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RCSI Medicine > Neurology > Flashcards

Neurology Flashcards

1
Q

BENZO S/e

A 
sedation 
resp depression 
Agitation 
ataxia 
sudden w/d - seizure 
tolerance
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2
Q

phenytoin s/e

A 
HYPERPLASIA GIGIVAL 
Hirtuism 
decrease BMD 
decrease folic acid 
drownsiness 
rash 
nystagmus
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3
Q

Primidone

A

biotransformation into metabolites phenobarbitone and phenylethylmalonamide → anticonvulsant activity
Use: GP FEM generalisedseizures, psychomotor (temporal lobe) epilepsy, focal seizures, myoclonic jerks
Adverse effects: Decreased bone mineral density, ataxia, drowsiness, fatigue, hyperirritability, suicidal ideation, vertigo, rash, GI upset, impotence, haematological, nystagmus, diplopia
Comments: May reduce effectiveness of hormonal contraception

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4
Q

s/e CARBAMAZEPINE

A

hyponatraemia, rash, pruritus, fluid retention, aplastic anaemia, hepatotoxicity, GI effects, sedation, ataxia, nystagmus, depression, dizziness, diplopia, lethargy, headache, idiosyncratic

May make primary generalised epilepsy worse.

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5
Q

Valproate moa and s/e

A 
inhibits na channel 
S/e 
- NTD 
- PCOS 
= hypothyroidism 
= insulin resistent DM
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6
Q

ETHOSUXAMIDE moa and s/e

A

nausea, vomiting, sleep disturbance, drowsiness, and hyperactivity
Comments: Rarely lupus-like reactions, SLE

MOA: iBlocks T-type calcium channels in thalamic neurons

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7
Q

lamotrigine s/e moa

A

Rash (Stevens-Johnson), tremor, headache, GI, insomnia, somnolence

moa blocks Na and decrease electrical emission

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8
Q

how is VIGABATRIN secreted

A

really

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9
Q

VIGABATRIN s/e

A

Sedation, fatigue, depression, psychosis,, headache, dizziness, weight gain

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10
Q

TOPIRAMATE s/e

A

Sedation, cognitive slowing, renal stones, weight loss, glaucoma, paresthesias, headache, fatigue, dizziness, depression, mood problems, metabolic acidosis

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11
Q

gabapentine moa and s/e

A

increase GABA in the brain binds to voltage dependent calcium channel
edation, dizziness, ataxia, GI upset, weight gain.

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12
Q

TIAGABINE moa and s/e

A

GABA uptake inhibitor

potential pro-convulsive effect
Dizziness, tiredness, mood changes, lack of energy, somnolence, nausea, nervousness, TREMOR , DIFFICULT CONCENTRATION , abdominal pain

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13
Q

ZONISAMIDE moa and s/e

A

blocks voltage-dependent sodium and T-type calcium channels

Somnolence, ataxia, cognitive slowing, weight loss, rash, ataxia, anorexia, confusion, abnormal thinking, nervousness, fatigue, and dizziness, nephrolithiasis (low risk)

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14
Q

what two anticonvulsants cause nephrolithiasis

A

ZONISAMIDE

TOPIRAMATE

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15
Q

LEVETIRACETAM moa s/e

A

Unclear, binds to a synaptic vesicle protein, may modulate synaptic transmission through alteration of vesicle fusion, may indirectly modulate GABA

Usually well tolerated
Sedation, mood disturbance, behavioural disturbance, fatigue, somnolence, dizziness, and infection (upper respiratory

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16
Q

what anticonvulsants mess the OCP effectiveness up

A

phenytoin

Primidone
Carbamazepine
lamotrigine

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17
Q

what three anticonvulsants are excreted renally vs. hepatic

A
  1. VIBigatrin
  2. Zonisamine
  3. Gabapentine
    4/ levetiracetam
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18
Q

Ulnar nerve Supplies and defect if damage

A 
C8 , T1
supplies
All small muscles of hands except LOAF
Wasting of small muscles of hand
Claw hand
Sensory loss over medial one and half fingers
Froment’s sign
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19
Q

Radial nerve Supplies and defect if damage

A 
C5-C8
Supplies
Triceps
Brachioradialis
Extensors of hand
Wrist drop
Sensory loss over anatomical snuffbox
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20
Q

Median nerve

A 
C6-T1
Supplies
Muscles of forearm  (except FCU, FDP)
LOAF
Sensory loss over palmar aspect of thumb and lateral two fingers
Ochsner’s clasping test
Tinel’s test
Phalen’s test
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21
Q

