Different Stages Of Parkinson's Disease Research Articles

Visual Hallucination and Pattern of Brain Degeneration in Parkinson's Disease

Background and Objectives: The incidence of visual hallucination (VH) increases with Parkinson's disease (PD) progression, and its development is thought to be related to a specific neurodegenerative process in PD. This study aimed to reveal brain degeneration related to VH in PD by analyzing neuroimaging data obtained from patients in their different stages of PD. Methods: Data from 48 PD patients - 21 nondemented without VH (PNV group), 10 nondemented with VH (PV group), and 17 demented with VH (PVD group) - and 30 age-matched healthy controls (HC group) were analyzed. Voxel-based morphometry and tract-based spatial statistics were conducted. Previous magnetic resonance volumetric studies on VH in PD were collectively reviewed. Results: The PV group showed gray matter atrophy in the right inferior parietal lobule and supramarginal gyrus compared with the HC and PNV groups. The PVD group showed a wider range of gray matter atrophies in the temporo-parieto-occipital regions than those in the PV group. White matter changes seemed to be an earlier event than gray matter changes. Fractional anisotropy values diffusely decreased in all three PD subgroups compared with the HC group without significant differences between the PD subgroups. Mean diffusivity was not different between the PNV and HC groups but increased in the parieto-temporal region in the PV group and increased diffusely in the PVD group, additionally including the fronto-occipital regions. A review of previous studies supported our observations. Conclusions: Gray matter degenerations from the parieto-temporal junction to the parieto-occipital and temporo-occipital regions may be responsible for VH on the typical timeline of PD progression.

Esophageal dysfunction in different stages of Parkinson's disease.

Dysphagia is a clinically relevant symptom in patients with Parkinson's disease (PD) leading to pronounced reduction in quality of life and other severe complications. Parkinson's disease-related dysphagia may affect the oral and pharyngeal, as well as the esophageal phase of swallowing. To examine the nature and extend of esophageal dysphagia in different stages of PD and their relation to oropharyngeal dysfunction, we examined 65 PD patients (mean age 66.3±9.7years, mean disease duration 7.9±5.8years, mean Hoehn & Yahr [H&Y] stage 2.89±0.91) and divided into three groups (early [H&Y I+II; n=21], intermediate [H&Y III; n=25], and advanced stadium [H&Y IV+V; n=19]), using esophageal high-resolution manometry (HRM) to detect esophageal motor disorders. Oropharyngeal impairment was assessed using fiberoptic endoscopic evaluation of swallowing. Major esophageal motor disorders were detected in nearly one third of the PD patients. Minor impairment of the esophageal body was present in 95% of participants and throughout all disease stages with pathological findings especially in peristalsis and intrabolus pressure (IBP). The IBP was found to significantly increase in the advanced stadium. Although dysfunction of the upper and lower esophageal sphincters was observed in individual patients, alterations in these esophageal segments revealed no statistical significance compared with normative data. No clear association was found between the occurrence of oropharyngeal dysphagia and esophageal impairment. Esophageal body impairment in PD is a frequent phenomenon during all disease stages, which possibly reflects α-synucleinopathy in the enteric nervous system.

Emerging preclinical pharmacological targets for Parkinson's disease.

Parkinson's disease (PD) is a progressive neurological condition caused by the degeneration of dopaminergic neurons in the basal ganglia. It is the most prevalent form of Parkinsonism, categorized by cardinal features such as bradykinesia, rigidity, tremors, and postural instability. Due to the multicentric pathology of PD involving inflammation, oxidative stress, excitotoxicity, apoptosis, and protein aggregation, it has become difficult to pin-point a single therapeutic target and evaluate its potential application. Currently available drugs for treating PD provide only symptomatic relief and do not decrease or avert disease progression resulting in poor patient satisfaction and compliance. Significant amount of understanding concerning the pathophysiology of PD has offered a range of potential targets for PD. Several emerging targets including AAV-hAADC gene therapy, phosphodiesterase-4, potassium channels, myeloperoxidase, acetylcholinesterase, MAO-B, dopamine, A2A, mGlu5, and 5-HT-1A/1B receptors are in different stages of clinical development. Additionally, alternative interventions such as deep brain stimulation, thalamotomy, transcranial magnetic stimulation, and gamma knife surgery, are also being developed for patients with advanced PD. As much as these therapeutic targets hold potential to delay the onset and reverse the disease, more targets and alternative interventions need to be examined in different stages of PD. In this review, we discuss various emerging preclinical pharmacological targets that may serve as a new promising neuroprotective strategy that could actually help alleviate PD and its symptoms.

