Overview
Isolation and fear of infection are two factors contribution to a rise in anxiety and depression amid the pandemic. As the COVID-19 pandemic enters its second year, new fast-spreading variants have caused a surge in infections in many countries, and renewed lockdowns. The devastation of the pandemic — millions of deaths, economic strife and unprecedented curbs on social interaction — has already had a marked effect on people’s mental health.
The COVID-19 pandemic has likely brought many changes to how you live your life, and with it uncertainty, altered daily routines, financial pressures and social isolation. You may worry about getting sick, how long the pandemic will last, whether you'll lose your job, and what the future will bring. Information overload, rumors and misinformation can make your life feel out of control and make it unclear what to do.
Severe Acute Respiratory Syndrome Corona virus 2 (Sars Cov 2) known for its varying cardiorespiratory impacts, has far reaching consequences on the nervous system, both central and peripheral. The presentations vary from mild to florid and may be limited to the respiratory tract causing lung fibrosis or may cause damage to multiple organs like the kidneys, gastrointestinal tract and the nervous system. The varied presentations and unpredictable duration of disease with delayed effects as well, pose serious treatment challenges to treating physicians and has added to the burden of healthcare across the world.
Multi-modal
Assessment
Signs
SARS- CoV-2 are single stranded RNA viruses with high rates of recombination and mutation. It enters the CNS through the olfactory nerve via the olfactory bulb or by crossing the blood brain barrier (BBB).
Neuroinflammation appears to be associated with excessive production of proinflammatory molecules causing disordered neuronal networks resulting in neuropsychiatric manifestations. As the viral load persists and lingers on in severe cases, IL-6 and chemokines cause reactive gliosis and damage to the neurons. The combination of systemic infection, neuroinflammation, viral neurotropism along with environmental stress appears to induce and promote existing psychiatric disorders such as major depressive disorder, bipolar disorder, psychoses, post-traumatic stress disorder (PTSD), and obsessive-compulsive disorder (OCD).
Parts of the CNS which lack BBB are more vulnerable to encephalopathy, neuroinfection and autoimmune encephalitis. SARS-CoV-2, infects the brainstem, resulting in hypoxia, hypercapnia and finally respiratory failure. The “cytokine storm” can injure the microcirculation and cause thrombosis. It also activates autonomic nerves, increasing the sympathetic tone, causing autonomic dysfunction.
Neuroinflammation and associated neurodegeneration, along with brain infection and ischemia, triggers and accelerates cognitive impairment and associated symptoms like onset of delirium and psychotic features and can bring about the onset of dementia.
Neuroinflammation and associated neurodegeneration, along with brain infection and ischemia, triggers and accelerates cognitive impairment and associated symptoms like onset of delirium and psychotic features and can bring about the onset of dementia.
CNS manifestations included ataxia, ischemic stroke, cerebral haemorrhage, and epilepsy and peripheral nervous system (PNS) symptoms such as ageusia, anosmia caused by direct contact and interaction of the virus with gustatory receptors or olfactory receptor cells, along with neuralgia and musculoskeletal symptoms. Covid -19 infection may make patients more vulnerable to Parkinson’s disease as it selectively damages the dopaminergic neurons. An acute paralytic disease-like Guillain-Barre syndrome (GBS), encephalomyelitis, Miller-Fisher syndrome or myositis-even without systemic symptoms, may represent the first manifestation of COVID-19.
Anxiety and other related disorders and mood disorders are psychiatric manifestations in covid patients and are linked to inflammatory injury to the brain, specifically in the elderly caused by pro-inflammatory factors such as TNF-α and IL-2 and neuroglial failure. In schizophrenic patients affected by Covid-19, high levels of IL-6 correlated to reduced hippocampal size and contributed to cognitive impairment.
Multi-modal
Diagnosis
Diagnosis
Elevated levels of inflammatory markers such as IL-6, CRP, ESR, ferritin, procalcitonin, LDH, lymphopenia are often seen in moderate to severe cases. Thrombocytopenia and elevated D-dimer levels may be indicative of coagulopathies. Computerized tomography (CT) chest Imaging may show ground glass opacities, bilateral or multilobar infiltration, pleural effusion, or short-term increase in lesions. PCR testing of SARS-CoV-2 is done in nasal and throat swabs and CSF. Diffusion tensor imaging (DTI) and 3D high-resolution T1WI sequences of recovered Covid-19 patients were more likely to have enlarged olfactory cortices, hippocampi, insulas, Heschl's gyrus, Rolandic operculum and cingulate gyrus, due to alterations in the microstructural and functional integrity of the brain.
Treatment
Anti-virals/anti-infectious agents: Among the broad-spectrum anti-virals, acyclovir, famciclovir and protease inhibitors such as nelfinavir, lopinavir, ritonavir, saquinavir, atazanavir have been used for treatment. Remdesivir, an RNA-dependent RNA polymerase (RdRp) inhibitor is used widely for symptomatic patients. Anti-IL-6 antibody therapies with tocilizumab, sarilumab have shown therapeutic benefit. Corticosteroids are used for their anti-inflammatory properties, along with Remdesivir, and are used as first line of treatment for those with lung lesions and elevated inflammatory markers. Due to the high rates of thromboembolism, prophylactic anticoagulation with low molecular weight heparin and is associated with decreased mortality in high-risk patients. Ivermectin, plasma exchange and IVIg have also been used with benefit.
