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. 2023 Apr 15;12(2):42–84.

Table 1.

Neuroimaging findings in COVID-19 disease and disorders

Central Nervous System (CNS)

Diseases or disorders First Author (Year) Sample Size (percentage of men and women) Mean Age (range) [years] Relative Frequency Percent MRI Findings
Headaches and dizziness [111] Lu (2020) 60 (56.7%, 43.3%) 44.10 Headache = 25% Patients with COVID-19 had statistically significant higher GM volumes (GMV) on both sides of the brain in the olfactory cortex, hippocampi, insula, left Rolandic operculum, left Heschl’s gyrus, and right cingulate gyrus.
[5] Kremer (2020) 64 (67%, 33%) 66 (20-92) Headache = 16% The severe acute respiratory syndrome coronavirus was suspected in 56% of the abnormal brain MRIs.
[140] Yoon (2020) 150 (65.33%, 34.67%) 63.6 (22-96) Headache = 8% Fourteen percent had an MRI, and twenty-six percent had both a CT and an MRA. Neuroimaging studies revealed anomalies in 17 percent of patients.
[68] Lersy (2020) 58 (66%, 34%) 62 (55-70) Headache = 5% In patients with neurological symptoms related to COVID-19, abnormalities, especially leptomeningeal enhancement, and increased inflammatory markers in CSF are common, whereas SARS-CoV-2 detection in CSF remains sparse.
[89] Karadaş (2020) 239 (55.6%, 44.4%) 46.46 (19-88) Headache = 27.6% In the frontal and posterior regions of the head, the symptoms of a headache were frequently observed.
Dizziness = 6.7%
[38] Jain (2020) 3218 (60.7%, 39.3%) 64 (2 weeks-105 years) Headache = 3.8% Patients with AMS or delirium, strokes, and mechanical falls or trauma were the most common reasons for neuroimaging studies. There were a few less common symptoms, including syncope (4%), headache (3.8%), dizziness (2.8%), seizures (2.1%), and ataxia (1.4%), among them.
Dizziness = 2.8%
[7] Scullen (2020) 27 (52%, 48%) 59.8 (35-91) Headache = 7.4% CT revealed 63% of neurologic findings, MRI showed 30%, and EEG showed 44%. Diffuse hypoattenuation, hemorrhages in the subcortical parenchyma, and hypodensities in deep structures are the most common findings. The corpus callosum, the basal ganglia, and deep WM were all found to be affected by MRI findings. There was only one patient with an irregular proximal focal stenosis of the supraclinoid internal carotid artery among patients with a large-territory stroke.
[81] Liottaa (2020) 509 (55.2%, 44.8%) 58.5 Headache = 37.7% A brain MRI was performed on 3.14% of the patients. In 42.2% of patients, neurologic symptoms were present at the onset of COVID-19, in 62.7 percent of patients, and at any time during the disease course in 82.3 percent of patients.
Dizziness = 29.7%
[16] García-Azorín (2021) 233 (57.9%, 42.1%) 61.1 Headache = 12.9% A brain MRI was performed in 26.0% of cases, and abnormal findings were found in 35.7%, including 16 cases of stroke-related findings, two cases of encephalitis-related changes, and two cases of non-specific WM lesions. A total of 13 patients underwent spinal MRIs, with 4 displaying degenerative signs and one displaying meningeal and nerve root enhancements.
[19] Altunisik (2021) 32 (40.6%, 59.4%) 39.94 (24-55) Daily Headache = 53.12% MRI results did not show an increase in intracranial pressure in patients with persistent headaches following COVID-19. The majority of the current data on elevated ICP findings come from small series and case reports of patients with a severe disease spectrum; thus, other factors other than elevated ICP may play a role in headache persistence. Patients with a wide range of severe illnesses have provided the majority of the current data on increased ICP. This suggests that increased ICP isn’t the only factor in the recurrence of headaches.
Migraine = 21.87%
Tension Headache = 25%
Dizziness = 37.5%
[128] Planchuelo-Gómez (2023) 42 (26%, 74%) 43.8 100% Individuals with chronic headache after COVID-19 resolution exhibited a variety of alterations in GM and WM structure. The changes in GM were minor, affecting anterior regions such as the pars orbitalis, fusiform gyrus, and frontal pole. On the one hand, the observed WM alterations were widespread, including the majority of the WM tracts, and seemed to be connected to WM fiber bundle degradation. The WM alterations, on the other hand, created a scenario similar to but milder than migraine.
Cerebrovascular Complications after Stroke [5] Kremer (2020) 64 (67%, 33%) 66 (20-92) 27% The severe acute respiratory syndrome coronavirus was suspected in 56 percent of the abnormal brain MRIs.