Regionally progressive accumulation of iron in Parkinson's disease as measured by quantitative susceptibility mapping.

The progression of Parkinson's disease (PD) seems to vary according to the disease stage, which greatly influences the management of PD patients. However, the underlying mechanism of progression in PD remains unclear. This study was designed to explore the progressive pattern of iron accumulation at different stages in PD patients. Sixty right-handed PD patients and 40 normal controls were recruited. According to the disease stage, 45 patients with Hoehn-Yahr stage ≤ 2.5 and 15 patients with Hoehn-Yahr stage ≥ 3 were grouped into early-stage PD (EPD) and late-stage PD (LPD) groups, respectively. The iron content in the cardinal subcortical nuclei covering the cerebrum, cerebellum and midbrain was measured using quantitative susceptibility mapping (QSM). The substantia nigra pars compacta (SNc) showed significantly increased QSM values in the EPD patients compared with the controls. In the LPD patients, while the SNc continued to show increased QSM values compared with the controls and EPD patients, the regions showing increased QSM values spread to include the substantia nigra pars reticulata (SNr), red nucleus (RN) and globus pallidus (GP). Our data also indicated that iron deposition was more significant in the GP internal segment (GPi) than in the GP external segment. No other regions showed significant changes in QSM values among the groups. Therefore, we were able to confirm a regionally progressive pattern of iron accumulation in the different stages of PD, indicating that iron deposition in the SNc is affected exclusively in the early stages of the disease, while the SNr, RN and GP, and particularly the GPi segment, become involved in advanced stages of the disease. This is a preliminary study providing objective evidence of the iron-related progression in PD. Copyright © 2016 John Wiley & Sons, Ltd.

Tandem Mass Spectrometry Multiplex Analysis of Glucosylceramide and Galactosylceramide Isoforms in Brain Tissues at Different Stages of Parkinson Disease.

Previous studies demonstrated that Parkinson disease (PD) is associated with a decreased activity of the glucocerebrosidase (GCase) enzyme in brain tissues. The objective of this study was to determine if GCase deficiency is associated with the accumulation of its glucosylceramide (GluCer) substrate in PD brain tissues. An ultra performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) method was developed, optimized, and validated for the multiplex analysis of GluCer isoforms (C18:0, C20:0, C22:0, C24:1, and C24:0) in brain tissue samples. These molecules were chromatographically separated from their isobaric galactosylceramide (GalCer) counterparts using normal phase chromatography. The analysis was performed by tandem mass spectrometry in the multiple reaction monitoring (MRM) acquisition mode. Limits of detection ranging from 0.4 to 1.1 nmol/g brain tissue were established for the different GluCer isoforms analyzed. For the first time, GluCer isoform levels were analyzed in temporal cortex brain tissue samples from 26 PD patients who were divided into three PD disease stages (IIa, III, and IV) according to the Unified Staging System for Lewy Body Disorders. These specimens were compared with brain tissue samples from 12 controls and 6 patients with Incidental Lewy Body Disease. No significant GluCer concentration differences were observed between the 5 sample groups. The GluCer isoform levels were also normalized with their matching GalCer isoforms. The normalized results showed a trend for GluCer levels which increased with PD severity. However, the differences observed between the groups were not significant, owing likely to the high standard deviations measured.

