CNS Examination — Masterclass
🔵 Examination method · 🟣 Mechanism/localisation · 🟡 Clinical pattern · 🟠 Examiner presentation · 🔴 Red flag · 🟢 Rapid revision
Bedside sequence
Begin with general observation and mental status, then higher functions, speech, cranial nerves, motor system, reflexes, sensory system, coordination, gait, meningeal signs and focused autonomic/cortical testing. The sequence should be adapted to consciousness, disability and the clinical question.
Higher mental functions
Assess level of consciousness, orientation, attention, memory, language, calculation, abstraction, judgement, neglect and behaviour. Separate impaired attention from true memory failure. Use bedside tasks appropriate to language, education and cultural background.
Speech and language
Distinguish dysarthria from aphasia. Assess fluency, comprehension, naming, repetition, reading and writing where appropriate. Broca-pattern aphasia is typically non-fluent with relatively preserved comprehension; Wernicke-pattern aphasia is fluent but poorly comprehended. Bedside patterns guide localisation but require clinical context.
Cranial nerves overview
Examine CN I when relevant; visual acuity/fields, pupils and fundus for CN II; ocular position and movements for III/IV/VI; facial sensation and mastication for V; facial movements for VII; hearing/vestibular function for VIII; palate, voice and swallowing for IX/X; shoulder shrug/head turn for XI; tongue for XII.
Pupils and light reflex
Record size, symmetry and reactivity. The afferent limb of the light reflex is CN II and the parasympathetic efferent limb is CN III. Assess direct and consensual responses and swinging-flashlight testing when an afferent defect is suspected.
Eye movements
Inspect for ptosis and resting deviation, then assess smooth pursuit through the cardinal directions without forcing extreme gaze. Identify diplopia, nystagmus and ophthalmoplegia. Interpret deficits using extraocular muscle actions, cranial nerves and internuclear pathways.
Facial nerve
Inspect facial symmetry at rest and during forehead wrinkling, tight eye closure, smiling and showing teeth. A typical supranuclear lesion relatively spares the forehead because of bilateral cortical innervation, whereas a peripheral VII lesion affects upper and lower face on that side.
Motor system
Assess bulk, involuntary movements, tone, power and functional movements. Grade strength systematically and compare sides. Interpret weakness by pattern: pyramidal, LMN, proximal myopathic, fatigable neuromuscular-junction or functional patterns require different corroborating signs.
Tone
Move relaxed joints passively. Spasticity is velocity-dependent and classically pyramidal; rigidity is less velocity-dependent and may be lead-pipe or cogwheel in parkinsonism. Hypotonia occurs with cerebellar, acute LMN and selected acute CNS lesions.
Power grading
Use the MRC 0–5 scale: 0 no contraction; 1 flicker; 2 movement with gravity eliminated; 3 movement against gravity; 4 movement against resistance; 5 normal power. Grade 4 has broad variability, so describe clinically meaningful asymmetry when needed.
Reflexes
Assess biceps, supinator/brachioradialis, triceps, knee and ankle jerks with the patient relaxed. Compare sides and use reinforcement if needed. Hyperreflexia with pathological reflexes supports UMN dysfunction; depressed reflexes suggest LMN/peripheral involvement but depend on context.
Plantar response
Stroke the lateral sole from heel toward forefoot and curve medially using an appropriate blunt stimulus. Extensor great-toe response with fanning in an adult supports corticospinal tract dysfunction. Withdrawal should not be mistaken for a true extensor plantar response.
Sensory examination
Test modalities according to the question: light touch, pinprick, temperature, vibration and joint position. Map abnormalities anatomically. Cortical sensory functions include stereognosis, graphesthesia, two-point discrimination and extinction, requiring intact primary sensation.
Coordination
Finger–nose, heel–shin and rapid alternating movements assess coordination. Look for dysmetria, intention tremor, decomposition and dysdiadochokinesia. Interpret apparent incoordination carefully when weakness, sensory loss or pain is present.
