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Y3 MedEd > Chronic Neuro 1 > Flashcards

Chronic Neuro 1 Flashcards

1
Q

What are the ascending tracts

A

Dorsal columns
Lateral spinothalamic tract
Ventral spinothalamic tract

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2
Q

What are the descending tracts

A

Lateral corticospinal tract

Ventral corticospinal tract

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3
Q

What does the lateral spinothalamic tract relay

A

Pain

Temperature

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4
Q

What do the dorsal columns relay

A

Deep touch
Vibration
Proprioception

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5
Q

What does the ventral spinothalamic tract relay

A

Light touch

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6
Q

What does the ventral corticospinal tract relay

A

Voluntary motor

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7
Q

What does the lateral corticospinal tract relay

A

Main voluntary motor

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8
Q

Generally are the upper limbs motor pathways more lateral or medial

A

Medial

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9
Q

What tract relays deep touch

A

Dorsal column

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10
Q

What tract relays vibration

A

Dorsal column

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11
Q

What tract relays proprioception

A

Dorsal column

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12
Q

What tract relays pain

A

Lateral spinothalamic tract

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13
Q

What tract relays temperature

A

Lateral spinothalamic tract

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14
Q

What tract relays light touch

A

Lateral spinothalamic tract

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15
Q

What tract relays motor signals

A

Lateral and ventral corticospinal

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16
Q

Define MS

A

A chronic inflammatory multifocal, demyelinating disease of the central nervous system of unknown cause, resulting in loss of myelin, and oligodendroglial and axonal pathology

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17
Q

4 main symptoms of MS

A

Optic neuritis
Motor weakness
Sensory disturbances
Fatigue

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18
Q

Other symptoms of MS (14)

A 
Weakness of limbs with spasticity and hyper-reflexia
Paraesthesiae, pain or sensory loss in limbs trunk, face or tongue
Ataxic and spastic gait
Urinary urgency and incontinence
Sexual dysfunction 
Diplopia
Vertigo and nystagmus
Dysarthria
Impairment of concentration or memory
Hemiparesis
Hemi sensory loss
Visual field defect
Seizures
Psychiatric disturbances
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19
Q

What eye symptoms can you see in MS (4)

A

papillitis. Diplopia, nystagmus, internuclear ophthalmoplegia

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20
Q

Where is MS most common

A

In America, Canada and Nordic countries and places with a higher latitude

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21
Q

Which allele is linked to MS

A

HLA DLRB1*15

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22
Q

Explain what happens during an acute relapse of MS

A

There is inflammation in response to myelin basic protein. The inflammation leads to demyelination, which causes delay of the nerve impulse and eventually the neurological symptoms. At first these completely resolve, but as disease progresses can often be left with residual symptoms.

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23
Q

Why are symptoms so variable in MS

A

Because the amount and location of damage to the NS is different in each person with MS

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24
Q

What are the three phenotypes of MS

A

Relapsing remitting
Secondary progressive
Primary progressive

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25
Q

What are the 3 criteria for MS

A

Absence of alternative diagnosis
Dissemination in time
Dissemination in space

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26
Q

What evidence is used to diagnose MS (4)

A

Clinical history and examination
Radiological evidence – MRI
Laboratory evidence – CSF
Electrophysiology – VEPs

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27
Q

What imaging can show DIT and DIS and how can it show DIT

A

MRI GAD contrast
Acute inflammation will light up brighter due to GAD crossing the barrier as inflammation makes it leakier. The BBB is leakier for 2-6 weeks.

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28
Q

What CSF evidence points towards MS

A

Presence of oligoclonal bands solely in the CSF and not plasma

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29
Q

How come there are oligoclonal bands in the CSF in MS

A

B cells release IgG antibodies targeting the myelin, these leak into the CSF producing these oligoclonal bands

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30
Q

Epidemiology MG

A

young adult women (under 40) and older men (over 60)

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31
Q

Common muscles affected by MG

A

Eye and eyelid movement, facial expression, chewing, talking, swallowing

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32
Q

Common symptoms of MG (5)

A 
Ptosis
Diplopia
Dysarthria
Dysphagia
±SOB
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33
Q

Signs in MG (2)

A

Fatigable muscles with Normal reflexes

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34
Q

What is the pathophysiology behind MG

A

antibodies block, alter, or destroy the receptors for acetylcholine at the neuromuscular junction, which prevents the muscle from contracting. In most this is caused by antibodies to the acetylcholine receptor itself

