Coronavirus disease (CoVID-19), caused by recently identified severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2), is characterized by inconsistent clinical presentations. While many infected individuals remain asymptomatic or show mild respiratory symptoms, others develop severe pneumonia or even respiratory distress syndrome. SARS-CoV-2 is reported to be able to infect the lungs, the intestines, blood vessels, the bile ducts, the conjunctiva, macrophages, T lymphocytes, the heart, liver, kidneys, and brain. More than a third of cases displayed neurological involvement, and many severely ill patients developed multiple organ infection and injury. However, less than 1% of patients had a detectable level of SARS-CoV-2 in the blood, raising a question of how the virus spreads throughout the body. We propose that nerve terminals in the orofacial mucosa, eyes, and olfactory neuroepithelium act as entry points for the brain invasion, allowing SARS-CoV-2 to infect the brainstem. By exploiting the subcellular membrane compartments of infected cells, a feature common to all coronaviruses, SARS-CoV-2 is capable to disseminate from the brain to periphery via vesicular axonal transport and passive diffusion through axonal endoplasmic reticula, causing multiple organ injury independently of an underlying respiratory infection. The proposed model clarifies a wide range of clinically observed phenomena in CoVID-19 patients, such as neurological symptoms unassociated with lung pathology, protracted presence of the virus in samples obtained from recovered patients, exaggerated immune response, and multiple organ failure in severe cases with variable course and dynamics of the disease. We believe that this model can provide novel insights into CoVID-19 and its long-term sequelae, and establish a framework for further research.
Cognitive impairment following SARS-CoV-2 infection is being increasingly recognized as an acute and possibly also long-term sequela of the disease. Direct viral entry as well as systemic mechanisms such as cytokine storm are thought to contribute to neuroinflammation in these patients. Biomarkers of COVID-19-induced cognitive impairment are currently lacking, but there is some limited evidence that SARS-CoV-2 could preferentially target the frontal lobes, as suggested by behavioral and dysexecutive symptoms, fronto-temporal hypoperfusion on MRI, EEG slowing in frontal regions, and frontal hypometabolism on 18F-FDG-PET. Possible confounders include cognitive impairment due to hypoxia and mechanical ventilation and post-traumatic stress disorder. Conversely, patients already suffering from dementia, as well as their caregivers, have been greatly impacted by the disruption of their care caused by COVID-19. Patients with dementia have experienced worsening of cognitive, behavioral, and psychological symptoms, and the rate of COVID-19-related deaths is disproportionately high among cognitively impaired people. Multiple factors, such as difficulties in remembering and executing safeguarding procedures, age, comorbidities, residing in care homes, and poorer access to hospital standard of care play a role in the increased morbidity and mortality. Non-pharmacological interventions and new technologies have shown a potential for the management of patients with dementia, and for the support of their caregivers.
Cervical dystonia is focal dystonia characterized by involuntary movement of the neck muscle, which leads to abnormal head posture. It can be accompanied with pain and tremor. In this study, we evaluated the presence of depression and anxiety in patients with cervical dystonia and the influence of dystonia symptoms on the quality of life. Psychiatric symptoms were evaluated by use of the Beck Depression Inventory (BDI-II) and Beck Anxiety Inventory. Toronto Western Spasmodic Torticollis Rating Scale (TWSTRS) was used to evaluate the cervical dystonia symptoms. Quality of life was assessed by the craniocervical dystonia questionnaire (CDQ-24) and short form 36 health survey (SF-36). Nineteen patients were analyzed. Most of the patients had mild cervical dystonia (mean TWSTRS 23.89). Depression was present in 42.1 % and anxiety in 57.9 % of the patients. Disability due to cervical dystonia correlated with the occurrence of depression (ρ = 0.534) and anxiety (r = 0.652). Disability was found to significantly influence the stigma, emotional state, pain, daily activity, social life, physical function, and physical and mental disability. Pain influenced some aspects of body pain, physical function, and physical and mental disability. Being associated with disability and pain, cervical dystonia decreases the quality of life in many aspects. Disability also influenced depression and anxiety, which were present in half of study patients. In addition to follow up for cervical dystonia symptoms, patients with cervical dystonia should also be assessed for psychiatric symptoms on routine clinical check-ups. In addition to botulinum toxin, psychopharmaceuticals should be considered as a treatment option in these patients.
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