Abstract:BackgroundMeningocele and meningoencephalocele of the skull are congenital deformities. Various species, such as pigs, dogs, and cats, are susceptible to congenital meningocele and meningoencephalocele and the incidence is higher in large white and landrace pigs.Case presentationIn this study, swelling was observed in the fontanel areas of the median planes of the skull cap in two female piglets of the same litter. Gross clinical examination, neurological examination, computed tomography (CT), and magnetic res… Show more
“…A number of congenital malformations have been reported in cattle and other domestic animal species with their development associated with either or a combination of hereditary and environmental factors [9, 12, 13, 15–17]. In meningocele or encephalomeningocele, the prime morphogenetic event that leads to the development of bone defects through which the meninges protrude, alone or together with neural tissue, has been traced to the focal failure of neural tube closure during fetal development [12, 14, 15].…”
Section: Discussionmentioning
confidence: 99%
“…Craniomeningocele can be hereditary as has been reported in a number of domestic animals including cattle, sheep and pigs [11–13]. Environmental factors linked to the development of this condition are numerous, including chemical agents, such as griseofulvin when administered during pregnancy [11–13, 18].…”
Section: Discussionmentioning
confidence: 99%
“…Cranial bifidum is one of the NTD that manifests as a focal bone defect in the cranium usually with protrusion of meninges to form a CSF-filled sac-like swelling called meningocele. In some instances, the protrusion may also include brain tissue thus called encephalomeningocele [10–13]. The morphogenesis of these bone defects is not simply due to defective ossification but have instead been reported to depend on primary neural tube defect whereby, focal neural tube dehiscence from embryonic ectoderm fails leading to a focal failure in the development of skeletal encasement [13–15].…”
Section: Introductionmentioning
confidence: 99%
“…In some instances, the protrusion may also include brain tissue thus called encephalomeningocele [10–13]. The morphogenesis of these bone defects is not simply due to defective ossification but have instead been reported to depend on primary neural tube defect whereby, focal neural tube dehiscence from embryonic ectoderm fails leading to a focal failure in the development of skeletal encasement [13–15]. Either or both the genetic and environmental factors have been associated with the development of these congenital defects [11, 14–16].…”
BackgroundCongenital cranial bone defects predispose to herniation of meninges, sometimes with brain tissue involvement, to form a cerebrospinal fluid (CSF)–filled cyst in the head. Such defects mainly results from focal failure of neural tube closure during fetal development and has been reported in various species of domestic mammals.Case presentationA one week old Ayrshire calf with a fluctuant swelling on parieto-occipital region of the head was referred to the faculty. The calf was always lying on lateral recumbency and exhibited resistance to deep palpation around the swelling and neck flexion. Embedded to the midline of the dorso-caudal surface of the cyst’s wall was a hard longitudinally oriented structure. The case was diagnosed as meningocele by means of radiographic examination. As the likelihood to full recovery was greatly reduced due to the negative impact already meted on brain tissue by intracranial pressure, the calf was euthanized on grounds of animal welfare and the diagnosis confirmed by anatomopathological findings which also revealed a circular bone defect in parieto-occipital region of the skull vault and a flattened bony structure embedded to the cyst’s wall.ConclusionAnatomopathological findings confirmed the diagnosis as cranial bifidum with meningocele at the parieto-occipital region of the skull vault. The presence of a bony structure embedded to the wall of meningeal sac was rather unusual and could not be sufficiently explained. It was however thought to, most likely, represent a part of interparietal bone that failed to get incorporated into squamous part of occipital bone as a result of the defect. The report also highlights challenges that work against timely delivery of urgent veterinary interventions in rural set ups of Africa and rest of the developing world, often leaving veterinarians with animal welfare consideration as main determinant of intervention measures.
