Brainscape's Knowledge GenomeTM

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


See full index

BPT Flashcards > Neurology > Flashcards

Neurology Flashcards

1
Q

Antibody associated with Miller Fisher syndrome

A

GQ1B antibodies - present in 90-95% of MFS cases

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

Antibodies associated with Acute Motor Axonal neuropathy

A

GD1a, GM1

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

Antibodies associated with sensory GBS

A

GD1b

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

Poor prognostic factors for GBS

A

Rapid onset prior to presentation (<7 dayys)
High disability nadir
Mechanical ventilation
Severely reduced CMAPs
Older than 40 yrs
Preceding diarrhoea illness - Campylobacter jejui
Preceding infection with CMV
Inexcitable nerves

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

Definition of epilepsy

A
  1. At least two unprovoked (or reflex) seizures occurring > 24 hours apart
  2. One unprovoked seizure and probability of further seizures similar to general recurrence risk after two unprovoked seizures, occurring over next 10 yrs
  3. Diagnosis of epilepsy syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Classification of seizures

A

Focal onset
- Aware vs impaired awareness
- Motor or non motor onset
- Focal to bilateral tonic-clonic

Generalised onset
- Motor - tonic clonic vs other motor
- Non-motor - absence

Unknown onset

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

Focal seizure semiology

A

Temporal - deja vu, olfactory aura, epigastric rising feeling, oral automatisms
Occipital - simple visual hallucinationrs
Primary auditory - buzzing/ringing
Primary motor - focal clonic activity
Frontal - complex motor behaviour

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

Management of focal seizures

A

1st line - Carbamazepine
Other agents - lamotrigine, topiramate, levetiracetam, gabapentin

Surgical procedures - temporal lobectomy, lesionectomy, cortisectomy, implanted devices

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

Childhood absence epilepsy

A

Onset between age 4-10
Dominant seizure type absence seizures (rare GTCS)

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

Juvenile absence epilepsy

A

Onset over age 10
Commonly absence, but more likely GTCS and may have myoclonus

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

Juvenile myoclonic epilepsy

A

Onset over age of 10
Myoclonus common - occurring early morning or shortly after walking
GTCS common and absence can occur

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

Lennox Gastaut syndrome

A

Occurring in early childhood
Multiple seizures types
Associated with developmental disability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Management of generalised epilepsy

A

Sodium valproate
Levetiracetam
Lamotrigine
Topiramate

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

Management of absence seizures

A

Ethosuximide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Structural lesions for epilepsy

A

Hippocampal sclerosis
- defined by increased T2 signal and reduced size
Benign tumours
- dysembryoplastic neuro-ectodermal tumour
- ganglioglioma
- cortical dysplasia
Vascular malformations
- cavernoma
- arterio-venous malformation
Malignant lesions
- metastatic
- primary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

AEDs in pregnancy

A

Lamotrigine
- 2-3 fold increase in metabolism during pregnancy
- metabolism enhanced by oestrogen
Levetiracetam
- increased renal clearance in 2nd-3rd TM

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

HLA association between SJS and carbamazepine

A

HLA B*1502
Associated greatest in Asian ancestry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Treatment of status epilepticus

A

1st line - IV/IM benzodiazepine (midaz, loraz)
2nd line - Levetiracetam, phenytoin, sodium valproate

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

Indication of cannabidiol in management of epilepsy

A

Dravet syndrome
Lennox Gastaut syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Dravet syndrome

A

Severe epilepsy syndrome due to Na+ gene mutation (SCN1A) treatment refractory seizures of multiple types

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Risk factors for SUDEP

A

Male gender
Young age
Non-compliance
Poorly controlled epilepsy
Prone sleeping
Sleeping alone

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

Risk and protective factors for Parkinson’s disorder

A

Risk factors:
- Age
- Pesticide/solvent exposure
- Farmers
- High levels of education
- History of TBI
- Low sunlight/vitamin D
- Melanoma
- Genetics

Protective:
- Smoking
- Artistic occupation

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

Genetic markers for PD

A

PARK 1-15

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

Pathogenesis of PD

A

a-synuclein key protein in pathogenesis of PD
- prone to mutate and form insoluble species which aggregate in neurons through genetic or environmental factors
- spread in prion-like fashion through CNS

