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Neurology Flashcards

1
Q

What is pyramidal weakness

A

Power seen in UMN lesions

Extension weakness in UL and flexor weakness in LL

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2
Q

Earliest sign seen in UMN lesions

A

Plantars

UMN lesions initally look like LMN lesions in hyperacute stage

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3
Q

Lentiform nucleus includes

A

Globus pallidus and putamen

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4
Q

Frontal lobe features

A 
Primary motor cortex - dictates movement
Personality
Primitive reflexes
Dysphasia Expressive (dominant)
Anosmia
Optic nerve compression
Gait apraxia (gait memory)
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5
Q

Parietal Lobe features

A 
Primary sensory cortex
Gerstmann syndrome
Sensory, visual, spatial inattention
Construction and dressing apraxia
Lower Quadrantanopia
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6
Q

Temporal lobe features

A

Pimary auditory cortex
REceptive dysphasia (dominant)
MEmory loss - hippocampus and amygdala
Upper quadrantanopia

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7
Q

Occipital Lobe Features

A

Homonymous Hemianopia
Anton’s Syndrome
Alexia without agraphia

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8
Q

Gerstman Syndrome

A

Dominant angular gyrus lesion

Acalculia, graphia, L-R disorientation, fingeragnosia (ALF)

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9
Q

Anton’s Syndrome

A

Bilateral occipital cortical lesion

Cortical blindness with confabulation

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10
Q

PITS

A

Parietal inferior quadrantanopia

Temporal superior quadrantanopia

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11
Q

Non- fluent/Expressive/Broca’s/Transocrtical motor aphasia

A

Able to comprehend, paucity of words, know what they want to say, but cant
+++Frustration

Dominant frontal lobe lesion

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12
Q

Fluent, repetitive, wernickes, transcortical sensory aphasia

A

Unable to comprehend, fluent but incomprehensible speech
Like a foreign language

Dominant temporal lobe lesion

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13
Q

Conduction aphasia

A

Mix between broncas an wernickes aphasia
-Able to comprehend with elements of fluent aphasia and poor repetition

Arcuate fasciculus lesion (connection between the 2 areas)

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14
Q

Most important part of the internal capsule and why

A

Posterior limb and Genu

-Carry the corticospinal trcts and some sensory fibres

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15
Q

Blood supply of the internal capsule

A

LEnticulostriate arteries which are penetrating branches of MCA (M1)

-Common areas of atherosclerosis

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16
Q

Stroke of lenticulostriate arteries in internal capsule presentation

A

pure motor stroke

Dense weakness, nil cortical signs

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17
Q

Thalamus Rule of 4s: Anterior nuclei

A

language and memory function (frontal/temporal input)

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18
Q

Thalamus Rule of 4s: Lateral nuclei

A

motor and sensory function

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19
Q

Thalamus Rule of 4s: Medial nuclei

A

maintaining arousal and memory (midbrain)

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20
Q

Thalamus Rule of 4s: Posterior nuclei

A

visual function

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21
Q

Issue with bilateral thalamic lesions

A

significant arousal issues

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22
Q

Thalamic stroke classical presentation

A

Pure sensory loss stroke

Terminal area for all sensory nerves

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23
Q

Arterial supply of thalamus

A

PCA

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24
Q

Cerebellum: Vermis lesion

A

Truncal ataxia

Nystagmus

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25
Q

Cerebellum: Hemisphere lesion

A 
Ipsilateral limb ataxia
Past pointing
Dysmetria
Intention tremor
Dysdiadokinesia
Nystagmus
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26
Q

Brain stem Rule of 4’s

A

4 Cranial nerves in the medulla, pons, and above pons
4 structures in the midline beginning with M
–Motor pathway, Medial lemniscus, medial longitudinal fasciculus, motor nucleus
4 structures on the side beginning with S
–Spinocerebellar pathway, spinothalamic pathway, sensory nucleus of 5th CN, Sympathetic tract
4 motor nuclei in the midline that divide equally into 12 (3.4.6.12)

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27
Q

Horner’s syndrome features

A

miosis, ptosis, anhidrosis

Points of terminals: C8/T1, then past lung apex, then superior cervical ganglion by bifurcation of ICA and ECA where sweat gland goes with ECA, then to eye along with ICA

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28
Q

CN 1

A

Olfactory

-Smell

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29
Q

CN 2

A

Optic

-Vision, afferent pathway for pupil

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30
Q

CN 3

A

Oculomotor

  • Superior, inferior, medial rectus, inferior oblique, levetor palpebrae
  • Efferent pathway for pupil
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31
Q

CN 4

A

Trochlear

-Superior oblique (depression, most in adduction, and intorsion)

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32
Q

CN 5

A

Trigeminal

-Facial sensation, muscles of mastication

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33
Q

CN 6

A

Abducens

-LAteral rectus

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34
Q

CN 7

A

Facial

  • Muscles of expression, stapedius
  • Sensation of anterior 2/3 of tongue
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35
Q

CN 8

A

Vestibulocochlear

-Hearing and balance

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36
Q

CN 9

A

Glossopharengeal

  • Sensation: middle ear, posterior 1/3 tongue
  • Some swallowing
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37
Q

CN 10

A

Vagus

  • Sensation of pharynx, larynx, oesphagus thoracic and abdominal viscera
  • Motor: soft palate, larynx, pharynx
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38
Q

CN 11

A

Accessory

-Sternocleidomastoid, trapezius

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39
Q

CN 12

A

Hypoglossal

-Tongue movement

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40
Q

Medial longitudinal fasciculus connects what 2 CN nuclei?

A

3 and 6

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41
Q

INO PAthyphysiology

A

Problem with MLF
Want to look to one side and signal sent to CN6 nuclei but due to damage to MLF cannot send signal to contralateral eyes CN3 nuclei to look in the same direction. So one eye abducts and the other does not move

Affected side is side which eye does not move
Normal eye then gets nystagmus to catch up with affected eye

Classically due to MS, but can be due to stroke in elderly

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42
Q

ACA territory stroke

A

Leg weakness >arm weakness

Pelvic floor dysfunction

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43
Q

Basilar stroke

A

Step wise stroke progression
Usually first medullary symptoms
Then diplopia
Then lose midbrain and drop in GCS

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44
Q

Lacunar Stroke: Pure motor stroke

A

Posterior limb of internal capsule r anterior portion of pons

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45
Q

Lacunar stroke: Ataxic hemiparesis stroke

A

Posterior limb of internal capsule, basis pontis, and corona radiata
Combination of cerebellar and motor Sx
Legs>arms

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46
Q

Lacunar stroke: Dysarthria/clumsy hand

A

Basis pontis lesion

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47
Q

Lacunar stroke: pure sensory

A

Thalamic infarct

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48
Q

Lacunar stroke: Mixed sensorimotor

A

Thalamus and posterior limb of internal capsule

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49
Q

Spinothalmic tract synapse and decussation

A

1st order neuron has cell body in dorsal root ganglion.
Synapse onto 2nd order neuron in posterior horn and that nerve then crosses over to the contralateral side and synapses in the thalamus.

