The Neurologic Examination and Neurologic Diagnosis

A neurologic exam answers two questions: is there a lesion, and where is it? Once you can place a lesion in the brain, brainstem, cord, root, plexus, peripheral nerve, junction or muscle, the differential shrinks to a handful of diagnoses, and the urgency becomes obvious. The board tests this localizing logic constantly, and in practice it is what separates the radiculopathy you can manage from the myelopathy, cauda equina syndrome or dissection you must refer today.

Section 1Cranial nerve and central nervous system examination

Mental status

Start with level of consciousness and orientation (person, place, time, situation), then attention (serial sevens, spelling WORLD backward), memory (three word recall at 5 minutes), language (naming, repetition, comprehension, reading, writing), visuospatial skill (clock drawing) and judgment. The Mini Mental State Examination scores 0 to 30, with 23 or below suggesting cognitive impairment; the Montreal Cognitive Assessment is more sensitive for mild impairment, with under 26 abnormal. In trauma or altered consciousness use the Glasgow Coma Scale: eyes 1 to 4, verbal 1 to 5, motor 1 to 6, total 3 to 15; 8 or less means coma and a threatened airway.

Two language deficits localize precisely. Broca (expressive) aphasia, from the inferior frontal gyrus of the dominant hemisphere, gives halting, effortful speech with good comprehension. Wernicke (receptive) aphasia, from the superior temporal gyrus, gives fluent but meaningless speech with poor comprehension. Both impair repetition; conduction aphasia (arcuate fasciculus) impairs repetition alone.

The twelve cranial nerves

Pupils, eyes and hearing

The pupillary light reflex uses CN II as the afferent limb and CN III (parasympathetic, via the Edinger Westphal nucleus) as the efferent limb; light in one eye constricts both pupils (direct and consensual). In the swinging flashlight test, a relative afferent pupillary defect (Marcus Gunn pupil) dilates paradoxically when the light swings to it, a sign of optic nerve disease such as optic neuritis. Horner syndrome, interruption of the oculosympathetic chain, gives ipsilateral ptosis, miosis and anhidrosis; causes include Pancoast tumor, carotid dissection and lateral medullary infarction. The Argyll Robertson pupil of neurosyphilis accommodates but does not react to light.

Extraocular movements are tested in an H pattern. Internuclear ophthalmoplegia from a lesion of the medial longitudinal fasciculus produces failure of adduction in the eye on the side of the lesion with nystagmus of the abducting eye; bilateral INO in a young adult strongly suggests multiple sclerosis.

Vertigo has a peripheral or central source. Benign paroxysmal positional vertigo causes brief spinning (under a minute) with head position change; the Dix Hallpike maneuver (head turned 45°, patient brought quickly supine with the head extended over the table edge) produces delayed, fatiguing, torsional upbeating nystagmus for the posterior canal, and the Epley maneuver treats it. Central vertigo from a cerebellar or brainstem stroke tends to have nonfatiguing, direction changing or vertical nystagmus, a normal head impulse test and other neurologic signs; this is a red flag.

Cerebellar examination

The cerebellum coordinates movement on the same side of the body, so a right hemisphere lesion causes right limb ataxia. The vermis controls the trunk and gait (truncal ataxia, wide based gait, typical of alcohol related degeneration); the hemispheres control the limbs. Signs are summarized by DANISH: dysdiadochokinesia, ataxia, nystagmus, intention tremor, slurred (scanning) speech and hypotonia.

Section 2Motor examination

Inspection and tone

Look first. Note posture, symmetry, atrophy (compare thenar eminences, first dorsal interossei, calves), fasciculations (spontaneous twitches of motor units, a lower motor neuron sign) and involuntary movements (resting tremor of Parkinson disease, chorea, myoclonus). Then assess tone, the resistance to passive movement of a relaxed limb.

The pronator drift test is a sensitive screen for subtle UMN weakness: arms held forward, palms up, eyes closed, for 20 to 30 seconds. The weak arm pronates and drifts downward.

Grading strength

Grade 3 is the pivotal grade: the limb can just overcome gravity. Test proximal and distal muscles, compare sides, and stabilize the proximal segment so that substitution does not hide weakness. Pain inhibition, poor effort and give way weakness (sudden collapse after initial full strength) are common causes of apparent weakness that are not neurologic.

