What is Dr. Zubair Khalid's research focus?

Dr. Zubair Khalid specializes in molecular virology, mRNA vaccine development, and computational biology, with a focus on avian pathogens like IBDV and Avian Reovirus.

Where is Dr. Zubair Khalid currently working?

Dr. Zubair Khalid is a Postdoctoral Research Associate at the University of Maryland (UMD), specifically within the Department of Animal and Avian Sciences.

Spastic Paresis: Causes and Presentation

Name: Spastic Paresis: Causes and Presentation
Creator: Dr. Zubair Khalid

By Dr. Zubair Khalid, DVM, MS, PhD · 2026-09-20

Spastic paresis is a neurologic syndrome defined by increased muscle tone, exaggerated spinal reflexes, and extensor rigidity resulting from damage to upper motor neurons. It is not a single disease. It is a clinical pattern that points to a lesion somewhere in the brain, brainstem, or spinal cord white matter above the level of the segment that supplies the affected limb.

The word "paresis" means partial loss of voluntary movement, as opposed to "plegia," which means complete loss. The word "spastic" describes the quality of that weakness. The limb is stiff, not floppy. When a clinician lifts a spastic limb and then lets go, it may snap back into extension rather than hang loosely. That stiffness is the visible signature of a nervous system that has lost its normal descending inhibition.

This article explains what upper motor neuron (UMN) lesions are, how they differ from lower motor neuron (LMN) lesions, what causes each pattern in dogs, cats, horses, and cattle, and why lesion localization matters for prognosis. It is written for veterinary students, technicians, and clinicians who need a working framework, and for owners who want to understand what their veterinarian is describing.

This article is educational and is not a substitute for veterinary diagnosis or treatment.

The Anatomy Behind the Signs

To understand spastic paresis, you need a working picture of the two-neuron motor system.

The upper motor neuron has its cell body in the cerebral cortex or brainstem. Its axon descends through the brainstem and spinal cord in tracts such as the corticospinal and rubrospinal tracts. It does not leave the central nervous system. It ends by synapsing on the lower motor neuron or on local interneurons that modulate that lower motor neuron.

The lower motor neuron has its cell body in the ventral gray matter of the spinal cord or in a brainstem motor nucleus. Its axon leaves the central nervous system, travels in a peripheral nerve, and ends on a skeletal muscle fiber at the neuromuscular junction. This is the final common pathway. Every movement command, voluntary or reflex, must pass through the lower motor neuron.

When the upper motor neuron system is damaged, the lower motor neuron survives but loses the descending input that normally calibrates its activity. The result is a release phenomenon: spinal reflex arcs that were once held in check now fire more readily. The muscle spindles remain intact and continue to report stretch. The stretch reflex becomes exaggerated. Tone rises. The limb stiffens in extension.

When the lower motor neuron itself is damaged, the reflex arc is broken. The muscle cannot receive commands and cannot generate a reflex. Tone falls. The muscle atrophies because it loses its trophic input. Reflexes diminish or disappear.

That single distinction, intact reflex arc versus broken reflex arc, explains nearly every difference between UMN and LMN signs.

UMN Versus LMN Signs: The Core Comparison

The four cardinal features to assess on neurologic examination are muscle tone, spinal reflexes, muscle mass, and gait. The table below summarizes how each pattern presents.

Feature	Upper Motor Neuron (UMN)	Lower Motor Neuron (LMN)
Muscle tone	Increased (spasticity, rigidity)	Decreased (flaccidity)
Spinal reflexes	Normal to increased (hyperreflexia)	Decreased to absent (hyporeflexia or areflexia)
Muscle atrophy	Absent or mild, from disuse	Rapid and pronounced
Gait	Stiff, spastic, wide-based, extensor rigidity	Weak, flaccid, easily fatigued
Proprioception	Often impaired	Often impaired
Pain perception	Variable, depends on sensory tract involvement	Variable
Bladder function	Difficult to express, spastic sphincter	Easily expressed, atonic bladder

A few practical points about this table.

Muscle atrophy in UMN lesions is slow and mild. It reflects disuse rather than denervation. In LMN lesions, atrophy can be visible within one to two weeks and becomes severe because the muscle has lost its nerve supply entirely.

