January 2006

Some Selected Abstracts:


1.                       Valyi-Nagy T, Dermody TS.  Role of oxidative damage in the pathogenesis of viral infections of the nervous system.  Histol Histopathol. 2005 Jul;20(3):957-67.

Department of Pathology, College of Medicine, University of Illinois at Chicago, Chicago, Illinois, USA.

Oxidative stress, primarily due to increased generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS), is a feature of many viral infections. ROS and RNS modulate the permissiveness of cells to viral replication, regulate host inflammatory and immune responses, and cause oxidative damage to both host tissue and progeny virus. The lipid-rich nervous system is particularly susceptible to lipid peroxidation, an autocatalytic process that damages lipid-containing structures and yields reactive by-products, which can covalently modify and damage cellular macromolecules. Oxidative injury is a component of acute encephalitis caused by herpes simplex virus type 1 and reovirus, neurodegenerative disease caused by human immunodeficiency virus and murine leukemia virus, and subacute sclerosing panencephalitis caused by measles virus. The extent to which oxidative damage plays a beneficial role for the host by limiting viral replication is largely unknown. An enhanced understanding of the role of oxidative damage in viral infections of the nervous system may lead to therapeutic strategies to reduce tissue damage during viral infection without impeding the host antiviral response.

Diagnosis, Diagnostics, Immunodiagnosis & Immunodiagnostics:

13228.  Busch MP, Caglioti S, Robertson EF, McAuley JD, Tobler LH, Kamel H, Linnen JM, Shyamala V, Tomasulo P, Kleinman SH. Screening the blood supply for West Nile virus RNA by nucleic acid amplification testing. N Engl J Med. 2005 Aug 4;353(5):460-7.

13229.  Colmenero JD, Queipo-Ortuno MI, Reguera JM, Baeza G, Salazar JA, Morata P.  Real time polymerase chain reaction: a new powerful tool for the diagnosis of neurobrucellosis. J Neurol Neurosurg Psychiatry. 2005 Jul;76(7):1025-7.

13230.   Courtioux B, Bisser S, M'belesso P, Ngoungou E, Girard M, Nangouma A, Josenando T, Jauberteau-Marchan MO, Bouteille B. Dot enzyme-linked immunosorbent assay for more reliable staging of patients with Human African trypanosomiasis. J Clin Microbiol. 2005 Sep;43(9):4789-95.

13231.  Ekmekci O, Karasoy H, Gokcay A, Ulku A. Atypical EEG findings in subacute sclerosing panencephalitis. Clin Neurophysiol. 2005 Aug;116(8):1762-7. 

13232.   Marzocchetti A, Di Giambenedetto S, Cingolani A, Ammassari A, Cauda R, De Luca A. Reduced rate of diagnostic positive detection of JC virus DNA in cerebrospinal fluid in cases of suspected progressive multifocal leukoencephalopathy in the era of potent antiretroviral therapy. J Clin Microbiol. 2005 Aug;43(8):4175-7.

13233.   Ng'walali PM, Kibayashi K, Mbonde MP, Harada S, Mwakagile D, Kitinya JN, Tsunenari S. Neuropathology of human immunodeficiency virus infection: a forensic autopsy study in Dar Es Salaam, Tanzania. Forensic Sci Int. 2005 Jul 16;151(2-3):133-8.

13234.  Prince HE, Lape-Nixon M, Busch MP, Tobler LH, Foster GA, Stramer SL.  Utilization of follow-up specimens from viremic blood donors to assess the value of west nile virus immunoglobulin G avidity as an indicator of recent infection. Clin Diagn Lab Immunol. 2005 Sep;12(9):1123-6.

13235.  Tilley PA, Walle R, Chow A, Jayaraman GC, Fonseca K, Drebot MA, Preiksaitis J, Fox J. Clinical utility of commercial enzyme immunoassays during the inaugural season of West Nile virus activity, Alberta, Canada. J Clin Microbiol. 2005 Sep;43(9):4691-5.

13236.  Tilley PA, Zachary GA, Walle R, Schnee PF. West Nile virus detection and commercial assays. Emerg Infect Dis. 2005 Jul;11(7):1154-5.

