Module I: Introduction to Psychopathology

 Normal development
 Common problems during normal development phase
 Etiology/Risk factors of psychopathology

The development of the brain has a long trajectory,

beginning within a few days after conception and
continuing through adolescence and beyond. The
nervous system undergoes its most dramatic
development during the first few years of life.
Brain development proceeds in overlapping
phases: making the brain cells (neurulation and
neurogenesis), getting the cells to where they need
to be (migration), growing axons and dendrites,
which are structures needed to link with other
nerve cells (neuronal differentiation and
pathfinding), developing synapses or points of
communication with other cells (synaptogenesis),
refining those synapses (maturation and pruning), and, finally, forming the supportive tissue that surrounds the nerve
cells and makes for efficient communication among them (gliagenesis or myelination).

1. Gastrulation
 Three important layers to remember
these are the ectoderm(nervous
system and skin),
mesoderm(muscles, skeleton,
kidneys, reproductive organs) and
endoderm(endocrine glands, lungs,
liver, digestive tract) and they form
early in development and so the
major event of the third week of
development is gastrulation.
 The three primary germ layers the
ectoderm mesoderm and endoderm fall and start becoming different types of tissues so the embryo is like a bowl.

2. Neurulation: Week 3-4

 The process of formation of a neural tube that takes a hollow shape that differentiates the brain and the spinal cord
of the Central Nervous System (CNS), the neural tube initially will be in a plate form and then later turns into a
tube form that is a neural tube.

Stage 1- Neural Tube Formation

 The neural plate creases inward until the edges come in contact and fuse.
 The process by which the neural plate develops a midline groove, the edges of which fold over, converge, and
close to form the neural tube
 Along the neural tube closure a ridge develops and forms the neural crest, which develops into a variety of
structures including spinal and brainstem ganglia, melanocytes, thymus, adrenal medulla, elements of the heart,
and the enteric nervous system. By 6 weeks, the rostral end of the neural tube begins to differentiate into three
primary sections, which develop into: the forebrain, midbrain, hindbrain, and cerebellum

 Spina Biforda- a birth defect in which an area of the spinal column doesn’t form properly, leaving a section of the
spinal cord and spinal nerves exposed through an opening in the back. Inability to move the lower legs (paralysis)
and other cognitive impairments are two symptoms.
  Encephalocele- a neural tube defect that occurs when the neural tube (the narrow channel that connects the brain
and the spinal cord) does not close completely during pregnancy.

Stage 2- Caudal Eminence Development

 The tube forms by hollowing out of the interior of a solid precursor.

 a series of events at the neural tube’s lower edge in which the caudal eminence develops into the bottom-most
spine segments and elements of the lower intestine.

 Caudal regression syndromes; sacral agenesis- sacrum bone that connects backbone to pelvis is partially or not
developed at all. The lower spine doesn’t fully form before birth.

3. Neurogenesis
 A multistage process in which neurons are generated and integrated into existing neuronal circuits.

A. Neural Proliferation:
 Neurogenesis refers to the birth of neurons and it starts in the spinal cord and brainstem.
 During this stage, neural progenitor cells undergo rapid cell division, generating a large number of neural cells.
 Neurons form from neural precursor cells, which can differentiate into various types of neurons based on genetic
and environmental cues.
 Proliferation peaks during the first trimester, with an estimated 250,000 neurons generated per minute at its peak.

 Aberrations in cell proliferation can lead to microcephaly (reduced head and brain size) or macrocephaly
(enlarged head), both of which can result in developmental and cognitive impairments.

B. Neuronal Migration:

 Due to proliferation of neurons, they start to migrate out toward the surface of the brain in waves between 12-20
weeks
 It brings cells into appropriate spatial relationships with other cells (Marín et al., 2010).
 Newborn neurons migrate from their germinal zone and disperse throughout the CNS to reach their final
destination where they subsequently become part of an appropriate lamination and neuronal circuit (Cooper,
2013). Cell polarity is required for neuronal migration
 Neurons that arrive at specific positions contribute to the formation of cortical columns—vertical structures that
play a role in processing sensory and motor information.

 A genetic lack of reelin causes lissencephaly, a “smooth” brain with a lack of development of folds (gyri) and
grooves (sulci)]
 Agenesis of corpus callosum is when the major connection between the two halves of the brain do not properly
form.
 Agenesis of cranial nerves is when the nerves controlling face and eye movements, hearing, balance, and
swallowing do not properly form.
 Focal cortical dysplasia is when a limited area of the brain forms abnormally.
 Macrogyria is when there are larger-than-normal folds of the brain.
 Microgyria is when there are smaller-than-normal folds of the brain.
 Polymicrogyria is when there are an abnormal number of small brain folds.
 In Neuronal heterotopias gray matter in the brain appears in the wrong places. It might appear around the
ventricles, the spaces of fluid inside the brain. Or it might appear in areas of white matter.
 Porencephaly results in an abnormal, fluid-filled cyst in the brain.
 Schizencephaly results in a slit or cleft in the brain.

4. Synaptogenesis:
 Synaptogenesis, the foundational process of forming synaptic connections between neurons, is pivotal for the
intricate architecture of brain connectivity. Commencing during prenatal development and extending into
early postnatal life, this dynamic process involves the extension and branching of axons and dendrites.
 Filopodia and dendritic spines undergo growth, creating synaptic connections that facilitate neural
communication. Simultaneously, synaptic pruning eliminates unnecessary or weak synapses, refining neural
circuits. Neurotrophic factors, exemplified by brain-derived neurotrophic factor (BDNF), play a vital role in
supporting neuron survival and growth during synaptogenesis. The establishment of synapses is a complex
interplay involving adhesion molecules, neurotransmitters, and intricate signaling pathways. Activity-
dependent processes, shaped by sensory experiences, contribute to the precise refinement of synaptic
connections, forming functional neural circuits.
 Disruptions in synaptogenesis have implications for neurodevelopmental disorders like autism, characterized
by atypical synaptic connectivity. The orchestration of genetic, environmental, and neurotrophic factors
collectively shapes the delicate and essential process of synaptogenesis, molding the functional architecture
of the nervous system.

