Neurological — Clinical Knowledge

GCS — Glasgow Coma Scale

The GCS measures level of consciousness across three components. Total score (3–15) guides TBI severity classification and clinical decision-making. Scores should be documented as component scores (e.g. E3V4M5) rather than the total alone.

Component	Response	Score
Eyes (E)	Spontaneous opening	4
	Opens to voice	3
	Opens to pain	2
	No response	1
Verbal (V)	Orientated	5
	Confused	4
	Inappropriate words	3
	Incomprehensible sounds	2
	No response	1
Motor (M)	Obeys commands	6
	Localises pain	5
	Withdraws from pain	4
	Abnormal flexion (decorticate)	3
	Extension (decerebrate)	2
	No response	1

Mild TBI

13–15

Headache, dizziness, memory and concentration problems, blurred vision. Patient typically alert and conversant.

Moderate TBI

9–12

Slurred speech, profound confusion. Requires close monitoring and transport to major trauma centre.

Severe TBI

3–8

Seizures, persistent headache, coma. High risk of secondary brain injury. Requires immediate intervention.

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GCS 8 or Below — Airway at Risk

A GCS ≤8 indicates significantly impaired consciousness. Protective airway reflexes are unreliable. Consider advanced airway management and evaluate for RSI. Also consider pharmacological management of seizures if GCS ≤12 with ongoing or suspected seizure activity.

AVPU Scale

Level	Description	Approx. GCS
A — Alert	Fully awake and responsive	15
V — Voice	Responds to verbal stimuli	~13
P — Pain	Responds only to painful stimuli	~8
U — Unresponsive	No response to any stimuli	3

Disability — Primary Survey

→Level of consciousness (AVPU or GCS)
→Pupillary assessment — size, equality, reactivity
→Blood glucose level (BGL) — rule out hypoglycaemia
→Posturing — decorticate vs decerebrate
→Lateralising signs — focal weakness, speech, gaze preference

Pupillary Assessment

Finding	Description	Clinical Significance
Equal and reactive	Both pupils constrict briskly to light	Normal finding
Unilateral fixed and dilated	One pupil unreactive, larger than the other	Uncal herniation — ipsilateral CN III compression; neurosurgical emergency
Bilateral fixed and dilated	Both pupils unreactive and large	Severe raised ICP, brainstem herniation, or cardiac arrest
Bilateral pinpoint	Both pupils very small, poorly reactive	Opioid toxicity, pontine lesion, organophosphate poisoning
Anisocoria	Unequal pupil size	May be benign (physiological) but new onset suggests pathology

Cerebral Perfusion Pressure (CPP)

The brain requires a constant supply of oxygen and glucose — accounting for approximately 20% of systemic blood flow. Cerebral blood flow depends on the cerebral perfusion pressure.

Cerebral Perfusion Pressure

CPP = MAP − ICP

Normal ICP

7–15 mmHg

Any rise must be compensated by reduction in brain, blood or CSF volume (Monroe-Kellie Doctrine)

Normal MAP

70–110 mmHg

MAP = Diastolic + (Systolic − Diastolic) ÷ 3

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Monroe-Kellie Doctrine

The total volume of intracranial contents (brain tissue, blood, CSF) must remain constant. Any increase in one component must be compensated by a decrease in another — otherwise ICP rises. Rising ICP compresses cerebral vasculature, reducing CPP and causing ischaemia.

Abnormal Posturing

Decorticate Posturing

→Arms flexed, wrists and fingers flexed inward
→Legs extended and internally rotated
→Indicates damage above the brainstem (cortical level)
→Less ominous than decerebrate but still serious

Decerebrate Posturing

!Arms extended, pronated and rigid
!Legs extended with plantar flexion
!Indicates brainstem dysfunction or compression
!More ominous — indicates severe neurological injury

Pathophysiology

Stroke occurs when blood flow to part of the brain is interrupted, leading to neuronal injury and cell death. Brain tissue requires a constant supply of oxygen and glucose — it has no energy stores and cell death begins within minutes of ischaemia. The chain of survival for stroke mirrors that of cardiac arrest: early recognition, activation, and definitive care are critical.

Ischaemic Stroke (Most Common)

→Thrombus — clot develops in situ within a cerebral artery (atherosclerosis)
→Embolus — clot travels from elsewhere (e.g. cardiac source in AF)
→Reduction in blood flow → decreased O₂ and glucose delivery → infarction
→Most clots occur in the middle cerebral artery
✓Outcomes can be positive with timely reperfusion therapy

Haemorrhagic Stroke (Less Common)

!Rupture of an intracranial vessel — hypertension, aneurysm, trauma, anticoagulants
!Intracranial haemorrhage → increased ICP → reduced cerebral perfusion
!Reduced O₂ and glucose → infarction
!ALOC is a red flag suggesting haemorrhagic cause
!Outcomes have not improved with modern treatment; thrombolysis is contraindicated

TIA — Transient Ischaemic Attack

A TIA is a brief episode of neurological dysfunction caused by temporary disruption to blood flow. It does not result in permanent damage, with symptoms typically resolving within minutes to a few hours. Despite symptom resolution, TIA is a critical warning sign of increased stroke risk and requires urgent clinical assessment. All patients with fluctuating symptoms at the time of assessment should be treated as if having a stroke.

