Criteria For Parkinson's Disease Research Articles

Síntomas no motores en pacientes con enfermedad de Parkinson Hospital de San José, Bogotá, DC Colombia

Introducción: la enfermedad de Parkinson (EP) es la segunda afección neurodegenerativa en frecuencia con una prevalencia en Colombia de 4.7 por mil habitantes. Los síntomas no motores (SNM) hacen parte del espectro ya que generan un aumento de la morbilidad e impactan la calidad de vida. Objetivo general: describir la frecuencia de SNM en pacientes con EP que asisten a la consulta externa de neurología en el Hospital de San José de Bogotá DC. Métodos: serie de adultos que consultaron entre abril y septiembre de 2011 cumpliendo criterios diagnósticos de EP según UKBrain Data Bank. Se utilizó el cuestionario de SNM para EP, PD NMS quest, validado en español. Resultados: se encuestaron SS pacientes con edad promedio de 68 años (DE 9.8), hombres 61.8%. El 51%, con un tiempo de evolución menor o igual a cinco años. El 85.5% tenían una puntuación en escala de Hoehn y Yahr entre 1-11. Los SNM más frecuentes son urgen­ cia urinaria 76.4%, tristeza 74.5%, sensación desagradable en las piernas durante la noche o necesidad de moverlas 67.2% y problemas para recordar cosas 61.8%. Conclusiones: los SNM son frecuentes en nuestra población siendo el sistema urinario es el más comprometido. Se debe indagar sobre estos para brindar un manejo integral al paciente. Se requieren más estudios en nuestra población que evalúen el impacto sobre la calidad de vida.

Presymptomatic Parkinson's disease: The Arizona experience

There is a growing interest in presymptomatic diagnosis of Parkinson's disease (PD), but the best and most practical method to screen and confirm asymptomatic individuals for PD needs further study. The Banner-Sun Health Brain and Body Donation program in Sun City, Arizona has studied primarily PD and Alzheimer's disease. Enrollees receive annual prospective standardized evaluation that includes clinical, biomarker testing, and at autopsy, neuropathological examination is performed followed by a consensus conference that determines final diagnosis. Since numerous Controls receive these assessments, these subjects become an excellent cohort to study presymptomatic PD. We found that Controls with partial diagnostic criteria for PD (1 of either rest tremor or bradykinesia) had a 6.6 relative risk for eventually developing full diagnostic criteria for PD. Neuropathologic examination has uncovered cases of "incidental Lewy body disease" (ILBD). We have shown that ILBD cases during life demonstrated no significant differences in clinical assessment versus similarly assessed controls. However, electrophysiological assessment showed subclinical low frequency rest discharges in some ILBD cases. Electroencephalography spectral frequency of ILBD cases was lower than for controls but not as low as for PD cases. The longitudinal assessments of this brain bank offer significant opportunities for the study of presymptomatic PD.

Neuropathology of sporadic Parkinson's disease: Evaluation and changes of concepts

Parkinson's disease (PD), one of the most frequent neurodegenerative disorders, is no longer considered a complex motor disorder characterized by extrapyramidal symptoms, but a progressive multisystem or-more correctly-multiorgan disease with variegated neurological and nonmotor deficiencies. It is morphologically featured not only by the degeneration of the dopaminergic nigrostriatal system, responsible for the core motor deficits, but by multifocal involvement of the central, peripheral and autonomic nervous system and other organs associated with widespread occurrence of Lewy bodies and dystrophic Lewy neurites. This results from deposition of abnormal α-synuclein (αSyn), the major protein marker of PD, and other synucleinopathies. Recent research has improved both the clinical and neuropathological diagnostic criteria of PD; it has further provided insights into the development and staging of αSyn and Lewy pathologies and has been useful in understanding the pathogenesis of PD. However, many challenges remain, for example, the role of Lewy bodies and the neurobiology of axons in the course of neurodegeneration, the relation between αSyn, Lewy pathology, and clinical deficits, as well as the interaction between αSyn and other pathologic proteins. Although genetic and experimental models have contributed to exploring the causes, pathomechanisms, and treatment options of PD, there is still a lack of an optimal animal model, and the etiology of this devastating disease is far from being elucidated.

