Infectious Disorders
Genital herpes: neurologic complications
May. 05, 2026
Worddefinition
At vero eos et accusamus et iusto odio dignissimos ducimus qui blanditiis praesentium voluptatum deleniti atque corrupti quos dolores et quas.
Neurologic complications of coronavirus infection …
- Updated 12.30.2025
- Released 04.10.2020
- Expires For CME 12.30.2028
Neurologic complications of coronavirus infections
Introduction
Overview
Coronaviruses are enveloped, positive-sense RNA viruses that cause respiratory and systemic symptoms in humans. Since late 2019, SARS-CoV-2 has revealed a wealth of observations that continue to be investigated to better understand its pathogenicity, phenotypic expression, and range of disease. Reported symptoms span a broad spectrum, including neurologic involvement ranging from common, self-limited findings to life-threatening complications. Many neurologic manifestations likely reflect systemic inflammation, immune-mediated mechanisms, and critical illness rather than direct viral neuroinvasion. Ongoing research is essential to clarify the mechanisms and distinguish true pathogen-related effects from coincidental or comorbid findings that may introduce observational bias.
This review summarizes acute, parainfectious, and post-acute neurologic manifestations, highlights the current understanding of proposed mechanisms, and outlines practical evaluation and management considerations for clinicians.
Key points
|
Neurologic manifestations span acute, immune-mediated, and post-acute phases, often overlapping within the same patient. | |
|
Evidence favors systemic inflammation, endothelial injury, and immune mechanisms over primary CNS infection in most cases; CSF PCR is rarely positive and often of uncertain significance. | |
|
Stroke risk increases during acute infection through converging pathways that include coagulopathy, endothelial dysfunction, patient immobility, and cardiac injury. | |
|
Olfactory dysfunction was frequent early in the pandemic and is less common with specific variants. Most patients recover within months, though a subset experience persistent, chronic symptoms. | |
|
Post-acute sequelae of COVID-19 have been reported to include cognitive dysfunction, dysautonomia, headache, and small fiber neuropathy. Patients presenting with these symptoms should be evaluated for alternative diagnoses and potentially treatable contributors. | |
|
Severe neurologic events after vaccination are rare, and the absolute neurologic risk is far higher after infection than after immunization. |
Historic note and terminology
Human coronaviruses were identified in the 1960s, with four endemic strains causing mild respiratory illness and three highly pathogenic Beta coronaviruses recognized in the modern era: SARS-CoV in 2002 to 2004, MERS-CoV from 2012, and SARS-CoV-2 from 2019. Early COVID-19 reports emphasized anosmia, encephalopathy, and cerebrovascular events. Subsequent clinicopathologic studies shifted emphasis toward immune and vascular mechanisms rather than direct neuroinvasion. Terminology for persistent symptoms varies across sources, including long COVID, post-COVID-19 condition, and post-acute sequelae of COVID-19. In this article, the term post-acute sequelae of COVID-19 (PASC) is used for consistency, and variant names follow World Health Organization labels.
Clinical manifestations
Systemic symptoms. Coronaviruses are known causes of respiratory, enteric, and systemic infections. Most human coronaviruses cause mild symptoms and resolve.
The most common symptoms of COVID-19 have shifted over the course of the pandemic, with fever now present in approximately 40% to 60% of cases and cough in 60% to 65%, both lower than early pandemic estimates. Fatigue, myalgia, sore throat, nasal congestion, and headache are frequently reported. Myalgia and fatigue are seen in about 50% and may persist even after recovery from other symptoms (44). Headache occurs in 8% (44). Diarrhea occurs in less than 5% and, in some patients, might be the major symptom (20). Lymphopenia and ground glass opacities on chest imaging are still observed in severe cases, but the proportion of severe pneumonia has declined with widespread vaccination and prior infection. Many infections are now mild or asymptomatic, especially in vaccinated individuals, but severe outcome persists in high-risk groups. These groups include but are not limited to people with diabetes, obesity, cardiac and respiratory disorders, and immunosuppressed states (08; 46; 52).
Neurologic symptoms. Although COVID-19 is largely a respiratory disorder, neurologic complications are frequently encountered throughout the course of the illness. Several acute neurologic syndromes have been associated with SARS-CoV-2 (Table 2). In some patients, neurologic manifestations may precede respiratory symptoms or be the sole manifestation of COVID-19 (16). There are multiple proposed mechanisms by which SARS-CoV-2 is theorized to cause neurologic effects, including direct viral infection, immune-mediated injury, blood-brain barrier dysfunction, cytokine toxicity, and indirect sequelae of critical illness (80). Given the heterogeneity of neurologic manifestations, the pathophysiology of the disease is likely multifactorial and involves multiple mechanisms. However, most evidence supports a systemic inflammatory response with CNS involvement and parainfectious phenomena rather than direct viral invasion of the CNS.
Table 2. Neurologic Complications of SARS-CoV-2 Infection
|
Acute neurologic complications | |
|
Anosmia and ageusia | |
|
Parainfectious and post-infectious complications | |
|
Acute disseminated encephalomyelitis | |
|
Post-acute sequalae of COVID-19 (PASC) | |
|
Cognitive dysfunction | |
Acute neurologic complications
Anosmia and ageusia. Anosmia and ageusia were initially reported as common complications in over 80% of patients with early infection, even in the absence of other nasal symptoms (36). The prevalence of this complication is highly variable, with rates ranging as high as 80% depending on the variant and population studied. The prevalence of anosmia and ageusia has declined significantly with the emergence of the Omicron variant. A meta-analysis estimated global prevalence as low as 3.7% for Omicron compared to 65% to 83% for earlier variants (79).
The virus is believed to invade the sustentacular cells in the vicinity of the olfactory nerve endings, which express SARS-CoV-2 receptor ACE2 (07). Ageusia results from anosmia. Anosmia and ageusia may, in turn, cause anorexia and weight loss. Transient edema of the olfactory nerves and bulbs may be seen on MRI. The prognosis for the recovery of olfactory function is favorable, with most individuals recovering within the first few months. According to a meta-analysis, approximately 95.7% of patients recover their sense of smell, and 98.0% recover their sense of taste by 180 days. An estimated 5.6% have ongoing smell loss, and 4.4% have ongoing taste loss beyond 6 months (74).
