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Case Report

Chronic Inflammatory Demyelinating Polyneuropathy after ChAdOx1 nCoV-19 Vaccination

Azienda Ospedaliero Universitaria Sassari, Unit of Neurology, Department of Medical, Surgical and Experimental Sciences, University of Sassari, 07100 Sassari, Italy
Parkinson and Movement Disorders Unit, Department of Clinical Neurosciences, Fondazione IRCCS Istituto Neurologico Carlo Besta, 20133 Milan, Italy
Authors to whom correspondence should be addressed.
Vaccines 2021, 9(12), 1502;
Submission received: 9 November 2021 / Revised: 29 November 2021 / Accepted: 7 December 2021 / Published: 19 December 2021
(This article belongs to the Special Issue The COVID Vaccine)


Recently several patients, who developed Guillain–Barré syndrome characterized by prominent bifacial weakness after ChAdOx1 nCoV-19 vaccination, were described from different centers. We recently observed a patient who developed a similar syndrome, later in the follow up he showed worsening of the neuropathy two months after the initial presentation. Repeat EMG showed reduced nerve sensory and motor conduction velocities of both upper and lower limbs, and a diagnosis of chronic inflammatory demyelinating polyneuropathy (typical CIDP) was made according to established criteria. Our report expands on the possible outcomes in patients who develop Guillain–Barrè syndrome after COVID-19 vaccinations and suggest that close monitoring after the acute phase is needed in these patients to exclude a chronic evolution of the disease, which has important implications for long-term treatment.

1. Introduction

Vaccines are the most cost-effective measures available against the COVID-19 pandemic with more than seven billion doses administered worldwide in November 2021 ( (accessed on 11 December 2021), thus monitoring of rare adverse events is of fundamental importance. COVID-19 vaccinations have mostly been associated with adverse events of little clinical significance such as injection site reaction or non-specific systemic symptoms such as fever and muscle aches, which usually resolve within days [1]. However, more severe adverse events have been reported in a minority of cases, including immune-mediated thrombocytopenia [2], and Guillain–Barrè syndrome, that is a potentially serious complication with a mortality rate of 3–5% despite intensive care treatment [3].
The incidence of GBS is estimated to be around 0.4–4.0 cases per 100,000 person-years [4]. The disease is more common in males especially over the age of 75, and less common among children [5]. GBS is generally classified into various subforms based on the pathophysiological profile and symptomatology (e.g., pharyngeal-cervical weakness syndrome, brachialis and bifacial paralysis with paresthesia) [6]. In some patients GBS can deteriorate again after some weeks from onset and several relapses can occur; in these patients a diagnosis of acute-onset chronic inflammatory demyelinating polyneuropathy (CIDP) should be considered [7].
In GBS an infectious trigger is recognized in >50% of cases while onset following vaccinations is debated [4]. Recently several patients who developed a GBS following CoV-19 vaccinations, were described from different centers [8,9,10,11,12]. In particular, most patients developed bifacial weakness with or without involvement of other peripheral nerves after ChAdOx1 nCoV-19 vaccination, suggesting this might represent a specific neuropathy phenotype associated with the vaccine. Clinical features of these patients are summarized in Table 1.
We recently observed a patient who developed a similar acute syndrome after the first dose of the ChAdOx1 nCoV-19 vaccine, but with worsening of the neuropathy two months after the initial presentation leading to a final diagnosis of CIDP.

