Upper Motor Neuron Syndrome: Lesions, Signs & Management

Last Updated on October 23, 2025

Upper motor neuron syndrome refers to the collection of clinical features that result from disruption of the descending motor pathways, principally the corticospinal and corticobulbar tracts. The syndrome consists of a loss of voluntary motor control, increased muscle tone (spasticity), exaggerated reflexes, and pathological signs such as the Babinski response. [1]

A neuron is a specialized nerve cell responsible for transmitting electrical impulses within the nervous system. Among them, motor neurons play a crucial role in controlling voluntary and reflex movements by conveying signals from the central nervous system to skeletal muscles.

Motor neurons are broadly divided into two hierarchical levels, the upper motor neurons (UMN) and lower motor neurons (LMN), each forming an essential link in the chain of motor control. The upper motor neurons originate in the motor cortex and brainstem, modulating voluntary activity through their influence on lower motor neurons, which directly innervate muscles and bring about contraction.

Damage to either of these pathways results in characteristic patterns. For instance, a patient presenting with upper limb weakness due to a stroke (an upper motor neuron lesion) will exhibit a markedly different set of signs compared with a brachial plexus injury (a lower motor neuron lesion). Recognizing these contrasting patterns helps localize the site of pathology and determine whether the lesion lies within the central or peripheral nervous system.

In this article, the anatomical basis, pathophysiology, and clinical manifestations of upper motor neuron syndrome are examined in detail, along with diagnostic differentiation from lower motor neuron lesions.

Relevant Anatomy

CNS- Gray and White Matter

The motor system is anatomically organized, with the central nervous system (CNS), comprising the brain and spinal cord, serving as the command and integration center, and the peripheral nervous system (PNS) carrying signals to and from the body.

The CNS is composed of gray matter and white matter.

• Gray matter consists mainly of neuronal cell bodies and unmyelinated fibers
• White matter is formed by myelinated axons and oligodendrocytes, which produce the myelin sheath.

In the brain, the gray matter forms the outer cerebral cortex and the deep nuclei, while the white matter lies beneath, forming tracts and commissures that interconnect the cortical and subcortical regions.

In the spinal cord, the arrangement is reversed. The gray matter occupies the central H-shaped region, surrounded by white matter that contains ascending and descending tracts. The gray matter is organized into anterior, posterior, and lateral columns.

[Read Anatomy of Spine]

Motor Neurons

Upper motor neurons originate in the motor cortex or brainstem motor centers. Their long axons descend through the brainstem and spinal cord, forming tracts that ultimately terminate on lower motor neurons or interneurons.

Lower motor neurons lie in the anterior horn of the spinal cord and in the motor nuclei of cranial nerves. Their axons exit via spinal or cranial nerves to innervate skeletal muscle fibers, the final common pathway for voluntary movement.[1]

Spinal and Cranial Nerve Connections

Each spinal nerve connects the spinal cord to skin, joints, and muscles, enabling both efferent (motor) output and afferent (sensory) input. The twelve cranial nerves are peripheral nerves that connect directly to the brain or brainstem, either directly or via intermediate ganglia.

(Of these, the olfactory and optic nerves are functionally part of the CNS rather than the PNS.)

Functional Integration

Every voluntary movement involves both components: Upper motor neurons generate, modulate, and direct motor commands, and Lower motor neurons transmit those commands to muscles, executing movement.

Upper Motor Neuron

Structural Arrangement

Upper motor neurons (UMNs) are neurons that originate in the cerebral cortex and descend through organized tracts to influence spinal and cranial lower motor neurons. Functionally, these pathways are grouped into two systems:

• The pyramidal system, responsible for voluntary motor control.
• The extrapyramidal system which regulates tone, posture, and automatic movements.

Pyramidal System

The pyramidal system consists of the corticospinal and corticobulbar tracts.

