Early Sign Of Parkinson's Disease Research Articles

A Comprehensive Review of Deep Learning Techniques for Identifying Parkinson's Disease from Gait Analysis

A group of neurological disorders that manifests in a wide range of motor and cognitive symptoms, Parkinson's Disease (PD) ranks second among those affecting older adults. Many people mistakenly believe that PD symptoms are caused by other conditions, such as essential tremor or natural aging. There may not be a cure for PD, but there are numerous medications that can help with symptoms. Since gait impairment is a prominent and early sign of PD in a clinical context, doctors typically use visual observations to analyse gait abnormalities as one of many manifestations to determine the severity of PD. Nevertheless, therapists' reliance on their own knowledge and judgment makes gait examination a difficult and subjective process. Extracting useful gait features from various input signals for gait analysis has recently been used Deep Learning (DL) models. Intermediate Medical Unit (IMU) patients with movement problems may benefit from a quick and clinically relevant evaluation of gait abnormalities performed automatically utilizing DL algorithms. Using gait analysis, this study provides a comprehensive overview of various DL frameworks that have been created for the purpose of PD prediction and categorization. At the outset, In the first part of the study, various PD prediction and classification systems that have been developed by various researchers and that rely on DL algorithms via gait analysis are reviewed briefly. To find a better way to identify and categorize the PD, we next undertake a comparative analysis to learn about the shortcomings of those algorithms.

Gut brain axis: an insight into microbiota role in Parkinson's disease.

Parkinson's disease (PD) is one of the most common progressive neurodegenerative diseases. It is characterized neuropathologically by the presence of alpha-synuclein containing Lewy Bodies in the substantia nigra of the brain with loss of dopaminergic neurons in the pars compacta of the substantia nigra. The presence of alpha-synuclein aggregates in the substantia nigra and the enteric nervous system (ENS) drew attention to the possibility of a correlation between the gut microbiota and Parkinson's disease. The gut-brain axis is a two-way communication system, which explains how through the vagus nerve, the gut microbiota can affect the central nervous system (CNS), including brain functions related to the ENS, as well as how CNS can alter various gut secretions and immune responses. As a result, this dysbiosis or alteration in gut microbiota can be an early sign of PD with reported changes in short chain fatty acids, bile acids, and lipids. This gave rise to the use of probiotics and faecal microbiota transplantation as alternative approaches to improve the symptoms of patients with PD. The aim of this review is to discuss investigations that have been done to explore the gastrointestinal involvement in Parkinson's disease, the effect of dysbiosis, and potential therapeutic strategies for PD.

Longitudinal change in autonomic symptoms predicts activities of daily living and depression in Parkinson's disease.

The primary objective of this study was to examine the relationship of longitudinal changes in autonomic symptom burden and longitudinal changes in activities of daily living (ADLs); a secondary analysis examined the impact of depressive symptoms in this relationship. Data were retrieved from the Parkinson's Progression Markers Initiative (PPMI), a dataset documenting the natural history of newly diagnosed Parkinson's disease (PD). The analysis focused on data from baseline, visit 6 (24months after enrollment), and visit 12 (60months after enrollment). The impact of longitudinal changes in autonomic symptom burden on longitudinal changes in ADLs function was examined. A secondary mediation analysis was performed to investigate whether longitudinal changes in depressive symptoms mediate the relationship between longitudinal changes in autonomic symptom burden and ADLs function. Changes in autonomic symptom burden, cognitive function, depressive symptoms, and motor function all correlated with ADLs. Only changes in ADLs and depression were found to be associated with changes in autonomic symptom burden. We found that longitudinal change in autonomic symptoms was a significant predictor of change in ADLs at 24 and 60months after enrollment, with the cardiovascular subscore being a major driver of this association. Mediation analysis revealed that the association between autonomic symptoms and ADLs is partially mediated by depressive symptoms. Longitudinal changes in autonomic symptoms impact ADLs function in patients with early signs of PD, both directly and indirectly through their impact on depressive symptoms. Future investigation into the influence of treatment of these symptoms on outcomes in PD is warranted.

Facial tremors in patients with and without parkinsonism.