[22] Chougar (2020) 73 (65.8%, 34.2%) 58.5 70.6% The MRI scans of 30 patients (22 non-ICU and 8 ICU) revealed no significant abnormalities aside from the changes common in elderly patients and pathological findings in 58.9% of patients.
[140] Yoon (2020) 150 (65.33%, 34.67%) 63.6 (22-96) 8% Fourteen percent had an MRI, and twenty-six percent had both a CT and an MRA. Neuroimaging tests revealed anomalies in the brains of 17% of people.
[51] Lin (2020) 2054 (57%, 43%) 64 (50-75) 11% There were six cases of abnormalities in the brain’s cranial nerves and three patients with a microhemorrhage pattern consistent with critical illness-associated microbleeds-in the 51 patients who underwent MR imaging examinations.
[52] Mahammedi (2020) 108 (63.8%, 36.2%) 69 (16-62) 31% Brain MRI was performed on 18% of patients, and 35% had acute abnormalities on brain MRIs.
[7] Scullen (2020) 27 (52%, 48%) 59.8 (35-91) 11.1% In patients with AD, MRI results frequently showed diffuse involvement of the deep WM, corpus callosum, and basal ganglia.
[48] Büttner (2021) 34 (76.5, 23.5%) 67.5 (7 months-82 years) 5.9% Some 38.2% had shown brain imaging abnormalities either on initial or follow-up neuroimaging.
[16] García-Azorín (2021) 233 (57.9%, 42.1%) 61.1 27% Brain MRI: 16 cases of stroke-related findings; 2 patients with encephalitis-related changes; and 2 cases of non-specific WM lesions. Degenerative signs were found in four of the cases, while meningeal and nerve root enhancement was found in one.
[100] Ray (2021) 52 (58%, 42%) 9 (1-17) 8% An abnormality in neuroimaging was found in 74% of those who underwent the procedure. One ischaemic involving the anterior and middle right cerebral artery, one intraparenchymal hemorrhage in the right frontal lobe, and one (1%) had bilateral hyperintensities within the claustra as a result of ADEM were found.
[77] Helms (2020) 140 (71.4%, 28.6%) 62 (52-70) 6.25% Some 28.57% had abnormalities in the WM of their brains that were found to be intraparenchymal.
Intracerebral Hemorrhage (ICH) [46] Katz (2020) 86 (56%, 44%) 67.4 (25-94) Pure intracranial hemorrhage = 16.3% An MR venogram revealed a hemorrhagic venous infarction in the left temporal lobe of a patient with a cerebral hemorrhage.
[88] Cleret de Langavant (2021) 26 (73%, 27%) 58.3 (16-86) Subdural hemorrhage = 3.8% All of the patients had normal brain MRIs.
[22] Chougar (2020) 73 (65.8%, 34.2%) 58.5 microhemorrhage = 11.3% MRIs revealed bilateral edematous changes in the thalami, basal ganglia, and midbrain, as well as variable contrast enhancement. One MRI case involved the substantia nigra. These findings include WM lesions with angiocentric enhancement as well as abnormalities in the basal ganglia, including substantia nigra involvement, which may indicate vasculitis and/or inflammation.
[52] Mahammedi (2020) 108 (64%, 36%) 71 (60.5-79) Intracranial hemorrhage = 6% Brain MRI was performed on 20 (18%) of the 108 patients. Seven of the MRIs (or 35% of the total) revealed acute abnormalities in the brain. Neuroimaging features in hospitalized COVID-19 patients were found to be variable, lacking specific patterns, but dominated by acute ischemic infarctions and intracranial hemorrhages, as shown in this research.
[5] Kremer (2020) 37 (81%, 19%) 61 (8-78) ICH lesion = 54% FLAIR and diffusion-weighted sequences show nonconfluent multifocal WM hyperintense lesions with variable enhancement, with associated hemorrhagic lesions in 11 of 37 patients and extensive and isolated WM microhemorrhages in nine of 37 patients. Microhemorrhages in a 57-year-old man with abnormal wakefulness after sedation were found by axial SWI in the WM of the brain. cerebellar peduncles, subcortical WM, internal capsule, and corpus callosum.
[48] Büttner (2021) 34 (75.8%, 24.2%) 67.5 (7 months, 82 years) Hemorrhagic manifestation = 26.5% It was discovered that a 57-year-old man had multiple microbleeds in the superficial and deep WM of his brain.
[129] Lersy (2020) 69 (67%, 33%) 65 (21-86) Extensive WM micro-hemorrhage = 9% Six of the patients had extensive WM microhemorrhages with atypical involvement of the corpus callosum. Imaging revealed vessel wall thickening with homogeneous and concentric enhancement, suggesting vasculitis.
