Neurological history, examination and localisation

• A neurological examination is not a checklist to be rushed through; it is a set of directed tests, each of which asks a specific question about where the nervous system is damaged.
• The order that protects against being misled is mental state, cranial nerves, motor, reflexes, sensation, cerebellar function and gait, with pauses to compare one side of the body with the other.
• Every finding is first interpreted as upper or lower motor neuron, sensory level, cranial nerve pattern or cerebellar pattern, and only then as a disease.
• Localisation comes first; diagnosis comes second. A stroke, a tumour and an abscess can look identical at the bedside if they occupy the same pathway.
• Write what you did and what you found, in that order, so the next clinician and you can compare later; a "normal neuro exam" written without the tests is not an examination.

By the end of this page you should be able to:

1. Take a neurological history that separates structure from time, progression and risk.
2. Perform a complete neurological examination in a reliable order and record it so that another clinician can follow your steps.
3. Test each cranial nerve with the correct method and remember which branches are motor, sensory or mixed.
4. Distinguish upper from lower motor neuron signs, and central from peripheral sensory loss.
5. Test coordination, gait and station and separate cerebellar from proprioceptive ataxia.
6. Turn a set of findings into a level of the nervous system and a side, and state what evidence you would look for on imaging or with a lumbar puncture.

A neurological examination is one of the few examinations in medicine where a calm, ordered look at the patient, with almost no equipment, can locate a lesion to within a few millimetres. The skill is learned as a sequence but is used as a language: each test corresponds to a pathway, and the pattern of abnormal results reveals where that pathway is interrupted. This page teaches the standard adult examination, the recording of it, and the reasoning that turns findings into a localisation. It is written for a medical student who is meeting the full examination for the first time; paediatric, unconscious and comatose examinations are noted as variations rather than being treated in full.

The emphasis throughout is on the patient's own words for symptoms and on the examiner's own hands for signs. A neurology story is best allowed to run: interrupt only to clarify time, distribution and pattern. Many important clues sit inside the order in which symptoms appeared, so the history is not a separate step from the examination, it is the first half of the localisation.

A full examination is indicated whenever there is a new neurological symptom, an unexplained change in a known long-term condition, a suspected stroke or transient loss of blood flow, new confusion, a fall, a suspected infection of the central nervous system, a suspected spinal cord or cauda equina problem, or any neurological sign picked up during a general examination. Headache with new features, sensory change that is not easily explained, and weakness that does not follow a joint distribution all demand it. A focused examination of one region is appropriate for a discrete peripheral nerve or root complaint, but the examiner should know the whole sequence well enough to extend it at any point.

There is no absolute contraindication to examining the nervous system, but several parts must be modified for safety. Do not extend the neck or rotate the head during examination if a cervical spine injury is suspected. Do not perform a passive neck flexion test for meningeal irritation if a mass or raised pressure inside the skull is a realistic possibility. Do not test plantar responses or use reflex hammers in a way that could upset an unstable patient, and do not force an examination on an agitated or distressed person; observe first and document what you could safely do. If a person is suspected to have an unstable spine or a possible vascular event in the neck arteries, gentle examination and imaging take priority over completeness.

The central nervous system consists of the brain and spinal cord; the peripheral nervous system is the cranial nerves, spinal nerve roots, plexuses, peripheral nerves and, functionally, the neuromuscular junction and muscle. The somatic nervous system carries voluntary movement and sensation; the autonomic part regulates blood pressure, sweating, bladder, bowel and pupillary responses. Three ideas underpin localisation.

First, the motor and sensory pathways in the brain run in opposite directions to one another in almost every region: they cross. The corticospinal tract, carrying voluntary movement, decussates in the medulla, so a hemisphere lesion produces weakness on the opposite side of the body. The dorsal column pathway, carrying position and vibration, crosses in the medulla as well, while the spinothalamic tract, carrying pain and temperature, crosses within one or two spinal segments of entry. Knowing where each crosses is what allows a lesion to be placed above or below the crossover.

