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The Spectrum of Neurologic Disease in the Severe Acute Respiratory Syndrome Coronavirus 2 Pandemic Infection
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from Jules: It seems that big inflammatory/immune responses accompany COVID & might be the cause of severe responses & as found & reported in this study below on neurologic sympyomology found in COVID infection. Out of China was report in HIV+ & COVID where PLWH did not respond worse than HIV- and some HIV+ seem to respond better in not getting COVID, or after getting COVID. There have been a few other anecdotal reports suggesting similarly, that HIV+ do not respond worse & the reason suggested is because HIV+ may not mount a normal or typical response due to HIV repressed immunity:
Survey for COVID-19 Among HIV/AIDS Patients in Two Districts of Wuhan, China
13 Mar 2020
https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3550029
Abstract
Background: There were over 49 thousand Coronavirus infected diseases-19(COVID-19) patients in Wuhan city, Hubei province, China, the center of epidemic of the disease. Over 5000 HIV/AIDS patients live in Wuhan. No data on the morbidity of COVID-19 in HIV/AIDS patients have been published to date.
Methods: In this study, we investigated 1178 HIV/AIDS patients in two central districts in Wuhan city. Whether they have any clinical presentations and whether they contacted any confirmed COVID-19 patients were inquired. The results for nucleic acid test (NAT) of SARS-CoV-2 and CT scan in those with clinical symptoms or contact history were investigated. The antiretroviral regimens of all these patients and other information, like age, sex, CD4+T cell counts (CD4 counts), HIV viral load (HIV-VL) were also collected. The risk factors for the COVID-19 in HIV/AIDS patients were analyzed.
Findings: We found 12 individuals in 1174 HIV/AIDS patients who presented clinical symptoms, and 8 of them were confirmed COVID-19. Six of them were NAT confirmed SARS-CoV-2 infection, and 2 were clinical confirmed cases. Six of the 8 COVID-19 patients had CD4 counts> 350/μl, and 2 with CD4 counts between 101-350/μl. All of the 8 patients have a low HIV-VL＜20 copies/ml. The older age is the risk factor to occur COVID-19 in HIV/AIDS. All the 8 COVID-19 patients were from 947 individuals (0.84%) who took NRTI+NNRTI as antiretroviral regimen. In those who have no symptoms, there were another 9 HIV/AIDS patients had close contact with confirmed COVID-19 patients, and only 1 of them was confirmed positive by NAT.
Interpretation: Our findings indicated that the compromised immunity might be the reason that HIV/AIDS patients did not occur inflammatory changes and clinical symptoms, which support the early usage of corticosteroids in treatment for COVID-19. At the same time, the usage of LPV/r may potentially help to prevent or treat COVID-19.
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April 10, 2020
Editorial
April 10, 2020
The Spectrum of Neurologic Disease in the Severe Acute Respiratory Syndrome Coronavirus 2 Pandemic Infection - Neurologists Move to the Frontlines
In this issue of JAMA Neurology, a retrospective consecutive case series1 of 214 patients from Wuhan, China, with either moderate or severe COVID-19 reports an early view of the incidence and types of neurologic complications and sets the stage for future longitudinal work in the area.
Prevalence of Neurologic Disease in SARS (SARS-CoV-1)
The typical clinical syndrome was a respiratory illness with severe lung injury and viral pneumonia, and there was a very high mortality in patients older than 65 years (approximately 50%).
Although the SARS epidemic was limited to about 8000 patients worldwide, there were some limited reports of neurologic complications of SARS that appeared in patients 2 to 3 weeks into the course of the illness, mainly consisting of either an axonal peripheral neuropathy or a myopathy with elevated creatinine kinase.4 At the time, it was unclear whether some of these manifestations might be owing to critical illness–related effects,5 but pathology subsequently showed that patients with SARS had widespread vasculitis seen in many organs, including striated muscle,6 suggesting that the clinical features in these neuromuscular patients might be more than just nonspecific complications of severe illness. Interestingly, there was a single report of a patient with SARS with olfactory neuropathy with onset 3 weeks into the illness.7
In addition to these peripheral syndromes, 5 of 206 patients with SARS in Singapore developed large-vessel strokes. Four of these patients had their strokes in the setting of critical illness owing to SARS, and 3 were associated with significant episodes of hypotension.