Subarachnoid hemorrhage = 4%
[45] Gorgulu (2021) 42 (50%, 50%) 73.5 (22-98) Cerebral hemorrhage = 28.6% Anatomical localization of ICH included 41.7% (n = 5) lobar, 16.7% (n = 2) basal ganglia, 16.7% (n = 2) cerebellum, and 25% (n = 3) other areas.
[59] Sawlani (2021) 3,403 (66%-33%) 59.7 (32-91) Microhaemorrhage = 12/20, 60% MRI abnormalities were found in 20 patients, and CT abnormalities were found in 18 patients, in 23% of the patients. The microhemorrhage in the corpus callosum splenium was the most recurrent and consistent finding on the MRI scans.
[40] Martin (2022) 7 (43%, 57%) 44 (11-74) Punctate brain hemorrhage = 43% One subject had a normal MRI and CT scan, while the other six had abnormal results. Five patients had abnormalities in the cerebrovascular system. Only one SAH, three microhemorrhages, and one stroke were reported.
[118] Mahammedi (2021) 135 (64%, 36%) 68.2 (17-94) Intracranial hemorrhage = 10% After subarachnoid and parenchymal hemorrhages, microhemorrhage was the most common intracranial hemorrhage. T2/FLAIR hyperintense lesions with associated microbleeds (with and without restricted diffusion) and confluent symmetric T2/FLAIR hyperintense lesions involving the deep and subcortical WM without restricted diffusion were the most common MR imaging findings of WM disease.
[140] Yoon (2020) 150 (65%, 35%) 63.6 (22-96) Hemorrhage = 7.3% A CT or MR scan found anomalies in 26 (17%) of the patients, and 11 (42%) of the patients had hemorrhages. There were microhemorrhages found in 7 of the 11 patients who had intracranial hemorrhage.
Cerebral Microbleeds (CMBs) [48] Büttner (2021) 34 (76%, 24%) 67.5 (7 months, 82 years) Microbleed = 20.6% The corpus callosum is the most severely affected area of the brain in this situation, with multiple microbleeds. Four patients in this group had a microbleed pattern that was consistent with critical illness encephalopathy. A similar neuroimaging pattern has been observed in other studies involving COVID-19 patients.
[56] Elizondo (2021) 47 - 12.5% Basal ganglia, cerebellum, cerebellum and/or juxtacortical cortex, cerebellum, and deep and periventricular WM were found to have microbleeds.
Encephalopathy [52] Mahammedi (2020) 108 (63.8%, 36.2%) 71 (16-62) Acute encephalopathy = 25% MRIs of the brain were performed on 20 of the 108 patients who were a part of the research. Of the 20 patients who had MRI scans, acute abnormalities in the brain were found in seven of them. Systemic toxemia, viremia, and/or hypoxic effects can all result in a non-specific cortical pattern of T2 FLAIR hyperintense signal with associated diffusion restriction.
PRES = 25%
Nonspecific encephalopathy = 50%
[7] Scullen (2020) 76 (52%, 48%) 59.8 (35-91) Encephalopathy = 74% The basal ganglia frequently showed FLAIR changes on MRI or CT, or discrete hypodensities, and SWI in several patients revealed petechial changes similar to necrotizing encephalopathy. In one patient, there were FLAIR changes in the cortical region of the bilateral precentral frontal gyri, as well as deep structural changes typical of anoxic ischemia.
Acute necrotizing encephalopathy = 7% An electrographic nonspecific encephalopathy with mild to moderate clinical AMS affected the majority of patients over the course of their illness. These patients frequently had non-specific imaging findings such as deep structure hypodensity or hypoattenuation. It was found that in severe cases, CT and MRI findings were consistent with idiopathic absence epilepsy (IAE) and acute necrotizing encephalopathy, two other viruses that can cause encephalitides.
[37] Meppiel (2020) 222 (61.3%, 38.7%) 65 (53-72) 30.2% Only six patients (9%) had small acute cerebral infarctions unrelated to symptoms, and one patient had a typical reversible lesion of the corpus callosum spleen.
[100] Ray (2021) 52 (58%, 42%) 9 (1-17) 52% of COVID-19 neurology patients had isolated encephalopathy. The abnormalities were found in 28 (58%) of the 46 MRI scans and 11 CT scans of the 52 patients. The corpus callosum splenium showed signs of mild encephalopathy in one case. Consistent symptoms in 22 of 25 cases have been found in children with the Pediatric Inflammatory Multisystem Syndrome (PIMS-TS). Patients with mild encephalopathy were found to have a reversible splenial lesion in the corpus callosum in more than 40% of cases.