Gait and station
Observe initiation, base, stride, arm swing, turning and tandem gait when safe. Test Romberg appropriately: worsening instability after eye closure suggests impaired proprioceptive/vestibular compensation rather than a primary cerebellar sign.
Meningeal signs
Assess neck stiffness when meningitis or subarachnoid irritation is suspected, while considering contraindications and cervical pathology. Kernig and Brudzinski signs have limited sensitivity; absence does not exclude meningitis.
UMN vs LMN
UMN pattern: weakness with increased tone, brisk reflexes and extensor plantar response after the acute phase. LMN pattern: weakness with wasting, fasciculation, reduced tone and depressed reflexes. Mixed patterns occur in disorders such as motor-neuron disease.
Localisation framework
Ask sequentially: cortex, subcortex/internal capsule, brainstem, cerebellum, spinal cord, root, plexus, peripheral nerve, neuromuscular junction or muscle? Use pattern of weakness, sensory level/distribution, cranial-nerve involvement, reflexes and sphincter findings to localise.
Rapid revision
CNS examination should end with localisation, not merely a list of signs. Present consciousness/higher function → cranial nerves → motor → reflexes → sensory → coordination/gait → localisation.
CVS Examination — Masterclass
🔵 Examination method · 🟣 Mechanism/localisation · 🟡 Clinical pattern · 🟠 Examiner presentation · 🔴 Red flag · 🟢 Rapid revision
Bedside sequence
General survey → hands and pulse → BP → face → neck/JVP → precordial inspection → palpation → auscultation → dynamic manoeuvres → lungs/peripheral oedema/abdomen as appropriate.
General and peripheral signs
Look for distress, cyanosis, pallor, cachexia, scars/devices, clubbing, splinter haemorrhages when relevant, peripheral temperature, capillary refill, oedema and signs suggesting systemic cardiac disease. Interpret individual peripheral signs cautiously.
Precordial inspection
Inspect chest shape, scars, pacemaker/ICD sites and visible pulsations. Note sternotomy or thoracotomy scars and deformity. Tangential lighting can help reveal impulses.
Apex beat
Locate the apex with the patient appropriately positioned. Describe site and character. A displaced apex may suggest cardiac enlargement; a sustained/heaving impulse suggests pressure loading; a hyperdynamic impulse suggests increased volume/flow. Body habitus and lung disease affect palpability.
Parasternal heave
Palpate the left sternal edge with the heel of the hand. A sustained lift suggests RV pressure/volume loading, often seen with pulmonary hypertension or significant RV enlargement.
Thrills
A thrill is a palpable murmur. Palpate valve areas and along expected radiation pathways when a loud murmur is suspected. Its location and timing should match auscultatory findings.
Heart sounds
Identify S1 and S2 and relate them to the carotid pulse. Assess intensity and splitting. Physiological S2 splitting widens on inspiration; abnormal splitting patterns can provide clues to conduction and haemodynamic disease.
Added sounds
S3 occurs in early diastole during rapid ventricular filling and can be physiological in younger people but in older symptomatic adults often suggests volume overload or systolic dysfunction. S4 occurs with atrial contraction into a stiff ventricle and is absent in atrial fibrillation.
Murmur description
Describe timing, site of maximal intensity, intensity/grade, character/pitch, radiation, relationship to respiration and response to manoeuvres. Do not jump directly from 'murmur' to diagnosis.
Aortic stenosis pattern
Classically an ejection systolic murmur at the aortic area radiating toward the carotids, with slow-rising pulse in significant disease. Severity cannot be determined reliably from murmur loudness alone; echocardiography is required.
Mitral regurgitation pattern
Classically a pansystolic murmur maximal at the apex with radiation toward the axilla, though direction varies with jet anatomy. Look for displaced/hyperdynamic apex and signs of pulmonary hypertension or heart failure.
Aortic regurgitation pattern
Classically an early diastolic decrescendo murmur along the left sternal border, often better with the patient sitting forward in expiration. A wide pulse pressure and collapsing pulse can support significant AR.
