Corpus Callosum
Agenesis of Corpus Callosum
Corpus Luteum
Acrocallosal Syndrome
Anisotropy
Diffusion Tensor Imaging
Nerve Fibers, Myelinated
Magnetic Resonance Imaging
Diffusion Magnetic Resonance Imaging
Brain
Nervous System Malformations
Internal Capsule
Diffuse Axonal Injury
Image Processing, Computer-Assisted
Functional Laterality
Fornix, Brain
Demyelinating Diseases
Myelin Sheath
Brain Diseases
Oligodendroglia
Brain Mapping
Cerebral Cortex
Septum Pellucidum
Atrophy
Leukoencephalopathies
Cerebral Ventricles
Hydrocephalus
Brain Injuries
Corpora Allata
Intellectual Disability
Aicardi Syndrome
Marchiafava-Bignami Disease
Malformations of Cortical Development
Neuroimaging
Cerebrum
Microcephaly
Spastic Paraplegia, Hereditary
Cebus
Lipoma
Image Interpretation, Computer-Assisted
Hyperglycinemia, Nonketotic
Neuroglia
Neuropsychological Tests
Penis
Pregnancy
Whale, Killer
Aging
Lateral Ventricles
Hypertelorism
Dichotic Listening Tests
Corpus Luteum Maintenance
Dandy-Walker Syndrome
Echoencephalography
Reference Values
Analysis of Variance
Sex Characteristics
Imaging, Three-Dimensional
Apraxias
Lissencephaly
Morphogenesis of callosal arbors in the parietal cortex of hamsters. (1/1216)
The morphogenesis of callosal axons originating in the parietal cortex was studied by anterograde labeling with Phaseolus lectin or biocytin injected in postnatal (P) hamsters aged 7-25 days. Some labeled fibers were serially reconstructed. At P7, some callosal fibers extended as far as the contralateral rhinal fissure, with simple arbors located in the homotopic region of the opposite cortical gray matter, and two or three unbranched sprouts along their trajectory. From P7 to P13, the homotopic arbors became more complex, with branches focused predominantly, but not exclusively, in the supra- and infragranular layers of the homotopic region. Simultaneously, the lateral extension of the trunk axon in the white matter became shorter, finally disappearing by P25. Arbors in the gray matter were either bilaminar (layers 2/3 and 5) or supragranular. A heterotopic projection to the lateral cortex was consistently seen at all ages; the heterotopic arbors follow a similar sequence of events to that seen in homotopic regions. These observations document that callosal axons undergo regressive tangential remodeling during the first postnatal month, as the lateral extension of the trunk fiber gets eliminated. Radially, however, significant arborization occurs in layer-specific locations. The protracted period of morphogenesis suggests a correspondingly long plastic period for this system of cortical fibers. (+info)The size and fibre composition of the corpus callosum with respect to gender and schizophrenia: a post-mortem study. (2/1216)
In this study the cross-sectional area (in n = 14 female controls, 15 male controls, 11 female patients with schizophrenia, 15 male patients with schizophrenia) and fibre composition (in n = 11 female controls, 10 male controls, 10 female patients with schizophrenia, 10 male patients with schizophrenia) of the corpus callosum in post-mortem control and schizophrenic brains was examined. A gender x diagnosis interaction (P = 0.005) was seen in the density of axons in all regions of the corpus callosum except the posterior midbody and splenium. Amongst controls, females had greater density than males; in patients with schizophrenia this difference was reversed. A reduction in the total number of fibres in all regions of the corpus callosum except the rostrum was observed in female schizophrenic patients (P = 0.006; when controlling for brain weight, P = 0.053). A trend towards a reduced cross-sectional area of the corpus callosum was seen in schizophrenia (P = 0.098); however, this is likely to be no more than a reflection of an overall reduction in brain size. With age, all subregions of the corpus callosum except the rostrum showed a significant reduction in cross-sectional area (P = 0.018) and total fibre number (P = 0.002). These findings suggest that in schizophrenia there is a subtle and gender-dependent alteration in the forebrain commissures that may relate to the deviations in asymmetry seen in other studies, but the precise anatomical explanation remains obscure. (+info)The role of ventral medial wall motor areas in bimanual co-ordination. A combined lesion and activation study. (3/1216)
Two patients with midline tumours and disturbances of bimanual co-ordination as the presenting symptoms were examined. Both reported difficulties whenever the two hands had to act together simultaneously, whereas they had no problems with unimanual dexterity or the use of both hands sequentially. In the first patient the lesion was confined to the cingulate gyrus; in the second it also invaded the corpus callosum and the supplementary motor area. Kinematic analysis of bimanual in-phase and anti-phase movements revealed an impairment of both the temporal adjustment between the hands and the independence of movements between the two hands. A functional imaging study in six volunteers, who performed the same bimanual in-phase and anti-phase tasks, showed strong activations of midline areas including the cingulate and ventral supplementary motor area. The prominent activation of the ventral medial wall motor areas in the volunteers in conjunction with the bimanual co-ordination disorder in the two patients with lesions compromising their function is evidence for their pivotal role in bimanual co-ordination. (+info)Functional neuropsychophysiological asymmetry in schizophrenia: a review and reorientation. (4/1216)
In reviewing the neuropsychophysiological evidence of functional asymmetry it is proposed that schizophrenia is characterized by a greater dispersion of leftward and rightward asymmetries. The two extremes are represented by active (left greater than right) and withdrawn (right greater than left) syndromes, as is the case with psychometric schizotypy. Syndrome-asymmetry relations extended beyond fronto-temporal systems to include posterior activity, infracortical motoneuron excitability, and individual differences in interhemispheric connectivity and directional biases. Central to these are lateral imbalances in thalamo-cortical and callosal arousal systems, while centrality to schizophrenia follows evidence of reversals in asymmetry with changes in symptom profile, clinical recovery, and neuroleptic treatment. Affinities are found in intact animals from challenge-induced turning tendencies representing coordinated activity of attentional, motor, and reinforcement systems. In both patients and animals, neuroleptics have reciprocal interhemispheric effects, with a bidirectionality that depends on syndrome or endogenous turning preference. Bidirectionality implicates nonspecific thalamic system (NSTS) and not limbic projections. It is proposed that the asymmetries arise from endogenous influences of genes, hormones, and early experience including stressors on NSTS asymmetry, and these underpin approach/withdrawal behavior that is manifested in temperament, personality, and clinical syndrome, and which precedes language development. (+info)Lipoma of the corpus callosum. (5/1216)
Lipoma of the corpus callosum is a rare congenital condition, often asymptomatic, but which may present as epilepsy, hemiplegia, dementia, or headaches. This paper reviews the condition and reports the only two cases which are known to the Hospital for Sick Children, Great Ormond Street, London. The second case demonstrated the value of computerised axial tomography (EMI scan) in making the diagnosis and showing associated anomalies. (+info)Genetic background changes the pattern of forebrain commissure defects in transgenic mice underexpressing the beta-amyloid-precursor protein. (6/1216)
