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Neurology > Neurology Course > Flashcards

Neurology Course Flashcards

1
Q

Gerstmann syndrome 4 symptoms

A

Acalculia, agraphia, L-R disorientation, finger agnosia

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2
Q

Foster-Kennedy Syndrome

A

Large meningioma compressing the olfactory bulb with raised ICP from frontal lobe

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3
Q

Pathway from cortex to peripheral nerves

A

Cortez, internal capsule, thalamus, basal ganglia, brain stem, spinal cord, peripheral nerve

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4
Q

Temporal lobe localising signs

A

Auditory cortex, receptive dysphasia, memory loss, upper quadrantanopia

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5
Q

Antons syndrome

A

Cortical blindness with bilateral occipital lobe lesions. Confabulation with blindness.
Single Basilar artery blood supply

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6
Q

Non-fluent aphasia

A

Brocas, transcorticol motor, usually frustrated, cominant frontal lobe

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7
Q

Fluent aphasia

A

Wernickes, transcorticol sensory. Unable to comprehent, not frustrated, dominant temporal lobe

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8
Q

Conduction aphasia

A

Mix between the 2, able to comprehend with elements of fluent aphasia - poor repetition. Arcuate fasciculus

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9
Q

Pathway of motor neurons

A

Cerebral cortex, corona radiata, internal capsule, crus cerebri, corticospinal tranct. Crosses in the lower medulla.

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10
Q

Blood supply of Internal capsule

A

Lenticulate arteries off of the penetrating branches of MCA

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11
Q

Blood supply and purpose Thalamus

A

Terminal for all sensory neurons, PCA is blood supply

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12
Q

Thalamus rule of 4s

A

Anterior - language and memory, lateral - motor and sensory function, medial (brain stem) arousal and memory, posterior involved with visual function

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13
Q

Spinothalamic tract

A

Pain, temperature, sensory tract to primary sensory cortex. Decussate immediately in spinal cord.

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14
Q

Dorsal collum

A

Proprioception, decussate in the medial lemniscus in the lower medulla.

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15
Q

Language differentiator of cortical involvement

A

Aphasia is always cortical - dysarthria can be lower or cortical

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16
Q

Internal capsule stroke pattern

A

Pure motor stroke

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17
Q

Differentiators cortical to sub-cortical

A

Neglect, inattention, language are all CORTICAL

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18
Q

Three regions of the cerebellum

A

2 hemispheres and vermis: everything in the cerebellum decussates twice. Left causes left, right causes right

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19
Q

Vermis lesion symptoms

A

Truncal ataxia, nustagmus - classic is with alcohol.

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20
Q

Brainstem rules of 4

A

4 cranial nerves in the medulla, 4 in the pons, 4 above the pons.
4 structures in the midline beginning with M
4 structures to the side beginning with S
4 motor nuclei that are in the midline are those that divide equally into 12 (3,4,6,12)

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21
Q

4 medial structure int he brainstem

A

Motor pathway, medial lemniscus, medial longitudinal fasciculus, motor nucleus

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22
Q

4 side structures are

A

Spinocerebellar pathway, spinothalamic pathway, sensory nucleus of the 5th CN, sympathetic tract

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23
Q

Cranial nerves

A

Olfactory, Optic, Oculomotor, trochlear, trigeminal,Abducens, Facial, Vestibulomorot, Glossopharyngeal, Vagus, Accessory, Hypoglossal

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24
Q

Olfactory purpose

A

Smell

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25
Q

Optic nerve

A

Vision, afferent pathway for pupil

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26
Q

Occulomotor

A

Superior, inferior, medial rectus, inferior oblique, levator palpebrae, efferent pathway for pupil

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27
Q

Trochlear

A

Supperior oblique

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28
Q

Trigeminal

A

Face sensation, muscle of mastecation

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29
Q

Bulbar nerves

A

9-12 i.e. nerves that come out of the medulla (the bulb(

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30
Q

Abducens

A

Lateral rectus

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31
Q

facial

A

Muscles of expression, stapedius, sensation ant 2/3rds tongue

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32
Q

vestibulocochlear

A

Hearing and balance

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33
Q

Glossopharengeal

A

Sensation of middle ear- posterior 1/3 tongue. Some swallow

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34
Q

Vagus

A

Sensation fo the pharynx, larynx, oedophagus, thoracic and abdo viscera. motor of soft palate