Second, the upper and lower motor neurons are different cells in series. The upper motor neuron sits in the cortex or its descending tract and modulates the lower motor neuron in the anterior horn of the spinal cord or the cranial nerve motor nucleus; the lower motor neuron is the final common path to the muscle. Damage at the upper level produces spasticity, brisk reflexes, clonus and an extensor plantar response, while damage at the lower level produces wasting, fasciculation, flaccidity and lost reflexes. This distinction is the single most useful split in clinical neurology.

Third, the cranial nerves are part of the peripheral nervous system but sit inside the skull. A lesion of one cranial nerve, or of the brainstem through which the nerve passes, produces a pattern that is localised by remembering which nerves travel together through each opening and by pairing a cranial nerve finding with a long-tract (motor or sensory) sign in the limbs.

Ask for the symptom in the patient's own words first, then shape it with the following questions. When did it start and was the onset sudden (over seconds), acute (over minutes to hours), subacute (days) or insidious (weeks to months)? Is it getting better, stable, or progressing, and is the progression constant or stepwise? Where exactly is it: one limb, one side, both legs, both arms and legs, or the whole body? What makes it better or worse: position, exertion, sleep, a specific movement? Are there associated symptoms: headache, visual change, speech change, swallowing, bladder or bowel change, fever, weight loss, numbness? What is the impact on walking, self-care, work and mood? Then ask about past medical history, vascular risk, medications, alcohol, smoking, family history, trauma, surgery and tetanus status, and about the person's occupation and whether they drive or work at heights.

Red flags in the history include a sudden worst-ever headache, a first seizure, rapidly progressive weakness over hours to days, new bladder or bowel dysfunction with back pain, a non-blanching rash with fever, and any new focal deficit. These do not wait for a complete examination; they trigger urgent action and referral in parallel with it. The most useful single question in neurology is not "what is wrong" but "what changed, and when"; a chronic symptom that changed character last week is more informative than a new symptom of identical character.

You need a torch (ideally bright, narrow beam), an ophthalmoscope, a tendon hammer, a pin or sterile safety pin for light touch and, where available, a cotton-wool wisp, tuning forks for vibration, a piece of cotton for temperature, a Snellen or near-vision chart, a ruler, and a scent such as coffee or peppermint for smell testing. A lower motor neuron screen also needs a tape measure to compare limb circumference. Keep the room quiet and warmly lit, and position the patient so that both arms and legs can be examined without the patient having to be turned repeatedly.

Introduce yourself, explain what the examination involves, how long it will take, and why it is needed. Obtain consent, offer a chaperone, and ask the patient to undress to underwear, keeping them covered between tests. Warn before any test that will feel sharp, cold or uncomfortable. Place the patient sitting on the edge of the couch with the legs dangling for reflexes, then lying if tone or sensation is to be tested in the lower limbs. Ask about pain before you begin and re-check it throughout.

The sequence below follows the conventional order; it can be shortened or re-ordered for a specific complaint, but the skill of extending it depends on knowing the whole sequence.

Start with the first sentence the patient speaks and whether it is sensible, since speech fluency, content and prosody tell you about frontal, temporal and subcortical function before any formal testing. A comprehensive neurologic examination should include evaluation of the sensorium, cognition, cranial nerves, motor function, sensory function ^[1]. Note orientation to person, place, time and purpose. Observe attention and concentration (for example, asking the person to repeat a short phrase, count backwards from twenty, or perform a serial subtraction task), register verbal memory by giving three unrelated words and testing recall immediately and after a delay, and assess language: fluency, comprehension, naming, repetition and reading. Test executive function by asking the patient to follow a two-step command, name as many words beginning with a letter as they can in one minute, or change from one rule to another. Visuospatial function is tested by copying intersecting shapes or drawing a clock. Mood, thought content and thought form, insight and judgement should be recorded, together with the risk of self-harm. Also record level of consciousness using eye, verbal and motor responses (the Glasgow Coma Scale), so that changes can be followed over time.

A full formal screen such as the Mini-Mental State Examination or the Montreal Cognitive Assessment (MoCA) is useful when you want a baseline or a number to follow over time. The MoCA is a 30-point screen in which 26 or more points is classified as normal cognitive performance, 18 to 25 as mild, 10 to 17 as moderate and 0 to 9 as severe impairment ^[6]; one point is added when the person has 12 or fewer years of education, with a maximum of 30 ^[6]. It has been validated for adults aged 55 to 85 ^[6]. The test and its administration instructions are copyrighted, so use a licensed copy and refer to local policy for the exact version.