Myotomes

A myotome is the group of muscles supplied mainly by one root. Most muscles receive two or three roots, so a single root lesion produces partial weakness, never paralysis; complete paralysis of a muscle points to a peripheral nerve.

Functional screens are fast: heel walking tests L4 and L5 dorsiflexors, toe walking tests S1 plantarflexors (ten single leg heel raises are needed to detect mild S1 weakness), and squatting and rising tests L3 and L4.

Upper versus lower motor neuron lesions

The upper motor neuron (UMN) runs from the motor cortex through the internal capsule, cerebral peduncle and pyramid, crosses at the pyramidal decussation in the lower medulla, and descends in the lateral corticospinal tract to synapse in the anterior horn. The lower motor neuron (LMN) runs from the anterior horn cell through the root, plexus and peripheral nerve to the muscle. Above the decussation a lesion produces contralateral signs; below it, ipsilateral signs.

Section 3Sensory examination

Two pathways, two sets of tests

Every bedside sensory test probes one of two ascending systems. The dorsal column medial lemniscus pathway carries fine touch, vibration, proprioception and two point discrimination. Its first order fibers enter the dorsal root and ascend ipsilaterally in the fasciculus gracilis (legs, medial) and fasciculus cuneatus (arms, lateral, present above T6), synapse in the nucleus gracilis and cuneatus of the medulla, cross as internal arcuate fibers, and ascend in the medial lemniscus to the ventral posterolateral (VPL) thalamus and postcentral gyrus. The anterolateral (spinothalamic) pathway carries pain, temperature and crude touch. Its fibers synapse in the dorsal horn, cross within one or two segments in the anterior white commissure and ascend contralaterally to the VPL thalamus.

Normal two point discrimination is about 2 to 5 mm at the fingertips, 8 to 15 mm on the palm and 40 mm or more on the back. Distal loss of vibration is often the earliest sign of a length dependent peripheral neuropathy, typically diabetic; the 10 g monofilament identifies a foot at risk of ulceration. Loss of stereognosis, graphesthesia or sensory extinction (a touch on one side is felt but missed when both sides are touched together) with intact primary sensation points to the contralateral parietal lobe.

Dermatomes and peripheral nerve fields

A dermatome is the skin area supplied by one spinal root. Adjacent dermatomes overlap, so a single root lesion causes a smaller and patchier deficit than the map suggests, and loss is usually greater for pain than for touch. A peripheral nerve field has sharper borders and usually combines fibers from several roots.

Sensory patterns that localize

• Stocking and glove loss, distal and symmetric, with reduced ankle reflexes: length dependent polyneuropathy (diabetes, alcohol, B12 deficiency, chemotherapy).
• A sensory level on the trunk (all modalities lost below a dermatome) with UMN signs below: spinal cord lesion; the true level may be a few segments higher.
• Brown Séquard syndrome (hemisection, often penetrating trauma): ipsilateral UMN weakness and loss of vibration and position below the lesion, contralateral loss of pain and temperature starting one or two segments below.
• Central cord syndrome (hyperextension in an older patient with a stenotic spondylotic canal): arms weaker than legs, hands worst, variable sensory loss; the commonest incomplete cord syndrome.
• Syringomyelia: a cavity at the center of the cervical cord interrupts crossing spinothalamic fibers, giving cape like loss of pain and temperature over the shoulders and arms with preserved touch (dissociated loss), later LMN atrophy of the hands; often associated with Chiari I malformation.
• Anterior cord syndrome (anterior spinal artery occlusion, flexion injury): loss of motor function and pain and temperature below the lesion with dorsal columns spared.
• Posterior column loss alone: tabes dorsalis, and with corticospinal involvement, subacute combined degeneration from B12 deficiency.
• Hemisensory loss of face, arm and leg on one side: contralateral thalamus or cortex.

Section 4Reflexes

Deep tendon reflexes

A deep tendon (muscle stretch) reflex is a monosynaptic arc: tendon tap, muscle spindle stretch, Ia afferent, synapse on the alpha motor neuron, contraction. Interruption anywhere in the loop (root, nerve, muscle) reduces it; loss of descending inhibition from an UMN lesion increases it. Test with the patient relaxed, the joint in mid position and both sides compared. If reflexes seem absent, use reinforcement (the Jendrassik maneuver: the patient hooks the fingers together and pulls, or clenches the teeth, just as the tendon is struck).

