Neurology Tutorial

Full Neurology Exam

  • Mental status
  • Cranial nerves
  • Motor examination
  • Gait and coordination
  • Sensory examination


Mental status

  • Level of consciousness, orientation, memory, and attention
  • There are a number of standardized tests of mental status that are used primarily in the detection and assessment of dementia such as the MMSE, MOCA and the SLUMS.
    • Level of consciousness
      • Are they alert, lethargic (sleepy), stuporous (can’t be aroused but may moan or withdraw) or comatose (no purposeful response to stimuli)?
    • Orientation
      • What is your name? Where are we? What is today’s date?
    • Memory
      • Ask them to remember 3 random words (pencil, umbrella, green) and ask them to repeat them (tests registration) and then ask them again after several minutes.
    • Attention
      • Digit span testing is performed by having them repeat a series of numbers- they should be able to easily remember 5 numbers (like a zip code).
      • Serial 7s is done by asking the patient to start from 100, subtract 7, and then subtract 7 from that number.
      • Have them spell the word world backwards.


Cranial Nerves

  • CN I
    • Test olfactory with easily recognizable scents one nostril at a time.
  • CN II
    • Assess far and near vision using an eye chart.
    • Assess visual fields in all 4 quadrants.
    • Funduscopic examination.
  • CN III
    • Assess pupils for size, and whether they constrict to light and near vision.
    • Swinging flashlight.
  • CN III, IV and VI
    • Assess extra ocular muscle movement by having them look in the 6 cardinal directions.
    • Assess diplopia with cover/uncover testing.
  • CN V
    • Test facial sensation in the 3 regions of the face (V1,2,3) with light touch, temperature with the tuning fork.
    • Test chewing muscle contraction by feeling clenched jaw muscles.
    • Jaw jerk if trying to differentiate the cause of UE hyperreflexia from cervical vs higher sources.
      • Normally the jaw jerk is minimal or absent.
    • CN VII
      • Test facial muscles by having patient raise eyebrow, keep eyes shut as you try to pry them open gently, puff cheeks with air, show their teeth, tense platysma by turning corners of the mouth down.
      • Taste (anterior 2/3rds) with sweet/salty/sour on a cotton applicator.
      • Test corneal reflex in comatose patients
    • CN VIII
      • Hearing assessment, Weber and Rinne.
      • Vestibular function if comatose or having vertigo with HINTS (head impulse, nystagmus, test of skew) with INFARCT predicting stroke (impulse normal, fast phase alternating, refixation on cover test more consistent with central causes).
      • COWS with caloric testing
    • CN IX, X
      • Have them open their mouth, say “ah”, look at the palate and uvula.
      • Gag in comatose.
    • CN XI
      • Shrug shoulders with you resisting them, have them turn their head to the side and push their chin towards the midline against your hand.
    • CN XII
      • Stick out their tongue, point it to left and right.


Motor Exam


  • Assess patient’s overall appearance.
  • Positioning (any posturing?); Movements (tremor, chorea).
  • Muscle bulk
    • Look for atrophy, abnormal hypertrophy. Atrophy can be seen in hand/feet muscles in neuropathic diseases such as diabetes.
  • Look for fasciculations.
  • Gait assessment.


Palpation and (rarely) percussion

  • This is not routinely performed but should be done if you suspect myositis (should have tenderness) and percussion can be performed if you suspect myotonia.



  • Findings in the assessment of tone:
    • Normal tone
    • Hypotonia
    • Hypertonia
      • Spasticity, rigidity, and paratonia
        • Spasticity is increased tone due to UMN disease that is most apparent in the mid-range of motion and is velocity-dependent.
        • Rigidity is a continuous resistance to passive movement, and is seen in diseases of the basal ganglia such as Parkinson’s.
          • Lead pipe rigidity is a continuous resistance to passive movement involving flexors and extensor muscles (no preference, as opposed to spasticity) throughout their full range of movement that is velocity-independent (does not matter if you move them fast or slow).
          • Cogwheel rigidity is a rigidity with superimposed tremor, leading to the cogwheel sensation, classically seen in Parkinsonism.
          • Tone can be increased or provoked by moving another part of the body while doing the exam, as by having the patient shake their head back and forth while testing for tremor or cogwheeling in the upper extremity.
          • Patients with cerebral palsy can have a mixture of spasticity and rigidity.
        • Paratonia (gegenhalten – German for against resistance) is the appearance of increased tone, seen in patients with dementing illness who resist all attempts at passive range of motion testing. The increased tone is not present at rest, and is equal and opposite to the force that you apply.
      • Myotonia is sustained contraction due to impaired relaxation, seen in myotonic dystrophy and myotonia congenita.
        • Patients with myotonic dystrophy may have a characteristic hand shake, where they are unable to relax their grip after squeezing your hand, and may exhibit percussion myotonia (sustained muscle contraction after inducing stretch reflex).



