lecture 6 - cognitive neuropsychology

Question 1

Study of functional deficits after acquired brain injury

Answer 1

• Brain injury due to stroke, infection, closed head injury, etc.
• Brain disease due to neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease etc
• Single case studies (or small groups)
• Generalisable?
• Difficulties knowing exact location and extent of damage?
  
  • Brain imaging with magnetic resonance imaging
• Impairments after damage doesn’t necessarily mean that the damaged region is the ‘locus’ of the function
• What precise function/process is being measured (e.g., a function isn’t the same as a task)
  An issue for all psychology – not just neuropsychology

Question 2

neuropsychology - cognitive neuroscience

Answer 2

• Study of the loss of cognitive functions after brain injury or disease
• To find out which regions of the brain are specialised for what functions “Localisation of cognition”
• To find out how cognitive functions are organised
• Modern neuroscience: All functions are mediated by networks of brain regions
  Impairments after damage doesn’t necessarily mean that the damaged region is the ‘locus’ of the function could be due to disconnection

Question 3

previous topic

Answer 3

• Attention and distraction -> 1. Neglect
• Learning and memory -> 2. Amnestic syndrome
• Speech and language -> 3. Aphasia
  Concepts and categories (aka semantic memory) -> 4. Semantic Dementia

Question 4

1 - impairments of attention

Answer 4

• Unilateral neglect - defects one size and usually arises due to a stroke
  
  • Patients don’t seem to notice (be able to attend to) information contralateral to the injury
    ○ Cancellation test
    ○ Copying test
• Hemispatial neglect syndrome - after stroke or in alzcheimers -representation issues on one side - either goes after a few weeks or long term. they are not aware they are missing something as imagination space is not on that side
• RE attention lecture: unable to move the ‘spotlight’ of attention to certain regions in order to process the information there.
• RE spatial cueing in Posner paradigm – unable to use cue that directs attention (not eyes) to one or other side of fixation leading to enhanced processing in congruent trials
  Looks as if people are unable to attend to a region of space, but it’s not space per se, but the region of individual objects, regardless of where in ‘space’ they are - neglect also effects internal representation

hemianopia - damage in occipital lobe and can’t see in LVF and are aware they can’t see it and move their heads

Question 5

Unilateral neglect

Answer 5

• Patients don’t seem to notice (be able to attend to) information contralateral to the injury
  ○ Cancellation test
  ○ Copying test
  
  • Do we attend to locations or to objects?
  • No explicit knowledge, but evidence that neglected information is processed
    ○ E.g., priming
    Contrast between explicit and implicit tests of processing. Explicit – explicitly tell P to attend to/act upon (cross out/copy) stimulus, P does it deliberately (explicitly). Implicit test – doesn’t explicitly require P to attend to/act upon stimulus as required in the explicit form. Whether or not information is processed isn’t judged by whether P can deliberately process it according to instructions. Processing revealed by indirect/implicit measure (re all other examples in attention, meory etc of explicit/implicit distinction

Question 6

‘representational’ neglect

Answer 6

Patient PS was asked to imaging standing on Piazza in front of dome and to describe
Scene -> reveals neglect of imagined information; when asked to turn around revealed
Neglect of imaged information on the other side -> attention to ”internal” information - described everything on right side and left out left side
As attention to “external” world
Bisiach, E. & Luzzati, C. (1978). Unilateral neglect of representational space. Cortex, 14, 129-133
* Neglect even when attending to ‘internal’ scenes. Ps required to imagine standing at one end (e.g., on steps of Duomo) of the Piazza and describe what they see – reveals neglect of info (buildings, shops, statues etc) on one side. Then imagine standing at the other end – now they describe the neglected info from the previous perspective and fail to describe the info they can describe when adopting the original perspective.
What does impaired attention tell us about unimpaired – role of objects, attention to ‘internal’ information similar to attention to external

damage to right side inferior parietal lobe causes the most severe problems

Question 7

memory impairments

Answer 7

anterograde and retrograde amnesia
diagram in notes

Question 8

organic amnestic syndrome

Answer 8

• Disorientation in time
• Profound anterograde amnesia
  
  • Loss of recent memory
  • Impairment in recall and recognition
• Retrograde amnesia to certain degree
• Intact IQ
• Preserved implicit memory/ procedural learning - skills
• Supposedly, anterograde amnesia – not being able to form ‘new memories’, but…
  RE importance of kind of test – whether something ‘leaves a trace’ depends on how we test if (RE different tests discussed in L&M lecture – recall, cued, recall, recognition). Plus implicit/explicit distinction again – if amnesic previously saw ‘rubble’ on a list, more likely to complete stem with that – vice versa if they saw ‘rubber’ previously. Evidence that the information has been learned/stored, even though there’s no conscious awareness that it has been.

Question 9

famous case HM

Answer 9

H.M. (died 3/12/08) Bilateral surgery 1953 aged 27 (first minor seizure at 10), medial temporal resections for epilepsy

HM important as (Corkin 2002)
1) Selectivity of memory loss – IQ spared – memory and language dissociable as comprehension spared
2) Short term memory spared, e.g., digit span, ability to hold a conversation
3) Sparing of skill learning – procedural memory – and sparing of most priming tasks
4) Directed attention to the importance of the hippocampus, but his pathology was not selective
5) Some debate about how much of his childhood memories remained intact, i.e., sparing of already stored memories – clearly some but unsure how much – seem to lack detail
Most studied amnesic – will remain unique for that reason alone

Question 10

case of Clive wearing

Answer 10

• English musician/musicologist
• In 1985 had brain infection due to herpes simplex encephalitis
• Herpes virus destroyed hippocampus and parts of frontal lobes
• This resulted in a dense amnestic syndrome with memory only lasting for a few seconds
• 8:31 AM: Now I am really, completely awake.
  9:06 AM: Now I am perfectly, overwhelmingly awake.
  9:34 AM: Now I am superlatively, actually awake.
• Supposedly, anterograde amnesia – not being able to form ‘new memories’, but…
  RE importance of kind of test – whether something ‘leaves a trace’ depends on how we test if (RE different tests discussed in L&M lecture – recall, cued, recall, recognition). Plus implicit/explicit distinction again – if amnesic previously saw ‘rubble’ on a list, more likely to complete stem with that – vice versa if they saw ‘rubber’ previously. Evidence that the information has been learned/stored, even though there’s no conscious awareness that it has been.

