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Classic stigmata of congenital syphilis SNHL, interstitial keratitis, Hutchinson teeth (notched incisors), mulberry molars, Clutton joints (bilateral painless knee effusions), nasal septal perforation & saddle deformity& frontal bossing. This recent issue is free to all users to allow everyone the opportunity to see the full scope and typical content of JNNP.
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Over the next few days DNS servers all across the internet will update themselves with your new domain name. Become part of the record-breaking IX Web Hosting Affiliate Program and receive up to INDUSTRY-LEADING $150 per Referral. Corresponding author: Eun Yeon Joo, Department of Neurology, Samsung, Medical Center, Sungkyunkwan, University School of Medicine, 81 Irwon-ro, Gangnam-gu, Seoul, 135-710, Korea, Tel. Acute retinal necrosis (ARN), a viral retinal disease with poor visual prognosis, following herpes simplex encephalitis (HSE) are uncommonly seen, and there has been no case yet reported of the reverse situation. A 57-year-old man was referred to Samsung Medical Center with abrupt confusion, fever, and loss of vision in both eyes. His brain magnetic resonance imaging (MRI) showed a hyper-intense lesion in the left medial temporal and bilateral medial occipital areas on T2-weight images, suggestive of HSE (Fig. After administration of intravenous acyclovir for 14 days, his systemic symptoms consistent with encephalitis slowly resolved, but his vision was not restored. Cases with ARN following HSE have been uncommonly reported,5a€“9 and to our knowledge, this is the first report of the reverse situation, HSE following ARN, in even an immune-competent patient. ARN usually presents as retinal necrosis with discrete borders located in the peripheral retina, rapid progression, circumferential spread, occlusive vasculopathy with arterial involvement, and a prominent inflammatory reaction in the vitreous and anterior chamber.3 Our patient was initially diagnosed with retinal vasculitis and treated with a high-dose systemic corticosteroid, which was not effective.
Skeletal findings osteochondritis& periostitis of long bones SNHL, interstitial keratitis, Hutchinson teeth (notched incisors), mulberry molars, Clutton joints (bilateral painless knee effusions), nasal septal perforation & saddle deformity& frontal bossing. We herein present the reverse situation, an immune-competent patient with HSE following ARN. The prevalence of the disease is equal in both genders, and it occurs in the 5tha€“7th decade of life.4 Though the diagnosis of ARN is made clinically in most patients, polymerase chain reaction (PCR) analysis of the aqueous humor or vitreous is known as a confirmative method to detect the causative virus. The patient was in his usual state of health until two weeks prior, when he began to develop sudden loss of vision in his right eye.
Fundus examination showed retinal hemorrhage, confluent retinal necrosis affecting almost the whole retina, vascular sheathing involving both arterioles and venules, optic disc swelling, and exudative retinal detachment in both eyes (Fig. On follow-up examination, retinal necrosis did not progress, but he still suffered from severe bilateral ocular pain with partial improvement of the exudative retinal detachment (Fig.
ARN associated with HSE is known to be caused by axonal transmission of a reactivated latent virus from the brain to the retina, and retinitis occasionally occurs after the encephalitis. Fluid-attenuated inversion recovery magnetic image revealed hyperintensity in the left medial temporal (arrow) and bilateral occipital cortices (arrow heads). He presented with seizures and cognitive impairment in the emergency department of our hospital. A 57-year-old man who had been under steroid therapy for retinal vasculitis the prior two weeks, presented with abrupt confusion and high fever. As shown by our patient, opposite direct transmission from the retina to the brain seems to be possible. Intraocular or systemic corticosteroids may induce retinal necrosis in patients with viral infection. Systemic steroid therapy may have exacerbated herpes viral infection in the retina, with subsequent spread to the contralateral eye and brain. Herpes simplex virus type 2 as a cause of acute retinal necrosis syndrome in young patients. Herpes simplex encephalitis and bilateral acute retinal necrosis syndrome after craniotomy. Three consecutive episodes of acute retinal necrosis due to herpes simplex-1 over twelve years following herpetic encephalitis. Initially clinical and brain MRI findings were in favor of herpes simplex virus (HSV) encephalitis. Thus, it is recommended that corticosteroids should be used in combination with antiviral agents or after beginning antiviral therapy.12 In this patient, the contralateral eye became infected, and HSE occurred during initial corticosteroid therapy without antiviral medication. Ophthalmic examination and polymerase chain reaction of the vitreous specimen revealed ARN by herpes simplex virus type 2. Two days after initiation of intravenous methylprednisolone, he complained of decreased vision in his left eye.