Mental state findings that should raise concern include disorientation, inattention that worsens in the evening, and new language or behavioural change; these may represent delirium, a stroke in the dominant hemisphere, or a mass or infection affecting the brain.

Cranial nerve testing is the physical functional assessment of the nerves arising from the brain and innervating the head, neck, and trunk ^[2]. Work from the top down; test the nerves that share a function together. A useful order is: smell (I), vision (II), pupils and eye movements (III, IV, VI), facial sensation and corneal reflex (V), facial strength and taste (VII), hearing and balance (VIII), palatal and pharyngeal movement, gag and voice (IX, X), sternocleidomastoid and trapezius (XI), tongue (XII). Where time is short, a brief screen still covers visual acuity, visual fields, pupils, fundi, eye movements, facial movement, hearing, palate and tongue.

Smell (I): test each nostril separately with a non-irritant scent such as coffee or peppermint, with the eyes closed; an irritant such as ammonia tests the trigeminal nerve instead. The olfactory nerve can be damaged by frontal skull-base fractures and tumours, and smell may be absent in ordinary viral illness.

Vision (II): test distance acuity with a Snellen chart and near vision, visual fields by confrontation, and examine the optic disc and retina. Record the fields by quadrant. Test colour vision if optic neuritis is suspected.

Eye movements, pupils and III, IV, VI: inspect the lids for ptosis; test pupil size, shape and reaction to light (direct and consensual) and accommodation; swing a torch from one eye to the other to look for a relative afferent pupillary defect, which points to optic nerve or retinal disease on the affected side. Test abduction (lateral rectus, VI), adduction, elevation and depression (III, plus superior oblique for IV, tested by asking the patient to look down and in). Watch for nystagmus and for diplopia in each direction of gaze.

Facial sensation and corneal reflex (V): test light touch and sharp sensation in the three trigeminal divisions on each side, compare left with right, and test the corneal reflex (afferent V, efferent VII). Test the jaw jerk and the chewing muscles by asking the patient to clench.

Facial strength (VII): test eye closure, eyebrow elevation and cheek puffing, and ask the patient to show teeth and whistle. Look for upper and lower face involvement; an upper motor neuron lesion spares the forehead, a lower motor neuron lesion affects the whole hemiface including the forehead and eye closure.

Hearing and balance (VIII): test hearing with a whispered voice or a tuning fork, using the Weber and Rinne tests to separate conductive from sensorineural loss. Test balance with Romberg and with standing on one foot. Nystagmus with a peripheral vestibular loss fatigues and is usually unidirectional, while central nystagmus is often persistent, vertical or changing direction.

Lower cranial nerves (IX, X, XII) and accessory nerve (XI): listen to the voice for hoarseness and nasal quality; inspect palatal movement as the patient says "ah" and test the gag reflex with caution. Ask the patient to shrug the shoulders against resistance (trapezius, XI) and turn the head against resistance (sternocleidomastoid, XI). The tongue (XII) is inspected at rest for wasting or fasciculation, and protrusion is observed for deviation toward the weaker side.

Cranial nerve findings are peripheral nervous system findings that sit inside the skull; they localise a lesion to one nerve, a combination of nerves (brainstem syndrome or skull-base process), or the nerve's nucleus in the brainstem.

Observe posture and movement as the patient enters the room, undresses and lies down: does one arm drift when both are held out at shoulder height with the palms up, and does the hand pronate and drift over a short time (pronator drift)? Are the limbs restless, tremulous or dystonic? Inspect and measure muscle bulk in the shoulders, upper arms, forearms, thighs and calves, comparing sides. Wasting suggests a lower motor neuron, myopathic or disuse problem; enlargement can be congenital or from compensatory work. Look for fasciculation, the fine, irregular twitches of small patches of muscle that point to lower motor neuron irritability.

