What Is Your Neurologic Diagnosis?

Ning-Wei Wei Department of Neurology and Neurosurgery, Gulf Coast Veterinary Specialists, Houston, TX

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Kara Sessums Department of Neurology and Neurosurgery, Gulf Coast Veterinary Specialists, Houston, TX

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Carley Giovanella Department of Neurology and Neurosurgery, Gulf Coast Veterinary Specialists, Houston, TX

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Melissa Jennings Department of Neurology and Neurosurgery, Gulf Coast Veterinary Specialists, Houston, TX

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Introduction

An 11-year-old 6-kg neutered male Lhasa Apso–Poodle mix was referred for evaluation of progressive ataxia, collapsing in the pelvic limbs, knuckling of the left thoracic and pelvic limbs, and severe pain. The owner reported that the dog was in a fight with another dog 4 days earlier and had sustained a puncture wound on the right rostral portion of the head. Radiographs obtained by the referring veterinarian revealed a possible fracture of the orbital bones and a fracture of the right maxilla at the level of the first premolar tooth. The referring veterinarian had cleaned the wound with chlorhexidine solution and prescribed carprofen (2 mg/kg, PO, q 12 h), gabapentin (16 mg/kg, PO, q 12 h), and cefpodoxime (8.3 mg/kg, PO, q 24 h). The treatment was unsuccessful in resolving the clinical signs, and the dog was referred for further evaluation.

Assessment

Anatomic diagnosis

The dog’s quiet to mildly dull mentation was attributed to a lesion involving the cerebral cortex or ascending reticular activating system. The head turn and circling to the right likely represented a lesion of the right forebrain (ie, prosencephalon [telencephalon and diencephalon]). The left-sided hemiparesis could have been caused by a lesion of the right forebrain, left brainstem, or left side of the cervical spinal cord. The absent proprioceptive positioning of the left thoracic and pelvic limbs could have been caused by a lesion of the right forebrain, right thalamus, left brain stem, or left side of the cervical spinal cord. The decreased palpebral reflex on the left suggested a lesion of left cranial nerve V and VII or the left brainstem.

Likely location of a single lesion

A lesion of the right forebrain was considered most likely.

Etiologic diagnosis

Differential diagnoses considered for this 11-year-old dog with post-traumatic, progressive, right-lateralizing encephalopathy and possible involvement of the left brainstem included inflammatory and infectious CNS diseases, skull fracture with ongoing intracranial hemorrhage, and, less likely, neoplasia.

Diagnostic Plan

The diagnostic plan included a CBC and serum biochemical profile to evaluate for evidence of systemic disease and advanced imaging (CT or MRI) of the brain for definitive diagnosis. Magnetic resonance imaging was elected because it provides greater detail of the brain.

Diagnostic Test Findings

The CBC revealed mild leukocytosis with mild mature neutrophilia (13,220 neutrophils/μL; reference range, 2,950 to 11,640 neutrophils/μL) and mild monocytosis (1,180 monocytes/μL; reference range, 160 to 1,120 monocytes/μL). Serum biochemical testing revealed mild hyperglobulinemia (4.8 g/dL; reference range, 2.5 to 4.5 g/dL).

Magnetic resonance imaging was performed with a 1.5 T unit; multiplanar T2-weighted, FLAIR, T2*-weighted gradient echo, and pre- and postcontrast T1-weighted images were acquired (Figure 1). Findings included severe swelling along the dorsum of the head that extended from the mid-dorsal nasal area caudally to the occipital protuberance and a 1.2-cm depressed fracture of the right frontal bone close to the dorsal midline. Contrast-enhancing meningeal changes were noted diffusely throughout the right cerebral hemisphere and, to a lesser degree, the left cerebral hemisphere. There was severe swelling of the adjacent right cerebral hemisphere and a mass effect with a thick, contrast-enhancing periphery that was hyperintense on T2-weighted images, of mixed intensity on FLAIR images, and hypointense to isointense on T1-weighted images. The MRI findings were suggestive of a right frontal or parietal bone fracture with severe cellulitis and myositis, a dorsal head abscess, and a large right cerebral abscess with intracranial meningitis. Cerebrospinal fluid was not collected because of the large mass effect in the brain and the need for immediate surgical intervention. Additionally, the surgical approach would provide direct access to the lesion for collection of material for bacterial culture and CSF collection might have resulted in rapid neurologic deterioration secondary to brain herniation.

