part of basal ganglia disturbances in the idiopathic Parkinson's syndrome. Disturbances in both frontal lobe functions (with effects on level of arousal and executive abilities such as planning) and memory (in particular free recall) are already demonstrable in the early stage of the disease in over 90 % of patients.There is however a high degree of variability in the literature published to date on the frequency of idiopathic Parkinson patients who subsequently develop clinically relevant dementia, ranging between 10 and 80 %. Very carefully detailed data were given for a community-based prevalence study [1] which found a prevalence of 27.7 % among Parkinson patients, who thus have a two-to three-fold higher risk for dementia than the general population.Particular risk factors for the development of dementia after the onset of idiopathic Parkinson's disease (IPD) have been identified: above-average age at the initial diagnosis of IPD, increased occurrence of dementia among other family members, higher level of severity in the extrapyramidal symptoms, early appearance of bilateral motor involvement, lower educational level, and the early development of confusional states or psychotic symptoms under L-dopa substitution.A considerable number of authors relate dementia developing after the onset of Parkinson's to the so-called subcortical dementias which are characterized by psychomotor bradyphrenia, forgetfulness, depression and alterations in personality, whereby primary cognitive disturbances such as amnesia, apraxia or aphasia are lacking. This intimate association of Parkinson's dementia with subcortical dementia is based on common neuropathological findings such as the presence of (1) Lewy bodies only in subcortical areas, and not in cortical areas, as well as (2) neuritic plaques. However, E. and H. Braak demonstrated extra-cellular amyloid deposits in all areas of the cortex, while neurofibrillary tangles were missing in the isocortex. Other elements which they considered essential for the development of dementia are (1) the decline of cholinergic neurons in the Nucleus basalis of Meynert and (2) distinct changes in the entorhinal region, whereas only minor damage should be found in the hippocampal areas. In addition, serotonergic neurons will be lost in the Nu-■ Abstract Approximately 25 % of patients with idiopathic Parkinson's disease (IPD) later develop