Coarse Face Research Articles

Enzyme Replacement Therapy with Idursulfase in Patients with Mucopolysaccharidosis Type II: Literature Review

Mucopolysaccharidosis type II (MPS II; Hunter syndrome) is X-linked hereditary disease from the group of lysosomal storage disease. Its prevalence is 3–7 cases per 1 million live-born boys. MPS II occurs due to the deficiency of iduronate-2-sulfatase enzyme because of pathological changes in the structure of the IDS gene. Enzyme deficiency leads to the accumulation of glycosaminoglycans (GAGs), dermatan sulfate and heparan sulfate, in lysosomes. This leads to the damage of various organs and systems in the body with further development of clinical picture of the disease: coarse face, recurrent infections of upper respiratory tract, hearing loss up to deafness, cardiovascular and respiratory systems pathologies, hepatosplenomegaly, musculoskeletal system abnormalities, low growth, central nervous system damage. Enzyme replacement therapy with idursulfase, that was introduced in clinical practice 15 years ago, has significantly changed the quality of life of these patients. Idursulfase is purified form of natural lysosomal enzyme iduronate-2-sulfatase obtained via human cell line. Exogenous enzyme entry promotes GAGs catabolism in cells. This article provides outcomes analysis of foreign and Russian studies on the efficacy and safety of this medication, and its effect on MPS II patients survivability.

3DFP-FCGAN: Face completion generative adversarial network with 3D facial prior

Face completion is a domain-specific image inpainting problem. Most existing face completion methods fail to synthesize fine-grained facial structures due to the undifferentiated treatment of face images and other scene images. To handle this problem, we propose an end-to-end deep generative model based approach which makes full use of the facial prior knowledge, including 2D facial geometry priors from facial parsing maps and landmarks, as well as the 3D depth prior. We adopt a coarse-to-fine inpainting framework where the 2D facial geometry priors based on coarse faces are extracted to guide the refinement network for better planar facial textures and structures. Moreover, a novel 3D regularized reconstruction loss is proposed for the enhancement of the stereo perception of generated faces. Experimental results on two large-scale benchmarks CelebA and CelebA-HQ show that our method significantly outperforms the state-of-the-arts in generating more visually realistic and pleasing faces. Code is available at .

Phenotypic and molecular spectra of patients with switch/sucrose nonfermenting complex-related intellectual disability disorders in Korea

BackgroundThe switch/sucrose nonfermenting (SWI/SNF) complex is an adenosine triphosphate-dependent chromatin-remodeling complex associated with the regulation of DNA accessibility. Germline mutations in the components of the SWI/SNF complex are related to human developmental disorders, including the Coffin–Siris syndrome (CSS), Nicolaides–Baraitser syndrome (NCBRS), and nonsyndromic intellectual disability. These disorders are collectively referred to as SWI/SNF complex-related intellectual disability disorders (SSRIDDs).MethodsWhole-exome sequencing was performed in 564 Korean patients with neurodevelopmental disorders. Twelve patients with SSRIDDs (2.1%) were identified and their medical records were retrospectively analyzed.ResultsARID1B, found in eight patients, was the most frequently altered gene. Four patients harbored pathogenic variants in SMARCA4, SMARCB1, ARID2, and SMARCA2. Ten patients were diagnosed with CSS, and one patient without a typical phenotype was diagnosed with ARID1B-related nonsyndromic intellectual disability. Another patient harboring the SMARCA2 pathogenic variant was diagnosed with NCBRS. All pathogenic variants in ARID1B were truncating, whereas variants in SMARCA2, SMARCB1, and SMARCA4 were nontruncating (missense). Frequently observed phenotypes were thick eyebrows (10/12), hypertrichosis (8/12), coarse face (8/12), thick lips (8/12), and long eyelashes (8/12). Developmental delay was observed in all patients, and profound speech delay was also characteristic. Agenesis or hypoplasia of the corpus callosum was observed in half of the patients (6/12).ConclusionsSSRIDDs have a broad disease spectrum, including NCBRS, CSS, and ARID1B-related nonsyndromic intellectual disability. Thus, SSRIDDs should be considered as a small but important cause of human developmental disorders.

