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]:

• Sensory and visceral inputs converge on the brainstem reticular formation, which projects through the thalamus to widespread cortex; this broad projection explains why a small strategic brainstem lesion can impair arousal profoundly
• Thalamic relay neurons activate cortical pyramidal neurons, while the descending reticular system influences tone and autonomic function
• 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 abolish behavioural evidence of awareness while leaving arousal intact—a pattern seen in VS/UWS. ^[2][12]

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. VS/UWS: VS/UWS has sleep-wake cycles (eyes open periodically) but no behavioural evidence of awareness
• VS/UWS vs. MCS: MCS 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
• A low GCS should trigger urgent airway assessment, but GCS alone does not prove inability to protect the airway; intubate when airway protection, ventilation or oxygenation is inadequate, using the whole clinical picture
• 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; intubate when airway protection, oxygenation or ventilation is inadequate. 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 mimics	Seizure; very rarely posterior-circulation ischaemia with focal neurological features. These are not mechanisms of true syncope
Orthostatic	Sustained fall in systolic BP ≥20 mmHg or diastolic BP ≥10 mmHg after standing (classically within 3 minutes) — drugs, volume loss, autonomic dysfunction [14]
Unknown	Need to rule out potential life-threatening causes

The visual hierarchy is the clinical lesson: reflex syncope is common, but cardiac syncope is the dangerous diagnosis not to miss. Obtain a 12-lead ECG and look for exertional/supine events, structural heart disease, family history of sudden death, chest pain or palpitations; jerks do not make the episode epileptic.

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% probability of further seizures over the next 10 years ^[16]

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

The third ILAE route is diagnosis of an epilepsy syndrome. A single seizure can therefore lead to an epilepsy diagnosis, but an epileptiform EEG or structural lesion does not automatically cross the ≥60% threshold; risk is individualized to the specific syndrome, lesion and clinical context. Diagnosis and the decision to start long-term treatment are related but distinct. ^[16]

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):

• The cap photograph shows that EEG records voltage differences between scalp electrodes; the displayed channels are a montage, not one trace per brain region
• The normal example shows an organized background without epileptiform discharges
• A left temporal epileptiform discharge is maximal over left temporal chains and supports a left temporal epileptogenic tendency; in the illustrated case it fits hippocampal sclerosis
• A generalized spike-and-wave discharge appears bilaterally synchronous across the montage and supports a generalized epilepsy such as JME
• Continuous 2 Hz lateralized sharp-and-wave activity and continuous generalized 3-4 Hz spike-and-wave activity illustrate patterns concerning for focal or generalized non-convulsive status, respectively—but EEG criteria require clinical context and expert interpretation

Do not use EEG as a screening test for unexplained blackout or to exclude epilepsy. When the history suggests an epileptic seizure, EEG supports diagnosis and classification; a normal routine EEG may be followed by sleep-deprived or ambulatory EEG if uncertainty persists. ^[18]

Look for structural lesions. Brain imaging may be normal in many patients. CT is useful acutely; epilepsy-protocol MRI is the preferred structural study when indicated. ^[1][18]

How to read the slide images ^[1]:

• Left frontal meningioma on CT: extra-axial frontal mass with surrounding low-density vasogenic oedema and local mass effect—a plausible structural seizure focus
• Mesial temporal (hippocampal) sclerosis on coronal T2 MRI: asymmetric hippocampal volume loss, increased T2/FLAIR signal and enlargement of the ipsilateral temporal horn; compare the two hippocampi rather than looking only at the arrow
• Left frontobasal cavernoma on MRI: a well-circumscribed mixed-signal “popcorn” lesion with a hemosiderin rim; prior microhaemorrhage makes it epileptogenic

Current NICE guidance offers MRI after an epilepsy diagnosis unless the presentation is a typical idiopathic generalized epilepsy or self-limited epilepsy with centrotemporal spikes; CT is an alternative when MRI is contraindicated and remains the practical acute test for haemorrhage or a large mass. ^[18]

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 Hong Kong: epilepsy is a specified condition in the Road Traffic (Driving Licences) Regulations. A licence holder who develops it must notify the Commissioner for Transport in writing; driving fitness/licensing is then an individual legal and medical determination. Do not replace this with the slide's blanket “cannot drive indefinitely” statement, and check the current Transport Department process. ^[19]

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]

Treat a convulsive seizure lasting 5 minutes, or recurrent seizures without recovery to baseline between events, as convulsive status epilepticus. Persistent impaired consciousness after convulsions stop also raises concern for non-convulsive status and should prompt urgent EEG when available. ^[1][21]

MEDICAL EMERGENCY. Do not wait for an hour: time and treat from the 5-minute threshold while managing ABC, glucose and reversible causes. Longer duration reduces the probability of medication response. ^[1][21]

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]

Current Hong Kong guidance (2023): all preconditions must remain satisfied through a minimum 4-hour observation period before the first formal examination. The total observation period is extended to 24 hours for hypoxic-ischaemic encephalopathy after cardiorespiratory arrest. After targeted temperature management below 35°C for more than 6 hours, testing is generally delayed until 24 hours after rewarming to ≥36°C, with longer delay considered after deeper hypothermia or prolonged sedatives. ^[22]

Certification requires two separate examinations, each by a different medical practitioner. One must be a designated specialist (usually intensive care/critical care, neurology or neurosurgery); the other should preferably have the same qualification and must be at least 6 years after registration with the required skill and knowledge. The transplant retrieval team must not determine brainstem death. ^[22]

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

The 2023 Hong Kong guideline makes the prerequisites operational: the patient must be apnoeic and mechanically ventilated; exclude lingering sedatives/poisons and neuromuscular blockade (confirm intact neuromuscular conduction); core temperature should be > 35°C; and major metabolic/endocrine derangements and hypotension (SBP ≤90 mmHg or MAP ≤60 mmHg) must not confound the examination. These notes are a conceptual summary, not a certification checklist—use the hospital form and current HKSCCM guidance. ^[22]

Objective demonstration of absent intracranial blood flow is required when clinical preconditions cannot be satisfied or brainstem testing is incomplete—for example unclear cause, possible metabolic/drug confounding, cranial nerves cannot be tested, cervical cord injury, or cardiovascular/respiratory instability precluding apnoea testing. A confirmatory study does not make an elicitable brainstem response acceptable. ^[22]

Accepted Hong Kong examples: four-vessel digital-subtraction angiography showing absent vertebrobasilar and supratentorial intracranial flow, or radionuclide perfusion imaging/SPECT with a tracer that crosses the blood-brain barrier. ^[22]

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.