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35
Q

What can antibodies be against in MG (2)

A

AChR

or muscle specific kinase (MuSK)

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36
Q

Things MG is associated with (2)

A

Thymic hyperplasia

Thymoma

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37
Q

Ix for MG (4)

A

Bloods – anti-AChR or anti-MuSK (but can also be seronegative MG)
EMG - demonstrates muscle weakness
CT/MRI

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38
Q

Difference between LEMS and MG (4)

A

Muscles improve after use and also LEMS has autonomic symptoms (dry mouth, constipation, incontinence)

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39
Q

Most common symptom in LEMS

A

Dry mouth due to the autonomic NS dysfunction

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40
Q

Pathophysiology of LEMS

A

There are antibodies for the voltage gated calcium channels that normally when opened lead to ACh exocytosis.
Only after repeated use of the muscle does weakness start to improve, as the incoming stimulus leads to cumulative opening of the few calcium channels not blocked by antibodies, eventually this is enough to release more acetylcholine.

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41
Q

What is LEMS associated with (2)

A

Small cell lung cancer (paraneoplastic syndrome LEMS)

AI disease

42
Q

Ix for LEMS (3)

A

Bloods – anti-VGCC
EMG
CT/MRI

43
Q

Define MND

A

Chronic neurodegenerative condition causing muscle wasting, paralysis and death

44
Q

Epidemiology of MND

A

More common in men

45
Q

What are the ‘bulbar signs’ in MND

A

Impaired swallowing and speech

46
Q

What is spared in MND

A

Oculomotor, sensory and autonomic function

47
Q

Is weakness seen in UMN, LMN or both

48
Q

Is atrophy in UMN, LMN or both

49
Q

How are reflexes affected in UMN and LMN

A

Increased in UMN

Decreased in LMN

50
Q

Are fasciculations seen in UMN, LMN or both

51
Q

How is tone affected in UMN and LMN

A

Increased in UMN

Decreased in LMN

52
Q

Is extensor response seen in UMN, LMN or both

A

UMN present

Absent in LMN

53
Q 
UMN:
Weakness
Atrophy
Reflexes
Fasciculations
Tone
Extensor response
A 
Weakness: yes
Atrophy: no
Reflexes: increased
Fasciculations: no
Tone: increased
Extensor response: present
54
Q 
LMN:
Weakness
Atrophy
Reflexes
Fasciculations
Tone
Extensor response
A 
Weakness: yes
Atrophy: yes
Reflexes: decreased
Fasciculations: yes
Tone: decreased
Extensor response: absent
55
Q

Does MND have UMN or LMN signs

56
Q

Signs of MND (to help differentiate from UMN conditions like stroke)

A

Wasting of thenar eminences and bulbar muscles of tongues

57
Q

What does bulbar mean

A

Related to the medulla oblongata

58
Q

What is the current theory behind MND

A

Over ubiquination (marking for degradation by the proteasome) of the proteins in the motor nerve fibre

59
Q

Which tract degenerates in MND

A

Lateral corticospinal tract

60
Q

Ix for MND and results (excluding bloods 4)

A

EMG - shows fasciculations and fibrillations
Nerve conduction studies - normal motor and sensory conduction
CT/MRI of brain and spinal cord
Blood tests
Muscle biopsy to exclude myopathic conditions

61
Q

What blood tests do we do for MND (7)

A 
Vitamin B12
Folate
HIV serology
Lyme disease serology 
Creatine kinase assay
Serum protein electrophoresis
Anti-GM1 (GBS)
62
Q

Progressive muscular atrophy:
Motor nerve affected
Presentation (2)

A

LMN only

LMN signs only (e.g. flail arm, flail foot syndrome)

63
Q

Progressive bulbar palsy:
Motor nerve affected
Presentation (3)

A

LMN lesion of CN IX-XII
Tongue: Flaccid, fasciculation of tongue
Jaw: Absent jaw-jerk
Voice: Nasal ‘Donald Duck’ voice

64
Q

Pseudobulbar palsy:
Motor nerve affected
Presentation

A

UMN lesion of cranial nerves IX-XII (9-12)
Tongue: Slow movements
Jaw: ↑jaw-jerk
Voice: ‘Hot potato’ speech

65
Q

Primary lateral sclerosis:
What happens in it
Motor nerve affected
Presentation (2)