Facial (lip and jaw) tremors can be an early sign of Parkinson's disease (PD), essential tremor and other parkinsonisms. Its response to acute dopaminergic therapy and further predictive clinical diagnosis has not been previously addressed. The aim of this study was to evaluate facial tremors response to acute dopaminergic therapy and further predictive value for clinical diagnosis. A retrospective review of medical records from patients with recent onset of facial tremor, with or without parkinsonism, submitted to acute levodopa challenge for clinical prediction of sustained long-term dopaminergic response was conducted. Twenty-eight out of 559 patients (5%) had facial tremors, which responded to levodopa in 46% of patients. Facial tremors response to acute levodopa challenge showed 92% sensitivity and 93% specificity to predict a final PD diagnosis. In PD patients, facial tremor magnitude of response to levodopa was not different from that of hand rest tremor (p=0.8). Facial tremors, although infrequent, can be an early sign of PD. Positive response to acute levodopa challenge predicts long-term PD diagnosis.

Anterior Temporal Atrophy and Posterior Progression in Patients with Parkinson's Disease

Background: Parkinson's disease (PD) is characterized by specific motor and nonmotor impairments. This suggests that PD is characterized by disease-specific regional cortical atrophy. Given the change of symptoms over time, a concurrent increase in regional atrophy may further be assumed to reflect the dynamic process of disease progression. Methods: In this study we retrospectively collected T1-weighted MRI scans from previous studies performed in our center, enabling the comparison of gray matter atrophy in 77 PD patients with 87 controls using voxel-based morphometry (VBM). This large VBM analysis provided the opportunity to investigate cortical atrophy in relation with disease progression. Results: We found significant PD-related reductions of gray matter density bilaterally in the anterior temporal cortex, the left inferior frontal and left extrastriate visual cortex, independent from normal aging. The anterior temporal cortex did not show major progression, whereas particularly the posterior parts of the lateral temporal cortex and adjacent extrastriate visual cortex occurred at a later stage of disease. Conclusions: Temporal pole atrophy as an early sign of PD is consistent with the PD pathology classification of Braak. The initial anterior temporal atrophy with spread to occipitotemporal and posterior parietal regions may subserve ‘emotion-based' sensorimotor transformations and deficits in the visual domain, respectively, which may be regarded as premotor symptoms.

Exploring the electrocardiogram as a potential tool to screen for premotor Parkinson's disease

The aim of this study was to test the hypothesis that patients with REM sleep behavior disorder, many of whom will develop Parkinson's disease (PD) or a related synucleinopathy, will demonstrate decreased heart rate variability (HRV) compared with a group of age-matched controls as measured by an electrocardiogram during wakefulness. We compared HRV in 11 untreated idiopathic REM sleep behavior disorder patients (9 men and 2 women; mean age, 63.3 years; SD, 7.5 years) and 11 control subjects with idiopathic insomnia without REM sleep behavior disorder (7 men and 4 women; mean age, 59.5 years; SD, 8.7 years). Subjects with other causes of reduced HRV were excluded. HRV was determined from 5-minute presleep segments of a single channel electrocardiogram recorded during polysomnographic evaluations, using R-R intervals during wakefulness. Time domain, geometric measures, and spectral analysis of the R-R intervals were significantly different between cases and controls. A discriminant function analysis correctly classified 95.5% of subjects (overall model fit, P = 0.016). Leave-one-out cross-validation correctly classified 77.3% of subjects. HRV during wakefulness is significantly decreased in patients with idiopathic REM sleep behavior disorder compared with control subjects, suggesting abnormalities of both sympathetic and parasympathetic function. Patients with RBD may later develop motor and cognitive features of a Lewy body disorder, such as PD. Cardiac autonomic dysfunction is also impaired in PD, suggesting that impaired HRV may be an early sign of PD. HRV measured by routine electrocardiograms could be used to screen for Lewy body disorders such as PD.

Perceived imbalance and risk of Parkinson's disease.

We prospectively examined associations between perceived imbalance and Parkinson's disease (PD) risk in the Health Professional Follow-up Study (HPFS), and Nurses' Health Study (NHS). We included 39,087 men and 82,299 women free of PD at baseline (1990) in the current analyses. We documented 449 incident PD cases during 12 years follow-up. Subjects who reported difficulty with balance before 1990 (baseline) were 1.8 more times likely to develop PD, relative to those who reported no balance difficulty (pooled multivariate RR = 1.8; 95% CI: 1.3, 2.5; P < 0.0001). When we further examined associations between perceived imbalance at baseline and PD onset during different time periods, we found a significant elevation of PD risk only during the first 4 years of follow-up. This result suggests that the imbalance may in some cases be an early sign of PD, and may represent the onset of motor symptoms although they have not been clinically recognized.