Prevalence and Timing of COVID-19 Neurologic Symptoms in Disease Course
In light of the sparse history of neurologic manifestations of SARS-CoV-1–associated disease, the report by Mao et al1 is important. In these 214 patients, they report 36.4% had some nervous system–related clinical finding.1 These neurologic manifestations ranged from fairly specific symptoms (eg, loss of sense of smell or taste, myopathy, and stroke) to more nonspecific symptoms (eg, headache, depressed level of consciousness, dizziness, or seizure).1 Whether these more nonspecific symptoms are manifestations of the disease itself or consistent with a systemic inflammatory response in patients who were quite ill will need to be defined in future studies. Importantly, the authors found that patients in their series with some of the more common specific symptoms, including smell or taste impairment and myopathy, tended to have these symptoms early in their clinical course; this appears to be quite distinct from SARS, where manifestations appeared quite late in established disease. A report8 of viral infiltration of the brainstem in a very limited number of pathologic specimens also raises the possibility that some of the crucial pathophysiology behind respiratory failure may be owing to central nervous system pathology, further expanding the view of which clinical manifestations of the current pandemic are truly neurologic in nature.
Most Stroke and Depressed Level of Consciousness Occurs Later and in More Severe Disease
Mao et al1 also found that neurologic symptoms were more common in patients with more severe disease (30.2% in nonsevere patients and 45.5% in severe patients). As has commonly been the case, they defined the severity based on respiratory features, defining mild as not requiring respiratory intervention, moderate as requiring some respiratory support, and severe as requiring mechanical ventilation. The more dramatic neurologic symptoms, such as stroke, ataxia, seizure, and depressed level of consciousness, all were more common in severely affected patients, accounting for the increased incidence in these patients.1 However, these associations should be considered in light of our understanding that patients with severe complications from SARS-COV-2 are more likely to have medical comorbidities, especially vascular risk factors such as hypertension.9 The occurrence of cerebrovascular events in critically ill patients with underlying high blood pressure and cardiovascular disease is therefore potentially unrelated to a direct effect of the infection itself or an inappropriate host response.
"In conclusion, SARS-CoV-2 may infect nervous system and skeletal muscle as well as the respiratory tract. In those with severe infection, neurologic involvement is greater, which includes acute cerebrovascular diseases, impaired consciousness, and skeletal muscle injury. .....In January 2020,3 ACE2 was identified as the functional receptor for SARS-CoV-2, which is present in multiple human organs, including nervous system and skeletal muscles....Central nervous system symptoms were the main form of neurologic injury in patients with COVID-19 in this study. The pathologic mechanism may be from the CNS invasion of SARS-CoV-2, similar to SARS and MERS viruses. As with other respiratory viruses, SARS-COV-2 may enter the CNS through the hematogenous or retrograde neuronal route. The latter can be supported by the fact that some patients in this study had smell impairment. We also found that the lymphocyte counts were lower for patients with CNS symptoms than without CNS symptoms. This phenomenon may be indicative of the immunosuppression in patients with COVID-19 with CNS symptoms, especially in the severe subgroup. Moreover, we found patients with severe infection had higher D-dimer levels than that of patients with nonsevere infection. This may be the reason why patients with severe infection are more likely to develop cerebrovascular disease.....Moreover, during the epidemic period of COVID-19, when seeing patients with these neurologic manifestations, clinicians should consider SARS-CoV-2 infection as a differential diagnosis to avoid delayed diagnosis or misdiagnosis and prevention of transmission.”
