ADD-ONS / GENERAL NEUROLOGY

Basic neurological examination

David Goldemund M.D.
Updated on 17/01/2024, published on 28/08/2023

the neurological examination consists of several components that assess various neurological functions
the purpose of the examination is to localize the lesion
the basic set of clinical tests is discussed in this chapter
- the level of detail of the examination depends on the actual setting (e.g., rapid evaluation in ER or CT scanner), the patient’s history, and symptoms
- a complete examination used to diagnose various neurological conditions is time-consuming; additional tests may be required, such as the Dix-Hallpike test, testing of specific symbolic functions, MMSE, brainstem reflexes, tests for detecting thoracic outlet syndrome, etc.)
- in acute stroke settings, the items that constitute the NIH stroke scale are of paramount importance

Example of a normal neurological finding

the patient is alert and has intact cognition, alertness, and orientation (to time, place, and person)
there is no dysarthria or aphasia
the visual field is intact, eye movements are unrestricted, without nystagmus and diplopia, pupils are isocoric with symmetrical and brisk reaction to light
facial innervation is intact, as are the remaining cranial nerves
extremities have normal tone and strength (5/5) bilaterally, there is no evidence of atrophy or fasciculations
deep tendon reflexes are normal (2+)
no ataxia and dysmetria, no pathologic reflexes
gait, balance, and coordination are normal
no meningeal signs
all sensory modalities are preserved

Mental status

rapid mental status assessment is an integral part of the acute stroke evaluation (most commonly LOC, attention, and orientation are tested as components of the NIH Stroke Scale (NIHSS)
level of consciousness (LOC)
- → Glasgow Coma Scale (GCS)
- AVPU scale (Alert, Verbal, Painful, Unresponsive)
attention and concentration
orientation (to person, time, and place)
- what day is it? (exact date or day of week)
- where are we?
- how old are you?
- where do you live?
memory – evaluate both short-term and long-term memory; add Mini-Mental Status Examination (MMSE) if needed
visuospatial functions
- ask the patient to draw a clock face with all the numbers in the correct positions
- ask the patient to copy a simple geometric figure (e.g., a triangle or square)
patient’s behavior and mood, note signs of delirium (
- Confusion Assessment Method for the ICU (CAM-ICU) is useful for detecting delirium in non-verbal or mechanically ventilated patients
- signs of delirium:
  - fluctuating levels of consciousness
  - disorientation to time and place
  - impaired attention and concentration
  - agitation or drowsiness
  - hallucinations or delusions

AVPU scale

scale is useful to rapidly grade a patient’s level of consciousness, responsiveness, or mental status:
- Alert – the patient is aware of the examiner, can respond to the environment around them, follow commands, open their eyes spontaneously, and track objects
- Verbally responsive – the patient’s eyes open only in response to a verbal stimulus directed toward them. The patient can react to that verbal stimulus directly and in a meaningful way
- Painfully responsive – the patient responds (move, moan, cry) to painful stimuli only
- Unresponsive – the patient does not react spontaneously to verbal or painful stimuli
correlation of AVPU and GCS
- GCS Score 15 – alert
- GCS 12 to 13 – verbally responsive
- GCS 5 to 6 – physically responsive
- GCS 3 – unresponsive

Speech

rapid evaluation of speech is essential, as it is a key component of the NIHSS score
during conversation, assess speech and focus on two main aspects:
- phatic functions (ability to understand spoken language, obey commands, name objects, and produce spontaneous fluent speech
- articulation and phonation (articulation, volume, phonation, melodicity)
aphasia typically suggests a lesion in the dominant cerebral hemisphere, often involving Broca’s or Wernicke’s area
dysarthria may indicate either cortical or subcortical lesions, making it a poor localizing sign

Cranial nerves (CN)

the cranial nerves (CN) innervate structures in the head and neck; they have motor, sensory, and autonomic functions
the olfactory nerve (CN I) and the optic nerve (CN II) originate from the cerebrum, while CN III-XII exit from the brainstem
abnormalities in cranial nerve function assist in localizing lesions to specific areas of the brain or brainstem
- a single cranial nerve lesion suggests peripheral neuropathy (very rarely caused by an isolated nuclear lesion)
- brainstem lesions usually involve multiple cranial nerves + motor/sensory tracts
  - a unique set of signs and symptoms (usually a combination of nuclear and fascicular lesions) form well-recognized brainstem syndromes (such as Wallenberg syndrome, Millard-Gubler syndrome, Weber’s Syndrome)
items usually examined in acute stroke settings are part of the NIH Stroke Scale
- LOC, orientation, and attention
- speech – dysartria x aphasia?
- visual impairment?
- conjugate or disconjugate gase palsy? diplopia?
- facial paresis?
- paresis?
- sensory impairment