In cases with an unusual clinical course, especially in retinal vasculitis with arterial involvement, viral uveitis including HSV infection should be suspected. After intravenous acyclovir therapy, retinal necrosis with hemorrhage was decreased, but vascular sheathing (black arrows) and exudative retinal detachment persisted.
One week after initiation of intravenous methylprednisolone, he became drowsy and high fever occurred, and he was then referred to Samsung Medical Center.
On the night of admission, the patient experienced a generalized tonic-clonic seizure during sleep. Bilateral rhegmatogenous retinal detachment with optic atrophy was found six weeks later, thus vitrectomy with silicone oil tamponade was done in the right eye. A follow-up brain MRI revealed marked increase in size of lesions and surrounding perilesional edema in the bilateral frontal lobes, cingulate gyrus and left insular cortex on T2-weighted images and lesions showed enhancement on post-contrast T1-weighted images.


This case implies that ARN may be a risk factor for HSE and the virus may reach the brain from the eye. Infectious retinitis including acute retinal necrosis was suspected, but in terms of the location of necrosis, his clinical features were not typical of ARN Diagnostic vitrectomy confirmed the presence of HSV-1. Patient underwent right frontal craniotomy and resection of lesion in right frontal region.
Inappropriate administration of a systemic steroid may exacerbate herpes viral infection in the retina, with subsequent spread to the brain. The rate of true multicentricity in gliomas is defined as lesions with no gross or microscopic linkage and has been reported to be 2-10% based on necropsy studies [1].
We discuss a case of multicentric glioblastoma multiforme (GBM) and review the relevant literature.
Multiple gliomas were first observed by Virchow in 1864 and Bradley in 1880 [3-5] in their seminal paper published in 1962.
The clinical presentation and imaging appearance of multicentric gliomas can mimic metastatic, encephalitis and other lesions.
On neurological examination at the time of admission, memory impairment was observed, and no other focal neurological deficits were noted. He had no familiar or personal history of psychiatric or neurological disorders, or in particular, of epileptic disease. Herpes simplex virus-polymerase chain reaction (HSV-PCR) assay in the CSF was negative.MRI study revealed asymmetrical multifocal lesions in bilateral frontal lobes, cingulate gyrus and left insular cortex with gyral swelling and effacement of sulci. Present a report a sporadic encephalitis associated with abnormal involuntary movements after.
No obvious restriction was seen on the diffusion-weighted sequence and no appreciable contrast was seen on T1-weighted Gd sequence (Fig. On the basis of acute history and imaging features, possibilities of HSV encephalitis were considered. However, other possibilities of multifocal lesions like gliomatosis cerebri and transient postictal signal changes were also considered in the differential diagnosis.
MRI of brain revealed multiple lesions at the same site and location of bilateral frontal lobes, cingulate gyrus and insular cortex, appearing iso- to hypointense on T1-weighted and hyperintense on T2-weighted (Fig. As imaging showed enhancement and increased size of lesions, there was suspicion of neoplastic lesion.
MRI after 3 months, showing multiple enhancing lesions arising suspicion of multicentric gliomas. A follow-up scan was done after 1 month of previous imaging which showed multiple lesions at the same site appearing iso- to hypointense on T1-weighted (Fig. These images were suggesting of multicentric glioma and differential diagnosis included metastases.Click for large imageFigure 3. Patient underwent right frontal craniotomy and resection of one of lesions in right frontal lobe was done. Histopathological examination of tissue showed gliofibrillary matrix and sheets of neoplastic astrocytes with moderate nuclear atypia and brisk mitosis. Postoperative MRI showed changes in the form of craniotomy defect in right frontal region, dural enhancement and hemorrhage in right frontal lobe and associated with abnormal signals at peripheral part of resection cavity and cingulated gyrus appearing isointense on T1-weighted (Fig.
There was abnormal signal in the left frontal lobe, extending into insular cortex appearing isointense on T1-weighted hyperintense on T2-weighted and FLAIR sequence.