13237.  Tonry JH, Brown CB, Cropp CB, Co JK, Bennett SN, Nerurkar VR, Kuberski T, Gubler DJ. West Nile virus detection in urine. Emerg Infect Dis. 2005 Aug;11(8):1294-6.


13238.   Kumar D, Humar A. Emerging viral infections in transplant recipients. Curr Opin Infect Dis. 2005 Aug;18(4):337-41. Review. 

13239.  Mandl CW. Steps of the tick-borne encephalitis virus replication cycle that affect neuropathogenesis. Virus Res. 2005 Aug;111(2):161-74. Review.

13240.  Rojanawiwat A, Miura T, Thaisri H, Pathipvanich P, Umnajsirisuk S, Koibuchi T, Vongsheree S, Iwamoto A, Ariyoshi K, Sawanpanyalert P. Frequent detection of Epstein-Barr Virus and cytomegalovirus but not JC virus DNA in cerebrospinal fluid samples from human immunodeficiency virus-infected patients in northern Thailand. J Clin Microbiol. 2005 Jul;43(7):3484-6.

13241.  Santagata S, Kinney HC. Mechanism of JCV entry into oligodendrocytes. Science. 2005 Jul 15;309(5733):381-2.

13242.     Takemoto M, Kira R, Kusuhara K, Torisu H, Sakai Y, Hara T. Gene expression profiles in peripheral blood mononuclear cells from patients with subacute sclerosing panencephalitis using oligonucleotide microarrays. J Neurovirol. 2005 Jul;11(3):299-305.

13243.  Valyi-Nagy T, Dermody TS. Role of oxidative damage in the pathogenesis of viral infections of the nervous system. Histol Histopathol. 2005 Jul;20(3):957-67. Review.


13244.    Chen L, Lin T, Zhang H, Su Y. Immune responses to foot-and-mouth disease DNA vaccines can be enhanced by coinjection with the Isatis indigotica extract. Intervirology. 2005 Jul-Aug;48(4):207-12.

13245.  Hayes EB, Sejvar JJ, Zaki SR, Lanciotti RS, Bode AV, Campbell GL. Virology, pathology, and clinical manifestations of West Nile virus disease. Emerg Infect Dis. 2005 Aug;11(8):1174-9. Review.

13246.   Yamshchikov G, Borisevich V, Kwok CW, Nistler R, Kohlmeier J, Seregin A, Chaporgina E, Benedict S, Yamshchikov V. The suitability of yellow fever and Japanese encephalitis vaccines for immunization against West Nile virus. Vaccine. 2005 Sep 15;23(39):4785-92.


13247.    Adelman B, Sandrock A, Panzara MA. Natalizumab and progressive multifocal leukoencephalopathy. N Engl J Med. 2005 Jul 28;353(4):432-3.

13248.  Aure K, Behin A, Louillet F, Lafitte C, Sanson M, Vernant JP. Dramatic improvement in non-AIDS related progressive multifocal leucoencephalopathy. J Neurol Neurosurg Psychiatry. 2005 Sep;76(9):1305-6.

13249.  Baeuerle M, Schmitt-Haendle M, Taubald A, Mueller S, Walter H, Pfeiffer C, Manger B, Harrer T. Severe HIV-1 encephalitis and development of cerebral non-Hodgkin lymphoma in a patient with persistent strong HIV-1 replication in the brain despite potent HAART -- case report and review of the literature. Eur J Med Res. 2005 Jul 29;10(7):309-16.

13250.    Berger JR, Koralnik IJ. Progressive multifocal leukoencephalopathy and natalizumab—unforeseen consequences. N Engl J Med. 2005 Jul 28;353(4):414-6.

13251.  Holcomb SS. Guidelines for West Nile virus. Nurse Pract. 2005 Sep;30(9):7, 11, 14.

13252.  Reilmann R, Imai T, Ringelstein EB, Gaubitz M, Niederstadt TU, Paulus W, Husstedt IW. Remission of progressive multifocal leucoencephalopathy in SLE after treatment with cidofovir: a 4 year follow up. J Neurol Neurosurg Psychiatry. 2005 Sep;76(9):1304-5.

