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Nimna's Flash Cards > Neurology > Flashcards

Neurology Flashcards

1
Q

Seizure classification

A
  1. Focal or generalised
  2. Aware or impaired awareness (focal only)
  3. Motor vs non-motor
  4. Provoked (reversible CNS insult) or unprovoked (genetic, structural, metabolic, immune, infectious causes of epilepsy).
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2
Q

Hippocampal sclerosis is seen in what type of epilepsy

A

Mesial Temporal lobe epilepsy

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3
Q

In epilepsy idiopathic seizures are caused by

A

idiopathic seizure = genetic cause

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4
Q

Location of haemorrhage causing focal jerking

A

Motor cortex

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5
Q

Seizuregenic neurotransmitter

A
  • Na
  • Glutamate
  • NMDA
  • AMPA
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6
Q

Anti-seizure neurotransmitters

inhibitory

A
  • GABA

- K

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7
Q

Management of Juvenile Myoclonic epilepsy

A

Sodium Valproate

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8
Q

Management of focal epilepsy

A

Carbamazepine

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9
Q

Management of absent seizures

A

Ethosuxamide

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10
Q

Antiepileptic which interact with OCP

A

Lamotrigine

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11
Q

Cause of further seizure while on anti-epileptics

A

Can be caused by anti-epileptics themselves. Particularly Carbamazepine.

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12
Q

Interaction of Valproate and Lamotrigine

A

Lamotrigine levels increase when used with Sodium Valproate due to enzyme inhibition.
Symptoms - cerebellar signs.

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13
Q

Best anti-epileptic for pregnancy

A

Lamotrigine
Levetriacetam

*DO NOT USE VALPROATE - highly teratogenic.

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14
Q

Carbamazepine and Steven Johnsons HLA associations

A

HLA 1502- asians

HLA

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15
Q

holepunch brain

A

neurocysticicosis

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16
Q

Herpes encephalitis EEG

A

Periodic lateralized epileptiform discharges (PLEDS)

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17
Q

Headache, hemiparesis and seizure in post-partum

A

Cerebral venous thrombosis.

Imaging - CT venogram or MR venogram

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18
Q

Anti-epileptics causing visual fields defects

A

Vigabatrin (blind as a bat)

Topiramate (Pirate eye patch)

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19
Q

Drugs which exert an effect on the CNS without crossing the blood-brain barrier

A

Domperidone

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20
Q

Antibody in stiff person syndrome

A

Anti-GAD65 (same as T1DM)

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21
Q

Features of Gertsmans syndrome (Dominant parietal lobe stroke)

A

Acalculia, Finger agnosia, Agraphia, L-R disorientation

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22
Q

Pathway of the sympathetic chain by neurons

A

1st order neuron - from posterolateral hypothalamus, through the midbrain and pons to the ciliospinal centre of budge at C8-T2

2nd order neuron - From T1 into sympathetic chain over apex of lung to the superior cervical ganglion at the level of the bifurcation of the carotid artery.

3rd order neuron- from superior cervical ganglion along the internal carotid artery to supply the eye.

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23
Q

Disease which is caused by JC virus

A

Progressive multifocal leukoencephalopathy

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24
Q

Management of PML

A

Cease biologic drugs (natalizumab/rituximab) + start plex.
commence hydrocortisone if IRIS develops.

Give Pembrolizumab

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25
Q

Unilateral temporal lobe enhancement on MRI

A

HSV encephalitis

Limbic encephalitis

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26
Q

Hummingbird sign on MRI

A

progressive supranuclear palsy

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27
Q

CJD symptoms

A

rapid onset dementia, behavioural changes, myoclonus.

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28
Q

CJD EEG and MRI findings

A

EEG - sharp wave pattern

MRI - cortical ribboning. Diffusion restriction in cortex and basal ganglia

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29
Q

Management of venous sinus thrombosis

A

Anticoagulate (even if there has been haemorrhage)

Use clexane/warfarin - no evidence for NOAC

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30
Q

What is the rule of 4’s

A
  1. 4 CN in the medulla, 4 in the Pons, 4 above the Pons
  2. 4 midline structures starting with M- medial longitudinal fasciculus, medial lemniscus, motor neuron bodies 3,4,6,12. Motor pathway.
  3. 4 side structures starting with S - sympathetic chain, sensory body of CN5, spinothalamic tract, spinocerebellar tract
  4. 4 motor nucleuses are factors of 12.
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31
Q