Question 11

Amnesia is not the same as not being able to learn new things - dissociation between explicit and implicit

Answer 11

• Incidental learning of 6-letter words
• Explicit test
  
  • Recall as many of the words as possible
  • Requires reference to previous learning event
• Implicit test
  
  • word stem completion
    ○ Say first word that comes to mind in response to first 3 letter
    □ E.g., RUB— (RUBBER/RUBBLE)
    Doesn’t require reference to past event but people with anterograde amnesia still show influence of previous words.

Question 12

3 - impairments of speech and language

Answer 12

• Broca’s aphasia - production
  Wernicke’s aphasia - comprehension

brain diagram in notes

Question 13

brocas aphasia

Answer 13

• Understands meaning of questions
• Knows what he wants to say
• Able to say individual words (no simple motor
  impairment)
• Great difficulty assembling utterances
• Impoverished speed limited to single words/short
  utterances such as “ don’t know”

Question 14

wernicke’s aphasia

Answer 14

• Very fluent speech production but meaningless
• Problem with understanding?
• Knows meaning of words/objects
  i.e. knows how to use them
• Poor at responding to meaning of spoken words
  Problem with producing meaningful speech

Question 15

Different regions seem to play different role in different aspects of a function

Answer 15

complexity of language/speech (as for any cognitive function) – fallacy of talking about the ‘speech centre’ or the ‘memory’ centre or any other broad ‘centre’ i.e., need to think carefully about what specific processes need to be accomplished in order to carry any task

Question 16

4 - impairments on conceptual processing

Answer 16

• Superordinate concepts less susceptible than ‘basic’ level concepts
  
  • e.g., Alzheimer’s patients refer to picture of an apple as ‘fruit’
    ‘Is a cabbage an animal, plant or man-made object?’ versus ‘Is a cabbage brown, grey, or green?’

Question 17

semantic dementia

Answer 17

• Progressive, selective loss of semantic knowledge (meaning) in any modality
• Profound loss of word meanings: evident in comprehension & production (empty speech)
• Inability to recognise objects (agnosia)
  Other cognitive abilities (e.g., episodic memory) and other aspects of language (syntax, phonology, pragmatics) seem to be much better preserved.

Question 18

Everyday effects of semantic difficulties

Answer 18

• DM (surgeon) presented because he couldn’t remember the names of his surgical instruments.
• AM presented with difficulties in naming people and objects.
  
  • Ate defrosting raw salmon for pudding after his lunch
  • Poured orange juice on his pasta and added sugar to his wine
• JL presented with similar difficulties as AM.
  
  • Asked his wife what the stuff was growing on his face everyday
    Frightened by finding a snail in the garden

Question 19

Impairments of conceptual processing

Answer 19

• Category-specific impairments
  
  • E.g., patients unable to name only body parts
  • Impaired knowledge for living things, with unimpaired knowledge of non-living things?
    ○ Different places in the brain for different categories?
    ○ Different types of defining attribute important for different categories?
    □ E.g., physical versus functional attributes
    ○ Different organisation of knowledge for different categories
    E.g., living things might share more features (be more similar to each other) than nonliving things

Question 20

Does losing knowledge of certain categories mean that those categories were stored in the damaged bit of the brain?

Answer 20

Or are there other differences between the impaired and unimpaired categories.
E.g., different kinds of features that are most important to our concepts: Artefacts/non-living things conceived mostly WRT their function attributes (e.g., what is a kettle? It’s for boiling water) versus living things, maybe physical features (what’s a giraffe? Long neck, brown and beige patched fur).
Or, different sizes/shapes of ‘clusters’ (RE exemplar/instance theories) of instances for different kinds of things – e.g., living things might tend to be more similar to each other (more shared features, closer together along dimensions) than artefacts? (dog, cat, cow…)

Question 21

key points

Answer 21

• Loss of function due to brain damage may highlight the various component processes involved in accomplishing functions in the ‘normal’ brain
• Caution needed in interpretation of findings - often there is more than one explanation - brain connectivity, individual differences in the developmental organisation of brain function.
  There’s always more than one interpretation of any finding

selective attention - neglect
episodic memory - amnesia
semantic memory - semantic dementia
language production - broca
language perception - wernicke

but very specific/ localised disorders are rare

Question 22

Methods in psychobiology and neuroscience

Answer 22

Researchers in neuroscience have a variety of techniques and methods they use to study behaviour. They can identify neurons that contain specific chemicals. They can take photographs of particular ions entering neurons when the appropriate ion channels open, as well as images of brain structure and function. They can inactivate individual genes to see what happens to behaviour when they no longer function. They can also witness the activity of the brain as it behaves, or can observe functions related to the behaviour of neurons such as blood flow or oxygen consumption.

Question 23

lesioning

Answer 23

• The earliest research methods in psychobiology – and one that is still the most commonly used – involves correlating an impairment in function with damage to a specific part of the nervous system. The damage can be studied in one of two ways.
  