We previously have reported corpus callosum defects in transgenic mice expressing the beta-amyloid precursor protein (betaAPP) with a deletion of exon 2 and at only 5% of normal levels. This finding indicates a possible involvement of betaAPP in the regulation or guidance of axon growth during neural development. To determine to what degree the betaAPP mutation interacts with genetic background alleles that predispose for forebrain commissure defects in some mouse lines, we have assessed the size of the forebrain commissures in a sample of 298 mice. Lines with mixed genetic background were compared with congenic lines obtained by backcrossing to the parental strains C57BL/6 and 129/SvEv. Mice bearing a null mutation of the betaAPP gene also were included in the analysis. We show that, independently of genetic background, both lack and underexpression of betaAPP are associated with reduced brain weight and reduced size of forebrain commissures, especially of the ventral hippocampal commissure. In addition, both mutations drastically increase the frequency and severity of callosal agenesis and hippocampal commissure defects in mouse lines with 129/SvEv or 129/Ola background. (+info)Brain involvement in Salla disease. (7/1216)
BACKGROUND AND PURPOSE: Our purpose was to document the nature and progression of brain abnormalities in Salla disease, a lysosomal storage disorder, with MR imaging. METHODS: Fifteen patients aged 1 month to 43 years underwent 26 brain MR examinations. In 10 examinations, signal intensity was measured and compared with that of healthy volunteers of comparable ages. RESULTS: MR images of a 1-month-old asymptomatic child showed no pathology. In all other patients, abnormal signal intensity was found: on T2-weighted images, the cerebral white matter had a higher signal intensity than the gray matter, except in the internal capsules. In six patients, the white matter was homogeneous on all images. In four patients, the periventricular white matter showed a somewhat lower signal intensity; in five patients, a higher signal intensity. In the peripheral cerebral white matter, the measured signal intensity remained at a high level throughout life. No abnormalities were seen in the cerebellar white matter. Atrophic changes, if present, were relatively mild but were found even in the cerebellum and brain stem. The corpus callosum was always thin. CONCLUSION: In Salla disease, the cerebral myelination process is defective. In some patients, a centrifugally progressive destructive process is also seen in the cerebral white matter. Better myelination in seen in patients with milder clinical symptoms. (+info)MR imaging of acute coccidioidal meningitis. (8/1216)
BACKGROUND AND PURPOSE: Our purpose was to describe the MR imaging findings in patients with acute coccidioidal meningitis. METHODS: Fourteen patients (11 men, three women; 22-78 years old; mean age, 47 years) with coccidioidal meningitis underwent neuroimaging within 2 months of diagnosis. Thirteen patients had MR imaging and one had an initial CT study with a follow-up MR examination 5 months later. Initial and follow-up MR images were evaluated for the presence of ventricular dilatation, signal abnormalities, enhancement characteristics, sites of involvement, and evidence of white matter or cortical infarction. The patterns of enhancement were characterized as focal or diffuse. Pathologic specimens were reviewed in two patients. RESULTS: Ten of the 14 images obtained at the time of initial diagnosis showed evidence of meningitis. All of the initially abnormal studies showed enhancement in the basal cisterns, sylvian fissures, or pericallosal region. Subsequent studies, which were available for three of the four patients with normal findings initially, all eventually became abnormal, with focal enhancement seen on the initial abnormal examination. Other abnormalities seen at presentation included ventricular dilatation (six patients) and deep infarcts (four patients). Pathologic specimens in two patients showed focal collections of the organism corresponding to the areas of intense enhancement on MR images. CONCLUSION: Early in its disease course, coccidioidal meningitis may show areas of focal enhancement in the basal cisterns, which may progress to diffuse disease. Pathologically, the areas of enhancement represent focal collections of the organism. Deep infarcts and communicating hydrocephalus are associated findings. (+info)The term "agenesis" refers to the failure of a structure to develop properly during fetal development. The corpus callosum is one of the largest white matter structures in the brain and plays a critical role in integrating sensory, motor, and cognitive information from both hemispheres.
Agenesis of Corpus Callosum can be caused by various genetic or environmental factors, such as:
1. Genetic mutations or deletions
2. Fetal exposure to certain drugs or infections during pregnancy
3. Maternal diabetes or other metabolic disorders
4. Trauma during pregnancy or childbirth
5. Brain injury or infection during early childhood.
Symptoms of Agenesis of Corpus Callosum can vary depending on the severity and location of the agenesis, but may include:
1. Delayed development of motor skills such as sitting, standing, and walking
2. Difficulty with language processing and speech articulation
3. Poor coordination and balance
4. Seizures or other neurological problems
5. Intellectual disability or developmental delays
6. Behavioral problems such as anxiety, depression, or autism spectrum disorder.
Diagnosis of Agenesis of Corpus Callosum typically involves a combination of physical examination, imaging studies such as MRI or CT scans, and genetic testing. Treatment for the condition may involve a multidisciplinary approach, including physical therapy, speech therapy, occupational therapy, and medication to control seizures or other symptoms. In some cases, surgery may be necessary to relieve pressure on the brain or to correct anatomical abnormalities.
Prognosis for individuals with Agenesis of Corpus Callosum varies depending on the severity of the condition and the presence of any additional health problems. However, early diagnosis and intervention can significantly improve outcomes and quality of life for these individuals. With appropriate treatment and support, many individuals with Agenesis of Corpus Callosum are able to lead fulfilling lives and achieve their goals.
The symptoms of acrocallosal syndrome can vary depending on the severity of the disorder, but may include:
* Delayed development and intellectual disability
* Seizures
* Vision problems
* Hearing loss or deafness
* Balance and coordination problems
* Abnormal facial features
* Distinctive skull shape
Acrocallosal syndrome is usually diagnosed using a combination of imaging tests, such as CT or MRI scans, and genetic testing. There is no cure for the disorder, but treatment may include surgery to remove the acoustic neuroma, physical therapy to improve balance and coordination, and special education to help with developmental delays.
Prognosis for individuals with acrocallosal syndrome varies depending on the severity of the disorder and the presence of other health problems. Some individuals may have mild symptoms and lead relatively normal lives, while others may have more severe symptoms and require ongoing medical care and support.
Some examples of nervous system malformations include:
1. Neural tube defects: These are among the most common types of nervous system malformations and occur when the neural tube, which forms the brain and spinal cord, fails to close properly during fetal development. Examples include anencephaly (absence of a major portion of the brain), spina bifida (incomplete closure of the spine), and encephalocele (protrusion of the brain or meninges through a skull defect).
2. Cerebral palsy: This is a group of disorders that affect movement, balance, and posture, often resulting from brain damage during fetal development or early childhood. The exact cause may not be known, but it can be related to genetic mutations, infections, or other factors.
3. Hydrocephalus: This is a condition in which there is an abnormal accumulation of cerebrospinal fluid (CSF) in the brain, leading to increased pressure and enlargement of the head. It can be caused by a variety of factors, including genetic mutations, infections, or blockages in the CSF circulatory system.