Vascular Territory Presentations

Artery	Area Supplied	Key Clinical Features
Middle Cerebral (MCA) Most Common	Frontal, temporal, parietal lobes; internal capsule	Contralateral hemiparesis (face/arm > leg), contralateral sensory loss, homonymous hemianopia, aphasia (dominant hemisphere), neglect (non-dominant hemisphere)
Anterior Cerebral (ACA)	Medial frontal and parietal lobes	Contralateral weakness and sensory loss (leg > arm), urinary incontinence, behavioural changes; uncommon
Posterior Cerebral (PCA)	Occipital and temporal lobes	Visual field defects (homonymous hemianopia), cortical blindness, memory impairment; possible hemiparesis and speech deficits
Vertebrobasilar — Cerebellar	Cerebellum	Impaired balance and coordination, gait ataxia, abnormal finger-nose test, vertigo, nausea, vomiting; often missed by standard tools
Vertebrobasilar — Brainstem	Pons, medulla, midbrain	Hemiparesis or quadriparesis, sensory loss, ALOC, cranial nerve deficits, abnormal respirations, "locked-in syndrome" (pontine); critically unwell

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Posterior Circulation — Frequently Missed

Posterior circulation strokes are commonly not captured by standard prehospital stroke tools such as FAST. Maintain suspicion in patients presenting with acute vertigo, ataxia, diplopia, or crossed syndromes (cranial nerve signs on one side, motor deficits on the other). The HINTS exam can assist in differentiating central from peripheral causes of vertigo.

Dominant vs Non-Dominant Hemisphere

Left Hemisphere (Dominant in most)

→Aphasia — expressive or receptive language deficit
→Right-sided motor and sensory deficits
→Alexia, agraphia (reading and writing impairment)

Right Hemisphere (Non-dominant)

→Left-sided motor and sensory deficits
→Neglect — patient unaware of left side of body/environment
→Gaze preference toward right; spatial and perceptual deficits

Stroke Mimics — MINT

Conditions that can present with stroke-like symptoms. Must be actively excluded before stroke management is initiated.

Category	Examples	Distinguishing Feature
M — Metabolic	Hyper/hypoglycaemia, hyponatraemia, hypoxia, encephalopathy	BGL check; corrects with treatment
I — Infectious	Bell's Palsy, CNS abscess, meningitis, encephalitis	Fever, infectious prodrome, rash
N — Neurological	Todd's paresis post-seizure, brain tumour, multiple sclerosis, migraine with aura	Prior seizure history; progressive rather than sudden onset
T — Toxins	Drug toxicity, carbon monoxide, alcohol intoxication	Exposure history; affects multiple systems

Stroke Chameleons — Presentations That Mimic Other Conditions

!Confusion or delirium (may be dismissed as dementia or psychiatric)
!Pinpoint pupils, ALOC, and respiratory depression (mimics opioid toxicity — brainstem stroke)
!Acute vertigo (may be attributed to BPPV — posterior circulation stroke)
!Severe hypertension without other features (can be cause or consequence of stroke)

Prehospital Assessment Tools

NIHSS-8 Stroke Tool

Severity Score

Scores level of consciousness, gaze, facial palsy, limb motor, ataxia, sensory, language, and neglect. Score ≥8 with MRS 0–3 and <60 min from EVT centre → refer for large vessel occlusion.

Modified Ranking Scale (MRS)

Baseline Function

Assesses pre-stroke functional status (0–6 scale). MRS 0–3 = independent or mildly dependent. Required alongside NIHSS-8 to determine EVT eligibility.

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ACT-FAST — Large Vessel Occlusion (LVO)

The ACT-FAST tool is used specifically to detect large vessel occlusions in anterior circulation strokes. It assesses arm weakness, leg weakness, and speech changes. LVO candidates are prioritised for direct transport to EVT-capable stroke centres.

Time Windows — Reperfusion Therapy

IV Thrombolysis

4.5 hrs

Alteplase (tPA). Potentially disabling ischaemic stroke within 4.5 hours. Must rule out haemorrhagic stroke. Not for mild stroke.

Endovascular Clot Retrieval (EVT)

24 hrs

Thrombectomy effective for occlusions of ICA, MCA ± basilar artery. One of the most effective treatments available. Requires NIHSS-8 ≥8 and MRS 0–3.

Haemorrhagic Stroke

No lysis

BP control, anticoagulant reversal, minimal surgical intervention. Thrombolysis is absolutely contraindicated.

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Time is Brain

Approximately 1.9 million neurons are lost every minute during a stroke. All stroke patients must be managed as time-critical emergencies with the highest dispatch priority. Code 1 transport with pre-notification is mandatory for all suspected strokes — early hospital activation significantly improves outcomes. Fast vs slow processors: some patients maintain perfusion via collateral pathways; others lose tissue rapidly.