Estudio piloto sobre la escala de convivencia con un proceso crónico en pacientes con enfermedad de Parkinson

To be able to provide patients with a chronic illness personalised care, it is necessary to know how they live with their disorder. Today, there is no validated scale that assesses this aspect. To present the pilot study of the preliminary version of the living with a chronic process scale (EC-PC, from the name in Spanish) carried out in patients with Parkinson's disease (PD) in Spain. A preliminary version of the scale was produced from a literature review and the participation of experts in chronic processes and in PD. Fifteen patients, in all the different stages of PD, answered the preliminary version of the EC-PC (39 items) and a questionnaire about the EC-PC. The viability/acceptability and preliminary aspects of internal consistency were analysed. No domain showed any floor or ceiling effects, but 43.6% of the items had a ceiling effect. The corrected item-total correlation was satisfactory, except in five items. The internal consistency of the five domains was satisfactory, with alpha indexes of 0.81-0.92 and item homogeneity coefficients of 0.19-0.43. The patients identified three items as ambiguous and difficult to answer. Based on these results, 12 items were eliminated and the final version of the EC-PC was drafted, its content being considered satisfactory following its evaluation by expert professionals. The EC-PC, pending validation, is a viable scale of potential interest in the clinical and community healthcare setting for assessing the ability to live with a chronic process like PD.

The heterogeneity of non-motor symptoms of Parkinson's disease.

In addition to motor symptoms, patients with Parkinson's disease (PD) may experience non-motor symptoms (NMS), more often with more advanced disease stage. However, the clinical feature of the NMS and potential risk factors that affect NMS in idiopathic PD patients remain unclear. 493 PD patients diagnosed with PD via the UK. Parkinson's Disease Society Brain Bank Clinical Diagnostic Criteria and 93 healthy control subjects (CN) were recruited in the current study. Questionnaires were used to assess the NMS, motor symptoms, cognitive function, and disease severity in both groups. Levodopa daily dose was calculated in PD patients. Multivariate linear regression analysis was used to identify the risk factors that potentially affect NMS in PD patients. The results showed that, the NMS occurrence and positive endorsement rate of PD patients were significantly higher compared to CN subjects. Multiple stepwise regression analysis found the motor symptom was the only factor that affected NMS in PD patients within five years of the disease course, whereas motor symptoms, cognitive function, disease severity and Levodopa daily dose significantly affected NMS if the disease course was more than five years. These findings demonstrated that NMS are affected by several risk factors at different stages of PD. The distribution of difference NMS is associated with the severity of motor symptoms and the dosage of anti-PD medications in Chinese PD patients.

Emerging therapies for Parkinson's disease: from bench to bedside.

The prevalence of Parkinson's disease (PD) increases with age and is projected to increase in parallel to the rising average age of the population. The disease can have significant health-related, social, and financial implications not only for the patient and the caregiver, but for the health care system as well. While the neuropathology of this neurodegenerative disorder is fairly well understood, its etiology remains a mystery, making it difficult to target therapy. The currently available drugs for treatment provide only symptomatic relief and do not control or prevent disease progression, and as a result patient compliance and satisfaction are low. Several emerging pharmacotherapies for PD are in different stages of clinical development. These therapies include adenosine A2A receptor antagonists, glutamate receptor antagonists, monoamine oxidase inhibitors, anti-apoptotic agents, and antioxidants such as coenzyme Q10, N-acetyl cysteine, and edaravone. Other emerging non-pharmacotherapies include viral vector gene therapy, microRNAs, transglutaminases, RTP801, stem cells and glial derived neurotrophic factor (GDNF). In addition, surgical procedures including deep brain stimulation, pallidotomy, thalamotomy and gamma knife surgery have emerged as alternative interventions for advanced PD patients who have completely utilized standard treatments and still suffer from persistent motor fluctuations. While several of these therapies hold much promise in delaying the onset of the disease and slowing its progression, more pharmacotherapies and surgical interventions need to be investigated in different stages of PD. It is hoped that these emerging therapies and surgical procedures will strengthen our clinical armamentarium for improved treatment of PD.

