Journal of Neuro-Ophthalmology, March 2003, Volume 23, Issue 1

Magnetic Resonance Imaging Abnormalities in Cat-Scratch Disease Encephalopathy

A 23-year-old woman who presented with a branch retinal artery occlusion followed by encephalopathy showed, by brain magnetic resonance imaging, a nonenhancing lesion in the right parietal gray matter with normal diffusion-weighted imaging. Of 64 reported cases of cat-scratch encephalopathy with documented neuroimaging findings, only 12 (18.8%) have had abnormal imaging findings. The abnormalities have included cerebral white matter lesions, basal ganglia and thalamic lesions, and multifocal lesions in immunocompromised patients, but no gray matter lesions similar to those in this patient. The variety of neuroimaging findings supports multiple pathophysiologic mechanisms of central nervous system involvement in this disorder.

ORIGINAL CONTRIBUTION Magnetic Resonance Imaging Abnormalities in Cat- Scratch Disease Encephalopathy Alvin B. H. Seah, MRCP, Marc S. Azran, Janet C. Rucker, MD, Valerie Biousse, MD, Daniel F. Martin, MD, and Nancy J. Newman, MD A 23- year- old woman who presented with a branch retinal artery occlusion followed by encephalopathy showed, by brain magnetic resonance imaging, a nonenhancing lesion in the right parietal gray matter with normal diffusion-weighted imaging. Of 64 reported cases of cat- scratch en­cephalopathy with documented neuroimaging findings, only 12 ( 18.8%) have had abnormal imaging findings. The abnormalities have included cerebral white matter lesions, basal ganglia and thalamic lesions, and multifocal lesions in immunocompromised patients, but no gray matter lesions similar to those in this patient. The variety of neuroimaging findings supports multiple pathophysiologic mechanisms of central nervous system involvement in this disorder. ( JNeuro- Ophthalmol 2003; 23: 16- 21) Cat- scratch disease ( CSD) is a relatively benign sys­temic zoonosis, manifesting with fever, lymphadenop-athy, and generalized malaise, usually with a history of prior contact with a cat or kitten ( 1). It is caused by Bar­tonella henselae in the majority of cases, although in a few reported cases, Bartonella quintana maybe responsible ( 2). Clinically, CSD usually starts with a papule at the site of inoculation, goes on to involve the regional draining lymph nodes by causing lymphadenopathy, and often resolves without treatment within 2 to 3 months. However, CSD may be complicated by involvement of other organs, in­cluding the eye and brain ( 1,2). Although cat- scratch encephalopathy is relatively benign compared with enceph­alopathy from other causes, it is the most important From the Departments of Ophthalmology ( ABHS, MSA, JCR, VB, DFM, NJN), Neurology ( VB, NJN), and Neurological Surgery ( NJN), Emory University School of Medicine, Atlanta, Georgia. Address correspondence to Nancy J. Newman, MD, Neuro-ophfhalmology Unit, Emory Eye Center, 1365- B Clifton Road NE, At­lanta, GA 30322, USA; E- mail: ophtnjn@ emory. edu This study was supported in part by a departmental grant ( Department of Ophthalmology) from Research to Prevent Blindness, Inc, New York, New York, and by core grant P30- EY06360 ( Department of Ophthal­mology) from the National Institutes of Health, Bethesda, Maryland. complication of CSD ( 1,3,4). No review has focused on the neuroimaging findings in this disorder. We describe un­usual neuroimaging findings in a patient with cat- scratch encephalopathy and review the literature regarding neu­roimaging of this disease. CASE REPORT A 23- year- old woman complained of blurred vision, nasally in the OD. Two weeks earlier she had been ill with fever but did not recall any lymphadenopathy. She had been bitten and scratched many times by her 12- week- old kitten. On examination, she had normal visual acuity, with an in-feronasal visual field defect in her OD. Funduscopy showed a small superotemporal branch retinal artery occlusion in the OD, with white spots in the inferonasal and inferotem-poral retina, and 1 to 2+ vitreous cells ( Fig. 