Prehospital Stroke Management

1

PPE and scene safety. Approach, assess scene, ensure safety.
2

Primary survey — ABCDE. Airway, breathing, circulation, disability (GCS, pupils), exposure. Request secondary officer to obtain 4-lead ECG, SpO₂, BP, temperature, BGL and RR simultaneously.
3

Secondary survey and history. Determine time of symptom onset — critical for thrombolysis/EVT eligibility. Medications, allergies, past medical history. Assess for stroke mimics (MINT).
4

Stroke screening. NIHSS-8 score and Modified Ranking Scale. If NIHSS-8 ≥8 AND MRS 0–3 AND <60 minutes from EVT centre — refer for LVO. Otherwise, acute stroke referral pathway.
5

Interventions. Supplemental O₂ only if SpO₂ <94%. IV access. Antiemetic if required. Do not administer antihypertensives unless specifically directed by stroke protocol — BP may be a protective response.
6

Positioning and transport. Position at 45° — balances cerebral perfusion and minimises oedema. Pre-notify receiving facility. Code 1 transport. Reassess during transport. Thrombolysis window: within 9 hours. EVT window: within 24 hours.

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Facility Selection

Not all hospitals can manage stroke patients. Choosing the right facility and pre-notification are critical. For suspected LVO, direct transport to an EVT-capable centre should be prioritised where within time window, even if it bypasses a closer facility. Retrieval Services QLD coordinates advanced transport as required.

Definition and Mechanisms

A seizure is a transient disturbance of cerebral function caused by abnormal, excessive neural electrical discharge. Mechanisms include: altered cell membrane permeability, abnormal ion distribution, reduced inhibitory neural activity (GABAergic suppression), and structural neuronal changes that increase excitability. Seizures may be provoked (identifiable cause) or unprovoked (no identifiable cause). Recurrent unprovoked seizures (≥2 in a year) lead to an epilepsy diagnosis.

Provoked Seizures — Common Causes

→Hypoglycaemia — most important reversible cause; always check BGL
→Electrolyte imbalance (sodium, calcium, magnesium)
→Fever (especially in children — febrile seizures)
→Drugs/toxins — recreational substances, withdrawal
→Hypoxia, CNS infection, TBI, stroke

AEIOU TIPS — Altered Consciousness Causes

→Alcohol/drugs, Epilepsy, Infection, Overdose, Uraemia
→Trauma, Insulin (BGL), Psych, Stroke/structural

Seizure Classification

Type	Onset	Clinical Features
Focal (Partial)	One brain area (frontal or temporal lobe most common)	Altered consciousness, dream-like state, automatisms (lip-smacking, blinking, pacing), sensory/visual/auditory phenomena; consciousness may or may not be impaired
Tonic–Clonic (Grand Mal)	Generalised — both hemispheres	Abrupt loss of consciousness, possible aura; tonic phase: rigidity, extended limbs, apnoea, cyanosis; clonic phase: rhythmic symmetric jerking; post-ictal flaccidity. Duration 60–90 seconds. Urinary incontinence common.
Absence (Petit Mal)	Generalised	Brief (seconds), abrupt loss of consciousness without loss of postural tone; staring, eyelid twitching; no post-ictal phase; resumes activity immediately on cessation
Tonic	Generalised	Sustained muscle stiffening without clonic phase
Myoclonic	Generalised	Brief, sudden muscle jerks/twitches; often bilateral; may occur in clusters
Atonic (Drop Attack)	Generalised	Sudden loss of muscle tone; patient falls abruptly; injury risk is high

Post-Ictal State

Following a seizure, it is common for the patient to have an altered level of consciousness with drowsiness, confusion, agitation or amnesia. This is the post-ictal state and typically lasts 5–60 minutes. Patients are not usually competent to consent during this phase. Subtle seizure activity may persist even when the patient appears post-ictal — suspect ongoing seizures if you observe:

!Rhythmic eye movements or deviation
!Persistently dilated pupils
!Persistent tachycardia without improvement
!Failure to improve in GCS over 20–30 minutes

Status Epilepticus

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Neurological Emergency

Status epilepticus is defined as a seizure lasting ≥5 minutes, or recurrent seizures without recovery of consciousness between episodes. Risks include hypoxia, hypercapnia, metabolic acidosis, hyperthermia, aspiration pneumonia and permanent neurological damage. Longer duration makes pharmacological termination increasingly difficult — early intervention is essential.

Escalating Management of Status Epilepticus

1

Airway, O₂, BGL. Protect airway, apply oxygen, check blood glucose — hypoglycaemia is a treatable cause. IV/IO access. Continuous monitoring.
2

Midazolam first-line. IM, IV or intranasal. Adult: 5–10 mg. Repeat dose if no effect. Enhanced GABA inhibition terminates seizure in most cases.
3

Levetiracetam second-line. IV infusion if midazolam fails. Sodium channel and GABA modulation. Less respiratory depression than benzodiazepines.
4

RSI / anaesthetic agents. If pharmacological benzodiazepine and second-line agents fail, RSI and propofol/thiopentone infusion under anaesthetic supervision. Requires retrieval or in-hospital escalation.