Encephalopathy. Encephalopathy is common in patients with COVID-19 and is likely multifactorial in etiology, potentially involving mechanisms of systemic inflammation, a cytokine storm, microvascular injury, and blood-brain barrier dysfunction. Encephalopathy is particularly common in critically ill patients with significant pulmonary involvement. Hypoxia and multiorgan involvement are thought to play a significant role in the pathogenesis of encephalopathy in patients with COVID-19. Rarely, encephalopathy may be the sole presenting sign of COVID-19, particularly in individuals older than 65 years of age (27).
Cerebrospinal fluid is usually normal or shows only mild nonspecific abnormality. Detection of SARS-CoV-2 RNA in CSF is rare and of uncertain clinical significance. Investigation into biomarkers to characterize disease severity and long-term disability is underway (37).
Neuroimaging and CSF examination are usually normal unless there are other coexisting neurologic complications of COVID-19. It is important to note that COVID-19-associated encephalopathy is associated with longer length of hospital stay and increased 30-day mortality (41).
Cerebrovascular disease. As with other viruses and severe infections, arterial and venous strokes may be encountered in patients with SARS-CoV-2 infection (Table 3). Interestingly, some studies have suggested a higher risk of stroke in patients with COVID-19 compared to influenza and bacterial pneumonia (86).
Altered coagulation pathways are often present in severe acute SARS-CoV-2, as suggested by elevated D-dimer levels, deranged prothrombin and activated partial thromboplastin times, and disseminated intravascular coagulation. However, in addition to altered coagulation, endothelial cell injury (as the ACE2 receptor is expressed on endothelial cells) and immobility (Virchow triad) are also probably contributory. Myocarditis may also increase stroke risk. Concordantly, strokes have also been reported in patients with no other risk factors.
Early single-center case series reported a prevalence of ischemic stroke in up to 4.6% and intracerebral hemorrhage in 0.5% (39). However, large studies have shown that acute ischemic stroke is not common in COVID-19 (1.3% in 8163 patients with SARS-CoV-2 infection versus 1.0% of 19,513 noninfected patients) (61). SARS-CoV-2 stroke patients are likely to have other comorbid risk factors as well. The management of stroke in the setting of COVID-19 should be approached similarly to stroke patients without COVID-19.
Table 3. Vascular Complications of SARS-CoV-2 Infection
Presentation | |
Cerebral venous thrombosis | |
Pathophysiology | |
Coagulopathy | |
Risk factors | |
Myocarditis | |
Meningoencephalitis. Although headache is a common symptom, direct viral invasion causing meningoencephalitis is rare with SARS-CoV-2, unlike the previously reported cases of SARS, MERS-CoV, and HCoV-OC43. An index case of SARS-CoV-2 meningoencephalitis was identified in Japan (54), and several additional cases have also been reported. Many reported cases of encephalitis and meningoencephalitis show negative cerebrospinal fluid PCR for the virus and lack clear evidence of direct neuroinvasion. In a systematic review and meta-analysis of COVID-19-associated encephalitis, the incidence of encephalitis as a complication of COVID-19 infection was estimated to be approximately 0.215% (71). In a postmortem analysis of 43 cases, SARS-CoV-2 RNA was identified in 53%, but with low copy numbers and a rare presence of infected cells (49). However, the presence of the virus showed no association with other neuropathological changes, such as astrogliosis or ischemic or inflammatory lesions. Most other reported autopsy series have been unable to identify the virus in the brain.
For this reason, it has been postulated that the pathophysiology of encephalitis seen in COVID-19 may be mediated by a cytokine release syndrome rather than direct viral invasion (60).
An additional, more recent meta-analysis reinforces the consensus that acute neurologic complications are largely driven by systemic inflammation, vascular injury, and an immune-mediated process rather than direct viral effects on the CNS, as direct detection of SARS-CoV-2 in neural tissue was rare, and when present, viral RNA pr protein was typically found at low levels. The work concluded that the neurologic injury is secondary to systemic effects with a predominance of vascular and inflammatory changes (85).
Seizures. Rarely, patients with COVID-19 infection may develop seizures. The reported incidence of seizures as a complication of COVID-19 is estimated to be less than 1% and is mostly seen in patients who are critically ill or have other neurologic complications of COVID-19, such as meningoencephalitis (34). The pathogenesis is likely multifactorial and often related to underlying toxic-metabolic disturbances and critical illness.
Myositis and other neuromuscular complications. Similar to other viral illnesses, myalgias are a commonly reported symptom in COVID-19 infection. However, myositis temporally associated with COVID-19 infection has also been reported, both as a complication associated with acute infection, with proximal weakness and highly elevated creatine kinase levels (48), as well as a later complication with subacute or chronic features consistent with an immune-mediated postinfectious process. Other neuromuscular complications can include polyneuropathy, facial nerve palsy, cranial neuropathy, and inflammatory plexopathies. Critically ill patients may also develop critical illness neuropathy and myopathy as a result of prolonged and severe illness.
The literature suggests type 2 fiber atrophy, necrotizing myopathy, and myositis, with some cases showing a dermatomyositis-like phenotype, such as perifascicular MHC expression. These features are not specific to COVID-19. Peripheral nerve involvement, including neuritis, has also been documented but without evidence of direct viral invasion (73).
Parainfectious and post-infectious complications
Acute disseminated encephalomyelitis. Acute disseminated encephalomyelitis (ADEM) is a post-viral syndrome that can be triggered by a variety of different viral infections, including coronaviruses. In fact, the pneumonia associated with SARS-CoV-2 usually occurs after a week or more of systemic or milder respiratory symptoms and is characterized by massive inflammation in the lungs, causing an acute respiratory distress syndrome that is fatal in many. In the pre-COVID-19 era, extensive inflammation involving the brain, cerebellum, and spinal cord was described in several patients with HCoV-OC43 a week or two after the infection, suggestive of ADEM (84). A similar syndrome may occur with SARS-CoV-2 in patients who survive the acute phase or may have minimal systemic symptoms during the acute phase (42; 58). In one MRI study of hospitalized patients with neurologic symptoms, 17% had leptomeningeal enhancement, and 13% had encephalitis (33). Neuropathological studies reveal perivascular macrophages and cytotoxic lymphocytes. These lesions were predominantly present in the brainstem and cerebellum as well as the meninges (62). Systematic reviews and meta-analyses have found that the median age of SARS-CoV-2-associated ADEM is significantly higher than that of classic (pre-pandemic) ADEM, which typically affects children, whereas COVID-19-associated cases are more common in adults and older individuals (47; 81).
