Chronic Neuro 1 Flashcards
(100 cards)
1
Q
What are the ascending tracts
A
Dorsal columns
Lateral spinothalamic tract
Ventral spinothalamic tract
2
Q
What are the descending tracts
A
Lateral corticospinal tract
Ventral corticospinal tract
3
Q
What does the lateral spinothalamic tract relay
A
Pain
Temperature
4
Q
What do the dorsal columns relay
A
Deep touch
Vibration
Proprioception
5
Q
What does the ventral spinothalamic tract relay
A
Light touch
6
Q
What does the ventral corticospinal tract relay
A
Voluntary motor
7
Q
What does the lateral corticospinal tract relay
A
Main voluntary motor
8
Q
Generally are the upper limbs motor pathways more lateral or medial
A
Medial
9
Q
What tract relays deep touch
A
Dorsal column
10
Q
What tract relays vibration
A
Dorsal column
11
Q
What tract relays proprioception
A
Dorsal column
12
Q
What tract relays pain
A
Lateral spinothalamic tract
13
Q
What tract relays temperature
A
Lateral spinothalamic tract
14
Q
What tract relays light touch
A
Lateral spinothalamic tract
15
Q
What tract relays motor signals
A
Lateral and ventral corticospinal
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
17
Q
4 main symptoms of MS
A
Optic neuritis
Motor weakness
Sensory disturbances
Fatigue
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
19
Q
What eye symptoms can you see in MS (4)
A
papillitis. Diplopia, nystagmus, internuclear ophthalmoplegia
20
Q
Where is MS most common
A
In America, Canada and Nordic countries and places with a higher latitude
21
Q
Which allele is linked to MS
A
HLA DLRB1*15
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.
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
24
Q
What are the three phenotypes of MS
A
Relapsing remitting
Secondary progressive
Primary progressive
25
What are the 3 criteria for MS
Absence of alternative diagnosis
Dissemination in time
Dissemination in space
26
What evidence is used to diagnose MS (4)
Clinical history and examination
Radiological evidence – MRI
Laboratory evidence – CSF
Electrophysiology – VEPs
27
What imaging can show DIT and DIS and how can it show DIT
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.
28
What CSF evidence points towards MS
Presence of oligoclonal bands solely in the CSF and not plasma
29
How come there are oligoclonal bands in the CSF in MS
B cells release IgG antibodies targeting the myelin, these leak into the CSF producing these oligoclonal bands
30
Epidemiology MG
young adult women (under 40) and older men (over 60)
31
Common muscles affected by MG
Eye and eyelid movement, facial expression, chewing, talking, swallowing
32
Common symptoms of MG (5)
```
Ptosis
Diplopia
Dysarthria
Dysphagia
±SOB
```
33
Signs in MG (2)
Fatigable muscles with Normal reflexes
34
What is the pathophysiology behind MG
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
35
What can antibodies be against in MG (2)
AChR
| or muscle specific kinase (MuSK)
36
Things MG is associated with (2)
Thymic hyperplasia
| Thymoma
37
Ix for MG (4)
Bloods – anti-AChR or anti-MuSK (but can also be seronegative MG)
EMG - demonstrates muscle weakness
CT/MRI
38
Difference between LEMS and MG (4)
Muscles improve after use and also LEMS has autonomic symptoms (dry mouth, constipation, incontinence)
39
Most common symptom in LEMS
Dry mouth due to the autonomic NS dysfunction
40
Pathophysiology of LEMS
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.
41
What is LEMS associated with (2)
Small cell lung cancer (paraneoplastic syndrome LEMS)
| AI disease
42
Ix for LEMS (3)
Bloods – anti-VGCC
EMG
CT/MRI
43
Define MND
Chronic neurodegenerative condition causing muscle wasting, paralysis and death
44
Epidemiology of MND
More common in men
45
What are the 'bulbar signs' in MND
Impaired swallowing and speech
46
What is spared in MND
Oculomotor, sensory and autonomic function
47
Is weakness seen in UMN, LMN or both
Both
48
Is atrophy in UMN, LMN or both
LMN
49
How are reflexes affected in UMN and LMN
Increased in UMN
| Decreased in LMN
50
Are fasciculations seen in UMN, LMN or both
Only LMN
51
How is tone affected in UMN and LMN
Increased in UMN
| Decreased in LMN
52
Is extensor response seen in UMN, LMN or both
UMN present
| Absent in LMN
53
```
UMN:
Weakness
Atrophy
Reflexes
Fasciculations
Tone
Extensor response
```
```
Weakness: yes
Atrophy: no
Reflexes: increased
Fasciculations: no
Tone: increased
Extensor response: present
```
54
```
LMN:
Weakness
Atrophy
Reflexes
Fasciculations
Tone
Extensor response
```
```
Weakness: yes
Atrophy: yes
Reflexes: decreased
Fasciculations: yes
Tone: decreased
Extensor response: absent
```
55
Does MND have UMN or LMN signs
