Upper Motor Neuron Syndromes

The upper motor neuron syndrome is marked by weakness, spasticity, hyperactivity of the tendon reflexes, and the presence of the flexor reflex (Babinski sign). This pattern of motor disturbance occurs when there is an interruption of the descending projections from the motor neurons in the

cerebral cortex and brain stem that modulate excitation of the internuncial pool of inhibitory interneurons and the alpha and gamma motor neurons. The net effect is a reduction of inhibitory influences and an increase in excitatory tone, producing exaggeration of the muscle stretch reflexes (hyperreflexia), increased muscle tone (spasticity), weakness, and disinhibition of the flexor reflex (Babinski sign). Several clinical syndromes affect the upper motor neurons.

The upper motor neuron syndrome is primarily a reflection of interruption of the corticospinal (pyramidal) tract. Because the corticospinal tract extends from the cerebral cortex to the lumbosacral spinal cord, the pattern of weakness and associated reflex abnormalities depends on the site of the lesion along the considerable length of this pathway. Because there are two halves to the brain and consequently two corticospinal tracts, the pattern also depends on which side is affected or whether both sides are affected. Also, the clinical signs on the affected side depend on whether the lesion is above or below the decussation of the tracts in the cervical medullary junction. A unilateral lesion of the cerebral motor cortex will affect the other side of the body. Depending on the size of the lesion, it might affect only one limb or even a part of one limb. For example, a small stroke in the arm area could produce a brachial monoplegia. Because the leg area is on the medial side of the hemisphere at the apex of the motor strip, the leg areas from each hemisphere face each other in the interhemispheric fissure. Therefore, a parasagittal lesion in the interhemispheric fissure could affect both legs and produce a syndrome of paraparesis, simulating a spinal cord lesion. This is most commonly produced by a parasagittal meningioma (...Table 15.-8 ).

Hemiparesis most commonly results from a lesion in the contralateral cerebral cortex. Depending on its location in the hemisphere and the side affected, other associated signs can further localize the lesion (.Table 1,5.i9.). Because of the considerable length of the corticospinal tract, hemiparesis can also result from lesions anywhere along its path (see T§b.le...1.5z9 ). Because the axons from the motor neurons gather together in the posterior limb of the internal capsule (...Fig, 15-21 ), a lesion in this location may be very small and still cause a complete hemiparesis (face, arm, body, and leg). Weakness that affects the entire side of the body equally without associated sensory signs (or aphasia if the lesion is in the left hemisphere) has been referred to by Fisher, in a clever redundancy, as a " pure motor hemiplegia.y " Less commonly, small strokes (lacunar infarcts)


Location of Lesion

Pattern of Weakness, Reflexes, and Associated Signs

Bilateral medial hemispheres (leg area motor cortex)

Spatic paraparesis with no sensory level


Paraparesis with hyperreflexia of legs, normal reflexes in arms; thoracic sensory level


Paraparesis, loss of reflexes, double incontinence with flaccid bladder and sphincters


Location of Lesion

Characteristics of Hemiparesis and Associated Signs

Cerebral cortex

Contralateral arm is affected more than leg or face; sometimes tongue (deviates to weak side).

Left hemisphere: aphasia, apraxia

Right hemisphere: inattention to left half of body, visual space; constructional apraxia

Homonymous hemianopia on weak side

Decreased graphesthesia, extinction of sensory stimuli

Internal capsule

Contralateral arm equal to leg; face may be spared

No sensory loss or aphasia

Brain stem

Contralateral arm equal to leg plus ipsilateral cranial nerve palsy


Third nerve palsy (Weber syndrome)


Sixth and seventh nerve palsies (peripheral); ipsilateral conjugate gaze palsy possible (Foville's syndrome)


Twelfth nerve palsy

Cervical spinal cord (hemicord)

Ipsilateral weakness of arm and leg, sparing face; Ipsilateral loss of propriocepton and vibration

Contralateral loss of pain and temperature (Brown-Sequard syndrome).

can produce more focal weakness depending on the region of the internal capsule involved. Weakness in the face and arm can produce the dysarthria-clumsy hand syndrome.33]

Lesions of the corticospinal tract as it traverses the brain stem also affect other structures in the brain stem, producing recognizable syndromes depending on the location and size of the lesion. Unilateral lesions of the pyramidal tract in the cerebral peduncle of the midbrain may involve the neighboring third nerve, red nucleus, or superior cerebellar peduncle (brachium conjunctivum). Lesions in this area are generally lacunar infarcts in hypertensive individuals that result from occlusion of small paramedian arteries supplying these structures. As the pyramidal tract enters the pons, the fibers become intermingled with other ascending and descending tracts in the basis pontis. It is still possible for lacunar infarctions to involve the pyramidal tracts primarily, producing a pure motor hemiparesis with or without facial involvement that is similar to the syndrome resulting from a lacunar infarct in the posterior limb of the internal capsule. The corticobulbar and corticopontocerebellar fibers are also present, and a lacunar infarction in the basis pontis, especially one at the junction of the upper third and lower two-thirds, may result in a dysarthria-clumsy hand syndrome that is similar to the clinical presentation of a lacune in the genu of the internal capsule. Another lacunar infarct syndrome is a homolateral ataxia and hemiparesis, which is more severe in the lower extremity. This also may be associated with dysarthria, nystagmus, and paresthesia from a lesion in the contralateral pons. Lesions (usually strokes) that include the pontine tegmentum produce a characteristic syndrome composed of an ipsilateral cranial nerve palsy and a contralateral hemiparesis (see Table 15.-9.). These uncommon clinical syndromes are described in more detail in Chapter.45 .

Figure 15-21 Cross section of the cortex showing the internal capsule and its fiber arrangemen(From Snell RS: Clinical Neuroanatomy for Medical Students. Boston, Little, Brown, 1987.)

Bilateral lesions of the basis pontis (infarction, hemorrhage, central pontine myelinolysis) produce the " locked-in syndrome" (.TableJ ,5-10 ). The patient is quadraparetic due to bilateral corticospinal tract involvement and aphonic due


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