Decussation occurs over 2-3 segments while ascending

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50
Q

Posterior column synapse and decussation

A

1st order neuron synapses on second order neuron in the medulla
2nd order neuron is called the medial lemniscus and decussates in the medulla
Then goes to thalamus and primary sensory cortex

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51
Q

Corticospinal tract synapse and decussation

A

1st order neuron from primary motor cortex to the anterior horn with decussation at the medulla
2nd order neuron from anterior horn through anterior nerve root to destination

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52
Q

Brown Sequard

A

Ipsilateral UMN weakness below lesion
Ipsilateral vibration and proprioception impairment below lesion
Contralateral pain and temp impairment 1-2 segments below lesion
Ipsilateral LMN weakness and sensory loss AT the level of lesion

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53
Q

Central Cord Syndrome

A

Loss of pain and temp bilaterally at the level of lesion
“Suspended sensory level” “Cape/vest distribution”

Increase in size of lesion: LMN lesion at the level of lesion

Further increase in size: UMN weakness and temp and sensation loss below the lesion

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54
Q

Spinal cord blood supply

A

Anterior and posterior spinal arteries supplied by:

  • Vertebral arteries of the neck
  • Intercostal branches of the aorta and midthoracic region
  • Great Radicular artery (of Adamkiewicz) in the lower thoracic or lumbar region
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55
Q

Anterior cord syndrome

A

Everything gone except posterior column

USually ischemic with occlusion of anterior spinal artery

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56
Q

Posterior cord syndrome

A

Only loss of dorsal column
Rarely ischemic given bilateral blood supply
Usually demyelination, nutritional, or genetic

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57
Q

T1

A

Grey is grey and white is white

Good for anatomy

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58
Q

T2

A

Grey is light
White is grey
Good for pathology

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59
Q

T2 Flair

A

Suppresses the CSF color
Grey is light and white is grey
Good for pathology

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60
Q

MRI DWI

A

For infarcts
Bright color is stroke

MRI ADC is the opposite and also good for strokes where dark color means stroke

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61
Q

Bloome artifact on MRI

A

Microhemorrhages

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62
Q

Contraindications for TPA

A
  • Ischemic stroke or head trauma in last 3 months
  • Previous ICH
  • Brain cancer
  • GI malignancy or hemorrhage in last 21 days
  • Intracranial/spinal surgery in last 3 months
  • Suspicion for SAH
  • BP >185/110
  • Active bleeding
  • Current IE
  • Suspicion of aortic arch dissection
  • Platelets <100,000
  • INR >1.7
  • APTT >40
  • Therapeutic clexane in last 24 hours
  • NOAC
  • Extensive hypoattenuation on CT
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63
Q

Timeframe for TPA in stroke

A

within 4.5 hours, sooner the better

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64
Q

Risk factors for hemorrhage post stroke

A 
Large infarct
Established infarctions
Grey matter infarctions
Higher NIHHS score
Poor collaterals
Hyperglycemia
Thrombocytopenia
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65
Q

Dose alteplase

A

0.9 mg/kg - 10% as bolus and the 90% over an hour

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66
Q

What is the penumbra and what imaging is used to determine its size

A

-Tissue at risk and potentially salvagable

CBV: Shows how much is dead

Tmax: showed the penumbra

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67
Q

Indication for clot retrieval in stroke

A

CTB: does not display extensive infarct
CTA: major vessel occlusion (ICA,M1,Basilar,M2)
CTP: Large penumbra, small core
Good premorbid function

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68
Q

Time frame for thrombectomy in stroke

A

up to 24 hours, with no difference in group getting treatment closer to 24 hours

DAWN trial - NEJM 2018

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69
Q

Tenectaplase vs alteplase before mechanical thrombectomy

A

Increased rates of perfusion with tenectaplase

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70
Q

Alteplase vs placebo in patients with unknown time of onset of stroke

A

Ischemic lesion on DWI with normal flair suggesting stroke <4.5 hours

Improved perfusion with alteplase, but increased risk of death

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71
Q

BP control in acute stroke

A

Increased BP as it will improve blood flow via collaterals, may reduce extent of irreversible ischemia

Upper limit with tPA: 180/105

Non tPA may go up to 220/120

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72
Q

Most important modifiable risk factor for strokes

A

HTN

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73
Q

Target BP after acute setting in strokes and Tx of choice

A

SBP 120-140

ACEi and Thiazide have the most evidence

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74
Q

When to commence BP Mx drugs post stroke

A

48-72 hours post stroke

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75
Q

Antiplatelets post stroke

A

Short term:
-Aspirin and clopidigrel for 3 weeks, then aspirin alone (most benefit of aspirin within 6 weeks)

Long term:

  • Only aspirin
  • No benefit of clopidigrel over aspirin and increased risk of bleeding if both A+C used
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76
Q

When is the highest risk of new stroke with large vessel atherosclerosis

A

First month, afterwards plaque stablises

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77
Q

CEA vs stenting

A

Higher risk of peri procedural stroke and death with stenting over the age of 70s

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78
Q

Indication for CEA

A

PAtients with non disabling carotid artery territory stroke or TIA with ipsilateral carotid stenosis measured 70-99%.

Ideally within 2 weeks

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79
Q

Indications for stenting over CEA

A

Unfavorable anatomy
Symptomatic restenosis post CEA
Previous radiotherapy
Only if Age < 70

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80
Q

Mx of intracranial large vessel atherosclerosis

A

DAPT
No role for warfarin
No role for stenting
Aggressive medical Mx

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81
Q

Risk factors for dissection

A

Trauma (can be minimal) with hyperextension of the neck
Genetic predisposition
Fibromuscular dysplasia
CTDs

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82
Q

Clinical features of dissection

A 
NEck pain
HEadache
Stroke
Partial Horner's Syndrome
SAH if rupture
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83
Q

Tx of dissection

A

Aspirin

Generally good prognosis with resolution of dissection in majority

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84
Q

When to start anticoagulation post acute stroke

A

0, 3, 6, 12 rule

0 days - TIA
3 days - Small stroke
6 days - medium stroke
12 days - large stroke

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85
Q

50% of cryptogenic strokes are due to:

A

PFO

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86
Q

Mx of PFO in stroke setting

A

PFO closure and antiplatelet therapy for patients <60 with no other cause of stroke found is indicated if associated with atrial septal aneurysm or moderate to large R to L shunt

Increased risk of AF in first 1-1.5 months post closure, but transient

0 % recurrence of stroke in PFO closure group

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87
Q

Risk of developing stroke post TIA

A

3.7% due to improved medical therapy

Risk stratification based on:

  • Age >60
  • BP >140/90
  • Clinical features: unilateral weakness, speech impairment
  • Duration: + points if >60 mins
  • Diabetes
  • Dual TIA
  • Imaging: >50% stenosis of ICA, acute DWI restriction
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88
Q

BP management in acute ICH

A

Aim 140-160 (closer to 140)

Higher renal adverse events in 7 days if intensive BP control

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89
Q

REducing haematoma size in ICH

A

Evidence for lowering bp to <160 and INR <1.3 within 4 hours

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90
Q

Platelets in ICH

A

Worse outcomes. Do not use

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91
Q

Tranexamic acid in ICH

A

Fewers deaths by day 7, but same amount of deaths by 90 days

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92
Q

Primary causes of ICH

A

Deep perforating vasculopathy (atheroscleosis of small vessels)

  • Basal ganglia or brainstem
  • White matter lesions, lacuna strokes

Cerebral amyloid angiopathy
-Lobar inctra cerebral hemorrhage (small vessel blockage)

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93
Q

Causes of secondary ICH

A 
Mets
AVM
aneurysm
Cerebral venous sinus thrombosis
IE
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94
Q

Cerebral Amyloid angiopathy Features

A

Symptomatic lobar hemorrhages
Cortical microhemorrages
White matter disease and cortical infarcts
Dementia
CAn present with TIA symptoms with positive symptoms

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95
Q

Cerebral Amyloid angiopathy Pathophysiology

A

Combo of ischemia and bleeds
Genetic association with APOE E4 and E3 allele
Amyloid deposition in capillaries, arterioles, and small arteries leads to necrosis of vessel wall and leads to rupture and small vessel occlusion

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96
Q

Mx of CAA

A

Avoid anticoagulation, antiplatelets, and thrombolysis

Mainstay BP control: Perindopril/Indapamide most evidence

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97
Q

Cerebral Venous thrombosis Risk factors

A 
Hormonal therapy
Post partum
Thrombophilia
Local infections
Chronic inflammatory diseases
Malignancy
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98
Q

Cerebral Venous thrombosis presentation

A

Isolated intracranial HTN (90% of cases)
SEizures
Focal neurology
Encephalopathy

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99
Q

Cerebral Venous thrombosis Mx

A

Heparin infusion or therapeutic clexane
Then transition to warfarin
3-6 month duration in provoked, 6-12 months if unprovoked

Increased risk of recurrence if occured during post partum and may require prophylactic anticoagulation in future pregnancy

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100
Q

Extradural haematoma on CT

A

Lemon

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101
Q

Subdural haematoma on CT

A

Banana

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102
Q

Heerfordt Syndrome

A

Sarcoid

Facial palsy combined with uveitis, fever, parotid enlargement, and transverse myelitis

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103
Q

Features of optic neuritis

A 
Subacute onset
Pain on eye movement
Decreased visual acuity and colour vision
Sparkles of light
Relative afferent pupillary defect

(Retrobulbar - no swelling, anterior -swellin)

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104
Q

Leber’s Optic neuritis

A

Acute onset visual loss and a week later the other eye too
Mitochondrial disorder
Nil pain on eye movement

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105
Q

Causes of bilateral optic disc swelling

A

HTN
Raised ICP (papillodema)
Bilateral ON/neuropathy - NMOSD

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106
Q

MS HLA type

A

HLA DR2 (HLA DRB1*15)

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107
Q

Environmental factors associated with MS

A

EBV
Smoking
Latitude

Sunlight exposure and Vit D are protective

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108
Q

Pathophysiology of MS

A

Early axonal loss as well as demyelination
Involves cortical grey matter lesions and white matter
Both T and B cell involvement

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109
Q

Duration of demylinating attack in MS

A

LAsting greater than 24-48 hours
Nadir within 2 weeks
Resolution by 4 weeks (may not return to baseline)

Pseudo relapse can occur in setting of fevers/heat

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110
Q

Lhermitte’s phenomenon

A

an electric shock-like sensation that occurs on flexion of the neck. This sensation radiates down the spine, often into the legs, arms, and sometimes to the trunk.

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111
Q

Uhthoff’s phenomenon

A

the worsening of neurologic symptoms in multiple sclerosis (MS) and other neurological, demyelinating conditions when the body gets overheated from hot weather, exercise, fever, or saunas and hot tubs.

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112
Q

63% of patients with a clinically isolated syndrome will develop MS. What are the RFs to develop MS

A 
Younger age
High cerebral lesion load
Asymptomatic infratentorial or spinal cord lesions
GAD enhancing lesions
Oligoclonal bands in CSF
Abnormal visual evoked potentials
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113
Q

Optic neuritis and MS

A

20% initial presentation of MS is optic neuritis

50% of MS patients will develop optic neuritis

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114
Q

MS on MRI

A 
T2 Flair is best modality
Contrast enhancing of acute lesions lasts up to 1 month
Typical location of lesions:
-Periventricular
-Juxtacortical
-Infratentorial
-Spinal cord
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115
Q

McDonalds Criteria

A

For Diagnosis of MS
NEED 2 LESIONS IN TIME AND SPACE

Time

  • 2 seperate attacks, or even a Hx of an attack
  • MRI with contrast enhancement of a lesion and no enhancement of another
  • Oligoclonal bands

Space:

  • 2 different locations in the CNS through objective clinical evidence
  • 2 different locations in the CNS through MRI
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116
Q

Oligoclonal bands in CSF with CIS

A

High predictor of conversion to MS

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117
Q

Factors that are associated with an increased risk of development of primary progressive MS in radiologically isolated syndrome

A

Older age
Man
Spinal cord lesions

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118
Q

Acute treatment of MS

A

3 days of IV/PO MEthyprednisolone

  • Accelerates rate of recovery from relapse
  • No change in disability or disease

PLEX for severe disease

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119
Q

Interferon Beta for MS

-MOA, SE, efficacy

A

Modualtes T cell and B cell function, decreases expression of matrix metalloproteinases and reverses BBB disruption

Annually ~30% reduction in relapses, disability, MRI lesion activity
Reduces mortality

SE:

  • Flu like symptoms
  • Injection site reaction
  • Depression, leukopenia, LFT derrangement, Thyroid disorders
  • Some will develop Abs
120
Q

Glatiramer Acetate for MS

-MOA, SE, efficacy

A

MOA

  • Functions as an altered peptide ligand for MHC Class II
  • Stimualtes TREG cells