4. Moyamoya disease: This is a rare condition caused by narrowing or blockage of the internal carotid artery and its branches, leading to reduced blood flow to the brain. It can result in stroke-like episodes, seizures, and cognitive impairment.
5. Spinal muscular atrophy: This is a genetic disorder that affects the nerve cells responsible for controlling voluntary muscle movement, leading to progressive muscle weakness and wasting. It can be diagnosed through blood tests or genetic analysis.
6. Neurofibromatosis: This is a genetic disorder that causes non-cancerous tumors to grow on nerve tissue, leading to symptoms such as skin changes, learning disabilities, and eye problems. It can be diagnosed through clinical evaluation and genetic testing.
7. Tuberous sclerosis: This is a rare genetic disorder that causes non-cancerous tumors to grow in the brain and other organs, leading to symptoms such as seizures, developmental delays, and skin changes. It can be diagnosed through clinical evaluation, imaging studies, and genetic testing.
8. Cerebral palsy: This is a group of disorders that affect movement, posture, and muscle tone, often resulting from brain damage sustained during fetal development or early childhood. It can be caused by a variety of factors, including premature birth, infections, and genetic mutations.
9. Down syndrome: This is a genetic disorder caused by an extra copy of chromosome 21, leading to intellectual disability, developmental delays, and physical characteristics such as a flat face and short stature. It can be diagnosed through blood tests or genetic analysis.
10. William syndrome: This is a rare genetic disorder caused by a deletion of genetic material on chromosome 7, leading to symptoms such as cardiovascular problems, growth delays, and learning disabilities. It can be diagnosed through clinical evaluation and genetic testing.
It's important to note that these are just a few examples of developmental disorders, and there are many other conditions that can affect cognitive and physical development in children. If you suspect your child may have a developmental disorder, it's important to speak with a qualified healthcare professional for an accurate diagnosis and appropriate treatment.
DAI is often seen in cases of mild traumatic brain injury (mTBI), also known as concussion, and is thought to be caused by the shearing forces that occur when the brain is subjected to rapid acceleration and deceleration, such as during a car accident or sports injury.
The symptoms of DAI can vary widely depending on the severity of the injury and may include:
* Memory loss
* Confusion
* Difficulty concentrating
* Dizziness and balance problems
* Sleep disturbances
* Mood changes, such as irritability or depression
* Changes in behavior, such as increased impulsivity or aggression
DAI is diagnosed through a combination of physical examination, medical history, and imaging tests, such as CT or MRI scans. Treatment for DAI typically focuses on managing symptoms and supporting the brain's natural healing process, and may include medication, physical therapy, and cognitive rehabilitation.
Prognosis for DAI varies depending on the severity of the injury, but in general, people with DAI can expect a full recovery within a few months to a year after the initial injury. However, some individuals may experience persistent symptoms or develop long-term cognitive and emotional changes as a result of the injury.
The most common demyelinating diseases include:
1. Multiple sclerosis (MS): An autoimmune disease that affects the CNS, including the brain, spinal cord, and optic nerves. MS causes inflammation and damage to the myelin sheath, leading to a range of symptoms such as muscle weakness, vision problems, and cognitive difficulties.
2. Acute demyelination: A sudden, severe loss of myelin that can be caused by infections, autoimmune disorders, or other factors. This condition can result in temporary or permanent nerve damage.
3. Chronic inflammatory demyelination (CIDP): A rare autoimmune disorder that causes progressive damage to the myelin sheath over time. CIDP can affect the CNS and the peripheral nervous system (PNS).
4. Moore's disease: A rare genetic disorder that results in progressive demyelination of the CNS, leading to a range of neurological symptoms including muscle weakness, seizures, and cognitive difficulties.
5. Leukodystrophies: A group of genetic disorders that affect the development or function of myelin-producing cells in the CNS. These conditions can cause progressive loss of myelin and result in a range of neurological symptoms.
Demyelinating diseases can be challenging to diagnose, as the symptoms can be similar to other conditions and the disease progression can be unpredictable. Treatment options vary depending on the specific condition and its severity, and may include medications to reduce inflammation and modulate the immune system, as well as rehabilitation therapies to help manage symptoms and improve quality of life.
Some examples of multiple abnormalities include:
1. Multiple chronic conditions: An individual may have multiple chronic conditions such as diabetes, hypertension, arthritis, and heart disease, which can affect their quality of life and increase their risk of complications.
2. Congenital anomalies: Some individuals may be born with multiple physical abnormalities or birth defects, such as heart defects, limb abnormalities, or facial deformities.
3. Mental health disorders: Individuals may experience multiple mental health disorders, such as depression, anxiety, and bipolar disorder, which can impact their cognitive functioning and daily life.
4. Neurological conditions: Some individuals may have multiple neurological conditions, such as epilepsy, Parkinson's disease, and stroke, which can affect their cognitive and physical functioning.
5. Genetic disorders: Individuals with genetic disorders, such as Down syndrome or Turner syndrome, may experience a range of physical and developmental abnormalities.
The term "multiple abnormalities" is often used in medical research and clinical practice to describe individuals who have complex health needs and require comprehensive care. It is important for healthcare providers to recognize and address the multiple needs of these individuals to improve their overall health outcomes.
Some common types of brain diseases include:
1. Neurodegenerative diseases: These are progressive conditions that damage or kill brain cells over time, leading to memory loss, cognitive decline, and movement disorders. Examples include Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis (ALS).
2. Stroke: This occurs when blood flow to the brain is interrupted, leading to cell death and potential long-term disability.
3. Traumatic brain injury (TBI): This refers to any type of head injury that causes damage to the brain, such as concussions, contusions, or penetrating wounds.
4. Infections: Viral, bacterial, and fungal infections can all affect the brain, leading to a range of symptoms including fever, seizures, and meningitis.
5. Tumors: Brain tumors can be benign or malignant and can cause a variety of symptoms depending on their location and size.
6. Cerebrovascular diseases: These conditions affect the blood vessels of the brain, leading to conditions such as aneurysms, arteriovenous malformations (AVMs), and Moyamoya disease.
7. Neurodevelopmental disorders: These are conditions that affect the development of the brain and nervous system, such as autism spectrum disorder, ADHD, and intellectual disability.
8. Sleep disorders: Conditions such as insomnia, narcolepsy, and sleep apnea can all have a significant impact on brain function.
9. Psychiatric disorders: Mental health conditions such as depression, anxiety, and schizophrenia can affect the brain and its functioning.
10. Neurodegenerative with brain iron accumulation: Conditions such as Parkinson's disease, Alzheimer's disease, and Huntington's disease are characterized by the accumulation of abnormal proteins and other substances in the brain, leading to progressive loss of brain function over time.
It is important to note that this is not an exhaustive list and there may be other conditions or factors that can affect the brain and its functioning. Additionally, many of these conditions can have a significant impact on a person's quality of life, and it is important to seek medical attention if symptoms persist or worsen over time.