Corticospinal Tract

Most of these neurons arise from the primary motor cortex (precentral gyrus), with contributions from the premotor and supplementary motor areas. Fibers converge in the corona radiata, pass through the posterior limb of the internal capsule, and descend through the midbrain and pons to form the medullary pyramids.

At the medulla, approximately 85–90 % of fibers decussate (cross), forming the lateral corticospinal tract, the main pathway for fine, skilled movement of distal limb muscles.

The remaining 10–15 % continue uncrossed as the anterior corticospinal tract, which primarily controls axial and proximal muscles and typically crosses near its spinal termination level.

Corticobulbar Tract

The corticobulbar tract projects from the motor cortex to the motor nuclei of cranial nerves within the pons and medulla. It governs muscles of the face, jaw, tongue, pharynx, and larynx, essential for speech, swallowing, and expression. Most cranial nerve nuclei receive bilateral cortical input (for example, the trigeminal and the upper half of the facial nucleus).

However, the lower facial nucleus and hypoglossal nucleus receive contralateral innervation, explaining contralateral lower facial weakness and tongue deviation in unilateral UMN lesions.
The cranial nerves themselves, once they exit the brainstem, are lower motor neurons, and their lesions produce LMN-type signs such as flaccid paralysis, atrophy, and fasciculations.

Extrapyramidal System

The extrapyramidal tracts, rubrospinal, reticulospinal, vestibulospinal, and tectospinal, originate from subcortical motor centers. They provide continuous modulation of muscle tone, posture, balance, and reflex movement patterns, ensuring fluid execution of voluntary commands from the pyramidal system.

Functional Role of Upper Motor Neurons

The upper motor neuron serves three principal functions by regulating the strength of spinal reflexes and fine-tuning muscle coordination

• Initiation and modulation of voluntary movement through activation of lower motor neurons.
• Inhibition of spinal reflex circuits prevents excessive tone or reflex hyperactivity.
• Integration of sensory feedback into adaptive postural and motor responses.

When upper motor pathways are damaged, this inhibitory control is lost, leading to hyperexcitability of spinal motor circuits, a hallmark of the upper motor neuron syndrome.

When the integrity of these pathways is lost, the balance between excitation and inhibition within spinal circuits collapses, resulting in the characteristic features of upper motor neuron syndrome- spasticity, hyperreflexia, loss of fine control, and abnormal reflex patterns.

The anterior grey column contains motor neurons that affect the skeletal muscles.

Pathophysiology of Upper Motor Neuron Syndrome

The fundamental role of upper motor neurons is to initiate, regulate, and inhibit activity in the spinal and cranial lower motor neurons. When disrupted, this delicate balance between excitation and inhibition collapses. The result is a constellation of changes in muscle tone, reflexes, and movement control collectively known as upper motor neuron syndrome. [2,3]

Loss of Inhibitory Control

Under normal circumstances, upper motor neurons exert a modulating inhibitory influence on the spinal reflex arcs. This control prevents excessive reflex activity and maintains smooth, coordinated motion. When a lesion interrupts these descending fibers, this happens:

• Inhibition of spinal interneurons and gamma motor neurons is lost.
• The stretch reflex loop becomes overactive, producing hyperreflexia and spasticity.
• Reciprocal inhibition between antagonist muscles diminishes, resulting in simultaneous contraction and stiffness.

In contrast, the reflex arc itself is destroyed in lower motor neuron lesions, leading to flaccidity and absent reflexes.

Excitatory Imbalance

Following UMN injury, segmental motor neurons receive unregulated excitatory input from preserved sensory afferents and interneurons. Over time, this leads to upregulation of receptor sensitivity in spinal motor circuits and enhanced synaptic transmission at the level of the anterior horn. This leads to the emergence of exaggerated deep tendon reflexes, clonus, and pathological reflexes such as the Babinski sign.

This hyperexcitability evolves as part of the plasticity that occurs after the initial phase of spinal shock.

Spasticity

Spasticity is a velocity-dependent (depends on the speed of the movement) increase in muscle tone. It involves increased excitability of alpha and gamma motor neurons and reduced presynaptic inhibition of afferent terminals in the stretch reflex arc.

