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Neurology Flashcards

1
Q

What does a sensory level suggest?

A

Location of injury is in spinal cord

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2
Q

What cell counts are significant on LP?

A

Lymphocyte >5
Polymorph >0

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3
Q

Will lesions in cranial nuclei in brainstem and anterior horn cell nuclei have UMN or LMN signs?

A

LMN, despite being within central nervous system

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4
Q

Pyramidal weakness

A

Weakness of
Upper limb extensors
Lower limbflexors

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5
Q

Frontal Lobe Signs

A

Primary motor cortex
Personality change
Primitive reflex (pout, moro, palmomental, glabellar tap)
Expressive dysphagia (dominant)
Anosmia
Optic nerve compression
Gait apraxia

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6
Q

Parietal Lobe

A

Primary sensory cortex
Gerstmann syndrome:
- Dominant, angular gyrus
- Acalculia, agraphia, L-R disorientation, finger agnosia (ALF)
Sensory, visual and spatial inattention (non dominant lesions)
Construction and dressing apraxia
Lower quadrantanopia

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7
Q

Temporal Lobe

A

Primary auditory cortex
Receptive aphasia (dominant)
Memory loss
Upper quadrantanopia

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8
Q

Foster Kennedy Syndrome

A

Tumour in frontal lobe
Altered vision in one eye
Papilloedema in opposite eye
Smell disturbance
Other frontal signs

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9
Q

Occipital Lobe

A

Homonymous Hemianopia
Anton’s Syndrome: cortical blindness with confabulation (bilateral lesions of occipital lobe)
Alexia without agraphia

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10
Q

What does the presence of quadrantanopia signify?

A

Cortical lesion

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11
Q

How to work out where the lesion is in quadrantanopia?

A

Flip everything
Up is down
Left is right

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12
Q

Broca Aphasia

A

Expressive, non fluent aphasia
Can comprehend, know what to say, but just can’t

Dominant frontal lobe

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13
Q

Wernicke’s Aphasia

A

Fluent, receptive aphasia
Not frustrated, can speak but incomprehensible

Dominant temporal lobe

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14
Q

Conduction Aphasia

A

Mix of Broca’s and Wernicke’s
Due to damage to the connection arcuate fasciculus)
Struggle with repetition, can comprehend some things,

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15
Q

Global Aphasia

A

Can’t comprehend, can’t express themselves
Left MCA stroke is classical cause

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16
Q

Transcortical aphasias

A

Can repeat things
So Transcortical motor: Broca’s but can repeat
Transcortical sensory: Wernicke’s but can repeat

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17
Q

Corticospinal Tract

A

Descending motor pathway
From primary motor cortex in frontal lobe → corona radiata → posterior limb and genu of internal capsule → pyramids → decussate in lower medulla

Blood supply from penetrating branches of MCA (M1)

Prone to damage from small vessel disease, hypertension.

Dense pure motor hemiparesis. No cortical signs. No aphasia, dysphasia, hemianopia/quadrantopia.

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18
Q

Thalamus

A

Largest nuclear mass of nervous system,
All sensory nerves come through here
PCA arterial supply
Pure sensory loss if stroke here

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19
Q

Pure Sensory Loss Stroke

A

PCA lesion affecting Thalamus

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20
Q

Pure dense motor stroke

A

M1 MCA affecting internal capsule if no additional cortical signs such as inattention, aphasia, etc.

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21
Q

Parts of Thalamus

A

Anterior: language, memory
Lateral: motor + sensory
Medial: arousal, memory
Posterior: visual

Think about where they’re pointing to. Can mimic other lesions

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22
Q

Spinothalamic Tract

A

Run contralateral in spinal cord
Decussate at level
Pain, temperature, crude touch
Peripheral nerve body is in dorsal root ganglion, synapse in dorsal horn
Another synapse in thalamus then to primary sensory cortex
Run generally lateral

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23
Q

Dorsal column

A

Run Ipsilateral in spinal cord
Proprioception, vibration, fine touch
Peripheral nerve penetrates into central nervous system up to lower medulla, running medially. Body still in dorsal root ganglion.
Decussates in lower medulla and synapses to 2nd order nerve here
Then again synapses in Thalamus

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24
Q

Rules of the Brainstem

A

Rule of 4s
- 4 Cranial nerves in the medulla, 4 in the pons and 4 above the pons
- 4 structures midline beginning with M
- 4 structures to side beginning with S
- The 4 motor nuclei are in the middle are those divide equally into 12 (except 1 and 2): 3, 4, 6, 12

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25
Q

Medial Brainstem Structures

A

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

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26
Q

Lateral (Side) Brainstem Structures

A

Spinocerebellar pathways, spinothalamic pathways, Sensory nucleus of 5th CN, Sympathetic tract

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27
Q

Medial Longitudinal Fasciculus

A

Links CN III and VI to coordinate eye movements

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28
Q

Cranial Nerve I - Olfactory

A

Smell

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29
Q

CN II - Optic

A

Vision, afferent pathway for pupil

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30
Q

CN III - Oculomotor

A

Superior, inferior, medial rectus, inferior oblique, Levator palpebrae

Efferent pathway for pupil

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31
Q

CN IV - Trochlear

A

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

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32
Q

CN V - Trigeminal

A

Facial sensation, muscles of mastication

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33
Q

CN VI - Abducens

A

Lateral rectus

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34
Q

CN VII - Facial

A

Muscles of expression, Stapedius, sensation to anterior 2/3 tongue

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35
Q

CN VIII - Vestibulocochlear

A

Hearing and balance

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36
Q

CN IX - Glossopharyngeal

A

Sensation: middle ear, posterior 1/3 tongue, some swallowing

?Carotid baroreceptor

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37
Q

CN X - Vagus

A

Sensation of pharynx, larynx, oesophagus, Thoracic and abdominal viscera
Motor: soft palate, larynx, pharynx

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38
Q

CN XI - Accessory

A

Sternocleidomastoid, Trapezius

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39
Q

CN XII - Hypoglossal

A

Tongue movement

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40
Q

Medial Lesion

A

Abnormal eye movements, tongue movements, motor weakness in limbs, fine touch.proprioception/vibration loss

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41
Q

Lateral Lesion

A

Loss of pain/temperature sensation
Loss of facial sensation and movement, loss of hearing/balance

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42
Q

Eye movement for CN IV palsy

A

Look down and out, eye opposite direction looking is being tested.

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43
Q

Eye movement for CN VI palsy

A

Lateral gaze
Eye towards direction trying to look is being tested.