There are several types of atrophy that can occur in different parts of the body. For example:
1. Muscular atrophy: This occurs when muscles weaken and shrink due to disuse or injury.
2. Neuronal atrophy: This occurs when nerve cells degenerate, leading to a loss of cognitive function and memory.
3. Cardiac atrophy: This occurs when the heart muscle weakens and becomes less efficient, leading to decreased cardiac output.
4. Atrophic gastritis: This is a type of stomach inflammation that can lead to the wasting away of the stomach lining.
5. Atrophy of the testes: This occurs when the testes shrink due to a lack of use or disorder, leading to decreased fertility.
Atrophy can be diagnosed through various medical tests and imaging studies, such as MRI or CT scans. Treatment for atrophy depends on the underlying cause and may involve physical therapy, medication, or surgery. In some cases, atrophy can be prevented or reversed with proper treatment and care.
In summary, atrophy is a degenerative process that can occur in various parts of the body due to injury, disease, or disuse. It can lead to a loss of function and decreased quality of life, but with proper diagnosis and treatment, it may be possible to prevent or reverse some forms of atrophy.
There are several types of leukoencephalopathies, each with its own unique set of causes and characteristics. Some of the most common include:
1. Adrenoleukodystrophy (ALD): A genetic disorder that affects the breakdown of fatty acids in the body, leading to the accumulation of toxic substances in the brain.
2. Metachromatic leukodystrophy (MLD): A genetic disorder that affects the metabolism of certain fats in the body, leading to the accumulation of toxic substances in the brain.
3. Krabbe disease: A rare genetic disorder that affects the breakdown of a substance called galactocerebroside in the brain, leading to the accumulation of toxic substances and progressive damage to the nervous system.
4. Niemann-Pick disease: A group of inherited disorders that affect the metabolism of certain fats in the body, leading to the accumulation of toxic substances in the brain and other organs.
5. Alexander disease: A rare genetic disorder that affects the breakdown of a substance called galactose in the brain, leading to the accumulation of toxic substances and progressive damage to the nervous system.
The symptoms of leukoencephalopathies can vary depending on the specific type of disorder and the severity of the disease. Common symptoms include:
* Cognitive impairment: Difficulty with learning, memory, and problem-solving skills.
* Motor dysfunction: Weakness, rigidity, or tremors in the muscles.
* Seizures: Abnormal electrical activity in the brain that can cause convulsions or other symptoms.
* Vision loss: Blindness or vision impairment due to damage to the optic nerve.
* Speech difficulties: Slurred speech, difficulty with articulation, or other communication challenges.
* Behavioral changes: Increased irritability, aggression, or other behavioral problems.
There is no cure for leukoencephalopathies, but treatment options are available to manage the symptoms and slow the progression of the disease. These may include:
1. Physical therapy: To improve motor function and reduce muscle weakness.
2. Occupational therapy: To improve daily living skills and cognitive function.
3. Speech therapy: To improve communication skills and address swallowing difficulties.
4. Medications: To control seizures, muscle spasms, or other symptoms.
5. Nutritional support: To ensure adequate nutrition and address any feeding challenges.
6. Respiratory support: To assist with breathing and manage respiratory infections.
7. Psychological support: To address behavioral changes and other psychological issues.
The prognosis for leukoencephalopathies is generally poor, as the diseases tend to progress rapidly and can lead to significant disability or death within a few years of onset. However, with appropriate management and support, many individuals with these conditions can achieve a good quality of life and live well into adulthood. It is important for families to work closely with healthcare providers to develop a comprehensive treatment plan that addresses their child's specific needs and provides ongoing support throughout their lives.
There are several types of hydrocephalus, including:
1. Aqueductal stenosis: This occurs when the aqueduct that connects the third and fourth ventricles becomes narrowed or blocked, leading to an accumulation of CSF in the brain.
2. Choroid plexus papilloma: This is a benign tumor that grows on the surface of the choroid plexus, which is a layer of tissue that produces CSF.
3. Hydrocephalus ex vacuo: This occurs when there is a decrease in the volume of brain tissue due to injury or disease, leading to an accumulation of CSF.
4. Normal pressure hydrocephalus (NPH): This is a type of hydrocephalus that occurs in adults and is characterized by an enlarged ventricle, gait disturbances, and cognitive decline, despite normal pressure levels.
5. Symptomatic hydrocephalus: This type of hydrocephalus is caused by other conditions such as brain tumors, cysts, or injuries.
Symptoms of hydrocephalus can include headache, nausea, vomiting, seizures, and difficulty walking or speaking. Treatment options for hydrocephalus depend on the underlying cause and may include medication, surgery, or a shunt to drain excess CSF. In some cases, hydrocephalus can be managed with lifestyle modifications such as regular exercise and a balanced diet.
Prognosis for hydrocephalus varies depending on the underlying cause and severity of the condition. However, with timely diagnosis and appropriate treatment, many people with hydrocephalus can lead active and fulfilling lives.
There are several different types of brain injuries that can occur, including:
1. Concussions: A concussion is a type of mild traumatic brain injury that occurs when the brain is jolted or shaken, often due to a blow to the head.
2. Contusions: A contusion is a bruise on the brain that can occur when the brain is struck by an object, such as during a car accident.
3. Coup-contrecoup injuries: This type of injury occurs when the brain is injured as a result of the force of the body striking another object, such as during a fall.
4. Penetrating injuries: A penetrating injury occurs when an object pierces the brain, such as during a gunshot wound or stab injury.
5. Blast injuries: This type of injury occurs when the brain is exposed to a sudden and explosive force, such as during a bombing.
The symptoms of brain injuries can vary depending on the severity of the injury and the location of the damage in the brain. Some common symptoms include:
* Headaches
* Dizziness or loss of balance
* Confusion or disorientation
* Memory loss or difficulty with concentration
* Slurred speech or difficulty with communication
* Vision problems, such as blurred vision or double vision
* Sleep disturbances
* Mood changes, such as irritability or depression
* Personality changes
* Difficulty with coordination and balance
In some cases, brain injuries can be treated with medication, physical therapy, and other forms of rehabilitation. However, in more severe cases, the damage may be permanent and long-lasting. It is important to seek medical attention immediately if symptoms persist or worsen over time.
There are various causes of intellectual disability, including:
1. Genetic disorders, such as Down syndrome, Fragile X syndrome, and Turner syndrome.
2. Congenital conditions, such as microcephaly and hydrocephalus.
3. Brain injuries, such as traumatic brain injury or hypoxic-ischemic injury.
4. Infections, such as meningitis or encephalitis.
5. Nutritional deficiencies, such as iron deficiency or iodine deficiency.
Intellectual disability can result in a range of cognitive and functional impairments, including:
1. Delayed language development and difficulty with communication.
2. Difficulty with social interactions and adapting to new situations.
3. Limited problem-solving skills and difficulty with abstract thinking.
4. Slow learning and memory difficulties.
5. Difficulty with fine motor skills and coordination.
There is no cure for intellectual disability, but early identification and intervention can significantly improve outcomes. Treatment options may include:
1. Special education programs tailored to the individual's needs.
2. Behavioral therapies, such as applied behavior analysis (ABA) and positive behavior support (PBS).
3. Speech and language therapy.
4. Occupational therapy to improve daily living skills.
5. Medications to manage associated behaviors or symptoms.
It is essential to recognize that intellectual disability is a lifelong condition, but with appropriate support and resources, individuals with ID can lead fulfilling lives and reach their full potential.
