Neuropsychology Short and Essay style questions and answers PDF

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Neuropsychology Short and Essay style questions and answers...

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Neuropsychology Short Questions Provide the key reasons for why we conduct assessments on patients in the field of clinical psychology. 

Determining the nature and location of any deficit.

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Providing information about onset, severity and progression of symptoms.

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Helping to discriminate between neurological and psychiatric symptoms.

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Helping to identify the focus for rehabilitation programmes.

What are the main 5 types of neurological disorder? 

Cerebral Infection

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Traumatic Brain Injury

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Cerebrovascular Accidents

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Brain Tumours

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Degenerative Disorders (Dementia)

What are the main forms of neurological degenerative disease? 

Alzheimer’s Disease

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Vascular Dementia

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Parkinson’s Disease

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Huntington’s Disease

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Multiple Sclerosis

What are the three main intervention approaches and give an example of each. 

Biological Treatments Programmes: Drug treatments, Deep Brain Stimulation, Surgery, Chemotherapy and Radiation Treatment.

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Cognitive Rehabilitation Programmes: Goal-management Training, Self-Instructional Training

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Caregiver Support Programmes: Alzheimer’s Society Advice for Caregivers.....ADD MORE PROGRAMMES AFTER EXTRA READING DONE.

When we ask the ‘main in the street’ what memory is, they would probably see it as a single construct. But it’s not. What different kinds of memory are there? 

Categorised by time: o Short term memory o Long term memory o Delayed memory o Recent memory o Prospective memory

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Categorised by type of information: o Semantic memory o Episodic memory o Prospective memory

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Categorised by the form: o Verbal memory o Visual memory o Olfactory memory o Gustatory memory o Kinaesthetic memory

What are the key features you would expect to see in an Amnesic case? 

Normal STM performance

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Normal general intellectual performance

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Normal procedural memory performance

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Dense anterograde amnesia

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Variable retrograde amnesia

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Near normal performance on measures of implicit memory

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Impaired performance on measures of explicit memory

Damage to which areas of the brain are often associated with amnesia? 

Medial temporal lobe: Hippocampus and adjacent structures.

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Midline diencephalon: Thalamus, mamilliary bodies.

What is confabulation – and why might it happen? 

Disturbance of memory, defined as the production of fabricated, distorted or misinterpreted memories about oneself or the world, without conscious intention to deceive.

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Korsakoff patients – frontal lesion

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Damage to prefrontal memory system.

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Can be provoked.

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Malfunction of interaction between familiarity and recollection, novel items seem familiar resulting in recollective confabulation.

What kinds of interventions could be employed to help someone with amnesia? 

Retraining of impaired function: 'The mental muscle' approach assumes that with sufficient training, underlying brain structures can be preserved or re-organised  neural plasticity.

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Functional adaptation: A ‘behavioural substitution’ approach. Alternative functions can be employed to achieve the same outcome. In other words, cognitive resources are focused on utilising and improving preserved function to substitute for impaired function.

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Compensation: Increasing efficiency of an impaired function. Similar to functional adaptation but focuses on the use of support from more artificial means.

What is semantic dementia? 

Progressive loss of verbal and non-verbal semantic memory.

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Preservation of other cognitive domains, e.g. working memory, non-verbal problem solving, syntax.

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Good orientation and recall of recent events.

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Atrophy to the infero-lateral temporal neocortex (anterior temporal lobes) with relative preservation of the hippocampus early in the disease.

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Impaired comprehension

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Associated deficits: Poor object recognition, abnormal social cognition and emotional regulation.

What are the category specific disorders of semantic memory? Provide a theoretical account of this impairment. 

Comprehension or semantic processing of a particular category of items (e.g. living things) is impaired relative to other categories of items.

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First patients reported with category specific impairments had survived herpes simplex encephalitis and in most cases damage to bilateral temporal, hippocampal and possibly frontal regions.

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Some closed head injury cases.

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Recognition deficit for living objects: Anterior, medial and inferior temporal regions.

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Recognition deficit for non-living: Posterior fontal-parietal regions.

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Sensory-Functional Theory: o Living things favour sensory representations. o Non-living favour functional representations. o Patients who demonstrate poor performance on animal relative to tools or vice versa reflect a specific impairment to either sensory/perceptual or functional semantic knowledge structures.

What is a ‘semantic hub’? 

The idea that there is a brain region where amodal semantic information is processed.

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Refers to the anterior temporal lobe which acts as a semantic hub, combining information from different sensory and motor areas to form amodal semantic representations.

What is a temporal gradient – why is it important in comparative discussions of semantic and episodic memory impairments? 

A trend of retrograde amnesia marked by a greater loss of memory for occurrences from the recent past than for occurrences from long ago.

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Semantic memory loss does follow the predicted temporal pattern??

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Episodic memory does not follow the temporal pattern??

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Patients with semantic dementia show a reverse step function with sparing of recall of events from the most recent 2 to 5 years but impairment on more distant life periods.

