Paraparesis

By | September 3, 2013

Paraparesis is a non-specific term for bilateral motor dysfunction of the pelvic limbs.

Paraparesis is a very common presentation in small animal veterinary practice and can be caused by orthopaedic, muscle, neuromuscular junction, nerve and spinal cord dysfunction. More rarely, systemic and metabolic disorders can present as episodic or progressive paraparesis (e.g. cardiac and pulmonary dysfunction, endocrine and electrolyte disturbances) and animals with drug-induced side-effects (e.g. phenobarbital and potassium bromide) may show pelvic limb dysfunction manifested as ataxia. Diseases of the thoracolumbar spinal cord are the most common cause of paraparesis and, as late or misdiagnosis of many of these disorders can have catastrophic consequences for the patient, it is important to fully understand how to evaluate and manage paraparetic animals.

Clinical signs

Paraparesis, by definition, represents motor deficits in the pelvic limbs. Abnormal gait descriptions include:

  • Ataxia ― loss of proprioception; incoordination
  • Fatigability applies when one or more muscles become weaker with repetitive but normal use and may imply neuromuscular dysfunction
  • Paresis ― reduced voluntary motor function
  • Paralysis or paraplegia ― absence of voluntary motor function
  • Weakness ― a non-specific term referring to an inability to carry out a desired movement with normal force because of a reduction in strength of the muscles necessary to carry out the movement.

Paraparesis may be accompanied by changes in muscle tone that are elicited by passive movements including flaccidity, spasticity and rigidity.

  • Flaccidity ― the absence of normal muscle tone.
  • Spasticity (in quadripeds) ― a selective increase in extensor tone.
  • Rigidity ― an increase of flexor and extensor tone.

Schiff-Sherrington posture is characterized by thoracic limb extension with normal to sometimes decreased tone in the pelvic limbs (). A lesion to the thoracolumbar spinal cord segments alters the ascending inhibitory pathways from the border cells in the lumbar grey matter (L2-L4). Axons from these cells cross to ascend in the contralateral fasciculus proprius to terminate in the cervical intumescence. Loss of this ascending inhibition to the thoracic limbs results in extension. In spite of this increase in extensor tone the thoracic limbs are normal neurologically with respect to motor function and proprioception. Schiff-Sherrington posture does not indicate that the spinal cord lesion is irreversible.

Clinical signs of thoracolumbar and lumbosacral spinal cord dysfunction

Evaluation Spinal cord segments T3-L3 Spinal cord segments L4-S3
Mental status Normal Normal
Posture Normal or pelvic limbs tucked under body and altered tail carriage Normal or pelvic limbs tucked under body and altered tail carriage
Gait Pelvic limb ataxia; symmetrical or asymmetrical paraparesis/plegia Pelvic limb ataxia, symmetrical or asymmetrical (more often with cauda equina) paraparesis and/or plegia
Cranial nerves Normal Normal
Postural reactions Mild to severe deficit or absent Mild to severe deficit or absent
Spinal reflexes Normal to hyperreflexic pelvic limb(s) Hyporeflexia or areflexia; pseudo-hyperreflexic patellar reflex with sciatic nerve dysfunction
Spinal hyperaesthesia Variable; dependent on disease process Variable; dependent on disease process
Pain perception Variable; dependent on disease severity Variable; dependent on disease severity
Micturition Usually affected with loss of motor function, detrusor areflexia-sphincter hypertonia None or mild to severe detrusor areflexia; sphincter hypotonia

Clinical signs of thoracolumbar spinal cord disorders reflect sensory, motor and autonomic dysfunctions of the pelvic limbs, tail, bladder and gastrointestinal tract (Clinical signs of thoracolumbar and lumbosacral spinal cord dysfunction). Depending upon the severity of pelvic limb dysfunction, the paresis may or may not be clinically obvious.

Gait

Gait should be evaluated at a slow and fast pace and when walking up and down steps.

