Submitted Successfully!
Thank you for your contribution! You can also upload a video entry related to this topic through the link below: https://encyclopedia.pub/user/video_add?id=23659
Check Note
2000/2000
Ver. Summary Created by Modification Content Size Created at Operation
1 -- 1931 2022-06-01 11:33:54 |
2 format correct Meta information modification 1931 2022-06-06 09:20:58 | |
3 References check OK. Meta information modification 1931 2022-06-06 13:36:57 |
Freezing of Gait
Edit
Upload a video

Parkinson Disease (PD) primarily affects older adults. It is the second-most common neurodegenerative disease after Alzheimer’s disease. Freezing of Gait (FoG) is a symptom present in approximately 80% of advanced-stage PD’s patients. FoG episodes alter the continuity of gait, and may be the cause of falls that can lead to injuries and even death. The recent advances in the development of hardware and software systems for the monitoring, stimulus, or rehabilitation of patients with FoG has been of great interest to researchers because detection and minimization of the duration of FoG events is an important factor in improving the quality of life. 

Parkinson Disease freezing of gait
Information
Subjects: Neurosciences
View Times: 137
Entry Collection: Neurodegeneration
Revisions: 3 times (View History)
Update Date: 06 Jun 2022
Table of Contents

    1. Introduction

    Parkinson Disease (PD) is the second-most common neurodegenerative disease, after Alzheimer’s disease, among the elderly. At present, there are 10 million people patients with PD worldwide [1][2]. Statistics show that the prevalence of PD is higher in Europe, North America, and South America in comparison with Africa and Asia, with an incidence of 13.4 per 100,000 people per year [2][3][4]. The causes of PD remain unknown, but some studies have attributed it to environmental exposure factors and genetic factors [5]. Moreover, sex and ethnicity have been shown to be influencing factors, with the male:female ratio of patients with PD being approximately 3:2 [3]. Age remains the main risk factor for the development of PD, and the prevalence and incidence of the disease increases exponentially after 60 years of age [3][6]. This trend has important implications for public health, since greater longevity, which is the trend in most countries, is expected to increase the number of people with PD by 50% in 2030 [3][7].
    Parkinson disease is associated with non-motor and motor symptoms. Non-motor symptoms include dementia, depression, psychotic characteristics, autonomic dysfunction, oculomotor abnormalities, and olfactory and visual impairments. The motor symptoms include tremor, stiffness, bradykinesia, postural instability, festination, decreased blink frequency, blepharospasm, and Freezing of Gait (FoG) [8]. Medical evaluation of non-motor symptoms is usually performed by a neuropsychologist, while motor symptoms are diagnosed by a neurologist on the basis of medical history, a review of signs and symptoms, and physical and neurological examinations.
    The FoG symptom is related on bradykinesia, rigidity, tremor, and postural instability, together with perceptive malfunction and frontal executive dysfunction [8][9]. It presents as a reduction in the forward progression of the feet, despite the person’s intention to walk [10][11][12]. This symptom occurs in 21–27% of patients in the early stages of PD [13][14], and this percentage continues to increase during PD evolution, with the symptom appearing in 80% of patients more than 17 years from the initial diagnosis. FoG may be the cause of falls that can lead to injuries and even death [15].
    FoG has its origin in the brain, specifically in the mesencephalic locomotive region (MLR), where the performance of the pedunculopontinal nucleus (PPN) diminishes their connections with basal ganglia. Similarly, the region of the brain stem is related to the condition of freezing, which has been validated with Functional Magnetic Resonance Imaging (FMRI) and ElectroEncephaloGraphy (EEG) data. FoG is no longer considered a strictly motor symptom but is a part of cognitive impairments that originate from areas of the brain that allow the body to be able to walk without hindrance [16][17].
    FoG does not respond to existing drugs, and neurorehabilitation exercises tend to be repetitive and tiring. Several invasive methods, such as deep brain stimulation (DBS) [18] or vagus nerve invasive stimulation (VNS) [19], have been developed for the treatment of FoG, but they are expensive, do not guarantee elimination of freezing, and may increase other symptoms. Patients with an episode of FoG can resume walking after receiving external stimulation, and non-invasive methods such as visual, vibratory, and tactile stimulation devices can provide such stimulation at a relatively low cost and without health risks.