Both
56
Signs of MND (to help differentiate from UMN conditions like stroke)
Wasting of thenar eminences and bulbar muscles of tongues
57
What does bulbar mean
Related to the medulla oblongata
58
What is the current theory behind MND
Over ubiquination (marking for degradation by the proteasome) of the proteins in the motor nerve fibre
59
Which tract degenerates in MND
Lateral corticospinal tract
60
Ix for MND and results (excluding bloods 4)
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
What blood tests do we do for MND (7)
```
Vitamin B12
Folate
HIV serology
Lyme disease serology
Creatine kinase assay
Serum protein electrophoresis
Anti-GM1 (GBS)
```
62
Progressive muscular atrophy:
Motor nerve affected
Presentation (2)
LMN only
| LMN signs only (e.g. flail arm, flail foot syndrome)
63
Progressive bulbar palsy:
Motor nerve affected
Presentation (3)
LMN lesion of CN IX-XII
Tongue: Flaccid, fasciculation of tongue
Jaw: Absent jaw-jerk
Voice: Nasal ‘Donald Duck’ voice
64
Pseudobulbar palsy:
Motor nerve affected
Presentation
UMN lesion of cranial nerves IX-XII (9-12)
Tongue: Slow movements
Jaw: ↑jaw-jerk
Voice: ‘Hot potato’ speech
65
Primary lateral sclerosis:
What happens in it
Motor nerve affected
Presentation (2)
Loss of Betz cells in motor cortex
= mainly UMN
UMN pattern of weakness
Brisk reflexes
Extensor planter response
No LMN signs
66
What is the classic triad of Parkinson's
Bradykinesia
Rigidity
Rest tremor
67
6M's of Parkinsons
```
Monotonous, hypotonic speech
Micrographia
HypomiMesis (expressionless face)
March a petit pas
Misery → depression
Memory loss → dementia
```
68
4 big signs of Parkinsons
Shuffling gait
Cogwheel rigidity
Hypomimia
Postural instability
69
What can cause Parkinsonism (give examples)
```
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
Which neurons die first in Parkinsons
Nigrostriatal pathway (nigra to striatum)
71
Death of which area of neurons leads to the cognitive impairment seen in Parkinson's
mesolimbic and mesocortical pathways
72
Why do neurons die in Parkinson's
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
What is a Lewy Body seen in
Parkinson's
74
RF of Parkinson's
Living in the countryside
Males
Ageing
FHx
75
What are the atypical Parkinsons
Progressive supranuclear palsy (PSP)
Multiple system atrophy (MSA)
Corticobasal degeneration (CBD)
Vascular Parkinson’s
Lewy Body Dementia (LBD)
76
What are the features of MSA (3)
Early autonomic and cerebellar features
| Papp-Lantos bodies
77
What are the features of PSP (2)
Early postural instability and vertical gaze palsy
78
What is a Papp-Lantos body
Alpha-synuclein in oligodendrocytes seen in MSA
79
What are Papp-Lantos bodies seen in
Oligodendrocytes in MSA
80
Early postural instability and vertical gaze palsy are features of...
Progressive supra nuclear palsy
81
Early autonomic and cerebellar features
| Papp-Lantos bodies are features of...
Multiple system atrophy
82
What is seen in corticobasal degeneration
Alien limb phenomenon
83
What is degenerated in corticobasal degeneration (3)
cerebral cortex (fronto-parietal atrophy), deep cerebellar nuclei and substantia nigra
84
Alien limb phenomenon occurs in what
Corticobasal degeneration
85
What are features of vascular dementia (2)
Legs particularly affected
Gait worse than tremor
Likely to have stroke RF
86
In what form of Parkinson's is:
Legs particularly affected
Gait worse than tremor
Vascular Parkinsons
87
Symptoms of Lewy Body dementia (6)
Amnestic, language deficits
Visuospatial Dysfunction
Hallucinations
Fluctuations
Aggression/Anxiety
Dementia onset same time as motor symptoms
88
In what do you see:
| Early dementia + visual hallucinations
Lewy body dementia
89
Symptoms of Parkinsons disease dementia (6)
Amnestic, language deficits
Visuospatial Dysfunction
Hallucinations
Fluctuations
Aggression/Anxiety
LATER ONSET
90
What is the difference between Lewy body dementia and PDD
Dementia develops a while after motor symptoms in PDD
LBD motor symptoms occur 1 year before or even after onset of dementia
91
What form of gait is seen in Wernicke's encephalopathy patients
Ataxic
92
What form of gait is seen in stroke patients
Hemiplegic
93
What form of gait is seen in cerebral palsy patients
Scissor
94
What form of gait is seen in Huntingtons patients
Choreiform
95
What disease has an ataxic gait
Wernicke's
96
What disease has a hemiplegic gait
Stroke
97
What disease has a scissor gait
Cerebral palsy
98
What disease has a choreiform gait
Huntington
99
Where does an ataxic gait suggest damage to
Cerebellum
100
What type of gait is a cerebellar sign
Ataxic