2. Case Presentation

The patient was a 49-year-old man who presented asymmetric bilateral facial weakness, and paresthesias in the tongue and face. Sixteen days before symptoms onset he received the first dose of ChAdOx1 nCoV-19 vaccine. He denied infections within the prior month. Neurologic examination showed severe bilateral facial paresis, more prominent on the right side, and lower limbs areflexia. Brain and spinal cord MRI showed enhancement of the facial nerves and of the cauda equina and lower thoracic nerve roots, respectively (Figure 1). Cerebrospinal fluid analysis revealed elevated proteins (110 mg/dL; normal range <45 mg/dL) without pleocytosis, and absence of intrathecal IgG synthesis. Serum search for ganglioside autoantibodies was negative, including anti-GQ1b, anti-GD1b, and anti-GM1 antibodies. Blink reflex test displayed bilateral impairment of the motor efferent pathway, while the remaining nerve conduction studies (NCS) and electromyography (EMG) examination were normal. A microbiological work-up of cerebrospinal fluid has ruled out infection of campylobacter jejuni, Epstein–Barr virus, cytomegalovirus, influenza A virus, and hepatitis A, B, C virus. An initial clinical diagnosis of GBS was made and intravenous immunoglobulins (IVI g; 0.4 g/kg/die for 5 days) were initiated 3 days after symptoms onset with mild improvement of the bifacial paresis and resolution of the hypoesthesia.
Two months after presentation, his symptoms worsened with painful paresthesias and progressive lower limbs weakness, more prominent during right foot dorsiflexion (4/5 MRC). He developed mild sensory ataxia with wide based gait and postural instability. Repeated nerve conduction study showed marked slowing of sensory and motor conduction velocities of both upper and lower limbs, prolonged distal latency, conduction blocks and absent F response, leading to a diagnosis of chronic inflammatory demyelinating polyneuropathy (CIDP) according to established criteria [13]. He received a second cycle of IVIg with improvement of paresthesias.
Later he was treated with IVIg cycles every six weeks. At last clinical evaluation, six months after presentation, the clinical features were characterized by complete resolution of left facial palsy with persistence of slight weakness in the right upper facial area. Gait ataxia improved but did not resolve completely. Paresthesias on the lower limbs were disabling and thus treatment with pregabalin and alpha lipoic acid was started with benefit. Clinical features and examinations of the patient are summarized in Table 1.

