Homonymus Hemianopia/Hemianopsia & Blindsight Rehabilitation + Neural Plasticity

Blindsight

Blindsight

Basic Visual Cortex

Primary Visual Cortex (Banich & Compton, 2011) -Also called as the STRIATE CORTEX (because of its stripy appearance under a microscope) -First Area where visual information gets processed -Location: BRODMANN'S AREA 17 in the occipital lobe which is located towards the back of the skull and contains a so called 'retinotopic map' in each half of the visual field -The visual cortex reverses the visual scene from left to right and also inverts it from top to bottom (turns it upside down which we don't realize) -Known for processing moving and still/static objects and pattern recognition -Right Visual Field: Info to the right fixation, projecting "to the left half of the retinas of both eyes" -Left Visual Field: Info to the left fixation, projecting "to the right half of the retinas of both eyes" -Far perhiperical information is only detected by the left eye (due to nose precluding, not allowing right eye detection) -Similarly, far right side is only detected by the right eye -Crossover (can be linked to contraletral occurence of hemineglect): Info from the left visual field only goes to the PVC (PRIMARY VISUAL CORTEX) of the right hemisphere, and info from the right visual field only goes to the PVC of the left hemisphere -Explanation: Retina has two sides, and information from each half of the inside retina (NASAL HEMIRETINA, as this part is closer to your nose, i guess that's why you can see the side of your nose when you close one of your eyes) crosses the mid part of the OPTIC CHIASM (OC) and directs itself in "the contralateral LATERAL GENICULATE NUCLEUS (LG) which is located in the THALAMUS which is the center part of it and is responsible for connecting with the optic nerve to the occipital lobe because the LG obtains great sensory input is received from the retina and the RAC (Reticular Activating Sytem) via the optic tract. It's a "stopover point that organizes that incoming information fom the retina and sends it to the cortex." -The duty of the OPTIC CHIASM is very important because it is the part that "allows information from a specific region of space detected by each eye to converge on the same region of brain tissue" (Banich & Compton) -The outside part of the retina called the TEMPORAL RETINA (TR) goes to the ipsilateral side of the LG -The PATHWAY from visual information in the brain to the eye is as follows: Left and Right visual field, infrom from both goes to the optic chiasm where they cross over and through the contralateral sides (left to righ primary cortex and right to left primary cortex) via the optic tract travels to either the right or left part of the LG of the Thalamus which receives the sensory input from the retinas in both visual fields, then they project to each visual cortex (ipsilateral because they cross over at the LG)! (Imagne how fast this must happen?!?! Jeez!) -Problems with visual processing can either occur from the brain or the eye. Determination of either is relatively easy because, problems resulting from the eyes will lead to a different view of the world depending on if it's viewed/looked at by the left or the right eye. Example: Partial retina damage to the left eye may lead to a noticable visual problem when only the left eye is open, if the only right is open, no problem would occur. Problems resulting from the brain (lesions etc.) would be the same regardless of which eye is open -Above fixation point: info goes to the ventral part of the visual cortex -Below fixation point: info goes to the dorsal part of th visual cortex -Damage to visual cortex leads to diability in terms of perceiving light and dark contrast -Far left periperhal visual damage: Damage to/in the left eye -Following on from this, the more serious vision disorder include homonymous hemianopsia/hemianopia, quadranopsia or scotomas (see below, we'll examine Hemianopia further however) -SCOTOMA: Normally a spot of missing visual information. If noticed above the fixation point it affects ventral regions and depending if it's located on the left or right, the damage would result from the contralateral side of the occipital lobe and hemisphere as usual. If notices below the fixation point on either side, the same applies, only it affects dorsal regions. Small parts of the visual cortex is damaged whereby problems occur with ligh-dark contrast detections.

Blindsight is...

