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Med 4 > CNS Week 5 Epilepsy > Flashcards

CNS Week 5 Epilepsy Flashcards

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1
Q

Define seizure

A

A transient occurrence of signs and or symptoms due to abnormal excessive or synchronous neuronal activity in the brain

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2
Q

Define epilepsy

A

A pathologic and enduring tendency to have recurrent seizures
And
By the neuro-biologic, cognitive, psychological and social consequences of this condition

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3
Q

What is the difference between seizures and epilepsy

A

Seizures are a pathological pattern of neural activity and epilepsy is a tendency to recurrent seizures

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4
Q

What are the 2 main types of seizure

A

Generalised seizures: starts simultaenously in both hemispheres

Focal seizures: seizure starts in a focus and then spreads

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5
Q

What are the 3 types of common generalised seizures

A

Typical absence

Myoclonic

Tonic- clonic

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6
Q

What are absence seizures

A

Mainly childhood in onset

Frequent brief attacks (1-30s)

Sudden loss and return of consciousness

No aura and no post-ictal state

Some involuntary movements

Respond to some anti-epileptic drugs and not others

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7
Q

What are myoclonus seizures

A

Sudden brief shock like muscle contractions

Usually bilateral arm jerks

Often worse in the mornings

Precipitated by sleep deprivation and alcohol

Respond to particular anti epileptics

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8
Q

Describe tonic clonic seizures

A

Sudden onset, gasp, fall

Tonic phase with cyanosis

Clonic phase

Post-ictal phase (recovery is not instant)

Tongue bitten and incontinence, fractured shoulder

Noisy breathing

Headache and muscle pain afterwards

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9
Q

What are focal seizures

A

Often aura or warning at onset

As seizures spreads -> loss of awareness and involuntary movement

Often caused by brain lesions -> tumour, abscess, trauma

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10
Q

Describe temporal lobe seizures

A

Auras: rising sensation in stomach, olfactory and gustatory hallucinations, deja vu

As the seizure spreads the person suddenly stops and blank stares, loss of responding and awareness, mouth movements, fidgeting or postures- automatisms

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11
Q

What is idiopathic epilepsy

A

No brain lesions, no intellectual impairment, often generalised seizures
Easy to treat, seizures usually controlled

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12
Q

What is symptomatic epilepsy

A

Sign of underlying lesion or brain disorder, often cognitive problems, abnormal MRI common
Seizures not controlled

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13
Q

What are the key regulators of neuronal excitability

A

Non gated ion channels
- resting membrane potential

Voltage gated ion chanels
- Na+, K+, Ca2+, Cl-
Dendrite information processing
Action potential and repolarisation

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14
Q

What are epileptiform discharges due to

A

Neuronal bursting (an ion channel property)

Synaptic effects (both glutamate and GABA)

Glia effects

Non synaptic effects (eg extracellular K+)

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15
Q

What is epileptogenesis

A

The process following an injury that leads to the first of a series of spontaenous and recurring seizures

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16
Q

What structural changes occur in epileptogenesis

A

Cell loss inhibitory

Axonal sprouting

Neurogenesis

Gliosis

Neuro - inflammation

BBB breakdown

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17
Q

What molecular changes occur in epileptogenesis

A

Neuronal changes (Na, K, Ca, Cl, HCO3)

Neurotransmitter transporters

Neuro-modulators

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18
Q

What functional changes occur in epileptogenesis

A

Gap junctions

Glia: buffering of extracellular environment

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19
Q

How was the first anti epileptic drug developed (phenytoin)

A

Electrodes to rodents head
Shocked with electricity to induce seizure

Loaded with drug beforehand to see if it prevents electrical current from causing a seizure

