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NEURO (Neurology) > Blackouts, Seizures & Epilepsy > Flashcards

Blackouts, Seizures & Epilepsy Flashcards

1
Q

What is a Blackout?

A

A transient loss of consciousness.

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2
Q

What is a Collapse?

A

An abrupt loss of postural tone with/without a loss of consciousness.

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3
Q

What is Syncope?

A

A transient loss of consciousness, caused by global impairment or cerebral hypoperfusion, resulting in a collapse.

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4
Q

Give 3 examples of Reflex Syncope.

A
  1. Vasovagal (Neurocardiogenic) Syncope.
  2. Situation Syncope.
  3. Carotid Sinus Syncope.
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5
Q

Give 1 example of Cardiac Syncope.

A
  1. Stokes-Adams Attacks.
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6
Q

Give 4 examples of Orthostatic Syncope.

A
  1. Orthostatic Hypotension.
  2. Primary Autonomic Failure.
  3. Secondary Autonomic Failure.
  4. Drug-Induced Autonomic Failure.
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7
Q

Aetiology of Vasovagal Syncope.

A

Reflex bradycardia with/without peripheral vasodilation that is provoked by emotion, pain or standing too long.

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8
Q

How does a Situation Syncope differ from Vasovagal Syncope?

A

Same symptoms but with a clear precipitant e.g. Cough Syncope, Effort Syncope (usually cardiac cause e.g. Aortic Stenosis), Micturition Syncope (commoner in men at night).

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9
Q

What happens in Carotid Sinus Syncope?

A

Hypersensitive baroreceptors cause excessive reflex bradycardia with/without vasodilation on minimal stimulation e.g. head-turning/shaving.

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10
Q

What happens in Stokes-Adams Attacks?

A

Transient arrhythmias e.g. Bradycardia due to complete heart block can cause a reduced CO and loss of consciousness.

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11
Q

What are the causes of Autonomic Failure?

A

Primary - Parkinson’s Disease, Lewy body Dementia.
Secondary - Diabetic Neuropathy, Amyloidosis, Uraemia.
Drug-Induced - Diuretics, Alcohol, Vasodilators.

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12
Q

Give 4 other causes of Syncope.

A
  1. Anxiety - Hyperventilation, Paraesthesiae, Tremor.
  2. Hypoglycaemia - rare in non-Diabetics.
  3. Drop Attacks - without LOC; mostly leg weakness but can be hydrocephalus, cataplexy or narcolepsy.
  4. Factitious - Pseudoseizures, Munchausen’s.
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13
Q

Investigations of Syncope (1).

A

Cardiac Assessment (ECG) if recurrent syncope/falls.

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14
Q

Acute Management of Syncope (5).

A
  1. Position on back.
  2. If breathing, restore blood flow to brain by raising legs above heart (30cm).
  3. Loosen belts, collars and constrictive clothing.
  4. Don’t make person get up quickly.
  5. ABCDE.
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15
Q

What is a seizure?

A

Transient episode of abnormal electrical activity in the brain.

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16
Q

What is Epilepsy?

A

An umbrella term for a condition where there is a recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifesting as seizures. Convulsions are the motor signs of electrical discharges.

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17
Q

Epidemiology of Epilepsy (1).

A

2/3 have achieved satisfactory seizure control with anti-epileptics.

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18
Q

What is a Post-Ictal Phase?

A

Patients feel drowsy and tired for at least 15 minutes.

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19
Q

Describe the pathophysiology of Seizures (2).

A
  1. Clusters of cortical neurones become temporarily impaired and become hyper excitable.
  2. The electrical discharges can be due to excessive excitation or limited inhibition : either faster/longer activation of Glutamate NMDA Receptors or dysfunctional GABA receptors.
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20
Q

Aetiology of Epilepsy (2B).

A
  1. Primary (2/3 - Idiopathic).
  2. Secondary - Cerebral Palsy, Tuberous Sclerosis, Mitochondrial Diseases.
    2B. Structural Causes - Cortical Scarring (Head Injury), SOLs, Strokes, Vascular Malformations.
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21
Q

What is the New Basic Seizure Classification based on?