Mitral stenosis pattern
Classically loud S1 when valve mobility is preserved, opening snap and low-pitched mid-diastolic rumble at the apex, best with the bell in left lateral position. AF and pulmonary hypertension are important associated findings.
Dynamic manoeuvres
Inspiration generally augments right-sided murmurs. Standing/Valsalva reduce venous return and can intensify HOCM while reducing many flow murmurs; squatting increases preload/afterload and tends to reduce HOCM. Use manoeuvres to refine, not replace, diagnosis.
Heart failure bedside integration
Combine JVP, hepatojugular reflux, oedema, lung crackles, S3, perfusion, BP and respiratory effort. No single sign is sufficiently sensitive to exclude heart failure.
Examiner presentation
Present pulse/BP/JVP first, then precordium and auscultation, followed by signs of congestion/perfusion. Conclude with the dominant lesion and haemodynamic consequence rather than reciting disconnected findings.
Rapid revision
CVS = peripheral haemodynamics + JVP + apex/heave/thrills + S1/S2/added sounds + murmur analysis + manoeuvres + congestion/perfusion.
Respiratory Examination — Masterclass
🔵 Examination method · 🟣 Mechanism/localisation · 🟡 Clinical pattern · 🟠 Examiner presentation · 🔴 Red flag · 🟢 Rapid revision
Bedside sequence
General observation → hands → face → neck → chest inspection → palpation → percussion → auscultation → vocal resonance → relevant peripheral signs. Compare corresponding areas side-to-side.
General observation
Assess respiratory rate, oxygen/device, ability to speak, work of breathing, posture, cough/sputum, cyanosis, cachexia and mental state. Severe respiratory disease can be recognised before touching the chest.
Hands and face
Look for clubbing, nicotine staining where relevant, tremor/asterixis, peripheral cyanosis and perfusion. Examine conjunctiva, central cyanosis and features suggesting systemic disease. Interpret signs in context.
Chest inspection
Assess shape, symmetry, scars, deformity, respiratory movement, accessory-muscle use and intercostal recession. Hyperinflation may increase AP diameter; unilateral reduced movement suggests focal pleural, pulmonary or chest-wall pathology.
Trachea
Assess tracheal position gently at the suprasternal notch. Deviation away from a lesion can occur with major pressure/volume effects such as tension pneumothorax or large effusion; deviation toward a lesion can accompany major volume loss.
Chest expansion
Place hands symmetrically and assess movement during deep inspiration. Reduced unilateral expansion suggests focal pathology; bilateral reduction may occur with hyperinflation, restrictive disease or poor effort.
Tactile vocal fremitus
Palpate transmitted vocal vibration over symmetrical chest areas. It tends to increase over consolidated lung with a patent bronchus and decrease with pleural effusion or pneumothorax. Technique and voice intensity influence the sign.
Percussion
Percuss comparable interspaces systematically. Dullness suggests increased density such as consolidation or fluid; stony dullness classically suggests pleural effusion; hyperresonance may occur with pneumothorax or marked hyperinflation.
Breath sounds
Normal vesicular breathing has a longer inspiratory component without a distinct pause. Bronchial breathing over peripheral lung suggests transmission through consolidated tissue or a cavity communicating with a bronchus, depending on context. Reduced/absent sounds suggest poor ventilation, pleural separation or obstruction.
Crackles
Fine late-inspiratory crackles may occur with interstitial fibrosis or pulmonary oedema; coarse crackles may reflect secretions/airway disease. Note timing, location, persistence and response to coughing rather than using 'crepitations' without description.
Wheeze and rhonchi
Wheeze is a musical continuous sound caused by narrowed airways and may be polyphonic or monophonic. A focal monophonic wheeze should raise concern for localised airway obstruction. Severe asthma can have minimal wheeze when airflow becomes critically reduced.
Pleural rub
A pleural friction rub is a superficial grating sound related to inflamed pleural surfaces, often heard in inspiration and expiration and localised. It should be distinguished from crackles and pericardial rub.