Lewy body
- pathological hallmark of PD
- composed of alpha synuclein

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

Clinical features of PD

A

In order of progression:
Change in bowel habits/constipation

RBD
EDS
Hyposmia
Depression

Motor symptoms

Urinary symptoms, postural hypotension

Hallucinations, psychosis, dementia

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

Non-motor features of PD

A

REM sleep disorder
Hyposmia
Depression
Urinary symptoms
Psychosis
Reduced libido
ED

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Motor features of PD

A

Presence of bradykinesia
Rigidity
Resting tremor
Postural instability
Unilateral onset
Progressive disorder
Persistent asymmetry
Responsive to levodopa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

MRI sign of MSA

A

Hot cross bun sign
T2 hyperintense cruciform appearance of pons
Increased signal in transverse pontocerebellar fibers

MSA-C (cerebellar types)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

MRI sign of PSP

A

Hummingbird sign
Midbrain strophy
Preserved pontine volume

Mickey mouse appearance
Reduction in AP diameter of midbrain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

MRI sign of Wilson’s disease

A

Giant panda sign
Relative hyperintensity of basal ganglia and mid brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Treatment of early PD

A

Exercise
Maintaining and improving mobility, flexibility, range of motion, speed of movement
Easing secondary symptoms i.e. depression and constipation
Commence treatment when functionally disabled - L-dopa, dopamine agonist, MAOI-B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Considerations with levodopa

A

Higher risk of dyskinesias over other PD treatments
Honeymoon period - beneficial effect in early phase of treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Consideration of dopamine agonist use

A

Initial therapy in patients < 60 yrs
In combination with L-dopa, motor fluctuations and dyskinesias reduced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Side effects of dopamine agonists

A

Sleepiness
Peripheral oedema
Neuropsychiatric SEs particularly in pts > 70 yrs
Impulse control disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Dopamine agonist examples

A

Pramipexole
Apomorphine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

MAO B inhibitors indications and considerations

A

Selegiline

Trial as initial therapy for mild disease in pts with bradykinesia or postural instability

May improve end of dose akinesias
May worsen dyskinesias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Indications and considerations of NMDA antagonist

A

Amantadine

Short term treatment of mild symptoms
Levodopa induced dyskinesia
Akinetic crisis

May cause adverse CNS effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Indications for functional neurosurgery

A

Motor complications not managed by medical treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Types of functional neurosurgeryy

A

Thalamic stimulation (DBS) - tremor
Pallidal stimulation - dyskinesias
Subthalamic stimulation - motor fluctuations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Advanced therapies for PD

A

Duodopa L-dopa gel
SC apomorphine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Pathophysiology of cognition impairment in PD

A

Lewy bodies spread in involve cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Pathophysiology of PD

A
  • Progressive dopaminergic neuron degeneration in the substantia nigra (part of the basal ganglia) and the locus coeruleus → dopamine deficiency at the respective receptors of the striatum with interrupted transmission to the thalamus and motor cortex → motor symptoms of PD
  • Indirect pathway of the basal ganglia is affected
  • Serotonin and noradrenaline depletion (in the raphe nuclei): likely cause of depressive symptoms
  • Acetylcholine surplus (in the nucleus basalis of Meynert): likely cause of dyskinesia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Pathophysiology of Lewy Body dementia

A

If motor symptoms precede by < 1 year + dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Clinical features of LBD

A

Visual hallucinations
Fluctuations in GCS
PD motor symptoms
Neuroleptic sensitivity (cog and motor)
Paranoia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Friederich’s ataxia features

A

Trinucleotide repeat expansion (of the nucleotide triplet GAA) in the FXN gene on chromosome 9

Progressive ataxia
Spastic paralysis
Nystagmus
Dysarthria
HOCM
DM
Scoliosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Fragile X associated tremor ataxia syndrome features

A

X-linked dominant disease caused by a CGG trinucleotide repeat expansion in the FMR1 gene (fragile X mental retardation 1 gene)

Late onset ataxia
Postural tremor
Executive deficits
Parkinsonism
Neuropathy

Increased T2 signal in cerebellar peduncles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Huntington disease features

A

Autosomal dominant
Increased number of CAG repeats (trinucleotide or triplet repeat expansion) in the huntingtin gene on chromosome 4

Mean age onset 45 yrs, median survival 18 yrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

