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MED627 > Epilepsy > Flashcards

Epilepsy Flashcards

1
Q

define seizure and epilepsy

A

Seizure - the clinical manifestation of an abnormal, excessive excitation and synchronization of a population of cortical neurons
Epilepsy - a tendency to recurrent seizures >24 hours apart which are not provoked by systemic or acute neurologic insults

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2
Q

what is an EEG?

A

Electroencephalography

  • Records cortical electrical activity, usually from the scalp.
  • The most important neurophysiological study for the diagnosis, prognosis, and treatment of epilepsy.
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3
Q

what is the difference between generalised and partial/focal seizures?

A

generalised - originate within networks distributed across both cerebral hemispheres + cellular/biochemical or structural abnormalities
focal - originate within networks limited to one cerebral hemisphere with semiology affecting the function of affected area + structural abnormalities

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4
Q

how are the seizures classified according to the ILAE 1981?

A
  • classified according to the clinical features of seizures and EEG findings
    1. generalised - absence, tonic, clonic, atonic, tonic-clonic, myoclonic
    2. partial - simple partial, complex partial (common, TLE) and secondary generalised (common in frontal lobe)
  • but simple and complex have been eliminated now
  • instead depends on cognitive impairment: focal seizure w or w/o dyscognitive features
    3. may be focal, generalised or unclear - epileptic spasms (uncladsifieable seizure)
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5
Q

what is the significance of classification of seizures?

A
  • Seizures can be classified based on their clinical and electrographic features (EEG recording).
  • Importantly, the diagnosis of a patient’s epilepsy syndrome is based on their clinical history and their seizure type(s).
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6
Q

what are the features of absence seizures?

A
  • formerly known as petit Mal
  • staring spell with impaired awareness: patient absent
  • brief episodes: 3-20 seconds
  • sudden onset and resolution
  • patients stop doing whatever he/she was doing, becomes unresponsive but maintains normal posture and muscle tone
  • blank expression with sometimes fine flickering of eyelids or face
  • often provoked by hyperventilation
  • onset typically b/w 4-14 hears if age (young childhood and resolves by age 18
  • normal development and intelligence
  • EEG: generalised 3Hz spike-wave discharges (slow activity on EEG)
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7
Q

what are the features of myoclonic seizures?

A
  • Brief, shock-like jerk of a muscle or group of muscles
  • Differentiate b/w benign, non-epileptic myoclonus (e.g., while falling asleep)
  • EEG: Generalised 4-6 Hz polyspike-wave discharges
  • muscle tone not normal (??)
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8
Q

what are the features of tonic seizures?

A
  • Symmetric, tonic muscle contraction of extremities with tonic flexion of waist and neck
  • Duration - 2-20 seconds.
  • EEG – Sudden attenuation with generalised, low-voltage fast activity (most common) or generalised polyspike-wave.
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9
Q

what are the features of atonic seizures?

A
  • Sudden loss of postural tone: severe - falls ; milder - head nods or jaw drops.
  • Duration - usually seconds, rarely more than 1 minute
  • EEG – sudden diffuse attenuation or generalised polyspike-wave
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10
Q

what are the features of tonic-clonic seizures?

A
  • Associated with LOC and post-ictal confusion/lethargy
  • Duration 30-120 seconds
  • Tonic phase (30 secs): Stiffening and fall; often associated with ictal cry (due to spams of larygeneal and respiratory muscle) and cyanosis (breathing ceases temporarily)
  • Clonic Phase (60 secs): symmetrical convulsions with muscular contraction and relaxation, noisy and poorly coordinated breathing w salivation that appears as frothing at the mouth. may have tongue bitting, other injuries, urine incontinence
  • postical coma (30 mins): seizure ends but patients remains unconsciousness, probably due to large-scale release neurochemicals like opiates and GABA
  • EEG – generalised polyspikes
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11
Q

what are simple partial seizures/focal seizures w/o dyscongitive features challenging to diagnose?

A

diverse range of manifestations

a. frontal: motor: clonic repetitive flexion/extension, limb jerking, headache or eye deviation
b. parietal: sensory disturbance - paresthesia (abnormal sensation: tingling, prickling, chilling, burning, numbness)
c. occipital - positive visual disturbance - coloured balls, flashing lights or hallucinations
d. auditory (crude or highly complex sounds)/ Olfactory (intense odours like burning rubber or kerosene)
e. Autonomic sensations- flushing, sweating, piloerection
- as there is a broad range of potential semiology linked to focal seizure so caution is advised before concluding the stereotypic episodes of bizarre or atypical behaviour is not due to seizure activity, thus in such cases, EEG may be helpful to confirm the diagnosis (motor focal seizure: 3-4Hz)

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12
Q

what are the features of complex partial seizures/focal seizures with dyscogntive features/focal seizure w impaired awarness?

A
  • most common TLE
  • LOC
  • semiology vary with site of origin and degree of spread
    1. Presence and nature of aura - peculiar smell, deja vu, jamais vu, euphoria (temporal: deja vu, jamais vu, memories, feeling dread, rising feeling)
    2. Automatisms - chewing, lip smacking, picking. at clothing or aimless reaching
    3. Other motor activity
  • Duration typically < 2 minutes
    4. postictal confusion or aphasia or anterograde amnesia
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13
Q

what are the features of secondary GTC seizures?

A
  • Begins focally, with or without focal neurological symptoms
  • Tonic and clonic phases with variable symmetry, typical duration 1-3 mins
  • Postictal confusion, somnolence
  • Can have transient focal deficit (Todd’s paresis)
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14
Q

how are epilepsy syndromes grouped?

A

Grouping of patients that share similar:

  1. Seizure type(s)
  2. Age of onset
  3. Natural history/Prognosis
  4. EEG patterns
  5. Aetiology / Genetics
  6. Response to treatment
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15
Q

what is epilepsy syndrome? describe the heterogeneity in epilepsy

A
  • Epilepsy is an umbrella term, under which many types of diseases and syndromes are included.
  • Some authors distinguish between epilepsies and epileptic syndromes, depending on whether seizures are the only neurologic disorder (an epilepsy) or are one of a group of symptoms (an epileptic syndrome).
  • Some of the epilepsies (e.g., juvenile myoclonic epilepsy) have well-defined genetics, clinical courses, and responses to medication.
  • Others (e.g., temporal lobe epilepsy) have natural histories which are highly variable, and which reflect differences in pathology as well as in host response to that pathologic process and to the treatments administered.
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16
Q

describe the epilepsy syndrome classification

A
  • The 1989 classification of epileptic syndromes: partial or generalised
  • depending on whether seizures arise in a circumscribed portion of the brain, or begin diffusely in the cortex and its deep connections
  • further subdivides into idiopathic, symptomatic and cryptogenic
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17
Q

describe the following terms

  1. symptomatic
  2. cryptogenic
  3. idiopathic
A
  1. symptomatic - known cause + associated w neurologic or neuropsychological abnormality + clear genetic, structural or metabolic cause
  2. cryptogenic - unknown cause + associated w neurologic or neuropsychological abnormality + assumed to be symptomatic
  3. idiopathic - unknown cause, suspected to be genetic
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18
Q

give examples of focal/partial epilepsy or epilepsy syndrome for

  1. idiopathic
  2. symptomatic
A
  1. idiopathic (age related onset) - benign childhood epilepsy with centrotemporal spikes (‘rolandic epilepsy’), childhood epilepsy with occipital paroxysms
  2. symptomatic - FL, PL, OL, TL epilepsy chronic progressive epilepsia partíais continua of childhood
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19
Q

give examples generalised epilepsy or epilepsy syndrome for

  1. idiopathic
  2. symptomatic
  3. cryptogenic
A
  1. idiopathic (age related onset)
    - Benign neonatal familial convulsions
    - Benign neonatal convulsions
    - Benign myoclonic epilepsy in childhood
    - Childhood absence epilepsy (pyknolepsy)
    - Juvenile absence epilepsy
    - Juvenile myoclonic epilepsy
  2. symptomatic or cryptogenic
    - west syndrome
    - Lennox-gastaut syndrome
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20
Q

what are the features of TLE?

A
  • most common in focal seizures w dyscognitive features
  • symptomatic or cryptogenic
  • onset at any age
  • EEG: temporal lobe epilpetiform discharges
  • common cause: sclerosis of hippocampus, small scared - detected T2W MRI
  • diagnosis essential as refractory to anticonvulsants treatment but responses well to surgical intervention
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21
Q

what are the features of JME?

A
  • juvenile/ early adolescent onset
  • bilateral myoclonic jerks
  • GTCS and absences (in 1/3)
  • common in the morning after waking up
  • exacerbated by sleep deprivation and alcohol
  • conserved consciousness unless myoclonus is severe
  • idiopathic: family history, genetic studies suggest polygenic cause
  • EEG: generalised spike or polyspike/wave discharges often photosensitive (30-40%)
  • complete remission uncommon but respond well to anticonvulsant medication
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22
Q

what are the features of west syndrome?

A
  • generalised
  • symptomatic or cryptogenic
  • infantile onset (begins in first year of life)
  • seizure disorder w progressive cognitive decline
  • also known as infantile spasms
  • Hypsarrhythmic EEG (random high voltage spikes and waves)
  • abrupt shock like episodes called salaam attacks
  • flexion of upper limbs + neck + hips w knees drawn up against the body
  • associated w developmental or perinatal brain injury such as anoxia or encephalitis
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23
Q

what is rate of prognosis in JME?

A
  1. longitudinal study of 81 CAE
    - 15% of participants w/o remission of CAE had developed JME
  2. longitudinal study of 5 years in 66 JME. in an arab population
    - 9 out 10 patients relapsed after VPA discontinuation
  3. longitudinal study of 24 JME
    - 11 discontinued treatment: 6 seizure free, 3 myoclonic seizure only, 2 w rare seizures
  4. study of 31 JME
    - 21 seizure free, 6 AED discontinued
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24
Q

what are the factors to be considered during choosing an epilepsy medication?

A
  1. Seizure type - partial or generalised
  2. Epilepsy syndrome
  3. Efficacy - best, ability to stop seizures
  4. Cost
  5. Pharmacokinetic profile
  6. Adverse effects - lowest likelihood
  7. Patient’s related medical conditions
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25
Q

what are the challenges associated while choosing an epilepsy medication?

A
  • several comparison studies: minimal differences in efficacy of standard AEDs
  • thus, differences in profile of expected adverse effect, pharmacokinetic and cost should guide AED choice
  • most patients can be optimally managed w single AED therefore, one mist be sure that drug oven has failed before moving on to alternative drug or two drug combination
  • if patient has persistent seizures but no adverse effects from the drug then the dose can be increased as tolerated or until seizure control in obtained
  • the “therapeutic range” of serum concentrations given is only a guideline—the patient’s clinical state determines the appropriate dose
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26
Q

what are choices of treatment for epilepsy?

A
  1. epilepsy medication

2. epilepsy surgery

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27
Q

what did the SANAD study find?

A

Marson et al. - an unblinded RCT, THE SANAD studied the effectiveness valproate, lamotrigine or topiramate for generalised and unclassifiable epilepsy and found valproate. was effective. for focal but. not generalised

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28
Q

what are the changes in terms after organising the epilepsies?

  1. partial
  2. simple partial
  3. complex partial
  4. secondary generalised TCS
  5. cryptogenic
  6. symptomatic
  7. idiopathic
A
  1. partial - focal
  2. simple partial - focal w/o impaired awareness
  3. complex partial - focal w impaired awareness
  4. secondary generalised TCS - focal evolving to bilateral convulsive seizure
  5. cryptogenic - unknown
  6. symptomatic - metabolic/structural
  7. idiopathic - genetic
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29
Q

what are the variables accounting for the different EEG?

A

Age - normal EEG of a child is very different from adult
Artefacts - chewing
Conscious Level - sharp waves seen in cortex while sleeping
Drugs - burst depression seen under anaethesia
Cerebral Pathology - cerebral palsy shows abnormal EEG but not necessarily seizures

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30
Q

what are the different activation techniques to induce/record a seizure/abnormal EEG?

A
  1. photo stimulation
  2. hyperventilation: vasoconstriction provokes seizure
  3. sleep and sleep deprivation
  4. long term monitoring: ambulatory and video-telemetry
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31
Q

what is the sensitivity of the following epileptiform activity during the following

  1. wake EEG
  2. Sleep EEG
  3. repeat wake and sleep EEG
A
  1. wake EEG - 50%
  2. Sleep EEG- 80%
  3. repeat wake and sleep EEG - 92%
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32
Q

what is the specificity of EEG?

A

EEG epileptiform in 0.5 – 4 % healthy adults however the population is not healthy

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33
Q

what are the uses of EEG in epilepsy?

A
  1. Diagnosis (ictal) - epilepsy vs non-epilepsy
    - interictal period reflecting epileptiform activity consists of bursts of abnormal discharges containing spikes or sharp waves
    - epileptiform activity not specific for epilepsy but has a greater prevalence in epileptic population than others
    - however, even in an epileptic patient, the initial interictal EEG may be normal up to 60%
    - thus, EEG cannot establish the diagnosis of epilepsy in many cases
  2. Classification (ictal/ interictal) - general or focal
    - however, absence of EEG seizure activity does not exclude seizure disorder as focal seizures may originate from a region in cortex that cannot be detected by standard scalp electrodes
    - since seizures typically infrequent and unpredictable often difficult to obtain EEG during a clinical event
    - thus, video EEG telemetry unit for hospitalised patients or use portable equipment to record EEG continuously on cassettes >24h in ambulatory patients
    - video approach now a routine approach for accurate diagnosis of epilepsy in patients w poorly characterised events or seizures that are difficult to control
  3. Classifying seizure disorders and aid in the selection of anticonvulsant medications e.g.
    - episodic generalised spike-wave activity seen for absence (3Hz) as well as epilepsy syndromes like JME + LGS
    - west syndrome: Hypsarrhythmia EEG
    - focal interictal epileptiform discharge seen in TLE and frontal lobe discharges
    a. frontal: limb jerking, headache or eye deviation
    b. parietal: sensory disturbance - spreading tingling
    c. temporal: deja vu, jamais vu, memories, feeling dread, rising feeling
    d. occipital - positive visual disturbance - coloured balls
  4. monitor the progress
    - normal EEG -> better prognosis
    - abnormal background or profuse epileptiform activity -> poor
    - however, this is also a limitation of EEG in epilepsy
  5. Work-Up for Epilepsy Surgery (ictal/ interictal)- concordance w MRI abnormality
  6. Management of Status Epilepticus - convulsive or non-convulsive ??
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34
Q

what are the abuses of EEG in epilepsy?

A
  1. monitoring of progress - not imp. if EEG changes or not after treatment but imp how patients reposed to the treatment
  2. anti-convulsant withdrawal in adults - anti-convulsants have better results in children
  3. diagnosis in the presence of intracerebral disease
  4. diagnosis where history is of syncope - EEG should not be done of its a blackout
  5. driving - the regulation change every few years of driving
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35
Q

what are the non-pharmacological epilepsy treatment options?

A
  1. Vagal nerve stimulation (VNS)
  2. Deep brain stimulation (DBS)
  3. Resective surgery
  4. Ketogenic diet
  5. Complementary therapies
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36
Q

what is VNS, when is it used and what are its aims?

A
  • an adjunctive treatment for epilepsy with focal or generalised onset
  • it is used for refractory patients who seizures have not been controlled after trial 2/3 medications and are not suitable for resective surgery
  • Aims to reduce the frequency and/or
    intensity of seizure activity, shorten recovery time and lessen side effects
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37
Q

how is a VNS embedded in the body and how does it work ?

A
  • a pulse generator is impacted into a pocket of skin normally not he left
  • wires and electrodes travel under the skin and are connected to the left vagus nerve in the neck
  • The stimulator is programmed to send regular, mild electrical impulses to the vagus nerve and can also be controlled by use of a magnet. The newest VNS model is also sensitive to a rise in HR (Eggleston et all, 2014).
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38
Q

what are the benefits of VNS?

A
  • aims to reduce seizure activity by up to 60% interrupting and preventing the electrical irregularities on the surface of the brain, that cause seizures.
  • improved alertness and memory and fewer mood problems.
  • Therapy is reported to improve over time, side effects lessen over time
  • proffered by patients over brain surgery
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39
Q

what are the limitations associated with VNS?

A
  • Not possible to know in advance who will have seizure reduction and to what extent
  • Can take up to 2yrs to achieve optimum seizure control
  • Mild side effects: laryngeal nerve travels within the mid cervical region of the left vagus nerve also so hoarseness of voice occurs each time the device activates + coughing
  • Battery changes every 6-8- years
40
Q

what is mode of action (MOA) (hypothesis and aim) of VNS in the brain?

A
  • hypothesis - CN10 afferents - numerous projects in CNS - so AP generated in vagal afferents have potential to affect the entire organism however, the precise MOA and how it suppresses seizures remains to be elucidated
  • aim: to induce AP within different types of fibres that constitute the nerve at the cervical level. however, the fibres responsible and/or necessary for its seizure suppressing effect are unknown
  • unidirectional stimulation activating afferent vagal fibres, is preferred, as epilepsy is considered a disease with cortical origin, and efferent stimulation may cause adverse side effects.
41
Q

which company developed VNS?

A
  • LivaNova developed VNS
  • reported that 2 year therapy 64% of patient has more than a 50% reduction in the frequency of their seizures.
  • There are patients that have become seizure free with VNS but that’s not what they vouch it can do
  • studies by LivaNova have shown that 82% of patients have inter-ictal tachycardia and so the device is sensitive to this rise and sends an additional boost of electrical stimulation to the nerve in an attempt to abort or shorten the seizure
  • Live Nova state that it can take up to 2 years to see the full impact of the VNS.
  • Side effects can re-emerge when we increase settings but usually settle after 24-48 hours, such as a cough upon stimulation.
  • after the initial surgery patients need to come back to see us every 2 weeks to build up the level of stimulation to a therapeutic level and then every 3-6 months depending on response to therapy/seizure control/battery life.
  • Licenced in states to treat depression but it improves mood
42
Q

how does vagus nerve stimulation have an anti-epileptic effect?

A
  • has an influence on the production of serotonin, (this has been proven via cerebral spinal fluid (CSF) samples)
  • VNS has de-syncronization function on the EEG rhythms and VNS has influence on the cerebral Blood flow (CBF) to both the thalamus and the cortex
  • All this together, has an anti-epileptic effect.
43
Q

what is DBS, when is it used and what are its aims?

A
  • an adjunctive treatment for epilepsy with focal onset
  • used for refractory patients who seizures have not been controlled after trial 2/3 medications and are not suitable for resective surgery
  • Aims to control excess electrical activity in the brain using regular electrical impulses to reduce the frequency and severity of seizures
  • involves implanting electrodes into specific areas in the brain
44
Q

what is the procedure for DBS?

A
  • thin wire implanted into the brain
  • wire is attached to an electrical stimulator placed under the skin
  • surgery takes few hours, 3-5 hrs hospital stay, switched on 2-4 wks after
45
Q

what are the risks and outcomes associated w DBS?

A
  • risks - haemorrhage (1-2%) and infection (3-5%)
  • following surgery, memory problems and depression may reduce over time
  • trials show seizures become less frequent in some people
  • in others, it may reduce the seizures a little or have no effect
46
Q

what are the limitations of DBS?

A
  • same as VNS
  • not widely available in the UK currently, still a relatively new treatment in field of epilepsy care and not currently available in shef
  • evidence on efficacy of DBS for refractory epilepsy is limited in both quantity and quality
  • evidence on safety shows serious but well-known side effects
  • therefore, this procedure should only be used w special arrangements for clinical governance, consent and audit or research according to nice guideline jan 2012
47
Q

when is surgery suitable for epilepsy?

A
  • suitable for focal seizures
  • if several AEDs trialled and none of them have stopped or reduced the seizure frequency by half
  • a physical cause for epilepsy such as scarring on brain or head injury or an infection like meningitis and this can be identified on scan and is only in one area of brain
48
Q

what is the aim of epilepsy surgery and its outcomes?

A
  • aim to dramatically reduce or stop the occurrence of seizures
  • around 70% of people become seizure-free
  • after surgery most people will still take their AEDs for 2 yrs
49
Q

what are the limitations associated with epilepsy surgery?

A
  • brain surgery so carries significant risks, i.e. death, stroke, paralysis, worsening of epilepsy
  • approx 50% of patients recommended for surgery are unable to proceed after formal testing
  • 2yr work up
  • investigations: MRI, EEG plus telemetry, PET, SPECT neuro-psychotherapy and psychiatry
50
Q

what is ketogenic diet? who and when is it mainly used for?

A
  • special high-fat, low-carbohydrate diet
  • one treatment option manly for children w epilepsy whose seizures are not controlled w AEDs
  • particularly recommended for children w Lennox-gastaut syndrome but useful in any seizure type
  • now available in adult service
51
Q

what is the procedure to get prescribed for ketogenic diet?

A
  • patients are first seen by neurologist and if suitable will be offered a low glycemic diet
  • if this works they can remains on this
  • if it does not work they are passed onto a specialist dietician for guidance on ketogenic diet
52
Q

what are the advantages of ketogenic diet?

A
  • may help to reduce the number or severity of seizures
  • can often have positive effects on behaviour
  • research also shows that it has an anti-epileptogenic effect on the brain
53
Q

what is mechanism of action of ketogenic diet?

A
  • ketones are formed when the body uses fat as its source of energy
  • the body usually carbohydrates (such as break, sugar, pasta) for its but because ketogenic diet is low in carbs, fats become the primary source of energy instead
  • when the body is in ketosis, the ketones can cross the BBB and cause an anti-epileptic effect
  • ketones are one of the more likely mechanisms of action of the diet; with higher ketone levels often leading to improved seizure control
54
Q

can the ketogenic diet ever be stopped?

A
  • If seizures have been well controlled for some time, usually 2 years, the doctor might suggest going off the diet
  • Usually, the patient is gradually taken off the diet over several months or even longer. Seizures may worsen if the ketogenic diet is stopped all at once
  • Children usually continue to take seizure medicines after they go off the diet
  • In many situations, the diet has led to significant, but not total, seizure control. Families may choose to remain on the ketogenic diet for many years in these situations
55
Q

what are the potential side effects associated with ketogenic diet

A
  1. Kidney stones
  2. High cholesterol levels in the blood
  3. Dehydration
  4. Constipation
  5. Slowed growth or weight gain
  6. Bone fractures
56
Q

what are the psychological factors associated with epilepsy?

A
  1. Co-morbid depression/anxiety – those with refractory epilepsy at high risk
  2. Low self-esteem
  3. Psycho-social problems: Education, Employment, Relationships. Social isolation
  4. Psychosis
  5. Self harm
  6. Anger, frustration & violence
  7. Adjustment/acceptance issues
  8. Suicidal thoughts, attempts and actual suicide
  9. Sleep disturbance
57
Q

the rates of psychiatric disorders are more prevalent in patients with epilepsy than controls
True or False

A

True, the main ones are - major depressive disorder, anxiety disorder, mood/anxiety disorder, suicidal ideation

58
Q

what are the cognitive and behavioural effects of epilepsy?

A
  1. Learning and educational problems
  2. Personality and behaviour difficulties
  3. Psychiatric disorders
  4. Cognitive slowing and memory problems
59
Q

which are the psychological interventions used in epilepsy?

A
  • relaxation, CBT, biofeedback
  • may be used in conjunction w AED therapy in adults where other the person or specialist considers seizure control to be inadequate w optimal AED therapy
  • this may be associated with an improved quality of life in some people (NICE,2012)
60
Q

what are the complementary therapies used in epilepsy?

A
  1. Aromatherapy – with caution
  2. Meditation – repeated can alter EEG patterns + or – effect on seizures
  3. Herbal remedies - CBD oil, studies in over 3000 people have shown 1 in every 8 will have a 50% reduction in seizures
61
Q

what is the risk of developing epilepsy?

A
  • Rochester et al. (2011), a population based study found that the cumulative incidence and life time risk of epilepsy increases with advancing age, this is crucial because:
    1. One in 26 people will develop epilepsy in their life time
    2. The lifetime risk provides an estimate of an individual’s risk for epilepsy over his or her remaining lifetime and assist heath care planners as they estimate service needs for epilepsy
  • at the age 20, there is RLR (relative lifetime risk) of 0.2 (2 in 1000)
62
Q

describe the changes in the incidence of TBI with advancing age

A
  • younger age (infants): skull is thin - highest risk of TBI, usually non-accidental perhaps birth trauma
  • middle age (teenagers): skulls gets steadier but irresponsible teens, especially men as they’re more prone to injuries
  • older age (elderly): have higher rates of falling therefore, high risk of TBI, men=women
63
Q

define mild, moderate and severe TBI?

A 
1. LOC 
mild TBI - less than 30 mins 
moderate TBI - more than 30 mins and less than 24 hours 
severe TBI - more than 24 hours 
2. Skull fracture 
mild TBI - absent 
moderate - could be present or absent 
severe TBI - contusion, hematite or skull fracture 
3. PTA (post traumatic amnesia)
mild TBI - less than 1 day 
moderate TBI - more than 1 day and less than 7 days 
severe TBI - more than 7 days
64
Q

why is the challenge associated with definition of TBI?

A

different definitions for different TBIs, not standardised

65
Q

define immediate, early and late seizures

A

immediate seizure - within the first day of injury; occur in less than 24 hours after injury
early seizure - within the first weeks of injury (acute symptomatic seizure)
late seizure - after one week of injury (constitute the diagnosis of PTE)

66
Q

what is rate of incidence of PTE?

A

Big sample sizes
Huge variation in incidence of PTE
Some retrospective and prospective

67
Q

what are the risk factors for PTE?

A
  1. sex: male
  2. history: alcohol abuse
  3. clinical findings: PTA, focal neurological signs, LOC at initial TBI,
  4. Abnormal neuro-imaging findings: skull fracture, midline shift, brain contusion, SDH, ICH
  5. Clinical severity of TBI: MBI, SBI and acute symptomatic seizure
68
Q

what is the risk of developing epilepsy/seziures after TBI?

A
  1. Huge sample size, prospective study
    - Risk of developing epilepsy is still higher after 20-30 years later
    Mild, moderate and severe
    - Severe brain injury carries a relatively higher risk of PTE
    - Epilepsy is highest in the first few years, risk continues to decline or separate from the baseline risk after 20 yrs of the moderate and mild
  2. 78000 population study in Denmark
    - High risk with severe brain injury and PTE
    - Shows relative risk rather than absolute proportion with epilepsy
    - RR is highest in the beginning and then falls but never falls down to the baseline
69
Q

why is the latent period b/w injury and developing epilepsy crucial?

A

provides an opportunity to study the therapeutic potentials

70
Q

what is the risk of developing epilepsy after penetrating brain injury?

A
  • higher risk of epilepsy after PBI, increases by >50%
  • famous example: Phineas gage
  • injury in 1848 but started seizures in 1860 - after 12 years, died from status epileptics a few months later
  • the 12 years highflying the latent period
71
Q

what is the role of temporal lobe injury and early seizures in predicting PTE?

A
  • a longitudinal study of 90 patients
  • studied the effect of two things on the development of PTE – acute symptomatic seizures (25%) and haemorrhagic temporal lobe epilepsy (75%)
  • Temporal lobe is a common site of onset of seizure
  • Half of them went for long term follow up – 45% developed PTE
    38% seizures on cEEG (continuous EEG)
  • Together highlighting, temporal lobe injury and early seizures predict the development of PTE
72
Q

what is the risk of developing early seizures?

A

vm

73
Q

what is status epilepticus?

A
  • seizure that lasts >30 mins (most seizures <5m)
  • or multiple seizures w/o recovery
  • w impaired LOC in inter-octal period
  • traditionally, by definition SE: 15-30m
  • practically, SE in which duration prompts acute use of ant-convulsant therapy for e.g. GCSE >5m
74
Q

what are the sub types of status epileptics and its features?

A
  1. generalised convulsive status epileptics (GCSE): rhythmic jerking, tonic-clonic movements, impaired mental status,
  2. non-convulsive status epileptics
75
Q

why is GCSE an emergency and must be treated immediately?

A
  • cardiorespiratory dysfunction, hyperthermic, metabolic derangements develop as a consequence of prolonged seizures resulting in irreversible neuronal injury
  • CNS injury could occur when patient is paralysed w neuromuscular blockade but continues to have seizure
76
Q

what are the common cause of GCSE?

A
  • anti-convulsant withdrawal or non-compliance
  • metabolic disturbances
  • drug toxicity
  • CNS infection
  • CNS tumours
  • refractory epilepsy
  • head trauma
77
Q

what is the significance of EEG is SE/GCSE?

A
  • GCSE is prominent initially when the patient is having convulsions however, the signs become subtle with increasing time
  • later, the patients might have only mild clonic movements of fingers or fine fine rapid eye movements
  • episodes of tachycardia, hypertension, pupillary dilation could also be present
  • in such cases, EEG is the only method of establishing the diagnosis
  • patients stops having prominent seizure but remains comatose due to being paralysed w neuromuscular blockage (to protect the airway), an EEG is essential to rule out the on going SE
78
Q

what are the management techniques in GCSE?

A
  • Stage 1 (0-10m): ABCD, BGC levels
  • samples ent to lab to identify metabolic abnormalities
  • anti-convulsant therapy w/o delay
79
Q

why is EEG not useful in focal seizures?

A
  • inter-ictal EEG for focal seizures often normal or may show brief discharges called as epileptiform spikes or sharp waves
  • since focal seizures arise from mTL or inferior frontal lobe (regions distant from the scalp), the EEG recorded during the seizure may be non-localising
  • however, the seizure focus if often detected using sphenoidal or surgically placed intracranial electrodes
80
Q

what are the three features of focal motor seizures?

A
  1. jacksonian march (secs): motor movements begin in a restricted region (fingers) and gradually progress to include larger portion of extremity
  2. Todd’s paralysis (min-hours): localised paresis
  3. epilepsia partíais continua (hours-days) - rare, often refractory to medical therapy
81
Q

why is it difficult to distinguish focal seizures evolved into generalised seizure and generalised onset tonic-clonic seizure and why is the distinguishing essential?

A
  • since the collateral witness tend to emphasise more on the dramatic generalised convulsive phase of the seizure and over look the more subtle focal symptoms present at onset
  • at times, focal onset is apparent only when a careful history identifies a preceding aura
  • distinguishing between the two is essential as there could be substantial differences in the evaluation and treatment b/w them
82
Q

why epileptic spams is an unclassifiable seizure? why is EMG useful for epileptic spasms? and when does it commonly occur and what is the cause?

A
  • EEG: hypsarrthymia consisting of diffuse, giant slow waves w chaotic background of irregular multifocal spikes and sharp waves
  • EEG background suppressed: electrode decremental response
  • EMG may help distinguish it from tonic and myoclonic seizures as it showed characteristic EMG pattern
  • occurs mainly in infants
  • could be due to neuronal function and connectivity in the developing CNS
83
Q

what are the features of Lennox gastaut syndrome?

A
  • children
  • triad
    1. multiple seizures: usually GTC, atonic and atypical absence
    2. EEG: <3Hz slow spike and wave discharges
    3. impaired cognitive function but not in all cases
  • associated w CNS disease or dysfunction like developmental abnormalities, perinatal hypoxia/ischemia, trauma, infection, acquired lesions
  • poor prognosis due to underlying diseases and consequences of sever poorly controlled epilepsy
84
Q

how does brain injury result in seizure?

A
  • changes in local structure ->
85
Q

what is the role of brain imaging in diagnosing epilepsy?

A
  • identifies any underlying structural abnormalities
  • exception: children w absence seizures
  • MRI superior than CT for detecting cerebral lesion associated w epilepsy
  • incidental findings like tumours, vascular malformation that need immediate therapy
  • new MRI methods has increased the sensitivity in detected cortex abnormalities including hippocampal atrophy associated w mTLE
  • but for suspected CNs infection or mass lesion: CT should be performed when MRI is not available, also CT is quicker
  • PET, SPECT used for some patients w refractory seizures
86
Q

what is impact of mensturation on epilepsy?

A
  • increase in seizure frequency around menses
  • either due to effects oestrogen + progesterone on neuronal excitability or changes in AED levels due to altered protein binding or metabolism
  • some may benefit from increase AED dosage during menses
  • natural projections or intramuscular medroxyprogesterone may benefit to some women
87
Q

what is the impact of pregnancy on epilepsy?

A
  • most women w epilepsy who become pregnant will have an uncomplicated gestation and deliver a normal baby
  • however, there are some risks
    1. seizure frequency
    = unchanged in 50%
    = increase in 20%
    = decrease in 30%
  • changes attributed to endocrine effects on CNS, variations in AED pharmacokinetics, changes in medical compliance
  • useful to see patients at frequent intervals during pregnancy to monitor serum AED levels
    2. fetal abnormalities in children born
    = 5-6% epileptic mothers as compared to
    = 2-3% healthy mothers
  • higher incidence in epileptic mothers due to teratogenic effects of AEDs and the risk increase with number of medications used (10-20% risk of malformations w 3 drugs) and possibly w higher doses
  • recent meta analysis, common malformations?: cardiovascular and musculoskeletal system (1-2%)
  • VPA strongly associated w increased risk of adverse fatal outcomes (7-20%)
  • little known about the safety of newer drugs although reports suggest, higher than expected risk of cleft lip or palate w use of lamotrigine during pregnancy
  • advisable to have patients on mono-therapy w low doses
  • type and frequency of seizures may allow them to safely come off the AEDs prior to contraception
  • patients should take folate as the anti-folate effect of anticonvulsant are thought to play a role in neural tube defects, although this benefit remains to be proved
  • AED medication are excreted into breast milk to a variable degree
  • the ratio ranges from 5% (VPA) to 300% (levetriacetam)
  • however, provided the known benefits of breast feeding and the lack of evidence of long term to infants by exposed to AEDs, mothers can be encouraged to breast feed
88
Q

what is the physiology of seizure?

A
  • 2 main phase: initiation and propagation
  • initiation phase:
    1. high frequency bouts of AP
  • extracellular Ca2+ influx -> long lasting depolarisation -> NGSC opening -> Na+ influx -> receptive AP -> followed by hyperpolsarisation mediated by GABA R or K+ channels (depending on cell type)
    2. hypersynchronisation: the synchronous bursts from a sufficient number of neurones result in spike discharge on EEG
  • normally, spread of bursting activity prevented by intact hyperpolarisation and inhibition by inhibitory neurones
  • normal seizure circumstances
89
Q

what is epidemiology of PNES?

A
  • UK: around 15,000 w NEAD excluding the misdiagnosis of epilepsy (NEAD society)
  • Epilepsy Foundation (US):
  • 20-30% seen an epileptic intractable seizures diagnosed w PNES
  • Prevalence rate in general population: 2-33 per 100,000 making PNES as prevalent as MS or trigeminal neuralgia
90
Q

why is PNES misdiagnosed or why is PNES difficult to diagnose?

A
  • misdiagnosis of epilepsy in people w PNES is very common
  • 25% of people previously diagnosed w epilepsy and are not responding to AEDs have been misdiagnosed
  • PNES difficult to diagnose cause:
    1. pshyicians taught almost exclusively to consider physical disorders as the cause of physical symptoms
    2. diagnosis of seizures mainly depends on the collateral witness who may not be trained to notice the subtle differences b/w seizures and non-epileptic seizures
    3. many neurologists do not have access to video EEG
91
Q

what is PNES? treatments?

A
  • attacks that resemble epileptic seizures but are not caused by abnormal brain electrical discharges
  • instead, are a manifestation of psychological distress
  • may look like they are experiencing GTC with falling and shaking.
  • less frequently, may mimic absence seizures or focal impaired awareness seizures
  • not a unique disorder but are a specific type of a larger group of psychiatric conditions that manifest as physical symptoms
  • used to be called somatoform disorders (DSM4) and are now termed somatic symptoms disorders (DSM5)
  • treatments: CBT, SSRIs
  • treatment issues: difficult to treat as when one symptom is extinguished, another symptom appears
92
Q

what causes PNES?

A
  • multifactorial, associated w abnormal emotional development in childhood
  • a specific traumatic event, such as physical or sexual abuse, incest, divorce, death of a loved one, or other great loss or sudden change, can be identified in some people with PNES
  • tend to develop during adolescence or early adulthood but may occur at any age, also appears to be more common in women
  • ICM: genetic predisposition -> NEAD vulnerable -> NEAD
93
Q

why is video EEG preferred over EEG for diagnosis of PNES?

A
  • EEG: less specific even for epilepsy as diagnosed epileptic patients have normal EEG
  • therefore, video EEG used to monitor the patient for hours or days till a seizure occurs
  • analysis of video and EEG could provide a certain diagnosis of PNES
  • traditionally, video EEG performed at hospital but w modern equipment it can be permed at home also
  • when videoEEG. unavailable, cell phone videos obtained by collateral witness also helpful in suspecting PNES
94
Q

how to differentiate NEAD from epilepsy?

A 
1. triggered by emotion 
NEAD - common 
epilepsy - rare 
2. onset 
NEAD - gradual
epilepsy - rapid
3. duration 
NEAD - prolonged 
epilepsy - secs-mins 
4. cyanosis 
NEAD - rare
epilepsy - common (GTC)
5. consciousness 
NEAD - may interact 
epilepsy - unconscious 
6. movements 
NEAD - semi-purposeful (avoid harm), pelvic thrusting 
epilepsy - commonly limbs + GTC 
7. eye opening 
NEAD - resist eye opening  
epilepsy - unable to resist 
8. post-ictal symptoms
NEAD - rare 
epilepsy - common 
9. breathing
NEAD - continuous 
epilepsy - periods pf apnoea
95
Q

what is the physiology of epilepsy?

A
  • normal seizures: glutamate induces excitatory bursts counteracted by inhibitory GABA release terminating the seizure
  • in SE, the seizure does not terminate leading to prolonged excitation due to glutamate
    1. early stage (mins)
  • increased glutamate release
  • decreased GABA release + inactivation of GABAa receptors
    2. middle stage
  • internalisation of GABAa receptors
  • increased AMPA receptor release onto the post-synapse
  • increased release of pro-convulsive peptides (glutamate)
    3. late changes
  • abnormal gene expression
  • plastic changes w synapses increasing the risk of future seizures

MED627 (6 decks)

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