brain dvpt 2

first trimester (wk 1-12)

development of major body structures & organs

by 4wk: brain & spinal cord starts to form

by end:

• heart beating regularly

• fingers & toes have formed

• nerves & muscles begin 2 work together

• eye lids have formed, remain closed until ~28wks

• fetus = 1oz

second trimester: wk 13-28

period of growth

by end:

• can hear, see, suck

• skin, hair, nails formed

• lungs formed, but dont work yet

• taste buds on tongue

• ovaries/testicles formed

• lanugo (fine hair) covers body

• can feel baby’s movements (flutters)

• weight = 1.5lbs

third trimester: wk 29-40

bones hardening

body fat increases

movements more noticable

lung formation complete

lanugo falls away

weight by end: average 6-9lbs

birth weight normality

normal → more than or equal to 2500grams/5.5lbs

low → less than 2500/5.5lbs

very low → less than 1500 grams/3.3lbs

extremely low → less than 1000 grams/2.2lbs

gestational age normality

normal → more than or equal to 37 weeks

preterm → less than 37 weeks

very preterm → less than 32 weeks

extremely preterm → less than 29 weeks

corrected age

chronological age in weeks - weeks premature

(when a child is born preterm their milestones r tracked but not the same way as normal babies so their age is corrected)

disparities between white, native, black, asian, pacific islander moms

Native and Black mothers additionally are 3x more likely to die of child-birth related causes than white

in 2021:

• black → 3% increase in preterm births

• native → 6% increase in preterm births

• asian & pacific islander → largest preterm birth increase at 8%

  • asian mothers saw decreased birth rate in yr of 2021 and have the lowest preterm birth rate overall

• covid → ppl w this r 40% more likely to go into preterm labor

medical factors associated with preterm births

previous preterm birth

family history of infertility

multiple gestation

placental abnormalities

uterine abnormalities/infections

preeclampsia: when pregnant woman dvp high blood pressure & protein in urine after 20th week

demographic differences

men have higher prevalence of neonatal complications and adverse neurodevelopment outcomes

rates of very low birth weight and very preterm birth:

• 2x as high in nonhispanic blacks as whites

• higher in single mothers

• higher in family of lower ses

differences hypothesized due to:

• effects of stress on neuron-endocrine system

• smoking + drug use

• underutilization of prenatal care

• susceptibilty to genital tract infections

• combined effect of low folate intake and GE interactions

medical interventions for preterm births

advances in neonatal intensive care in 1960s resulted in increased survival and reduced morbidity [markedly in VLBW AND ELBW cohorts]

resuscitation

assisted ventilation and high pressure ventilation

drug treatments

IV nutrition

phototherapy for jaundice

surfactant for immature lungs (introduced in 1990s)

antenatal steroids and antibiotics

environmental interventions for pre term interventions

environmental controls over exposure to light, loud noise, sleep interruptions

positioning and handling procedures

parent education and counseling

effects of pre term birth on brain

brain growth is rapid in late fetal period

• increases in total brain volume

• proliferation of glial cells

• formation of myelin

• growth of axial and dendritic spines

• synaptogenesis

• axonal pruning

primary processes responsible for brain damage in neonates with VLBW/VPTB:

1. hypoxic ischemia (INADEQUATE FLOW OF BLOOD AND OXYGEN TO THE BRAIN)

2. associated oxygen & glucose deprivation

common brain abnormalities

PVL (periventricular leukomalacia)

• involves death of small areas of brain tissue (white matter) around ventricles

  • death around ventricles can enlarge space in brain and not as much gray and white matter in the brain as we want

• creates holes in the brain

hemorrhagic infarctions (IVH=intraventricular hemorrhage)

• infarctions are tissue areas in the body that have died because they did not receive proper oxygen - in this case in the brain

• major complication of premature birth

• cause of CEREBRAL PALSY and HYDROCEPHALUS

ventriculomegaly

• lateral ventricles are dilated

brain regions most affected by preterm birth

subcortical structures and circuits connecting these to frontal and parietal regions

diffuse reduction in white matter

cortical atrophy

lesions in basal ganglia, hippo campus, brainstem, cerebellum

larger ventricular volumes

structural abnormalities in school age kids & adults

thinning of corpus callosum

diffuse reductions in white matter

ventricular dilation

porencephaly (very extreme birth weight kids)

