Gait variability and basal ganglia disorders: Stride-to-stride variations of gait cycle timing in parkinson's disease and Huntington's disease

1998 ◽  
Vol 13 (3) ◽  
pp. 428-437 ◽  
Author(s):  
Jeffrey M. Hausdorff ◽  
Merit E. Cudkowicz ◽  
Renée Firtion ◽  
Jeanne Y. Wei ◽  
Ary L. Goldberger
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Gait Cycle ◽  
Gait Variability ◽  
Basal Ganglia Disorders

scholarly journals Insight Into the Emerging Role of Striatal Neurotransmitters in the Pathophysiology of Parkinson’s Disease and Huntington’s Disease: A Review

2019 ◽  
Vol 17 (2) ◽  
pp. 165-175 ◽  
Author(s):  
Sumit Jamwal ◽  
Puneet Kumar
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Neuronal Death ◽  
Critical Role ◽  
Altered Level ◽  
Excitotoxic Neuronal Death

Alteration in neurotransmitters signaling in basal ganglia has been consistently shown to significantly contribute to the pathophysiological basis of Parkinson’s disease and Huntington’s disease. Dopamine is an important neurotransmitter which plays a critical role in coordinated body movements. Alteration in the level of brain dopamine and receptor radically contributes to irregular movements, glutamate mediated excitotoxic neuronal death and further leads to imbalance in the levels of other neurotransmitters viz. GABA, adenosine, acetylcholine and endocannabinoids. This review is based upon the data from clinical and preclinical studies to characterize the role of various striatal neurotransmitters in the pathogenesis of Parkinson’s disease and Huntington’s disease. Further, we have collected data of altered level of various neurotransmitters and their metabolites and receptor density in basal ganglia region. Although the exact mechanisms underlying neuropathology of movement disorders are not fully understood, but several mechanisms related to neurotransmitters alteration, excitotoxic neuronal death, oxidative stress, mitochondrial dysfunction, neuroinflammation are being put forward. Restoring neurotransmitters level and downstream signaling has been considered to be beneficial in the treatment of Parkinson’s disease and Huntington’s disease. Therefore, there is an urgent need to identify more specific drugs and drug targets that can restore the altered neurotransmitters level in brain and prevent/delay neurodegeneration.

Movement disorders

2011 ◽  
Author(s):  
Nicholas Fletcher
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Movement Disorders ◽  
Involuntary Movement ◽  
Neuroleptic Drug ◽  
Involuntary Movements ◽  
Different Types

Almost any neurological disorder can produce a disorder of movement but the ‘movement disorders’ include the akinetic rigid syndromes, hyperkinesias, and some tremors. It can sometimes seem, especially with the use of videotape recordings, that diagnosis of movement disorders is mainly a matter of correct visual recognition. Such an approach is not recommended and can lead to mistakes unless, as in other areas of medicine, the history is considered first and the physical signs second. Obvious examples include the family history in Huntington’s disease, developmental history in dystonic cerebral palsy, and neuroleptic drug treatment in patients with tardive dyskinesia. In addition, a single disorder may give rise to several different types of involuntary movement. For example, Huntington’s disease may give rise to an akinetic rigid state, chorea, myoclonus, tics, or dystonia. Patients with Parkinson’s disease taking levodopa may show different types of movement disorder at different times of the day.In akinetic rigid states the diagnostic issue will be whether the patient has idiopathic Parkinson’s disease or one of the other Parkinsonian syndromes. With involuntary movements, the first step in diagnosis is to classify these as dystonia, tics, tremor, chorea, or myoclonus. It must be remembered that involuntary movements are merely physical signs, not diagnostic entities, and that they do not always occur in a pure form; for example, patients with dystonia may have additional choreiform movements or tremor. If more than one form of abnormal movement seems to be present, the diagnosis should be based on the most obvious one. The next step is to decide on the cause of the movements and at this stage the diagnosis must be based upon an accurate and complete history as noted above.The movement disorders are often associated with abnormalities of the basal ganglia and, to some extent, vice versa. This is not entirely correct. Disturbances of basal ganglia function certainly have profound effects on movement with the development of bradykinesia, rigidity, tremor, or the various forms of dyskinesia. However, it is not correct when considering the pathophysiology of movement disorders to regard the basal ganglia as an isolated movement control centre. In fact, they are an important but poorly understood component of a much wider motor system. It is also important to remember that the basal ganglia are involved in the processing of limbic and other cognitive processes which may also be disturbed by basal ganglia dysfunction.

scholarly journals Hypernasality associated with basal ganglia dysfunction: evidence from Parkinson’s disease and Huntington’s disease

PeerJ ◽  
2016 ◽  
Vol 4 ◽  
pp. e2530 ◽  
Author(s):  
Michal Novotný ◽  
Jan Rusz ◽  
Roman Čmejla ◽  
Hana Růžičková ◽  
Jiří Klempíř ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Rating Scale ◽  
Acoustic Parameter ◽  
Perceptual Analysis ◽  
Healthy Control ◽  
Perceptual Assessment

BackgroundAlthough increased nasality can originate from basal ganglia dysfunction, data regarding hypernasality in Parkinson’s disease (PD) and Huntington’s disease (HD) are very sparse. The aim of the current study was to analyze acoustic and perceptual correlates of velopharyngeal seal closure in 37 PD and 37 HD participants in comparison to 37 healthy control speakers.MethodsAcoustical analysis was based on sustained phonation of the vowel /i/ and perceptual analysis was based on monologue. Perceptual analysis was performed by 10 raters using The Great Ormond Street Speech Assessment ’98. Acoustic parameters related to changes in a 1/3-octave band centered on 1 kHz were proposed to reflect nasality level and behavior through utterance.ResultsPerceptual analysis showed the occurrence of mild to moderate hypernasality in 65% of PD, 89% of HD and 22% of control speakers. Based on acoustic analyses, 27% of PD, 54% of HD and 19% of control speakers showed an increased occurrence of hypernasality. In addition, 78% of HD patients demonstrated a high occurrence of intermittent hypernasality. Further results indicated relationships between the acoustic parameter representing fluctuation of nasality and perceptual assessment (r= 0.51,p< 0.001) as well as the Unified Huntington Disease Rating Scale chorea composite subscore (r= 0.42,p= 0.01).ConclusionsIn conclusion the acoustic assessment showed that abnormal nasality was not a common feature of PD, whereas patients with HD manifested intermittent hypernasality associated with chorea.

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