3. Discussion

Acute demyelinating polyneuropathy is a rare, but well recognized complication of COVID-19 vaccines. The disease variant with bifacial weakness has recently been recognized to be more common in patients with adenoviral-vectored (Oxford AstraZeneca, Johnson and Johnson) vs. mRNA-based (Pfizer BioNTech, Moderna) vaccines [14]. In line with these findings, our patients developed an acute demyelinating polyneuropathy with bifacial palsy 2 weeks after the ChAdOx1 nCoV-19 vaccine, but subsequent clinical and EMG worsening prompted a diagnostic revision to CIDP with acute onset. To date, only one patient who developed CIDP after COVID-19 vaccination was reported, with typical gradual onset of ascending lower limb weakness and sensory changes without facial involvement [15].
A difference of the previously described cases of bifacial palsy, in which the clinical course is reported favorable or stabilized or which have been described in the acute phase, in our patient is available the most prolonged follow-up, that is of 6 months. This pro-longed clinical observation led to diagnose a chronic form of demyelinating polyneuropathy, which was an unexpected clinical evolution. Therefore, our report expands on the possible outcomes in patients who develop Guillain–Barrè syndrome after COVID-19 vaccinations and suggest that close monitoring after the acute phase is needed in these patients to exclude a chronic evolution of the disease, which has important implications for long-term treatment.
Our patient presented a clinical onset of GBS with bifacial weakness with paresthesias phenotype; 8 weeks later he presented a clinical deterioration, thus a diagnosis of CIDP was made, supported by neurophysiological findings. The distinction between GBS with fluctuations after start of treatment and CIDP is difficult but it has been recommended that diagnosis of CIDP should be considered when a patient thought to have GBS deteriorates again after 8 weeks from onset or when deterioration occurs 3 times or more [7].
In GBS, acute motor neuropathy may involve facial nerves in various clinical presentations that include unilateral, bilateral facial palsy, bifacial palsy associated with involvement of other cranial nerves and bifacial palsy associated with limb paresthesia, moreover facial involvement is also possible in patients with classical forms of GBS. Interestingly it has been proposed that Bell’s palsy may share similar pathogenic mechanisms with autoimmune neuropathies [16].
The specific clinical phenotype of bifacial weakness with paresthesias is quite uncommon and accounts for about less of 5% of the patients affected with GBS or Miller Fisher spectrum disorders [17], whereas in those patients who have a fluctuating GBS with treatment related fluctuations, who later may become a CIDP, facial involvement was reported to be very common and it is present in about 63% of the patients [7]. On the other hand, CIDP at onset presents uncommonly with cranial nerve involvement, which is reported in about 11% of typical forms mostly with ophthalmological implications rather than facial palsy [13].
GBS and CIDP are immune-mediated disorders in which the exact mechanism of the immune response linked to the pathogenesis is still not clear. In GBS, the pathogenic events are associated with the immune response usually to a previous infection, which subsequently leads to a cross-reaction with the production of antibodies directed to epitopes of the myelin sheath or to peripheral nerves and roots, thus causing an autoimmune process. Antecedent infections are reported in about two-thirds of patients with GBS [17], therefore molecular mimicry between microbial proteins and nerve cell surface has been one of the suggested pathophysiologic mechanisms. CIDP is typically an idiopathic disease, in which an immune response targeting myelin components of the peripheral nervous system develops due to an autoimmune process, which mainly involves immune mechanisms mediated by T cells. In CIDP, the finding of an infection that precedes the onset is rare and unlikely [18]. Numerous antibodies are associated with GBS (such as GD1a, GD1b, GM1, GQ1b), while usually no autoantibodies are identified in CIDP patients, even if variants with antibodies directed against myelin or proteins localized to the Ranvier node have been also described (such as neurofascin, gliomedin, and contactin-1), which appear to result in a more severe disease phenotype [18].
Neuropathies after vaccination are rare event and CIDP developing in the postvaccination period is distinctly unusual, accounting for about 1.5% of patients [19], and poorly described [20]. In our patient, the temporal association between the first dose of ChAdOx1 nCoV-19 vaccine and onset of neuropathy is remarkable so that a triggering role of the vaccine appears to be in causal association. It has been proposed that a postvaccination neurological syndrome could result from the generation of host antibodies that cross-react with proteins present in peripheral myelin [8]. These antibodies may be generated in direct response to the SARS-CoV-2 spike protein, because there is evidence of a cross-reactivity between the SARS-CoV-2 spike protein and peripheral nerve glycolipids [8,21]. This hypothesis is supported by reports of some patients with GBS with bifacial weakness and paresthesias subtype also among patients affected by GBS post COVID-19 [22], even if in these series it does not appear to be the most common phenotype [23]. Therefore, an immune response to other components of the vaccine should be considered, such as a response against the chimpanzee adenovirus vector.
The optimal management and long-term outcomes of these patients remain to be determined. We treated our patient according to the available recommendation with IVIg administration at earliest convenience [17], however, he developed treatment related fluctuations as observed in about 6–10% of all patients with GBS [17]. This may be due to the possibility that the treatment effect has worn off while the inflammatory phase of the disease is still ongoing, and thus further treatment with repeating IVIg cycles was administered and nonetheless, the patient developed a form of CIDP. To our knowledge this is the first case, among GBS with bifacial palsy onset post COVID-19 vaccination, that shows this evolution of the disease, on this regard, it would be interesting to have additional details on the clinical and EMG follow-up of the previous reported cases with short follow up [8,9,12].
In recent months, several case reports have shown that some variants of GBS can occur after the administration of the ChAdOx1 nCoV-19 vaccine, and in particular the bifacial weakness and paresthesia appears to be the prevalent form. This case report clearly shows the need for close monitoring of patients developing GBS after COVID-19 vaccination after the acute phase. We highlight that adequate long-term clinical follow-up is essential in these cases, as evolution to a chronic form is possible, despite adequate treatment. While an eventual causal relationship between different types of COVID-19 vaccines and autoimmune neuropathies remains to be determined, neurologists should be aware of this possibility as prompt diagnosis and treatment is crucial to improve outcomes in patients with GBS or CIDP and other potentially serious neurologic disorders.