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https://jamanetwork.com/journals/jamaneurology/fullarticle/2764548
Neurologic Manifestations of Hospitalized Patients With Coronavirus Disease 2019 in Wuhan, China
JAMA Neurol. Published online April 10, 2020
https://jamanetwork.com/journals/jamaneurology/fullarticle/2764549
Key Points
Question
What are neurologic manifestations of patients with coronavirus disease 2019?
Findings
In a case series of 214 patients with coronavirus disease 2019, neurologic symptoms were seen in 36.4% of patients and were more common in patients with severe infection (45.5%) according to their respiratory status, which included acute cerebrovascular events, impaired consciousness, and muscle injury.
Meaning
Neurologic symptoms manifest in a notable proportion of patients with coronavirus disease 2019.
Abstract
Importance
The outbreak of coronavirus disease 2019 (COVID-19) in Wuhan, China, is serious and has the potential to become an epidemic worldwide. Several studies have described typical clinical manifestations including fever, cough, diarrhea, and fatigue. However, to our knowledge, it has not been reported that patients with COVID-19 had any neurologic manifestations.
Objective
To study the neurologic manifestations of patients with COVID-19.
Design, Setting, and Participants
This is a retrospective, observational case series. Data were collected from January 16, 2020, to February 19, 2020, at 3 designated special care centers for COVID-19 (Main District, West Branch, and Tumor Center) of the Union Hospital of Huazhong University of Science and Technology in Wuhan, China. The study included 214 consecutive hospitalized patients with laboratory-confirmed diagnosis of severe acute respiratory syndrome coronavirus 2 infection.
Main Outcomes and Measures
Clinical data were extracted from electronic medical records, and data of all neurologic symptoms were checked by 2 trained neurologists. Neurologic manifestations fell into 3 categories: central nervous system manifestations (dizziness, headache, impaired consciousness, acute cerebrovascular disease, ataxia, and seizure), peripheral nervous system manifestations (taste impairment, smell impairment, vision impairment, and nerve pain), and skeletal muscular injury manifestations.
Results
Of 214 patients (mean [SD] age, 52.7 [15.5] years; 87 men [40.7%]) with COVID-19,
126 patients (58.9%) had nonsevere infection
and 88 patients (41.1%) had severe infection according to their respiratory status.
Overall, 78 patients (36.4%) had neurologic manifestations.
Compared with patients with nonsevere infection, patients with severe infection were older, had more underlying disorders, especially hypertension, and showed fewer typical symptoms of COVID-19, such as fever and cough. Patients with more severe infection had neurologic manifestations, such as acute cerebrovascular diseases (5 [5.7%] vs 1 [0.8%]), impaired consciousness (13 [14.8%] vs 3 [2.4%]), and skeletal muscle injury (17 [19.3%] vs 6 [4.8%]).
- Patients with severe infection had more increased inflammatory response, including higher white blood cell counts, neutrophil counts, lower lymphocyte counts, and increased C-reactive protein levels compared with those patients with nonsevere infection.
- In addition, patients with severe infection had multiple organ involvement, such as serious liver (increased lactate dehydrogenase, alanine aminotransferase, and aspartate aminotransferase levels), kidney (increased blood urea nitrogen and creatinine levels), and skeletal muscle damage (increased creatinine kinase levels).
- Moreover, nervous system manifestations were significantly more common in severe infections compared with nonsevere infections (40 [45.5%] vs 38 [30.2%], P =n .02). They included acute cerebrovascular disease (5 [5.7%]; 4 patients with ischemic stroke and 1 with cerebral hemorrhage who died later of respiratory failure; vs 1 [0.8%]; 1 patient with ischemic stroke; P = .03, Figure), impaired consciousness (13 [14.8%] vs 3 [2.4%]; P < .001), and skeletal muscle injury (17 [19.3%] vs 6 [4.8%]; P < .001). In the severe group, 1 patient had a seizure characterized by a sudden onset of limb twitching, foaming in the mouth, and loss of consciousness, which lasted for 3 minutes.