Bimanual coordination dysfunction in early, untreated Parkinson's disease

Bimanual coordination involves the simultaneous performance of either symmetrical (in-phase) or asymmetrical (anti-phase) movements with both hands and is known to be impaired in Parkinson's disease (PD). At present, it is unclear whether this aspect of motor function is already impaired in early stage, untreated PD patients. Therefore, we investigated the accuracy of bimanual coordination in 13 early stage, untreated PD patients and 13 age- and sex-matched healthy controls. Each subject performed bimanual coordination tasks at two different movement frequencies (1 and 1.75 Hz) and with two different phase relationships (in-phase and anti-phase). The percentage of unsuccessful trials (as a measure of overall task performance) in PD patients was significantly higher than in healthy subjects. PD patients performed high frequency in-phase and anti-phase bimanual coordination tasks less accurately with their non-dominant hand than healthy subjects. Furthermore, PD patients had more difficulty than healthy subjects in maintaining a constant phase relationship between the hands in the anti-phase condition at low movement frequency. This study demonstrates that bimanual coordination dysfunction is a very early sign of PD. Bimanual coordination tasks, in particular those involving high frequency anti-phase movements, might prove useful in the early diagnosis of PD.

SELF-REPORTED EARLIEST SYMPTOMS OF PARKINSON DISEASE.

Purpose/Hypothesis: Parkinson disease (PD) is caused by cell death in the substantia nigra pars compacta of the midbrain. Although the classic diagnostic signs of PD are muscle rigidity, tremor, and bradykinesia, these signs only appear after approximately 90% of the neurons within the pars compacta have degenerated. Currently, research is focused on developing neuroprotective treatments to halt the progression of cell death in PD. Neuroprotective treatments will only be effective if the cell death can be recognized by signs that precede the cardinal signs of PD. Physical therapists, trained to observe movement, are well-suited to develop early detection tests for PD. The purpose of this study was to ask persons with PD directly about their earliest symptoms, to obtain clues for early detection. To date, no one has methodically queried persons with the disease about pre-diagnostic symptoms. Number of Subjects: 45. Materials/Methods: Surveys were distributed at support groups, physician offices, and on an internet website, and were completed anonymously by persons with idio-pathic PD. The survey included basic demographic data, multiple-choice questions, and open-ended questions related to pre-diagnostic physical and emotional symptoms. Subjects were required to order the onset of symptoms in each section. Results: Forty-five people (16 females, 29 males, aged 73.2 ± 8.9) responded to the survey. The average number of years with PD was 8 ± 6.53. Thirty-five percent of respondents reported tremor as the first sign of PD. The remaining subjects reported diminished olfaction, depression, voice changes, and bradykinesia. An analysis of all early signs revealed that 1) as a cluster of early symptoms, sleep disorders, fatigue, depression and tiredness occurred in 50% of subjects, and 2) males and females had different early signs: males more often reported classic signs of the disease, and females more often reported fatigue, tiredness, depression and voice-weakening. Ten-percent of all subjects also reported that symptoms first appeared after major medical events, such as surgery or trauma. Conclusions: This study had 2 major findings. First, most people with PD reported a classic symptom as the first symptom of PD, suggesting that they were unable to detect any subtle earlier symptoms of impending PD. Second, females especially, reported fatigue, depression, tiredness and sleep disturbances as early signs of PD. This cluster of symptoms should be added to previously reported micrographia and diminished olfaction, as early indicators of PD. Clinical Relevance: Because individuals may not be able to detect the early symptoms of PD, physical therapists should be aware that pre-diagnostic signs of PD may include fatigue, depression, tiredness, and sleep disturbances, in addition to the previously reported micrographia and diminished olfaction. In addition, physical therapists need to conduct more research to develop clinical test batteries for early detection. The ultimate goal would be to halt disease progression with new neuroprotective treatments, such as drug, gene, or physical therapy.

Respiration and heart rate variability during sleep in untreated Parkinson patients.

Twenty-six patients with untreated mild to moderate Parkinson's disease (PD) lasting 5 years or less, were investigated in the sleep laboratory. Sleep architecture and respiration during sleep did not significantly differ from age-matched controls. PD patients showed defective cardiac autonomic control during sleep, mainly parasympathetic but also sympathetic in nature, although they had normal results in conventional autonomic tests during wakefulness. Therefore, autonomic cardiac involvement seems to be an early sign of PD.