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J Vet Clin 2023; 40(1): 56-61

https://doi.org/10.17555/jvc.2023.40.1.56

Published online February 28, 2023

Successful Management of Post-Traumatic Hydrocephalus and Pseudomeningocele Following Traumatic Brain Injury in a Cat

Hyoung-Won Seo1 , Jeong-Min Lee1 , Hae-Boem Lee2 , Yoon-Ho Roh3 , Tae-Sung Hwang4 , Kun-Ho Song1 , Joong-Hyun Song1,*

1Department of Veterinary Internal Medicine, College of Veterinary Medicine, Chungnam National University, Daejeon 34134, South Korea
2Department of Veterinary Surgery, College of Veterinary Medicine, Chungnam National University, Daejeon 34134, South Korea
3Division of Animal Surgery, Department of Clinical Veterinary Medicine, Vetsuisse Faculty, University of Bern, Bern 3012, Switzerland
4Institute of Animal Medicine, College of Veterinary Medicine, Gyeongsang National University, Jinju 52828, South Korea

Correspondence to:*jh.song@cnu.ac.kr

Received: December 6, 2022; Revised: January 9, 2023; Accepted: January 24, 2023

Copyright © The Korean Society of Veterinary Clinics.

A 5-month-old female domestic short-haired cat presented with a history of seizure episodes for two months following an animal bite injury to the head. There were no remarkable findings on physical and neurological examination or blood analysis. Computed tomography revealed a fracture of the left parietal bone with an inward displacement of the bone fragment while magnetic resonance imaging revealed an enlarged temporal horn of the left lateral ventricle and a pseudomeningocele compressing the adjacent cerebral parenchyma. Subsequently, cerebrospinal fluid analysis results were normal. The patient was diagnosed with traumatic brain injury (TBI), with subsequent post-traumatic hydrocephalus (PTH) and pseudomeningocele. Despite treatment with phenobarbital and levetiracetam, seizures were not sufficiently controlled. Craniectomy for bone fragment removal and duraplasty were performed after a week. The patient then returned to normal condition with no further seizure activity. On repeated MRI two months after discharge, the hydrocephalus of the lateral ventricle and pseudomeningocele were enlarged; however, the patient maintained a good clinical status without any neurological signs. To the best of our knowledge, PTH and intracranial pseudomeningoceles have not yet been reported in cats. PTH and pseudomeningocele are among the complications of TBI and may not have any significant relevance with the clinical signs in this case. Thus, to broaden our knowledge about PTH and pseudomeningocele in cats, we describe serial changes in the clinical findings of this cat over the treatment period.

Keywords: cat, craniectomy, duraplasty, pseudomeningocele, post-traumatic hydrocephalus.

Post-traumatic hydrocephalus (PTH) is a progressive process characterized by excessive cerebrospinal fluid (CSF) accumulation due to liquor-dynamic disturbances following a traumatic brain injury (TBI), which is defined as damage to the brain by external forces (3,11,13,21). Pseudomeningocele is an abnormal collection of CSF in the soft tissue, within a fibrous capsule, unlike meningocele, which is surrounded by a dura layer (10). Usually neurologic signs, including a decreased level of consciousness, alteration in mental state, and neurological deficits (e.g., weakness, paresis/paraplegia, seizure) (1), are closely related to the injury (2). Various criteria have been suggested for PTH diagnosis; an universal criteria has not been established, even in human medicine (6,21). However, it can be confirmed by combining clinical assessment and advanced diagnostic imaging, which involves a history of TBI and identification of skull damage and enlargement of the ventricular system via computed tomography (CT) and magnetic resonance imaging (MRI) (18). PTH and pseudomeningocele can be managed with surgical intervention and conservative management using analgesics, antiepileptic and anti-inflammatory drugs. The clinical symptoms can be improved by treatment of the underlying causes, and a conservative approach is preferred. In human medicine, the incidence of PTH among TBI patients was reported to be 0.7 to 29%, with a wide variation owing to the differences in the evaluation criteria (15). In this study, we reviewed the clinical features, MRI findings, and therapeutic outcomes in a cat with PTH and pseudomeningocele and evaluated their clinical significance. To the best of our knowledge, this is the first case report of PTH and pseudomeningocele in a cat which was successfully treated with surgical intervention and conservative therapy.

A 5-month-old female domestic short-haired cat was referred to the Veterinary Medical Teaching Hospital of the Chungnam National University. Four months prior to presentation, the cat was found on a street with a penetrating injury, suspected to be a brain-bite wound (Fig. 1A). The cat had multiple complex partial seizures, characterized by orofacial motor signs (chewing and eye and facial twitching) and a generalized tonic-clonic episode. The seizures did not improve with administration of zonisamide 5 mg/kg, per os [PO], q 12 h or levetiracetam (Keppra, UCB Pharma, Brussels, Belgium) 20 mg/kg, PO, q 8 h. Further, no remarkable findings were observed during physical examination. The results of the complete blood count and serum chemistry analysis were within the normal ranges. Neurological examination revealed unremarkable results, except for intermittent facial twitching.

