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Therapeutic use of hydroxyprogesterone in the management of acute spinal cord injury in a bull: A case report

Abstract

A 4-year-old black, non-descript bull was presented to the Large Animal Medicine Unit, Veterinary Clinical Complex, Veterinary College and Research Institute, Orathanadu, with a history of acute lateral recumbency and generalized stiffness. Clinical examination revealed dullness and congested mucous membranes, though vital parameters were within normal limits. Neurological evaluation indicated diminished thoracic reflexes and exaggerated pelvic limb reflexes, localizing the lesion to the cervical spinal cord (C6-T2). Radiographic findings were unremarkable. The case was tentatively diagnosed as acute spinal cord injury. Initial treatment included antibiotics, corticosteroids, and methylcobalamin. From the third day, intramuscular hydroxyprogesterone was administered on alternate days. Marked improvement was observed, and by the seventh day, the bull was ambulatory without assistance. This case highlights the potential therapeutic role of hydroxyprogesterone in large animal neurology.

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Introduction

Progesterone, traditionally recognized as a reproductive hormone, also functions as a neuroprotective steroid synthesized within the nervous system by glial cells and neurons (Guennoun et al., 2014) [2] . Neurosteroids, including progesterone were involved in neuronal repair and regeneration through enzymatic steroidogenesis. In veterinary medicine, progesterone has been reported to support recovery in spinal cord injuries, particularly in dogs, due to its cost-effectiveness and minimal side effects compared to corticosteroids (Ramkumar et al., 2023) [5] . This case report describes the clinical application of hydroxyprogesterone in the management of spinal cord injury in a bull.

Case Presentation

A 4-year-old black, non-descript bull was presented with lateral recumbency and generalized rigidity that began earlier the same day. The owner suspected trauma. On examination, the bull was dull with congested mucous membranes. Vital signs were normal. Neurologically, the animal was stuporous with an unstable head position, diminished thoracic reflexes, and exaggerated hindlimb reflexes. Hematology revealed neutrophilia and reduced LDH levels (Table 1 &2). Tests for blood parasites were negative. Radiographs showed no skeletal abnormalities. Based on neurological signs, the lesion was localized to the cervical spinal cord (C6-T 2 ). Neurological grading (modified from Scott, 1977) [6] categorized the bull as grade III. A presumptive diagnosis of acute spinal cord injury was made.

Treatment and Progression

Initial management included IV normal saline (2L), IV ceftriaxone-tazobactam (10 mg/kg), IM prednisone (0.5 mg/kg), IM ranitidine (2 mg/kg), and IV Methylcobalamin (60 mL). By the second day, the animal could lift its head and eat, though it remained recumbent. A sling was used for support. On day 3, hydroxyprogesterone (5 mg/kg IM) was introduced. The following day, the bull stood unsteadily. Hydroxyprogesterone was continued on alternate days. By day 7, the animal was able to walk independently.