Reflex testing is the single most useful bedside discriminator. A patellar reflex that is brisk and exaggerated suggests a lesion above the relevant spinal segment. A patellar reflex that is weak or absent suggests a lesion at or below the segment.

Bladder function deserves special mention. In cats with upper motor neuron injury between T3 and L3, urinary retention is common because the detrusor muscle and sphincter lose coordinated control. A study of 34 cats with UMN injury found that adding tactile stimulation of the perigenital region during manual bladder expression improved the urine stream. In cats with chronic UMN injury, the time to obtain a urine stream fell from 9.3 seconds with manual expression alone to 3.1 seconds with added tactile stimulation. In acute cases, a urine stream was achieved in 54 percent of cats managed with manual expression alone versus 100 percent with added stimulation [1]. This is a practical, low-cost technique that any owner can be taught.

What Causes Spastic Paresis

Spastic paresis is a syndrome, not a diagnosis. The underlying cause determines treatment and prognosis. Causes fall into several broad categories.

Structural Lesions of the Brain or Brainstem

Tumors, abscesses, granulomas, and inflammatory lesions in the motor cortex or brainstem can interrupt descending motor tracts. In dogs, brainstem neoplasia is an uncommon but recognized cause of tetraparesis with spasticity. In cattle, a recent transcriptomic and immunohistochemical study found that bovine spastic paresis is associated with downregulation of genes specific for inhibitory neurons in the brainstem, including cholecystokinin (CCK), neuropeptide Y (NPY), and somatostatin (SST) [2]. These inhibitory neurotransmitters normally help modulate movement. Their loss may release brainstem motor circuits from inhibition, producing the persistent hindlimb stiffness that defines the condition.

Spinal Cord Compression

Compression of the spinal cord by an intervertebral disc, a vertebral malformation, or a mass interrupts descending tracts and produces UMN signs caudal to the lesion. This is the most common cause of spastic paresis in small animal practice. A dog with a thoracolumbar disc extrusion may have normal tone and reflexes in the forelimbs and spastic paresis with hyperreflexia in the hindlimbs. The lesion is between the two.

Cervical spondylomyelopathy in dogs, often called wobbler syndrome, is another classic example. The compression occurs in the cervical spine and produces a characteristic two-engine gait: short, stiff strides in the forelimbs and a wide-based, ataxic, spastic gait in the hindlimbs.

Cervical Stenotic Myelopathy in Horses

Equine cervical stenotic myelopathy, also known as wobbler syndrome, is a developmental or degenerative narrowing of the cervical vertebral canal that compresses the spinal cord. Affected horses show progressive ataxia and spastic paresis, particularly in the hindlimbs. The gait is often described as floating or hypermetric. Proprioceptive deficits are common. The condition is more frequent in young, rapidly growing horses of certain breeds, including Thoroughbreds and Warmbloods. Diagnosis requires careful neurologic examination and imaging. Prognosis depends on the severity and number of compressive sites.

Bovine Spastic Paresis (Elso Heel)

Bovine spastic paresis is a progressive neuromuscular disorder characterized by hypertension and stiffness of the hindlimbs [3]. The condition is also known as Elso heel. It occurs worldwide with an estimated prevalence of less than 1 percent, though in Germany alone approximately 20,000 Holstein cattle are thought to be affected [2].

The clinical presentation is striking. Affected calves develop a characteristic posture in which the affected hindlimb is extended caudally and the hock is flexed. The gastrocnemius muscle is rigid. When the calf moves, the limb may jerk or hop. The condition can be unilateral or bilateral.

The pathogenesis has been debated for decades. Electromyographic studies in calves with spastic paresis found marked increases in activity in several muscles but no characteristic EMG changes [4]. This suggested that the disorder is not a simple myopathy. More recent work points to an autoimmune or inflammatory process targeting brainstem inhibitory interneurons [2]. The gastrocnemius and superficial digital flexor muscles are consistently involved, and their motor neurons are located in the L6 to S2 spinal cord segments [5]. This segmental localization helps explain why surgical treatments that target the tibial nerve can be effective.

