Respiratory disorders of Parkinson's Disease

Author(s):  
Yasmin C Aquino ◽  
Lais M Cabral ◽  
Nicole C Miranda ◽  
Monique C Naccarato ◽  
Barbara Falquetto ◽  
...  

Parkinson's disease (PD) is characterized by the progressive loss of dopaminergic neurons in the substantia nigra, mainly affecting people over 60 years of age. Patients develop both classic symptoms (tremors, muscle rigidity, bradykinesia and postural instability) and nonclassical symptoms (orthostatic hypotension, neuropsychiatric deficiency, sleep disturbances and respiratory disorders). Thus, patients with PD can have a significantly impaired quality of life, especially when they do not have multi-modality therapeutic follow-up. The respiratory alterations associated with this syndrome are the main cause of mortality in PD. They can be classified as peripheral when caused by disorders of the upper airways or muscles involved in breathing and as central when triggered by functional deficits of important neurons located in the brainstem and involved in respiratory control. Currently, there is little research describing these disorders, and therefore, there is no well-established knowledge about the subject, making the treatment of patients with respiratory symptoms difficult. In this review, the history of the pathology and data about the respiratory changes in PD obtained thus far will be addressed.

Genes ◽  
2021 ◽  
Vol 12 (3) ◽  
pp. 430
Author(s):  
Steven R. Bentley ◽  
Ilaria Guella ◽  
Holly E. Sherman ◽  
Hannah M. Neuendorf ◽  
Alex M. Sykes ◽  
...  

Parkinson’s disease (PD) is typically sporadic; however, multi-incident families provide a powerful platform to discover novel genetic forms of disease. Their identification supports deciphering molecular processes leading to disease and may inform of new therapeutic targets. The LRRK2 p.G2019S mutation causes PD in 42.5–68% of carriers by the age of 80 years. We hypothesise similarly intermediately penetrant mutations may present in multi-incident families with a generally strong family history of disease. We have analysed six multiplex families for missense variants using whole exome sequencing to find 32 rare heterozygous mutations shared amongst affected members. Included in these mutations was the KCNJ15 p.R28C variant, identified in five affected members of the same family, two elderly unaffected members of the same family, and two unrelated PD cases. Additionally, the SIPA1L1 p.R236Q variant was identified in three related affected members and an unrelated familial case. While the evidence presented here is not sufficient to assign causality to these rare variants, it does provide novel candidates for hypothesis testing in other modestly sized families with a strong family history. Future analysis will include characterisation of functional consequences and assessment of carriers in other familial cases.


2021 ◽  
Vol 182 ◽  
pp. 106396
Author(s):  
David A. Kaminsky ◽  
Donald G. Grosset ◽  
Deena M. Kegler-Ebo ◽  
Salvador Cangiamilla ◽  
Michael Klingler ◽  
...  

Author(s):  
Hector Riquelme-Heras

Background: Parkinson's disease was described for the first time by James Parkinson in 1817 in the trial "Shaking Palsy," and thus there is also evidence of this disease in the Indian medical system 4500 years ago, for the diagnosis and its management with Mucuna pruriens.Years later, it was subsequently determined to contain levodopa. Two types of manifestations of Parkinson's disease are currently known, such as motor and non-motor, the first being the one that usually leads to diagnosis. Success in this will depend on the skill of the primary care physician, the ability to recognize the first symptoms by the patient, and the health systems in the management of care for the timely referral. This work shows the comprehensive management of a patient who arrives at Primary Care services, presenting vague and specific symptoms. These symptoms were treated with medications or remedies in order to calm the condition temporarily. It is convenient to call the specific symptoms such as headache, nausea, pain, dizziness, tiredness and weakness, poor motivation, sadness, easy crying, and sleep disturbances; A large percentage go to their health centers for presenting motor alterations, many times identified by their relatives or by themselves and despite being recognized as something abnormal, many of them come when the tremor intervenes with the activities of daily life. At this point, the management of the disease would begin, making clear the importance of education for the population to attend abnormal situations on time and not in late stages, significantly improving the quality of life or the prognosis of the disease Parkinson's, as is the case that occurred in our institution; A 64-year-old female patient who presents with tremor in the fifth finger of the right hand, she mentions that it is more intense when there are apparently stress situations, hyposmia and sleep disturbances, going to different health centers where they were controlled the discomfort with essential medications, many of these not requiring a prescription, temporarily decreasing in intensity; This being the beginning of multi-causality for proper management from considering the first contact doctor as a resource manager with the use of diagnostic skills to recognize characteristic signs in early stages of the disease and the ability to maintain continuity with the patients and their families as a model of family system. Studies were determined that non-motor manifestations could appear months or years before they manifest as motor symptoms to give comprehensive management to patients from their first contact with the health centers closest to them. The diagnostic presumption and its referral to the neurology and timely treatment service, until evaluating the functionality and efficacy of health policies, avoiding the delay in pharmacological treatment and access to specific neuroimaging studies at any stage of the disease. Objective: The objective of this report is to present a clinical case of a patient diagnosed with Parkinson's disease, from its management in the first contact medical services to have comprehensive management by a neurologist, thus in this way the period of latency to start treatment. Methods: We present a clinical case of a 64-year-old patient who came to consultation due to a tremor in the fifth finger of the right hand.A review of her medical history is performed, and management by different specialties is identified, for mood disorders, insomnia, essential tremor in addition to allergic rhinitis, already with drug treatment with slight or no improvement. The patient underwent a neurological examination and imaging and laboratory studies. She was referred to the neurology service as soon as possible. Result: After the interrogation and physical examination, the patient was referred to the Neurology service to confirm the presumption of diagnosis as a movement disorder under study. This process is often called the "latency period" of the diagnosis. The present work is shown as a decisive factor in giving a verdict on this problem. It is known that this level of resolution takes into account the pillars of first contact medicine as health resource managers. In this way, pharmacological treatment was started with a decrease in tremor as a motor symptom and an increase in quality and amount of sleep, increased mood, and affect as non-motor symptoms. Conclusion: The patient is under established medical and pharmacological control, and the long diagnostic latency period could be evidenced, as it usually happens in many movement disorders or their early stages, in this case, Parkinson's disease. Likewise, the family doctor is an instrument that allows the resolution of more than 90% of health problems in general, and the proper management of the remaining percentage is multifactorial, as well as medical skill and experience, the capacity of the patient or the family members. in recognizing early-stage motor disorders and health systems that often make a referral to other medical specialties difficult.


