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Sem 1 Year 2 > Movement, language, neuroinflammation and stroke > Flashcards

Movement, language, neuroinflammation and stroke Flashcards

1
Q

What is apraxia?

A

The clinical manifestation of a praxis disorder
Is an inability to perform purposeful movement despite motivation, and preserved overall neurological function

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2
Q

What are the different types of apraxias?

A

Executive apraxias= deficit in sequencing complex movements
Posterior apraxias= deficit in the spatial (spacial) construction of complex movements

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3
Q

What injury is more likely to cause apraxia?

A

More common with left brain injuries

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4
Q

What are the different types of executive apraxia?

A

Speech apraxia (slowing and incoordination of speech), limb kinetic (inability to do fine motor movements)

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5
Q

What are the different types of posterior apraxias?

A

Optic- inability to reach for objects due to visual guidance impairment
Ideomotor- failure to perform a complex motor action
Ideatinional- an inability to conceptionalise an action

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6
Q

What are the 3 systems mainly involved in human movement?

A

The corticospinal tract
Basal ganglia loop
Cerebellar loop

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7
Q

What is the diagram that shows how motor responses are generated through the different loops?

A
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8
Q

What are the things that need to be considered when a patient presents with problems in moving?

A
  • Do they have good sensory inputs- good vision, vestibular function, proprioception
    Planning and praxis centres- can they make a plan, sequence it and orientate it in 3D space
    Disorder of effector systems- e.g. corticospinal tracts
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9
Q

What is the Wernicke-Geschwind model of language production?

A

Broca area= production
Wernicke area= comprehension
Arcuate fasiculus= connects them

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10
Q

Where is Wernickes area located?

A

In the parietal-occipital junction

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11
Q

What can damage to Broca’s area lead to?

A

Expressive aphasia; patients have a problem with speech production and are unable to find the words they are trying to say

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12
Q

What can damage to Wernickes area lead to?

A

Receptive aphasia; patients are unable to understand speech and although they can talk, is nonsence

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13
Q

What can damage to the arcuate fasiculus lead to?

A

Conductive aphasia; can be subtle- patients cannot repeat phases spoken to them

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14
Q

Where is language typically comprehended and generated in the brain?

A

85% of people- left hemisphere

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15
Q

What is fluent aphasia?

A

The patient can speak with or without sensible meaning of words

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16
Q

What is non-fluent aphasia?

A

No speaking, damage to Broca’s areas but also to the frontal lobe or connections to the vocal chords

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17
Q

What are movement disorders?

A

The term movement disorders refers to a group of nervous system (neurological) conditions that cause either increased movements or reduced or slow movements.

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18
Q

What are the two ways that movement disorders present?

A

Hypokinetic (too little movement) or hyperkinetic (too much movement)

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19
Q

What are examples of hypokinetic movement disorders?

A

Akinesia = lack of movement
Hypokinesia = reduced amplitudes of movement
Bradykinesia = slow movement
Rigidity = stiffness or inflexibility of the muscles.

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20
Q

What is muscle tone?

A

Muscle tone is the amount of tension (or resistance to movement) in muscles.

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21
Q

What are patterns to recognise if muscle tone is increased?

A

Spasticity or ‘clasp knife’
Disorders of the extra-pyramidal system
Paratonia/Gegenhalten

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22
Q

What is spasticity or ‘clasp knife’?

A

Muscle movement feels maximally stiff at the beginning and end of range
Problem with corticospinal tract/pyramidal tract
Will see a pyramidal pattern of weakness- big muscles will be relatively well conserved compared to smaller muscles

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23
Q

Why does spasticity occur?

A

Reflex pathways are always primed to contract, but there is usually descending inhibition from the cortex.
If there is a problem, no inhibition

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24
Q

What happens in disorders of extrapyramidal systems?

A

Lead pipe rigidity- leads to increased tone throughout the range of movement of muscle

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25
Q

What is paratonia/gegenhalten?

A

The patient is voluntarily resisting the attempt to examine tone- problem with executive systems; seen in delirium and dementia

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26
Q

What is Parkinson’s disease?