CN I – Olfactory nerve

testing involves evaluating the patient’s sense of smell; test is often omitted in emergency settings
one nostril at a time is tested while the other is covered (odor detection and then identification)
most common pathologies:
- anosmia (COVID and other infections, nasal polyps, allergies, traumatic lesion of the cribriform plate, Parkinson’s disease, lesions at the base of the skull)
- hyposmia – reduced ability to smell, may be due to partial nerve damage or other non-neurological factors

CN II – Optic nerve

visual acuity (each eye separately, using Snellen chart or a similar tool)
visual fields
- test all quadrants, including simultaneous stimulation (neglect)
- perimetry
pupillary light reflex – evaluate direct and consensual pupillary responses to light (CN II serves as an afferent pathway)
- altered light reflex involves an abnormal constriction in response to light stimulation; it indicates either an optic nerve lesion or a lesion of the efferent path
fundoscopy – check the optic disc for signs of swelling, pallor, or hemorrhage
color vision (using Ishihara plates or a similar method)

Altered light reflex

afferent pathway lesions: optic nerve damage may result in a poor or absent light reflex
efferent pathway lesions: oculomotor nerve (CN III) dysfunction can lead to sluggish or absent pupillary constriction
- transtentorial herniation may cause unilateral or bilateral fixed, dilated pupils (due to the CN III compression)
sympathetic Pathway: Horner’s syndrome may result in miosis and a slower dilation response
pharmacological agents
- atropine or phenylephrine may cause mydriasis
- opioids may cause miosis

CN III, IV, and VI – Oculomotor, trochlear, and abducens nerves

these cranial nerves control the extraocular muscles and facilitate coordinated eye movements
inspection – assess for ptosis, strabismus, or other abnormal eye position
testing:
- extraocular movements
  - smooth pursuit – the patient is asked to follow the examiner’s finger with their eyes; test movement in all directions, including vergence (focusing on a near object)
  - saccades (fast eye movements involved in acquiring new visual targets) – instruct the patient to quickly shift gaze between two horizontally or vertically aligned targets without moving the head
  - during the examination, ask about diplopia and note any strabism or involuntary eye movements (indicating vestibular or central nervous system involvement)
- pupillary response
  - direct and consensual light reflex (see CN II) – normal, poor or absent reaction
  - assess miosis and convergence facilitated by the near vision
abnormal findings:
- disconjugate eye movements
  - uncoordinated or asymmetrical movements, often indicative of a lesion affecting either the brainstem or the peripheral nerves involved in ocular motility
  - the oculomotor nerve lesion leads to ipsilateral dilated pupil, ptosis, and outward and downward deviation of the eye
  - lateral deviation of the eye (lateral rectus muscle palsy) is typical for the lesion of the CN VI; bilateral palsy may be caused by intracranial hypertension
  - Internuclear Ophthalmoplegia (INO) – a brainstem lesion affecting the medial longitudinal fasciculus leads to impaired adduction in the eye ipsilateral to the lesion during horizontal gaze, with nystagmus in the abducting contralateral eye
  - skew deviation – a vertical misalignment of the eyes due to a brainstem or cerebellar lesion
  - One-and-a-half syndrome – a combination of INO and a horizontal gaze palsy, typically due to a unilateral brainstem lesion
- conjugate gaze palsy (vertical, horizontal)
  - impairment of coordinated (horizontal or vertical) eye movements due to a lesion affecting the supranuclear pathways or gaze centers; both eyes are affected symmetrically
  - horizontal gaze palsy – lesions affecting the cortex or the paramedian pontine reticular formation (PPRF) and the abducens nucleus
    - contralateral cortical lesion (“patient looks at the infarct lesion”); eyes are deviated toward the lesion
    - contralateral brainstem lesion; eyes are deviated from the lesion
  - vertical gaze palsy – lesions in the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) or the posterior commissure can impair upward and/or downward gaze
nuclear lesion may be associated with involvement of brainstem pathways (Weber syndrome) → brainstem syndromes

