1
Q
epidemiology
A
0.6% of canadian population; 15500 new cases each year in Canada
2
Q
seizure
A
- temporary neurological reaction to sudden excessive electrical excitation of cortical neurons
- loss of awareness or consciousness, movement or sensation disturbances, changed mood or mental function
- results from either known or idiopathic (unknown) origins
3
Q
is the stratum corneum involved in seizures?
A
NO - this is in psoriasis (outer layer of epidermis)
said he made an exam q with this
4
Q
epilepsy
A
- CHRONIC neurological disorder affecting the brain (although some can “get out of it”)
- symptoms are RECURRENT seizures
- IDIOPATHIC: no known cause
5
Q
What must occur for a person to be diagnosed with epilepsy?
A
- an individual must have had 2 or more seizures of unknown aetiology to be diagnosed
- therefore if they are diagnosed with epilepsy, we don’t know the root of the origin of the disease!
- first they will go through all the differential diagnosis procedures (tumour, meningitis, head trauma, metabolic, etc)
(i. e. if they have 2 seizures all from separate, KNOWN causes this is NOT epilepsy)
6
Q
describe the flow chart of “questions” that one must go through to diagnose epilepsy
A
1) More than one seizure?
- no-> can’t diagnose epilepsy at this time
- yes-> …
2) provoked?
- yes-> therefore secondary seizure-> investigate underlying cause
- no-> therefore primary seizure-> examine patient history-> diagnostic tests-> determine epilepsy syndrome-> examine treatment options (AKA THEY HAVE EPILEPSY)
7
Q
Diagnostic tests
A
Brain imaging:
- electroencephalograph
- computerized tomography scanning
- magnetic resonance imaging
- positron emission tomography
Blood tests
Lumbar puncture
8
Q
electnoenecphalograph
A
- EEG
- looks at the wave pattern-> is it normal or not
- non-invasive
- record electrical activity on brain surface
- locate area of irregularly firing cortical neurons
- determine severity and type of seizure disorder
- does not diagnose or exclude epilepsy
- person with epilepsy may have normal EEG
9
Q
computerized tomography scanning
A
- CT scan
- this is a generalized snapshot of the area
- look for gross structural abnormalities
10
Q
magnetic resonance tomography
A
- MRI
- get the detail-> repeated slice of the body to get a full image
- gets the exact size, depth, etc for the abnormality
11
Q
positron emission tomography
A
- PET scan
- ask person to pick up a pen and the scan will highlight the specific part of the brain that made you pick it up (i.e. any specific function/movement)
12
Q
what do blood tests check for when diagnosing epilepsy
A
-check for infections, anemia (low iron is a trigger), minerals, poisons that may have caused a seizure (secondary causes)
13
Q
what does a lumbar puncture check for when diagnosing epilepsy
A
-seizure caused by infection of bleeding in the brain
14
Q
4 mains stages to an action potential
A
1) resting
2) depolarization
3) repolarization
4) hyperpolarization
15
Q
resting membrane potential
A
= -70mV
- more Na, Ca, Cl outside
- more K inside
16
Q
depolarization
A
- Ca influx creates partial depolarization
- Na channels open and Na rushes into cortical neuron
- becomes more positive
17
Q
repolarization
A
- K rushes out of cortical neuron, leaving behind a negative charge
- Cl rushes into cortical neuron, bringing in a negative charge
- going back toward resting state
18
Q
hyperpolarization
A
- some K channels remain open
- slows K to leak through
- membrane becomes more negative than resting membrane potential
19
Q
pathophysiology
generic
A
-cluster of cortical neutrons in a localized area simultaneously fire abnormally and this may spread to other regions of the brain
20
Q
pathophysiology
initiation
A
- bursts of APs from a cluster of cortical neurons
- synchronization of these neurons
- prolonged neuronal depolarization-> reptitive APs
- hyperexcitability due to imbalance of neuronal membrane
21
Q
balanced neuron
A
excite= inhibit
- Na and Ca in= Cl in and K out
- aspartate and glutamate= GABA
22
Q
imbalanced neuron
A
EXCITE>inhibit (blocked)
- defective voltage gaed ion channels-> hyperexcitability
- Na: excessive influx
- Ca: excessive influx
- K: insufficient efflux
- Cl: insufficient influx
- excessive excitatory NTs-> glutamate and aspartate
- insufficient inhibitory NT-> GABA
23
Q
Pathophysiology
Termination
A
- seizure ends after a few seconds/minutes depending on type of seizure
- YOU WANT THEM TO BE AS SHORT AS POSSIBLE*
- spontaneous
- unknown mechanism
24
Q
what it is called if there is not termination of the seizure
A
status epilepticus-> a dangerous condition in which epileptic seizures follow one another without recovery of consciousness between them.
25
2 main seizure categories
1) partial
| 2) generalized
26
partial seizure
- originates in a localized part of the brain in one hemisphere or a specific lobe
- only small part of the brain!
a) simple partial
b) complex partial
c) secondarily generalized
- 80% of people at least start off with partial seizures
27
generalized seizure
- occurs in both hemispheres of the brain-> throughout ENTIRE brain
a) absence
b) atonic
c) myoclonic
d) tonic- clonic
28
simple partial
-most benign seizure
Before:
-aura- physiological warning sign before experiencing a seizure (i.e. various scents, anxiousness, deja vu)
During:
-symptoms depend on which area of the brain in affected; they are most likely just an abnormality:
Motor- ie jerking movements, tonic movements (stiffening)
Sensory- ie tingling/ numbness
Autonomic- ie abdominal discomfort
psychic- ie hallucinations, fear, sadness
-no loss of consciousness, awake, aware
After:
-memory intact, can recall what happened
29
what is important when it comes to simple partial seizures?
-early detection so that it doesn't progress into a more severe type of seizure
30
Complex partial
-more invasive- bigger area, more severe and complex than simple
Complex b/c lose consciousness
before:
-may be preceded by an aura (simple partial)
During:
-impaired consciousness (unaware of environment)- makes it even more dangerous
-involves automatisms, ie mumbling, picking at clothes, random walking
-may progress into a generalized seizure
After:
-doesnt recall event
-may be confused or tired immediately after
31
Secondarily generalized
- partial seizure that evolves into a generalized seizure (keep expanding into different parts of the brain)
- can start as simple partial seizure (aura)-> complex partial-> secondarily generalized (tonic-clonic)
- tonic-clonic convulsions
- aka starts off small, but finishes like generalized (hyper excitability of entire brain)
32
Absence
-petit mal
-more common in children (2-18)
-keep this in mind for children (i.e. having trouble concentrating- may not just be ADHD
Before: no aura
During:
-brief lapse of consciousness, blank stare, unaware, then continue on with activity
-begins and ends suddenly, lasting a couple of seconds
-may involve automatisms
-may occur many times throughout the day, thus interfere with learning
After:
-continue on with activity
-prompt recovery
*this can happen 200-300 times a day-> aka blips that you miss through the day
33
Atonic
```
ATONIC= absence of tone
Before:
-no warning-> completely out of blue (could even be walking and then fall over)
During:
-abruptly lose muscle tone
-brief loss of consciousness
-collapse and fall (drop attack)
After:
-recover after a few seconds
-regain consciousness
```
34
Myoclonic
*opposite to atonic-> walking and then stiffen up
Before: no warning
During:
-muscle jerks- foot kicking, hand flings out suddenly, whole body jerks
-may have 1 seizure or many in a row
-consciousness intact
After: memory intact
35
Tonic Clonic
-grand mal
Before: no warning
During:
-epileptic cry, lose consciousness, collapse
-Tonic phase: body stiffens
-Clonic phase: body jerks (muscles contract and relax)
-convulsive
-change in breathing, bite tongue, incontinsence
After:
-no recollection
-fatigued, confused, tired
* this is what a "normal" seizure is seen as"
36
Status epilepticus
(-recall: usually, seizures last only a couple seconds, no more than 5 minutes)
- seizure lasts for long
- may repeat without recovery
- can lead to neurological disability
- can be convulsive or non-convulsive
37
secondary seizures
```
can be triggered by:
-head trauma
-head injury
-stress
-lack of sleep
-drug use
-alcohol withdrawal
-poor nutrition
-disease of infection
(if one of these is what causes a person's seizure, it rules out epilepsy
```
38
alcohol and its effect on seizures
- its a CNS depressant and an inducer of the liver
- induces production of hepatic enzymes that triggers the breakdown of the drugs that treat seizures, therefore:
- heavy consumption decreases seizure threshold (could happen to anyone)
- chronic consumers likely to experience seizures upon withdrawal from alcohol
- patients with epilepsy advised not to consume large amounts
- can react negatively with AEDs- less effective, have side effects-> vulnerable to have seizure
39
febrile seizure
- convulsions (tonic-clonic) due to fever
- common in infants and children, usually harmless
- most last for a few minutes
- therefore not considered to have epilepsy
40
is there a cure for epilepsy?
no- BUT there IS a cure for seizure disorder-> i.e. you find whatever the cause is for you and treat towards that
41
treatment goals
- decrease frequency and severity of seizures
- pharmacological treatment-> anti-epileptic drugs (AEDs)
- nonpharm treatment:
- surgery
- vagal nerve stimulation
- ketogenic diet
42
vagal nerve stimulation
- brief jolts of electrical energy sent to brain via left vagus nerve
- prevent or interrupt electrical disturbances in brain
- decrease frequency and duration of seizures
- pulse generator implanted under skin on upper left side of chest to left side of neck
- unknown mechanism
43
ketogenic diet
- high in fat, low in CHO
- by tricking body into thinking its starving it make brains burn fats to metabolize instead of glucose
- for children
- unknown mechanism
44
pharmacological treatment
- AEDs
- 3 basic mechanisms of action:
1) modification of voltage-gated ion channel
2) increasing gamma-aminobutyric (GABA)- mediated inhibitory neurotransmission
3) decreasing glutamate-mediated excitatory neurotransmission
45
What is the most commonly used path for AEDs
-voltage gated Na channel blockers (mainly during the hyper polarized stage of an AP)
-prevents influx of Na and decreases the frequency of recurrent APs
(voltage gated Ca channel blockers work similarly- limits depolarization of the cortical neuron by restricting entrance of Ca)
46
Other than Na and Ca channel blockers, what is another possible site of action of AEDs?