The palliative IMRT was given at high dose on left frontal lobe, moderate dose at resection site and mild dose covering the entire brain sparing the vital structures like optic nerve, optic chiasma and pituitary gland. Postoperative MRI showing postoperative changes in the form of craniotomy defect (red arrow), hemorrhage (white arrow), residual lesion in right frontal lobe (green arrow) and lesion with internal necrosis in left frontal lobe (blue arrow) which increased in size compared to preoperative MRI. However, similar clinicoradiological findings for glioblastoma and HSE can lead to delays in the diagnosis of glioblastoma and treatment of patients, and thus resulting in significant cerebral morbidity and poor prognosis.HSE is the major cause of serious sporadic encephalitis with a predilection for the limbic system [4].
Therefore, intravenous acyclovir should be continued until the limbic system lesion is diagnosed as any other diseases except HSE, because failure to consider the possibility of HSE can lead to a delay in accurate diagnosis and proper treatment, with a significant risk of mortality and morbidity [1].
The HSV-PCR assay of the CSF is an invaluable test in the diagnosis of a patient with suspected HSE. However, it sometimes tends to remain false-negative in the acute phase of HSE because the intensity of the PCR product band of an earlier CSF sample is weak [7]. For this reason, the negative result of the HSV-PCR assay in our case was overlooked and acyclovir continued to be intravenously administrated.
In retrospect, it may have been due to the corticosteroid effect but not acyclovir administration.Primary and metastatic brain tumors, including glioblastoma, can present as acute encephalitis or encephalopathy, although the frequency is very low.
Jasen [8] reported that one (1.5%) out of 65 patients with acute encephalitis actually had a brain tumor (oligodendroglioma).
Chen et al [9] reported that five (5.3%) of 95 patients who were biopsy-negative for HSE had brain tumors, of whom three had primary CNS tumors (two patients with glioblastomas and one patient with primary CNS lymphoma) and two had metastatic colon adenocarcinoma. Further, Kimberlin [10] reported three patients with high grade gliomas mimicking acute viral encephalitis. They suggested that stereotactic brain biopsy should be considered in patients with temporal lobe masses if a definitive diagnosis using PCR assays for common viruses is unavailable. If we had performed stereotactic brain biopsy on our patient based on the initial CNS manifestations, functional deficits would have been much less severe.First, MRI is more sensitive than CT in the detection of brain tumors.
However, patients whose initial MRIs were negative or had mild abnormalities, and soon thereafter had high grade glioma, were occasionally encountered.
After all, in suspected tumors, serial brain imaging studies are needed to document the evolution of brain tumor and to rule out underlying encephalitis.The imaging appearance of multifocal and multicentric GBM is indistinct from that of metastases, with MRI displaying multiple contrast-enhancing masses [9, 11].


Certain MRI features such as variable lesion morphology, mild peritumoral edema, and irregular tumor margins can suggest the diagnosis of multifocal or multicentric GBM [12-14]. Since metastasis from extracranial primary tumors is the most common diagnosis associated with multiple brain masses, histopathological verification is imperative before making a diagnosis of metastasis, especially in patients with no known primary neoplasm [3, 11].
The diagnostic workup for multifocal and multicentric GBM is generally the same as that for solitary GBM. Dissemination of GBM, however, can occur intracranially or throughout the spinal axis [15]. In such cases of GBM with leptomeningeal gliomatosis, either suspected clinically or radiographically due to the presence of leptomeningeal enhancement or hydrocephalus, complete neuroaxis MRI should be obtained. Batzdorf and Malamud characterized the modes of growth in gliomas by establishing criteria to distinguish multiple and multicentric gliomas [16]. Others have attempted additional classifications based on pathologic and radiologic criteria [4, 17].
Therefore, multifocal glioma consists of tumors separated by white matter tracts within the same hemisphere, whereas multicentric glioma consists of tumors in opposite hemispheres or separated by the tentorium.Multifocal and multicentric GBMs do not exhibit any histopathologic characteristics that differentiate them from typical, solitary supratentorial GBM [16, 18]. Pathognomonic features of GBM include pseudopalisading necrosis and neovascularization [19].