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35
Q

Accessory

A

Sternocleidomastoid and trapezius

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36
Q

Hypoglossal

A

Tongue movement

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37
Q

How to differentiate a MLF lesions

A

Medial longitudinal fasciculus: unable on command to look to the medial portion i.e. 6th nerve to 3rd nerve on contralateral side not communicating. STILL ABLE TO CONVERGE as 3rd to 3rd reflex without issue. The side that can’t move is the side that the lesion is on

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38
Q

Intranuclear opthalmoplegia

A

INO lesion - meaning that on adduction of the eye, the eye is unable to adduction but can conjugate gaze. Issue with the side that is affected. MLF lesion

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39
Q

“Cross signs” rule of thumb

A

Highly likely brainstem localisation

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40
Q

Typical laterally medullary syndrome

A

Bulbar signs, horners, ipsilateral numberness (large CN5 nucleus), occasionally disinterested with dysmetria due to PICA infarct.

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41
Q

Area postrema, location and purpose

A

The area postrema, a paired structure in the medulla oblongata of the brainstem, is a circumventricular organ having permeable capillaries and sensory neurons that enable its dual role to detect circulating chemical messengers in the blood and transduce them into neural signals and networks.

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42
Q

Five classical lacunar syndrome

A

Pure motor, ataxic hermiparesis, dysarthria/clumsy hand, pure sensory, mixed sensorimotor

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43
Q

Pure motor stroke

A

Lacunar stroke, 30-50% of lacunar strokes. Posterior limb of internal capsule

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44
Q

Lacunar Pure sensory

A

Thalamic infarct

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45
Q

Lacunar ataxic hemipareiss

A

Post. limb of internal capsule, basis pontis and corona radiata. Combination of cerebellar and motor symptoms

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46
Q

Lacunar Dysarthria location

A

Basis pontis

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47
Q

Mixed sensorimotor lacunar

A

Thalamus, posterior limb of internal capsule

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48
Q

Staccato progression with drop in GCA

A

Basilar stroke

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49
Q

Leg > arm stroke blood supply

A

ACA territory. Often get urinary problems as pelvic floor muscles knocked off

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50
Q

Alexia without agraphia location

A

Often hemianopia - i.e. occipital lesion. Posterior cerebral artery, specifically the collosal branches

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51
Q

Location of spinal nerves

A

Come out above the vertebrae in the C spine, below past that as there is a C8 nerve but no vertebrae

52
Q

Spinal cord posterior vs. anterior

A

Posterior horn/root is sensory, anterior is motor.

53
Q

Posterior collumn

A

Proprioception and vibration. Decussatie in the lower medulla

54
Q

Spinothalamic tract

A

Pain and temperature. decussate immediately

55
Q

Dorsal root ganglia

A

Home of the sensory bodies

56
Q

Corticospinal tract

A

Descending motor fibers - Also decussate int eh lower medulla

57
Q

Brown-sequard lesion

A

Hemi-disection of the cord: Loss of ipsilateral motor and dorsal column + loss of pain and temp on contralateral side

58
Q

Central cord syndrome

A

AFFECTS the crossing fibers at that level - but NOT the tracts. Classic is the formation of a syrinx post traumatically

59
Q

Vascular supply of spinal cord

A

a single anterior and two paired posterior arteries.

60
Q

Anterior cord syndrome

A

Lose everything except the dorsal collumn (proprioception and vibration)

61
Q

How to look at MRI

A

T1 first: Grey is grey, white is white, CSF black
T2 image: Grey matter is lighter and white matter is greyand CSF white
T2 flair: suppressing intensity of T2, CSF is not black

62
Q

T1 image good for

A

Anatomical pathology

63
Q

T2 and flair use

A

T2 for acute pathology such as inflammation, infarct etc.

64
Q

DWI use

A

Stroke, mismatch ‘wild water is white’

65
Q

ADC use

A

ADC decreased intensity in stroke which matches the DWI mismatch

66
Q

SWI use

A

Used for blood - very sensitive. Appears like a black dot for haemorrhage or blood. Picks up on iron

67
Q

Omega sign

A

Omega sign is the central sulcus - i.e. the line delineating the frontal lobe

68
Q

MCA artery branching position

A

Sylvian fissure

69
Q

Front abutting the region of the anterior or genu of corpus collosum

A

Location of the Caudate, to the side of this is the putamen and globus pallidus. (lenticuloform nucleus)

70
Q

‘Micky mouse’