Vocal resonance
Increased vocal resonance/bronchophony supports consolidation; reduced transmission occurs with pleural fluid or air. Whispered pectoriloquy and egophony are additional transmitted-voice phenomena.
Consolidation syndrome
Typical cluster: reduced expansion, dull percussion, increased fremitus/vocal resonance, bronchial breathing and crackles. Real patients may not display every textbook sign.
Pleural effusion syndrome
Typical cluster: reduced expansion, stony dull percussion, reduced/absent breath sounds and reduced vocal fremitus/resonance over the fluid. Large effusions can displace mediastinal structures.
Pneumothorax syndrome
Reduced expansion, hyperresonance, reduced breath sounds and reduced vocal transmission. Tension physiology adds haemodynamic compromise and requires emergency treatment; do not delay for elaborate examination.
COPD/hyperinflation
Look for hyperinflated chest, reduced expansion, hyperresonance, quiet breath sounds, prolonged expiration, wheeze and accessory-muscle use. Signs vary with phenotype and severity.
Rapid revision
Respiratory localisation often comes from the combination of expansion + percussion + breath sounds + vocal transmission. Compare sides systematically and integrate with RR/SpO₂.
GI / Abdominal Examination — Masterclass
🔵 Examination method · 🟣 Mechanism/localisation · 🟡 Clinical pattern · 🟠 Examiner presentation · 🔴 Red flag · 🟢 Rapid revision
Bedside sequence
General survey → hands/arms → face/mouth → chest when relevant → abdominal inspection → palpation → percussion → auscultation → organ-specific manoeuvres → groins/hernial or rectal examination when indicated.
General and peripheral signs
Assess nutrition, pallor, icterus, hydration, oedema, bruising, scratch marks, clubbing and selected chronic liver-disease stigmata. Avoid treating nonspecific peripheral signs as diagnostic by themselves.
Abdominal inspection
Expose appropriately while maintaining dignity. Inspect contour, symmetry, movement with respiration, scars, striae, dilated veins, hernias, visible masses/peristalsis and umbilicus.
Palpation principles
Ask about pain first, warm the hands and begin away from tenderness. Use light palpation for tenderness/guarding and deeper palpation for masses and organs. Distinguish voluntary guarding from involuntary rigidity.
Abdominal mass
Describe site, size, shape, surface, edge, consistency, tenderness, mobility, movement with respiration, pulsatility and relationship to surrounding structures. Determine whether it is intra-abdominal or abdominal-wall where possible.
Liver
Palpate from the right iliac fossa toward the costal margin during inspiration. Describe edge, surface, tenderness and consistency. Percussion can estimate span. A palpable liver is not automatically enlarged, and an enlarged liver may not always be palpable.
Spleen
Begin palpation from the right lower abdomen toward the left hypochondrium as the patient inspires. Splenomegaly typically enlarges inferomedially, moves with respiration and may have a palpable notch. Percussion and alternative positioning can assist.
Kidneys
Use bimanual palpation/ballottement when indicated. An enlarged kidney may be ballotable and a band of colonic resonance may lie anteriorly. Distinguishing renal from splenic masses is a classic bedside exercise.
Ascites
Look for distension and flank fullness; assess shifting dullness for clinically significant free fluid. Fluid thrill may be useful in larger-volume ascites. Ultrasound is more sensitive than bedside signs for small volumes.
Tenderness and peritonism
Localised tenderness helps anatomical localisation. Rebound tenderness is not always necessary and can cause pain; percussion/cough tenderness and involuntary guarding can demonstrate peritoneal irritation more gently. Rigidity or systemic instability requires urgent evaluation.
Bowel sounds
Auscultate when clinically relevant, especially suspected obstruction/ileus. Bowel sounds are variable and have limited diagnostic specificity. Do not use a brief period of silence alone to declare absent bowel sounds.
Portal hypertension clues
Assess splenomegaly, ascites, abdominal-wall veins and signs of chronic liver disease. JVP helps distinguish some causes of ascites and hepatomegaly related to right-sided cardiac congestion.
