scholarly journals Parkinson’s disease and affective disorder: The temporal relationship

2012 ◽  
Vol 02 (02) ◽  
pp. 96-109
Author(s):  
Flemming Mørkeberg Nilsson
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Affective Disorder ◽  
Temporal Relationship

scholarly journals Case Studies in Neuroscience: Lack of inhibitory synaptic plasticity in the substantia nigra pars reticulata of a patient with lithium-induced tremor

2019 ◽  
Vol 122 (4) ◽  
pp. 1367-1372 ◽  
Author(s):  
Luka Milosevic ◽  
Robert F. Dallapiazza ◽  
Renato P. Munhoz ◽  
Suneil K. Kalia ◽  
Milos R. Popovic ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Deep Brain Stimulation ◽  
Affective Disorder ◽  
Brain Stimulation ◽  
Bipolar Affective Disorder ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Therapeutic Mechanism ◽  
Deep Brain

Tremor is a well-known side effect from many psychiatric medications, including lithium and dopamine antagonists. In patients whose psychiatric symptoms are stabilized and only respond to certain medications, deep brain stimulation may offer relief of the consequent motor complications. We report the case of an elderly male with disabling tremor related to lithium therapy for bipolar affective disorder, who was subsequently treated with deep brain stimulation. In this patient, we obtained recordings from the substantia nigra pars reticulata and performed a high-frequency stimulation protocol that robustly elicits long-term potentiation (LTP)-like changes in patients with Parkinson’s disease. We hypothesized that in this patient, who did not have Parkinson’s disease, the levels of inhibitory plasticity would be much greater. However, we found an unanticipated lack of plasticity in the patient with lithium-induced tremor, compared with two de novo control patients with Parkinson’s disease. This patient was successfully treated with deep brain stimulation in the vicinity of the ventral oral posterior nucleus, an area of the thalamus that receives inputs from the basal ganglia. We postulate that the lithium-induced blockade of LTP may bring about motor complications such as tremor while simultaneously contributing to the therapeutic mechanism for treating the symptoms of psychiatric disorders such as bipolar affective disorder. NEW & NOTEWORTHY Use of a dual-microelectrode technique enabled us to compare long-term potentiation (LTP)-like changes in a patient with lithium-induced tremor to that of patients with Parkinson’s disease. This study corroborated the findings in rodent brain slices that chronic lithium treatment may block LTP. Whereas a deficit in LTP may underlie the therapeutic mechanism for treating psychiatric disorders such as bipolar affective disorder, it may simultaneously contribute to consequent appearance of tremor.

Bipolar affective disorder and Parkinson's disease: a rare, insidious and often unrecognized association

2002 ◽  
Vol 23 (0) ◽  
pp. s67-s68 ◽  
Author(s):  
A. Cannas ◽  
A. Spissu ◽  
G.L. Floris ◽  
S. Congia ◽  
M.V. Saddi ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Affective Disorder ◽  
Bipolar Affective Disorder

Electroconvulsive Therapy in Parkinsonism with Affective Disorder

1988 ◽  
Vol 152 (1) ◽  
pp. 55-58 ◽  
Author(s):  
Nutan Atre-Vaidya ◽  
V. Chowdary Jampala
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Effective Treatment ◽  
Affective Disorder ◽  
Electroconvulsive Therapy ◽  
Poor Prognosis ◽  
First Report

The authors report a patient whose Parkinson's disease and mania both responded well to electroconvulsive therapy (ECT) after failing to respond to chemotherapy. The authors review the literature and suggest that ECTis a safe and effective treatment for affective syndromes associated with Parkinsonism. The presence of dementia in these patients appears to be an indicator of poor prognosis. This paper is believed to be the first report of successful use of ECT in mania occurring together with Parkinsonism.

scholarly journals Temporal evolution of inflammation and neurodegeneration with alpha-synuclein propagation in Parkinson’s disease mouse model