Figure 1.(A) Image showing penetrating injury and suspected brain-bite wound (arrow). (B) Transverse CT image at the temporal bone level showing a depressed fracture of the temporal bone on the left side (arrow). (C) Left caudolateral 3D-reconstruction CT image (arrow). L, left.

CT (Alexion TM, Canon Medical Systems, Japan) revealed a fracture of the left parietal bone with inward displacement of the bone fragment (Fig. 1B, C). On MRI (1.5 Tesla unit, Vantage ElanTM, Canon, Medical) (Fig. 2), a linear structure was observed at the level of the left parietal bone with a hypointense signal on T1-weighted image (T1WI) and T2-weighted image (T2WI), resembling a bone fragment extending to the level of the left thalamus. An atypical and circular intracranial cyst with a hyperintense signal on T2WI and a hypointense signal on T1WI and Fluid-attenuated inversion recovery (FLAIR) was observed in the lateral and ventral brain parenchyma of the embedded bone fragment, respectively. The lateral and ventral cysts measured 0.95 × 0.3 × 0.82 cm, 1.6 × 1.5 × 1.2 cm, respectively (L × W × H). A midline shift which slightly displaced the left thalamus and interthalamic adhesions to the right side was also seen. In addition, hyperintense signals on T2WI and FLAIR, and isointense signals on T1W1 were observed around the bone fragment with evident contrast enhancement, which was considered an inflammatory change. In summary, inflammatory changes in the brain parenchyma were caused by bone fragments, resulting in an enlarged temporal horn of the left lateral ventricle and a pseudomeningocele. Cerebrospinal fluid (CSF) analysis revealed a normal nucleated cell count (4 cells/μL, reference range, <5) and protein concentration (10 mg/dL, reference range, <25), and negative polymerase chain reaction results for infectious agents. Cytological examination of the CSF revealed a predominance of mononuclear cells.

Figure 2.(A) Transverse T2WI, (B) FLAIR image, and (C) Sagittal T2WI of the head. These images reveal PTH (arrow), and pseudomeningocele (arrowhead) with inflammatory changes within the left parietal lobe. L, left.

Based on the history and results of diagnostic imaging, the patient was diagnosed with TBI and subsequent PTH and pseudomeningocele. Despite treatment with phenobarbital (Phenobarbital, Hana Pharm., Seoul, Korea) 2.5 mg/kg, PO, q 12 h and levetiracetam 20 mg/kg, PO, q 8 h, the seizure was not well-controlled. Craniectomy and duraplasty were performed after a week, to remove the bone fragment and relieve intracranial pressure (Fig. 3A). The tissue sample surrounding the bone fragment was sent to a commercial laboratory (IDEXX Laboratories, Inc., USA) for histopathological examination, which revealed pyogranulomatous and eosinophilic inflammatory infiltrates with fibrin aggregation and absence of infectious organisms (Fig. 3B).

Figure 3.(A) Intraoperative image of the bone fragment embedded in the brain parenchyma (arrow). (B) The histopathologic examination revealed pyogranulomatous and eosinophilic infiltrate and aggregates of fibrin with no infection.

After surgical correction, the patient returned to a normal condition without further seizure activities. A repeated MRI scan two months after discharge, the inflammatory changes related to the bone fragment had entirely alleviated; however, the ventriculomegaly and pseudomeningocele had enlarged (1.8 × 1.9 × 2.2 cm and 1.1 × 0.38 × 1.6 cm, respectively, L × W × H) (Fig. 4). Despite these findings, the patient maintained a good clinical status without any neurological signs. There was no recurrence of any clinical signs following the four-month follow-up period owing to treatment with phenobarbital 3.5 mg/kg, PO, q 12 h and levetiracetam 30 mg/kg, PO, q 8 h.

Figure 4.(A) Transverse T2WI, (B) FLAIR image, and (C) Sagittal T2WI of the head after removing the bone fragment. These images reveal PTH (arrow), and pseudomeningocele (arrowhead) without inflammatory changes within the left parietal lobe. L, left.

TBI is divided into primary and secondary injuries of the brain parenchyma. Primary injury occurs immediately as a result of direct mechanical damage during traumatic events, whereas secondary injury occurs minutes to days after the trauma, due to a combination of systemic extracranial damage and intracranial physical and biochemical changes. Guidelines for TBI treatment in humans have been established and focus on maintaining adequate cerebral perfusion. However, currently, no recommended guidelines exist in veterinary medicine. Most clinical recommendations are based on in vivo experiments, human studies, or personal experience (16). This classification is important since primary injuries are unmanageable, whereas secondary injuries are predictable and preventable. The prevention and treatment of secondary injuries can reduce mortality and improve outcomes. Therefore, attention must be focused on blood pressure optimization, brain tissue oxygenation, maintenance of adequate cerebral perfusion pressures, and prevention of seizures (7,20).