Sciatic nerve

A 
Supplies
Hamstrings
All muscles below knee
Footdrop
Weak knee flexion
Normal knee jerk, absent/weak ankle jerk
Sensory loss posterior thigh, lateral and posterior calf and foot
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22
Q

Common peritoneal nerve

A 
L4-S1
Terminal branch of sciatic nerbe
Supplies
Anterior and lateral leg compartments
Weak dorsiflexion/eversion
Normal reflexes
Sensory loss lateral dorsum of foot
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23
Q

Brown Squard Syndrome

A

IPSILATERAL - UMN sign below lesion, LMN at level of lesion and VIBRATION AND propioperception

CONTROLATERAL temp and pain

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24
Q

SACD spinal cord

A 
Symmetrical UMN signs in lower limbs
Exaggerated knee jerks
Absent ankle jerks
Symmetrical proprioception/vibration loss
Peripheral neuropathy
Optic atrophy
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25
Q

CAUSE OF SACD SPINAL CORD

A

B 12

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26
Q

SYRINGOMYELIA

A

A fluid-filled, gliosis-lined cavity within the spinal cord
Pain/temperature loss over neck/shoulders/arm (cape)
Arm atrophy
UMN lesions in LL

Causes
Congenital malformations (e.g. Chiari malformation Type 1)
Postinfectious
Postinflammatory (e.g. transverse myelitis, MS)
Posttraumatic

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27
Q

CONUS MEDULARIS

A

Lesions at vertebral level L2
flaccid paralysis of the bladder and rectum
impotence
saddle (S3-S5) anaesthesia, usually more localised to perianal area.

Causes
disc herniation
spinal fracture
Space occupying lesion

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28
Q

seizure

A

sudden change in behaviour or function due to neurological dysfunction

epilepsy - recurrent seizures (at least 2) due to excessive electrical activity in the brain

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29
Q

Complication of epilepsy

A 
AAA CDD T 
AED S/e 
anorexia 
Acidosis 
Cognitive impairment 
Depression 
death 
Trauma / personal injury
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30
Q

Risk of epilepsy recurrence

A
  • structural brain disease
  • cognitive impairment
  • multiple seizure type
  • age onset in 1st decade ( 10 years)
  • family history
  • not responding to treatment
  • combo treatment needed
  • abnormal neuro exam
  • epileptiform foci on EEG
  • Abnormal MRI
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31
Q

Seizure biomarkers

A 
CLP 
cortisol 
creatinine kinase 
LDL 
Prolactin 
Ph
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32
Q

provocation testing for seizures on EEG

A
  • sleep deprivation

- hyperventilation

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33
Q

what classification is used for seizure

A

ILAE 2010

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34
Q

definition of MND

A

Progressive group of neurological conditions which affects motor neurons at the anterior horn cell. characterized by both UMN and LMN lesions and sensory invovlemt is unlikely

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35
Q

what does bulbar involvement mean

A

Means the medulla is affected and it involves CN 9-12

RESULTS IN : dysarthria, dysphasia and laryngospasm

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36
Q

pathogenesis of MND

A 
Nerve damage and loss
Both axonal and myelin damage
Subsequent gliosis occurs 
Spinal cord atrophy
Muscle atrophy
Intracellular inclusions
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37
Q

Epidemiology of MND

A

2 types
- sporadic
- Familial - SOD1, TARDBP , CaORFT2
OLDER AGE

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38
Q

what are the additional symptoms you can get in MND

A
  1. Cognitive impairment - 3 types: 1. Pseudobulbar palsy
    dementia and
    frontal Temporal lob (executive function and memory
  2. Autonomic dysfunction
    - falls
    - urinary retention - catheter - recurrent UTI
    - constipation - bowl obstruction
  3. Parkinsonian features
  4. Sensory - complain 20%, but no exam finding
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39
Q

UMN and LMN symp in MND

A

UMNL

  • stiffness (HEAVY , Dragging)
  • clonus
  • spasm

LMNL
- weakness and atropin
fasciculation
cramps

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40
Q

UMN and LMN signs in MND

A 
UMN
Spasticity
Slowed rapid alternating movements
Increased reflexes
Gait disorder
Spastic
LMN
Weakness
Gait disorder
Reduced reflexes
Muscle atrophy and fasciculations
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41
Q

Distal spread UMNL

A

contraction of muscles that produce motions other than the one associated with the test muscle

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42
Q

Hoffman’s sign

A

tapping the nail or flicking the terminalphalanxof the middle or ring finger. A positive response is seen with flexion of the terminal phalanx of the thumb.