CAG repeats in Huntington disease and interpretation

A

Normal: < 26
Intermediate: 27-35 –> no development of symptoms, but children at risk
Reduced penetrance: 36-39 –> may or may not develop symptoms at any age
Full penetrance: > 40 –> have disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Imaging for Huntington disease

A

Neuronal loss and atrophy of caudate putamen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Clinical features of Huntington disease

A

Motor - chorea, motor impersistence, dysarthria, ataxia, trouble walking, dystonia

Psych - depression, anxiety, apathy, paranoia

Dementia - Impulsive, personality change, social withdrawal, cognitive slowing, weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Findings of demyelinating lesions in NCS

A

Slowed conduction velocity
Conduction block
Temporal dispersion
Lower amplitudes due to distal dispersion or conduction block
Delayed or absent F-waves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Findings of axonal lesions in NCS

A

Low amplitudes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Recovery of neurapraxia/demyelination

A

Remyelination of local Schwann cells
Weeks to months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Recovery of axonal loss/axonotmesis/neurotmesis

A

Axonal regrowth -1mm/day, 1 inch/month
Distal branch sprouting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Carpal tunnel syndrome clinical features

A

Sensory disturbances (pain, tingling, and numbness) and motor symptoms (weakened thenar muscles leading to weakened pinch and grip of the thumb) in the area innervated by the median nerve distal to the carpal tunnel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Radial neuropathy clinical features

A

Sudden painless wrist and finger drop
Compression at spiral grooves, triceps spared
Sensory loss of dorsum of hand, especially thumb and index

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

EMG findings in acute denervation

A

Prominent fibrillation/positive sharp waves
Reduced recruitment in proportion to number of motor units lost

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

EMG findings of chronic denervation

A

No fibrillation potentials
Increased duration
Increased amplitude
Reduced recruiment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

EMG findings of myopathy

A

Minimal fibrillations, may be present in some myopathies
Decreased duration
Decreased amplitude
Small amplitude, recruited early

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Clinical manifestations of anterior horn cell disease

A

Progressive, asymmetric motor disorder with mixed proximal/distal, UMN and LMN signs

One of four body segments (cranial/bulbar, cervical, thoracic, and lumbosacral)
- Sparing eye movements, bowel and ladder
- Tongue fasciculations
- Painless
- Region spread within and to adjacent regions
- “Split hand syndrome”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

MND epidemiology

A

Sporadic - 5% dominantly inherited
Mean age of onset 55 yrs
Median survival from diagnosis 3-5 yrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Variants of MND

A

Amyotrophic lateral sclerosis - mixed UMN and LMN
Spinal muscular atrophy - predominant LMN
Primary lateral sclerosis - predominant UMN, better prognosis
Progressive bulbar palsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

MND EMG findings

A

Findings of acute and chronic denervation and reinnervation
- Fasciculations in muscles with chronic denervation
- Fibrillations and positive sharp waves with acute denervation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

MND NCS findings

A

No conduction block
Normal or near normal motor conduction velocities
Normal sensory studies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Gold coast criteria for ALS

A
  1. Progressive motor impairment documented by history of repeated clinical assessment, preceded by normal motor function
    AND
  2. Presence of UMN and LMN dysfunction in at least 1 body region with
    - UMN and LMN dysfunction noted in same body region OR LMN in at least 2 body regions
    AND
  3. Investigations excluding other disease processes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Clinical features of multifocal motor neuropathy with conduction block

A

Progressive, asymmetrical, predominantly distal, pure motor, LMN pattern with some atrophy

Upper limbs > lower
Cramps and fasciculations common
CN involvement rare
Absent sensory symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Clues to diagnosis of MMCB

A

Age
Weakness > atrophy
Peripheral nerve pattern of weakness
Absence of CN or UMN signs
Depressed or absent tendon reflexes
Unusual sites of focal demyelination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Investigation findings of multifocal motor neuropathy w/ conduction block

A

NCS - partial conduction block in one or more nerves, sensory nerves normal

IgM anti-GM1 antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Management of MMCB

A

IVIg
IV cyclophosphamide
Plasma exchange
Rituximab

Prednisone can worsen it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

MMN clinical features

A

Stepwise, multifocal, asymmetric, can be distal or proximal
Eventually becomes symmetrical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