Bovine spastic paresis has been classified into three forms based on which muscle groups are involved: gastrocnemius (BSP-G), quadriceps femoris (BSP-Q), and mixed (BSP-M). A retrospective study of 79 calves found that BSP-M was the most common form at 47 percent, followed by BSP-G at 33 percent and BSP-Q at 20 percent. BSP-M and BSP-Q calves were significantly more likely to be bilaterally affected than BSP-G calves [6]. This classification matters because treatment response differs by form.

Nutritional and Toxic Causes

Not all spastic paresis is inherited or structural. Nutritional imbalances can produce similar signs. An outbreak of disease in intensively fattened calves fed concentrate mixtures rich in phosphorus was characterized by joint swelling, deformations, and spastic paresis of the posterior body. Affected calves had hyperphosphatemia and relative or absolute hypocalcemia. The condition responded to correction of the calcium-to-phosphorus ratio and vitamin D supplementation [7]. This is a reminder that metabolic causes should be on the differential list, especially in herd outbreaks.

A separate condition called bovine asymmetric hind limb paresis has been described in calves born or raised on flood plain pastures in a restricted area of northwestern New South Wales. Calves were either born with clinical signs or developed them by four months of age. The disease was slowly progressive, irreversible, and asymmetrical, with persistent hyperextension of the hip and stifle joints. No gross or microscopic lesions were found in the nervous or musculoskeletal system to account for the signs. An in-utero plant poisoning was suspected but no specific plant was identified [8]. This condition shares many features with bovine spastic paresis and illustrates how environmental causes can mimic genetic ones.

Degenerative and Age-Related Causes

In older animals, degenerative conditions can produce spastic paresis. A five-year-old Friesian bull developed a progressive locomotor disorder with rigid Achilles tendons and excessively straight hindlimbs. Necropsy showed degenerative arthropathy in all hindlimb joints below the hip, along with tendon and muscle lesions. The superficial digital flexor muscle had severe type II fiber atrophy with many abnormal type I fibers [9]. This case shows that chronic orthopedic disease can secondarily produce a gait that resembles spastic paresis, even when the primary problem is not neurologic.

Localization Determines Prognosis

The single most important clinical skill in evaluating spastic paresis is lesion localization. The prognosis for a dog with a single thoracolumbar disc extrusion is very different from the prognosis for a dog with a diffuse brainstem tumor. The prognosis for a calf with unilateral gastrocnemius involvement is very different from the prognosis for a calf with mixed bilateral involvement.

Localization requires a systematic neurologic examination. The clinician assesses mentation, cranial nerves, postural reactions, spinal reflexes, tone, and pain perception in each limb. The pattern of deficits reveals the level of the lesion.

A lesion in the cervical spinal cord produces UMN signs in all four limbs. A lesion in the thoracolumbar spinal cord produces UMN signs in the hindlimbs and normal signs in the forelimbs. A lesion in the lumbar intumescence produces LMN signs in the hindlimbs. A lesion in the brainstem produces cranial nerve deficits plus UMN signs in all limbs.

For bovine spastic paresis, localization is more specific. The gastrocnemius and superficial digital flexor muscles are innervated by motor neurons in the L6 to S2 segments [5]. A femoral nerve block can be used diagnostically to determine whether the quadriceps femoris is involved. In a study of 13 calf cadavers, a dorsal paravertebral approach provided the best access to the femoral nerve for anesthetic blockade [10]. In live calves, this technique has been used to identify animals suitable for partial tibial neurectomy [11].

Treatment Options and Outcomes

Treatment of spastic paresis depends on the underlying cause and the species.

In cattle with bovine spastic paresis, partial tibial neurectomy is the most commonly reported surgical treatment. In a study of 113 double-muscled Belgian Blue calves, good results were obtained in 83.2 percent of cases, with considerable improvement in another 4.4 percent. Severe hyperflexion of the hock necessitating early slaughter occurred in 4.4 percent, and 8 percent showed little or no improvement [12]. A separate study of 79 calves found that 86 percent of BSP-G calves treated surgically had complete resolution of clinical signs. Among BSP-M calves treated surgically, 81.5 percent improved but none completely recovered. Conservatively managed BSP-M calves all worsened over time. None of the BSP-Q calves were treated surgically, and 66.7 percent worsened while 33.3 percent spontaneously improved [6].