48%
PIMS-TS neurology group: encephalopathy
[18] Lindan (2021) 38 0-18 2.6% Patients with fever and encephalopathy were observed. MRI revealed an unexpected pattern of cerebral microhemorrhages and infarct foci.
[140] Yoon (2020) 150 (65.3%, 34.7%) 63.6 (22-96) Leukoencephalopathy = 27% CT scans were performed on 141 patients; MRI scans were performed on 21 others; and a combination of CT and MRI scans was performed on another 31 patients. Twenty-six (17%) of the patients had abnormal neuroimaging studies, including hemorrhage, infarction, and leukoencephalopathies.
[41] Klironomos (2020) 185 (74.5%, 25.5%) 62 Leukoencephalopathy = 44% Both patients showed signs of dynamic processes, with leukoencephalopathy regressing and leptomeningeal enhancement growing in the same time period. One patient with diffuse symmetric leukoencephalopathy improved clinically and partially resolved during follow-up. There were symmetrical WM changes in both the occipital and frontal regions of one patient, as well as reduced diffusion in those regions. These findings could point to hypoxic-induced diffuse leukoencephalopathy.
[126] Lang (2021) 93 (67%, 33%) 63 Leukoencephalopathy = 6.4% Neuroimaging findings such as intracranial hemorrhage (n = 24), infarction (n = 4), or a combination of these were found in 26% of the patients studied.
[51] Lin (2020) 2054 (57%, 43%) 64 (50-75) PRES = 1.1% T2 FLAIR hyperintensity or CT hypoattenuation in confluence was used to determine PRES from prior literature.
[71] Azab (2021) 977 (45.4%, 54.6%) 60.15 Acute necrotizing encephalopathy = 13.7% SARS-CoV-2 encephalitis was detected in the CSF, and brain MRI showed increased intensity in the right mesial temporal lobe. Another case of acute necrotizing encephalitis has been reported. It appeared on MRI scans as a “ring enhancement”.
[70] Pons-Escoda (2020) 103 (61%, 39%) 74 (50.2-90) Encephalopathy = 23.5% The brains of 17 patients were imaged using MRI. One patient was left out of this study. There were no abnormalities found in the brain images of four patients who had suffered from encephalopathy due to prolonged sedation.
[124] Uginet (2022) 39 (89.7% 10.3%) 66.5 85% In 29 of the 34 patients with COVID-19 encephalopathy who had high-resolution vessel wall imaging, they found a circular enhancement and thickening of the basilar and vertebral arteries (85%), but no correlation with ischemia or microbleeds.
[58] Uginet (2021) 707 64.6 4.4% COVID-19 encephalopathy severity was not related to pneumonia severity. 92% of patients (23/25) had abnormal MRI findings, and 85% (17/20) had intracranial vessel gadolinium enhancement, indicating that the blood-brain barrier had been disrupted, while 85.7 percent (6/7 patients) had increased CSF/serum quotient of albumin. The SARS-CoV2-induced endotheliitis is consistent with altered brain homeostasis and vascular dysfunction, even though other pathophysiological mechanisms may be at play.
[141] Espindola (2021) 58 (43.1%, 56.9%) 51.6 41.4% Only 12.1% of the 58 participants in the study were found to have CVD in their brain MRI, six of whom had intracranial hemorrhage, and one had a TIA.
[65] Helms (2020) 32 62 (52-70) 18.7% Of the 118 patients examined, 32 underwent brain MRI. A subarachnoid contrast enhancement on brain images in six of the 32 patients with encephalopathy suggests that the blood meningeal barrier has abnormal permeability.
Meningitis, encephalitis and myelitis [38] Jain (2020) 3218 (60.7%, 39.3%) 64 (2 weeks-105 years) Encephalitis = 2.5% Imaging findings consistent with encephalitis were seen in only one patient (2.5%).
[91] Kandemirli (2021) 27 (44.4%, 55.6%) 63 (34-87) Leptomeningeal enhancement = 18.5% Only post-contrast 3D FLAIR images showed leptomeningeal enhancement in one case; post-contrast T1WI or TurboFlash T1WI images did not show any evidence of this enhancement whatsoever.
[68] Lersy (2021) 58 (66%, 34%) 62 (55-70) Leptomeningeal enhancement = 38% Brain MR images showed leptomeningeal enhancement in 20% of patients.
4% of demyelinating lesions have acute inflammation.
[63] Sanchez (2020) 841 (56.2%, 43.8%) 66.42 Encephalitis < 1% To rule out inflammation, one patient had encephalitis, which manifested as an apparent stroke mimic in FLAIR sequences of brain MRI (14th day from onset, stage IIA) with bilateral temporal hyperintensity.