MMN causes

A

Diabetes
Infectious - leprosy, HIV
Arteritis - CTD, vasculitis
Trauma
Hereditary liability to pressure palsies
Sarcoidosis
Malignancy

72
Q

Causes of peripheral neuropathy

A

Metabolic - diabetes, uraemia, porphyria, hypothyroidism, acromegaly, EtOH, B1/B6/B12/niacin deficiency
Infections - HIV, lyme, leprosy
Toxic - drugs, poisons
Inherited - CMT, Frederich’s ataxia
CTD - RA, PAN, SLE, Sjogren’s, Wegener’s, Churg-Strass
Paraproteinaemias - MM, MGUS, POEMS, amyloid
Immune mediated - GBS, CIDP, MMCB, POEMS, Amyloid

73
Q

Charcot Marie Tooth disease subtypes

A

CMT I - demyelinating (AD/X linked)
- Due to duplication of PMP 22 gene: CMT1A

Hereditary neuropathy with pressure palsies
- PMP 22 deletion/point mutation

CMT IX - X linked dominant

CMT II- axonal

74
Q

CMT genetics

A

PMP22
GJB1 - CMT1X
MFN2 - CMT 2A
MPZ - CMT1B

75
Q

Types of diabetic neuropathies

A

Symmetric polyneuropathies
- sensory
- sensorimotor
–> distal, length dependent
–> sensory > motor. axonal > demyelinating
- autonomic

Focal and multifocal
- CN palsies
- Radiculopathies
- Mononeuritis
- Asymmetric proximal neuropathy (amyotrophy)
- Treatment induced

76
Q

Investigations of peripheral neuropathy

A

NCS
Metabolic screens
Autoimmune and paraprotein screens
ESR, CRP
Toxic screen
LP
Consider cancer screen, HIV, sural nerve biopsy

77
Q

What feature on NCS most sensitive in detection of early diabetic polyneuropathy?

A

F wave latency

78
Q

GBS features

A

Acute, demyelinating, autoimmune neuropathy
Asymmetric, patchy and global
Weakness, sensory features and autonomic disturbance developing over days

79
Q

Triggers for GBS

A

URTI, GIT infection, immunisation, surgery, trauma
Specific agents: campylobacter jejuni, EBV, CMV, mycoplasma, viral hepatitis, HIV, seroconversion

80
Q

Clinical variants of GBS

A

Miller Fisher syndrome
- External ophthalmoplegia, ataxia, areflexia
- GQ1B
Polyneuritis cranialis
Pure sensory variant
Acute autonomic neuropahty
Acute axonal variant
- Acute motor axonal neuropathy (AMAN) (AMSAN)
- Pharyngeal-cervical-brachial variant

81
Q

Investigations of GBS

A

CSF
- Elevated protein
NCS
- conduction slowing, block, long latencies and delayed F waves
EMG
- may shown denervation changes 2-4 weeks

82
Q

Treatment of GBS

A

IVIg
Plasma exchange

83
Q

Clinical criteria for typical CIDP

A

Chronically progressive, stepwise or recurrent
Symmetric proximal and distal weakness
Less prominent sensory dysfunction
Absent or reduced reflexes
Minimal autonomic involvement

84
Q

Clinical criteria for atypical CIDP

A

Predominantly distal (DADS)
Asymmetric (MADSAM)
Focal
Pure motor
Pure sensory

85
Q

Clinical features of CIDP

A

Progress or relapse/remit over > 8 weeks
Symmetric weakness of both proximal and distal muscles
↓ Deep tendon reflexes in both upper and lower extremities
Sensory involvement (e.g., paresthesias)
Autonomic dysfunction and cranial nerve involvement are rare.
CIDP variants can manifest with asymmetric symptoms and/or purely sensory or motor symptoms.