13253.   Secko D. Immunotherapy for West Nile virus infection. CMAJ. 2005 Sep 13;173(6):591.

13254. Wyen C, Lehmann C, Fatkenheuer G, Hoffmann C. AIDS-related progressive multifocal leukoencephalopathy in the era of HAART: report of two cases and review of the literature. AIDS Patient Care STDS. 2005 Aug; 19(8):486-94. Review.



 April 2006

Some Selected Abstracts:


Bellini WJ, Harcourt BH, Bowden N, Rota PA. Nipah virus: an emergent paramyxovirus causing     severe encephalitis in humans. J Neurovirol. 2005 Oct;11(5):481-7. Review.

Respiratory and Enteric Viruses Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia 30333, USA. wbellini@cdc.gov

Nipah virus is a recently emergent paramyxovirus that is capable of causing severe disease in both humans and animals. The first outbreak of Nipah virus occurred in Malaysia and Singapore in 1999 and, more recently, outbreaks were detected in Bangladesh. In humans, Nipah virus causes febrile encephalitis with respiratory syndrome that has a high mortality rate. The reservoir for Nipah virus is believed to be fruit bats, and humans are infected by contact with infected bats or by contact with an intermediate animal host such as pigs. Person to person spread of the virus has also been described. Nipah virus retains many of the genetic and biologic properties found in other paramyxoviruses, though it also has several unique characteristics. However, the virologic characteristics that allow the virus to cause severe disease over a broad host range, and the epidemiologic, environmental and virologic features that favor transmission to humans are unknown. This review summarizes what is known about the virology, epidemiology, pathology, diagnosis and control of this novel pathogen.







1.                   Hasko G, Pacher P, Vizi ES, Illes P. Adenosine receptor signaling in the brain immune system. Trends Pharmacol Sci. 2005 Oct;26(10):511-6. Review.

Department of Surgery, UMDNJ-New Jersey Medical School, Newark, NJ 07103, USA. haskoge@umdnj.edu

The brain immune system, which consists mainly of astrocytes, microglia and infiltrating immune cells, is quiescent normally, but it is activated in response to pathophysiological events such as ischemia, trauma, inflammation and infection. Adenosine is an endogenous purine nucleoside that is generated at sites that are subjected to these "stressful" conditions. Adenosine interacts with specific G-protein- coupled receptors on astrocytes, microglia and infiltrating immune cells to regulate the function of the immune system in the brain. Although many of the effects of adenosine on immune-  competent cells in the brain protect neuronal integrity, adenosine might also aggravate neuronal injury by promoting inflammatory processes. A more complete understanding of adenosine receptor function in the brain immune system should help develop novel therapeutic ways to treat brain disorders that are associated with a dysfunctional immune response.         


             Mackenzie JS. Emerging zoonotic encephalitis viruses: lessons from Southeast Asia and Oceania. J Neurovirol. 2005 Oct;11(5):434-40. Review.

Australian Biosecurity CRC, Curtin University of Technology, Perth, Western Australia, Australia. Mackenzie@curtin.edu.au

The last decade of the 20th Century saw the introduction of an unprecedented number of encephalitic viruses emerge or spread in the Southeast Asian and Western Pacific regions (Mackenzie et al, 2001; Solomon, 2003a). Most of these viruses are zoonotic, either being arthropod-borne viruses or bat-borne viruses. Thus Japanese encephalitis virus (JEV), a mosquito-borne flavivirus, has spread through the Indonesian archipelago to Papua New Guinea (PNG) and to the islands of the Torres Strait of northern Australia, to Pakistan, and to new areas in the Indian subcontinent; a strain of tick-borne encephalitis virus (TBEV) was described for the first time in Hokkaido, Japan; and a novel mosquito-borne alphavirus, Me Tri virus, was described from Vietnam. Three novel bat-borne viruses emerged in Australia and Malaysia; two, Hendra and Nipah viruses, represent the first examples of a new genus in the family Paramyxoviridae, the genus Henipaviruses, and the third, Australian bat lyssavirus (ABLV) is new lyssavirus closely related to classical rabies virus. These viruses will form the body of this brief review.