[37] Meppiel (2020) 222 (61.3%, 38.7%) 65 (53-72) Encephalitis = 9.5% Neuroimaging revealed various acute nonvascular lesions in 14 of the 21 people with encephalitis who underwent the procedure.
[62] Rifino (2021) 137 (66%, 34%) 64.9 (30-95) Encephalitis = 3.6% The vigilance and/or consciousness of 49 patients were disturbed. They all had a CT scan or an MRI of the brain. SARS-CoV-2 RT-PCR was performed in the CSF of twenty-one patients. Clinical features, CSF data, and neuroimaging led us to conclude that encephalitis was present in five of the patients, one of whom had been infected with HSV-1 and another had been diagnosed with necrotizing encephalitis.
Necrotizing encephalitis < 1%
[71] Azab (2021) 977 (45%, 55%) 60.15 Viral encephalitis = 16.2% Only 34 patients with encephalitis had MRIs done because of the limited availability. The MRI findings of COVID-19 encephalitis included WM lesions, demyelinating hyperintensities, leptomeningeal enhancement, and necrotic hemorrhage. MRI microvascular brain lesions were found in approximately 21 patients with encephalitis. There is a possibility that this is the result of a COVID-19-mediated vascular brain injury.
Acute necrotizing encephalopathy = 13.7%
[16] García-Azorín (2021) 233 (57.9%, 42.1%) 61.1 Meningoencephalitis = 3.6% Two patients were diagnosed with encephalitis after abnormal findings were found in 57 of 219 (26.0%) patients who underwent a brain MRI.
Encephalitis < 1%
[18] Lindan (2021) 38 0-18 Encephalomyelitis-like changes of the brain = 42% Anti-N-methyl-D-aspartate receptor (anti-NMDAR) autoimmune encephalitis was diagnosed in a patient with brain changes similar to those seen in ADEM. When the term “ADEM-like” is used to describe an imaging phenotype that resembles an ADEM pattern, it means that the pattern is similar in some way. As a result, one patient developed a long-term, T2 hyperintense central cord myelitis.
Myelitis = 21%
[9] Khedr (2021) 117 Patients with definite COVID-19, n = 55 (50%, 50%) Definite Encephalitis = 5% An MRI can show brain edema and inflammation as evidence of encephalitis.
Patients with probable COVID-19, n = 62 (56%, 44%) COVID-19 = 51.5 Meningoencephalitis < 1%
Probable = 60.3
Altered mental status and delirium [5] Kremer (2020) 37 (81%, 19%) 61 (8-78) Alteration of consciousness = 73% There were three distinct patterns in the brain MRI of patients with severe COVID-19: signal abnormalities in the medial temporal lobe, non-confluent multifocal WM hyperintense lesions on FLAIR and diffusion with variable enhancement, and extensive and isolated WM microhemorrhages.
Confusion = 32%
Agitation = 19%
[65] Helms (2020) 140 (71.4%, 28.6%) 62 (52-70) Delirium with a combination of acute attention, awareness, and cognition disturbances = 84.3% Patients with WM microhemorrhages and one with a left frontal intraparenchymal hematoma were found in the 28 MRI scans; these were found in eight of the 28 patients. A total of four patients had FLAIR hyperintensities, with two patients showing small foci of contrast enhancement and two patients showing diffusion hyperintensities. During postcontrast T1 or FLAIR imaging, a hyperintensity and/or enhancement in the subarachnoid space was observed in 17 of these patients (60.7%).
Unexpected state of agitation = 69.3%
[100] Ray (2021) 52 (58%, 42%) 9 (1-17) Acute psychosis = 3.84% One had an abnormal T2 signal in the hippocampus and cortical diffusion restriction due to limbic encephalitis; one had an abnormal T2 signal in the periventricular; and one had signal changes in the intraorbital segment of the right optic nerve consistent with demyelination in a child with acute demyelinating syndrome.
[91] Kandemirli (2021) 27 patients with MRI (78%, 22%) The median age of patients with MRI: 63 (34-87) - The right frontal cortical hyperintensity and symmetrical WM hyperintensity were clearly visible on axial FLAIR images taken at the midbrain and centrum semiovale. Linear hyperintensity was also visible on the frontal sulci. Axial b2000 DWI showed a frontal increase in signal with a correspondingly low ADC. Axial T1WI revealed effacement of the right frontal sulcal region. The pial-subarachnoid enhancement on post-contrast T1WI was mild. Radial and centro semiovale axial SWI revealed blooming artifacts in the frontal sulci. FLAIR showed bilateral leptomeningeal enhancement after contrast.