    2. Brain Activity during a FoG Episode

    To understand the parameters to be measured by those systems, it was necessary to analyze the brain motor activity involved in PD during episodes FoG. Brain activity occurs when the brain generates electrical impulses known as action potentials, which travel through neurons. Electrical impulses contain information that travels from neuron to neuron making use of hundreds of thousands of them to get transported and perform a specific function, any alteration provokes a change in their contiguous connections [20]. When the brain generates an impulse to move a muscle, the impulse passes through the basal ganglia that help to smooth muscle movements and coordinate changes in posture, such as the gait.
    A statistical parametric mapping analysis applied to healthy subjects during the gait revealed that the following areas were activated in their brain activity: supplementary motor, medial primary sensorimotor, striatum, cerebellar vermis, and visual cortex. These results indicate that the cerebral cortexes that control: motor functions, visual cortex, basal ganglia, and cerebellum, may be involved in the bipedal locomotor activities in humans [21]. When a person has PD, there is a degeneration in the cells of the basal ganglia that causes a decrease production of dopamine and reduces connectivity between nerve cells and muscles [22].
    Encephalography was used to understand the bioelectrical connections of those who suffer from PD and present FoG. The Figure 1 shows the electrode arranged system in a 10–20 scheme. This scheme was used to analyze brain activity utilizing electrodes on the hair scalp in FOG patients. The presence of FOG episodes generates different levels of energy in the brain waves of the parietal zone (P4), suggesting that this zone has been deeply affected by the disease. Measurements of P4 and the central zone (Cz) are the features that most contributed to the analysis for detecting FoG transition in PD patients [23][24][25].
    Figure 1. The international 10–20 system seen above the head. A = Ear lobe, C = central, Pg = nasopharyngeal, P = parietal, F = frontal, Fp = frontal polar, O = occipital [23].
    When the fronto-parietal zone is affected, there is a decrease in executive functions (including cognitive skills), aggravating the problems in people with FoG, who also have failures in their visuospatial network. Some authors such as Amboni et al. compared the progression of cognitive impairment in 26 Parkinsonian patients with FoG (FoG+) and without FoG (FoG-) over a follow-up period of 2 years, finding that FoG+ patients had a faster progression of cognitive impairment, while in FoG- patients, cognitive alteration remained unchanged during this period [26]. Another technique used is magnetic resonance imaging, where it was concluded that FoG+ patients present predominantly frontal-executive dysfunction compared to FoG- patients [27]. At the same time, the right hemisphere of the brain looked more affected in FoG+ patients, which would make sense due to the great influence of this hemisphere on visuospatial abilities [28].
    At a neuronal level, the important role of the pedunculopontine nucleus (PPN) located in the MLR, likely play a crucial role in the appearance of axial symptoms in PD. The aim was to activate the remaining PPN cholinergic neurons to improve axial symptoms including FoG and balance deficits in PD patients. Its importance resides in that it is the main center of the mesencephalic locomotor region and controls the initiation, maintenance, and modulation of posture and gait [29]. The presence of FoG was associated with altered functional connectivity between the PPN and the corticopontine-cerebellar pathways (in the bilateral cerebellum and in the pons) and visual temporal areas compared to healthy subjects, additionally marked abnormalities in white matter extending to motor, sensory and cognitive regions [30].
    A significant number of PD patients increasingly rely on visual and auditory signals to control the locomotion [31], which creates a problem because visual impairments have been correlated with gait disturbance, deficits in visual attention, memory, and visuospatial abilities [32][33]. Lenka et al. managed to establish that a reduction in inter-hemispheric connectivity between bilateral parietal operculum, somatosensory cortex, and primary auditory areas are correlated with FoG [34]. The hearing deficiency was tested with the Rey Auditory-Verbal Learning Test (RAVLT) [35]. This shows a decline in vision and hearing in those who have episodes of FoG.