Screening LRRK2 gene mutations in patients with Parkinson’s disease in Ghana

The leucine-rich repeat kinase 2 (LRRK2) gene is associated with autosomal dominant Parkinson disease (PD) [1]. Its most common mutation G2019S may account for 3–6% of familial and 1–2% of sporadic PD cases. This mutation’s frequency may range from\0.1% in Asia to 43% in North Africa, even in apparently sporadic cases [2, 3] because of its low penetrance [4]. To date, this is the first screening of LRRK2 mutations in Ghana and only the third in a subSaharan African country [5, 6]. Fifty-four black African individuals meeting the UK Brain Bank criteria for PD were consecutively recruited between December 2008 and March 2011 from three outpatient clinics in Ghana. Every index case was reviewed by a neurologist specialized in movement disorders (R.C.). PD individuals were unrelated, with the exception of two sisters. At least one first-degree relative with tremors/possible PD has been reported in ten families (11 cases), suggesting a potential autosomal dominant (n = 7) or recessive (n = 3) pattern of inheritance. Control subjects (n = 46) had similar age and the same ethnicity as the cases, and no neurological disease or family history of tremors/PD (Table 1). Cases and controls were equally balanced among the three hospitals. The study was approved by the local ethics committee and all participants gave written consent before recruitment. Genomic DNA extraction was performed from saliva using the Oragene method (DNA Genotek, Ottawa, ON, Canada). The LRRK2 analysis was based on sequencing of exon41 (including G2019S and I2020T) and exon31 (including R1441G/C/H). LRRK2 exon41 and exon31 with their intron–exon boundaries were amplified by PCR using primers and condition previously reported [7]. Mutation analysis of the PCR purified product was performed by direct sequencing using the Big Dye Terminator Kit (version1.1, Applied Biosystems). Sequences were run on an ABI Prism 3130 XL Genetic Analyzer (PE Applied Biosystem) and the electropherograms analyzed with SeqScape software (Applied Biosystems). LRRK2 exon41 and exon31 screening did not reveal any mutation in cases and controls. We identified one heterozygous intron substitution IVS41 ? 30A [ G in a healthy subject and heterozygous IVS30-6C [ T in two PD and one healthy control. These variants have never been associated to a pathogenic mechanism and they are likely to be rare polymorphisms. Electronic supplementary material The online version of this article (doi:10.1007/s00415-011-6210-y) contains supplementary material, which is available to authorized users.

MF.02 The prevalence and clinical characteristics of pathological gambling in patients with Parkinson's disease: an evidence based review

AimsTo identify the prevalence of pathological gambling (PG) in patients with Parkinson's disease (PD) from studies using comparable methodology to the best general population estimates. Additionally, to collate case-control based...

Epidemiology and etiology of Parkinson’s disease: a review of the evidence

The etiology of Parkinson's disease (PD) is not well understood but likely to involve both genetic and environmental factors. Incidence and prevalence estimates vary to a large extent-at least partly due to methodological differences between studies-but are consistently higher in men than in women. Several genes that cause familial as well as sporadic PD have been identified and familial aggregation studies support a genetic component. Despite a vast literature on lifestyle and environmental possible risk or protection factors, consistent findings are few. There is compelling evidence for protective effects of smoking and coffee, but the biologic mechanisms for these possibly causal relations are poorly understood. Uric acid also seems to be associated with lower PD risk. Evidence that one or several pesticides increase PD risk is suggestive but further research is needed to identify specific compounds that may play a causal role. Evidence is limited on the role of metals, other chemicals and magnetic fields. Important methodological limitations include crude classification of exposure, low frequency and intensity of exposure, inadequate sample size, potential for confounding, retrospective study designs and lack of consistent diagnostic criteria for PD. Studies that assessed possible shared etiological components between PD and other diseases show that REM sleep behavior disorder and mental illness increase PD risk and that PD patients have lower cancer risk, but methodological concerns exist. Future epidemiologic studies of PD should be large, include detailed quantifications of exposure, and collect information on environmental exposures as well as genetic polymorphisms.

Spinal cord stimulation failed to relieve akinesia or restore locomotion in Parkinson disease