         Marchetti B, Abbracchio MP. To be or not to be (inflamed)--is that the question in anti-inflammatory drug therapy of neurodegenerative disorders? Trends Pharmacol Sci. 2005 Oct;26(10):517-25. Review.

Department of Pharmacology, University of Sassari Medical School, Sassari, Sardinia, Italy. biancamarchetti@libero.it

A sustained inflammatory reaction is present in acute (e.g. stroke) and chronic (e.g. Alzheimer's disease, Parkinson's disease and multiple sclerosis) neurodegenerative disorders. Inflammation, which is fostered by both residential glial cells and blood-circulating cells that infiltrate the diseased brain, probably starts as a time- and site-specific defense mechanism that could later evolve into a destructive and uncontrolled reaction. In this article, we review the crucial dichotomy of brain inflammation, where failure to resolve an acute beneficial response could lead to a vicious and anarchic state of chronic activation. The possible use of non-steroidal anti-inflammatory drugs for the management of neurode- generative diseases is discussed in light of recent data demonstrating a neuroprotective role of local innate and adaptive immune responses. Novel therapeutic approaches must rely on potentiation of endogenous anti-inflammatory pathways, identification of early markers of neuronal deterioration and a combination treatment involving immune modulation and anti-inflammatory therapies.3.                   


            McIver CJ, Jacques CF, Chow SS, Munro SC, Scott GM, Roberts JA, Craig ME, Rawlinson WD. Development of multiplex PCRs for detection of common viral pathogens and agents of congenital infections. J Clin Microbiol. 2005 Oct;43(10):5102-10.

             Department of Microbiology, South Eastern Area Laboratory Service, Prince of Wales Hospital, New South Wales 2031, Australia.

            Potential causes of congenital infection include Toxoplasma gondii and viruses such as cytome- galovirus  (CMV), enterovirus, hepatitis C virus, herpes simplex virus types 1 and 2 (HSV-1 and -2), human herpesvirus types 6, 7, and 8, lymphocytic choriomeningitis virus, parvovirus, rubella virus, and varicella-zoster virus. Testing for each of these agents using nucleic acid tests is time consuming and the availability of clinical samples such as amniotic fluid or neonatal blood is often limited. The aim of this study was to develop multiplex PCRs (mPCRs) for detection of DNA and RNA agents in the investigation of congenital infection and an mPCR for the viruses most commonly requested in a diagnostic virology laboratory (CMV, Epstein-Barr virus, enterovirus, HSV-1, HSV-2, and varicella-zoster virus). The assays were assessed using known pathogen-positive tissues (cultures, placentae, plasma, and amniotic fluid) and limits of detection were determined for all the agents studied using serial dilutions of plasmid targets. Nested PCR was performed as the most sensitive assay currently available, and detection of the amplicons using hybridization to labeled probes and enzyme-linked immunosorbent assay detection was incorporated into three of the four assays. This allowed detection of 10 to 10(2) copies of each agent in the samples processed. In several patients, an unexpected infection was diagnosed, including a case of encephalitis where HSV was the initial clinical suspicion but CMV was detected. In the majority of these cases the alternative agent could be confirmed using reference culture, serology, or fluorescence methods and was of relevance to clinical care of the patient. The methods described here provide useful techniques for diagnosing congenital infections and a paradigm for assessment of new multiplex PCRs for use in the diagnostic laboratory

Diagnosis, Diagnostics, Immunodiagnosis & Immunodiagnostics:

 13768.     Chanama S, Sukprasert W, Sa-ngasang A, A-nuegoonpipat A, Sangkitporn S, Kurane I, Anantapreecha S. Detection of Japanese encephalitis (JE) virus-specific IgM in cerebrospinal fluid and serum samples from JE patients. Jpn J Infect Dis. 2005 Oct;58(5):294-6.