• cyst or cavity filled with CSF dvps in brain

• very rare central nervous system disorder

• usually result of damage from stroke or infection after birth

intraparenchymal cysts secondary to IVH & PVL

neuropsychological outcomes of preterm births

risk of cognitive, learning, and behavior problems

persist into school - age and adulthood

lower bw & preterm birth related to poorer outcomes

lower outcomes also related to neonatal complications

• ivh, pv, chronic lung disease

performances on tests of executive functions and perceptual-motor abilities more closely related to biological risks

environmental/social risk factors better predict verbal ability, IQ, and behavioral outcomes

VLBW/VPTB vs NBW

mildly reduced global cognitive ability

areas of neuropsychological functioning most affected:

• executive functioning (EF)

• perceptual-motor skills

• memory

high rates of learning disorders (LDs), special education plactice, and grade repetition

weaknesses in math are prominent

behavior difficulties most often involve inattention

late pre term birth vs very preterm birth and normal term birth

lptb vs vptb kids → experience fewer medical complications/lower morbidity risk

• neuropsychological deficits are more mild

lptb vs ntb kids → still have more intellectual/neuropsychological deficits

• subtle negative effect on intelligence, academic performance, ef, visuospatial/visuomotor functioning, language, and internalizing behavior problems

• developmental and neuropsychological group differences have not been found to be universally common

parents health at the time of having child will GREATLY impact the health of the child

current research → NEUROPSYCH OUTCOMES IN PREK KIDS (baron et al. 2011)

aimed to examine the specific neuropsych deficits in pre term and extremely low birth weight kids born btwn 2004-2006 of varying gestational ages

preschool age is an important neuromaturation time neglected by past lit

interested in knowing if deficits expected in premature kids would remain when the corrected age was accounted for

PT and ELBW preschoolers had significant immaturities in their neuropsych dvpt, but most performed within norm limits

some deficits are apparent despite age correction, tho scores vastly improved

research highlihts the importance of early interventions and positive impact on outcomes

neuropsych outcomes for LATE preterm birth

for many years it was thot that ppl born near full term (ie 34-36 6/7 weeks) did not suffer neuropsych consequences of LBW & VLBW kids

current research points out that although these kids are not at risk for the most harmful deficits, significant risks do exist for birth just a few weeks premature

baron et al 2012

near full term birth infants r at risk for problematic medical complications, neurological development, and subtle neuropsychological weakness

outcomes are significantly different for those born near full term when cmopared to those born LBW/VLBW and full term, but more research incorporating this age bracket is needed

auditory system in steps

1. begins with cochlear nerve to dorsal and ventral cochlea

2. travels through superior olivary nucleus & trapezoid body (pons)

3. travels through lateral lemniscus

4. ascends to the inferior colliculus in midbrain

5. medial gen nucleus of the thalamus

6. primary auditory cortex in temporal lobe (heschel’s gyrus)

auditory system areas

ventral cochlea

dorsal cochlea

superior olivary nucleus & trapezoid body

lateral lemniscus

inferior colliculus

medial geniculate nucleus of thalamus

primary auditory cortex

ventral cochlea

encodes intensity info

dorsal cochlea

encodes information and analyzes quality of sounds

superior olivary nucleus & trapezoid body

modulates localization of sound and the intensity of sounds

lateral lemniscus

acoustic startle and likely modulates the amplitude of sounds

inferior colliculus

integrating auditory stimuli and actions

medial geniculate nucleus of thalamus

further processing and integration of auditory stimuli

relays to aud cortx

primary auditory cortex

cortical processing of sounds, noise & auditory info

temporal lobe

primary auditory cortex

TONOTOPIC ORGANIZATION (ie low freq processed ANTERIOR and high freq sounds processed POSTERIOR)

