Week 1 Flashcards
List aspects of assessment at the cellular level, structural (system) level, regions, and functional divisions
- Cellular level
What are functional units of the nervous system?
How do ions influence nerve cell function?
How does a nerve cell convey information? - Structural (system) level
Central nervous system
Peripheral nervous system - Regions
Peripheral, spinal, brainstem, cerebellar, and cerebral regions - Functional divisions
Somatic system:
Somatic sensory
Somatic motor
Autonomic system
Define neurons
specialized cells that form the basis of the nervous system
- Referred to as a nerve cell
- Send signals throughout the body rapidly
Label and define these
1) Neuron, 2) Oligodendrocyte (glial cell), 3) Astrocyte (glial cell)
Cell types: Neurons and Glia (glial cells)
A) Neurons: anatomical and functional units for signal transmission
B) Glia (non-neuronal cells): supporting matrix, maintaining homeostasis, nourishment, regulating neuronal functions
Label the structure of a neuron
1) Dendrite, 2) nucleus, 3) Sensory: first node of Ranvier Motor: axon Hillock, 4) cell body, 5) axon, 6) myelin sheath, 7) Schwan cell, 8) node of ranvier, 9) axon terminal
Anatomical components
* Dendrites (receives signals)
* Soma (cell body, axon hillock)
* Axon (transports signal to other neurons)
* Axon terminal
Functional components
* Receiving zone
* Trigger zone
* Conducting zone
* Effector zone
Identify and describe the types of neurons
A) Bipolar, B) Bipolar “pseudounipolar”, C) multipolar
Anatomical classifications:
* Bipolar: one dendrite root and one
axon
Pseudounipolar
* Multipolar: multiple dendrites and single axon (most common)
What are the functional classifications of neurons?
motor neurons
Sensory neurons
Interneurons (up or downgrades information before relaying it to other neurons)
What are the types of glial cells?
Glia: Greek word for “glue” – supporting cells
- Macroglia:
A) Astrocytes (CNS) – star-shapes cells that involve neuronal signaling (liaison, communications and pathways for neuronal migration), housekeeping, and nutritive function for neurons
B) Oligodendrocytes (CNS) – form myelin sheath
C) Schwann cells (PNS) – form myelin sheath - Microglia: (immune system of the CNS)
Functions as phagocytes
Activate during nervous system development and following injury, infection, or disease
What is the function of the myelin sheath?
insulation and improves signal conduction speed
Explain Oligodendrocytes and Schwann cells
contribute to the myelination of the neurons in CNS and PNS.
Myelin is an effective insulator, shielding neurons from extracellular environment.
Schwann cells is the only supporting cell of the PNS, providing all of the functions performed by other classes of glial cells in the CNS (e.x. phagocytes, signaling pathway for the regrowth of PNS)
Explain what is happening in the image
No blood supply to the neuron. Astrocyte detects it and signals microglia
label these events
1) sensory receptor in the skin
2) afferent pathway
3) integrating center
4) efferent pathway
5) effector organs
Label and explain the sequence of events
1) local potential, 2) Action potential, 3) Synaptic events, 4) Local potential, 5) Action potential, 6) Synaptic events
- Local potential
A) Small, graded potential (amplitude & duration)
B) Receptor or Synaptic potential
C) Spread passively and confined to a small area of membrane - Action Potential
A) Large, all-or-none, depolarizing signal
B) Actively propagate along the axon of a nerve cell and travel one-way to the terminal - Synaptic Events
A) transport signal to the other neurons via the release of neurotransmitters
Explain the transmission of information by neurons and the causes of membrane potential
- Neurons have a selectively permeable membrane
- Membrane potential: separation of different charges across a membrane
creating a electrical potential (-70mV “resting”) - Causes of membrane potential:
- Non-uniformed distribution of ions (Outside/Inside: Na+/ K+ and A-)
- Differential permeability of ions (cell membrane is more permeable to K+ and very impermeable to Na+)
List and describe the gradients affecting membrane potential
- Electrical Gradient (Electrical force):
Represents the difference in electrical charge across the membrane - Chemical Gradient (Diffusion force):
Represents the difference in the concentration of a specific ion across the membrane
What type of equilibrium is maintained? What rules of movement do ions follow?
1) Dynamic equilibrium
2) negative attracts positive, high concentration to low concentration
When is resting membrane potential established?