2021 ◽  
Vol 90 ◽  
pp. 161-164
Author(s):  
Seong-Min Choi ◽  
Soo Hyun Cho ◽  
Kyung Wook Kang ◽  
Jae-Myung Kim ◽  
Byeong C. Kim

2016 ◽  
Vol 10 (1) ◽  
pp. 42-58 ◽  
Author(s):  
Mohsin H.K. Roshan ◽  
Amos Tambo ◽  
Nikolai P. Pace

Parkinson’s disease [PD] is the second most common neurodegenerative disorder after Alzheimer’s disease, affecting 1% of the population over the age of 55. The underlying neuropathology seen in PD is characterised by progressive loss of dopaminergic neurons in the substantia nigra pars compacta with the presence of Lewy bodies. The Lewy bodies are composed of aggregates of α-synuclein. The motor manifestations of PD include a resting tremor, bradykinesia, and muscle rigidity. Currently there is no cure for PD and motor symptoms are treated with a number of drugs including levodopa [L-dopa]. These drugs do not delay progression of the disease and often provide only temporary relief. Their use is often accompanied by severe adverse effects. Emerging evidence from bothin vivoandin vitrostudies suggests that caffeine may reduce parkinsonian motor symptoms by antagonising the adenosine A2Areceptor, which is predominately expressed in the basal ganglia. It is hypothesised that caffeine may increase the excitatory activity in local areas by inhibiting the astrocytic inflammatory processes but evidence remains inconclusive. In addition, the co-administration of caffeine with currently available PD drugs helps to reduce drug tolerance, suggesting that caffeine may be used as an adjuvant in treating PD. In conclusion, caffeine may have a wide range of therapeutic effects which are yet to be explored, and therefore warrants further investigation in randomized clinical trials.


Author(s):  
Ajay Chaudhary ◽  
Noopur Khare ◽  
Yamini Dixit ◽  
Abhimanyu Kumar Jha

Parkinson’s disease (PD), a neurodegenerative disease is becoming major health concern mainly for elder people of age over 60 years. The main cause of PD is permanent loss/death of dopaminergic nerve cells present in brain part called substantia nigra, which is responsible for dopamine synthesis. MAO-B, monoamine oxidase B, regulates dopamine metabolism and increased activity of MAO-B causes dopamine degradation which in turn promotes the accumulation of glutamate and oxidative stress with free radical liberation. Several factors like oxidative stress, free radical formation, increased cholesterol, mitochondrial dysfunction, nitric oxide toxicity, signal-mediated apoptosis, head trauma, and environmental toxins and gene mutations like VPS35, SNCA, EIF4G1, GBA, CHCHD, LRRK2, PINK1, DNAJC13 and SOD2 are associated with PD. Symptoms of PD include bradykinesia, muscle rigidity, resting tremors, postural instability and shuffling gait, constipation, sleep problems, fatigue, apathy, loss of smell and taste, excessive sweating, frequent nightmares, dream enacting behaviour, anxiety, depression, daytime drowsiness. In PD, low levels of ceruloplasmin were observed in people with early onset of PD. Ceruloplasmin, a ferroxidase enzyme which is synthesized in liver parenchymal cell, regulates iron metabolism and lower level of which causes iron accumulation in brain which is responsible for the early onset of PD. Levodopa-based preparations, Dopamine agonists, Catechol-o-methyltransferase (COMT) inhibitors, MOA-B inhibitors, Adjunctive therapy, Antiglutamatergics drugs are currently used for the treatment of PD.


2011 ◽  
Vol 82 (10) ◽  
pp. 1112-1118 ◽  
Author(s):  
J. R. Evans ◽  
S. L. Mason ◽  
C. H. Williams-Gray ◽  
T. Foltynie ◽  
C. Brayne ◽  
...  

2021 ◽  
Vol 14 (9) ◽  
pp. e243938
Author(s):  
Mariana Barbosa ◽  
Vera Fernandes

Clozapine is an atypical antipsychotic used in refractory schizophrenia, also efficient in alleviating dyskinesia in Parkinson’s disease. Despite its potency, this drug is associated with severe metabolic side effects, including increased risk for diabetes. We report the case of a 45-year-old overweight woman with Parkinson’s disease who presented with rapid-onset hyperglycaemia within 2 months after starting clozapine for refractory dyskinaesia. She had a history of gestational diabetes. At presentation, her blood glucose level was 505 mg/dL and glycated haemoglobin 12.4%, with no catabolic symptoms. Clozapine was suspended and metformin was started, but adequate glycaemic control was achieved only with insulin therapy, along with exenatide and empagliflozin afterwards. We assume that clozapine acted as a trigger for rapid deterioration of glycaemic control through direct pathophysiological mechanisms, rather than an indirect slowly evolving weight gain-related metabolic syndrome pathway. Clinicians should be aware of this complication, enabling timely diagnosis and proper treatment.


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