 13769.     Lee DH, Mathew J, Pfahler W, Ma D, Valinsky J, Prince AM, Andrus L. Individual donor nucleic acid amplification testing for detection of West Nile virus. J Clin Microbiol. 2005 Oct;43(10):5111-6.

 13770.     Lolli F, Mazzanti B, Pazzagli M, Peroni E, Alcaro MC, Sabatino G, Lanzillo R, Brescia Morra V, Santoro L, Gasperini C, Galgani S, D'Elios MM, Zipoli V, Sotgiu S, Pugliatti M, Rovero P, Chelli M, Papini AM. The glycopeptide CSF114(Glc) detects serum antibodies in multiple sclerosis. J Neuroimmunol. 2005 Oct;167(1-2):131-7.

 13771.     Marciniak C, Rosenfeld EL. Serial electrodiagnostic studies in West Nile virus-associated acute flaccid paralysis. Am J Phys Med Rehabil. 2005 Nov;84(11):904-10.

 13772.     Pawar SD, Singh A, Gangodkar SV, Rao BL. Propagation of Chandipura virus in chick embryos. Indian J Exp Biol. 2005 Oct;43(10):930-2.

 13773.     Rand K, Houck H, Lawrence R. Real-time polymerase chain reaction detection of herpes simplex virus in cerebrospinal fluid and cost savings from earlier hospital discharge. J Mol Diagn. 2005 Oct;7(4):511-6.


 13774.     Best SM, Morris KL, Shannon JG, Robertson SJ, Mitzel DN, Park GS, Boer E, Wolfinbarger JB, Bloom ME. Inhibition of interferon-stimulated JAK-STAT signaling by a tick-borne flavivirus and identification of NS5 as an interferon antagonist. J Virol. 2005 Oct;79(20):12828-39.

 13775.     Briese T, Bernard KA. West Nile virus--an old virus learning new tricks? J Neurovirol. 2005 Oct;11(5):469-75. Review.

 13776.     Chatterjee P. Japanese encephalitis outbreak in India. Lancet Neurol. 2005 Nov;4(11):700.

 13777.     Cruz-Pacheco G, Esteva L, Montano-Hirose JA, Vargas C. Modelling the dynamics of West Nile Virus. Bull Math Biol. 2005 Nov;67(6):1157-72.

 13778.     Custer B, Busch MP, Marfin AA, Petersen LR. The cost-effectiveness of screening the U.S. blood supply for West Nile virus. Ann Intern Med. 2005 Oct 4;143(7):486-92. Summary for patients in: Ann Intern Med. 2005 Oct 4;143(7):I44.

 13779.     Hanna SL, Pierson TC, Sanchez MD, Ahmed AA, Murtadha MM, Doms RW. N-linked glycosylation of west nile virus envelope proteins influences particle assembly and infectivity. J Virol. 2005 Nov;79(21):13262-74. 

 13780.     Lee DH, Mathew J, Pfahler W, Ma D, Valinsky J, Prince AM, Andrus L. Individual donor nucleic acid amplification testing for detection of West Nile virus. J Clin Microbiol. 2005 Oct;43(10):5111-6.

 13781.     Olival KJ, Daszak P. The ecology of emerging neurotropic viruses. J Neurovirol. 2005 Oct;11(5):441-6. Review.

 13782.     Ota MO, Moss WJ, Griffin DE. Emerging diseases: measles. J Neurovirol. 2005 Oct;11(5):447-54. Review.

 13783.     Soldan SS, Gonzalez-Scarano F. Emerging infectious diseases: the Bunyaviridae. J Neurovirol. 2005 Oct;11(5):412-23. Review.


 13784.     Hombach J, Solomon T, Kurane I, Jacobson J, Wood D. Report on a WHO consultation on immunological endpoints for evaluation of new Japanese encephalitis vaccines, WHO, Geneva, 2-3 September, 2004. Vaccine. 2005 Nov 1;23(45):5205-11.

 13785.     Marfin AA, Gubler DJ. Japanese encephalitis: the need for a more effective vaccine. Lancet. 2005 Oct 15-21;366(9494):1335-7.

