Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

SA Clinical Neuroscience > S9) Cortical Dysfunction and Dementia > Flashcards

S9) Cortical Dysfunction and Dementia Flashcards

1
Q

What is dementia?

A

Dementia is the progressive decline in higher cortical function leading to a global impairment of memory, intellect and personality which affects the individual’s ability to cope with activities of daily living

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Identify four common causes of dementia

A
  • Alzheimer’s disease
  • Dementia with Lewy bodies
  • Vascular dementia
  • Fronto-temporal dementia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the reversible causes of dementia?

A
  • Depression
  • Trauma
  • Vitamin deficiency
  • Alcohol
  • Thyroid disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Identify a rare cause of dementia

A

Creutzfeldt-Jacob disease – a rare and fatal condition that affects the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does dementia present?

A
  • Memory deficit
  • Behavioural changes
  • Physical changes
  • Language disorder
  • Visuospatial disorder (temporal)
  • Apraxia (temporal)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Explain how dementia presents with a memory deficit

A

Memory deficit – struggle to learn new information, short term memory loss

Hippocampus/temporal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Explain how dementia presents with behavioural changes

A

Behavioural changes – altered personality, disinhibition, labile emotions, wandering

pre frontal cortex atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Explain how dementia presents with physical changes

A

Physical changes – incontinence, reduced oral intake, difficulty swallowing

limbic system (hippocampus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Explain how dementia presents with a language disorder

A

Language disorder – anomic aphasia, difficulty understanding language

primary motor cortex, brooks and wernickers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Explain how dementia presents with a visuospatial disorder

A

Visuospatial disorder – unable to identify visual and spatial relationships between objects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Explain how dementia presents with apraxia

A

Apraxia – difficulty with motor planning resulting in inability to perform learned purposeful movements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What investigations would one request for a patient presenting with dementia?

A
  • Full history + MMSE (collateral from family)
  • Full neurological examination
  • Blood tests – TFTs, Vitamin B12 (reversible causes)
  • CT/MRI head
    Pet Ct
  • Memory Clinic follow
    up
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which method is used to differentiate between delirium and dementia?

A

Confusion assessment method (CAM score)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

A CAM Score of 2/more indicates delirium rather than dementia.

What does the CAM score entail?

A
  • Acute change / fluctuating mental status
  • Altered consciousness – hypo/hyperactive
  • Inattention
  • Disorganised thinking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does a patient with dementia’s brain present on CT scans?

A
  • Transverse CT head showing dilation of ventricles and generalised atrophy
  • NB. features on scan don’t always correlate with clinical picture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Explain how a patient’s brain with dementia presents on an MRI scan

A

Axial and coronal sections of T1 weighted MRI brain showing hippocampal atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe the rate of progression of cognitive decline in the following forms of dementia:

  • Vascular dementia
  • Alzheimer’s disease
  • Lewy-body dementia
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe the macroscopic pathology of Alzheimer’s disease

A
  • Loss of cortical and subcortical white matter causing gyral atrophy with narrow gyri and wide sulci
  • Marked ventricular dilation reflecting loss of white matter

→ hippocampus often affected first

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the microscopic pathology of Alzheimer’s disease

A
  • Amyloid-Beta plaques
  • Neurofibrillary tangles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Outline the mild, moderate and severe stages of Alzheimer’s disease

A
  • Mild: 2-4 years, minor memory loss, difficulty learning and remembering new information, long term memory and reasoning intact
  • Moderate: 2-10 years, withdrawal, confusion, poor judgement, increasing difficulty in self-care, anger, anxiety, frustration
  • Severe: 1-3 years, incapacitated, patients do not recognise people, loss of bodily functional control, violent episodes of aggression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe the pathophysiology of dementia with Lewy bodies

A

Lewy bodies in the cortex and substantia nigra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Identify four clinical features of dementia with Lewy Bodies

A
  • Substantial fluctuations in the degree of cognitive impairment over time
  • Parkinson’s symptoms (repeated falls)
  • Visual hallucinations
  • Frequent falls

(if movement disorders follow after dementia we call it Parkinson’s, if it precedes movement disorder we call it dementia with Lewy bodies)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe the pathology of vascular dementia

A
  • Arteriosclerosis of the blood vessels supplying the brain
  • Diffuse small vessel disease vs infarcts (large vessel disease)
  • Results in decreased/cut off blood supply to specific part of brain

→ can occur in multiple sites In the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Describe the clinical features of vascular dementia

A

Abrupt, step-wise decline in cognitive function related to vascular episode

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe the management of vascular dementia?

A

Assess cardiovascular risk – treat hypertension/high cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Frontotemporal dementias are a diverse group of conditions with similar presentation but different pathologies.