In nerve conduction studies reduced amplitude is due to

A

axonal loss

can also be issues with NMJ or muscle

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32
Q

In nerve conduction studies reduced velocity/ increased latency is due to

A

demyelination

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33
Q

Nerve lesions that cannot be tested in NCS

A

pre-ganglionic sensory nerve lesions

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34
Q

In nerve conduction studies reduced f-waves is due to

A

defect anywhere along the neuron

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35
Q

Interferon beta MOA and SE

A

Decreases T and B cell function by decreasing matrix metalloproteinases

SE - flu like symptoms, leukopenia, LFTs, thyroid.

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36
Q

Glatiramer acetate MOA and SE

A

Ligand for MHC II, stimulates Tregs

SE: injection reactions

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37
Q

Teriflunomide MOA and SE

A

Inhibits pyrimadine synthesis

SE - hair thinning, GI, teratogenic

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38
Q

Dimethyl fumarate MOA and SE

A

Lowers lymphocyte count
SE - flushing, diarrhoea.
Risk of PML

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39
Q

Fingolimod MOA and SE

A

Sphingosine 1 phosphate receptor modulator
Traps T cells in lymphnodes

SE - bradycardia, macular oedema, shingles.

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40
Q

Cladribine MOA and SE

A

Purine antimetabolite - causes DNA strand breakage and activates p53
SE- headache, shingles, malignancy.

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41
Q

Natalizumab MOA and SE

A

Targets a4b1 integrin, stops leukocytes crossing the BBB.

SE: PML, pharyngitis, peripheral oedema

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42
Q

Alemtuzumab MOA and SE

A

Targets CD52 - causes lymphopenia

SE: autoimmune disease

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43
Q

Ocrelizumab MOA and SE

A

Targets CD20

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44
Q

MS drugs in pregnancy

A

Interferron beta
Glatiramer acetate
All biologics

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45
Q

Pathophysiology of migraine

A

Cortical spreading depression(of Leao)

Self propagating wave of neuronal and glial depolarisation

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46
Q

Cause of headache in migraine vs cause of aura

A

Aura = due to cortical spreading neuronal and glial depolarisation

Headache = activation of trigeminal afferent nociception.

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47
Q

Molecular cascade in migraine

A

Neuronal pannexin 1 -> Caspase 1 -> kappa B - > pro-inflammatory mediators -> calcitonin gene related peptide.

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48
Q

Acquired loss of color vision, dyschromatopsia, indicates injury/pathology in which vessel/part of the eye.

A

Optic nerve! - this is caused by optic neuropathy.

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49
Q

Types of optic neuropathy

A

Anterior - ie involving the optic disc. Optic disc appears inflamed. Can be non-arteritis or srteritis (associated with GCA). NAION will typically have some or all of the signs of an optic neuropathy including decreased visual acuity, dyschromatopsia, an RAPD, a swollen optic nerve with splinter hemorrhages and a visual field defect.

Posterior ischemic optic neuropathy (PION) encompasses those conditions that result in ischemia to any portion of the optic nerve posterior to the optic disc.

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50
Q

How to differentiate Conus Medullaris from Cauda equina

A

Conus medullaris - both upper and lower motor signs.

Cauda equina - lower motor only

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51
Q

Difference between post-ictal and inter-ictal psychosis

A

Postictal psychosis usually begins within 48 to 72 hours of a seizure or cluster of seizures, following a lucid interval. Postictal psychosis is often associated with positive symptoms including paranoid or referential delusions, hallucinations, and aggression

interictal psychosis may be more likely to manifest with disorganization and negative symptoms.

52
Q

3rd nerve palsy cause if pupil is involved

A

Aneurysm compressing the 3rd nerve intracranially - can be posterior communicating artery.

53
Q

3rd nerve palsy cause if pupil spared.

A

GCA
Ischaemic injury.

Needs MRI.

54
Q

Type of patient who gets idiopathic intracranial hypertension

A

overweight young female

55
Q

Risk factors for idiopathic intracranial hypertension

A

Overweight, OCP, Vit A use, tetracyclines.