A
  1. Where does the seizure begin in the brain?
  2. How is the level of awareness during a seizure?
  3. What other features are present?
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22
Q

What is a convulsion?

A

Motor manifestation of a seizure.

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23
Q

What type of seizure is usually associated with aura (in the prodromal phase)?

A

Focal Seizure.

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24
Q

Give 4 post-ictal features.

A
  1. Headache.
  2. Confusion.
  3. Myalgia/Temporary Weakness e.g. Todd’s Palsy.
  4. Dysphasia.
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25
Q

Investigations of Epilepsy (6).

A
  1. Referral for Specialist Assessment and Investigation within 2 weeks.
  2. Prolactin Levels are raised following a true epileptic seizure.
  3. Diagnosis - Specialist.
  4. EEG - typical patterns in different forms of epilepsy.
  5. ECG - exclude cardiovascular causes.
  6. MRI - structural causes e.g. tumours.
26
Q

General Management of Epilepsy (4).

A
  1. Aim : Seizure-Free on Minimum Anti-Epileptics : Monotherapy.
  2. Initiated and Guided by a Specialist.
  3. Can stop AED usage under Specialist Supervision if seizure-free for more than 2 years after risk assessment by dose reduction (2-3 months for most drugs; 6 months for Benzodiazepines and Barbiturates).
  4. AEDs started only following a second seizure usually unless neurological deficit, structural abnormality, EEG shows epileptic activity or if family/patient consider risk unacceptable in 1st seizure.
27
Q

Prognosis of Epilepsy (3).

A
  1. Sudden Unexpected Death is commoner in uncontrolled epilepsy and can be related to nocturnal seizure-associated apnoea or systole.
  2. 3x mortality.
  3. 5% risk of foetal abnormalities so good seizure control prior to conception and during pregnancy is important.
28
Q

Give 5 types of Generalised Seizures.

A
  1. Tonic-Clonic Seizures.
  2. Myoclonic Seizures.
  3. Absence Seizures.
  4. Atonic/Akinetic Seizures.
  5. Infantile Spasms.
29
Q

Pathophysiology of Generalised Seizures.

A

They originate at some point within and rapidly engaging bilaterally distributed networks lead to the simultaneous onset of widespread electrical discharge with no localising features to a single hemisphere.

30
Q

Tonic-Clonic Seizures :-
- Clinical Features (5).
- Management (2).

A

Clinical Features :
1. Tonic (Muscle-Tensing) precedes Clonic (Muscle-Jerking) Phases.
2. Tongue-Biting.
3. Incontinence.
4. Irregular Breathing.
5. Post-Ictal State.

Management :
1st Line : Sodium Valproate.
2nd Line : Lamotrigine or Carbamazepine.

31
Q

Myoclonic Seizures :-
- Epidemiology.
- Clinical Features (4).
- Management (2).

A

Epidemiology : Typically Kids (Juvenile Myoclonic Epilepsy) - Teenage Onset and commoner in Girls.

Clinical Features :
1. Sudden brief muscle contractions like a sudden jump.
2. Usually remains awake.
3. Infrequent generalised seizures, often in the morning with daytime absences.
4. Examples : Thrown suddenly to the ground or violently disobedient limb.

Management :
1st Line : Sodium Valproate.
2nd Line : Lamotrigine, Levatiracetam, Topiramate, Clonazepam.

32
Q

Absence Seizures :-
- Name.
- Epidemiology.
- Aetiology.
- Clinical Features (4).
- Investigations.
- Management.
- Prognosis.

A

Name : Petit Mal.

Epidemiology : Kids, typically between 3-10 and girls 2:1 boys.

Aetiology : Can be provoked by stress or hyperventilation.

Clinical Features :
1. Blank, staring into space before abruptly returning to normal.
2. Unaware of surroundings and unresponsive.
3. 10-20 seconds and quick recovery.
4. Unaware of seizure.

Investigations : EEG - Bilateral, Symmetrical 3Hz. spike and wave pattern.

