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Neuro Flashcards

1
Q

What are the criteria for thrombolysis?

A

Presentation within 4.5 hours
Not haemorrhage

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2
Q

What are the components of NIHSS score?

A

Consciousness
Month + age
Follow commands
Horizontal gaze palsy (remember oculocephalic reflex)
Visual loss
Facial palsy
Arm drift (10s)
Leg drift (10s)
UL/LL Ataxia
Sensation
Aphasia (recognise items, read sentence)
Dysarthria
Inattention

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3
Q

What are the contra-indications for thrombolysis?

A

Absolute
Intra-cranial haemorrhage
Seizure at onset
Stroke/TBI <3m
LP <7d
GI bleed <3w
Active bleeding
Pregnancy
Varices
Uncontrolled HTN

Relative
Concurrent anticoag
Bleeding disorder
Retinal haemorrahge
Suspected intracranial thrombus
Major surgery <2w

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4
Q

What is the MRS score?

A

Modified Rankin Score (MRS) of DISABILITY not frailty.

0 = nil
1 = symptoms without disability
2 = Can look after own self for 1 week
3 = Cannot look after own self for 1 week
4 = Needs help with ADL’s
5 = Bed-bound

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5
Q

What do you do if a patient is on a DOAC and needs thrombolysis?

A

Contra-indicated if received DOAC within 24 hours of stroke (move towards 48 hours)

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6
Q

How do you manage blood pressure control in a candidate for thrombolysis?

A

No clear evidence that high blood pressure is a risk - there is a theoretical risk of bleeding.
Blood pressure is a protective mechanism in stroke. I
If thrombolysing, - need to bring the blood pressure down
In thrombolysis - Labetolol boluses then infusion (provided HR>60)

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7
Q

How do you manage blood sugars in a candidate for thrombolysis?

A

Hyperglycaemia related to poor outcomes
Sliding scale, stat novorapid, long-acting low dose insulin - no right answer.
(bear in mind volumes of infusions if on sliding scale and labetolol infusions!)

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8
Q

Can you ever thrombolyse a wake up stroke?

A

Theory is that the stroke wakes patients up.
Can thrombolyse if you can get an urgent MRI to look at the T2/DWI mismatch to assess penumbra.

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9
Q

What are the indications for thrombectomy?

A
  1. Ischaemic stroke
  2. Large vessel occlusion - intra-cranial carotid, MCA (M1, M2), basilar, and most recently posterior circulation strokes.
  3. Need CTA!!!! Not just non-contrast CT. Need the scan BEFORE you refer.
  4. MRS 0-1 (latest guidelines)
  5. NIHSS >6 (or >10 for basilar)

Patients will get thrombolysis + thrombectomy together.

After 12 hours - need CT or MR perfusion scan to assess flow to brain and salvageable brain.

Even the larger strokes with large cores will now get thrombolysed - there isn’t actually as big a risk of bleeding as we predicted, so if there is a potentially salvageable penumbra - thrombolysis is on the table (based on data from 2023 trials)

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10
Q

What are the causes for spastic paraparesis?

A

Inflammatory
Autoimmune: Multiple Sclerosis (cerebellar signs)
Vasculitis
Sarcoidosis

Infection
Tropical spastic paraparesis

Post infection: Dengue, Schistosomiasis, Mycoplasma

Ischaemic
Anterior spinal artery occlusion

Trauma

Metabolic
B1,6,12 deficiency
SCDC
Taboparesis
Copper deficiency

Structural
Tumours (intramedullary) - ependymoma, astrocytoma, glioblastoma
(extramedullary) - schwannoma, meningioma, neurofibroma
Cord compression (sensory level)
Cervical myelopathy/disc prolapse

Hereditary
Hereditary spastic paraparesis

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11
Q

Differential for peripheral neuropathy?

A

Toxin
Alcohol
Chemotherapy

Idiopathic
Sarcoidosis

Inflammatory
CIDP
ANCA+ Vasculitis

Inherited
Hereditary Sensory motor neuropathy (CMT) - muscle wasting

Metabolic
Diabetes
SCDC
B1,6,12 deficiency
Uraemia

Endocrine
Hypothyroidism

Paraneoplastic
Lung cancer
Paraproteinaemia

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12
Q

What do you know about HSMN?