Apathy in Parkinson's disease patients

pathy in Parkinson's disease (PD) patients is one of the least studied manifestations of a broad range of neuropsychic disorders. According to numerous researchers, the rate of apathy in PD patients is 17–80%. The structural and neurochemical changes associated with PD have been considered to be the leading pathophysiological factors of apathy. The possible general pathophysiological mechanisms are discussed for apathy and hypokinesia, depression, executive (frontal) cognitive functions, and sleep disorders in PD patients. The pathophysiological commonality of apathy, hypokinesia, and executive functions is probably based on bilateral disorders of functional links of the striatum and dorsolateral, medial parts of the prefrontal cortex. A combination of apathy and depression in PD patients may be due to dysfunction of the structures of the limbic system and medial orbital prefrontal cortex, which are responsible for the motivationally driven behavior. Variability of relationships of apathy with hypokinesia, depression, cognitive impairments, sleep disorders at different stages of PD may be associated with the phenomenological heterogeneity of apathy. Apathy reduces quality of life, makes a significant contribution to disturbances of both everyday and social adaptation of PD patients. A study of the possibility for apathy correction using dopaminergic therapy is rather promising. Twenty patients with PD (the middle stage according to the Hoehn and Yahr scale, 2.5) received pramipexole (1.5–3.0 mg/day) to correct motor disorders. A statistically significant positive trend in the time course of apathy, according to the overall assessment by the Starkstein apathy scale (AS), was noted after 4–6 weeks of the therapy. Based on the results, no statistically significant correlation was observed between the dynamics of the overall apathy score and the dynamics of motor symptoms of PD on the unified rating scale for PD assessment («Motor functions»). We believe that this fact demonstrates the independent effect of pramipexole therapy against motivational disorders.

The Experiences of Taiwanese Older Individuals at Different Stages of Parkinson Disease

Parkinson disease (PD) is a progressive neurological condition, usually occurring among older individuals. Along with increasing handicaps in daily life, patients with PD also face problems with psychosocial adjustment. This study explored the experiences of older Taiwanese individuals at different stages of PD. Qualitative design with in-depth interviews was conducted with participants being treated at the neurology outpatient department in a teaching hospital in northern Taiwan. The study included nine men and six women, aged 65-80 years, with PD at stages 1-4. Comparative analysis of the interviews revealed four themes: ignorance of symptoms, loss of control, gradual deterioration, and a deep sense of helplessness. In stage 1, symptoms were not significant at the onset of PD. For most participants, others first detected the symptoms, rather than themselves. During stage 2, although they could still care for themselves, they became very anxious when the effects of medication disappeared and their reactions slowed before they took the next dose. During stage 3, the physical capacity of the body decreased gradually and affected the patient's participation in social activities. In stage 4, older patients gradually became dependent on others in their daily lives. They were upset and worried that the symptoms would worsen and make them become a burden for their children. By understanding the perceptions of elderly patients at different stages of PD, this study has organized the key care requirements into four stages. These include the following: (1) provide more information on the disease in stage 1, (2) increase guidance on regular medication usage and establish a support system in stage 2, (3) highlight the importance of a safe living environment and encourage participation in support groups in stage 3, and (4) assist patients to find the meaning of life and value of existence in stage 4.

Clinical syndromes: Parkinsonian gait

Disturbances of gait manifest in almost all cases of Parkinson's disease (PD), often leading to loss of mobility and increased mortality. In this review a clinically oriented approach to gait disorders in different stages of PD is presented. In addition, interactions between motor behavior and mental processing will be discussed. Analyzing the clinical features of gait can be helpful to differentiate PD from atypical forms of parkinsonism. Bedside tests to distinguish parkinsonian gait disorders are reviewed. There is still an unmet need to effectively treat complex gait disturbances, which are frequently not responsive to dopamine replacement medication. We thus present current approaches for the management of dopa-refractory gait disorders.