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44
Q

Lateral Medullary Syndrome

A

Ipsilateral facial numbness
Contralateral limb numbness
Ipsilateral Horner Syndrome
Ipsilateral dysmetria
Difficulty swallowing
Hiccups

Can have disinterest and vagueness if PICA artery stroke is causing it, get some cerebellar involvement

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45
Q

Staccato stroke syndrome

A

Tip of basilar lesion:
Medulla
Pons
Cortical

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46
Q

Brown Sequard

A

Ipsilateral LMN weakness and complete sensory loss at level of lesion
Ipsilateral UMN lesion below level
Ipsilateral loss of vibration and proprioception below lesion
Contralateral pain and temperature sensation 1-2 levels below
No bladder dysfunction

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47
Q

Central Cord Syndrome

A

Dysfunction of spinothalamic tracts on both sides at the level - “Cape sensory change”

As it enlarges, affects anterior horn cells → segmental LMN weakness at the level
Then UMN weakness below level

Typically seen after trauma, syrinx

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48
Q

Anterior Cord Syndrome

A

Loss of everything below level except proprioception and vibration (i.e. dorsal columns preserved)

Mostly due to ischaemia due to anterior spinal artery occlusion

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49
Q

Posterior Cord Syndrome

A

Loss of dorsal column only

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50
Q

Hyperacute treatment of ischaemic stroke without large vessel occlusion

A

0-4.5hr: CTB → Alteplase/Tenecteplase
4.5-9hr: CTP/MRI perfusion → Alteplase
Wake up: MRI/DWI and if markers to suggest <4.5hr (Ischaemia on DWI, normal FLAIR) → Alteplase

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51
Q

Risk Factors for haemorrhage post Thrombolysis

A

Happens regardless of tPA, but certain factors increase risk:
- Large infarcts
- Established infarct
- Grey matter infarcts
- Higher NIHHS
- Poor collaterals
- Hyperglycaemia
- Thrtombocytopaenia

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52
Q

Absolute contraindications to Thrombolysis

A

Extensive hypoattenuation on CT
Suspicion of SAH
Current or previous ICH
Intracranial neoplasms
Severe head trauma last 3 months
Intracranial or intraspinal surgery
Platelets <100
INR >1.7
APTT >40
Clexane last 24hr
Suspicion for current endocarditis
Active GI or internal bleed
Aortic arch dissection

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53
Q

Patients on which form of anticoagulation can be thrombolysed?

A

Dabigatran. Can be reversed fast enough to then thrombolyse.

Warfarin too slow to reverse
Apixaban’s reversal agent causes incomplete reversal

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54
Q

Choice of tPA

A

Tenecteplase superior to Alteplase on meta-analysis - standard of care for prior to 4.5hr

New study for Reteplase: superior to alteplase prior to 4.5hr

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55
Q

Indications for Clot Retrieval

A

Salvageable tissue and large vessel occlusion (ICA, M1, M2, ACA, PCA, Basilar)
Benefit even with large core
tPA eligible or ineligible (if eligible still give tPA)
Good premorbid function
No specific age cutoff

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56
Q

Management of large vessel occlusion stroke

A

If no access to clot retrieval, essentially as for stroke without large vessel occlusion.

0-4.5hr: CTA + CTP → Thrombectomy + Tenecteplase/Alteplase
4.5-9hr: Thrombectomy (or if not in centre with thrombectomy can give tPA if meets perfusion mismatch criteria, then transfer to centre with access to thrombectomy)
4.5-20hr: CTA + CTP → Thrombectomy

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57
Q

Predictors of good outcomes for clot retrieval

A

Younger
NIHHS Score
SBP
History of ischaemic stroke
Premorbid function
Location of thrombosis
Collaterals
Size of infarct (smaller better)
Time to treatment

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58
Q

Blood pressure targets in stroke

A

Too low = bad

Post tPA: keep below 185/110
No tPA: keep below 220/120

Intensive control <140 → worse outcomes

IV Labetalol 10mg often used

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59
Q

Hemicraniectomy in Ischaemic Stroke

A

When there is significant swelling.

For patients <60, with >50% MCA strokes, leads to 39% fewer deaths. But increases disability. (i.e. if you do survive you’re more impaired)

Works for older patients. but none >70 get back to mRS 0-2. In this group however it increases survival with no change in disability.

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60
Q

Who should be considered for an internal loop recorder post stroke?

A

Older patients
Higher CHADS-VASc
MRI characteristics
Left atrial cardiomyopathy

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61
Q

Benefit of DOACs over Warfarin in AF and Stroke

A

Dabigatran 150mg BD and Apixaban 5mg BD both superior to Warfarin
Rivaroxaban non inferior to warfarin
ICH risk lower for all
GI bleed more common in Riva and Dabi
Apixaban has mortality benefit

Embolic stroke of unknown cause - don’t anticoagulate: no benefit and increases bleeding

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62
Q

PFO

A

25% of population have it
PFO present in 50% of cryptogenic strokes
Most likely to be the cause if the patient is younger and has few other risk factors
Increases risk of perioperative stroke

Closure indicated in:
- <60 year olds
- With no other cause found and have atrial septal aneurysm or moderate to large right to left shunt

These patient should have closure + antiplatelets

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63
Q

When should Carotid Endarterectomy be done?

A

Patients with non disabling carotid artery territory stroke or TIA with ipsilateral carotid stenosis 70-99%

Consider if 50-69% and symptomatic (i.e. had a stroke in right territory)

Perform within 14 days, or within 3 months at the absolute most. Can be done as early as 48hr.

All then get usual secondary prevention

Asymptomatic stenosis only intervened upon if very high risk.

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64
Q

When to stent carotids post stroke

A

Selected patients with unfavourable anatomy, symptomatic restenosis, previous radiotherapy

Only in patients <70.

Don’t stent intracranial stenosis. No benefit over DAPT and risk factor management.

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65
Q

Most common vessels for dissection leading to stroke?

A

Carotid, Vertebral arteries

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66
Q

Post acute treatment for carotid/vertebral artery dissection leading to stroke

A

Aspirin

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67
Q

Most important risk factor to manage for stroke risk and when to do it

A

Hypertension (for both types)

Wait 48-72hr, then start. Risk benefit in reduction even if don’t have hypertension

Others:
Dyslipidaemia
Diabetes
Smoking
Alcohol

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68
Q

platelet use post stroke

A

Aspirin or Clopidogrel

DAPT if TIA or small stroke for 3 weeks then monotherapy

Long term DAPT increases bleeding risk without benefit

Ticagrelor better than Clopidogrel in patients who are CYP2C19 carriers (Reduces Clopidogrel metabolism, increases bleeding)

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69
Q

TIA Management

A

Workup like a stroke

DAPT for 21 days then monotherapy ongoing

If AF present, just start anticoagulation

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70
Q

Amaurosis Fugax

A

Form of TIA leading to transient monocular vision loss.