Acute necrotizing hemorrhagic encephalopathy. This is a feared complication of several viruses, most notably influenza. It is thought to result from cytokine release syndrome rather than direct viral invasion of brain parenchyma, which is especially salient given the propensity of SARS-CoV-2 for causing similar cytokine storms in the lungs. Cases have included bilateral lesions, including those of the thalami, cerebral hemispheres, and the cerebellum, in patients who presented with several days of more typical COVID-19 symptoms (58; 55).
Myelitis. Cases of acute transverse myelitis associated with SARS-CoV-2 have been reported. In a case series of 43 patients, the latency period from the onset of COVID-19 symptoms to the onset of transverse myelitis symptoms was bimodal, with one group presenting concurrently (15 hours to 5 days in 11 of 34 patients) and a separate group presenting as a more postinfectious phenomenon (10 days to 6 weeks in 23 of 34 patients) (65). The majority of cases were longitudinally extensive, with three or more vertebral segments involved. Lesions had extended into the brainstem in some patients, whereas others had lesions that extended caudally into the conus medullaris. Additionally, myelitis may be a presenting feature of another post-infectious immune-mediated process, such as neuromyelitis optica spectrum disorder (NMOSD) or myelin-oligodendrocyte glycoprotein antibody-associated disease (MOGAD) (18).
Autoimmune encephalitis. Although rare, there are numerous reports of autoimmune encephalitis developing after COVID-19 infection. A systematic review identified 23 definite and 48 possible cases of autoimmune encephalitis associated with COVID-19 infection or vaccination (67). Anti-NMDAR encephalitis was the most common type of definite autoimmune encephalitis reported in this meta-analysis (12 cases total). Molecular mimicry has been proposed as a possible pathophysiological mechanism. Reports of seronegative anti-NMDAR encephalitis following COVID-19 infection should be interpreted with caution.
Another study, emphasizing the rarity of post-COVID autoimmune encephalitis, demonstrated that 0.05% of patients with COVID-19-related diagnoses in 2020 included post-COVID autoimmune encephalitis (78). This study examined residual sera from 556 consecutive Mayo Clinic Rochester patients who underwent autoimmune encephalopathy neural antibody evaluations and were tested for total antibodies against SARS-CoV-2, and medical records were reviewed. From the laboratory SARS-CoV-2 antibody cohort, diagnoses included post-sequelae of SARS-CoV-2 infection (PASC), toxic-metabolic encephalopathy during COVID-19 pneumonia, diverse non-COVID-19 relatable neurologic diagnoses, and autoimmune encephalitis.
Guillain-Barré syndrome. Postinfectious brainstem encephalitis and Guillain-Barré syndrome had previously been described with MERS (29). In a case series from Italy during the SARS-CoV-2 epidemic, five patients developed symptoms of Guillain-Barré syndrome 5 to 10 days after first developing COVID-19 symptoms, with both axonal and demyelinating features (77). A later, more comprehensive review of 73 patients showed that more than three quarters had predominantly demyelinating features (03). In that large series, the time to neurologic nadir was a median of 4 days. Prognosis for a worse outcome was associated with the severity of COVID-associated pneumonia. Miller-Fisher syndrome with ophthalmoparesis has also been reported (21).
The incidence of Guillain-Barré syndrome was increased in certain regions, such as northern Italy, during the early COVID -19 pandemic, with a 2.6- to 2.85-fold higher risk compared to the pre-pandemic persons, but the increase was not observed universally, and in some countries the risk was slightly reduced due to decreased circulation during lock downs of other infections that can commonly precede Guillain-Barré syndrome (13; 12; 10).
Myositis. Myositis temporally associated with COVID-19 infection has been reported, both as a complication associated with acute infection, with proximal weakness and highly elevated creatine kinase levels (48), as well as a later complication with subacute or chronic features consistent with an immune-mediated postinfectious process. Multiple autopsy studies and systematic reviews, however, have failed to demonstrate a direct SARS-CoV-2 invasion of skeletal muscle fibers (04).
Multisystem inflammatory syndrome. This is a rare but severe syndrome in patients infected with SARS-CoV-2. It is more well-defined in children and adolescents (MIS-C) as a hyperinflammatory syndrome resembling Kawasaki disease and is characterized by fever, marked elevation of inflammatory biomarkers (CRP, D-dimer, and ferritin), and multiple organ system involvement (64). Gastrointestinal complaints are frequently reported, and myocardial injury with left ventricular dysfunction and shock requiring inotropic support may occur. A similar syndrome may also occur in adults (MIS-A), with greater complexity. It usually follows within 2 to 3 weeks after the acute infection. Neurologic manifestations typically include encephalopathy and generalized weakness, dysarthria, and dysphagia. MRI may reveal abnormal signals in the splenium of the corpus callosum on diffusion-weighted imaging (35). Cerebrospinal fluid analysis is usually normal. The pathophysiology of this syndrome is incompletely understood. The American College of Rheumatology now recommends initial therapy for MIS-C with both IVIG at 2 g/kg and a low-to-moderate dose of glucocorticoids (1 to 2 mg/kg/day), particularly in patients with shock or organ-threatening disease, rather than IVIG alone (22).
Post-acute sequelae of COVID-19 (PASC)
Many patients who recover from COVID-19 continue to experience symptoms months to years after recovery from the acute infection. Several terms have emerged to describe this phenomenon, including post-acute sequelae of COVID-19 (PASC), long haul COVID, and post-COVID-19 syndrome. Frequently reported symptoms include fatigue, cognitive dysfunction, dyspnea, headache, and dizziness. A meta-analysis found that nearly 50% of patients with COVID-19 infection reported at least one post-COVID symptom, and nearly 20% of patients reported at least one neurologic symptom (87). The pathophysiologic mechanism underlying PASC remains unclear, and it is likely that multiple mechanisms may contribute. When evaluating patients with PASC, it is important to ensure that an alternate diagnosis would not better explain the patients symptoms.
Headache. Approximately 10% of patients report persisting headaches after COVID-19 infection (87). This can be either new-onset headaches or exacerbation of a previous headache disorder. There is no unique headache phenotype related to COVID-19 infection, though migraine and tension-type headaches are the most commonly reported. The management of headaches in this setting is similar to that in patients without COVID-19.
