EMT neurology A&p

ANATOMY

1

For anatomy, you must be able to name, label, pronounce and describe the location and function of the following:

  • Central Nervous System (CNS):

    • Brain:

      • Cerebrum:

        • Frontal lobe

        • Parietal lobe

        • Temporal lobe

        • Occipital lobe

        • Cerebral cortex

        • Central sulcus

        • Parieto-occipital sulcus

        • Corpus callosum

        • Thalamus

        • Hypothalamus

        • Pituitary gland

        • Pineal gland

        • Optic chiasma

        • Lateral ventricles

        • Third ventricle

        • Choroid plexus

      • Cerebellum

      • Brainstem

        • Midbrain

        • Pons

        • Medulla oblongata

    • Spinal cord

      • Cervical region

      • Thoracic region

      • Lumbar region

      • Sacral region

    • Protective structures:

      • Skull

      • Meninges (dura mater, arachnoid mater, pia mater)

      • Cerebrospinal fluid (CSF)

  • Peripheral Nervous System (PNS):

    Two main subdivisions:

    • Somatic Nervous System (Voluntary control):

      • Sensory nerves (afferent)

      • Association nerves (interneurons)

      • Motor nerves (efferent)

    • Autonomic Nervous System (Involuntary control):

      • Sympathetic nervous system:

        • Fight, flight and freeze

      • Parasympathetic nervous system:

        • Rest, digest, sex and read

  • 12 Cranial nerves:

    • You do not need to memorise the full sequence in order, but you must understand the clinically relevant cranial nerves marked with a star below:

      • Somatic:

        • CN I – Olfactory (sensory)

        • *CN II – Optic (sensory)

        • *CN V – Trigeminal (facial sensation + chewing muscles)

        • *CN VII – Facial (facial expression muscles)

        • *CN VIII – Vestibulocochlear (hearing + balance)

        • *CN XI – Accessory (sternocleidomastoid + trapezius)

        • *CN XII – Hypoglossal (tongue movement)

      • Autonomic:

        • *CN III – Oculomotor (pupil constriction)

        • CN VII – Facial (salivary + lacrimal glands)

        • *CN IX – Glossopharyngeal (salivary gland)

        • *CN X – Vagus (major parasympathetic supply to heart, lungs, GI)

    • You must also be able to identify and explain which nerves are responsible for balance and taste.

      • Balance:

        • CN VIII – Vestibulocochlear

      • Taste:

        • CN VII – Facial

        • CN IX – Glossopharyngeal

        • CN X – Vagus

    • NB: Not all the cranial nerves are solely somatic or autonomic, most have dual somatic and autonomic functions.

2

PHYSIOLOGY

For physiology, you should be able to understand the underlying pathophysiology behind:

  • Consciousness and awareness:

    • Role of the cerebral cortex in cognition, awareness and higher function

    • Role of brainstem in maintaining alertness

    • Difference between focal neurological deficit and global impairment

  • Causes of unconsciousness – Remember the mnemonic FISH SHAPED:

    • F – Fainting (syncope):

      • Transient cerebral hypoperfusion

        • Vasovagal syncope

        • Simple syncope

        • Heart failure

    • I – Infections, for example:

      • Sepsis

      • Meningitis

      • Acute Disseminated Encephalomyelitis (ADEM)

    • S – Stroke (Cerebrovascular Events - CVEs):

      • Ischaemic

      • Haemorrhagic

    • H – Head injury (Traumatic brain Injuries - TBIs)

      • Primary injury - Blunt force trauma, rapid deceleration etc

      • secondary injury - Hypoxia, hypotension, raised ICP etc

    • S – Shock

      • Reduced cerebral perfusion pressure

    • H – Hypoxia

      • Reduced oxygen delivery to brain tissue

    • A – Alcohol

      • CNS depression

    • P – Poisoning

      • Drugs, toxins, CO exposure etc

    • E – Epilepsy

      • Abnormal electrical cortical discharge broke into two categories:

        • Generalised seizures

        • Focal Seizures

    • D – Diabetes

      • Hypoglycaemia

      • Severe hyperglycaemia

  • You must understand the difference between:

    • Structural causes (bleed, tumour, stroke, trauma) and;

    • Metabolic/toxic causes (hypoxia, hypoglycaemia, drugs, sepsis)

  • Cerebral perfusion and oxygenation:

    • Cerebral perfusion pressure (conceptual understanding only)

    • Relationship between systemic blood pressure and brain oxygen delivery

    • Effect of hypotension on neuronal survival

    • Effect of hypoxia on neuronal survival

    • Loss of autoregulation in severe illness

  • Intracranial pressure (ICP):

    • Monro-Kellie principle (fixed skull volume: brain tissue, blood, CSF)

    • Cushings response (Hypertension, Bradycardia, Bradypnoea)

    • Compensation vs decompensation

    • How bleeding, swelling or blocked CSF flow increases ICP

  • Consequences of raised ICP:

    • Headache

    • Vomiting

    • Reduced GCS

    • Unequal or non-reactive pupils

    • Abnormal posturing

    • Brainstem compression

  • Stroke pathophysiology:

    • Ischaemic stroke (thrombus vs embolus)

    • Haemorrhagic stroke

    • Transient ischaemic attack (TIA)

    • Penumbra concept (basic awareness only)

    • Large vessel occlusion (conceptual understanding)

  • Seizure physiology:

    • Abnormal electrical discharge in the cerebral cortex

    • Generalised vs focal onset

    • Post-ictal suppression

    • Risk of airway compromise

  • Spinal cord injury:

    • Disruption of ascending and descending pathways

    • Loss of sympathetic tone

    • Neurogenic shock

    • Babinski’s repsonse and priapism

  • Autonomic nervous system physiology:

    • Sympathetic activation

    • Parasympathetic dominance

    • Vagus nerve influence on heart rate

    • Autonomic instability in brainstem injury

  • Balance and coordination:

    • Role of cerebellum

    • Role of vestibular system (CN VIII)

    • Cerebellar stroke → ataxia, dysmetria, imbalance

  • Taste physiology:

    • Anterior 2/3 tongue – CN VII

    • Posterior 1/3 tongue – CN IX

    • Minor contribution – CN X

  • Infection of the nervous system:

    • Meningitis: meningeal inflammation → raised ICP → altered consciousness and possibly death

    • Encephalitis: inflammation of brain tissue → seizures → behavioural change → reduced GCS and possibly death

    • Acute disseminated encephalomyelitis: Immune-mediated demyelinating disorder, usually following viral infection → inflammatory response against CNS myelin → widespread demyelination → impaired nerve conduction → neurological deficit → altered consciousness.

  • You must understand the progression of:

    • Hypoxia or hypotension → reduced cerebral perfusion → confusion → reduced GCS → coma → cardiac arrest

    • Ischaemic stroke → vessel occlusion → ischaemia → infarction → cerebral oedema → raised ICP → deterioration

    • Intracranial bleed → expanding volume → increased ICP → brainstem compression → respiratory compromise → cardiac arrest

    • Meningitis → inflammation → raised ICP ± septic shock → multi-organ failure

    • Prolonged seizure → hypoxia → acidosis → exhaustion → post-ictal coma → airway compromise → possible death

  • For Level 5, you must be able to:

    • Recognise structural vs metabolic causes of unconsciousness

    • Identify time-critical stroke patterns using exams such as:

      • BEFAST Test

      • MEND Exam

      • HIT Exam

    • Understand why hypotension and hypoxia worsen brain injury

    • Protect the brain from secondary injury

    • Recognise early neurological deterioration before arrest occurs

Why do emt’s need to know this?

3

Altered level of consciousness is one of the most common and highest-risk presentations in prehospital care. Without understanding neurological physiology, assessment becomes guesswork.

  • GCS interpretation relies on knowing:

    • Which part of the brain controls eye opening

    • Which structures generate speech

    • Which pathways produce purposeful movement

    • Why a falling GCS indicates deterioration

  • Stroke assessment depends on understanding:

    • Why unilateral weakness occurs

    • Why facial droop happens

    • Why speech disturbance localises to specific hemispheres

    • Why posterior circulation strokes may present with imbalance rather than weakness

    • Why time equals brain

  • Recognising focal neurological deficit vs global impairment determines:

    • Stroke vs hypoglycaemia

    • Head injury vs intoxication

    • Sepsis vs intracranial bleed

    • Metabolic collapse vs structural brain injury

  • Unconsciousness assessment requires rapid application of FISH SHAPED to avoid missing reversible causes such as:

    • Hypoglycaemia

    • Hypoxia

    • Shock

    • Opioid toxicity

  • Cerebral perfusion knowledge explains:

    • Why hypotension worsens brain injury

    • Why hypoxia accelerates neuronal death
      Why maintaining blood pressure and oxygenation prevents secondary brain injury

  • Understanding intracranial pressure allows you to recognise:

    • Cushing’s response

    • Unequal pupils

    • Abnormal posturing

    • Sudden deterioration after head injury

    • These directly influences urgency of transport and pre-alert decisions.

  • Head injury management depends on knowing:

    • Primary injury cannot be reversed

    • Secondary injury can be prevented

    • Airway, oxygenation and perfusion are neuroprotective

  • Seizure management requires understanding:

    • Why prolonged seizures cause hypoxia and acidosis

    • Why airway compromise is common

    • Why post-ictal states must not be mistaken for ongoing seizure

  • Spinal cord injury physiology explains:

    • Neurogenic shock (hypotension without blood loss)

    • Priapism as a sign of cord injury

    • Why immobilisation decisions matter

  • Autonomic understanding clarifies:

    • Bradycardia in raised ICP

    • Vagal influence on heart rate

    • Autonomic instability in brainstem injury

  • Balance and cerebellar function knowledge prevents:

    • Missing posterior stroke

    • Mislabelling neurological deficit as “vertigo” or anxiety

  • Infection-related neurology is time critical:

    • Meningitis and encephalitis can deteriorate rapidly

    • Sepsis can cause altered consciousness without focal deficit

    • Early recognition improves outcome

  • Differentiating between life-threatening and stable neurological presentations determines:

    • Treat and discharge

    • Treat and refer

    • Urgent ED conveyance

    • Blue light transport

    • Stroke centre pre-alert

  • Neurological deterioration can be subtle and rapid. EMTs must recognise:

    • Confusion before collapse

    • Behaviour change before reduced GCS

    • New imbalance before hemiparesis

    • Early stroke before complete deficit

  • Ultimately, neurological A&P allows you to answer three critical questions on scene:

    • Is the brain perfused?

    • Is the brain oxygenated?

    • Is this structural or metabolic?

    If you can answer those confidently, you prevent secondary brain injury and improve survival and long-term neurological outcome.

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