Dorsal column spinal stimulation in dopamine-depleted rodents was recently reported to disrupt pathologic corticostriatal synchronization, alleviate akinesia, and restore locomotion.1 This claim has prompted consideration that spinal stimulation “might become an efficient and less invasive alternative for treatment of Parkinson disease (PD) in the future.” In this study, we investigated whether dorsal column stimulation was of therapeutic benefit in 2 patients with PD. ### Level of evidence. This study provides Class II evidence that for patients with moderate to severe motor impairment from PD, high-frequency epidural cervical spinal cord stimulation does not significantly improve motor function as measured by the motor subsection of the Unified Parkinson's Disease Rating Scale (UPDRS). ### Methods. Two patients with PD had spinal stimulators (Medtronic models 3487a or 3898) implanted surgically into the high cervical epidural space without complication, as described previously.2 Patient 1, 75 years old, had moderate motor impairment (off/on medication motor UPDRS = 30/18). Patient 2, 77 years old, had more severe motor impairment (off/on medication UPDRS = 51/38) and was unable to walk without dopaminergic medication. Both patients met UK Brain Bank criteria for PD.3 Ten days postoperatively, both patients participated in a double-blind crossover study of the motor effects of spinal stimulation. In an initial exploratory phase, an antiparkinsonian effect of spinal stimulation was sought over a range of frequencies (30–300 Hz) and intensities (up to 4.0 V and 240 μs). Having failed to establish a clear benefit for any particular set of parameters, for the purposes of the study, patient 1 was …

Co-existence of Parkinson’s disease and progressive supranuclear palsy: case report and a review of the literature

Idiopathic Parkinson's disease (PD) and progressive supranuclear palsy (PSP) are distinct clinicopathological entities characterized by α-synuclein and tau pathology, respectively. They have occasionally been reported to co-exist in the same patient. We describe a rare case of a 73-year-old Caucasian woman diagnosed as idiopathic PD 5 years before her death yet at autopsy had not only PD, but also PSP. Although this patient fulfilled clinical criteria for idiopathic PD and did not have supranuclear ophthalmoplegia, she had several atypical features, including early postural instability with falls, early dysphagia, and a relatively rapid course. In conclusion, this case and a literature review highlight the co-existence of synuclein and tau pathology in the same patient and demonstrate that multiple diagnoses may exist in patients presenting with parkinsonism. The clinical heterogeneity seen in parkinsonism may reflect the occurrence of combined pathology.

Dopaminergic and non‐dopaminergic pharmacological hypotheses for gait disorders in Parkinson’s disease

Gait disorders form one component of the axial disorders observed in Parkinson's disease (PD). Indeed, short steps with a forward-leaning stance are diagnostic criteria for PD in the early stages of the condition. Gait disorders also represent a major source of therapeutic failure in the advanced stages of PD (with the appearance of freezing of gait and falls) because they do not respond optimally to the two hand late-stage therapeutics--levodopa and electrical subthalamic nucleus (STN) stimulation. The late onset of doparesistance in these disorders may be linked to propagation of neurodegeneration to structures directly involved in gait control and to non-dopaminergic neurotransmitter systems. The coeruleus locus (a source of noradrenaline) is rapidly and severely affected, leading to a major motor impact. The pedunculopontine nucleus (PPN) and lateral pontine tegmentum (rich in acetylcholine) are both involved in gait. Degenerative damage to the serotoninergic raphe nuclei appears to be less severe, although serotonin-dopamine interactions are numerous and complex. Lastly, dopaminergic depletion leads to glutamatergic hyperactivity of the efferent pathways from the the STN to the PPN. However, the relationships between the various parkinsonian symptoms (and particularly gait disorders) and these pharmacological targets have yet to be fully elucidated. The goal of this review is to develop the various pathophysiological hypotheses published to date, in order to underpin and justify ongoing fundamental research and clinical trials in this disease area.

Intérêt de la tomoscintigraphie cardiaque à la 123I-mIBG couplée à la perfusion myocardique dans le diagnostic de l’atrophie multisystématisée