Since PTH was first described in human medicine by Dandy and Blackman in 1914 (4), several studies have investigated various ways to identify the mechanism, pathophysiology, risk factors, and treatment underlying PTH. However, it is rarely discussed in veterinary medicine and has only been reported once. In 2018, PTH was diagnosed in a 2-month-old female Yorkshire Terrier dog following a forensic necropsy (8). The mechanism of PTH involves mechanical obstruction of the CSF, laceration of the ventricle, increased number of inflammatory cells and proteins in the CSF, and subsequent blockage of arachnoid granulation and CSF flow. In TBI, there is a disturbance in the normal dynamic balance between CSF production and absorption (15,21). However, the exact etiology of PTH is not fully understood. Several risk factors for PTH have been investigated, including older age, lower Glasgow Coma Scale score at admission, intraventricular/subarachnoid hemorrhage, and meningitis with positive cerebrospinal fluid culture in human studies (13,19,21). Although several scoring systems exist for grading conventional hydrocephalus, they cannot be applied to cases in which a mass lesion distorts the brain anatomy. Hence, the severity of hydrocephalus should be judged by visual inspection of the ventricles and sulci compared with the expected size (9).

PTH has proven to be associated with the formation of cranial pseudomeningocele in humans (10). Pirouzmand et al. (14) found a 17.4% incidence rate of pseudomeningocele in patients with hydrocephalus compared with a 0.5% incidence rate in patients without hydrocephalus. The pathophysiology of a pseudomeningocele may involve the leakage of CSF into the surrounding soft tissue following dural and arachnoid tears induced by surgery or trauma (10). The most important indication for treatment is leakage of CSF from the body or clinical symptoms (5). The clinical presentation of a pseudomeningocele is dependent on the location (12). Treatment of pseudomeningocele includes spontaneous remission, lumbar drainage, and surgical intervention (10). However, the treatment must be specific to each patient, depending on the timing, size, symptoms, and location of the dural defect (5). In this case, the patient presumably had a dural tear from TBI. Upon development of hydrocephalus, CSF leaked from the tear, forming a pseudomeningocele and allowing slight decompression.

In human studies, PTH and pseudomeningocele following TBI are usually treated concurrently to promote rapid stabilization. Furthermore, clinical symptoms due to PTH and pseudomeningocele were significantly alleviated following an improvement in TBI. The clinical severity of hydrocephalus and pseudomeningocele did not correlate with the type of lesions evaluated by initial CT or with the type, size, and location of the lesions evaluated by MRI in the post-acute phase (9). In the present case, PTH and pseudomeningocele observed by MRI did not improve, despite the absence of any neurological symptoms after removal of the suspected origin of PTH. We propose that although the patient experienced PTH and pseudomeningocele which caused midline shifting, it was less likely to be related to clinical symptoms. Rather, the patient showed clinical symptoms due to inflammation caused by an embedded bone fragment in the brain parenchyma.

There are no consensus or standardized guidelines about using or tapering anti-epileptic drugs (AED) in cases of post-traumatic epilepsy (PTE) because of the complexity of PTE and the new unknown mechanisms that regulate epileptogenesis after TBI. Prospective longitudinal studies and randomized controlled trials are warranted to establish the correct PTE pharmacologic treatment (17). In this case, since PTH and pseudomeningocele, which are risk factors for seizures, remain after surgery, it is cautious to reduce AED. However, if the seizure-free interval is sufficiently maintained, the AED will be gradually tapered.

Altogether, the possibility of PTH and pseudomeningocele should be considered in patients with TBI, and it has been surmised that the presence of PTH and pseudomeningocele does not always correlate with the clinical status of patients with TBI. However, depending on the underlying mechanism or severity of PTH and pseudomeningocele, a comprehensive treatment of both PTH and pseudomeningocele might be needed.

TBI is a common neurological disease encountered in veterinary medicine. Although PTH and pseudomeningocele are among the common complications of TBI in human medicine, they have not been well documented in veterinary literature. PTH and pseudomeningocele can develop by various mechanisms following TBI, and MRI might be a helpful diagnostic tool to identify PTH and pseudomeningocele in patients with TBI. Further studies are required to understand the exact mechanism and clinical significance of PTH and pseudomeningocele in veterinary patients and to establish efficient treatment strategies for these patients with PTH and pseudomeningocele.

This research was supported by the National Research Foundation of Korea, funded by a grant from the Korean Government (NRF-2022R1G1A10036821131482092640101).