CN V – Trigeminal nerve

CN V is responsible for facial sensation and masticatory muscle control
- examination is essential for diagnosing conditions like trigeminal neuralgia, tumors affecting the cerebellopontine angle, etc.
sensory testing: evaluate light touch, pain, and temperature sensation in the three divisions (ophthalmic, maxillary, mandibular) on both sides of the face
corneal reflex: gently touch the cornea with a cotton wisp and observe for a blink response (move from side to avoid triggering the blink reflex)
- corneal reflex is tested in comatose patients to assess the level of brainstem lesion
- absence of the reflex in an awake patient suggests a lesion of the trigeminal or facial nerve or both
jaw-jerk reflex: tap the jaw with a reflex hammer while the mouth is slightly open (exaggerated reflex is a sign of upper motor neuron lesion)
motor testing: assess the strength of the masseter and temporalis muscles by asking the patient to clench their teeth and move the jaw from side to side; palpate and visually inspect for muscle wasting and asymmetry

CN VII – Facial nerve

supplies the facial muscles, stapedius muscle, and sensory (taste) information from the anterior 2/3 of the tongue (via the chorda tympani branch)
- the general somatic sensations like touch, temperature, and pain from this region are conveyed via the lingual nerve, a branch of the mandibular division of the trigeminal nerve
patient is asked to raise their eyebrows, close their eyes tightly, smile, and blow up their cheeks
weakness of the entire side of the face is indicative of either a peripheral lesion or damage to the facial nucleus on the ipsilateral side (like in Bell’s palsy or a pontine infarct)
- peripheral lesion can also present with hyperacusis and loss of taste to the anterior 2/3 of the tongue
weakness of the lower half of the face with sparing of the forehead is suggestive of a supranuclear lesion contralateral to the palsy (motor cortex)
- forehead has innervation from both the left and right sides of the motor cortex

CN VIII – Vestibulocochlear nerve

examination involves the assessment of both auditory and vestibular functions
assessment of hearing
- asses ability to discern words or sentences at a low volume or rubbing fingers close to the ear
- audiometry (gold standard)
- if a hearing deficit is established, doing the Weber and Rinne tests enables conductive vs. sensorineural hearing loss differentiation
  - a normal Rinne exam will exhibit air conduction (AC) greater than bone conduction (BC), a conductive hearing loss will show BC greater than AC; in patients with sensorineural hearing loss, AC will be greater than BC, but for a shorter duration when compared to a normal subject
  - a normal Weber test shows hearing the sound/vibration equally in both ears. A conductive hearing loss will lateralize the sound to the abnormal ear, while a sensorineural hearing loss will lateralize to the normal ear
vestibular testing
- note any nystagmus, imbalance (tonic deviation of arms or while standing), or other signs of vestibular dysfunction
- Head Impulse Test (HIT) – assesses the horizontal vestibulo-ocular reflex (VOR); particularly useful for diagnosing acute unilateral vestibular lesions
- caloric stimulation (evaluates a unilateral vestibular dysfunction) – warm or cold water irrigation of the external auditory canal is used to stimulate the vestibular apparatus, observing for nystagmus
- Dix-Hallpike Maneuver (used to diagnose benign paroxysmal positional vertigo)

Head Impulse Test (HIT)

HIT is a diagnostic maneuver employed to assess the vestibulo-ocular reflex (VOR) and evaluate acute peripheral vestibular function
The procedure involves the following steps:
- the patient is seated and instructed to fixate on a target directly ahead
- the examiner quickly rotates the patient’s head horizontally to one side, approximately 15-20 degrees, without warning
- the examiner observes the patient’s eyes for corrective saccades
results:
- negative HIT – eyes remain fixated on the target, indicating a functional VOR and suggesting that peripheral vestibular function is intact
- positive HIT – eyes make a corrective saccade to re-fixate on the target, indicative of a deficient VOR and suggestive of a peripheral vestibular lesion on the side to which the head was turned

CN IX and X – Glossopharyngeal and vagus nerves

CN IX and X innervate the pharynx and posterior third of the tongue
the vagus nerve also innervates the larynx and upper portion of the gastrointestinal tract
assess the patient’s speech, seek for hoarseness or nasal speech
the patient may also be asked to swallow some water and observed for coughing or gurgling, which may indicate weakness of the muscles involved in swallowing
ask the patient to open the mouth and say “aaaa,” and observe the symmetry of the palatal arch
- the deviation of the uvula to one side indicates a vagal nerve lesion on the opposite side