Tenotomy is an alternative surgical approach. In two Korean native Hanwoo calves with spastic paresis, tenotomy of the superficial tendon of the medial head and the deep tendon of the lateral head of the gastrocnemius was performed. A cast was applied postoperatively and removed three weeks later. Neither calf showed postoperative sequelae, and prognosis was evaluated at three weeks, six months, and eighteen months [3].

These surgical options are not curative for the underlying neurologic disease. They relieve the mechanical consequence of muscle contracture. The best outcomes occur in calves with unilateral gastrocnemius involvement.

In dogs and cats, treatment targets the underlying cause. Spinal cord compression from a disc extrusion may be treated with rest, anti-inflammatory medication, or surgery. Inflammatory or infectious causes may respond to specific therapy. Degenerative conditions are managed supportively.

In horses with cervical stenotic myelopathy, treatment options include conservative management with restricted exercise and anti-inflammatory medication, or surgical stabilization. Prognosis is guarded to poor for performance horses with severe compression.

Clinical Relevance, Limitations and Common Mistakes

The most common mistake in evaluating spastic paresis is failing to distinguish UMN from LMN signs. A dog with a thoracolumbar disc extrusion may have hyperreflexia in the hindlimbs, but if the clinician tests the patellar reflex and finds it reduced, the lesion may be lower than expected. Similarly, a cat with a lumbar lesion may have a flaccid bladder rather than a spastic one.

Another common mistake is attributing all stiffness to neurologic disease. Orthopedic conditions, tendon contracture, and muscle disease can produce gaits that resemble spastic paresis. The Friesian bull with degenerative arthropathy is a case in point [9]. A complete examination that includes orthopedic and musculoskeletal assessment is essential.

A third mistake is assuming that a diagnosis of bovine spastic paresis means the animal must be culled. Unilateral gastrocnemius cases have a good prognosis with surgery. Mixed and quadriceps cases have a more guarded prognosis, but some calves improve spontaneously [6].

A fourth mistake is overlooking nutritional causes. Herd outbreaks of spastic paresis should prompt evaluation of the ration, particularly the calcium-to-phosphorus ratio [7].

Limitations of current knowledge include the incomplete understanding of the pathogenesis of bovine spastic paresis. The autoimmune hypothesis is supported by transcriptomic evidence [2], but the trigger and the full mechanism remain unknown. There is no genetic test or breeding program that reliably prevents the condition. Electromyography does not show characteristic changes [4], so diagnosis remains clinical.

Individual cases require veterinary assessment. The information here is a framework for understanding, not a substitute for examination.

Frequently Asked Questions

What is spastic paresis?

Spastic paresis is increased muscle tone with exaggerated reflexes and extensor rigidity caused by damage to upper motor neurons. It is a clinical syndrome, not a specific disease.

What is the difference between UMN and LMN signs?

UMN signs include increased tone, normal to increased reflexes, and minimal atrophy. LMN signs include decreased tone, reduced or absent reflexes, and rapid, pronounced muscle atrophy.

What causes spastic paresis in dogs?

The most common cause in dogs is spinal cord compression, such as a thoracolumbar disc extrusion or cervical spondylomyelopathy. Brainstem lesions and inflammatory diseases can also produce the pattern.

What is Elso heel in cattle?

Elso heel is another name for bovine spastic paresis, a progressive disorder of hindlimb stiffness and rigidity. It is most common in double-muscled breeds such as Belgian Blue and can be unilateral or bilateral.

Can spastic paresis be treated?

Treatment depends on the cause. In cattle with the gastrocnemius form, partial tibial neurectomy or tenotomy can produce good outcomes. In dogs and cats, treatment targets the underlying spinal or brain lesion.

Is spastic paresis painful?

Spastic paresis itself is not typically painful, but the underlying cause may be. Spinal cord compression, disc extrusion, and joint disease can all cause pain alongside the neurologic signs.

What is the prognosis for a horse with cervical stenotic myelopathy?

Prognosis is guarded to poor for performance horses with severe compression. Mild cases managed conservatively may remain stable, but progressive cases often deteriorate.

Can nutrition cause spastic paresis?

Yes. Calves fed rations with severely imbalanced calcium-to-phosphorus ratios have developed spastic paresis along with joint swelling and deformities. Correcting the ration and supplementing vitamin D resolved the condition in reported outbreaks.