A

2 types
Type 1: demyelinating
Type 2: axonal pathology

Type 1 is more common and inherited in an AD pattern
Defect in PMP 22 gene
Motor symptoms predominate
Distal muscle wasting

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13
Q

What are some causes for demyelinating polyneuropathies?

A

CIDP
MM
MGUS
HSMN
HIV

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14
Q

Investigations for a peripheral neuropathy?

A
  1. Blood glucose, urinalysis
  2. Fundoscopy
  3. Urea
  4. LFTs
  5. Thyroid function
  6. Immunoglobulins
  7. HbA1c
  8. Nerve conduction studies (is this demyelinating - eg. inflam or axonal)
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15
Q

Talk to me about nerve conduction and EMG studies

A

Nerve conduction - problem with nerve
EMG - problem with muscle response to nerve stimulus

Nerve conduction studies
Axon problem or myelin problem and evaluation of conduction blocks

Axon problem:
Reduced amplitude of conduction
Trauma, toxin, ischaemia, metabolic, genetic

Myelin problem (usually immune mediated)
Slow conduction velocity
GBS, CIDP

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16
Q

What types of peripheral nerves do you know?

A

Pain: thinly myelinated A-delta
Warmth: unmyelinated C
Vibration/proprioception: large calibre myelinated

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17
Q

What causes a predominant motor disturbance?

A

Porphyria
Lead toxicity
Diphtheria
CIDP/GBS
Drugs

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18
Q

What are the neurophysiology test findings of CMT?

A

Severe and uniformly reduced responses
Might be possible to differentiate an axonal vs. myelin pathology to direct genetic testing (Type 1 is pred. demyelinating and inherited in AD with mutation in PMP22)

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19
Q

What is your differential for cerebellar ataxia?

A

Acute:
Stroke

Chronic:
MS
Drugs (lithium, carbamazapine, chemotherapy)
Alcoholic cerebellar degeneration
SOL
Vit E deficiency
Friedreichs ataxia (cerebellum, cord, peripheral nerves)
MSA
Paraneoplastic

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20
Q

What are the causes of myelopathy by time frame?

A

Hyper-acute
Vascular infarct

Acute
Disc prolapse

Weeks
Inflammatory: MS
Infective: VZV

Months
Metabolic
Infective (HIV), HLTV-1
Tumours
MND
Hereditary Spastic Paraparesis

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21
Q

What are the clinical signs of Friedrich’s Ataxia?

A

Brain:
Cerebellar syndrome

Cord:
Upgoing plantars
Dorsal column signs
Pyramidal pattern of weakness that affects the lower limbs more than upper limbs

Peripheral nerves:
Depressed DTR’s
Muscle weakness

Non-neuro:
Diabetes
Optic atrophy
Sensorineuronal deafness
HOCM
Conduction defects

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22
Q

What do you know about Friedrich’s ataxia’s genetic inheritence and pathophysiology?

A

AR trinucleotide repeat disorder that does not demonstrate anticipation

Mutation in the Frataxin gene that regulates iron and oxidative phosphorylation

Particularly affects the spinocerebellar tract and peripheral nerves

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23
Q

What types of inherited cerebellar ataxias do you know?

A

Friedrich’s
AD Cerebellar ataxia
AR Ataxic telangiectasia
AR Ataxia with Vitamin E deficiency
AR Ataxia with Occulomotor apraxia
AR Mitochondrial recessive ataxic syndrome

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24
Q

What do you know about the genetics of Myotonic Dystrophy

A

AD trinucleotide repeat disorder that DOES demonstrate anticipation and expansion

CTG TNR in myotin protein kinase

Manifests age 20-30

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25
Q

What are the non-cardiac manifestations of myotonic dystrophy?

A

Cardiac: prolonged QT, mitral valve prolapse, cardiomyopathy

Endocrine: DM, Hypogonadism, nodular thyroid enlargement

Neuro: mild cognitive impairment

GI: dysphagia, reflux, delayed gastric empyting, SIBO

Resp: Hypoventilation

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26
Q

Clinical signs of myotonic dystrophy?

A

Frontal balding with smoothened forehead and ptosis
Wasting of facial muscles
Depressed DTRs
High stepping gait
Distal to proximal pattern of weakness
Dorsal guttering of hands
Inability to relax clenched hand

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27
Q

Are there any treatments for Myotonic Dystrophy?

A

Phenytoin
Maxilitine (however concern due to cardiac safety profile)
MDT to address home, work, and transport environments and make adaptations.

