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3. The clinical profile of NMOSD in Australia and New Zealand

Author

Bukhari, Wajih, Clarke, Laura, O’Gorman, Cullen, Khalilidehkordi, Elham, Arnett, Simon, Prain, Kerri M., Woodhall, Mark, Silvestrini, Roger, Bundell, Christine S., Ramanathan, Sudarshini, Abernethy, David, Bhuta, Sandeep, Blum, Stefan, Boggild, Mike, Boundy, Karyn, Brew, Bruce J., Brownlee, Wallace, Butzkueven, Helmut, Carroll, William M., Chen, Celia, Coulthard, Alan, Dale, Russell C., Das, Chandi, Dear, Keith, Fabis-Pedrini, Marzena J., Fulcher, David, Gillis, David, Hawke, Simon, Heard, Robert, Henderson, Andrew P. D., Heshmat, Saman, Hodgkinson, Suzanne, Jimenez-Sanchez, Sofia, Kilpatrick, Trevor J., King, John, Kneebone, Chris, Kornberg, Andrew J., Lechner-Scott, Jeannette, Lin, Ming-Wei, Lynch, Christopher, Macdonnell, Richard A. L., Mason, Deborah F., McCombe, Pamela A., Pereira, Jennifer, Pollard, John D., Reddel, Stephen W., Shaw, Cameron, Spies, Judith, Stankovich, James, Sutton, Ian, Vucic, Steve, Walsh, Michael, Wong, Richard C., Yiu, Eppie M., Barnett, Michael H., Kermode, Allan G., Marriott, Mark P., Parratt, John, Slee, Mark, Taylor, Bruce V., Willoughby, Ernest, Wilson, Robert J., Brilot, Fabienne, Vincent, Angela, Waters, Patrick, and Broadley, Simon A.

Published
2020
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11. Anti-glutamic acid decarboxylase antibody screening in first-episode psychosis.

Author

Warren, Nicola, Freier, Karen, Siskind, Dan, O'Gorman, Cullen, Blum, Stefan, Gillis, David, and Scott, James G

Subjects
GLUTAMIC acid, ONLINE information services, PSYCHOLOGY information storage & retrieval systems, CINAHL database, ENCEPHALITIS, IMMUNOGLOBULINS, META-analysis, MEDICAL information storage & retrieval systems, CONFIDENCE intervals, PSYCHOSES, SYSTEMATIC reviews, MEDICAL screening, ENZYMES, QUALITY assurance, DESCRIPTIVE statistics, MEDLINE, ODDS ratio
Abstract

Objective: The Royal Australian and New Zealand College of Psychiatrists recommends screening for a range of antibodies in first-episode psychosis, including anti-glutamic acid decarboxylase antibodies. Glutamic acid decarboxylase antibody–associated encephalitis occurs with high antibody titres and may cause cognitive dysfunction, seizures and psychiatric symptoms. However, glutamic acid decarboxylase antibodies are more frequently found in lower titre in association with other autoimmune disorders (such as diabetes mellitus type 1) and in healthy individuals. The utility of testing unselected populations of consumers with psychosis is unclear. The psychiatric manifestations of this disorder are also poorly described. Methods: First, systematic review of cohort and case–control studies that tested for IgG glutamic acid decarboxylase antibodies in psychiatric populations was conducted. Random-effects meta-analysis of odds ratio for antibody positivity in cases with psychosis and controls assessed prevalence. Second, literature review of all published cases and case series of glutamic acid decarboxylase antibody–associated limbic encephalitis was assessed for frequency and description of psychotic symptoms. Results: There were 17 studies, in which 2754 individuals with psychotic disorders were tested for glutamic acid decarboxylase IgG antibodies. Thirty-one consumers with psychosis (0.7%) had positive glutamic acid decarboxylase antibodies compared to 24 controls (1.0%), all at low titre and not fulfilling diagnostic criteria for autoimmune encephalitis. Meta-analysis found no significant difference in rates of glutamic acid decarboxylase antibody positivity (odds ratio = 1.8, 95% confidence interval: [0.90, 3.63]). Literature review found 321 cases of glutamic acid decarboxylase antibody–associated limbic encephalitis, with psychosis in 15 (4.3%) cases. Clinical screening would have identified all cases that presented to psychiatric services. Conclusion: Glutamic acid decarboxylase antibodies were uncommon in consumers with psychosis, with no significant difference in prevalence from controls and no cases of encephalitis identified. In cases with established glutamic acid decarboxylase antibody–associated limbic encephalitis, psychotic symptoms were uncommon and identifiable by clinical assessment. Targeted antibody testing guidelines should be further considered. [ABSTRACT FROM AUTHOR]

Published
2023
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13. sj-docx-1-anp-10.1177_00048674221089560 – Supplemental material for Anti-glutamic acid decarboxylase antibody screening in first-episode psychosis

Author

Warren, Nicola, Freier, Karen, Siskind, Dan, O’Gorman, Cullen, Blum, Stefan, Gillis, David, and Scott, James G