Figure 1
Figure 1

Midsagittal T2-weighted (A) and transverse T2-weighted (B), T1-weighted (C), and postcontrast T1-weighted (D) MRI images of the brain of an 11-year-old Lhasa Apso–Poodle mix that developed progressive ataxia, collapsing in the hind limbs, knuckling of the left thoracic and pelvic limbs, and severe pain after sustaining a puncture wound on the right rostral portion of the head in a dog fight 4 days earlier. A large subcutaneous lesion (asterisk) that is hyperintense on T2-weighted images (A and B) and hypointense to isointense on T1-weighted images (C) is apparent, along with marked swelling of the temporal musculature (arrowhead; B and D). There is a large, triangular defect extending through the calvarium that primarily involves the right frontal and parietal bones and is causing a focal deformity of the adjacent brain tissue (arrow; B). There is generalized swelling of the brain tissue, with a mass effect (circle; B through D) that is hyperintense on T2-weighted images and hypointense to isointense on T1-weighted images and shows postcontrast ring enhancement (D). This mass effect is approximately 1.4 cm in length, 1.5 cm in height, and 1.6 cm in width and is causing a midline shift to the left with compression and distortion of the right lateral ventricle.

Citation: Journal of the American Veterinary Medical Association 260, 11; 10.2460/javma.20.10.0598

Treatment

Immediately after MRI was completed, mannitol (1 g/kg) and dexamethasone sodium phosphate (0.14 mg/kg) were given IV, and a modified right rostrotentorial craniectomy was performed. A large volume of mucopurulent discharge drained out while the skin incision was made. Freer and Adson periosteal elevators were used to reflect the temporalis muscle laterally. A puncture wound was evident in the right frontal bone slightly off midline, and 3 bone chips were removed from the surgical site. A firm piece of abnormal tissue was removed from within the brain and submitted for histologic examination, and swab specimens of the tissue overlying the frontal bone were collected. The entire surgical area was copiously lavaged with sterile saline (0.9% NaCl) solution and evaluated for continued hemorrhage. Hemostatic surgical foam was placed over the craniectomy site, and the right temporalis muscle was elevated and rotated rostrally to cover the craniectomy site. A continuous suction (grenade) drain was placed in a U shape over the left and right temporalis muscles prior to skin closure.

Immediate postoperative treatment consisted of enrofloxacin (10 mg/kg, IV, q 24 h), ampicillin-sulbactam (30 mg/kg, IV, q 8 h), gabapentin (17 mg/kg, PO, q 8 h), levetiracetam (21 mg/kg, PO, q 8 h), dexamethasone (0.07 mg/kg, IV, q 12 h), and fentanyl (3 μg/kg/h, as a continuous rate infusion). Supplemental oxygen was provided, and syringe feeding was performed because of masticatory muscle pain. A fentanyl transdermal patch (25 μg) was applied to the skin for postoperative pain management. The dog was weaned off the fentanyl continuous rate infusion and moved out of the oxygen cage the following day. Regurgitation was noticed 3 days after the surgery; therefore, administration of dexamethasone was discontinued and the dog was treated with maropitant (1 mg/kg, IV, q 24 h), metoclopramide (0.4 mg/kg, SC, q 24 h), ondansetron (1 mg/kg, PO, q 12 h), pantoprazole (1 mg/kg, IV, q 24 h), and sucralfate (250 mg, PO, q 8 h). The dog was discharged 4 days after surgery with prescriptions for amoxicillin-clavulanate (21 mg/kg, PO, q 12 h), enrofloxacin (10 mg/kg, PO, q 24 h), gabapentin (17 mg/kg, PO, q 8 to 12 hours), maropitant (2 mg/kg, PO, q 24 h), metoclopramide (2 mg/kg, PO, q 8 h), ondansetron (0.7 mg/kg, PO, q 12 h), sucralfate (250 mg, PO, q 8 h), and famotidine (1 mg/kg, PO, q 24 h).