[125] Gunbey (2021) 354 (42%, 58%) 65.2 Syncope = 13% CT and MR imaging detected abnormalities in 4.7% and 28% of cases, respectively. Neuroimaging results showed infarcts, parenchymal hemorrhages, and encephalitis, as well as cortical signal abnormalities, the PRES, and cranial nerve involvement. MRI results (n = 103 total) showed that the WML classification ratios in patients were as follows: none 31% (n = 32), mild 16.9% (n = 17), moderate 19.7% (n = 20), and severe 32.4% (n = 34).
Altered mental status = 3%
[131] Radmanesh (2020) 242 (62%, 38%) 68.7 Altered mental status = 42.1% 42 (41.2% of the patients) had WM microangiopathic changes, 29 (28.4% of the patients) had chronic infarcts, and 1 patient had a meningioma that was found by chance.The imaging of the brains of no patients with AMS revealed any cases of acute or subacute infarction or acute intracranial hemorrhage.
Syncope/fall = 32.6%
[5] Kremer (2020) 64 (67%, 33%) 66 (20-92) Confusion = 53% A total of 36 (56%) brain MRIs were deemed abnormal, possibly due to the SARS-CoV-2 virus.
Impaired consciousness = 39%
Agitation = 31%
Seizure [67] Khedr (2021) 19 (36.8%, 63.2%) 47 (35-65) 100% There was diffuse cerebral oedema, leptomeningeal enhancement with T2 and FLAIR hyperintensities in the frontal lobes and/or bilateral medial temporal and/or thalamic oedema.
[68] Lersy (2021) 58 (66%, 34%) 62 (55-70) 10% MR images of the brains of five of the six patients who had seizures yielded GM lesions in one (2%) and FLAIR hyperintensities in the mesial temporal lobes in one (2%) of the patients.
Neuropsychiatric Symptoms [79] Du (2022) 19 (42%, 58%) 50.5 Dyspnea = 42% The RecCOVID group had significantly higher amplitude of ALFF values in the left precentral gyrus (PreCG), middle frontal gyrus, inferior frontal gyrus of the operculum, inferior frontal gyrus of the triangle, insula, hippocampus, parahippocampal gyrus, fusiform gyrus, and postcentral.
Fatigue = 37%
Myalgia = 21%
[142] Voruz (2022) 50 - Severe = 18% Long-term memory and executive dysfunctions are caused by SARS-CoV-2 infection, which is linked to changes in large-scale functional brain connections.
Moderate = 42% Mild = 40%
Peripheral Nervous System (PNS)
Guillain-Barre Syndrome (GBS) and its Variants [68] Lersy (2021) 58 (66%, 34%) 62 (55-70) 2% Neuroimaging was performed on the patient with Guillain-Barré syndrome. Guillain-Barré syndrome-related multiple cranial nerve enhancement was seen in brain MRI images, but spinal MRIs were found to be normal.
[51] Lin (2020) 2054 (57%, 43%) 64 (50-75) 1 patient with MFS CT or MR imaging of the brain was performed on 278 (14%) patients. Neuronal enhancement after IV gadobutrol administration was clearly visible in an enlarged, T2-hyperintense left oculomotor nerve on MR imaging of the brain.
[52] Mahammedi (2020) 108 (63.8%, 36.2%) 69 (16-62) 2 cases of GBS, 1 case of MFS Acute neuroimaging abnormalities were found in 51 out of 108 patients. Two GBs patients and one MFS patient had cranial nerve and cauda equina enhancement, respectively.
Smell and Taste Disorders [51] Lin (2020) 2054 (57%, 43%) 64 (50-75) 33% Each of the diagnostic olfactory bulb sequences was performed on all 12 patients. The olfactory bulb volume in none of the patients was altered. However, 4 of 12 patients had an abnormally increased olfactory bulb signal on post-contrast T2 FLAIR, which could indicate intrinsic T2 prolongation or, potentially, contrast enhancement. On post-contrast T2 FLAIR images of the olfactory bulb, they discovered evidence of olfactory neuritis in four patients with COVID-19.
[17] Strauss (2020) 12 (50%, 50%) 58.25 100% The T2 FLAIR signal intensity in the normalized olfactory bulb was significantly different between patients with COVID-19 and controls with anosmia. Intraneural T2 signal hyperintensity was seen in four of the 12 COVID-19 patients compared to none of the 12 anosmia-free controls. The 3D FLAIR signal intensity in the olfactory bulb was higher in patients with COVID-19 and neurologic symptoms when compared to a control group of patients who had olfactory dysfunction of the same age.
