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SAM Module C Neurology > Epilepsy > Flashcards

Epilepsy Flashcards

1
Q

What percentage of cats with seizures have suspected idiopathic epilepsy

A

Approx 1/3

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2
Q

What are possible vascular causes of epilepsy in cats?

A 
Hypertensive encephalopathy
Feline ischemic encephalopathy
Thromboembolic diseases
Polycythemia
Coagulopathy
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3
Q

What inflammatory conditions are associated with epilepsy in cats?

A 
Meningoencephalitis of unknown origin
Cuterebriasis, dirofilariasis
Rabies, pseudorabies
Feline immunodeficiency virus‐infection
Feline leukemia virus‐infection
Feline infectious peritonitis
Cryptococcosis, blastomycosis
Toxoplasmosis
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4
Q

What are the main metabolic causes of seizures in ccats?

A 
Hyperthyroidism
Renal encephalopathy
Thiamin deficiency
Hepatic encephalopathy
Hypoglycemia
Hypocalcemia
Electrolyte imbalance
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5
Q

What are the 4 stages of a seizure?

A

prodrome, aura, ictus, and postictal stages.

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6
Q

What are feline seizures typically like?

A

frequently complex focal seizures with or without secondary generalization. The ictal signs frequently include drooling, facial twitching, tremor, rapid running, mydriasis, hypersalivation, urination, and defecation. During focal seizure, a cat can remain in sternal recumbency or can show running or climbing activity. Seizures might be particularly violent

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7
Q

What are the main differential diagnoses for a seizure in cats (things that are not epilpsy)

A

behavioral changes, obsessive‐compulsive disorder, movement disorders, narcolepsy/cataplexy, sleep disorders, increased intracranial pressure, pain‐associated behavior, tremor syndromes, syncope, feline orofacial pain syndrome, vestibular or neuromuscular disorder, and other encephalopathies

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8
Q

How responsive are cats to epilepsy tx?

A

40% of cats with IE become seizure‐free, 40% show decreases of over 50% in frequency of seizure, and 20% are resistant to treatment

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9
Q

What is epilepsy?

A

not a single disease but a collection of conditions with a wide range of underlying aetiologies and pathologies resulting in recurrent seizures

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10
Q

What do you need to check in the hx?

A
  1. description, duration and frequency. V short or v long make a fit unlikely
  2. time of the day (normally at rest)
  3. postictal effects (disorientation, ataxia and polyphagia)
  4. behaviour between seizures
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11
Q

What signs are typical of a seizure?

A

 more common at rest
 prodrome - restlessness, anxiety
 ictus - consciousness may be impared; autonomic signs (salivation, urination and defaecation)
 postictal signs - confusion, blindness, ataxia

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12
Q

What is a focal seizure?

A

due to activation of only one part of one cerebral hemisphere;
called complex when there is alteration of awareness

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13
Q

What is a generalised seizure?

A

due to initial activation of both cerebral hemispheres simultaneously;
consciousness may be impaired and motor manifestations are bilateral

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14
Q

What stimulates narcolepsy?

A

Excitement

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15
Q

What is an audiogenic reflex seizure?

A

Fits in cats triggered by high pitched noises

Leviteracetam more useful than pheno for tx

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16
Q

What are the main classifications of seizures

A
  • Reactive seizures
     response from normal brain to transient disturbance in function from metabolic disorders or intoxication
     reversible
  • Idiopathic Epilepsy
     genetic (e.g. Lagotto Romagnolo)
     suspected genetic (high breed prevalence)
     of unknown cause
  • Structural Epilepsy
     seizures provoked by intracranial pathology
     vascular, inflammatory/infectious, traumatic,
    anomalous, neoplastic, degenerative
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17
Q

Outline idiopathic epilepsy

A

 presumed to be of genetic origin
 channelopathies (mutations of genes that encode either voltagegated or ligand-gated ion channels) or other genetic diseases
 most common in purebred dogs, between 6m-6y (3m-10y), normal in interictal period

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18
Q

What are the main ddx for structural epilepsy?

