Session 9 Flashcards

1
Q

What is the role of the limbic association area?

A

Attaches emotional connotations to our sensory input and consequent behaviour. Rewards appropriate behaviour with pleasure sensations. Closely related with the ability to learn.

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2
Q

What is lateralisation within the brain?

A

Whereby individuals have a dominant and a non-dominant hemisphere.

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3
Q

What is the function of the dominant hemisphere?

A

Language, maths, logic and motor skills.

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4
Q

What is the function of the non-dominant hemisphere?

A

Emotion, music/art, visuospatial and body awareness.

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5
Q

How is language lateralised?

A

Input into the system is via Wernicke’s area of the temporal lobe. This interprets written and spoken words.
Output is via Broca’s area of the frontal lobe, which formulated the language components.

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6
Q

Describe the pathway for speaking a heard word.

A

Primary auditory area to Wernicke’s area, to Broca’s area, to the motor cortex.

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7
Q

Describe the pathway for speaking a written word.

A

Primary visual area to Wernicke’s area, to Broca’s area, to the motor cortex.

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8
Q

What connects Wernicke’s area to Broca’s area?

A

Arcuate Fasciculus.

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9
Q

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

A

Wernicke’s: Disorder of comprehension, hence fluent but unintelligible speech.

Broca’s: Poorly constructed sentenced and disjointed, yet their comprehension is fine.

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10
Q

Name the two types of memory.

A

Declarative and procedural.

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11
Q

What is the difference between the two types of memory?

A

Declarative: naming of objects/recognition of places/remembering events etc. Rapidly learned but also rapidly forgotten.
Procedural: performance of motor skills that are learnt and perfected with practice, e.g. riding a bike.

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12
Q

How do memories form?

A

Via synaptic links between the cortical and sensory areas, amygdala and hippocampus, and the diencephalon, basal forebrain and the pre-frontal cortex.

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13
Q

How can memories be committed from short to long term memory?

A

Via consolidation. E.g. if there’s emotion involved, rehearsal, repetition, association etc.

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14
Q

What is long-term potentiation?

A

Long-lasting enhancement in signal transmission between two neurones that results from stimulating them synchronously. Makes memories stronger by allowing circuits to adapt.

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15
Q

What is the difference between anterograde and retrograde amnesia?

A

Anterograde: cannot form new memories.
Retrograde: cannot remember previous memories.

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16
Q

Give two causes of amnesia.

A

Vascular interruptions, tumours, trauma, infections or vitamin B deficiency.

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17
Q

What is dementia?

A

Progressive decline of cognitive function, usually affecting the whole cortex.

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18
Q

What are the three most common causes of dementia?

A

Alzheimer’s disease, dementia with Lewy bodies and vascular dementia.

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19
Q

Describe Alzheimer’s disease.

A

Exaggerated ageing process with loss of memory, aphasia, apraxia and behavioural changes. Presents with neurofibrillary tangles and senile plaques. Tau protein become hyperphosphorylated. Reduction in neurotransmitters, loss of connection between cells and death of brain tissue.

20
Q

Describe dementia with Lewy bodies.

A

Fluctuation in cognition, especially in attention and alertness. Cortical Lewy bodies are seen at autopsy. Very rapid onset of symptoms.

21
Q

Describe vascular dementia.

A

Caused by multiple infarcts throughout the cortex, causing neuronal death. Memory loss is not so prominent in early stages. Often issues with planning.

22
Q

What investigations are used to diagnose dementia?

A

Confusion screen, urine dip, mental state examination, refer to local memory clinic. , and an MRI of the head.

23
Q

What treatments are available for Alzheimer’s disease?

A
  • ACh esterase inhbitors, e.g. Donepezil.

- NMDA receptor antagonists, e.g. memantine. Used in severe AD.

24
Q

What do they look at during a confusion screen?

A

FBC, UandEs, LFT, CRP, glucose, calcium, thyroid function tests, B12 and folate.

25
Q

What symptoms are seen with early stage Alzheimer’s disease?

A

Mislaying items, forgetting recent events, slow at grasping new ideas, poor judgement.

26
Q

What symptoms are seen with middle stage Alzheimer’s disease?

A

Not recognising people, confused about where they are, wandering, delusions and hallucinations.

27
Q

What symptoms are seen with late stage Alzheimer’s disease?

A

Weak and unstable, difficulty eating and swallowing, weight loss, incontinence, gradual loss of speech.

28
Q

What causes epilepsy?

A

Excessive neuronal activity in the brain.

29
Q

Name three types of generalized epileptic seizures.

A

Tonic-clonic, atonic, myoclonic and absence seizures.

30
Q

What is given if an epileptic seizure lasts over 5 minutes?

A

Buccal midazolam or rectal diazepam.

31
Q

Give three routes that microorganisms can enter the CNS.

A

Direct spread, blood-borne, iatrogenic.

32
Q

What is meningitis?

A

Inflammation of the leptomeninges (pia mater and arachnoid mater). Presents with headache, neck stiffness and a fever.

33
Q

What are the main causes of meningitis?

A

Neonates: E.Coli and L.Monocytogenes.
2-5: H.influenza.
5-30: N.meningitides
Over 30: S.pneumoniae.

34
Q

What is chronic meningitis commonly caused by?

A

Post-primary non-pulmonary mycobacterium tuberculosis.

35
Q

Give two complications of meningitis.

A

Raised ICP, cerebral infarction, cerebral abscesses, subdural empyema and epilepsy.

36
Q

What is encephalitis?

A

Infection of the neural parenchyma, resulting in a headache, fever, confusion, drowsiness or fatigue.

37
Q

What are the main causes of encephalitis?

A

Herpes virus, cytomegalovirus or HIV.

38
Q

What is prion disease?

A

Result of mutated prion proteins, which are normal constituents at neuronal synapses. These then cause conformational post-translational processes, causing aggregation of the PrPs, which causes neuronal death and holes in the grey mater.

39
Q

How can the brain accommodate for raised ICP?

A
  • Spatial (brain atrophy/shrinkage)
  • Reduced blood flow
  • Reduced CSF volume
40
Q

Give two causes of RICP

A

Expanding focal lesions (tumours, haematomas, abscesses), or global increase in brain mass.

41
Q

What will RICP present with?

A

Headache, vomiting, papilloedema.

42
Q

What are the three main types of brain herniation?

A

Subfalcine, tentorial and tonsillar.

43
Q

Describe a subfalcine herniation.

A

Cingulate gyrus pushed under free edge of the falx cerebri. Ischaemia in parts of the parietal and frontal lobes.

44
Q

Describe tentorial herniation.

A

Uncus herniates through the tentorial notch, resulting in damage to CNIII. Also occlusion of the cerebellar arteries. Commonly fatal due to haemorrhage into the brainstem.

45
Q

Describe tonsillar herniation.

A

Cerebellar tonsils are pushed into the foramen magnum, with associated compression of the brainstem. Can result in a coma. Compression of the cerebral peduncles can cause hemiparesis.