Discussion

Spinal cord injuries (SCIs) in cattle may arise from trauma, infectious causes, metabolic disorders, or congenital anomalies. Neurological deficits vary based on lesion location, with C6-T 2 lesions typically causing reduced forelimb reflexes and exaggerated hindlimb responses (Simpson et al., 2019) [7] . Secondary spinal damage-such as edema, demyelination, and ischemia-may exacerbate injury severity via inflammatory mediators (Thomas, 2021) [8] . Spinal cord injury (SCI) in cattle is relatively uncommon but carries significant clinical and economic implications. In the present case, neurological examination localized the lesion to the C6-T 2 spinal cord segments, as evidenced by diminished thoracic limb reflexes with exaggerated pelvic limb reflexes, consistent with lower motor neuron involvement at the level of the lesion and upper motor neuron signs caudal to it. The absence of radiographic abnormalities suggests a functional or compressive spinal cord insult without overt vertebral fracture. In large animal practice, where advanced imaging such as MRI is rarely feasible, systematic neurological examination remains the primary diagnostic tool. Early recognition and grading (modified Scott grading -Grade III) indicated preserved deep pain perception, supporting a guarded-to-favourable prognosis with prompt therapeutic intervention. Hematological evaluation revealed leukocytosis (17.4 ×10³/µl) with neutrophilia (60%), suggesting an acute stress or inflammatory response, possibly secondary to trauma and tissue injury. The absence of eosinophilia and basophilia ruled out parasitic or hypersensitivity etiologies. Red blood cell count, hemoglobin, and packed cell volume were within normal limits, indicating that anemia or hemorrhagic shock was unlikely. Serum biochemical parameters were largely within reference ranges, supporting systemic stability. Blood urea nitrogen and creatinine were normal, excluding renal compromise. Liver enzymes (AST 86 U/L; ALP 258 U/L) were mildly elevated, which may reflect muscle injury or stress-related hepatic enzyme induction. Lactate dehydrogenase (LDH 675 U/L), although not markedly elevated, can be associated with muscle and tissue damage following trauma. Electrolyte levels, including calcium, phosphorus, and magnesium, were within normal limits, ruling out metabolic causes of recumbency such as hypocalcemia or hypomagnesemia (Weiss and Wardrop, 2010) [9] . Thus, clinicopathological findings supported a traumatic-inflammatory etiology rather than metabolic or infectious neurological disease. The multimodal therapeutic approach likely contributed synergistically to recovery. Corticosteroid therapy may have reduced spinal cord edema and inflammatory mediator release during the early phase of secondary injury. Methylcobalamin could have supported neuronal repair and remyelination. The introduction of hydroxyprogesterone on day three coincided with marked clinical improvement, with progression from sternal recumbency to assisted standing and eventual independent ambulation by day seven. Progesterone's recognized neuroprotective properties including antiinflammatory action, membrane stabilization, reduction of lipid peroxidation, and promotion of remyelination may have played a pivotal role in limiting secondary neuronal damage and enhancing axonal recovery. Further controlled studies are warranted to validate its clinical efficacy and establish standardized treatment protocols. Accurate neurological localization is key in large animals, though diagnostic imaging is often limited due to logistical and financial constraints (Achard et al., 2017) [1] . CSF analysis, though helpful, was not possible in this case due to the bull's temperament. Therapeutic protocols typically involve anti-inflammatory agents, antimicrobials, and vitamin supplementation (Ramkumar et al., 2023) [5] . Corticosteroids like prednisone are effective in reducing inflammation and secondary nerve damage (Lu et al., 2016) [3] . Methylcobalamin has been used for neural regeneration and myelin repair (Nishimoto et al., 2015) [4] . Recent studies suggest that neuro-steroids, particularly progesterone, have regenerative and neurotrophic effects, promoting remyelination and axonal regrowth (Ramkumar et al., 2023) [5] . The favourable response observed in this bull supports the neuroprotective role of progesterone in managing spinal cord injuries.

Conclusion

This case demonstrates successful recovery from acute spinal cord injury in a bull using a multimodal approach, including hydroxyprogesterone. While advanced imaging is often impractical in large animals, clinical neurology and basic supportive care remain essential. Further research into the field application of progesterone for neurological disorders in large animals is warranted.

References

  1. Achard D, Steiner A, Meylan M. Neurological examination in ruminants: a review. Veterinary Journal. 2017;221:36-45. doi:10.1016/j.tvjl.2017.01.007
  2. Guennoun R, Labombarda F, Gonzalez Deniselle MC, Liere P, De Nicola AF, Schumacher M. Progesterone and its metabolites as neuroprotective agents in CNS trauma and neurodegeneration. Journal of Molecular Neuroscience. 2014;54(3):366-377. doi:10.1007/s12031014-0307-2
  3. Lu J, Ashwell KW, Waite PM. Advances in corticosteroid therapy for spinal cord injury: Clinical relevance and translational potential. Neuroscience Bulletin. 2016;32(2):144-152. doi:10.1007/s12264-0160012-1
  4. Nishimoto S, Tanaka H, Fujita K, Nakamura S, Niimi H. Methylcobalamin: A potential treatment for peripheral nerve degeneration and pain. Current Neuropharmacology. 2015;13(4):509-520. doi:10.2174/1570159X13666150416221701
  5. Ramkumar PK, Saravanan M, Vijayakaran K, Kamalesh SL, Abimanyu G. Medical management of acute spinal cord injury with aspiration pneumonia in a kid. Indian Journal of Veterinary Medicine. 2023;43(2):74-77.
  6. Scott HW. Neurological grading of spinal cord lesions in dogs. Veterinary Record. 1977;101(14):288-290.
  7. Simpson KM, Henthorn PS, Smith-Maxie L. Disorders of the bovine spinal cord. In: Smith RL, editor. Large Animal Internal Medicine. 5th ed. Elsevier; 2019. p. 1092-1097.
  8. Thomas JA. Pathophysiology of spinal cord injury: Primary and secondary mechanisms. Neurosurgical Focus. 2021;50(1):E1. doi:10.3171/2021.1.FOCUS20793
  9. Weiss DJ, Wardrop KJ, editors. Schalm's veterinary hematology. 6th ed. Wiley-Blackwell; 2010.
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