  • Scale:
    • 0 = no movement
    • 1 = flicker or fasciculations
    • 2 = movement with gravity removed
    • 3 = movement against gravity alone, but not against any added resistance
    • 4 = movement against some resistance but abnormally weak
    • 5 = normal strength
  • When testing muscle strength, the following observations may be helpful:
    • Muscles are strongest when they are acting from their shortest position, and are weakest when they are fully lengthened (the opposite of Starling’s law with the heart).
    • The biceps and hamstrings are strongest when flexed, triceps and quadriceps are strongest when extended.
      • In strong patients, most examiners will be overpowered by testing in their shortest, strongest position, so test them with the muscle lengthened (elbow bent while testing triceps, straight when testing biceps)
        • Extend the flexors, flex the extensors to get the strong muscles into a weaker position
      • In general, the antigravity muscles are the strongest. These include the neck extensors, arm extensors, wrist and finger flexors, leg extensors and plantar flexors.
      • When testing strength, have an organized approach, starting from the neck and ending with the toes.
        • In a simple screening exam, when your suspicion for significant deficits is low, you will just be testing the main muscles of the limbs, while in patients you suspect have a neurologic illness a more complete exam may be appropriate.
          • In myopathies, concentrate on the proximal muscles.
          • Axonal neuropathies, the distal.
        • Test the following muscle groups:


Deltoid Triceps Bicep Wrist Ext Wrist Flex Digital Interossei Hip Flex Hip Ext Knee Flex Knee Ext Ankle Plantar flex Ankle


Left 5 5 5 5 5 5 5 5 5 5 5 5
Right 5 5 5 5 5 5 5 5 5 5 5 5



  • Muscle stretch reflexes assess the integrity of both the sensory neurons on the muscle as well as the motor neurons to the muscle and the connections to and from the brain.
  • When a muscle is stretched, as by striking it or its tendon, it will reflexively contract.
    • Hyperreflexia
      • Hyperreflexia is a classic sign of UMN disease and hyperthyroidism.
      • Hyperreflexia in one limb or in lower but not upper extremities can help localize lesions.
    • Hyporeflexia
      • Hyporeflexia or areflexia can be seen in LMN disease, myopathies, peripheral neuropathies.
      • Patterns of hyporeflexia or areflexia can also localize lesions or suggest a category of disease.
        • Peripheral neuropathies are length-dependent, with loss of distal > proximal reflexes.
      • Absent reflexes is a cardinal feature of Guillain-Barré.
      • Remember that hypothyroidism can cause hung up reflexes, often best seen in the Achilles tendon.
    • Reflexes are graded on a 0-4 scale with 2 being normal
      • 0 – No response
      • 1 – Present but only with reinforcement
      • 2 – Normal
      • 3 – Brisk but no clonus
      • 4 – Markedly abnormal, with clonus
    • Technique
      • It is all in the wrist – swing the hammer smoothly and briskly. The amount of force needed varies as some patients have reflexes with even light percussion, while others may require a stronger blow.
      • The muscle needs to be as relaxed as possible – try to distract your patient, move the joint a few times to loosen the muscle.
        • Reinforcement is the contraction of other muscle groups away from the stretched muscle that may bring out the reflex, such as having the patient clench their teeth when checking upper limb reflexes, or having them grip their fingers and try to pull them apart (Jendrassik maneuver) when checking lower limb reflexes.
      • Sometimes the muscle can be felt better than seen.
        • Feel the quadriceps rather than looking for a dramatic leg kick.
      • Some reflexes are better obtained by tapping your own finger or thumb rather than the tendon.
        • This is true for the jaw jerk, biceps, and brachioradialis.


