Event-related mu-rhythm desynchronization during movement observation is impaired in Parkinson’s disease

ObjectivePatients with Parkinson’s disease often experience difficulties in adapting movements and learning alternative movements to compensate for symptoms. Since observation of movement has been demonstrated to lead to the formation of a lasting specific motor memory that resembled that elicited by physical training we hypothesize that mu-rhythm desynchronization in response to movement observation is impaired in Parkinson’s disease.MethodIn a pilot study with nine patients with Parkinson’s disease at a Hoehn and Yahr stage of I or II and eleven age-matched controls, we tested this hypothesis by comparing the event related desynchronization (ERD) patterns from the EEG recorded during the observation of hand action and baseline videos.ResultsHealthy subjects showed normal bilateral ERD of the mu-rhythm. In patients with Parkinson’s disease this distinct ERD pattern was lacking.ConclusionThe results of this study suggest that event-related mu-rhythm desynchronization is impaired in Parkinson’s disease, even at early stages of the disease.SignificanceStudying event-related mu-rhythm desynchronization dysfunction in Parkinson’s disease patients may enhance our understanding of symptoms as impaired motor learning.     

Dopaminergic modulation of emotional memory in Parkinson’s disease

The aim of this study was to assess the effect of dopaminergic treatment on emotional memory in patients with Parkinson's disease (PD). We tested memory for emotional and neutral visual stimuli in ten non-demented PD patients on and off dopaminergic medication. Patients recalled significantly more emotional items during the off- than on-medication testing session. In contrast, treatment condition did not affect memory for neutral items. These findings demonstrate that emotional memory deficits observed in PD may result from dopaminergic treatment and suggest an involvement of dopaminergic neurotransmission in emotional processing.     

Hand function is impaired in healthy older adults at risk of Parkinson’s disease

Abnormal substantia nigra morphology in healthy individuals, viewed with transcranial ultrasound, is a significant risk factor for Parkinson’s disease. However, little is known about the functional consequences of this abnormality (termed ‘hyperechogenicity’) on movement. The aim of the current study was to investigate hand function in healthy older adults with (SN+) and without (SN?) substantia nigra hyperechogenicity during object manipulation. We hypothesised that SN+ subjects would exhibit increased grip force and a slower rate of force application compared to SN? subjects. Twenty-six healthy older adults (8 SN+ aged 58 ± 8 years, 18 SN? aged 57 ± 6 years) were asked to grip and lift a light-weight object with the dominant hand. Horizontal grip force, vertical lift force, acceleration, and first dorsal interosseus EMG were recorded during three trials. During the first trial, SN+ subjects exhibited a longer period between grip onset and lift onset (i.e. preload duration; 0.27 ± 0.25 s) than SN? subjects (0.13 ± 0.08 s; P = 0.046). They also exerted a greater downward force prior to lift off (?0.54 ± 0.42 N vs. ?0.21 ± 0.12 N; P = 0.005) and used a greater grip force to lift the object (19.5 ± 7.0 N vs. 14.0 ± 4.3 N; P = 0.022) than SN? subjects. No between group differences were observed in subsequent trials. SN+ subjects exhibit impaired planning for manipulation of new objects. SN+ individuals over-estimate the grip force required, despite a longer contact period prior to lifting the object. The pattern of impairment observed in SN+ subjects shares similarities with de novo Parkinson’s disease patients.     

Chocolate consumption is increased in Parkinson’s disease

Clinical observations in Parkinson’s disease (PD) patients suggested an increased chocolate consumption. Chocolate contains high contents of various biogenic amines potentially influencing brain monoamine metabolism. 498 PD patients and their partners were evaluated by a structured self-questionnaire asking for consumption of chocolate and non-chocolate sweets, changes in chocolate consumption during the disease course, and depressive symptoms. Questionnaires from 274 patients (55 %) and 234 controls were eligible for further analysis. Consumption of chocolate was significantly higher in PD patients compared to controls, while consumption of non-chocolate sweets was similar in both groups. Our study suggests that chocolate consumption is increased in PD independent of concomitant depressive symptoms measured by BDI-1. Although reasons for increased chocolate consumption in PD remain elusive, it may hypothetically be a consequence of the high content of various biogenic amines and/or caffeine analogues with potential antiparkinsonian effects.     