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28
Q

What other causes of myotonia do you know?

A

Startle myotonia
Paramyotonia congenita
Hyperkalaemic periodic paralysis

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29
Q

what are the common types of muscular dystrophy?

A

Fascioscapulohumeral dystrophy
Becker’s
Duchenne’s

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30
Q

What are the clinical signs of fascio-scapulo-humeral dystrophy?

A

Facial weakness
NO ptosis/balding
Weakness in upper limb girdle - shoulder weakness, winging of scapula. Forearms spared.
Weakness and protuberance of abdomen
Weakness in foot dorsiflexion with foot drop
Sensosineuronal deafness
Retinal telangiectasia

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31
Q

What is the inheritence of facio-scapulo-humeral dystrophy?

A

AD
Presents age 20
Normal life expectancy

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32
Q

What do you know about Duchenne’s?

A

More severe than Becker’s
X-lined recessive inactivating mutation in the dystrophin gene that leads to muscle loss in skeletal, cardiac, smooth muscle, and brain tissue
Proximal to distal weakness
Calf pseudohypertrophy with wasting in anterior shin
Contractures
Loss of DTRs
Kyphoscoliosis

Non-cardaic
Dilated cardiomyopathy
Pulmonary hypertension
Resp failure

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33
Q

What do you know about Becker’s?

A

X-linked recessive inactivating mutation in dystrophin gene that leads to muscle breakdown in skeletal, cardiac, smooth, brain
Less severe than Duchenne’s
Survive into 40’s
Proximal to distal weakness
Hyper-lordosis (to offset hip extensor weakness)
Loss of DTR’s
Mild pseudohypertrophy

Non-neuro comps
Dilated cardiomyopathy
Pulmonary Hypertension
Respiratory failure

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34
Q

What are some causes for median nerve palsy/carpel tunnel syndrome?

A

Endocrine
Acromegaly
Hypothyroidism

Metabolic
Gout
Renal Failure
Diabetes
Paget’s

Trauma

Occupational

Idiopathic

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35
Q

What are common sites of compression of the median nerve?

A

Elbow
Pronator teres
Carpel tunnel

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36
Q

What are common sites of injury of the radial nerve?

A

Axilla
Spiral groove (ulnar side)
Arcade of Frohse
Wrist

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37
Q

How do you differentiate a C8/T1 radiculopathy vs. ulnar nerve lesion?

A
  1. Both with have weakness in ulnar innervated muscles
  2. In C8/T1 there will be weakness of thumb abduction, and finger extension
  3. There will be more diffuse sensory loss with a C8/T1 radiculopathy
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38
Q

Motor neuropathy

A

Anterior Horn cells
-MND
Peripheral nerves
-Multifocal peripheral neuropathy

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39
Q

What do you know about Kennedy’s disease

A

X linked recessive
Chronic and insidious onset
Peri-oral fasciculations

40
Q

What is the PD triad?

A

Bradykinesia
Rigidity
Tremor

41
Q

What PD plus syndromes do you know?

A

Multi-system atrophy (Autonomic+Cerebellar+Parkinonian)
Progressive Supranuclear palsy
Lewy Body Dementia

42
Q

Cerebellar signs to elicit:

A
  1. Dysarthria (scanning dysarthria)
  2. Dysmetria (past-pointing with intension tremor)
  3. Hypotonia
  4. Dysdiadochokinesia
  5. Coarse horizontal nystagmus
  6. Broken pursuit
  7. Abnormal saccades
43
Q

What is the pathophys of idiopathic PD?

A

Disruption of dopaminergic transmission in basal ganglia. Loss of melanin containing dopaminergic neurons in the substantia nigra that are replaced by cytoplasmic inclusion bodies caused Lewy bodies. Predominantly affects the ventrolateral substantia nigra

44
Q

What treatments for PD do you know?

A
  1. Co-careldopa (dopa-decarboxylase inhibitor + levodoa)
  2. Non-ergot dopamine agonists (rotigotine, pramipexole, ropinorole)
  3. Ergot derived dopamine agonists (bromocrptine and carbegoline) - fibrosis
    MAO-B inhibitors (selegeline, rasegeline). Cognitive side effects
  4. Anti-cholinergics (procyclodine, benzatropine) - for tremor
  5. COMT inhibitors (entacapone - inhibit GI breakdown of levodopa)
45
Q

How do you assess speech and language?