Identify some

A
  • Frontotemporal lobar degeneration (FTLD) with tau pathology
  • Pick’s disease
  • Familial tauopathies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe three clinical features of fronto-temporal dementias

A
  • Alteration of social behaviour and personality: agitation, depression
  • Impaired judgment and insight – gambling, taking off clothes, inappropriate comments
  • Speech output falls eventually to a state of mutism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Outline the holistic approach for managing dementia in terms of:

  • Memory aid
  • Therapies
  • Drugs
  • Social care
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is a seizure?

A

A seizure is a sudden irregular discharge of electrical activity in the brain causing a physical manifestation such as sensory disturbance, unconsciousness or convulsions

30
Q

What are convulsions?

A

Convulsions are uncontrolled shaking movements of the body due to rapid and repeated contraction and relaxation of muscles

31
Q

What is an aura?

A

An aura is a perceptual disturbance experienced by some prior to a seizure e.g. strange light, unpleasant smell, confusing thoughts

32
Q

What is epilepsy?

A

Epilepsy is a neurological disorder marked by sudden recurrent episodes of sensory disturbance, LOC or convulsions, associated with abnormal electrical activity in the brain

33
Q

What is status epilepticus?

A

Status epilepticus are epileptic seizures occurring continuously without recovery of consciousness in between (generalised seizure – medical emergency)

34
Q

How can seizures be classified?

A
35
Q

Partial seizures only occur in part of the brain.

What are the two types of partial seizures and how do they differ?

A
  • Simple – same consciousness
  • Complex — consciousness is impaired
36
Q

Identify two types of partial seizures

A
  • Temporal lobe epilepsy – following seizure with fever or an early injury to the brain
  • Frontal lobe epilepsy
37
Q

Describe the five different types of generalised seizures

A
  • Tonic-clonic – 1st tonic (muscles tense) 2nd clonic (convulsions)
  • Absence – daydreaming
  • Myoclonic – brief shock-like muscle jerks
  • Atonic – ‘without tone’, drop attack
  • Tonic – increased tone
38
Q

What investigations can one request for a patient presenting with epilepsy?

A
  • Clinical history
  • EEG
  • MRI
39
Q

Describe the clinical history one must take before, during and after a seizure

A
  • Before – PMH, FH, triggers, aura, first sign/symptom
  • During – description of seizure, duration, abrupt/gradual end
  • After – post-ictal state, tongue-biting, incontinence, neurological deficit
40
Q

What is the differential diagnosis for a patient seeming to present with epilepsy?

A
  • Vascular: stroke, TIA
  • Infection – abscess, meningitis
  • Trauma – intracerebral haemorrhage
  • Autoimmune – SLE
  • Metabolic – hypoxia, electrolyte imbalance, hypoglycaemia, thyroid dysfunction
  • Iatrogenic – drugs, alcohol withdrawal
  • Neoplastic – Intracerebral mass
41
Q

The EEG is not diagnostic but supports a diagnosis.

Explain when an EEG is used to assess a patient presenting with epilepsy

A
  • In first unprovoked seizure – assess risk of seizure recurrence (unequivocal epileptiform activity on EEG)
  • Standard EEG assessment involves photic stimulation and hyperventilation – patient warned that it may induce a seizure
42
Q

What are the contra-indications for an EEG?

A

Do not use if:

  • Probable syncope (risk of false positive result)
  • Clinical presentation supports diagnosis of non-epileptic event
  • In isolation to make a diagnosis of epilepsy
43
Q

What should be considered if an EEG is unclear?

A
  • Repeated standard EEGs
  • Sleep EEGs (sleep deprivation or melatonin in children/young people)
  • Long-term video or ambulatory EEG
44
Q

What other investigations can one request for a patient presenting with epilepsy?

A

To exclude other suspected causes of seizure:

  • ECG as standard in adults
  • MRI – in all patients with new-onset seizures
45
Q

Outline the initial management for a patient presenting with epilepsy

A
46
Q

What are the restrictions on driving with epilepsy?

A
  • If suffers epilepsy when awake → licence is taken away until 1 year seizure-free
  • If due to medication change → licence is taken away until 6 months seizure-free
  • Seizures whilst asleep or don’t affect driving or consciousness → assessment of case by DVLA
  • If one-off seizure then → licence is taken away until ​6 months seizure-free and assessment by DVLA
47
Q

What is an amyloid precursor protein?