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20
Q

Mode of action of vigabatrin

A

GABA transaminase inhibitor

Higher GABA levels prevent fading of inhibiton

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21
Q

Mode of action of tiagabine

A

GABA reuptake inhibitor

Higher GABA levels prevent fading of inhibition

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22
Q

In summary what are seizures caused by

A

Abnormal burst firing and synchronisation in normal / modified neural circuits

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23
Q

Steps for the management of epilepsy

A

Ensuring a correct diagnosis

Determining the cause

Deciding on treatment

Advising on lifestyle issues

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24
Q

4 different types of seizures

A

Absences

Myoclonus

Tonic clonic

Focal

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25
Q

Differentials for blackouts and funny turns

A

Epilepsy

Fainting

Cardiac causes

Psychological causes

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26
Q

Why is valporate a risk in women

A

Has a 6-10% malformation rate in pregnancy with subtle facial abnormalities
30-40% associated with low IQ and autism

Never give valporate to a woman 12-55 without specialist adivce
There is a valporate pregnancy prevention program where it is not prescribed unless the woman is fitted with a highly active contraceptive coil

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27
Q

Non pharmacological epilepsy treatments

A

Resection of epileptic focus

Vagal nerve stimulation

Ketogenic diet

28
Q

Social consequences of epilepsy

A

Loss of driving licence

Loss of employment

Stigmatization and anxiety

Needing antiepileptic drugs

Problems with contraception and conception

29
Q

Describe idiopathic epilepsy

A

Milder

No lesion

Easier to control

Often generalised

30
Q

Describe symptomatic epilepsy

A

Can vary with age:

  • brain malformations
  • inherited metabolic / gene disorders
  • birth trauma / stroke
  • infection and immune disorders
  • trauma
  • tumours
  • stroke
31
Q

What is language lateralisation

A

Most humans (70-95%) have a left hemisphere lateralisation for language abilities

Broca identified area in left hemisphere that plays primary role in speech production

Wernicke identified another part of left hemisphere associated with speech comprehension

32
Q

Different tests used for determining language lateralisation

A

Wada test

Functional imaging

Event related potentials

Transcranial magnetic stimulation

33
Q

Describe the wada / sodium amytal test

A

Procedure used by neuropsychologists prior to surgery for temporal lobe epilepsy to determine hemispheric specialisation for key language skills

Injection of sodium amytal into 1 of the hemispheres produces transient ipsilateral hemiparesis
- when the speech dominant hemisphere is injected there is clear but transient speech impairment

34
Q

What are the 4 types of hearing impairment

A

Normal hearing: you can hear quiet sounds of less than 20dB

Mild hearing loss: loss between 20-40 dB
(Difficulty following speech in noisy situations

Moderate hearing loss: between 41-70 dB
(Difficulty following speech)

Severe hearing loss: between 71-95 dB
(Severe difficulty following speech without a hearing aid)

35
Q

Describe the make up of the external auditory meatus

A

Lateral third- cartilaginous, ceruminous and sebaceous glands produce cerumen (earwax)

Medial 2/3s - bony lined with thin skin continuous with the tympanic membrane

36
Q

What is the tympanic membrane

A

Thin semitransparent membrane externally lined by thin skin and internally lined by mucous membrane all sandwiching radial and circumferential collagen fibres

37
Q

Measurements of the tympanic membrane

A

Not quite 1cm across and 0.1mm thick

38
Q

What are the 3 ossicles

A

Malleus (hammer) 8mm, 0.025g

Incus (anvil) 10mm, 0.025g

Stapes (stirrup) 3x1mm, 0.002g

39
Q

Combined role of the ossicles

A

Increase the force and reduce the amplitude of vibrations needed to drive the inner ear

40
Q

What is the stapedius

A

The bodys smallest muscle. Inserts to the stapes and when tense reduces the amplitude of vibrations

41
Q

What is the tensor tympani

A

Inserts into the malleus and when tense it reduces the amplitude of the vibrations

42
Q

Describe the process of ear syringing

A

Used to clear blocked ear canals from wax
Water 37c is forced into the external auditory meatus

Aimed posterosuperiorly to prevent perforation of the tympanic membrane

Hold a bowl inferiorly to the auricle to catch any material dislodged from the meatus including the returning water