Detection of passive movement in lower limb joints is impaired in individuals with Parkinson’s disease

ObjectiveSensory information is crucial when performing daily activities, and Parkinson’s disease may diminish sensitivity to sensory cues. This study aimed to examine the detection threshold of passive motion of knee and ankle joints in individuals with Parkinson’s disease.MethodsEighteen individuals in the early stages of idiopathic Parkinson’s disease (age: 62.7 ± 7.3 years) and 18 healthy matched controls (age: 62.5 ± 7.1 years) first performed a simple reaction time test. Participants were asked to perform ten trials, during which they had to watch a square on a screen and press a button as quickly as possible when the square lit up. Thereafter, the participants were tested for their detection threshold of passive motion of their lower limb joints. Participants were seated in a specially designed chair and their knee or ankle joint was passively moved at a velocity of 0.5º/s. Participants kept their eyes closed and were instructed to press a button as quickly as possible when any joint motion was detected.ResultsIndividuals with Parkinson’s disease needed more time to perform the reaction time test than did the control participants. Individuals with Parkinson’s disease also needed larger angular displacement, even when reaction time was used as a covariate measure, to detect any passive motion, in both knee (0.70º ± 0.20º) and ankle (1.03º ± 0.23º) joints than did the control participants [(0.57º ± 0.20º) and (0.84º ± 0.27º), respectively].ConclusionImpaired joint proprioception can be observed in the early stages of Parkinson’s disease, which may compromise the use of proprioception cues from lower limbs.     

Depression in Parkinson’s disease

Among the recently well appreciated non-motor symptoms in Parkinson’s disease (PD), depression plays a prominent role due to its frequency and impact on quality of life. However, depression may be confounded by motor symptoms, especially akinesia and other non-motor symptoms such as apathy, anxiety and dementia. Data on specific diagnostic tools or treatment for depressive symptoms in PD patients are still sparse. Here we summarize an expert opinion based on available data and clinical experience.

     

Neuroimaging in Parkinson’s disease

In this review, the potential role of positron emission tomography and single photon emission computed tomography as biological markers for diagnosing and following the progression of Parkinson’s disease (PD) is discussed. Their value for assessing the efficacy of putative neuroprotective agents in PD and for revealing the pharmacological changes underlying the symptomatology and complications of this disorder is also considered. It is concluded that in the future functional imaging will provide a valuable adjunct to clinical assessment when judging the efficacy of putative neuroprotective approaches to PD.     

Depression in Parkinson’s disease

Depression is common in Parkinson’s disease (PD), and its identification and treatment are critically important in disease management. Despite depression’s high prevalence and major impact on patient quality of life, questions remain regarding its epidemiology and preferred treatment. The authors of this paper summarize available information on the epidemiology of depression in PD, review treatment options, and discuss possible interactions between antidepressants and other agents. This information may help guide clinical treatment and define the need for further studies.     

Depression in Parkinson’s disease

Abstract Objectives The pathophysiology of depression and anxiety in Parkinson's disease remains obscure. We aimed to compare the fractional anisotropy (FA) values of Parkinson's disease (PD) patients with and without depression to investigate the nature of depression in PD. Methods Twenty-eight patients were divided into two groups: those with depression and those without. Diagnosis of depression was made using the DSM-IV criteria. Patients in the two groups were matched for Hoehn Yahr stage. Results There were significant reductions in FA values in the bilateral frontal ROIs possibly representing anterior cingulate bundles. Conclusions The anterior cingulate bundles play an important role in depression in PD, and some aspects of depression in PD have pathological processes in common with de novo depression.     