Woolly hair nevus caused by somatic mutation and Costello syndrome caused by germline mutation in HRAS: Consider parental mosaicism in prenatal counseling

Germline mutations in HRAS cause Costello syndrome (CS), while mosaic mutations in HRAS show a variability of phenotypes, ranging from mild features such as keratinocytic epidermal nevus (KEN), sebaceous nevus (SN), woolly hair nevus (WHN) with KEN, to severe manifestations of CS with cutis laxa. We report two individuals. The first was a 2-year-old boy with woolly hair nevus (WHN) without any other cutaneous involvement, in whom somatic HRAS mutation (c.34G>A; p.Gly12Ser) was identified in his affected scalp and hair follicle specimens. This is the first reported WHN type 1 (no cutaneous involvement) patient caused by somatic HRAS mutation. The other individual was a 12-year-old girl with CS caused by germline HRAS mutation (c.34G>A), that manifested with coarse face, palmoplantar keratoderma, deep palmar and plantar creases, hyperpigmented patches, asymmetry and deformity of lower limbs, atopic dermatitis, as well as mental retardation. Of note, a linear hyperpigmented plaque was observed in her father's lumbosacral region. Although the father refused to provide semen and skin tissue for further examination, this reminds us of possible mosaicism in parents of individuals with germline de novo HRAS mutation and underlines the importance of parental evaluation for prenatal counseling.

Social cognition in individuals born preterm

Faces hold a substantial value for effective social interactions and sharing. Covering faces with masks, due to COVID-19 regulations, may lead to difficulties in using social signals, in particular, in individuals with neurodevelopmental conditions. Daily-life social participation of individuals who were born preterm is of immense importance for their quality of life. Here we examined face tuning in individuals (aged 12.79 ± 1.89 years) who were born preterm and exhibited signs of periventricular leukomalacia (PVL), a dominant form of brain injury in preterm birth survivors. For assessing the face sensitivity in this population, we implemented a recently developed experimental tool, a set of Face-n-Food images bordering on the style of Giuseppe Arcimboldo. The key benefit of these images is that single components do not trigger face processing. Although a coarse face schema is thought to be hardwired in the brain, former preterms exhibit substantial shortages in the face tuning not only compared with typically developing controls but also with individuals with autistic spectrum disorders. The lack of correlations between the face sensitivity and other cognitive abilities indicates that these deficits are domain-specific. This underscores impact of preterm birth sequelae for social functioning at large. Comparison of the findings with data in individuals with other neurodevelopmental and neuropsychiatric conditions provides novel insights into the origins of deficient face processing.

Face inpainting based on GAN by facial prediction and fusion as guidance information

Face inpainting, a special case of image inpainting, aims to complete the occluded facial regions with unconstrained pose and orientation. However, existing methods generate unsatisfying results with easily detectable flaws. There are often fuzzy boundaries and details near the holes. Especially, for face inpainting, the face region semantic information (face structure, contour, and content information) has not been fully utilized, which leads to unnatural face images, such as asymmetry eyebrow and different sizes of eyes. This is unrealistic in many practical applications. To solve the problems, a new generative adversarial network by facial prediction and fusion as guidance information, is proposed for large missing regions of face inpainting. In the proposed method, two stages are adopted to complete coarse inpainting and refinement of the face. In Stage-I, we combine generator with a new encoder–decoder network with variational autoencoder-based backbone to predict the face region semantic information (including face structure, contour and content information) and do facial fusion for face inpainting. This could fully explore face region semantic information and generate coordinated coarse face images. Stage-II builds upon Stage-I results to refine face image. Both global and patch discriminators are used to synthesize high-quality photo-realistic inpainting. Experimental results on both CelebA and CelebA-HQ datasets demonstrate the effectiveness and efficiency of our method.

Mucopolysaccharidosis VII in Brazil: natural history and clinical findings

BackgroundMucopolysaccharidosis type VII (MPS VII), also known as Sly syndrome, caused by deficiency of the lysosomal enzyme β-glucuronidase, is an ultra-rare disorder with scarce epidemiological data and few publications about natural history and clinical spectrum.MethodsWe conducted a case series report which included retrospective data from all MPS VII patients diagnosed through the “MPS Brazil Network” who were known to be alive in 2020 in Brazil (N = 13). Clinical data were obtained from a review of the medical records and descriptive statistics and variables were summarized using counts and percentages of the total population.ResultsThe majority of the patients were from the Northeast region of Brazil. Among the signs and symptoms that raised the clinical suspicion of MPS, coarse face was the most frequent; 58% of the patients had a history of non-immune hydrops fetalis. All the subjects presented short neck and trunk. The majority presented typical phenotypical signs of MPS disorders. They all presented neurodevelopmental delay and cognitive impairment. About half of this cohort had knees deformities. Dysostosis multiplex was identified in almost all patients and cardiomyopathy was less frequent than observed in other types of MPSs. The mean age at diagnosis was 5 years, ranging from 1 to 14 years. Almost all patients (12/13) were homozygous for the c.526C>T (p.Leu176Phe) mutation. A novel variant of the GUSB gene was found, the c.875T>C (p.Leu292Pro), in a compound heterozygous with the c.526C>T (p.Leu176Phe) variant.ConclusionsThis case series is the biggest data collection of MPS VII patients alive in Latin America. The overall clinical picture of the MPS VII patients is very similar to other MPS disorders, including a spectrum of severity and delayed diagnosis.