Cognitive dysfunction. Many patients with COVID-19 report symptoms of brain fog after infection, similar to recovery from other viral infections. The pathophysiology is not well understood but is suspected to be multifactorial, and investigation into the underlying etiology and predominant causative factors in many cases may establish a more specific description. Neuropsychological testing may help quantify the degree of cognitive dysfunction, if present. Comorbid psychiatric conditions, such as depression, anxiety, or posttraumatic stress disorder, may further contribute to cognitive symptoms and diagnostic clarity, as many cases may reside in the border zone of organic and nonorganic etiologies. For patients with objective cognitive dysfunction or significant disability, it is important to evaluate for other underlying causes of cognitive decline that may have been exacerbated or unmasked with COVID-19 infection. Although high quality evidence has demonstrated that SARS-CoV2 can infect brain cells (astrocytes) and cause metabolic and structure changes, thus, supporting a neurotropism in severe cases, the abundance of autopsy and neuroimaging studies has indicated that the predominant mechanisms of injury is indirect via hypoxia neuroinflammation, microvascular injury, and blood-brain barrier disruptive mechanisms rather than a widespread direct viral invasion of neurons and support cells (11; 14).
Dysautonomia. Symptoms related to autonomic dysfunction are not infrequently reported after COVID-19 infection. These symptoms include lightheadedness, dizziness, small fiber neuropathy, exercise intolerance, and fatigue, among others. As many of these symptoms overlap with symptoms seen in postural orthostatic tachycardia syndrome (POTS), the diagnosis of POTS has been increasingly made in this patient population (57). The management of POTS is similar in patients with or without preceding COVID-19 infection.
Small fiber neuropathy has emerged as a potential mechanism for autonomic and sensory symptoms in some patients with long COVID. However, the pathogenesis of persistent myalgia remains unclear (02).
Dizziness. Dizziness is frequently reported both during and after COVID-19 infection. Descriptions of dizziness are often variable and nonspecific. Objective vestibular dysfunction is reported, but definitive objective evidence demonstrating a causal relationship is lacking. The American Academy of Physical Medicine and Rehabilitation recognizes vestibular rehabilitation as a beneficial management strategy for post-COVID-19 dizziness and vestibular disorders endorsed in their consensus guidelines (68; 51).
Neuropathy and pain. Patients who recover from COVID-19 often report the development of neuropathic symptoms. Neuropathy distribution can vary among patients and may be length-dependent, focal, or patchy. It has been proposed that small fiber neuropathy may be the underlying etiology of neuropathy in a proportion of these patients (01). Management is largely symptomatic, and there is no specific treatment for COVID-19-related neuropathy and pain.
Sleep disturbance. Some patients report significant sleep disturbances after COVID-19 infection, particularly insomnia. This may further exacerbate other symptoms, such as fatigue. Management is similar to that for patients without COVID-19 infection.
Other complications
Risk factors for neurologic complications. Advanced age, obesity, cardiac and respiratory disorders, hypertension, and diabetes are the most common comorbidities present in patients with more severe manifestations of the infection. Marked elevation in D-dimer levels, unvaccinated status, and admission hyperglycemia are now recognized as independent risk factors for developing serous neurologic complications in hospitalized patients with COVID-19 (05).
An interesting hypothesis has emerged around the use of ACE inhibitors to treat hypertension and diabetes to explain this phenomenon. ACE2 is the receptor for SARS-CoV-2 (83). The use of ACE inhibitors may lead to increased expression of ACE2, theoretically making the cells more vulnerable to infection with the virus. However, there is no evidence that stopping ACE inhibitors or angiotensin receptor blockers (ARBs) improves outcomes in COVID-19 infection, and it may potentially worsen outcomes (43). Therefore, patients receiving treatment with these agents should continue unless there is another strong indication to discontinue.
Risks of COVID-19 for patients with neurologic diseases. Patients with neurologic diseases tend to be older than those without, so risks associated with COVID-19 are of particular concern for neurologists who care for these patients. Additionally, inflammatory-mediated neurologic diseases necessitate immunosuppressive medications. In myasthenia gravis, for example, a registry study of 91 patients reported that 22 (24%) died from COVID-19 (56). Also, because patients with neurologic disability often require physical assistance and care from loved ones or from specialized facilities, there are additional risks of infection from this loss of independence.
Biological basis
Coronaviruses are enveloped viruses with a positive-sense single-stranded RNA genome. The word corona is derived from crown, which describes the spike-like proteins on the viral surface. They are classified as four genera: Alpha, Beta, Gamma, and Delta. The Alpha and Beta coronaviruses primarily infect mammals, the Gamma coronaviruses primarily infect birds, and the Delta coronaviruses infect mammals and birds. Cross-species transmission has led to the emergence of clinically severe human coronavirus infections, including the Middle East respiratory syndrome (MERS) caused by MERS-CoV, severe acute respiratory syndrome (SARS) caused by SARS-CoV-1, and COVID-19 caused by SARS-CoV-2, with widespread transmission and deadly consequences (38).
To date, seven human coronaviruses have been identified (Table 1). Among these, SARS and SARS-CoV-2 are thought to have originated from bats (66), with a possible intermediate host facilitating zoonotic transmission. Entry into the host cell is facilitated by the spike proteins that attach to angiotensin-converting enzyme receptor type 2 (ACE2), which is highly expressed in the respiratory tract. ACE2 receptors are also known to be expressed in both neurons and glia in several CNS areas, most notably in the choroid plexus and the thalamus.
The landscape of identified variants and sub-lineages of SARS-CoV-2 continues to expand. The World Health Organization and the Centers for Disease Control and Prevention have designated major strains as variants of concern or interest, and those are being monitored. The most predominant variant worldwide with multiple sub-lineages is the Omicron variant. Other important globally recognized variants include Alpha, Beta, Gamma, and Delta. Neurotropism and neurovirulence differences between strains and sublineages are under investigation.
The most predominant strain is the Omicron strain (06; 45; 09).
Table 1. Types of Human Coronaviruses and Their Receptors
Alpha coronaviruses | Receptor |
HCoV-NL63 | ACE2 |
HCoV229E | hAPN |
Beta coronaviruses | |
SARS-CoV1 | ACE2 |
SARS-CoV-2 | ACE2 |
MERS | DPP4 |
HCoV-OC43 | 9-O-acetylsialic acid plus other sialoglycan-based receptors |
HCoV-HKU1 | |
| 9-O-acetylsialic acid |
ACE=angiotensin converting enzyme; hAPN=human aminopeptidase N (CD13); DPP4=dipeptidyl peptidase 4 | |
The virus has four main structural proteins: spike (S), envelope (E), membrane(M), and nucleocapsid (N). The S protein is a trimeric glycoprotein composed of two separate polypeptides called S1 (binding domain) and S2 (stalk) (24). They mediate attachment to the host receptor and are the primary target for neutralizing antibodies and vaccines. The M protein is the most abundant structural protein in the virion. The envelope protein facilitates the assembly and release of the virus. The ion channel activity in the SARS-CoV envelope protein plays a critical role in pathogenesis. The N protein constitutes the nucleocapsid that binds the viral RNA (70; 82; 25; 26; 53).