Cancer in Parkinson’s disease

INTRODUCTIONWe examined the prevalence of cancer in patients with Parkinson’s disease (PD) and controls evaluated at the Mayo Clinic in Jacksonville, Florida, between 2003 and 2014.METHODSWe retrospectively collected information regarding cancer diagnoses and diagnosis of PD from 971 unrelated PD patients and 478 controls, and all were white. For PD patients, we examined cancers diagnosed before and after PD diagnosis separately in addition to considering all cancer diagnoses.RESULTSTwenty different cancers were identified. In PD patients, the most common types of cancer were skin cancer (17.3% overall; 10.6% before PD), followed by nonmelanoma skin cancer (16.0% overall; 9.7% before PD), prostate cancer in men (12.8% overall; 9.2% before PD), breast cancer in women (10.6% overall; 6.3% before PD), and melanoma (2.4% overall; 1.1% before PD). Compared to controls, a significantly lower frequency of nonmelanoma skin cancer (odds ratio [OR]: 0.62, P = 0.0024) and any skin cancer (OR: 0.57, P = 0.0002) was observed in PD patients. These differences were greater when considering only cases with cancers that occurred before PD diagnosis (OR: 0.49, P < 0.0001; OR: 0.45, P < 0.0001, respectively), and there was a lower frequency of melanoma and any cancer preceding PD diagnosis compared to controls (OR: 0.31, P = 0.003; OR: 0.36, P < 0.0001). There was no evidence of a frequency difference for any other cancer.CONCLUSIONSPD patients had a lower frequency of skin cancers or any cancer prior to PD diagnosis compared to controls, suggesting that cancer may have a protective effect on PD risk.     

Fatigue in Parkinson’s disease

Abstract. Fatigue is a recognized problem in Parkinsons disease and other clinical conditions. We characterized this symptom in 19 patients and 19 age- and sex-matched controls, using the Multidimensional Fatigue Inventory (MFI) and the Geriatric Depression Scale. Fatigue may be an independent symptom in Parkinsons disease, frequently associated with depression. Our analysis showed the usefulness of the MFI in discriminating between different dimensions of fatigue for a better therapeutic approach.     

Which memory system is impaired first in Alzheimer's disease?

Diagnosis of Alzheimer's disease (AD) in its earliest stages becomes increasingly important as disease modifying agents are being developed. In this area of research, many clinical and neuroimaging studies focus on markers of hippocampal dysfunction. However, during the "transentorhinal stage" of AD, neurofibrillary tangles (NFT), related to tau protein pathology, develop in the anterior subhippocampal (perirhinal/entorhinal) cortex before the hippocampus. NFT are tightly correlated with clinical symptoms. Therefore, an accurate understanding of the behavioral correlate of transentorhinal dysfunction could critically contribute to the early diagnosis of the disease. Recent findings from studies in animals and human brain-damaged patients suggest that the anterior subhippocampal region, functionally integrated into an anterior mesiotemporal network, is involved in object based context-free memory. In this article, we evaluate the hypothesis according to which tau deposition in the anterior subhippocampal region during the earliest stages of the most common form of AD, with predominant MTL dysfunction, will lead to dysfunction of neural networks implicated in context-free memory. We challenge the view that impaired episodic memory is the hallmark of early AD. Instead, a model that integrates the localization and temporal sequence of NFT within the mesial temporal lobe (MTL) is proposed. Paralleling the development of NFT in anterior subhippocampal areas, impaired context-free, object-based, memory could be the first detectable sign in AD. In a subsequent, "hippocampal" stage, context-rich, episodic and spatial memory, becomes altered as well. The question as to the "episodic" nature of "episodic memory tasks" is also addressed.     

