Table 2.

COVID-19 associated neurological complications and potential pathophysiology

Clinical syndrome	Potential pathophysiology	Refs.
Parainfectious manifestations
Anosmia	Infection of olfactory epithelium or nerve	[14–16]
Ischemic stroke	Cytokine overproduction; Vascular endothelial damage, Endothelial dysfunction; Hypercoagulable state	[17–26]
Hemorrhagic stroke	Decrease in ACE2 levels; Blood pressure increase; Coagulopathy; CVST	[27–30]
Encephalopathy, encephalitis	Cytokine overproduction; Vascular endothelial damage; Direct CNS invasion; Hypoxia; Autoimmunity; Medication effects	[17, 28, 31–41]
Myalgia/rhabdomyolysis	Infection of muscle; Metabolic derangements; Medication effects	[15]
Myoclonus	Autoimmune cerebellar/brainstem damage; Hypoxia	[47]
Seizure	Fever; Hypoxia; Multiorgan failure; Metabolic derangements; Cytokine overproduction; Direct CNS invasion	[14, 32]
Headache	Hypoxia; Activation of peripheral trigeminal nerve endings; Cytokine overproduction; Direct CNS invasion; Hypercoagulable state	[44, 45]
Post-viral syndromes
Brain fog/Long Covid	Autoimmune; Neuroinflammation; Neurodegeneration	[42–47]
Guillain–Barre syndrome/polyneuropathy	Autoimmunity/Molecular mimicry	[46]
Depression, anxiety and sleep disorders	Cytokine overproduction/Neuroinflammation; Direct CNS invasion	[48–51]
Transverse myelitis	Immune cell mediated	[14–16]
Acute disseminated encephalomyelitis	T cell mediated	[15, 16]

ACE2 angiotensin-converting enzyme-2; CVST cerebral venous sinus thrombosis; CNS central nervous system