Important lessons from the COVID-19 pandemic
Teleneurology. The barriers to physical contact necessitated by the pandemic have altered the landscape for providing neurologic care. In order to continue providing both inpatient and outpatient services, neurologists at many centers quickly adopted teleneurology protocols that were previously limited to telestroke or for geographically isolated settings. Teleneurology has to date included emergency department consults done remotely from other areas of the hospital, policy restrictions being relaxed at both a hospital level and a government level, and some states allowing remote practice of medicine across state lines. These changes were adapted quickly, using the existing infrastructure in many cases, and could potentially alter the care and practice of neurology if many of the changes persist beyond the pandemic (31).
Ethical dilemma. The COVID-19 pandemic brought to light numerous ethical issues involving neurologists and their patients, notably that many of our patients are unable to advocate for themselves because of neurologic disease, or that, because of neurologic disease, their lives are considered less valuable. In times when medications and life-saving devices may be limited, patients with neurologic diseases have often been at the forefront of scenarios, eg, the idea that patients with COVID-19 and comorbid dementia may be removed from a ventilator because of resource scarcity (30). These scenarios are difficult to imagine, but as neurologists, we have a responsibility to remain advocates for our patients, especially when they are at their most vulnerable.
Unique ethical challenges were also introduced by teleneurology, including concerns about privacy, data security, and equitable access. Ongoing proactive collaboration among government leaders, hospital systems, providers, and patients is needed to ensure responsible development and access to this technology.
Prevention and considerations
Vaccine-associated adverse neurologic events. Remarkably, severe COVID-19 has become a largely preventable disease since the introduction and widespread availability of several SARS-CoV-2 vaccines, including mRNA-based vaccines and recombinant spike protein subunit-based vaccines. As with other vaccines, there have been rare reports of neurologic complications. Neurologic adverse events are estimated to occur in 0.03% of all doses administered based on data from the Vaccine Adverse Event Reporting System (VAERS). Most adverse events are transient and include headache, myalgia, fatigue, and syncope. Rare reports of immune-mediated and cerebrovascular events are briefly outlined below. It is important for patients to know that neurologic complications following COVID-19 infection are estimated to be 617-fold higher than neurologic complications following COVID-19 vaccination (15).
Immune-mediated events. Similar to other vaccines, several immune-mediated events have been reported in association with COVID-19 vaccines. These syndromes typically present several days to weeks after vaccination and include Guillain-Barré syndrome, Bell palsy, and a wide variety of demyelinating events (multiple sclerosis, NMOSD, MOGAD, ADEM, transverse myelitis, optic neuritis) (15). These complications are quite rare and, importantly, were most frequently encountered with the adenoviral vector-based vaccine, which is no longer approved for use in the United States (59; 40).
Cerebrovascular events. There are rare reports of ischemic stroke, hemorrhagic stroke, and cerebral venous sinus thrombosis following COVID-19 vaccination, though the causal relationship is unclear. A systematic review concluded that the proportion of acute ischemic stroke following COVID-19 vaccination is similar to the general population and significantly less than the risk associated with COVID-19 infection (72). It is important to note that most reported cases describing venous sinus thrombosis following COVID-19 vaccination were associated with the adenoviral vector-based vaccine, which is no longer available in the United States.
In summary, although rare immune-mediated and cerebrovascular complications can occur after COVID-19 vaccination, the absolute risk is low and is far outweighed by the risk associated with SARS-CoV-2 infection.
References
- 01
- Abrams RM, Simpson DM, Navis A, Jette N, Zhou L, Shin SC. Small fiber neuropathy associated with SARS-CoV-2 infection. Muscle Nerve 2022;65(4):440-3. PMID 34766365
- 02
- Abrams RM, Zhou L, Shin SC. Persistent post-COVID-19 neuromuscular symptoms. Muscle Nerve 2023;68(4):350-5. PMID 37466117
- 03
- Abu-Rumeileh S, Abdelhak A, Foschi M, Tumani H, Otto M. Guillain-Barré syndrome spectrum associated with COVID-19: an up-to-date systematic review of 73 cases. J Neurol 2021;268(4):1133-70. PMID 32840686
- 04
- Aschman T, Schneider J, Greuel S, et al. Association between SARS-CoV-2 infection and immune-mediated myopathy in patients who have died. JAMA Neurol 2021;78(8):948-60. PMID 34115106
- 05
- Aslam J, Luqman S, Nazly S, et al. Predictors of fatal neurological complications among admitted COVID-19 patients with their implication in outcome: a case control study. PLoS One 2022;17(9):e0274485. PMID 36156595
- 06
- Barouch DH. Covid-19 vaccines: immunity, variants, boosters. N Engl J Med 2022;387(11):1011-20. PMID 36044620
- 07
- Brann DH, Tsukahara T, Weinreb C, et al. Non-neuronal expression of SARS-CoV-2 entry genes in the olfactory system suggests mechanisms underlying COVID-19-associated anosmia. Sci Adv 2020;6(31):eabc5801. PMID 32937591
- 08
- Burkert FR, Lanser L, Bellmann-Weiler R, Weiss G. Coronavirus disease 2019: clinics, treatment, and prevention. Front Microbiol 2021;12:761887. PMID 34858373
- 09
- Chakraborty C, Bhattacharya M, Abdelhameed AS. Recent SARS-CoV-2 evolution trajectories indicate the emergence of Omicron's several subvariants and the current rise of KP.3.1.1 and XEC. Virology 2025;607:110508. PMID 40187091
- 10
- Censi S, Bisaccia G, Gallina S, Tomassini V, Uncini A. Guillain-Barré syndrome and SARS-CoV-2 infection: a systematic review and meta-analysis on a debated issue and evidence for the Italian factor. Eur J Neurol 2024;31(2):e16094. PMID 37823707
- 11
- Crunfli F, Carregari VC, Veras FP, et al. Morphological, cellular, and molecular basis of brain infection in COVID-19 patients. Proc Natl Acad Sci U S A 2022;119(35):e2200960119. PMID 35951647
- 12
- Filosto M, Cotti Piccinelli S, Gazzina S, et al. Guillain-Barré syndrome and COVID-19: a 1-year observational multicenter study. Eur J Neurol 2022;29(11):3358-67. PMID 35837806
- 13
- Filosto M, Cotti Piccinelli S, Gazzina S, et al. Guillain-Barré syndrome and COVID-19: an observational multicentre study from two Italian hotspot regions. J Neurol Neurosurg Psychiatry 2021;92(7):751-6. PMID 33158914
- 14
- Frontera JA, Simon NM. Bridging knowledge gaps in the diagnosis and management of neuropsychiatric sequelae of COVID-19. JAMA Psychiatry 2022;79(8):811-17. PMID 35767287
- 15
- Frontera JA, Tamborska AA, Doheim MF, et al. Neurological events reported after COVID-19 vaccines: an analysis of VAERS. Ann Neurol 2022;91(6):756-71. PMID 35233819
- 16
- Ganesh A, Reis IR, Varma M, Patry DG, Cooke LJ. Neurological and head/ears/eyes/nose/throat manifestations of COVID-19: a systematic review and meta-analysis. Can J Neurol Sci 2022;49(4):514-31. PMID 34287109
- 17
- Gao L, Zheng C, Shi Q, et al. Evolving trend change during the COVID-19 pandemic. Front Public Health 2022;10:957265. PMID 36203708
- 18
- Garg RK, Paliwal VK, Gupta A. Spinal cord involvement in COVID-19: a review. J Spinal Cord Med 2023;46(3):390-404. PMID 33705268
- 19
- Gregory CO, Hall A. COVID-19. In: Brunette GW, editor. CDC Yellow Book 2024: Health Information for International Travel. Oxford University Press, 2024.