Tone is the resistance to passive movement. Test by moving each limb slowly and then quickly, watching for increased resistance that is constant (rigidity) or that increases at speed (spasticity). Cogwheel rigidity, most obvious in movement around one axis, suggests a disorder of the basal ganglia. Test tone in the arms (flexion and extension at shoulder, elbow and wrist) and the legs (hip, knee and ankle). Always include the trunk and neck if a generalised disorder or meningitic irritation is suspected.

Power is tested against gravity and resistance. Ask the patient to move against gravity, then against your hand, and attempt to quantify with the Medical Research Council scale, in which grade 0 is no contraction, 1 a flicker or trace of contraction, 2 movement through the full range with gravity eliminated, 3 active movement against gravity, 4 active movement against gravity and resistance, and 5 normal power ^{[4] [5]}. The scale is ordinal rather than a true measurement, so a comment about the pattern (fatiguing, pain-limited, give-way) is often more useful than the number, and a suspected pain-limited weakness should be recorded as such. Always test the major movements at each joint: shoulder abduction and adduction, elbow flexion and extension, wrist and finger flexion and extension, grip, hip flexion and extension, knee flexion and extension, and ankle dorsiflexion and plantar flexion. Compare side with side in the same movement rather than testing absolute strength.

Test the tendon (deep) reflexes by briskly tapping the tendon with the hammer while the muscle is relaxed and the joint is slightly flexed: biceps (C5 and C6), triceps (C7), supinator (C5 and C6), knee (L3 and L4) and ankle (S1). Document them as absent, diminished, normal, brisk or clonic, using the same wording throughout your notes. In a person whose reflexes are difficult to elicit, use reinforcement (the Jendrassik manoeuvre for the lower limbs, or asking the patient to clench the teeth for the upper) before concluding that they are absent. Test the superficial reflexes if relevant: abdominal (T8 to T12), cremasteric (L1 and L2) and anal (S2 to S4), noting that these depend on patient relaxation and abdominal wall function as much as on the nervous system.

Test the plantar response by stroking the lateral sole and across the ball of the foot with a blunt stimulus. In a healthy adult the big toe goes down (flexor response). An upgoing big toe with fanning of the other toes is an extensor plantar response (Babinski sign) and is a valuable upper motor neuron sign when it is present and correctly elicited. A withdrawal or flexor response is not the same thing and should be described as such.

Explain each test before you perform it. Test primary sensation with light touch (cotton wool), pain (pin, using the same pressure each time), temperature (a cold metal or plastic object) and vibration (tuning fork on bony points), and test proprioception by moving the distal interphalangeal joint up and down with the eyes closed. Compare symmetrical points. Map any sensory loss onto the dermatome and peripheral nerve distributions, recording exactly where the boundary is; the exact level of impaired pinprick or temperature is more important than the quality of the sensation in many cases, because disease of the spinal cord and cauda equina are often defined by levels.

Cortical (sensory) function is tested with two-point discrimination, graphesthesia, stereognosis and sensory extinction by simultaneous bilateral touch. These are disturbed by lesions in the parietal cortex or its sensory relay, even when primary sensation is intact.

Sensory findings are interpreted as: a peripheral nerve territory (for example, loss over the thumb and index finger in a median nerve lesion), a root territory (dermatomal), a sensory level across the trunk or legs (spinal cord), a hemisensory loss on one side of the body (brainstem or thalamus/cortex) or a glove-and-stocking pattern (peripheral neuropathy or functional presentation).

Ask the person to hold both arms out with the eyes closed and look for tremor and drift. Test rapid alternating movements (pronation and supination, finger tapping) and targeted movements (finger-to-nose, heel-to-shin) on each side, comparing speed and accuracy. Test dysdiadochokinesia and rebound if weakness is not present. Observe the eyes for nystagmus and the speech for scanning dysarthria. The cerebellum is not the only structure that coordinates movement, so a pure cerebellar picture requires that weakness, sensory loss and rigidity have been excluded. Cerebellar lesions tend to produce ipsilateral incoordination, while a lesion in the cerebellar peduncle or brainstem can produce a mixed picture.