A
  1. Comprehension - one, two, three stage commands
  2. Repetition (arcuate fasciculus)
  3. Spontaneous speech (fluency, dysarthria)
  4. Naming (anomia)
  5. Reading + writing
46
Q

How do you localise a problem to the NMJ/muscle?

A

Weakness
Normal sensation
Normal reflexes

47
Q

What is the pathophysiology of PD?

A

Disruption of dopamine transmission in the basal ganglia. Loss of melanin containing dopaminergic neurons in substantia nigra and remaining neurons are replaced by cytoplasmic inclusion bodies called Lewy bodies. Predominantly affects the ventro-lateral substantia nigra

48
Q

What PD Plus syndromes do you know?

A

Multiple Systems atrophy (cerebellum+autonomic+PD)
PSNP (more proximal axial rigidity) - poor response to levodopa
Cortico-basal degeneration (frontoparietal involvement - limb apraxia)

49
Q

What is the tremor of PD?

A

RESTING
Note that some patients with PD have a postural component to the tremor - differentiate by asking patient to write

50
Q

Does CMT involve prox or distal limbs?

A

Distal. Affects arms and legs. Mostly affects legs first, except in Type 2D that affects arms first.

In the arms, the weakness stops abruptly at the lower third of thigh

51
Q

What is the pattern of sensory loss in CMT?

A

Depends on the type. Demyelinating type will pred. affect proprioception and vibration

52
Q

Reflexes and Plantars in CMT?

A

Absent reflexes, normal or absent plantars

53
Q

Do you know of any conditions that cause a demyelinating polyneuropathy?

A

CIDP
MM
HSMN
HIV
HNPP (hereditary neuropathy with pressure palsy)

54
Q

Do you know of any drugs that cause a predominently sensory neuropathy?

A

Isoniazid
Metronidazole
Hydralazine

55
Q

Do you know of any drugs that cause a motor neuropathy?

A

Dapsone

56
Q

Do you know of any drugs that cause a sensorimotor neuropathy?

A

Vincristine
Vinblastine
CIsplatin

57
Q

What investigations would you perform for a peripheral neuropathy workup?

A

Bloods: FBC, UE, CRP, ESR, TFT, LFT, vasculitis screen
Urine: Glucose, Bence jones
Nerve conduction studies

58
Q

How do you differentiate a common peroneal nerve palsy from an L5/S1 root lesion?

A

Common peroneal nerve comes off the sciatic nerve and wraps around the fibular head where it is prone to injury. The common peroneal nerve supplies the motor nerves for big toe dorsiflexion (toe to face) and foot eversion (will be apparent when asking patient to stand on tip toes). Reflexes will be normal. There is limited sensory loss involving the lateral calf (superficial) or just the web spaces (deep)

There will be preserved sensation in the tips of toes (tibial) and lateral ankle (sural) that are also L5/S1

There will be preserved ankle inversion and hip abduction which are both lost in L5/S1 nerve root

In both conditions, DTRs are preserved

To assess for an L5 root problem that is not a common peroneal nerve problem, you can test the tibialis posterior

59
Q

What is the pattern of disease in facio-scapulo-humeral muscular dystrophy?

A

Weakness of upper limb and upper arms, preserved forearm strength
Visible scapula due to weakness
Abdominal weakness (Beevor’s sign)
50% of patients will develop lower limb weakness
Sensorineuronal deafness
Retinal telangiectasia

60
Q

What is the inheritance of muscular dystrophy?

A

X-lined recessive mutation in Dystrophin gene
Dystrophin is expressed in skeletal, cardiac, smooth muscle, and brain tissue

61
Q

What are the clinical findings of Becker’s and Duchenne’s muscular dystrophy?

A

Beckers has a ‘better’ prognosis
Proximal to distal pattern of weakness
Legs > neck > arms > distal
Waddling gait
Hyper-lordoisis
Calf pseudohypertrophy (more so in Duchenne’s)

Dilated cardiomyopathy
Pul HTN
Respiratory failure

62
Q

What is Devic’s disease?

A

Now considered distinct from MS
More frequently seen in Asian populations
Central cord lesions (cervical) and optic tract
Vomiting is a frequent presenting complaint
IgG Aquaporin-4 positive
Acute attacks treated with steroids, plasmapharesis and immune supression (rituximab)

63
Q

What treatments for MS do you know?

A

Acute flares are treated with steroids. These do not affect the degree of RECOVERY, but do shorten the length of the relapse.