  1. Annegers JF, Coan SP. The risks of epilepsy after traumatic brain injury. Seizure 2000; 9: 453-457.
    Pubmed CrossRef
  2. Chapman JC, Diaz-Arrastia R. Military traumatic brain injury: a review. Alzheimers Dement 2014; 10(3 Suppl): S97-S104.
    Pubmed CrossRef
  3. Choi I, Park HK, Chang JC, Cho SJ, Choi SK, Byun BJ. Clinical factors for the development of posttraumatic hydrocephalus after decompressive craniectomy. J Korean Neurosurg Soc 2008; 43: 227-231.
    Pubmed KoreaMed CrossRef
  4. Dandy WE, Blackman KD. Internal hydrocephalus: an experimental, clinical and pathological study. Am J Dis Child 1914; 8: 406-482.
    CrossRef
  5. Han SR, Lee SJ, Yee GT, Choi CY, Sohn MJ, Lee CH. An unusual cervical post-traumatic pseudomeningocele - a case report -. J Korean Neurotraumatol Soc 2009; 5: 115-117.
    CrossRef
  6. Heinonen A, Rauhala M, Isokuortti H, Kataja A, Nikula M, Öhman J, et al. Incidence of surgically treated post-traumatic hydrocephalus 6 months following head injury in patients undergoing acute head computed tomography. Acta Neurochir (Wien) 2022; 164: 2357-2365.
    Pubmed KoreaMed CrossRef
  7. Lee HC, Choi ES, Cho KW, Kang BT, Kim JW, Yu CH, et al. Traumatic brain injury in a Pomeranian dog: clinical, computed tomography, and necropsy findings. J Vet Clin 2010; 27: 579-583.
  8. Lopes C, Viana D, Matos M, Rodrigues F, Pimentel S. Post-traumatic hydrocephalus in a dog. Rev Educ Contin Med Vet Zootec CRMV-SP 2018; 16: 85-86.
  9. Mazzini L, Campini R, Angelino E, Rognone F, Pastore I, Oliveri G. Posttraumatic hydrocephalus: a clinical, neuroradiologic, and neuropsychologic assessment of long-term outcome. Arch Phys Med Rehabil 2003; 84: 1637-1641.
    Pubmed CrossRef
  10. Mehendale NH, Samy RN, Roland PS. Management of pseudomeningocele following neurotologic procedures. Otolaryngol Head Neck Surg 2004; 131: 253-262.
    Pubmed CrossRef
  11. Menon DK, Schwab K, Wright DW, Maas AI. Position statement: definition of traumatic brain injury. Arch Phys Med Rehabil 2010; 91: 1637-1640.
    Pubmed CrossRef
  12. Pahys JM, Chicorelli AM, Asghar J, Betz RR, Samdani AF. Cervical pseudomeningocele due to occult hydrocephalus. Spine (Phila Pa 1976) 2008; 33: E394-E396.
    Pubmed CrossRef
  13. Park S, Park J, Kim J, Kim J, Son J, Chang D, et al. Penetrating cranial injury due to gunshot in a dog: a case report. Vet Med 2010; 55: 253-257.
    CrossRef
  14. Pirouzmand F, Tator CH, Rutka J. Management of hydrocephalus associated with vestibular schwannoma and other cerebellopontine angle tumors. Neurosurgery 2001; 48: 1246-1253; discussion 1253-1254.
    Pubmed CrossRef
  15. Rufus P, Moorthy RK, Joseph M, Rajshekhar V. Post traumatic hydrocephalus: incidence, pathophysiology and outcomes. Neurol India 2021; 69(Supplement): S420-S428.
    Pubmed CrossRef
  16. Sande A, West C. Traumatic brain injury: a review of pathophysiology and management. J Vet Emerg Crit Care (San Antonio) 2010; 20: 177-190.
    Pubmed CrossRef
  17. Sharma S, Tiarks G, Haight J, Bassuk AG. Neuropathophysiological mechanisms and treatment strategies for post-traumatic epilepsy. Front Mol Neurosci 2021; 14: 612073.
    Pubmed KoreaMed CrossRef
  18. Smith LGF, Milliron E, Ho ML, Hu HH, Rusin J, Leonard J, et al. Advanced neuroimaging in traumatic brain injury: an overview. Neurosurg Focus 2019; 47: E17. Erratum in: Neurosurg Focus 2021; 50: E22.
    Pubmed CrossRef
  19. Svedung Wettervik T, Lewén A, Enblad P. Post-traumatic hydrocephalus - incidence, risk factors, treatment, and clinical outcome. Br J Neurosurg 2022; 36: 400-406.
    Pubmed CrossRef
  20. Tang ME, Lobel DA. Severe traumatic brain injury: maximizing outcomes. Mt Sinai J Med 2009; 76: 119-128.
    Pubmed CrossRef
  21. Yoon JE, Lee CY, Sin EG, Song J, Kim HW. Clinical feature and outcomes of secondary hydrocephalus caused by head trauma. Korean J Neurotrauma 2018; 14: 86-92.
    Pubmed KoreaMed CrossRef

Article

Case Report

J Vet Clin 2023; 40(1): 56-61

Published online February 28, 2023 https://doi.org/10.17555/jvc.2023.40.1.56

Copyright © The Korean Society of Veterinary Clinics.

