Sem 2 L3 - Epilepsy and Neuroplasticity Flashcards

(33 cards)

1
Q

What is Epilepsy?

A

A chronic medical condition produced by temporary changes in the electrical function of the brain, causing seizures which affect
awareness
movement
sensation

affecting 0.5-1% of population (mainly children and elderly)

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2
Q

what type of disease is epilepsy?

A

An idiopathic disease - no single cause of epilepsy

Wide range of symptoms
Symptoms depend on:
the type of epilepsy
the area(s) of the brain being affected

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3
Q

What are the types of epilepsy?

A

Partial Epilepsy - simple partial seizures + complex partial seizures

Generalised Epilepsy - grand mal seizures + petit mal seizures

A diagnosis of epilepsy isnt very informative / useful bc of the heterogeneity of disease types, that will affect the individual and require treatment / adjustment in quite different ways

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4
Q

What are Simple Partial Seizures? (a branch of Partial Epilepsy)

A

Localised to specific areas of the brain (partial)
Accordingly, localised effects that are usually sensory and/or motor
eg - localised jerking beginningin right hand and progressing to clonic movements (jerks) of entire right arm (a focal motor seizure)

this progression (Jacksonian March) up the arm is produced by epileptiform activity in the motor cortex that controls the arm

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5
Q

What are Complex Partial Seizures? (a branch of partial seizures)

A

Localised to specific areas of the brain (partial)
Their effects are complex and diverse (hence the name)

AKA as Focal Onset impaired awareness seizures
Inappropriate motor behaviour although may be associated w ordered/co-ordinated
eg running, chewing, buttoning
may be absent (impaired consciousness)
lasts just a few minutes
often no memory of the episode

often referred to as temporal lobe epilepsy due to common localisation in temporal lobe
approx half of all adult epilepsies

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6
Q

What are auras in partial epilepsy?

A

Occasionally there are symptoms preceding partial seizures
Auras are abnormal sensations eg
sense of fear
rising feeling in abdomen
strange tastes of odours (metallic)
visual sensations akin to hallucinations

Aura due to early abnormal electrical activity originating from seizure focus - earliest manifestation of partial seizure

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7
Q

What are Petit Mal (absence) seizures? (part of Generalised Epilepsy)

A

involves entire brain (generalised)
the person is briefly absent - disrupted consciousness (might not know they were absent)

more common in children and disappear w age

widely underdiagnosed

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8
Q

What are Grand Mal seizures? (generalised epilepsy)

A

Can involve entire brain
Patient may lose consciousness, fall to ground, rigid extension of limbs (tonic phase)
jerk in all extremities (clonic phase)
Tonic-clonic seizure or “Grand Mal”

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9
Q

Partial seizures can what?

A

Generalise

u can start w a partial seizure and the electrical activity can spread to be not localised and lead to generalised epilepsy

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10
Q

A small and quite specific part can be the source of the seizure activity. This may be the case for what?

A

Localised brain damage (stroke, head injury) or following an infection, or the presence of a tumour

surgery to remove the problematic tissue can be an option for these cases

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11
Q

What does an EEG detect during a seizure?

A

Synchronised activity of many neurons - field potentials
Diagnosis based on EEG measures, plus neuropsychological symptoms

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12
Q

What is happening to the brain during a seizure?

A

Extensive synchronisation of firing across a number of neurons

can be seen by EEG measures, as well as from other invasive measures, including cell-specific recording

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13
Q

What are we interested in in EEG data?

A

The frequency components of the signal (how fast the waveforms are oscillating)
not just in the signal over time

Spike and Wave (at 3Hz) associated with petit mal generalised seizures

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14
Q

What are the treatments of epilepsy?

A

Pharmacological

Drugs that target GABA or Na+ channels (an inhibitory neurotransmitter GABA makes whichever neuron it is connected to fire less)

The above strategies seek to dampen the excessive neural firing (eg increasing release of inhibitory nt GABA in a way not unlike some general anaesthetics)

Surgery (in severe of drug treatment resistant cases)

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15
Q

What are the Pharmacological treatments of epilepsy?

A

Carbamazepine
Phenobarbital
Phenytoin (Dilantin)
Valproic acid

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16
Q

What is Neuroplasticity?

A

Changes to brain structure, connectivity and function over time in response to change in environment (internal or external)

changes in the way the neuron is firing
loss in connection etc

(like evolution where what already exists is modified to better suit requirements)

17
Q

What are the 3 key principles in Neuroplasticity?