86
Q

Investigation findings of CIDP

A

LP
- Increased protein, low cell count
NCS
- slow CV, conduction block or temporal dispersion, prolonged DML, absent/prolonged F-waves

87
Q

Treatment of CIDP

A

Prednisone
Plasma exchange
IVIg
Azathioprine

88
Q

Features of distal acquired demyelinating symmetric neuropathy (DADS-M)

A

Elderly males
Predominant distal sensory loss
Mild distal weakness - foot drop, ataxia
Associated unsteadiness/falls/tremor

89
Q

Investigation findings of DADS-M

A

Prolongation of distal latencies on NCS
IgM paraproteinaemia in 2/3
Anti MAG

90
Q

Features of myasthenia gravis

A

Fatiguable weakness
90% of cases involve extraocular muscles
80% involve facial and bublar muscles
50% involve purely ocular disease
50% progress to generalised myasthenia

91
Q

Myasthenia and thymoma

A

Almost all thymoma associated with MG
Thymic lymphoid hyperplasia in 70%
Thyrotoxicosis in 5%

92
Q

Diagnosis of MG

A

Repetitive stimulation - decremental response at low frequency
ACh receptor antibodies
- 85% of pts with generalised MG, 60% with ocular MG
Anti-MuSK
- high frequency in bulbar involvement and respiratory crises
Tensilon test
- Positive in 80%

93
Q

Features of LEMS

A

Antibody to presynaptic voltage gated calcium channel, reducing number of vesicles released

Proximal muscle weakness; muscle strength improves with repetitive or ongoing use
Reduced or absent reflexes
Autonomic symptoms

94
Q

Causes of LEMS

A

Paraneoplastic - SCLC
AI disorder

95
Q

Diagnosis of LEMS

A

EMG: Repetitive nerve stimulation results in incremental responses.
NCS: Small initial CMAP, increases after voluntary contraction or high frequency stimulation
Confirmatory test: anti-VGCC antibodies in serum
Other: CT chest, abdomen, and pelvis to screen for underlying malignancy

96
Q

Treatment of LEMS

A

Plasma exchange
Prednisone
Azathioprine
Guanidine
Diaminopyridine

97
Q

Features of statin myopathy

A

Symptom onset at any time - 25% after > 12 month usage
Mild myalgias –> severe rhabdomyolosis
Self-limiting, lasting ~2-3 months
Elevated CK levels
Myalgias common symptom

98
Q

General principles of stroke anatomy

A

ACA - leg weakness
MCA - hemiplegia, hemiparesis with cortical signs. if dominant side, can have speech deficits.
PCA - visual field deficits
Penetrating vessels in subcortical - hemiplegia or hemiparesis without cortical signs

99
Q

Causes of ICH

A

Idiopathic
Hypertensive
Amyloid angiopathy –> microhaemorrhage, SAH, cortical calcification
Vascular abnormality
Secondary to ischaemic stroke
Trauma
Underlying bleeding disorder
Anticoagulation related
Drug related

100
Q

Management of cerebral haemorrhage

A

Surgery for significant compression
Aim SBP < 140mmHg
Reversing agents for anticoagulation
Fibrinolytics beneficial in first 24 hours from onset

101
Q

Risk factor screening for stroke

A

HTN
Hypercholesterolaemia
Diabetes
Precoagulant states/IE
AF or other source of cardio-embolic source
Collagen disorders, vascular dissection, rare genetic causes

102
Q

Risk of stroke in TIA

A

In 48 hours - 6%
In 1 week - 10%
In 6 months - 17%

103
Q

Stroke prevention strategies

A

Early carotid surgery for symptomatic stenosis after TIA and mild stroke
Antiplatelet agents
Anticoagulation for non valvular AF
Antihypertensives aiming BP < 130/85
High dose cholesterol lowering agents
Lifestyle advice

104
Q

DAPT duration

A

Usual DAPT for 3 weeks and then stepdown to SAPT

If high risk intracranial atherosclerosis, consider longer duration of 90 days

105
Q

Time windows for acute stroke therapy

A

IV thrombolysis up to 9 hours if evidence of salvageable tissue
Endovascular therapy up to 24 hours

106
Q

DOACs for embolic stroke

A

ARISTOPHANES study

Apixaban - less stroke/embolic events, less major bleeds

Rivaroxiban - higher bleeding risk

107
Q

Most likely location for thrombus in AF

A

Left atrial appendage

108
Q

Device for AF if DOAC not appropriate

A

Left atrial appendage oclusion

109
Q

Evidence re: LAAO compared to DOACs

A

Prague 17 study
Left atrial appendage occlusion non-inferior to DOAC at preventing embolic events/bleeding

110
Q

Risk stratification of PFO and stroke

A

Characteristics
- Large shunt
- septal aneurysm

Clinical
- age
- stroke features
- ROPE score
- hypercoagulopathy
- Concomitant VTE
- competing risks