1). The OS showed a single white spot. The work- up, which had nega­tive findings, included transthoracic echocardiography, complete blood cell count, sedimentation rate, rapid plasma reagin, prothrombin time, partial thromboplastin time, fac­tor VIII, protein C and S levels, antinuclear antibody, lupus anticoagulant, and Lyme and toxoplasma titers. Bartonella IgG titers were elevated at 1: 1024, and the patient was prescribed a course of ciprofloxacin 500 mg twice a day for 10 days. During the next month, the patient had two nocturnal seizures, clumsiness, and a decrease in memory and atten­tion. Magnetic resonance imaging ( MRI) of the brain ( Fig. 2) performed 5 weeks after the onset of the branch retinal artery occlusion and 5 days after the onset of neurologic symptoms, showed increased signal intensity in the right parietal lobe on T2- weighted, fluid attenuation inversion re­covery, and proton density sequences. The lesion did not become enhanced. Diffusion- weighted imaging findings were normal. The complete blood cell count, sedimentation rate, prothrombin time, partial thromboplastin time, thyroid-stimulating hormone, and antinuclear antibody test results were again normal. A repeat Bartonella IgG titer was 1: 2048. A lumbar puncture showed two white blood cells per microliter, no red blood cells per microliter, a protein Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. 16 J Neuro- Ophthalmol, Vol. 23, No. 1, 2003 MRI ABNORMALITIES IN CA T- SCRA TCH DISEASE ENCEPHALOPA THY JNeuro- Ophthalmol, Vol. 23, No. 1, 2003 FIG. 1. Fundus photograph of OD showing an acute branch retinal artery occlusion in a patient with cat- scratch disease. level of 17 mg/ dL, and a glucose level of 58 mg/ dL. An awake and an asleep electroencephalogram did not reveal any epileptiform activity. Repeat MRI performed a week after the initial imaging showed that the lesion in the right parietal lobe gray matter was resolving, and diffusion-weighted imaging findings remained normal. A cervical and intracranial magnetic resonance angiography scan was also normal. The patient was treated with azithromycin 250 mg every day for 3 days, another course of ciprofloxacin 500 mg twice a day for 21 days, and enteric- coated aspirin. She recovered neurologic function and has remained sei­zure free. Her visual function remains unchanged. DISCUSSION Cat- scratch disease is a systemic infectious disease manifesting with fever, tender lymphadenopathy, and gen­eralized malaise ( 1,5). The causative organism is a pleo­morphic, gram- negative bacillus ( 6) initially thought to be Aflpiafelis ( 7) but recognized in 1992 to be a newly iden­tified organism, Bartonella ( formerly Rochalimaea) hense­lae ( 2,8- 10). A closely related organism, B. quintana can also cause clinical CSD ( 2,11,12). Serologic testing ( 13) is currently the main investigational modality for confirming this diagnosis ( 2). The incidence of CSD in the United States has been estimated at approximately 22,000 cases per year ( 14). The pathologic response is variable and depends on the patient's immune status. Immunocompetent patients show a suppurative, granulomatous response ( 6), and the CSD bacilli can be seen inside blood vessel walls with spe­cial stains ( 6) and electron microscopy ( 15). Immunocom­promised patients show a vasculoproliferative response termed bacillary angiomatosis ( 16). A typical case of CSD in the immunocompetent host has a characteristic clinical course ( 1,2). It starts with a scratch from a kitten, followed by development of a non-tender papule at the site of the scratch over the next week, then regional lymph node enlargement over the next 2 weeks, which may be tender. Patients may be relatively well and afebrile or may experience a variety of systemic complaints, including fever, anorexia, malaise, arthralgia, myalgia, and abdominal, neck, and back pain. Other com­plications of CSD include ophthalmic, neurologic, bone, and abdominal involvement. The eye is the most commonly affected nonlymphatic organ ( 17). Parinaud oculoglandular syndrome is the