Symmetric 1+ or 3+ reflexes can be normal; asymmetry and the company a reflex keeps matter more than its absolute grade. Hyperreflexia also occurs in hyperthyroidism and anxiety; generalized hyporeflexia in hypothyroidism (with a slow relaxation phase), polyneuropathy and Guillain Barré syndrome.

Superficial reflexes

Superficial reflexes are polysynaptic and travel partly through the corticospinal system, so they are lost on the side of an UMN lesion while deep reflexes become brisk, and they are lost with a segmental lesion. Absent abdominal reflexes in a young adult may be an early clue to MS; they are often absent normally after abdominal surgery, in obesity and in multiparous women. Absent anal wink and bulbocavernosus reflexes point to a conus or cauda equina lesion.

Pathological reflexes

Section 5Neurologic diagnosis

Radiculopathy by level

Radiculopathy is dysfunction of a nerve root, most often from disc herniation or foraminal stenosis (uncovertebral and facet osteophytes). It produces radicular pain in a dermatomal band (sharp, shooting, often worse with cough, sneeze or Valsalva and with neural tension tests), with variable dermatomal sensory loss, myotomal weakness and a reduced reflex. In the cervical spine the roots exit above the pedicle of the same numbered vertebra (C6 exits between C5 and C6, so a C5 to C6 disc compresses C6), and C8 exits between C7 and T1. In the lumbar spine roots exit below their pedicle, and a posterolateral disc compresses the traversing root of the level below (L4 to L5 disc, L5 root).

C7 is the most commonly affected cervical root and L5 and S1 account for most lumbar radiculopathies, because the L4 to L5 and L5 to S1 discs bear the most load. Radicular pain often improves with shoulder abduction (Bakody sign) in the neck and with lying in the lumbar spine. Most radiculopathies improve with conservative care; progressive or severe motor deficit (grade 3 or worse), intractable pain or any sign of cord or cauda equina involvement require referral.

Myelopathy

Cervical spondylotic myelopathy, cord compression from disc osteophyte complexes, ligamentum flavum hypertrophy, ossification of the posterior longitudinal ligament and a congenitally narrow canal, is the commonest cause of spinal cord dysfunction in adults over 55. It is often painless and insidious: clumsy hands (dropping things, trouble with buttons), diffuse nondermatomal hand numbness, a broad based spastic gait and falls, Lhermitte sign, and late bladder urgency. Signs are UMN below the level: hyperreflexia, Hoffmann, Babinski, clonus, the inverted supinator reflex, and in the hand the finger escape sign and a slowed grip and release test (fewer than about 20 cycles in 10 seconds). An anteroposterior canal diameter under about 10 mm (or a Torg Pavlov ratio under 0.8) indicates stenosis. MRI shows cord compression and sometimes T2 signal change. Myelopathy is a contraindication to cervical manipulation and requires spine surgical referral; progression is stepwise and often irreversible.

Thoracic myelopathy (disc, metastasis, meningioma) gives a sensory level and spastic legs with normal arms. Spinal cord compression from metastasis usually begins with back pain, often worse lying down and at night, before weakness appears: in a patient with cancer, new back pain is metastasis until proven otherwise, and established weakness is an emergency.

Cauda equina and conus medullaris syndromes

The cord ends at about L1 to L2 in adults (the conus medullaris); below that the canal holds the cauda equina, a bundle of lumbosacral roots. Compression of the cauda equina, most often by a large central L4 to L5 or L5 to S1 disc herniation, also by tumor, epidural abscess, hematoma or severe stenosis, is a surgical emergency.

The key red flags to ask every patient with low back pain are saddle numbness, new urinary retention or incontinence, fecal incontinence, sexual dysfunction and bilateral or progressive leg weakness. Urinary retention is the most consistent finding, and a post void residual over about 200 mL is supportive. Examine perianal sensation and anal tone. Suspected cauda equina syndrome needs same day emergency MRI and surgical decompression, ideally within 48 hours, because outcome depends on bladder function at the time of surgery.