- 20
- Guan WJ, Ni ZY, Hu Y, et al. Clinical characteristics of coronavirus disease 2019 in China. N Engl J Med 2020;382(18):1708-20. PMID 32109013
- 21
- Gutierrez-Ortiz C, Méndez-Guerrero A, Rodrigo-Rey S, et al. Miller Fisher syndrome and polyneuritis cranialis in COVID-19. Neurology 2020;95(5):e601-5. PMID 32303650
- 22
- Henderson LA, Canna SW, Friedman KG, et al. American College of Rheumatology clinical guidance for multisystem inflammatory syndrome in children associated with sars-cov-2 and hyperinflammation in pediatric COVID-19: version 2. Arthritis Rheumatol 2021;73(4):e13-29. PMID 33277976
- 23
- Holshue ML, DeBolt C, Lindquist S. First case of 2019 novel coronavirus in the United States. N Engl J Med 2020;382(10):929-36. PMID 32004427
- 24
- Huang Y, Yang C, Xu XF, Xu W, Liu SW. Structural and functional properties of SARS-CoV-2 spike protein: potential antivirus drug development for COVID-19. Acta Pharmacol Sin 2020;41(9):1141-9. PMID 32747721
- 25
- Jahirul Islam M, Nawal Islam N, Siddik Alom M, Kabir M, Halim MA. A review on structural, non-structural, and accessory proteins of SARS-CoV-2: Highlighting drug target sites. Immunobiology 2023;228(1):152302. PMID 36434912
- 26
- Kakavandi S, Zare I, VaezJalali M, et al. Structural and non-structural proteins in SARS-CoV-2: potential aspects to COVID-19 treatment or prevention of progression of related diseases. Cell Commun Signal 2023;21(1):110. PMID 37189112
- 27
- Kennedy M, Helfand BKI, Gou RY, et al. Delirium in older patients with COVID-19 presenting to the emergency department. JAMA Netw Open 2020;3(11):e2029540. PMID 33211114
- 28
- Kesheh MM, Hosseini P, Soltani S, Zandi M. An overview on the seven pathogenic human coronaviruses. Rev Med Virol 2022;32(2):e2282. PMID 34339073
- 29
- Kim JE, Heo JH, Kim HO, et al. Neurological complications during treatment of Middle East respiratory syndrome. J Clin Neurol 2017;13(3):227-33. PMID 28748673
- 30
- Kim SY, Grady C. Ethics in the time of COVID: What remains the same and what is different. Neurology 2020;94(23):1007-8. PMID 32253351
- 31
- Klein BC, Busis NA. COVID-19 is catalyzing the adoption of teleneurology. Neurology 2020;94(21):903-4. PMID 32238505
- 32
- Krause PR, Fleming TR, Longini IM, et al. SARS-CoV-2 variants and vaccines. N Engl J Med 2021;385(2):179-86. PMID 34161052
- 33
- Kremer S, Lersy F, Anheim M, et al. Neurologic and neuroimaging findings in COVID-19 patients: A retrospective multicenter study. Neurology 2020;95(13):e1868-82. PMID 32680942
- 34
- Kuroda N. Epilepsy and COVID-19: updated evidence and narrative review. Epilepsy Behav 2021;116:107785. PMID 33515934
- 35
- LaRovere KL, Riggs BJ, Poussaint TY, et al. Neurologic involvement in children and adolescents hospitalized in the United States for COVID-19 or multisystem inflammatory syndrome. JAMA Neurol 2021;78(5):536-47. PMID 33666649
- 36
- Lechien JR, Chiesa-Estomba CM, De Siati DR, et al. Olfactory and gustatory dysfunctions as a clinical presentation of mild-to-moderate forms of the coronavirus disease (COVID-19): a multicenter European study. Eur Arch Otorhinolaryngol 2020;277(8):2251-61. PMID 32253535
- 37
- Lersy F, Benotmane I, Helms J, et al. Cerebrospinal fluid features in patients with coronavirus disease 2019 and neurological manifestations: correlation with brain magnetic resonance imaging findings in 58 patients. J Infect Dis 2021;223(4):600-9. PMID 33249438
- 38
- Li F. Structure, function, and evolution of coronavirus spike proteins. Ann Rev Virol 2016;3(1):237-61. PMID 27578435
- 39
- Li Y, Li M, Wang M, et al. Acute cerebrovascular disease following COVID-19: a single center, retrospective, observational study. Stroke Vasc Neurol 2020;5(3):279-84. PMID 32616524
- 40
- Li X, Raventós B, Roel E, et al. Association between COVID-19 vaccination, SARS-CoV-2 infection, and risk of immune mediated neurological events: population based cohort and self-controlled case series analysis. BMJ 2022;376:e068373. PMID 35296468
- 41
- Liotta EM, Batra A, Clark JR, et al. Frequent neurologic manifestations and encephalopathy-associated morbidity in Covid-19 patients. Ann Clin Transl Neurol 2020;7(11):2221-30. PMID 33016619
- 42
- Lopes CCB, Brucki SMD, Neto CEBP, et al. Acute disseminated encephalomyelitis in COVID-19: presentation of two cases and review of the literature. Arq Neuropsiquiatr 2020;78(12):805-10. PMID 33295423
- 43
- Lopes RD, Macedo AVS, de Barros E Silva PGM, et al. Effect of discontinuing vs continuing angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers on days alive and out of the hospital in patients admitted with COVID-19: a randomized clinical trial. JAMA 2021;325(3):254-64. PMID 33464336
- 44
- Lu R, Zhao X, Li J, et al. Genomic characterisation and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding. Lancet 2020;395(10224):565-74. PMID 32007145