most common ocular manifestation, occurring in up to 5% of pa­tients, and manifesting with unilateral eye redness, foreign body sensation, and tearing, with associated cervical or preauricular lymph node enlargement ( 1,2). Other ophthal­mic manifestations include uveitis, vitreous inflammation, retinitis, neuroretinitis, and optic disc edema ( 18). Focal re-tinochoroiditis may occur in the absence of disc edema or macular exudates, and this may give rise to intraretinal hemorrhage, branch retinal artery or vein occlusions, or lo­calized serous retinal detachment. Our patient's ocular in­volvement with branch retinal artery occlusion and associ­ated vitreous cells is typical. Neurologic complications occur in only about 2% to 3% of patients with CSD ( 4) and include encephalopathy, cranial nerve paresis, spinal cord involvement, and periph­eral neuritis ( 3,4,19). Encephalopathy, first described in CSD in 1952 ( 20), is the most common, occurring in about 90% of all patients with neurologic manifestations ( 4,19). Although relatively benign compared with other causes of encephalopathy, it is an important complication, with pa­tients presenting with seizures, often leading to status epi-lepticus, which may be difficult to control. The mental state of these patients ranges from lethargy or even coma to agi­tation and confusion ( 3,4,19). Carithers and Margileth ( 3) described a " transient combative behavior" in which pa­tients reacted to physical contact by hitting out at medical staff and parents, a behavior that they claim was undocu­mented in other forms of encephalopathy. Focal neurologic signs such as weakness, numbness, or ataxia may be present. The prognosis for cat- scratch encephalopathy is generally good, and the vast majority of patients recover without sequelae ( 3,4,19). Some patients, however, have persistent seizures ( 19,21) or focal neurologic deficits ( 22), and a case has been described in which the patient became demented ( 23). This report extends the range of intracerebral in­volvement and neuroimaging findings that can be attributed to bartonellosis. The majority of case series regarding cat-scratch encephalopathy date from before the modern era of neuroimaging. In the largest reported series, by Carithers Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. 17 JNeuro- Ophthalmol, Vol. 23, No. 1, 2003 Seah et al. SI. ft /• a? ( 4. L 1 ItWr s r L : . C • i ^ I ^ 1 L 1 J 0M / • i y • N . » A * 1 1 1 L \ • ^_ fe 1 r j •_• i Jul % M 41: 53: 39 PH Ksj = 1.0 • - 6 la; 17 Cf « ct, ss. a il; l'Vi'. j / « J p 1 5 0 SE/ EPI t x : i / i S* MZ ru. J < 1 • CM F0V; 26r26 5.4tN</ e. 6sp/ C 30/ OOttO 1 i 120X123/ 1.< M IEX 01 1 * V - ^ r ^ . . . 1 . . , . t . . . FIG. 2. Magnetic resonance imaging of the brain. A: Fluid attenuation inversion recovery and B: enhanced T1- weighted magnetic resonance imaging scans show a nonenhancing gray matter lesion in the right parietal lobe. C: Diffusion- weighted imaging findings are normal, showing that this is not an ischemic process. Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. 18 © 2003 Lippincott Williams & Wilkins MRI ABNORMALITIES IN CA T- SCRA TCH DISEASE ENCEPHALOPA THY JNeuro- Ophthalmol, Vol. 23, No. 1, 2003 and Margileth ( 3), 61 cases of patients with cat- scratch en­cephalopathy were collected from 1959 to 1987 ( 3). Of these, only 33 patients, slightly more than half, received a computed tomographic ( CT) brain scan, and these scans were described as " not diagnostic or showed transient ab­normalities." Only six patients had MRI performed; five of these scans were normal and one abnormal. The abnormality was localized to the occipital lobe and was also noted on a CT scan of the brain. Unfortunately, there are no further descrip­tions of the lesion and no indication as to whether those pa­tients who had normal MRI scans also had CT scans. To date, 64 patients have been reported with cat-scratch encephalopathy about whom imaging information is documented ( Table 1) ( 3,11,12,19,21- 37). Only 12 of these patients ( 18.8%) had imaging abnormalities. ( Two