Annually ~30% reduction in relapses, disability, MRI lesion activity

SE:
-Injection site reaction

121
Q

Laquinimod for MS

-MOA, SE, efficacy

A

unknown MOA
-reduces leuks in CNS or modualtes cytokines

23% reduction in relapse and reduces disability and MRI lesions

SE
0Mild LFT derrangeent

122
Q

Teriflunomide for MS

-MOA, SE, efficacy

A

From LEF
-Antimetabolite that interferes with de novo synthesis of pyramidines, blocks replication and rapidly dividing cells

31% reduction in relapse, disability progression and MRI lesions reduced by 80%

SE
-Thinning hair, GI upset, teratogenic

123
Q

Dimethyl Fumerate for MS

-MOA, SE, efficacy

A

MOA:

  • Hydrolyzed into monomethyl fumerate
  • Unknown mechansm

53% reduction in relapse, 90% reduction in MRI lesions

SE:
Flushing and diarrhea
Nausea and abdo pain
PML

124
Q

Fingolimod

-MOA, SE, efficacy

A

MOA

  • Sphingosine 1 phosphate receptor modulator
  • Inhibits the migration of T cells from lymphoid tissue into peripheral circulation and CNS

54% reduction in relapse and 82% reduction in MRI lesions

SE:

  • First dose bradycardia
  • VZV reactivation
  • Macular oedema (need 3 monthly OCT)
  • HTN
  • LFT derrangment
  • Lymphopenia
  • Risk of rebound relapse after ceasing (1-2 months post) that can be more severe than prev. relapses
  • PML
125
Q

Cladribine for MS

-MOA, SE, efficacy

A

MOA

  • Immunosuppresive purine antimetabolite that targets lymphocytes, folloed by reconstitution
  • 2x5 da treatment one month apart then yearly

58% reduction in relase, 82% reduction in MRI lesions

SE

  • HEadaches
  • Lymphopenia
  • Herpes Zoster
  • Malignancy (increased risk with treatment >2 years)
126
Q

Natalizumab for MS

-MOA, SE, efficacy

A

MOA

  • targets a4b1 integrin
  • Inhibits the leucocyte migration across the BBB by blocking the interaction between a4 integrin on leuks and the vascular cell adhesion molecule 1 on endothelial cells

68% reduction in relapse, 92% reduction in MRI lesions

SE:

  • Anxiety, pharyngitis, peripheral oedema, infusion related symptoms
  • 6% develop persistant anti natalizumab ab
  • PML
  • Risk of rebound relapse with cessation
127
Q

PML features

A

Subacute worsening visual, motor, or cognitive change with gradually enlarging T2 hyperintensities with minimal or no gad enhancement

128
Q

Mx of PML

A

PLEX
CAn trial Pembrolizumab

Can develop IRIS post PLEX abou 2-5 weeks post PLEX

129
Q

Alemtuzumab for MS

-MOA, SE, efficacy

A

MOA

  • Targets CD52 (T and B cells) and leads to lyphopenia
  • yearly infusion for 2 years

SE:

  • Infusion reaction
  • ITP
  • Graves disease
  • Anti GBM
  • Increased infection risk, herpes
130
Q

Ocrelizumab for MS

-MOA, SE, efficacy

A

MOA

  • Targets CD20
  • Similar mechanism to rituximab

Effective in Primary Progressive MS (need Hx of OGB in CSF previously)
Slows the disability, doesn’t cure it.

131
Q

Siponimod for MS

-MOA, SE, efficacy

A

MOA

  • Selective Sphingosine 1 phosphate receptor 1 and 5 modulator
  • 2nd gen Fingolimod
  • may prevent neurdegeneratio nand promote remyelination

Indication: Secondary progressive MS

SE:
-First dose bradycardia
-VZV dissemination
-Macualr oedema
HTN
-LFT derrangement
Lypmhopenia
132
Q

Mitoxantrone for MS

-MOA, SE, efficacy

A

MOA
-Chemo agent: inhibition of B cell, T cell, and macropage proliferation

For aggressive RRMS, secondary progressive MS

SE: 
Cardiac toxicity (CI if EF <50%) or drop during treatment
133
Q

MS and pregnancy

A

MS relapses are reduced in pregnancy, but not completely.

Increased risk of relapse post partum

134
Q

Tx of MS in pregnancy

A 
CAn use:
IFB
Glateramer Acetate
Alemtuxumab
Rituximab/Ocrelizumab - avoid in 2nd/3rd trimester
135
Q

Features of NMO

A

Relapsing B cell mediated disease targeted agaisnt astrocytes
-More severe than MS with likely permanent residual damage

PRsentation

  • Optic neuritis
  • Acute myelitis (contiguous spinal cord MRI lesion over 3 vertebral segments)
  • Area postrema syndrome (episodes of otherwise unexplained hiccups or nausea and vomiting)
136
Q

Anti AQP4

A

NMO

137
Q

MOG Ab

A

NMO, ADEM

-Steroid responsive

138
Q

Tx of NMO

A

Acute: IV Methylpred or PLEX

Chronic:

  • Eculizumab, Ritux, AZA, MTX
  • Inebilizumab (CD19 depletion)
  • Satralizumab (Anti IL 6 receptor)
139
Q

ADEM

A

USually preceeded by viral infection
Resolves after 3 months
Neurological symptoms assocaited with encephalopathy

140
Q

SOD1 mutation

A

Gain of function mutation for motor neuron disease

141
Q

C9orf72

A

Motor neuron disease

142
Q

TDP-43 cytoplasmic inclusions

A

Dementia in ALS - Tau process
ALS patients get frontotemporal dementia - executive function and verbal fluency loss

Ocassional overlap with PSP/PArkinsons

143
Q

NCS in Motor neuron disease

A

Decreased CMAP

Normal SNAP

144
Q

Tx of MND

A

Riluzole - inhibitor of glutamate relase
-Extends survival by 3-6 months

Edaravone

  • Potential free radical scavenger to reduce oxidative stress
  • Mild reduction in progression (only safe to use up to 6 months)
145
Q

What is a motor unit

A

a single motor nerve and all of the muscle fibres it innervates

146
Q

Fibrillation potentials and positive sharp waves on EMG

A

Spontaneous firing of individual muscle fibres
Sign of ACTIVE DEMYELINATION
Can occur in inflammatory myopathies

147
Q

Faciculations on EMG

A

Firing of all parts of the motor unit

  • MND
  • CIDP
  • Chronic nerve entrapment
  • Cal also occur in benign fasciculation syndrome
148
Q

EMG - Neurogenic changes

A

Spontaneous: Faciculations
Morphology: Large amplitude , widened duration
Recruitment: Decrased

149
Q

EMG - Myogenic changes

A

Morphology: small amplitude
Recruitment: Increased

150
Q

MG Antibodies

A

AChR (85%) - Correlates with thymoma or thymic hyperplasia

MuSK (6-10%)

151
Q

Features of MG with MuSK ab

A

Non-white, young female
Early onset
Not related to thymoma
Generalised MG
Severe disease with resp and bulbar involvement
Poor response to treatment, good response to rituximab