Management : 1st Line - Sodium Valproate or Ethosuximide.

Prognosis : >90% stop having seizures as they age.

33
Q

Atonic/Akinetic Seizures :-
- Name.
- Epidemiology.
- Clinical Features.
- Management.
- Prognosis.

A

Name : Drop Attacks.

Epidemiology : Typically begin in childhood.

Clinical Features : Brief lapses in muscle tone, less than 3 minutes, with no LOC.

Management :
1st Line - Sodium Valproate.
2nd Line - Lamotrigine.

Prognosis : Could be indicative of Lennox-Gastaut Syndrome.

34
Q

Infantile Spasms :-
- Name.
- Epidemiology.
- Aetiology.
- Clinical Features.
- Investigations.
- Management (2).
- Prognosis (2).

A

Definition : West Syndrome.

Epidemiology : Rare disorder starting in infancy at 6 months of age.

Aetiology : Usually secondary to serious neurological abnormality e.g. Tuberous Sclerosis, Encephalitis, Birth Asphyxia.

Clinical Features : Clusters of full-body spasms, e.g. flexion of head and trunk and extension of arms. Each spasm is 1-2 seconds but repeated up to 50x.

Investigation : EEG - Hypsarrhythmia.

Management :
1. Difficult to treat.
2. 1st Line - Prednisolone or Vigabatrin.

Prognosis :
1. 1/3 die by 25.
2. 1/3 become seizure free.

35
Q

Aetiology of Focal/Partial Seizures.

A

Originate within networks linked to one hemisphere on one side of the brain.

36
Q

Clinical Features of Focal/Partial Seizures :
- Frontal Lobe (5).
- Parietal Lobe.
- Occipital Lobe.
- Temporal Lobe.

A

Frontal Lobe :
1. Posturing/Peddling Movements in Legs.
2. Jacksonian March.
3. Motor Arrest.
4. Subtle Behavioural Disturbances.
5. Dysphasia.

Parietal Lobe : Sensory disturbances.

Occipital Lobe : Visual phenomena e.g. spots, lines, flashes.

Temporal Lobe : Automatisms and impaired consciousness.

37
Q

What is a Jacksonian March?

A

Spreading focal motor seizure with retained awareness, often starting with the face/thumb.

38
Q

What is an Automatism?

A

Complex motor phenomena with impaired awareness, varying from primitive oral movements e.g. lip-smacking, chewing or manual movements e.g. fiddling to complex actions.

39
Q

What are the levels of awareness in a focal seizure?

A
  1. Focal Aware.
  2. Focal Impaired Awareness.
  3. Unknown Awareness.
40
Q

Management of Focal/Partial Seizures (2).

A

1st Line : Carbamazepine or Lamotrigine.
2nd Line : Sodium Valproate or Levetiracetam.

41
Q

What is Status Epilepticus?
Prognosis of Status Epilepticus.

A

Medical emergency : state involving seizures lasting more than 5 minutes or more than 3 seizures in one hour. It is a tonic-clonic seizure.
Prognosis : Mortality and risk of permanent brain damage increases with the length of attack.

42
Q

Aetiology of Status Epilepticus (5).

A
  1. Usually in patients with known epilepsy.
  2. If 1st presentation, chance of a structural brain lesion is more than 50%.
  3. Withdrawal from AEDs.
  4. Metabolic Disturbances.
  5. Drug-Toxicity e.g. TCAs.
43
Q

Management of Status Epilepticus.

A
  1. ABCDE management.
  2. IV Access (Cannula).
  3. IV Lorazepam/Diazepam (Benzodiazepine) 4mg as a slow-bolus into a large vein.
  4. Repeat after 10 minutes if seizure continues.

If in community : Buccal Midazolam (Mouth - M); Rectal Diazepam. Half the volume is squirted between lower gum and cheek on each side.

If ongoing/’Established’ - start a second line e.g. Phenytoin or Phenobarbital infusion. BP/ECG monitoring (Hypotension and avoid if Bradycardia/Heart Block).

If no response/’Refractory Status’ - achieve rapid control of seizure activity using induction of general anaesthesia.