CN XI – Spinal accessory nerve

innervates the sternocleidomastoid and trapezius muscles
assess for tone, muscle atrophy, or asymmetry in the neck and shoulder regions
test motor function and compare both sides:
- instruct the patient to rotate the head against resistance
- ask the patient to shrug the shoulders against resistance
- examine the extent of cervical rotation and shoulder elevation

CN XII – Hypoglossal nerve (nervus hypoglossus)

provides motor innervation to the tongue
examination involves inspecting the tongue in the relaxed position within the oral cavity
- the presence of increased corrugation and fasciculations may indicate a lower motor neuron disease (MND)
- deviation to one side is a marker of contralateral peripheral lesion
instruct the patient to protrude the tongue and move it laterally
- the deviation to one side upon protrusion suggests either a contralateral central lesion or an ipsilateral peripheral lesion (due to the predominance of the intact genioglossus muscle)
- the central lesion is less pronounced than a nuclear lesion, given that the corticobulbar tract has both contralateral and homolateral components
- peripheral lesions are accompanied by atrophy; fasciculations indicate nuclear involvement – usually MND)

Cerebellum

these tests evaluate cerebellar functions (coordination, balance, and fine motor skills)
finger-to-nose / finger-to-finger test
- tested with the eyes open; the patient is instructed to touch their nose and then the examiner’s extended finger, alternating between the two in a repetitive manner
  - you can increase the difficulty of this test by adding resistance to the patient’s movements or moving your finger to different locations
- normal finding: the task is performed with precision, touching both the nose and the examiner’s finger accurately
- abnormal finding: the patient’s finger overshoots or undershoots the target (dysmetria), an intention tremor may be observed
heel-to-shin test
- the patient is asked to place the heel on the knee of the opposite leg and then slide the heel in a straight line down the shin
- normal finding: the movement is smooth and accurate, with the heel maintaining contact with the tibia throughout the movement
- abnormal finding: dysmetria, or a lack of coordinated movement (ataxia), tremor or decomposition of movement
rapid alternating movements (tests for dysdiadochokinesia)
- foot or finger tapping
- pronation-supination test (the patient is asked to pronate (turn the palm down) and supinate (turn the palm up) their hands as quickly and smoothly as possible for 5 seconds)
- protrusion-retraction of tongue
Romberg test and gait analysis (see separate tab)
speech (scanning speech in cerebellar disorders causes enunciation of individual syllables
assess tonus (hypotonia in cerebellar syndrome)

Motor exam

muscle inspection (look for deformities, fasciculations, hypertrophy, or atrophy)
palpate muscles to assess for mass lesions or localized pain
assess the tonus (resistance to passive motion in the major joints)
- differentiate between normal tonus, flaccidity, spasticity, or rigidity
assess strength
- scored 0-5, from “none” to “normal”
- compare left and right sides and differentiate between proximal x distal weakness
- arm tests
  - Mingazzini test – extremities are extended horizontally with palms down and eyes closed; assess for drop (which indicates weakness)
  - grip strength and fine motor skills of the hand
    - perform fine motor tasks, such as writing or picking up small objects
  - Dufour test – both extremities are extended horizontally in maximum supination with eyes closed; assess for possible pronation and drop
- legs tests
  - Mingazzini test – the patient lies supine and raises the legs with the knees bent at 90 degrees. Failure to maintain the position indicates weakness (exclude pain, etc.)
  - test hip and knee flexion, extension, plantar and dorsal ankle flexion
  - tiptoe and heel walking (see gait)
estimate lesion type: cortical, brainstem, spinal cord, peripheral nerve, or muscle disease

Deep tendon reflexes / pathologic reflexes

reflexes help differentiate upper from lower motor neuron lesions
- deep tendon reflexes (DTR)
- pathologic reflexes

Deep tendon reflexes

assessed by tapping specific tendons with a reflex hammer
- biceps reflex (C5-6) – striking the biceps tendon while the patient’s arm is partially flexed at the elbow elicits flexion of the elbow
- brachioradialis reflex (C5-6) – striking the tendon near the wrist elicits the flexion and supination of the forearm at the elbow joint
- triceps reflex (C7-8) – striking the triceps tendon just above the olecranon process while the patient’s arm is flexed at the elbow elicits a contraction of the triceps brachii muscle, leading to extension of the elbow
- patellar/knee-jerk reflex (L2-L4) – striking the patellar tendon below the patella while the patient’s leg is relaxed and slightly bent at the knee elicits a contraction of the quadriceps femoris muscle, leading to a brief extension of the knee
- Achilles tendon reflex (S1-S2) – striking the Achilles tendon at the level of the ankle joint elicits a contraction of the gastrocnemius and soleus muscles, leading to plantarflexion of the foot
reflex scoring: 0 – absent, 1+ – hypoactive, 2+ – normal, 3+ – brisk, 4+ – nonsustained clonus, 5+ – sustained clonus
- hypo-/areflexia indicates a lower motor neuron lesion or spinal shock
- hyperreflexia and clonus indicate an upper motor neuron lesion
  - when an upper motor neuron lesion occurs, the cortical inhibition of lower motor neurons is reduced, which can cause the reflexes to become hyperactive and clonus to occur

