Upper Motor Neuron

Rules for localization of weakness

Upper motor neuron

  • Includes nervous tissue from the cortex down to (but not including) the anterior horn cells.
  • 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.o

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.
  • CNVIII 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 discis 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.

Upper motor neuron signs

Hyperreflexia

  • 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

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 anklebecause ofdisinhibition 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.

Babinski’s

  • 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 thelateralfoot from the heel to the ball of the foot then across the ball of the foot(not all the way to thebase 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.

Hoffman’s

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 signis present, suggesting UMN disease.

Spasticity

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.