43
Q

What are otoscopes

A

Used to view the tympanic membrane

Straighten out the meatus by pulling the tip of the pinna posteriorly and superiorly

Use little finger against the patients cheek as a guage of depth

44
Q

3 problems that can arise in the external auditory meatus

A

Wax: 50% skin, 50% cerumen which is translucent on secretion but turns yellow golden brown black in time

Otitis externa: inflammation of the ear canal- eg caused when a foreign body becomes dislodged

Bony growths: arise by the formation of the benign new bone

45
Q

2 conditions that can arise in the tympanic membrane

A

Tympanosclerosis- scarring of the tympanic membrane causing calcium deposits to form

Perforation in the membrane

46
Q

What is conductive hearing loss

A

Loss by air conduction but not by bone conduction (an air borne gap)
Generally indicates a problme in the outer / middle ears that hinders normal sound getting ot the inner ear

Can usually be fixed by ENT surgery

47
Q

What is otitis media and how can it be treated

A

Inflammation of the mucus membrane lining the middle ear

Treated by a grommet surgically inserted in the tympanic membrane (commonest surgery for young children)

48
Q

What are some abnormalities of the outer ear

A

Microtia: congenital abnormality. Failure of the auricle and external auditory meatus to develop

Pre-auriciular appendage - accessory cartilaginous appendage formed just anterior and superior to the tragus

Haematoma- result of blunt trauma causing subcutaenous bleeding (cauliflower ear)

49
Q

Describe the method of sound delivery

A

The outer hair cells actively amplify sounds

Which releases energy into the cochlea

Which vibrate everything in reverse order

Which vibrates the eardrum and so vibrates the air

Which is sound emissions

50
Q

What is tinnitus

A

The conscious perception of an auditory sensation in the absence of a corresponding external stimulus

No treatment to successfully eliminate

51
Q

Negatives of hearing aids

A

They dont restore normal hearing
They dont sound natural or transparent
Dont distinguish wanted vs unwanted sounds
Dont properly fix the difficulty focusing on wanted sounds

52
Q

Features of a temporal lobe seizure

A

Olfactory hallucinations (imagining smells) and smacking lips together

53
Q

Features of an occipital lobe seizure

A

Flashes / floaters

54
Q

Features of a juvenile myoclonic seizure

A

Infrequent generalised seizures and daytime absences

55
Q

Features of a parietal lobe seizure

A

Paraesthesia (burning or prickling sensation in hands, arms, legs or feet)

56
Q

Features of frontal lobe seizures

A

Posturing and head / leg movements

57
Q

Symptoms of idiopathic intracranial hypertension

A

Blurred vision and headache worsened by coughing and changing position
Difficulty abducting right eye (lateral rectus eye muscle impaired)
and bilateral papilloedema visible on fundoscopy

Classically seen in overweight women

58
Q

Symptoms of giant cell arteritis

A

Left sided vision loss, headache and scalp tenderness
High temperature
Jaw claudication
Relative afferent pupillary defect

59
Q

Treatment for giant cell arteritis

A

High dose prednisolone

60
Q

Which monoclonal antibody treatment is directed against vascular endothelial growth factor (VEGF)

A

Bevacizumab

61
Q

What is conduction dysphasia

A

Fluent speech but poor repetition with relatively intact comprehension

Is the result of a lesion to the arcuate fasciculus which connects broca and wernicke’s areas

62
Q

What is drusen

A

Yellow deposits on the retina

Is a characteristic sign of dry age related macular degeneration

63
Q

Role of astrocytes

A

Remove excess potassium ions from CSF in the CNS
Provide physical support for neurons
Help form BBB
Help with physical repair of neuronal tissues

64
Q

What neurotransmitter is involved in photophobia, lacrimation and redness and pupil constriction

A

Acetylcholine

As these are parasympathetic pathway activity and acetylcholine is the main transmitter of this pathway

65
Q

What is the ordinary function of ependymal cells

A

Provide the inner lining of the ventricles and are responsible for CNS production

Med 4 (12 decks)

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