Subjects
FOS: Psychology, FOS: Clinical medicine, 170199 Psychology not elsewhere classified, 110319 Psychiatry (incl. Psychotherapy), Neuroscience
Abstract

Supplemental material, sj-docx-1-anp-10.1177_00048674221089560 for Anti-glutamic acid decarboxylase antibody screening in first-episode psychosis by Nicola Warren, Karen Freier, Dan Siskind, Cullen O’Gorman, Stefan Blum, David Gillis and James G Scott in Australian & New Zealand Journal of Psychiatry

Published
2022
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15. Response to treatment in NMOSD: the Australasian experience

Author

Clarke, Laura, primary, Bukhari, Wajih, additional, O'Gorman, Cullen M., additional, Khalilidehkordi, Elham, additional, Arnett, Simon, additional, Woodhall, Mark, additional, Prain, Kerri M., additional, Parratt, John D.E., additional, Barnett, Michael H., additional, Marriott, Mark P., additional, McCombe, Pamela A., additional, Sutton, Ian, additional, Boggild, Mike, additional, Brownlee, Wallace, additional, Carroll, William M., additional, Hodgkinson, Suzanne, additional, Macdonell, Richard A.L., additional, Mason, Deborah F., additional, Pereira, Jennifer, additional, Slee, Mark, additional, Das, Chandi, additional, Henderson, Andrew P.D., additional, Kermode, Allan G., additional, Lechner-Scott, Jeannette, additional, Waters, Patrick, additional, Sun, Jing, additional, and Broadley, Simon A., additional

Published
2022
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17. Bi-allelic loss-of-function OBSCN variants predispose individuals to severe recurrent rhabdomyolysis

Author

Cabrera-Serrano, Macarena, primary, Caccavelli, Laure, additional, Savarese, Marco, additional, Vihola, Anna, additional, Jokela, Manu, additional, Johari, Mridul, additional, Capiod, Thierry, additional, Madrange, Marine, additional, Bugiardini, Enrico, additional, Brady, Stefen, additional, Quinlivan, Rosaline, additional, Merve, Ashirwad, additional, Scalco, Renata, additional, Hilton-Jones, David, additional, Houlden, Henry, additional, Aydin, Halil Ibrahim, additional, Ceylaner, Serdar, additional, Drewes, Sarah, additional, Vockley, Jerry, additional, Taylor, Rhonda L, additional, Folland, Chiara, additional, Kelly, Aasta, additional, Goullee, Hayley, additional, Ylikallio, Emil, additional, Auranen, Mari, additional, Tyynismaa, Henna, additional, Udd, Bjarne, additional, Forrest, Alistair R R, additional, Davis, Mark R, additional, Bratkovic, Drago, additional, Manton, Nicholas, additional, Robertson, Thomas, additional, O’Gorman, Cullen, additional, McCombe, Pamela, additional, Laing, Nigel G, additional, Phillips, Liza, additional, de Lonlay, Pascale, additional, and Ravenscroft, Gianina, additional

Published
2021
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18. MRI Patterns Distinguish AQP4 Antibody Positive Neuromyelitis Optica Spectrum Disorder From Multiple Sclerosis

Author

Clarke, Laura, primary, Arnett, Simon, additional, Bukhari, Wajih, additional, Khalilidehkordi, Elham, additional, Jimenez Sanchez, Sofia, additional, O'Gorman, Cullen, additional, Sun, Jing, additional, Prain, Kerri M., additional, Woodhall, Mark, additional, Silvestrini, Roger, additional, Bundell, Christine S., additional, Abernethy, David A., additional, Bhuta, Sandeep, additional, Blum, Stefan, additional, Boggild, Mike, additional, Boundy, Karyn, additional, Brew, Bruce J., additional, Brownlee, Wallace, additional, Butzkueven, Helmut, additional, Carroll, William M., additional, Chen, Cella, additional, Coulthard, Alan, additional, Dale, Russell C., additional, Das, Chandi, additional, Fabis-Pedrini, Marzena J., additional, Gillis, David, additional, Hawke, Simon, additional, Heard, Robert, additional, Henderson, Andrew P. D., additional, Heshmat, Saman, additional, Hodgkinson, Suzanne, additional, Kilpatrick, Trevor J., additional, King, John, additional, Kneebone, Christopher, additional, Kornberg, Andrew J., additional, Lechner-Scott, Jeannette, additional, Lin, Ming-Wei, additional, Lynch, Christopher, additional, Macdonell, Richard A. L., additional, Mason, Deborah F., additional, McCombe, Pamela A., additional, Pereira, Jennifer, additional, Pollard, John D., additional, Ramanathan, Sudarshini, additional, Reddel, Stephen W., additional, Shaw, Cameron P., additional, Spies, Judith M., additional, Stankovich, James, additional, Sutton, Ian, additional, Vucic, Steve, additional, Walsh, Michael, additional, Wong, Richard C., additional, Yiu, Eppie M., additional, Barnett, Michael H., additional, Kermode, Allan G. K., additional, Marriott, Mark P., additional, Parratt, John D. E., additional, Slee, Mark, additional, Taylor, Bruce V., additional, Willoughby, Ernest, additional, Brilot, Fabienne, additional, Vincent, Angela, additional, Waters, Patrick, additional, and Broadley, Simon A., additional