    3. Motor Characteristics during FoG

    Although FoG originates in the brain, it manifests as an irregularity in gait. As PD progresses, this irregularity becomes more frequent and disabling for the patient, which results in longer FoG episodes. These episodes can present as complete akinesia when the patient is not medicated (off state, FoG-). When the patient is medicated (on state, FoG+), the FoG episodes are shorter and rarely become akinetic. FoG+ patients present deficiencies during motor initiation that are not present in FoG- patients or healthy people. Additionally, FoG+ patients are slower to initiate motor activity, and in particular, to respond to the signal from the brain to initiate walking. Moreover, these patients require more time to react to stop walking in comparison with FoG- patients and healthy people [36][37].
    In muscular-system analyses, FoG is characterized by co-contraction of agonist and antagonist muscles [10][38]. The patients show changes in the pressure of the foot and the behavior of the distance between the steps, as these become shorter compared to those in a slow walk. The frequency of this type of walk is between 4 and 5 Hz [39][40]. Patients with FoG respond to classic auditory, visual, and tactile stimulations [41]. However, these stimulations cannot effectively induce the muscular system to react to bradykinesia [42], which results in alterations in symmetry, rhythm, and bilateral coordination in the patients’ walk with FoG [43][44].
    On the other hand, dysfunction in cognitive networks and interictal gait changes may contribute to Parkinson’s disease patients presenting with episodes of FoG. An analysis of patients performing two activities at the same time is presented in one study [45], and the FoG+ patients showed a shorter stride length and slower speed, except during postural balance, in that study. In contrast, during the turn, both groups (FoG+ and FoG-) showed a slower turning speed in the tests involving double activities compared to the findings for the single-task condition.
    Analyses of the FoG to date have focused on the lower extremities. However, some studies have revealed determining characteristics in the upper limbs, specifically in the wrists, which show FoG earlier than the legs and feet [36][46]. These studies revealed that FoG can be detected using wrist motion and machine learning models with an FoG hit rate of 0.9 and specificity between 0.66–0.8. Additionally, the standard deviation, acceleration, and rotation were analyzed, in addition to the power between the frequency ranges of 0 to 1 Hz, 5 to 6 Hz, and in the intervals of 0 to 4 Hz, 5 to 8 Hz, and 9 to 12 Hz [46][47].
    Some studies have focused on analyzing single-leg posture using portable inertial sensors and performing statistical calculations. The results of these studies indicate that the acceleration peak of the medial-lateral trunk in FoG+ and FoG- patients was significantly lower than that of healthy patients (p < 0.05), and the equilibrium was longer in FoG- patients in comparison with that in FoG+ patients [48].
    Various studies have revealed significant differences in the duration of the balanced phase of the feet during walking in FoG+ and FoG- patients and healthy subjects. This reduction in the duration of equilibrium is generally associated with an increased risk of falls [49][50][51][52][53].
    In one study [54], the two main reasons for falls in PD patients were identified as FoG and impaired balance. This argument is supported by other investigations [55][56][57], which validated the relationship between FoG and falls. These falls are consequences of FoG and appear from the early stages of the disease [58][59][60]. Additionally, falls could be disabling and can deteriorate the quality of life of patients [61][62][63][64]. These falls can occur in multiple directions and are associated with motor symptoms but also with non-motor symptoms, such as mood and cognitive disorders [65]. When the FoG occurs, the center of gravity continues to advance due to the effect of inertia, but the feet stop moving body while the body continues forward, which causes the majority of falls. Therefore, to initiate the walk, FoG+ patients require wider movements than FoG- patients [17].