111
Q

COVID-19 and stroke

A

Associated with hypercoagulable state +/- direct infection/inflammation of blood vessels

Mostly causing large vessel occlusion

More likely to develop:
- AKI
- Hepatic failure
- Respiratory failure

112
Q

Stroke mimics

A

Focal seizures
Migraines
Tumour
SDH
Hypotension/syncope
Peripheral vestibular conditions
Panic attacks
Conversion disorders/FND

113
Q

Tenectoplase vs alteplase for acute stroke therapy

A

Alteplase = tenectoplaste - equally more effective up to 4.5 hours

114
Q

Hypertension in stroke population

A

Up to 70%

115
Q

Definition of MS

A

Chronic inflammatory autoimmune disease of CNS characterised by inflammation, demyelination and axonal loss

116
Q

Braak staging

A

Lower brainstem and olfactory system (dorsal motor nucleus of vagus nerve, anterior olfactory nucleus) > medulla oblongata > pontine tegmentum > basal mid- and forebrain, hypothalamus, thalamus > mesocortex, allocortex > neocortex

117
Q

Risk factors for MS

A

Caucasian
Female
If affected sibling
High latitude of residence
Low vitamin D levels
Smoking
Obese
Inadequate sleep in adolescence

118
Q

Genetic risks of MS

A

HLA-DRB1+15:01 confers greatest risk

119
Q

EBV and MS

A

Increased risk of MS linked to antibody response to EBV nuclear antigen

120
Q

Role of myelin and oligodendrocytes

A

Oligodendrocytes responsible for myelinating axons in CNS
Myelin increases speed of electrical conduction
Oligodendrocyte provides trophic support to neurons

121
Q

Immunopathogenesis of MS

A
  1. Peripheral activated autoreactive T cells (especially Th17) migrate across blood brain barrier
  2. Reactivation by local antigen presenting cells
  3. Clonal expansion
  4. Secretion of proinflammatory cytokines
  5. Stimulation of microglia and astrocytes
  6. Destruction of myelin, oligodendrocyte loss, and axonal loss
122
Q

Acute vs chronic demyelinated plaque

A

Acute plaque
- indistinct margin
- inflammatory cells centred around vessels in ‘perivascular cuff’
- oedema and demyelination throughout plaque
- oligodendrocyte and axonal loss varialbe

Chronic plaque
- more distinct borders
- hypocellular core with thickened vessels and enlarged perivascular spaces
- loss of myelin and glial scarring prominent

123
Q

Clinical phenotypes of MS

A

Relapsing remitting MS (85-90%)
Primary progressive (10%)
Secondary progressive MS
Primary relapsing MS

124
Q

Definition of relapse

A

Any new or worsening neuro symptoms that last longer than 24 hours, or shorter than 24 hours but recurs repeatedly over days

125
Q

Definition of pseudorelapse

A

Previous neuro symptoms may temporarily worsen if body temperature is elevated –> reflects conduction block in previously demyelinated axons

126
Q

Typical MRI lesions in MS

A

Corpus callosal
Periventricular “Dawson fingers”
Infratentorial

127
Q

Role of oligoclonal bands

A

Represents immunoglobulins to specific antigens within CNS
Found in CNS

128
Q

Role of VEP

A

Measures time taken for visual stimulus to be recorded over occiput
Normal VEP virtually excludes a lesion of optic nerve or along visual pathways in anterior brain

129
Q

Diagnostic criteria for RRMS

A

> /2 clinical attacks + MRI findings or good historical evidence
1 clinical attack with typical MRI + follow up MRI with new lesion and/or OCB present in CSF

130
Q

Diagnostic criteria for PPMS

A

1 year of disability progression independent of clinical relapse + two of following criteria
- >1 T2 hyperintensive lesion characteristic of MS in one or more following brain regions (periventricular, cortical or juxtacortical or infratentorial)
- >2 T2 hyperintense lesions in spinal cord
- Presence of CSF specific oligoclonal bands

131
Q

Definition of neuromyelitis optica spectrum disorder (NMOSD)

A

Immune mediated disease causing demyelination and axonal damage or optic nerves and spinal cord