Pathologic reflexes

the presence of these reflexes is generally considered abnormal in adults and is indicative of the upper motor neuron or central pathways lesion)
Hoffman’s sign: pathologic flexion of the thumb and/or index finger upon flicking the nail of the middle finger
Babinski sign: lateral plantar stimulation provokes the upgoing of the great toe
Chaddock’s sign: similar to Babinski, elicited by stroking lateral malleolus with a blunt object
- in a positive Chaddock’s sign, the great toe will extend upward
- not as common as Babinski’s sign
Oppenheim’s sign: dorsiflexion of the great toe elicited by pressure along the medial tibia
clonus: rhythmic oscillations following sustained stretch, commonly at the ankle

Sensory examination

sensory exam evaluates the integrity of the sensory pathways, distinguishing normal, diminished (hypesthesia/anesthesia), or exaggerated sensation (hyperesthesia, dysesthesia)
modalities tested:
- light touch (using a cotton wisp or fingertip, the examiner gently touches the patient’s skin to assess their ability to feel the stimulus.)
- pain and temperature (using a sharp object and warm/cold objects)
- vibration (using a tuning fork placed on bony prominences)
- two-point discrimination (assessed using calipers or a paperclip)
- proprioception (positional sensation) (tested by moving the patient’s finger or toe up and down, touching the nose with eyes closed)
- higher-order sensory functions like stereognosis, graphesthesia, and tactile neglect may also be evaluated (not part of the basic neurological exam)
  - stereognosis is the ability to recognize objects by touch, graphesthesia is the ability to identify numbers or letters traced on the skin, and tactile neglect is the inability to perceive stimuli on one side of the body
  - these higher-order sensory functions are not typically part of the basic neurological exam
in the acute stroke setting, commonly only touch sensation and tactile neglect are assessed
examination often follows a dermatomal pattern to identify lesions in specific spinal cord segments or peripheral nerves
focus on the patient’s symptoms, describe the extent of the deficit and its characteristics
topical diagnosis:
- cortical lesion (typically contralateral hemihypesthesia + higher-order sensory dysfunction
- brainstem lesion (d
- spinal cord lesion (sensory level, d)
- radiculopathies (specific dermatome lesions)
- neuropathies (glove-stocking pattern, usually in the lower extremities)

Gait and standing

Bracht-Romberg test (used to test proprioception and cerebellar function)

B-R I – patient standing with feet apart, eyes open
B-R II – patient standing with feet together, eyes open
- sharpened B-R – feet in tandem
BR III – patient standing with feet together, eyes closed
- loss of balance in this position may indicate deficits in proprioceptive pathways
Romberg IV, V – patient standing with feet together, eyes closed, head turned to the right (IV) or left (V)

Gait

assess walking at least 3 meters and back
gait indicates the patient’s level of function – look at the base, stride length, arm swing, turns (how many steps are needed), and symmetry
- consider comorbidities and other factors (arthritis, obesity, pain, etc.) into account
test modification – walking with eyes closed, tandem gait, tiptoe, heel walking, etc.
examples of abnormal gait:
- paretic
- spastic
- antalgic (pain-induced)
- ataxic (cerebellar or sensory impairment)
- hypokinetic (slow, short steps):
- dyskinetic (involuntary movements, such as dystonia or athetosis)
- myopathic

Meningeal signs

meningeal signs indicate irritation of the meninges (most commonly due to infection, subarachnoid hemorrhage, or meningeal carcinomatosis)
the following tests are used:
- assessment of nuchal rigidity: if positive, passive flexion of the patient’s neck causes pain and resistance (also check rotation and lateroflexion to rule out cervical-cranial syndrome)
- Kernig sign: passive extension of the knee, while the leg is flexed at the hip in a supine patient, causes pain
- Brudzinki sign: passive neck flexion causes reflex knee flexion in the supine position