A

Midbrain on MRI

71
Q

Micky mouse eyes

A

Red nucleus - mouth is aqueduct

72
Q

Most common transverse myelitis

A

MS

73
Q

NMO antibodies

A

Neuromyelitis optica

74
Q

Optic neuritis

A

Loss of colour vision, pain on eye movement, decreased visual acuity, cecocentral scotoma, relative afferent pupillary defect

75
Q

Relative afferent pupillary defect

A

Swinging torch test and efferent affect of affected eye overwhelms with the UNAFFECTED eye dilating inappropriately

76
Q

HLA associated with MS

A

HLA DR2 and DRB1*15

77
Q

Common strong risk factor association with MS

A

EBV strong, smoking, latitude (further from the equator the higher the risk)
Vit D protective

78
Q

Pathophysiology of MS

A

Early axonal loss, involving cortical grey matter lesions. B and T cells involved. Progression starts from the onset of disease

79
Q

Definition of MS

A

Need dissemination of MS in time and space: meaning, progression and multiple lesions within a space.

80
Q

Criteria used for 1st clinical presentation in MS

A

McDonalds criteria

81
Q

Specific clinical finding for MS

A

Bilateral INO. Also think of it in trigeminal neuralgia

82
Q

How many CIS progress to MS

A

63% - abnormal evoked potentials, younger age, OCBs all higher risk

83
Q

20% first clinical event in MS is

A

Optic neuritis - if normal MRI-B have 25% of MS, if abnormal MRI-B then 70% risk

84
Q

Radiology in MS

A

T2 flair white matter lesions. T2 hyperintense, T1 hypointense.
Dissemination in space with 1 or more T2 lesions in at least 2 of the following 4 areas:
Periventircular, cortical, infratentorial, spinal cord

85
Q

Dissemination in Time

A

New T2 and or Gad enhancing lesion on follow up MRI. Simultaneous enhancing of an enhancing lesion.

86
Q

Primary Immunoglobulin of the CSF

A

IgG. OCBs is the increase of IgGs, can also occur with severe disruption of the bbb. Non-specific however does fit for MS. It can also be used to define dissemination in time - they take time to occur

87
Q

Acute treatment MS

A

Corticosteroids (1g IV methylpred. 3 days) No benefit from oral steroid tail.
Can now give oral methylprednisolone: 1g methylprednisolone for 3 days in form of pred
In severe attacks, plasmapheresis is the go.

88
Q

Long term treatment MS

A

New model is efficacy>safety

Monoclonal antibodies are the most efficacious

89
Q

Dimethyl fumarate MOA

A

MMF up-regulates the Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) pathway

90
Q

Leflunomide MOA

A

nhibiting the mitochondrial enzyme dihydroorotate dehydrogenase (DHODH)

91
Q

Fingolimod MOA

A

Sphingosine-1-phosphate receptor modulator. Inhibits migration of T cells from Lymphoid tissues into CNS and peripheral circulation
Can induce arrythmias
Also can cause high risk of rebound relapse - ensure that when stopping or ceasing that something else is onboard
Ozanimod is the same MOA but only subtypes 1 and 5

92
Q

Natalizumab MOA

A

Alpha4beta1-integrin inhibitor. This blocks the function of the integrin, which typically helps lymphocytes cross the BBB

93
Q

PML definition

A

Sub-acute progressive demyelinating process to the JC virus (john-cunningham virus)
50-60% of population have this virus, no issue in immunocompetant people
Destroys oligodendrocytes leading to demyelination.
Associated with natalizumab use.
20% mortality

94
Q

PML presentation

A 
Subacute deterioration of visual, motor or cognitive change. T2 hyperintensities enlarging. No gad enhancement. 
Cease Natalizumab (plasma exchange to remove)
CSF for JCV
95
Q

IRIS definition

A

Immune reconstitution inflammatory syndrome: paradoxical deterioration in clinical status attributed to recovery of the immune system vital for controlling JCV (also occurs in HIV or other immunocompromised states)

96
Q

Alemtuzumab MOA

A

Targets CD52 expressed on lymphocytes and monocytes and causes a rapid profound lymphopenia.
Increased risk of all autoimmune conditions

97
Q

Ocrelizumab MOA

A

CD20 reducer with presenvation of lymphoid stem cells. Similar mechanism to rituximab
First trial that was proven to be efficacious against Primary progressive MS rather than RR MS