  • A neuropsychologist may examine the effects of brain damage caused by injury or disease on function (acquired brain injury), such as the effect of damage to the front part of the brain on a person’s ability to create and adhere to plans, for example.
  • The second way involves the investigator producing an experimental brain lesion or ablation, -damage to a particular part of the brain, but only in an animal’s brain. Of course, neurosurgeons do lesion parts of the brain to alleviate some forms of suffering.
  • One recent, successful treatment for the movement disorder Parkinson’s disease, for example, has involved lesioning a small structure deep within the brain. A similar technique ‘lesions’ in another way (the procedure is called deep brain stimulation, DBS).
  • In Parkinson’s disease, a person may behave rigidly or be unable to walk properly or exhibit tremors or engage in excessive, repetitive, involuntary motor behaviour. Treatment by Levodopa (mentioned earlier) provides some respite but there are off periods when the drug does not work. DBS overstimulates parts of a collection of structures called the basal ganglia, described below. This has been found to be more successful than lesioning the parts directly (Liu et al, 2008). Why lesioning and overstimulation seem to work (i.e. produce the same effect) is still a mystery.
  • One theory is that surgery reduces the inhibitory effects of neurons in the basal ganglia and increases them in another structure, the thalamus and cortex (Liu et al, 2008).
  • When an animal’s brain is experimentally lesioned, the investigator hypothesises that this lesion might have specific consequences; they then study the effects of the lesion on the animal’s behaviour. If particular behaviours are disrupted, then the reasoning suggests, the damaged part of the brain must be involved in those behaviours.
  • Some lesioning techniques are used in both experimental and neurosurgical work. For example, to reach the region to be lesioned, the experimenter or surgeon uses a device called a stereotaxic apparatus to insert a fine wire (called an electrode) into a particular location in the brain. The term ‘stereotaxic’ refers to the ability to manipulate an object in three-dimensional space. The researcher passes an electrical current through the electrode, which produces heat that destroys a small portion of the brain around the tip of the electrode. After a few days, the animal recovers from the operation, and the researcher can assess its behaviour.
  • A stereotaxic apparatus can also be used to insert wires for recording the electrical activity of neurons in particular regions of the brain. But an electrode placed in an animal’s brain can also be used to lead electrical current into the brain as well as out of it. If an electrical connector on the animal’s skull is attached to an electrical stimulator, current can be sent to a portion of the animal’s brain. This current activates neurons located near the tip of the electrode. The experimenter can then see how this artificial stimulation affects the animal’s behaviour
    Neurosurgeons sometimes use stereotaxic apparatus to operate on humans. Neurosurgeons can also insert electrodes into the human brain and record the electrical activity of particular regions to try to find locations that might be responsible for triggering epileptic seizures.

Question 24

Studying brain injury - clinical neuropsychology

Answer 24

• Although we can, under very careful conditions, experimentally lesion the brains of non-humans, we cannot do this in humans, for obvious reasons. We have, therefore, relied on studies of accidental brain injury to help us build a picture of the role of damaged brain regions in specific functional impairments.
  
  • This approach usually utilises the single-case study design. Brain injury usually results from accident or disease and, because it is more difficult to obtain information of this kind, scientists have studied a small number of individuals intensively over a long period of time. The approach allows neuroscientists to observe how localised brain damage can impair intellectual or emotional function.
  • Most human brain lesions are the result of natural causes, such as a stroke. A stroke (also known as a cerebrovascular accident, or CVA) occurs when a blood clot obstructs an artery in the brain or when a blood vessel in the brain bursts open. In the first case, the clot blocks the supply of oxygen and nutrients to a particular region and causes that region to die. In the second case, the blood that accumulates in the brain directly damages neural tissue, partly by exerting pressure on the tissue and partly through its toxic effects on cells. The most common causes of strokes are high blood pressure and high levels of cholesterol in the blood.
    Lesions also occur as a result of injury to the brain by missiles or objects. Approximately 750 in every 100,000 people will experience traumatic brain injury annually (Anderson et al, 2011). Young men and boys are at a higher risk of brain injury than are girls and young women: 1.4 times higher in the under 10s and 2.2 times higher in those between 10 and 20 years old (Thurman, 2016). The most common cause of injury in the under 5s is falls; in the over 15s, it is motor vehicle accidents (Thurman, 2016).

Question 25

The consequences of brain injury in such patients have given rise to many neuropsychological disorders which have helped shape theories of cognitive function

Answer 25

These disorders include the inability to produce or comprehend speech (aphasia), inability to produce speech (fluent or Broca’s aphasia), inability to comprehend speech, specifically (Wernicke’s aphasia), inability to recognise objects (visual agnosia), inability to follow motor commands (apraxia), reading impairment (acquired dyslexia), inability to recognise familiar faces (prosopagnosia), inability to attend to stimuli in one half of the visual field (spatial neglect) and a lack of awareness of visual objects, among many others (and you will read more about them in later chapters). Other impairments have no specific name but involve an inability to perform a specific function, such as recognising specific emotions in faces and voices; placing events in sequence; planning; learning new material or retrieving old material from memory.
* One of the most famous – if not the most famous – single-case study in neuropsychology is HM. HM underwent surgery for uncontrollable epilepsy in the late 1950s. The surgery involved removal of a part of the brain called the temporal lobe which includes a structure called the hippocampus (this has been implicated in various memory functions). After the surgery and beyond, HM exhibited a form of memory impairment called anterograde amnesia; he was unable to learn new material. The intensive study of HM led to a neurobiological theory of human memory which involved the temporal lobe and the hippocampus, and the study has since been supplemented by other case studies and neuroimaging studies of memory in healthy participants. He is also one of psychology’s most controversial case studies, and you will find out why in Chapter 8.
* There have been arguments for and against the single-case study approach in neuropsychology. One argument against is that damage to a brain region does not necessarily demonstrate that this region is responsible for any function that is disrupted following injury. Other areas connected to the damaged region may be responsible for the specific function but connections to the intact areas from the lesioned area have been disrupted. There is also the need to specify exactly what function is being measured (this is a problem for psychology in general, rather than neuropsychology in particular).
* When we say that a region may be ‘responsible’ for phonological processing, what exactly is meant by phonological processing? Could the region be responsible for some other function which allows phonological processing, rather than being responsible for phonological processing itself?
* There are also obvious methodological and practical problems such as the extent, variability and locus of the lesion – factors that are uncontrollable. There is also great variation in regional brain structure between individuals. Amunts et al (1999), for example, found that the size of Broca’s area varied enormously in a group of 10 individuals: there was a tenfold difference between participants in some cases.
When such brain injury occurs, it is also unlikely to be limited to one specific region or structure; it may extend to more than one and so conclusions drawn about the significance of findings in studies such as these need to be done circumspectly. There are other factors such as sex, personality, handedness, intellectual ability and culture which may need to be taken into account. And it is culture that is the focus of the International Perspectives section.

Question 26

rehabilitation after brain injury

Answer 26

• Rehabilitation is an ‘active process whereby people who are disabled by injury or disease work together with professional staff, relatives and members of the wider community to achieve their optimum physical, psychological, social and vocational well-being’ (McLellan, 1991, p. 785) and programmes have been designed for reading disorders resulting from brain injury (acquired reading disorders) (Patterson, 1994), the inability to produce or understand speech (aphasia) (Berndt and Mitchum, 1995), an inability to attend to or ‘see’ one half of the world (spatial neglect) (Robertson et al, 1993) and memory disorders (Wilson and Powell, 1994; Glisky, 1997). The process of helping functional recovery following brain injury is called neuropsychological rehabilitation.
  