Parkinson’s disease is not associated with gastrointestinal myenteric ganglion neuron loss

Gastrointestinal dysfunction is a prominent non-motor feature of Parkinson’s disease (PD) that contributes directly to the morbidity of patients, complicates management of motor symptoms, and may herald incipient PD in patients without motor disability. Although PD has traditionally been considered a disease of dopaminergic neurons in the substantia nigra, analyses of gastrointestinal samples from PD patients have consistently revealed pathology in the enteric nervous system. The relationship of PD pathology to GI dysmotility is poorly understood, and this lack of understanding has led to limited success in developing treatments for PD-related GI symptoms. We have quantitatively compared myenteric neuron density and relative abundance of NO, VIP, and catecholamine neurons between patients with PD and control individuals along the length of the GI tract. In addition, we have examined the frequency of GI α-synuclein neuritic pathology and its co-localization with the same neuronal markers. We have included a comparison with a small population of patients with incidental Lewy bodies found at autopsy. These data indicate that there is no neuronal loss in the myenteric plexus in PD. Lewy body pathology parallels parasympathetic autonomic input from the dorsal motor nucleus of the vagus, not the distribution of extrinsic sympathetic input or intrinsic enteric neurons, and is only rarely co-localized with tyrosine hydroxylase. These data provide a critical background to which further analyses of the effect of PD on the GI tract may be compared and suggest that neuropathology in myenteric neurons is unlikely to be a causative factor in PD-related GI dysmotility.     

Pallidotomy does not ameliorate abnormal intracortical inhibition in Parkinson’s disease

Motor cortex excitability was assessed in 12 patients with Parkinson’s disease (PD) using transcranial magnetic stimulation. Patients were studied when mobile and medicated (“ON”) and when immobile after medication withdrawal (“OFF”). Results were compared to eight age-matched and 11 young controls. Cortical excitability was assessed by measurement of resting motor threshold (RMT), intracortical inhibition and cortical silent period duration. In five patients, the studies included assessments following pallidotomy. Cortical excitability was abnormal in patients with PD with reduced RMT in “ON” and “OFF” states, and less effective intracortical inhibition. Pallidotomy did not affect cortical excitability in either “ON” or “OFF” states, indicating that enhanced motor cortex excitability in patients with PD is unaffected by pallidotomy despite clinical improvement in motor scores.     

Sleep disturbances in Parkinson’s disease

Disorders of sleep and daytime alertness are frequent in Parkinson’s disease patients and arise from a number of diverse factors. The most common complaint of night-time sleep disturbance in Parkinson’s disease is sleep fragmentation. Sleep fragmentation can be associated with recurrent parkinsonian symptoms, the effect of medications, concomitant medical disorders such as nocturia, or psychiatric disorders such as depression or anxiety. Likewise, nocturnal sleep disturbance may arise from sleep apnea, periodic limb movements of sleep, or rapid eye movement (REM) sleep behavior disorder. Nocturnal sleep deprivation may lead to excessive daytime sleepiness. Other potential sources of daytime sleepiness include the effects of medications or disruption of central sleep mechanisms due to the pathologic processes of Parkinson’s disease itself. Diagnosis of sleep disturbances and daytime sleepiness requires a direct interview of the patient and the caregiver, and may involve consultation with the sleep specialist or medical physician. Treatment is aimed toward improving night-time sleep and daytime drowsiness by addressing the causative factors.     

Gastrointestinal dysfunction in Parkinson’s disease

Journal of Neurology - Gastrointestinal (GI) dysfunction is prevalent in Parkinson’s disease (PD). Symptoms are evident throughout the disease course, affect the length of the GI tract and...     

Musculoskeletal problems in Parkinson’s disease

Musculoskeletal problems are very common and are an important contributor to poor quality of life in Parkinson’s disease. However, they are under-appreciated, under-evaluated, and under-treated. This paper will address the prevalence of musculoskeletal problems in Parkinson’s disease, and review the clinical characteristics of selected musculoskeletal conditions, such as shoulder problems, low back pain, arthritis, deformity, osteoporosis and fracture. Finally, a variety of treatment modalities for musculoskeletal problems will be reviewed.