56
Q

Mx of idiopathic intracranial hypertension

A

Weight loss

Acetazolomide

57
Q

Small fibre nerves

A

C- fibres - pain and temperature

58
Q

Neurological effect of EtOH and EtOH withdrawal

A

EtOH use - releases GABA, causes GABA receptor upregulation.
Inhibits NMDA receptors, causes NMDA receptor upregulation.

EtOH withdrawal - Low levels of GABA, Increased NMDA and high NMDA receptors.

59
Q

Neurological effect of Nicotine.

A

binds stereo-selectively to nicotinic-cholinergic receptors.
stimulating effect = locus ceruleus
reward effect = limbic system

60
Q

Examination sign of poor prognosis in subarachnoid haemorrhage

A

Terson syndrome (preretinal hemorrhages) may be seen and implies a poorer prognosis.

61
Q

Driving limitation on seizures

A

Standard - 12 months

Variation - 6 months if clear trigger or first seizure now treated.

62
Q

Adrenal disease and progressive spastic paresis

A

X-linked adrenoleukodystrophy and adrenomyeloneuropathy - peroxisomal disorder of beta-oxidation that results in accumulation of very long-chain fatty acids (VLCFAs) in all tissues. Accumulation of abnormal VLCFAs in affected organs (central nervous system, Leydig cells of the testes, and the adrenal cortex) is presumed to underlie the pathologic process of ALD/AMN

63
Q

Test for X-linked adrenoleukodystrophy and adrenomyeloneuropathy

A

ABCD1 mutation

64
Q

Symptoms of X-linked adrenoleukodystrophy and adrenomyeloneuropathy in men

A

spastic paraparesis, abnormal sphincter control, neurogenic bladder, sexual dysfunction. Numbness and pain from polyneuropathy. Adrenal insufficiency.

65
Q

Symptoms of X-linked adrenoleukodystrophy and adrenomyeloneuropathy in women

A

peripheral neuropathy and myelopathy, often with a gait disorder and fecal incontinence and sometimes with mild spastic paraparesis

66
Q

Management of contraception with AED use

A
  1. Mirena

2. Increase oestrogen dose in OCP

67
Q

Endocrine function of the hypothalamus

A

supraoptic and paraventricular nuclei secrete ADH. The paraventricular nucleus also
secretes oxytocin.

68
Q

Interaction of Lamotrigine and Carbamazepine

A

Lamotrigine levels decrease (unlike the increase seen with sodium valproate) - this is because Carbamazepine is an enzyme inducer.

69
Q

Drugs which lower the seizure threshold

A 
Propofol 
Beta-Lactam Abx 
Amphotericin 
Antidepressants 
Clozapine 
Theophylline 
Cyclosporine
Pethidine
70
Q

Role of Nimodipine in Subarachnoid haemorrhage

A

Theoretically to prevent vasospasm.

goal = to decrease neurological deficits that develop as a result of distal infarction of brain from site of vasospasm

71
Q

Which AEDs reduce concentration in pregnancy due to reduced protein binding?

A

Phenytoin, Phenobarbital, Valproate

72
Q

Which AED has the most stable levels in pregnancy

A

Carbamazepine

73
Q

AEDs with the least stable levels in pregnancy

A

Levetiracetam, Lamotrigine, Oxcarbazine

74
Q

Stroke causing loss of Ant 2/3 tongue taste

A

Marie Foix - AICA stroke - Facial nuclei involved rather than just facial nerve

75
Q

How to differentiate medial medullary syndrome from lateral medullary syndrome

A

Medial = motor loss, tongue motor palsy, medial lemniscus (vibration + proprioception).
Lateral (side) = sensory loss, side nuclei - CN 9,10,11, Sympathetic chain.

76
Q

Types of nerve fibres and function

A

Aa fibres - myelinated 15mm - muscle spindles (proprioception) + alpha motor
Ab fibres - myelinated 8mm - mechanoreceptors
Ac (gamma) fibres - myelinated 5mm - muscle spindles (proprioception)
Ad fibres - myelinated 3mm - pain (rapid response), temp.