  • A review of the content of treatment in 95 randomised control trials with 4,068 patients found that most rehabilitation programmes were created for language, visuospatial and memory function, and most patients had suffered a stroke (van Heugten et al, 2012). The mean number of hours of treatment provided was 4.1 a week. If traumatic brain injury is mild, cognitive performance can be impaired after three months on tasks testing attention, memory, executive function and information processing, although other studies find no impairment (Anderson et al, 2011; Dean and Sterr, 2013).
  • The mechanism that underpins rehabilitation is thought to be plasticity (Kolb and Gibb, 2013). According to Cramer et al (2011), plasticity is ‘the ability of the nervous system to respond to intrinsic or extrinsic stimuli by recognizing its structure, function and connections’. It reflects the capacity of the brain to be flexibly organised and reorganised during the early years and seems to explain why cognitive development and speech are better able to recover from a brain injury sustained in early childhood than from one sustained during adolescence or adulthood. We know, for example, that when the brain undergoes rehabilitation after injury that the uninjured areas might take over the function of the damaged area, which is why performance is often never as completely proficient as it once was. The brain’s reorganisation helps the person to undertake the impaired function.
  • The most common type of rehabilitation programme is cognitive rehabilitation (Parente and Stapleton, 1997). Here, the patient is encouraged to engage in two types of activity: (1) ‘the reinforcing, strengthening or establishing of previously learned behaviour’, and (2) the establishment of ‘new patterns of cognitive activity or mechanisms to compensate’ for the impairment (Bergqvist and Malec, 1997). It shows consistently successful results in the majority of cases of mild to severe brain injury (Ho and Bennett, 1997).
  • The most common form of impairment following brain injury is memory disorder. Specific problems include deficits in learning new material and in retaining other kinds of information (Wilson and Powell, 1994). Some techniques of rehabilitation used to improve memory include exercises and drills, use of external aids and the use of mnemonic strategies.
    Julia Cogan was a 23-year-old first-class physics graduate who was studying for a PhD in neuroimaging and oncology when she suffered brain injury (Oddy and Cogan, 2005). She made a full physical recovery, but her memory was severely impaired. Her everyday problems were familiar ones; she was unable to remember what she had for breakfast, for example, and relied on the strategies she had developed so that she could lead as normal a life as possible. Like JC, she made extremely good use of her Filofax and, if she could not remember a piece of information, then she could find it quickly in her pad. The pad included extensive notes on people she had met, her travel arrangements, her recipes, and so on. If she was asked how work was going, then she would flick to a page which described her last assignment and her next. Julia is young, well-motivated, intelligent and very well-organised. The evidence suggests that all these characteristics can help recovery following rehabilitation.

Question 27

plasticity in people without brain injury 1

Answer 27

• Some studies have suggested that if the brain is trained – even over a period of hours and minutes – then the training will result in changes in its structure. (Holzel et al, 2011; Tang et al, 2012). The idea is not new in neuroscience. One of the oldest theories of learning suggests that our learning is enhanced if the connections between neurons are strengthened by repeated exposure to stimuli. Repeatedly stimulating the fingertips of monkeys has been found to result in an increase in the part of the somatosensory cortex responsible for the representation of fingers (Jenkins et al, 1990).
  
  • In a well-known experiment, Draganski et al (2004) divided 21 men and 3 women into two groups: juggling-training or no-training. The jugglers were given three months to learn a three-ball cascade. Magnetic resonance imaging (MRI) was used to measure brain structure before the training, when participants could juggle for 60 minutes, and after three months. Between the first and second scan, there was an increase in volume in grey matter on both sides of the middle temporal lobe (a region known as the visual motion area – hMT/V5) and a specific area, the left posterior intraparietal sulcus. This increase correlated with performance: as performance increased so did brain volume. No change was seen in jugglers.
    The study has received limited replication success, even from the same researchers (Boyke et al, 2008; Driemeyer et al, 2008) with results showing increases in area near the right V5. The increases declined after three months if the practice was not sustained.

Question 28

Plasticity in people without brain injury 2

Answer 28

There is evidence in support of the effects of training on brain structure. One study found that training people to undertake a complex finger sequence task across several weeks was associated with increased volume on the primary motor cortex (Karni et al, 1995). White matter volume increases have been seen in people who undertook two months’ worth of working memory training (Takeuchi et al, 2010) and in people being taught balancing skills over six weeks (Taubert et al, 2010). Scholz et al (2009) found that training was associated with grey matter increases and changes in the visual cortex have been found when people spent two hours remembering colour name categories. Studies have found increases in hippocampus volume after three months of foreign language training, learning to spatially navigate, and after 12 months of aerobic exercise (Erickson et al, 2011).

Question 29

Plasticity in people without brain injury 3

Answer 29

• In their review of neuroimaging studies and plasticity in 2013, Lovden et al found that 33 such studies had been published. The mechanism responsible for the structural change, if the change does happen, is unknown but candidate explanations have included: remodelling of existing neurons, neurogenesis (see the section earlier), an increase in glial cells, changes in the spines of dendrites, and changes in axonal buttons (Zatorre et al, 2012; Thomas and Baker, 2013).
  
  • It seems, therefore, as if the overwhelming evidence suggests that experience and training can alter brain structure. Or does it?
  • In their review of the literature, Thomas and Baker (2013) found that the majority of the studies they reviewed contained flaws. Four of 20 studies did not include a control group, for example. Perhaps just as important, because the error was so common, was the failure to include a proper experimental control.
  • Most studies divided participants into a training or control condition but did not have another condition in which participants did something like the experimental group but not exactly the same thing. Groups were not given different tasks so that the specific effect of training could be distinguished from the effect of just undertaking any task.
  • They also note another problem with these studies and that is the experimental group can differ from the control group in another way. Because they are engaged in a task for weeks, these participants may be more invested and, therefore, more motivated than are those who do nothing. Any change could be attributable to this characteristic of the sample, rather than to training. Only three studies they reviewed employed a separate training task condition although those studies showed benefits of the training.
    They conclude that only one study shows effects that are specific to training (Erickson et al, 2011). Erickson (2013) himself has pointed out that there has also been great variation in the lengths of time people spend in training; this has ranged from three days to one year.

