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CPT > Epilepsy > Flashcards

Epilepsy Flashcards

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1
Q

What is a seizure?

A

Transient occurrence of signs/symptoms due to abnormal activity in the brain, leading to a disturbance of consciousness, behaviour, emotion, motor function or sensation

  • clinical manifestation of abnormal and excessive excitation and synchronisation of a group of neurones within the brain
  • so a loss of GABA signals or too strong an excitatory Glutamate ions
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2
Q

What can cause seizures?

A
  • genetic differences in brain chemistry/receptor structure: genetic epilepsy syndromes
  • by exogenous activation of receptors-drugs (something that normally isnt there, activates the receptors)
  • acquired changes in brain chemistry: drug withdrawal, metabolic changes
  • damage to any of these networks: strokes, tumours
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3
Q

What are the symptoms and signs of a seizure?

A
  • loss of consciousness often (but not always) with changes in muscle tone, tongue biting
  • for tonic-clinic seizures initial hypersonic phase, followed by rapid clonus (shaking/jerking)
  • post-ictal period present: can last minutes to hours
  • often an aura prior to seizure (like déjà vu)
  • may be more varied or subtle depending on type of seizure
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4
Q

What is epilepsy?

A
  • repeated series of seizures that is unprovoked by a systemic or neurological insult
  • not only a disease of the young, over 60s almost as common (increases as they age due to cerebrovascular disease)
  • must have at least 2 unprovoked seizures occuring more than 24 hours a apart
  • one unprovoked seizure and probability of further seizures (at least 60% over the next 10 years)
  • diagnosis of epilepsy syndrome
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5
Q

What are the types of reflex seizures?

A
  • brough by a particular stimulius
  • photogenic
  • musicogenic
  • thinking
  • eating
  • hot water immersion
  • reading
  • orgasm
  • movement
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6
Q

What are the classifications of seizures?

A
  • focal onset: aware and impaired awareness, motor and non motor onset
  • Generalised onset: motor (tonic-clinic, myoclonic, atonic) and non motor (absence)
  • Unknown onse
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7
Q

What are generalised seizures?

A
  • no consciousness at all
  • originate at some point within and rapidly engage bilaterally distributed networks
  • can include cortical and subcortical structures but not necessarily the entire cortex
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8
Q

What are focal seizures?

A
  • originate within networks limited to one hemisphere
  • may be discretely localized or more widely distributed
  • only spread locally, gives unilateral motor symptoms, can be conscious
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9
Q

What are provoked seizures?

A
  • seizures as a result of another medical condition such as:
  • drug use or withdrawal
  • alcohol withdrawal
  • head trauma and intracranial bleeding
  • metabolic disturbances
  • CNS infections
  • febrile seizures in infants
  • uncontrolled hypertension
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10
Q

What are the differential diagnoses of seizures?

A
  • syncopal episodes (ex. Vasovagal syncope)
  • cardiac issues including reflex anoxia seizures, arrhythmia
  • movement disorders (ex. Parkinson’s, Huntington’s)
  • TIA
  • Migraines
  • non-epileptic attack disorder (formerly pseudo-seizures) which often occurs in druggies
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11
Q

What is the initial management of a seizure?

A 
ABCDE
Airway
Breathing
Circulation
Disability
E: recovery position
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12
Q

When do you give drugs to terminate a seizure?

A
  • wait after 5 minutes

- most seizures will self terminate

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13
Q

What is status epilepticus?

A
  • seizure of any variety lasting 5 min or more, or multiple seizures without a complete recovery between them
  • status is a medical emergency
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14
Q

What is the pharmacological treatment for Status?

A
  • wait 5 minutes
  • benzodiazepine
  • benzodiazepines again
  • phenytoin (or maybe Levetiracetam?)
  • thiopentone/anaesthesia (call intensive care)
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15
Q

Benzodiazepines as treatment for Status Epilepticus (lorazepam, midazolam, diazepam)

A
  • GABA agonists so work best when membrane positive in order to hyperpolarize (in seizures)
  • work best as a preventative measure
  • no firing neurones=no more seizures
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16
Q

What inevestigstions can you do for epilepsy?