Descending curtain of visual loss

Never forget giant cell arteritis

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71
Q

Location of ICH and cause

A

Deep: Hypertension, other vascular risk factors

Lobar/peripheral: Cerebral Amyloid Angiopathy

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72
Q

Management of ICH

A

Intubate if dropping GCS
Aim for BP around 140 but not much lower
Manage hyperglycaemia
Reverse any anticoagulation (benefit limited for DOACs)
Don’t give platelets to reverse antiplatelet therapy
Can resume anticoagulation 4-8 weeks post, maybe longer if critical area/large

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73
Q

When to decompress ICH surgically

A

Cerebellar haemorrhage >3cm, deteriorating, brainstem compression, hydrocephalus

For supratentorial haemorrhage, only life threatening conditions where haemorrhage is 2cm from surface

If there is blood in ventricles and get blocked causing hydrocephalus, EVD is indicated

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74
Q

Management of CAA

A

Avoid anticoagulation, antiplatelet and thrombolysis

Hypertension control leads to 77% risk reduction

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75
Q

Risk Factors for Central Venous Sinus Thrombosis

A

Obesity
Thrombophilia (including OCP)
Local infection
Chronic inflammatory disease
Malignancy

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76
Q

Central Venous Sinus Thrombosis

A

Venous back pressure is the problem essentiall,y then CSF can’t be absorbed, there is ischaemia due to lack of venous outflow too.

Often present as intracranial hypertension.

Seizure with stroke, think CVST.

Management
Anticoagulation even if there is haemorrhage to prevent clot propagation. Clexane generally best, but Heparin sometimes used as more easily reversed/stopped.
DOACs long term. 3-6 months if severe, 6-12 if unprovoked.
Indefinite if severe thrombophilia or systemic thrombosis
Mechanical thrombectomy/direct fibrinolysis an option but no good evidence.
Hemicraniectomy if large
Other measures to bring down pressure - hypercapnia, etc.

Generally do reasonably well.

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77
Q

Internal Capsule Stroke

A

Classical Lacunar Syndrome

Typically pure motor

Due to M1 - Lenticulostriate artery occlusion

Can also get ataxic hemiparesis

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78
Q

Thalamic Stroke

A

Pure sensory lacunar syndrome

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79
Q

Basis Pontis Stroke

A

Dysarthria/clumsy hand

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80
Q

Causes of Transverse Myelitis

A

Primary Neurological conditions
- MS
- Neuromyelitis Optica (NMOSD)
- Myelin Oligodendrocyte glycoprotein associated disease (MOGAD)
- Acute demyelinating encephalomyelitis (ADEM)

Systemic inflammatory conditions: SLE, Sjogren’s Behcets, Sarcoid (Heerfordt syndrome)

OthersL Syphilis, TB, HIV, HSV, VZV, Paraneoplastic

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81
Q

Non Arteritic Ischaemic Optic Neuropathy

A

Cause of intrinsic optic neuropathy

Painless vision loss

Loss of blood flow to anterior aspect of the eye

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82
Q

Arteritic Ischaemic Optic Neuropathy

A

Typically painful vision loss, this is GCA

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83
Q

Leber’s Optic Neuropathy

A

Mitochondrial disorder which leads to fairly sudden onset vision loss

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84
Q

Optic Neuritis

A

Subacute onset with pain on eye movement

Visual acuity decreased, particularly colour vision. May be sparkles of light and a central scotoma can be present.

Relative Afferent Pupillary defect is classic finding

Disc swelling may or may not be present

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85
Q

Causes of bilateral Optic Disc Swelling

A
  • Hypertension
  • Raised ICP
  • Bilateral optic neuritis/neuropathy → NMOSD

Papilloedema specifically means bilateral optic disc swelling secondary to raised intracranial pressure

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86
Q

MS Epidemiology

A

By far most common neuroimmiunology condition, develops in geneticslly suceptible individuals as result of environmental exposure.

Not hereditary, polygenetic, but there are clusters.

  • HLA DR-2 (HLA-DRB1*15) Northern Europeans
  • Female > Male

Environmental Factors
- EBV is key → new paper HOT TOPIC
- Smoking
- Latitude
- Sunlight exposure and Vitamin D is protective for MS
- Immigrants who migrate before adolescence acquire risk of the new country
- Obesity

EBV + defect in dendritic cells is likely the key mechanistic driver of MS

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87
Q

Risk factors for developing MS post CIS

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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88
Q

McDonald’s Criteria

A
  • 2 lesions in time and space
  • Clinical diagnosis with radiological findings to help fulfil criteria

Time:
- 2 separate attacks, or even a history of an attack
- MRI with contrast enhancing and non enhancing lesions
- Oligoclonal bands (take up to a year to develop)

Space
- 2 different locations in the CNS through objective clinical evidence
- 2 different locations in the CNS through MRI

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89
Q

Acute MS Treatment

A

3 day Methylprednisolone pulse
No steroid taper required

Only benefit is accelerating recovery from relapse, but no benefit in terms of final outcomes i.e. no changes to disability or disease modification.

Can give oral with same outcomes.

Plasmapheresis for severe attacks

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90
Q

Interferon Beta

A

Modulate T and B cell function, reverses blood brain barrier disruption.

Reduces MS relapses 30% annually

Side Effects: Flu like symptoms, may worsen neurology. Depression, leukopaenia, liver abnormalities, thyroid disorders

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91
Q

Glatiramer

A

For MS

Stimulates Treg cells with synthetic mimics of MHC class II, rarely used now.

May be used in cancer patients.

Injection site reactions key

92
Q

Teriflunomide

A

For MS

Dervied from leflunomide. Antimetabolite, interfering with de novo pyrimidine synthesis, inhibiting lymphocytes.

Similar efficacy to Interferon annual reuction of relapse around 30%

SEs: hair thinning, teratogenic.

93
Q

Dimethyl Fumarate

A

For MS

Unknown mechanism, but lowers lymphocyte count

Reduces annual relapse rate by 53%, also reduces disability and reduces gad enhancing lesions

SEs: Flushing (use aspirin), diarrhoea, nausea.

Can cause PML

94
Q

Fingolimod

A

Sphingosine-1-phosphate receptor modulator → inhibits migration of T and B cells from lymphoid tissue into peripheral circulation and CNS

(So low Lymphocytes in blood and some immunosuppression, but lymphocytes still there)

Reduces annual MS relapse rate by 54%, slows disability and gad enhancing lesions

SEs: First dose bradycardia, VZV reactivation, macular oedema, HTN, LFT derangement.

Monitoring for first dose due to bradycardia

Risk of rebound relapse with cessation (as Lymphocytes still present, just being held in lymphoid tissue)

95
Q

Ozanimod

A

Another sphingosine-1-phosphate receptor modulate (subtypes 1 + 5) → more specific for lymphocyte migration

48% reduction of MS relapse

Dose escalation reduces bradycardia risk and macular oedema.

96
Q

Cladribine

A

Purine antimetabolite targeting lymphocytes → immunomodulatory

Two 5 day courses then repeated a year later

58% MS reduction in relapse

SEs: VZV/HSV elapse, headaches, however increases malignancy risk if used past 2 years

Generally relapse starts to develop around 4 years, some get to 10 years. Need frequent MRIs to monitor.

97
Q

Natalizumab

A

alpha4 beta1 integrin inhibitor → prevents leukocyte migration across BBB

Reduced annual MS relapse rate 68%, reduced disability, reduced new lesions

SEs: Anxiety, pharyngitis, peripheral oedema, PML, rebound relapse, anti drug antibodies

98
Q

Progressive Multifocal Leukoencephalopathy

A

JC Virus related subacute demyelinating process. Polyomavirus, usually dormant, present in 50-60% of population.