The symptoms of Aicardi Syndrome can vary widely, but may include:
* Developmental delays and intellectual disability
* Seizures, which can be severe and difficult to control
* Vision loss or blindness
* Abnormalities in the structure of the brain and spinal cord, such as abnormal formation of the cerebral hemispheres or spina bifida
* Congenital heart defects
* Other congenital anomalies
Aicardi Syndrome is a rare condition, and the exact prevalence is not known. However, it is estimated to affect about 1 in 100,000 to 1 in 200,000 individuals worldwide. The syndrome can be diagnosed through a combination of clinical evaluations, imaging studies such as MRI or CT scans, and genetic testing.
There is currently no cure for Aicardi Syndrome, but various treatments can be used to manage the symptoms and improve quality of life. These may include medications to control seizures, physical therapy to improve mobility and coordination, and other supportive measures such as speech and language therapy and occupational therapy. In some cases, surgery may be necessary to correct anatomical abnormalities or to relieve pressure on the brain or spinal cord.
The prognosis for individuals with Aicardi Syndrome varies widely, depending on the severity of the symptoms and the presence of other health issues. Some individuals with the syndrome may have a relatively mild course, while others may experience significant developmental delays and disability. With appropriate medical care and support, however, many individuals with Aicardi Syndrome can lead fulfilling lives and achieve their full potential.
The condition was first described in 1925 by Italian neurologists Ugo Marchiafava and Ermanno Bignami. It is estimated to affect approximately one to two people per million population per year, with a higher prevalence among men than women.
Clinical features of Marchiafava-Bignami disease can include confusion, disorientation, memory loss, difficulty with speech and language, involuntary movements, and changes in mood and behavior. As the condition progresses, patients may experience seizures, weakness or paralysis, and vision problems.
The exact cause of Marchiafava-Bignami disease is not fully understood, but it is believed to be an immune response to certain compounds found in alcohol, particularly congeners, which are substances other than ethanol that are present in fermented beverages. Risk factors for developing the condition include heavy and long-term alcohol consumption, poor nutrition, and certain genetic predispositions.
There is no cure for Marchiafava-Bignami disease, but treatment options may include corticosteroids to reduce inflammation in the brain, anticonvulsants to control seizures, and rehabilitation therapy to improve cognitive and motor functions. In severe cases, the condition can be fatal, with mortality rates ranging from 20% to 80%.
In summary, Marchiafava-Bignami disease is a rare and progressive neurological disorder caused by an immune response to alcohol consumption, leading to inflammation of the brain and a range of cognitive, motor, and behavioral symptoms. While there is no cure for the condition, treatment options are available to manage its symptoms and improve quality of life.
It is important to note that Marchiafava-Bignami disease is a very rare condition, and the majority of people who consume alcohol will not develop the disorder. However, excessive alcohol consumption can have serious health consequences, including an increased risk of liver disease, heart disease, and certain types of cancer. It is important to drink responsibly and in moderation to reduce the risk of developing these conditions.
Types of Malformations of Cortical Development:
There are several types of malformations of cortical development, including:
1. Cerebral palsy: a group of disorders that affect movement, balance, and posture, often resulting from brain damage during fetal development or birth.
2. Hydrocephalus: a condition in which there is an abnormal accumulation of cerebrospinal fluid (CSF) in the brain, leading to increased intracranial pressure and enlargement of the head.
3. Microcephaly: a condition in which the brain and skull are smaller than normal, often resulting in developmental delays, intellectual disability, and seizures.
4. Macrocephaly: a condition in which the brain and skull are larger than normal, often resulting from an overproduction of CSF or a brain tumor.
5. Cortical dysplasia: a condition in which there is abnormal development of the cerebral cortex, leading to problems with movement, cognition, and behavior.
6. Fetal alcohol spectrum disorders (FASD): a group of conditions that result from exposure to alcohol during fetal development, often causing malformations of the cerebral cortex and other brain structures.
7. Genetic mutations: some genetic mutations can lead to malformations of cortical development, such as those caused by maternal infection or exposure to certain medications.
8. Infections during pregnancy: certain infections, such as rubella or toxoplasmosis, can cause malformations of cortical development if contracted during pregnancy.
9. Traumatic brain injury: a head injury during fetal development or early childhood can disrupt normal cortical development and lead to developmental delays and cognitive impairments.
10. Exposure to toxins: exposure to certain toxins, such as lead or pesticides, during fetal development can damage the developing brain and result in malformations of cortical development.
These are just a few examples of conditions that can cause malformations of cortical development. It's important to note that many of these conditions can be diagnosed through imaging studies such as MRI or CT scans, and some may require specialized testing or monitoring throughout childhood. Early detection and intervention can help improve outcomes for children with these conditions.
* Genetic mutations or chromosomal abnormalities
* Infections during pregnancy, such as rubella or toxoplasmosis
* Exposure to certain medications or chemicals during pregnancy
* Maternal malnutrition or poor nutrition during pregnancy
* Certain medical conditions, such as hypothyroidism or anemia.
Microcephaly can be diagnosed by measuring the baby's head circumference and comparing it to established norms for their age and gender. Other signs of microcephaly may include:
* A small, misshapen head
* Small eyes and ears
* Developmental delays or intellectual disability
* Seizures or other neurological problems
* Difficulty feeding or sucking
There is no cure for microcephaly, but early diagnosis and intervention can help manage the associated symptoms and improve quality of life. Treatment may include:
* Monitoring growth and development
* Physical therapy to improve muscle tone and coordination
* Occupational therapy to develop fine motor skills and coordination
* Speech therapy to improve communication skills
* Medication to control seizures or other neurological problems.
In some cases, microcephaly may be associated with other medical conditions, such as intellectual disability, autism, or vision or hearing loss. It is important for individuals with microcephaly to receive regular monitoring and care from a team of healthcare professionals to address any related medical issues.
The hallmark symptoms of SPH are difficulty walking (ataxia), weakness or paralysis of the lower limbs, and spasms or twitching of the muscles. Other common features may include:
1. Intellectual disability: Some individuals with SPH may have mild to moderate intellectual disability, which can range from learning difficulties to more severe cognitive impairments.
2. Autism spectrum disorder: Some individuals with SPH may also have autism spectrum disorder (ASD), which is characterized by difficulties in social interaction and communication, as well as repetitive behaviors or interests.
3. Seizures: Some people with SPH may experience seizures, which can be a significant source of concern for families and caregivers.
4. Vision problems: Some individuals with SPH may have vision loss or other eye problems, such as nystagmus (involuntary eye movements).