-- Compared with the patients without muscle injury, patients with muscle injury had significantly higher levels of creatine kinase (median, 400.0 U/L [range 203.0-12216.0] vs median, 58.5 U/L [range 8.8-212.0]; P < .001), regardless of their severity. Meanwhile, patients with muscle injury had higher neutrophil counts, lower lymphocyte counts, higher C-reactive protein levels, and higher D-dimer levels. The abnormalities were manifestations of increased inflammatory response and blood coagulation function. In addition, we found that patients with muscle injury had multiorgan damage, including more serious liver (increased lactate dehydrogenase, alanine aminotransferase, and aspartate aminotransferase levels) and kidney (increased blood urea nitrogen and creatinine levels) abnormalities.
Conclusions and Relevance
Patients with COVID-19 commonly have neurologic manifestations. During the epidemic period of COVID-19, when seeing patients with neurologic manifestations, clinicians should suspect severe acute respiratory syndrome coronavirus 2 infection as a differential diagnosis to avoid delayed diagnosis or misdiagnosis and lose the chance to treat and prevent further transmission.
Introduction
In December 2019, many unexplained pneumonia cases occurred in Wuhan, China, and rapidly spread to other parts of China, then to Europe, North America, and Asia. This outbreak was confirmed to be caused by a novel coronavirus (CoV).1 The novel CoV was reported to have symptoms resembling that of severe acute respiratory syndrome CoV (SARS-CoV) in 2003.2 Both shared the same receptor, angiotensin-converting enzyme 2 (ACE2).3 Therefore, this virus was named SARS-CoV-2, and in February 2020, the World Health Organization (WHO) named the disease coronavirus disease 2019 (COVID-19). As of March 5, 2020, there were 95 333 confirmed cases of COVID-19 and 3282 deaths globally.4
Coronaviruses can cause multiple systemic infections or injuries in various animals.5 The CoVs can adapt quickly and cross the species barrier, such as with SARS-CoV and Middle East respiratory syndrome CoV (MERS-CoV), causing epidemics or pandemics. Infection in humans often leads to severe clinical symptoms and high mortality.6 As for COVID-19, several studies have described typical clinical manifestations including fever, cough, diarrhea, and fatigue. Coronavirus disease 2019 also has characteristic laboratory findings and lung computed tomography (CT) abnormalities.7 However, to our knowledge, it has not been reported that patients with COVID-19 had any neurologic manifestations. Here, we report the characteristic neurologic manifestations of SARS-CoV-2 infection in 78 of 214 patients with laboratory-confirmed diagnosis of COVID-19 and treated at our hospitals, which are located in the epicenter of Wuhan.
Results
Demographic and Clinical Characteristics
A total of 214 hospitalized patients with confirmed SARS-CoV-2 infection were included in the analysis. Their demographic and clinical characteristics were shown in Table 1. Their mean (SD) age was 52.7 (15.5) years, and 87 were men (40.7%).
Of these patients, 83 (38.8%) had at least 1 of the following underlying disorders: hypertension (51 [23.8%]), diabetes (30 [14.0%]), cardiac or cerebrovascular disease (15 [7.0%]), and malignancy (13 [6.1%]).
The most common symptoms at onset of illness were fever (132 [61.7%]), cough (107 [50.0%]), and anorexia (68 [31.8%]).
Seventy-eight patients (36.4%) had nervous system manifestations: CNS (53 [24.8%]), PNS (19 [8.9%]), and skeletal muscle injury (23 [10.7%]). In patients with CNS manifestations, the most common reported symptoms were dizziness (36 [16.8%]) and headache (28 [13.1%]). In patients with PNS symptoms, the most common reported symptoms were taste impairment (12 [5.6%]) and smell impairment (11 [5.1%]).
According to the American Thoracic Society guidelines for community-acquired pneumonia,10 88 patients (41.1%) had severe infection and 126 patients (58.9%) had nonsevere infection.