Reactivated in immunosuppression, crosses BBB then destroys oligodendrocytes.

Subacute worsening of symptoms. Not inflammatory.

20% mortality risk. Increased risk with longterm use, previous immunosuppression. Check for JC virus prior to treatment, if positive don’t give. Check 6 monthly on treatment

Treat by stopping causative drug, PLEX,

Pembrolizumab used to allow immune system to respond to the infection. Also BK virus specific T cells can be done. Only do this if there is an additional cause that can’t be removed (e.g. haematological reason for immunosuppression).

99
Q

Alemtuzumab

A

CD52 Inhibitor on lymphocytes → immunomodulatory effect

Reduces MS relapse 50% compared to IFN

SEs: ITP, Graves, anti-GBM, Infections

100
Q

Ocrelizumab

A

Anti-CD20 → B cell depletion (same as Rituximab)

47% MS relapse reduction compared to IFN

SEs: increased risk of URTI, severe COVID, HBV reactivation, hypogammaglobulinaemia

Works in primary progressive MS but not on PBS

101
Q

Siponimod

A

Works for secondary progressive MS

Selective sphingosine 1-phosphate receptor 1 +5 modulator (2nd gen fingolimod) → crosses BBB

Same first dose bradycardia as Fingolimod, VZV, macular oedema, HTN, LFT dernagement

Contraindicated with CYP2C93/3 → must do genotyping

102
Q

Ofatumumab

A

CD-20 depleting agent

51-59% reduction in relapse compared to teriflunomide

SEs: URTI, UTI

103
Q

Autologous SCT in MS

A

For highly active MS that breaks through high efficacy therapy

Similar efficacy to Ocrelizumab at 3 year mark.

65% have no disease activity at 10 years

104
Q

Pregnancy and MS

A

Relapse risk drops during pregnancy
But increased risk postpartum, usually severe and starting treatment post delivery isn’t protective

IFN-beta and Glatarimer safe.

Natalizumab can continue to around 34 weeks then resume post partum.

Best option is CD20 depletion dosed just prior to conception (i.e. Ocrelizumab/Ofatumumab/Ritux)

Don’t use Fingolimod and Teriflunomide.

105
Q

Neuromyelitis Optica Spectrum Disorders

A

B cell mediated disease against AQP4 with complement activation.
Astrocytopathy

Optic neuritis (often bilateral), longitudinally extensive transverse myelitis (>3 levels), Area postrema syndrome (unexplained nausea, hiccups, vomiting). Acute brainstem syndrome.

Test for AQP4 (75-80% sensitive, >99% specific) and MOG (present in 50% of AQP4 -ve cases) antibodies. Few have oligoclonal bands.

IV Methylpred or PLEX for acute attack.

Long term: AZA, MMF, RTX.
Then disease specific MABs: Eculizumab (complement inhibitor), Inebilizumab (anti-CD19), Satralizumab (anti IL-6)

106
Q

Eculizumab

A

Terminal complement inhibitor

Remarkably effective for NMOSD
NNT 2.5

Must have meningococcal vaccination prior

107
Q

Myelin Oligodendrocyte Glycoprotein Associated Disease (MOGAD)

A

Pathophysiology not fully understood
MOG protein is in CNS
Demyelinating disease

1:1 gender ratio
Commonly post infectious/post vaccine

Test for MOG Ab in serum prior to immunosuppression

Need to have high PPV - lots of false positives with MOG Ab. Positive in lots of other things, not super specific

Optic neuritis (mostly anterior unlike MS and NMOSD), transverse myelitis, ADEM, brainstem lesions, cortical encephalitis

Treatment: IV Methylprednisolone with steroid taper. IVIG is treatment of choice. RTX, MMF other options

108
Q

ADEM (Acute disseminated encephalomyelitis)

A

Monophasic disorder of the brain and sometimes cord

Mostly children or young adults

Encephalopathy is key

Usually preceded by viral infection or other systemic infection

Usually resolves after 3 months.

25% develop MS

Subset are MOG positive

109
Q

Limbic Encephalitis

A

Hippocampus, Amygdala, Cingulate Gyrus

  • Subacute psychiatric manifestations
  • Poor short term memory
  • Temporal lobe seizures
  • MRI changes in unilateral or bilateral lobes
110
Q

Rhomboencephalitis

A

Encephalitis of the brainstem

  • Decreased conscious state
  • Cranial nerve and brainstem signs
111
Q

Cerebellitis/Cerebellar degeneration

A

Cerebellar symptoms and signs

Essentially present as a subacute onset of a movement disorder

112
Q

Key infective causes of Encephalitis

A

HSV (esp 1)
Enterovirus

Flavivirus
HIV

Bacterial: Listeria, TB, Syphilis

Fungal: Cryptococcus

113
Q

HSV Encephalitis

A

Most common cause in Australia
50% of patients > 50

Primarily HSV1, via trigeminal ganglion where reactivation goes to temporal lobe and back to original superficial site of infection

Acute to subacute onset of encephalitis.

Focal seizures very common

HSV PCR can be negative if done in first 48hr and MRI can also be normal early. But temporal lobe involvement classic. Lymphocyte predominant LP.
EEG: focal slowing, epileptiform discharges

IV Aciclovir for 14-21 days
No benefit (or harm) from Dexamethasone

114
Q

Key infective cause of brainstem encephalitis

A

Listeria

Can cause microabscesses, moreso in immunocompetent patients.

Most testing is poorly sensitive

Cranial nerve exam going to be more sensitive.

Benpen for management

115
Q

Japanese Encephalitis Virus

A

Bilateral Thalamic Encephalitis

Flavivirus
Most cases are asymptomatic but can be severe
Serum is more sensitive than CSF (moves into parenchyma so CSF can be negative)

NGS to test for it

116
Q

Autoimmune versus Paraneoplastic Encephalitis

(key differentiators)

A

Paraneoplastic:
- T cell mediated
- Intracellular epitope
- Poorer prognosis

Autoimmune:
- B cell mediated
- Extracellular/Surface epitope
- Generally good prognosis

117
Q

Paraneoplastic Antibodies

A

They are not causative, they are bystanders. Lots of overlap so just send the full panel. Panel is the anti-neuronal antibodies.

Hu:
- Limbic encephalitis, peripheral neuropathy
- Small cell lung cancer

Yo:
- Cerebellar degeneration
- Breast/Ovarian cancer

Ri:
- Opsoclonus myoclonus (random jerking of eyes), Rhomboencephalitis
- SCLC

Ma/Ta:
- Rhomboencephalitis
- Testicular cancer

118
Q

KELCH-11

A

Cerebellar autoimmune encephalitis in testicular seminoma

119
Q

NMDA Encephalitis

A
  • 95% young people, and mostly women
  • 50% have ovarian teratomas
  • Older patients often have carcinoma, cancer less frequent in men and children
  • 20% of HSV encephalitis develop NMDA encephalitis

Most common autoimmune encephalitis
B cell mediated, often linked to malignancy with antigen coming from the apoptotic tumour

Limbic encephalitis typically with preceding viral prodrome.
Orofacial dyskinesia, autonomic instability, insomnia, speech disturbance

Then drop GCS

Test on CSF. Serum has bulk false positives. MRI can be normal. Lymphocytes in CSF.

