Nervensystem II: ausgewählte Kapitel

1. Developmental differentiation view:
   1. low level basic, multisensory integration present at birth
2. Developmental integration view:
   1. multisensory skills are absent at birth
   2. emerge and imporve slowly with increasing sensorimotor experience

• before 8, children do not integrate information between the senses, one merely dominates the other
• after a time, the more robust one educates the other

Older age:

• older adults have greater MSI (not better) than young adults
• reduced sensitivity in unisensory systems increases the inverse effectiveness effect
• have a larger time window integration -> less precise MSI

• Non-autistic subjects focus more on linguistic stimuli

Autistic subjects:

• focus more on non-linquistic stimuli
• have impairments in audiovisual integration -> McGurk effect is weaker: seeing the person say somehting makes less of a difference
• have a larger temporal integration window (binding impairment)-> less temporally precise integration (it is better to have focalized MSI)
• relatively intact intersensory processing for simple events, but impaired for complex events -> especially in the social context
• Unisensory impairments which limit intersensory functioning:
  • reduced lipreading
  • face processing
    • detection of speech in a mix
• In general a weak central coherence -> focus more on the components rather than the global picture of things

1. Phonological Hypothesis: specific impairment in the representation, storage and/or retrieval of speech sounds
2. Rapid auditory processing Hypothesis: deficits in the ability to properly process rapidly changing acoustical cues
3. magnocellular hypothesis: importance of temporal processes within the visual system (visual representation of the printed word)
4. cerebellar hypothesis: highly automatic processes are impaired -> timing mechanisms controlled by cerebellar circuits. 

• reduced coupling of auditory and visual responses in the auditory association cortex and superior temporal sulcus
• do not show modulation of the auditory mismatch negativity -> no efficient integration of letter-speech sound information
• have a wider MSI window -> are more easily distracted and have less efficient MSI

Positive symptoms = things that appear

• hallucinations
• delusions
• disorganized behaviour
• disorganized speech

Negative Symptoms = things that disappear

• emotional withdrawal
• anhediona -> inability to feel pleasure during normally pleasurable behaviours
• social avoidance

Structural changes = gray matter contraction

• parieto-occipital regions
• temporal lobes
• frontal lobes

Unisensory: severe deficits in the basic:

• auditory
• visual
• somatosensory

MS Integration:

• decrease of multisensory facilitation
• decrease in the susceptibility to McGurk illusion
• benefit from speech reading/visual articulation is reduced
• cross-sensory gating is impaired (visuoacoustic -> filtering of unnecessary information)

all have sensory defecits extending beyond a single modality and appear rooted in changes in temporal processes

-> timing of the sensory information transmission within sensory systems could be at the origin of multisensory malfunction

Sensory processing disorder = a condition where multisensory integration is not adequatly processed in order to provide appropriate responses to the demands of the environment

• could be due to sympathetic overactivity or less parasympathetic activity
• timing of ERP (event related potentials differ between SPD and normal developing children

Yes, it is necessary for normal tactile perception. If you inhibit the occipital cortex using TMS, you have reduced tactile performance.

-> the Lateral occipital complex = is responsible for visual and taktile integration -> is a bimodal cortex region (tactile-visual)

Then the visual input dominates the tactile input -> the movement of the visual input is perceived, while the tactile overruled. 

In this case, the premotor and occipital cortex(V5 V3/3A) are recruited

1. Hypercompensation: when the absence of one sensory modality leads to changes in the remaining intact senses
2. Cross-modal compensation: when the sensory-deprived cognitive system has compensated (or substituted) to perform at the same level as healthy individuals
3. Perceptual deficiency hypothesis: when the lack of one modality results in detrimental effects in the intact modality

1. Intramodal plasticity: when intact sensory systems change to mediate behavioral changes 
   1. Example: increase in represented pitches in the normally afferented auditory cortex of the blind
2. Reorganisation of multisensory brain structures: recruitment of neurons with multisensory properties to process intact modalities
   1. Example: increase in the recqruitment of posterior Superior temporal sulcus (STS) in deaf individuals monitoring visual displays of moving stimuli
3. cross-modal (or intermodal) changes: when the brain regions predominantly associated with the impaired system become recruited for tasks involving the intact systems
   1. activation of auditory cortices in deaf individuals

• losing a primarily spatial sense like vision -> triggers perceptual learning through the remaining sensory systems
• losing a primarily communicative sense like hearing -> triggers perceptual learning of visuospatial abilities
• deafferented cortical regions are recruited for both blindness and deafness.

