Consciousness = state of awareness of self and environment. It has two components: Arousal (brainstem function — reticular activating system) and Awareness (high-level integration of multiple sensory inputs — resides in the cerebral cortex). ^[1]

Think of it as a two-layer system:

• Arousal = the "power switch" — is the brain turned on? This is a primitive brainstem function controlled by the ascending reticular activating system (ARAS).
• Awareness = the "software" — can the brain process and integrate information? This resides in the cerebral cortex.

You need BOTH for normal consciousness. Damage to either can produce different clinical states.

The reticular formation is a complex network of brainstem nuclei and neurons spanning the entire brainstem. ^[1]

How the ARAS maintains consciousness ^[1]:

• Projects to the thalamus
• Thalamic relay neurons activate cortical pyramidal neurons
• Tonic mode (desynchronized firing) → wakefulness or REM sleep
• Burst mode (rhythmic, bilateral synchronous firing) → non-REM sleep (produces sleep spindles on EEG)

Why this matters: A lesion in the brainstem (e.g., basilar artery stroke) can knock out the ARAS and produce coma, even though the cortex itself is undamaged. Conversely, diffuse cortical damage (e.g., from hypoxia) can destroy awareness while leaving arousal intact — this is the vegetative state. ^[2]

A same condition, e.g. stroke, can result in any of these states depending on the location and severity. ^[1]

Key discriminators for exams:

• Coma vs. Vegetative state: Vegetative state has sleep-wake cycles (eyes open periodically) but NO awareness
• Vegetative vs. Minimal conscious state: Minimal conscious state shows reproducible purposeful behavior (e.g., visual pursuit, localizing to pain)
• Locked-in syndrome: Full awareness, vertical eye movements preserved — test by asking patient to blink

History to identify potential cause. PE: ABC → GCS → Pupillary reflexes → Obvious focal weakness → Plantar responses → Any trauma → Fever → Neck stiffness ^[1]

The order matters: ABC first (airway, breathing, circulation), then neurological assessment. This is your "30-second survey."

GCS 13-15: Mild | 9-12: Moderate | 3-8: Severe ^[1]

Total range: 3–15

Clinical pearls for GCS:

• Always record the best response
• GCS ≤ 8 → intubation usually indicated (cannot protect airway) ^[1]
• Elicit pain at supraorbital ridge, earlobe, or trapezius squeeze — avoid sternal rub (bruising) ^[2]
• Localizing to pain (M5): hand comes up above the clavicle toward the stimulus
• Flexion withdrawal (M4): elbow flexes but hand does NOT cross the clavicle
• Abnormal flexion/decorticate (M3): internal rotation + pronation + shoulder adduction ± spastic wrist flexion
• Extension/decerebrate (M2): elbow extension + shoulder adduction

Blood/urine tests (routines, glucose, toxins/drug screen), Neuroimaging (based on clinical suspicion), Lumbar puncture, EEG ^[1]

Supportive: ABC, intubation if indicated especially GCS < 8 and cannot protect airway. Specific management depends on the cause identified. ^[1]

Loss of consciousness with complete recovery. Syncope (cardio or cerebrovascular cause) vs. Seizure. History from witness is vital. ^[1]

LOC + muscle jerk does NOT mean seizure. Syncopal myoclonus occurs in up to 20% of patients with syncope. ^[1]

Classification	Remarks
Neurocardiogenic (most common)	Increased vagal tone — vasovagal syncope, situational syncope (micturition/defecation)
Cardiac (most lethal)	MI, arrhythmia, valvular heart disease, cardiac tamponade, PE
Neurological	Seizure; Others (less common): posterior circulation TIA, subclavian steal, complex migraine
Orthostatic	Drop in systolic BP > 20 mmHg on standing — Drug, volume loss, autonomic dysfunction
Unknown	Need to rule out potential life-threatening causes

This table is directly from the lecture slides and is extremely high yield ^[1]:

Seizure: Sudden burst of electrical activity in the brain leading to changes in movement, behavior, feeling and/or consciousness. ^[1]

Diagnosis of seizure: CAREFUL HISTORY IS MOST IMPORTANT. Suggestive features: transient occurrence of abnormal behavior, involuntary movements, recurrent/stereotypical attack. ^[1]

Epilepsy: Brain disorder that causes recurring, unprovoked seizures. ^[1]

Abnormal synchronous brain activity caused by abnormal spread & neuronal recruitment secondary to: (1) Enhanced excitatory transmission, (2) Failure of inhibitory mechanism, (3) Changes in intrinsic neuronal properties. ^[1]

In simple terms: neurons that normally fire independently get "recruited" into synchronized, self-sustaining bursts of activity. This can happen because excitation (glutamate) is too high, inhibition (GABA) is too low, or the neurons themselves have abnormal membrane properties (e.g., ion channel mutations).