A

Loss of Betz cells in motor cortex
= mainly UMN

UMN pattern of weakness
Brisk reflexes
Extensor planter response
No LMN signs

66
Q

What is the classic triad of Parkinson’s

A

Bradykinesia
Rigidity
Rest tremor

67
Q

6M’s of Parkinsons

A 
Monotonous, hypotonic speech
Micrographia
HypomiMesis (expressionless face)
March a petit pas
Misery → depression 
Memory loss → dementia
68
Q

4 big signs of Parkinsons

A

Shuffling gait
Cogwheel rigidity
Hypomimia
Postural instability

69
Q

What can cause Parkinsonism (give examples)

A 
PD
Drug induced (drugs that lower dopamine levels like antipsychotics or antiemetics)
Atypical Parkinsons (Vascular Parkinson's (due to multiple small stroke like infarcts in the striatum area)
70
Q

Which neurons die first in Parkinsons

A

Nigrostriatal pathway (nigra to striatum)

71
Q

Death of which area of neurons leads to the cognitive impairment seen in Parkinson’s

A

mesolimbic and mesocortical pathways

72
Q

Why do neurons die in Parkinson’s

A

alpha synuclein – misfolds and begins to accumulate in cells. Eventually cells lose there ability to degrade such protein and so they end up packed away inside the cell to minimise damage. These packages are called Lewy Bodies and Lewy Neurites (Lewy discovered them).

73
Q

What is a Lewy Body seen in

A

Parkinson’s

74
Q

RF of Parkinson’s

A

Living in the countryside
Males
Ageing
FHx

75
Q

What are the atypical Parkinsons

A

Progressive supranuclear palsy (PSP)
Multiple system atrophy (MSA)
Corticobasal degeneration (CBD)

Vascular Parkinson’s
Lewy Body Dementia (LBD)

76
Q

What are the features of MSA (3)

A

Early autonomic and cerebellar features

Papp-Lantos bodies

77
Q

What are the features of PSP (2)

A

Early postural instability and vertical gaze palsy

78
Q

What is a Papp-Lantos body

A

Alpha-synuclein in oligodendrocytes seen in MSA

79
Q

What are Papp-Lantos bodies seen in

A

Oligodendrocytes in MSA

80
Q

Early postural instability and vertical gaze palsy are features of…

A

Progressive supra nuclear palsy

81
Q

Early autonomic and cerebellar features

Papp-Lantos bodies are features of…

A

Multiple system atrophy

82
Q

What is seen in corticobasal degeneration

A

Alien limb phenomenon

83
Q

What is degenerated in corticobasal degeneration (3)

A

cerebral cortex (fronto-parietal atrophy), deep cerebellar nuclei and substantia nigra

84
Q

Alien limb phenomenon occurs in what

A

Corticobasal degeneration

85
Q

What are features of vascular dementia (2)

A

Legs particularly affected
Gait worse than tremor
Likely to have stroke RF

86
Q

In what form of Parkinson’s is:

Legs particularly affected
Gait worse than tremor

A

Vascular Parkinsons

87
Q

Symptoms of Lewy Body dementia (6)

A

Amnestic, language deficits

Visuospatial Dysfunction

Hallucinations

Fluctuations

Aggression/Anxiety

Dementia onset same time as motor symptoms

88
Q

In what do you see:

Early dementia + visual hallucinations

A

Lewy body dementia

89
Q

Symptoms of Parkinsons disease dementia (6)

A

Amnestic, language deficits

Visuospatial Dysfunction

Hallucinations

Fluctuations

Aggression/Anxiety

LATER ONSET

90
Q

What is the difference between Lewy body dementia and PDD

A

Dementia develops a while after motor symptoms in PDD

LBD motor symptoms occur 1 year before or even after onset of dementia

91
Q

What form of gait is seen in Wernicke’s encephalopathy patients

92
Q

What form of gait is seen in stroke patients

A

Hemiplegic

93
Q

What form of gait is seen in cerebral palsy patients

94
Q

What form of gait is seen in Huntingtons patients

A

Choreiform

95
Q

What disease has an ataxic gait

A

Wernicke’s

96
Q

What disease has a hemiplegic gait

97
Q

What disease has a scissor gait

A

Cerebral palsy

98
Q

What disease has a choreiform gait

A

Huntington

99
Q

Where does an ataxic gait suggest damage to

A

Cerebellum

100
Q

What type of gait is a cerebellar sign

Y3 MedEd (34 decks)

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