How Does COVID-19 Affect the Brain: Neurological Complications and Cognitive Effects of COVID-19

The coronavirus disease (COVID-19) with its rapid spread and high mortality rate has caused major disruptions. It involves the nervous system. COVID-19 also causes infection in the brain stem which may influence chemosensory neural cells related with respiratory and cardiovascular regulation and also neurons of the respiratory center. This study evaluates the effects of COVID-19 on neurological complications and cognitive. Several studies were reviewed for the effects of COVID-19 on neurological complications and cognitive function. COVID-19 causes signs such as headache, altered mental status, anosmia, myalgia, ischemic stroke, developed cerebral hemorrhage, and cerebral venous sinus thrombosis, olfactory disorders, anosmia, losing taste, mental retardation, migraine, Guillain-Barre syndrome, encephalopathy, severe abduction deficits in both eyes, esotropia, epilepsy, hypogeusia, hyposmia, faulted consciousness and seizures. It also caused cognitive function such as Alzheimer's disease, cognitive worsening, depression, anxiety, tiredness, anxiety, decrease in BDNF, stress and fatigue. In conclusion, COVID-19 causes negative effects on neurological system and cognitive function which must be considered for the treatment of the disease in alongside clinical treatments. Copyright © 2022 Wolters Kluwer Medknow Publications. All rights reserved.

LDA-CNN: Linear Discriminant Analysis Convolution Neural Network for Periocular Recognition in the Wild

Due to the COVID-19 pandemic, the necessity for a contactless biometric system able to recognize masked faces drew attention to the periocular region as a valuable biometric trait. However, periocular recognition remains challenging for deployments in the wild or in unconstrained environments where images are captured under non-ideal conditions with large variations in illumination, occlusion, pose, and resolution. These variations increase within-class variability and between-class similarity, which degrades the discriminative power of the features extracted from the periocular trait. Despite the remarkable success of convolutional neural network (CNN) training, CNN requires a huge volume of data, which is not available for periocular recognition. In addition, the focus is on reducing the loss between the actual class and the predicted class but not on learning the discriminative features. To address these problems, in this paper we used a pre-trained CNN model as a backbone and introduced an effective deep CNN periocular recognition model, called linear discriminant analysis CNN (LDA-CNN), where an LDA layer was incorporated after the last convolution layer of the backbone model. The LDA layer enforced the model to learn features so that the within-class variation was small, and the between-class separation was large. Finally, a new fully connected (FC) layer with softmax activation was added after the LDA layer, and it was fine-tuned in an end-to-end manner. Our proposed model was extensively evaluated using the following four benchmark unconstrained periocular datasets: UFPR, UBIRIS.v2, VISOB, and UBIPr. The experimental results indicated that LDA-CNN outperformed the state-of-the-art methods for periocular recognition in unconstrained environments. To interpret the performance, we visualized the discriminative power of the features extracted from different layers of the LDA-CNN model using the t-distributed Stochastic Neighboring Embedding (t-SNE) visualization technique. Moreover, we conducted cross-condition experiments (cross-light, cross-sensor, cross-eye, cross-pose, and cross-database) that proved the ability of the proposed model to generalize well to different unconstrained conditions. [ FROM AUTHOR]

Multiple Cranial Neuropathies After COVID-19 Vaccination

Objective: To present a patient with acute-onset of multiple cranial neuropathies associated with recent COVID-19 vaccination. Background: Vaccine-associated neurologic adverse effects have been well-described over the decades;the influenza vaccine as well as others have been thought to precede Guillain-BarréSyndrome (GBS), Miller-Fisher Syndrome (MFS), and similar processes. Hyper-inflammatory responses have been frequently reported with SARS-CoV-2 infection and immunization, along with various neurologic pathologies. In this case report we describe a cranial polyneuropathy (3, 6, 7 and 12) associated with the COVID-19 vaccine. Design/Methods: Case Report with Video/Photos Results: A 52-year-old R-handed female presented with acute-onset, rapidly progressive deficits including left upper lid ptosis, left eye ophthalmoplegia, leftward tongue deviation, left facial paresis and dysarthria. History includes congenital left eye cataract s/p lens exchange, remote strabismus surgery and slight ptosis at baseline. She denied recent illness or injuries, though had completed single-dose vaccination for SARSCoV-2 11 days prior to symptom onset. Exam revealed new L eye esotropia with restriction in abduction and supraduction. Also noted was worsening of baseline ptosis, weak tongue protrusion with right-sided fasciculations and leftward deviation. Patient endorsed dysphagia and dysarthria. Workup consisted of three unexplanatory MRIs during week of symptom onset, lumbar puncture, evaluation by ENT and neuro-ophthalmology as well as other serum and CSF studies to investigate other autoimmune causes. Consent-obtained videos and photographs were taken for documentation/educational purposes. Follow-up visits revealed slow improvement starting three months after symptom onset. Conclusions: We outline a case of a female patient who presented with progressive, multiple cranial neuropathies with onset 11 days after single-dose SARS-CoV-2 vaccination. This constellation of symptoms in the setting of COVID-19 vaccination suggests propensity towards autoimmune neurologic processes. Further investigation is needed to determine the true incidence of similar polyneuropathies with the COVID-19 vaccine and to guide providers and patients to make informed decisions.

eP455: Fetal ultrasound presentation and neonatal diagnosis of Freeman-Sheldon syndrome in son of previously undiagnosed adult male

