What Is Your Neurologic Diagnosis?

Dylan M. Djani Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996.

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William B. Thomas Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996.

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A 4-month-old 1.4-kg (3.1-lb) castrated male domestic shorthair cat was evaluated because of sudden-onset and progressive ataxia, weakness, and altered mental status characterized by obtundation over a 24-hour period. The cat had a propulsive gait with movement in short bursts. Three weeks earlier, the cat had developed decreased appetite and fever and had an inflammatory leukogram. Assessment of serum Toxoplasma IgG and IgM titers performed at that time yielded negative results. The fever resolved with administration of amoxicillin–clavulanic acid for 4 days. The day before the evaluation, the cat became nonambulatory. On examination, the cat had signs of depression and difficulty rising from lateral recumbency. No signs of pain were elicited on skull or vertebral column palpation. After examination, the cat had a seizure that responded to diazepam.

What is the problem? Where is the lesion? What are the most probable causes of this problem? What is your plan to establish a diagnosis? Please turn the page.

Assessment

Anatomic diagnosis

ProblemRule out location
Mental obtundationProsencephalon (cerebral cortex, thalamus, or internal capsule) or brainstem (ascending reticular activating system)
Propulsive gaitProsencephalon (cerebral cortex, thalamus, or limbic system)
SeizuresProsencephalon (cerebral cortex or thalamus)
Decreased nasal sensationProsencephalon (cerebral cortex or thalamus), brainstem (trigeminal sensory nucleus), or trigeminal nerve (maxillary and ophthalmic branches)
Decreased palpebral reflexBrainstem (trigeminal sensory nucleus or facial nerve nucleus), trigeminal nerve (maxillary branch), facial nerve, or orbicularis oculi muscle
Tetraparesis and pelvic limb hypermetriaBrainstem, cerebellum, or cervical spinal cord (C1-T2 segments)
Falling to the right and left into laterally recumbent postureVestibular apparatus, vestibulocochlear nerve, brainstem (vestibular nuclei), thalamus, or cerebellum

Likely location of 1 lesion

Multifocal to diffuse disease affecting the forebrain, brainstem, cerebellum, and spinal cord was suspected.

Etiologic diagnosis—Given the cat's signalment and history and the course of the disease, differential diagnoses included metabolic disease (hypoglycemia), congenital CNS anomalies (hydrocephalus, hydranencephaly, or porencephaly), infectious or inflammatory disease of the CNS (toxoplasmosis or feline infectious peritonitis [FIP]), and neurodegenerative diseases (globoid cell leukodystrophy or gangliosidosis). Diagnostic evaluation included a CBC and plasma biochemical panel to screen for metabolic disease and assess organ function prior to anesthesia, followed by MRI of the brain to assess for structural disease. Further diagnostic workup including analysis of a CSF sample and specific infectious disease testing were to be performed on the basis of results of MRI.

Diagnostic test findings—Clinicopathologic findings included leukocytosis (30,700 WBCs/μL; reference interval, 4,700 to 15,300 WBCs/μL) characterized by neutrophilia (25,790 neutrophils/μL; reference interval, 2,000 to 9,200 neutrophils/μL) and monocytosis (740 monocytes/μL; reference interval, 80 to 320 monocytes/μL) as well as mild hypocholesterolemia (68 mg/dL; reference interval, 74 to 255 mg/dL), hyperphosphatemia (5.6 mg/dL; reference interval, 2.2 to 5.3 mg/dL), and low BUN concentration (11 mg/dL; reference interval, 18 to 40 mg/dL). Magnetic resonance imaging (T1-weighted, T2-weighted, and fluid-attenuated inversion recovery images and T1-weighted images after administration of contrast agent in the sagittal, transverse, and dorsal planes) of the brain performed with a 1.5-T magneta revealed symmetric dilation of the ventricular system and central canal of the cranial cervical spinal segments with triangular distortion of the interthalamic adhesion, dorsocaudal displacement of the cerebellum, and ventral compression of the brainstem (Figure 1). There were multifocal hyperintensities of the parenchyma adjacent to the ventricles on the T2-weighted and fluid-attenuated inversion recovery sequences. There was contrast enhancement of the ependymal lining of the olfactory recesses, fourth ventricle, and central canal. The imaging findings were consistent with severe hydrocephalus, multifocal ependymitis, and meningitis. On the basis of the cat's age, history, and MRI findings, FIP was suspected. The cat was euthanized with an IV injection of pentobarbital sodium prior to recovery from anesthesia, and a CSF sample was not collected. Gross abnormalities at necropsy included chronic, focally extensive necrotizing periventriculitis and encephalomyelitis with hydrocephalus and multifocal hemorrhage. Histologic examination of samples of the brain and cervical spinal cord revealed chronic granulomatous and lymphoplasmacytic periventriculitis, meningoencephalomyelitis, ependymitis, and choroiditis with hydrocephalus, consistent with FIP.