(Banich & Compton, 2011 & other sources too and me) -Blindsight is a disorder when patients became cortically blind due to a lesion in the PVC/SC, damage to area V1 (Visual Cortex) disrupting optic nevres to carry visual info to the striate colliculus and hence losing sight in the relative visual area/field -Term was coined by Weiskrantz (1974) with the case of patient D.B. who could see almost nothing in his LVF (left visual field) he has been blind for a long time to his left eye I assume he had lesions in his right hemisphere then. He had surgery to remove which destroyed his PVC. However, in the upper left quadrant of his eye, he started to exhibit residual vision/preseverd visual activity, some tests then revealed that he could eventually guess colours, shapes and motions of some stimuli.He told the researches surprised that he did not see anything and completely guessed it all, when he got informed that he got quite a few right. (links with the intact pathway hypothesis for preserved visual knowledge). It was revealed later by Weiskrantz and colleagues that D.B. had a "superior vision" in his blind visual field for stimuli that was almost impossible to see (quadrant). -Cortical Blindness resulting from "blindness of cortical origin" rather than resulting from an eye problem or an optic nerve disruption -Patients have no "conscous experience" of "seeing" something, this is regarded to the widespread damage to the striate cortex -The area that is the actual blindness itself is called SCOTOMA which may present itself in various ways, as a spot or taking up the whole visual field. It is located int the visual field contralaterally to the damaged hemisphere -The visual cortex and some nerve fibres carrying information to the eye get damaged in the case of Blindsight -It can occur on one side of the visual field only or both visual fields too, cortical blindness can cover the whole visual field (this occurs when both sides/hemispheres of the PVC/SC are damaged) if only one hemisphere is damaged reaching one side of the PVC/SC then the patient will only be affected on the contralateral visual field to the damage,becoming HEMIANOPIC -Symptoms usually include being blind to visual stimuli in the affected visual area not being able to sense light-dark contrasts -Interestingly, according to Carlson, (2013) sensory (visual) info is able to control the behaviour of a patient without them consciously realising and demonstrate this/sensation inferring that: conscousness itself is not owned/does not belong to all regions of the brain suggesting that only specific brain areas are responsible and play a role in the case of consciousness -However, some patients who have blindsight experience blindness in their affected contralateral visual field to their lesion, yet a lot of patients demonstrate some "rudimentary visual capacities" retained even though they are blind to one of their visual fields. -A lot of patient with cortical blindness do not demonstrate/exhibit blindsight actually. Vision/Visual Cortex studies reveal that some areas of vision are still preserved regardless of a lesion/deficit in the PVC, and that the patient reports no physical experience of vision. -Blindsight reveals that the PVC/SC is vital in terms of seeing the visual world around us,however, it also reveals that NOT ALL parts/features of the PVC/SC is needed/vital for vision because some still gets preserved regardless that the PVC/SC is damaged. -According to Weiskrantz (2004), blindsighted patients are able to locate spots of light by moving their eyes to the stimuli or pointing at it. Furthermore, they are able to make some "colour judgements" from each other, like a red or a grey square in the visual field and determine whether a target/object/stimuli is moving or stationery. This all inferring that patients with blindsight still have preserved visual knowledge in certain forms. (cited in Banich & Compton, 2011) -Interestingly, usually in all studies, patients say that they have no conscious visual awareness about what they are doing, they are unable to see what is presented and they are likely to guess what is in their affected visual field completely/all the time. -It is not certain whether residual vision is due to a path called tectopulvinar pathway and the concept that this pathway has remained intact, or whether it's due to the intact path from the LGN extending to the extrastriate regions or whether it's acocunted for some spared fucntionw within the striate cortex. There is still a great debate about thiw between researchers. -Evidence regarding this, which supports the tectopulvinar pathway hypothesis may illustrate it with a study by Leh et al., 2006/ if you can remember: Leh, Johansen-Berg & Ptito, 2006 as cited in Banich and Compton) which used "diffusion tensor imaging" on patients with blindsight whereby the "projections" coming from the superior corriculus within the damaged/lesioned hemisphere was examined with patients who had blindsight followed by hemispherectomy, patients who had no lasting visual abilitrs in the affected visual field but having hemispherectomy, and control patients with no visual damage. The study found the following: 1. Patients with blindsight, hemispherectomy: connections was spotted in the damaged hemisphere between the superior colliculus and fiber pathways leading to various cortical areas in the intact hemisphere (PVC and some other visual areas) Connections looked very prominent, even more prominent that those with non-brain damage (control group) 2. Patients with no lasting visual abilities, hemispherectomy: Observations were made about the superior colliculus yet again, which in their case in their damaged hemisphere did not show particularly significant activity in its connections with other cortical regions. 3. Control patients: N.A. Results infer and are even with the idea/concept that blindsight itself is dependent on the "projections" /signalling of the tectopulvinar pathway to the cortical regions. All in all, this infers that visual information that is still intact in these patients with visual deficits, is narrowed down to the sort of information that only the superior colliculus can access. -The other pathway that may be responsibe for residual vision and researches are still debating about is the possibility of the intact path of LGN extending to the extrastriate cortex and its regions. This might also mediate intact visual abilites in patients and it thus seems like that the LGN sends visual information to certain cortical visual areas. -In animal studies for example by Sincich et al. (2004), they looked at monkeys and showed that in monkeys, K-cell layers of the LGN transmit/pass on straight into the extrastriate cortex and its cortical areas "that process motion". This infers that motion detection my be preserved in blindsight which is through the geniculate pathway going around the PVC/SC when it is damaged and hence, leaving motion detection intact in blindsighted patients. -To finish off, arguing against the above, some researches demonstrated that in the cases where blindsight have been observed in patients and have had hemispherectomy/removal of the entire cerebral hemisphere (unilateral removal of the hemisphere) there is almost never any preserved SC tissue that would support any reamining visual ability/vision (Stoerig, 1993; Ptito & Leh, 2007 cited in Banich & Compton). Additionally, some other researches tested blindsight patients for reamining SC activity, some found evidence for this, and some did not find anything. This explains that preserved Striate tissue or activity may occur in some patients but cannot be accounted for all the cases where visual ability was preserved to a certain extent. -There may be more than one pathways that could aid preserved visual abilities or support residual vision when they have damage to their PVC/SC -Blindsight still has a lot of gaps, not many blindsighted patients have been examined so far, and it must be noted that evry patient has a slightly different deficit, the pattern is different, and often other areas are affected too. There is a great heterogenetiy within patients; some say they still detect something without seeing it in their affected field whereas other state that they are fully blind in that field. Only some generalizations (altalnositas) can be made. (Weiskkrantz, 2004 cited in Banich & Compton, 2011). -The field of blindsight still seeks a lot of answers and needs more research.