Background: Freeman-Sheldon syndrome [distal arthrogryposis type 2A (OMIM #193700), DA2A, Freeman-Burian syndrome] is a rare autosomal dominant multiple pterygium syndrome caused by alterations in MYH3. The phenotypic features, particularly of the face, are distinct and easily recognizable, and the diagnosis can be confirmed with molecular gene analysis. Fetal ultrasound imaging may provide important diagnostic clues to facilitate the diagnostic process. Informed consent and parental permission were provided by the parents. Case presentation: The infant’s mother presented for a Maternal Fetal Medicine genetic counseling telehealth appointment (due to COVID-19 pandemic restrictions) as a G7P2132, 32-year old female who had insulin-dependent diabetes and thrombocytosis. Her partner was a 24-year old male with a history of hearing loss, a V-shaped palate, and a lower lip cleft. Gestational age was 14 4/7 weeks and the indications were: increased nuchal translucency, paternal complex medical history, maternal G6PD heterozygote, and recurrent pregnancy loss. During the genetic counseling session, the following were addressed: 1) Maternal heterozygote status for G6PD indicated that if the fetus was male, there was a 50% chance he would be affected with G6PD-deficiency;2) Increased nuchal translucency on fetal ultrasound (US) with measurement at 98th percentile is associated with an increased risk of chromosomal abnormalities, microdeletion/duplications, and Noonan syndrome. The patient reportedly had low risk cell-free DNA but results were not available to the counselor at the time of consult. The option for additional genetic screening and diagnostic testing was declined;3) Three first trimester pregnancy losses with the father of this baby (FOB) were addressed, and parents deferred chromosome analyses at the time;4) Mother shared FOB’s complex history of bilateral sensorineural hearing loss, V-shaped cleft palate, lower lip cleft, and micrognathia. However, father was not present during the telehealth encounter. Mother was counseled regarding the possibility of an autosomal dominant condition with the potential risk to the pregnancy of up to 50%. It was recommended that the FOB have a clinical genetics evaluation, which could potentially provide a specific diagnosis and inform recurrence risk and management guidance. Follow-up MFM genetic counseling telephone visit occurred with the mother at 31 6/7 weeks gestation due to multiple congenital anomalies evident on fetal ultrasound. A 25 week fetal ultrasound revealed hypotelorism and a thickened nuchal translucency. A repeat study at 29 weeks revealed a V-shaped palate with a possible cleft, micrognathia, and midline mandibular cleft. FOB’s history was revisited. It was determined that he had 3 previous “no shows” to Genetics clinic appointments and did not pursue evaluation after the last counseling appointment. Again, it was emphasized that in order to best make a diagnosis for the family, an affected person would need to undergo a thorough evaluation, including medical and family history review, physical examination, and any indicated genetic testing. The parents were comfortable with the likelihood that the baby had the same condition as the father, but variable expressivity and broad range pf phenotypic presentation were explained. Recommendations for postnatal evaluation of the infant and pertinent genetic testing were provided. Consultative Genetics evaluation of the infant at 2 days of age revealed a short, broad forehead with supraorbital fullness leading to a horizontal brow indentation;mask-like facial appearance;hypotelorism;very deep set eyes with blepharophimosis;deep, creased nasal bridge;small, upturned nose with hypoplastic alae and narrow nares;microstomia with pursed lips;glossoptosis;micrognathia;2 deep vertical chin creases;short neck with excess nuchal skin;inverted and wide spaced nipples;clenched hands with 5th digits overlying 4th and 2nd overlying 3rd, bilaterally;bilateral vertical talus;2nd toes longer and overlying rd toes;clinodactyly of 4th and 5th toes bilaterally;and deep gluteal crease with no visible sinus. There were no evident contractures. The father has a complex history with no medical assessments prior to age 18. He reported that he did “not look like anyone else” in his family. He has a diagnosis of autistic spectrum disorder, a submucous cleft, vision issues, hearing loss necessitating a hearing aid on the left, and a history of cholesteatomas and of mastoidectomy. On brief examination, he had a mask-like face, blepharophimosis, left microphthalmia, left esotropia, narrowing of his midface, deep vertical crease on the mandibular region, microstomia, broad great toes, single flexor creases on the thumbs, and contracture of right thumb. Maxillofacial CT of the infant revealed hypoplastic mandibular body, ramus, and condyles bilaterally with micrognathia and retrognathia;hypoplastic maxilla bilaterally;and enophthalmos with retracted appearance of globes in the bony orbits bilaterally. Multiple facial bone abnormalities were seen, including microsomia, micrognathia, retrognathia, orbital hypotelorism and enophthalmos Genetic testing was performed via a custom Whole Exome Slice at GeneDx laboratories and included the MYH3 and TNNI2 genes. Results revealed a heterozygous pathogenic change in MYH3 (c.2015 G>A;p. R6724) consistent with the diagnosis of Freeman-Sheldon syndrome. Conclusion: The presentation of “midline mandibular cleft” on fetal ultrasound was the most specific prenatal finding. This is a very rare fetal finding. Thus, it should prompt further evaluation to assess for true clefting versus ridging or creasing. Additionally, targeted assessment for other findings or clinical clues for Freeman-Sheldon syndrome, such as contractures, “windmill vane” hand, and mouth size, could aid in the differential diagnosis considerations and the diagnostic process. Admittedly, these are position and quality dependent, and are challenging to assess even in ideal situations. The phenotype of the father was immediately recognizable. However, due to COVID-19 pandemic restrictions, prior to the infant’s birth, only telehealth visits were conducted and the father’s participation was by telephone. This limited the ability to narrow the differential diagnosis without visualization of his distinct phenotypic features. Finally, missed opportunities to diagnose the father prior to this pregnancy occurred. Many clinics send “no show” letters to referring providers and patients, as we do. Emphasizing the importance of diagnosis prior to pregnancy for individuals concerned about having a genetic disorder should be considered as part of the information shared in these letters.