Parkinson Disease (PD) is a neurodegenerative disorder of the central nervous system that often impairs the patient’s motor skills, speech and other functions. The four cardinal signs of parkinsonism are resting tremor, bradykinesia, cogwheel rigidity and postural instability. The prevalence of depression in PD ranges from 4% to 75%. However depression in PD is often mistakenly as the presentation of the disease itself. Therefore this paper reviewed the clinical feature of depression in PD and explored the aetiology of depression in PD.
Acute mountain sickness is an illness caused by climbing to a high altitude without prior acclimatization. Neurological consequences, like parkinsonism following acute mountain sickness without lesion of brain MRI have been reported rarely. A healthy 56-year-old man presented with dysarthria and gait disturbance. Neurological examination revealed tremor of hands, limb rigidity, and bradykinesia. The symptoms developed approximately 30 days following a 3,500 m climb of the Annapurna in the Himalayas. Brain MRI did not reveal any abnormalities including globus pallidus. The parkinsonism symptoms persisted for about 3 months before a complete recovered was made. We suggest that parkinsonism can develop after climbing to a high altitude but that the symptoms can be transient if a brain MRI detects no abnormalities.
A 31-year-old male, apparently well, presented with typical chest pain. His ECG showed ST-elevation from V1-V4 and echocardiogram revealed anteroseptal wall hypokinesia with ejection fraction of 45%. Normal coronary arteries were seen on coronary angiogram. A thyroid function test showed elevated free T4 levels with suppressed thyroid stimulating hormone (TSH). Treatment with thionamides and beta-blockers improved symptoms. Upon review 4 months later he was well. Repeat echocardiogram showed good ejection fraction with no hypokinetic area.
Delayed neuropsychiatric sequelae is an important condition which commonly occur during recovery from acute carbon monoxide poisoning. Typical presentation would be apathy, disorientation, amnesia, hypokinesia, bizarre behavior, insomnia and neurological manifestations such as gait disturbance, hypertonia and tremor. We report here a case of a man presented with delayed neuropsychiatric sequelae one month after the carbon monoxide poisoning in his suicidal attempt. He presented with the typical presentation and diagnosis confirmed with the MRI findings. His MRI showed abnormal signal in subcortical hemisphere white matter of both temporo-fronto-parietal-occipital regions along the insula and both globus pallidus. He was treated with Olanzapine, Fluvoxamine, Chlorpromazine and Levodopa and his condition slowly improved. It is important for clinicians to recognize the symptoms and risk factors to develop delayed neuropsychiatric sequelae in patients who previously had carbon monoxide poisoning.
Parkinson's disease (PD) is a severely debilitating neurodegenerative disease, affecting the motor system, leading to resting tremor, cogwheel rigidity, bradykinesia, walking and gait difficulties, and postural instability. The severe loss of dopaminergic neurons in the substantia nigra pars compacta causes striatal dopamine deficiency and the presence of Lewy bodies indicates a pathological hallmark of PD. Although the current treatment of PD aims to preserve dopaminergic neurons or to replace dopamine depletion in the brain, it is notable that complete recovery from the disease is yet to be achieved. Given the complexity and multisystem effects of PD, the underlying mechanisms of PD pathogenesis are yet to be elucidated. The advancement of medical technologies has given some insights in understanding the mechanism and potential treatment of PD with a special interest in the role of microRNAs (miRNAs) to unravel the pathophysiology of PD. In PD patients, it was found that striatal brain tissue and dopaminergic neurons from the substantia nigra demonstrated dysregulated miRNAs expression profiles. Hence, dysregulation of miRNAs may contribute to the pathogenesis of PD through modulation of PD-associated gene and protein expression. This review will discuss recent findings on PD-associated miRNAs dysregulation, from the regulation of PD-associated genes, dopaminergic neuron survival, α-synuclein-induced inflammation and circulating miRNAs. The next section of this review also provides an update on the potential uses of miRNAs as diagnostic biomarkers and therapeutic tools for PD.