5. Scoliosis: Some people with SPH may develop scoliosis, a condition in which the spine curves abnormally to one side.
6. Other health issues: Depending on the specific type of SPH, individuals may also experience other health problems, such as kidney or liver disease, or gastrointestinal issues.
SPH is caused by mutations in various genes, including those involved in the functioning of nerve cells and the formation of the nervous system. These mutations can be inherited from one's parents or may occur spontaneously. There is currently no cure for SPH, but various treatments can help manage the symptoms and improve quality of life. These treatments may include:
1. Physical therapy: To help maintain muscle strength and flexibility, as well as to improve mobility and balance.
2. Occupational therapy: To develop skills for daily living and to assist with adapting to vision loss or other disabilities.
3. Speech therapy: To address communication difficulties and swallowing problems.
4. Medications: To control seizures, muscle spasms, or other symptoms.
5. Assistive technology: Such as canes, walkers, or wheelchairs, to assist with mobility.
6. Surgery: May be necessary to correct eye problems, such as cataracts or strabismus (crossed eyes), or to relieve pressure on the brain caused by hydrocephalus.
It is essential for individuals with SPH to receive regular medical care and monitoring from a multidisciplinary team of healthcare professionals, including neurologists, ophthalmologists, orthopedists, and other specialists as needed. With appropriate management and support, many people with SPH can lead fulfilling lives and achieve their goals.
There are many types of lipoma, with different names depending on their location and the tissues in which they grow. Common types include:
-Intramuscular lipoma: These occur within muscles and can feel firm or hard to the touch.
-Subcutaneous lipoma: These grow just beneath the skin and are usually soft to the touch.
-Mixed lipoma: These contain both fat cells and other types of tissue, such as muscle fibers.
-Spindle cell lipoma: These lipomas have a characteristic spindle or cylindrical shape under a microscope.
There are several ways to diagnose a lipoma, including physical examination, ultrasound imaging, and biopsy. Treatment for lipoma usually involves monitoring the tumor over time, as it will likely shrink or stay the same size without any intervention. However, if a lipoma grows quickly, becomes painful, or is causing discomfort or functional problems, surgical removal may be necessary.
In conclusion, lipomas are noncancerous growths that occur just beneath the skin or within muscles and connective tissues. They are usually painless unless pressed, but they can still cause discomfort or functional problems if large enough. While surgery is sometimes required to remove a lipoma, it is usually not necessary as long as the tumor remains small and doesn't grow rapidly over time.
The exact cause of hypertelorism is not known, but it is thought to be related to genetic mutations that affect the development of the skull and face during fetal development. The condition can run in families, and there may be a higher risk of recurrence if there is a family history of hypertelorism or other similar conditions.
There are several distinct types of hypertelorism, including:
* Isolated hypertelorism: This is the most common type and is characterized by an abnormal distance between the orbits without any other facial anomalies.
* Syndromic hypertelorism: This type is associated with other congenital anomalies, such as cleft lip and palate, hearing loss, and intellectual disability.
* Familial hypertelorism: This type runs in families and may be associated with other genetic conditions.
There is no specific treatment for hypertelorism, but rather a multidisciplinary approach that includes:
* Monitoring and management of any associated conditions, such as hearing loss or intellectual disability.
* Orthodontic treatment to help align the teeth and improve the appearance of the smile.
* Ophthalmological monitoring to ensure proper eye care and vision development.
* Surgical intervention to correct any facial anomalies, such as cleft lip and palate, or to improve the appearance of the face.
The prognosis for individuals with hypertelorism varies depending on the severity of the condition and the presence of any associated anomalies. In general, early diagnosis and appropriate management can help improve the outcomes and quality of life for individuals with this condition.
The syndrome is named after the American neurologist Dr. Arthur Dandy and British pediatrician Dr. Norman Walker, who first described it in the early 20th century. It is also known as hydrocephalus type I or cerebellar hydrocephalus.
DWS typically affects children, usually girls, between 3 and 18 months of age. The symptoms can vary in severity and may include:
* Enlarged skull
* Abnormal posture and gait
* Delayed development of motor skills
* Intellectual disability
* Seizures
* Vision problems
The exact cause of Dandy-Walker Syndrome is not known, but it is believed to be related to genetic mutations or environmental factors during fetal development. It can occur as an isolated condition or in combination with other congenital anomalies.
There is no cure for DWS, but treatment options may include:
* Shunts to drain excess CSF
* Physical therapy and occupational therapy
* Speech and language therapy
* Seizure medication
* Monitoring with regular imaging studies
The prognosis for children with Dandy-Walker Syndrome varies depending on the severity of the condition and the presence of other medical issues. Some individuals may experience significant developmental delays and intellectual disability, while others may have milder symptoms. With appropriate treatment and support, many individuals with DWS can lead fulfilling lives.
Examples of syndromes include:
1. Down syndrome: A genetic disorder caused by an extra copy of chromosome 21 that affects intellectual and physical development.
2. Turner syndrome: A genetic disorder caused by a missing or partially deleted X chromosome that affects physical growth and development in females.
3. Marfan syndrome: A genetic disorder affecting the body's connective tissue, causing tall stature, long limbs, and cardiovascular problems.
4. Alzheimer's disease: A neurodegenerative disorder characterized by memory loss, confusion, and changes in personality and behavior.
5. Parkinson's disease: A neurological disorder characterized by tremors, rigidity, and difficulty with movement.
6. Klinefelter syndrome: A genetic disorder caused by an extra X chromosome in males, leading to infertility and other physical characteristics.
7. Williams syndrome: A rare genetic disorder caused by a deletion of genetic material on chromosome 7, characterized by cardiovascular problems, developmental delays, and a distinctive facial appearance.
8. Fragile X syndrome: The most common form of inherited intellectual disability, caused by an expansion of a specific gene on the X chromosome.
9. Prader-Willi syndrome: A genetic disorder caused by a defect in the hypothalamus, leading to problems with appetite regulation and obesity.
10. Sjogren's syndrome: An autoimmune disorder that affects the glands that produce tears and saliva, causing dry eyes and mouth.
Syndromes can be diagnosed through a combination of physical examination, medical history, laboratory tests, and imaging studies. Treatment for a syndrome depends on the underlying cause and the specific symptoms and signs presented by the patient.
There are several types of apraxias, each with distinct symptoms and characteristics:
1. Ideomotor apraxia: Difficulty performing specific movements or gestures, such as grasping and manipulating objects, due to a lack of understanding of the intended purpose or meaning of the action.
2. Ideational apraxia: Inability to initiate or perform movements due to a lack of understanding of the task or goal.
3. Kinesthetic apraxia: Difficulty judging the weight, shape, size, and position of objects in space, leading to difficulties with grasping, manipulating, or coordinating movements.
4. Graphomotor apraxia: Difficulty writing or drawing due to a lack of coordination between the hand and the intended movement.
5. Dressing apraxia: Difficulty dressing oneself due to a lack of coordination and planning for the movements required to put on clothes.