 13786.     Ohrr H, Tandan JB, Sohn YM, Shin SH, Pradhan DP, Halstead SB. Effect of single dose of SA 14-14-2 vaccine 1 year after immunisation in Nepalese children with Japanese encephalitis: a case-control study. Lancet. 2005 Oct 15-21;366(9494):1375-8.

 13787.     Pugachev KV, Guirakhoo F, Monath TP. New developments in flavivirus vaccines with special attention to yellow fever. Curr Opin Infect Dis. 2005 Oct;18(5):387-94. Review. 

 13788.     Sejvar JJ, Labutta RJ, Chapman LE, Grabenstein JD, Iskander J, Lane JM.  Neurologic adverse events associated with smallpox vaccination in the United States, 2002-2004. JAMA. 2005 Dec 7;294(21):2744-50. Erratum in: JAMA. 2005 Dec 28;294(24):3092.

 13789.     Zenz W, Pansi H, Zoehrer B, Mutz I, Holzmann H, Kraigher A, Berghold A, Spork D.  Tick-borne encephalitis in children in Styria and Slovenia between 1980 and 2003. Pediatr Infect Dis J. 2005 Oct;24(10):892-6.


 13790.     Hanly JG, Harrison MJ. Management of neuropsychiatric lupus. Best Pract Res Clin Rheumatol. 2005 Oct;19(5):799-821. Review.

 13791.     Openshaw H, Cantin EM. Corticosteroids in herpes simplex virus encephalitis. J Neurol Neurosurg Psychiatry. 2005 Nov;76(11):1469.   

 13792.     RamachandranNair R, Parameswaran M, Girija AS. Acute disseminated encephalomyelitis treated with plasmapheresis. Singapore Med J. 2005 Oct;46(10):561-3. 



 July 2006

Some Selected Abstracts:


Centers for Disease Control and Prevention (CDC). Human rabies--Mississippi, 2005. MMWR Morb Mortal Wkly Rep. 2006 Mar 3;55(8):207-8.

On September 27, 2005, a previously healthy boy aged 10 years in Mississippi died from encephalitis later attributed to rabies. This report summarizes the patient's clinical course and the subsequent epidemiologic investigation, which implicated exposure to bats at the boy's home as the likely source of rabies. The findings underscore the importance of
recognizing the risk for rabies from direct contact with bats and seeking prompt medical attention when exposure occurs.

Diagnosis, Diagnostics, Immunodiagnosis & Immunodiagnostics:

14319. Civen R, Villacorte F, Robles DT, Dassey DE, Croker C, Borenstein L, Harvey SM, Mascola L. West Nile virus infection in the pediatric population. Pediatr Infect Dis J. 2006 Jan;25(1):75-8.

14320. Gunduz A, Beskardes AF, Kutlu A, Ozkara C, Karaagac N, Yeni SN. Herpes encephalitis as a cause of nonconvulsive status epilepticus. Epileptic Disord. 2006 Mar;8(1):57-60.

14321. Mort DJ, Bronstein AM. Sudden deafness. Curr Opin Neurol. 2006 Feb;19(1):1-3.

14322. Sharma V, Chan YC, Ong, Teoh HL, Wilder-Smith EP. Bickerstaff's brainstem encephalitis: can it recur? J Clin Neurosci. 2006 Feb;13(2):277-9.

14323. Wang DS, Tang Y, Wang Y. A case of overlapping Bickerstaff's brainstem encephalitis and Guillain-Barre syndrome. J Zhejiang Univ Sci B. 2006 Feb;7(2):138-41.


14324. Hsu YH, Cho LC, Wang LS, Chen LK, Lee JJ, Yang HH. Acute respiratory distress syndrome associated with rabies: a case report. Kaohsiung J Med Sci. 2006 Feb;22(2):94-8.