2021 ◽  
Author(s):  
Thuy Thi Lai ◽  
Yun Joong Kim ◽  
Phuong Thi Nguyen ◽  
Young Ho Koh ◽  
Tinh Thi Nguyen ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Inflammatory Response ◽  
Mouse Model ◽  
Temporal Relationship ◽  
Temporal Evolution ◽  
Inflammatory Responses ◽  
Alpha Synuclein ◽  
Motor Dysfunction ◽  
Whole Brain

Abstract Alpha-synuclein (αSyn) propagation has been determined to play a key role in the pathomechanism of Parkinson’s disease (PD), but neurodegeneration and the involvement of inflammation in its pathologic progression are yet to be well understood with regard to temporal relationship. In this study, by means of PD mouse model injected with intrastriatal αSyn preformed fibril (PFF), the temporal evolution of αSyn propagation, inflammation, and neurodegeneration was explored in the perspective of the striatum and the whole brain. In the PFF-injected striatum, inflammatory responses including the microglia and astrocyte were activated at the earliest stage and reduced with time, and the phosphorylated form of αSyn accumulation increased behind it. Thereafter, the degeneration of striatal dopaminergic neurons became significant with the conspicuity of behavior phenotype. Similar pattern of forefront eruption of inflammation and following αSyn propagation was noted in the opposite striatum, which was not injected with PFF. Meanwhile, in analyzing the whole brain, inflammatory responses were determined to have activated at the earliest stage, and the soluble αSyn expression then increased concurrently. Inflammatory response decreased afterward, and the accumulation of the insoluble form of αSyn increased behind it. Our results suggested that the inflammatory response may precede the accumulation of the pathologic form of αSyn; thereafter, the neurodegeneration and motor dysfunction followed αSyn proliferation in PD mouse model. From this model, recognizing the temporal relationship between inflammation, αSyn propagation, and neurodegeneration may be helpful in establishing PD animal model and monitoring the effect of interventional therapy.

scholarly journals Temporal Evolution of Inflammation and Neurodegeneration With Alpha-Synuclein Propagation in Parkinson's Disease Mouse Model

2021 ◽  
Vol 15 ◽  
Author(s):  
Thuy Thi Lai ◽  
Yun Joong Kim ◽  
Phuong Thi Nguyen ◽  
Young Ho Koh ◽  
Tinh Thi Nguyen ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Inflammatory Response ◽  
Mouse Model ◽  
Temporal Relationship ◽  
Temporal Evolution ◽  
Inflammatory Responses ◽  
Alpha Synuclein ◽  
Motor Dysfunction ◽  
Whole Brain

According to a few studies, α-synuclein (αSyn) propagation has been suggested to play a key role in the pathomechanism of Parkinson's disease (PD), but neurodegeneration and the involvement of inflammation in its pathologic progression are not well understood with regard to temporal relationship. In this study, with the help of the PD mouse model injected with intrastriatal αSyn preformed fibril (PFF), the temporal evolution of αSyn propagation, inflammation, and neurodegeneration was explored in the perspective of the striatum and the whole brain. In the PFF-injected striatum, inflammatory response cells, including microglia and astrocytes, were activated at the earliest stage and reduced with time, and the phosphorylated form of αSyn accumulation increased behind it. Afterward, the degeneration of striatal dopaminergic neurons became significant with the conspicuity of behavioral phenotype. Similar patterns of forefront eruption of inflammation and then followed by αSyn propagation were noted in the opposite striatum, which were not injured by PFF injection. In analyzing the whole brain, inflammatory responses were activated at the earliest stage, and the soluble αSyn expression increased concurrently. The inflammatory response decreased afterward, and the accumulation of the insoluble form of αSyn increased behind it. Our results suggested that the inflammatory response may precede the accumulation of the pathologic form of αSyn; thereafter, the neurodegeneration and motor dysfunction followed αSyn proliferation in the PD mouse model. From this model, recognizing the temporal relationship between inflammation, αSyn propagation, and neurodegeneration may be helpful in establishing the PD animal model and monitoring the effect of interventional therapy.

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