How is membrane potential regulated?
ion channels, 4 types
- Leak channels (non-gated):
diffusion of a small number of ions through the membrane at a slow continuous rate - Modality-gated channels:
specific to sensory neurons, in response to mechanical stimulations, temperature changes or chemicals - Ligand-gated channels:
in response to a neurotransmitter binding to the receptor of the channel - Voltage-gated channels:
in response to changes in electrical potential
Can the electrical potential across an atonal membrane be measured?
yes, the differences in positive and negative charges in and out of the neuron can be measured by electrodes = resting membrane potential (RP, -70 mV)
Most important ions: Na+, K+
List the ions that are at a higher concentration in the extracellular matrix when resting
Na+ ( 145 millimoles/liter)
Cl- (105 millimoles/liter)
Ca2+ (5 millimoles/liter)
List the ions that are at a higher concentration in the intracellular matrix when resting
K+ (155 millimoles/liter)
Mg2+ (26 millimoles/liter)
Describe how the resting membrane potential of a neuron is maintained
A) At rest, the inside of the neuron contains more negative charges than the outside
inside: ↑ [K+] , Anions [A-]
outside: ↑ [Na+] , [Cl-]
B) Dynamic equilibrium of RP is maintained by:
Negative charged molecules (anions) trapped inside the cell
Passive diffusion of ions through leak channels (K+ & Na+)
The Na+- K+ pump: require ATP; two K+ into the cell & three Na+ out
Explain local potentials
- Small, graded potentials (amplitude & duration)
- Membrane is depolarized or hyper-polarized
- spread passively within receptors or synaptic membrane
- Travel only 1-2 mm
Label these
A) inhibited neuron
B) spatial summation (multiple spots receive signals)
C) Temporal summation (same spot receives signals)
Explain action potential
- Large depolarizing signal; all-or-none
- Actively propagated along an axon
- Repeated generation of a signal
- Travel in one-direction only (away form cell body)
Label these stages
temporal summation, action potential
1) Excitatory post synaptic potentials (EPSP)
2) Temporal summation of 2 EPSPs
3) 3 EPSPs combine to exceed threshold
4) simultaneous EPSPs combine spatially to exceed threshold
5) Inhibitory post synaptic potentials (IPSP)
6) resting potential
Describe the all or none principle
AP can only be produced when the stimulation reaches “threshold stimulus intensity” meaning that the stimulation is sufficient to brings the membrane potential up to -55mV.
Further increasing stimulation intensity will NOT change the size and duration of the AP (i.e. stronger stimulation will still produce the same size and duration of AP)
Label these
1) depolarizing phase (rising phase): more positive, from -70 mV to +30 mV
2) repolarizing phase (falling phase): more negative, from +30 mV, to -70 mV)
3) hyper-polarizing phase (re-setting phase): even more negative than its resting potential, at -90 mV instead of -70 mV)
Describe the depolarization phase
- A small change in the membrane voltage will depolarize the membrane enough to flip open Na+ channels
- These are called voltage-gated Na+ channels
- As Na+ moves into the cell more and more Na+ channels open
- Change polarity rapidly: from (-) to (+)
Describe repolarization phase
- The Na+ channels start to close
- At the same time voltage-gated K+ channels open – they are a bit slower to respond to the depolarization than the Na+ channels
- The K+ ions move out and the membrane potential falls toward the resting potential (i.e -70 mV); from (+) to (-)
- K+ channels remain “open”, leading to hyperpolarized membrane potential
Describe hyperpolarization phase
- The membrane potential falls below the resting potential of –70mV
- It is said to be hyperpolarized (≤ -70 mV; more negative than its resting potential)
- Gradually active Na+-K+ pumps: pumping of the ions (2K+ in and 3Na+ out) to restore the resting potential ( i.e. back to –70mV again)
Does Na+ or K+ increase first when an action potential is being initiated
Na+
Label these
A) & E) resting steady potential = -70 mV
B) depolarizing
C) repolarizing
D) hyperpolarizing
Explain which ions act in each stage
A) voltage gated Na+ and K+ channels closed
B) voltage gated Na+ channels open and Na+ enters axon beginning depolarization
C) more voltage gated Na+ channels open further depolarizing the membrane. Na+ channels close 1 msec after opening
D) many voltage gated K+ channels open, K+ exits, taking positive charges out of axon
E) voltage gated K+ channels remain open, K+ continues to go out of axon, restoring the polarized membrane potential
What are the refractory periods?