Delayed Diagnosis of Congenital Hypothyroidism in a 6-month-old Male Infant in Tamale, Ghana.

Congenital hypothyroidism is a common inborn endocrine disorder. Asymptomatic presentation in majority of cases mean that its diagnosis may be missed especially in settings where newborn screening is absent. We present a case of delayed diagnosis of congenital hypothyroidism and emphasize on need for high level of suspicion to aid prompt diagnosis and treatment. Our case is a 3 year, 4 months old male, who was first seen at 5 months of age on account of poor growth. He passed meconium after day four of life, developed jaundice in first week of life, and slept a lot in neonatal period. He had coarse faces, protruding tongue, widened anterior fontanelle and herniation of umbilicus. He was started on oral levothyroxine 50 microgram daily. In resources limited settings where universal newborn screening is absent, healthcare workers should have a high level of suspicion in picking up the early signs of the condition.

Clinical Features of Infantile GM1 Gangliosidosis: Report of an Iranian Patient

Background: GM1 gangliosidosis is an autosomal recessive lysosomal storage disease due to a lack of β-galactosidase activity, exactly because of mutations in the GLB1 gene. GM1 gangliosidosis is a rare disease that could occur either during infancy (infantile type 1), as a juvenile (type 2), or in adulthood (type 3) in both nervous and skeletal systems. Type 1 is characterized by premature psychomotor deterioration, visceromegaly, macular cherry-red spot, skeletal deformities, and death in the first 2 years of life. Case Presentation: We reported an Iranian infant who, on initial check-up, had coarse face, visceromegaly, dystonia, and hepatosplenomegaly that increased at 15 months of age. At the initial check-up, a genetic test was performed and GM1 gangliosidosis type 1 was diagnosed. Conclusion: infant form is characterized by early-onset before the age of 6 months and rapidly progressive psychomotor deterioration, facial abnormalities, and visceromegaly.

Antenatal sonographic diagnosis of fryns syndrome: A case report

Fryns et al described a syndrome in the year 1979.1 Fryns syndrome is characterized by diaphragmatic defects, facial dysmorphism including coarse face, hypertelorism, broad and flat nasal bridge, with thick nasal tip, long philtrum, tented upper lip, wide mouth, micrognathia, low set and poorly formed ears and distal digital hypoplasia, pulmonary hypoplasia and others.2 We report a case of fryns syndrome in twenty- nine years old, Chinese, primigravida diagnosed during antenatal ultrasound scan at 26 weeks of gestation. The diagnosis has been confirmed by clinical finding, ultrasound, X-ray chest, CT brain, and ECHO at the postnatal period. Keywords: Fryns syndrome, Diaphragmatic hernia, Microphthalmia, Lung hypoplasia polyhydramnios.

Comorbid Cardiovascular Malformation and Type II Mucolipidosis: Clinical Case

Background . Type II mucolipidosis (I-cell disease, ICD) is one of the lysosomal storage diseases. It is very rare disease; the literature describes only few cases with confirmed diagnosis of mucolipidosis. Cardiovascular changes in children with such pathology are even less often. Clinical case description . The article describes the clinical case of type II mucolipidosis alongside with cardiovascular pathology — valvular heart apparatus defect with abdominal aortic hypoplasia and reversible myocardial dysfunction on the therapy of chronic heart failure (CHF). The patient has coarse face, gingival hyperplasia, macroglossia, dysostosis multiplex, diffuse muscular hypotonia, and mass of subcutaneous tissue. Arterial hypertension, heart cavities dilatation, left ventricular (LV) walls hypertrophy, and data of CT aortography let us to diagnosis abdominal aortic hypoplasia. Conclusion . Cardiovascular malformation in patients with mucolipidosis leads to severe, life-threatening conditions development. Untimely diagnosis can worsen the course of disease. Multidisciplinary approach is needed for the patient management.