Objective The aim of this prospective study is to assess the pertinence of using 123I-mIBG myocardial tomoscintigraphy coupled with perfusion scintigraphy as a diagnostic tool, to discriminate between multiple system atrophy (MSA) and idiopathic Parkinson's disease (PD) at first guided by clinical data and L-DOPA tests. Material and methods Forty patients, aged from 43 to 78 years (median 62 years) with Parkinson's syndrome were studied. Nineteen had a diagnosis of PD (criteria of brain bank) and 21 AMS (Gibbs criteria). All were given test to acute L-DOPA. Chest-centered planar imaging (128 × 128 matrix, 5 minutes of duration) is performed at 1 hour and 4 hours after injection of 220 MBq of 123I-mIBG, in addition a non-synchronised tomoscintigraphy (64 × 64 matrix, 32 images of 50 seconds , zoom 1.45) was performed after the 4th hour and 15 minutes after injection of 200 to 400 MBq of 99mTc-tetrofosmin. Besides neurological data, the parameters retained for comparison purposes with 123I-mIBG cardiac tomoscintigraphy were patients’ age, duration of disease and L-DOPA test results. Two regions of interest (ROI) identical in size and in shape are used for 123I-mIBG uptake quantifications (H/M and washout [Wo]). The first one was placed in projection of mediastinum (M) and the other one in projection of heart (H). Results We found an overall decreased uptake of the myocardial 123I-mIBG without perfusion abnormality in 15 of 19 patients with PD and 11 among them were L-DOPA sensitive (L-DOPA test greater than 30%). Normal tracer uptake with 123I-mIBG associated with an almost quite normal perfusion was seen in 15 of 21 patients with MSA and they were little or not L-DOPA sensitive (L-DOPA test less than 30%). Therefore, 10 discordant cases (25%) between cardiac scintigraphy and clinical evolution of disease with also discordant L-DOPA tests were observed. In the PD group, quantification of data enhanced the diagnostic decision with low heart to mediastinum ratio (H/M) (1.32 ± 0.15 at the early stage and 1.25 ± 0.13 at the later stage). In the MSA group, the uptake of 123I-mIBG (1.66 ± 0.43 at the early stage and 1.72 ± 0.42 at the later stage) was comparable to literature data, however, with significant inter-individual variations. The association of data of scintigraphy with L-DOPA test allows to improve sensitivity in 84% and specificity in 90.5%. Conclusion Our prospective study of 40 cases shows the relevance of cardiac sympathetic postganglionic imaging with 123I-mIBG coupled with myocardial perfusion scintigraphy to discriminate between MSA and PD with a higher sensitivity (71.4%) compared to the test with L-DOPA but a lower specificity (78.9%) than the L-DOPA. The difficulty of diagnosis is firstly linked to damage occurring to both the pre- and postganglionic sympathetic systems in patients with MSA and secondly to the integrity of the sympathetic nerve endings in patients with PD. However, the association of data of scintigraphy with L-DOPA test show a significant improvement of sensibility (84%).

What features improve the accuracy of the clinical diagnosis of progressive supranuclear palsy‐parkinsonism (PSP‐P)?

Progressive supranuclear palsy-parkinsonism (PSP-P) is a primary tauopathy characterised by neurofibrillary degeneration, which is frequently mistaken for Parkinson's disease (PD), multiple system atrophy (MSA), and vascular parkinsonism (VP) at presentation. The aim of this study was to identify particular clinical features (green flags) that may be helpful in differentiating PSP-P from these other disorders. We identified 37 patients with PSP-P from 726 patients archived at the Queen Square Brain Bank. Using a retrospective case notes review the clinical features were compared between the PSP-P group and Lewy body associated parkinsonism (PD, n = 444 and dementia with Lewy bodies (DLB), n = 46), MSA (n = 90), and VP (n = 19), using the chi(2)-test for proportions for a two-by-two contingency table. The sensitivity, specificity, and positive predictive values (PPV) and negative predictive values (NPV) were calculated for individual clinical features. A specificity of >0.85 or a PPV of >0.85 were considered reliable discriminators. No clinical features were predictive of PSP-P, but late drug induced dyskinesias (specificity 0.92, PPV 0.99), late autonomic dysfunction (specificity 0.94, PPV 0.99) and any visual hallucinations (specificity 0.94, PPV 0.99) were better in distinguishing PD and PSP-P than predicted using operational diagnostic criteria for PD. PSP-P shares many clinical features with PD and DLB, MSA and VP, but visual hallucinations, drug induced dyskinesias and autonomic dysfunction are very uncommon and may be helpful exclusion criteria.

Sleep disturbances in patients with Parkinson's disease

Sleep problems, common in Parkinson's disease (PD), are the consequence of the neurodegenerative process, as well as of neurochemical changes on one side, and of drug intake on the other side. To estimate the frequency of sleep problems and its correlation with the disease, therapy and demographic factors in patients with idiopathic Parkinson's disease. The study enrolled 65 consecutive patients who fulfilled criteria for idiopathic PD. The original questionnaire was performed to obtain demographic, disease and treatment data. The patients were tested with standardized scales: unified PD rating scale (UPDRS) and Hoehn and Yahr staging scale (HY scale). Mini mental stage examination (MMSE) was performed for the evaluation of cognitive status. Parkinson's disease sleep scale (PDSS) was applied for the assessment of sleep problems. There were 37 male and 28 female patients. Negative correlations (p < 0.01) were found between mean total PDSS and mean total UPDRS, as well as the mean scores of each part of UPDRS and HY stage. There was no difference in PDSS scores regarding gender. Analyzing each item in the PDSS scale, the lowest score was obtained for item 8 (nocturia). We did not find any difference in total PDSS scores between the patients on d-agonist and those who did not take d-agonist. Regarding amantadin, intake there were differences between groups for items concerning nocturnal motor symptoms. Patients in advanced stages of the disease and worse motility have more prominent sleep problems. Drug therapy has important impact on sleep quality in patients with PD.