[134] Altundag (2021) 24 with anosmia due to COVID-19 39.3 100% anosmia There were CT measurements of the cleft width and volumes and MRI measurements of the signal intensity, the bulb volumes, and the olfactory depths of the nasal passages, as well as the T2-weighted signal intensity. Anosmic patients with SARS-CoV-2 (group 1) or non-SARS-CoV-2 viral infection (group 2) had significantly wider olfactory clefts (OCs) than healthy controls. Healthy controls had lower OC volumes, and the T2 signal in the OC area was higher in groups 1 and 2 compared to groups 2. Between groups 1, 2, and 3, there was no discernible difference in olfactory bulb volume or sulci depth as measured by MRI.
[91] Kandemirl (2021) 23 (39.10%, 60.9%) 29 (22-41) 100% Olfactory bulb volumes, sulcus depth, morphology, signal intensity, and nerve filia architecture were all assessed quantitatively and qualitatively using MRI. An abnormality in signal intensity in 91.3% of cases was found to be diffusely increased or scattered hyperintense foci or microhemorrhages. 34.8% of cases had clumping of the olfactory filia, and 17.4% had thinning and scarcity of the filia. A primary abnormality in olfactory cortical signals was found in 21.7% of cases. Olfactory bulb volume was 62 millimeters in diameter on average. On the right, the median olfactory sulcus depth was 6.8 mm, while on the left, it was 6.3 mm.
[136] Yildirim (2022) Persistent COVID-19 related OD: 31 (32%, 68%) COVID-19-related persistent OD: 32.5 100% There was a significant difference in COVID-19-related olfactory dysfunction (OD) compared to post-infectious olfactory dysfunction. On the other hand, there was no significant difference in the proportion of COVID-19-related and post-infectious OD with deformed bulb morphology and elevated olfactory bulb signal intensity in the other OD groups.
Post-Infectious OD: 97 (39%, 61%) Post-Infectious: 45.9
[41] Klironomos (2020) 185 (74%, 26%) 62 19% Slight contrast enhancement was seen in two patients, and seven of 37 (or 19%) had abnormally high T2-weighted FLAIR sequence signals in the olfactory bulb.
[111] Lu (2020) 60 (56.67%, 43.32%) 44.10 3.33% loss of smell and 6.67% loss of taste Significantly larger volumes were found in the bilateral olfactory, hippocampal, insula, left Heschl’s gyrus, left Rolandic operculum, and right cingulate gyrus.
[133] Eliezer (2020) 20 (50%, 50%) 34.6 (21-53) - The severity of the olfactory score was found to be significantly correlated with the degree of OC obstruction. The olfactory bulb (OB) volume in COVID-19 patients and healthy subjects did not differ significantly. Between the first and second MRIs, there was no significant difference in the OB volume (OBV). Olfactory function loss is linked to reversible OC obstruction in SARS-CoV2-infected patients.
[137] Guney (2021) 41 (48.72%, 51.22%) 40.27 Approximately 100% had a history of smell disorder Patients with COVID-19 had significantly smaller left, right, and mean olfactory bulb volumes and olfactory sulcus depths (OSDs) than control individuals. People with COVID-19 infection and a smell disorder who are in the chronic phase of their illness see a significant decrease in OBV. When compared to normal healthy cases, OSD values were found to be lower during the chronic period.
[132] Burulday (2021) 23 (56.5%, 43.5%) 37.08 (19-73) Smell = 100% COVID-19 disease affects the Obs’ periphery but not the center smell regions of the insular gyrus and corpus amygdala. The significance of their research is to identify MRI abnormalities in individuals with COVID-19 who have olfactory issues.
[136] Yildirim (2022) 31 (67.7%, 32.3%) 32.5 Olfactory dysfunction = 100% Whereas COVID-19-related anosmia has reduced OB volume and white matter tract integrity of olfactory areas, it is not as severe as other post-infectious OD. In COVID-19-related OD, trigeminosensory activation was stronger. These results may indicate that COVID-19 related OD has a better maintained central olfactory system than COVID-19 related OD. Persistent COVID-19-related anosmia may be caused by OB injury.
[143] Esposito (2022) 27 (37%, 63%) - Olfactory loss = 100% More segregated processing within areas more functionally related to the anterior piriform cortex was associated with more residual olfactory impairment. While olfactory loss was a lasting COVID19 symptom, greater neural connection within the olfactory brain was connected with a recent SARSCoV2 infection. The functional connectivity of the anterior piriform cortex, the greatest cortical receiver of olfactory bulb afferent axons, explained the interindividual diversity in sensory impairment.