Ask the person to walk a few metres, turn and walk back, watching arm swing, base, step length and symmetry, and whether the foot slaps the floor. Test heel-to-toe walking, walking on toes and heels, hopping and standing on one foot; ask the person to walk tandem. Test station by asking them to stand with feet together, then close the eyes (Romberg): a positive Romberg (increasing sway or fall with the eyes closed) points to proprioceptive loss rather than cerebellar disease, because the vestibular and motor systems are not enough on their own. Ask about falls, turning style (en bloc turning suggests parkinsonism) and seat-to-stand transfers. Do not ask a patient to do any manoeuvre that puts them at risk of falling; use a wall or a second person and stay close.

Upper motor neuron damage produces spasticity (velocity-dependent increase in tone), hyperreflexia, clonus, weakness that is worse for fine movements and extension than for flexion in the arm, and an extensor plantar response. It may be accompanied by wasting late, from disuse. Lower motor neuron damage produces wasting and fasciculation, reduced tone, weakness for the movements that the muscle performs, and reduced or absent reflexes in the same distribution as the weakness. A lesion of a nerve root produces a dermatomal sensory disturbance and a myotomal weakness; a peripheral nerve lesion produces a territory that does not match a dermatome or myotome.

Work backwards from the sensory loss to the anatomy. A single limb territory with motor findings and trophic change suggests a mononeuropathy or nerve root. Symmetrical glove-and-stocking loss suggests a length-dependent peripheral neuropathy. A sensory level across the trunk and symmetric lower limb loss suggests disease of the spinal cord. Dissociated sensory loss (loss of pain and temperature with preserved vibration and proprioception, or vice versa) suggests a lesion inside the spinal cord, such as a syrinx, or a lesion in the brainstem. Hemisensory loss with normal power points to thalamic or parietal disease.

A lesion of one cranial nerve is a peripheral (or skull-base) problem until proved otherwise. A combination of ipsilateral cranial nerve findings with contralateral long-tract signs points to the brainstem on the side of the cranial nerve finding. Multiple bilateral lower cranial nerve palsies with limb weakness raise the possibility of a problem at the foramen magnum or upper cervical spine. A sixth nerve palsy in isolation, especially if it appears with raised pressure inside the skull, can be a false localising sign rather than a pointer to the sixth nerve's own pathway.

Cerebellar ataxia is present whatever the eyes are doing, and is accompanied by nystagmus, dysarthria and incoordination of the arms. Proprioceptive (sensory) ataxia is worse with the eyes closed (positive Romberg) and is accompanied by loss of joint position and vibration sense. A patient with both sensory loss and an apparently cerebellar gait may have a lesion of the posterior columns or a peripheral neuropathy.

A localisation is a statement of level, side, and the evidence that supports it, rather than a diagnosis. The following algorithm is a teaching version of what experienced clinicians do; it is not a substitute for supervised practice.

When two possible levels remain, choose the one that explains more findings, and state what would change your mind. Write the localisation as a sentence, for example: "Right cerebral hemisphere infarct is most likely, on the basis of sudden onset, non-fluent aphasia and right hemiparesis with upper motor neuron signs, with no level suggesting the spinal cord or a peripheral process."

Write notes so that another clinician can repeat your examination. Use a standard layout: appearance and behaviour; orientation and speech; cranial nerves I to XII; arms (tone, bulk, power, coordination, reflexes, sensation); legs (same); gait and Romberg; plantar responses; summary and plan. For each abnormality record objective findings, not interpretations: "grade 3 power at left ankle dorsiflexion" rather than "weak".

Muscle power should be recorded on the Medical Research Council scale from 0 to 5, defined above, with the caveat that grade 4 covers a very wide band and that grades 4 minus, 4 and 4 plus were proposed by the Medical Research Council as a way of marking slight, moderate and strong resistance ^[5]. Scales such as these are ordinal descriptions, so add a clinical comment whenever a grade sits near the bottom of a category. ^[4]

Reflexes should be recorded with a consistent convention; many notes use absent, diminished, normal, brisk and clonic. Deep tendon reflexes are named by nerve root (biceps C5 to C6, triceps C7, supinator C5 to C6, quadriceps L3 to L4, Achilles S1) so that findings lead naturally to a level.