NO strict contralateral rep of auditory world in way that visual and somatosensory cort

types of hearing loss

conductive

sensorineural

mixed

conductive hearing loss

occurs when sound is not conducted properly from the outer ear to the middle ear

results in a reduction of sound level

caused by → foreign body, cold, ear infection, fluid in middle ear, etc

sensorineural hearing loss

occurs when there is damage to the inner ear (cochlea) or neural pathways

often irreversible reduction or loss of sound

caused by → toxins, aging, head trauma, exposure to loud noises, illness, etc

mixed hearing loss

combo of conductive and sensorineural hearing loss

neuroanatomy of langauge

the left hemisphere is dominant in more than 95% of right handers and in more than 60-70% of left handers

two main regions (broca & wernicke) lie adjacent to the sylvian fissure, separating the temporal and frontal lobes and language disorders associated with these associated areas have led to the concept of “perisylvian” aphasias

language areas

initial steps of language processing is the ability to identify sound based sequences (phonological awareness) and comprehend them as words

• broca’s area plans and activates the production of sequences of speech sounds

• ability to repeat language requires that the phonological representations generated by processing in WA be converted to motor articulatory sequences and utterances in BA

damage to wernicke’s area

fluent aphasia (bc motor articulatory regions in the frontal lobe are intact and the disturbance in convo)

characterized primarily by disturbance in production of sequences of speech sounds

damage to broca’s area

nonfluent aphasia (with intact comprehension)

able 2 comprehend, but when they go to speak it is choppy and disflient like broken language)

broca and wernicke’s areas are connected by

arcuate fasciculus - a large subcortical white matter pathway

damage to this = conduction aphasia

language lateralization

the speech/langauge zones are located in BOTH hemispheres

LEFT = dominant in over 95% of right handers and 60-70% of left handers

RIGHT = some aspects of language like prosody (flavor / intonation/ emotional valence/ intensity of loudness & softness / playfulness)

nondominant hemisphere: recognition and production of affective elements of speech

subcortical structures = THAMALUS + BASAL GANGLIA

the language areas

the speech zones (ie broca, wernicke, sensory/motor areas of face and supplementary speech areas) are located in both hempispheres

stimulation of speech zones resulted in positive (vocalizations but not speech) & negative (inability to vocalize or use words appropriately)

however these studies did not support a strict localization model

• [stim outside of speech zones can disrupt speech and stim of speech zones affects more than just speech]

thus, subcortical structures and right hemisphere areas have inputs to lang (ie prosody

DVPTL LANG DSRDRS IE dyslexia/apraxia of speech/dysarthria R NOT APHASIC DSRDRS

aphasia

term reserved for acquired disorder that disturbs language functions

broca’s aphasia

expressive aphasia

nonfluent speech, grammar problems, comprehension GOOD

wernicke’s aphasia

receptive aphasia

fluent speech, grammar okay, but meaningless & comprehension POOR

conduction aphasia

arcuate fasiculus affected - bridge between broca and wernickes

impaired repetition and paraphasic errors

global aphasia

both speech AND comprehension affected

anomia or dysnomia

normal fluency, comprehension & repetition

naming diffuculties (tip of the tongue phenomenon)

NURTURE theories of language development

environmental behaviorism

b.f. skinner

• language shaped by reinforcement when child imitates speech

  • correct words are rewarded

• trial and error

  • child gets the bottle after saying “milk”

• learning process

  • mom says “daddy” every time he walks into room

• however, how would one explain a new utterance?

NATURE theories of language development

nativist

noam chomsky

• language is innate — etched into the structure of the mind

• language acquisition device

  • proposed this was a neurological system that contained a set of rules

  • we chunk info and theres a way that we organize it and are naturally able to use it

  • universal grammar → common to all language

  • speak in a rule-oriented fashion as soon as enough words are acquired

NATURE + NURTURE theories of language dvpt

interaction btwn inner capacity and environmental influence

lev vygotsky

• zone of proximal development

• social context and social exchange are the sources of language acquisition

• language leads to thought

when kids are around others who are similar and slightly more advanced in dvpt, those kids tend 2 learn at faster rate than kids w diff expce bc they are in proximity of that expsure

overtaxing can be too much tho so u need the right chemistry within group to have right kind of learning

current research about language development

kids transition from BABBLING @6MONTHS to FULL SENTENCES BY 3YRS regardless of culture

young infants exhibit universal capacity to detect diffs btwn phonetic contrasts used in worlds langs

by age 1 → native lang phonetic abilities increase & non native discrimination decreases

• parallel structure diffs in brain (pruning)

better discrimination assocaited with faster vocab growth (bidirectional)

social intxns play role in learning language

• motherese (high pitch slow + exaggerated) = good for child

language as a system

language is not just communciation but a structured system with a finite set of elements BUT infinite set of possibilities → makes language unique to humans

these elements include words which r composed of phonemes (sounds of language)

words are combined in predictable ways to yeild a potentially infinite number of sentences

structural components of language

phonology (sound system)

syntax (grammar)

semantics (vocab)

functional components of language

discourse processing

pragmatics (social rules)

structure in dvpt of functional

phonology

• phonological awareness

• phonemic segments

morphology

• study of structure and form of words in language

• including inflection, derivation, and the formation of compounds

• prefixes, suffixes, roots

syntax

• word order

• sentence patterns

sound element of language development

speech sound (phonological) awareness

ability to segment language into sounds which makes up words

conscious focus on the acoustic signal

language play serves as practice and facilitates the acquisition of form

deficit is dx as speech sound disorder

speech sound disorders

phonological development

incidence 5% of young kids

ca 2-5yrs

• deletion of final consonant ca/cat

• fronting: t/k, d/g → “mommy, div me tiss”

• most kids outgrow or “suppress” phonological processes

  • for those who don’t, association w later phonological deficits, specific learning disorder, with impairment in reading

• amenable to treatment

word element of language development

segmenting sentences into words

seek word meanings

• words are tied to communicative functions

• awareness that words represent concepts independent of the functions they serve

• words r symbols

content in language system development

knowledge of objects

relationship between objects and events

content categories

concept development

• temporal

• spatial

• causal

• quantitative

use of functional language system

communicative intent

conversational rules

• turn taking

• topic control

cohesion

• ordering of ideas

• inflection

• pronoun reference

pragmatics

involve three major communication skills

• using language for diff purposes

• changing language according to needs of lisstener or situation

• following rules for convos and storytelling

language disorders

language deficits → deficiency in set of language skills that develop with exposure

language delays → slowed acquisition in set of language skills that develop with exposure

disorders (impact functioning)

• aphasias

• communication disorders

• specific learning disorder, with impairment in written expression and/or reading

speeded access to verbal codes

access to phonemic or semantic categories and speed of recall

• word retrieval or naming difficulties

• can also affect reading

verbal fluency

speeded naming

importance of language

verbal deficits tend to have more obvious and widespread cognitive consequences than deficits in other functional systems

• task instructions are frequently verbal

• self regulating and self critiquing mechanisms are verbal

• most of the school day is all verbal

self talk → verbal probs limit us in what we can do to motivate ourselves to do something

communication disorders

most common developmental disorder in kids under age 5

75-80% of early intervention cases involve speech and language issues

disorders:

• language disorder

• social (pragmatic) communication disorder

• speech sound disorder

• childhood onset fluency disorder (stuttering)

• unspecified communication disorder

childhood disorders

language disorder

speech sound disorder

social (pragmatic) communication disorder

• not associated with ID, autism, hearing impairment, or specific social-environmental factors

• incidence rates: 7.6% of 5 year olds

• heritable

• gender diffs → 4boys:1girl

afferent nerve fibers

carry sensory nerve impulses toward the CNS

affects what you feel

approaches the brain

efferent nerve fibers

carry motor nerve impulses away from the CNS to muscles

effect on what you do

exits the brain

spinal cord dorsal/posterior column

ascending sensory fibers

spinal cord ventral/anterior column

descending motor fibers

how does motor info travel from the brain to the body?

primary motor brain regions

• primary motor cortex/motor strip

• premotor & supplementary motor areas

• basal ganglia

• cerebellum

descending motor pathways

• spinal cord

primary structures involved in motor development

cerebellum

• coordination of movement and posture

• adaption of movement to changing external and internal conditions

• has been implicated in attention and decision making

• organized ipsilaterally (on the same side - ie right side of cerebellum manages right side of body)

basal ganglia

• subcortical nuclei (cluster of neurons) involved in initiation and control of movement

• located deep beneath the cerebral cortex

basal ganglia is comprised of

caudate nucleus

putamen

globus pallidus (pallidum)

associate areas include substantia nigra, subthalamic nucleus, and projections from basal ganglia to thalamic nuclei

cerebellum

“little brain”

recieves sensory input from spinal cord and other parts of brain

functions: smoothly coordinates motor movements and assists with motor planning

integrates inputs to fine tune movement

• coordination

• precision

• accurate timing

damage causes problems with fine movement, equilibrium, posture & motor learning on the side of the body ipsilateral to the lesion

practicing learning motor patterns

circular expereince of practice coupled with novel experience = motor fluency

complex movements are result of “smoothing” out a motor movement in terms of fluidity (timing) and accuracy

ie walking toy thing & playpen with dangling things = practice and opportunities for better motor control

motor transfer and motor memory

transfer = learned motor movements can b adapted and applied to new learning

motor memories are retrieved, modified to adapt to the new skill, and then acquired = new motor learning

cerebellum thought to be a big contributor to motor memory development

the fact that we can ride a bike after not riding it for a long time is because of the motor memory

primary motor cortex

strip of tissue located on the frontal lobe alongside precentral gyrus

generates neural impulses that initiate and control the execution of purposeful movements based on input from sensory cues

(ie sends out signals that cause movement)

somatotopic organization aka body is mapped across motor cortex

• classic homunculus but not as clearcut as initially believed

• contralateral organization

hemiplegia

loss of voluntary movements on the contralateral side of the body, particularly in the distal effectores (ie fingers)

[aka paralysis of one side of body]

• frequently experienced secondary to a hemorrhage of the middle cerebral artery

• reflexes are initially absent, but return within a couple of weeks and may become exaggerated

• spasticity is evident — muscles that oppose the effects of gravity become extremely rigid

• in the absence of cortical inhibition, primitive reflex mechanisms meant to maintain postural stability take hold

• hemiplegic patients can no longer generate an action based on internal goals and desires

supplementary motor area

helps with organizing & planning out the steps of complex movements

located in front of primary cortex

has some nerve projections to the spinal cord and brainstem

prefrontal cortex

higher order structure involved in complex thinking and decision making (has subdivisions that play specific roles)

• movement + motor aspects of speech

• behavior programming

• integration of sensory info

• integration of arousal, emotion, motivation & behavior/movement

• executive functions

prefrontal cortex subdivisions

primary motor cortex + supplementary motor areas

orbital prefrontal cortex → executive control of social and emotional behavior (decisions about social interactions; not automatic)

lateral prefrontal cortex → executive control of cognition (attention, focus, planning, working memory)

medial prefrontal cortex → executive control of motor behavior

multiple sclerosis

affects approximately 400,000 people in the u.s. (200 ppl diagnosed weekly)

multifocial demyelinating disease → causes destruction of myelin sheath of nerve fibers - scar like lesions called sclerotic plaques form in the areas where demyelination has occurred and block or distort the normal transmission of nerve impulses

cerebral palsy

10,000 babies diagnosed annually in the u.s.

non progressive heterogeneous group of movement, postural, and muscular disorders

• the area of the brain that had the insult wont change / get worse in those regions, but the demands of life will get higher so we may see the skills get weaker over time

• this will happen in utero, but wont see the muscles coming online as much as would expect only when we need to use them in dvpt

types of cerebral palsy

muscular dystrophy

progressive muscle weakness and wasting

huntington’s disease

affects ~30k ppl in u.s.

affects striatum/basal ganglia (especially caudate nucleus)

symptoms include motor, cognitive, behavioral

diagnosis relies on emergence of choreoform movements

adult onset, progressively disabling, lethal disease

there is no effective treatment to delay onset or to slow decline

parkinson’s disease

affects ~ 1 million ppl in u.s.

affects production of motor neurotransmitter

symptoms include tremor, rigidity, slowed movement, and instability

no known cure but some treatments can mitigate the effects

dopamine

produced in substantia nigra

decreased dopamine due to damage to substantia nigra leads to parkinson’s

excess dopamine has been implicated in schizophrenia

pathway of visual stimuli

each eye is divided into 2 “visual fields” — a right side and a left side = “hemifields”

via optic chiasm, visual signals from LEFT hemifields of both eyes are sent to the right hemisphere and the signals from the RIGHT hemifields of both eyes are sent to the left hemisphere

optic chiasm

x shaped structure formed by the crossing of optic nerves in the brain (known as the optic commissure)

optic nerves connect eyes to the brain

• left primary visual cortex (occipital lobe) receives images from the right visual field of the right and left eyes

• right primary visual cortex (occipital lobe) receives images from the left visual field of right and left eye

• this is due to the sorting of optic nerves at the optic chiasm so the right side of the brain controls the view of objects in the left side of visual space (+vice versa)

• REMEMBER the image is inverted onto the retina when passing through the lens

summary of visual pathways

from retina

through optic nerve

crossing at optic chiasm

travelling to lateral geniculate nucleus

LGN connected to primary visual cortex via optic radiations/tracts

to the primary visual cortex (occipital lobe)

role of superior colliculus

as input “travels” to primary visual cortex, ~10% of tracts target here [aka the optic tectum]

these areas appear central to directing attention and motor functions to points of light within the visual periphery —- aka orient eyes (+other sensory stimuli) to respond to new stimuli in visual fields

• van coming toward u while sitting on nyc bench

• trying to catch incoming football

role of lateral geniculate nucleus

this is the major target of the two optic tracts, located in the dorsal area of the thalamus (aka relay station btwn subcortical areas of the brain and the cortex)

• several of cell layers here r specialized to respond to diff types of cells in the retina, but these layers process incoming info in parallel / simultaneously

• thus the unitary nature of our visual perception does not occur bc the info is being processed all at one time by one structure

• from the LGN the optic radiations send “visual info” to be processed in the primary visual cortex in the occipital lobe

occipital lobe

topographic/retinotopic map → orderly spatial relationship of info, 2D representation of retinal map of visual world; axons of each retina preserve their orde as they travel back to V1

2V1s in each person (left and right hemispheres)

each has representation of opposite half of the visual field

each V1 does not j receive input from the opposite eye, but from the opposite visual field of each eye

primary visual cortex (v1)

just as image of world is inverted when projected onto retina, retinotopic v1 map is upside down and from the opposite visual field of each eye than the side of the brain

cortical magnification → MORE CORTICAL SPACE DEDICATED TO FOVEA THAN PERIPHERY (higher density of photoreceptors in fovea, thus clearer vision — resp 4 sharp, central vision)

LGN integrates temporal and spatial correlations that contribute to successful vision

• recieves feed-forward input from retina AND feed-back input from v1 & other non retinal areas

LGN r not just feed forward areas, but receive 80% of their projections from the primary visual cortex

occipital lobe neuroanatomy

differentiated from parietal lobe via parietal occipital sulcus

on lateral surface of brain, no clear divisions btwn temporal and parietal lobes from the occipital lobe

while specialized for visual material, other lobes also contain visual functions

surface of occipital libe has calcarine fissure which separates upper and lower halves of visual system + fusiform gyrus on ventral surfave

2 streams for processing visual info

ungerleider + mishkin

where? → dorsal pathways projecting to parieto-occipital association cortex

• analyze motion and spatial relationships between objects and between body and visual stimuli

what? → ventral pathways projecting to occipito-temporal association cortex

• analyze form and specific regions for colors, faces, letters, etc

object perception

involves the ventral stream but distinct areas have been implicated for object perception

process of recognizing images is pre organized

prosopagnosia

cognitive disorder that results in an inability to recognize faces

aka face blindness

occurs when there is damage to the fusiform face area