Coordination and Gait

Tests of Cerebellar function

  • Arms
    • Have the patient hold their arm outstretched with eyes closed, and suddenly push them up or down, looking for oscillations, over correction.
    • Finger to nose.
    • Dysdiadochokinesis.
  • Legs
    • Heel to shin.
    • Heel tapping.
  • Trunk
    • Have the patient sit up from a supine position without using their arms, looking for truncal ataxia.
    • Tandem gait.


Sensory Exam

  • Test light touch bilaterally with your fingers or a piece of cotton.
  • One approach is to check both sides in a variety of dermatomes, such as:
    • Shoulders (C4)
    • Inner/outer forearm (C6/T1)
    • Thumb/pinky (C6/C8)
    • Front of thigh (L2)
    • Medial/lateral calf (L4/5)
    • Little toe (S1)
    • Medial buttock (S3)
  • Test pain with a disposable pin or a broken tongue blade.
  • Test temperature by comparing the cool tuning fork to your (presumably) warm finger, or to something warmed up (like another tuning fork) again with their eyes closed, having them say warm or cold.
    • Test vibration with a 128 Hz tuning fork on the distal phalanx of the fingers and toes below the nail bed (a 256 Hz may also be used but there are some standards developed around the 128).
    • Test proprioception by holding the sides of the fingers and toes and moving them up or down and seeing if the patient can tell which direction they are moved , again with eyes closed.


Cortical Sensory Functions:

  • Two-point
  • Stereognosis
  • Graphesthesia
  • Extinction



Two questions you should ask when dealing with a neurological problem are; where is the lesion and what is the lesion? The answer to the first question can help in answering the second question, both by narrowing the differential diagnosis, and also by helping you to choose the best follow up imaging or laboratory tests.


Time course: Can help answer what the lesion is.

  • Acute (seconds to hours)
    • Suggests ischemia, hemorrhage, seizure, or trauma.
  • Subacute (days to months)
    • Suggests an expanding lesion, as in tumors or infection, or demyelination.


 Rules for localization of weakness

Upper motor neuron

    • Includes nervous tissue from the cortex down to (but not including) the anterior horn cells.
    • Features:
  • Increased tone, especially in the UE flexors and LE extensors.
  • Hyperactive reflexes.
  • “Pyramidal pattern” of weakness (weak UE extensors/abductors, weak LE flexors/adductors).
  • Positive Babinski, Hoffman’s, pronator drift, or rolling tests.
  • Decrease in the superficial reflexes (abdominal, cremasteric, anal).
  • May have sensory findings, which may be cortical (astereognosis, agraphesthesia) or may affect entire limb.
    • Motor cortex lesions
      • Can affect the contralateral half the body or just one part of the body.
      • Presence of aphasia, visual field defects, cortical sensory loss or seizures locate the lesion in the cortex.There may also be sensory loss if the sensory cortex is also involved.
    • Internal capsule
      • Remember FATL (face, arm, trunk, leg) as they all run close together in the posterior limb. There is no cortical sensory loss or any of the above cortical signs with a stroke here.
    • Brainstem
      • Face involvement means brainstem or above (exception is CN V which extends to upper cervical cord).
      • Look for cranial nerve involvement on the ipsilateral side, body contralateral.
        • CN III and IV in midbrain.
        • CN VI and VII in pons.
        • CN VIII in pontomedullary junction.
        • CN IX-XII in medulla.
    • Cord lesions
      • Spinal cord lesion suggested by findings of a sensory level, pain and temperature loss on contralateral side of body, no deficits in face, presence of LMN findings as well (atrophy, fasciculations).
      • Above C5, ipsilateral hemiparesis that spares the face (face means brainstem).
      • Between C5 and T1, variable ipsilateral arm with paresis of the leg.
      • Below T1, just the leg.
      • Trauma, demyelinating diseases, epidural abscess, other infections, infarctions (anterior spinal artery supplies anterior 2/3rds of cord), B12 deficiency, tumors (cord compression), disc herniation.
        • In cervical disc herniation, there may be LMN findings at the level of where the disc compresses (laterally) the nerve root, and often UMN findings below that level from myelopathy (compression of the cord, from herniation centrally) along with sensory disturbances.
        • The classic presentation of cervical myelopathy is weakness in the upper and lower extremities, possibly urine/bowel incontinence and a spastic gait (only 1/3rd complain of neck pain).
          • Compression of the cord from a herniated disc is seen in cervical disc herniations not lumbar, as the spinal cord ends at about the L2 vertebrae (thoracic discs rarely herniate).
            • Central herniation of the lumbar vertebra can cause cauda equina syndrome by impinging upon the sacral nerve roots.