Histopathologic findings were consistent with severe, locally extensive, subacute, necrosuppurative meningoencephalitis with hemorrhage and vasculitis. Irregular blood vessels were surrounded by lymphoplasmacytic cuffs and infiltrated by neutrophils that contained necrotic debris. Some areas of the neuroparenchyma showed a complete loss of architecture. Clostridium perfringens and a Bacteroides sp were isolated on anaerobic culture; both were susceptible to amoxicillin-clavulanate.

A recheck examination 2 weeks after surgery revealed improved mentation but persistent circling to the right with diminished proprioceptive placing on the left side. Treatment with amoxicillin-clavulanate was continued for 3.5 months. The dog had a seizure 2 months after the surgery, and treatment with levetiracetam (21 mg/kg, PO, q 8 h) was instituted. The dog had a second seizure 4 months after surgery, and anticonvulsant treatment was transitioned to zonisamide (9 mg/kg, PO, q 12 h).

Five months after surgery, the dog was reportedly doing well at home with a normal personality and activity level. There were no further seizures reported by the owner.

Comments

A brain abscess forms when an area of cerebral inflammation becomes necrotic and encapsulated by glial cells and fibroblasts. Although brain abscesses are uncommon findings in dogs and cats, such abscesses can result from direct extension of cranial infections (eg, sinusitis, rhinitis, otitis interna, etc), a penetrating head wound or foreign body, or hematogenous spread or can be a result of iatrogenic causes (eg, CSF collection or craniotomy).15 Aerobic bacteria, including Staphylococcus spp, Streptococcus spp, Pasteurella multocida (especially in cats), Actinomyces spp, and Nocardia spp, and anaerobic bacteria, including Escherichia coli, Klebsiella spp, Bacteroides spp, Peptostreptococcus spp, Fusobacterium spp, and Eubacterium spp, have both been reported. Fungal and protozoal infections can also result in abscess formation.

A brain abscess is considered life-threatening owing to local tissue destruction and increased intracranial pressure. Clinical signs usually reflect a focal space-occupying lesion, a multifocal syndrome associated with many small microabscesses, or increased intracranial pressure. The diagnosis can be made on the basis of advanced diagnostic imaging findings. Typical findings on CT images include skull fracture, postcontrast ring enhancement, low attenuation of the center of the lesion, and a mass effect. The lesion is typically hypointense on T1-weighted MRI images and hyperintense with a hypointense rim on T2-weighted images. Strong postcontrast peripheral ring enhancement with associated vasogenic edema is usually seen. Susceptibility artifacts may be seen on T2*-weighted images, appearing as signal voids in the wall of the abscess. Computed tomography scanning is often faster; however, MRI can provide more detail of the brain. Cerebrospinal fluid analysis commonly reveals a suppurative pattern with degenerative and toxic-appearing neutrophils, and the CSF protein concentration is often high. The presence of intracellular bacteria in a CSF sample confirms the diagnosis, but intracellular bacteria are not commonly seen. Bacterial culture of a CSF sample can be performed; however, negative results cannot be used to rule out a brain abscess.

In dogs with a brain abscess, timely surgical intervention should be considered to reduce intracranial pressure, confirm the diagnosis, obtain samples for bacterial culture, and enhance the efficacy of antimicrobial treatment.6,7 Antimicrobials should be selected on the basis of results of susceptibility testing of organisms isolated from the abscess. However, when such testing cannot be performed, broad-spectrum antimicrobial treatment, such as use of a penicillin in conjunction with a fluoroquinolone or even a third-generation cephalosporin, should be considered. Metronidazole can also be considered because it readily enters the CNS and has excellent bactericidal activity against many anaerobes. Short-term (3 to 4 days) use of a corticosteroid should be considered to attenuate inflammatory responses and reduce vasogenic edema. Overall, the prognosis for dogs with a brain abscess is poor, given the limited published information currently available. Early recognition, appropriate antimicrobial treatment, seizure management, and surgical intervention may improve the outcome in dogs with a brain abscess.

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