patients were subsequently proven by polymerase chain re­action to have B. quintana rather than B. henselae as the etiologic agent of CSD [ 11,12]). Of the 12 patients with imaging abnormalities ( Table 1), 4 had abnormalities on CT scan, with MRI either not performed or not reported ( 19,22,30,31), 2 had abnormalities on both CT and MRI scans ( 3,11), 2 had abnormalities on MRI scan undetectable by CT ( 23,37), and 4 had abnormalities on MRI scan with no information provided regarding brain CT ( 12,21,34,36). Of the abnormalities, one was described as " focal changes in the occipital area" ( 3), two were believed to be occipital infarctions ( 19,22), two were diffuse white matter lesions ( 23,34), and three were abnormalities involving the basal ganglia and thalami ( 11,12,21). In three patients who were immunocompromised and, properly speaking, had cerebral bacillary angiomatosis rather than cat- scratch encephalop­athy, imaging revealed a left temporal lesion in one patient ( 30), multifocal parenchymal and leptomeningeal involve­ment in another ( 36), and a left basal ganglia lesion in the third ( 31). There were no details on the MRI abnormalities in the last case ( 37). In none of the imaging reports is there a description of a gray- matter lesion similar to that of our patient- a lesion involving the gray matter, seen on T2- weighted, fluid attenuation inversion recovery, and proton density sequences, lacking enhancement or evidence of acutely restricted diffusion. The wide range of cerebral pathologic lesions that may manifest in patients with cat- scratch encephalopathy has led to a number of theories regarding pathophysiology. It has been suggested that there are two forms of central nervous system involvement: ( 1) a diffuse, reversible en­cephalopathy with absence of focal neurologic findings, normal imaging, and benign outcome; and ( 2) a focal en­cephalopathy, with lateralizing findings on both examina­tion and imaging, with the potential for long- term neuro­logic sequelae ( 19). The " diffuse encephalopathy" is thought to be the result of remote effects such as a neuro­toxin or an immune- mediated process rather than from direct invasion of brain parenchyma. Other authorities ( 4,35) agree that direct invasion of the central nervous sys­tem seems unlikely, because cerebrospinal fluid analysis is usually normal and because recovery is generally rapid even in the absence of antibiotic therapy. Lewis and Tucker ( 19) favor a toxic mechanism because of the abrupt onset of neurologic dysfunction and equally prompt resolution of symptoms. To date, however, there have been no further data to support their hypothesis. In support of the mechanism of direct bacterial inva­sion, recent polymerase chain reaction techniques have identified Bartonella DNA in cerebrospinal fluid, beyond the blood- cerebrospinal fluid barrier, in both immunocom­petent ( 11) and immunocompromised ( 31) patients. In two immunocompromised patients, direct bacterial invasion has also been proven on brain biopsy, by the Warthin- Starry stain in one patient ( 30) and using polymerase chain reac­tion techniques in the other ( 36). Bartonella- specific immu­noglobulin has also been found in the cerebrospinal fluid, clearly supporting the hypothesis that bacterial invasion can occur ( 31). These reports have included patients with both normal ( 11,30) and abnormal ( 36) cerebrospinal fluid, as well as normal ( 11) and abnormal neuroimaging findings ( 11,30,31,36). A vasculitic process as a basis for " focal encephalop­athy" was also proposed by Lewis and Tucker ( 19). Indeed, one patient reported with a " stroke" was the first case of cat- scratch encephalopathy with an imaging abnormality, presumably secondary to " vasculitis" ( 22). This 7- year- old girl presented with the sudden onset of expressive aphasia and a dense right hemiparesis. A brain CT scan showed a hypodense area around the left internal capsule consistent with an infarction. An angiogram performed 6 days later showed beading and irregularity of the left internal