Lower motor neuron

    • Includes the anterior horn cell, root/plexus, and peripheral nerve.
    • Motor neuron diseases
      • ALS, mixed upper and lower motor neuron findings.
      • Polio, Coxsackie, West Nile virus, and a newer enterovirus can also cause anterior horn disease.
    • Radiculopathy or polyradiculopathy (single or multiple nerve roots)
      • Radiculopathy causes sensory loss in a dermatomal distribution, weakness in a myotome distribution.
      • Disc prolapse (as above).
        • Lumbar is usually in the L5-S1 distribution, with back pain along with radicular pain/paresthesias/numbness in the distribution of the nerve root.
          • L4 leads to weak quadriceps, loss of patellar reflex.
          • L5 leads to weak dorsiflexion of foot and great toe, loss of medial hamstring reflex.
          • S1 leads to weak plantar flexion and loss of Achilles reflex.
      • Polyradiculopathy may be difficult to distinguish from a polyneuropathy, imaging and lab studies may be needed
        •  (Main causes are infections such as herpes, Lyme disease, cancers, sarcoid)
    • Plexopathy
      • Trauma, autoimmune, inflammatory, tumor (weakness/sensory loss in more than one spinal or peripheral nerve distribution).
      • Traumatic evulsion of C5-6 nerve roots.
        • From birth trauma or trauma separating head and shoulder leads to Erb-Duchenne paralysis.
          • Recall C5-6 innervate the suprascapular, axillary and musculocutaneous nerves to the supra/infraspinatus, deltoid, biceps and brachialis, so the arm hangs at the side (weak supraspinatus or deltoid), the arm is extended (weak biceps/brachialis), shoulder is internally rotated (weak infraspinatus) – called  “waiter’s tip” position.
        • Klumpke paralysis is from C8-T1, can be seen after a fall arrested by grabbing an object or by traction on an abducted arm, or by a Pancoast tumor, leading to wasting of the small muscles of the hand and a claw handed appearance.
    • Peripheral mononeuropathy
      • Entrapment, trauma, diabetes – carpal tunnel is classic.
      • Deficits in the distribution of a single peripheral nerve.
    • Mononeuritis multiplex
      • Multiple single nerves affected, seen in diabetes, vasculitis (granulomatous polyangiitis, PAN, Churg-Strauss), sarcoidosis and infections such as Lyme, HIV and leprosy.
    • Polyneuropathy
      • Toxic, metabolic, nutritional, etc.
      • Usual presentation is symmetric distal sensory loss, burning sensations, or weakness (stocking/glove distribution).
      • In axonal, sensory loss predominates; in demyelinating, motor predominates.
      • Demyelinating neuropathies
        • MS, ADEM, Guillain-Barré, CIDP, many inherited conditions including Charcot Marie Tooth.
        • Affects motor and sensory (the large myelinated fibers, not the unmyelinated).
        • Not length dependent so not distal > proximal.
        • Reflexes lost early.
        • Nerve conduction velocities slowed.
      • Axonal neuropathies
        • Often nutritional, metabolic, and toxic causes.
        • Charcot Marie Tooth (1 is demyelinating, 2 is axonal).
        • Distal > proximal loss (length dependent).
        • Reflexes present until late.
        • Small > large fiber involvement.
        • Usually symmetric.
        • Nerve conduction velocities may be normal.