Remove cancer if present
Pulse MP, IVIG, RTX
Cyclo 2nd line

120
Q

LGI1 Encephalitis

A
  • Previously VGKC Encephalitis
  • Cognitive and memory changes
  • Faciobrachial dystonic seizures (First feature)
  • Seizures

Disease of the elderly
Responds well to treatment, but recovery of cognition and memory often poor. (Hippocampal damage key)

Treatment:
- IVIG, steroids
- Can prevent cognitive change if treat when seizures present

121
Q

Posterior Reversible Encephalopathy Syndrome

A

Predominantly due to hypertension exceeding limits of cerebral autoregulation.

Immunosuppression, pre-eclampsia, renal failure, autoimmune disease, infection can all cause it too.

MRI: white matter changes on MRI in posterior circulation

Acute mental state changes, headaches, visual change, seizures (most common symptom, 90%)

Treatment:
- Aggressive blood pressure management, get MAP + diastolic down
- Seizure management
- Treat other reversible causes

122
Q

Differential for rest tremor

A

Idiopathic Parkinson’s Disease is key, and is less common in Parkinson’s Plus syndromes.

Others:
- Dystonic Tremor
- Essential Tremor (late)

123
Q

Differential for postural tremor

A
  • Essential tremor is key
  • Dystonic tremor
  • Enhanced physiological tremor (worsened by anxiety, drugs, hyperthyroidism - fine tremor)
  • Drug induced tremor
  • Neuropathies
124
Q

Essential Tremor

A

A clinical syndrome. Thought to be pathology of connection between cerebellum, thalamus and cortex.

Bimodal presentation in 20s and 60s, and is a familial form which presents earlier. Pesticides and heavy metals classic triggers.

Bilateral, largely symmetrical postural and kinetic tremor of hands and forearms. May have concomitant head and jaw tremor. Alcohol tends to help but not diagnostic. Smoking also helps.

“yes yes” tremor

Exclude physiological/drug/dystonia

125
Q

Essential Tremor treatment

A

Not everyone needs treatment

First line: propranolol, primidone, topiramate
Second line: Benzodiazepine, Gabapentin, zonisamide

Botox for head tremor (NEJM article this year)

Third line: DBS, Focal ultrasound (essentially burn a hole in the thalamus)

126
Q

Holmes Tremor

A

Due to lesion just outside the red nucleus, blocking cerebellar outflow pathways.

Big kinetic tremor, coarse, fast.

Occurs in Wilson’s Disease, Stroke, MS.’

Responds to Levodopa

127
Q

Dystonia

A

Cramping, twisting, patterned movements.

Due to sustained or intermittent muscle contractions.

“no no” tremor (repetitive contraction pulling head to the side)

Worsened by voluntary action, Worse if fighting the muscle that’s contracting

128
Q

Chorea

A

Involuntary movements of limbs/trunk/neck/face, irregular, no repetition, unpredictable

Can look like fidgeting or multifocal myoclonus.

Can’t maintain motor activity

Drug induced chorea, termed dyskinesia, occurs in Idiopathic PD with too many drugs

129
Q

Myoclonus

A

Fast, brief movements due to sudden increase or decrease in tone.

Asterixis is a negative myoclonus

Mostly metabolic, e.g. hepatic encephalopathy, CO2 narcosis, Cefepime

130
Q

Idiopathic Parkinson’s Disease Background

A

Some genes associated: LRRK2 is key, others CHCHD2

Environmental risk factors: dietary dairy intake, pesticides, air pollution
Environmental protective factors: smoking, coffee

131
Q

Idiopathic Parkinson’s Disease Pathophysiology

A

Synucleinopathy: insoluble forms of alpha synuclein accumulate, forming neuronal inclusions called Lewy Bodies.

These are toxic and lead to cell disruption.

Normally the proteins regulate synaptic vesicle transport.

132
Q

Diagnosis of Parkinson’s Disease

A

Bradykinesia must be present
Accompanied by rigidity or rest tremor

Absence of absolute exclusion criteria and presence of at least two supportive criteria.

No red flags

133
Q

Rigidity versus Spasticity

A

Rigidity: increased resistance to passive movement about a joint that is not velocity dependent

Spasticity: velocity dependent resistance to movement about a joint

134
Q

What condition is likely if a patient has a movement disorder and can still ride a bike?

A

Parkinson’s Disease

135
Q

Which form of Idiopathic Parkinson’s Disease has more falls?

A

Akinetic-rigid

136
Q

What type of movement disorder is REM Sleep Behaviour Disorder suggestive of?

How to manage?

A

Synucleinopathy:
- Idiopathic Parkinson’s Disease
- Multiple Systems Atrophy
- Lewy Body Dementia

Treatment: SSRI makes it worse, so get rid of this.
Levodopa can make symptoms worse, particularly evening dose.

Melatonin and Clonazepam can help, Best evidence is for Melatonin

137
Q

Benefits of Levodopa

A

Motor function
ADLs
Quality of life

Compared to other medications for Parkinson’s. By far best drug for Idiopathic Parkinson’s Disease.

Works for many years, but short acting so lots of doses needed.

Not disease modifying

Generally “honeymoon period” for a couple of years, in which management works easily. Then gets harder due to motor fluctuations.

138
Q

Risk Factors for Motor Fluctuations in Parkinson’s Disease

A

Risk is higher with longer disease duration and higher levels of Levodopa used. Younger onset associated with higher risk.

Duration of Levodopa therapy is not associated.

Management: Divide dose to increase frequency, add COMT or MAO

139
Q

Dyskinesia in Parkinson’s Disease

A

Chorea-type movement associated with too much Levodopa, linked to disease duration as well.

Treatment:
- Minimise dopaminergic medication dose/split into more frequent smaller doses
- Extended release Amantadine

140
Q

Dopamine Agonists

A

Pramipexole (oral), Rotigotine (patch), Apomorphine (infusion)

Effective, but not as good as Levodopa. However long acting.

Good as a night time medication to help overnight and reduce early morning off.

SEs: Nausea, somnolenfe, dizziness, hallucinations, worsens delirium, impulse control disorders.

Due to delirium issues, best used in younger patients.

Must ask about impulse control problems before prescribing

141
Q

Monoamine Oxidase B Inhibitors

A

Rasagiline, Selagiline

Essentially blocks breakdown of Dopamine to increase concentration

Probably slightly better than Dopamine Agonists.

Used for mild/early symptoms or young patients.

Cause insomnia and higher overall mortality.