A

-EEG
-record of electrical pattern of activity in the brain
Imaging
-MRI
-can detect vascular or structural abnormalities

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17
Q

Carbamazepine (Tegretol)

A
  • sodium channel blocker
  • also used for bipolar and sometimes chronic pain
  • side effects: suicidal thoughts, joint pain, bone marrow failure
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18
Q

Phenytoin

A
  • sodium channel blocker
  • used mainly in status epilepticus or as an adjunct in generalised seizures
  • has zero order kinetics so no half life (care when adjusting doses)
  • specific side effects: bone marrow suppression, hypotension, arrhythmia (give IV)
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19
Q

Sodium Valproate (Epilim, Depakote)

A
  • probably a mix of GABAa effects and sodium channel blockade
  • 1st line for GENERALISED epilepsies
  • specific side effects: liver failure, pancreatitis, lethargy
  • really old and dirty drug
20
Q

Lamotrigine

A
  • primarily a sodium channel blocker, may also affect calcium channels
  • good for focal epilepsy
  • used often where valproate contraindicated in generalised epilepsy
21
Q

Levetiracetam (Keppra)

A
  • novel MOA and is well tolerated
  • synaptic vesicle glycoprotein binder, stops the release of neurotransmitters into synapse and reduces neuronal activity
  • option for focal seizures and generalized seizures
  • anecdotally being use more frequently, easy dosing and well tolerated
  • safe in pregnancy
22
Q

What are the side effects of AEDs?

A
  • tiredness/drowsiness
  • nausea and vomiting
  • mood changes and suicidal ideation
  • osteoporosis
  • rashes including Steven Johnson syndrome (most likely caused by carbamazepine or phenytoin)
  • many can cause anaemia, thrombocytopenia or bone marrow failure
23
Q

What should patient do regarding the side effects?

A
  • patients on anti-epileptics and warfarin will need close monitoring
  • ideally patients on AEDs shouldn’t consume alcohol
  • carbamazepine and phenytoin ay decrease the effectiveness of oral contraceptive pills and some antibiotics
  • valproate can increase the plasma conc. Of other AEDS
  • newer AEDs have less side effects, or are metabolised in other ways (Levetiracetam)
24
Q

What are some DDIs with AEDs?

A

CYP inducers

  • phenytoin
  • carbamazepine
  • barbituates

CYP inhibitors
-valproate

25
Q

What drug has the greatest risk of congenital malformations?

A
  • valproate
  • shouldn’t be prescribed to any woman of child-bearing age
  • if prescribed, women must have hysterectomy and on a highly effective contraceptive
  • lamotrigine and Levetiracetam are safest
26
Q

What is the pathology iof Idiopathic Parkinson’s Disease

A
  • neurdegneration
  • lewy bodies (synucleinopathy)
  • loss of pigment: 50% loss leads to symptoms, increased turnover, upregulate receptors
  • reduced dopamine
27
Q

What are the drug classes in IPD?

A
  • levodopa (L-DOPA)
  • dopamine receptor agonists
  • MAOI type B inhibitors
  • COMT inhibitors
  • anticholinergic
  • amantidine
28
Q

Why do we not just use dopamine in IPD??

A
  • dopamine cannot cross BBB

- L—DOPA crosses by active transport and is absorbed by active transport

29
Q

Levodopa (L-DOPAMINE)

A
  • must be taken up by dopaminergic cells in substantia nigra to be converted to dopamine
  • fewer remaining cells means less reliable effect of l-dopa
  • given oral
  • absorbed by active transport
  • 90% inactivated in intestinal wall by monoamine oxidase and DOPA decarboxylase
  • half life of 2 hours so must be given frequently
  • 9% converted to dopamine in peripheral tissues by DOPA decarboxylase
  • <1% enters CNS
30
Q

What are the formulations of L-DOPA?

A
  • used in combo with PERIPHERAL DOPA decarboxylase inhibitor:
  • co-careldopa (Sinemet)
  • co-beneldopa (Madopar)
  • reduced dose required
  • reduced side effects
  • increased L-DOPA reaching brain
  • given in tablet formulations only
  • standard dosage-variable strengths
  • controlled released preparations
  • dispersible Madopar (not soluble)
31
Q

What are the advantages and disadvantages of L-DOPA?

A

Advantages

  • highly efficacious
  • low side effects: nausea/anorexia, hypotension, psychosis, tachycardia

Disadvantages

  • precursor: needs enzyme conversion
  • long term: loss of efficacy, involuntary movements, motor complications
32
Q

What are the interactions of L-DOPA?

A
  • pyridoxine (vitamin B6) increases peripheral breakdown of L-DOPA
  • MAOIs risk hypertensive crisis
  • many antipsychotic drugs block dopamine receptors and Parkinsonism is a side effects (newer, “atypical” antipsychotics less so)
33
Q

Dopamine Receptor Agonists

A
  • non ergot: ropinirole, pramipexole
  • patch: rotigotine
  • subcutaneous: apomorphine
  • first line therapy
  • add on therapy
  • apomorphine: only for patients with severe motor fluctuations
34
Q

What are the advantages and disadvantages of dopamine receptor agonists?