Figure 1—
Figure 1—

Magnetic resonance images of the brain in a cat that had sudden-onset and progressive decreased mentation, weakness, and ataxia and a generalized seizure over a 24-hour period. Marked dilation of the entire ventricular system with displacement of the cerebellum and compression of the brainstem is apparent on both the sagittal T1-weighted postcontrast (A) and sagittal T2-weighted precontrast (B) images. Moderate contrast enhancement is noted along the ependymal lining of the fourth ventricle on the sagittal T1-weighted postcontrast sequence image (A). Dilation of the lateral ventricles and mesencephalic aqueduct is evident in the axial T2-weighted image (C).

Citation: Journal of the American Veterinary Medical Association 254, 5; 10.2460/javma.254.5.587

Comments

Feline infectious peritonitis is the most common infection of the CNS in cats, with neurologic involvement detected in up to 38% of cats with the dry form of FIP and in 5% of cats with the wet form of FIP.1 Neurologic examination of affected cats typically reveals a multifocal neuroanatomic localization of abnormalities, with the most common clinical signs being ataxia, paraparesis, tetraparesis, abnormal mentation, head tilt, pathological nystagmus, and seizures.1,2 Neurologic abnormalities are related to the brain and spinal cord regions affected by the pyogranulomatous vasculitis and resultant hydrocephalus.3

In cats, antemortem diagnosis of FIP represents a diagnostic challenge, particularly with the dry form, because of the inability to serologically or genetically distinguish FIP virus (a monocyte-macrophage tropic mutant of feline enteric coronavirus) from the nonmutated feline enteric coronavirus.1,3–5 Definitive diagnosis requires histologic evaluation of affected tissues for evidence of pyogranulomatous vasculitis. Pathological lesions within the CNS chiefly involve the leptomeninges (arachnoid and pia mater) and ventricular system, specifically the ependymal lining and choroid plexuses, and result in secondary hydrocephalus.1 Therefore, results of MRI of the brain and analysis of CSF samples are helpful in determining a diagnosis. Recently, the usefulness of immunocytochemical reactivity of CSF preparations for feline enteric coronavirus antigen was investigated.5 Findings indicated that procedure had sensitivity of 85% and specificity of 83.3% for detection of feline enteric coronavirus antigen, and it was concluded that the specificity of the immunocytochemical staining was too low to definitively diagnose FIP affecting the CNS. A neurologic form of FIP should be considered as a differential diagnosis for young cats with multifocal neurologic signs, and results of diagnostic testing should be interpreted in light of the patient's signalment and history when FIP is suspected.

Footnotes

a

1.5-T Siemens Magnetom Espree, Siemens Healthcare, Malvern, Pa.

References

  • 1. Crawford AH, Stoll AL, Sanchez-Masian D, et al. Clinicopathologic features and magnetic resonance imaging findings in 24 cats with histopathologically confirmed neurologic feline infectious peritonitis. J Vet Intern Med 2017;31:14771486.

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  • 2. Rand JS, Parent J, Percy D, et al. Clinical, cerebrospinal fluid, and histological data from twenty-seven cats with primary inflammatory disease of the central nervous system. Can Vet J 1994;35:103110.

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  • 3. Diaz JV, Poma R. Diagnosis and clinical signs of feline infectious peritonitis in the central nervous system. Can Vet J 2009;50:10911093.

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  • 4. Foley JE, Lapointe JM, Koblik P, et al. Diagnostic features of clinical neurologic feline infectious peritonitis. J Vet Intern Med 1998;12:415423.

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  • 5. Gruendl S, Matiasek K, Matiasek L, et al. Diagnostic utility of cerebrospinal fluid immunocytochemistry for diagnosis of feline infectious peritonitis manifesting in the central nervous system. J Feline Med Surg 2017;19:576585.

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