There is also enhanced cutaneous and propriospinal reflex coupling (reflex responses triggered by stimulation of skin receptors), causing co-contraction of muscles.

In contrast, rigidity seen in extrapyramidal disorders (e.g., Parkinson’s disease) is not velocity-dependent and reflects basal ganglia dysfunction rather than corticospinal interruption.

Loss of Fine Motor Control

Upper motor lesions result in loss of dexterity, particularly in distal limb muscles. This effect is most pronounced in the upper limbs, where fine motor tasks depend heavily on intact corticospinal modulation.

Clinical Features of Upper Motor Neuron Syndrome

The features evolve in two phases: an initial phase of hypotonia and areflexia (spinal shock), followed by the chronic phase marked by spasticity and hyperreflexia. [4]

Phases of Response

• Acute Phase (Spinal Shock): Immediately after injury, especially in spinal cord lesions, there is a sudden loss of all reflexes and tone below the lesion. The affected limbs become flaccid, like a lower motor neuron lesion. This occurs because of the abrupt withdrawal of supraspinal facilitation to spinal neurons.
• Chronic Phase: Over days to weeks, the spinal circuits regain autonomous activity in the absence of cortical control. Reflexes return, but with increased amplitude and abnormal distribution. Muscle tone increases, producing spastic paralysis, a combination of weakness, stiffness, and hyperreflexia.

Positive and Negative Signs (Terminology)

The manifestations of upper motor neuron syndrome can be divided into 

• Positive signs: Represent excess or release phenomena that appear when inhibitory control from the brain is lost, such as spasticity, hyperreflexia, clonus, or a Babinski response.
• Negative signs: Reflect loss of normal motor function, such as weakness, loss of dexterity, or diminished reflexes.

Positive Signs

• Spasticity: Spasticity is a velocity-dependent increase in muscle tone caused by the loss of descending inhibitory control over spinal reflexes. The resistance felt during passive stretch rises with the speed of movement and suddenly releases, the so-called “clasp-knife” phenomenon.
  The involved muscles show stiffness and limited mobility. The distribution of spasticity is more prominent in the flexors of the upper limb and extensors of the lower limb.
• Hyperreflexia: Deep tendon reflexes (biceps, triceps, knee, ankle) become exaggerated. The threshold for eliciting a reflex is reduced, and the response amplitude is increased. In severe cases, repeated muscle contractions follow a single tap.
• Clonus: Clonus is a series of rhythmic, involuntary contractions following sudden stretching of a muscle, classically elicited at the ankle or patella. Clonus indicates sustained hyperexcitability of the stretch reflex arc.
• Babinski sign: Stroking the sole produces extension of the great toe and fanning of the other toes, instead of normal flexion. Hoffmann and Tromner signs may be elicited in the upper limb as corticospinal tract indicators.
• Synkinesis: Voluntary movement in one limb may trigger involuntary motion in another, reflecting loss of inhibitory modulation. For instance, flexion of one arm may elicit flexion of the opposite limb.

Negative Signs

• Weakness (Paresis): Although muscle tone is increased, true power is reduced. The weakness is most prominent in distal and fine motor muscles, leading to impaired manual dexterity and awkward gait.
• Loss of Fine Movements: The ability to perform precise, fractionated actions, such as manipulating small objects or performing isolated finger movements, is markedly impaired. This arises from the disruption of corticospinal projections to individual motor units.
• Bradykinesia: Movements become slower and less coordinated, especially for alternating or sequential tasks.
• Fatigability: Due to impaired motor recruitment, affected muscles tire rapidly during repetitive use.