The standard anatomical reference for peripheral nerve and root territories is the Medical Research Council's Aids to the Examination of the Peripheral Nervous System ^[4]. Dermatomes are the territories of skin supplied by single spinal nerve roots; the commonly used anchor points are C5 over the deltoid, C6 thumb, C7 middle finger, C8 little finger, T1 medial forearm, T4 nipples, T10 umbilicus, L1 inguinal, L4 medial calf, L5 dorsum of foot, and S1 lateral foot and sole. Test the boundaries rather than naming a single spot, because dermatomes overlap.

The Glasgow Coma Scale is useful for describing the level of eye, verbal and motor responses serially when a person is drowsy, and should be recorded alongside the underlying examination rather than replacing it.

For mental state, the MoCA ranges quoted above can be recorded with the total score out of 30, the education correction, and the date, so that change is visible; the MoCA has been validated for ages 55 to 85 ^[6]. Screening scores are screening tools and should not be translated directly into a diagnosis.

The examination should be followed by a decision about urgency. Sudden-onset limb or facial weakness suggests a stroke or transient ischaemic attack and needs assessment against the NICE guidance on stroke and TIA in adults ^[3]. A facial pain with persistent facial numbness or abnormal neurological signs warrants neuroimaging using a suspected cancer pathway referral ^[3]. Rapidly progressive gait ataxia over days to weeks warrants urgent neurological assessment on a suspected cancer pathway ^[3]. A person with gradually progressive gait ataxia should be referred for neurological assessment with an alcohol history, thyroid function, vitamin B12 and folate, and serological testing for gluten sensitivity where local guidelines suggest it ^[3]. A person with gait apraxia, that is difficulty initiating and coordinating walking, should be referred to neurology or an elderly care clinic to exclude normal pressure hydrocephalus ^[3]. Blackouts with clear features of vasovagal syncope, even with brief jerking of the limbs, do not usually need routine neurological referral ^[3]. Red flags should be declared loudly in the notes and the plan, and if a finding is time-critical, act and record in parallel rather than after the rest of the examination.

Children: the examination changes with age and cooperation. The head circumference, neonatal reflexes and primitive reflexes, tone in flexion and extension, and the Hammersmith Infant Neurological Examination are the core, and developmental milestones belong alongside it. An infant who is hypotonic with poor social engagement needs urgent specialist assessment.

Older adults: dizziness, fear of falling, and visual or cognitive impairment often dominate, and the examination must be performed where the person can walk safely. Peripheral neuropathy, B12 deficiency and medication effects are common contributors.

People with communication difficulties: use visual cards, writing, pointing and proxy history, and record what method was used. A person with aphasia after a stroke may be neurologically intact in all other domains.

The longest part of a neurology examination costs nothing: observation, detailed history, ophthalmoscopy, tendon hammer work, paper and pen, and repeated comparison of one side with the other. Vibration sense can be tested with a tuning fork or even a struck table leg. If brain imaging is not available, localisation and a careful watch for red flags become more, not less, important; write the plan so that a clinician at the referral hospital can see your reasoning. Equipment that is often missing, such as a strong torch for fundoscopy, can be improvised or borrowed before a transfer.

• The examination follows a fixed order, but each step is a question: mental state, cranial nerves, motor, reflexes, sensation, cerebellar function, gait.
• Define every abnormality by which function is lost, by which side, and at what level, before thinking about a diagnosis.
• Upper motor neuron signs are spasticity, hyperreflexia, clonus and an extensor plantar response; lower motor neuron signs are wasting, fasciculation, flaccidity and lost reflexes.
• MRC grades are an ordinal scale; a number without a description of how it was obtained is not useful.
• Sensory level and pattern localise better than a single sensory symptom; map dermatomes precisely.
• A positive Romberg implies proprioceptive loss; cerebellar ataxia is present with the eyes open.
• Cranial nerve findings combined with crossed long-tract signs localise to the brainstem.
• Write what you did, not only what you concluded, and explain your localisation as a sentence with the evidence.
• Screening scores such as the MoCA support but do not replace clinical judgement.

Neuroanatomy, neuroimaging, stroke and transient ischaemic attack, traumatic brain injury, brain death and determination of death by neurological criteria, coma and unconsciousness, headache, epilepsy, peripheral neuropathy, motor neuron disease, Parkinson disease, multiple sclerosis, cerebellar disorders, and functional neurological disorder.