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MBBS IV - Junior Clerkship WCS > JC29 (Medicine) - Seizure and LOC > Flashcards

JC29 (Medicine) - Seizure and LOC Flashcards

1
Q

4 major disease entities that cause sudden LOC +

A

Syncope
Seizure
Pseudo-seizure
Toxic/ Metabolic coma

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2
Q

Syncope +

  • Pathophysiology/ Mechanism
  • S/S, Precipitating factors
  • Subtypes
A

Pathophysiology/ Mechanism: Generalized hypoperfusion to the brain

Features

  • Brief lightheadedness
  • LOC < 1 min, Fast recovery with no confusion
  • Precipitated by pain, emotion or standing position (vasovagal)
  • S/S: darkening of vision, tinnitus, hyperventilation, distal tingling, nausea, clamminess or sweating

Subtypes

  • Neurocardiogenic: Situational, Vasovagal, Hypertensive carotid sinus syndrome
  • Postural hypotension
  • Cardiogenic: poor cardiac output causes
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3
Q

Seizure

  • Pathophysiology/ Mechanism
  • Different S/S and presentations
  • Causes
A

Pathophysiology/ Mechanism: abnormally excessive or synchronous activity in brain

Features: Transient altered awareness + abnormal behavior + involuntary movement

  • Preceded by aura (eg. peculiar taste/smell, déjà vu feeling, auditory hallucination, anxiety, nausea, abdominal pain)
  • LOC + falling + clonic movement = generalized tonic clonic
  • LOC + stare blankly into space = absence
  • LOC + Localized contractions = focal
  • Lasts > 1 min with slow recovery
  • S/S incontinence, uprolling eyeball, tongue-biting

Causes:

  • Epilepsy (unprovoked)
  • Provoked seizures
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4
Q

Causes of provoked seizures

A

Provoked seizures:

  • Drugs or toxin-related
  • Metabolic, eg. hypoGly, hypoCa, hypoNa
  • CNS infection
  • Acute stroke or haemorrhage
  • Head trauma
  • Febrile convulsion in children

Provoked seizure means NOT EPILEPSY

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5
Q

Pseudo-seizure

  • Pathophysiology/ Mechanism
  • Features
A

Mechanism - Psychogenic, non-epileptic attack

Features

  • Long episodes >30 mins, rapid recovery/ emotional distress
  • Precipitate by emotional triggers
  • Retain awareness, only 10% LOC
  • Eyes cannot be opened
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6
Q

Differentiate seizures from syncope

A

Features Specific to seizure, not syncope:

  • Aura
  • Cyanosis
  • Tongue-biting
  • Post-ictal confusion, amnesia, headache

Features specific to syncope, not seizure:

  • Rapid recovery
  • +/- minor tongue biting
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7
Q

Compare toxic and metabolic coma S/S

Causes of each type of coma

A

Toxic coma

  • transient, intermittent coma
  • Cause by alcohol, solvent, barbituates

Metabolic coma

  • LOC
  • Preceded by sweating, confusion, weakness
  • Cause by insulin, fasting, anti-diabetics
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8
Q

Likely causes of sudden LOC precipitated by micturition, sleep, standing, and exercise

A

→ During blood-taking, micturition - syncope
→ During sleep - seizure
→ Standing - orthostatic hypotension
→ During exercise - outflow obstruction

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9
Q

Common forms of aura

A
  • Peculiar taste or smell
  • Feeling of déjà vu
  • Feeling of jamais vu (never seen)
  • Hearing of familiar music
  • Feeling of fear or anxiety welling up in chest
  • Visceral feelings, eg. nausea, abdominal pain
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10
Q

Presentation:

Short LOC with rapid recovery

Under 1 minute

Brief, asynchronous jerking

Pallor

Light-headedness, sweating, visual darkening

Most likely dx?

A

Syncope

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11
Q

Presentation:

Few minutes of LOC with slow recovery and confusion

With aura

Incontinence

Tongue-biting

Tonic-clonic movement

Most likely Dx

A

Generalized seizure

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12
Q

Presentation:

Several hours episode, no LOC

Partially retain awareness

Eyes cannot be open

Preceded by emotional distress

Most likely dx?

