Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three patients with a hypokinetic-rigid syndrome, a woman aged 69 years and two men aged 62 and 67 years, were admitted because of frequent falling. In two patients Parkinson's disease was diagnosed, the third had progressive supranuclear palsy. Balance impairment and falls typically emerge late in the course of Parkinson's disease. Falls can have dramatic physical consequences, such as (hip) fractures, and often induce a fear of additional falls which further impairs mobility and social contacts. The pathophysiology of falls in Parkinson's disease is complex and appears to result from both impaired balance regulation and commonly occurring balance disturbances (due to the shuffling gait and dyskinesias). Balance impairment often responds insufficiently to pharmacological treatment. Aspecific measures such as physical therapy, walking aids and reduction of domestic hazards can reduce the number of falls. Because patients often fail to voluntarily report their falls, physicians must actively pay attention to balance impairment in Parkinson's disease.
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PMID:[Don't let the patient with Parkinson's disease fall!]. 1022 Nov 2

Parkinson's disease (PD) is a neurodegenerative disorder caused by a progressive loss of dopaminergic neurons of the substantia nigra, resulting from an oxidative stress. The lack of dopaminergic neurons is reflected by a disturbed balance of the neural circuitry in the basal ganglia. Cannabinoids might alleviate some parkinsonian symptoms by their remarkable receptor-mediated modulatory action in the basal ganglia output nuclei. Moreover, it was recently observed that some cannabinoids are potent antioxidants that can protect neurons from death even without cannabinoid receptor activation. It seems that cannabinoids could delay or even stop progressive degeneration of brain dopaminergic systems, a process for which there is presently no prevention. In combination with currently used drugs, cannabinoids might represent, qualitatively, a new approach to the treatment of PD, making it more effective.
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PMID:Potential role of cannabinoids in Parkinson's disease. 1093 5

Postural instability is a sign of progression of Parkinson's disease (PD) and often resistant to levodopa treatment. To explore the effect of bilateral deep brain stimulation (DBS) of the subthalamic nucleus (STN) on postural stability and gait, full body gait analyses were performed without medication, OFF and ON DBS in eight PD patients and 12 healthy age-matched controls. DBS setting was changed at least 3 hours before gait analysis. To describe asymmetry most and least affected sides (MAS and LAS) were rated with the Unified Parkinson's Disease Rating Scale, motor part and quantitative gait analysis with the Vicon 612 gait analysis system. Stride length and gait velocity but not cadence improved ON DBS. The distances between the heel markers and center of mass (COM) were asymmetric and reduced OFF DBS. STN DBS increased the distances significantly and reduced asymmetry. The improvement in heel to COM distance was larger on the MAS compared with the LAS. OFF DBS knee momentum asymmetry was inversed so that LAS was more impaired than MAS. ON DBS asymmetry improved. PD patients OFF DBS place the heel too close to COM. The most affected body side has the most impaired swing and the result is a smaller knee moment on the opposite and least affected body side and an asymmetric gait pattern with disturbed balance OFF STN DBS. The asymmetry OFF DBS improved ON DBS. We suggest that DBS facilitates symmetric gait and thereby improves balance during gait.
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PMID:Improved asymmetry of gait in Parkinson's disease with DBS: gait and postural instability in Parkinson's disease treated with bilateral deep brain stimulation in the subthalamic nucleus. 1909 89

The aim of this study is to determine whether the balance problems experienced by Parkinson's disease (PD) patients may in part be due to dysfunctional processing of vestibular information, and to search for factors that may help predict the risk of falls. We evaluated the balance of 45 idiopathic PD patients and 20 healthy subjects by means of computerized dynamic posturography using sensory organization tests (SOT), rhythmic weight shift (RWS) tests and limits of stability (LOS) tests; and by the timed up-and-go (TUG) test. PD patients had poorer scores in the SOT than controls for overall balance and vestibular and visual inputs. They also performed worse in RWS and LOS tests, and were slower in performing the TUG test. Hoehn-Yahr stage did not correlate with vestibular input. Balance impairment in PD patients involves deteriorated processing of vestibular input, but this deterioration is independent of disease progression. Falls are related to PD patients' reduced limits of stability.
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PMID:A prospective study of alterations in balance among patients with Parkinson's Disease. Protocol of the postural evaluation. 1912 4