  • Neuromuscular junction
    • NMJ diseases (MG, Lambert Eaton, botulism) tend to fluctuate during the day or over days, and may fatigue (as in MG) or improve (as in Lambert Eaton) with repetitive activity.
    • Variable weakness is the hallmark of NMJ disorders.
    • NMJ diseases also usually affect the ocular muscles (ptosis, diplopia).
    • Patchy involvement that doesn’t conform with an anatomic distribution.
    • Tone normal or decreased.
    • Reflexes usually normal in MG, and reduced or absent in LE.
    • No sensory loss.


  • Myopathies
    •  Same as LMN lesions except no fasciculations and reflexes are decreased or absent.
    • Affect the large proximal muscles (shoulder/hip), and can have associated pain.
      • Look for the rash of dermatomyositis, medications such as statins, family history of muscular dystrophy or myotonic dystrophy.


  • Functional
    • Normal tone, bulk, reflexes
    • Erratic weakness


Upper motor neuron signs



  • Muscle stretch reflexes assess the integrity of both the sensory neurons on the muscle as well as the motor neurons to the muscle and the connections to and from the brain.
  • When a muscle is stretched, as by striking it or its tendon, it will reflexively contract.
  • Hyperreflexia is a classic sign of UMN disease and hyperthyroidism
    • Hyperreflexia in one limb or in lower but not upper extremities can help localize lesions



Clonus is the repeating contraction of a stretched muscle. Normally, if a muscle is stretched rapidly, it will contract, which then puts a stretch on the antagonistic muscle, which contracts. For example, rapidly dorsiflexing the ankle stretches the gastrocnemius, causing it to contract, resulting in plantar flexion, which stretches the anterior tibialis, causing dorsiflexion, which stretches the gastrocnemius, which may cause another planar flexion. In UMN disease this process may continue for several beats (non-sustained) or indefinitely (sustained) so long as steady stretch is applied to the gastrocnemius by dorsiflexing the ankle because of disinhibition that normally quells the excessive contractions. To elicit clonus, for example in the ankle, briskly dorsiflex the ankle, and maintain some pressure on the foot.



  • An assessment for upper motor neuron disease.
  • Before performing this exam, which can feel noxious, explain to the patient what you are doing and why – it may be helpful to demonstrate it in their hand.
  • Stroke the lateral foot from the heel to the ball of the foot then across the ball of the foot (not all the way to the base of the toes) towards the big toe.
  • The normal response is for the toes to plantar flex (downward).
  • Dorsiflexion of the great toe (up going) and downward fanning of the other toes indicates disease in the upper motor neuron tract.


Nail of middle finger is flicked downward, flexing the finger, causing it to rebound into extension; if their thumb and index finger flexes the Hoffman’s sign is present, suggesting UMN disease.



Spasticity is increased tone due to UMN disease that is most apparent in the mid-range of motion and is velocity-dependent.


Pronator drift

  • Sometimes patients with subtle weakness won’t have any deficits detectable on strength examination. Subtle weakness may be detected on pronator drift.
  • Have the patient hold their arms stretched out in front of them with the palms up, close their eyes and have them maintain this position for about 10 seconds (some sources advocate a minute or more).
    • Inability to hold this position, especially any downward pronation or flexion is a sign of upper motor neuron weakness.


Crossed adductor reflex

Spread of a reflex to other muscles not being tested. A sign of upper motor neuron disease.


Lower motor neuron signs



  • These are subtle, subcutaneous movements that represent contractions of a motor unit, seen in LMN disease (especially those involving anterior horn cells), but can be entirely benign.
  • In LMN lesions they are thought to represent the repetitive discharges of dying motor units.
  • Myokymia is the state of nearly continuous fasciculations causing a rippling appearance, associated with demyelinating diseases such as Guillain-Barre and MS.



  • Reduced bulk (atrophy) suggests LMN disease or muscle disuse.
    • Places to look for atrophy include the thenar eminence and the dorsal interosseous muscles in length dependent neuropathies (as in long standing, poorly controlled diabetes). Patterns of atrophy can suggest the site of nerve or muscle disease.
      • Peroneal muscles in Charcot-Marie-Tooth, the most common inherited neuromuscular disorder (1/2500).
      • Temporal muscles in myotonic dystrophy.


Weakness or paralysis of the muscles of the eye.