Tyramine hypertensive crisis is serious complication to know: MOAI inhibits noradrenaline breakdown → adrenergic crisis

142
Q

Management of Delirium in a Parkinson’s patient

A

Stop in this order (essentially order of potency)

  • Anticholinergic medications
  • Amantadine
  • Dopamine agonists
  • Monoamine oxidase inhibitors
  • Levodopa
143
Q

Management of Hallucinations in Parkinson’s Disease

A

Remove perpetuating agents
Quetiapine
Pimavanserin
Clozapine - best drug

144
Q

Dementia with Lewy Bodies

A

Fluctuating cognition
Recurrent visual hallucinations, typically well formed and detailed (small animals, etc.)
Spontaneous features of parkinsonism, which respond poorly to L-Dopa

The delineation in terms of timing of movement and cognitive symptoms is less important rather than the phenotype above.

Very sensitive to neuroleptics.
Treat with anti-cholinesterases.

145
Q

Mimics of Akinetic-Rigid Parkinson’s Phenotype

A

Neuroleptics
Vascular parkinsonism (see lower limb UMN signs)
Brain tumours
Carbon Disulphide
Mangansim
Huntingtons

146
Q

Mimics of Tremor Phenotype

A

Dystonic tremor
Essential Tremor
FXTAS
Valproate toxicity
Functional

147
Q

Progressive Supranuclear Palsy

A

Syndrome of supranuclear palsy, postural instability, dementia

Tauopathy

Slowed vertical saccades (specifically downgaze palsy), decreased blinking, staring gaze.

Wide based gait and axial rigidity, with early falls due to postural instability.

Personality changes and cognitive changes within first 2 years. FTD phenotype.

Pseudobulbar palsy - dysarthria, dysphasia

Minimal tremor, bradykinesia

MRI: hummingbird sign, mickey mouse sign.

20% responsive to L-dopa
most die within 5-8 years.

148
Q

Multisystem Atrophy

A

Alpha synucleinopathy
Onset usually in 60s
Mean survival 6-10 years
Autonomic failue, Parkinsonism, Cerebellar signs

Erectile dysfunction, urinary dysfunction, REM sleep disturbance, dystonia, antecollis, pyramidal signs, dysphonia, parkinsonism

149
Q

Corticobasal Syndrome

A

Wide phenotype, varying presentation. Syndrome can be casued by PSP, AD, FTD, etc.

But also Corticobasal Degeneration which is a specific Tauopathy involving basal ganglia degeneration.

Asymmetric progressive ideomotor apraxia affecting hand. Loss of two point discrimination, agraphia, rigidity, myoclonus.

Alien hand syndrome

150
Q

Management of Restless Legs

A
  • Correct any iron deficiency
  • Levodopa
  • Dopamine agonists (Pramipexole)

However augementation occurs with Levodopa and Dopamine agonists

Gabapentin/Pregabalin

151
Q

Fragile X Associated Tremor Ataxia Syndrome (FXTAS)

A

Due to premutation of fragile X mental retardation 1 gene. Essentially 55-199 CGG repeats, (not enough to cause fragile X syndrome of intellectual disability, seizures, autism). Once pass 200 no protein, but below this the long protein is toxic.

F > M

Action tremor, cerebellar gait

Parkinsonism, moderate to severe STML, executive function deficit, neuropathy.

MRI: lesion in peduncles, corpus callosum.

Also linked to primary ovarian failure.

152
Q

Huntington’s Disease

A

30-50 year olds

AD inherited expansion of CAG repeats on Huntingtin gene. Normal 6-26, Huntington >35, definite >40

Age of onset inversely linked to size of repeat → anticipation occurs with each generation

Long protein leads to degeneration of neurons.

Psychiatric: depression, irritability, psychosis, social withdrawal, OCD
Motor: INitial distal involuntary movements, chorea (face and axial), bradykinesia, dystonia
Cognitive: can predate motor, often executive dysfunction

153
Q

Westphal Variant

A

Juvenile Huntington’s
High repeat count
Generally inherited from father
Can get seizures, progresses quickly

154
Q

Spinocerebellar Ataxia

A

CAG repeat disorder
Many different SCAs, different inheritance

Predominantly Ataxia and upper motor neuron signs

155
Q

Serotonin Syndrome

A

Mental status change: agitation, hypervigilance, delirium
Neuromuscular hyperactivity: hyperreflexia, rigidity, clonus (mostly lower limbs)
Autonomic hyperactivity: hypertension, tachycardia, diaphoresis, temp >40

Think of it as mostly UMN (pyramidal)

SSRI, SNRI, MOI, TCAs

156
Q

Neuroleptic Malignant Syndrome

A

Due to antipsychotics (multiple drugs, rapid escalation, long acting), also cessation of them or PD drugs

Triad of:
- Autonomic dysfunction
- Altered conscious state
- Extrapyramidal symptoms

Highest specificity: hyperthermia, rigidity, elevated CK

Also a leukocytosis

157
Q

What is the classic mutation in familial Motor Neuron Disease?

A

SOD1 - gain of function mutation

Also C9orf72 - phenotype of PSP/FTD symptoms

158
Q

Pathophysiology of Motor Neuron Disease

A

Dying forward and dying backwards hypotheses

But essentially oxidative stress involving anterior horn leading to death of corticospinal tract and motor neurons

159
Q

Most common Phenotype on MND

A

Limb onset with combination of upper and lower motor neuron signs in the limbs

Second most:
Bulbar onset, presenting with speech and swallowing difficulties, limb featues later

Primary lateral sclerosis with pure UMN
Also a pure LMN

160
Q

MND Clinical

A

Mix of UMN and LMN
Asymmetric weakness, working proximally
Generally limb by limb
Split hand
Fasciculations (rare without weakness)
Pseudobulbar (UMN)
Respiratory muscle involvement

Prognosis
- 50% dead within 30 months
- 20% survive 5-10 years
- Poor prognosis: older age at onset, early resp muscle input, bulbar onset

161
Q

Dementia in MND

A
  • Tauopathy
  • TDP-43-positive ubiquinated cytoplasmic inclusions
  • Overlap with FTD - loss of executive function and verbal fluency
162
Q

Investigations in MNDq

A

Decreased CMAP
Normal SNAP
EMG: fasciculations, fibrillations, positive sharp waves, chronic neurogenic changes
MRI: Corticospinal tract hyperintensity, rule out myelopathy

163
Q

Riluzole

A

Indicated for MND
Inhibits Glutamate release
Disease modifying
Prolongs survival 3-6 months

164
Q

Benefits of PEG in MND

A

Survival benefit, as not aspirating or dying from malnutrition

165
Q

Regulation of horizontal and vertical linear movement

A

Utricle and Saccule

166
Q

Regulation of rotational movement

A

Semicircular canal and ampulla

167
Q

Peripheral Nystagmus

A

Loss of input from one vestibular apparatus makes brain think head is turning towards normal side, so eyes drift towards abnormal side then saccade back to centre

Tends to be unilateral

168
Q

Central Nystagmus

A

Loss of input to maintain a fixed gaze, eyes drift back to centre, then rapidly saccade back to point of fixation

So often direction changing

169
Q

Acute Vestibular Syndrome

A
  • Acute, continuous dizziness lasting days
  • Nausea, vomiting, nystagmus, head motion intolerance, gait unsteadiness
  • Always symptoms
  • Must have spontaneous nystagmus
170
Q

Causes of Acute Vestibular Syndrome

A

Peripheral:
- Vestibular neuritis/labyrinthitis

Central
- Stroke: brainstem or cerebellar
- MS
- Rare: autoimmune, infection, metabolic, thiamine deficiency

171
Q

Role of HINTS Plus exam

A

To discriminate between peripheral and central causes in acute vestibular syndrome only.