A

A lack of dopamine supply to the striatum in the basal ganglia.
Cells of the substantial Niagara are degenerating because of alpha- synucleinopathy (abnormal accumulation of α-synuclein in neurons and glial cells), no longer release dopamine

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27
Q

What are the motor features of Parkinson’s?

A

Causes bradykinesia, rigidity, tremor, postural instability

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28
Q

What is the role of dopamine in basal ganglia?

A

Dopamine is released from the substantial Niagara, and either inhibits or excites the striatum, causing the indirect or the direct pathway to occur in the basal ganglia. This either reinforces or stops movement

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29
Q

What is the diagram in how the basal ganglia affects the motor cortex?

A
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30
Q

What medication is used to treat Parkinson’s?

A

Replacement of dopamine- Levo-DOPA, when given with DOPA decarboxylase inhibitor, allows it to be converted to dopamine in only the CNS

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31
Q

What are examples of hyperkinetic disorders?

A

Jerky movements e.g tremor, chorea (takes the form of dance) or tics (quick twitches of muscle)
Non-jerky movements e.g. dystonia (uncontrolled muscle movements- spasms), myoclonus (brief twitches) and stereotypies (patterned movements such as head nodding)

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32
Q

What are the different signs of cerebellar damage?

A

V = Vertigo
A = ataxia
N = nystagmus (a rhythmical, repetitive and involuntary movement of the eyes)
I = Intention tremor
S = slurred/staccato speech
H = hypotonia (decreased muscle tone)
D = Dysdiodochokinesis (the inability to perform rapid alternating muscle movements)

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33
Q

What is an intention tremor?

A

A tremor that is worse towards the end of a movement

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34
Q

What are the causes of meningitis?

A
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35
Q

What are the equivalent of phagocytes in the neural system?

A

Glial cells in CNS and macrophages in the PNS

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36
Q

What is Uhthoff’s phenomenon?

A

A transient worsening of neurological symptoms related to a demyelinating disorder such as multiple sclerosis when the body becomes overheated in hot weather, exercise, fever, saunas, or hot tubs.

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37
Q

What can diffuse inflammation in the CNS do to patients?

A

Makes patients confused e.g. delirium (can occur in urinary infections in elderly who have leaky blood brain barriers)

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38
Q

What is Gillian Barre syndrome?

A

A rare disorder in which the immune system attacks the nervous system
Immune system attacks myelin or axon which damages PNS

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39
Q

What are the symptoms of Gullian Barre syndrome?

A

Firstly, symptoms are paresthesias (tingling/numbness) in hands and feet, then muscle weakness, flaccid paralysis and absent reflexes. All appear first in hands and feet.
Sometimes pain in back, shoulder and thighs
Symptoms are symmetrical

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40
Q

When does Gullian barre syndrome often happen?

A

After gastro-intestional or respiratory infections

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41
Q

What is multiple sclerosis?

A

Chronic inflammatory and degenerative disease of the CNS

42
Q

What is multiple sclerosis characterised by?

A

Inflammation, demyelination, a variable extent of demyelination (myelin repair), neuroaxonal injury and atrogliosis

43
Q

How does the incidence of MS change with the equator?

A

Incidence of MS increases further away from the equator (related to sunshine and Vit D during puberty possibly)

44
Q

What age is the peak age of MS in Scotland?

A

30s-40s

45
Q

What environmental risks may lead to MS?

A

Vit D
Smoking
EBV
Obesity

45
Q

What is a trigger of MS?

A

Molecular mimicry- the immune system has to face a virus with antigens similar to those in the CNS, and then can no longer tell the difference between them and host antigens.

46
Q

What are the symptoms of MS?

A
  • Trouble seeing.
  • Sensitivity to heat.
  • Numbness, especially in the feet.
  • Weakness.
  • Fatigue.
  • Difficulty thinking clearly and memory loss
  • Depression.
  • Needing to urinate urgently.
  • Walking (gait) difficulties
  • Spasticity
  • Dizziness
47
Q

What are the different stages of MS?

A
  1. Relapsing-remitting stage
  2. Relapsing with persistent deficits
  3. Progressive
48
Q

What percent of patients do not go through the relapse stage?