This is a classic exam topic — "what else could it be?" ^[1]

These four clinical vignettes from the lecture are extremely exam-relevant ^[1]:

At least two unprovoked seizures occurring > 24 hours apart ^[1]

OR One unprovoked seizure and > 60% chance of recurrence in the next 10 years, supported by: ^[1]

• Abnormal epileptiform discharges on EEG
• Structural brain pathology
• Abnormal neurological examination beyond postictal period (focal findings or intellectual disability)
• Nocturnal seizure

This means a single seizure CAN lead to a diagnosis of epilepsy if the recurrence risk is sufficiently high — you don't always need to wait for a second seizure.

Incidence has two peaks: (1) Childhood — genetic/polygenetic/unknown, (2) ≥65 years — structural (including neurodegenerative diseases). Prevalence ~1% in adults; in ≥65 years: 2-6%. ^[1]

The lecture uses a structured etiological framework ^[1]:

Common cause of temporal lobe seizure. Onset typically adolescent/young adult. ^[1]

Common idiopathic generalized epilepsy syndrome. Onset typically 10-24 years, female preponderance. Normal development and cognition. ^[1]

Previously known as epilepsy with grand mal seizure. Onset 10-25 years. Normal development and cognition. Precipitated by sleep deprivation/alcohol. ^[1]

To detect abnormal electrical activities (epileptiform discharges) in the brain. ^[1]

The diagnosis of seizure/epilepsy is almost ALWAYS based on clinical history (usually from witness). ^[1]

Key points from lecture ^[1]:

• Around 50% of epilepsy patients have normal interictal EEG → A normal EEG does NOT rule out epilepsy
• Common to have false positive/borderline positive EEG → overdiagnosis of epilepsy
• Main uses of EEG:
  1. Support diagnosis of epilepsy
  2. Risk stratification for initiation of ASM
  3. Diagnosis of ongoing seizure / non-convulsive status epilepticus
• You are NOT expected to know how to interpret EEG, but only know WHEN to order one ^[1]

EEG patterns mentioned in lecture (for recognition, not interpretation):

• Left temporal epileptiform discharge → hippocampal sclerosis
• Generalized spike-and-wave discharge → JME
• Continuous 2 Hz sharp-and-wave over R brain → focal status epilepticus
• Continuous generalized 3-4 Hz spike-and-wave → generalized non-convulsive status epilepticus

Look for structural lesions. Brain imaging may be normal in many patients. CT for obvious lesions. MRI would probably be needed for ALL patients without obvious structural lesion on CT. ^[1]

Imaging examples from slides: Left frontal meningioma, mesial temporal sclerosis, left frontobasal cavernoma ^[1]

Blood test for electrolytes, glucose, kidney/liver function; further blood test like immune workup/autoimmune encephalitis antibody panel/toxicology screen as appropriate. Lumbar puncture for CSF as appropriate. ^[1]

1. Ensure full recovery (not in status epilepticus). 2. Rule out acute, potentially reversible causes (vascular, infection, inflammation, metabolic, toxic). 3. Make sure it's the FIRST seizure (patient may have recurrent behavioral arrest/myoclonus that family/patient is unaware is relevant). 4. Assess risk of recurrence (epilepsy diagnosis) — EEG/neuroimaging. ^[1]

Diagnosis of epilepsy has considerable effect on mood, interpersonal relationship, employment, quality of life and ability to drive. ^[1]

Driving in HK → report to transport department. No specific regulation for when patients with epilepsy can drive, hence usually cannot drive indefinitely. ^[1]

Avoid activities with ↑ risk of injury if seizure occurs: driving, operating high-risk equipment, working at heights, swimming/hiking alone, cooking over fire alone. ^[1]

Risk of SUDEP (Sudden Unexpected Death in Epilepsy) ~1/1000. Risk reduced with better control of epilepsy. ^[1]

Used to be known as antiepileptic drugs (AED). Drugs that suppress seizure by changing neurotransmission. ^[1]

Most act through a primary pathway but also have effect on other pathways. ^[1]

Factors: Drug effectiveness (focal vs. generalized), potential adverse effects, childbearing plans, drug interactions, comorbid medical conditions (hepatic/renal disease), patient preference, cost. ^[1]

Response to 1st ASM: ~50%. Response to 2nd ASM: additional ~15%. Response to 3rd ASM or multiple drug: additional ~5%. ^[1]

Drug-resistant/refractory epilepsy: 1/3 of patients. Defined as failed to become seizure free with adequate trial of TWO antiseizure medications (either monotherapy or combination). ^[1]

Continuous convulsive seizure for more than 5 minutes; OR Failed to regain consciousness after seizure. Non-convulsive status epilepticus (up to 60% of SE are non-convulsive). Frequent, recurrent seizures close together. ^[1]

MEDICAL EMERGENCY. Recognition of status epilepticus is important, as prolonged seizure will lead to neuronal damage. Aim to abort seizure within the 1st hour. The longer the seizure, the more difficult it can be aborted. ^[1]

