Thursday, 27 October 2011

Week 5 - Movement Disorders

Among many neurological deficits, movement disorders seriously inhibit a person’s day to day life. Movement disorders are caused by damage to the central nervous system (CNS). This includes damage to neurons in subcortical structures or lesions to the cortex. Damage to the two subcortical structures causes the most harm to motor dysfunction. These are; the cerebellar loop, which controls the timings and trajectory of movement using sensory and motor information and; the basal ganglia loop, which controls the excitability of the frontal motor structures and will decide the likelihood of movement and the strength of the movement. The basal ganglia is a collection of nuclei which includes; the caudate, putamen and the globus pallidus. These nuclei are often involved in severe movement disorders such as Huntington’s disease and tourette syndrome, which is caused by excessive motor activity, and Parkinson’s disease which is caused by restricted movement.
This shows that the subcortical structures are extremely important for motor control because any damage or lesion affecting this area leads to some serious inhibitory movement problems.
Below I will discuss movement disorders (including Parkinson’s disease, Huntington disease and tourettes syndrome) and the methods used to treat these disorders.

Parkinson’s disease

The characteristics of Parkinson’s disease include akinesia (general loss of movement) rigidity and tremors when resting; Akinesia involves bradykinesia (a slowness of movement) and hypokinesia, which is a reduction in movement.
Age of onset - Is between 40 and 70 years of age.
Symptoms - Stooped posture, difficulty with speech and trouble turning their bodies, and also trouble with writing.
Treatment - L-dopa (penetrates the blood/brain barrier) Dopamine receptor agonists and MAO B inhibitors.

Huntington’s disease

This is an inherited disease and causes a person to perform involuntary (dance-like) movements and causes dementia.
Age of onset - Is between 40 and 50 years of age.
Symptoms - Difficulty with speech and standing, changes to personality, clumsiness.
Treatment - No long term treatments. Dopamine antagonists relieve a small amount of symptoms for a temporary amount of time. Treatments aim is to restore balance to neurotransmitters in the basal ganglia but in the long run this is not enough to prevent the disease from progressing.

Tourettes syndrome

Has been proposed as the result of dysfunction between the basal ganglia and its connections to the orbito-frontal cortex.
Age of onset - Begins in childhood (typically before the age of 15)
Symptoms - Head jerking, shrugging of the shoulders and the most obvious is the repetition of words and swearing.
Treatment - A drug called haloperidal is administered to patients with tourettes syndrome.

Important revision notes from the article (week 5) - 'Abnormalities in the awareness of action'

- Researchers have proposed that the central nervous system (CNS) holds internal models that interact our own bodies and the external world in order to optimize motor control. The two internal models proposed are; 'The forward model' this predicts the sensory consequences of motor commands. The second model proposed is the 'inverse model' this provides the motor commands to achieve the desired outcome.

- Although we are aware of the goals underlying most of our movement it has been suggested that we are unlikely to have conscious access to all of our motor commands and adjustments that are made in order to carry out a command. This leads to the speculation that we do not have conscious access to the inverse model/motor commands. However this field of research is not conclusive.

- On the other hand the 'forward model' has been proposed as being available to awareness.
-The 'forward model' compares the actual outcome of motor commands to the desired outcome, all of which is made before a movement is made this allows for adjustments to be made before the action is carried out.

- The second job of the 'forward model' is to compare the prediction of the sensory consequences of movement to the actual feedback - this comparison is made after the movement is made. This allows for the body to compensate for the sensory effects of the movements being made.

  • An experiment took place to demonstrate that the motor system can function in the absence of awareness.
  • Goodale etal ran an experiment where participants were asked to point at a visual target. It was reported that during a saccade the target was displaced, this went unnoticed by the participants, however their arm moved in the correct direction.
  • Castiello etal found that participants were only aware of a target jump 200ms after the motor system had made appropriate adjustments.
  • An interesting study was ran by knoblich & Kircher. Participants were instructed to draw circles which they then saw reproduced by dots. The dots were slowly increased therefore making the circle bigger, participants were asked to lift their pen when they saw a change. Results found that participants compensated for the changes well before they were actually aware of the change. This shows that we are not conscious of all the fine adjustments made by the inverse model, and it's only when a change becomes so big that we notice any change. Overall so long as our desired intentions have been met, we are unaware of sensory feedback about the state of our motor systems.
Neurological abnormalities

Optic ataxia

- This is where patients have trouble with grasping objects that they can see before them. Although their actions are carried out in a clumsy manner the movement the patient is making matches their intention. The patient is aware of their problem in reaching and grasping. This condition is caused because the 'inverse model' is not properly tuned.

Anarchic hand sign

- This is where patient’s hands move of their own accord without the will of the patient. It seems that simply seeing an object is enough to trigger a movement. The patient clearly recognises a problem between desired actions and actions that do take place.