Special Seizure Types

Type	Context	Key Management Points
Febrile Seizure	Age 6 months–5 years; associated with rapid rise in temperature (≥38°C), usually viral	Generally self-limiting. Do not aggressively cool unless temp >40°C. Must rule out bacterial causes (meningitis, UTI, pneumonia). Reassure caregivers.
Eclamptic Seizure	Seizures in pregnancy or postpartum associated with pre-eclampsia (hypertension + proteinuria)	High risk to mother and foetus. First-line: magnesium sulphate. Position in left lateral decubitus. Urgent transport. Fetal monitoring.
Drug-Induced Seizure	Synthetic cannabinoids, cocaine, MDMA, amphetamines, opioid withdrawal; often self-limiting	Usually self-limiting. Clinical judgement needed around transport — forcible assessment may require sedation which can be more harmful. Benzodiazepines if prolonged.
PNES (Psychogenic Non-Epileptic Seizure)	Psychological origin, not abnormal electrical activity; caused by stress, trauma, anxiety	Eyes often closed; trembling with limp (not rigid) body; prolonged duration; sharp recovery without post-ictal confusion. Sensitive handling; referral to specialist required.

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PNES vs Epileptic Seizure — Cannot Be Reliably Distinguished Clinically

Healthcare personnel cannot reliably distinguish PNES from epileptic seizures in the prehospital environment without EEG confirmation. Treat as presumed epileptic if clinically indistinguishable, particularly in a first-presentation patient. PNES requires sensitive, non-confrontational management and specialist follow-up.

Prehospital Seizure Management

1

Scene safety and differential diagnosis. Consider whether the event is a seizure, syncope, hypoglycaemia, cardiac event or intoxication. Gather collateral history from bystanders.
2

Protect from injury. Clear surrounding hazards. Do not restrain limbs. Place in lateral position if airway is at risk. Cushion head. Do not insert anything into the mouth.
3

Vital signs and BGL. GCS, SpO₂, blood pressure, temperature. BGL — administer glucose if hypoglycaemic. Time the seizure duration.
4

Pharmacological intervention if seizure is ongoing or GCS ≤12. Follow benzodiazepine protocol (Midazolam). Maintain oxygen and airway adjuncts. Support ventilation if required.
5

Assess for status epilepticus. If ≥5 minutes without recovery, escalate to status epilepticus protocol. Consider levetiracetam. Transport to ED with pre-notification.

Overview

TBI is defined as an acute brain injury resulting from mechanical energy to the head from external forces. It is the largest contributor to morbidity and mortality in trauma, and the leading cause of mortality in individuals under 45 years. A significant external force can cause bleeding, swelling, tearing and contusions of the meninges and brain parenchyma. The brain is normally protected by the skull, CSF and meninges — disruption of any of these layers can be catastrophic.

Primary Brain Injury

Relates to the initial mechanical injury — occurring at the moment of impact. Cannot be reversed in the prehospital setting. Classified as focal or diffuse.

Focal Injuries

→Cerebral contusion — bruising of brain tissue following significant impact
→Cerebral laceration — penetrating impact tears brain tissue
→Extradural (epidural) haematoma — haemorrhage between dura mater and inner skull; often associated with skull fracture and arterial bleeding (middle meningeal artery). Classic "lucid interval" then rapid deterioration.
→Subdural haematoma — haematoma between dura and brain surface; rupture of bridging veins; common in elderly with brain atrophy
→Intracerebral haemorrhage — usually due to haemorrhagic stroke or aneurysm

Diffuse Axonal Injury (DAI)

→Affects large areas of the brain simultaneously
→Caused by rapid acceleration-deceleration — shearing, tearing and stretching forces applied to axons
→Widespread microscopic damage to white matter
→Associated with immediate loss of consciousness; CT may appear deceptively normal
→Major cause of persistent vegetative state and long-term disability

Secondary Brain Injury

Secondary injury develops in the hours to days after the primary insult. Unlike primary injury, it is potentially preventable — and is the primary focus of prehospital neuroprotection.

Intracranial Causes

!Expanding extradural/subdural haematoma → rising ICP
!Vasogenic oedema — disruption of capillary integrity → fluid leaks into extracellular space
!Cytotoxic oedema — disruption of cell membrane → intracellular swelling (ischaemia-driven)
!Seizures → increased metabolic demand → worsens ischaemia

Extracranial (Systemic) Causes

!Hypoxia — injured brain needs more O₂; any SpO₂ drop rapidly worsens outcome
!Hypotension — reduces MAP → reduces CPP → cerebral ischaemia
!Hypercarbia — CO₂ retention causes cerebral vasodilation → worsens ICP
!Hypocarbia — excessive ventilation causes cerebral vasoconstriction → ischaemia
!Hypertension, acidosis, hyperthermia — each impairs cerebral autoregulation

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The Lethal Triad of Secondary Brain Injury

Hypoxia + Hypotension + Hypercarbia — each independently worsens outcome. Even a single episode of hypotension (SBP <90 mmHg) or hypoxia (SpO₂ <90%) in the prehospital phase is associated with significantly increased mortality. Prevent and correct aggressively.