Other Important Signs

Gait and Posture

Depending on lesion distribution:

• Hemiplegic posture: Seen in unilateral upper motor neuron lesions involving the cerebral hemisphere. The upper limb is flexed and adducted, while the lower limb is extended and circumducts during walking.
• Spastic (scissoring) gait: Occurs in bilateral lesions of the corticospinal tracts, typically from spinal cord or brainstem involvement, leading to adduction and crossing of the lower limbs during ambulation.
• Paraplegia or quadriplegia: Results from bilateral spinal cord lesions, paraplegia when the lesion is below the cervical level, and quadriplegia when it involves the cervical cord.

Superficial Reflexes

Superficial (cutaneous) reflexes such as the abdominal, cremasteric, and plantar flexor responses are diminished or absent, reflecting loss of descending facilitation. These must be distinguished from hyperactive deep tendon reflexes, which are segmental.

Pronator Drift

A subtle but reliable sign of a UMN lesion affecting the upper limb. When the patient stands with both arms extended forward, palms up, and eyes closed, the affected arm pronates and drifts downward due to unopposed pronator tone.

Locating the Lesion in a Patient

In orthopedic and trauma practice, the main concern when faced with upper motor neuron syndrome signs is where along the motor pathway the lesion lies. Precise localization determines whether the pathology is supraspinal (intracranial) or spinal.

Supraspinal and Spinal Lesions

The central motor pathway, or corticospinal tract, forms a continuous neural axis extending from the cerebral cortex to the spinal cord.

Functionally, supraspinal refers to the portion of this pathway above the point where fibers decussate, that is, within the motor cortex, internal capsule, brainstem, and upper medulla. At these levels, descending fibers have not yet crossed to the opposite side, so a lesion produces contralateral weakness.

The fibers decussate at the pyramidal decussation, located at the cervicomedullary junction, the transitional zone between the medulla oblongata and the cervical spinal cord. This junction lies a few millimeters above the first cervical spinal segment (C1), often within the region of the foramen magnum. The foramen magnum is the practical boundary between the brain and the spinal cord.

Below the cervicomedullary junction, the corticospinal fibers have crossed and descend in the lateral and anterior funiculi of the cord. Lesions here produce ipsilateral upper motor neuron signs below the level of injury, often with a sensory level or sphincter disturbance.

The foramen magnum remains a convenient surgical marker for this neural transition, but the true physiological divide is defined by the pyramidal decussation itself. The lesions above have contralateral signs, whereas the lesions below have ipsilateral signs.

Identifying Different Lesions

Supraspinal (Intracranial) Lesions

Common causes include stroke, head injury, intracranial tumor, or abscess. The pattern typically shows

• Contralateral weakness involving the face and limbs
• Weakness is more marked in the upper limb and lower face.
• Fine movements are disproportionately affected compared to overall strength.
• Tone and reflex changes develop after an initial flaccid phase
• There is no sensory level or segmental pattern.
• Lower motor neuron signs are absent.
• Associated features such as speech disturbance, facial asymmetry, or seizures may appear depending on cortical involvement.
• Bladder function is usually preserved.

Spinal Cord Lesions

Common causes include trauma, compressive myelopathy due to disc or tumor, spondylotic myelopathy, transverse myelitis, and demyelinating disorders.

The pattern is characterized by bilateral involvement below a clearly defined level. Lower motor neuron signs, such as flaccidity and atrophy, occur at the level of the lesion due to anterior horn cell damage, while upper motor neuron signs ( spasticity, hyperreflexia, and Babinski response) appear below the lesion.

A sensory level helps localize the height of the cord lesion. Bladder and bowel dysfunction are common in complete or high lesions, and gait may be spastic or paraparetic. The coexistence of lower motor neuron signs at the level of the lesion and upper motor neuron signs below it is diagnostic of a spinal cord lesion.

Extraspinal Lesions or Lower Motor Lesions

These lesions also need to be excluded when UMN presents. Common causes include peripheral nerve injury, plexus injury, motor neuron disease, primary muscle pathology, or functional disorders. The pattern typically presents as localized or asymmetric weakness not conforming to an upper motor neuron distribution.There is flaccidity, loss of reflexes, and absence of the Babinski sign. Sensory loss, if present, corresponds to a nerve or root distribution, and muscle wasting often appears early.