Bi-allelic Pathogenic Variants in HS2ST1 Cause a Syndrome Characterized by Developmental Delay and Corpus Callosum, Skeletal, and Renal Abnormalities

Heparan sulfate belongs to the group of glycosaminoglycans (GAGs), highly sulfated linear polysaccharides. Heparan sulfate 2-O-sulfotransferase 1 (HS2ST1) is one of several specialized enzymes required for heparan sulfate synthesis and catalyzes the transfer of the sulfate groups to the sugar moiety of heparan sulfate. We report bi-allelic pathogenic variants in HS2ST1 in four individuals from three unrelated families. Affected individuals showed facial dysmorphism with coarse face, upslanted palpebral fissures, broad nasal tip, and wide mouth, developmental delay and/or intellectual disability, corpus callosum agenesis or hypoplasia, flexion contractures, brachydactyly of hands and feet with broad fingertips and toes, and uni- or bilateral renal agenesis in three individuals. HS2ST1 variants cause a reduction in HS2ST1 mRNA and decreased or absent heparan sulfate 2-O-sulfotransferase 1 in two of three fibroblast cell lines derived from affected individuals. The heparan sulfate synthesized by the individual 1 cell line lacks 2-O-sulfated domains but had an increase in N- and 6-O-sulfated domains demonstrating functional impairment of the HS2ST1. As heparan sulfate modulates FGF-mediated signaling, we found a significantly decreased activation of the MAP kinases ERK1/2 in FGF-2-stimulated cell lines of affected individuals that could be restored by addition of heparin, a GAG similar to heparan sulfate. Focal adhesions in FGF-2-stimulated fibroblasts of affected individuals concentrated at the cell periphery. Our data demonstrate that a heparan sulfate synthesis deficit causes a recognizable syndrome and emphasize a role for 2-O-sulfated heparan sulfate in human neuronal, skeletal, and renal development.

Distinct mechanisms of face representation by enhancive and suppressive neurons of the inferior temporal cortex.

Face-selective neurons in the inferior temporal (IT) cortex respond to faces by either increasing (ENH) or decreasing (SUP) their spiking activities compared with their baseline. Although nearly half of IT face neurons are selectively suppressed by face stimulation, their role in face representation is not clear. To address this issue, we recorded the spiking activities and local field potential (LFP) from IT cortex of three monkeys while they viewed a large set of visual stimuli. LFP high-gamma (HG-LFP) power indicated the presence of both ENH and SUP face-selective neural clusters in IT cortex. The magnitude of HG-LFP power of the recording sites was correlated with the magnitude of change in the evoked spiking activities of its constituent neurons for both ENH and SUP face clusters. Spatial distribution of the ENH and SUP face clusters suggests the presence of a complex and heterogeneous face hypercluster organization in IT cortex. Importantly, ENH neurons conveyed more face category and SUP neurons conveyed more face identity information at both the single-unit and neuronal population levels. Onset and peak of suppressive single-unit, neuronal population, and HG-LFP power activities lagged those of the ENH ones. These results demonstrate that IT neuronal code for face representation is optimized by increasing sparseness through selective suppression of a subset of face neurons. We suggest that IT cortex contains spatial clusters of both ENH and SUP face neurons with distinct specialized functional role in face representation.NEW & NOTEWORTHY Electrophysiological and imaging studies have suggested that face information is encoded by a network of clusters of enhancive face-selective neurons in the visual cortex of man and monkey. We show that nearly half of face-selective neurons are suppressed by face stimulation. The suppressive neurons form spatial clusters and convey more face identity information than the enhancive face neurons. Our results suggest the presence of two neuronal subsystems for coarse and fine face information processing.

Mutation and Phenotypic Spectrum of Patients With RASopathies

To examine the common and specific clinical features, mutation spectrum and genotype-phenotype correlation in Noonan syndrome and related RASopathies. Records of 30 patients with clinical diagnosis of Noonan syndrome and related RASopathies presenting over a six-year period at a Tertiary care Medical Genetics centre were reviewed. Detailed clinical phenotype evaluation and genetic testing (PTPN11 sequencing or next generation sequencing) was done. The genetic results were used to classify the patients. Noonan syndrome was confirmed in 22 patients, 5 had cardiofaciocutaneous syndrome and 3 had Noonan syndrome like disorder with loose anagen hair. The molecular diagnosis was confirmed in 27 patients. Mutations in PTPN11 gene were confirmed in 57.8 % patients. Developmental delay, cardiac defects, ectodermal abnormalities and coarse face was the predominant phenotype. Noonan syndrome like disorder with loose anagen hair was clinically identifiable by the sparse, slow growing hair and caused by one recurrent SHOC2, c.4A>G mutation. Noonan syndrome and other RASopathies should be suspected in patients with short stature, cardiac defects, typical facial dysmorphism with or without ectodermal involvement.