Question 30

visuospatial neglect

Answer 30

• Patients with lesions in the right posterior parietal cortex sometimes have difficulty in perceiving objects to their left (Vallar, 1998; Guariglia et al, 2014). Around 50–80 per cent of patients with right hemisphere stroke are unable to attend automatically to any stimuli in left space (Halligan and Marshall, 1994; Guariglia et al, 2014). This is called visuospatial neglect (or unilateral spatial hemineglect) and occurs on the side of the body that is contralateral to the side of the brain damage. It is called neglect because patients cannot, or show an impairment in the ability to, respond to stimuli in the visual field opposite to the area of brain injury.
  
  • Neglect for the left side is more common than right neglect (which would be caused by damage to the left hemisphere). Recent research suggests that a large number of other, subcortical structures may also result in neglect if damaged (Molenberghs et al, 2011). The variety of structures involved may explain why some patients show different types of neglect depending on the medium of impairment – personal, perceptual or representational.
    Patients may ignore visual stimuli in the left visual field; not putting the left arm of a pair of glasses on the ear, or not eating what is on the left side of a plate of food or not reading the left side of a newspaper. Problems in the representational domain involve being unable to describe the left side of stimuli mentally imagined (such as remembering the location of a landmark). For this reason, psychologists administer a battery of tests, rather than one individual test (as this would not measure all types of neglect) (Guariglia et al, 2014). Guariglia et al suggested that differences in tests may explain the variety of degrees of reported neglect.

Question 31

Spatial-neglect patients show a characteristic pattern of behaviour on visuospatial tests.

Answer 31

• Spatial-neglect patients show a characteristic pattern of behaviour on visuospatial tests. For example, if they are required to bisect lines of varying length, they will err to the right. If they are presented with an array of stimuli (such as small lines) and asked to mark off as many as possible, they mark off those on the right-hand side but fail to mark off those on the left. Patients find this even more difficult if there are more target stimuli present (Tan Brink et al, 2020).
  When asked to draw (or mentally imagine a scene), patients fail to draw or report details from the left side of the object or image (Guariglia et al, 1993; Halligan and Marshall, 1994). Sometimes, patients will transfer details from the left to the right-hand side. See Figures 6.34 and 6.35. This is called allesthesia or allochiria (Meador et al, 1991).

Question 32

visuospatial neglect Guariglia et al (2014)

Answer 32

• Guariglia et al (2014) found that in their study of 287 patients with right-sided brain injury, 45 per cent showed evidence of neglect based on standard test battery administration. Line bisection performance correlated with cancellation task, writing and perceptual task performance, but not with personal neglect suggesting, as other data have, that personal neglect might be a variation of – or a different disorder to –perceptual neglect.
  
  • The reasons for spatial neglect are unclear (see Halligan and Marshall, 1994, and Mozer et al, 1997, for a discussion) but there are various methods for reducing the symptoms of the disorder, including optokinetic stimulation (we think our bodies rotate to the right if our field of vision is full and the stimuli move to the left and we try to compensate for this by moving to the left), neck-muscle vibration (stimulating the left neck-muscles making us think that our muscles are extended and moving to the left), caloric stimulation (inserting cold or warm water into the contralesional ear – this stimulates the vestibular nerve, creating movement of the eyeball), and prism adaptation (patients wear prisms that automatically shift attention to the right) (Kerkhoff and Schenk, 2012).
  • A review of these methods used in studies from 1997 to 2012 found that only 12 randomised control trials had been published and that the prism adaptation technique was the most effective (Yang et al, 2013). There are significant effects of the disorder on patients’ lives and on the lives of their caregivers, including lack of independence, problems with looking after themselves, undertaking household chores, walking, reading and using a wheelchair (Bosma et al, 2020).
    Recovery from neglect is variable. One review recently reported that 98/142 of patients showed recovery at six months; their cancellation task performance recovered (Moore et al, 2021). Patients with allocentric neglect recovered more slowly than did patients with egocentric neglect.

Question 33

biological basis of memory

Answer 33

Much of what we know about the biology of human memory has been derived from studies of people who suffer from memory loss – amnesia – or from studies of animals in which amnesia is surgically induced to learn more about the specific brain mechanisms involved in memory (Parkin, 1996). But with the development of neuroimaging techniques, psychologists and neuroscientists have begun to outline the regions of the healthy brain that are active during the various memory processes of encoding, retrieval and working memory. Before reviewing this material, however, we need to go back to the beginning – to learning.

Question 34

Before memory - learning

Answer 34

• Before material can be remembered (and forgotten), it must first be learned. Learning involves three basic processes: the acquisition of material, its consolidation and its retrieval. Retrieval can involve free recall, where the participant is asked to remember previously presented stimuli, unaided by cues (or recognition) where the participant has, for example, to determine which of two stimuli had been previously presented (where one stimulus is a distractor and not experienced before and the other is the stimulus previously seen/heard/etc.).
  
  • During instrumental learning the organism identifies a link between a stimulus and the response. It learns that by making a certain number of behavioural responses or making these responses at certain intervals it will be rewarded (or reinforced; the reward reinforces the behaviour and encourages it to be repeated to achieve the same outcome).
  • In classical conditioning, the organism learns that if two previously unassociated stimuli are paired often enough, then the response normally elicited by the first will also be elicited by the other (although before they were paired it would not have done this).
  • Learning seems to involve a strengthening of connections between neurons. The theory was proposed by Hebb (1949) in his famous book, The Organization of Behaviour. Hebb proposed that each psychologically important event is conceived of as the flow of activity in a neuronal loop. This loop is made up of the interconnections among dendrite, cell body and the synapses on these structures. The synapses in a particular path become functionally connected to form what Hebb called a cell assembly. The assumption he made was that if two neurons are excited together, they become linked functionally. If the synapse between two neurons is repeatedly activated as the postsynaptic neuron fires, then the structure or chemistry of the synapse changes. This change strengthens the connection between neurons.
    Hebb proposed that short-term memory resulted from reverberation of the closed loops of the cell assembly; long-term memory is the more structural, lasting change in synaptic connections. This long-term change in structure is thought to reflect long-term potentiation (LTP), a term which describes the strengthening of neuronal connections via repeated stimulation (Lomo, 1966). Lomo found that if the axonal pathway from the entorhinal cortex to the dendate gyrus was repeatedly, electrically stimulated, then there was a long-term increase in the size of potentials generated by the postsynaptic neurons. LTP, therefore, was produced by the activation of synapses and the depolarisation of postsynaptic neurons. Psychologists agree that long-term memory involves to a varying or undetermined extent or degree more or less permanent changes in the structure of the brain (Fuster, 1995; Horn, 1998). But where and how?