A

Neurodegeneration (loss of connections and synapses and neurons)

Neural Regeneration (generating new connections and neurons)

Neural Reorganisation (larger scale reorganisation involving both neurodegeneration and neural regeneration)

18
Q

What is Neurodegeneration?

A

Up to 100 billion neurons in the adult brain
Number remains relatively stable over time w normal aging
But the number of connections change dramatically

the connections between neurons die - good bc it optimises the network

Grey matter volume (cell bodies) does decline with age though, this is in part due to reduction in connections and in numbers of other support cells (eg glial cells, which represent about 50% of all cells in the brain)

White matter volume increases for a while as the connections get better insulated with myelin - connections to/from frontal cortex amongst the last to become fully myelinated

19
Q

What are the different types of neurodegeneration?

A

When the neuron is damaged, the axon gets damaged and 2 things happen. if the neuron has been damaged, the neurons it projects to are also affected

Retrograde transneuronal degeneration - dying backward

Anterograde transneuronal degeneration - dying forward -

neighbours are affected by the death of that neuron - bc env around neuron has become damaged

one neuron existing networks - damage neuron within network, it will spread and affect other connections within that network

20
Q

What does neurodegeneration result from?

A

A disruption to the homeostatic environment within and surrounding the neuron - in the context of brain disease and most brain damage or brain injury

21
Q

What causes neurodegeneration? (Neuronal death)

A

A loss of fuel supply (oxygen, glucose)

Disruption of normal NT function (eg loss of input, excitoxicity) - neuron can die off

Attack from infections, toxins or own immune system

Faulty genetic signalling

22
Q

What are the 2 types of Neuronal death?

A

Necrosis - death due to cellular ill health (unmanaged)

Apoptosis - The cellular self destruct option (adaptive)

23
Q

What is Neural Regeneration?

A

some weird and wonderful examples of (neural) regeneration in non-mammalian and invertebrate species
(not so good in mammals - things are chopped off and do not grow back)

There is clear capacity for regrowth / regeneration in the peripheral nervous system but more complex / difficult in the central nervous system

24
Q

What is the central nervous system? (CNS)

A

The brain and spinal cord

commands decisions and shite

25
What is the Peripheral Nervous System? (PNS)
Everything else (besides brain and spinal cord) - located outside the skull and spine/ Two divisions - Somatic nervous system (interacts w external environment) Autonomic nervous system( interacts and regulates the body's internal environment)
26
What does neural regeneration depend on?
The tissue environment - ie has the cause of degeneration been removed? eg disease, injury hypoxia
27
assuming the cause of degeneration has been resolved..
Myelination of cells improve transmission of signals along axons Myelin sheath wrapped around axon when there is a damage to the cell the myelin can break down. in the pns there is a growth cone (end of the damage end of the axon) start shooting out and form 10 drills to grow in different directions to reach out and make a connection w target cell) shwann cells are needed tho and myelination for this to happen in the pns - CRITICAL FOR REGENERATION (regrowth) of pns neurons distance to the target - any key factors in whether there is effective regeneration
28
why is regrowth not always helpful?
the wiring gets messed up if the remaining Schwann cells are not able to guide it properly
29
What are implications for spinal cord injury?
spinal cord is part of cns remember (myelin from oligodendrocytes) target of spinal cord axons is usually quite distant regeneration potential for seriously injured spinal cord neurons therefore much reduced whereas peripheral nerve targets such as muscle stand a much better chance
30
there may be little regrowth and regeneration potential in the mammalian central nervous system because of????
Different pressures Increased adaptability - more pns Increased stability - more cns Intrinsic factors and Extrinsic factors
31
What do treatment strategies focus on ?
Guiding regrowth and enhancing tissue environment (trying to support or replicate the existing pns strategies)
32
low and high frequency tones are mapped across what?
the brain eg auditory cortex visual cortex
33
After damage, what do the maps need to be?
Reconfigured for muscle control the homunculus is a reasonable representation, but an oversimplification: damage to a single finger area doesn't mean loss of voluntary control of that finger representations are more complex and overlapping - this is a good thing for neural re-organisation following damage in case of damage to the body (eg loss of limb) the neural system loses input, but the cells/structures are still intact and connected to the rest of the nervous system creating problems like phantom limb