Successful Management of Post-Traumatic Hydrocephalus and Pseudomeningocele Following Traumatic Brain Injury in a Cat

Hyoung-Won Seo1 , Jeong-Min Lee1 , Hae-Boem Lee2 , Yoon-Ho Roh3 , Tae-Sung Hwang4 , Kun-Ho Song1 , Joong-Hyun Song1,*

1Department of Veterinary Internal Medicine, College of Veterinary Medicine, Chungnam National University, Daejeon 34134, South Korea
2Department of Veterinary Surgery, College of Veterinary Medicine, Chungnam National University, Daejeon 34134, South Korea
3Division of Animal Surgery, Department of Clinical Veterinary Medicine, Vetsuisse Faculty, University of Bern, Bern 3012, Switzerland
4Institute of Animal Medicine, College of Veterinary Medicine, Gyeongsang National University, Jinju 52828, South Korea

Correspondence to:*jh.song@cnu.ac.kr

Received: December 6, 2022; Revised: January 9, 2023; Accepted: January 24, 2023

This is an open access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

A 5-month-old female domestic short-haired cat presented with a history of seizure episodes for two months following an animal bite injury to the head. There were no remarkable findings on physical and neurological examination or blood analysis. Computed tomography revealed a fracture of the left parietal bone with an inward displacement of the bone fragment while magnetic resonance imaging revealed an enlarged temporal horn of the left lateral ventricle and a pseudomeningocele compressing the adjacent cerebral parenchyma. Subsequently, cerebrospinal fluid analysis results were normal. The patient was diagnosed with traumatic brain injury (TBI), with subsequent post-traumatic hydrocephalus (PTH) and pseudomeningocele. Despite treatment with phenobarbital and levetiracetam, seizures were not sufficiently controlled. Craniectomy for bone fragment removal and duraplasty were performed after a week. The patient then returned to normal condition with no further seizure activity. On repeated MRI two months after discharge, the hydrocephalus of the lateral ventricle and pseudomeningocele were enlarged; however, the patient maintained a good clinical status without any neurological signs. To the best of our knowledge, PTH and intracranial pseudomeningoceles have not yet been reported in cats. PTH and pseudomeningocele are among the complications of TBI and may not have any significant relevance with the clinical signs in this case. Thus, to broaden our knowledge about PTH and pseudomeningocele in cats, we describe serial changes in the clinical findings of this cat over the treatment period.

Keywords: cat, craniectomy, duraplasty, pseudomeningocele, post-traumatic hydrocephalus.

Introduction

Post-traumatic hydrocephalus (PTH) is a progressive process characterized by excessive cerebrospinal fluid (CSF) accumulation due to liquor-dynamic disturbances following a traumatic brain injury (TBI), which is defined as damage to the brain by external forces (3,11,13,21). Pseudomeningocele is an abnormal collection of CSF in the soft tissue, within a fibrous capsule, unlike meningocele, which is surrounded by a dura layer (10). Usually neurologic signs, including a decreased level of consciousness, alteration in mental state, and neurological deficits (e.g., weakness, paresis/paraplegia, seizure) (1), are closely related to the injury (2). Various criteria have been suggested for PTH diagnosis; an universal criteria has not been established, even in human medicine (6,21). However, it can be confirmed by combining clinical assessment and advanced diagnostic imaging, which involves a history of TBI and identification of skull damage and enlargement of the ventricular system via computed tomography (CT) and magnetic resonance imaging (MRI) (18). PTH and pseudomeningocele can be managed with surgical intervention and conservative management using analgesics, antiepileptic and anti-inflammatory drugs. The clinical symptoms can be improved by treatment of the underlying causes, and a conservative approach is preferred. In human medicine, the incidence of PTH among TBI patients was reported to be 0.7 to 29%, with a wide variation owing to the differences in the evaluation criteria (15). In this study, we reviewed the clinical features, MRI findings, and therapeutic outcomes in a cat with PTH and pseudomeningocele and evaluated their clinical significance. To the best of our knowledge, this is the first case report of PTH and pseudomeningocele in a cat which was successfully treated with surgical intervention and conservative therapy.

Case Report

A 5-month-old female domestic short-haired cat was referred to the Veterinary Medical Teaching Hospital of the Chungnam National University. Four months prior to presentation, the cat was found on a street with a penetrating injury, suspected to be a brain-bite wound (Fig. 1A). The cat had multiple complex partial seizures, characterized by orofacial motor signs (chewing and eye and facial twitching) and a generalized tonic-clonic episode. The seizures did not improve with administration of zonisamide 5 mg/kg, per os [PO], q 12 h or levetiracetam (Keppra, UCB Pharma, Brussels, Belgium) 20 mg/kg, PO, q 8 h. Further, no remarkable findings were observed during physical examination. The results of the complete blood count and serum chemistry analysis were within the normal ranges. Neurological examination revealed unremarkable results, except for intermittent facial twitching.

Figure 1. (A) Image showing penetrating injury and suspected brain-bite wound (arrow). (B) Transverse CT image at the temporal bone level showing a depressed fracture of the temporal bone on the left side (arrow). (C) Left caudolateral 3D-reconstruction CT image (arrow). L, left.

