BCI for Cerebral Palsy

Stuff I am working on
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Daniel Wee
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BCI for Cerebral Palsy

Post by Daniel Wee »

1. Determination of type of CP
- spastic quadriplegia/hemiplegia/diplegia
- suggests that degree of motor impairment may vary

2. Determination of granularity of EEG based neuro-feedback BCI
- desire output controls

3. Possibility of using neural networks to learn and classify EEG signals
- some sort of RNN/LSTM sequence to sequence classifier/translator

Javier's case sounds like spastic quadriplegia
- all four limbs affected
- torso and face may also be affected
- co-occurring disorders such as epilepsy

Neurological issues
- damage to motor cortex (regulation of voluntary movement)
- damage to pyramidal tracts (signal pathways between cerebral cortex and CNS)

Possible causes
- prenatal brain haemorrhage or infection
- lack of oxygen to brain during birth
- brain trauma or infection after birth

Prevailing therapies
- PT to improve overall motor function
- OT to teach skills and perform tasks
- Speech therapy to strengthen vocal/speech muscles
- medication to relieve muscle stiffness and improve movement (relaxants)
Daniel Wee
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Re: BCI for Cerebral Palsy

Post by Daniel Wee »

A child with cerebral palsy often has other conditions related to developmental brain abnormalities, such as intellectual disabilities. Almost 50% of children with CP have an average intelligence, 20% have an intelligence slightly lower than average (borderline intelligence). The rest 30% its not mentioned if its more inteligent or not than average. Most patients that have spastic tetraparetic, discinetic and ataxic have a severe mental discapacity (SCPE Working Group 2002)

There have been studies that prove that children with CP with average intelligence have attentional deficits or problems with the executive functions, which may partially account for the behavioral problems that sometimes present. (Guzzetta 2001) They might have deficits in visioperceptive functioning. The child has difficulties recognizing the spatial relations between objects, as well as between objects and his own body. This results frequently in a constructive dyspraxia. The saccadic movement of the eye to focus on an object that appears periferically at the previous point of focus are slow and dyspraxic, which constitutes an added difficulty in order to achieve the perceptive integration. The proprioceptive-visual integration of the parietal lobe is necessary in order to orient the movements and postures of the upper limbs to reach for and manipulate the surrounding objects and starting the proceeding automatic movement that experience and repetition offers. These deficits are completely independent from the vision problems that may coexist (Guzzetta 2001).

Language problems are also common and their severity depends on the timing that the lesion took place, in the prelinguistic period or later, when the linguistic function has already started to form.
Daniel Wee
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Re: BCI for Cerebral Palsy

Post by Daniel Wee »

For discussion on factors impacting effectiveness of BCI with CP

https://www.intechopen.com/books/cerebr ... bral-palsy
Daniel Wee
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Re: BCI for Cerebral Palsy

Post by Daniel Wee »

tDCS = trans-cranial direct current stimulation
tMS - trans-cranial magnetic stimulation

https://www.frontiersin.org/articles/10 ... 00533/full
Daniel Wee
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Re: BCI for Cerebral Palsy

Post by Daniel Wee »

DIscussion on various types of headwear (Neurosky, Emotiv):-

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4806709/

Should also look up MUSE.
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Re: BCI for Cerebral Palsy

Post by Daniel Wee »

Employment of TMS (transcranial magnetic stimulation) for excitation or inhibiting of pyramidal neurons/dendrites in motor cortex:-

https://elifesciences.org/articles/13598
https://www.ncbi.nlm.nih.gov/pubmed/10680569

Spasticity

http://jn.physiology.org/content/jn/99/2/1041.full.pdf
Daniel Wee
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Re: BCI for Cerebral Palsy

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Prefrontal cortex makes cognitive decisions on movement that is passed to the motor cortex, consisting of the Supplementary motor cortex, the pre-motor cortex and the Primary motor cortex (M1). These signals are passed through the pyramidal tract, consisting of the corticospinal and the corticobulbar pathways leading to the spinal cord and the brain stem (medulla oblongata) respectively, which in turn passes the signals to the lower motor neurons for activation. However, there is secondary motor loop that involves the basal ganglia that serves to regulate motor functions that includes inhibitory signals. These signals go through extra-pyramidal tracts.

Corticobulbar pathways carry facial control signals, separately from corticospinal pathways which handle the rest of the body.

On the role of basal ganglia:-
http://www.neuroanatomy.wisc.edu/coursebook/motor2.pdf

Impaired motor function and spasticity in CP patients could arise at the motor cortex level, possibly with associated damage in the adjacent somatosensory cortex. It could also arise in the pyramidal tracts and/or extra-pyramidal tracts. Problems could also arise from the basal ganglia itself ([caudate, [putamen, global pallidus [internal and external]] forming the lenticular nucleus] forming the striatum, substantia nigra, subthalamic nucleus).

Lenticular nuclei damage in dyskinetic CP patients:-
https://www.ncbi.nlm.nih.gov/pubmed/26706479

Striatum (input - afferents)
- Caudate
- Lenticular nucleus
- - putamen
- - global pallidus
Substantia nigra (output - efferents)
Subthalamic nucleus (output - efferents)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3543080/

Gross functions and circuits surrounding the basal ganglia (in relation to primary motor cortex):-
http://www.indiana.edu/~m131/lectures/B ... 202016.pdf
https://www.youtube.com/watch?v=RtXU11ueKkQ
https://www.youtube.com/watch?v=82oIHBGDoiI

The basal ganglia has non-motor functions - seeing as to how it is tied to the nucleus accumbens and the proximity to the amygdala.
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Re: BCI for Cerebral Palsy

Post by Daniel Wee »

Types of CP disablity:-

1.0 (Athetoid) Dyskinetic CP - inability to control muscle tone (contraction): having both hypertonia and hypotonia (paralysis)
- damage to basal ganglia
- damage in extra-pyramidal areas or corticospinal areas
- does this mean that corticobulbar pathways are unaffected?
- non-spastic

2.0 Spastic CP - hypertonia (stiff muscles: contraction?)
- spastic hemiplegia
- spastic diplegia
- spastic quadriplegia, triplegia, monoplegia
- possibly due to GABAergic dysfunction
- damage to motor cortex, probably related to the cortical motor homunculus
- map areas damaged leading to dysfunction of limbs
https://www.ncbi.nlm.nih.gov/pubmed/19740221

3.0 Ataxic CP
- damage to cerebellar structures?
- non-spastic
Daniel Wee
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Re: BCI for Cerebral Palsy

Post by Daniel Wee »

Use of TMS to probe and map cortical plasticity in CP patients.
http://www.nature.com/pr/journal/v45/n4 ... lback=true
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