Association areas and Dementia Flashcards

1
Q

What are the three main association areas?

A

Parieto-occipital-temporal
Limbic
Pre-frontal

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2
Q

Parieto-occipito-temporal assocaition cortex

A

Includes parietal, occipital and temporal lobes

Interacts with the pimary sensory and motor araes. Lesions cause sensorimotor disorders and cognitive disorders

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3
Q

Limbic association area

A

The limbic system is involved with learning, memory, spacial perception, motivation and emotional processing.

Cortex includes the frontal and temporal lobes. interacts with hippocampus, amygdala, thalamus and hypothalamus

Lesions cause cognitive and affective disorders.

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4
Q

Prefrontal association cortex

A

Includes all frontal areas outside those involved in motor control.

Linked to other association areas.

Involved in higher cognition, reasoning, rationale, motivation and moods.

Lesions cause affective and cognitive disorders

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5
Q

Name 3 disconnection syndromes and their effects

A

Pure word deafness: Lesion between primary auditory cortex and auditory association area. Impaired comprehension of spoken words.

Conduction dysphasia: Lesion of arcuate fasciculus linking Broca’s area to Wernike’s ara. Causes fluent dysphasic speech. Understands written and spoken words but poor repitition.

Pure word blindness: Lesion of the posteror corpus callosum and dominant occipital lobe. Interruption of the connection between the visual cortex and the angular gyrus. Inability to read, name colours or copy writing.

Hemispacial neglect: Lesion to the right parietal lobe causes a loss of visual acuity of the left. Patients only deal with the ipsilateral side of the body.

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6
Q

Cortical regions associated with speech deficits

A

Wernicke’s area: Temporal-parietal region. Involved in formulation of speech. Lesions involving the superior temporal gyrus and surrouding parts of the parietal cortex produce receptive/sensory aphasia. Patients are unable to understand written or spoken language. They may be able to speak but it does not make sense

Broca’s area: Frontal lobe. Involved in motor control of speech. Lesions in the frontal gyrus causes motor/non-fluent aphasia. Patients are unable to express their ideas in spoken words.

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7
Q

Describe the interactions between Broca’s and Wernicke’s areas to repead spoken and written words

A

Repeating spoken word:
Word is perceived and information transferred to the primary auditory cortex. Signal passes though Wernike’s area where information is integrated and processed. Signal then passes through the arcuate fasciculus to Broca’s area where the motor pattern is formed and information is transmitted to te primary motor cortex.

Repeating a writen word:
Visual information reaches the primary visual cortex and passes to Wernike’s area via the angular gyrus. Then via the arcuate fasciculus to Broca’s area for speech.

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8
Q

Name three types of dysphasia

A

Expressive dysphasia: Non-fluent. Due to lesion of Broca’s area. Can understand what is being said but loss of motor control of speech = problems producing written and spoken words in response

Receptive dysphasia: Fluent: Due to lesion in Wernike’s area. Able to produce words but incomprehensible language - random sentences.

Conductive dysphasia: lesion of the arcuate fasciculus that links Wernicke’s and Broca’s areas together. The patient cannot repeat statements or name objects, but is able to perform commands.

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9
Q

Visual agnosia

A

Inability to recognise familiar objects. Lesions in occipital and temporal lobe

Includes:
faces (prosopagnosia)
reading (agnostic alexia)
Colour agnosia
Object agnosia

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10
Q

Forms of long term memory

A

Declarative: Allows conscious recall of facts and knowledge. Episodic - personal experiences. Semantic - facts. Involves the hippocampus and prefrontal cortex

Procedural - Memories that are accessed without conscious control e.g. motor learning, reading. Involves cerebellum

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11
Q

Forms of amnesia

A

Anterograde: loss of memory of events following trauma

Retrograde: loss of events occuring prior to the incident

Useful clinically to determine the extent of damage. The more serious the amnesia, the more serious the underlying damage - particularly retrograde.

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12
Q

Types of neuronal degeneration

A

Wallerian - distal generation of the axon and myelin (normally due to trauma)

Axonal - death of the axon proximal to the cell body. Some regeneration possible. e.g. diabetic nephropathy

Myelin - loss of oligodendrocytes and schwann cells. Affects conduction velocity

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13
Q

Dementia

A

Progressive global deterioration in cognition, behaviour and personality. Sufficient to affect work, social functioning and relationships

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14
Q

Classification of dementia types

A

Cortical: Higher cortical abnormalities, dysphasia, agnosia, apraxia.
can be due to frontotemporal dementia, CJD, alzheimers

Subcortical: Apathetic, forgetful and slow, impaired visuospacial abilities, depression of mood. Can be due to normal pressure hydrocephalus, Parkinson’s, huntinton’s

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15
Q

Histological characteristics of Alzheimers

A

Neurofibrillary tau tangles

beta amyeloid plaques.

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16
Q

Vascular dementia

A

Can be stroke related - step-wise deterioration due to multiple successive events. Multi-infarct or single-infarct

Small vessel dementia (Biswangers disease). Impairment of executive functions.

17
Q

Frontotemproal dementia

A

Focal atrophy of frontal and temporal lobes.

Aftrophy of frontal cortex produce changes in personality, social behaviour and judgement.

Semantic dementia: Atrophy of temporal lobes results in expressive and sensory dysphasia. Reduced vocabulary and memory

Atrophy of the insula produces non-fluent dysphasia.

18
Q

Area of the brain paricularl affected in Alzheimers

A

Hippocampus and basal forebrain

19
Q

Drug treatment in Alzheimers

A

Loss of cholinergic neurones in Alzheimers.

Anti-cholinesterase drugs can improve symptoms.

E.g. tacrine, donepezil, memantine