CT (Alexion TM, Canon Medical Systems, Japan) revealed a fracture of the left parietal bone with inward displacement of the bone fragment (Fig. 1B, C). On MRI (1.5 Tesla unit, Vantage ElanTM, Canon, Medical) (Fig. 2), a linear structure was observed at the level of the left parietal bone with a hypointense signal on T1-weighted image (T1WI) and T2-weighted image (T2WI), resembling a bone fragment extending to the level of the left thalamus. An atypical and circular intracranial cyst with a hyperintense signal on T2WI and a hypointense signal on T1WI and Fluid-attenuated inversion recovery (FLAIR) was observed in the lateral and ventral brain parenchyma of the embedded bone fragment, respectively. The lateral and ventral cysts measured 0.95 × 0.3 × 0.82 cm, 1.6 × 1.5 × 1.2 cm, respectively (L × W × H). A midline shift which slightly displaced the left thalamus and interthalamic adhesions to the right side was also seen. In addition, hyperintense signals on T2WI and FLAIR, and isointense signals on T1W1 were observed around the bone fragment with evident contrast enhancement, which was considered an inflammatory change. In summary, inflammatory changes in the brain parenchyma were caused by bone fragments, resulting in an enlarged temporal horn of the left lateral ventricle and a pseudomeningocele. Cerebrospinal fluid (CSF) analysis revealed a normal nucleated cell count (4 cells/μL, reference range, <5) and protein concentration (10 mg/dL, reference range, <25), and negative polymerase chain reaction results for infectious agents. Cytological examination of the CSF revealed a predominance of mononuclear cells.

Figure 2. (A) Transverse T2WI, (B) FLAIR image, and (C) Sagittal T2WI of the head. These images reveal PTH (arrow), and pseudomeningocele (arrowhead) with inflammatory changes within the left parietal lobe. L, left.

Based on the history and results of diagnostic imaging, the patient was diagnosed with TBI and subsequent PTH and pseudomeningocele. Despite treatment with phenobarbital (Phenobarbital, Hana Pharm., Seoul, Korea) 2.5 mg/kg, PO, q 12 h and levetiracetam 20 mg/kg, PO, q 8 h, the seizure was not well-controlled. Craniectomy and duraplasty were performed after a week, to remove the bone fragment and relieve intracranial pressure (Fig. 3A). The tissue sample surrounding the bone fragment was sent to a commercial laboratory (IDEXX Laboratories, Inc., USA) for histopathological examination, which revealed pyogranulomatous and eosinophilic inflammatory infiltrates with fibrin aggregation and absence of infectious organisms (Fig. 3B).

Figure 3. (A) Intraoperative image of the bone fragment embedded in the brain parenchyma (arrow). (B) The histopathologic examination revealed pyogranulomatous and eosinophilic infiltrate and aggregates of fibrin with no infection.

After surgical correction, the patient returned to a normal condition without further seizure activities. A repeated MRI scan two months after discharge, the inflammatory changes related to the bone fragment had entirely alleviated; however, the ventriculomegaly and pseudomeningocele had enlarged (1.8 × 1.9 × 2.2 cm and 1.1 × 0.38 × 1.6 cm, respectively, L × W × H) (Fig. 4). Despite these findings, the patient maintained a good clinical status without any neurological signs. There was no recurrence of any clinical signs following the four-month follow-up period owing to treatment with phenobarbital 3.5 mg/kg, PO, q 12 h and levetiracetam 30 mg/kg, PO, q 8 h.

Figure 4. (A) Transverse T2WI, (B) FLAIR image, and (C) Sagittal T2WI of the head after removing the bone fragment. These images reveal PTH (arrow), and pseudomeningocele (arrowhead) without inflammatory changes within the left parietal lobe. L, left.

Discussion

TBI is divided into primary and secondary injuries of the brain parenchyma. Primary injury occurs immediately as a result of direct mechanical damage during traumatic events, whereas secondary injury occurs minutes to days after the trauma, due to a combination of systemic extracranial damage and intracranial physical and biochemical changes. Guidelines for TBI treatment in humans have been established and focus on maintaining adequate cerebral perfusion. However, currently, no recommended guidelines exist in veterinary medicine. Most clinical recommendations are based on in vivo experiments, human studies, or personal experience (16). This classification is important since primary injuries are unmanageable, whereas secondary injuries are predictable and preventable. The prevention and treatment of secondary injuries can reduce mortality and improve outcomes. Therefore, attention must be focused on blood pressure optimization, brain tissue oxygenation, maintenance of adequate cerebral perfusion pressures, and prevention of seizures (7,20).

Since PTH was first described in human medicine by Dandy and Blackman in 1914 (4), several studies have investigated various ways to identify the mechanism, pathophysiology, risk factors, and treatment underlying PTH. However, it is rarely discussed in veterinary medicine and has only been reported once. In 2018, PTH was diagnosed in a 2-month-old female Yorkshire Terrier dog following a forensic necropsy (8). The mechanism of PTH involves mechanical obstruction of the CSF, laceration of the ventricle, increased number of inflammatory cells and proteins in the CSF, and subsequent blockage of arachnoid granulation and CSF flow. In TBI, there is a disturbance in the normal dynamic balance between CSF production and absorption (15,21). However, the exact etiology of PTH is not fully understood. Several risk factors for PTH have been investigated, including older age, lower Glasgow Coma Scale score at admission, intraventricular/subarachnoid hemorrhage, and meningitis with positive cerebrospinal fluid culture in human studies (13,19,21). Although several scoring systems exist for grading conventional hydrocephalus, they cannot be applied to cases in which a mass lesion distorts the brain anatomy. Hence, the severity of hydrocephalus should be judged by visual inspection of the ventricles and sulci compared with the expected size (9).