“…A number of congenital malformations have been reported in cattle and other domestic animal species with their development associated with either or a combination of hereditary and environmental factors [9, 12, 13, 15–17]. In meningocele or encephalomeningocele, the prime morphogenetic event that leads to the development of bone defects through which the meninges protrude, alone or together with neural tissue, has been traced to the focal failure of neural tube closure during fetal development [12, 14, 15].…”
Section: Discussionmentioning
confidence: 99%
“…Craniomeningocele can be hereditary as has been reported in a number of domestic animals including cattle, sheep and pigs [11–13]. Environmental factors linked to the development of this condition are numerous, including chemical agents, such as griseofulvin when administered during pregnancy [11–13, 18].…”
Section: Discussionmentioning
confidence: 99%
“…Cranial bifidum is one of the NTD that manifests as a focal bone defect in the cranium usually with protrusion of meninges to form a CSF-filled sac-like swelling called meningocele. In some instances, the protrusion may also include brain tissue thus called encephalomeningocele [10–13]. The morphogenesis of these bone defects is not simply due to defective ossification but have instead been reported to depend on primary neural tube defect whereby, focal neural tube dehiscence from embryonic ectoderm fails leading to a focal failure in the development of skeletal encasement [13–15].…”
Section: Introductionmentioning
confidence: 99%
“…In some instances, the protrusion may also include brain tissue thus called encephalomeningocele [10–13]. The morphogenesis of these bone defects is not simply due to defective ossification but have instead been reported to depend on primary neural tube defect whereby, focal neural tube dehiscence from embryonic ectoderm fails leading to a focal failure in the development of skeletal encasement [13–15]. Either or both the genetic and environmental factors have been associated with the development of these congenital defects [11, 14–16].…”
BackgroundCongenital cranial bone defects predispose to herniation of meninges, sometimes with brain tissue involvement, to form a cerebrospinal fluid (CSF)–filled cyst in the head. Such defects mainly results from focal failure of neural tube closure during fetal development and has been reported in various species of domestic mammals.Case presentationA one week old Ayrshire calf with a fluctuant swelling on parieto-occipital region of the head was referred to the faculty. The calf was always lying on lateral recumbency and exhibited resistance to deep palpation around the swelling and neck flexion. Embedded to the midline of the dorso-caudal surface of the cyst’s wall was a hard longitudinally oriented structure. The case was diagnosed as meningocele by means of radiographic examination. As the likelihood to full recovery was greatly reduced due to the negative impact already meted on brain tissue by intracranial pressure, the calf was euthanized on grounds of animal welfare and the diagnosis confirmed by anatomopathological findings which also revealed a circular bone defect in parieto-occipital region of the skull vault and a flattened bony structure embedded to the cyst’s wall.ConclusionAnatomopathological findings confirmed the diagnosis as cranial bifidum with meningocele at the parieto-occipital region of the skull vault. The presence of a bony structure embedded to the wall of meningeal sac was rather unusual and could not be sufficiently explained. It was however thought to, most likely, represent a part of interparietal bone that failed to get incorporated into squamous part of occipital bone as a result of the defect. The report also highlights challenges that work against timely delivery of urgent veterinary interventions in rural set ups of Africa and rest of the developing world, often leaving veterinarians with animal welfare consideration as main determinant of intervention measures.
“…Congenital MCs and MECs have been reported in humans and various domestic animals. 15,16 A hereditary predisposition has been shown in Burmese cats, 16 but teratogenic factors and nutritional deficiencies may play a role in the development of such malformations. 17,18 Based on the small number of cases collected throughout Europe in this study, it appears to be a sporadically occurring disease, that might be underdiagnosed because diagnosis requires advanced imaging and some dogs may not have any neurologic signs, as occurred in the dog diagnosed with lymphoma and an incidental MEC.…”
Background: The term meningoencephalocele (MEC) describes a herniation of cerebral tissue and meninges through a defect in the cranium, whereas a meningocele (MC) is a herniation of the meninges alone.Hypothesis/Objectives: To describe the clinical features, magnetic resonance imaging (MRI) characteristics, and outcomes of dogs with cranial MC and MEC.Animals: Twenty-two client-owned dogs diagnosed with cranial MC or MEC.Methods: Multicentric retrospective descriptive study. Clinical records of 13 institutions were reviewed. Signalment, clinical history, neurologic findings and MRI characteristics as well as treatment and outcome were recorded and evaluated.Results: Most affected dogs were presented at a young age (median, 6.5 months; range, 1 month -8 years). The most common presenting complaints were seizures and behavioral abnormalities. Intranasal MEC was more common than parietal MC. Magnetic resonance imaging identified meningeal enhancement of the protruded tissue in 77% of the cases. Porencephaly was seen in all cases with parietal MC. Cerebrospinal fluid (CSF) analysis identified mild abnormalities in 4 of 11 cases. Surgery was not performed in any affected dog. Seventeen patients were treated medically, and seizures were adequately controlled with anti-epileptic drugs in 10 dogs. Dogs with intranasal MEC and mild neurologic signs had a fair prognosis with medical treatment.Conclusion and clinical importance: Although uncommon, MC and MEC should be considered as a differential diagnosis in young dogs presenting with seizures or alterations in behavior. Medical treatment is a valid option with a fair prognosis when the neurologic signs are mild.
Neural tube defects (NTDs) are congenital malformations resulting from the improper or incomplete closure of the neural tube during embryonic development. A number of similar malformations of the protective coverings surrounding the central nervous system are also often included under this umbrella term, which may not strictly fit this definition. A range of NTD phenotypes exist and have been reported in humans and a wide range of domestic and livestock species. In the veterinary literature, these include cases of anencephaly, encephalocele, dermoid sinus, spina bifida, and craniorachischisis. While environmental factors have a role, genetic predisposition may account for a significant part of the risk of NTDs in these animal cases. Studies of laboratory model species (fish, birds, amphibians, and rodents) have been instrumental in improving our understanding of the neurulation process. In mice, over 200 genes that may be involved in this process have been identified and variant phenotypes investigated. Like laboratory mouse models, domestic animals and livestock species display a wide range of NTD phenotypes. They remain, however, a largely underutilized population and could complement already established laboratory models. Here we review reports of NTDs in companion animals and livestock, and compare these to other animal species and human cases. We aim to highlight the potential of nonlaboratory animal models for mutation discovery as well as general insights into the mechanisms of neurulation and the development of NTDs.
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