The patients with severe infection were significantly older (mean [SD] age, 58.2 [15.0] years vs 48.9 [14.7] years; P < .001) and more likely to have other underlying disorders (42 [47.7%] vs 41 [32.5%]; P = .03), especially hypertension (32 [36.4%] vs 19 [15.1%]; P < .001), and had fewer typical symptoms of COVID-19 such as fever (40 [45.5%] vs 92 [73%]; P < .001) and dry cough (30 [34.1%] vs 77 [61.1%]; P < .001).
Moreover, nervous system manifestations were significantly more common in severe infections compared with nonsevere infections (40 [45.5%] vs 38 [30.2%], P =n .02). They included acute cerebrovascular disease (5 [5.7%]; 4 patients with ischemic stroke and 1 with cerebral hemorrhage who died later of respiratory failure; vs 1 [0.8%]; 1 patient with ischemic stroke; P = .03, Figure), impaired consciousness (13 [14.8%] vs 3 [2.4%]; P < .001), and skeletal muscle injury (17 [19.3%] vs 6 [4.8%]; P < .001). In the severe group, 1 patient had a seizure characterized by a sudden onset of limb twitching, foaming in the mouth, and loss of consciousness, which lasted for 3 minutes.
Apart from cerebrovascular disease and impaired consciousness, most neurologic manifestations occurred early in the illness (median time, 1-2 days). Of 6 patients with acute cerebrovascular disease, 2 arrived at the emergency department owing to sudden onset of hemiplegia but without any typical symptoms (fever, cough, anorexia, and diarrhea) of COVID-19. Their lung lesions were found by an emergent lung CT and were diagnosed as having COVID-19 by a positive SARS-CoV-2 nucleic acid detection in the later stage. Some patients with fever and headache were admitted to the neurology ward after initially being ruled out of COVID-19 by routine blood test results and a screening lung CT in the clinic. However, several days later, they had typical COVID-19 symptoms such as cough, throat pain, lower lymphocyte count, and ground-glass opacity appearance on lung CT. Their diagnosis of COVID-19 was confirmed by a positive nucleic acid test and then they were transferred to the isolation ward.
Laboratory Findings in Patients and With Severe and Nonsevere Infection
Table 2 showed the laboratory findings in severe and nonsevere subgroups. Patients with severe infection had more increased inflammatory response, including higher white blood cell counts, neutrophil counts, lower lymphocyte counts, and increased C-reactive protein levels compared with those patients with nonsevere infection (white blood cell count: median, 5.4 x 109/L [range, 0.1-20.4] vs 4.5 x 109/L [range, 1.8-14.0]; P < .001; neutrophil: median, 3.8 x 109/L [range, 0.0-18.7] vs 2.6 x 109/L [range, 0.7-11.8]; P < .001; lymphocyte count: median, 0.9 x 109/L [range, 0.1-2.6] vs 1.3 x 109/L [range, 0.4-2.6]; P < .001; C-reactive protein: median, 37.1 mg/L [range, 0.1-212.0] vs 9.4 mg/L [range, 0.2-126.0]; P < .001). The patients with severe infection had higher D-dimer levels than patients with nonsevere infection (median, 0.9 mg/L [range, 0.1-20.0] vs 0.4 mg/L [range, 0.2-8.7]; P < .001), which was indicative of consumptive coagulation system. In addition, patients with severe infection had multiple organ involvement, such as serious liver (increased lactate dehydrogenase, alanine aminotransferase, and aspartate aminotransferase levels), kidney (increased blood urea nitrogen and creatinine levels), and skeletal muscle damage (increased creatinine kinase levels).