Not for episodic vestibular syndrome

172
Q

Vestibular Neuritis

A

Presumed post infectious or viral (Ramsay Hunt Syndrome classic)

Clinical diagnosis, MRI normal

Resolves over weeks

Labyrinthitis if hearing involved → need to consider alternate aetiology (i.e. stroke)

173
Q

Stroke and Acute Vestibular Syndrome

A

25% of all AVS, 96% are Ischaemic Strokes
No role for CT
Exam better than MRI DWI in first 48hr
So may need to repeat in a few days

174
Q

HINTS Plus Exam

A
  1. Head Impulse Test
  2. Nystagmus
  3. Test for Skew deviation
  4. Neurological exam including hearing and gait
175
Q

Nystagmus and Vestibular Neuritis

A

Dominantly fixed direction horizontal nystagmus (with torsional component).

Follows Alexander’s Law (worse towards fast phase)

Fixation tends to dampen it, so may need to attempt to remove it:

Cover one eye, shine torch in other eye → can show nystagmus. Can do the same with fundal exam

176
Q

Stroke and Nystagmus

A

Dominantly vertical, torsional

Horizontal nystagmus that is direction changing (gaze evoked)

However half of all posterior fossa strokes have direction fixed horizontal nystagmus

177
Q

Skew Deviation

A

Vertical double vision due to disruption of tracts in brainstem

Due to lesions in brainstem or cerebellum

Cover uncover test → correction present (i.e. eyes bounce up an down) → suggestive of central cause

178
Q

HINTS Exam in Stroke

A

Vertical Nystagmus
Positive Test of Skew
No catch up Saccade on HIT
Anything focal on neurological exam

179
Q

Head Impulse Test

A

Assessing Vestibulo-Ocular Reflex

Slow movement of head, then flick head back to centre

Catch up saccade: vestibular (eyes stay fixed with head, then catch up)

AICA stroke can lead to positive HIT as the Labyrinth knocked out → will have hearing loss

180
Q

HINTS Exam in Peripheral AVS

A

All criteria must be met

Nystagmus: horizontal dominant, direction fixed, respects Alexander’s Law
No skew deviation
Positive head impulse test with catchup saccade
No other signs on neuro exam

181
Q

Treatment of Vestibular Neuritis

A

1 week oral Prednisolone 60mg
Symptomatic
Any concern for VZV give antivirals

10-15% develop BPPV
Persistent postural perceptual dizziness may develop - functional

182
Q

Spontaneous Episodic Vestibular Syndrome

A

No triggers, spontaneous. Tricky on first occasion, often worked up as AVS as don’t know it’s episodic.

Symptoms cannot be triggered by manoeuvres or exam

Causes: Vestibular Migraine, recurrent posterior circulation TIA (super uncommon), Meniere’s Disease

Consider medical causes: Vasovagal, arrhythmias, panic attacks, unstable angina, hypoglycaemia

183
Q

Vestibular Migraine

A

Second most common cause episodic vestibular syndromes

Migraines can cause vestibular symptoms, and primary vestibular disease can cause migraines

Can develop nystagmus, and mixed picture

At least 5 episodes, 5min to 72hr. Hx of migraines, and migraine featues with at least 50% of vestibular episodes.

Treat like migraines. Can develop PPPD

184
Q

Meniere’s Disease

A

Over diagnosed, not that common a cause of vertigo.

Endolymph ionic derangement and accumulation. Can become bilateral.

Spontaneous non triggered vertigo, hearing loss/tinnitus during attack, aural fullness.

Rule out other causes. Initialy episodic but can become fixed.

Direction fixed nystagmus, then swaps direction as resolving. Some HIT positive

Symptomatic treatment, vestibular rehab. Other things don’t help.

185
Q

Key feature of triggered episodic vertigo

A

Can trigger the symptoms at bedside

186
Q

Key differential for BPPV

A

Orthostatic hypotension

Others:
Central Paroxysmal positional vertigo (lesion causing compression with head movement)

187
Q

BPPV

A

Most common cause of vestibular dysfunction. Any age, more common as get older.

Brief episodes, lasts less than a minute.

Most specific symptom: get dizziness when turn head while lying in bed

188
Q

Dix-Hallpike

A

Usually delay 1-5s from doing movement and symptoms starting
Last <30s (fatigues as fluid movement settled)
Then nystagmus develops once symptoms have started. Mixed upbeat, torsional

Lack of latency, fatiguability suggestive of CPPV. Also downbeat in CPPV.

189
Q

Central Paroxysmal Positional Vertigo

A

Central mimic of BPPV

Posterior fossa masses key issue, also stroke or demyelination in posterior fossa.

190
Q

Superior Semicircular Canal Dehiscence

A

Rare, likely developmental. Thinning of temporal bone around semicircular canal.

Develop third window within the semicircular canals which becomes a pressure outlet essentially and sound waves move through the semicircular canals.

Triggered by sound, raised ICP.

Bone conducted sound is transmitted very well, e.g. can hear eyes move, heartbeat, pulsatile tinnitus, bowel sounds.

High resolution CT scan

Nystagmus between episodes.

191
Q

Pathophysiology of Epilepsy

A

Paroxysmal depolarisation shift: rapidly repetitive action potentials not followed by refractory period leading to prolonged depolarisation.

Seizures occur when large numbers of neurons in one region undergo the same.

192
Q

Types of Generalised Seizure

A

Tonic Clonic
Absence (a very specific syndrome)
Myoclonic
Atonic

193
Q

Focal Seizure Features

A

Subjective sensory or psychic phenomena
Motor
+/- impaired awareness
+/- generalisation (focal to bilateral tonic-clonic

194
Q

Incontinence and seizures

A

Urinary incontinence is non specific and commonly occurs in syncope

Faecal incontinence very rare in seizures, more likely in syncope

195
Q

Provoked Seizure

A

Acute precipitant that may or may not occur: SAH, stroke, TBI, meningitis, Alcohol withdrawal, hypoglycaemia, hyponatraemia, uraemic encephalopathy, chronic liver disease

If can be reversed, may not need AED. If likely to have ongoing seizures then may need AED

196
Q

Juvenile Myoclonic Epilepsy

A

2ndf most common form of epilepsy
7% have ICK mutation
Start during teens, normal development
Myoclonic jerks in early waking states
90% GTCS, 30% have absence
Worse with sleep deprivation and alcohol

3Hz spike/polyspike wave
Photic stimulation and hyperventilation

First line: Valproate
Women of child bearing age: Lamotrigine

Unlikely to go into remission

197
Q

Childhood and Juvenile Absence Epilepsies

A

Onset 8-12 years old
Normal development
Absence seizures, occasional GTCS
80% of patients’ seizures resolve by adulthood
Sodium Valproate