Question 35

Where are long-term memories formed?

Answer 35

• Long-term potentiation seems to predominate in the hippocampus. If the hippocampus is stimulated, long-term physical changes are observed (Bliss and Gardner-Medwin, 1973). The entorhinal cortex provides inputs to the hippocampus. The axons from the entorhinal cortex pass through a part of the subcortex called the perforant path and form synapses with cells in the dendate gyrus, a part of the hippocampal formation.
  
  • The hippocampal formation itself is composed of two distinct structures: Ammon’s horn (often referred to as the hippocampus) and the dendate gyrus. Ammon’s horn comprises the substructures CA1, CA2 and CA3. CA1 is sometimes referred to as ‘Sommer’s sector’. There is also significant hippocampal output to the mammillary body via a tract called the fornix. Damage to each of these structures is sometimes associated with memory loss although the evidence for the involvement of the fornix is mixed (Calabrese et al, 1995).
  • Translating this process into the behaviour seen in classical conditioning, the unconditioned stimulus (the puff of air) makes strong synaptic connections with the neurons which produce the unconditioned response (the blink). Presenting the conditioned stimulus (the tone) alone, generates weak synapses. But pairing the tone with the unconditioned stimulus leads to the conditioned stimulus forming very strong synaptic connections. The more often the pairing is made, the stronger the connection becomes. For this type of classical conditioning to occur, a functioning hippocampus appears to be necessary, and the involvement of the structure would appear to be that of acquiring conscious knowledge of the relationship between the conditioned and unconditioned stimulus.
  • The hippocampus is also involved in learning the relationship between the unconditioned and conditioned stimulus when there is a delay between the presentation of each, a process called trace conditioning (Clark and Squire, 1998).
    The consolidation of memory seems to be time dependent. For example, the initial period and the few hours after the learning of UCS and CS pairings appears to be the moment when memory is consolidated. Therefore, interruption of the process at these times will impede consolidation (Bourtchouladze et al, 1998). The first period of consolidation may be dependent on a different neurotransmitter system to that involved in the second. These are the NMDA and dopaminergic systems, respectively

Question 36

Chemical modulation of long-term potentiation

Answer 36

• The most important excitatory neurotransmitter in the nervous system is glutamic acid or glutamate. One subtype of glutamate, N-methyl-D-aspartate (NMDA), appears to be important for producing long-term potentiation (LTP) (Abel and Lattal, 2001). NMDA receptors are found in the CA1 sector of the hippocampus; blocking activity in NMDA receptors prevents long-term potentiation in CA1 and the dendate gyrus. Blocking activity does not prevent or reverse LTP that has already occurred. The key process is the entry of calcium ions through ion channels, a phenomenon mediated by NMDA receptors.
  
  • When calcium enters an ion channel, changes in the structure of the neuron are produced by an enzyme, called a calcium-dependent enzyme, CDE (Lynch et al, 1988). One CDE is called calpain which breaks down proteins in the spines of dendrites. Without this entry of calcium, LTP does not occur. Weak synapses, resulting from weak activation, do not lead to depolarisation that allows calcium ions to enter ion channels. Strong synapses that are activated do lead to this depolarisation, suggesting that the NMDA receptor is vital for the process of learning acquisition (Steele and Morris, 1999).
  • However, LTP can occur in other parts of the brain, apart from the hippocampus, and not all forms of LTP involve the NMDA receptors. So, although the hippocampus and the NMDA receptors seem to be prime mechanisms for LTP, they may not be the only ones.
  • There are structures such as the amygdala, for example, that are involved in the conditioning of fear. Temporarily inactivating part of the amygdala, for example, can impair an organism’s ability to learn to fear whereas inactivating the same area after conditioning has taken place still results in a fear response in the organism (Wilensky et al, 1999). This finding suggests that this part of the amygdala may be involved in the acquisition, but not consolidation, of memory.
  • One of the most important findings in the physiology of memory in recent decades has been that the hippocampal formation is essential for the formation or learning of new memories, but it may not be involved in the long-term retention or retrieval of memory (Shors, 2004). What is unclear is why this dissociation should be.
  • Lee et al (2004) have discovered that a type of gene, called Zif268, is needed for the reconsolidation of context-dependent fear memory but another factor (called brain-derived neurotrophic factor or BDNF) is needed for initial consolidation. This shows how different physiological processes are involved in different aspects of memory formation: one type of factor is needed for immediate consolidation (but not reconsolidation) and another is involved in reconsolidation (but not immediate consolidation).
  • The retrieval of fear memory also appears to recruit Zif268 but in another region of the brain – the anterior cingulate cortex (ACC) (Frankland et al, 2004). Frankland et al found that remote memory for fear was associated with anterior cingulate involvement in mice. Both the studies report changes in the brain during fear conditioning.
    Studies of memory in animals have now associated around 47 specific genes with good memory performance. In research with human participants, genetic clusters were examined in participants who learned a series of semantically unrelated words for immediate free recall and then completed an unexpected delayed free-recall test five minutes later (de Quervain and Papassotiropoulos, 2006). The genes that encoded a certain protein (ADCY8), and five others, were related to better memory performance and with greater activation in those brain regions involved in autobiographical memory and delayed recall (areas described below).

Question 37

amnesia

Answer 37

• Damage to particular parts of the brain can permanently impair the ability to form new long-term memories while leaving language and perception intact. The inability to form new memories is called anterograde amnesia.
  
  • The impairment in the ability to retrieve memories from before the brain injury is called retrograde amnesia. The brain damage can be caused by the effects of long-term alcoholism, severe malnutrition, stroke, head trauma or surgery.
  • In general, people with anterograde amnesia can still remember events that occurred prior to the damage. They can talk about things that happened before the onset of their amnesia, but they cannot remember what has happened since. They never learn the names of people they subsequently meet, even if they see them daily for years.
    Amnesia is not an all-or-nothing phenomenon, however. Severe amnesia, for example, can leave facial familiarity recognition, the acquisition of school knowledge or knowledge of the meaning of words intact. The fact that amnesic patients can remember facts and describe experiences that occurred before the brain injury indicates that their ability to recall explicit memories acquired earlier is not severely disrupted. Of those parts of the brain necessary for establishing new explicit memories, the most important part seems to be the hippocampus, a structure located deep within the temporal lobe, and which forms part of the limbic system.

