Impact of COVID-19 on Parkinson’s disease
Impact of COVID-19 on Parkinson’s disease

Impact of COVID-19 on Parkinson’s disease

The pandemic with coronavirus disease 2019 (COVID-19) has devastated entire regions of the world, leaving over 6 million dead at the last count. The greatest impact has been on those with underlying diseases and those with old age, heavier body weight and cardiovascular risk factors. in fact, over half of COVID-19 patients have such diseases.

The long-term complications or sequelae of COVID-19 have been increasingly reported, ranging from mild fatigue to debilitating fatigue, chest pain and neurological symptoms. Among the latter has been the concern about whether COVID-19 affects patients with Parkinson’s disease (PD). The latter are among the most common neurodegenerative disorders among the elderly worldwide, characterized by bradykinesia or a reduction in movement, stiffness, resting tremor, and postural instability.

The common factors for advanced age and cardiovascular disease in both COVID-19 and PD make it important to examine the association between these conditions. Recent research shows that the virus can affect the brain and enter through the olfactory nerves. It can also affect the vagus nerve and other brainstem nuclei and thus penetrate the central nervous system.

The involvement of the brainstem would also explain the severe respiratory symptoms seen in a significant minority of cases.

In previous viral pandemics, such as the Spanish flu from 1918 to 1920, parkinsonism was observed to become more common as a post-encephalitic successor following an epidemic of encephalitis lethargica. Again, bird flu led to parkinsonism in many survivors. Transient or prolonged parkinsonism has also been reported to follow many other viral infections, including coxsackie virus, West Nile virus, and the Japanese encephalitis B virus.

In most cases, it is attributed to the occurrence of neuroinflammation with or without hypoxic brain damage, associated with damage to the basal ganglia, either structural or functional. Other research suggests that in addition to genetic factors, viral infections contribute to the risk of PD in the long run.

Possible connections between COVID-19 and PD

Several observations suggest a link between COVID-19 and neurodegeneration. First, SARS-CoV-2 can enter the central nervous system (CNS) via the nasal epithelium, causing neuronal death. Hyposmia or anosmia have been reported in both preclinical PD and COVID-19. COVID-19 can cause damage to the basal ganglia via thrombotic lesions.

In addition, cross-reactive antibodies against endemic seasonal humans coronaviruses at higher levels in PD patients compared to healthy controls could indicate a role of viral infection in the pathogenesis of this condition. Hyper-inflammation can activate resident immune cells in the CNS or trigger immune cell infiltration into the brain, causing them to attack and kill neurons and associated cells.

Parkinsons

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Relationship between PD and COVID-19

Because PD is associated with weakness of the respiratory muscles, abnormal posture and stiffness of the respiratory muscles, and poor chest wall movement during respiration, PD patients who develop severe COVID-19 may be at a higher risk of not responding to mechanical ventilation if necessary.

In addition, it may appear that the presence of chronic inflammation due to the presence of cardiovascular risk factors such as obesity, hypertension and end-organ disease will predispose to a cytokine storm when the PD patient encounters the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the pathogen behind the current pandemic.

Pneumonia is the most common cause of hospitalization among PD patients and of death, but despite the common association between COVID-19 and pneumonia, there is little evidence that COVID-19 increases the risk of death in PD patients.

Other presumed mechanisms by which COVID-19 may exacerbate PD include the risk of a systemic hyperinflammatory response to the infection, the increased fragility of PD patients compared to the general population, and possible interactions between the dopaminergic neurons and those regulating renin-angiotensin. the system.

Does PD increase the risk of severe COVID-19?

Some studies show that the presence of PD does not increase the risk of testing positive for COVID-19. The age group of PD patients affected by COVID-19 corresponds to the age group of the general population.

Again, in most cases, the infection gives no to mild symptoms and few deaths. The hospitalization rate and mortality rate are similar to those of the general population.

Does COVID-19 increase the severity of PD symptoms?

Compared to non-COVID-19 patients, PD patients with COVID-19 had more severe motor symptoms and more on-off fluctuations, as well as non-motor symptoms.

Motor symptoms worsened with COVID-19, including an increase in leisure time over an entire day, compared with non-COVID-19-PD patients. The increase is so remarkable that it causes an increase in the dose of dopaminergic medication in up to one in three cases.

Diarrhea is more common among COVID-19 patients with PD, and occurs in half of the cases. This may interfere with normal dosing with levodopa and other dopaminergic drugs. This contributes to the aggravation of motor symptoms in COVID-19-PD patients along with the infection itself. In fact, diarrhea may fully explain the increase in leisure time among these patients compared to PD patients without COVID-19.

But COVID-19 in itself, rather than the presence of diarrhea, accounts for the deterioration of engine on-off oscillations.

The negative effect of COVID-19 on PD symptoms may be due to high fever, difficulty breathing and hypoxia, involvement of the coagulation system, myalgias and other stressors. The risk of respiratory failure may be greater due to the bradykinesia and stiffness that may be thought to reduce vital capacity and maximal expiratory flow.

Pain, sleep disturbances and fatigue can also aggravate certain symptoms of PD. Particularly prominent is the effect of anxiety and isolation. In case of severe infection, hospitalization may require mechanical ventilation, especially if the PD patient is elderly and has more than one comorbidity. This is made more difficult if the patient is on other treatments, such as deep brain stimulation or intrajejunal levodopa infusion, and mortality may be higher in such cases.

Non-motor symptoms such as fatigue are due to COVID-19 itself, possibly due to systemic inflammation. Urinary symptoms such as urge incontinence and nycturia worsen both due to the increased on-off motor fluctuations and the presence of the infection itself.

Cognitive impairment was not observed and autonomic functions remained unaffected. Non-motor symptoms also show a general worsening with the onset of COVID-19. However, the psychiatric symptoms worsened among those with pre-existing psychiatric illnesses, mostly insomnia and depression. Such patients were more likely to be younger and female.

Elderly with COVID-19

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The effect of the pandemic on PD patients

The COVID-19 pandemic caused PD patients to experience many changes in the way they received medical attention. Teleconsultations came into vogue as resources were redistributed to meet emergency patients. This was accompanied by some limitations such as the difficulty of assessing mood or cognitive status or rigidity level, via telemedicine.

DBS proved feasible via remote computer programs that could assess the patient’s symptoms to improve motor performance in these patients. The COVID-19 vaccines could also help protect PD patients despite a short-term intensification of symptoms.

Conclusions

There is no evidence that PD increases the risk of severe COVID-19. “While a role for the virus in causing or exacerbating Parkinson’s disease appears unlikely at present, exacerbation of specific motor and non-motor symptoms has been reported.. “

This should require careful adherence to currently appropriate PD medication to avoid worsening of symptoms. In addition, the presence of diarrhea should make caregivers assess patients for the presence of dehydration, which may be due to fever, diarrhea, or loss of appetite.

Further research will be required to show how far the direct effects of viral invasion in the brain account for these findings and how much is due to systemic inflammation. Careful follow-up of COVID-19 survivors may help establish a link between this infection and future PD or other neurological disorders in the future.

Through PD-tailored home equipment, adjustments and routine habit integration, patients may be able to manage the disease well during and after the COVID-19 pandemic. “

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