A

→ protein that helps repair damaged neurones

→ periodically replaced and chopped up into smaller soluble parts via enzymes

→ These allow them to be disposed

48
Q

what enzymes break down the amyloid precursor protein

A

alpha and gamma secretase

49
Q

if Beta amylase gets involved in amyloid proteins what happens

A

→ amyloid proteins are broken down into insoluble molecules

they then start to form beta amyloid plaques

these fill space in between neurones and so slow down transmission

50
Q

what pathological functions can plaques do

A

→ cause inflammatory response

→ neuronal death

→ if they deposit around blood vessels they can cause antipathy, weakened blood vessels can bleed

51
Q

what are tau proteins

A

→ They stabilise microtubules within the neuronal cytoskeleton (these mobilise nutrients around the cytoskeleton)

52
Q

how do beta amyloid plaques damage tau proteins

A

→ hyperphosphorylation of tau proteins (picks disease)

→ change shape of tau proteins

→ Tau proteins can’t support cytoskeleton = neuronal death

→ Tau proteins start to tangle = tau tangles

53
Q

what medication removes amyloid plaques

A

aducanumab

54
Q

which neurotransmitter is reduced in alzhimers

A

Ach

it is essential for processing memories and learning

55
Q

types of Alzheimer’s

A
56
Q

what psychotic features does dementia have

A

→ hallucinations

→ delusions (false beliefs)

57
Q

why do people with dementia have insomnia and drowsiness

A

reduced cortical activity

58
Q

what other disease could be giving a similar presentation to dementia

A

o Hypothyroidism
o Hypercalcaemia
o B12 deficiency
o Normal pressure hydrocephalus

 Abnormal gait  Incontinence  Confusion

59
Q

neurones involved With dementia

A

o Cholinergic (treatments target

this)
o Noradrenergic
o Serotonergic
o Those expressing

somatostatin

60
Q

risk factors for vascular dementia

A

Previous stroke / MI etc o Hypertension
o Hypercholesterolaemia
o Diabetes

o Smoking

61
Q

what is the pathology of Lewy body dementia

A

→ misfolding of protein alpha - synuclein

→ Forms spherical intracytoplasmic inclusions

→ Deposits found:

Substantia nigra

T emporal lobe

Frontal lobe

Cingulate gyrus (found just above the

corpus callosum)

62
Q

why should you avoid giving someone with dementia with Lewy bodies antipsycotics

A

Do not give antipsychotics (dopamine antagonists)

as can cause neuroleptic malignant syndrome, a psychiatric emergency

 Fever

 Encephalopathy (confusion)

 Vital signs instability (tachycardia,

tachypnoea (v.sensitive sign), fluctuating

BP)

 Elevated creatine phosphokinase

 Rigidity (caused by dopamine antagonism)

63
Q

what is the second most common type of dementia and their symptoms

A

Fronto-temporal

→ effect younger patients

Behavioural disinhibition
o Inappropriate social behaviour
o Loss of motivation without depression (caused by

damage to anterior cingulate cortex) o Repetitive/ritualistic behaviours
o Non fluent (Broca type) aphasia

have an MI scan you will see either bi-temporal or unilateral atrophy

64
Q

pathology of AIDS dementia complex

A

→ patients with AIDS more likely to live longer due to meds

→ Entry of HIV infected macrophages into the brain is thought to lead to indirect damage to neurones

Clinical features:

o Cognitive impairment

Psychomotor retardation (slow thoughts and

movements, also seen in depression) o Tremor

o Ataxia
o Dysarthria
o Incontinence

65
Q

drugs to treat dementia with

A

Drugs
o Acetylcholinesterase inhibitors (e.g. donepezil,

rivastigmine, galantamine)

Alzheimer’s disease
o NMDA antagonists (e.g. memantine)

 Useful for treating agitation  NMDA antagonist

66
Q

what is delirium

A

→ acute confused state, reversible and an organic cause

→ neuronal damage and inflammation

Rapid onset of confusion

Clouded consciousness (may be drowsy)

Fluctuating course

Maybe transient visual hallucinations

Often exaggerated emotional responses (e.g. aggression)

67
Q

types of delirium

A

→ hypoactive

→ hyperactive

68
Q

describe features of hypoactive delirium

A

Withdrawn

Quiet

Sleepy

Consequently more likely to be missed / confused with

something else

69
Q

describe features of hyperactive delirium

A
  • Restless
  • Agitated
  • Aggressive

 Mood may rapidly fluctuate
 Persecutory delusions (narrative of elusion often not coherent)

 Symptoms worse at start and end of day

Maybe related to changes in endogenous cortisol levels

70
Q

Causes of delirium

A
71
Q

management of people suffering with delirium

A

 Find and treat the underlying cause

 Prognosis

Increases risk of dementia

Associated with mortality

These patients often have lengthy hospital stays and

have a high risk of re-admission

SA Clinical Neuroscience (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions