Epilepsy Flashcards
seizure
- 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
epilepsy
- 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
epileptic aura (and why it’s important)
- 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)
focal seizures
- 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)
generalized seizures
- 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
4 types of seizures
- Simple partial (focal)
- Complex partial (focal)
- Absence seizure (generalized)
- Tonic-clonic (generalized)
Risk factors for epilepsy: specific examples
- 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)
Immediate vs. Early vs. Late Seizures
- 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
Overlapping risk factors
- 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)
potential mechanisms of epileptogenesis (post-TBI)
- 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
Comorbidities
- 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
3 common treatments for epilepsy
- Anticonvulsants
- Vagus Nerve Stimulation
- Ketogenic Diet
less common treatments for epilepsy
- Cannabidiol treatment (weakly binds to endocannabinoid receptors, positive anecdotal/case study evidence)
- Surgical procedures (for severe intractable epilepsy)
Treatment: Anticonvulsants
- can lessen frequency and severity of seizures, but do not cure epilepsy
- Side effects can impact motor and cognitive speed, memory, mood, and psychosis
Treatment: vagus nerve stimulation
- Putting pacemaker style pulse generator in chest to stimulate vagus nerve and prevent overactivity
- Only moderately effective
Treatment: ketogenic diet
Increases ketones, which may be beneficial
Surgical procedures
- 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)
What are the most likely locations of Epileptic Focus?
- 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
Cartesian Dualiasm (Hustvedt article)
- 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)
psychogenic non-epileptic seizures (PNES) vs. epilepsy (Hustvedt article)
- 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
why does philosophy matter in modern psychological science? (Hustvedt article)
- philosophy informs diagnosis
- - terms like “functional” and “organic” reflect less nuanced understandings of biological processes
implications of psychogenic vs. organic debate for neuroscientists (Hustvedt article)
neurologists/medical professions must examine their implicit prejudices against psychogenic/emotional/psychiatric
illnesses as less “real” simply because they have no apparent physical cause
state of research in TBI (Mahler study)
- 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
Mahler study: key points
- 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
Mahler study: methods and results
- 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)
ictal spikes
Seizures have characteristic form of EEG activity -> commonly measured by inter-ictal spikes (distance between spikes/pulses)