Laboratory Findings in Patients With and Without CNS Symptoms
Table 3 showed the laboratory findings of patients with and without CNS symptoms. We found that patients with CNS symptoms had lower lymphocyte levels, platelet counts, and higher blood urea nitrogen levels compared with those without CNS symptoms (lymphocyte count: median, 1.0 x 109/L [range, 0.1-2.3] vs 1.2 x 109/L [range, 0.2-2.6], P = .049; platelet count: median, 180.0 x 109/L [range, 18.0-564.0] vs 227.0 x 109/L [range, 42.0-583.0], P = .005; blood urea nitrogen: median, 4.5 mmol/L [range, 1.6-48.1] vs 4.1 mmol/L [range, 1.5-19.1], P = .04). For the severe subgroup, patients with CNS symptoms also had lower lymphocyte levels and platelet counts and higher blood urea nitrogen levels compared with those without CNS symptoms (lymphocyte count: median, 0.7 x 109/L [range, 0.1-1.6] vs 0.9 x 109/L [range, 0.2-2.6], P = .007; platelet count: median, 169.0 x 109/L [range, 18.0-564.0] vs 220.0 x 109/L [range, 109.0-576.0], P = .04; blood urea nitrogen: median, 5.0 mmol/L [range, 2.3-48.1] vs 4.4 mmol/L [range, 1.5-19.1], P = .04). For the nonsevere subgroup, there were no significant differences in laboratory findings of patients with and without CNS symptoms.
Laboratory Findings in Patients With and Without PNS Symptoms
Table 4 showed the laboratory findings of patients with and without PNS symptoms. We found that there were no significant differences in laboratory findings of patients with PNS and those without PNS. Similar results were also found in the severe subgroup and nonsevere subgroup, respectively.
Laboratory Findings in Patients With and Without Skeletal Muscle Injury
The eTable in the Supplement shows the laboratory findings of patients with and without skeletal muscle injury. Compared with the patients without muscle injury, patients with muscle injury had significantly higher levels of creatine kinase (median, 400.0 U/L [range 203.0-12216.0] vs median, 58.5 U/L [range 8.8-212.0]; P < .001), regardless of their severity. Meanwhile, patients with muscle injury had higher neutrophil counts, lower lymphocyte counts, higher C-reactive protein levels, and higher D-dimer levels. The abnormalities were manifestations of increased inflammatory response and blood coagulation function. In addition, we found that patients with muscle injury had multiorgan damage, including more serious liver (increased lactate dehydrogenase, alanine aminotransferase, and aspartate aminotransferase levels) and kidney (increased blood urea nitrogen and creatinine levels) abnormalities.
For the severe group, patients with skeletal muscle injury had decreased lymphocyte counts and more serious liver injury (increased lactate dehydrogenase, alanine aminotransferase, and aspartate aminotransferase levels) and kidney injury (increased creatinine levels).
Discussion
To our knowledge, this is the first report on detailed neurologic manifestations of the hospitalized patients with COVID-19. As of February 19, 2020, of 214 patients included in this study, 88 (41.1%) had severe infection and 126 (58.9%) had nonsevere infection. Of these, 78 (36.4%) had various neurologic manifestations that involved CNS, PNS, and skeletal muscles. Compared with patients with nonsevere infection, patients with severe infection were older and had more hypertension but fewer typical symptoms such as fever and cough. Patients with severe infection were more likely to develop neurologic manifestations, especially acute cerebrovascular disease, conscious disturbance, and skeletal muscle injury. Most neurologic manifestations occurred early in the illness (the median time to hospital admission was 1-2 days). Some patients without typical symptoms (fever, cough, anorexia, and diarrhea) of COVID-19 came to the hospital with only neurologic manifestation as their presenting symptoms. Therefore, for patients with COVID-19, we need to pay close attention to their neurologic manifestations, especially for those with severe infections, which may have contributed to their death. Moreover, during the epidemic period of COVID-19, when seeing patients with these neurologic manifestations, physicians should consider SARS-CoV-2 infection as a differential diagnosis to avoid delayed diagnosis or misdiagnosis and prevention of transmission.