Peripheral entrapments and thoracic outlet syndrome

Thoracic outlet syndrome is compression of the brachial plexus or subclavian vessels in the interscalene triangle, costoclavicular space or beneath pectoralis minor. Neurogenic TOS (over 90 percent) affects the lower trunk (C8 and T1): aching and paresthesia in the medial forearm and ulnar hand, worse with overhead activity, and in true neurogenic TOS a cervical rib or band with wasting of the thenar muscles (the Gilliatt Sumner hand). Arterial TOS gives a cold, pale hand, claudication and emboli, often with a cervical rib; venous TOS (effort thrombosis, Paget Schroetter syndrome) gives arm swelling and cyanosis after vigorous overhead activity and is an emergency. The provocative tests (Adson, Wright, Roos, costoclavicular) are discussed with the thoracic exam; they have high false positive rates, so diagnosis rests on the whole picture. TOS is distinguished from C8 radiculopathy by the absence of neck signs and from ulnar neuropathy by medial forearm involvement.

Vertebrobasilar insufficiency and cervical artery dissection

Cervical artery dissection is a tear in the intima of the vertebral or internal carotid artery, allowing blood into the wall. It may follow trivial or major trauma, sports or occur spontaneously, especially with connective tissue disorders, migraine and recent infection. It is a leading cause of stroke in adults under 45. The early symptoms are often new, unusual neck pain or headache, the very complaints that bring patients to a chiropractor, and ischemic symptoms may follow hours to days later.

Posterior circulation ischemia (vertebrobasilar insufficiency) is remembered as the five Ds and three Ns: dizziness or vertigo, diplopia, dysarthria, dysphagia and drop attacks; nystagmus, nausea and numbness (often of the face or perioral area), plus ataxia. Sudden onset of these, especially in combination with new neck pain or headache, requires emergency referral.

The question of manipulation and stroke deserves a precise answer. Population case control and case crossover studies have found that patients with vertebrobasilar stroke are more likely to have seen a chiropractor in the preceding days, but they are equally likely to have seen a primary care physician, which is consistent with patients consulting for the neck pain and headache of an evolving dissection. A small causal contribution in rare cases cannot be excluded, and the absolute risk is very low. Premanipulative positional tests (sustained rotation and extension, such as the George or DeKleyn tests) have poor sensitivity and are not reliable screens; a careful history for dissection symptoms and risk factors, and a neurologic and cranial nerve screen, are what protect the patient. Any patient with signs of an evolving dissection must not be manipulated and needs emergency care.

Stroke

About 85 percent of strokes are ischemic (thrombotic, embolic from the heart or carotid, lacunar) and 15 percent hemorrhagic (intracerebral from hypertension, or subarachnoid from aneurysm with a thunderclap headache). A transient ischemic attack is a temporary deficit without infarction and carries a high early stroke risk. Recognize stroke with BE FAST (balance, eyes, face droop, arm weakness, speech, time to call). Time is brain: thrombolysis is given within 4.5 hours of onset and thrombectomy in selected patients up to 24 hours, so note the time last known well and call emergency services.

Multiple sclerosis, ALS and other CNS disease

Multiple sclerosis is immune mediated demyelination of the CNS, most often beginning in women aged 20 to 40. Hallmarks are lesions disseminated in time and space: optic neuritis (painful monocular vision loss, central scotoma, afferent pupillary defect), internuclear ophthalmoplegia, sensory symptoms, Lhermitte sign, spastic weakness with hyperreflexia, bladder urgency, fatigue and Uhthoff phenomenon (worsening with heat). Most patients start with a relapsing remitting course. MRI shows T2 and FLAIR white matter lesions that are periventricular (perpendicular Dawson fingers), juxtacortical, infratentorial and spinal; CSF shows oligoclonal bands.

Amyotrophic lateral sclerosis degenerates both upper and lower motor neurons. It presents with asymmetric painless weakness of a hand or foot, fasciculations and atrophy alongside hyperreflexia and Babinski in the same region, and bulbar dysarthria and dysphagia. Sensation, eye movements and sphincters are spared. Death from respiratory failure typically follows in 3 to 5 years.

Words worth knowing