    References

    1. Dauer, W.; Przedborski, S. Parkinson’s Disease. Neuron 2003, 39, 889–909.
    2. Kalia, L.; Lang, A. Parkinson’s disease. Lancet 2015, 386, 896–912.
    3. Pringsheim, T.; Jette, N.; Frolkis, A.; Steeves, T. The prevalence of Parkinson’s disease: A systematic review and meta-analysis. Mov. Disord. 2014, 29, 1583–1590.
    4. Van Den Eeden, S. Incidence of Parkinson’s Disease: Variation by Age, Gender, and Race/Ethnicity. Am. J. Epidemiol. 2003, 157, 1015–1022.
    5. Lee, A.; Gilbert, R. Epidemiology of Parkinson Disease. Neurol. Clin. 2016, 34, 955–965.
    6. Driver, J.; Logroscino, G.; Gaziano, J.; Kurth, T. Incidence and remaining lifetime risk of Parkinson disease in advanced age. Neurology 2009, 72, 432–438.
    7. Calabrese, V.; Dorsey, E.; Constantinescu, R.; Thompson, J.; Biglan, K.; Holloway, R.; Kieburtz, K.; Marshall, F.; Ravina, B.; Schifitto, G.; et al. Projected Number of People With Parkinson Disease in the Most Populous Nations, 2005 Through 2030. Neurology 2007, 69, 223–224.
    8. Gelb, D.; Oliver, E.; Gilman, S. Diagnostic Criteria for Parkinson Disease. Arch. Neurol. 1999, 56, 33.
    9. Heremans, E.; Nieuwboer, A.; Vercruysse, S. Freezing of Gait in Parkinson’s Disease: Where Are We Now? Curr. Neurol. Neurosci. Rep. 2013, 13, 350.
    10. Nutt, J.; Bloem, B.; Giladi, N.; Hallett, M.; Horak, F.; Nieuwboer, A. Freezing of gait: Moving forward on a mysterious clinical phenomenon. Lancet Neurol. 2011, 10, 734–744.
    11. Rahman, S.; Griffin, H.; Quinn, N.; Jahanshahi, M. Quality of life in Parkinson’s disease: The relative importance of the symptoms. Mov. Disord. 2008, 23, 1428–1434.
    12. Tan, D.; Danoudis, M.; McGinley, J.; Morris, M. Relationships between motor aspects of gait impairments and activity limitations in people with Parkinson’s disease: A systematic review. Park. Relat. Disord. 2012, 18, 117–124.
    13. Giladi, N.; McDermott, M.; Fahn, S.; Przedborski, S.; Jankovic, J.; Stern, M.; Tanner, C. Freezing of gait in PD: Prospective assessment in the DATATOP cohort. Neurology 2001, 56, 1712–1721.
    14. Tan, D.; McGinley, J.; Danoudis, M.; Iansek, R.; Morris, M. Freezing of Gait and Activity Limitations in People With Parkinson’s Disease. Arch. Phys. Med. Rehabil. 2011, 92, 1159–1165.
    15. Hely, M.; Morris, J.; Reid, W.; Trafficante, R. Sydney multicenter study of Parkinson’s disease: Non-L-dopa-responsive problems dominate at 15 years. Mov. Disord. 2005, 20, 190–199.
    16. Peterson, D.; Pickett, K.; Duncan, R.; Perlmutter, J.; Earhart, G. Gait-Related Brain Activity in People with Parkinson Disease with Freezing of Gait. PLoS ONE 2014, 9, e90634.
    17. Peterson, D.; Fling, B.; Mancini, M.; Cohen, R.; Nutt, J.; Horak, F. Dual-task interference and brain structural connectivity in people with Parkinson’s disease who freeze. J. Neurol. Neurosurg. Psychiatry 2014, 86, 786–792.
    18. Perlmutter, J.S.; Mink, J.W. Deep brain stimulation. Annu. Rev. Neurosci. 2006, 29, 229–257.
    19. George, M.S.; Sackeim, H.A.; Rush, A.J.; Marangell, L.B.; Nahas, Z.; Husain, M.M.; Lisanby, S.; Burt, T.; Goldman, J.; Ballenger, J.C. Vagus nerve stimulation: A new tool for brain research and therapy. Biol. Psychiatry 2000, 47, 287–295.
    20. Rattay, F. The basic mechanism for the electrical stimulation of the nervous system. Neuroscience 1999, 89, 335–346.
    21. Fukuyama, H.; Ouchi, Y.; Matsuzaki, S.; Nagahama, Y.; Yamauchi, H.; Ogawa, M.; Kimura, J.; Shibasaki, H. Brain functional activity during gait in normal subjects: A SPECT study. Neurosci. Lett. 1997, 228, 183–186.
