Neurologic Complications and Manifestations-
SARS-CoV-2 virus enters the nervous system by hematogenous spread or
retrograde neuronal transmission via the olfactory bulb and enters
neuronal and glial cells by attaching to the angiotensin-converting
enzyme 2 (ACE2) receptor, widely expressed in various neuronal
populations (15). A wide range of neurologic manifestations have been
reported in more than a third of the Covid-19 patients, particularly
those with a severe infection (16). In addition, neurologic
complications, particularly cerebrovascular diseases, represent a major
cause of morbidity and mortality for ECMO patients (17, 18).
All Covid-19 patients on ECMO support underwent routine neurological
examination. Sixty percent of the ECMO patients developed significant
neurologic complications affecting both central and peripheral nervous
systems. The most common neurological complications were encephalopathy,
seizures, autonomic dysfunction, and critical illness polyneuropathy
(Table 5).
Encephalopathy, defined broadly as an alteration in mental status, was
seen in 6 patients and can be attributed to a variety of etiologies. All
9 extubated patients can follow commands and show gradual improvement in
mental status. Six patients underwent continuous electroencephalography
(EEG) monitoring using leads placed into the subgaleal space.
Neurologists with advanced EEG training reviewed both raw and
quantitative EEG data in correlation with patients’ neurologic exam and
hemodynamic parameters. All six patients showed abnormal epileptiform
activity. (Figure 5) In three patients, the epileptiform activity
correlated with a change in neurologic exam, and both EEG findings and
neurologic exams improved after the administration of antiseizure
medication. Two patients, who remain on ECMO support at the time of this
report, had epileptiform activity without a clinical correlate that also
resolved with antiseizure medication. Seven patients developed wide
fluctuations of heart rate and blood pressure out of proportion to known
stimuli that was suggestive of autonomic dysfunction. Four of these
patients had poorly controlled DM rendering it difficult discern between
diabetic autonomic neuropathy versus other etiology. We did not find any
clinical or radiographic evidence of brain ischemia or hemorrhage in our
patients. Transcranial Doppler, obtained in one patient, did not reveal
any high-intensity signal transients suggestive of cerebral micro
emboli. Brain MRI obtained in two of the patients with seizure activity
did not show any acute intracranial finding.
Six patients developed generalized weakness concerning for critical
illness myopathy and or polyneuropathy; however, confirmatory nerve
conduction and electromyographic studies were not obtained to limit
provider exposure. The four patients who have been discharged from the
hospital have shown continued improvement in their muscle strength. As
this is a preliminary report, the patients’ functional neurologic
outcome remains in evolution. Cerebral Performance Category (CPC) will
be obtained during follow up visits after discharge.
The underlying mechanisms of neurological complications in Covid-19
patients is still unclear and may involve both direct and indirect
effects of SARS-CoV-2 infection as part of the systemic inflammatory
response. Coagulopathy, myocardial injury, and pre-morbid risk factors,
such as hypertension and diabetes, may also contribute to the
development of neurological complications in these patients.