Author Contributions

Conceptualization, C.F.B. and D.G.C.; methodology, C.F.B. and A.E.E.; software, P.Z.; validation, A.E.E., E.S. and P.S.; investigation, C.F.B. and E.R.; resources, P.S.; data curation, C.F.B., E.R. and P.Z.; writing—original draft preparation, C.F.B. and D.G.C.; writing—review and editing, C.F.B., D.G.C. and A.E.E.; supervision, P.S.; All authors have read and agreed to the published version of the manuscript.


This research received no external funding.

Institutional Review Board Statement

The study was conducted according to the guidelines of the Declaration of Helsinki, and approved by the Institutional Review Board of University of Sassari.

Informed Consent Statement

Informed consent was obtained from the patient involved in the study.

Data Availability Statement

The datasets used and analyzed during the current study are available from the corresponding author on reasonable request.

Conflicts of Interest

The authors declare no conflict of interest.


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Figure 1. Brain and spinal cord MRI findings. Axial post-gadolinium T1-weighted images of the brain showing enhancement of the right ((A), arrow) and left ((B), arrow) facial nerves. Sagittal T1-weighted images before (C) and after (D) gadolinium administration showing diffuse enhancement of the cauda equina and lower thoracic nerve roots.
Figure 1. Brain and spinal cord MRI findings. Axial post-gadolinium T1-weighted images of the brain showing enhancement of the right ((A), arrow) and left ((B), arrow) facial nerves. Sagittal T1-weighted images before (C) and after (D) gadolinium administration showing diffuse enhancement of the cauda equina and lower thoracic nerve roots.
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Table 1. Clinical and MRI characteristics of patients with bifacial weakness after ChAdOx1 nCoV-19 vaccination.
Table 1. Clinical and MRI characteristics of patients with bifacial weakness after ChAdOx1 nCoV-19 vaccination.
Symptoms/SignsRespiratory FailureDays from First Dose of VaccineCSF FindingsEMG FindingsMRITreatmentOutcome
Ascending distal limbs dysesthesias; bifacial paresisNone16P: 163 mg/dL;
C: 19/mL
Day 16: Facial NCS showed severely reduced compound muscle action potential amplitude responses and normal terminal latencies bilaterally; sensory and motor NCS: normalEnhancement of facial nervesPrednisolone 60 mg/day × 5 daysStabilized
Headache, LL dysesthesias, and bifacial paresisNone26P: 123 mg/dL;
C: 14/mL
Day 13: Facial NCS showed borderline normal amplitude responses and normal terminal latencies bilaterally; sensory and motor NCS: normalNormal non-contrast brain MRI
Prednisolone 60 mg/day × 5 daysStabilized
Lumbar back pain, dysarthria and bifacial paresis; lower limb dysesthesias; proximal limb weakness on examNone21P: 247 mg/dL;
C: 8/mL
Day 13: Facial NCS, not performed; sensory and motor NCS: normalNormal non-contrast brain MRIIVIgStabilized
LL paresthesias; bifacial paresisNone29P: 89 mg/dL;
C: <5/mL
NAEnhancement of facial nervesNoneSubjective improvement of numbness
Bifacial paresis, areflexic quadriparesis, upper back painYes10P: 72.2 mg/dL
C: 5/mL
Demyelinating neuropathyNAIVIg
Bifacial paresis, right abducense palsy, bulbar palsy, Distal sensory impairment in the legs, areflexia, limb weaknessYes14P: 345 mg/dL
C: 3/mL
Axonal motor-sensory neuropathyNormal brain and spine MRIIVIg
Still hospitalized
Bilateral LL numbness, weakness, right-sided facial, tongue numbness, and back pain, right trigeminal V2-V3 sensory impairment, areflexiaYes12P: 120 mg/dL
C: 3/mL