1) Absolute: (~ 1 ms) unresponsive to stimuli (i.e. no AP can be generated)
2) Relative: may response to stronger stimuli (i.e. AP may be generated)
What are the causes of refractory period in neurons?
1) Absolute: Majority of Na+ channels are inactive because they have been open and not yet been reset back to the resting state.
2) Relative: Most of Na+ channels are reset back to the resting state; AP can be triggered with stronger stimuli.
What are the 3 phases of communication with a neuron?
What is the advantage of having a refractory period?
Promote forward propagation of the action potential while preventing its backward flow. (From cell body to axon terminal)
How can a toilet represent action potential?
- Full Toilet – Resting Potential
- Push Flush Lever – Threshold Stimulus triggering Action Potential.
- Toilet Refilling/Can’t Flush – Repolarization/Refractory Period
- Sewer Pipes – One-way communication like action potential only goes from dendrite end to axon terminal end.
Describe action potential conduction
Propagation of the action potential (typical velocity: 40-60 m/sec)
1) Orthodromic: Action potential travels in one direction - down axon to the axon terminal
2) Antidromic (experimental “lab setting”): Backward propagation is possible if the initiation of AP occurs in the middle of axon
What happens to conduction velocity as we age?
General information:
(Motor nerves have higher conduction velocity)
(Average: 40-60 m/s)
conduction velocity slows down as we age
Describe factors influencing conduction velocity
1) Diameter of the axon
larger diameter, faster action potential propagation
allow greater current flow with less time required to change the electrical charge of the adjacent membrane
2) Myelination
presence of a sheath of protein and fats surrounding an axon
provide insulation that prevent current flow across the axonal membrane
a greater separation of charges across the axon membrane and therefore preserve the amplitude of the impulse
3) Temperature
Warm membrane proteins react faster
−Cold (ice) used to block pain sensation “gate control theory”
What can myelin help prevent during action potential conduction?
Layers of myelin sheaths insulate the leakage of charges and facilitate current flow
* Schwann cells in the PNS
* Oligodendroglia in CNS
What are the properties of nodes of ranvier?
*Every 0.2-2.0 mm
*Place of AP generation
*Place of voltage-gated sodium channels
describe saltatory conduction
Saltatory conduction – the process by which an action potential appears to jump from node to node along an axon. (AP travels by leaping)
Depolarization only at nodes of Ranvier - areas along the axon that are unmyelinated and where there is a high density of voltage-gated ion channels; current carried by ions flows through extracellular fluid from node to node
Depolarizing potential spreads quickly across myelinated region, appearing jump from node to node.
Describe unmyelinated conduction
An action potential propagates along the membrane of the axon
step-by-step depolarization of each portion of the length of the axon as Na+ flows into the cell during depolarization, the voltage of adjacent areas is effected and their voltage gated Na+ channels open
Describe speed of conduction of myelinated vs unmyelinated fibers
large myelinated fibers:
1) 100-150 m/sec
2) Peripheral sensory and motor axons
Thin unmyelinated fibers:
1) ~1 m/sec
2) short axons in gray matter of CNS
Some visceral autonomic axons
What is the clinical implication of membrane potential issues from electrolyte imbalance?
Electrolyte imbalances – increased general weakness
[Na+], [K+], and [Ca+] influence the function of neurons
Sodium and water balance (normal range = 135 – 145 mEq/L)
Physical therapy is contraindicated when potassium levels are below 3.0 mEq/L or above 5.1 mEq/L (normal range = 3.5 - 5.0 mEq/L).
Hypocalcemia: “lower” [Ca+] may cause hypersensitive nerves with muscle cramping (tetanic contraction; spasm) and tingling sensations (normal range = 4.3- 5.3 mEq/L).
Hypercalcemia: “increases” [Ca+] decrease neuronal excitability, leading to hypotonicity of smooth and striated muscles; symptoms include fatigue, muscle weakness, low tone and sluggish reflexes.
- Cause of electrolyte imbalance
Dehydration
Kidney diseases
Chronic disease (i.e. DM)
What is the clinical implication of damaged myelin?
