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What the experts said
In the first week of embryonic development, blastogenesis occurs with the embryo containing 2 layers.
In gastrulation during the 3rd week, the two embryonic layers become 3 layers by adding mesoderm.
Defects in the gastrulation stage can lead to two main neurosurgically relevant conditions: neuroenteric cyst and split cord malformation.
A neuroenteric cyst is a CNS cyst lined by epithelium mimicking the GI tract.
Neuroenteric cysts usually persist and cause recurrent infections and need to be excised with the whole tract.
Split cord malformation (diastematomyelia) has two types: Type 1 is the severe type and Type 2 is the mild type.
In split cord malformation Type 1, there are two separate spinal cords, each in its own dural sac, while in Type 2 there is a single dural sac with two hemicords.
Split cord malformation Type 1 has a bony cartilage spur, while Type 2 has no such structure.
In split cord malformation Type 1, patients more frequently present with weakness and back pain, while Type 2 may be discovered only incidentally.
Surgery for split cord malformation involves removing the bony spur to avoid more traction to the cord.
Dorsal induction and primary neurulation occur between the 3rd and 4th week of embryonic development.
During primary neurulation, the neural plate folds to form a neural tube with a cranial pore and caudal pore.
The neural crest, part of the neural plate, forms the peripheral nervous system.
A small notochord persists and forms the nucleus pulposus of the intervertebral disc.
The cranial neuropore closes on the 24th day and the caudal neuropore closes on the 26th day.
Failure of cranial neuropore closure causes anencephaly or encephaloceles.
Failure of caudal neuropore closure causes spina bifida, either occulta or aperta.
Failure of disjunction leads to dermal sinus tract.
Anencephaly is failure of the neural tube to form in the neuropore, leading to failure of the skull and part of the brain to form, and is usually fatal and typically detected before birth.
In encephalocele, brain tissue, dura, and CSF protrude through a defect in the back of the head, usually, and the sac needs to be closed; repair is possible and outcomes vary according to size and location.
Spina bifida can be two types: occulta (hidden) and aperta (myelomeningocele), which is an open spinal defect with a protruding sac containing spinal cord, meninges, and CSF.
Myelomeningocele requires urgent surgery to close the defect to prevent infection, especially when ruptured.
In the last few years, prenatal surgery is being attempted for myelomeningocele, operating and closing it while in the prenatal stage, based on the MOMS trial.
Spina bifida aperta (myelomeningocele) is usually associated with hydrocephalus and may need VP shunt.
Spina bifida occulta is a small vertebral defect with maybe a skin stigmata but no symptoms, can be incidentally discovered or develop tethered cord syndrome in the future.
Spina bifida aperta is a large protruding defect needing urgent surgery after birth or prenatal surgery, usually associated with hydrocephalus, and requires lifelong follow-up for shunt, leg weakness, and sometimes urinary incontinence.
Dermal sinus tract is a tube tract from the skin to the deeper spine, intradural, lined by epithelium, based on failure of disjunction between cutaneous ectoderm and neuroectoderm.
Dermal sinus tract can present with recurrent infection leading to meningitis and potential leg weakness; surgical removal of the whole tract is important.
Secondary neurulation occurs between the 20th and 48th days of embryonic development and forms the caudal portion of the neural tube, specifically structures lower in the spinal cord (sacral and coccygeal segments).
Abnormalities of secondary neurulation include persistent terminal ventricle (fifth ventricle), tight filum terminale, and terminal myelocystocele.
Ventral induction, including vesiculation, occurs between the 5th and 10th week of embryonic development.
In ventral induction, there are 3 primary brain vesicles (forebrain, midbrain, hindbrain) that differentiate into 5 secondary vesicles.
The forebrain divides into telencephalon (which forms the cerebrum) and diencephalon (which forms the thalamus, hypothalamus, and epithalamus).
The midbrain (mesencephalon) forms the midbrain structures.
The hindbrain divides into metencephalon (which forms the pons and cerebellum) and myelencephalon (which forms the medulla oblongata).
Holoprosencephaly is a forebrain abnormality representing failure of the forebrain to divide, resulting in a single lobed brain structure with facial abnormalities and severe neurological deficits.
Septo-optic-pituitary dysplasia is another forebrain abnormality involving incomplete development of midline brain structures, affecting vision, pituitary hormones, and causing developmental delay.
Dandy-Walker malformation is a hindbrain abnormality characterized by vermian agenesis or enlargement of the fourth ventricle, leading to issues with motor coordination, balance, and sometimes hydrocephalus.
Neuroproliferation occurs between the 6th and 12th week of embryonic development and involves rapid increase of neural precursor cells in the developing brain.
Hypoproliferation during neuroproliferation causes microcephaly, while hyperproliferation causes macrocephaly.
Neural migration occurs between the 8th and 20th week (or 2nd and 5th month) of embryonic development, during which neuroblasts migrate to specific brain locations to form neurons and establish brain layer structure.
Polymicrogyria is characterized by multiple small gyri separated by small sulci, generating an irregularly bumpy cortical surface with excessive small folds, causing intellectual disability and sometimes epilepsy.
Schizencephaly is an abnormal cleft or split lined by gray matter, resulting in developmental delay and motor impairment, and can be closed-lip or open-lip.
Gray matter heterotopia is gray matter in abnormal locations in the brain, such as intraventricular or periventricular areas.
Lissencephaly (smooth brain in Latin) is characterized by lack of normal folds and gyri, leading to severe developmental and motor issues, with only 2 or 3 gyri visible.
Porencephaly is a rare congenital disease that occurs from encephalomalacia during early life, usually seen on CT or MRI, usually communicating with the ventricles, and results from ischemic insults.
Porencephaly consists of cystic cavities within the cerebral hemisphere that often communicate with the ventricular system or subarachnoid space, usually caused by vascular insults like stroke during fetal or neonatal period.
Arachnoid cysts are cerebrospinal fluid sacs located in the arachnoid membrane, resulting from arachnoid membrane splitting abnormality or CSF abnormalities, defined as extra-axial CSF-filled cysts that typically don't enhance and typically don't communicate with the ventricles.
Schizencephaly consists of gray matter-lined clefts splitting the cerebral cortex, usually extending from the ventricular surface to the pial surface, leading to developmental malformation.
Clinical presentation of porencephaly is based on the size and location of the porencephalic cyst; arachnoid cysts are usually asymptomatic and incidentally discovered; schizencephaly usually presents with developmental delay, seizures, or motor deficits.
Agenesis of corpus callosum occurs between the 8th and 20th week due to defective tissue and issues in neural migration, usually presenting with developmental delay, seizures, and motor incoordination.
The Viking helmet sign is a unique MRI appearance in agenesis of corpus callosum where the lateral ventricles' frontal horns are shaped like a Viking helmet, flaring outwards.
The posterior (caudal) neuropore closes on the 28th day during primary neurulation.
The neural tube closes at the middle around day 20, and the anterior (cranial) neuropore closes on day 24.
Agenesis of corpus callosum can be due to defective neural migration occurring between the 8th and 20th week.
Myelomeningocele is caused by failure of closure of the caudal neuropore, usually at the 28th day, during primary neurulation.