44
Q

Mechanism of Action of Sodium Valproate (2).

A
  1. Increases the brain content/activity of GABA which has a relaxing effect.
  2. Weak inhibitor of Sodium channels to stabilise resting membrane potentials and reduce neuronal excitability.
45
Q

Indication of Sodium Valproate (2).

A
  1. Generalised Seizures & Epilepsy (not Focal).
  2. Bipolar Disorder.
46
Q

Contraindication/Cautions of Sodium Valproate (2).

A
  1. Females (Teratogenicity/Significant Risk of Neurodevelopmental Delay in Kids).
  2. CYP450 Inhibitor.
47
Q

Adverse Effects of Sodium Valproate (6).

A
  1. Teratogenicity.
  2. Liver Damage and Hepatitis.
  3. Hair Loss.
  4. Tremors.
  5. Thrombocytopenia.
  6. GI, Neurological and Psychiatric Effects.
48
Q

Mechanism of Action of Carbamazepine (1).

A

Binds to Sodium Ion channels to increase their refractory period.

49
Q

Indication of Carbamazepine (4).

A
  1. 1st Line in Focal Seizures.
  2. Least Teratogenic of AEDs.
  3. 1st Line in Trigeminal Neuralgia.
  4. Bipolar Disorder.
50
Q

Cautions of Carbamazepine (1).

A
  1. Inducer of CYP450 System.
51
Q

Adverse Effects of Carbamazepine (2).

A

2As.
1. Agranulocytosis.
2. Aplastic Anaemia.

52
Q

Mechanism of Action of Lamotrigine.

A

Sodium-Channel Blocker.

53
Q

Adverse Effects of Lamotrigine (2).

A

2Ls.
1. Leukopenia.
2. Life-Threatening Rashes : Stevens-Johnson Syndrome, DRESS Syndrome.

54
Q

Mechanism of Action of Phenytoin.

A

Binds to Sodium-Ion Channels and increases their refractory period.

55
Q

Indications of Phenytoin (2).

A
  1. 2nd Line in Status Epilepticus.
  2. Epilepsy (but other AEDs are preferred due to side effect profile).
56
Q

Cautions of Phenytoin (2).

A
  1. Give Vitamin K in last month of pregnancy to prevent clotting disorders in neonate.
  2. CYP450 Inducer.
57
Q

Adverse Effects of Phenytoin (6).

A
  1. Folate Deficiency - Megaloblastic Anaemia.
  2. Vitamin D Deficiency - Osteomalacia.
  3. Dizziness.
  4. Ataxia.
  5. Gingival Hyperplasia Hirsutism (Coarsening of Facial Features).
  6. Cleft Palate.
58
Q

Adverse Effects of Ethosuximide.

A
  1. Night Terrors.
  2. Rashes.
59
Q

Surgery in Epilepsy (2).

A
  1. Considered if single epileptogenic focus e.g. Hippocampal Sclerosis or low-grade Tumour.
  2. Up to 70% chance of seizure resolution but carries risk of focal neurological deficits.
60
Q

Febrile Convulsions :
- Epidemiology.
- Clinical Features (2).

A

Epidemiology : Children between 6 months and 5 years.

Clinical Features : Viral infection - temperature rise rapidly can cause an episode. Brief generalised tonic-clonic.

61
Q

Alcohol Withdrawal Seizures :
- Aetiology.
- Peak Incidence.

A

Aetiology : Chronic Alcohol consumption enhances GABA-mediated inhibition in the CNS (like Benzodiazepines) and inhibits NMDA-type Glutamate receptors. Withdrawal causes decreased inhibitory GABA and increased NMDA Glutamate transmission.

Peak Incidence : 36 hours following the cessation of drinking.

62
Q

Psychogenic Non-Epileptic Seizures :
- Pathophysiology.
- Clinical Features.
- Epidemiology.

A

Pathophysiology : No characteristic electrical discharges.

Clinical Features : Gradual onset and pelvic thrusting.

Epidemiology : Commoner in psychiatric patients and females.

NEURO (Neurology) (54 decks)

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