Coarse face, hypotonia, and neurodevelopmental regression

Inborn errors of metabolism are a heterogeneous class of multisystemic diseases which, although individually rare, are collectively quite common. Central nervous system is usually affected.The authors report the case of a five-month-old girl, daughter of non-consanguineous parents, born after an unremarkable full-term pregnancy and delivery. Hypotonia and neurodevelopmental regression were noted from the age of five months, along with progressive onset of facial dysmorphism, hepatomegaly, seizures, and dilated cardiomyopathy. Gangliosidosis type 1 diagnosis was confirmed by biochemical, enzymatic, and genetic findings.This report enhances the relevance of multidisciplinary approach and follow-up.

Look More Into Occlusion: Realistic Face Frontalization and Recognition With BoostGAN.

Many factors can affect face recognition, such as occlusion, pose, aging, and illumination. First and foremost are occlusion and large-pose problems, which may even lead to more than 10% accuracy degradation. Recently, generative adversarial net (GAN) and its variants have been proved to be effective in processing pose and occlusion. For the former, pose-invariant feature representation and face frontalization based on GAN models have been studied to solve the pose variation problem. For the latter, frontal face completion on occlusions based on GAN models have also been presented, which is much concerned with facial structure and realistic pixel details rather than identity preservation. However, synthesizing and recognizing the occluded but profile faces is still an understudied problem. Therefore, in this article, to address this problem, we contribute an efficient but effective solution on how to synthesize and recognize faces with large-pose variations and simultaneously corrupted regions (e.g., nose and eyes). Specifically, we propose a boosting GAN (BoostGAN) for occluded but profile face frontalization, deocclusion, and recognition, which has two aspects: 1) with the assumption that face occlusion is incomplete and partial, multiple images with patch occlusion are fed into our model for knowledge boosting, i.e., identity and texture information and 2) a new aggregation structure integrated with a deep encoder-decoder network for coarse face synthesis and a boosting network for fine face generation is carefully designed. Exhaustive experiments on benchmark data sets with regular and irregular occlusions demonstrate that the proposed model not only shows clear photorealistic images but also presents powerful recognition performance over state-of-the-art GAN models for occlusive but profile face recognition in both the controlled and uncontrolled environments. To the best of our knowledge, this article proposes to solve face synthesis and recognition under poses and occlusions for the first time.

Face pareidolia in schizophrenia

BackgroundFaces convey valuable daily life social signals. As in most psychiatric conditions, non-verbal social cognition or its components including face processing may be aberrant in schizophrenia (SZ). Social participation of individuals with SZ is vital for their quality of life, and remediation of social abilities in this population is of high relevance both for society and clinical care. MethodTuning to faces in non-face images such as shadows, grilled toasts, or ink blots is called face pareidolia. Humans possess high sensitivity to facial signals: even fetuses and infants are well tuned to coarse face cues. Here we assessed face tuning in individuals with SZ and person-by-person matched controls by using a new experimental tool, a set of food-plate images bordering on the Giuseppe Arcimboldo style. The key benefit of these images is that single components do not trigger face processing. Results and conclusionsThe outcome indicates that individuals with SZ exhibit aberrant face tuning in face-like non-face images (χ2(1) = 17.44, p = 0.0001) that can hamper adaptive interaction with peers and social participation hindering, in turn, clinical remediation. Face response rate in SZ patients was related to the scores on the event arrangement task tapping social cognition (Pearson product-moment correlation, r = 0.602, p = 0.01) and on picture completion task assessing visual perceptual organization (Spearman's rho = 0.614, p = 0.009). Therefore, poor performance on the face tuning task is unlikely to be accounted for by deviant general cognitive abilities, but rather by impairments in perceptual integration and social cognition. Comparison of these findings with data in autism and other neuropsychiatric conditions provides novel insights on the origins of face tuning in SZ and triggers brain imaging research.