Utilization behaviour

- This is where a patient utilizes an object inappropriately, however in contrast to the 'anarchic hand sign' the patient does not see the discrepancy, this is because the patient will rationalize their movement by saying they thought someone wanted them to do it, their actions are involuntary however they feel like the movement was intended.

Phantom limbs

- This occurs after a patient has had a limb amputated, but still feels like they have still got the limb, and report feeling like they can move it or that it feels paralysed. An explanation put forward is that the estimated position of a limb is not entirely based on sensory information but also the stream of motor commands to the limb. The 'forward' model estimates the position of the limb before sensory information has been received. Therefore motor commands may be issued to the limb therefore making the phantom limb feel like its moving. In time the motor control system will adapt to changes therefore many patients report losing the ability to move their phantom limbs.

Thursday, 20 October 2011

Week 4 revision blog - Visual perception

Lesions to the parietal cortex results in a deficit to a person’s spatial perception abilities. Neglect after stroke appears to have high consequences, an example of this is when a patient has a right hemisphere stroke they lose awareness of any left side stimulus when there is a competing right stimulus. It is reported that patients are only aware of half of the world. This disorder causes difficulties in most everyday life events, e.g. difficulty dressing one side of the body, reading things on only one side of the page, and often only eating from one side of their plate. Some patients are unaware that they are neglecting information on one hemifield, this is called 'anosagnosia' this is obviously detrimental to the recovery of the patient. Spatial neglect can be simply tested using a task that involves copying a drawing. A person with spatial neglect will only copy one half of a drawing. Blindsight is another sensory impairment, this is caused by damage to the striate cortex and involves the ability to locate an unseen object, even though reporting they could not see the object itself. Riddoch (1917) reported that patients with blindsight could tell the direction an object was moving, but could not actually see the object. Research has hypothesised that this happens due to 'extraocular scatter' which is when light reflects off of the stimuli therefore allowing it to be picked up by the visual system. The subcortical pathway that carries information from the retina to the superior colliculus could help explain blindsight, as this neural pathway only provides rough information at a quick pace, therefore the patient picks up rough movement, but cannot distinguish any fine detail.

Revision material from the article (week 4) – ‘Implicit face perception in a patient with visual agnosia? Evidence from behavioural and eye-tracking analyses’.

Le. S & Raufaste. E etal (2002)
investigate whether a patient with a face perception deficit can recognise faces in the absence of their awareness. Prosopagnosia is the inability to recognise faces that the person previously knew. It has been suggested that although prosopagnosia patients report not feeling familiarity when viewing a face it has been shown that the processing of familiar faces can still happen without the patients awareness (this has been shown by skin conductance test).
It has been shown that
object recognition and face recognition activate different loci in the same cortical area therefore although one type of recognition may stay intact, the other becomes severely damaged. The article puts forward two hypotheses to explain why a patient with visual agnosia and prosopagnosia was still capable of some visual processing. The two hypothesis are; 'The spared hypothesis' this suggest that the patients abilities are due to spared modules of implicit face processing. The second hypothesis is the 'general strategy hypothesis' this suggests the patient’s ability was due to compensatory strategies. Experiment one saw the patient along with control participants having to distinguish if the picture being shown to them was a face or a vegetable and experiment two saw the patient and control participants having to state whether the picture they were being shown was a face or not. Results showed that the patient was not aware of faces, however it showed that he processed them differently to non-faces. Eye tracking shows that facial features were processed similarly to the control participants, therefore it was discussed that the results rejected the 'general compensatory strategy hypothesis' therefore supporting the 'spared module hypothesis'. These results suggest that a patient with severe deficits to visual perception can recognise faces without conscious awareness.

Important info from lecture

- Lesions of the parietal cortex lead to spatial deficits.
-When a patient has had a right hemisphere stroke they lose awareness of any left stimulus when there is a competing right stimulus.

Neglect is a directional bias modulated by competing stimuli not a lack of awareness of one half of space.

- Patients with right parietal lesions have impaired detection on their right side and often revisit locations on the right side because they cannot remember where they have looked before.
- Neglect patients also show deficits on non-spatial tasks, therefore sustained attention & selective attention are impaired.

- The optic nerves from each eye meet at the optic chiasm - Information from the left part of the visual field goes to the right side of the brain & information from the right part of the visual field goes to the left side of the brain.

Homonymous hemianopia

- This is a loss of vision on the corresponding area of visual field in both eyes.


This includes; a loss of half of the field of vision and can detect/discriminate visual stimuli in their blind field e.g. colour, motion etc.

- The visual pathway is fast and unconscious and provides only rough information about the location and identity of stimuli not fine detail - this could explain why the patient can detect colour and motion but not actually able to fully detect/see the stimuli.