    22. Rivlin-Etzion, M.; Marmor, O.; Saban, G.; Rosin, B.; Haber, S.N.; Vaadia, E.; Prut, Y.; Bergman, H. Low-Pass filter properties of basal ganglia–cortical–muscle loops in the normal and MPTP primate model of Parkinsonism. J. Neurosci. 2008, 28, 633–649.
    23. Bhavsar, R.; Sun, Y.; Helian, N.; Davey, N.; Mayor, D.; Steffert, T. The correlation between EEG signals as measured in different positions on scalp varying with distance. Procedia Comput. Sci. 2018, 123, 92–97.
    24. Handojoseno, M.A.; Shine, J.M.; Nguyen, T.N.; Tran, Y.; Lewis, S.J.G.; Nguyen, H.T. The detection of Freezing of Gait in Parkinson’s disease patients using EEG signals based on Wavelet decomposition. In Proceedings of the 2012 Annual International Conference of the IEEE Engineering in Medicine and Biology Society, San Diego, CA, USA, 28 August–1 September 2012; pp. 69–72.
    25. Handojoseno, A.M.A.; Shine, J.M.; Nguyen, T.N.; Tran, Y.; Lewis, S.J.G.; Nguyen, H.T. Using EEG spatial correlation, cross frequency energy, and wavelet coefficients for the prediction of Freezing of Gait in Parkinson’s Disease patients. In Proceedings of the 2013 35th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC), Osaka, Japan, 3–7 July 2013; pp. 4263–4266.
    26. Amboni, M.; Barone, P.; Picillo, M.; Cozzolino, A.; Longo, K.; Erro, R.; Iavarone, A. A two-year follow-up study of executive dysfunctions in Parkinsonian patients with freezing of gait at on-state. Mov. Disord. 2010, 25, 800–802.
    27. Tessitore, A.; Amboni, M.; Esposito, F.; Russo, A.; Picillo, M.; Marcuccio, L.; Pellecchia, M.; Vitale, C.; Cirillo, M.; Tedeschi, G.; et al. Resting-state brain connectivity in patients with Parkinson’s disease and freezing of gait. Park. Relat. Disord. 2012, 18, 781–787.
    28. Almeida, Q.; Lebold, C. Freezing of gait in Parkinson’s disease: A perceptual cause for a motor impairment? J. Neurol. Neurosurg. Psychiatry 2009, 81, 513–518.
    29. Grabli, D.; Karachi, C.; Welter, M.; Lau, B.; Hirsch, E.; Vidailhet, M.; François, C. Normal and pathological gait: What we learn from Parkinson’s disease. J. Neurol. Neurosurg. Psychiatry 2012, 83, 979–985.
    30. Wang, M.; Jiang, S.; Yuan, Y.; Zhang, L.; Ding, J.; Wang, J.; Zhang, J.; Zhang, K.; Wang, J. Alterations of functional and structural connectivity of freezing of gait in Parkinson’s disease. J. Neurol. 2016, 263, 1583–1592.
    31. Sage, M.; Almeida, Q. A positive influence of vision on motor symptoms during sensory attention focused exercise for Parkinson’s disease. Mov. Disord. 2010, 25, 64–69.
    32. Uc, E.; Rizzo, M.; Anderson, S.; Qian, S.; Rodnitzky, R.; Dawson, J. Visual dysfunction in Parkinson disease without dementia. Neurology 2005, 65, 1907–1913.
    33. Yogev-Seligmann, G.; Hausdorff, J.; Giladi, N. The role of executive function and attention in gait. Mov. Disord. 2008, 23, 329–342.
    34. Lenka, A.; Naduthota, R.; Jha, M.; Panda, R.; Prajapati, A.; Jhunjhunwala, K.; Saini, J.; Yadav, R.; Bharath, R.; Pal, P. Freezing of gait in Parkinson’s disease is associated with altered functional brain connectivity. Park. Relat. Disord. 2016, 24, 100–106.
    35. Ricciardi, L.; Bloem, B.R.; Snijders, A.H.; Daniele, A.; Quaranta, D.; Bentivoglio, A.R.; Fasano, A. Freezing of gait in Parkinson’s disease: The paradoxical interplay between gait and cognition. Park. Relat. Disord. 2014, 20, 824–829.