Question 38

role of the hippocampus in memory 1

Answer 38

• The hippocampus, like many structures of the brain, is not fully mature at birth. In fact, it is not until a child is 2–3 years old that most of these structures are fully developed. As a result, many cognitive activities, such as the formation of semantic memories, are not particularly well developed until this age (Liston and Kagan, 2002). One reason that few people remember events that occurred during infancy may be the immaturity of the hippocampus.
  
  • The hippocampus receives information from all association areas of the brain and sends information back to them. In addition, the hippocampus has two-way connections with many regions in the interior of the cerebral hemispheres. Thus, the hippocampal formation is in a position to ‘know’ – and to influence – what is going on in the rest of the brain (Gluck and Myers, 1995). Presumably, it uses this information to influence the establishment of explicit long-term memories.
  • The structure appears to be very important for navigating or exploring our way around a spatial environment or in forming representations of the locations of objects (O’Keefe and Nadel, 1978). Morris et al (1982), for example, placed rats in a pool of milky water that contained a platform just underneath the water. In order to avoid swimming constantly, the rats had to find the platform hidden beneath the milky water.
  • Eventually, through trial and error, the rats would find the platform. Then, the researchers performed a series of experimental ablations. One group of rats received lesions to the hippocampus, another received lesions to the cerebral cortex and another received no lesion. When the rats were then allowed into the pool, the pattern of behaviour seen in was observed.
  • Notice how those rats with the hippocampus lesion had extremely poor navigation compared with the cortex lesion and control group. Similarly, when rats had learned that there was a platform under water and were then allowed to explore the water with the platform removed, those with an intact hippocampus would spend longer in the part of the pool where the platform had been previously positioned. Those rats with hippocampal lesions, however, did not engage in this ‘dwell time’ in the quadrant where the platform once was (Gerlai, 2001). This suggests an important role for the hippocampus in spatial learning.
  • Both rodents and primates show deficits in what has been called spatial memory (Redish and Touretzky, 1997). Spatial memory, the ability to encode and retrieve information about locations and routes is, like memory itself, not a unitary function. Kessels et al (2001), for example, noted that there is a difference between memory for routes and paths and the knowledge of spatial layouts which enables a person to find an object or a location.
  • The role of the hippocampus in aspects of spatial memory has been well documented in animals, but O’Keefe and Nadel’s view (1978) of hippocampal function has not gone unchallenged.
    Olton et al (1979), for example, argued that the hippocampus was not exclusively responsible for spatial memory but was more involved in working memory. Tasks used to study spatial memory were, according to the theory, tests of short-term or working memory rather than spatial memory: all required the organism to keep information in mind while they engaged in another behaviour that used such information and this is the feature that was disrupted by damage.

Question 39

role of the hippocampus in memory 2

Answer 39

• Others have argued that rather than being primarily responsible for memory formation, the hippocampus’s role is the perception and construction of scenes (Maguire et al, 2015). Patients with bilateral hippocampal damage, for example, presented with the typical autobiographical memory problems and spatial navigation difficulties but were also poor at perceiving scenes and constructing them in the imagination (Graham et al, 2010). They were not impaired at perceiving or imagining single objects. This is called the scene construction theory of hippocampal function (Hassabis and Maguire, 2007; Maguire and Mullally, 2013). The hippocampus, in this theory, brings together details of a scene to construct a coherent perception.
  
  • The authors based their theory, in part, on the behaviour of people when they recall episodic memories; these memories will normally involve the retrieval of scenes. Squire et al (2010) found that patients with hippocampal damage with spared autobiographical memory also had spared scene construction ability.
  • Kim et al (2015) have argued that the role of the hippocampus is purely mnemonic; patients with bilateral damage can show preserved spatial navigation, scene construction and imagining and boundary extension. They attribute scene perception problems to underlying memory problems and that scene construction may be a function of the parahippocampal gyrus, rather than the hippocampus.
  • Some researchers have also suggested that different parts of the hippocampus may undertake different types of memory and imagination functions; the posterior part is responsible for retrieval of memory whereas the anterior part undertakes the function of re-combining or re-encoding details when people imagine stimuli from memory (Addis and Schacter, 2011).
  • Some research suggests that there are positive and large correlations between spatial navigation ability and hippocampal volume. Woollett & Maguire (2011) found that the posterior hippocampus grey matter volume was larger in taxi drivers who had studied The Knowledge and passed it. Others do not. Why?
    Weisberg & Ekstrom (2021) suggest this could be because these volume increases are only found in individuals who have extreme navigational ability, that the increases depend on the type of navigation ability test administered or that the hippocampus is not involved in navigation ability but that connections between the hippocampus and nearby regions are. Good navigators, they argue, are good because they are good spatial problem solvers and can solve problems flexibly. This is reflected in strengthened connections between the hippocampus and other brain regions and structures (Kong et al, 2017). They also note, as the section on developmental topological disorientation showed, that these individuals who find it almost impossible to navigate real world environments have weaker hippocampus-prefrontal cortex connectivity.

Question 40

Neuropsychology of language and language disorders

Answer 40

Neuropsychology aims to localise not only basic perceptual and sensory functions, such as touching, seeing, recognising objects and so on, but also quite sophisticated cognitive functions. The most extensively studied cognitive function is language, and our knowledge of the neuropsychology of language has come from three sources: studies of individuals with brain injury who show language impairment, individuals who do not develop language adequately, and neuroimaging studies in which activation of the brain in healthy individuals is monitored while they complete language tasks. These sources indicate that the mechanisms involved in perception, comprehension and production of speech are located in different areas of the cerebral cortex.

Question 41

language disorders

Answer 41

Brain damage can result from many factors and can cause a wide variety of impairments in cognitive function. Some of the most pronounced impairments are those related to language. Some language impairments result directly from brain injury, others do not but are likely to be the result of disorganised or abnormal brain activity or structure. The most common language disorders are called the aphasias. The key feature of the aphasias is the loss of language function; the patient is unable to produce or comprehend speech. Another important disorder of language is reading impairment (dyslexia).