- Some researchers found that after training homonymous hemianopia patients with visual search everyday for a month the patients improved and became faster at finding targets - eye tracking also revealed that patients more effectively made allocation of fixations after training, therefore suggesting that this visual problem can be improved with visual training.

-Milner & goodale (1995) suggest that there are two vision systems; visual perception and visuomotor control only the first is involved in conscious awareness. Blindsight has been suggested as dissociation between fast motor reactions and conscious perception.

What and where

What = Bilateral lesion of the temporal lobe leads to a deficit in the discrimination of objects.
Where = Bilateral lesion of the parietal lobe leads to a deficit in the discrimination of locations.

Thursday, 13 October 2011

Week Three - Visual Perception

Visual perception is a person’s eye sight it allows the sensory and perceptual systems to interpret information from their environment and therefore begin the process of how to react to the visual stimuli before them. Brain damage and lesions to the visual system consequently result in a severe deficit to a person’s visual abilities and can cause many perceptual disorders. These include; Agnosias, visual agnosias and prosopagnosia. Agnosia is an impaired ability to recognise basic objects, this is however not attributed to sensory or attentional deficits. The most common cause of agnosia is due to brain damage causing sensations such as light and colour to become confused. Interestingly patients with agnosia that cannot recognise an object can more than likely specify what the object is if they are allowed to touch it, therefore showing that the patient has an intact memory about the object, but just cannot visually recognise it. Visual agnosia is caused by right inferior parietal lobe lesions. Patients with visual object agnosia may experience symptoms such as difficulty with copying drawings, and finding it hard to match objects . Stroke and heart attack can cause this perceptual disorder. Prosopagnosia patients find it difficult to recognise faces, however the ability to recognise objects stays intact. Interestingly it was reported by Hecaen & Angelergues (1962) that patients with this disorder have difficulty recognising the faces of people they previously knew or even pictures of their own face. Although prosopagnosia patients have an inability to recognise faces they can however still identify individuals by peripheral cues such as voice, hair, silhouette etc. It has been recognised that the reason for some patients to report not being able to recognise faces but still being able to recognise objects or vice versa is due to object and face recognition activating different parts of the brain.

Questions for week three;

  • Q1 - Why do we need to move our eyes across a scene?
- The movement of our eyes helps direct focus and attention to stimuli of high salient importance, therefore making it easier to take in visual information and process it in the brain.

  • Q2 - Would it not be easier if we could see the whole scene in front of us at once?
- This would not be ideal because the brain cannot cope with an overload of visual information, therefore it is best to focus attention on information of high salience.

  • Q3 - What does FEF mean? And what is its role in vision?
- FEF means frontal eye field and it is an area in the frontal cortex involved in the generation of motor commands for pointing the eyes , and therefore the foveas toward desired target locations.

Week 3 article reading - 'Cognitive Physiology: Moving the mind's eye before the head's eye'.

- It is said that when we shift our spatial attention it is most often followed by a matching eye movement. Evidence has suggested that this reflects the ability of the same cortical area to shift eye position and the locus of attention.
-It has been suggested that the visual system has evolved greatly over time and in a very selective way. It has been noted that the most evolved is the high spatial resolution being confined to a small fraction of the retina, the fovea. This is very instrumental as if the abilities of the fovea were spread across the whole retina this would have been difficult, and resulted in a flood of information reaching the brain, which would have been impossible to accommodate.
-The visual system now identifies the object and reflexively or voluntarily foveates them for detailed analysis, therefore a dedicated motor system has been developed. The motor system is only activated when a worthwhile target for an eye movement has been identified. This all highlights how much the human brain has evolved.

-Because of an overload of information arriving at the eyes with little of this being of importance, an attentional system has been developed.

-Voluntary attention enhances the activity of neurons in extrastriate cortex when something seems of importance.

-The central mechanism that directs attention still seems unclear because although the link between extrafoveal attentional location & eye movement appears strong it has not been shown that one causes the other.

-However Moore& Armstrong tried to demonstrate that there was a link. In a study with monkeys they found that the absolute response enhancement was stronger if presented with a preferred stimulus then when presented with a non-preferred stimulus, showing that attention is directed at things that are appealing to us.

-Findings have found that the FEF plays a central role in directing spatial attention and that this process is linked directly to the generation of eye movement commands.

-Stimulation of the FEF shifts attention.

-A criticism of this theory is that attention can also be directed to a low-salience portion of the visual field which can cause eye movements.

-Attention can also be directed at features as well as locations.

-It seems that the FEF plays the main role in stimulus salience, however other cortical areas are also involved in carrying salient signals.

Important info from lecture 3

Two cortical routes = what & where
The two crucial functions are;

Object Perception = Where is it?
  • A lesion to this part of the brain causes optic ataxia, resulting in problems with reaching and grasping things.
Saccades = Rapid eye movements (lasts between 25 & 100 msec)
Fixations = Pauses between saccades where the eye takes in visual information.

