Introduction

• Definitions:
  • Paresis is the loss of power of voluntary movement; it is also called partial paralysis.
  • Paralysis is the loss of voluntary motor function.
  • Paraparesis/paraplegia refers to the weakness or absence of voluntary movement in the pelvic limbs.
  • Quadriparesis/quadriplegia (tetraparesis/tetraplegia) refers to the weakness or absence of voluntary movement in all limbs.
  • Hemiparesis refers to motor dysfunction of two limbs on the same side of the body affected.
  • Monoparesis refers to motor dysfunction of a single limb.
• Cause: most common causes in reptiles are trauma/injury and metabolic bone disease. Also, other bacterial, viral, CNS and toxic causes.
• Signs: can be peracute, acute, chronic, intermittent, static or progressive. Abnormal gait, use of limb(s). Can include falling, dragging a limb(s), leaning to one side, inability to stand or walk.
• Diagnosis: neurologic examination; CBC/chemistries; specific bloodwork for lead levels, cholinesterase testing; radiography, including skull to evaluate bullae disease (radiography is considered a poor diagnostic tool for imaging of tympanic bullae or visualization of fluid within the cavity, CT and MRI are superior and should be recommended). Computed tomography (CT) or magnetic resonance imaging (MRI) to evaluate brain infiltrate, spinal cord compression, bony lesions. CSF: in reptiles CSF is found below the dura and is collected from the atlanto-occipital space. Electromyelogram/nerve conduction velocity (EMG/NCV) to compare affected limb to unaffected.
• Treatment: hospitalize if neurologic signs, non-ambulatory, severe infections, anorexia. Supportive care includes fluid therapy, nutritional support, activity restriction. Analgesics and non-steroidal anti-inflammatory drugs (NSAID). Corticosteroids are controversial in reptiles and contraindicated with NSAIDs. Broad-spectrum antibiotics that penetrate the CNS if suspected or confirmed bacterial infection. Surgical repair of spinal fractures or trauma: may be of limited value.
• Prognosis: depends on etiology. Poor: loss of deep pain perception.

Pathogenesis

Etiology

• Most commonly trauma/injury Traumatic injuries and metabolic bone disease Metabolic bone disease.
• Infectious meningitis/encephalitis (bacterial, viral).
• Neoplasia of brain/spinal cord.
• Abscess in central nervous system (CNS).
• Cerebrovascular accident.
• Toxoplasmosis Toxoplasmosis.
• Toxicosis: lead, ivermectin (chelonians) Ivermectin, Clostridium botulinum Botulism, organophosphate if there is a history of ingestion or exposure.

Predisposing factors

General

• Trauma from improper handling or housing which results in fractures or luxations.
• Husbandry deficits (lack of heat/UVB/calcium supplementation) Chelonia husbandry Lizard husbandry Snake husbandry leading to nutritional secondary hyperparathyroidism.

Specific

• Existing skeletal abnormalities such as arthritis, spondylosis which may compromise neuromuscular function.
• Hypocalcemia Hypocalcemia.

Pathophysiology

Lesions of the central and/or peripheral nervous system

• CNS (brain, spinal cord):
  • Cell bodies and nuclei in the brain are responsible for initiating movement.
  • Axons transmit impulses to various locations in the spinal cord.
• PNS (sensory, motor neurons innervating various muscle groups):
  • Impulses to the limbs received from the spinal cord through the ventral nerve roots into spinal nerves and then to peripheral nerves.
  • Collections of lower motor neurons (LMN), divergence to the peripheral nerves of the limbs is in the cervical intumescence and the lumbar intumescence.
  • Upper motor neurons (UMN): maintain muscle tone, normal spinal reflexes:
    • Control or inhibit LMNs.
    • When injured, spinal reflexes no longer inhibited: loss or decrease of voluntary movement.
    • Hyperreflexia: LMN and peripheral nerves maintain muscle tone, control spinal reflexes. When injured: loss or decreased movement; diminished or absent reflexes.
• Spinal reflexes: peripheral nerve function and local spinal cord segment evaluation. Do not involve conscious awareness of a stimulus.

Timecourse

• Depends on etiology.
• If there is neurologic damage, muscle disuse atrophy and wasting occurs in as little as 5-7 days.
• Trauma: onset of signs may be immediate.

Diagnosis

Treatment

Prevention

Outcomes