A

Pseudo-seizure/ Psychogenic seizure

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13
Q

First-line investigations for sudden LOC

A

Ix
 EEG for epilepsy
 ECG ± Holter monitor for arrhythmia
 Tilt-table test for neurogenic syncope and orthostatic hypotension
 Echocardiography for cardiomyopathy
 Blood glucose for hypoglycaemia

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14
Q

Physiological control of consciousness

  • Define consciousness
  • Components of consciousness
  • Areas of brain involved
A

Consciousness: state of awareness of self and surrounding

Components:
□ Arousal: state of being ‘awake’ → from ascending reticular formation + thalamus
□ Awareness: cognitive and affective mental function (i.e. the ‘content’) → from anterior cingulate and precuneus

Dependent on:
□ Reticular activating system (RAS) in brainstem, hypothalamus, thalamus
□ Cerebral hemisphere

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15
Q

Reticular activating system (RAS)

  • Location in brain
  • Function
  • EEG patterns in wakefulness and sleep
  • Physiological mechanisms
A

Location: Upper brainstem and medial thalamus

Function: Maintain cerebral cortex in state of wakeful consciousness

EEG pattern:

  • Awake/ REM sleep = desynchronized waves
  • Non-REM sleep = Regular spindles

Mechanisms:

  • Thalamic relay neurons from brain stem to thalamus > activate cortical pyramidal neurons > control level of consciousness
  • Tonic mode: thalamic neurons fire and activate cortex in desynchronized way > maintain wakefulness/ REM sleep
  • Burst mode: thalamic neurons fire and active cortex in synchronous way > non-REM sleep
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16
Q

Coma

  • Definition
  • GCS cut-off
  • Critical brain structure involved
A

Coma: severe impairment of arousal ± awareness

Definition: GCS ≤8 (E≤1, V≤2, M≤5)

  1. Diffuse bilateral cortical/ hemispheric damage
  2. Direct damage/suppression of RAS or its projections)
  3. Suppression of reticulo-cerebral function: drugs, toxins, metabolic causes
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17
Q

Intracranial causes of coma

A

□ Traumatic: diffuse white matter injury, haematoma
□ Vascular: SAH, ICH, cerebral infarct with ↑ICP, brainstem infarct/haemorrhage
□ Neoplastic: tumour with oedema
□ Infective: meningitis, abscess, encephalitis
□ Others: epilepsy, hydrocephalus

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18
Q

Extracranial causes of coma

A

□ Metabolic: electrolyte imbalances, liver/renal failure, endocrine disorders
□ Drugs/toxins: sedatives, anticonvulsants, anaesthetics, alcohol, heavy metals, CO…
□ Vascular occlusion: vertebral artery disease, bilateral carotid disease
□ Cardiorespiratory insufficiency
□ Psychiatric: hysteria, catatonia

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19
Q

Structural causes of coma

A
  • Bilateral internal carotid artery occlusion
  • Bilateral anterior cerebral artery occlusion
  • Basilar occlusion
  • Subarachnoid hemorrhage
  • Thalamic hemorrhage
  • Pontine hemorrhage
  • Trauma - contusion, concussion
  • Hydrocephalus
  • Midline brainstem tumor
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20
Q

List disorders of conscioussness

A

Coma

Stupor - baseline unresponsiveness, only aroused by vigorous stimuli

Persistent Vegetative State (PVS)

Akinetic Mutism and Abulia

Inattention

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21
Q

Persistent vegetative state

Definition

Area of brain involved

Common causes

Prognosis

A

Definition

  • Awake but unresponsive state
  • No cognitive neurological function but retain non-cognitive function (cardiac, respiration, vascular)
  • Head and neck movement may persist
  • No meaningful response to external and internal environment

Area:

  • Extensive cortical gray or subcortical white matter lesion
  • Preservation of brainstem function

Common causes: Cardiac arrest and head trauma

Prognosis: Regaining mental function after months of PVS is almost zero

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22
Q

Define akinetic mutism and abulia

A

Akinetic mutism:

  • Partially or fully awake, able to form impression and think
  • Immobile and mute
  • Damage in medial thalamic nuclei, frontal lobes or hydrocephalus

Abulia: (mild akinetic mutism)

  • Mental and physical slowness, diminished ability to initiate activity
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23
Q

GCS scale

A
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24
Q

Conditions that mimic coma

A
  1. PVS
  2. Locked-in syndrome - Alert, aware, quadriplegic with lower cranial nerve palsy due to bilateral ventral pontine syndrome)
  3. Akinetic mutism and abulia
  4. Catatonia - appear awake with eyes open, hypomobile and mute syndrome with major psychosis
  5. Pseudocoma - awake, eye cannot be opened, emotional distress
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25
Q