Cushing's Triad — Raised ICP

Cushing's Triad is the body's response to critically raised ICP — a final compensatory attempt to maintain cerebral perfusion. Its appearance is a precursor to brain herniation and potential fatal outcome.

Hypertension

Raised BP

Body increases MAP to overcome rising ICP and maintain CPP. Widened pulse pressure.

Bradycardia

Slow HR

Baroreceptor response to hypertension triggers compensatory vagal bradycardia.

Irregular Respirations

Abnormal RR

Brainstem compression disrupts respiratory centres. May present as Cheyne-Stokes or agonal breathing.

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Herniation — Immediately Life-Threatening

Cushing's Triad signals impending transtentorial (uncal) herniation — the temporal lobe herniates through the tentorium cerebelli, compressing CN III (ipsilateral fixed dilated pupil) and the descending corticospinal tract (contralateral hemiplegia). Treat with hyperventilation to reduce PaCO₂ (target 35 mmHg) and urgent transport. Mannitol may be considered at CCP level.

Signs and Symptoms of Raised ICP

Early Signs

→Headache (typically worse in morning)
→Nausea and vomiting
→Restlessness, agitation, drowsiness
→Slurred speech
→Papilloedema (swelling of optic nerve)

Late / Critical Signs

!Reduced GCS / Coma
!Seizures
!Abnormal posturing (decorticate or decerebrate)
!Unequal or fixed/dilated pupils
!Cushing's Triad — herniation imminent

Prehospital TBI Management

1

Recognise severity. GCS — mild (13–15), moderate (9–12), severe (≤8). Mechanism of injury, presence of LOC, amnesia.
2

Airway and oxygenation. Maintain SpO₂ ≥95%. Any hypoxia worsens outcome. Intubation if GCS ≤8 or unable to protect airway. Avoid hyperventilation unless herniation signs — target EtCO₂ 35–40 mmHg (or 30–35 mmHg if herniation).
3

Maintain blood pressure. Avoid hypotension (SBP <90 mmHg). IV fluid to maintain CPP. Avoid hypotonic fluids. A single episode of hypotension significantly increases mortality.
4

Treat other life-threatening injuries. TBI frequently co-exists with thoracic, abdominal and spinal injuries. Haemorrhage control, chest decompression, pelvic stabilisation as indicated.
5

Neurological monitoring. GCS trend is more important than a single score. Pupillary reactivity, posturing. Manage seizures with benzodiazepines. Request CCP/HARU backup for severe TBI.
6

Transport to major trauma centre. Pre-notify. Code 1. Minimise on-scene time for severe TBI.

Overview and Risk Factors

Spinal cord injury (SCI) results in loss of motor, sensory and autonomic function below the level of the injury. Common mechanisms involve flexion and hyperextension injuries. High-risk mechanisms include:

→RTC involving rollover or ejection
→Fall from significant height
→Diving head first into shallow water
→Axial loading of the spine (rugby, sports impact)
→Pre-existing cervical spine abnormalities increase risk significantly

SCI Classification Patterns

Pattern	Mechanism	Clinical Features
Complete Transection	Severing of the cord	Complete loss of motor, sensory and autonomic function below injury. No recovery expected below level.
Central Cord Syndrome	Hyperextension — compresses cord centrally	Arms > legs in weakness; sacral sensation often spared. Common in elderly with pre-existing cervical disease.
Anterior Cord Syndrome	Compromise of anterior spinal artery	Motor paralysis + pain/temperature loss below injury; vibration and proprioception preserved.
Brown-Séquard Syndrome	Hemisection (one side) of cord — penetrating injury	Ipsilateral motor loss and proprioception; contralateral pain and temperature loss.

Effects by Spinal Level

Level	Key Effects
Cervical (C1–C7)	Most debilitating. Quadriplegia. Respiratory compromise (C3–5 → phrenic nerve → diaphragm). Dependent on mechanical ventilation at high cervical levels.
Thoracic (T1–T12)	Affects trunk, chest and abdomen. Intercostal muscle dysfunction → respiratory compromise. Paralysis of lower limbs (paraplegia). Important internal organs affected.
Lumbar (L1–L5)	Upper extremities unaffected. Weakness or paralysis in lower limbs. Bowel and bladder function may be affected.
Sacral	Upper body and most lower limb function preserved. Bowel/bladder dysfunction. Sexual dysfunction. Partial lower limb impairment.

Spinal Shock vs Neurogenic Shock

Spinal Shock

→Temporary, transient loss of all spinal cord function below the level of injury
→Suppression of all spinal reflexes below injury — flaccid paralysis
→Neurological — not haemodynamic in nature
→Can last hours to weeks; reflexes return as spinal shock resolves

Neurogenic Shock

!Damage to nervous system (typically above T6) causes loss of sympathetic control of vascular tone
!Vasodilation below injury → distributive hypotension
!Paradoxical bradycardia (loss of cardiac sympathetics) with hypotension
!Warm, dry, pink skin (vasodilated) — distinguishes from hypovolaemic shock (cold, clammy)
!Treatment: IV fluid cautiously + vasopressors (noradrenaline). Avoid aggressive fluid loading.