5. Apoptosis:
 Apoptosis, a fundamental process in cellular development and maintenance, is the programmed cell death that
plays a crucial role in sculpting the intricate landscape of tissues and organs. Occurring throughout various stages
of development and in response to physiological cues, apoptosis is essential for eliminating unwanted or damaged
cells, ensuring proper tissue formation. This tightly regulated process involves a series of molecular events,
including cell shrinkage, chromatin condensation, and the formation of membrane-bound apoptotic bodies.
Caspases, key executioner proteins, orchestrate these cellular changes. Apoptosis contributes to tissue
homeostasis by removing surplus cells, shaping organ structures, and refining connections in the nervous system.
 Disruptions in apoptosis can lead to pathological conditions, such as cancer or neurodegenerative diseases. The
interplay of genetic, environmental, and signaling factors collectively governs apoptosis, underscoring its
significance in maintaining cellular balance and functional integrity in biological systems.

6. Gliogenesis:
 Gliogenesis, a pivotal process in neural development, involves the generation and maturation of glial cells,
essential components of the nervous system that support and modulate neuronal function. Beginning during
embryonic development and continuing into postnatal life, gliogenesis complements neurogenesis, contributing to
the intricate cellular composition of the brain. Glial cells, including astrocytes, oligodendrocytes, and microglia,
play diverse roles in neuronal health, synaptic function, and immune response. The process of gliogenesis
encompasses the migration, differentiation, and maturation of precursor cells into distinct glial cell types.
Astrocytes provide structural support and contribute to neurotransmitter homeostasis, while oligodendrocytes
form myelin sheaths crucial for efficient neuronal communication. Microglia serve as the resident immune cells,
participating in immune surveillance and response in the central nervous system. The orchestrated interplay of
genetic factors, environmental cues, and signaling pathways governs gliogenesis, ensuring the proper formation
and maintenance of glial cells to support the overall function and health of the nervous system.
 Disruptions in gliogenesis can have implications for various neurological disorders, highlighting the significance
of this process in neural development and homeostasis.

7. Myelination:
 Myelination, a crucial process in nervous system development, involves the formation of myelin sheaths around
axons, enhancing the efficiency of signal transmission between neurons. This intricate process begins during late
prenatal development and continues into early adulthood. Specialized glial cells, primarily oligodendrocytes in the
central nervous system and Schwann cells in the peripheral nervous system, play a pivotal role in myelination.
These cells wrap layers of myelin around axons, forming a protective insulating sheath. Myelination not only
accelerates nerve impulse conduction but also provides metabolic support to axons. The timing and progression of
myelination vary across different regions of the nervous system, contributing to the maturation of neural circuits.
 Demyelinating Diseases: Conditions like multiple sclerosis involve the immune system attacking and damaging
the myelin sheath, resulting in impaired signal transmission. This leads to symptoms such as weakness,
coordination difficulties, and cognitive impairment.
  Hypomyelination: Insufficient myelin formation, or hypomyelination, can occur due to genetic mutations or
environmental factors. This condition may manifest as delayed motor development, muscle weakness, and
cognitive deficits.
 Dysmyelination: Abnormalities in the myelination process, known as dysmyelination, can lead to the formation of
structurally and functionally abnormal myelin. This may result in a range of neurological symptoms depending on
the affected regions of the nervous system.
 White Matter Disorders: Disruptions in myelination can contribute to white matter disorders, affecting the
integrity of the brain's white matter, where myelinated axons are concentrated. These disorders may lead to
impairments in motor function, sensory processing, and cognitive abilities.

Month Bodily Development Neurological and Sensory Development

Initiation of basic organ formation, heart begins beating (Weight: Early neural tube development, foundational stage of
1 Not specified, Length: 1/10 inch) brain formation

Formation of distinct fingers, visible veins, heart divides into Continued limb development, early brain structure,
2 chambers (Weight: Not specified, Length: About 1 inch) development of sensory organs

Fully formed body, swallowing, kicking, organs and muscles Increased organ functionality, basic neurological
3 active (Weight: Not specified, Length: 2.5 to 3 inches) activity, sensory development
 Covered with lanugo, audible heartbeat, fetal movements Ongoing skin development, auditory sensory
4 (Weight: Not specified, Length: Not specified) development, increased fetal activity

Vernix caseosa forms, baby's first kick felt (Weight: Almost a Continued growth, protective coating development,
5 pound, Length: Nearly 8 inches) enhanced sensory perception

Eyebrows and eyelids visible, lungs filled with amniotic fluid Auditory and visual sensory development, lung
6 (Weight: Not specified, Length: Not specified) function initiation

Well-formed body, fingernails present (Weight: About 3.5 Continued body maturation, sensory organ
7 pounds, Length: About 12 inches) refinement, increased brain activity

Rapid weight gain, fat layers accumulate, head-down position Accumulation of adipose tissue, positioning for birth,
8 (Weight: Between 4 and 6 pounds, Length: Not specified) ongoing brain maturation

Increased crowding, decreased fetal movement, lung maturation Final stages of development, preparation for birth,
9 (Weight: 6 to 9 pounds, Length: Between 19 and 22 inches) enhanced neurological functions