Recognition & response are filters of attention - Hearing, seeing & touching can aid attention.

Attention impairments

Agnosia = Unattended stimuli is not available to conscious awareness.

Agnosias: Impairments of recognition
It's the inability to recognize basic objects, this is caused by brain damage.

Object agnosia

Patients cannot recognise common objects, yet have no problem in recognizing faces.

  • Some patients have trouble recognizing common objects whilst others have trouble recognizing faces, suggesting that objects & faces may be processed by separate perceptual mechanisms/brain areas.
Prosopagnosia ('face blindness')
  • Although patients have basic recognition they cannot recognise faces.
  • With object agnosia- visual acuity is spared.
  • Because patients with prosopagnosia have difficulty recognising faces they often rely on other factors such as hair, voice or other peripheral cues.
  • In an experiment using an FMRI machine, it showed that when patients viewed pictures of objects their PPA became more active and when viewing faces their FFA became more active, showing that faces and objects use different parts of the brain.

Wednesday, 5 October 2011

Week 2 - How do we study our brain and it's cognitive functions?

Article for lecture two

In this article it is pointed out that neurological disorders cannot solely be explained by just medical neurology alone.
Mental Illness is generally approached by (a) chemical imbalances and changes in transmitters & receptors in the brain which is corrected by drugs, which has been very successful. And (b) The Freudian approach which suggests that mental illness is because of your up-bringing. A third approach has been proposed in this article which is evolutionary neuro-psychiatry, it explains why symptoms are different for different types of mental illness.
Hysteria is a medical term for paralysis in a part of the body, but when neurologically tested there is no evidence of deficits or lesions in the brain. Therefore this condition is often described as psychological. However PET & FMRI scans now show us what parts of the brain are active or inactive, so therefore shows when a patient makes a specific action or mental process. The parts of the brain that are active will light up when an action is performed.
An action such as wiggling a finger lights up two parts of the brain; the motor cortex which sends messages to execute the action and the pre-frontal cortex that prepares your finger to move. For a patient with hysteria the pre-motor area lights up which shows they are pre-paring to do the action however the anterior cingular and ventromedial frontal lobes (parts of the frontal cortex) show up which are inhibiting the attempt of moving the arm. This latter part of the brain mentioned that lights up are linked to the emotional centres of the brain which makes sense because hysteria is caused by an emotional trauma. This highlights the causation of hysteria and also the brain malfunctions that may maintain hysteria.

If there is damage to the limbic system and the amygdala this could cause major damage to a person’s emotion. A gut-level emotional reaction to a visual stimulus can be measured by the amount a person sweats. When shown something emotionally important or exciting we sweat more - this can be measured by the Galvanic skin response (involves two electrodes in your skin) The Galvanic skin response can be used to assess damage connected to the emotional centres of the brain.

Derealisation and Depersonalisation involve the limbic system. It is known as feeling like you are not real or feeling like a zombie. Here it is explained as an evolutionary adaptive mechanism. It is said that in dire emergencies such as soldiers in battle the anterior cingular in the brain becomes extremely active. This inhibits the amygdala and other emotional centres, therefore suppressing emotions and fear. It also makes you really alert for action. It is described as an adaption from evolution because it can keep you out of harm’s way, however chemical imbalances can cause this to happen frequently, therefore causing you to become depersonalised.

Overall an understanding of brain mechanisms helps make sense of different symptoms for different mental illnesses.

This shows that there are many tools we can use to study our brain and its cognitive functions; these include the different scans and tests that highlight brain functioning, and what parts of the brain are responsible for what cognitive functions such as emotion.

Important info from lecture:

Cognitive Psychology = the study of mental processes and is needed for everyday life.
Neuropsychology = focuses on brain structures & processes that cause behaviour - e.g. appetite & emotion.

It is beneficial to study brain damaged patients  because it may help understand the role of that particular brain region, however a criticism of this is that the previous levels of functioning may not be known so it would be hard to make comparisons before and after a brain lesion.

EEG - Electroencephalography

  • Non invasive, easy & cheap to operate, used on healthy humans
  • Not sure what EEG changes signify, mass neuronal activity, weak function localisation.
PET - Positron Emission Tomography
  • It is a gamma ray detector, Measures changes in local blood flow correlated with mental activity (Blood flow is the most reliable measurement)
  • However it is invasive & expensive.
MRI - Magnetic Resonance Imaging
  • Non-invasive, good spatial resolution, participants can still take part in cognitive testing whilst being scanned.
  • Downfalls include claustrophobia and it is reported to be noisy, radio frequencies must be shielded.
FMRI - Functional Magnetic Resonance Imaging
  • Measures blood oxygen level dependent responses (BOLD)
  • This is non-invasive and has good spatial resolution however analysis is complex, this too is claustrophobic and expensive and produces low temporal resolution.