132
Q

Pathology of NMOSD

A

Necrosis and cavitation involving both gray and white matter
Majority of patients have aquaporin-4 antibodies
- crosses BBB and binds to water channels on astrocytes
- activates complement system/MAC causing complement dependent cytotoxicity
- stimulates Ab-dep cellular toxicity
- death to astrocytes followed by oligodendrocytes and neurons
- oligodendrocytes loss leads to demyelination

133
Q

Neuroimaging in NMOSD

A

Longitudinally extensive spinal cord lesion (LETM)
Long optic nerve lesion, often involving posterior aspects of nerve or optic chiasm
Lesions involving dorsal medulla
Lesions involving hypothalamus/thalamus

134
Q

Clinical characteristics of NMOSD

A
  1. Optic neuritis
  2. Acute myelitis
  3. Area postrema syndrome (intractable hiccups, N+V)
  4. Acute brainstem syndrome
  5. Symptomatic cerebral syndrome with NMOSD-typical brain lesions
135
Q

Treatment of NMOSD

A

IV methylpred + oral corticosteroids
+/- PLEX
Steroid sparing agents (MMF, azathioprine)
B cell depleting therapy

136
Q

Pathophysiology of MOGAD

A

Myelin oligodendrocyte glycoprotein exclusively expressed on oligodendrocytes and myelin. inCNS
Anti-MOG Ab –> demyelination

137
Q

Presentation of MOGAD

A

Bilateral (consecutive) optic neuritis
Typically very severe
Steroid responsive with good recovery of vision

138
Q

Poor prognostic factors in MS

A

Frequent relapses within first 2 years of diagnosis
Short interval between first 2 relapses
Rapid early disability progression
High lesion load (especially spinal cord or infratentorial)
Cerebral atrophy
Male gender
Later age of onset

139
Q

MOA of natalizumab

A

alpha 4 integrin monoclonal Ab (found on monocytes and lymphocytes)

140
Q

Natalizumab SEs

A

Increased risk of herpes virus reactivation
Risk of progressive multifocal leukoencephalopathy, caused by JC virus

141
Q

Higher risk of PML if

A

JCV serology positive and:
- Any prior immunosuppression
- >2 yrs on natalizumab
- JCV index (level of positivity)

142
Q

MOA of alemtuzumab

A

Anti-CD52 (found on differentiated lymphocytes and monocytes) –> eliminates pathogenic T cells

143
Q

Alemtuzumab SEs

A

Infusion reactions common
Increased infection risk
Risk of secondary autoimmunity (thyroid disease, ITP)

144
Q

MOA of ocrelizumab

A

Anti-CD20 fully humanised monoclonal Ab

145
Q

Ocrelizumab SEs

A

Infusion reactions common
Increased infection risk
Risk of PML
Increased risk of malignancies (though not significant)

146
Q

MOA of ofatumumab

A

Fully humanised monoclonal antibody against CD20+ B cells

147
Q

MOA of cladribine

A

Selective immune reconstitution therapy
Deoxyadenosine analogue prodrug selectively targets lymphocytes due to preferential intracellular activation

148
Q

Cladribine SEs

A

Lymphopenia
Increased risk of infections (whilst lymphopenic)

149
Q

MOA of fingolimod

A

Binds to S-1-P receptors on lymphocytes and blocking their egress from lymph nodes

150
Q

Fingolimod SEs

A

First dose bradycardia - requires cardiac monitoring when first given
LFT derangement
Lymphopenia
Increased infection risk especially herpes virus
Increased risk of non-melanomatous skin cancers
PML risk

151
Q

Ozanimod MOA

A

Sphingosine-1-phosphate inhibitor
Slightly different receptor specificity and lower risk of cardiac complications

152
Q

Dimethyl fumarate MOA

A

Modulates antioxidative pathways via activation of Nrf2

153
Q

Dimethyl fumarate SEs

A

Flushing
GIT upset
Lymphopenia
Rare LFT deranagements
Risk of PML

154
Q

MOA of teriflunomide

A

Inhibits dihydroorotate dehydrogenase and interferes with pyrimidine synthesis

155
Q

SEs of teriflunomide

A

Hepatotoxicity
Hair thinning
HTN
GI upset
Teratogenic

156
Q

MOA of glatiramer acetate

A

Synthetic polypeptide antigenically similar to myelin basic protein

157
Q

MOA of interferon beta 1a and 1b

A

Diverts immune system away from proinflammatory Th1 and Th17 pathways to more anti-inflammatory Th2 pathway
Also effects T-reg, NK cells, B-cells and lymphocyte migration into BBB