Olfactory testing combined with dopamine transporter imaging as a method to detect prodromal Parkinson's disease

ObjectiveOlfactory dysfunction is an early and common symptom in Parkinson disease (PD). Previously, the authors demonstrated that idiopathic olfactory dysfunction in first-degree relatives of PD patients is associated with an...

Therapeutic extradural cortical stimulation for Parkinson's Disease: Report of six cases and review of the literature

Objectives We report our experience and results with extradural cortical stimulation (ECS) in the surgical treatment of Parkinson's Disease (PD). Besides, we review the literature supporting the use of this technique. Materials and methods Six patients with advanced PD and exclusion criteria for Deep Brain Stimulation (DBS) were included in our ECS protocol. With the aid of functional MRI and somato-sensory evoked potentials monitoring, the motor cortex projection over the scalp was drawn. Finally, under local anesthesia a stimulation lead was placed in the epidural space overlying the central sulcus. Results Patients showed mild daily life activities improvement with a slightly lower levodopa equivalent dose, but UPDRS part III scores showed no significant modification. Conclusions Despite ECS is a minimally invasive surgical technique, our results only support its use in selected patients with advanced PD, in whom this therapy may be modestly effective. More experimental studies regarding the neuromodulation of the basal ganglia-cortex loops are required to optimize its clinical application.

Alpha‐synuclein and familial Parkinson's disease

Whole gene duplications and triplications of alpha-synuclein (SNCA) can cause Parkinson's disease (PD), and variation in the promoter region (Rep1) and 3' region of SNCA has been reported to increase disease susceptibility. Within our cohort, one affected individual from each of 92 multiplex PD families showing the greatest evidence of linkage to the region around SNCA was screened for dosage alterations and sequence changes; no dosage or non-synonymous sequence changes were found. In addition, 737 individuals (from 450 multiplex PD families) that met strict diagnostic criteria for PD and did not harbor a known causative mutation, as well as 359 neurologically normal controls, were genotyped for the Rep1 polymorphism and four SNPs in the 3' region of SNCA. The four SNPs were in high LD (r(2) > 0.95) and were analyzed as a haplotype. The effects of the Rep1 genotype and the 3' haplotype were evaluated using regression models employing only one individual per family. Cases had a 3% higher frequency of the Rep1 263 bp allele compared with controls (OR = 1.54; empirical P-value = 0.02). There was an inverse linear relationship between the number of 263 bp alleles and age of onset (empirical P-value = 0.0004). The 3' haplotype was also associated with disease (OR = 1.29; empirical P-value = 0.01), but not age of onset (P = 0.40). These data suggest that dosage and sequence changes are a rare cause of PD, but variation in the promoter and 3' region of SNCA convey an increased risk for PD.

Clinical and molecular neuroimaging characteristics of Brazilian patients with Parkinson's disease and mutations in PARK2 or PARK8 genes

To describe clinical and neuroimaging (SPECT) characteristics of Brazilian patients with Parkinson's disease (PD) and mutations in PARK2 or PARK8 genes. A total of 119 patients meeting clinical criteria for PD were evaluated. Of all patients studied, 13 had mutations in either PARK2 (n=9) or PARK8 genes (n=4). No statistically significant differences in clinical characteristics in both groups were seen. SPECT with [99mTc] TRODAT-1 showed significant differences between patient and control and the most remarkable difference was between PARK2 and control. The study found a frequency of mutation of 10.1% and it was most commonly seen in women. These patients had long disease course and high rates of dyskinesia after L-DOPA use. PARK8 patients did not have a relevant family history of PD.