Système nerveux autonome : une source de biomarqueurs dans la maladie de Parkinson

No validated biomarker is yet available for Parkinson's disease (PD). Clinical PD symptoms include dopa-responsive motor symptoms and dopa-resistant non motor symptoms. Some of the non motor symptoms begin during the premotor stage, like constipation, hyposmia or REM-sleep disorders. Dementia, gait disorders and dysarthria occur in later stages of the disease. PD pathology extends well beyond the substantia nigra. It affects autonomic and non autonomic nuclei in the brainstem and in the medulla, the olfactory bulb and the peripheral autonomic nervous system. Alpha-synuclein aggregates, called Lewy bodies and Lewy neurites, are detectable in these structures at early stages. The study of the enteric nervous system (ENS) displays the Lewy pathology in living patients through the digestive biopsies. Minor salivary glands analysis could be a good marker as well, but this needs confirmation. An anatomopathologic PD biomarker would be interesting at different stages of PD: for the positive diagnosis, to follow the progression and to develop neuroprotective treatments.

The Intranasal Administration of 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine (MPTP): A New Rodent Model to Test Palliative and Neuroprotective Agents for Parkinson's disease

Parkinson's disease (PD) is the second most common neurodegenerative disorder affecting approximately 1% of the population older than 60 years. Classically, PD is considered to be a motor system disease and its diagnosis is based on the presence of a set of cardinal motor signs that are consequence of a pronounced death of dopaminergic neurons in the substantia nigra pars compacta (SNc). Nowadays there is considerable evidence showing that non-dopaminergic degeneration also occurs in other brain areas which seems to be responsible for the deficits in olfactory, emotional and memory functions that precede the classical motor symptoms in PD. Dopamine-replacement therapy has dominated the treatment of PD and although the currently approved antiparkinsonian agents offer effective relief of the motor deficits, they have not been found to alleviate the non-motor features as well as the underlying dopaminergic neuron degeneration and thus drug efficacy is gradually lost. Another major limitation of chronic dopaminergic therapy is the numerous adverse effects such as dyskinesias, psychosis and behavioral disturbance. The development of new therapies in PD depends on the existence of representative animal models to facilitate the evaluation of new pharmacological agents before they are applied in clinical trials. We have recently proposed a new experimental model of PD consisting of a single intranasal (i.n.) administration of the proneurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 1 mg/nostril) in rodents. Our findings demonstrated that rats and mice treated intranasally with MPTP suffer impairments in olfactory, cognitive, emotional and motor functions conceivably analogous to those observed during different stages of PD. Such infusion causes time-dependent loss of tyrosine hydroxylase in the olfactory bulb and SNc, resulting in significant dopamine depletion in different brain areas. We have also identified some pathogenic mechanisms possibly involved in the neurodegeneration induced by i.n. administration of MPTP including mitochondrial dysfunction, oxidative stress, activation of apoptotic cell death mechanisms and glutamatergic excitotoxicity. Therefore, the present review attempts to provide a comprehensive picture of the i.n. MPTP model and to highlight recent findings from our group showing its potential as a valuable rodent model for testing novel drugs that may provide alternative or adjunctive treatment for both motor and non-motor symptoms relief with a reduced side-effect profile as well as the discovery of compounds to modify the course of PD.

Quantitative lateralized measures of bradykinesia at different stages of Parkinson's disease: The role of the less affected side

The onset of motor abnormalities in Parkinson's disease (PD) is usually unilateral. However, current therapeutic trials do not analyze separately the performance of the more affected (MA) and less affected (LA) limbs. From a cohort of 85 subjects at different stages of PD, we asked whether the relationship between bradykinesia and disease severity was similar on both limbs and if the MA side remained more bradykinetic than the LA side in advanced PD. MA and LA limb determination was made from the history of the side first affected. Twenty-one age-matched subjects were used as controls. The velocities of finger and arm movements on both sides were inversely correlated with disease severity (P < 0.03). The slope of the decline in wrist movement velocity was steeper on the LA side (P = 0.029). When the regression lines were extrapolated to the y-axis (UPDRS III = 0) the performance of the LA side was not different from that of controls (P = 0.954 and P = 0.829 for finger and arm movements, respectively), whereas that of the MA side was slower (P = 0.019 and P = 0.016), suggesting that at the theoretical state of no disease the LA side would reflect less or no contralateral nigral pathology. With increasing disease severity, there was less difference between MA and LA sides in both finger and arm bradykinesia (P < 0.004). These findings highlight the value of analyzing separately the MA and LA sides in subjects with PD, especially for clinical trials of potential disease modifying agents in early stages of disease.