152
Q

How does Tensilon Test work

A

Administration of edrophonium (short acting acetylcholinesterase inhibitor)
Given with atropine at bedside

153
Q

Diagnostic findings on Repetitive nerve stimulation for MG

A

10% decline in amplitude with repitation
-Good for generalised MG

Single fibre EMG best for ocular MG

154
Q

Mx of MG

A
  1. Pyridostigmine (Cholinesterase inhibitor)
  2. Steroids - reduce risk of developing generalised MG - can worsen before improving usually after 4-5 days of starting
  3. AZA/MMF/Tac/RTX/IVIG/PLEX
  4. Eculizumab in severe cases

Thymoma removal if present

MG Crisis: IVIG, PLEX, Steroids, Supportive care and intubation

155
Q

Meds that can cause G crisis

A 
BB
CCB (verapamil)
Aminoglycosides
Fluroquinolones
Tetracyclines
Macrolides
Phenytoin
Lithium
156
Q

MG and pregnancy

A

Exacerbation in 1st trimester and post partum

Settled during 2nd and 3rd trimester

157
Q

LEMS Clinical features

A

Prosimal weakness - improved post exercise
Autonomic features - Dry mouth, erectile dysfunction, constipation, urinary issues, orthostatic hypotension
Areflexia

158
Q

VGCC antibodies

A

LEMS

159
Q

Tx of LEMS

A

Tumor resection (SCLC usually paraneoplastic)
3-4 diaminopyridine - Blocks efflux of K+ ions prolonging duration of depolarisation
IVIG
PRed

160
Q

MOA of Botulism

A

Anaerobic spore forming Gram positive bacillus

Inhibition of presynaptic acytelcholine release

161
Q

Features of Botulism

A 
Incubation 2 days
N+V
Symmetric descending flaccid paralysis
Autonomic involvement - Dry eyes, mouth, paralytic ileus, urinary retention
Mentation and reflexes preserved
162
Q

Mx of botulism

A

Equine antitoxin

  • Avoid aminoglycosides
  • REmove toxin if ileus and not absorbed

Recovery over months

163
Q

Anti synthetase syndrome

A 
ILD
FEver
Polyarthritis
MEchanic hands
Raynauds

Anti Jo1 ab

164
Q

Anti cN1A

A

Inclusion body myositis

165
Q

Anti SRP

A

Necrotising autoimmune myositis

166
Q

Types of generalised seizures

A

Tonic clonic
Absence
Myoclonic
Atonic

167
Q

Juvenile absence epilepsy features and Mx

A

Absece seizures and occasional GTCS
Generally cease in late teens
Mx - Valproate

168
Q

JME features and Mx

A

ICK Gene in 7 % (Intestinal cell kinase)
Myoclonus in nearly waking states
CAn have GTCS and absence seizures
Wose with sleep deprivation and ETOH

Mx

  1. Valproate
  2. Lamotrigine - women of child bearign age
  3. Zonisamide

Prognosis - poor remission

169
Q

3 Hz spike/polyspike wave discharges

A

Buzzword for JME

170
Q

Mesial Temporal Lobe Epilepsy with Hippocampal Sclerosis

A

Most common form of epilepsy
Risk factors: Prolonged febrile convulsions, CNS infections
Typical auras, focal seizures with impaired awareness with or without automatisms
-Deja vu, gustatory/olfactory hallucinations, epigastric rising sensation

Usually medically refractory and requiring surgery

171
Q

EEG: Alpha 9-12 Hz

A

Normal Wakefullness

172
Q

EEG: Beta 13-15 Hx

A

Too much Benzos

173
Q

EEG: Theta 5-8 Hz

A

Drowsy or encephalopathic

174
Q

EEG: Delta 1-4 Hz

A

Sleep or encephalopathic

175
Q

EEG: Spike and wave

A

Epileptogenic

176
Q

When to treat seizures

A

After 2 seizures no more than 1-2 years a part

EArly treatment if high risk of recurrence or in vulnerable population

177
Q

Tx of choice for focal seizures

A
  1. Carbamazepine
  2. Lamotrigine
  3. Gabapentin
  4. Keppra
  5. Valproate
  6. Phenytoin
178
Q

Tx if choice for absence seizures

A
  1. Valproate

2. Ethosuzimide

179
Q

Tx of choice for Generalised epilepy

A
  1. Valproate
  2. Lamotrigine for women of child bearing age
  3. Zonisamide
180
Q

Carbamazepine and SJS HLA type

A

HLA B*1502 - Han Chinese, thai, malay, filopino

HLA A *3103 - Europeans

181
Q

Best known combo for dual therapy in epilepsy

A

lamotrigine and valproate

182
Q

Role of hormones in epilepsy

A

Estrogen promotes neuroexcitatory properties
Progresterone promotes neuroinhibitory properties

Lamotrigine levels lowered by OCP
OTher AEDs induce rapid clearance of OCP

183
Q

Best tolerated AEds in pregnancy

A

Lamotrigine and carbamazepine

Note that lamotrigine and keppra undergo increased clearance and will need increased dose at some point in pregnancy

184
Q

Risk factors for SUDEP

A

GTCS > 2 years
Nocturnal seizures
Treatment resistant seizures
Long duration of epilepsy and early stage of onset
Dravet Syndrome - Na channel gene mutation

185
Q

Mx of Status epilepticus

A
  1. Benzos - IV Loraze 2-4 mg; Midaze 10 mg IM
  2. Load with AED - Rule of thumb 20 mg/kg
  3. Midaze/propofol infusion
  4. Pentobarbitol

Monitor BSL as will drop with prolonged status

186
Q

MOA Carbamazepine and SE

A

Sodium channel

SE:
-Diplopia/dizziness/drowsiness
-SJS/Rash
-Aplastic anaemia
Hyponatremia
-Hepatotoxicity
-Lupus like syndrome
-WEight gain
-Decreased bone mineral density
187
Q

MOA and SE Keppra

A

Inhibits presynaptic calcium channels reducing neurotransmitter release and acting as a neuromodulator

SE:

  • Psychosis/irritability/hostility/depression
  • Dizziness
188
Q

MOA and SE Phenytoin

A

Sodium channel

SE:

  • CAn worsen absence and myoclonic seizures
  • Ataxia, nystagmus, diplopia
  • Blood dyscrasia
  • Behavior changes
  • Skin thickening/gingival hyperplasia/hirsutism/corsening facial features/Acne
  • Peripheral neuropathy
  • Bone disease
189
Q

MOA and SE Valproate

A

PIP3 reduction, sodium channel, Increases GABA

SE:

  • WEight Gan/PCOS like syndrome/ menstrual cycle issues
  • Thrombocytopenia
  • Teratogenic ++
  • Acute liver failure/pancreatitis
  • Alopecia
  • PArkinsons/dementia
190
Q