Neural Mechanisms (mediating blindsight, some you've already written)

(Copied from lec slides) -There is residual visual function without awareness. It can generate affective awareness without perceptual awareness. -There is cortical activation going through an alternate route. It reaches both the dorsal ('action') stream and the ventral ('shape') stream. -The Dorsal Stream is thought to mediate much spatial processing and interaction with the environment -But the neural activity in these structures does not (is not alone sufficient to) enter into consciousness -Residual Functions: types and what ways can patients preserve it (explained above) -Pathways: tectopulvinar or lateral genicular nucles pathways to the superior colliculus

Hemianopia is....

-A certain type of damage in a part of the visual cortex, normally occurs in one half of the visual field in the left or the right eye, sometimes both eyes -Complete los occurs when one visual side of the optic nerve is damaged so the contralateral eye will be blind -A visual field disorder/condition, affecting all regions of the right or the left occipital lobe (contralateral if regions of the right occipital lobe is affected, left eye/visual field will be blind/gone, and if left regions of the occipital lobe is affecten then the right eye/visual field of the visual cortex will be blind/gone and no visual information may be detected. This is a result of the damage to the entire occipital cortex of one hemisphere: leading to he inability to detect visual information int he contralaterla field (similar to hemineglect) -QUADRANOPSIA: Occurs in either the ventral regions of the left occipital lobe (if above fixation point) or if below it occurs in the dorsal regions, similar to hemianopia, only it is either only a ventral or the dorsal part damage/deficit of the occipital lobe and hence, only "one quadrant of the visual world is lost" -Also referred to as decreased vision or partial blindness, belongs to the visual deficit group of ANOPSIA

Neuroanatomy

-Also occurs in the PVC or in other name, the Striate Cortex, area V1 -Two pathways from the retina to the brain: tectopulvinar pathway coming from the retina and extending to the superior colliculus of the Midbrain and the geniculostriate pathway coming from the retina and extending to the LGN/LG (Lateral Geniculate Nucleus) of the Thalamus -Branches of the optic nerve carrying visual info to the superior colliculus and other regions of the cerebral cortex -Many patients however, who have a damage to area V1 in the cerebral cortex, don't show complete blindsight often only in some parts of the visual field, this might be because some healthy tissue may remain even thought there are lesions -Scotoma: It is the type of area for blindness in the visual field that is affected by the lesioned hemisphere, which may take up a blind spot or the whole visual field as a big blind space abd hence, cause the patient to have no consious vision, it's either a partial blind spot or a degeneration of vision ina larger spot surrounded by intact vision from either the same eye as well or the other eye. Scotomas are "simply reduced information within the visual field" (Fletcher et al., 2012) -Patients with damage to area V1 state that they see no visual imagery, no dreams of visual material and they don't have conscious vision, but according to Kalat, 2009, some patients still exhibit the phenomenon of blindsight