The scientific and clinical basis for the treatment of Parkinson disease (2009)

Parkinson disease (PD) is an age-related neurodegenerative disorder that affects as many as 1-2% of persons aged 60 years and older. With the aging of the population, the frequency of PD is expected to increase dramatically in the coming decades. Current therapy is largely based on a dopamine replacement strategy, primarily using the dopamine precursor levodopa. However, chronic treatment is associated with the development of motor complications, and the disease is inexorably progressive. Further, advancing disease is associated with the emergence of features such as freezing, falling, and dementia which are not adequately controlled with dopaminergic therapies. Indeed, it is now appreciated that these nondopaminergic features are common and the major source of disability for patients with advanced disease. Many different therapeutic agents and treatment strategies have been evaluated over the past several years to try and address these unmet medical needs, and many promising approaches are currently being tested in the laboratory and in the clinic. As a result, there are now many new therapies and strategic approaches available for the treatment of the different stages of PD, with which the treating physician must be familiar in order to provide patients with optimal care. This monograph provides an overview of the management of PD patients, with an emphasis on pathophysiology, and the results of recent clinical trials. It is intended to provide physicians with an understanding of the different treatment options that are available for managing the different stages of the disease and the scientific rationale of the different approaches.

Dopamine transporter distribution in patients with Parkinson disease of different stages detected using single-photon emission computed tomography brain imaging

Background Literatures have reported that the density changes of dopamine transporter is negatively correlated with the severity degree and grading of disease condition of Parkinson disease (PD). However, the distribution of dopamine transporter in each nucleus of corpora striatum at each period is still unclear. Objective To observe the radioactive uptake distribution of dopamine transporter in bilateral corpora striata of patients with different stages of PD using single photon emission computed tomography (SPECT), and make a comparison with healthy controls. Design Case-control analysis. Setting Department of Imageology, Second Hospital Affiliated to Guangzhou University of Chinese Medicine. Participants Thirty patients with PD admitted to Second Hospital Affiliated to Guangzhou University of Traditional Chinese Medicine between January and December 2005 were recruited. The involved patients, 19 male and 11 female, were aged from 36 to 80 years and with disease course of 2.5 months to 10 years. They all met the clinical diagnosis criteria of Britain Parkinson's disease Association Think Tank; Following Hoehn-Yahr grading: grade I: unilateral morbidity; grade II: bilateral morbidity, but without balance disorder; grade III: bilateral morbidity, accompanied with early posture balance disorder; grade IV: severe morbidity, needs more help; grade V: without help, only in bed or wheelchair. There were 11 patients with mild PD (grade I–II), 9 patients with moderate PD (grade III) and 10 patients with advanced PD (grade IV–V). Meanwhile, 6 healthy persons were selected as normal controls. Informed consents were obtained from all the subjects. Methods Twenty-four hours after withdrawal of PD drugs, 30 patients with PD and 6 healthy controls took kalium perchloricum 400 mg orally. After lying down for 30 minutes, all the subjects were intravenously injected with 740 MBq 99Tc m-TRODAT-1 (Jiangsu Institute of Atomic Medicine, Batch No. 20040310) at elbow part. Following injection, image was collected using scanner for single photon emission computed tomography (ADAC Company, USA). Matrix was 64×64, each detecting head revolved 180°, 1 frame/60 s. Sixty-four frames were collected with double detecting heads, 50 K/frame. Faultages with clearest image of corpora striatum were selected. Regions of interest (ROI) of caudate nucleus, anterior and posterior putamen and thalamic region in bilateral corpora striata were radioactively counted, and mean value of radioactive counting of ROI was used as the mean value of pixel in each region of bilateral corpora striata. Main outcome measures Comparison of radioactive uptake in each region of brain between healthy persons and patients with PD. Results Thirty patients with PD and six healthy persons who received body examination participated in the final result. Comparison of radioactive uptake in each region between healthy persons and patients with PD: ▪In the healthy persons, high-density radioactive uptake was found in bilateral corpora striata; Structures of caudate nucleus, anterior and posterior putamen, and thalamus were clear with eudipleural radioactive distribution, and the background of peripheral brain tissue was very low. ▪Radioactive intakes in opposite anterior and posterior putamen of patients with mild PD were significantly inferior to those in homolateral ones(70.45±3.35,87.64±2.65, t =15.82, P < 0.05). Structures of bilateral caudate nucleus and thalamus were clear with eudipleural radioactive distribution ( P > 0.05). ▪ Radioactive intakes in anterior and posterior putamen and thalamus of patients with moderate PD were significantly reduced as compared with healthy persons. There were significant differences in mean radioactive counting of ROI between patients with PD and healthy persons ( t =5.20, P < 0.05; t =3.95, P < 0.05); The structure of opposite caudate nucleus was not very clear, radioactive distribution of opposite caudate nucleus was significantly reduced as compared with homolateral one (81.11±4.25,104.56±3.64, t = 14.65, P < 0.05). ▪As for patients with advanced PD, the structure of bilateral corpora striata was not clear, radioactive intake was significantly reduced and peripheral background was heightened, even higher than the distribution of the whole corpora striatum. Conclusion SPECT DAT imaging of brain can show the distribution of radioactive uptake in each region of bilateral corpora striata of patients with different stages of PD, which is helpful to diagnose and evaluate the severity of PD.