Internuclear ophthalmoplegia

  • Seen in multiple sclerosis, due to a lesion in the medial longitudinal fasciculus, a pathway that connects the nuclei of cranial nerve III and VI to allow for coordinated abduction and adduction, essentially yoking the eyes together.
  • On lateral gaze, abduction occurs but adduction is impaired producing diplopia, with jerk nystagmus in the contralateral abducting eye.
  • Unlike 3rd nerve palsy, normal adduction is maintained during convergence as the lesion isn’t with the medial rectus muscle, which works normally, but in the MLF – in convergence the signals don’t go through the heavily myelinated MLF.



  • Involuntary jerking movements of the eyes. Can occur side to side, up and down, or in a circular pattern.
  • Nystagmus can be a sign of cerebellar disease, drug toxicities, vestibular disease, multiple sclerosis or other CNS diseases.
  • In malnourished patients, alcoholics, bariatric surgery patients, and others with nystagmus, especially with gait disturbances and mental status changes, think of Wernicke’s encephalopathy, which is a medical emergency.
    • Responds to thiamine.
    • Can be induced in susceptible patients by the infusion of dextrose without thiamine.

 Gait abnormalities

  • Gait evaluation can be informative, revealing evidence of conditions such as UMN disease (scissoring gait or hemiplegic gait) myopathy (waddling gait), and peripheral sensory neuropathy or foot drop (high stepping).
  • Walking on toes and heels screens for weakness in the plantar flexors (S1, S2) and dorsiflexors (L4, L5)


Antalgic gait

Caused by a painful leg, the patient with an antalgic gait spends less time bearing weight on the affected side (shortened stance phase) and more time with the affected leg in the air (enhanced swing phase).


Hemiplegic (spastic) gait

The patient holds the affected leg stiffly without flexing freely at the hip, knee, or ankle. The leg rotates outward in a semicircular fashion, first away from and then toward the body (circumduction).


Magnetic gait

 Associated with normal pressure hydrocephalus, the patient does not lift the legs far off the floor, as if they are attached to it by a “magnet”.


Shuffling gait

The Parkinsonian shuffling gait is characterized by reduced or absent arm swing, forward bent torso, short or shuffling steps, hesitation in initiation, festination (quickening of steps), and “freezing” when encountering obstacles.


Steppage gait

Caused by paralysis of the pretibial and peroneal muscles, leading to the inability to dorsiflex the foot (foot drop). Steps are regular and even but there is overlifting and slapping of the involved foot.


Cerebellar gait

There is a wide base (separation of legs), irregular cadence, unsteadiness, and lateral veering. Sometimes referred to as a “drunken” gait.


Waddling gait

Slightly widened base with overlifting of hip(s), characteristic of myopathies.

Parkinson’s disease

Masked facies

Reduced facial muscle movement.


Shuffling gait

The Parkinsonian shuffling gait is characterized by reduced or absent arm swing, forward bent torso, short or shuffling steps, hesitation in initiation, festination (quickening of steps), and “freezing” when encountering obstacles.


 Pill-rolling tremor

The tremor of Parkinson’s disease occurs at rest, is coarse, rhythmic, and low frequency (3 to 5 Hz), often involving the hands, as if the patient is rolling a pill between their fingers. The tremor subsides upon willful movement.

Horner’s syndrome

Characterized by miosis, anhidrosis and ptosis 



Bell’s palsy

  • Bell’s palsy is a peripheral nerve injury leading to paralysis of the entire half of the face.
  • In strokes, only one of the 2 UMNs are affected, so the upper face is still innervated, and the patient can raise their eyebrows (strokes spare the forehead).
  • Bell’s palsy is often associated with other CN VII deficits such as decreased taste, hyperacusis, and either increased or decreased tearing
  • Bell’s palsy can also result in synkinesis, in which the damaged nerves regenerate aberrantly and supply different muscles.



Synkinesis describes the involuntary movement of a muscle that occurs with the voluntary movement of a different muscle. It is thought to develop primarily as a result of aberrant regeneration of nerve fibers after traumatic injury and can be a sequela of Bell’s palsy.