CGRP

A

Calcitonin Gene Related Peptide

  • Produced by trigeminal ganglion and released in nerve endings
  • Most potent dilator of cerebral and diral blood vessels
  • Release of inflammatory mediators from mast cells
  • Increased levels during a MIGRAINE
191
Q

Hemiplegic migraine

A

weakness tkes up to 72 hours to reseolve
Need to rule out stroke or TIA
FMH1 mutation of CANCNL1A4 gene (coding for calcium channel)

192
Q

Migraine prophylaxis medication options

A 
Amitryptylline
Propanolol
Topiramate
Candesartan
Pizotifen

New role for CGRP inhibitors

193
Q

Cluster headaches

A

Male predominence
Occur nearly daily lasting 15-180 mins
Follow circadian cycle - predominantly nocturnal
Sharp stabbing pain with ipsilateral autonomic features
Restlessness and agitation

Acute Tx - Triptans, High flow O2 with non rebreather
Bridging Tx - steroids, occipital nerve block
Prevention - Verapamil SR TDS

194
Q

Paroxsymal Hemicrania

A

Similar to cluster but..
Female predominant
5-10 times per day lasting 2-20 mins
Complete an absolute response to indomethocin (diagnostic)

Melatonin trial if indomethocin responsive

195
Q

Hemicrania continua

A

Constant unilateral, side locked headache
assoacited with autonomic features and restlessness
Daily to near daily lasting 30 mins to 3 days
Tx: indomethicin responsive

196
Q

SUNCT/SUNA

Short lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing

A

Stabbing lancinating burning pain, orbital pain
Up to 100 times per day lasting 1-600 seconds
Tx: Lamotrigine

O2 and indomethocin do nothing for this

197
Q

Trigeminal neuralgia

A

20 x increase risk in MS - esp. bilateral TN
V2 distribution most common
Usually due to neurovascular compression

Tx: CArbamazepine, microvascular decompression

198
Q

Idiopathic intracranial HTN RF and secondary causes

A

Unknown cause

RF: Female, obese, reproductive age

SEcondary causes:
Venous sinus thrombosis
Tetracycliens, fluroquinolones
Vit A - tretinoin
Iron deficiency
OSA
Raised CSF protein
199
Q

Diagnsotic criteria for IIH

A

Papillodema
Normal neuro exam except CN abnormalities
Normal MRI and CSF
CSF opening pressure > 25 mmHg

200
Q

IIH management

A 
WEight loss
Acetazolamide
Topiramate
VP shunt
Optic nerve seath fenestration
Venous stenting
201
Q

Aceazolamide MOA

A

Potent ezyme inhibitor of carbonic anhydrase, and it impedes the activity at the choroid plexus reducing CSF secretion

202
Q

Intracranial hypotension

A

Postural headache worse on standing or sitting and better when laying flat
Most common is post LP headache

Mx:
bed rest, fluids, coffee, epidural blood patch, surgical repair

203
Q

Eseential tremor

A

Bilateral, slow progression
ETOH may help, but not diagnostic

Mx: Propanolol, DBS, USS Thalamotomy, Primidone

204
Q

Intention tremor

A

Worse on end of movement and suggests cerebellar involvement

205
Q

Holmes tremor

A

Unilateal, rest, postural, movement, and worse on intention

Seen in wilson’s disease, stroke, MS

206
Q

Dystonia

A

Sustained r intermittant muscle contractions causing abnormal often repetitive movements, postures, or both
Movments are typically twisting
Initiated or worsened by voluntary action

Mx: Botox

207
Q

Chorea

A

Involuntary movmeent of limbs, trunk, neck, or face wjich rapidly flit from region to region in an irregular pattern

208
Q

Dyskinesia

A

Chorea movement with parkinsons

209
Q

FEatures of presymptomatic stage of PArkinsons

A

Anosmia
Constipation
REM sleep disorder
Mood changes, increasing fatigue

210
Q

Inclusion criteria for PArkinsons

A

Decrementing bradykinesia
Rigiditiy
4-6 Hx rest tremor

211
Q

Side effects of L Dopa

A 
Sedation, N+V
Dyskinesia, mtor fluctuations
Impulse control disorders (in high doses)
Punding
Dopamine dysregulation - abuse
212
Q

Motor complications in PArkinsons

A

On - Well
Off - Full blown parkinsons
Dyskinesias - too much drugs

Will have mtr fluctuations and dyskinesias after 5 years of treatment

213
Q

Risk factors for motor fluctuations in PD

A

Longer disease duration
Higher levels of L Dopa used
Younger onset of PArkinsons

214
Q

Mx of motor fluctiations in PD

A

Divide dose into increased freq.

Add on COMT or MAO

215
Q

Dyskinesia treatment in PD

A

minimise dopaminergic meds
Amantadine
Break up doses into higher frequency

216
Q

Amantadine MOA

A

Weak antagnist of the NMDA type glutamate receptor, Increases dopamine release and blocks dopamine reuptake

217
Q

DA agonist - names, MOA

A

MOA: Stimulate dopamine by binding directly to post synaptic dopamine receptors in the striatum

MEds:
-Non Ergot DAs: Pramiprexole, Ropinirole, Transdermal rotigotine, Apomorphine

-Ergot derived: CAbergoline, bromocriptine, pergolide

218
Q

SE of CAbergoline, bromocriptine, pergolide

A

Heart valve complications and retroperitoneal fibrosis

219
Q

SE DA agonists

A

Nausea, somnolence, oedema, dizziness, hallucinations, hypotension
Worsens delirium
Impulse control disorders

220
Q

MAO B inhibitors names and SE

A

Rasagline, selagiline

USed in early/young patients

SE: 
LFT derrangement
INSOMNIA - most common
Higher overall mortality
Tyrasine hypertensive crisis
-Tyrasine releases NA and ordinarily MAO A breaks down excess, if MAOI then adrenergic crisis
221
Q

Exenatide in Parkinsons

A

GLP1 receptor agonst

Improves medication motor scores
Likely symptomatic improvement rather than neuroprotective

222
Q

Order of ceasing PD meds in setting of delirium and hallucinations

A
  1. Anticholinergic meds
  2. Amantadine
  3. DA
  4. MAOI
  5. L Dopa
223
Q

Why can meds not be stopped abruptly in PD

A

PArkonsonian crisis - NMS

224
Q

Strongest predictor of dementia in PD

A

Age not duration

225
Q

Alpha synneuclianopathies

A

PD
DLB
MSA

226
Q

Tau protein opathies

A

PSP

Corticobasalar degeneration

227
Q

PSP Triad and MRI findings

A

Supranuclear palsy, postural instability, dementia

  • Early falls
  • Psuedobulabar palsy: dysarthria anddysphasia

Hummingbird sign on MRI (midbrain atrophy)