Parkinson's disease (PD) is traditionally viewed as a mainly hypodopaminergic syndrome, with symptoms resulting predominantly from loss of dopamine-producing neurons in the substantia nigra. However, while most of the cardinal motor features of PD respond well to dopaminergic therapy, many other features of the disease do not. Balance impairment and the associated risk of falling represent one of the most prominent and potentially disabling features that are typically refractory to dopaminergic treatment. Therefore, it is possible that lesions in nondopaminergic systems contribute to the pathophysiology of postural instability in PD. Such nondopaminergic lesions are well recognized, certainly in advanced stages of PD where postural instability and falls dominate the clinical presentation. However, it remains unclear which of the identified nondopaminergic lesions is specifically responsible for postural instability and balance impairment. In this review, we argue that cell loss in the locus coeruleus and a resultant central norepinephrine deficit are intimately involved in the pathophysiology of postural instability in PD. If proven to be correct, this link between defective noradrenergic neurotransmission and postural instability could have important implications for the future development of new symptomatic treatments aimed to correct postural instability and preventing falls. Studies in the next 5 years could test this hypothesis, using a battery of complementary research techniques, including advanced neuroimaging (structural, functional imaging and nuclear), neurochemical studies of cerebrospinal fluid, post-mortem clinicopathological analyses and detailed clinical balance evaluations supplemented by posturography studies.
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PMID:Postural instability in Parkinson's disease: the adrenergic hypothesis and the locus coeruleus. 1921 Feb 1

In early disease stages, it can be difficult to differentiate clinically between Parkinson's disease and the various forms of atypical parkinsonism, like multiple system atrophy or progressive supranuclear palsy. Balance impairment in the medio-lateral plane (i.e. sideways) is often seen in patients with a form of atypical parkinsonism, but not in patients with Parkinson's disease. This is reflected by the distance between the feet during gait, which is typically normal (or even narrow) in Parkinson's disease, but widened in atypical parkinsonism. Estimating this stance width depends on subjective judgement, and is difficult to quantify in clinical practice. Here, we emphasize that this medio-lateral balance impairment can also be revealed using two simple tests: (1) inability to perform tandem gait (taking one or more side steps being abnormal); and (2) self-report by patients who have lost the ability to ride a bicycle. Both tests have a good diagnostic yield in differentiating between Parkinson's disease and atypical parkinsonism, even early in the course of the disease.
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PMID:Medio-lateral balance impairment differentiates between Parkinson's disease and atypical parkinsonism. 2512 84

Impaired balance is a major contributor to falls and diminished quality of life in Parkinson's disease, yet the pathophysiology is poorly understood. Here, we assessed if patients with Parkinson's disease and severe clinical balance impairment have deficits in the intermittent and continuous control systems proposed to maintain upright stance, and furthermore, whether such deficits are potentially reversible, with the experimental therapy of pedunculopontine nucleus deep brain stimulation. Two subject groups were assessed: (i) 13 patients with Parkinson's disease and severe clinical balance impairment, implanted with pedunculopontine nucleus deep brain stimulators; and (ii) 13 healthy control subjects. Patients were assessed in the OFF medication state and blinded to two conditions; off and on pedunculopontine nucleus stimulation. Postural sway data (deviations in centre of pressure) were collected during quiet stance using posturography. Intermittent control of sway was assessed by calculating the frequency of intermittent switching behaviour (discontinuities), derived using a wavelet-based transformation of the sway time series. Continuous control of sway was assessed with a proportional-integral-derivative (PID) controller model using ballistic reaction time as a measure of feedback delay. Clinical balance impairment was assessed using the 'pull test' to rate postural reflexes and by rating attempts to arise from sitting to standing. Patients with Parkinson's disease demonstrated reduced intermittent switching of postural sway compared with healthy controls. Patients also had abnormal feedback gains in postural sway according to the PID model. Pedunculopontine nucleus stimulation improved intermittent switching of postural sway, feedback gains in the PID model and clinical balance impairment. Clinical balance impairment correlated with intermittent switching of postural sway (rho = - 0.705, P < 0.001) and feedback gains in the PID model (rho = 0.619, P = 0.011). These results suggest that dysfunctional intermittent and continuous control systems may contribute to the pathophysiology of clinical balance impairment in Parkinson's disease. Clinical balance impairment and their related control system deficits are potentially reversible, as demonstrated by their improvement with pedunculopontine nucleus deep brain stimulation.
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PMID:Balance control systems in Parkinson's disease and the impact of pedunculopontine area stimulation. 3136 48

Balance impairment is a major mechanism behind falling along with environmental hazards. Under physiological conditions, ageing leads to a progressive decline in balance control per se. Moreover, various neurological disorders further increase the risk of falls by deteriorating specific nervous system functions contributing to balance. Over the last 15 years, significant advancements in technology have provided wearable solutions for balance evaluation and the management of postural instability in patients with neurological disorders. This narrative review aims to address the topic of balance and wireless sensors in several neurological disorders, including Alzheimer's disease, Parkinson's disease, multiple sclerosis, stroke, and other neurodegenerative and acute clinical syndromes. The review discusses the physiological and pathophysiological bases of balance in neurological disorders as well as the traditional and innovative instruments currently available for balance assessment. The technical and clinical perspectives of wearable technologies, as well as current challenges in the field of teleneurology, are also examined.
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PMID:Fifteen Years of Wireless Sensors for Balance Assessment in Neurological Disorders. 3251 15