Neuroanatomy

-Builds upon the systems of the basic visual cortex -This includes the basic pathway of vision: 1. Info from retina is sent to the occipital lobe where it then travel simultaneously parallel to each other on the left and the righ visual fields 2.They reach the point of the LGN (lateral geniculate nucleus) and then travel through the optic tract until they reach the OC (optic chiasm) which is responsible for the crossover and turning inversely the visual information. 3. The left visual field projects to the right hemisphere and the right visual field projects to the left hemisphere 4. Once the visual information crosses to the contralateral side at the OC, it hits the optic nerve and reaches the eyes ans allows for vision and putting a visual image of the world together. -Main areas are the Visual Cortex or area V1, the Superior Colliculum and the Lateral Geniculate Nucleus

Homonymous Hemianopia is...

-Homonymous means same or having the same -Homonymous Hemianopia is when both half of the visual field in each eye is affected (visual deficit/loss in the same side of both eyes), there is a hemianopic deficit in each half of the eye unfortunately. (Sounds like shit) -Important to note, that loss of visual field occurs in half of the eye, but in both eyes on the same side -If the left visual field was damaged in the occipital lobe the image would feature a person only seeing the right half of the picture in both eyes (see wiki if confused), and then the patient would officially have: Left Homonymous Hemianopsia/Hemianopia -The visual information seen on the left, does not cross over and travel to both right side of the visual cortex/field/right side of the brain, one of the respoinding pathways to visual information is lost unfortunateley. DOUUU :( :D

Additionally, if time allows look at:

-Motion Area (MT) V5 -Semir Zeki

Rehabilitation (see other recovery methods below Blindsight)