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43
Q

Crossed adduction

A

contraction of the adductors of the thigh and inward rotation of the limb elicited by tapping the sole.

44
Q

Triple flexion

A

Flexion at the hip, knee, and ankle, in response to stimulation of the sole of the foot.

45
Q

palmomental sign

A

stroke palm see twitching - bulbar uMN L

46
Q

ALS pulse syndrome

A 
Frontotemporal dementia, 
Autonomic dysfunction
Parkinsonism
Supranuclear gaze paresis
Sensory loss
47
Q

Ddx MND

A
  1. multifocal motor neuropathies
  2. multifocal myopathies (dermatomyositis, polymyositis)
  3. Hereditary neuropathies (hereditary spastic paralysis, spinobulbar muscular dystrophy)
  4. inflammatory neuropathies (incision body myositis)

Others:
post polio syndrome
paraneoplastic (ovaries, lung, renal)

48
Q

Exclusion Criteria

A

Clinical or electrophysiological - suggest other condition (e.g.hx of poliomyelitis)
Neuroradiological evidence of a condition that could otherwise account for the clinical syndrome (e.g. evidence of cervical myelopathy)
Failure of the condition to progress

49
Q

El escorital criteria

A

LMN degeneration by clinical, electrophysiological, or neuropathological examination
UMN degeneration by clinical examination
Progressive spread

50
Q

investigation of MND

A 
Electrophysiology (EMG)
- fibrillation 
- positive sharp waves 
Nerve Conduction studies (do repetitive test to look for fatiguability) 
potential 
Imaging
Blood and CSF analysis  - HIV, Septic screen, serum cA2+, TFT, SPEP and LP 
MRI BRAIN
51
Q

investigation for complication of MND

A
  1. RESPIRATORY FUNCTION
  2. MSU - infection
    renal US - stone
  3. full swallow assessment (video fluoroscopy)
  4. Constipation - PFA
52
Q

treatment

A
  1. RILUZOLE
  2. Symptoms:
    Spasticity - Baclofen, Tizanidine
    Cramping & fasciculation - Quinine sulphate
    Salivation & drooling - Amitriptyline,Scopolamine, irradiation
    Pseudo bulbar affect - Amitriptyline
  3. Resp dysfunction - NIV
  4. Swallow difficulty - thicken fluids, NPO, peg
53
Q

long term survival in MND

A

Younger
male
limb symptoms (better than bulbar)

54
Q

resp symp in MND that may be missed

A 
Breathnessness
Early morning headaches
Daytime sleepiness, nocturnal agitation
Nightmares
Confusion

Hypoxic signs

55
Q

Chorhea 2 types

A

Athetosis - slower, writhing movements

Ballism - proximal and large amplitude

56
Q

Dystonia

A

Involuntary, sustained muscle contractions that result in twisting and repetitive movements or abnormal posture. [2]

57
Q

tic

A

Brief, repeated, stereotyped movements which patients can suppress for a period of tim

58
Q

Myoclonus

A

Brief, shock-like, involuntary movements caused by muscular contractions or inhibitions

59
Q

Tardive Dyskinesia

A

Orobuccolingual, truncal or choreiform movements (grimacing/chewing)
Chronic exposure to antipsychotics/antiemetics (dopamine receptor blockers)

60
Q

4 hypokinesia disorders

A

Parkinsons
Progressive nuclear palsy
Portico-Basal degneration
Multiple system atrophy

61
Q

wha trinucelar repeat in fridrich’s ataxia

A

GAA

62
Q

hereditary spinocerbral ataxia

A

progressive cerebellar syndrome

oculomotor retinal and pyramidal EP sensory cognitive and behavioural sam

63
Q

what trinucelar repeat for huntigton

A

CAG

64
Q

multiple sclerosis

A

immune-mediated inflammatory disease of the central nervous system, characterised by demyelination

65
Q

proven risk factors

A 
Female gender
age 25-35
other A.I disease 
 MHC 1 and 2 alleles
HLA DRB1
MZT concordance: 20-40%
66
Q

what is a relapse in MS called

A

Episode of neurological dysfunction lasting >24 hours in the absence of fever
Often lasts weeks to months
May gradually improve (remission)
May have residual disability following relapse

67
Q

disseminated in space

A 
Dissemination in space requires
 ≥1 T2 bright lesions in 2 or more locations: 
- Periventricular
- infratentorial
- juxtacortical
- spinal cord
68
Q

