Manal Merbouh,Ghizlane El Aidouni,Houssam Bkiyar,Brahim Housni
Post COVID-19 trigeminal neuritis: Case report
COVID-19,Trigeminal neuritis,Case report
Neurological symptoms are prevalent in Coronavirus disease 2019 (COVID-19) cases, ranging from 30% to 80% depending on the severity of the disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). We have documented a case of a 26-year-old woman who suffered from trigeminal neuritis caused by COVID-19, but responded well to corticotherapy. Two primary mechanisms may explain the neuroinvasive and neurovirulent properties of human coronaviruses. Neurological symptoms can persist long after recovery from COVID-19.
Post COVID-19 trigeminal neuritis: Case report

Neurological symptoms are prevalent in Coronavirus disease 2019 (COVID-19) cases, ranging from 30% to 80% depending on the severity of the disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). We have documented a case of a 26-year-old woman who suffered from trigeminal neuritis caused by COVID-19, but responded well to corticotherapy. Two primary mechanisms may explain the neuroinvasive and neurovirulent properties of human coronaviruses. Neurological symptoms can persist long after recovery from COVID-19.

The Coronavirus disease 2019 (COVID-19) is caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Throughout the pandemic, numerous cases of neurological disorders impacting both the central and peripheral nervous systems have emerged [1]. It has been reported that roughly 30% of patients with confirmed COVID-19 experience neurological symptoms. However, this number increases dramatically to 85% for those who are admitted to intensive care or have acute respiratory distress syndrome (ARDS) [2]. These acute neurological complications are prevalent and contribute to the ongoing burden of COVID-19 even in the long term [3].

We report the case of a 26-year-old patient with no medical or surgical history who was admitted to the neurology department for a decrease in sensitivity of the right hemiface that appeared after 5 days of flu-like symptoms. The examination at admission found a patient stable on the hemodynamic and respiratory plan with a systolic blood pressure (PAS) of 130 mm Hg, diastolic blood pressure (PAD) of 70 mm Hg, and oxygen saturation (Spo2) of 98% at room air. The neurological examination found right facial hypoesthesia of the mandibular territory with preservation of sensitivity at the level of the masseterine notch, evoking an attack of the third territory of the trigeminal nerve. A cerebral medullary MRI was carried out (Fig. 1), which showed an anomaly of the signal and linear enhancement of the intracisternal portion of the right trigeminal nerve, extended to its apparent origin on the pons, without tumefaction or mass syndrome, evoking more a trigeminal neuritis than a schwannoma. The biological workup showed lymphopenia at 800/μL. The rest of the workup in search of autoimmune diseases, infections, and neoplasia was without particularity (lumbar puncture, cytobacteriological examination of urine, CRP, glycated hemoglobin, ionogram, liver workup, hepatitis serologies, HIV and syphilis, CEA, AFP, CA 125, CA15-3, CA 19-9, Vit D,Vit B12,Vit B9,Ferritin,TSH,T4,T3,ANA,ANCA, anti-Ro/SSA, anti La/ SSB, Anti Ds DNA, ACE in blood and CSF, iso-electrofocalisation of CSF proteins, biopsy of the salivary glands). In front of the nonindividualization of an etiology and the influenza syndrome which preceded the neurological symptomatology, a PCR COVID-19 was carried out returning positive. The patient received 5 days of intravenous corticotherapy at a rate of 1g/d associated with carbamazepine 200 mg/d for 10 days. Then the patient was declared discharged after 5 days. The evolution was marked by the disappearance of symptoms after 7 days, the follow-up did not objectify any reappearance of the neurological symptoms, a cerebral MRI of control is envisaged after 6 months. This case reports follows CARE guidelines [4].

There is growing concern about the increased occurrence of neuropsychiatric conditions after a COVID-19 diagnosis, as it raises the question of whether it is a significant risk factor for neurological symptoms associated with multi-organ syndrome [3]. While initial descriptions were suggestive, they could not confirm a direct causal relationship between infection and neurological disease [5]. However, the emerging epidemiological literature suggests that COVID-19 infection is responsible for causing some neurological symptoms in both the acute and long-term phases of the disease. Neurological impairment or malfunction can arise from various indirect mechanisms, often related to immune dysregulation. The cytokine storm induced by SARS-CoV-2 can result in delayed severity of COVID-19 and is probably responsible for many of its neurological complications. These disorders may be linked to antibodies targeting self-antigens or tissues causing pathology at the neuronal synapse, neuromuscular junction, or myelin sheath. Nevertheless, attributing causality in the context of COVID-19 may be particularly challenging as it requires demonstrating 2 causally relevant processes, primary infection, and secondary autoimmunity [6], [7]. The virus can have an impact on the nervous system through both direct and indirect mechanisms. It can potentially enter the central nervous system through various pathways, such as retrograde axonal transport, crossing the blood-brain barrier or being transported by infected immune cells. The virus binds to ACE2, a protein that is highly expressed in various cell types such as neurons and choroid plexus, which can lead to cell death or inflammatory infiltration. Autopsy studies have revealed that some COVID-19 patients experience microglia activation and immune-mediated encephalitis. Additionally, the virus can indirectly affect the nervous system by triggering hyperinflammation and activating the immune system [3]. Helena Arino and her team discovered a vast array of lesions that affected multiple parts of the brain, including confluent subcortical FLAIR/T2 hyperintensities, focal cortical and subcortical diffusion restriction, white matter enhancing lesions, microhemorrhages, necrotic hemorrhagic lesions, and leptomeningeal enhancement. Their research also revealed that leptomeningeal enhancement with bilateral frontotemporal hypoperfusion was one of the earliest imaging findings observed in COVID-19 patients with ARDS and neurological symptoms upon admission [8]. A retrospective observational study examining the neuroimaging findings in COVID-19 patients revealed that the most common features were the involvement of the medial temporal lobe, nonconfluent multifocal white matter, hyperintense lesions on fluid-attenuated inversion recovery images with varying enhancement, and hemorrhagic lesions, as well as extensive and isolated microhemorrhages. Furthermore, the study demonstrated that intracerebral hemorrhagic lesions were present in the majority of patients and were linked to a worse clinical status [9]. The patient was satisfied with the treatment. These findings highlight the potential neurological complications of COVID-19 and the need for further research in this area in order to establish a causal link.

The diversity of neurological symptoms that arise in COVID-19 patients can affect both the central and peripheral nervous systems, further research is needed to better understand the different mechanisms that cause these symptoms and investigate potential long-term complications.

The article type (case report), the ethical approval was not necessary.

This is not an original research project involving human participants in an interventional or an observational study but a case report. This registration was not required.

Not commissioned, externally peer reviewed.

Written informed consent was obtained from the parent's patient. for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal on request.