-No established therapy (there is no single profound therapy that ensures success) (copied from lec slides + WIKI as I had no more time) 1.Vision Restitution/Restoration Therapy?(lec slide):Repeated photostimulation is applied at the border between the seeing and the blind field. -Patients typically undergo several months of training. Functional improvement in terms of reading and visual search tests, structured questionaire reports. -Variable proportion of patients show improvement but no pattern to predict efficacy; age, time since lesion, type of visual field defects are not good predictors. -fMRI studies suggest increased activities in attentional areas after VRT (Marshall et al, 2008). -Henriksson et al. (2007) & Nelles et al (2007) found that visual field training stimulation induced bilateral activation within the extrastriate cortex, and this activation was stronger in the ipsilateral (contralesional) hemisphere. -Plow et al. (2012) studied a 3-month regime of VRT in two patients suffering from a left occipital lesion (Right HH). They coupled sessions of visual training with TMS of the occipital area. They observed better recovery in the patients (who had received TMS) compared to control patients (who had received sham stimulations). -Conclusion: visual training in the blind visual field, regardless of whether it is coupled to TMS, can induce cortical reorganization. 2. Audivisual Stimulation Training (no time, copied from wiki) (WIKI, no time) -Audiovisual stimulation training has been developed as an effective treatment for patients suffering from Homonymous Hemianopia which uses multi-sensory stimulation to improve vision. Patients can go through an intensive program of up to 4 hours a day for 2 weeks, in which areas of their visual field, both intact and affected, are stimulated using sound and light. -Many patients have seen lasting results from Audio-visual Stimulation Training, allowing them some recovery. This training affects different parts of the patients' saccades, including spatial and temporal aspects (Passamonti et al., 2009). Patients with Right Hemianopia tend to show fewer progressive and regressive saccades, larger amplitude of these saccades, and reduced duration of fixation time (Passamonti et al., 2009). They also show improved accuracy on reading performance tasks. However, performance is still impaired (Passamonti et al., 2009). Left Hemianopia patients show even greater improvements, showing a significantly smaller number of saccades, and following reading tasks their ocular responses are comparable to 'normal' vision patients (Passamonti et al.,2009).There are also some negative aspects of Audio-visual stimulation Therapy, being that the field of vision is not improved (Windsor et al., n.d.). Studies have shown that sensitivity of perception showed no significant difference when the patient was told to keep their eye stationary from the original treatment which allowed the patient to move their eye will adjusting their gaze(Passamonti et al.,2009).. If visual field had been increased, the sensitivity should have increased when the eye was held in one position. 3. Explorative Saccade Training (WIKI,no time) -Explorative Saccade Training was developed to train patients to make exploratory saccades without head movement in the area of the visual field which has been lost, and sometimes may be referred to as Scanning Therapy (Koons et al., 2010). Many methods have been developed for performing this type of therapy, most of which are performed by an occupational therapists, and the individual patient. These patients learn to apply these search strategies to everyday tasks. -Explorative Saccade Training begins with the development of large saccades, followed by the development of smaller saccades. The patient should start to try to improve the speed of these saccades in order to develop a natural flow to their visual perception. -Attention may play a very important role in saccadic visual rehabilitation (Lane et al, 2008) -Explorative Saccade Training improves exploratory behavior, and enhances performance of digit search tasks (Roth et al., 2009). Lasting effects are shown for improvement of natural search performance on the patients' blind side after only about six weeks of training (Windsor et al., n.d); with scanning improvements of up to 35° into the affected side of vision (Koons et al., 2010). An advantage Explorative Saccade Training is that it has been shown to be affective for patients who have been living with Hemianopia for many years and have had the time to come up with their own adaptive strategies to deal with their vision (Roth et al., 2009). 4. Hemianopic Alexia (http://link.springer.com/chapter/10.1007%2F978-1-4471-5529-4_2) -Hemianopic alexia is the most peripheral of the alexias and also the most common. It is caused by a hemianopia that mildly interferes with single-word reading but has its main impact on upon text reading. This is because the visuomotor system is robbed of visual information away from the point of fixation that it requires in order to plan efficient reading eye movements. Herein we discuss the anatomy of the visual system, including how the visual word is represented in primary visual cortex, and why the most common cause of a hemianopia is a posterior cerebral artery infarct. We cover visual field assessment and the pattern of inefficient eye movements made when patients with hemianopic alexia read text. In the second half, we provide a detailed critical review of the main therapeutic approaches including visual restoration (blindsight and conscious vision) and eye-movement-based methods.

Other

-Other Hemianopia may include quadranopsia (see above), bitemporal hemianopsia (patient sees left half with left eye only and right half with right half only, kibaszott chameleon!):D, or binasal hemianopia (patient sees only closer to his/her nose, left inside half only with left eye, and right inside half only with right eye, KANCSAL! :D)

Causes

-Stroke -Brain Tumor -Some sort of serious Trauma -Lesions in the optic tract signaling to the visual cortex leading to contralateral homonymous hemianopsia -In rare cases, it has also been observed in patients with cerebral cancer -Sometimes, serious migraines may achieve the same effect (aura phase) leading to some people losing their sight for a while, or see in patches

Rehabilitation and Techniques

1.Leh et al. (2006) Unconscious vision: new insights into the neuronal correlate of blindsight using diffusion tractography (Copied from lecture slide) -Alternative Method: Via the SC (superior collliculs or Striate Cortex?) -Strong ipsilateral and contralateral projections from the SC to primary visual areas, visual association areas, precentral areas/FEF only in those hemispherectomized subjects with 'Type I' or 'attention blindsight'. -No such connections without 'Type I' or 'attention blindsight'. These results strongly support an essential role of the SC in blindsight. -This study demonstrates the usefulness of DTI tractography in investigating cerebral plasticity, compensation and reorganization following various cerebral lesions. 2.Anders et al. (2004) Affective blindsight: pairing unseeing stimulus with averse feeling -Some faces were paired with an averse human scream. Following training, subject reported averse feeling when presented with the face in the blind region. They were not visually aware of the face. -BOLD responses were significantly increased in the left anterior parietal cortex -Negative emotional feelings significantly enhanced All patients denied any visual sensation fMRI: no visual activity in the region corresponding to the calcarine sulcus (From Lec. Slides) -Sahraie et al. (2006) claimed that visual sensitivity in the blind hemifield could be improved without the patient's awareness, and that this could be done even in the very depth of the impaired hemifield. Trained patients over 3 months Overall, the patients exhibited improved sensitivity in target detection at various contrast sensitivity levels and spatial frequencies, and objective improvements at clinical perimetry tests. Therefore, authors con- cluded that training blindsight could be a way to improve visual field defect in hemianopia. -Raninen et al. (2007) trained patients to detect flickering stimuli and to discriminate letters at various eccentricities within the blind hemifield. The patients were tested twice weekly for roughly 1 year, Patients improved in these tasks, but not in Goldman perimetry. -Chokron et al. (2008) trained nine brain damaged patients on various forced-choice tasks in their blind hemifield, including visual- target pointing, letter recognition, comparison of two stimuli presented in both hemifields and target location. They all improved in behavioral tasks, and eight of the nine patients exhibited a significant enlargement of their visual field (as determined by classical perimetry examination).