158
Q

Washout periods for MS drugs prior to conception

A

None
- Glatiramer acetate
- Interferon beta
- Dimethyl fumarate
- Natalizumab

2 months
- Fingolimod

4 months
- Alemtuzumab

6 months
- Cladribine
- Ocrelizumab/Ofatumumab

Accelerated elimination
- Teriflunomide

159
Q

Prognosis of MS

A

Untreated MS, ~50% of pts develop SPMS after 10-20 yrs of RRMS diagnosis

160
Q

Cortical signs of frontal lobe

A

Personality
Primitive reflexes
Dysphasia expressive
Anosmia
Optic nerve compression
Gait apraxia

161
Q

Cortical signs of parietal lobe

A

Gerstmann syndrome - acalculia, agraphia, L-R disorientation, fingeragnosia
Sensory, visual and spatial inattention
Construction and dressing apraxia
Lower quandrantanopia

162
Q

Signs of Gerstmann syndrome

A

Dominant, angular gyrus
Acalculia
Agraphia
L-R disorientation
Fingeragnosia

163
Q

Cortical signs of temproal lobe

A

Receptive dysphasia (dominant)
Memory loss
Upper quandrantanopia

164
Q

Cortical signs of occipital lobe

A

Homonymous hemianopia
Anton’s syndrome
Alexia without agraphia

165
Q

Signs of Anton’s syndrome

A

Cortical blindness with confabulation

166
Q

Types of aphasia

A

Non-fluent, Expressive, Broca’s, transcortical motor
- Able to comprehend, paucity of word
- Usually frustrated
- Dominant frontal lobe

Fluent, receptive, Wernicke’s, transcortical sensory
- Unable to comprehend, fluent but incomprehensible speech
- Not frustrated
- Dominant temporal lobe

Conduction aphasia
- Mix between the two
- Able to comprehend elements of fluent aphasia and poor repetition

167
Q

Thalamus sign and functions

A

Terminal for all sensory nerves
Arterial supply from PCA

Anterior nuclei - language and memory function
Lateral nuclei - motor and sensory function
Medial nuclei - maintaining arousal and memory
Posterior nuclei - visual function

168
Q

Peripheral cerebellum signs

A

Ipsilateral limb ataxia
Past pointing
Dysmetria
Intention tremor
Dysdiadochokinesia
Nystagmus

169
Q

Vermis cerebellum signs

A

Truncal ataxia
Nystagmus (flocculonodular lobe)

170
Q

4 rules of brainstem

A
  1. 4 cranial nerves in medulla, 4 in pons, 4 above pons
  2. 4 structures in midline beginning with M
  3. 4 structures to side beginning with S
  4. 4 motor nuclei in midline
171
Q

4 medial structures

A

Motor pathway
Medial lemniscus
Medial longitudinal fasciculus
Motor nucleus

172
Q

4 side structures

A

Spinocerebellar pathways
Spinothalamic pathways
Sensory nucleus of 5th CN
Sympathetic tract

173
Q

CN location in brainstem

A

Midbrain - III, IV
Pons - V, VI, VII, VIII
Medulla - IX, X, XI, XII

174
Q

Brown-Sequard syndrome

A

Ipsilateral UMN weakness below level of lesion
Ipsilateral impairment of vibration and position sense below level of lesion

Contralateral pain and temperature sensation from one to two segments below lesion

Ipsilateral LMN weakness and complete sensory loss at level of lesion

175
Q

Central cord syndrome

A

Loss of pain and temperature in one or more adjacent dermatomes bilaterally at level of lesion

Sensory classically seen in “cape” or “vest” distribution across neck and shoulders or trunk

Further expansion affects lateral corticospinal tracts causing UMN weakness and temperature and sensation loss below lesion

176
Q

Anterior cord syndrome

A

Dorsal columns preserved
Proprioception and vibration preserved
Usually ischaemic with occlusion on anterior spinal artery

177
Q

Posterior cord syndrome

A

Just loss of dorsal column
Rarely ischaemic given bilateral blood supply
Demyelination, nutritional, genetic

BPT Flashcards (32 decks)

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