Conditions that mimic epileptic seizures

A
  1. Hyperventilation - Anxiety, peripheral cyanosis, hand paresthesia, carpopedal spasm
  2. Migraine
  3. Panic attack - intense dread or fear, inability to breathe, no LOC, autonomic features
  4. Psychogenic seizures - motionless with forceful eye closure, thrashing limb movement and pelvic thrusting
  5. Syncope
  6. Transient global amnesia - Hours of isolated amnesic syndrome, no confusion, no negative features
  7. Transient ischemic attack - predominant negative features: weakness, loss of sensation…etc
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26
Q

Diagnostic criteria of epilepsy

A

2 or more seizures NOT PROVOKED by illnesses or circumstances, occur 24 hours apart

OR
Single unprovoked seizure if recurrence risk is high

OR

Diagnosis of an epilepsy syndrome

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27
Q

Causes of Epilepsy

A

Epilepsy = unprovoked seizure

  1. Idiopathic (62%) - genetic mutations in cellular and synaptic proteins and ion channels
  2. Stroke (9%)
  3. Head trauma (9%)
  4. Alcohol (6%)
  5. Neurodegenerative diseases (4%)
  6. Static encephalopathy (3.5%) - e.g. hepatic or uremic encephalopathy
  7. Brain tumor (3%)
  8. Infection (2%)
  9. Autoimmune - NMDAR autoantibodies encephalitis
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28
Q

Clinical Classification of Seizures

A

Partial (focal, local) seizures

  • Simple partial seizure (SPS) - normal consciousness
  • Complex partial seizure - impaired consciousness
  • Partial seizure secondarily generalized

Generalized seizures

  • Myoclonic seizure
  • Absence seizure
  • Clonic seizure
  • Tonic-clonic seizure
  • Tonic seizure
  • Atonic/ Astatic seizure
29
Q

epilepsy syndrome

  • Definition
  • How to classify which syndrome?
  • Main Classes
A

Syndrome with predisposition to Recurrent, Unprovoked seizures

Classification according to:

  1. Types of seizure
  2. Any neurological and developmental abnormalities
  3. EEG findings

Main classes:

  1. Generalized epilepsy syndrome (Genetic) - seizure begin simultaneously in both cerebral hemispheres
  2. Partial/ Localized-related epilepsy syndrome (CNS lesions) - seizure originate in 1 or more localized foci
30
Q

General Mechanism of seizure

A

Abnormal/ excessive synchronous electrical activity in brain

High spread and neuronal recruitment due to:

  • Enhanced connectivity
  • Enhanced excitatory transmission
  • Failure of inhibitory mechanisms
  • Changes in intrinsic neuronal properties
31
Q

Specific mechanisms of Epilepsy (unprovoked seizure)

A

Generalized epilepsies asso. with mutations of:

  • Ion-channels
  • Neurotransmitter receptors
  • Synaptic support protein
  • mTOR pathway regulators
  • Chromatin remodeling and transcription regulators

Mostly complex inheritance patterns, some Mendelian inheritance of single gene mutation

32
Q

Generalized epilepsy with febrile seizures plus (GEFS+)

Definition

Associated mutations

A

syndromic autosomal dominant disorder, can exhibit numerous epilepsy phenotypes (e.g. absence, myoclonic, atonic, afebrile GTCS)

Usually present in childhood, most disappear by adulthood

Mutation in voltage-gated Na Channel B1 subunit (SCN1B), SCN1A, and GABRG2 genes > high depolarization rate and hyperexcitability

33
Q

List some epilepsy syndrome asso. with single gene mutations

A

Generalized epilepsy with febrile seizures plus (GEFS+) - SCN1A, SCN1B, SCN2A, GABRG2

Benign familial neonatal convulsions - KCNQ2, KCNQ3

Autosomal dominant nocturnal frontal lobe epilepsy - CHRNA4, CHRNB2

Childhood absence epilepsy and febrile seizures - GABRG2

Autosomal dominant partial epilepsy with auditory features - LGI2

34
Q

Complex partial seizures

Cause

S/S

A

Cause: Temporal Lobe Epilepsy (TLE)

Onset S/S:

  • Olfactory/ gustatory hallucinations
  • Epigastric sensation
  • Psychiatric symptoms: deja vu/ jamais vu
  • Stare blankly

Progress to LOC with S/S:

  • Unintelligible speech, lip smacking
  • Picking at clothes
  • Automatism: coordinated involuntary motor activity during clouded consciousness e.g. screaming, crying, laughing
35
Q

Partial Seizure

Causes

Most common type and brain areas involved

A

Causes: Most common seizure in adults

  • Head trauma
  • Stroke
  • Tumor

Mesial temporal lobe epilepsy (mTLE)

  • Complex partial seizure from mesial temporal lobe
  • Common lesion: hippocampal sclerosis
  • Areas involved: mesial temporal lobe structures: hippocampus, amygdala, parahippocampal cortex
36
Q

Investigations for epilepsy

A
  1. Neurological exam
  2. Skin lesions in neurocutaneous syndromes - Neurofibromatosis, Tuberous sclerosis
  3. For unprovoked first seizure:
  • EEG
  • MRI for structural lesions
  • Blood: CBC, electrolyte, L/RFT, Ammonia
  • Substance abuse screen
37
Q

Investigations for epilepsy (+)

A
  1. Neurological exam
  2. Skin lesions in neurocutaneous syndromes - Neurofibromatosis, Tuberous sclerosis
  3. For unprovoked first seizure:
  • EEG
  • MRI for structural lesions
  • Blood: CBC, electrolyte, L/RFT, Ammonia
  • Substance abuse screen
38
Q

EEG for Dx of epilepsy (-)

Pros and Cons

A

Pros:

  • Epileptiform EEG patterns (spikes and sharp waves) help Dx and Classification of seizure
  • Video EEG monitoring possible to find epileptogenic focus (ictal EEG)

Cons:

  • Abnormal EEG only in 50% of unprovoked first seizure
  • Interictal EEG abnormalities cannot Dx epilepsy
  • Normal EEG cannot exclude epilepsy
  • Sleep deprivation is confounding factor of abnormal EEG
39
Q

Epilepsy management options

Indications

A

Lifestyle modification

  • Avoid potentially dangerous activities: Driving, power equipment, hiking, swimming, cooking over fire..etc

Neuromodulation therapy

  • Electrical pulses to brain/ nerves to enhance rhythmic pulses against seizure generation
  • e.g. Vagus nerve stimulation

Pharmacological - Anti-epileptic drugs

  • Indicated for recurrent seizure dx by EEG or known seizure cause
  • Broad-spectrum or narrow-spectrum AED

Surgery

  • Refractory to AED after 2nd, 3rd line - Drug-resistant epilepsy
40
Q

2 major categories of anti-epileptic drugs and examples

A

Broad-spectrum AED

  • Valproate
  • Lamotrigine
  • Levetiracetam
  • Topiramate
  • Perampanel

Narrow-spectrum AED

  • Carbamazepine, Oxcarbazepine
  • Phenytoin
  • Lacosamide
  • Gabapentin, Pregabalin
41
Q

Indication and contraindication of narrow-spectrum AED

A

Indication:

Focal/ Localized epilepsy with Partial and secondarily generalized seizures

C/I:

Some types of Idiopathic generalized epilepsy syndrome: Absence epilepsy and Myoclonic seizures

42
Q

AEDs for absence seizure only

A

Ethosuximide

43
Q

AED for focal seizures only

A

Narrow AED*

Carbamazepine, Oxcarbazepine

Gabapentin, Pregabalin

Lacosamide

Phenytoin

44
Q

First-line AED for All focal and most generalized seizures (+)

A

BDZs

Levetiracetam

Perampanel

Topiramte

Sodium Valproate

45
Q

Valproate (-)

  • Indication
  • MoA
  • Metabolism
  • S/E
  • C/I
A

Indication: Primary GTCS, absence and myoclonic seizures, 2nd line for partial seizures

MoA: Voltage-dependent blockade of Na channels

Metabolism: Protein-bound, T½ 7-17h, Liver metabolism

S/E: Tremor, weight gain, sedation, pancreatitis, BM suppression, thrombocytopenia, urea cycle dysfunction (increase NH3)

C/I: Teratogenic! Children, female of child-bearing age

46
Q

Phenytoin (-)