Key Terms (Alphabetical order!)

Anopsia Primary Visual Cortex Occipital Lobe Brodmann Area 17 Nasal Hemiretina (inside part of retina closer to the nose) Temporal Hemiretina (outside part of retina) Retina Homonymous Optic Chiasm Lateral Geniculate Nucleus Optic Nerve Superior Colliculus Thalamus Optic Tract Nasal/Binasal Hemianopia Temporal/Bitemporal/Bipolar Hemianopia Blindsight Striate Cortex (PVC) Cortical Blindness Tectopulvinar Path Receptive Field Photoreceptor Fovea Ganglion Cells Scotoma Extrastriate Cortex Hemianopic Alexia

Recovery

Can blindsight produce functional vision? Can blindsight be improved with training? Does neural plasticity have a role in rehabilitation from Homonymou Heminopia (HH)? Can we teach strategies to improve effective vision in HH?

Plasticity is associated with... (Adjacent fckin neurons appear here,whyyyyyyyyyyyyyyyyy)

Decreases, increases, and shifts in brain activation to facilitate the behavioral improvement: -Take over of function by adjacent neurons Think of an example: -Reallocation in hemispheric resources Think of an example: -Recruitment of additional brain regions Think of an example: -Strengthening of an anatomical structure /connection Think of an example: -Functional Connections Hebbs rule: "Neurons that fire together, wire together." *Learning- induced plasticity can be associated with the idea that supports that behavioral improvement would likely be supported by stronger, longer, and expanded activation in a specific brain region. Recovery of Function following Brain Damage -In cases of relatively small lesions to motor cortex regions adjacent to the damaged tissue may take over function -Changes in gene function in a ring located around the lesion result in an increase in proteins that promote growth and a decrease in proteins that inhibit growth

Questions

Do we rehabilitate hemi-spatial neglect e.g. via TMS or teach alternative strategies? Do we target disordered memory functions or do we re-design the environment? If we can't answer these... We may waste precious therapy on ineffective treatments Damage the patient through harmful therapy Allow atrophy of brain tissues by failing to give correct stimulation

Symptoms

Firstly, CT and MRI can be used to examine the underlying causes of hemianopia (whether it's a tumor, stroke, a lesion etc.) Symptoms may include: -It can affect mobility -Feel of uncomforted in big crowds and anxiety -Partial vision loss, full vision loss (Copied from lec slides) -Impaired visual search/orientation in 2D and 3D space, reading difficulties and slowed and inaccurate performance in functional visual activities (Pambakian et al., 2005; Leff et al., 2006; McDonald et al., 2006) -Bump into other pedestrians or obstacles in their blind hemifield.

Principles of Neural Plasticity (Kleim & Jones, 2008; Ludlow, et al., 2008)

