Basic neurological examination

• 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
• the odor should be detected and identified
• 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 (to detect 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)

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)

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 motor neuron disease (MND)
    
  • look for possible deviation
• 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 peripheral lesion, given that the corticobulbar tract has both contralateral and homolateral components
    
  • peripheral lesions are accompanied by atrophy;  fasciculations indicate nuclear involvement – usually MND)