Epilepsy Flashcards

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1
Q

seizure

A
  • occasional, excessive, unprovoked discharge of nerve tissue on muscles
  • can alter consciousness, sensation, and behaviour
  • Seizure is technically the activity going on in the brain (relies on EEG); convulsion is the behavioural manifestation (ie. Tonus (rigidity), clonus (tremors))
    • Pre-ictal, interictal, and post-ictal activity
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2
Q

epilepsy

A
  • recurrent unprovoked seizures (at least 2 seizures on 2 separate days with 24-hour period separating them)
  • due to atypical, excessive, or synchronous neuronal activity in the brain
  • Reflex epilepsy: some specific activity triggers seizures (ie. Brushing teeth)
  • Intractable epilepsy: does not respond to treatment/medication
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3
Q

epileptic aura (and why it’s important)

A
  • Intense moment right before seizure arrives, indicating that a seizure is imminent (ex. A certain feeling, smell, etc.)
  • Important for 2 reasons:
    • They warn the epileptic of an impending seizure
    • The nature of the aura is predictive of the epileptic focus (the place where it starts before it spreads, can be helpful for surgical treatment/removal)
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4
Q

focal seizures

A
  • start in one brain area and stay in that area (ie. Motor cortex seizure)
    • Simple partial seizure: symptoms are primarily sensory or motor or both; typically no loss of consciousness (ie. Mouth twitching during seizure, but no loss of consciousness)
    • Complex partial seizure: patients engage in compulsive, repetitive, simple behaviours (automatisms) and more complex behaviours that can appear perfectly normal; disruption and/or alteration of consciousness is common (ie. Tugging at shirt)
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5
Q

generalized seizures

A
  • involves entire brain
  • Secondary generalization: when a focal seizure evolves into a generalized seizure
  • Types:
    • Absence seizure (“petit mal”): no significant convulsion. Primary symptoms are: loss of consciousness, cessation of ongoing behaviour, vacant look, fluttering eyelids
    • Tonic-clonic (“grand mal”): muscle rigidity and tremors; loss of consciousness and equilibrium; tongue-biting, urination, and cyanosis are also common
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6
Q

4 types of seizures

A
  • Simple partial (focal)
  • Complex partial (focal)
  • Absence seizure (generalized)
  • Tonic-clonic (generalized)
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7
Q

Risk factors for epilepsy: specific examples

A
  • Vascular (ex. malformations)
  • Congenital (ex. family history and genetics)
  • Trauma (ex. head trauma)
  • Tumor (ex. in CNS)
  • Degenerative (ex. neurodegeneation)
  • Infection
  • Cryptogenic/idiopathic (no apparent mechanism; vast majority of cases)
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8
Q

Immediate vs. Early vs. Late Seizures

A
  • Immediate seizures = occurring within 24 h after injury
  • Early seizures = occur less than 1 week after injury
  • Late seizures = occur more than 1 week after injury
  • Latent period = time between injury and onset of late seizures
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9
Q

Overlapping risk factors

A
  • Overlapping risk factors for early and late seizures indicate that we don’t really know what’s causing it (ie. Intracranial hematoma, post-traumatic amnesia, depressed skull fractures)
  • Glasgow Coma Scale score of 3-8 (3 is almost comatose)
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10
Q

potential mechanisms of epileptogenesis (post-TBI)

A
  • overabundance of glutamate being released due to TBI damage -> leads to excitotoxicity (cellular loss), tau, and increased calcium
  • tau interacts with free radicals to reduce the threshold for seizures
  • to much calcium leads to excessive apoptosis
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11
Q

Comorbidities

A
  • People with epilepsy are more likely to experience the following co-existing medical conditions:
    • Diabetes
    • Major depressive disorder
    • Anxiety disorders
    • Migraine headaches
    • Stroke
    • Heart disease
    • Asthma
    • Arthritis
    • Suicide
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12
Q

3 common treatments for epilepsy

A
  • Anticonvulsants
  • Vagus Nerve Stimulation
  • Ketogenic Diet
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13
Q

less common treatments for epilepsy

A
  • Cannabidiol treatment (weakly binds to endocannabinoid receptors, positive anecdotal/case study evidence)
  • Surgical procedures (for severe intractable epilepsy)
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14
Q

Treatment: Anticonvulsants

A
  • can lessen frequency and severity of seizures, but do not cure epilepsy
  • Side effects can impact motor and cognitive speed, memory, mood, and psychosis
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15
Q

Treatment: vagus nerve stimulation

A
  • Putting pacemaker style pulse generator in chest to stimulate vagus nerve and prevent overactivity
  • Only moderately effective
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16
Q

Treatment: ketogenic diet

A

Increases ketones, which may be beneficial

17
Q

Surgical procedures

A
  • treatment for severe intractible epilepsy only
  • Prior to surgery, electrodes are sometimes inserted into/onto the cortex to find the epileptic focus (“subdermal grids”)
    • These electrodes are very helpful in research (ex. “The Halle Berry neuron” -> finding out that some neurons are responsible for categories)
18
Q

What are the most likely locations of Epileptic Focus?

A
  • Epileptic focus is much more likely to be found in the frontal or temporal lobes than other parts of the cortex
  • Why? Research has shown that regions associated with learning and memory are more likely to have an epileptic focus
19
Q

Cartesian Dualiasm (Hustvedt article)

A
  • Notion proposed by Descartes that the human mind and body are seperate entities (gap between pysche and soma)
  • Generally rejected by current neuroscientists, but still present in the field through terms like “psychogenic” (due to psychic/mental factors and not to detectible somatic/organic factors)
20
Q

psychogenic non-epileptic seizures (PNES) vs. epilepsy (Hustvedt article)

A
  • epilepsy = organic disease
  • PNES = functional disorder (no physical site of injury can be found)
    • ex. headaches, recurrence of add semlls, shortness of breath, fatigues, and seizures
21
Q

why does philosophy matter in modern psychological science? (Hustvedt article)

A
  • philosophy informs diagnosis

- - terms like “functional” and “organic” reflect less nuanced understandings of biological processes

22
Q

implications of psychogenic vs. organic debate for neuroscientists (Hustvedt article)

A

neurologists/medical professions must examine their implicit prejudices against psychogenic/emotional/psychiatric
illnesses as less “real” simply because they have no apparent physical cause

23
Q

state of research in TBI (Mahler study)

A
  • fairly limited
  • most research done on cohort of select TBI patients -> difficult to generalize
  • few population-based cohort studies done; those done have lots of attrition, no validation of TBI diagnosis, or include young patients only
24
Q

Mahler study: key points

A
  • population based study
  • suggests risk of epileptic seizures is increased 2x after mild TBI and 9x after severe TBI
  • 5x-6x greater risk after isolated intracranial hemorrhage or contusion; combination of the two leads to 43x increased risk
  • During first 6 months after severe TBI, risk increased 50x
  • risk is still increased >10 years after trauma
25
Q

Mahler study: methods and results

A
  • looked at patients newly identified with an unprovoked seizure or epilepsy, used statistical analyses to determine relative risk regarding different combinations of head injuries and time intervals after trauma
  • risk of epilepsy higher afer severe TBI, combined head injuries, and within first 6 months post-trauma (and remains elevated for >10 yrs)
26
Q

ictal spikes

A

Seizures have characteristic form of EEG activity -> commonly measured by inter-ictal spikes (distance between spikes/pulses)