Damage to myelin:
Increase resistance to the electrical signal
Propagation of action potential slows down and may stop before it reaches the next site of conduction (i.e. fail to transport signal)
Demyelinating diseases:
* Peripheral neuropathy – any pathological change involving peripheral nerves, which mostly occurs in largest, myelinated sensory & motor nerves - Guillain-Barre Syndrome
* CNS demyelination
- brain & spinal cord nerves
- Multiple sclerosis (MS)
- Spinal cord injury (SCI)
Describe causes, sensory & motor deficits, as well as medical treatments for GBS
- Caused by virus infections
activates the immune system
to mistakenly attack the nerve resulting in demyelination - Sensory and motor deficits
Progressively lose sensation and motor function
Weakness is typically greater than sensory loss
Abnormal sensations: tingling, burning, pain, hypersensitivity to touch - Medical Treatments
Plasmapheresis –filter blood plasma to remove circulating anti-bodies
Intravenous immunoglobulin
infusions of immune globulin
Describe multiple sclerosis and its treatment
- Autoimmune disease cause destruction of oligodendrocytes resulting in patches of demyelination, plaques, scar tissues
- MS has affected women three times more frequently than men
- Weakness, lack of coordination, double vision, impaired sensation, and slurred speech
- Medical Treatments
no known cure for multiple sclerosis
Medications used to slow down the progression of MS
Maintain optimal functions
What are the 3 prenatal developmental stages in utero?
Single fertilized cell to an entire human being (three stages):
1) Pre-embryonic (Conception to 14 days):
Ovum (single cell) to embryo (multiple cells)
2) Embryonic (Day 15 to the end of 8th week):
Organs formed (sensory organs, epidermis, the nervous system)
3) Fetal ( 9th week to birth):
the nervous system continue to develop more fully
Myelination:
A) Begins in the 4th month and completed by the 3rd year of life
B) Myelination occurs at different rates in each system: motor roots of the spinal cord are myelinated at approximately 1 month of age, but descending motor tracts are not completely myelinated until 2 years old.
C) Growing into deficit – nervous system damage that occurred earlier is not evident until the damaged system would normally have become functional.
Label these and describe the pre embryonic stage
1) ovum, 2) placenta, 3) embryonic disk, 4) ectoderm, 5) endoderm
Pre-embryonic (Conception to 14 days):
Ovum (single cell)
Sphere of cells (multiple cells)
Outer layer: placenta
Inner cell mass becomes two-layered embryonic disk (ectoderm and endoderm)
Mesoderm soon develops between two layers (in embryonic stage)
Describe the embryonic stage
Embryonic (Day 15 to the end of 8 weeks):
A) Organs formed:
Ectoderm: sensory organs, epidermis, the nervous system
Mesoderm: dermis, muscles, skeleton, excretory and circulatory systems
Endoderm: gut, liver, pancreas, and respiratory system
Formation of the Nervous System
Formation of a tube “neural tube” (Day 18-26): form CNS (brain & spinal cord)
Formation of the brain (Day 28 –the end of 8th wk)
Label these and describe the formation of the neural tube
1) neural plate, 2) ectoderm, 3) mesoderm, 4) endoderm, 5) neural groove, 6) somite, 7) superior, 8) inferior, 9) neural tube, 10) neural crest, 11) outer layer, 12) inner layer
Occurs in embryonic stage (Day 16-26): develops from the ectoderm
Neural plate (figure A): A longitudinal thickening of the ectoderm (Day 16)
Neural groove (figure B): folding of the plate (Day 18)
Neural tube (figure C): the folds touch each other (Day 21)
A) Open ends of the tube called “neuropore” (superior and inferior, close by Day 27 and 30)
B) Differentiate into two layers by Day 26 (inner- gray matter; outer- white matter: axon & glial cells)
Label these and describe the formation of ectoderm and mesoderm in the embryonic stage
1) somite, 2) neural groove
Ectoderm
Neural crest: cells adjacent to the tube (PNS)
Epidermis (epidermal layer of skin): enclose neural tube and crest
Somite
Mesoderm
Somites
A) Anteromedial part: called “sclerotome” – becomes vertebrae and skull
B) Posteromedial part: called “myotome” – becomes skeletal muscles
C) Lateral part: called “dermatome”- becomes dermis
Describe motor innervation in embryonic development
The neurons connecting the neural tube with the somite
Neural tube:
Inner layer divides into dorsal and ventral sections
A) Ventral: motor plate innervates the myotome regions of the somites; neurons in this part become lower motor neurons and interneruons in the ventral horn
B) Dorsal: association plate (alar plate) forms interneurons and projection neurons that process sensory information
After the embryonic stage:
Formation of a myotome - a group of muscles derived from one somite and innervated by a segmental spinal nerve
Describe sensory innervation in embryonic development