The individual tumors in cases of multicentric GBM usually have the same pathologic appearance [16, 20].
Although there is still no unified theory regarding the pathogenesis of multifocal and multicentric GBM, several hypotheses have been developed.
The first stage is neoplastic transformation, in which a wide field becomes more susceptible to neoplastic growth. The second stage is tumor proliferation at two or more activated sites that can occur simultaneously in response to various stimuli including biochemical, hormonal, and viral triggers. For example, there is a reported association between p53 mutations and multifocal GBM that correlates the pattern of p53 mutation to tumor migration and augmented growth. This molecular and genetic characterization of multifocal GBM has thereby implicated particular oncogenes and growth factors in the pathogenesis of multifocal and multicentric GBM.In addition to the molecular pathways involved in multifocality and multicentricity, studies have correlated the tumor pattern at diagnosis and recurrence with the spatial relationship to the subventricular zone (SVZ) and cortex as seen on MRI [4]. More specifically, patients with a contrast-enhancing lesion contacting the SVZ and infiltrating the cortex were most likely to have multifocal disease at the time of diagnosis and distant tumor recurrence. On the other hand, patients with a contrast-enhancing lesion neither contacting the SVZ nor infiltrating the cortex always had solitary lesions and contiguous tumor recurrences. Neural stem cells have been found to express matrix metalloproteinases, which are proteolytic enzymes implicated in tumor spread [4]. Furthermore, the SVZ is thought to be a highly permissive environment for tumor growth and cellular migration.Currently, there are no clear guidelines regarding the optimal management of multifocal and multicentric GBM [12]. While the extent of resection is established as an independent determinant of survival in patients with solitary GBM, the role of surgery for multifocal and multicentric GBM remains controversial [8, 12, 22]. First one is surgery done in our patient, aggressive resection of one tumor focus, biopsy alone followed by chemotherapy and radiation treatment, and second one is multiple craniotomies during a single operation with no clear indication of which modality is superior [12, 23-25]. The standard radiation treatment for GBM includes conformal radiotherapy that encompasses the tumor volume and margin along with concurrent and adjuvant temozolomide [2, 25, 26]. Regarding radiotherapy for multifocal and multicentric GBM, a study found no significant difference in the median time to progression or median survival time between conformal radiotherapy and whole brain radiation treatment [25].Additionally, the role of radiotherapy to control infratentorial GBM is not yet defined [7, 27, 28]. Some studies support the use of craniospinal radiotherapy with posterior fossa boost for malignant cerebellar gliomas, especially in children [27]. However, other studies have found no benefit with craniospinal radiotherapy in GBM in adults and support whole brain radiation treatment with or without posterior fossa boost [7].
Most authors agree that craniospinal irradiation is reasonable if CSF dissemination occurs [28]. In patients with leptomeningeal gliomatosis, other treatments could also include intrathecal chemotherapy and CSF shunting for associated hydrocephalus.ConclusionMulticentric glioblastoma is a rare entity.
The clinical presentation may develop extremely fast and can be characterized quite exclusively by cognitive symptoms; such symptoms can be very difficult to place, especially when focal neurological signs are not present.
It is rare that high-grade brain tumors may present as acute encephalopathy with limbic system involvement by brain imaging.In this particular case, the initial imaging was mimicking with acute HSV encephalitis and we could not expect a so relevant evolution in such short time.
Therefore, an intensive follow-up with short repeat brain imaging as well as stereotactic biopsy is necessary in such patients if definite evidence for the diagnosis of HSE can not be obtained.AcknowledgementWe would like to express our special thanks of gratitude to Dr.
Sunil Gupta for his constant encouragement without which this assignment would not have been possible. Multicentric glioblastoma multiforme occurring in the supra- and the infratentorial regions--case report. 1967.Hassaneen W, Levine NB, Suki D, Salaskar AL, de Moura Lima A, McCutcheon IE, Prabhu SS, et al.
Prognostic significance of intracranial dissemination of glioblastoma multiforme in adults. Genetic analysis of a multifocal glioblastoma multiforme: a suitable tool to gain new aspects in glioma development. Relationship of glioblastoma multiforme to neural stem cell regions predicts invasive and multifocal tumor phenotype.
Independent association of extent of resection with survival in patients with malignant brain astrocytoma.



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