  • Indication
  • MoA
  • Metabolism
  • S/E
A

Indication: GTCS, Partial seizure

MoA: Voltage-dependent blockade of Na channels

Metabolism: Hepatic CYP450, Protein bound, diseases can change unbound fraction, disproportionate serum amount after saturation

S/E: Dose-related neuro-toxicity, Hypersensitive skin reactions, Gingival Hyperplasia and Coarse facial feature, Hirsutism, Hypocalcemia, Megaloblastic anaemia

47
Q

Carbamazepine (-)

  • Indication
  • MoA
  • Metabolism
  • S/E
  • C/I
A

Indication: GTCS, Partial seizure

MoA: Prevent repetitive firing in depolarized neurons through blocking Na channels

Metabolism: hepatic, need increasing dose over time

S/E: Significant D/D interaction with lots of drugs, Dose-related neurotoxicity, Allergic morbilliform rash, SJS, Reversible leukopenia, HypoNa, Toxic hepatitis, Orofacial dyskinesia, Arrhythmia

C/I: Absence and myoclonic seizure

48
Q

Lamotrigine (-)

  • Indication
  • MoA
  • Metabolism
  • S/E
A

Indication: GTCS, Partial seizure, 1st line for Elderly

MoA: Anti-folate activity (inhibit dihydrofolate reductase) + Inhibit voltage-dependent Na channels

Metabolism: Protein-bound, hepatic metabolism, Urine excretion, T½ 30h, No D/D interaction with other AED

S/E: Rash, drowsiness, dizziness, unsteady gait, headache, tremor, nausea

49
Q

Levetiracetam

  • Indication +
  • MoA
  • Metabolism
  • S/E
A

Indication: adjunct for ALL partial seizure +/- secondary generalized seizure

MoA: Bind to synaptic vesicle protein SV2A > modulate exocytotic function of presynaptic neuron

Metabolism: Enzymatic hydrolysis, urine excretion, No D/D interactions with any AED or cardiac drugs

S/E: Hyperactivity, Somnolence, Asthenia, Dizziness, Infection

50
Q

Reasons for cautionary use of AED on women and children

A
  1. Valproate (high risk): Teratogenic, PCOS, Anovulation, Hyperandrogenism
  2. AED use increase Fetal Malformation, Poor cognitive outcomes (Low IQ)
  3. Lamotrigine interacts with OC pills
51
Q

Which AED to use in pregnant women?

A

All AEDs have risk

Lowest risk = Lamotrigine, Levetiracetam

52
Q

Epilepsy surgery

  • Indications
  • Types
  • Complications
A

Indication:

  • Drug-resistant AED (refractory to 2 or more AED)
  • TLE (most common drug-resistant AED)

Types:

  • Standard anterior temporal lobectomy
  • Selective amygalo-hippocampectomy
  • Laser Interstitial Thermal Therapy
  • Steotactic Radiosurgery

Complications:

  • short-term memory loss (dominant temporal lobe surgery)
  • Infection
  • Visual field defects
  • CN palsies
  • Hemiparesis
  • Death
53
Q

Status Epilepticus

  • Definition
  • Subtypes (-)
  • Causes
  • Prognosis (-)
A

Definition: Prolonged (>5 mins) or repeated seizure without full recovery of consciousness between attacks

Subtypes:

  • Convulsive status epilepticus (generalized tonic clonic) - most common
  • Non-convulsive status epilepticus (absence)
  • Complex partial Status Epilepticus

Causes:

  • Acute cerebral insult: CNS infection, Neurotoxins, Autoimmune encephalitis
  • Rapid withdrawal of AED

Prognosis: 3-20% mortality

54
Q

Status Epilepticus

Treatment and monitoring

A

Medical Emergency!

  • ABC: airway protection, oxygen, intubation with ventilation, IV fluid, BP
  • Observe vitals
  • ECG
  • EEG
  • Terminate seizure: IV AED
  • Look for underlying causes: AED withdrawal? CNS infection? Neurotoxins? Autoimmune encephalitis?
55
Q

Status Epilepticus

Drug options and indications

A

IV AEDs:

  • Phenytoin , Valproate, Levetiracetam, Lacosamidem, Perampanel

Anesthesia and hypnotics:

  • Phenobarbital (caution respiratory arrest)
  • Propofol
  • Thiopental
  • Midazolam (refractory to IV AED)
56
Q