A
  • Vascular (stroke)
  • Infectious/inflammatory (viral, protozoal, bacterial; immune- mediated – MUOs)
  • Traumatic (TBI)
  • Anomalous (porencephaly, hydranencephaly, hydrocephalus, lissencephaly…)
  • M
  • I
  • Neoplasia (primary or metastatic)
  • Degenerative (storage diseases, CDS)
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19
Q

What are the main work ups of reactive seizures?

A
  1. hepatic
  2. electrolyte imbalance (Na, Ca)
  3. hypoglycaemia
  4. hypoxemia
  5. thiamine deficiency
  6. renal
  7. toxins and drugs
     ~10% of all seizures
     ~40% intoxications, 30% hypoglycemia in dogs
     ~40% present in SE
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20
Q

What are the indications for advanced investigations?

A

 MRI and CSF
 age at seizure onset ˂6m or ˃6y
 interictal neurological abnormalities
 Status or clusters
 presumptive diagnosis of IE but drug‐resistance
to 1 AED titrated to highest tolerated dose
 Cats?

21
Q

What are the criteria for the diagnosis of idiopathic epilepsy?

A
  • Tier I confidence level
     CBC, biochem, urinalysis
     age at seizure onset ˃6m and ˂ 6y
     normal neurological examination
- Tier II confidence level
 Tier I +
 BA stimulation
 MRI
 CSF
  • Tier III confidence level
     Tier I + II +
     EEG abnormalities
22
Q

What are the aims for treating epilepsy?

A
  1. improve frequency and severity of seizures
  2. without causing significant side effects
  3. rarely can stop seizures altogether
  4. some breeds trickier (e.g. Border Collie)
  5. clusters hard to stop
23
Q

How are border collies harder to tx for epilepsy?

A

Prone to clusters

Poor tolerance of phenobarb

24
Q

What are the main treatment options for dogs?

A

 Phenobarbital
 Potassium bromide
 Imepitoin

If refractory:
 Levetiracetam
 Zonizamide
 Gabapentin and Pregabalin
 Topiramate and Felbamate
25
Q

What are the main treatment options for cats?

A 
 Phenobarbital
 Levetiracetam
 Gabapentin
 No diazepam - fulminant hepatotoxicity
 No potassium bromide - allergic pneumonitis
 No imepitoin?
26
Q

Outline the mechanism of phenobarb and the dose

A

 prolongs opening of the chloride channel at the GABAA receptor; effective in 60-80% of dogs with IE
 auto-induction usually results in the need for increases in dose to maintain therapeutical levels
 initial dose 3mg/kg BID in dog and 2mg/kg in cat; therapeutical serum concentration 15-40µg/ml (aim for 25-30µg/ml)
 steady-state 10-14d, ideally measure trough levels
 loading dose: 3mg/kg slow IV q30-60min for a total of up to 20mg/kg

27
Q

What are the s/e of phenobarb and how do you monitor it?

A

 sedation (worse after starting therapy or increase of dose), ataxia,
PU/PD, polyphagia
 mild to moderate increases in ALP and ALT
 main adverse effects (usually reversible):
1. potential for hepatotoxicity (check BAs, biochemistry)
2. blood dyscrasias (probably idiosynchratic)
• neutropaenia, anaemia, thrombocypaenia
 check serum concentrations, biochemistry and haematology
 2 weeks
 3 months
 q6 months

28
Q

How does imepitoin work?