Dissemination in time

A

Dissemination in time can be established in one of two ways:

  1. a new T2 bright lesion and/or gadolinium-enhancing lesion when compared to a previous scan (irrespective of timing)
  2. presence of asymptomatic enhancing lesion and a non-enhancing T2 bright lesion on any one scan
69
Q

B-interferon S/e

A

site necrosis, flu-like symptoms, abnormal LFTs (ALT), leukopaenia, anaemia

70
Q

Gatiramer-acetate

A

injection site-reaction, post-injection chest pain, flushing, dyspnoea, palpitations, and/or anxiety

71
Q

Natalizumab moa s/e

A

evelopment of progressive multifocal leukoencephalopathy

T cell lymphocyte inhibitor

72
Q

Alemtuzumab S/e and moa

A

depletion of CD52
-expressing T cells, B cells, natural killer cells, and monocytes
S/e autoimmune disorders, including immune thrombocytopenia

73
Q

Mitoxantrone s/e and use

A

Side-effects: cardiotoxicity, immunosuppression, possible link with colorectal Ca

USE Reserved for patients with rapidly advancing disease who have failed other therapies

74
Q

Dimethyl Fumarate (oral)

A

neuroprotective and immunomodulatory properties

flushing and gastrointestinal symptoms, lymphopaenia, PML

75
Q

Teriflunomide (oral)

A

disrupts the interaction of T cells with antigen presenting cells

diarrhoea, nausea, hair thinning, hepatotoxicity, teratogenicity

76
Q

Fingolimod (oral)

A

alters lymphocyte migration, sequestration of lymphocytes in lymph nodes

small increased risk of infection, atrioventricular block, and possibly basal cell carcinoma.

77
Q

spasticity in MS treatment

A

Baclofen (may also be given via intra-thecal pump)
Tizanidine :
Gabapentin
Clonazepam/diazepam: For cerebral-mediated spasticity
Botulinum toxin
Surgery: chronic epidural stimulation

78
Q

Fatigue in MS

A

Amantidine
4 Aminopyridine
Antidepressnants
Modafinil

79
Q

Bladder sphincter dysfunction

A

Anticholinergics/antimuscarinics
Botulinum toxin
Self intermittent catherisation
Suprapubic catheterisation

80
Q

Bowel sphincter dysfunction

A 
Laxatives
Pro-kinetics
Bowel stimulants
Bulking agents
Manual evacuation
81
Q

Poor prognosis of MS

A 
Early onset
High lesion load
Short interval between relapse
Primary progressive MS
Bowel/bladder symptoms at onset
82
Q

Muscular disease definition

A

Neuromuscular disorders in which the primary symptom is muscle weakness due to dysfunction of muscle fiber
People with muscular disorders describe weakness doing specific movements (distinct from patients who complain of generalised weakness)

83
Q

Ddx muscle weakness

A 
CNS damage- Stroke, SOL
Spinal cord injury or disease
Anterior horn cell disease- MND, polio
Peripheral nerve disease
Neuromuscular junction disease- myasthenia gravis, Eaton Lambert syndrome
84
Q

Myotonic dystrophy definition

A

Inherited (autosomal dominant) disease characterized by adult onset muscular dystrophy.
DM1: Trinucleotide repeat on chrom 19
DM2: tetranucleotide repeat - chromosome 3

85
Q

Definition of myotonia

A

Slow relaxation of muscle following contraction (myotonia diminishes as disease progresses)

86
Q

how to make diagnosis of muscle dystrophy

A

Genetic testing
CTG repeat in DM1
CCTG repeat in DM2

EMG
repetitive myotonia (sounds like “dive-bomber”)
Predominant in distal muscles

Muscle biopsy
Atrophy
Necrosis
Increased nuclei

87
Q

signs of myotonic dystrophy

A

Finger grip myotonia- delay in letting go when shaking hand, or delay in loosening grip when asked to grips fingers
Percusssion myotonia- tapping over thenar eminence causes
Distal muscle weakness
Impaired extra-ocular muscle usage
Gynaecomastia
CF of cardiomyopathy- displaxed apex, murmurs, crepitations, etc.
Testicular atrophy

88
Q

Ddx : TIA

A 
Migraine
Partial Seizure
Syncope
Vestibular Disorders
Neuropathy and Radiculopathy
Ocular Disorders
Hypoglycaemia
CNS Tumours
89
Q