Abnormal pupils

  • If pupils are unequal (anisocoria), test them in dim light and with bright light and assess the pupil’s response.
    • If the greatest difference between the pupils is in dim light, the smaller pupil isn’t dilating normally (as in Horner’s or simple anisocoria)
    • If the greatest difference is in bright light, the larger pupil isn’t constricting (as in Adie’s or parasympathetic inhibition).
    • If they respond normally but are unequal in size, this is called essential anisocoria.
  • When testing the pupils, shine a light into them and look to see if they constrict, both directly (when the light is shone into the eye) and consensually (when you shine a light into one eye, the other should also constrict).
  • Check for pupil constriction when the patient looks at objects up close after shifting their gaze from far away objects (accommodation) -you can do this by moving your finger from a few feet away towards the patient’s nose while observing their pupils-easier to see in dim light, where the pupils start out bigger.



  • Marcus Gunn pupil (relative afferent pupil defect)

    • This is the most common pupil defect, characterized by asymmetric pupillary constriction to light, but these pupils are equal (no anisocoria).
    • Main etiology is optic neuritis, but other diseases of the optic nerve or retina may cause it.
      • The swinging flashlight test is performed by shining a light for 1-2 seconds in one eye and then moving the light to the other. Have the patient look at a distant object to not cause confounding pupil constriction due to accommodation
      • Normally, the direct and consensual responses are equal but in diseases of the optic nerve or retina, the direct response is less than normal, so that when the light passes from the “good” eye, rather than constriction one will see a slight, paradoxical dilation of the pupil, as the perceived light is dimmer than in the good eye, and the consensual response will also be decreased symmetrically
      • The consensual response in the affected eye, however, is intact, so when light is shone in the good eye, even the bad eye constricts normally (since the consensual response is independent of the optic nerve and retina from the bad eye)


  • Anisocoria

    • Adie’s (tonic) pupil

      • This is due to denervation of parasympathetics from the ciliary ganglion, impairing pupillary constriction to light, but with preserved accommodation (so called light: near dissociation, also seen in the Argyll-Robertson pupil)
      • There is either no constriction to light or delayed constriction, followed by delayed dilation once the light is removed from the eye
      • Classically seen in women in their 30s/40s, may be associated with absent lower extremity reflexes (Holmes-Adie syndrome)
      • Will constrict with unusual sensitivity to low dosepilocarpine (non-selective muscarinic agonist), which would have a minimal effect on the normal pupil, but in Adie’s has marked response due to denervation hypersensitivity
    • Argyll Robertson pupil

      • Classically due to tertiary syphilis, causing damage to nerve fibers in the midbrain, resulting in bilateral small, irregularly shaped pupils that like Adie’s pupil, have light: near dissociation; they accommodate but don’t react (to light)
    • Horner’s syndrome

      • This triad of unilateral ptosis, miosis, anhydrosis (eyelid droop, small pupil and lack of sweating) is caused by compression of the sympathetics along their pathway from the hypothalamus down to the second order neuron that passes over the apex of the lung and then up to the third order neuron via the sympathetic chain to the third order neuron that passes in the internal carotid where the long ciliary nerve goes to the orbit to innervate the pupillary dilator muscle.
      • The miosis in Horner’s is due to loss of sympathetics to the pupillary dilator muscle, and unlike CN III lesions and Adie’s pupil the miosis is more apparent in the dark than the light.


Progressive supranuclear palsy

  • Characterized by impaired vertical eye movements, usually with impaired downgaze then up gaze and eventually leading to global gaze paresis
  • Preserved involuntary (VOR) movements but impaired voluntary (saccades, pursuit)
  • Parkinsonian signs are present, although the tremor is not as pronounced
  • Patients develop frontal lobe dementia, postural instability, pseudobulbar palsy, and an extensor axial rigidity, especially of the neck.


Charcot-Marie-Tooth disease

  • Charcot-Marie-Tooth disease is the most common inherited cause of polyneuropathy
  • Pes cavus (high arched feet) and hammertoes (the proximal interphalangeal joint of the toe is bent upward) are commonly found on physical examination.


Sources and further reading:

  • Ropper AH, Samuels MA, Klein JP, eds. Adam and Victor’s Principles of Neurology. 10th ed. China: McGraw-Hill Education; 2014.