- 45
- Ma KC, Shirk P, Lambrou AS, et al. Genomic surveillance for SARS-CoV-2 variants: circulation of Omicron lineages - United States, January 2022-May 2023. MMWR Morb Mortal Wkly Rep 2023;72(24):651-6. PMID 37319011
- 46
- Mainali S, Darsie ME. Neurologic and neuroscientific evidence in aged COVID-19 patients. Front Aging Neurosci 2021;13:648662. PMID 33833676
- 47
- Manzano GS, McEntire CR, Martinez-Lage M, Mateen FJ, Hutto SK. Acute disseminated encephalomyelitis and acute hemorrhagic leukoencephalitis following COVID-19: systematic review and meta-synthesis. Neurol Neuroimmunol Neuroinflamm 2021;8(6):e1080. PMID 34452974
- 48
- Manzano GS, Woods JK, Amato AA. Covid-19-associated myopathy caused by type I interferonopathy. N Engl J Med 2020;383(24):2389-90. PMID 33216474
- 49
- Matschke J, Lütgehetmann M, Hagel C, et al. Neuropathology of patients with COVID-19 in Germany: a post-mortem case series. Lancet Neurol 2020;19(11):919-29. PMID 33031735
- 50
- McArdle AJ, Vito O, Patel H, et al. Treatment of multisystem inflammatory syndrome in children. N Engl J Med 2021;385(1):11-22. PMID 34133854
- 51
- Melamed E, Rydberg L, Ambrose AF, et al. Multidisciplinary collaborative consensus guidance statement on the assessment and treatment of neurologic sequelae in patients with post-acute sequelae of SARS-CoV-2 infection (PASC). PM R 2023;15(5):640-62. PMID 36989078
- 52
- Meyerowitz EA, Scott J, Richterman A, Male V, Cevik M. Clinical course and management of COVID-19 in the era of widespread population immunity. Nat Rev Microbiol 2024;22(2):75-88. PMID 38114838
- 53
- Minigulov N, Boranbayev K, Bekbossynova A, Gadilgereyeva B, Filchakova O. Structural proteins of human coronaviruses: what makes them different? Front Cell Infect Microbiol 2024;14:1458383. PMID 39711780
- 54
- Moriguchi T, Harii N, Goto J, et al. A first case of meningitis/encephalitis associated with SARS-coronavirus-2. Int J Infect Dis 2020;94:55-8. PMID 32251791
- 55
- Mullaguri N, Sivakumar S, Battineni A, Anand S, Vanderwerf J. COVID-19 related acute hemorrhagic necrotizing encephalitis: a report of two cases and literature review. Cureus 2021;13(4):e14236. PMID 33948421
- 56
- Muppidi S, Guptill JT, Jacob S, et al. COVID-19-associated risks and effects in myasthenia gravis (CARE-MG). Lancet Neurol 2020;19(12):970-1. PMID 33212055
- 57
- Ormiston CK, Świątkiewicz I, Taub PR. Postural orthostatic tachycardia syndrome as a sequela of COVID-19. Heart Rhythm 2022;19(11):1880-9. PMID 35853576
- 58
- Paterson RW, Brown RL, Benjamin L, et al. The emerging spectrum of COVID-19 neurology: clinical, radiological and laboratory findings. Brain 2020;143(10):3104-20.** PMID 32637987
- 59
- Patone M, Handunnetthi L, Saatci D, et al. Neurological complications after first dose of COVID-19 vaccines and SARS-CoV-2 infection. Nat Med 2021;27(12):2144-2153. PMID 34697502
- 60
- Pilotto A, Masciocchi S, Volonghi I, et al. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) encephalitis is a cytokine release syndrome: evidences from cerebrospinal fluid analyses. Clin Infect Dis 2021;73(9):e3019-26. PMID 33395482
- 61
- Qureshi AI, Baskett WI, Huang W, et al. Acute ischemic stroke and COVID-19: an analysis of 27 676 patients. Stroke 2021;52(3):905-12. PMID 33535779
- 62
- Reichart S, Behrens-Baumann WJ, Dirschmind H, Gallastroni LP, Mennel S. Severe acute respiratory syndrome coronavirus 2, face mask and keratitis: can extended use of face masks trigger keratitis? Ophthalmologe 2020;1-3. PMID 33252770
- 63
- Renaud M, Thibault C, Le Normand F, et al. Clinical outcomes for patients with anosmia 1 year after COVID-19 diagnosis. JAMA Netw Open 2021;4(6):e2115352. PMID 34165581
- 64
- Riphagen S, Gomez X, Gonzalez-Martinez C, Wilkinson N, Theocharis P. Hyperinflammatory shock in children during COVID-19 pandemic. Lancet 2020;395(10237):1607-8. PMID 32386565
- 65
- Roman GC, Gracia F, Torres A, Palacios A, Gracia K, Harris D. Acute transverse myelitis (ATM): clinical review of 43 patients with COVID-19-associated ATM and 3 post-vaccination ATM serious adverse events with the ChAdOx1 nCoV-19 vaccine (AZD1222). Front Immunol 2021;12:653786. PMID 33981305
- 66
- Ruiz-Aravena M, McKee C, Gamble A, et al. Ecology, evolution and spillover of coronaviruses from bats. Nat Rev Microbiol 2022;20(5):299-314. PMID 34799704
- 67
- Samim MM, Dhar D, Goyal S, et al. AI-CoV study: autoimmune encephalitis associated with COVID-19 and its vaccines-a systematic review. J Clin Neurol 2022;18(6):692-710. PMID 36367067
- 68
- Saniasiaya J, Kulasegarah J. Dizziness and COVID-19. Ear Nose Throat J 2021;100(1):29-30. PMID 32931322
- 69
- Schiffmann A. Coronavirus dashboard. Available from: https://ncov2019.live/data. Accessed 2021.