[138] Campabadal (2022) 23 (13%, 87%) 51.96 Olfactory dysfunction = 100% Reduced GM volume and higher MD in olfactory-related regions explain post-acute COVID-19 patients’ chronic olfactory impairments.
[139] Ammar (2022) 11 (64%, 36%) 41.5 Olfactory dysfunction = 100% Individuals with anosmia reported OB imaging abnormalities that may be quantitatively assessed using the T2 FLAIR-Signal intensity ratio (SIR) and OB volumes. After the patient regained smell, the T2 FLAIR-SIR and OB volumes substantially normalized. This lends credence to the underlying mechanism of transitory OB inflammation as a cause of Olfactory Dysfunction in COVID-19 patients.
[135] Çetin (2022) 15 (73.3%, 26.7%) 25.1 Ansomia = 100% According to the conclusions of this research, there is a link between loss of taste and smell and MRI findings.
Peripheral neuropathy [62] Rifino (2021) 1760 (66%, 34%) 64.9 (30-95) 22.6% In one case, the brain MRI was normal, but the spine MRI showed diffuse degeneration. When the brain MRI was normal, the roots of the cauda appeared conglutinate and showed a slight hyperintense signal in T2 sequences in another case.
[144] Michaelson (2021) 14 (100%) 57 (33-82) 100% Plexopathies, peripheral neuropathies, and entrapment neuropathies are examples of peripheral neurological problems.
Cognitive-behavioral Disorders
Mild Cognitive Impairment [96] Hosp (2021) 29 (62%, 38%) 65.2 - In order to examine the effects of atrophy on partial volume effects, MRI scans were performed. In addition, the raters were made aware of four cases of cerebral (micro) infarctions and given instructions to rate any abnormalities that went beyond the scope of structural defects and possibly expected diaschisis.
[5] Kremer (2020) 37 (81%, 19%) 61 (8-78) Alteration of consciousnes = 73% FLAIR and diffusion-weighted sequences with variable enhancement, associated hemorrhagic lesions, and extensive and isolated white-matter micro-hematomas in the medial temporal lobe were used to identify signal abnormalities in the temporal lobe. Patients with ICH lesions had more severe clinical presentations and higher admission rates to ICUs (20 of 20 patients [100%] vs. 12 of 17 patients without hemorrhage).
Confusion = 32%
[16] García-Azorín (2021) 233 (54.9%, 45.1%) 61.1 Altered mental status = 23.6% A brain MRI revealed abnormal findings, including stroke-related changes and WM lesions caused by encephalitis. A total of 13 patients underwent a spinal MRI, which revealed signs of degeneration, as well as enhancement of the meninges and nerve roots.
[65] Helms (2020) 140 (100% men) 62 Delirium (84.3%) with a combination of acute attention, awareness, and cognition disturbance Associating FLAIR and diffusion hyperintensities with multiple infra and supratentorial white-matter microhemorrhages in the brain. FLAIR hyperintensities in WM that are confluent, with small contrast enhancement foci.
Neuromuscular Disorders
Myopathy and Myositis [63] Sanchez (2020) 841 (56.2%, 43.8%) 66.4 Myopathy = 3.1% In addition to reviewing electronic medical records, laboratory parameters, radiologic examinations (head CT or brain MRI), and neurophysiologic tests, if necessary, such as EEG and EMG, they also conducted neuropsychological evaluations. In 26 patients (3.1%), we found evidence of myopathy in the form of hyperCKemia in three of the patients.
[9] Khedr (2021) 117 Patients with definite COVID-19, n = 55 (50%, 50%) Definite Myositis = 4.8% A C4-T4 cervicalodorsal myelopathy was found on an imaging study; it was most likely caused by secondary occlusion of the anterior spinal artery following acute COVID-19 pneumonia, according to results from an imaging study performed after the patient had been hospitalized.
Patients with probable COVID-19, n = 62 (56%, 44%) COVID-19 = 51.5
Probable = 60.3
[18] Lindan (2021) 38 0-18 Myositis = 10% Multifocal T2 bright lesions in the brain WM, vasculitic patterns with ischaemic lesions, enhancing neuritis or polyradiculitis, venous thrombosis, splenial lesions of the corpus callosum, longitudinally extensive myelitis, and myositis were found in the brain, cranial nerves, and spinal cord, respectively. Myositis of the visible musculature of the neck or face was found in 36% of patients with the multisystem inflammatory syndrome in children (MIS-C). There have been reports of myositis in adults who have COVID-19. Neuroradiologists should be aware of the possibility of myositis as a possible cause of neck swelling in children with MIS-C. Finally, splenial lesions and myositis of the neck and face were the most common findings in children with MIS-C.