A

 partial agonist at the benzodiazepine site of the GABA receptor, weak Ca channel blocker
 anxiolytic effects – useful?
 immediate effect?
 10-30mg/kg BID; start 10-15mg/kg and increase if necessary
 no need to do serum levels, just increase to effect but no improvement in seizure control above 30mg/kg…

29
Q

Outline the s/e of imepitoin

A

 side-effects less common and short-lived
 hyperactivity, polyphagia, polyuria, polydipsia, sedation, hypersalivation, vomiting, ataxia, change in behaviour, anorexia, diarrhoea
 routine bloods? – at 4 weeks and then q6m…
 no data for cats
 useful for clusters? Last study says not so good…
 no IV formulation so cannot use in status

30
Q

Outline the pharmacokinetics of KBr

A

 filtered by glomerulus then reabsorbed by kidneys in competition with Cl-
 competes with Cl- for renal elimination – ↑ Cl- intake increases bromide elimination - NO DIET CHANGES!!
 20-30mg/kg SID with food, therapeutical serum concentration 1-2 mg/ml (with PB) or 1-3mg/ml alone
 steady-state at 2.5-3m, measure at any time of day (1-3m)
 loading dose if in a hurry (40mg/kg TID for 3-5d) – NOT EASY…

31
Q

What are the s/e of KBr

A

 sedation, ataxia, weakness, PU/PD, polyphagia
 nausea, vomiting (direct gastric irritation)
- liquid form and with food
- divide into BID
- increased risk of pancreatitis
 coughing and allergic pneumonitis in cats
 Bromism: stupor or coma, disorientation, ataxia, paresis, blindness, dysphagia
 stop bromide, in severe cases administer NaCl slowly

32
Q

Outline the use of leviteracetam

A

 initial dose 20-25mg/kg TID (possibly higher dose if on PB)
 70% to 90% excreted unchanged in urine; remainder hydrolyzed in serum and other organs
 IV loading dose 60mg/kg
 very few side-effects, transient sedation
1. myoclonic seizures, possibly also focal
2. patients with hepatic problems (e.g. PSS)
3. cats (mild sedation and decreased appetite uncommon)
4. possibly used as pulse therapy in CS?
5. SE as IV formulation
6. potential antiepileptogenic effect

33
Q

Outline the use of zonisamide

A

 initial dose 5mg/kg BID (10mg/kg if on PB)
 metabolised by liver
 steady-state in 3-4 days
 transient sedation, anorexia
 hepatotoxicity and haematological changes (neutropaenia)
 possibly useful in cats
 very expensive

34
Q

When should AEDs be monitored?

A
  1. steady-state after starting treatment or after loading
  2. if seizure frequency worsens
  3. if there are signs of toxicity
  4. q6-12m to check if changes in pharmacokinetics have affected
    blood concentrations
  5. mainly phenobarbital and potassium bromide – not just within range but at appropriate level for seizure frequency!
35
Q

What is refractory epilepsy

A 
 therapeutical levels of 2 medications but less than 50% reduction in seizures
 ~30% of cases with epilepsy
 Look for:
 diagnostic errors:
1. non-epileptic paroxysmal event
2. symptomatic epilepsy
 ineffective drugs
 incorrect dosing, timing, diet
 poor owner compliance
36
Q

What are the main theories behind what causes refractor epilepsy?

A

 altered expression of drug transporters in brain, which pump AEDs away
 changing drug targets in patients with recurrent seizures, making them resistant to AEDs

37
Q

What should you do with refractory epilepsy?

A

 start with most appropriate AED or if unknown the one you have the most experience with
 measure levels when appropriate and increase dose if still seizures and no significant side-effects; keep repeating
 add 2nd AED (aim for monotherapy if possible)
 add 3rd AED if necessary; if not working, try a different 3rd AED and keep rotating
 diet?
 look for mistakes

38
Q

What are the stages of status/ cluster fits?

A

 1st stage - ↑ autonomic activity:
 hypertension, hyperglycaemia, hyperthermia, ↑CBF
 2nd stage (after ~30min):
 hypotension, hypoglycaemia, ↓CBF
 excessive electrical activity starts causing brain damage

39
Q

What are clusters/ status?

A

 SE – seizure lasting at least 5min or ≥2 seizures without full recovery of consciousness
 CS – multiple seizures over a short period of time with recovery of consciousness between them

40
Q

How do you deal with multiple seizures at home?

A 
rectal diazepam (1-2 mg/kg)
 can use levetiracetam as pulse in case of cluster seizures (20mg/kg TID for 48-72h)
41
Q

How do you deal with clusters/ status in hosp?