Neural crest:
Break up into segments connecting to the dermal areas of the somites (Dermatome)
Forms peripheral sensory neurons (Dorsal root ganglia)
A) Two processes: connects to the spinal cord and innervates the dermal region of the somite
After the embryonic stage:
Formation of a dermatome - the dermis innervated by a single spinal nerve
Sensory neurons (DRG) – convey information from sensory receptors to the association plate
Describe normal CNS development vs normal bone growth
Throughout normal development, bone growth outpace nerve growth:
Until the 3rd month, spinal cord segments and spinal nerves adjacent to corresponding vertebrae
The disparity between vertebral levels and spinal cord levels increases from 3 months in utero to adulthood
A) Spinal cord ends at L4 at birth
B) The adult spinal cord ends at the L1–L2 vertebral level
C) The end of the spinal cord is the conus medullaris
When does brain development start? Describe it
Brain Formation: Begins Day 28:
When the superior neuropore closes, the future brain region of the neural tube expands to form three enlargements (brain and ventricles)
1) Hindbrain: medulla, pons, and cerebellum (4th ventricle)
2) Midbrain: midbrain (cerebral aqueduct)
3) Forebrain: posterior part - diencephalon (thalamus and hypothalamus, 3rd ventricle); anterior part – telencephalon (cerebrum, basal ganglia, lateral ventricles)
Why do we check reflexes as a PT?
to look for intact local neuro circuitry
Describe ATNR, STNR, & TLR reflexes
Asymmetric tonic neck reflex (ATNR)
appears 18 wks in utero; disappear by 3-9 months of age
Head is rotated: limbs on the nose side extend, and limbs on the skull side flex
Symmetric tonic neck reflex (STNR)
appears 6 to 9 months after birth until 9 to 11 months of age
Neck is flexed: flexion of the upper limbs and extension of the lower limbs
Tonic labyrinthine reflex (TLR)
response opposite to the neck reflex
emerges at birth and disappears completely in 2–4 months
after birth
Tilting the head back: flexion of the upper limbs and extension of lower limbs
when are prenatal developmental disorders most likely to cause major malformations?
most susceptible between day 14 and week 20
Major deformities of the nervous system occur before week 20 because the gross structure is developing during this time.
After 20 weeks of normal development, damage to the immature nervous system causes minor malformations and/or disorders of function
Describe neural tube defects
1) Anencephaly:
cranial end of the tube remains open and the forebrain does not develop
malformed brainstem without cerebral and cerebellar hemispheres (incomplete brain)
Caused by chromosomal abnormalities, maternal nutritional deficiencies, and maternal hyperthermia
Fetus died before birth
2) Spina bifida: inferior neuropore does not close; commonly caused by folic acid deficits during early pregnancy
Spinal bifida occulta: bone does not close “distal neural tube” and nervous tissue remain inside the vertebra; spinal cord function is normal (no motor or sensory deficits, just a bone issue)
Spinal bifida cystica (aperta): cystlike sac; spinal cord protrudes
* Meningocele (meninges only)
* Myelomeningocele (meninges and spinal cord)
* Myeloschisis
(ranked least to most severe)
Label and describe these
1) Spina Bifida Occulta
2) Meningocele
protrusion of the meninges through the bony defect.
3) Myelomeningocele
neural tissue and meninges protrude outside the body, resulting in paresis of LE, bowl and bladder dysfunction
4) Myeloschisis
malformed spinal cord open to the surface of the body, resulting in paralysis of LE, bowl and bladder dysfunction
Describe the etiology, signs & symptoms, consciousness, cognition, and somatosensation in lower limbs for Spina Bifida Aperta
Describe the autonomic, motor, cranial nerves, region affected, incidence, and prognosis for Spina Bifida Aperta
Describe tethered cord syndrome
Tethering the spinal cord to the bone: the end of the spinal cord adheres to one of the lower vertebra
As the person grows, resulting traction on the inferior spinal cord causes dermatomal and myotomal deficits in the lower limbs
pain in the saddle region (the part of the body that would contact a horse saddle) and lower limbs, and bowel and bladder dysfunction
Clinical signs may not occur until adolescence or later
progressive lower limb weakness
deterioration of walking,
back pain, leg pain
excessive muscle resistance to stretch
increasing scoliosis
increasing foot deformity
deterioration in bladder and bowel function
Describe normal, hypotonic, and hypertonic muscle tone
(Muscle tone is tested through PROM of full available range)
1) Normal muscle tone: The state of muscle tension at rest that allows for proper posture, movement, and responsiveness to external forces. It reflects a balance between muscle stiffness and flexibility.