98
Q

Best predictor of MS during pregnancy

A

Activity of disease pre-conception is the highest predictor of relapse

99
Q

Safe MAB in pregnancy

A

Ritux or ocrelizumab in the first trimester - not 2nd or 3rd

100
Q

Neuromielitis optica Spectrum disorder (NMOSD)

A

AKA Devics disease: longitudinal transverse myelitis with optic neuritis. B cell disease. Targets astrocytes. Longitudinally extensive.
Necrotic spinal cord

101
Q

NMOSD prognosis

A

50% blind and 50% at 5 years unable to walk

102
Q

NMOSD atibody

A

75% sensitive and 99% specific for NMO is AQP4 antibody
MOG antibody 50% of all AQP4 negative cases. Poor response to ritux.
Test in serum not CSF

103
Q

NMOSD treatment

A 
PLEX, methylpred: long term therapy, aza and mycophenolate antiquated now. 
MAB use (Eculizumab, inebilizumab, satarizumab)
104
Q

Eculizumab MOA

A

Terminal compliment inhibitor: Must have meningicoccal vaccine. Risk of encapsulated organisms.
Only given to AQP4 +ve patients.

105
Q

ADEM

A

Monophasic disorder that affects the brain and occasionally the spinal cord. Usually preceded by viral infection or other systemic infection. Usually resolve after 3 months.
Big chunky lesions on MRI

106
Q

Parminson pathophysiology

A

Alpha-synuclein is a protein that, in humans, is encoded by the SNCA gene. It is deposited in peripheral nerves in parkinsons. It eventually migrates to central system

107
Q

BRAAK stages

A 
Parkinsons stages
Pre-symptomatic
Anosmia, constipation, REM sleep behaviour
Symptomatic:
(3-4 stage)
Parkinsonism
Late - stage 5-6 neuropsych features
108
Q

Diagnosing criteria for parkinsons

A

Decrementing bradykinesia + rigidity or 4-6 hz rest tremor

109
Q

Difference between spasticity and rigidity

A

Spasticity is a spinothalamic or central lesion and is Rate or velocity dependant.
Rigidity is a constant without velocity dependance

110
Q

Palilalia

A

Repetition of a phrase or word with increasing rapidity

111
Q

Synucleopathies

A

LBD, parkinsons, MSA

112
Q

Treatment parkinsons

A

Levodopa with dopa decarboxylase inhibitor. Dopamine produces a lot of peripheral side effects - so needs to make it centrally without being broken down.

113
Q

Three motor phases of parkinsons

A

On Well treated
Off Undertreated
Dyskinesia - over treated.

114
Q

Non-ergot Dopamine agonists

A

Newer dopamine agonists are known as non-ergot. These are pramipexole, ropinirole, rotigotine and apomorphine. Rotigotine comes as a PATCH

115
Q

Side effects of Dopamine agonists

A

Impulse control disorders and pundits

116
Q

Selagiline and raseagling

A

MOA B inhibitors: as effective as dopamine agonists if not slightly better

117
Q

Treatment paradigm Parkinsons

A

Young = MAO I
Most patients LCOPA
Too parkinsonian increase dose

118
Q

Advanced stages of Parkinsons milestones

A

Unable to draw intersecting pentagons

119
Q

TAU-opathy

A

PSP (syndrome of posutral instability, supranucleua palsy and dementia)
CTE (Chronic traumatic encephalopathies)
Alzheimers

120
Q

Supranuclear gase palsy

A

Slowed vertical saccades are most specific feature
Specific down gaze palsy
Eye signs poor sensitivity aside from saccades. Blink rate decreased and over activation of frontalis.

121
Q

Multisystem atrophy symptoms and cause

A

Alpha synucelin disorder: autonomic dysfunction, tremors, slow movement, muscle rigidity, and postural instability

122
Q

Fragile X ataxia/tremor syndrome

A

FMR1 protein deficiency

123
Q

Huntingtons disease

A

Autosomal dominant. Trinucleotide repeat gene.

Triad of Psychiatric, motor and cognitive

124
Q

Serotonin syndrome

A

Mental status change, neuromuscular activity (resembles upper motor neuron), autonomic hyperactivity.
SSRI, SNRIs, MOAs, TCAs

125
Q

Neuroleptic malignant syndrome

A

Secondary to antipsychotics: rapid escalation of abrupt cessation of anti-psychotics or parkinsons: autonomic dysfunction, lower motor neurons signs.

Neurology (4 decks)

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