A

15%

49
Q

How does disease progression of MS happen for the majority of patients?

A

Majority of patients start with attacks- relapsing and remitting disease. Over time, patients no longer fully recover from these relapses, then progresses to a progressive stage

50
Q

How is MS diagnosed?

A

Need history and examination that show dissemination in space and time (as its a disease that affects different parts of the nervous system at different times)

51
Q

How can you see if different parts of the nervous system are affected at different times in MS?

A

MRI shows different parts
Contrast and lumbar punctures can show different times

52
Q

How does contrast show different time for MS diagnosis?

A

Use contrast- gadolinium, an acute lesion will show leakiness of BBB and the gadolinium will leak into brain and different areas will light up. If some light up and others do not, then you can tell that some are acute and some are longstanding

53
Q

How do lumbar punctures show different time for MS?

A

If there is oliogoclonal bands in the CSF to fulfill that criteria.
Oliogoclonal bands- non-specific antibodies that are picked up in the CSF- generally not there without MS.

54
Q

How may stem cells be used as a cure for MS?

A

Patient has own bone marrow ablated, then replaced with new stem cells- hoping the immune system reboots and stop attacking self cells

55
Q

What is the difference between an ischaemic stroke and TIA?

A

TIAs and ischaemic strokes are both caused by an interruption of blood supply to an area of the brain, however the symptoms of TIA fully resolve within 24 hours (usually a lot less time)

56
Q

What is dysarthria?

A

a motor speech disorder resulting in poor articulation

57
Q

What is dysphasia?

A

a language disorder resulting in difficulties of generating speech (expressive) or comprehension of speech (receptive)

58
Q

What are some associated features of TIA and stroke?

A

Headache, nausea, vomiting, neck stiffness, numbness, tingling, incontinence,

59
Q

What is ataxia?

A

group of disorders that affect co-ordination, balance and speech

60
Q

What are the symptoms of stroke?

A

Weakness, sensory disturbance, visual disturbance, speech disturbance, ataxia, dysphagia and reduced level of consciousness

61
Q

What is dysphagia?

A

Swallowing problems

62
Q

If swallowing is not checked on a patient, what may occur?

A

May lead to aspiration pneumonia and choking

63
Q

What are risk factors of stroke?

A

-Hypertension
-Diabetes
-Previous stroke/TIA
-Smoking
-Excessive alcohol intake
-Combined oral contraceptive pill
-Weight

64
Q

How may ischaemic strokes occur?

A

Can be caused by atheroma or thromboembolism

65
Q

Why is atrial fibrillation a risk factor for stroke?

A

Atrial fibrilalion may cause clots which can turn into emboli and lead to the brain

66
Q

What does FAST stand for?

A

FACE
ARMS
SPEECH
TIME

67
Q

What can damage to the motor area of the right cerebral hemisphere cause?

A

Weakness of the left arm, leg and face

68
Q

What can damage to Broca’s and Wernicke’s areas in a stroke cause?

A

Broca’s= speech problems
Wernicke’s= difficulty in understanding speech, reading and naming objects

69
Q

What must be done to determine the cause of a stroke?

A

A brain CT usually

70
Q

What is a doppler ultrasound?

A

An ultrasound of the carotid arteries in the neck- in stroke can check for patches of atheroma

71
Q

What is the initial treatment for those with ischaemic strokes?

A

300 mg aspirin daily for two weeks- longer term treatment is clopidogrel (anti-platelet medication)

72
Q

What is thromboectomy?

A

Surgery to remove clots

73
Q

What medication may be given to patients with atrial fibrillation to reduce the chance of stroke?

A

Anticoagulant medication such as warfarin, apixaban or rivaroxaban

74
Q

What is CNS infarction?

A

brain, spinal cord or retinal cell death attributable to ischemia based on pathological, imaging or other objective evidence of ischemic injury.

75
Q

What is the global lifetime risk for stroke?

A

For > 25 years, is 25%

76
Q

Where do the internal carotid artery and the vertebral artery lead to?

A

ICA= anterior circulation
VA= posterior circulation

77
Q

What are the non-modifiable risk factors for stroke?