- 70
- Shajahan A, Pepi LE, Rouhani DS, Heiss C, Azadi P. Glycosylation of SARS-CoV-2: structural and functional insights. Anal Bioanal Chem 2021;413(29):7179-93. PMID 34235568
- 71
- Siow I, Lee KS, Zhang JJY, Saffari SE, Ng A. Encephalitis as a neurological complication of COVID-19: a systematic review and meta-analysis of incidence, outcomes, and predictors. Eur J Neurol 2021;28(10):3491-502. PMID 33982853
- 72
- Stefanou MI, Palaiodimou L, Aguiar de Sousa D, et al. Acute arterial ischemic stroke following COVID-19 vaccination: a systematic review and meta-analysis. Neurology 2022;99(14):e1465-74. PMID 36002319
- 73
- Suh J, Mukerji SS, Collens SI, et al. Skeletal muscle and peripheral nerve histopathology in COVID-19. Neurology 2021;97(8):e849-58. PMID 34099523
- 74
- Tan BK, Han R, Zhao JJ, et al. Prognosis and persistence of smell and taste dysfunction in patients with covid-19: meta-analysis with parametric cure modelling of recovery curves. BMJ 2022;378:e069503. PMID 35896188
- 75
- Tang G, Liu Z, Chen D. Human coronaviruses: Origin, host and receptor. J Clin Virol 2022;155:105246. PMID 35930858
- 76
- Tian S, Hu N, Lou J, et al. Characteristics of COVID-19 infection in Beijing. J Infect 2020;80(4):401-6. PMID 32112886
- 77
- Toscano G, Palmerini F, Ravaglia S, et al. Guillain-Barre syndrome associated with SARS-CoV-2. N Engl J Med 2020;382(26):2574-6. PMID 32302082
- 78
- Valencia Sanchez C, Theel E, Binnicker M, Toledano M, McKeon A. Autoimmune encephalitis after SARS-CoV-2 infection: case frequency, findings, and outcomes. Neurology 2021;97(23):e2262-8. PMID 34635560
- 79
- von Bartheld CS, Wang L. Prevalence of olfactory dysfunction with the Omicron variant of SARS-CoV-2: a systematic review and meta-analysis. Cells 2023;12(3):430. PMID 36766771
- 80
- Wan D, Du T, Hong W, et al. Neurological complications and infection mechanism of SARS-COV-2. Signal Transduct Target Ther 2021;6(1):406. PMID 34815399
- 81
- Wang Y, Wang Y, Huo L, Li Q, Chen J, Wang H. SARS-CoV-2-associated acute disseminated encephalomyelitis: a systematic review of the literature. J Neurol 2022;269(3):1071-92. PMID 34459986
- 82
- Yadav R, Chaudhary JK, Jain N, et al. Role of structural and non-structural proteins and therapeutic targets of SARS-CoV-2 for COVID-19. Cells 2021;10(4):821. PMID 33917481
- 83
- Yan R, Zhang Y, Li Y, Xia L, Guo Y, Zhou Q. Structural basis for the recognition of SARS-CoV-2 by full-length human ACE2. Science 2020;367(6485):1444-8. PMID 32253352
- 84
- Yeh EA, Collins A, Cohen ME, Duffner PK, Faden H. Detection of coronavirus in the central nervous system of a child with acute disseminated encephalomyelitis. Pediatrics 2004;113(1 Pt 1):e73-6. PMID 14702500
- 85
- Younger DS. COVID-19 postmortem neuropathology: insights of a meta-analysis of 464 cases. Neurol Sci 2025;46(9):4703-6. PMID 40560519
- 86
- Zarifkar P, Peinkhofer C, Benros ME, et al. Frequency of neurological diseases after COVID-19, influenza A/B and bacterial pneumonia. Front Neurol 2022;13:904796. PMID 35812108
- 87
- Zeng N, Zhao YM, Yan W, et al. A systematic review and meta-analysis of long term physical and mental sequelae of COVID-19 pandemic: call for research priority and action. Mol Psychiatry 2023;28(1):423-33. PMID 35668159
- 88
- References especially recommended by the author or editor for general reading.
Contributors
All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.
Author
-
Paul Crane MD
Dr. Crand of University of Utah Health has no relevant financial relationships to disclose.
See Profile
Editor
-
John E Greenlee MD
Dr. Greenlee of the University of Utah School of Medicine has no relevant financial relationships to disclose.
See Profile
Former Authors
- Avindra Nath MD
- Rohit Benjamin MD
- Bryan Smith MD
- Rumyar V Ardakani MD
- Amanda L Piquet MD
ICD & OMIM codes
- ICD-10
-
- U07.1: COVID-19, virus identified (confirmed by laboratory testing)
- ICD-11
-
- RA01.0: COVID-19 (confirmed)
- RA01.1: COVID-19 (suspected or probable)
This is an article preview.
Start a Free Account
to access the full version.
-
Nearly 3,000 illustrations, including video clips of neurologic disorders.
-
Every article is reviewed by our esteemed Editorial Board for accuracy and currency.
-
Full spectrum of neurology in 1,200 comprehensive articles.
-
Listen to MedLink on the go with Audio versions of each article.
Questions or Comment?
MedLink, LLC
3525 Del Mar Heights Rd, Ste 304
San Diego, CA 92130-2122
Toll Free (U.S. + Canada): 800-452-2400
US Number: +1-619-640-4660
Support: service@medlink.com
Editor: editor@medlink.com
ISSN: 2831-9125
Also in This Category
-
-
Infectious Disorders
Cryptococcal meningitis
May. 01, 2026
-
Infectious Disorders
Tuberculosis of the CNS
Apr. 30, 2026
-
Headache & Pain
Headache associated with HIV and AIDS
Apr. 10, 2026
-
Infectious Disorders
Whipple disease
Apr. 08, 2026
-
Infectious Disorders
Post-polio syndrome
Mar. 28, 2026
-
Infectious Disorders
Coccidioidomycosis: neurologic manifestations
Mar. 27, 2026
-
Infectious Disorders
Viral meningitis
Mar. 13, 2026