Difference between revisions of "2014 Group Project 7"

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In this study, maps of local variation in tissue expansion are created for the first time in the living fetal human brain, in order to examine how structural complexity emerges in fetal brain. Previous studies have described overall growth of brain based upon ''in utero'' imaging studies with the use of magnetic resonance imaging (MRI) and ultrasound; however, complicated folding of the cortex in adult brain is due to different rates of regional tissue growth. Recent development in fetal MRI motion correction and computational image analysis techniques were employed in this study to help with the understanding of the patterns of local tissue growth. These techniques were applied to 40 normal fetal human brains in the period of primary sulcal formation (20–28 gestational weeks). This time period covers a developmental stage from the point at which only few primary sulci have developed until the time at which most of the primary sulci have formed, but before the emergence of secondary sulci on MRI. This developmental period is also important clinically, since the clinical MRI scans are also performed at this gestational age. Therefore it is important to describe the normal growth patterns in this period in order to be able to recognise abnormalities in the formation of sulci and gyri.
 
In this study, maps of local variation in tissue expansion are created for the first time in the living fetal human brain, in order to examine how structural complexity emerges in fetal brain. Previous studies have described overall growth of brain based upon ''in utero'' imaging studies with the use of magnetic resonance imaging (MRI) and ultrasound; however, complicated folding of the cortex in adult brain is due to different rates of regional tissue growth. Recent development in fetal MRI motion correction and computational image analysis techniques were employed in this study to help with the understanding of the patterns of local tissue growth. These techniques were applied to 40 normal fetal human brains in the period of primary sulcal formation (20–28 gestational weeks). This time period covers a developmental stage from the point at which only few primary sulci have developed until the time at which most of the primary sulci have formed, but before the emergence of secondary sulci on MRI. This developmental period is also important clinically, since the clinical MRI scans are also performed at this gestational age. Therefore it is important to describe the normal growth patterns in this period in order to be able to recognise abnormalities in the formation of sulci and gyri.

Revision as of 23:33, 4 October 2014

2014 Student Projects
2014 Student Projects: Group 1 | Group 2 | Group 3 | Group 4 | Group 5 | Group 6 | Group 7 | Group 8
The Group assessment for 2014 will be an online project on Fetal Development of a specific System.

This page is an undergraduate science embryology student and may contain inaccuracies in either description or acknowledgements.

Neural - CNS

--Mark Hill (talk) 15:19, 26 August 2014 (EST) OK you have nothing here, not even a project title (that I added). I will be asking your group questions in the lab tomorrow. How about some content, references, sources for each section. See Lab 3 Assessment.

--Mark Hill (talk) 11:36, 6 September 2014 (EST) Better, but still just references and no content.

Introduction

- definition of CNS - brain and spinal cord

- Neural development before fetal period First trimester development: Neurulation = ectoderm (outer layer) forms initial structure of the CNS, and folds upon itself to form neural tube towards the end of week 3. head portion- becomes the brain, further differentiates into forebrain, midbrain and hindbrain (recognizable by the 5th week of gestation) middle portion- becomes the brain stem (about 5th week) neural tube differentiates into 3 primary structural units of the brain: the proencephalon (forebrain), the mesencephalon (midbrain) and the rhombencephalon (hindbrain) (by the 7th week) The prosencephalon divides into the telencephalon and the diencephalon, the rhombencephalon divides into the metencephalon and the myelencephalon. formation of 2 additional structures and creating 5 primary units that will become the mature brain

- this webpage focuses on development of CNS of fetal neural system.

Research History/Historic findings

<pubmed>19339620</pubmed> <pubmed>8005032</pubmed> <pubmed>9311417</pubmed> <pubmed>17848161</pubmed> <pubmed>12768653</pubmed> <pubmed>17060425</pubmed>


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Development during fetal period

<pubmed>21042938</pubmed> <pubmed>12060827</pubmed> <pubmed>23727529</pubmed> <pubmed>16905335</pubmed> <pubmed>17848161</pubmed> <pubmed>18760424</pubmed> <pubmed>16971596</pubmed> <pubmed>17032846</pubmed>

Neural-development.jpg

Timeline of human neural development [1]


1. cell proliferation

- Formation of neurons and glia

- Begins around 40th embryonic day and is almost complete around the 6th month of gestation [2]