B fibres - moderately myelinated 2mm - preganglionic sympathetic

C fibres - unmyelinated 1mm - pain

77
Q

Nerve fibre most affected by hypoxia

A

b- fibres - therefore hypoxia causes autonomic effects

78
Q

Nerve fibre most affected by pressure

A

a- fibres - eg carpal tunnel

79
Q

Nerve fibre most affected by anaesthetic

A

c-fibres

80
Q

CN with parasympathetic activity

A

3 - pupil parasympathetics
7 - lacrimal gland, sublingual gland, submandibular gland
9 - parotid gland
10 - vagus

81
Q

Miller Fishcer triad and Ab

A

ophthalmoplegia with ataxia and areflexia

GQ1B

82
Q

Biggest RF for SUDEP (unexplained death in epilepsy)

A

frequency of GTCS

83
Q

4 symptoms of PRES syndrome

A
  • CCCV = confusion, cephalgias, convulsions, visual disturbance
84
Q

Treatment for NMO

A

Eculizumab -prevention

Methyl pred- acute attack

85
Q

Risk Factors for PRES

A
  • severe HTN
  • Pre-eclampsia
  • Immunosuppression - Tac, cyclo, cisplatin, VEGF
  • renal failure
  • autoimmune disease
86
Q

PRES MRI finding

A

vasogenic oedema in bilateral posterior hemispheres.

87
Q

What does each part of the HINTS exam test?

A

Head impulse - POSITIVE IF PERIPHERAL - abnormal due to disease with the 8th cranial nerve (vestibulocochlear nerve). Lesion of vestibulocochlear nerve should be unilateral, and patient will correct with saccade if peripheral.

Nystagmus - BIDIRECTIONAL/ VERTICAL = CENTRAL.
UNIDIRECTIONAL = PERIPHERAL

Test of skew - If present = CENTRAL

88
Q

Trigeminal autonomic cephalgias

A
  1. SCUNT/SUNA - 60secs
  2. Paroxysmal hemicrania - 15mins
  3. Cluster headache - 1hr
  4. Continuous hemicrania - days

Have unilateral autonoic signs - tearing, nasal drip, miosis, ptosis, tinnitus

89
Q

Condition that cluster headaches and Trigeminal autonomic cephalgias are associated with

A

Pituitary adenomas

90
Q

Management of Cluster headaches

A
  • Triptans
  • Occipital nerve injection
  • Steroids
  • Verapamil

NOT indomethicin

91
Q

Management of Paroxysmal hemicrania/ continuous hemicrania

A

Indomethacin

92
Q

Management of SCUNT/SUNA - acute and preventer

A

Acute - Lignocaine

Lamotrigine is preventer for SCUNT/SUNA

93
Q

Migraine preventers

A
  • propanolol
  • pizotifen
  • topiramate
  • valproate
  • verapamil
  • clonidine
  • candesartan
  • amitriptyline
94
Q

CGRP mabs (name 3)

A
  • Fremanezumab
  • Galcanezumab
  • Erenumab
95
Q

Target of Ergots and triptans

A
  • 5HT
96
Q

Stroke syndromes:

  • Contralateral weakness and sensory loss more marked in the upper limbs and lower half of the face than in lower limbs
  • Gaze deviates toward the side of infarction
  • Contralateral homonymous hemianopia without macular sparing
  • Aphasia if in dominant hemisphere
  • Broca aphasia (lesion to inferior frontal gyrus)
  • Wernicke aphasia -Occurs in lesion to superior temporal gyrus
  • Conduction aphasia
  • Hemineglect if in nondominant hemisphere
  • Sensory neglect
A

MCA

97
Q

Stroke syndromes:

  • Contralateral weakness and sensory loss in the lower limbs more marked than in upper limbs
  • Abulia (lack of will)
  • Urinary incontinence
  • Dysarthria/ Transcortical motor aphasia
  • Frontal release signs
  • Limb apraxia
A

ACA

98
Q

Stroke syndromes:

  • Contralateral homonymous hemianopia with macular sparing due to occipital lobe involvement
  • Contralateral sensory loss due to lateral thalamic involvement: light touch, pinprick, and positional sense may be reduced.
  • Memory deficits
  • Vertigo, nausea
A

PCA

99
Q

Stroke syndromes:

  • Ipsilateral bulbar palsy (dysphagia, dysphonia, hiccups, decreased gag reflex)
  • Ipsilateral nystagmus and vertigo (vestibular nuclei)
  • Pain and temperature - contralateral to body and ipsilateral to face.
  • limb ataxia
  • Horners syndrome
A

PICA = lateral medulla affected

100
Q

Stroke syndromes:

  • Contralateral body pain and temp loss
  • ipsilateral ataxia
  • ipsilateral face pain + temp loss - 5thCN
  • ipsilateral weakness - 7th CN
  • Loss of anterior 2/3 tongue sensation
  • Ipsilateral horners and vestibular nuclei
A

AICA

101
Q

Stroke syndromes:
- Locked in syndrome
-

A

Basilar

102
Q

Stroke syndromes:

Amaurosis Fugax

A

Internal carotid

103
Q

Stroke syndromes:

Horner’s syndrome alone

A

Common carotid

104
Q

Area of brain causing hemibalismus

A

Subthalamic nucleus

105
Q

Stroke syndromes:

  • Ipsilateral internuclear ophthalmoplegia
  • Ipsilateral facial muscle weakness
  • Contralateral hemiparesis
A

Medial pontine - supplied by paramedian branches of the basilar

106
Q

Stroke syndromes:
Contralateral hemiplegia and paresthesia
Gaze palsy and ipsilateral deviation of the eyes
Stupor and coma

A

Putamen

107
Q

Stroke syndromes:
Contralateral hemiparesis and paresthesia
Miotic and unreactive pupils, upgaze palsy with gaze deviation away from the side of the lesion (wrong way eyes)

A

Thalamus

108
Q

VGKC disease and presentation

A
  • Includes LGI1 and CASPR2 encephalitis
  • faciobrachial dystonic seizures
  • hyponatremia
  • REM sleep disorder
  • severe impairment of short-term memory
  • neuromytonia - muscle twitching at rest
  • associated with lung, breast and thymus cancers.
109
Q

LGI1 disease and presentation

A

LGI1 encephalitis

  • faciobrachial dystonic seizures
  • hyponatremia
  • REM sleep disorder
110
Q

LGI1 disease and presentation

A

LGI1 encephalitis

  • faciobrachial dystonic seizures
  • hyponatremia
  • REM sleep disorder
111
Q

CASPR2 disease and presentation

A

limbic encephalitis

  • severe impairment of short-term memory
  • neuromytonia - muscle twitching at rest

Associated with thymoma

112
Q

AMPA disease and presentation

A

AMPA encephalitis

  • females, with a median age of onset of 50 to 60 years
  • limbic encephalitis
113
Q

VG calcium channel disease and presentation

A

Lambert-Eaton myasthenia

recovery of lost deep tendon reflexes or improvement in muscle strength with vigorous, brief muscle activation.

114
Q

MND/ALS pattern

A

both UMN and LMN disease with patchy involvement and both acute and chronic denervation. Can get split hand syndrome or isolated foot drop etc. Needs evidence that there isn’t structural compression.

115
Q

EMG findings for acute denervation

A

Fibrillations and positive sharp waves with increased insertional activity.

116
Q

EMG findings for chronic denervation

A

Large amplitude, long duration complex motor unit action potentials with neurogenic recruitment.

117
Q

Which disease does ALS/MND have overlap with?

A

Frontotemporal dementia

118
Q

Genes associated with ALS

A
  • SOD1
  • C9ORF72
  • FUS
119
Q

Histology in ALS

A

TDP-43 accumulation and inclusion formation is observed in most sporadic cases of ALS and fronto-temporal dementia.

120
Q

Mechanism of central sensitization

A
  • increased c-fibre stimulus leads to upregulation of NMDA and glutamate in the spinal cord.
  • Dorsal horn becomes disorganised.
  • Increased substance P production - lowers nociception threshold.
  • can cause sympathetic responses due to disorganised/crossed fibres.
121
Q

Hockey stick sign on brain imaging

A

CJD

122
Q

CJD finding in CSF

A

CSF 14-3-3 protein

123
Q

CJD EEG

A

periodic synchronous bi- or triphasic periodic sharp wave complexes

124
Q

GBS antibodies

A
  • GM3 - motor axonal
  • GM1 - Multifocal motor neuropathy and dementia
  • GQ1b - Miller Fischer syndrome - ataxia, ophthalmoplegia, areflexia.
125
Q

Symptoms of normal pressure hydrocephalus

A

Ataxia, Cognitive impairment, urinary incontinence.

126
Q

Effect of extending thrombolysis time frame to 9 hours.

A

Increased proportion of patients with regained function. Increased cerebral haemorrhage

Nimna's Flash Cards (15 decks)

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