A

 IV or rectal diazepam or midazolam up to 3x
 load IV with PB or continue q12h
Diazepam (0.5-1mg/kg IV or 1-2mg/kg PR) or Midazolam (0.2mg/kg IV) repeat up to 3 times while loading with PB (3mg/kg slow IV q15m-4h up to a
total of 20mg/kg in 24h in dogs and 15mg/kg in cats; then 3mg/kg BID)

If this fails, 
 can use levetiracetam
• loading dose 60mg/kg IV (slowly)
• 20mg/kg TID IV or PO
• 40mg/kg rectal (solution through urinary catheter)
 can load on KBr
• rectally if cannot swallow or orally
• 30-40mg/kg TID for 3-5 days
• significant sedation, ataxia, confusion for a few weeks
42
Q

What are the 4 stages of status epilepticus?

A

 early - ongoing seizure due to failure of mechanisms responsible for seizure termination
 established – SE that persists after treatment with benzodiazepines
 refractory – SE that fails to abort after a first line (usually a benzodiazepine) and a second-line antiseizure drug
 super-refractory – SE that continues or recurs 24 h or more after onset of anaesthetic therapy

43
Q

Outline the use of benzodiazepines

A

enhance GABA effect at GABAa receptor
 not good as maintenance therapy:
1. short half-life
2. development of tolerance over a few weeks
3. cross-tolerance: won’t work in an emergency!!!
 diazepam (0.5mg/kg/h) or midazolam CRI (0.3mg/kg/h), taper over 18- 24h
 ++ strong anti-epileptic action
 – tendency for rapid and acute tolerance to develop, risks of hepatic and renal impairment, milder respiratory and cardiac depressant

44
Q

Outline the use of propofol

A

 direct activation of the c-aminobutyric receptor–chloride ionophore complex and by inhibiting NMDA glutamate receptors
 may be more suited in cases with hepatic encephalopathy, established SE and some intoxications
 care with possibility of Heinz body anaemia in cats -
 2-8mg/kg bolus, then 4-12mg/kg/h and slowly taper over 18-24h
 if using infusion – use preservative free formulation (≥ 40ml/kg)
 ++ very rapid onset and recovery even after prolonged infusion, responsiveness allows greater control of the level of anaesthesia no serious drug–drug interactions
 – mild hypotension or cardiocirculatory depression, risk of misinterpreting common drug-induced involuntary movements as seizures

45
Q

What are the aims of monitoring AED therapy?

A

(i) Determine effective drug concentrations after initiation of successful treatment (as appropriate);
(ii) Determine if drug failure is because of pharmacokinetic factors so as to focus on a change
in dose (metabolic tolerance) or pharmacodynamic factors so as to focus on a change of drugs (functional tolerance);
(iii) Determine if treatment failure is caused by poor compliance or an inadequate or changed drug concentration;
(iv) Prevent toxic effects; and
(v) Aid with individualization of treatment

46
Q

When should phenobarb testing be done

A

Ideally in the am prior to eating or getting meds

47
Q

How does phenobarb affect other drugs?

A

increase clearance of several other AEDs, including levetiracetam, zonisamide and clorazepate

48
Q

When are KBr measurements recommended to be taken?

A

recommended at the first steady-state concentration point between 6 and 12 weeks then on an
annual basis or if > 3 seizures occur before the next
scheduled evaluation, or if signs of toxicity are suspected. Because of the long elimination half-life, samples can be collected at any time point >2 h after
dosing to avoid any peak effect variability

49
Q

What are the 4 types of adverse events?

A

Type I: Predictable and directly related to pharmacologic effects in a dose-dependent fashion
Type II: Unpredictable (idiosyncratic) and potentially life-threatening
Type III: Cumulative with long-term treatment and
potentially life-threatening
Type IV: Delayed (carcinogenic or teratogenic) and
life-threatening

SAM Module C Neurology (14 decks)

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