ABCD2 score

A

Age > 60
Blood Pressure > 140/80
Clinical (2 points for hemiparesis , 1 point for speech problem w/o weakness)
Duration 2 points > 60 minutes, 1 point 10-60 minutes
Diabetes

90
Q

Interpretation of ABCD2 score

A

Score 6 to 7: High two-day stroke risk (8 percent)
Score 4 to 5: Moderate two-day stroke risk (4 percent)
Score 0 to 3: Low two-day stroke risk (1 percent)

91
Q

Agnosia

A

inability to interpret sensation

92
Q

MCA stroke presentation

A 
Contralateral paralysis (Face and limbs)
Contralateral sensory loss (Face and limbs)
Aphasia/Dysphasia
Homonymous hemianopia
Agnosia
Sensory neglect
Apraxia (dressing/constructional)
93
Q

Apraxia

A

Apraxia (dressing/constructional

94
Q

Agnosia

A

inability to interpret sensation

95
Q

Abulia

A

inability to act decisively

96
Q

Posterior cerebral artery stroke

A 
CENTRAL 
Mild hemiparesis
Choreathetosis
Intention tremor
Thalamic syndrome- simultaneous sensory loss and anaesthesiae/parasthesiae
PHERIPHERAL 
Homonymous hemianopia/quadrantanopia
Visual neglect
Visual apraxia
Prosopagnosia
Visual hallucinations
Memory abnormalities
97
Q

BP should only be treated acutely in stroke if:

A 
BP should only be treated acutely if:
Patient is candidate for thrombolysis
Severe HTN (SBP>220mmHg, DBP > 120mmHg)
Co-existing ACS, AKI, acute CCF, acute aortic dissection
Haemorrhagic stroke

Otherwise a higher BP - tolerated in ischemic stroke its permissive HTN

98
Q

Lateral Medullary Syndrome

A 
Ipsilateral 
Facial pain
Impaired facial/limb sensation
Nystagmus
Ataxia
Vertigo
Diplopia
Oscillopsia
Impaired gag reflex
Dysphagia
Horner’s syndrome

Contralateral -Impaired pain and temperature sensation

99
Q

Posterior cerebral artery stroke

A 
CENTRAL 
Mild hemiparesis
Choreathetosis
Intention tremor
Thalamic syndrome- simultaneous sensory loss and anaesthesiae/parasthesiae
PHERIPHERAL 
Homonymous hemianopia/quadrantanopia
Visual neglect
Visual apraxia
Prosopagnosia
Visual hallucinations
Memory abnormalities
100
Q

BP should only be treated acutely in stroke if:

A 
BP should only be treated acutely if:
Patient is candidate for thrombolysis
Severe HTN (SBP>220mmHg, DBP > 120mmHg)
Co-existing ACS, AKI, acute CCF, acute aortic dissection
Haemorrhagic stroke

Otherwise a higher BP - tolerated in ischemic stroke its permissive HTN

101
Q

blood pressure is >185/110 mmHg, treat with:

A

Labetalol IV, up to twice OR

Nicardipine drip

102
Q

Malignant MCA syndrome

A 
2-5 days post stroke
Mortality 50-80%
Clinical Predictors:
Young age
History of hypertension, heart failure,
Raised WCC,
Coma on admission
Nausea, vomiting
SBP> 180mmHg within first 24hrs
103
Q

criteria for hemicrainectomy

A
  • Age< 60
  • NIHSS>15
  • Decrease LOC >/=1 on item 1a of the NIHSS
    < 45 hrs from onset(surgery should be undertaken < 48hrs from onset)
  • space occupying cerebellar infarcts
  • At least 50% MCA territory involved on CT, with / without additional infarction in the territory of the anterior or posterior cerebral artery on the same side, or 145cm3 on DWI MRI
104
Q

what location of stroke is worse

A

ACA and PCA

Best = lacunar

105
Q

prognosis post stroke

A

Severity of stroke (NIHSS scale)
Site of stroke
co-morbidities,
Baseline function
Presence of continued risk factors (smoking, poor DM control, AF, etc.)
BMI - low or normal BMI confer poor prognosis

106
Q

treatment of heamorragic stroke

A

Reversal of anticoagulant
- ABC, Tx infection, Early SALT review, BP monitor, seizure prophylactic,
Possible craniotomy

107
Q

what is better for stroke CT OR MRI

A 
Non-contrast CT brain ±CT angiogram (intracranial ± carotids/vertebrals)
MRI brain (more sensitive for early infarct with FLAIR, less widely available)

RCSI Medicine (6 decks)

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