Drug options for non-convulsive Status Epilepticus

A
  • Lorazepam
  • Diazepam
  • IV Valproate
  • Levetiracetam
57
Q

Acute confusion/ Delirium

Diagnostic criteria

A

Dx criteria (DSM-IV)

At least 2 of:

  • Perceptual disturbance (misinterpretation, illusion, hallucination)
  • Incoherent speech
  • Disturbance of sleep-wake cycle
  • Increased or decreased psychomotor activity
58
Q

List all mental function impairments in Acute confusion state (-)

A

Memory

Perception

Comprehension

Problem-solving

Language

Praxis

Visuospatial function

Emotional behavior

59
Q

Delirium

  • Definition
  • Prognosis
  • S/S
A

Definition: Acute Confusion state with acute decline in attention and cognition

Mortality rate 1-year = 35-40%

S/S:

  • Acute onset with fluctuating course
  • Inattention
  • Disorganized thinking
  • Altered level of consciousness
  • Cognitive deficits
  • Perceptual illusions/ hallucinations
  • Psychomotor disturbance: hyperactive/ hypoactive/ mixed
  • Altered sleep
  • Emotional disturbances
60
Q

Why is delirium underdiagnosed -

A

Features causing under-diagnosis

  • Fluctuating S/S
  • Overlap with dementia
  • No formal system for cognitive assessment
  • Underappreciation of clinical consequences and significance/ importance
61
Q

Delirium -

Pathogenesis

Areas of brain involved

A

Diffuse slowing of cortical background activity, Generalized disruption of higher cortical functions

Disturbances in brain chemistry: Cholinergic deficiency, Dopaminergic excess, Cytokines breakdown BBB, Chronic hypercortisolism

Areas involved:

  • Prefrontal cortex
  • Subcortical structures
  • Thalamus
  • Basal ganglia
  • Frontal and temporoparietal cortex
  • Fusiform cortex
  • Lingual gyri
62
Q

Approach for Delirium

A
  • Formal cognitive testing with MMSE
  • Determine acuity of mental state changes
  • Look for underlying causes: esp. Dementia (major RF)
  • Review medication and alcohol abuse
  • (EEG and neuroimaging have low yield)

Investigations:

Basic Blood baseline, glucose, ketone

ABG for respiratory failure

LP

Septic workup with blood culture

63
Q

Precipitating factors for Delirium

A
64
Q

Conditions that lead to delirium

A

Drugs: sedatives, hypnotics, narcotics, anticholinergics, alcohol or drug withdrawal

Primary neurological diseases: Stroke, Intracranial bleed, meningitis or encephalitis

Intercurrent illness: Infection, AMI, DKA, Hypoxia, Shock, Fever, Anemia, Dehydration, Starvation, Metabolic derangement

Surgeries

Hospital environment: use of physical restraints, use of bladder catheter, admit to ICU

Psychological: Stress, sleep deprivation, chronic pain

65
Q

Prevention of delirium

A
  1. Orientation and therapeutic activities for cognitive impairment
  2. Early mobilization
  3. Use non-pharmacological Tx
  4. Improve sleep
  5. Hydration
  6. Better communication if visual or hearing impairment
66
Q

Management of Delirium

A
  1. Find underlying cause
  2. Supportive
  • ABC, hydration, nutrition
  • No immobilization, Prevent DVT, pressure sores
  • Avoid restraints
  • Provide calm environment with orientating things (clock, calendars, pictures)
  • Frequent communication with staff
  • Improve sleep/ normal sleep
  • Coordinated drug schedule, vitals assessments, procedures

3. Prevent complications

  1. Treat behavioral symptoms: Antipsychotics, Antidepressants, BDZ
67
Q

List 4 drugs for delirium

Indication

A

Only for behavior symptoms with harm to self or others

Antipsychotics - Haloperidol (1st line)

Atypical antipsychotic - Riseperidone, Olanzapine, Quetiapine

BDZ - Lorazepam (2nd line)

Antidepressant - Trazodone

68
Q

Brain Death

Clinical Criteria

A
  1. Coma
  2. No spontaneous respiration/ absolute apnea (CO2 tension above 60 mmHg)
  3. No brainstem reflexes (pupillary, oculocephalic, corneal, gag)
  4. No reversible causes of CNS depression (drug, hypothermia, electrolyte disturbance)
  5. Electrocerebral silence - Isoelectric EEG signal with no cerebrocortical function

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