In January 2020,3 ACE2 was identified as the functional receptor for SARS-CoV-2, which is present in multiple human organs, including nervous system and skeletal muscles.11 The expression and distribution of ACE2 remind us that the SARS-CoV-2 may cause some neurologic manifestations through direct or indirect mechanisms. Autopsy results of patients with COVID-19 showed that the brain tissue was hyperemic and edematous and some neurons degenerated.12 Neurologic injury has been confirmed in the infection of other CoVs such as in SARS-CoV and MERS-CoV. The researchers detected SARS-CoV nucleic acid in the cerebrospinal fluid of those patients and also in their brain tissue on autopsy.13,14
Central nervous system symptoms were the main form of neurologic injury in patients with COVID-19 in this study. The pathologic mechanism may be from the CNS invasion of SARS-CoV-2, similar to SARS and MERS viruses. As with other respiratory viruses, SARS-COV-2 may enter the CNS through the hematogenous or retrograde neuronal route. The latter can be supported by the fact that some patients in this study had smell impairment. We also found that the lymphocyte counts were lower for patients with CNS symptoms than without CNS symptoms. This phenomenon may be indicative of the immunosuppression in patients with COVID-19 with CNS symptoms, especially in the severe subgroup. Moreover, we found patients with severe infection had higher D-dimer levels than that of patients with nonsevere infection. This may be the reason why patients with severe infection are more likely to develop cerebrovascular disease.
Consistent with the previous studies,7 muscle symptoms were also common in our study. We speculate that the symptom was owing to skeletal muscle injury, as confirmed by elevated creatine kinase levels. We found that patients with muscle symptoms had higher creatine kinase and lactate dehydrogenase levels than those without muscle symptoms. Furthermore, creatine kinase and lactate dehydrogenase levels in patients with severe infection were much higher than those of patients with nonsevere infection. This injury could be associated with ACE2 in skeletal muscle.15 However, SARS-CoV, using the same receptor, was not detected in skeletal muscle by postmortem examination.16 Therefore, whether SARS-CoV-2 infects skeletal muscle cells by binding with ACE2 needs to be further studied. One other reason was the infection-mediated harmful immune response that caused the nervous system abnormalities. Significantly elevated proinflammatory cytokines in serum may cause skeletal muscle damage.
Limitations
This study has several limitations. First, only 214 patients were studied, which could cause biases in clinical observation. It would be better to include more patients from Wuhan, other cities in China, and even other countries. Second, all data were abstracted from the electronic medical records; certain patients with neurologic symptoms might not be captured if their neurologic manifestations were too mild, such as with taste impairment and smell impairment. Third, because most patients were still hospitalized and information regarding clinical outcomes was unavailable at the time of analysis, it was difficult to assess the effect of these neurologic manifestations on their outcome, and continued observations of the natural history of disease are needed. Fourth, during the outbreak period of COVID-19, because of the influx of many patients infected with SARS-CoV-2, advanced neuroimaging, such as magnetic resonance imaging and diagnostic procedures such as lumbar puncture and electromyography/nerve conduction velocity, was purposefully avoided to reduce the risk of cross infection. Therefore, in our study, most of the symptoms were a patient’s subjective descriptions. We could not distinguish whether these neurologic manifestations are caused by the virus directly or by the pulmonary disease or other organ damage indirectly.
Conclusions
In conclusion, SARS-CoV-2 may infect nervous system and skeletal muscle as well as the respiratory tract. In those with severe infection, neurologic involvement is greater, which includes acute cerebrovascular diseases, impaired consciousness, and skeletal muscle injury. Their clinical conditions may worsen, and patients may die sooner. This study may offer important new clinical information on COVID-19 that would help clinicians raise awareness of its involvement of neurologic manifestations. It is especially meaningful to learn that for those with severe COVID-19, rapid clinical deterioration or worsening could be associated with a neurologic event such as stroke, which would contribute to its high mortality rate. Moreover, during the epidemic period of COVID-19, when seeing patients with these neurologic manifestations, clinicians should consider SARS-CoV-2 infection as a differential diagnosis to avoid delayed diagnosis or misdiagnosis and prevention of transmission.
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