PTH has proven to be associated with the formation of cranial pseudomeningocele in humans (10). Pirouzmand et al. (14) found a 17.4% incidence rate of pseudomeningocele in patients with hydrocephalus compared with a 0.5% incidence rate in patients without hydrocephalus. The pathophysiology of a pseudomeningocele may involve the leakage of CSF into the surrounding soft tissue following dural and arachnoid tears induced by surgery or trauma (10). The most important indication for treatment is leakage of CSF from the body or clinical symptoms (5). The clinical presentation of a pseudomeningocele is dependent on the location (12). Treatment of pseudomeningocele includes spontaneous remission, lumbar drainage, and surgical intervention (10). However, the treatment must be specific to each patient, depending on the timing, size, symptoms, and location of the dural defect (5). In this case, the patient presumably had a dural tear from TBI. Upon development of hydrocephalus, CSF leaked from the tear, forming a pseudomeningocele and allowing slight decompression.

In human studies, PTH and pseudomeningocele following TBI are usually treated concurrently to promote rapid stabilization. Furthermore, clinical symptoms due to PTH and pseudomeningocele were significantly alleviated following an improvement in TBI. The clinical severity of hydrocephalus and pseudomeningocele did not correlate with the type of lesions evaluated by initial CT or with the type, size, and location of the lesions evaluated by MRI in the post-acute phase (9). In the present case, PTH and pseudomeningocele observed by MRI did not improve, despite the absence of any neurological symptoms after removal of the suspected origin of PTH. We propose that although the patient experienced PTH and pseudomeningocele which caused midline shifting, it was less likely to be related to clinical symptoms. Rather, the patient showed clinical symptoms due to inflammation caused by an embedded bone fragment in the brain parenchyma.

There are no consensus or standardized guidelines about using or tapering anti-epileptic drugs (AED) in cases of post-traumatic epilepsy (PTE) because of the complexity of PTE and the new unknown mechanisms that regulate epileptogenesis after TBI. Prospective longitudinal studies and randomized controlled trials are warranted to establish the correct PTE pharmacologic treatment (17). In this case, since PTH and pseudomeningocele, which are risk factors for seizures, remain after surgery, it is cautious to reduce AED. However, if the seizure-free interval is sufficiently maintained, the AED will be gradually tapered.

Altogether, the possibility of PTH and pseudomeningocele should be considered in patients with TBI, and it has been surmised that the presence of PTH and pseudomeningocele does not always correlate with the clinical status of patients with TBI. However, depending on the underlying mechanism or severity of PTH and pseudomeningocele, a comprehensive treatment of both PTH and pseudomeningocele might be needed.

Conclusions

TBI is a common neurological disease encountered in veterinary medicine. Although PTH and pseudomeningocele are among the common complications of TBI in human medicine, they have not been well documented in veterinary literature. PTH and pseudomeningocele can develop by various mechanisms following TBI, and MRI might be a helpful diagnostic tool to identify PTH and pseudomeningocele in patients with TBI. Further studies are required to understand the exact mechanism and clinical significance of PTH and pseudomeningocele in veterinary patients and to establish efficient treatment strategies for these patients with PTH and pseudomeningocele.

Source of Funding

This study received no external funding.

Acknowledgements

This research was supported by the National Research Foundation of Korea, funded by a grant from the Korean Government (NRF-2022R1G1A10036821131482092640101).

Conflicts of Interest

The authors have no conflicting interests.

Fig 1.

Figure 1.(A) Image showing penetrating injury and suspected brain-bite wound (arrow). (B) Transverse CT image at the temporal bone level showing a depressed fracture of the temporal bone on the left side (arrow). (C) Left caudolateral 3D-reconstruction CT image (arrow). L, left.
Journal of Veterinary Clinics 2023; 40: 56-61https://doi.org/10.17555/jvc.2023.40.1.56

Fig 2.

Figure 2.(A) Transverse T2WI, (B) FLAIR image, and (C) Sagittal T2WI of the head. These images reveal PTH (arrow), and pseudomeningocele (arrowhead) with inflammatory changes within the left parietal lobe. L, left.
Journal of Veterinary Clinics 2023; 40: 56-61https://doi.org/10.17555/jvc.2023.40.1.56

Fig 3.

Figure 3.(A) Intraoperative image of the bone fragment embedded in the brain parenchyma (arrow). (B) The histopathologic examination revealed pyogranulomatous and eosinophilic infiltrate and aggregates of fibrin with no infection.
Journal of Veterinary Clinics 2023; 40: 56-61https://doi.org/10.17555/jvc.2023.40.1.56

Fig 4.