228
Q

MSA FEatures and MRI findings

A

Autonomic failure, Parkinsonism, Cerebellar signs

Hot cross bun sign

229
Q

Corticobasal syndrome

A

Cortical dysfunction and basal ganaglia dysfunction

Asymetric progressive ideomotor aprazia that frequently affects the hand and is associated with rigidity myoclonus and dystonia

Alien hand

230
Q

FMR protein deficiency

A

FXTAS/Fragile X syndrome

231
Q

HTT Protein

A

Huntingtons
-CAG repeat, paternal anticipation

HTT protein is toxic to striatal neurons

232
Q

Spinocerebellar ataxia

A

CAG repeat disorder
CAn be AD, AR, X linked
Variable syndromes, but predominantly ataxia and UMN signs

233
Q

Differentiating Serotonin syndrome from NMS

A

SS:

  • Acute onset <24 hours
  • Myoclonus, Hyperreflexia, rigidity

NMS

  • Slower onset
  • CK rise and rigidity
234
Q

HSV encephalitis

A

Herpes PCR can be negative in first 24-48 hours and should recheck if high suspicion

MRI: Y2 hyperintensity in medial and inferior temporal lobe extending up insular cortex

EEG: focal slowing

Tx: IV Aciclovir 14-21 days

235
Q

Listeria encephalitis

A

Most commonly rhomboencephalitis - brainstem involvement
Incidence higher in pregnancy, elderly, immunosuppressed

Tx: Benpen, ampicillin

236
Q

Anti Hu

A

Limbic encephalitis, peripheral neuropathy

SCLC

237
Q

Anti Yo

A

Cerebellar degeneration

Breast/Ovarian cancer

238
Q

Anti Ri

A

Opsoclonus myoclonus, rhomboencephalitis

SCLC

239
Q

Anti Ma/Ta

A

Rhomboencephalitis - NArcolepsy, Vertical gaze disorder

Testicular cancer

240
Q

NMDA encephalitis

A

F>M
50% of young women have ovarian teratoma
Most common cause of AI encephalitis
PResent with preceeding viral prodrome and then associated with psychosis, hallucinations, behavioral changes

NMDA antibodies oresent
MRI: Temporal lobe limbic changes

241
Q

Tx of NMDA encephalitis

A 
Remove cancer
IV methylpred, then PO pred
IVIG or PLEX
Rituximab
Cyclophophamide
242
Q

LGI1 antibody

A

Voltage gate potassium channel encephalitis
Cognitive and memory changes
Faciobracial dystonic seizures

243
Q

CASPR2 ab

A

Voltage gate potassium channel encephalitis

244
Q

VGKC Ab

A

Voltage gate potassium channel encephalitis

245
Q

PRES RFs

A

Clincial and radiological syndrome of encephalopathy and posterior circulation oedema

RFs:
HTN
Pre-eclampsia
REnal failure
Autoimmune conditions
246
Q

PRES Tx

A

Aggressive BP control

Seizure Mx

247
Q

Effect on NCS in radiculopathy and pre ganglionic lesions

A

Normal NCS

248
Q

What does a low amplitude on NCS represent

A

Axonal loss

249
Q

What does increased latency or decreased conduction velocity on NCS represent

A

Demyelination

250
Q

NCS in Compression lesions

A

Focal demyelination - drop in velocity at lesion site

Oeer time will get drop in amplitude, then change in motor conduction

251
Q

What is SNAP for NCS

A

Sensory nerve action potentials - the sum of the resultant APs

252
Q

What is CMAP for NCS

A

Compound muscle action potential - sum of all the APs in the muscle fibre

253
Q

Conduction Block on NCS

A

Specific point that the nerve has slowed conduction

Drop in CMAP amplitude between proximal and distal sites of the same nerve

254
Q

F wave on NCS

A

Only way of looking at proximal segment of nerve
May be only abnormality in early GBS
Delayed F wave if dysfunction

255
Q

Risk factors for carpel tunnel

A 
Female
Diabetes
PRegnancy
RA
Hypothyroidism
HAemodialysis
Steroid use
256
Q

Mononeuritis multiplex presentation

A

painful neuropathy which is not at a place of compression
Due to inflammation of blood vessel within the nerve - both small and large fibres are affected - motor and sensory

Definitive testing is biopsy

257
Q

3rd nerve palsy determining compression vs vascultitis

A

Compression - dilates first

Vasculitis - Motor, then pupil dilates later or can be pupil sparing altogether

258
Q

Sarcoid induced neuropathies

A

Polyradiculopathy
Peripheral neuropathy
Mononeuropathy multiplex

Bilateral CN7 palsies - Always consider sarcoid

259
Q

Hereditary neuropathy with liability to pressure palsy

HNPP

A

PMP22 gene reciprocal deletion
AD
Characterised by transient and recurrent motor and sensory mononeuropathies, typically occuring at entrapment sites

260
Q

Peripheral neuropathy always affects feet before hands. If it is the other way around who do you need to consider as the cause

A

Dorsal root ganglion or cervical injury

261
Q

DDX for autonomic failure

A

Diabetes
MSA
Amyloid

262
Q

Paraproteinemic Peripheral neurpathy causes

A
  • MGUS - If present not always cause - IgM most common
  • Waldenstroms - distal acquired demyelinating symmetric neuropathy
  • MM
  • POEMS
  • Amyloidosis - Painful length dependent PN with generalised autonomic failure
263
Q

Chemo agents that cause PN

A

Platinum based chemo
Taxanes
Vinca ankaloids
Bortezomib

264
Q

Neuropathies in B12 deficiency

A

PN
Corticospinal tract
Dorsal column

265
Q

RAdiculopathy features

A

Asymmetric
Follow a dermatome or myotome
PAINFUL
Can be sensory or motor

266
Q

Zoster sine herpete

A

Neuralgiform pain with no rash

267
Q

Miller Fisher Syndrome

A

Type Of GBS

Opthalmoplegia, areflexia, ataxia

268
Q

Anti GQ1b

A

Miller Fisher Syndrome

269
Q

GBS presentation

A

Prodrome in the 4 weeks prior to onset of symptoms
Symmetric ascending weakness
CAn be associated with radicular pain
Proximal and distal weakness is usually the predominant feature
Hyporeflexia or areflexia can be delayed by 1 week
WEakness nadir by 2-4 weeks
–If progressive Sx post 4 weeks then rethink Diagnosis ?CDIP

270
Q

NCS in GBS

A

Prolonged F wave latency
Prolonged distal latencies (demyelinating) - motor before sensory
Sural nerve is often preserved

271
Q

Anti GD1a and GM1

A

Acute motor axonal neuropathy/Multifocal motor neuropathy with conduction block
(GBS varient)