Ataxic gait

Animals with spinal cord disease have an ataxic gait and postural reaction deficits (specifically conscious proprioception deficits). Conscious proprioception is a non-weight-bearing test used to discriminate between orthopaedic and neurological lameness. Subtle proprioceptive loss and paresis may become more apparent during postural reaction testing (i.e. hopping, extensor postural thrust and wheel-barrow reaction).

  • Spinal reflexes, myotatic and withdrawal (flexor) reflex can assist further with neuroanatomical localization ().
  • The cutaneous trunci reflex can assist with localization of a thoracolumbar lesion but is not always a reliable indicator.
  • Assessment of pelvic limb pain perception () is extremely important in paraplegic animals as it provides critical prognostic information ().
  • Asymmetry of neurological deficits is common with vascular, inflammatory and compressive myelopathies.

Disorders of the thoracolumbar spinal region by onset and pain status

Diseases exhibiting no paraspinal hyperaesthesia Onset
Degenerative

Degenerative myelopathies; spinal muscular atrophies; central axonopathies; hereditary ataxia in Smooth Fox and Jack Russell Terriers; leucoencephalomyelopathy of Rottweilers; neuroaxonal dystrophies; nervous system degeneration in Ibizan Hounds; Afghan Hound myelopathy; hypomyelinogenesis; dysmyelinogenesis; storage diseases; spondylosis deformans; dural ossification

Chronic
Anomalous

Myelodysplasia

Chronic
Neoplasia

Primary: Intramedullary (ependymoma, glioma)

Chronic; may have acute manifestation
Inflammatory

Infectious myelitis (viral, protozoal)

Usually acute
Vascular

Fibrocartilaginous embolic (FCE) myelopathy; thrombosis; infarction

Acute
Diseases exhibiting paraspinal hyperaesthesia
Degenerative

Calcinosis circumscripta; inten/ertebral disc disease; spinal extrasynovial cyst; mucopolysaccharidosis

Acute or chronic
Anomalous

Vertebral malformations; spina bifitia: syringohydromyelia

Chronic
Metabolic

Hyperchylomicronaemia

Chronic
Neoplastic

Primary: Extradural (vertebral, lymphoreticular); Intradural-extramedullary (nerve sheath tumour, meningioma, nephroblastoma) Secondary: Metastatic (mammary carcinoma, haemangiosarcoma)

Acute or chronic
Idiopathic

Diffuse idiopathic skeletal hyperostosis

Usually chronic
Inflammatory

Infectious: Meningitis/myelitis (viral, fungal, bacterial, protozoal, rickettsial, algal, spinal empyema); discospondylitis (bacterial,fungal); vertebral physitis

Non-infectious: Granulomatous meningoencephalomyeiitis; steroid-responsive meningitis; vasculitis

Usually acute
Trauma

Traumatic disc herniation; vertebral fractures/luxations

Acute

Presence of paraspinal hyperaesthesia also assists with the differential diagnoses (Disorders of the thoracolumbar spinal region by onset and pain status). Paraspinal hyperaesthesia usually indicates a compressive and/or an inflammatory cause. Pain sensitive structures include the periosteum of the vertebrae, meninges, nerve roots and intervertebral disc (). Disorders that classically do not manifest paraspinal hyperaesthesia are degenerative spinal cord diseases, intramedullary neoplasia and fibrocartilaginous em-bolic (FCE) myelopathy.

Stiff gait

A stiff or stilted gait is characteristic for an animal with orthopaedic, muscle or neuromuscular junction disease. In order to differentiate orthopaedic from neurological disease, the animal will often be required to undergo strenuous exercise. In cases of neurological disease this will exacerbate the paraparesis; whereas, clinical signs often improve with exercise in animals with orthopaedic disease. In addition, the following should be noted to help differentiate the origin of the gait deficit:

  • Animals with orthopaedic disease will not have conscious proprioceptive deficits, although the associated loss of strength with these conditions may make interpretation of these tests difficult
  • Myopathic disease usually presents with generalized weakness and exercise intolerance that can be episodic or persistent. Gait is usually stiff and stilted or ‘bunny-hopping’. Exercise intolerance and episodic weakness are often not obvious until the animal is exercised. Commonly in myopathic disease, the pelvic limbs are affected first and more severely than the thoracic limbs, and may therefore initially present as paraparesis (). Muscle palpation may reveal severe atrophy or hypertrophy with or without tremors and/or fasciculations. In addition, myopathies (and polyneuropathies) can result in dysphagia, dyspnoea and dysphonia. Depending upon the severity of atrophy the range of joint movement may be limited. Pain may also be evident upon palpation of the muscles
  • The neuromuscular junction disorder that is most often confused with other paraparetic disorders is generalized myasthenia gravis (MG). Although rare, MG may manifest as an episodic weakness with pelvic limb involvement only. The gait of affected animals can show a shortened stride or ‘bunny-hop’ that progresses to collapse. Strength returns with rest ().
  • Neuropathies are characterized by flaccid paresis, postural reaction deficits and neurogenic muscle atrophy. Paraesthesia or analgesia may be evident with involvement of the sensory component of the nerve. Gait evaluation commonly reveals moderate to severe ataxia. Distal limbs may have a flaccid appearance. Muscle palpation reveals severe atrophy and in chroniccases, joint contractu re. Musclefasciculations may be present. Spinal reflexes often are decreased or absent. Neuropathies can be responsible for dysphagia, dysphonia and dyspnoea.

Lesion localization

Thorough physical, orthopaedic and neurological examinations of the patient are crucial for localizing the clinical signs and avoiding unnecessary diagnostic testing and client expense. A patient with suspected orthopaedic disease should have a neurological examination.

Neuroanatomical localization of paraparesis is specified to the spinal cord segments T3-L3 or L4-S3 () based upon signs of upper motor neuron (UMN) or lower motor neuron (LMN) limb weakness, respectively (). UMN weakness refers to a lesion that interrupts the descending motor pathways from supraspinal neurons that converge on the LMN pool. Clinical signs of UMN weakness manifest as paresis and/or plegia with normal to increased spinal reflexes (hyperreflexia) and muscular hypertonia. LMN weakness refers to a lesion of the ventral spinal cord grey matter and its axon coursing to the muscle through the spinal nerve roots and peripheral nerve. LMN weakness clinically manifests as paresis and/or plegia, decreased to absent spinal reflexes (hyporeflexia to areflexia), decreased muscle tone (flaccidity) and muscle atrophy that is severe and rapid in onset. The sacral and coccygeal regions are localized according to LMN signs involving the perineal region, bladder function, urethral tone and tail tone ().

A stiff or stilted gait, muscle atrophy and lack of proprioceptive deficits are suggestive of orthopaedic, junctional or myopathic disease. LMN signs relevant to the pelvic limbs, with a lack of involvement of the tail and bladder, lead to the suspicion of a peripheral neuropathy rather than a process affecting the spinal cord or cauda equina. Neuropathies may be associated with signs of megaoesophagus.

Due to the multiplicity of anatomical dysfunctions that can produce clinically similar disorders, the clinician faces a diagnostic dilemma. Aged patients often have concurrent orthopaedic and neurological disorders, which further complicate the examination process. For example, in middle-aged, large-breed dogs, disorders that often mimic each other and coexist include:

  • Degenerative lumbosacral stenosis
  • Degenerative myelopathy
  • Type II intervertebral disc disease
  • Degenerative joint disease as a result of hip dysplasia or rupture of the anterior cruciate ligament.

To furthercomplicate matters aspecificante-mortem diagnostictest is lacking for some diseases. For example, in German Shepherd Dogs the diagnosis of degenerative myelopathy should always be a consideration for paraparesis, even in the face of other causes. It is important to note that signs of pelvic limb dysfunction can present prior to signs of thoracic limb paresis in some cases of cervical spinal cord disease (e.g. giant breed wobbler syndrome) and in generalized peripheral neuropathies, junctionopathies and myopathies.

It is important to remember that localization refers to spinal cord segments rather than vertebrae. Thus, a lesion that localized to the L4-S3 spinal cord segments could lie anywhere caudal to the second lumbar vertebra (the approximate site of the L4 spinal cord segment) ().