    36. Tripoliti, E.; Tzallas, A.; Tsipouras, M.; Rigas, G.; Bougia, P.; Leontiou, M.; Konitsiotis, S.; Chondrogiorgi, M.; Tsouli, S.; Fotiadis, D. Automatic detection of freezing of gait events in patients with Parkinson’s disease. Comput. Methods Programs Biomed. 2013, 110, 12–26.
    37. Schaafsma, J.; Balash, Y.; Gurevich, T.; Bartels, A.; Hausdorff, J.; Giladi, N. Characterization of freezing of gait subtypes and the response of each to levodopa in Parkinson’s disease. Eur. J. Neurol. 2003, 10, 391–398.
    38. Dietz, M.; Goetz, C.; Stebbins, G. Evaluation of a modified inverted walking stick as a treatment for Parkinsonian freezing episodes. Mov. Disord. 1990, 5, 243–247.
    39. Okuma, Y. Freezing of gait in Parkinson’s disease. J. Neurol. 2006, 253, vii27–vii32.
    40. Freeman, J.S.; Cody, F.W.; Schady, W. The influence of external timing cues upon the rhythm of voluntary movements in Parkinsonś disease. J. Neurol. Neurosurg. Psychiatry 1993, 56, 1078–1084.
    41. Rutz, D.G.; Benninger, D.H. Physical therapy for freezing of gait and gait impairments in Parkinson disease: A systematic review. PM&R 2020, 12, 1140–1156.
    42. Bartels, A.; Balash, Y.; Gurevich, T.; Schaafsma, J.; Hausdorff, J.; Giladi, N. Relationship between freezing of gait (FOG) and other features of Parkinson’s: FOG is not correlated with bradykinesia. J. Clin. Neurosci. 2003, 10, 584–588.
    43. Hausdorff, J.; Schaafsma, J.; Balash, Y.; Bartels, A.; Gurevich, T.; Giladi, N. Impaired regulation of stride variability in Parkinson’s disease subjects with freezing of gait. Exp. Brain Res. 2003, 149, 187–194.
    44. Plotnik, M.; Giladi, N.; Hausdorff, J. Bilateral coordination of walking and freezing of gait in Parkinson’s disease. Eur. J. Neurosci. 2008, 27, 1999–2006.
    45. Fortaleza, A.d.; Mancini, M.; Carlson-Kuhta, P.; King, L.; Nutt, J.; Chagas, E.; Freitas, I.; Horak, F. Dual task interference on postural sway, postural transitions and gait in people with Parkinson’s disease and freezing of gait. Gait Posture 2017, 56, 76–81.
    46. Mazilu, S.; Blanke, U.; Calatroni, A.; Gazit, E.; Hausdorff, J.; Tröster, G. The role of wrist-mounted inertial sensors in detecting gait freeze episodes in Parkinson’s disease. Pervasive Mob. Comput. 2016, 33, 1–16.
    47. Daneault, J.F.; Vergara-Diaz, G.; Parisi, F.; Admati, C.; Alfonso, C.; Bertoli, M.; Bonizzoni, E.; Carvalho, G.F.; Costante, G.; Fabara, E.E.; et al. Accelerometer data collected with a minimum set of wearable sensors from subjects with Parkinson’s disease. Sci. Data 2021, 8, 48.
    48. Bonora, G.; Mancini, M.; Carpinella, I.; Chiari, L.; Ferrarin, M.; Nutt, J.; Horak, F. Investigation of Anticipatory Postural Adjustments during One-Leg Stance Using Inertial Sensors: Evidence from Subjects with Parkinsonism. Front. Neurol. 2017, 8, 361.
    49. Jacobs, J. Multiple balance tests improve the assessment of postural stability in subjects with Parkinson’s disease. J. Neurol. Neurosurg. Psychiatry 2005, 77, 322–326.
    50. Smithson, F.; Morris, M.; Iansek, R. Performance on Clinical Tests of Balance in Parkinson’s Disease. Phys. Ther. 1998, 78, 577–592.
    51. Morris, M.; Iansek, R.; Smithson, F.; Huxham, F. Postural instability in Parkinson’s disease: A comparison with and without a concurrent task. Gait Posture 2000, 12, 205–216.
    52. Adkin, A.; Frank, J.; Jog, M. Fear of falling and postural control in Parkinson’s disease. Mov. Disord. 2003, 18, 496–502.
    53. Vellas, B.; Wayne, S.; Romero, L.; Baumgartner, R.; Rubenstein, L.; Garry, P. One-Leg Balance Is an Important Predictor of Injurious Falls in Older Persons. J. Am. Geriatr. Soc. 1997, 45, 735–738.