Differentiating Upper Motor Neuron Syndrome From Lower

Upper Motor Neuron Syndrome affects the neural pathways that originate in the motor cortex or brainstem and descend to the spinal cord or cranial nerve nuclei. The lesion is above the level of the anterior horn cell or cranial nerve motor nucleus. The reflex arc remains intact but disinhibited, leading to hyperactivity.

Lower Motor Neuron Lesions involve the anterior horn cells, cranial motor nuclei, or peripheral motor axons that connect directly to skeletal muscle. The reflex arc is interrupted, resulting in flaccidity and loss of muscle response.

Distinguishing between upper motor neuron and lower motor neuron lesions is necessary for neurological localization. Clinical signs enable the clinician to infer whether weakness originates from cortical–spinal tract dysfunction or peripheral motor neuron disruption.

The following is a summary of these signs. [2]

In case of spinal injury Mixed UMN–LMN picture may appear at the lesion level (e.g., cervical cord injury damaging anterior horn cells). So the areas affected by injured fibers will have lower motor signs, whereas areas below will have upper motor signs.

Common Causes of Upper Motor Neuron Syndrome

Upper motor neuron syndrome can result from any process that disrupts the descending motor pathways from the motor cortex through the internal capsule and brainstem to the spinal cord. The pattern of weakness, reflex change, and associated features depends on the level, extent, and nature of the lesion. [2]

Supraspinal lesions arise above the foramen magnum, typically producing contralateral weakness with associated cortical features such as aphasia, facial asymmetry, or sensory loss.

Spinal lesions cause ipsilateral weakness below the level of the lesion, often accompanied by a sensory level and sphincter disturbance.

Supraspinal Lesions

These refer to lesions above the foramen magnum or the cervicomedullay junction. Lesions involving the motor cortex, internal capsule, or brainstem lead to contralateral weakness and characteristic cortical signs. Tone and reflex changes evolve after an initial flaccid phase.

• Cerebrovascular Accidents (Stroke): It is the most common supraspinal cause, often due to infarction or hemorrhage in the internal capsule or motor cortex. It leads to contralateral hemiplegia or hemiparesis. Immediately after the lesion, there is flaccidity, which later evolves into spasticity and hyperreflexia. There is lower facial weakness contralateral to the lesion, while the upper face is spared. Cortical features like aphasia, neglect, and sensory loss help localize the region.
• Traumatic Brain Injury: Contusion or diffuse axonal injury involving descending tracts leads to contralateral hemiparesis or hemiplegia with later spasticity. It is often associated with other cortical or cranial nerve deficits.
• Space-Occupying or Inflammatory Lesions: These include tumors, abscesses, or encephalitis damaging the motor cortex or internal capsule. The weakness is a gradual or subacute onset. Seizures or signs of raised intracranial pressure may be present.
• Congenital and Perinatal Lesions: Cerebral palsy (spastic type) occurs due to non-progressive perinatal injury to corticospinal tracts, causing spastic diplegia or quadriplegia, often with developmental delay or seizures.

Spinal Lesions

The Lesions are at or below the foramen magnum. The lesions cause damage to descending corticospinal tracts within the spinal cord, leading to spastic weakness below the level of the lesion, often with sensory involvement.

• Spinal Cord Injury: The acute spinal injury may lead to compression, contusion, or transection. It immediately results in acute flaccid paralysis (spinal shock) and then evolves into chronic spasticity and hyperreflexia. The injury may show upper and lower motor patterns at the lesion level and upper motor patterns below the lesion.
• Myelopathies: Compressive myelopathies are generally caused by disc prolapse, spondylotic changes, tumors, or epidural abscess. At the level of compression, there will be lower motor neuron signs, whereas there will be upper motor neuron signs below the level. Sensations and the bladder are often involved. HIV myelopathy, tuberculous meningomyelitis, or post-viral myelitis may lead to progressive spastic paraparesis or quadriparesis.
• Neurological Disorders: Multiple sclerosis may lead to patchy, asymmetric upper motor signs due to plaques in the brain and cord. Transverse myelitis may cause acute bilateral upper motor signs below the lesion, sensory and sphincter dysfunction.
  