6. Gait apraxia: Difficulty walking or maintaining balance due to a lack of coordinated movement of the legs, trunk, and arms.
7. Speech apraxia: Difficulty articulating words or sounds due to a lack of coordination between the mouth, tongue, and lips.
The diagnosis of apraxias typically involves a comprehensive neurological examination, including assessments of motor function, language, and cognitive abilities. Treatment options vary depending on the underlying cause and severity of the apraxia, but may include physical therapy, speech therapy, occupational therapy, and medication.
Lissencephaly is a rare genetic disorder characterized by a smooth, thin layer of brain tissue. It is caused by mutations in genes that regulate brain cell growth and development. The condition can result in intellectual disability, seizures, and other neurological symptoms. While there is no cure for lissencephaly, various treatments such as medication, surgery, and therapy can help manage its symptoms.
Lissencephaly is a rare genetic brain disorder that affects the cerebral cortex, which is the outer layer of the brain responsible for thinking, learning, and movement. The condition is characterized by a smooth, abnormally thin layer of brain tissue, which can lead to intellectual disability, seizures, and other neurological symptoms.
Lissencephaly is caused by mutations in genes that regulate brain cell growth and development. These mutations can occur randomly or be inherited from one's parents. The condition is estimated to affect approximately 1 in 100,000 people worldwide.
There is currently no cure for lissencephaly, but various treatments can help manage its symptoms. Medications such as anticonvulsants can help control seizures, while therapy and special education can help improve cognitive function and development. In some cases, surgery may be necessary to relieve pressure on the brain or correct anatomical abnormalities.
While the outlook for individuals with lissencephaly can vary depending on the severity of their condition, many people with the disorder lead fulfilling lives with appropriate support and management. Early diagnosis and intervention are key to improving outcomes for individuals with this condition.
Corpus callosum
Corpus Callosum
Agenesis of the corpus callosum
X-linked complicated corpus callosum dysgenesis
List of avant-garde films of the 2000s
Glossary of medicine
FAM43A
MASA syndrome
Lipoma
Longitudinal fissure
Alien hand syndrome
List of OMIM disorder codes
Linda Richards (neuroscientist)
Roger Wolcott Sperry
Leukoencephalopathy with neuroaxonal spheroids
Corpus callosotomy
Andermann syndrome
Susac's syndrome
Cave of septum pellucidum
Neuroanatomy of handedness
Joubert syndrome
Tuber cinereum
The Tale of the Dueling Neurosurgeons
Cat intelligence
François Chaussier
Spatial hearing loss
Ganglionic eminence
Perivascular space
Neuroscience and intelligence
Warren S. Brown
Strømme syndrome
FAM178B
List of diseases (C)
ZTTK syndrome
Congenital mirror movement disorder
NFIA
Of Two Minds (book)
Free will
Monotreme
Role of chance in scientific discoveries
Pallister-Killian syndrome
Risk factors of schizophrenia
Sex differences in human physiology
High-altitude cerebral edema
Axon
Trisynaptic circuit
Child psychopathology
Frederick Andermann
Shapiro syndrome
Associative visual agnosia
Supplementary motor area
Frontonasal dysplasia
Saal Bulas syndrome
Commissural fiber
Monosomy 9p
Functional specialization (brain)
Agenesis of the Corpus Callosum | National Institute of Neurological Disorders and Stroke
Corpus callosum agenesis - About the Disease - Genetic and Rare Diseases Information Center
NIMH » Corpus Callosum
Agenesis of the Corpus Callosum Imaging: Practice Essentials, Computed Tomography, Magnetic Resonance Imaging
Corpus callosum of the brain: MedlinePlus Medical Encyclopedia Image
Total Protein - Alzheimer's Disease: Brain: Corpus Callosum | P1236045Alz | Biochain
A Cross-Sectional Study on the Impact of Arterial Stiffness on the Corpus Callosum, a Key White Matter Tract Implicated in...
Haploinsufficiency of ZNF462 is associated with craniofacial anomalies, corpus callosum dysgenesis, ptosis, and developmental...
Unilateral whisker denervation drives synaptic remodeling across the corpus callosum | NIH Research Festival
corpus callosum
Subjects: Corpus Callosum - Digital Collections - National Library of Medicine Search Results
corpus callosum Archives • Ollibean
Dissected Corpus Callosum and Fornix | Neuroanatomy | The Neurosurgical Atlas
Corpus callosum size and shape alterations in adolescent inhalant users
Misaligned Genu of Corpus Callosum in version 3.2 | TORTOISE group
Congenital agenesis of the corpus callosum in mice is associated with altered regional sleep EEG dynamics in mice - Nuffield...
Plus it
Association between corpus callosum development on magnetic resonance imaging and diffusion tensor imaging, and...
MEDLINE Data Changes 2012: Revised Entry Combinations Table. NLM Technical Bulletin. 2011 Nov-Dec
Pediatric Neurological Disorders | Lurie Children's
The Interplay between Reproductive Social Stimuli and Adult Olfactory Bulb Neurogenesis
K-means Clustering Approach for Segmentation of Corpus Callosum from Brain Magnetic Resonance Images - Wellcome Centre for...
Table 3 - Zika Virus-Associated Birth Defects, Costa Rica, 2016-2018 - Volume 27, Number 2-February 2021 - Emerging Infectious...
Corpus callosum damage in heavy marijuana use: preliminary evidence from diffusion tensor tractography and tract-based spatial...
Browse in Images in Clinical Tropical Medicine | AJTMH
NICHD/NIDCD * Network on the Neurobiology and Genetics of Autism Collaborative Programs of Excellence in Autism (CPEAs):...
Asymmetric thinning of the cerebral cortex across the adult lifespan is accelerated in Alzheimer's disease | Nature...