DMARD’s are started in
-Relapsing-remitting with 2 relapses in 2 years
-Secondary progressive disease

Anti-CD20 Ocrelizumab
Anti-α4β1 Natalizumab
S1P modulator Fingolimod
Fatigue: Amantadine

64
Q

How do you differentiate an INO from a III palsy?

A

INO is a problem with the ipsilateral MLF that prevents eye adduction on conjugate gaze. If you cover the abducting eye, the pathological eye will now adduct. This will not be the case in a III palsy.

65
Q

What structures go through the carvenous sinus?

A

III
IV
Va
Vb
Carotid
Sympathetic carotid plexus

66
Q

What is an Argyl Robertson pupil?

A

Neuro-syphillis
Problem with communication between pre-tectal nucleus and EW nucleus
Preserved near reaction (doesnt need pre-tectal nuclei) but no light reaction (needs pre-tectal nuclei)
Resting pupils are small and irregular
Ptosis may be present with compensatory forehead wrinkling

67
Q

What is a RAPD?

A
  1. Defect in AFFERENT side
  2. Shining light in the normal eye will result in bilateral constriction. When you swing the light to the affected side, there will be bilateral dilation
    If there is a RAPD with no visual loss, the problem is in the tectal midbrain (dorsal midbrain)
    If there is visual loss + RAPD = problem is in the retina or the optic nerve
68
Q

What are the clinical features of a CPA tumour?

A

Usually an acoustic neuroma, or less commonly a meningioma

CPA borders
Medial: V, VI, VII, VIII CNs
Roof: cerebellum
Lateral: bone
Floor: IX, X, XI, XII CNs

69
Q

What is Webber Syndrome?

A

Bran of posterior cerebral artery that supply the midbrain.
Ipsilateral III
Contralateral hemiparesis

70
Q

What is lateral medullary syndrome?

A

Most common brainstem vascular syndrome

Lateral medulla is suppled by posterior inferior cerebellar artery and vertebral artery.

  1. Ipsilateral Horner’s
  2. Ipsilateral cerebellar signs
  3. Ipsilateral V spinothalamic
  4. Contralateral spinothalamic
71
Q

What are common sites of ulnar nerve injury?

A

Back of ulnar olecranon
Guyon’s canal

72
Q

Where is Brocca’s area?

A

Posterior part of inferior frontal gyrus

73
Q

Where is Wernicke’s area?

A

Posterior part of superior temporal gyrus

74
Q

What is the genetics of Huntington’s?

A

AD CAG TNR on chromosome 4

75
Q

What are the clinical features of Huntington’s?

A

Presents in 3-4th decade
Degeneration of motor cortex and striatum (caudate + putamen) with early caudate atrophy seen on MRI
Manifests are chorea
In younger patients, may be rigid with PD signs and slow saccadic eye movements
Fronto-cortical cognitive impairment leads to behavioural disturbances

76
Q

What is your differential diagnosis for chorea?

A

Inherited
Huntingtons (AD)
Wilson’s (AR)
Spinocerebellar ataxia (AD)

Acquired
SLE
PRV
Levodopa
Syndenham’s chorea (late feature of Strep pyogens rheumatic fever)

77
Q

What is the gene implicated in Wilson’s disease and how is it inherited?

A

ATP 7B. AR. Failure of biliary copper excretion

78
Q

Diagnostic criteria for wilsons?

A

<40: low caeruloplasmin
>40: high 24-hour urinary copper excretion

79
Q

What are the clinical signs of Wilsons?

A

Children usually present with liver disease, and adults present with neurological disease.

Neuro
Tremor
Chorea
Bradykinesia
Psychiatric disturbances
Seizures

Liver
Hepatitis
Cirrhosis

Metabolic
Hypoparathyroidism
Type 2 RTA (Proximal) Fanconi

Other
Haemolysis
Arthropathy

80
Q

What is the Bamford Clasification of Stroke?

A

TACS
-Higher function
-Unilateral hemiparesis and/or sensory
-Homonomous Hemianopia

PACS
-Two of TACS

Lacunar
-Pure motor
-Pure sensory
-Sensori-motor
-Ataxic hemiparesis

Posterior (one of the following)
-CN + contralateral motor/sensory deficit
-Bilateral motor/sensory deficit
-Horizontal gaze palsy
-Cerebellum
-ISOLATED homonomous hemianopia

81
Q

What is macular sparing?