Demyelinating neuropathyNormal brain and spine MRIIVIg
Still hospitalized
Facial diplegia, bulbar palsy, bilateral facial numbness, bilateral distal lower and UL numbness, and bilaterally trigeminal sensory loss, areflexiaYes14P: 75 mg/dL
C: 4/mL
Demyelinating neuropathyNormal brain and spine MRIIVIg
Still hospitalized
Facial diplegia, bulbar palsy. Bilateral distal UL and LL numbness, areflexiaYes11P: NA
Demyelinating neuropathyNAIVIg
Still hospitalized
Facial diplegia, bulbar palsy, complete ophthalmoplegia,
UL and LL distal numbness, UL and LL weakness, areflexia
Yes12P: NA
Demyelinating neuropathyNAIVIg
Still hospitalized
Facial diplegia, bulbar palsy, bilateral UL and LL numbness, areflexiaNone13P: 83 mg/dL
C: 2/mL
Demyelinating neuropathyNAIVIg
Still hospitalized
Bilateral facial weakness with numbness of the tongue and mouth, interscapular back and LL pain, paresthesia of both hands and feet
Normal tone, power and reflexes in both UL and LL, except absent right ankle jerk. Reduced light touch and pinprick sensation symmetrically in LL to the knee and vibration to the ankles. Gait was ataxic
None7P: 1.99 g/L
C: 2/mL
Sensory NCS: UL and LL: reduced SNAP amplitude
Motor NCS:
UL and LL:
Prolonged DMLs, and F-wave latencies
Slow CV
Dispersed CMAPs and CB.
Facial NCS: Prolonged DMLs
MRI pre and post GAD contrast: normal except for bilateral smooth contrast enhancement along whole facial nerveIVIgFacial weakness resolved
Pain and paresthesia improving.
Intact reflexes including right ankle jerk
Severe bilateral facial weakness, Myalgia, paresthesia of both hands and feet, severe neck pain, urinary retention, dysphagia, altered taste and paresthesia of tongue
Normal limb tone, with full power except mild weakness in right hip flexion. Reflexes initially present but then subsequently lost. Flexor plantar responses. Patchy, asymmetrical glove and stocking reduction in pinprick sensation and a sensory ataxia
None11P: 2.81 g/L
C: 23/mL
Sensory NCS: UL: absent SNAPs
LL: normal
Motor NCS: UL and LL:
Prolonged DMLs, and F-wave latencies
Slow CV
Dispersed CMAPs and CB
Facial NCS: Absent.
Facial EMG: Few fibrillations, no volitional motor units
MRI pre and post GAD contrast: normal except for bilateral smooth contrast enhancement along whole facial nerveIVIg20% improvement in facial weakness.
Ataxic gait and pain static. Areflexia persists.
No longer in urinary retention
3-week history of severe LL cramping pain. Numbness in feet and hands, spreading proximally to the ankles. Progressive right facial weakness became severe and bilateral after 5 days.
Tone, power, and reflexes in limbs were normal. Impaired sensation in all modalities in UL and LL with a sensory ataxia
None7P: 5.14 g/L
C: 1/mL
Sensory NCS: UL: reduced SNAP amplitudes
LL: normal
Motor NCS: UL and LL:
Dispersed CMAPs
Tibial F wave latencies prolonged
Facial NCS: Normal except blink reflexes absent
Facial EMG: Very reduced volitional motor units
MRI pre and post GAD contrast: normal except for bilateral smooth contrast enhancement along whole facial nerveNone95% improvement in facial weakness.
Ataxic gait 80% better.
25% improvement in pain and paresthesia
Lower back and abdominal pain. Altered taste and sequential facial weakness within 24 h. Mild proximal LL weakness.
Slight weakness in hip flexion bilaterally. Absent knee and left ankle reflexes with normal sensory examination
None12P: 0.96 g/L
C: 1/mL
Sensory NCS: UL and LL: reduced/absent SNAP amplitudes and velocities
Motor NCS: UL and LL:
Prolonged DMLs
Dispersed CMAPs
Facial NCS: Not tested
Facial EMG: Not tested
Normal MRI. NO post contrast study.
Normal CT performed