Agenesis of Corpus Callosum1
- Absence of the septum pellucidum is found with many cerebral malformations, including holoprosencephaly, agenesis of corpus callosum, ventriculomegaly, open spina bifida, cortical malformations. (isuog.org)
Genu of the c1
- However, when we use DIFFPREP from Tortoise 3.2, one subject becomes corrupted in the genu of the corpus callosum. (nih.gov)
Body of the corpus callosum2
- The genu and anterior body of the corpus callosum are visualized, whereas the posterior body, splenium, and rostrum are absent. (medscape.com)
- In particular, significant associations were found between the cfPWV, an alteration of the extracellular water diffusion, and a neuronal density increase in the body of the corpus callosum which was also correlated with the performance in cognitive flexibility. (nih.gov)
Dysgenesis3
- Other disorders of the corpus callosum include dysgenesis, in which the corpus callosum is developed in a malformed or incomplete way, and hypoplasia, in which the corpus callosum is thinner than usual. (nih.gov)
- Because the corpus callosum may be partially or completely absent, the term dysgenesis has also been used to describe the spectrum of callosal anomalies. (medscape.com)
- People with Aicardi syndrome have absent or underdeveloped tissue connecting the left and right halves of the brain (agenesis or dysgenesis of the corpus callosum ). (nih.gov)
Partially or completely absent1
- Corpus callosum agenesis is a birth defect in which the structure that connects the two sides of the brain (the corpus callosum) is partially or completely absent. (nih.gov)
Brain11
- Agenesis of the corpus callosum (ACC) is a brain disorder in which the tissue that connects the left and right sides of the brain (its hemispheres) is partially or completely missing. (nih.gov)
- Many people with agenesis of the corpus callosum do not have any symptoms or the symptoms may range from subtle or mild to severe, depending on whether and which associated brain abnormalities are present. (nih.gov)
- The corpus callosum is the largest white matter structure of the brain. (medscape.com)
- Sagittal T1-weighted MRI of the brain shows the normal appearance of the corpus callosum. (medscape.com)
- The corpus callosum is the structure deep in the brain that connects the right and left hemispheres of the cerebrum, coordinating the functions of the two halves. (medlineplus.gov)
- These bundles, called the corpus callosum, house the fibers enabling communication between left and right sides of the brain. (nih.gov)
- The optic pathway and corpus callosum are two axonal pathways which distribute information between the left and right sides of the brain. (jneurosci.org)
- In newborn infants born very preterm, brain injury is associated with changes in simple metrics of corpus callosum development. (bvsalud.org)
- The corpus callosum - a collection of many millions of nerve fibers in the middle of the brain - is the largest connection between the two sides of the brain, or hemispheres. (luriechildrens.org)
- We used an MRI technique that is sensitive to the structural integrity of brain tissue combined with a white matter mapping tractography technique to investigate structural changes in the corpus callosum (CC). Diffusion tensor imaging (DTI) was obtained in eleven heavy marijuana users who started using marijuana in early adolescence and eleven age matched controls. (ox.ac.uk)
- The corpus callosum is the part of the brain that bridges the two hemispheres and enables communication between them. (nih.gov)
Diffusion3
- Association between corpus callosum development on magnetic resonance imaging and diffusion tensor imaging, and neurodevelopmental outcome in neonates born very preterm. (bvsalud.org)
- In a prospective cohort of 193 neonates born preterm, 24 to 32 weeks' gestation , we used magnetic resonance imaging and diffusion tensor imaging acquired early in life (n=193) and at term-equivalent age (n=159) to measure corpus callosum development mid-sagittal area (including corpus callosum subdivisions) and length, and fractional anisotropy from the genu and splenium. (bvsalud.org)
- Corpus callosum damage in heavy marijuana use: preliminary evidence from diffusion tensor tractography and tract-based spatial statistics. (ox.ac.uk)
Fornix1
- The C-shaped cingulum, corpus callosum and fornix have been aggressively dissected from surrounding structures and are well demonstrated. (neurosurgicalatlas.com)
Congenital1
- Agenesis of the corpus callosum (ACC) is the complete or partial absence of corpus callosum and is one of the most common congenital cerebral malformations. (medscape.com)
Seizures1
- This may occur secondary to porencephaly or schizencephaly , as a surgical complication in cases involving the transcallosal approach to the lateral and third ventricle, or with hemisection of the callosum for the treatment of seizures. (medscape.com)
Posterior3
- With pseudo-corpus callosum, which involves conditions of complete or partial agenesis, the hippocampal commissure may become enlarged and appear like the posterior part of the corpus callosum. (medscape.com)
- Secondary destruction of the corpus callosum occurs when the genu and anterior body are destroyed, leaving the posterior portion of the corpus callosum intact. (medscape.com)
- Adverse motor outcome was associated with smaller corpus callosum size in the posterior subdivision (p=0.003). (bvsalud.org)
Microstructure2
- The aims of the study are to better understand the relationship between arterial stiffness, white matter microstructure, and perfusion of the corpus callosum in older adults. (nih.gov)
- In this population , the development of the corpus callosum , as reflected by size and microstructure, is associated with neurodevelopmental outcomes at 18 months corrected age. (bvsalud.org)
Symptoms1
- When Do Symptoms of Corpus callosum agenesis Begin? (nih.gov)
Deficits1
- Since normal children have incomplete myelination of the corpus callosum, it was hypothesized that paralanguage deficits in children with ACC would be less apparent relative to their peers. (caltech.edu)
Magnetic1
- The normal appearance of the corpus callosum, along with the appearance on magnetic resonance imaging (MRI) of partial and complete ACC, are shown below. (medscape.com)
Mice3
- In the corpus callosum of mice engineered with a human stuttering mutation (lower panel), there are fewer astrocytes, shown in green, than in normal mice (upper panel). (nih.gov)
- The loss of astrocytes was most pronounced in the corpus callosum of the mutant mice. (nih.gov)
- Using advanced MRI methods, the researchers detected a slightly reduced volume of the corpus callosum in the mutant mice. (nih.gov)
Investigate1
- Here we further explore the role of these Hsts at the optic chiasm and investigate their function in corpus callosum development. (jneurosci.org)
Incomplete1
- The differences in results between adults and children with ACC are thought to reflect incomplete callosal development in normal children, and the importance of the corpus callosum in the early stages of the development of the ability to process literal language. (caltech.edu)
Integrity2
- cfPWV better predicts the microstructural integrity of the corpus callosum when compared with other index of vascular aging (the augmentation index, the systolic blood pressure, and the pulse pressure). (nih.gov)
- Mean diffusivity (MD) and fractional anisotropy (FA) (which measure structural integrity and tract coherence, respectively) were analysed within the corpus callosum which was spatially defined using tractography and tract-based spatial statistics (TBSS). (ox.ac.uk)
Cognitive1
- Abnormal cognitive outcomes were associated with lower corpus callosum fractional anisotropy (p=0.008). (bvsalud.org)
Development2
- To characterize corpus callosum development in neonates born very preterm from early in life to term-equivalent age and its relationship with neurodevelopmental outcome at 18 months corrected age. (bvsalud.org)
- We examined the association of (1) intraventricular haemorrhage (IVH) and white matter injury (WMI) severity, and (2) neurodevelopmental outcome at 18 months corrected age with corpus callosum development. (bvsalud.org)
White matter1
- However, the impact of arterial stiffness to white matter structure involved in the etiology of AD, including the corpus callosum remains poorly understood. (nih.gov)
Normal2
- Recent research revealed impaired processing of both nonliteral meaning and affective prosody in adults with agenesis of the corpus callosum (ACC) and normal intelligence. (caltech.edu)
- Is this corpus callosum normal? (isuog.org)
Structure1
- Agenesis (absence) of the corpus callosum is a condition in which this structure is either partially or completely missing. (luriechildrens.org)
Rare1
- Unfortunately, agenesis of the corpus callosum is a rare disorder. (nih.gov)
Find2
- Where can I find more information about agenesis of the corpus callosum? (nih.gov)
- At the corpus callosum we find that Hs6st1 has Slit -independent functions and our data indicate additional roles in FGF signaling. (jneurosci.org)
Children1
- 13. Corpus Callosum Lipomas in Children. (nih.gov)