272
Q

Tx of GBS

A
  1. PLEX - Reduces time to walk unaided and time on ventilator - USe within 2-4 week onset
  2. IVIG -use within 2 weeks onset for most benefit in those unable to walk unaided

NO STEROIDS - worse outcomes

273
Q

Poor prognostic markers in GBS

A 
Rapid onset prior to presentation
High diability nadir
Severely reduced CMP
Older than 40 yo
PReceeding diarrheal illness, C. Jejuni
PReceeding CMV infection
Inexcitable nerves
274
Q

CIDP

Chronic inflammatory demylinating polyradiculopathy

A

Chronic version of AIDP
Nadir > 4 weeks
Usually milder phenotype and rarely has resp involvement
Similar NCS findings to AIDP

Tx
-Steroids, steroid sparing agents, IVIG, PLEX

275
Q

NF155

Contactin 1 Ab

A

Severe CIDP

Mx: Rituximab

276
Q

Multifocal Motor neuropathy with conduction block

A

Immune mediated condition with asymmetric peripharl motor loss
Usually upper extremeties
Atrophy and EMG evidence of axon loss over time
Deep tendon reflexes usually decreased
Anti GM1 in 40-80%

IVIG and steroids can worsen the condition

277
Q

Dorsal root Gangiolopathy

A

Pure sensory loss
UL before LL or same time as LL
Causes: Sjogrens, Anti Hu, B6 deficiency

278
Q

Parsonage-Turner Syndrome

A

Neuralgic amyotrophy, brachial neuritisL Pain and muscle atrophy
-Severe shoulder and arm pain followed by weakness and numbness
Usually middle aged men, but can be anyone

Tx: steroids and analgesics

279
Q

Diabetic Amyotrophy (Lumbosacral Radiculoplexopathy)

A

Age >50 and men usually
SEvere unilateral pain in the back, hip, or thigh that spreads to involve the entire limb and can involve the other leg within weeks or months
-Proximal weakness shortly after the onset of pain, and then can become widespread

Not related to glucose control or duration of diabetes

280
Q

LEvel above which consciousness is associated

A

medulla

281
Q

Topiramate MOA and SE

A

stabilises presynaptic neuronal membranes by blocking voltage-dependent sodium channels. Enhances activity of GABA on postsynaptic chloride channels.

SE:
-Psych stuff
Renal stones

282
Q

by rapidly progressive dementia, myoclonus and periodic tri-phasic sharp waves on EEG?

A

JC Virus

283
Q

Stroke Syndrome:

MCA inferior devision

A

Contralateral visual loss - homonymous hemianopia Contralateral visual loss - upper quadrant anopia
Contralateral constructional apraxia (non-dominant hemisphere)
Contralateral aphasia - receptive (dominant hemisphere - Wernicke’s area)

284
Q

Stroke Syndrome:

MCA superior devision

A

Contralateral weakness - upper and lower limb (Face, arm>leg) Contralateral weakness - face - lower half Contralateral hemisensory loss - upper and lower limb Contralateral sensory loss - face - all modalities Contralateral hemineglect (non-dominant hemisphere) Contralateral aphasia - expressive (dominant hemisphere - Broca’s area)

285
Q

Balint Syndrome

A

If affecting bilateral posterior cerebral arteries
Affects bilateral parietal-occipital lobes
Bilateral loss of voluntary but not reflex eye movements
Bilateral optic ataxia - poor visual-motor coordination
Bilateral asimultagnosia - inability to understand visual objects

286
Q

Claude syndrome

A

Ipsilateral eye movement weakness (oculomotor palsy)
Contralateral ataxia - arm and leg (cerebellar tracts)
Contralateral tremor

287
Q

Posterior cerebral artery - Unilateral occipital

A

Contralateral visual loss - homonymous hemianopia (optic pathway, calcarine cortex)

288
Q

Thalamic Pain syndrome

Dejerine-Roussy Syndrome

A

Penetrating branches to thalamus
Contralateral hemisensory loss - all modalities
Contralateral hemi-body pain

289
Q

Weber Syndrome

A

Penetrating arteries to midbrain

Contralateral weakness - upper and lower limb (corticospinal tract) Ipsilateral lateral gaze weakness (CnIII)

290
Q

Lateral pontine syndrome

Marie-Foix syndrome

A

AICA
Ipsilateral ataxia - arm and leg (cerebellar tracts) Contralateral weakness - upper and lower limbs (corticospinal tracts) Contralateral pain and temperature loss (spinothalamic tracts)

291
Q

Lateral medullary syndrome

Wallenberg syndrome

A

PICA

Small penetrating arteries
Ipsilateral loss of pain and temperature from face + facial pain (Cn5 nucleus)
Ipsilateral ataxia - arm and leg, gait ataxia (Restiform body, cerebellum)
Ipsilateral nystagmus, N&V, vertigo (Vestibular nucleus)
Ipsilateral hoarseness and dysphagia (nucleus ambiguus)
Ipsilateral Horner’s syndrome (descending sympathetics)
Contralateral loss of pain and temperature from body (Spinothalamic tract)
Hiccoughs

292
Q

Medial medullary syndrome

Dejerine syndrome

A

Vertebral ARtery/anterior spinal

Contralateral weakness of upper and lower extremity (Pyramidal tract) Contralateral hemisensory loss - vibration and proprioception (Medial lemniscus) Ipsilateral tongue weakness +/- atrophy (Cn12 nucleus)

293
Q

Inferior medial pontine syndrome

Foville syndrome

A

Basilar artery

Unilateral lesion affecting the dorsal pontine tegmentum in caudal third of pons
Contralateral weakness - upper and lower limbs (corticospinal tract)
Ipsilateral weakness - face - entire side (CnVII nucleus/fascicle) Ipsilateral lateral gaze weakness (PPRF or CnVI nucleus)

294
Q

Locked-in syndrome

A

Basilar artery

Affects bilateral ventral pons Bilateral weakness - upper and lower limb (Bilateral cortical spinal tracts) - quadriplegia Bilateral weakness - face - entire side (bilateral corticobulbar tracts) Bilateral lateral gaze weakness (bilateral fascicles of CnVI)
Dysarthria (bilateral corticobulbar tracts)

295
Q

Ventral pontine syndrome

Raymond syndrome

A

Basilar artery

Affects ventral medial pons
Ipsilateral lateral gaze weakness (CnVI) Contralateral weakness - upper and lower limb (pyramidal tract)

296
Q

Ventral pontine syndrome

Millard-Gubler syndrome

A

Basilar artery

Affects basis pontis and fascicles of CN VI and VII Contralateral weakness - upper and lower limb (pyramidal tract) Ipsilateral lateral gaze weakness (CnVI) Ipsilateral facial weakness (whole side) (CnVII)

Bpt (15 decks)

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