Figure 4.(A) Transverse T2WI, (B) FLAIR image, and (C) Sagittal T2WI of the head after removing the bone fragment. These images reveal PTH (arrow), and pseudomeningocele (arrowhead) without inflammatory changes within the left parietal lobe. L, left.
Journal of Veterinary Clinics 2023; 40: 56-61https://doi.org/10.17555/jvc.2023.40.1.56

References

  1. Annegers JF, Coan SP. The risks of epilepsy after traumatic brain injury. Seizure 2000; 9: 453-457.
    Pubmed CrossRef
  2. Chapman JC, Diaz-Arrastia R. Military traumatic brain injury: a review. Alzheimers Dement 2014; 10(3 Suppl): S97-S104.
    Pubmed CrossRef
  3. Choi I, Park HK, Chang JC, Cho SJ, Choi SK, Byun BJ. Clinical factors for the development of posttraumatic hydrocephalus after decompressive craniectomy. J Korean Neurosurg Soc 2008; 43: 227-231.
    Pubmed KoreaMed CrossRef
  4. Dandy WE, Blackman KD. Internal hydrocephalus: an experimental, clinical and pathological study. Am J Dis Child 1914; 8: 406-482.
    CrossRef
  5. Han SR, Lee SJ, Yee GT, Choi CY, Sohn MJ, Lee CH. An unusual cervical post-traumatic pseudomeningocele - a case report -. J Korean Neurotraumatol Soc 2009; 5: 115-117.
    CrossRef
  6. Heinonen A, Rauhala M, Isokuortti H, Kataja A, Nikula M, Öhman J, et al. Incidence of surgically treated post-traumatic hydrocephalus 6 months following head injury in patients undergoing acute head computed tomography. Acta Neurochir (Wien) 2022; 164: 2357-2365.
    Pubmed KoreaMed CrossRef
  7. Lee HC, Choi ES, Cho KW, Kang BT, Kim JW, Yu CH, et al. Traumatic brain injury in a Pomeranian dog: clinical, computed tomography, and necropsy findings. J Vet Clin 2010; 27: 579-583.
  8. Lopes C, Viana D, Matos M, Rodrigues F, Pimentel S. Post-traumatic hydrocephalus in a dog. Rev Educ Contin Med Vet Zootec CRMV-SP 2018; 16: 85-86.
  9. Mazzini L, Campini R, Angelino E, Rognone F, Pastore I, Oliveri G. Posttraumatic hydrocephalus: a clinical, neuroradiologic, and neuropsychologic assessment of long-term outcome. Arch Phys Med Rehabil 2003; 84: 1637-1641.
    Pubmed CrossRef
  10. Mehendale NH, Samy RN, Roland PS. Management of pseudomeningocele following neurotologic procedures. Otolaryngol Head Neck Surg 2004; 131: 253-262.
    Pubmed CrossRef
  11. Menon DK, Schwab K, Wright DW, Maas AI. Position statement: definition of traumatic brain injury. Arch Phys Med Rehabil 2010; 91: 1637-1640.
    Pubmed CrossRef
  12. Pahys JM, Chicorelli AM, Asghar J, Betz RR, Samdani AF. Cervical pseudomeningocele due to occult hydrocephalus. Spine (Phila Pa 1976) 2008; 33: E394-E396.
    Pubmed CrossRef
  13. Park S, Park J, Kim J, Kim J, Son J, Chang D, et al. Penetrating cranial injury due to gunshot in a dog: a case report. Vet Med 2010; 55: 253-257.
    CrossRef
  14. Pirouzmand F, Tator CH, Rutka J. Management of hydrocephalus associated with vestibular schwannoma and other cerebellopontine angle tumors. Neurosurgery 2001; 48: 1246-1253; discussion 1253-1254.
    Pubmed CrossRef
  15. Rufus P, Moorthy RK, Joseph M, Rajshekhar V. Post traumatic hydrocephalus: incidence, pathophysiology and outcomes. Neurol India 2021; 69(Supplement): S420-S428.
    Pubmed CrossRef
  16. Sande A, West C. Traumatic brain injury: a review of pathophysiology and management. J Vet Emerg Crit Care (San Antonio) 2010; 20: 177-190.
    Pubmed CrossRef
  17. Sharma S, Tiarks G, Haight J, Bassuk AG. Neuropathophysiological mechanisms and treatment strategies for post-traumatic epilepsy. Front Mol Neurosci 2021; 14: 612073.
    Pubmed KoreaMed CrossRef
  18. Smith LGF, Milliron E, Ho ML, Hu HH, Rusin J, Leonard J, et al. Advanced neuroimaging in traumatic brain injury: an overview. Neurosurg Focus 2019; 47: E17. Erratum in: Neurosurg Focus 2021; 50: E22.
    Pubmed CrossRef
  19. Svedung Wettervik T, Lewén A, Enblad P. Post-traumatic hydrocephalus - incidence, risk factors, treatment, and clinical outcome. Br J Neurosurg 2022; 36: 400-406.
    Pubmed CrossRef
  20. Tang ME, Lobel DA. Severe traumatic brain injury: maximizing outcomes. Mt Sinai J Med 2009; 76: 119-128.
    Pubmed CrossRef
  21. Yoon JE, Lee CY, Sin EG, Song J, Kim HW. Clinical feature and outcomes of secondary hydrocephalus caused by head trauma. Korean J Neurotrauma 2018; 14: 86-92.
    Pubmed KoreaMed CrossRef

Vol.41 No.1 February 2024

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The Korean Society of Veterinary Clinics

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eISSN 2384-0749

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