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The most plausible account at present is that semantic and episodic memories are dependent on different but interacting systems with different half-lives and which can be separately damaged.

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Earlier reverse temporal gradient and normal temporal gradients might have been contaminated by semantic memory information.

What is the difference between Broca’s aphasia and Wernicke’s aphasia? 

Broca’s is located in the motor speech area (frontal lobe) and it helps in movements required to produce speech, can understand speech but cannot produce speech. o Expressive aphasia (non-fluent aphasia)

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Wernicke’s is located in the sensory area (parietal and temporal lobe), helps understanding speech and using the correct words, may be able to produce speech but cannot understand speech. o Receptive aphasia (fluent aphasia)

How many ‘processing routes’ are there for word repetition? (Conduction aphasia) How many ‘processing routes’ are there for word reading? (Surface vs Phonological dyslexia) What is anomia? How can it be diagnosed? 

A disorder of object naming

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A form of aphasia in which the patient is unable to recall the names of everyday objects

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Fluent, good comprehension, good repetition, poor naming.

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Damage to the angular gyrus and inferior parietal lobe.

Previous exam questions What is confabulation? Provide a short account of how this may occur? 

Disturbance of memory, defined as the production of fabricated, distorted or misinterpreted memories about oneself or the world, without conscious intention to deceive.

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Generally very confident about their recollections, despite contradictory evidence.

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Research suggests that confabulation is associated with dysfunction of cognitive processes that control the retrieval from long-term memory.

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Frontal lobe damage often disrupts this process, as seen with Korsakoff patients (Moscovitch, 1992).

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Researchers also argue that it is a disorder resulting from failed ‘reality monitoring/source monitoring’, i.e. deciding whether a memory is based on an actual event or imagination.

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Two subtypes: o Simple confabulation – Errors in the temporal ordering of real events. Damage to memory systems in the medial temporal lobe.

o Fantastic confabulation – Bizarre and patently impossible statements not rooted in true memory. Reveal a dysfunction of the supervisory system, believed to be a function of the frontal cortex. List the key clinical features of amnesia and provide examples of neuropsychological tests utilised with such cases. 

Normal STM performance



Normal general intellectual performance



Normal procedural memory performance



Near normal performance on measures of implicit memory



Impaired performance on measures of explicit memory.



Dense anterograde amnesia



Variable retrograde amnesia

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Rivermead Behavioural Memory Test (RBMT): Aims to measure the level of practical memory problems patients experience.

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Memory assessment tests: Weschler memory scale, California verbal learning test.

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However, worth noting that memory assessment should always be taken in conjunction with wider neuropsychological assessment as impaired memory testing performance could reflect: impaired language, impaired EFs, impaired attention/concentration, mood or motivational factors.

Describe the condition known as ‘semantic dementia’ – provide a list of key clinical features and examples of relevant neuropsychological assessments. 

Frontal-temporal lobes damage.

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Atrophy to the infero-lateral temporal neocortex (anterior temporal lobes – ATL) with relative preservation of the hippocampus early in the disease.



Progressive loss of verbal and non-verbal semantic memory.



Preservation of other cognitive domains (e.g. working memory, non-verbal problem solving ability).



Good orientation and recall of recent events.

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Production: Fluent but with semantic errors.

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Comprehension: Impaired

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Repetition: Intact

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Associated deficits: Poor object recognition, abnormal social cognition and emotional regulation.

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Executive and Social Cognition Battery including Theory of Mind tests (Mind in the Eyes, Faux Pas), the Hotel Task, Multiple Errands Task-hospital version and the Iowa Gambling Task for complex decision-making for fronto-temporal dementia.

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Memory assessments: Weschler memory scale, California verbal learning test.

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Neuropsychological examination to assess language, behaviour, memory, executive and visual-spatial functions.

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Neuroimaging, e.g. MRI to determine where and how extensively brain regions have atrophied.

What is the condition known as semantic dementia and how is it diagnosed? 

See previous.

What are the key clinical features of Broca’s and Wernicke’s aphasia? 

Broca’s o Severely non-fluent o Production reduce in grammatical complexity. o Poor articulation o Poor melodic line o Poor speech volume o Aetiology: Non-fluent cases  Dorsolateral frontal lesions, focused on dominant hemisphere, region for motor speech representations.

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Wernicke’s o Severe auditory comprehension deficits o Speech output rapid (fluent) but often meaningless o Phonemic (“stool”=”pool”) o Semantic (“stool”=”chair”) o Neologisms (“stool”=”gwool”) o Aetiology: Fluent cases  Superior temporal lesions

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Broca’s is located in the motor speech area (frontal lobe) and it helps in movements required to produce speech, can understand speech but cannot produce speech. o Expressive aphasia (non-fluent aphasia)

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Wernicke’s is located in the sensory area (parietal and temporal lobe), helps understanding speech and using the correct words, may be able to produce speech but cannot understand speech. o Receptive aphasia (fluent aphasia)

What is the difference between retrograde and anterograde amnesia? Provide examples with reference to neuropsychological evidence. 