A

Central field representation in the occipital cortex receives blood supply from MCA and PCA. So if PCA is interrupted, the central field portion is still supplied by the MCA and you get ‘macular sparing’.

82
Q

What are the clinical findings of a third nerve palsy?

A

Mydriasis
Hypotropic
Exotropic
Divergent strabismus
Intorsion on medial gaze

83
Q

What are the clinical findings of Horner’s syndrome?

A
  1. Partial ptosis that is overcome by upward gaze
  2. Miosis
  3. Preserved light and accomodation reflexes
  4. May be associated with anhidrosis if first and second order neurons are affected
84
Q

What are the three neurons in the sympathetic chain to the eye?

A

1st: From hypothalamus to ciliospinal centre of Budge (C8-T2)
2nd: From Budge to Superior cervical ganglion
3rd: From Superior cervical ganglion to ciliary ganglion and levator palpebrae

85
Q

What are some causes for Horner’s syndrome?

A

1st order neuron: Syrinx, MS, Neck trauma
2nd order neuron: Pancoast, cardiothoracic surgery
3rd order neuron: Caroticocavernous fistula

86
Q

How can you differentiate a surgical from medical III palsy?

A

Not always possible, but surgical causes usually result in a dilated pupil, and medical causes sometimes the pupil isnt dilated. This is because the parasympathetic fibres run on the outside of the III nerve

87
Q

What are the medical and surgical causes for a III palsy?

A

Medical (M’s)
Mononeuritis
GCA
Midbrain infarct
Midbrain demyelination
Migraine

Surgical (C’s)
PCOMA = urgent CTA
Cavernous sinus pathology
Cerebral uncal herniation

88
Q

Causes for an upgaze palsy?

A

Miller Fisher variant of GBS
Parinaud syndrome (pineal tumour)
PSNP
MG
Grave’s

89
Q

What causes Myasthenia Gravis?

A

Anti-bodies agasinst the post-synaptic acetylcholine receptor, or rarely anti muscle specific tyrosine receptor antibodies

It affects occular, bulbar, limb, and respiratory muscles

90
Q

Are there any other conditions associated with Myasthenia?

A

Thymomas
Thymic hyperplasia
Pernicious anaemia
Autoimmune thyroid disorders
RA
SLE

91
Q

How do you investigate Myasthenia?

A

Single fibre EMG - diagnostic
Antibodies (ACh receptor, muscle specific tyrosine receptor antibodies
CT chest
FBC (Pernicious anaemia)
Lung function testing

92
Q

How do you treat Myasthenia?

A
  1. Long-acting acetylcholinesterase inhibitors
  2. The majority of patients eventually require immunosuppression - pred, then aza, cyclo, myco, ciclo

When starting pred - admit - might worsen symptoms and precipitate a crisis

  1. Thymectomy

Crisis: Immunoglobulins, plasmapharesis

93
Q

Do you know of any factors that exacerbate Myasthenia?

A

Infection
Stress
Exertion
Medication:
Beta blockers
Penicillamine
Procainamide
Aminoglycoside antibiotics
Quinolones
Macrolides
Tetracycline

94
Q

Lamotrigine comms

A

‘Slows electrical signals down’
Comes as a tablet
Can take up to 6 weeks to work
Common side effects - skin rashes (SJS), headaches, mood changes, sleep, GI
Rashes are most common in the first 8 weeks and at dose changes, especially when dose increased too quickly
Long-term risk of osteoporosis
Need to check kidney and liver function
Safe in pregnancy
Advise 5mg folic acid for 3 months before conception
Safe in breastfeeding (can be found in breastmilk and can lead to drowsiness)
Might stop the COMBINED pill working - advise changing contraception or using condoms

95
Q

Valproate

A

Epilem
Comes as tablets or liquid
Side effects - GI, oral ulcers, tremors, sleepy, weight gain. Rare - hepatic, suicidal thoughts, pancreatitis
CONTRAINDICATED in pregnancy
Safe in breastfeeding
No effect on contraception
Reduces fertility

96
Q

Leviteracetam

A

Keppra
Takes a few weeks
Headaches, blocked nose, feeling sleepy
Safe in pregnancy
Usual folic acid 5mg 3/12 before
Does NOT affect contraception
Safe in pregnancy

97
Q

Ethosuximide

A

Absence seizures first line

PACES (6 decks)

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