- Occurs in germinal matrix that comprised of ventricular and subventricular proliferative zones of cells


2. cell migration

- migration of cells from the 2 ventricular zones to their final positions

- 2 migrations

1) primary migration: occurs from week 8 to 16 of gestation, and continues to week 25 with lesser activity

2) passive migration: result in the oldest cells locating farthest from the proliferative zone as they are pushed away by recently generated cells, this lead to midline structures including thalamus and regions of the brain stem


Internurons migration in cerebral cortex.jpg Image of interneurons migration and interactions with radial glia in the developing cerebral cortex [3]

3. cell differentiation

- begins after the migration of neuronal and glial cells to the final positions

- starts about the 25th month of gestation until adolescence

- axonal and dendritic properties become fine-tuned as cells transform into committed members of specialized systems

4. cell death (apoptosis)

- 2 mechanisms: axonal retraction and neuronal pruning [4]

- Axonal retraction: recession of the collaterals of a neuron’s axon or shrinking of the terminal arborization of the axon

- Other connections are removed through selective cell death in which neurons die as a result of failing to establish appropriate connections

- critical for appropriate brain development

Brain

(focusing on the early development --> fetal development stages)

Spinal Cord

Current research models and findings

<pubmed>19786578</pubmed> <pubmed>21501576</pubmed> <pubmed>21492152</pubmed> <pubmed>24664314</pubmed> <pubmed>24639464</pubmed> <pubmed>24284205</pubmed> <pubmed>24177053</pubmed> <pubmed>24051984</pubmed> <pubmed>24996922</pubmed>


<pubmed>21414909</pubmed>

In this study, maps of local variation in tissue expansion are created for the first time in the living fetal human brain, in order to examine how structural complexity emerges in fetal brain. Previous studies have described overall growth of brain based upon in utero imaging studies with the use of magnetic resonance imaging (MRI) and ultrasound; however, complicated folding of the cortex in adult brain is due to different rates of regional tissue growth. Recent development in fetal MRI motion correction and computational image analysis techniques were employed in this study to help with the understanding of the patterns of local tissue growth. These techniques were applied to 40 normal fetal human brains in the period of primary sulcal formation (20–28 gestational weeks). This time period covers a developmental stage from the point at which only few primary sulci have developed until the time at which most of the primary sulci have formed, but before the emergence of secondary sulci on MRI. This developmental period is also important clinically, since the clinical MRI scans are also performed at this gestational age. Therefore it is important to describe the normal growth patterns in this period in order to be able to recognise abnormalities in the formation of sulci and gyri.

In this study, techniques mentioned previously were utilised to quantify tissue locations in order to map the tissues that were expanding with a higher or lower growth rate than the overall cerebral growth rate. It was found that relatively higher growth rates were detected in the formation of precentral and postcentral gyri, right superior temporal gyrus, and opercula whereas slower growth rates were found in the germinal matrix and ventricles. Additionally, analysis of the cortex illustrated greater volume increases in parietal and occipital regions compared to the frontal lobe. It was also found that gyrification was more active after 24 gestational weeks. These maps of the fetal brain were used to create a three-dimensional model of developmental biomarkers with which abnormal development in human brain can be compared.[5]

Abnormalities

<pubmed>12454899</pubmed> <pubmed>25007063</pubmed> <pubmed>16530991</pubmed> <pubmed>7504639</pubmed> <pubmed>19651588</pubmed> <pubmed>25135350</pubmed> <pubmed>25128525</pubmed> <pubmed>24397701</pubmed>

Microcephaly, Macrocephaly and Hydrocephalus

Microcephaly and macrocephaly refer to abnormal head size. These abnormalities are seen in less than 2% of all newborns. Learning abnormalities and neurophysiological malfunctioning associated with these abnormalities are dependent on etiology, severity and patient’s age. The most frequent cause of macrocephaly is hydrocephalus.

Microcephaly

Noticeable reduction in the size of brain is observed due to factors that kill the dividing cells in the ventricular germinal zone. These dividing cells give rise to brain cells (both neurons and glia). Microcephaly is specifically defined as a head size more than two standard deviations below the mean for age, gender and race.There are two diagnostic types of primary and secondary microcephaly. In primary microcephaly, abnormal development is observed in the first seven months of gestation while abnormal development occurs during the last 2 months of gestation (prenatal period) in the secondary type.