carotid artery and the left middle cerebral artery, suggestive of a localized cerebral arteritis. Another patient with a " stroke" underwent cerebral arteriography 14 days after the onset of symptoms ( 19), but this proved normal, and it was specu­lated that an earlier arteriogram might have demonstrated a transient arteritis. Certainly, in the retina, a vasculitic ap­pearance with focal retinochoroiditis, cotton wool spots, and arterial and venous thrombosis, such as in our patient, is well described ( 17). One immunocompromised patient de­veloped intraretinal hemorrhages and cotton wool spots in the retina consistent with B. henselae infection, and a retinal biopsy detected B. henselae DNA ( 38). Thus, it seems pos­sible that a " vasculitis" may represent either an immune-mediated phenomenon or direct invasion of the bacteria into the blood vessels. This would not be surprising, espe­cially given the known affinity of B. henselae for epithelial cells ( 14) and the demonstrated presence of the bacilli within blood vessel walls on pathologic specimens ( 6,14). Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. 19 J Neuro- Ophthalmol, Vol. 23, No. 1, 2003 Seah et al. TABLE 1. Cat- scratch encephalopathy cases with abnormal neuri No. 1 2 3 4 5 6 7 8 9 10 11 12 13 Source ( reference) Selby and Walker, 1979( 22), case 2 Lewis and Tucker, 1986( 19) Carithers and Margileth, 1991 ( 3) Revol et al, 1992( 23) Spach et al, 1992( 30) Hahn et al, 1994( 21) Schwartzmann etal, 1994 ( 31) Hopkins et al, 1996( 34) Parrott et al, 1997( 11), case 1 Rivello et al, 1998( 12) George et al, 1998( 36) Armengol et al, 1999 ( 37), case 6 This report Age 7 7 NR 47 49 4 39 2 19 11 39 6 23 Gender F M NR M M F M M M M M F F Neurologic features Aphasia, R hemi-paresis Lhemi-paresis NR Confusion Perseveration, anomic aphasia, R homony­mous hemianopia Comatose Disorientation, hallucin­ations Not given Clumsiness and left sided weakness Agitated and combative Altered mental status NR Decrease in memory and attention Seizures No Focal NR No No Gener­alized No Yes Gener­alized Focal None Gener­alized seizures Gener­alized seizures '- imaging CT L parietal stroke R parietal stroke Imaging MRI Not done Not done Focal changes Focal changes in in the occipital area Normal L temporal lobe lesion NR L basal ganglia lesion NR Lesion in R thalamus NR NR Normal Not done the occipital area White matter abnor­malities NR Bilateral thalamic hyper-intensity NR White matter hyper-intensity Lesion in R thalamus Hyperintense lesions in pulvinar and L thalamus Multifocal brain and lepto-meningeal abnormalities Abnormal, but no details reported R parietal lobe gray matter Sequelae Rhemi-paresis Frequent seizures, mildL hemiparesis NR Persistent dementia Resolution of lesions after treatment Frequent seizures Died NR Recovered Recovered Recovered Recovered Recovered Comments Vasculitis on angi­ography Part of a series of 61 patients HIV+ HIV+ Bquintana byPCR Bquintana byPCR HIV+ Part of a series of 6 cases cq$ mt ^ Tprap? y; v^^ M^^ mwMi?^ mmfh^ Mi T^ fMradfi ^ m ^ ^ g ^ ranted. TCH7 polymerase chain reaction; K = right. r MRI ABNORMALITIES IN CA T- SCRA TCH DISEASE ENCEPHALOPA THY JNeuro- Ophthalmol, Vol. 23, No. 1, 2003 In our patient, the parietal lobe lesion demonstrated on im­aging cannot represent acute ischemia, given the normal diffusion- weighted imaging findings 5 days after the onset of neurologic symptoms. There was no gross evidence of vasculitis by magnetic resonance angiography, but cerebral arteriography was not performed. The patient's MRI find­ings might be compatible with direct invasion of the cere­bral cortex, but no biopsy confirmation is available. Our patient would also appear to be an exception to the gener­alization that patients with focal encephalopathy and with im­aging abnormalities have permanent neurologic sequelae. REFERENCES 1. Carithers HA. Cat- scratch disease: an overview based on a study of 1200 patients. Am JDis Child 1985; 139: 1124- 33. 2. Bass JW, Vincent JM, Person DA. 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