Question 42

aphasia

Answer 42

• Around 250,000 people in the UK and a million people in the US suffer from aphasia (Geranmayeh et al, 2014). Aphasia literally means ‘total loss of language function’, although patients with the disorder do not lose all language: they are able to perform some language tasks, for example, depending on the site of the brain injury. Because of this, the term ‘dysphasia’ is sometimes used (dys – means ‘partial loss of’).
  
  • There are different types of aphasia. Two of the most common types are non-fluent (Broca’s) aphasia and receptive (Wernicke’s) aphasia. The areas of the brain which, when damaged, cause these aphasias. Aphasia is not a unitary disorder; it is heterogeneous and often the simple classifications do not capture the full extent of the disorder nor the nature of the language and communication impairment. This is likely to be due to the different brain regions involved.
  • Stroke tends to affect the left hemisphere, which is why its effects are most strongly and debilitatingly seen in language and speech specifically. But does right-hemisphere stroke exist and, if it does, what effects does it have on language function?
  • Right-hemisphere strokes do exist and to answer the second question, Gajardo-Vidal et al (2018) examined the effect of left-hemisphere and right-hemisphere based stroke on language performance in 478 patients (109 of whom had right-hemisphere stroke).They found that the most impaired task after right-hemisphere stroke was an auditory sentence-to-picture matching task; the most impaired function after left damage was spoken picture description. This does not mean that all patients demonstrated these impairments, only that they were the most commonly impaired tasks. For example,13 per cent of right-hemisphere and 54 per cent of left hemisphere stroke patients showed those impairments.
  • The impairment was not a universal deficit. When the 13 per cent was examined in more detail (N = 9), it was found to have more damage to specific parts of the frontal lobe than the group that did not show the auditory deficit (specifically, dorsal parts of the superior longitudinal fasciculus and right inferior frontal sulcus).
    In a final study, they sought to confirm the involvement of these areas in the impaired task in an fMRI study of 25 healthy adults. This study found activation in the right inferior frontal sulcus during the auditory picture matching task used in the stroke study.

Question 43

recovery from damage to speech areas

Answer 43

• When the left hemisphere is injured, does the right hemisphere take over the left’s language function and can this be confirmed using fMRI? One of the accepted hypotheses of recovery after brain injury is that when a function is disrupted, reorganisation within the brain helps the person recover some of that function. It is imperfect – because the brain region was previously uninvolved in the function, it is a ‘silent area’ – but the recovery of speech and language function has been attributable to other cortical areas undertaking the function of the damaged hemisphere. You saw from the two case studies discussed earlier that patients born without a left or a right hemisphere were able to develop, functionally, relatively well. This, of course, is different to having developed both hemispheres and then one is consequently injured.
  
  • Wilson and Schneck (2020) undertook an analysis of the fMRI studies of aphasia and reorganisation following injury and their conclusions suggest that support for this hypothesis is weak. They examined 86 studies and found there were methodological problems – such as confounds and failure to correct for multiple comparisons – throughout the sample. Often, it was unclear from the studies whether individuals could perform the tasks administered. Reaction times and accuracy were rarely matched between aphasic groups and controls.
    The strongest conclusions were that the language areas were less activated in individuals with aphasia than in controls, and that activity in the left-hemisphere language areas and perhaps a temporal area in the right hemisphere is seen in aphasic individuals during language tasks. The evidence for the right hemisphere taking

Question 44

specific language impairment

Answer 44

Some children have difficulties in producing or understanding spoken language, in the absence of known brain injury. The 7 per cent who exhibit this impairment are said to show specific language impairment (SLI) (van der Lely, 2005). There is some overlap between this disorder and autism and dyslexia, but some have argued that children with SLI show non-phonology and phonology impairments, whereas children with dyslexia have intact non-phonological language skills but impaired phonological ability, that is, an inability to categorise sounds and map letters to sounds (Krishnan et al, 2016).
Grammar and phonology are the most affected aspects in SLI but individuals’ intelligence is within the normal range (van der Lely and Marshall, 2010). When a 6-year-old with adequate hearing but SLI is asked to repeat the sentence, ‘Goldilocks ran away from the three bears because she thought they might chase her’, she says, ‘Doedilot when away from berd. Them gonna chate her’ (Bishop, 1997).
Some language impairments, however, seem to occur in the absence of such auditory impairment. These impairments arise from a child’s inability to acquire the rules of language early (Gopnik, 1997). One example of such a language impairment is the inability to produce the past tense. For example, in the following statement,

‘Everyday he walks eight miles. Yesterday he . . . ’

Some children would not be able to supply the past tense for ‘walk’ to complete the second sentence.
These problems are seen in children who have normal auditory acuity and non-verbal and psychosocial skills, and, although they may have other difficulties such as dyslexia and depression, none of these factors has been reliably associated with these specific language impairments.
An early, theoretical interpretation of the deficits in SLI suggested that the deficit was one of procedural memory, rather than in language specifically. That is, these individuals experienced problems with the acquisition of skills required for sequencing more generally, not those specific to language (Ullman and Pierpont, 2005). A meta-analysis of non-linguistic tasks requiring procedural learning found that SLI was associated with impaired performance on these measures, especially if children were young (Lum et al, 2014). Dyslexic children and adults with SLI have difficulty in extracting structures from sequences when learning artificial grammars (Pavlidou and Williams, 2014). These studies suggest that individuals with SLIs have problems in learning regularities in sequences of stimuli which are not necessarily linguistic (Krishnan et al, 2016).
Some have suggested that the deficits seen in SLI may involve two types of grammar processing – basic and extended and that extended grammar is the most seriously affected. Extended grammar involves an awareness of the hierarchy of words in sentences and being able to understand this across whole clauses such as ‘Who did Baloo give the long carrot to at the farm?’ (ven der Lely and Pinker, 2014).
A meta-analysis has found that two regions are implicated in specific learning difficulty: the frontal cortex, including Broca’s area and the equivalent area in the right hemisphere, and the caudate nucleus. Others suggest that regions such as the basal ganglia and striatum are implicated and that there is a reduction in some nuclei of the basal ganglia seen in children with SLI (Krishnan et al, 2016). As Krishnan et al acknowledge, some other studies show the opposite pattern (larger volumes, or no differences in adolescents).