Microcephaly is caused by various factors that prevent normal proliferation and migration of cells during CNS development. These factors are divided into physical (irradiation, raised maternal temperature), chemical (anticancer drugs) and biological (infection of uterus due to rubella, cytomegalovirus and herpes simplex virus). Genetic defects and chromosomal disorders can also play a role.All of these factors result in destruction of the brain tissue (encephalopathy) with multiple areas of scarring and cyst formation.

Occipital encephalocele associated with microcephaly.jpg

Clinical photograph showing the giant occipital encephalocele associated with microcephaly and micrognathia[6]


Macrocephaly

In patients with macrocephaly the head is enlarged. Macrocephaly is specifically defined as a head size more than two standard deviations above the mean for age, gender and race. Macrocephaly is a syndrome of diverse aetiologies rather than a disease and the most frequent cause is hydrocephalus.

Hydrocephalus

Progressive enlargement of head due to accumulation of cerebrospinal fluid in ventricles is known as hydrocephalus. Excessive accumulation of cerebrospinal fluid is due to an imbalance between the formation and absorption of cerebrospinal fluid (communicating hydrocephalus) or obstruction of circulation of cerebrospinal fluid (non-communicating hydrocephalus). Multiple abnormalities such as brain tumours, congenital malformations and inflammatory lesions are associated with hydrocephalus.

In a patient with hydrocephalus, cerebrospinal fluid accumulation results in raised intracranial pressure which in turn results in enlarged ventricles and skull. Raised intracranial pressure is further associated with behavioural change, headache, papilloedema (oedema of the optic nerve) and herniation syndromes (subfalcine, uncal and cerebellar).

Enlargement of cranial sutures, progressive thinning of cerebral walls and lamination of cerebral cortex are all manifestations of hydrocephalus. Symptoms include significant deficits in motor skills (damage to pyramidal tracts) and cognitive functioning. The extent of brain damage depends on the underlying factor and developmental stage in which damage occurs. Hydrocephalus can be treated by shunting the excess fluid from the lateral ventricles into the heart or peritoneal cavity.


Arachnoid cyst with hydrocephalus.jpg

Fetal Alcohol Syndrome

[7]

Severe alcohol consumption during pregnancy and especially at critical stages of development (i.e. just after neural tube closure) can result in fetal alcohol syndrome (FAS). FAS is the most severe form of a spectrum of physical, cognitive and behavioural disabilities, collectively known as fetal alcohol spectrum disorders (FASD).

Mental retardation is the most serious abnormality associated with FAS. In addition, FAS is typically associated with central nervous system abnormalities, impaired sensation, impaired motor skills and lack of coordination. Patients diagnosed with FAS have a small head size relative to height, and demonstrate minor abnormalities of the face, eye, heart, joints, and external genitalia.

Ethanol in alcohol directly damages neurons by acting as an agonist for GABA receptors in the brain as well as interfering with many other receptors. Ethanol can also alter body’s metabolism by an indirect effect on neurons that modulate the secretion of hormones. In addition, it is postulated that malnutrition intensified by alcohol abuse is another cause of FAS since FAS is more common in individuals with low socioeconomic status. Nutritional deficiency and alcohol abuse inhibit the metabolism of folate, choline and vitamin A which are necessary for neurodevelopment. Therefore supplementation of these three nutrients to mothers with Disorder Binge drinking or low socioeconomic status may reduce the severity of FAS. Therefore pregnant mothers need to be aware of the risk associated with consuming even small amounts of alcohol. FASD and FAS represent a serious problem for both the individuals and society but are easily preventable.

References

  1. Report of the Workshop on Acute Perinatal Asphyxia in Term Infants, U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health, National Institute of Child Health and Human Development, NIH Publication No. 96-3823, March 1996.
  2. <pubmed>4203033</pubmed>
  3. <pubmed>17726524</pubmed>
  4. <pubmed>10532616</pubmed>
  5. <pubmed> 21414909 </pubmed>
  6. <pubmed>3271622</pubmed>|[1]
  7. <pubmed> 23809349 </pubmed>