  Primary lateral sclerosis causes pure UMN degeneration, progressive spasticity, and pseudobulbar symptoms. Amyotrophic lateral sclerosis (ALS) has both upper and lower motor signs. Thus, one may see spasticity with fasciculations and wasting.

Management in Upper Motor Neuron Syndrome

The management aims to decrease abnormal muscle tone, restore functional mobility, and prevent secondary complications. Often, the underlying cause is irreversible, and treatment focuses on optimizing residual function.

Physical therapy, pharmacologic agents, and occasionally surgical or neuromodulatory procedures are the options that may be tailored to each patient. [4]

Physical Rehabilitation

It is the cornerstone of the management of upper motor neuron syndrome.

• Exercises: Regular passive and active stretching helps maintain muscle length and joint mobility, and prevents the development of contractures and minimizes reflex-mediated stiffness. Strengthening and functional training include residual voluntary control and task-oriented training like hand manipulation, gait retraining.
• Posture and Splinting: Correct postural alignment reduces abnormal tone and prevents deformity. Splints may be used at rest or during movement as required. Night splints may be used to maintain a neutral joint position.
• Neuromuscular electrical stimulation: It involves the application of controlled electrical impulses to motor nerves or directly to muscle fibers to evoke contraction. It facilitates voluntary activation of weak muscles and may temporarily reduce spasticity by reciprocal inhibition.
• Gait and Mobility Training: Body-weight–supported treadmill training and robotic-assisted gait devices help in lower limb involvement by providing repetitive, task-specific practice under controlled conditions.
  The use of ankle-foot orthoses or knee-ankle-foot orthoses further enhances stability and safety during walking by preventing foot drop, improving limb alignment, and reducing the energy expenditure of ambulation. Orthotic and assistive devices like wheelchairs may be used by non-ambulatory persons.

Pharmacologic Management

Drug therapy aims at the management of spasticity. Therapy is indicated when spasticity causes pain, interferes with hygiene or movement, or risks contractures. The drugs commonly employed are baclofen, tizanidine, diazepam, dantrolene sodium, and botulinum toxin type A.
For severe, generalized spasticity unresponsive to oral medication, intrathecal baclofen via pump is given.

Surgical Interventions

Reserved for selected cases where spasticity is severe and refractory. The procedures are sectioning dorsal spinal roots (rhizotomy) to reduce afferent drive, tendon lengthening or joint release for fixed contractures, and neurotomies.

Follow-up and Prognosis

Chronic upper motor neuron syndromes, particularly after stroke or spinal cord injury, are associated with depression, anxiety, and loss of independence. Psychological counseling, social support, and community rehabilitation programs are vital. Follow-up includes regular reassessment of tone, strength, and functional status. Continuous adjustment of the therapy is needed.

Prognosis depends on the cause and extent of damage. Functional improvement significantly enhances the quality of life with consistent rehabilitation.

References

1. In: Kumar V, Abbas AK, Aster JC, eds. Robbins & Cotran: Pathologic Basis of Disease (Robbins Pathology). 10th ed. 2020. Chapter 28:Page: 1266, 1287-1289.
2. Purves D, Augustine GJ, Fitzpatrick D, et al., editors. Neuroscience. 2nd edition. Sunderland (MA): Sinauer Associates; 2001. Damage to Descending Motor Pathways: The Upper Motor Neuron Syndrome. Available from: [PubMed]
3. Burke D, Wissel J,  Donnan GA.. Pathophysiology of spasticity in Stroke.  Neurology 2013; 80:S20–6.[PubMed]
4. Emos MC, Agarwal S. Neuroanatomy, Upper Motor Neuron Lesion. [Updated 2023 Aug 14]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: [PubMed]