Современные возможности пренатальной и постнатальной диагностики синдрома Фринса: собственные наблюдения и обзор литературы

Fryns syndrome (FS, OMIM#194050) is a rare lethal autosomal recessive disorder with unknown genetic defect, manifested the distinct complex of the multiply congenital abnormalities (MCA), including diaphragmatic hernia. There was made the world literature overview for the FS phenotypic features, clinical and genealogical data of the published familial cases, ultrasound and morphological characteristics of affected fetuses. Aim . Analysis of the clinical, morphological and prenatal ultrasound data of 12 FS cases, detected in Belarus during 2009-2018 years, and families’ reproduction results. Material and methods . Genetic counseling of 10 families with affected outcome was performed. All the pregnants underwent the combined (biochemical and ultrasound) screening. Prenatal and postnatal cytogenetical studies (GTG-banding) and the morphological investigations of the 10 aborted fetuses and 2 deceased infants were fulfilled. Results and Discussion . All the patients presented typical FS phenotypic features correlated with the diagnostic criteria. The spectrum of prenatal findings diagnosed at 1-st trimester included nuchal skin enlargement/cystic hygroma (5 cases), at the 2-ed trimester – diaphragmatic hernia (11 cases), omphalocele (1), other malformations (4 fetuses). The facial dysmorphisms (coarse face) were detected in all the patients. Lungs hypoplasia was found in all cases, 5 patients additionally dysplayed other abnormalities: pulmonary sequestration, cystic-adenomatoid malformation, lobular aplasia. Characteristic phalanges and nails hypoplasia or aplasia were registered in 11 cases, 3 sibs presented rare malformations – polydactyly (hands) and ectrodactyly (feet). Associated malformations spectrum included cleft palate, brain abnormalities (ventricular dilatation, arhinencephaly), cardiac defects, omphalocele, Meckel diverticule, hydronephroses, renal cysts, bicornuate uterus and hypospadia. The familial case with 3 affected sibs demonstrated a similarity in main diagnostic criteria. The couples reproduction analysis illulustrated a serious failure. Outcome of 29 pregnancies were as follows: 12 – FS cases, 4 – miscarries at 1-st trimester, 11 – healthy offspring and 2 cases – pregnancies are going on currently (both fetuses without malformations). Conclusion . Clinical diagnosis of FS may be noted in patients (either fetuses or newborns), which display the conjunction of typical MCA pattern with a normal karyotype. Additional investigations must be used in order to exclude the associated abnormalities if diaphragmatic hernia has been detected in fetus. In our opinion polydactyly and ectrodactyly may be added to the FS phenotypic spectrum.

Online Mixed Multiscale Finite Element Method with Oversampling and Its Applications

In this paper, we consider an online basis enrichment mixed generalized multiscale method with oversampling, for solving flow problems in highly heterogeneous porous media. This is an exten- sion of the online mixed generalized multiscale method [6]. The multiscale online basis functions are computed by solving a Neumann problem in an over-sampled domain, instead of a standard neighborhood of a coarse face. We are motivated by the restricted domain decomposition method. Extensive numerical experiments are presented to demonstrate the performance of our methods for both steady-state flow, and two-phase flow and transport problems.

Rapid and coarse face detection: With a lack of evidence for a nasal-temporal asymmetry

Humans have structures dedicated to the processing of faces, which include cortical components (e.g., areas in occipital and temporal lobes) and subcortical components (e.g., superior colliculus and amygdala). Although faces are processed more quickly than stimuli from other categories, there is a lack of consensus regarding whether subcortical structures are responsible for rapid face processing. In order to probe this, we exploited the asymmetry in the strength of projections to subcortical structures between the nasal and temporal hemiretina. Participants detected faces from unrecognizable control stimuli and performed the same task for houses. In Experiments 1 and 3, at the fastest reaction times, participants detected faces more accurately than houses. However, there was no benefit of presenting to the subcortical pathway. In Experiment 2, we probed the coarseness of the rapid pathway, making the foil stimuli more similar to faces and houses. This eliminated the rapid detection advantage, suggesting that rapid face processing is limited to coarse representations. In Experiment 4, we sought to determine whether the natural difference between spatial frequencies of faces and houses were driving the effects seen in Experiments 1 and 3. We spatially filtered the faces and houses so that they were matched. Better rapid detection was again found for faces relative to houses, but we found no benefit of preferentially presenting to the subcortical pathway. Taken together, the results of our experiments suggest a coarse rapid detection mechanism, which was not dependent on spatial frequency, with no advantage for presenting preferentially to subcortical structures.