Retrograde: Loss of access to events that happened in the past, prior to a trauma.

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Anterograde: A deficit encoding, storing or retrieving new events occurring after a trauma. Ability to memorise new things is impaired or lost because data does not transfer successfully from the conscious short-term memory into long-term. o More common o Can be caused by a number of potential factors, e.g. HM case, Korsakoffs syndrome. o HM: Removal of hippocampus to alleviate epilepsy symptoms. o Anterograde amnesia is symptom of KS, thiamine (vitamin B1) deficiency, damage across thalamus, cerebellum and frontal lobe. o Primarily anterograde with KS but could be retrograde.

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Retrograde amnesia there is almost always a gradual restoration of most of the lost information, with anterograde there is quite often no such recovery and patients are left with a permanent condition.

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ADD NEUROPSYCH EVIDENCE?

Describe the key clinical features of Broca’s asphasia, Wernicke’s aphasia and Conduction aphasia. 

Broca’s o Severely non-fluent o Production reduce in grammatical complexity.

o Poor articulation o Poor melodic line o Poor speech volume o Aetiology: Non-fluent cases  Dorsolateral frontal lesions, focused on dominant hemisphere, region for motor speech representations. 

Wernicke’s o Severe auditory comprehension deficits o Speech output rapid (fluent) but often meaningless o Phonemic (“stool”=”pool”) o Semantic (“stool”=”chair”) o Neologisms (“stool”=”gwool”) o Aetiology: Fluent cases  Superior temporal lesions

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Broca’s is located in the motor speech area (frontal lobe) and it helps in movements required to produce speech, can understand speech but cannot produce speech. o Expressive aphasia (non-fluent aphasia)



Wernicke’s is located in the sensory area (parietal and temporal lobe), helps understanding speech and using the correct words, may be able to produce speech but cannot understand speech. o Receptive aphasia (fluent aphasia)

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Conduction o Also called associative aphasia, an acquired language disorder characterised by intact auditory comprehension, fluent speech production but poor speech repetition. o Fluent, good comprehension, poor repetition. o Lesions in the left temporoparietal region. o Damage to dorsal projections, disruption to auditory input-speech output mappings.

Provide a list of the key motivations for why neuropsychologists conduct cognitive assessments of patients. 

Determining the nature and location of any deficits.



Providing information about onset, severity and progression of symptoms.



Helping to discriminate between neurological and psychiatric symptoms



Helping to identify the focus for rehabilitation programmes.

What are the 5 main types of neurological disorder? 

Cerebral infection



TBI



Cerebrovascular accidents



Brain tumours



Degenerative disorders (dementia)

What is semantic dementia – describe the key clinical features of such cases. 

Frontal-temporal lobes damage.



Atrophy to the infero-lateral temporal neocortex (anterior temporal lobes – ATL) with relative preservation of the hippocampus early in the disease.



Progressive loss of verbal and non-verbal semantic memory.



Preservation of other cognitive domains (e.g. working memory, non-verbal problem solving ability).



Good orientation and recall of recent events.



Production: Fluent but with semantic errors.



Comprehension: Impaired



Repetition: Intact



Associated deficits: Poor object recognition, abnormal social cognition and emotional regulation.

What is meant by the term ‘malingering’ and in what ways can it be identified? 

Purposeful production of falsely or grossly exaggerated physical or psychological complaints with the goal of receiving a reward, e.g. attention.

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Assessment of malingering with the M-FAST.

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Computerised assessment of response bias-97

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Symptom validity test.

What is the condition known as Aphasia? Provide examples of all the different classifications of this disorder identifiable by the Boston Diagnostic Aphasia Examination. 

Speech disorder resulting in difficulties producing or comprehending speech.

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Language centres of the left hemisphere (usually Broca’s or Wernicke’s area).

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Damage typically caused by a cerebral vascular accident (stroke), head trauma however are other causes.

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Broca’s aphasia

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Wernicke’s aphasia

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Conduction aphasia

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Anomia

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Global aphasia

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Transcortical motor aphasia: Affects speech production, mapping meaning onto form.

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Transcortical sensory aphasia: Affects speech comprehension, mapping form onto meanings.

Define the terms retrograde and anterograde amnesia? Provide examples of each pattern of impairment with reference to neuropsychological case studies.

Interventions: Treatment and Rehabilitation for Neurological Disorders 

Biological Treatment Programmes

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Cognitive Rehabilitation Programmes

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Caregiver Support Programmes

Rehabilitation Procedures In most cases, neurological damage is permanent, so rehabilitation procedures provide: 

Exercises to improve impaired functions

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Training in the use of cognitive and behavioural aids

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Assistive technology

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Basic drug treatment and psychotherapy to help deal with related mood disorders.

Biological Treatments 

Drug treatments

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...