Principle 1: Use it or Lose it: If a neural circuit is not actively engaged in task performance for an extended period of time, it will degrade in function Principle 2: Use it & Improve it Training that drives a specific brain function can lead to an enhancement of both function & structure of the neural mechanisms involved in that behavior Principle 3: Specificity The nature of the training experience dictates the nature of the plasticity.Changes in neural functions may be limited to the specific function being trained.For example consider the case of "blindsight.Can blindsight be trained to produce function vision? Targeted stimulation for hemispatial neglect -Constraint -induced movement therapy -Limb activation training -Prism adapation training -Neck muscle vibration -Facilitated movement (harness and treadmill) Principle 4: Repetition Matters Induction of plasticity requires sufficient repetition.Repetition of a newly learned or relearned behavior may be required to induce lasting neural change.Therefore, the number of repetitions per session and the number of sessions required for a behavior to become consolidated needs to be established.Simply engaging a neural circuit in task performance is not sufficient to drive plasticity. There is a need to obtain a level of improvement and brain reorganization sufficient for the patient to continue to use the affect function outside of therapy and to maintain and make further functional gains. Principle 5: Intensity Matters Induction of plasticity requires sufficient training intensity But remember...May not be appropriate for patients that are easily fatigued.Medical status & other factors should be considered before assuming that intensive training can produce behavioral changes and neural plasticity Maladaptive responses to intense treatment programs may cause further damage Principle 6: Time Matters Different forms of neural plasticity may occur at different times in response to treatment.Therapy promoting neural restructuring should work anytime, but there may be time windows in which it is particularly effective in direction the lesion-induced reactive plasticity.Time delays may also allow for the greater establishment of self-taught compensatory behaviors, some of which may interfere with rehabilitative training efforts. Principle 7: Salience Matters Training experience must be sufficiently salient to induce plasticity.Neural plasticity may be enhanced when the training is purposeful & related to the behavior being trained.Saliency is already an important consideration in the treatment of many neurological disorders, including aphasia and motor speech disorders. Functional brain imaging could address the degree to which meaningful speech communication may activate a different brain network than that used for syllable repetition. Principle 8: Age Matters Adult brains are capable of plastic adaptation to injury including some degree of structural reorganization.Training-induced plasticity occurs more readily in younger brains.For example -can you think of any examples where age of the patient appears to have an effect on brain plasticity? Kennard principle (1936,1942): The earlier in life damage is sustained, the better the recovery The crowding hypothesis: Deficits may emerge in later childhood with the child falling behind peers in cognitive development Language vs spatial cognition Principle 9: Transference Ability of plasticity following training in one set of neural circuits may promote concurrent or subsequent plasticity. It is important to determine if a particular therapy is responsible for the enhancement of another behavior or whether transference occurs regardless of the type of therapy. Principle 10: Interference Plasticity causing changes in neural function can also impede the induction of other behaviors or skills Therapy that benefits one skill may interfere with performance of another. Perhaps enhancing some speech skills such as articulation might interfere with other aspects such as prosody or rate. Retained functions may interfere with the recovery of lost functions after injury.

Neural Plasticity (All copied from lecture slides)

WHAT IS NEURAL PLASTICITY? -Also called Neural Adaptation -Neuroscience research has characterize this as an adaptive capacity of the CNS -It is the ability of the CNS to change & adapt in response to environmental cues, experience, behavior, injury or disease -Neurons possess the ability to alter their structure and function in response to a variety of internal & external pressures, including behavioral training -Thus, it the mechanism by which the brain encodes experience & learns new behaviors, and by which a damaged brain relearns lost behavior in response to rehabilitation MECHANISM OF NEURAL PLASTICITY 1.Angiogenesis 2.Axonal sprouting (neurogenesis) 3.Unmasking of latent synapses (synaptogenesis) 4.Regeneration from neural stem cells in the subventricular regions migrating to the periinfarct area. IPSILATERAL EFFECTS - Decreased dendritic branching - Increased dendritic branching - Neuronal sprouting - Synaptogenesis - GABAa receptor downregulation - NMDA receptor enhancement - Facilitation of LTP - Neuronal hyperexcitability - Alteration of cortical maps CONTRALATERAL EFFECTS - Increased cortical thickness - Dendritic growth (short term) - Dendritic pruning (longer term) - Increased spine density (longer term) - Synpatogenesis (longer term) - GABAa receptor downregulation -NMDA receptor enhancement -Neuronal hyperexcitability

Type I (Do we need examples?)

WIKI "Type 1 blindsight is the term given to this ability to guess—at levels significantly above chance—aspects of a visual stimulus (such as location or type of movement) without any conscious awareness of any stimuli."

Type II (Do we need examples?)

WIKI "Type 2 blindsight occurs when patients claim to have a feeling that there has been a change within their blind area—e.g. movement—but that it was not a visual percept."