2) Hypotonic: Decreased muscle tone, leading to floppiness, reduced resistance to movement, and difficulty maintaining posture. Common in conditions like Down syndrome or peripheral nerve damage.
3) Hypertonic: Increased muscle tone, resulting in stiffness, resistance to movement, and sometimes spasticity or rigidity. It is often seen in conditions like cerebral palsy or after a stroke.
Summary: Muscle tone describes the resting tension in muscles. Normal tone supports movement and posture, while hypotonic muscles are too loose, and hypertonic muscles are excessively stiff.
Describe cerebral palsy (CP)
Caused by abnormal brain development or permanent, nonprogressive damage to a developing brain
1) Hypotonic CP - very low muscle tone, often described as floppy
associated with inadequate muscle contraction to maintain normal head and trunk posture; has little or no
ability to actively move
2) Spastic CP - Spasticity is velocity-dependent hypertonia; excess muscle stiffness often leads to contractures,
toe walking and a scissor gait
hemiplegia affects both limbs on one side of the body
tetraplegia affects all four limbs equally
diplegia: the upper limbs are less severely affected than both lower limbs
3) Dyskinetic CP - muscle tone fluctuates, ranging from hypotonia to hypertonia; consisting of involuntary
movements
choreiform (jerky, abrupt, irregular)
athetoid (slow, writhing)
dystonic (involuntary sustained skeletal muscle contractions)
4) Mixed type CP - If spasticity and dyskinesias coexist
5) Ataxic type CP - normal muscle tone; incoordination and shaking during voluntary movement
Describe the etiology, consciousness, cognition, sensory, motor, and autonomic abnormalities of CP
Describe the cranial nerves, vision, associated disorders, region affected, prevalence, demographics, and prognosis of CP
Describe Abusive head trauma (formerly Shaken Baby Syndrome)
Caused by a blow to the head or falls
Brain scans show hemorrhage and edema
Various sensory, motor, cognitive deficits
Describe Attention Deficit Hyperactivity Disorder (ADHD)
reduced volume of the prefrontal cortex, caudate and putamen, and cerebellum; Inadequate myelination of axons connecting these areas
developmentally inappropriate inattention, impulsivity, and motor restlessness
50% of people with ADHD have impaired handwriting or clumsiness and are delayed in achieving motor milestones
Describe Autism Spectrum Disorders
Autism begins in utero with abnormal development of brain structures
Disorganized arrangement of cells in the prefrontal and temporal cortex
Abnormal synaptogenesis and imbalance between excitatory and inhibitory neurons occur during the third trimester and early postnatal periods
Abnormal communication among cerebral areas, increased gray matter volume in frontal and temporal cortices (crucial in decision-making and social understanding networks)
Larger than normal amygdala during childhood, although the amygdalas size difference does not persist into adolescence.
Sensory over-responsiveness correlates with abnormal strong activation of the sensory cortices and the amygdalae.
Half of people with autism have normal or better intelligence
Present with a range of abnormal behaviors
impaired social skills – difficulty with communication and social interactions
repetitive behaviors - body rocking, banging toy cars, hand flapping
limited interests - obsession with certain subjects
abnormal reactions to sensations – under- or over-responsiveness
list the peak time of occurrence and disorders secondary to interference with neural tube formation
peak time of occurrence:
in utero weeks 3 - 4
Disorders secondary o interference:
Anencephaly, arnold-chiari malformation, spina bifida occulta, meningocele, mylomeningocele, myeloschisis
list the peak time of occurrence and disorders secondary to interference with cellular proliferation
peak time of occurrence:
in utero month 3 - 4
Disorders secondary o interference:
Fetal alcohol syndrome, cocaine-affected nervous system
list the peak time of occurrence and disorders secondary to interference with neural migration
peak time of occurrence:
in utero month 3 - 5
Disorders secondary to interference:
Heterotopia, seizures, autism
list the peak time of occurrence and disorders secondary to interference with organization (differentiation, growth,…)
peak time of occurrence:
In utero month 5 - early childhood
Disorders secondary o interference:
Intellectual disability, trisomy 21, cerebral palsy, autism
list the peak time of occurrence and disorders secondary to interference with myelination
peak time of occurrence:
Birth - 3 years
Disorders secondary to interference:
Unkown