October 2006


Some selected abstract:


Clarke M, Newton RW, Klapper PE, Sutcliffe H, Laing I, Wallace G. Childhood encephalopathy: viruses, immune response, and outcome. Dev Med Child Neurol. 2006 Apr;48(4):294-300.
Department of Paediatric Neurology, Leeds General Infirmary
, UK.
This study examined children with an acute encephalopathy illness for evidence of viral infection, disordered blood-brain barrier function, intrathecal immunoglobulin synthesis, and interferon (IFN) production, and related their temporal occurrence to outcome. A prospective study of 22 children (13 males, 9 females; age range 1mo to 13y, median 2y 4mo), recorded clinical details, with serum and cerebrospinal fluid (CSF) analysis near presentation and then on convalescent specimens taken up to day 39 of the neurological illness. Outcome was assessed with standard scales between 18 months and 3 years after presentation. A history consistent with viral infection was given in 17 children but laboratory evidence of viral infection was found in only 7 (7/17). In 18 out of 21 children, an elevated CSF:serum albumin ratio indicative of impairment of the blood-CSF and blood-brain barriers was detected at some stage of the illness. In 14 of the 15 children with a raised immunoglobulin G index, and in 12 of the 14 children where the CSF was positive for oligoclonal bands, this was preceded by, or was observed at the same time as, an abnormal albumin ratio. Sixteen children (16/18) had elevated IFN-alpha levels in serum, or CSF, or in both. We conclude that these findings indicate an initial disruption of the blood-brain barrier followed by intrathecal antibody production by activated lymphocytes, clonally restricted to a few antigens. This is the first in vivo study to show this as an important pathogenetic mechanism of encephalitis in children. Poor outcome was associated with young age, a deteriorating electroencephalogram pattern from grade 1 to grade 2, and the degree of blood-brain barrier impairment, particularly when prolonged, but not with Glasgow Coma Scale score. The persistence of IFN-alpha was associated with a good prognosis.


Keogh JM, Badawi N.  The origins of cerebral palsy. Curr Opin Neurol. 2006 Apr;19(2):129-34. Review. 
Hornsby Ku-Ring Gai Hospital, University of Sydney, Sydney, New South Wales, Australia.

PURPOSE OF REVIEW: Cerebral palsy is the most common and visible motor disability of childhood. Its aetiology remains a topic of hot debate between those who see it as a reflection of medical mismanagement of an avoidable complication and those who see its origins in the development of the fetal brain affected at many points along a causal pathway to damage. This review outlines the themes of research publications over the year 2004/2005. RECENT FINDINGS: The review looks at recent findings relating to epidemiology, infection and inflammation, prematurity, multiple pregnancy, thrombophilias, genetics, placenta, neuroimaging and rescue therapies in cerebral palsy. SUMMARY: Papers this year have helped clarify risk groups and identify some areas (e.g. the management of thrombophilias and the potential of induced hypothermia) with the potential to be rapidly introduced into clinical practice. In this enigmatic and multifactorial condition, however, progress remains slow. New tools such as magnetic resonance imaging are providing valuable insights into the lesions that result in cerebral palsy but the pathways to injury remain unclear. The future of cerebral palsy research lies in understanding the complex interactions of multiple factors on the road to cerebral palsy or in looking for final common pathways such as inflammation which may be amenable to manipulation.

Diagnosis, Diagnostics, Immunodiagnosis & Immunodiagnostics:

14704.  Dutta A, Tonkin T, Gelman W. Postpartum convulsions--a diagnostic enigma. J R Soc Med. 2006 Apr;99(4):203-4.

14705.  Merkler D, Horvath E, Bruck W, Zinkernagel RM, Del la Torre JC, Pinschewer DD. "Viral deja vu" elicits organ-specific immune disease independent of reactivity to self. J Clin Invest. 2006 May;116(5):1254-63.


14706.  Anlar B, Waye JS, Eng B, Oguz KK.  Atypical clinical course in juvenile metachromatic leukodystrophy involving novel arylsulfatase A gene mutations. Dev Med Child Neurol. 2006 May;48(5):383-7. 


14707.  Clarke M, Newton RW, Klapper PE, Sutcliffe H, Laing I, Wallace G. Childhood encephalopathy: viruses, immune response, and outcome. Dev Med Child Neurol. 2006 Apr;48(4):294-300. 

14708.  Keogh JM, Badawi N.  The origins of cerebral palsy. Curr Opin Neurol. 2006 Apr;19(2):129-34. Review