Chronic liver disease
Look for jaundice, muscle wasting, bruising, spider telangiectasia, palmar erythema, gynaecomastia/testicular changes where appropriate, asterixis, hepatosplenomegaly, ascites and oedema. Many signs are neither sensitive nor specific individually.
Examiner presentation
Present abdomen by inspection, tenderness/masses, liver/spleen/kidneys, percussion/ascites and bowel sounds, then relevant extra-abdominal signs. Conclude with a syndrome such as portal hypertension rather than listing signs without synthesis.
Rapid revision
Abdomen = look → gentle palpation → deep/organ palpation → percussion/ascites → auscultation → targeted special examination. Always integrate abdominal findings with general examination.
Locomotor Examination — Masterclass
🔵 Examination method · 🟣 Mechanism/localisation · 🟡 Clinical pattern · 🟠 Examiner presentation · 🔴 Red flag · 🟢 Rapid revision
Core approach
Use Look–Feel–Move, then function and special tests. Compare sides. Determine whether pathology is articular, periarticular, muscular, neurological or referred.
Screening: GALS
GALS is a rapid locomotor screen: Gait, Arms, Legs, Spine. Ask screening questions about pain/stiffness and difficulty dressing or climbing stairs, then perform the standard screening movements. Abnormalities trigger a detailed regional examination.
Look
Inspect posture, gait, swelling, erythema, deformity, scars, muscle wasting and alignment. Observe the joint above and below when relevant.
Feel
Assess temperature, tenderness, swelling, effusion, bony landmarks, crepitus and soft tissues. Identify whether swelling is bony, synovial, effusive or periarticular.
Move
Assess active movement first, then passive movement when appropriate. Record range, pain, restriction, end-feel and crepitus. Active limitation greater than passive limitation can suggest muscle/tendon or pain-related dysfunction; both may be restricted in joint disease.
Function
Functional testing reveals disability not captured by isolated range-of-motion measurements. Examples include gait, sit-to-stand, grip, reaching behind the head/back and task-specific movements.
Inflammatory vs mechanical pattern
Inflammatory disease often produces prolonged morning stiffness, swelling and improvement with activity; mechanical disease more often worsens with use and has shorter stiffness. These are patterns rather than absolute rules.
Shoulder
Inspect, palpate SC/AC joints and shoulder landmarks, assess active/passive flexion, extension, abduction, adduction and rotation. Use targeted tests for impingement, rotator cuff, instability or AC pathology only when indicated.
Elbow, wrist and hand
Assess deformity, swelling, nodules, muscle wasting and grip. Examine elbow flexion/extension and forearm rotation; wrist movements; MCP/PIP/DIP joints; thumb function. In inflammatory arthritis, document distribution and synovitis.
Hip
Observe gait and leg position; assess flexion, extension, abduction, adduction and internal/external rotation. Internal rotation is often affected early in hip joint pathology. Consider referred pain from spine or knee.
Knee
Inspect alignment, quadriceps wasting and swelling. Palpate joint lines and patella, assess effusion and range. Ligament and meniscal tests should be performed according to injury history and patient comfort.
Ankle and foot
Inspect arches, alignment, swelling, callosities and deformity. Assess ankle and subtalar movement and targeted tendon/ligament structures. Foot findings can reflect inflammatory, neuropathic, vascular or mechanical disease.
Spine
Inspect alignment and curvature; assess cervical and lumbar movement as appropriate. Neurological examination is required when radiculopathy, myelopathy or cauda equina pathology is suspected.
Red flags
Urgent assessment is required for a hot swollen joint with systemic illness, suspected septic arthritis, acute neurovascular compromise, major trauma, suspected compartment syndrome, or spinal symptoms with progressive neurological deficit/sphincter disturbance.
Examiner presentation
State gait/function, visible abnormalities, tenderness/swelling, active/passive ROM and targeted special tests. Finish with whether the pattern is inflammatory/mechanical and the likely anatomical structure.
Rapid revision
Locomotor = Look + Feel + Move + Function + joint above/below + neurovascular status when relevant. GALS screens; regional examination defines the abnormality.