C-Spine Clearance

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Clinical Clearance Criteria

C-spine can be clinically cleared (no collar required) if ALL of the following are met: (1) Normal level of alertness, (2) No tenderness at the posterior midline of the cervical spine, (3) No signs or symptoms of SCI, (4) No pain or distracting injury that might prevent the patient from identifying cervical pain.

If C-Spine Cannot Be Cleared

→Apply soft cervical collar if significant posterior midline tenderness or symptoms of SCI
→Maintain manual in-line stabilisation (MILS) during airway management
→Head blocks, rolled towels or manual stabilisation of the neck during extrication and transport
→Log-roll with spinal precautions when repositioning is required

Autonomic Dysreflexia

Autonomic dysreflexia (hyperreflexia) is an abnormal, exaggerated stimulation of the autonomic nervous system in patients with chronic SCI above T6. The lower sympathetic system is disconnected from brain control. A noxious stimulus below the injury level triggers uncontrolled sympathetic discharge — causing massive vasoconstriction below the injury and severe hypertension. The brain attempts to correct via vagal bradycardia and vasodilation above the lesion, but cannot suppress the sympathetic surge below.

Common Triggers

→Bladder distension (most common — blocked catheter, urinary retention)
→Bowel distension or impaction
→Acute injury or pain below level of SCI
→Infection (e.g. UTI)
→Labour (childbirth)
→Pressure sores, tight clothing

Signs and Symptoms

!Severe hypertension (can be life-threatening)
!Pounding headache
!Bradycardia (paradoxical — vagal response above lesion)
!Flushing and sweating above lesion; pallor and piloerection below
!Anxiety, nasal congestion, blurred vision

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Complications of Untreated Autonomic Dysreflexia

If left untreated, the hypertensive crisis can cause cerebral haemorrhage, myocardial infarction, or seizures. Management: remove the triggering stimulus (decompress bladder/bowel), position upright, GTN 0.4 mg SL, and consider labetalol or GTN infusion if refractory. Urgent transport.

Cauda Equina Syndrome

Cauda equina syndrome (CES) is a spinal surgical emergency caused by acute or progressive compression of the nerve bundle in the lumbar/sacral spinal canal. Most common cause is a large lumbar disc prolapse (L4–L5 or L5–S1). Requires urgent specialist assessment — failure to treat carries significant risk of permanent disability.

Clinical Presentation

!Back or leg pain (often bilateral)
!Difficulty urinating — urinary retention
!Altered sensation in the saddle area (perineum)
!Altered sensation or weakness in both legs
!Sexual dysfunction

Red Flags in Back Pain

!Loss of bladder or bowel control
!Saddle anaesthesia / bilateral leg symptoms
!Fever >38°C, rigors
!Unable to mobilise; abnormal vitals
!Signs of generalised illness or malignancy

Overview

Vertigo is the false sensation that the body or its surroundings are moving or spinning. It is usually accompanied by nausea, vomiting, nystagmus and loss of balance. Symptoms are commonly triggered or worsened by changes in head position. The key clinical task is differentiating peripheral vertigo (benign, inner ear origin) from central vertigo (potentially life-threatening, brainstem/cerebellar origin).

Peripheral vs Central Vertigo

Feature	Peripheral Vertigo	Central Vertigo
Origin	Inner ear / vestibular system	Brainstem or cerebellum (stroke, MS, tumour)
Onset	Sudden or gradual (over 12–24 hrs)	Sudden or gradual onset
Severity	Intense spinning	Often milder dizziness but worse gait disturbance
Hearing changes	May be present (Ménière's, labyrinthitis)	Absent
Headache	Uncommon	Possible — especially in cerebellar stroke
Cranial nerve palsies	Absent	May be present (diplopia, dysarthria, facial weakness)
Head movement effect	Symptoms significantly worse with movement	Symptoms worse with movement
Finger-nose test	Normal	Abnormal — ataxia, past-pointing
Unsteady gait	Mild — can often walk	Severe — cannot walk unaided (cerebellar)

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Inability to Walk Unaided — Treat as Central Until Proven Otherwise

A patient with acute vertigo who cannot walk unaided should be presumed to have a central cause (cerebellar or brainstem stroke) until proven otherwise. Cerebellar stroke characteristically presents with vertigo not altered by head position, loss of coordination, and an abnormal finger-nose test — unlike BPPV.

Peripheral Causes — Common Conditions

Condition	Mechanism	Distinguishing Features
BPPV Benign Paroxysmal Positional Vertigo	Calcium carbonate particles (otoconia) dislodged from utricle into semicircular canals	Symptoms onset over 12–24 hours, strongly triggered by head position changes. Nausea common, vomiting rare. Normal finger-nose test. Treated with Epley manoeuvre.
Vestibular Neuritis	Inflammation of the vestibular nerve, typically post-viral	Onset over 12–24 hours. Vertigo less dramatically altered by position than BPPV. Nausea and vomiting. No hearing loss. Normal finger-nose test.
Labyrinthitis	Inflammation of the labyrinth (fluid-filled inner ear channels)	Similar to vestibular neuritis but with reduced hearing or tinnitus on affected side — key differentiator. Onset over 12–24 hours.
Ménière's Disease	Increased fluid in the endolymphatic compartment of the cochlea	Episodes of vertigo >20 minutes, tinnitus, fluctuating hearing loss, and aural fullness (congested ear feeling). Uncommon cause overall.