- glutamate receptors
| - drugs that act at these receptors reduce receptor activity- inhibits glutamate-mediated excitatory neurotransmission
47
What are some common side effects of AEDs?
-drowsiness
-irritability
-nausea
-skin rash
-lack of coordination
(but side effects of each drug may vary)
48
Why are doses of AEDs titrated up?
- these drugs hyperactive the metabolic activity of the liver, therefore:
- takes a long time to saturate the liver of a full dose needed to control seizures (titrate up until this happens)
49
When do we turn to surgery to treat seizures
-considered when seizures are not responsive to pharmaceutical treatment
50
what are the 2 goals of surgery
1) maximize seizure control
| 2) minimize disruption of normal brain functioning
51
what are the 2 main types of surgery
1) resection/resective surgery
| 2) disconnection surgery
52
resection/ resective surgery
- removal of the area of brain involved in seizure activity
| goal: cure seizure disorder
53
disconnection surgery
- interrupts nerve pathways that allow seizures to spread
- useful when seizure activity occurs in critical areas of the brain that cannot be removed
goal: provide relief
54
If a woman who experiences seizures is pregnant will her children be healthy?
- most likely (>90%)
| - depends on severity of epilepsy
55
what is the biggest danger to the fetus from their mom being epileptic?
- AEDs can affect fetus
- risk of malformation in child
- risk still present even with disuse of AED
- seizures can still endanger the mom and fetus so taking AEDs at lowest dose is safest option for both
56
can pregnancy effect seizure patterns?
yes
- there are increased seizures even with AED use
- concentration of AED in blood can change
57
what is the GENERAL thing to do if you see someone having a seizure
1) look at a clock and know how long they have had a seizure, as after 5 mins their brain nerves start to die and could have major permanent damage
3) can put something soft under head (prevent more trauma-> could trigger another episode), cover up mid-section (lose control of bowel movement), but other than this don't hold them or put anything in mouth
* ONLY turn them SLIGHTLY on SIDE-> don't want to choke on tongue or saliva
3) call 911 if over 5 mins (or other certain circumstances)
58
first aid for complex partial
- guide person away from danger
| - do not restrain person
59
atonic
-call 911 if any injuries from fall
60
tonic-clonic
- protect from head injury
- turn person on side to clear airway
- dont restrain
- dont put anything in mouth
- cover in case of incontinence
61
Why do we call 911 if their seizure lasts longer than 5 minutes?
-this is now status epileptics
62
in what other cases do we call 911
- continuous seizures
- consciousness does not return
- occurred in water
- difficulty breathing
- chest pain
- injured
- individual is not known to have epilepsy
63
A patient has 3 seizures this year. First one had UNKNOWN cause. 2nd one was caused by FEVER. The 3rd had IDIOPATHIC origin. Can this person be diagnosed with epilepsy?
yes
64
You are a pharmacist and someone approaches you with a new Rx. This patient has been diagnosed with epilepsy and his physician wants to treat him with Drug X, a Cl- channel antagonist. Using your understanding of the pathophysiology of seizures, would this be an appropriate treatment? If not, what would you recommend?
No- b/c we want chloride to go into the cell b/c it is negative! (this will therefore dampen the excitation)
Recommend a Na or K channel antagonist/ or glutamate, NMDA receptor blocker, a K channel efflux agonist -> ALL work!
65
A patient with epilepsy had five seizures last year and was put on Drug X, which is Na+ channel blocker. This year, she had five seizures while still taking Drug X. What would be the best treatment strategy for this patient?
A) Immediately discontinue use of Drug X and start patient on Drug Y, which is a Ca2+ channel blocker.
B) Slowly decrease dose of Drug X, while simultaneously introducing and slowly increasing dose of Drug Y.
C) Introduce Drug Y while continuing Drug X at same dose.
D) No change in treatment is necessary.
technically C and D is correct-> C is more correct:
-it is definitely not A or B, b/c this drug has clearly been working (disease has not gotten worse- a plateau of seizure #s= treatment success)
-however, not adding a new drug is also not a terrible thing
-it is good to try tho as this might even REDUCE # of seizures
(if this had been on exam, the answer would have been E- 2 of the above, or C&D)
66
Are patients with epilepsy treated with mono-pharmacy?
NO
-poly-pharmacy b/c there is no cure therefore we just have to manage it the best that we can
(this also applies for pain