Locomotor Training in People With Parkinson Disease

The purpose of this article is to consider the role of the physical therapist in locomotor training for people with Parkinson disease. The ways in which disease progression, medication status, environmental conditions, individual factors, and the goals of locomotor tasks contribute to clinical decision making are explored. Using the International Classification of Functioning, Disability and Health, gait training will be considered in relation to impairments of body structure and function, activity limitations, and participation restrictions in people who are newly diagnosed through to those with end-stage disease. Based on the principles of neural adaptation and clinical research findings, practical suggestions are made on how to provide the most efficient and effective physical therapy services at different stages of Parkinson disease.

Comparison of FP-CIT SPECT with F-DOPA PET in patients with de novo and advanced Parkinson’s disease

Diagnosis of Parkinson's disease (PD) can be difficult. F-DOPA PET is able to quantify striatal dopa decarboxylase activity and storage capacity of F-dopamine, but is expensive and not generally available. FP-CIT binds to the dopamine transporter, and FP-CIT SPECT is cheaper and more widely available, but has a lower resolution. The aim of this study was to compare these two methods in the same patients with different stages of PD to assess their power in demonstrating deficits of the striatal dopaminergic system. Thirteen patients with de novo PD and 17 patients with advanced PD underwent FP-CIT SPECT and static F-DOPA PET. After data transfer to standard stereotactic space, a template with regions of interest was used to sample values of the caudate, putamen and an occipital reference region. The outcome value was striato-occipital ratios. Patients were clinically examined in the "off state" (UPDRS-III and H&Y stage). Good correlations were found between striatal F-DOPA uptake and striatal FP-CIT uptake (r = 0.78) and between putaminal F-DOPA uptake and putaminal FP-CIT uptake (r = 0.84, both p < 0.0001). Both striatal uptake of FP-CIT and that of F-DOPA correlated moderately with H&Y stage (rho = -0.52 for both techniques), UPDRS-III (rho = -0.38 for F-DOPA; rho = -0.45 for FP-CIT) and disease duration (rho = -0.59 for F-DOPA; rho = -0.49 for FP-CIT, all p < 0.05). FP-CIT values correlate well with F-DOPA values. Both methods correlate moderately with motor scores and are equally able to distinguish patients with advanced PD from patients with de novo PD.