HINTS Examination

The HINTS exam is used for patients presenting with persistent vertigo over hours/days, nystagmus, and a normal neurological exam. It distinguishes between peripheral and central causes with high sensitivity for posterior circulation stroke.

H — Head Impulse Test

Rapidly rotate the head to one side while patient fixates on your nose. In peripheral vertigo: corrective saccade (eyes slip then snap back) — reassuring. In central: normal head impulse test — concerning for stroke.

N — Evaluation of Nystagmus

Peripheral: horizontal, unidirectional nystagmus that fatigues. Central: direction-changing, vertical or purely rotary nystagmus that does not fatigue. Vertical nystagmus strongly suggests central pathology.

TS — Test of Skew

Cover-uncover test. In central lesions: vertical deviation (skew deviation) of one eye as the cover is removed. Skew deviation strongly suggests brainstem or cerebellar pathology.

Nystagmus Classification

Nystagmus is involuntary rhythmic eye movement with a slow drift phase and a fast corrective phase. It can often be suppressed by visual fixation — monitor the patient when they are not fixating on an object.

Feature	Peripheral Nystagmus	Central Nystagmus
Frequency	High frequency	Low frequency
Amplitude	Low amplitude (small drift)	High amplitude (large drift)
Direction	Horizontal; unidirectional	Vertical, pendular or rotary; may be direction-changing
Fatiguability	Yes — exhausts with sustained gaze	No — does not fatigue
Visual fixation	Suppresses nystagmus	Does not suppress nystagmus

Red Flags in Vertigo Assessment

Central / Stroke Red Flags

!Unable to walk unaided
!Abnormal finger-nose test (cerebellar ataxia)
!Signs of stroke — facial droop, arm weakness, speech disturbance
!New headache (especially severe or thunderclap)
!Diplopia, dysarthria, dysphagia
!ALOC or altered vital signs

Additional Red Flags

!Acute hearing loss (labyrinthitis, perilymph fistula)
!Neck pain (vertebrobasilar dissection)
!Visual disturbance
!Persistent nystagmus that does not fatigue
!Recent head or neck trauma
!Symptoms that do not improve when head is still

Bedside Tests

Finger-Nose Test

1

Ask patient to place their index finger on their nose.
2

Hold your finger 30 cm away and ask them to touch your finger.
3

Slowly move your finger and ask them to alternate between nose and your finger. Test both sides.

Peripheral vertigo: normal. Cerebellar/central: past-pointing, intention tremor, dysmetria.

Dix-Hallpike Test — BPPV Diagnosis

Used to identify BPPV and confirm the affected ear. Patient is brought from sitting to supine with head turned 45° to one side. Positive if rotary/upbeat nystagmus reproduces vertigo with a latency and fatigability. A positive test confirms BPPV.

Epley Manoeuvre — BPPV Treatment

A canalith repositioning manoeuvre performed after a positive Dix-Hallpike. Moves displaced otoconia back to the utricle via sequential head positioning. Highly effective for posterior canal BPPV.

Midazolam

Benzodiazepine — GABA-A Positive Allosteric Modulator

First-Line Seizure

Dose

5–10 mg

Adult IM/IV/IN

0.1–0.2 mg/kg

Paeds (max 5 mg)

Routes

IM (preferred prehospital — no IV required), IV, or intranasal. IM onset 5–10 min. Intranasal onset 3–5 min. Short acting — effects last 1–2 hours.

Indications

Active generalised seizure, status epilepticus (first-line), procedural sedation, acute agitation

Precautions

Monitor respiratory rate and SpO₂. Risk of respiratory depression, especially with concurrent opioids or alcohol. Resuscitation equipment must be available.

Mechanism of Action

Positive allosteric modulator at GABA-A receptors → enhances inhibitory chloride current → hyperpolarisation of neuronal membranes → suppresses abnormal electrical discharge and terminates seizure activity.

Levetiracetam

Anti-Epileptic — SV2A Ligand

Second-Line Seizure

Dose

1,000–3,000 mg

Adult IV infusion

20–60 mg/kg

Paeds IV

Administration

IV infusion over 15 minutes. Also available as IV bolus. Less respiratory depression than benzodiazepines — important advantage in airway-compromised patients.

Indications

Status epilepticus refractory to benzodiazepines. Also used for long-term epilepsy management.

Advantages over Benzodiazepines

Minimal sedation, minimal respiratory depression, no drug interactions via CYP450 system, can be used safely with CNS depressants

Mechanism of Action

Binds to synaptic vesicle glycoprotein 2A (SV2A) → modulates neurotransmitter release (reduces glutamate, augments GABA) → reduces neuronal hyperexcitability and seizure propagation. Also modulates sodium and potassium channels.