A

Advantages

  • direct acting
  • less dyskinesia/motor complications
  • possible neuroprotection

Disadvantages

  • less efficacy than L-DOPA
  • impulse control disorders
  • more psychiatric s/e (dose limiting)
  • expensive
35
Q

What are some impulse control disorders (dopamine dysregulation syndrome)

A
  • pathological gambling
  • hypersexuality
  • compulsive shopping
  • desire to increase dosage
  • punding
36
Q

What are the side effects of dopamine receptor agonists?

A
  • sedation
  • hallucinations
  • confusion
  • nausea
  • hypotension
  • secondary narcolepsy
37
Q

MAOI type B inhibitors (selegiline, rasagaline)

A

Monoamine oxidase B

  • metabolised dopamine
  • predominates in dopamine containing regions in brain
  • MAOB inhibitors enhance dopamine

Monoamine Oxidase B inhibitors

  • can be used alone
  • prolonged action of L-DOPA
  • smooths out motor response
  • may be neuroprotective
38
Q

What are COMT inhibitors

A
  • reduces the breakdown of L-DOPA
  • but has no therapeutic effect on its own
  • entacapone: doesnt cross BBB
  • reduce peripheral breakdown of L-DOPA to 3-O-methyldopa since 3-O-methyldopa competes with L-DOPA active transport into CNS
  • no therapeutic effect alone
  • can use combination tablets COMT inhibitor and L-DOPA and peripheral dopa decarboxylase inhibitor (Stalevo)
  • have L-DOPA “sparing” effect
  • prolongs motor response to L-DOPA (reduces symptoms of “wearing off”)
39
Q

What are anticholinergics?

A
  • may have antagonistic effects to dopamine
  • trihexyphenidydyl
  • orphenadrine
  • procyclidine
  • minor role in treatment of pD
  • not very useful because it doesnt solve the main problems in PD: Bradykinesia and PD
40
Q

What are the advantages and disadvantages of anticholinergics?

A 
Advantages
-treat tremor
-not acting via dopamine systems 
Disadvtanges 
-no effect on bradykinesia
-side effects: confusion, drowsiness, usual anticholinergic s/e, blurred vision, urinary retention
41
Q

Amantadine

A
  • MOA uncertain
  • possibly enhances dopamine release or anticholinergic NMDA inhibition
  • poorly effective
  • few side effects
  • little effect on tremor
  • not used as much anymore
42
Q

Surgery for IPD

A
  • carried out stereotactically
  • of value in highly selected cases: must be dopamine responsive, significant side effects with L-DOPA, no psychiatric illness
  • controlled trials
  • Lesion: thalamus for tremor, GPi for dyskinesia
  • deep brain stimulation: subthalamic nucleus
43
Q

What is Myasthenia Gravis?

A
  • fluctuation, fatiguable, weakness in skeletal muscle
  • commonly presents in extraocular muscle (get double vision and ptosis)
  • bulbar involvement: dysphagia, dysphagia, dysarthria
  • limb weakness: proximal symmetric
  • respiratory muscle involvement: will get type 2 resp failre
44
Q

What are the drugs affecting neuromuscular transmission which exacerbates Myasthenia Gravis?

A
  • aminoglycosides
  • beta-blockers
  • CCBs
  • quinidine
  • procainamide
  • chloroquine, penicillamine
  • succinylcholine
  • magnesium
  • ACE inhibitors
45
Q

What is the therapeutic management of myasthenia gravis?

A

Acetylcholinesterase inhibitors

  • enhance neuromuscular transmission
  • skeletal and smooth muscle
  • excess dose can cause depolarizing block: cholinergic crisis
  • cholinergic side effects

Pyridostigmine-oral

Neostigmine- oral and IV preparations (ITU)

  • quicker action, duration up to 4 hours
  • significant cholinergic side effects
46
Q

Pyridostigmine

A

-prevents breakdown of ACh in NMJ
-ACh more likely to engage with remaining receptors
-onset 30min; peak 60-120min; duration 3-6hours
-dose interval and timing crucial
-give several times a day
Cholinergic side effects: miosis and the SSLUDGE syndrome
Salivation
Sweating
Lacrimation
Urinary incontinence
Diarrhoea
GI upset and hypermotility
Emesis

47
Q

What is a DAT scan?

A
  • labelled tracer
  • presynaptic uptake
  • abnormal in PD
  • not diagnostic
  • tremor
  • neuroleptic
  • vascular

CPT (16 decks)

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