Acute cerebral insult: CNS infection (e.g., HSV encephalitis), autoimmune encephalitis, stroke, brain tumor, metabolic encephalopathy. Withdrawal/Stop ASM. ^[1]

Close neuro-observation. Consider ICU admission. Ensure ABC. Prompt initiation of ASM. Continuous EEG monitoring. Workup and treat possible underlying cause (tumor, infection, CNS infection, autoimmune encephalitis, metabolic). Prevent complications. ^[1]

Brain death = brainstem death = irreversible cessation of brainstem function. Despite philosophical arguments, brain death = death legally in common law jurisdiction. After certified brain death, patient is medically certified dead. ^[1]

Brain death is diagnosed when there is: (1) Severe, irreversible brain injury (patient in coma, usually confirmed with neuroimaging); (2) Exclusion of potentially reversible causes; (3) Absent brainstem reflexes. ^[1]

Waiting time after brain injury: at least 4 hours; 24 hours for CPR. ^[1]

Hong Kong brain death certification: Done by 2 separate doctors — one specialist of appropriate college (ICU, Neurologist, Neurosurgery) and another at least 6 years after registration. ^[1]

Before testing brainstem reflexes, you MUST confirm: ^[1]

1. Irreversible severe brain injury
2. Neuromuscular function is intact (no paralytic agents)
3. Absence of depressant drugs
4. Absence of reversible causes contributing to comatose state
5. Ensure normothermic, correct metabolic/electrolyte disturbance, stable hemodynamic

Only done when: (1) No clear cause of coma; (2) Possible metabolic/drug effect; (3) Any brainstem test cannot be completed. ^[1]

Neuroimaging: Brain perfusion imaging or four-vessel DSA to demonstrate absent brain perfusion/flow. ^[1]

The lecture defines altered mental state/delirium as any acute change in attention/awareness or cognition ^[1]. Key features from supporting material ^[2]:

• Acute onset with fluctuating course (hallmark)
• Impaired attention (cardinal feature — test with serial 7s, digit span)
• Disturbed sleep-wake cycle
• Perceptual disturbances (visual hallucinations common)
• Hyperactive vs. hypoactive vs. mixed subtypes

Delirium vs. Dementia: Delirium is acute with fluctuating attention; dementia is chronic with preserved attention early on. But they frequently co-exist — 2/3 of delirium occurs in patients with underlying dementia. ^[2]

From GC 051: Anti-NMDA receptor encephalitis — most commonly affects young women and children, associated with ovarian teratomas. Presents with: viral prodrome → neuropsychiatric symptoms → abnormal movements (orofacial/limb dyskinesias) → seizures → altered consciousness → autonomic dysfunction.

From supporting material: West Haven Criteria grades 0-4. Grade 2+ = asterixis (flapping tremor). Mechanism: ↑ ammonia crosses BBB → astrocyte swelling → cerebral edema. Management: lactulose, rifaximin, treat precipitants.

1. A 70-year-old man collapses while shaving and has brief limb jerking lasting 5 seconds. He recovers within 2 minutes and is fully oriented. What is the most likely diagnosis?

   • Answer: Syncope with syncopal myoclonus (NOT seizure — jerking was brief, after LOC, rapid recovery)

2. An 18-year-old woman has morning myoclonic jerks and a GTCS. EEG shows 3-5 Hz generalized spike-wave. Which drug should be AVOIDED?

   • Answer: Carbamazepine/Phenytoin (can worsen myoclonic seizures in JME)

3. Which ASM follows zero-order kinetics?

   • Answer: Phenytoin

4. Which ASM must require HLA-B*1502 testing before prescription?

   • Answer: Carbamazepine (risk of SJS/TEN if positive)

5. A patient with epilepsy and liver cirrhosis needs an ASM. Which is preferred?

   • Answer: Levetiracetam (not P450 dependent, renally excreted)

6. Describe the step-wise management of status epilepticus. (5 marks)

   • ABC + O2; Hstix → thiamine → dextrose if low; Resume usual AED if known epilepsy; Stage 1: IV lorazepam 4mg; Stage 2: IV phenytoin 20mg/kg or IV valproate 20-40mg/kg; Stage 3: consider GA; Continuous EEG; Identify cause; Prevent complications

7. List the preconditions that must be met before brain death testing. (5 marks)

   • Irreversible severe brain injury; intact neuromuscular function; absence of depressant drugs; absence of reversible causes; normothermic; correct metabolic/electrolyte disturbance; stable hemodynamics

8. A 25-year-old woman has recurrent epigastric aura → behavioral arrest → oral automatisms. MRI shows right hippocampal sclerosis. (a) What is the diagnosis? (b) What is the first-line ASM? (c) If drug-resistant, what is the surgical option?

   • (a) Mesial temporal lobe epilepsy with hippocampal sclerosis; (b) Lamotrigine or levetiracetam (woman of childbearing age); (c) Anterior temporal lobectomy or hippocampectomy (60-70% seizure freedom)