    54. Youn, J.; Okuma, Y.; Hwang, M.; Kim, D.; Cho, J. Falling Direction can Predict the Mechanism of Recurrent Falls in Advanced Parkinson’s Disease. Sci. Rep. 2017, 7, 3921.
    55. Kerr, G.; Worringham, C.; Cole, M.; Lacherez, P.; Wood, J.; Silburn, P. Predictors of future falls in Parkinson disease. Neurology 2010, 75, 116–124.
    56. Matinolli, M.; Korpelainen, J.; Sotaniemi, K.; Myllylä, V.; Korpelainen, R. Recurrent falls and mortality in Parkinson’s disease: A prospective two-year follow-up study. Acta Neurol. Scand. 2011, 123, 193–200.
    57. Bloem, B.; Hausdorff, J.; Visser, J.; Giladi, N. Falls and freezing of gait in Parkinson’s disease: A review of two interconnected, episodic phenomena. Mov. Disord. 2004, 19, 871–884.
    58. Voss, T.; Elm, J.; Wielinski, C.; Aminoff, M.; Bandyopadhyay, D.; Chou, K.; Sudarsky, L.; Tilley, B. Fall frequency and risk assessment in early Parkinson’s disease. Park. Relat. Disord. 2012, 18, 837–841.
    59. Bloem, B.; Grimbergen, Y.; Cramer, M.; Willemsen, M.; Zwinderman, A. Prospective assessment of falls in Parkinson’s disease. J. Neurol. 2001, 248, 950–958.
    60. Lindholm, B.; Hagell, P.; Hansson, O.; Nilsson, M. Prediction of Falls and/or Near Falls in People with Mild Parkinson’s Disease. PLoS ONE 2015, 10, e0117018.
    61. Wood, B. Incidence and prediction of falls in Parkinson’s disease: A prospective multidisciplinary study. J. Neurol. Neurosurg. Psychiatry 2002, 72, 721–725.
    62. Bloem, B.; Munneke, M.; Carpenter, M.; Allum, J.; Pressley, J. The impact of comorbid disease and injuries on resource use and expenditures in parkinsonism. Neurology 2003, 61, 1023.
    63. Gazibara, T.; Pekmezovic, T.; Tepavcevic, D.K.; Svetel, M.; Tomic, A.; Stankovic, I.; Kostic, V. Health-related quality of life in patients with Parkinson’s disease: Implications for falling. Park. Relat. Disord. 2015, 21, 573–576.
    64. Walton, C.; Shine, J.; Hall, J.; O’Callaghan, C.; Mowszowski, L.; Gilat, M.; Szeto, J.; Naismith, S.; Lewis, S. The major impact of freezing of gait on quality of life in Parkinson’s disease. J. Neurol. 2002, 72, 721–725.
    65. Parihar, R.; Mahoney, J.; Verghese, J. Relationship of Gait and Cognition in the Elderly. Curr. Transl. Geriatr. Exp. Gerontol. Rep. 2013, 2, 167–173.
    More
    Information
    Subjects: Neurosciences
    Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register : , , ,
    View Times: 137
    Entry Collection: Neurodegeneration
    Revisions: 3 times (View History)
    Update Date: 06 Jun 2022
    Table of Contents
      1000/1000

      Confirm

      Are you sure you want to delete?

      Video Upload Options

      Do you have a full video?
      Cite
      If you have any further questions, please contact Encyclopedia Editorial Office.
      Clotet, R.; Huerta, M.; Barzallo, B.; Punin, C. Freezing of Gait. Encyclopedia. Available online: https://encyclopedia.pub/entry/23659 (accessed on 06 February 2023).
      Clotet R, Huerta M, Barzallo B, Punin C. Freezing of Gait. Encyclopedia. Available at: https://encyclopedia.pub/entry/23659. Accessed February 06, 2023.
      Clotet, Roger, Mónica Huerta, Boris Barzallo, Catalina Punin. "Freezing of Gait," Encyclopedia, https://encyclopedia.pub/entry/23659 (accessed February 06, 2023).
      Clotet, R., Huerta, M., Barzallo, B., & Punin, C. (2022, June 01). Freezing of Gait. In Encyclopedia. https://encyclopedia.pub/entry/23659
      Clotet, Roger, et al. ''Freezing of Gait.'' Encyclopedia. Web. 01 June, 2022.
      Top
      Feedback