Magnesium Sulphate

Anticonvulsant — NMDA Receptor Antagonist

Eclampsia / Refractory

Dose

4 g

Eclampsia IV loading

1–2 g/hr

Maintenance infusion

Onset / Duration

IV onset: immediate. Monitor for toxicity — loss of patellar reflex (first sign), respiratory depression (severe toxicity). Antidote: calcium gluconate 10 mL of 10% IV.

Indications

Eclamptic seizures (first-line — preferred over benzodiazepines in pregnancy). Refractory seizures. Also used for refractory asthma bronchospasm and torsades de pointes.

Side Effects

Flushing, nausea, diaphoresis, hypotension. At toxic levels: loss of reflexes, respiratory depression, cardiac arrest.

Mechanism of Action

Antagonises NMDA glutamate receptors → reduces excitatory neuronal transmission. Also blocks voltage-gated calcium channels → reduces cerebral vasospasm in eclampsia. Physiological calcium antagonism reduces smooth muscle contractility and neuromuscular transmission.

Glucose 10%

Carbohydrate — Dextrose Solution

Hypoglycaemia

Dose

100–200 mL

Adult IV

2 mL/kg

Paeds IV

Target BGL

Treat if BGL ≤4 mmol/L with symptoms. Target BGL 4–8 mmol/L post-treatment. Recheck BGL 10–15 minutes after administration.

Indications

Hypoglycaemia (BGL ≤4 mmol/L) with ALOC, seizure activity, or inability to take oral glucose. Also indicated where BGL is the likely cause of neurological presentation.

Important Note

Always check BGL before administering neurological drugs — hypoglycaemia is the most important reversible cause of ALOC and seizures. If unable to establish IV access, glucagon 1 mg IM may be used (less effective for paediatrics).

Mechanism of Action

Direct replenishment of circulating glucose → restored substrate for cerebral metabolic function → rapid reversal of neuroglycopaenia. The brain is entirely dependent on glucose for energy production and cannot synthesise or store it.

GTN (Glyceryl Trinitrate)

Nitrate — Vasodilator

Autonomic Dysreflexia

Dose

0.4 mg

SL (sublingual)

2 mg/hr

IV infusion

Onset

SL: onset 1–3 minutes. Duration 30 min. Titrate to blood pressure response. Repeat SL dose after 5 minutes if no improvement.

Indications (Neurological Context)

Autonomic dysreflexia — hypertensive crisis in patients with SCI above T6. First, remove triggering stimulus (catheterise, decompress bowel). Then GTN SL if BP remains elevated.

Contraindications

Hypotension, recent use of PDE5 inhibitors (sildenafil, tadalafil), severe aortic stenosis, raised ICP

Mechanism of Action

Converts to nitric oxide (NO) in vascular smooth muscle → activates guanylyl cyclase → increases cGMP → smooth muscle relaxation → venodilation (primarily) and arteriodilation → rapid reduction in preload and afterload → blood pressure reduction.

Labetalol

Alpha-1 / Non-Selective Beta Blocker

Autonomic Dysreflexia

Dose

10–20 mg

IV every 5 min

Onset

IV: onset 2–5 min. Duration 2–4 hours. Can repeat every 5 minutes to a maximum of 300 mg cumulative dose.

Indications

Refractory autonomic dysreflexia not responding to GTN. Hypertensive urgency/emergency. Acute aortic dissection.

Contraindications

Asthma (non-selective beta blockade), decompensated cardiac failure, bradycardia, heart block, cocaine-induced hypertension

Mechanism of Action

Competitive antagonism at alpha-1 receptors → peripheral vasodilation (reduces afterload). Non-selective beta blockade → reduces heart rate, myocardial contractility and renin release. Combined effect achieves controlled, titratable blood pressure reduction without reflex tachycardia.

Key Neurological Drug Summary

Drug	Class	Primary Indication	Route	Adult Dose
Midazolam	Benzodiazepine	Active seizure, status epilepticus (1st line)	IM / IV / IN	5–10 mg
Levetiracetam	Anti-epileptic (SV2A)	Status epilepticus refractory to BZD	IV infusion	1,000–3,000 mg
Magnesium Sulphate	NMDA antagonist	Eclamptic seizure (1st line)	IV	4 g loading
Glucose 10%	Carbohydrate	Hypoglycaemia (BGL ≤4 mmol/L)	IV	100–200 mL
GTN	Nitrate	Autonomic dysreflexia (1st line)	SL / IV	0.4 mg SL
Labetalol	Alpha/Beta blocker	Refractory autonomic dysreflexia	IV	10–20 mg q5min
Alteplase (tPA)	Thrombolytic	Ischaemic stroke (hospital; within 4.5–9 hrs)	IV	0.9 mg/kg (max 90 mg)

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Check BGL Before All Neurological Drug Administration

Hypoglycaemia is a stroke mimic, seizure trigger, and cause of ALOC. Always measure blood glucose before attributing altered consciousness to a neurological cause. A BGL ≤4 mmol/L requires glucose administration before any further neurological workup.

Neurological Emergencies

Neurological Assessment

Stroke

Seizures

Traumatic Brain Injury

Spinal Cord Injury

Vertigo

Pharmacology