NoneResidual mild facial weakness, proximal leg weakness and mild paresthesia.
Reflexes regained
Lower back discomfort and radicular pain. Facial, perioral and LL paresthesia progressing to severe simultaneous bilateral facial weakness.
Depressed UL reflexes. Normal LL reflexes. Mild distal LL sensory loss to vibration and pinprick
None8P: 1.22 g/L
C: 0/mL
Sensory NCS: Not tested
Motor NCS: Not tested
Facial NCS: Not tested
Facial EMG: Not tested
Normal MRI. NO post contrast study.
Normal CT performed
None95% resolution of facial weakness, pain and paresthesia
Severe back pain. Bilateral facial weaknessNone10P: (1264 mg/L
C: 8 × 10 × 6
/L lymphocytes
Severe, multifocal sensorimotor
demyelinating polyneuropathy, with reduced compound
motor action potentials, reflecting likely hypoexcitability
Normal CT and MRI of the brainIVIgs
Oral Prednisolone
Rapid improvement following the treatment
Four limb distal paresthesia and postural instability. Bilateral facial palsy (House–Brackmann grade V). Gait ataxia, global areflexia, and distal paresthesia both at the LL and UL; Normal pallesthesia. Segmental strength diffusely preserved (MRC: 5/5). No spine sensory level. No vegetative, or sphincter involvementNone10P: 140 mg/dL
C: normal white blood cell count
Motor polyradiculoneuropathy with temporal dispersion of the tibial nerve cMAP bilaterally, with F reflex absent in all districts. No sensory involvement, particularly no temporal dispersion of the sural nerve SNAP bilaterallyUnremarkable brain and cervical MRI with gadoliniumIVIgSlowly improved
(Present case report)
Headache, bifacial paresis and paresthesias; lower limbs areflexia, lumbar back painNone16P: 110 mg/dL
C: <5/mL
First admission:
Blink reflex: absence of all potentials (R1i, R2i, R2c) with right-sided stimulation and normal findings after left supraorbital stimulation.
NCS: absence of demyelinating/axonal neuropathy at upper and lower extremities
Second admission:
Blink reflex: delay of R1i, R2i after stimulation of left side and R2c delay with right supraorbital stimulation. Absence of R1i and R2i after right stimulation and absence of R2c with left-sided stimulation.
NCS: demyelinating sensorimotor polyneuropathy at upper and lower extremities
Enhancement of facial nerves and cauda equinaIVIgProgressed to CIDP
Abbreviations: C: white cell count; CB: conduction block; CIDP: chronic inflammatory demyelinating polyneuropathy; CMAP: compound muscle action potential; CSF: cerebrospinal fluid; CV: conduction velocities; DML: distal motor latency; EMG: electromyography; F: female; GAD: gadolinium; IVIg; intravenous immunoglobulins; LL: lower limb; M: male; NCS: nerve conduction studies; NA: not available; P: protein levels; PLEX: plasmapheresis; R1i: ipsilateral R1; R2i: ipsilateral R2; R2c: contralateral R2; SNAP: sensory nerve action potential; UL: upper limbs.
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Bagella, C.F.; Corda, D.G.; Zara, P.; Elia, A.E.; Ruiu, E.; Sechi, E.; Solla, P. Chronic Inflammatory Demyelinating Polyneuropathy after ChAdOx1 nCoV-19 Vaccination. Vaccines 2021, 9, 1502.

AMA Style

Bagella CF, Corda DG, Zara P, Elia AE, Ruiu E, Sechi E, Solla P. Chronic Inflammatory Demyelinating Polyneuropathy after ChAdOx1 nCoV-19 Vaccination. Vaccines. 2021; 9(12):1502.

Chicago/Turabian Style

Bagella, Caterina Francesca, Davide G. Corda, Pietro Zara, Antonio Emanuele Elia, Elisa Ruiu, Elia Sechi, and Paolo Solla. 2021. "Chronic Inflammatory Demyelinating Polyneuropathy after ChAdOx1 nCoV-19 Vaccination" Vaccines 9, no. 12: 1502.

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