Pathophysiology

The severity of the motor and sensory deficits from spinal cord disease is dependent upon the rapidity of disease onset, extent of spinal cord involvement and the area within the vertebral column that is affected. Spinal cord dysfunction can be a secondary consequence of extrinsic or intrinsic injuries to the spinal column. Traumatic aetiologies, such as vertebral fractures, luxation and penetrating injuries from missiles or animal bites, are examples of extrinsic injuries. Intrinsic injuries include embolization of the spinal cord vasculature, extrusion of the nucleus pulposus and developmental anomalies. As for tetraparesis () disease processes affecting the spinal cord and peripheral nerves and muscles may be compressive, concussive, inflammatory, vascular, metabolic or degenerative.

Animals with acute, severe thoracolumbar spinal cord injuries may develop an unusual systemic complication known as neurogenic shock.

Neurogenic shock is associated with cervical or cranial thoracic injury to the spinal column. This has been observed in people and experimentally in dogs and cats but is rarely evident in clinical patients.

This syndrome results from sympathetic loss (decreased blood pressure and heart rate resulting from unopposed vagal tone) and continual vagal tone. This phenomenon results in a loss of spinal cord blood flow regulation and subsequent ischaemia. Neurogenic shock resolves with fluid therapy and pressor agents.

Neurodiagnostic investigation

History and findings of physical and neurological examinations will identify a neurological problem and assist with neuroanatomical localization and consideration of differentials. The onset (acute or insidious), rate of progression (rapid or gradual) and temporal relation (intermittent and/or episodic, stable or chronic) can be established. A recommended diagnostic approach to spinal cord diseases is as follows:

  • Complete blood count (CBC), serum biochemistry profile and urinalysis
  • Thoracic radiographs in animals >5 years of age, and after trauma
  • Survey spinal radiographs can assist with recognition of obvious abnormalities such as discospondylitis, luxations and bone neoplasia. If an abnormality is not seen, advanced imaging and cerebrospinal fluid (CSF) analysis are indicated
  • CSF collection ― preferably from the cerebellomedullary cistern and caudal lumbar region
  • Myelography and epidurography are useful for the detection and characterization of compressive spinal cord lesions (extradural, intradural and intramedullary) and for determining the extent of the compression ().
  • Computed tomography (CT) is used as a primary method to evaluate the spine or assist with determining lesion extent after myelography
  • Magnetic resonance imaging (MRI) is becoming a more common diagnostic technique as it is particularly useful in the detection of lesions within the spinal cord.

Additional diagnostic procedures include electrodiagnostic evaluation (electromyography and nerve conduction studies), nerve and muscle biopsy, CSF protein electrophoresis, serology and exploratory surgery.

Differential diagnosis

The anatomical localization and distinguishing features of lesions that cause paraparesis are summarized in Anatomical localization of lesions that can cause paraparesis.

Anatomical localization of lesions that can cause paraparesis. CP = conscious proprioception.

Location Distinguishing factors on examination
T3-L3 Paraparesis, postural reaction and CP deficits (pelvic limbs); intact to increased spinal reflexes; + focal spinal hyperaesthesia
L4-S3 Paraparesis, postural reaction and CP deficits (pelvic limbs); decreased to absent spinal reflexes; + change in tail carriage and/or tone; + incontinence; + focal spinal hyperaesthesia
Bilateral orthopaedic disease of pelvic limbs Paraparesis but stilted gait; normal CPs; abnormal findings on orthopaedic examination
C1-T2 As for T3-L3 plus subtle postural reaction or gait deficits in thoracic limbs; neck pain.
Peripheral neuropathy As for L4-S3 but no change in tail function or continence; + laryngeal paralysis; + megaoesophagus; ± thoracic limb involvement
Junctional disease Normal CP; spinal reflexes may be initially normal but decrease with repetition; often see paraparesis ± thoracic limb involvement that is exacerbated by exercise or activity; no evidence of spinal pain + laryngeal paralysis; + megaoesophagus; no evidence of incontinence

Diseases that cause paraparesis

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