Frequency of heterozygous Parkin mutations in healthy subjects: Need for careful prospective follow-up examination of mutation carriers

The role of single heterozygous mutations in the putatively recessive Parkin gene in Parkinson disease (PD) is a vividly debated issue, partly caused by the largely unknown frequency of these mutations in healthy individuals. We investigated mutations in all 12 Parkin exons in 356 controls from two European populations including individuals from South Tyrol and Germany. None of the controls carried a homozygous or compound heterozygous mutation. Seventeen carriers of rare heterozygous alterations were detected, of which 13 (13/356; 3.7%) are considered to alter protein structure including four different gene dosage alterations, four missense mutations, and two frameshift mutations. Two of the mutations occurred recurrently in the South Tyrolean population. There was no obvious difference in the mutation frequency between the two populations. One of the presumably healthy mutation carrier was available for re-examination at the age of 67 years. He presented with mild signs of parkinsonism but not fulfilling diagnostic criteria for definite PD. To elucidate the role of heterozygosity is important for genetic testing and counseling of mutation carriers. A detailed clinical prospective and follow-up examination of mutation carriers is required for a better understanding of the role of heterozygous Parkin mutations.

Motor and non-motor features of Parkinson\'s disease

Parkinson's disease (PD) is a common neurodegenerative brain disease in developed countries where population of the elderly is high. PD is increasingly being documented in developing countries where there are rapid demographic changes. Motor features of PD have been documented in Africans in previous studies. However non-motor features such as depression and sleep disturbance have not been well documented. To study the motor and non-motor features of idiopathic Parkinson's disease in Tanzania. A descriptive consecutive referral of patients to the national tertiary care hospital. Neurology clinic at Muhimbili National Hospital a major teaching and national referral hospital. Forty two of 1,908 (2.2%) new referralpatients over four years of study satisfied the criteria for idiopathic PD. Of these 25 (59.5%) were males and 17 females. There was no significant difference between sex, in demographic and clinical features. Nevertheless females tended to be older; and the majority of whom were housewives. Three male patients were in advanced stage five and six or UPDRS above 61/108. Thirty nine (92.8%) patients completed BDI and none of these had a BDI score of more than ten. Insomnia was reported in 14(33%) of patients. There was no significant difference between age, sex, clinical stage or UPDRS score. However 12 (28.6%) of 42 patients had been noted to have at least one sleep behaviour disorder and all had mild to moderate disease at stages one to three or UPDRS score of 60/108 or less. Idiopathic Parkinson's disease is increasingly being seen in Tanzania due to the ageing population. Majority of patients in this series were in early stage of disease. Depression was conspicuously absent. However sleep behaviour disorder, which is potentially harmful to the patient, bed partners and requires different management, was a common feature that was elicited by direct enquiry in patients with Parkinson's disease.

Prevalence of Parkinson's disease and other types of parkinsonism in the Aeolian Archipelago, Sicily

Objective To estimate prevalence of Parkinson's disease (PD) and other types of parkinsonism in the Aeolian Archipelago, Sicily. Methods We studied the frequency of PD and other types of parkinsonism in the Aeolian Archipelago (population 13,431). All potential cases were identified from available medical information sources. To ensure the completeness of the case-findings, a screening questionnaire was also mailed to residents aged 40 years and over. Subjects were considered prevalent if they fulfilled the SNES diagnostic criteria for PD, on prevalence day (January 1, 2001). Results We identified 17 patients with parkinsonism from medical sources, and 4 from mail-survey. Prevalence for all types of parkinsonism was 156.3/100,000 (95% CI 99.4–234.8). Fourteen subjects fulfilled diagnostic criteria for PD giving a crude prevalence of 104.2/100,000 (95% CI 59.4–170.7) and 422.5/100,000 in the population aged 60 years and over. Conclusions Prevalence of all types of parkinsonism and PD found in the Aeolian Archipelago is lower than that previously reported in Sicily.

Role of DAT‐SPECT in diagnostic work‐up of Parkinsonism

The diagnosis of idiopathic Parkinson's disease (PD) can be achieved with high degrees of accuracy in cases with full expression of classical clinical features. However, diagnostic uncertainty remains in early disease with subtle or ambiguous signs. Functional imaging has been suggested to increase the diagnostic yield in parkinsonian syndromes with uncertain clinical classification. Loss of striatal dopamine nerve terminal function, a hallmark of neurodegenerative Parkinsonism, is strongly related to decreases of dopamine transporter (DAT) density, which can be measured by single photon emission computed tomography (SPECT). The use of DAT-SPECT facilitates the differential diagnosis in patients with isolated tremor symptoms not fulfilling PD or essential tremor criteria, drug-induced, psychogenic and vascular Parkinsonism as well as dementia when associated with Parkinsonism. This review addresses the value of DAT-SPECT in early differential diagnosis, and its potential as a screening tool for subjects at risk of developing PD as well as issues around the assessment of disease progression. (c) 2007 Movement Disorder Society