A
  • Age
  • Sex
  • Low birth weight
  • Race/ethnicity
  • Family history
78
Q

What are the labels on the diagram?

A
79
Q

What are the labels on the diagram? (ignore 5,6,13,14)

A
80
Q

Where does the anterior, middle and posterior cerebral arteries supply?

A
81
Q

What are the different classifications of ischaemic strokes?

A

Can have a total or partial anterior circulation stroke- affects the anterior or middle cerebral arteries
Can have a posterior circulation stroke- posterior cerebral artery or vertebral artery
Lacunar- affects small deep perforating arteries

82
Q

What are the signs of an anterior stroke?

A

Ulilateral weakness and/or sensory deficit of the face/arms/legs
Higher cerebral dysfunction

83
Q

What are the signs of a posterior circulation stroke?

A

Vertigo, imbalance, unilateral limb weakness, slurred speech, double vision, headache, nausea, and vomiting

84
Q

What are the signs of a lacunar stroke?

A

Pure motor, or sensory affects

85
Q

What is the initial treatment for ischaemic stroke?

A

300 mg aspirin daily

86
Q

What tests are used in patients presenting with stroke?

A

CT scan

87
Q

What is thrombectomy?

A

Surgical removal of a clot- sometimes offered to patients with a posterior circulation stroke

88
Q

When do you suspect TIA?

A

When the person presents with sudden onset, focal neurological deficit which has completely resolved within 24 hours of onset and cannot be explained by another condition such as hypoglycaemia

89
Q

What are focal deficits that can occur in TIAs?

A
  • Unilateral weakness or sensory loss.
  • Dysphasia.
  • Ataxia, vertigo, or loss of balance.
  • Syncope.
  • Sudden transient loss of vision in one eye (amaurosis fugax), diplopia, or homonymous hemianopia.
  • Cranial nerve defects.
90
Q

What are the clinical features of stroke?

A
  • Confusion, altered state of consciousness and coma
  • Headache
  • Unilateral weakness or paralysis in arm, face or leg
  • Sensory loss
  • Ataxia
  • Dysphasia
  • Specific cranial nerve deficits such as unilateral tongue weakness or Horner’s syndrome
  • Difficulty with fine motor coordination and gait.
91
Q

What is ataxia?

A

Ataxia is a term for a group of disorders that affect co-ordination, balance and speech

92
Q

What are some differential causes of stroke?

A
  • Hypoglycaemia
  • Drug/alcohol toxcity
  • Syncope
  • Vertigo
  • Seizure
  • Migraine with aura
  • MS
  • Trauma
  • Systemic or local infection (sepsis, encephalitis)
93
Q

What is myasthenia gravis?

A

Myasthenia gravis causes muscle weakness that typically has times when it improves and other times when it gets worse.

It often affects the eyes and face first, but usually spreads to other parts of the body over time.

94
Q

What are the symptoms of myasthenia gravis?

A

Droopy eyelids
Double vision
Trouble making facial expressions
Problems chewing and swallowing
Slurred speech
Weak arms, legs or neck

95
Q

What causes myasthenia gravis?

A

Myasthenia gravis is caused by an error in the transmission of nerve impulses to muscles.

96
Q

What can be given during the relapse stage of MS?

A

Immunomodulatory and immunosuppressive therapies.

97
Q

What occurs in the relapse and progressive stage of MS?

A
  • Relapses= driven by focal areas of BBB leakage where the immune system gets in an causes damage to axons and myelin- then is repaired.
  • Progressive stage- more diffuse activation of microglia, also a diffuse loss of nerve cell tissue- neurodegeneration
98
Q

What is risk with using higher efficacy drugs for MS?

A
  • The more we suppress immune system, MS is more under control but there is a bigger risk of opportunistic infection and risk of malignancy.
  • Can still use drugs- escalation or induction then maintenance approach
99
Q

What is the induction and maintenance approach and the escalation approach?

A

Induction then maintenance approach= large dose at beginning then backing off to maintain control.
escalation approach- start with lower treatment then gradually increase- mostly used today

Sem 1 Year 2 (18 decks)

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