Sensory substitution devices = transform the characteristics of one sensory modality into the stimuli of another modality

For istance:

• present visual information as touch
• present visual information by audition

Examples:

• Tongue display unit: vision is replaced through tactile information
• vision can also be replaced through auditory information

1. multipotent, undifferentiated neuroepithelium surrounds the ventricular system
2. regulation by genes -> conserve a constant ratio of synaptically related cells
3. in the adult brain -> Dendate gyrus of the hippocampus and in the olfactory bulb
4. 3 Zones:
   1. vetricular zone: apical radial glial cells; apical intermediate progenitors
   2. subventricular zone: basal intermediate progenitor
   3. intermediate zone: migrating neurons

1. GABAergic interneurons:
   1. originiate in the ganglionic eminence of the SVZ
   2. migrate tangentially along axons
   3. comprise 20% of total cortical neurons
2. Glioblast: are the majority of radial migratory cells to the cortex in the second half of gestation
3. Ogrganization mostly by the gene Reelen: expressed by Cajal-Retzius cells of the molecular zone

= are classified by their effects on sulcation and gyration of the cortex. They develop earlier than the formation of the gyri.

Examples: lissencephaly, Polymicrogyria, pachygyria

Causes: congenital infections: CMV, congenital rubella etc. 

• axons always form earlier than dendrites
• growth cone = growing axon -> is guided by chemical signals that attract or repell (secreted by ependynal cell basal process)
• the axonal terminal proliferates to innervate many neurons
• Disorders: 
  • defective guidance -> axons that project to aberrant sites
    • agenesis of the corpus callosum

1. the dendritic tree of each neuron proliferates only after the neuron is in its final site within the CNS

2. Disorders of dendrites and synapses?

1. Down syndrome --> same as FAS
2. Fetal alcohol syndrome --> abnormal dendritic spines and lack of dendritic branches in the cerebral cortical neurons
3. Autism spectrum disorder
4. Epilepsy

You have impaired social and communicative skills& repetitive behaviours

Converging problem: connectivity:

1. Decrease in connectivity between specific brain regions --> Hypoconnectivity (defective axon growth and guidance)
   1. Increase in connectivit within regions --> Hyperconnectivity (to many neurons, dendrites, spines -> lack of apoptosis)

1. Seizures induce changes in axon guidance proteins -> rewiring of neuronal circuits in later stages of epillepsy

2. recurrent seizures in the hippocampus -> new mossy fibre collaterals which abberrantly innervate the molecular layer and synapse with their own dendrites -> self-stimulation

1. Fissures generally form earlier than sulci and are often longer or deeper
2. Fissures --> formed by external forces
   1. include forces from within the ventricular system
3. Sulci --> formed by internal forces
   1. from within the parenchyma of the brain itself
   2. proliferation and growth of individual cells, neurons and glial processes

1. Interhemispheric fissure: divides the telencephalon into two hemispheres
2. hippocampal fissure: between the dentate gyrus and ammons horn
3. sylvian fissure
4. calcarine fissure: is on the medial side of the occipital lobe

Neural connectivity forms after the radial, inside out proliferation and migration of neurons. The connectivity begins in Layer 6 and goes inwards. 

The connectivity driven tangential growth mainly affects superficial layers and triggers the formation of gyri and sulci.

The SVZ is thicker at sites where gyri form and thinner where sulci will form. 

1. Holoprosencephaly: is the failure of the hemispheric fissure -> earliest cerebral defect.
2. Fetal Alcohol Syndrom:
   • most common retardation cause
   • changes in brain structures and behaviour:
     • Learning defecit
     • memory
     • executive functioning
   • microcephally

• Myelin sheath is generated by Oligodendrocytes
• does not occur before the growth cone reaches its final destination
• Timeline:
  • earliest myelination: 24 weeks of gestation
  • corticospinal tract: fully at 2 years
  • corpus callosum: late adolescence is when it finished
  • ipsilateral frontotemporal association bunlde: not until 32 years old (emotions and decisions)
• can be detected by MRI

1. Is the formation of synapses between individual neurons
2. it begins before the 27th week, but mainly occurs after birth
   1. happens at the same time as growth of axons and dendrites&myelination of axons in the subcortical white matter
3. Three Phases of Synaptogenesis:
   1. immature synapses form between axons and dendrites
   2. synapses convert from a silent to an active state
   3. reduction in the number of synapses -> refining of the neuronal connections within the circuit (Synaptic pruning)

= is the selective elimination of a portion of neurons and synapses -> allows us to become experts

Happens mainly at 3 times in our lives:

1. at two years of age (when we speak our first words)
2. Adolescence
3. at 40 years of age (midlife crisis).