198
Q

Mesial Temporal Lobe Epilepsy with Hippocampal Sclerosis

A

Most common form of epilepsy

Risk factors: prolonged febrile convulsions and CNS infections

Typical auras, focal seizures with impaired awareness, with or without automatisms

Can have dreamy states with perceived unreality or deja vu or jamais vu phenomena, gustatory/olfactory hallucinations, epigastric rising sensations

Eventually can evolve into bilateral TCS

MRI: unilateral (sometimes bilateral) hippocampal atrophy, T2 signal increase

60-90% of patients medically refractory → surgery (most common drug refractory epilepsy)

199
Q

EEG Frequency

A

Alpha 9-12Hz: Normal
Beta 13-15Hz: Too much Benzos
Theta: 5-8Hz: Drowsy, encephalopathic
Delta 1-4Hz: Sleep or encephalopathic

Spike and wave pattern is epileptogenic pattern

200
Q

Epilepsy versus Seizures

A

A disorder of the brain characterised by enduring predisposition to generate epileptic seizures

201
Q

Risk of recurrence of seizures and when to treat

A

After 1st seizure: 46%
After 2nd seizure: 70%

Thus, treat after 2nd unprovoked seizure (as long as within a year or two)

Treat after first seizure if EEF is abnormal, neurological exam is abnormal, or MRI shows structural abnormality

Or if further seizures expected to be severe or vulnerable population

202
Q

Focal Seizure AED choice

A

Carbamazepine
Lamotrigine

Carbamazepine not ideal in elderly, Lamotrigine probably better but Carbamazepine is first on PBS

Levetiracetam also effective, but more expensive

203
Q

Absence Seizure AED Choice

A

Valproate

Ethosuximide for pure Absence seizures in kids

204
Q

Idiopathic Generalised Epilepsy AED Choice

A

Valproate
Lamotrigine for women of child bearing age
Zonisamide

205
Q

GTCS AED Choice

A

Valproate
Levetiracetam (inferior and more expensive)

206
Q

AED to avoid in Mitochondrial Disorders

A

Valproate

207
Q

Key serious risk of Carbamazepine

A

SJS in patients with HLA B*1502

Common in Han Chinese, Thai, Indian, Malay, Filipino, Indonesians

8% of population

OR 895 if mutation present

HLA A*3101 mutation in Europeans, but less serious

208
Q

AED choice if rapid response needed

A

Phenytoin
Levetiracetam
Valproate

Otherwise start low and go slow

209
Q

Role of drug levels in AEDs

A

Reference range is not therapeutic range. May be therapeutic below and toxic within.

Uses:
1. Establish an individual therapeutic concentration once working
2. Diagnose toxicity
3. Assess compliance
4. Guide dose adjustment (pregnancy, drug interactions, etc.)

210
Q

Best combination of AED for refractory Epilepsy

A

Lamotrigine + Valproate

211
Q

Drug resistant epilepsy

A

Those with ongoing seizures despite 2 or more AEDs tried

Refer to epilepsy unit
Consider surgery
10-28% reach seizure freedom with further adjustments

212
Q

Predictors of high risk of seizure recurrence

A

Long duration of epilepsy prior to remission
Short seizure free interval before ceasing AEDs
Late age of onset
History of febrile seiures
>10 seizure before remission
Developmental delay
Ongoing EEG abnormalities

213
Q

Epilepsy and Pregnancy

A

Oestrogen is neuroexcitatory
Progesterone is neuroinhibitory

Thus seizures more common during certain phases of menstrual cycle

Epilepsy may increase risk of infertility, and polypharmacy certainly does

Most AED induce hormonal contraception leading to rapid clearance. (Lamotrigine is key exception).

High mortality with seizures during pregnancy.

214
Q

Typical congenital anomalies with AEDs

A

Neural Tube Defects
Congenital heart disease
Cleft lip/palate
Urogenital defects

Valproate key offender, plus Phenytoin.

Carbamazepine, Phenobarb, lamotrigine some risk.

Ideally go to monotherapy Lamotrigine. Levetiracetam being increasingly used.

Polypharmacy is the key problem.

215
Q

AEDs undergoing increased clearance during pregnancy

A

Lamotrigine
Levetiracetam

216
Q

Epilepsy and Osteoporosis

A

Epilepsy an independent RF for osteoporosis

2-6x higher rates if on an AED

Longer duration = higher risk

Increased Vit D metabolism, and lower oestrogen levels due to altered metabolism

217
Q

Risk Factors for SUDEP

A

GTCS >2 years
Nocturnal seizures
treatment resistant (or not taking)
Long duration of epilepsy
Early age of onset
Dravet Syndrome (Sodium channel gene mutation)

Young people wth convulsive seizures mostly.

Possibly some centrally mediated cardiopulmonary dysfunction

218
Q

Inter Ictal Psychosis

A

Chronic schizophrenia like psychosis

RF: bilateral temporal lobe epilepsy, age of onset, refractory disease

Responds to antipsychotics, and seizure activity doesn’t really influence psychosis

219
Q

Post Ictal Seizures

A

2-10% of patients

Cluster of focal seizures with impaired awareness or GTCS followed by onset of psychosis hours to days afterwards, lasting for weeks

220
Q

Definition of Status Epilepticus

A

5 minutes of continuous seizure, or two or more seizures between which there is incomplete recovery of consciousness

20% mortality

Seizures >30 minutes unlikely to terminate spontaneously → increased mortality

longer = harder to terminate

221
Q

Implication of convulsive status epilepticus

A

Leads to permanent brain damage which becomes an epileptogenic focus → drivers further seizure activity → increased resistance to treatment

CO increases initially with raised BP, glucose and lactate

Then all start to drop after 30 minutes

Then becomes malignant with hyperthermia, rhabdo and multiorgan failure

222
Q

Treatment of Status Epilepticus

A

First line: Lorazepam 2-4mg IV (fast, superior); Midazolam 10mg IM then repeat if still seizing

Second line: Phenytoin 15-20mg/kg; Valproate 20-40mg/kg; Keppra 20-60mg/kg

Third line: Midazolam loading then infusion or Propofol load and infusion

223
Q

Serious consequence of sudden withdrawal of Benzodiazepines

A

Treatment resistant status epilepticus

224
Q

Treatment of benzo refractory status

A

Keppra/Valproate/Phenytoin all similar

225
Q

Non convulsive status

A

After or independent of convulsive seizure

Either focal status or absence status

Change in behaviour and cognition with no motor symptoms

EEG key

Risks: known Epilepsy Hx, structural brain abnormality, benzo withdrawal

Not life threatening, but can lead to neuronal damage.

Treat as for convulsive status

226
Q

Pathophysiology of Migraine

A

Brainstem ion channel dysfunction, involved in regulation of sensory/pain inputs and cranial vascular tone

227
Q

Menstruation and Migraine

A

Risk factor for migraine without aura specifically

Predictable, can manage around cycles and give prophylaxis/treatment on this basis

BPT (15 decks)

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