Published
2021
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20. 077 Acute monoplegia

Author

Lefever, Kristen, primary, Eisemann, Jared, additional, Gore, Letitia, additional, Clarke, Laura, additional, O’Gorman, Cullen, additional, Swayne, Andrew, additional, and Schweitzer, Daniel, additional

Published
2021
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21. MRI Patterns Distinguish Neuromyelitis Optica Spectrum Disorder From Multiple Sclerosis (4128)

Author

Clarke, Laura, primary, Arnett, Simon, additional, Bukhari, Wajih, additional, Khalilidehkordi, Elham, additional, Sanchez, Sofia Jimenez, additional, O’Gorman, Cullen, additional, Prain, Kerri, additional, Woodhall, Mark, additional, Silvestrini, Roger, additional, Bundell, Christine, additional, Abernethy, David, additional, Bhuta, Sandeep, additional, Blum, Stefan, additional, Boggild, Mike, additional, Boundy, Karyn, additional, Brew, Bruce, additional, Brownlee, Wallace, additional, Butzkueven, Helmut, additional, Carroll, William, additional, Chen, Celia, additional, Coulthard, Alan, additional, Dale, Russell, additional, Das, Chandi, additional, Fabis-Pedrini, Marzena, additional, Fulcher, David, additional, Gillis, David, additional, Hawke, Simon, additional, Heard, Robert, additional, Henderson, Andrew, additional, Heshmat, Saman, additional, Hodgkinson, Suzanne, additional, Kilpatrick, Trevor, additional, King, John, additional, Kneebone, Christopher, additional, Kornberg, Andrew, additional, Lechner-Scott, Jeannette, additional, Lin, Ming-Wei, additional, Lynch, Christopher, additional, Macdonell, Richard, additional, Mason, Deborah, additional, McCombe, Pamela, additional, Pereira, Jennifer, additional, Pollard, John, additional, Ramanathan, Sudarshini, additional, Reddel, Stephen, additional, Shaw, Cameron, additional, Spies, Judith, additional, Stankovich, James, additional, Sutton, Ian, additional, Vucic, Steve, additional, Walsh, Michael, additional, Wong, Richard, additional, Yiu, Eppie, additional, Barnett, Michael, additional, Kermode, Allan, additional, Marriott, Mark, additional, Parratt, John, additional, Slee, Mark, additional, Taylor, Bruce, additional, Willoughby, Ernest, additional, Brilot, Fabienne, additional, Vincent, Angela, additional, Waters, Patrick, additional, and Broadley, Simon, additional

Published
2021
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24. An Australian State-Based Cohort Study of Autoimmune Encephalitis Cases Detailing Clinical Presentation, Investigation Results, and Response to Therapy

Author

Swayne, Andrew, primary, Warren, Nicola, additional, Prain, Kerri, additional, Gillis, David, additional, O'Gorman, Cullen, additional, Tsang, Benjamin K-T., additional, Muller, Claire, additional, Broadley, Simon, additional, Adam, Robert J., additional, McCombe, Pamela, additional, Wong, Richard C., additional, and Blum, Stefan, additional

Published
2021
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27. Relapse Patterns in NMOSD: Evidence for Earlier Occurrence of Optic Neuritis and Possible Seasonal Variation

Author

Khalilidehkordi, Elham, primary, Clarke, Laura, additional, Arnett, Simon, additional, Bukhari, Wajih, additional, Jimenez Sanchez, Sofia, additional, O'Gorman, Cullen, additional, Sun, Jing, additional, Prain, Kerri M., additional, Woodhall, Mark, additional, Silvestrini, Roger, additional, Bundell, Christine S., additional, Abernethy, David, additional, Bhuta, Sandeep, additional, Blum, Stefan, additional, Boggild, Mike, additional, Boundy, Karyn, additional, Brew, Bruce J., additional, Brown, Matthew, additional, Brownlee, Wallace, additional, Butzkueven, Helmut, additional, Carroll, William M., additional, Chen, Celia, additional, Coulthard, Alan, additional, Dale, Russell C., additional, Das, Chandi, additional, Fabis-Pedrini, Marzena J., additional, Fulcher, David, additional, Gillis, David, additional, Hawke, Simon, additional, Heard, Robert, additional, Henderson, Andrew P. D., additional, Heshmat, Saman, additional, Hodgkinson, Suzanne, additional, Kilpatrick, Trevor J., additional, King, John, additional, Kneebone, Chris, additional, Kornberg, Andrew J., additional, Lechner-Scott, Jeannette, additional, Lin, Ming-Wei, additional, Lynch, Christopher, additional, Macdonell, Richard A. L., additional, Mason, Deborah F., additional, McCombe, Pamela A., additional, Pereira, Jennifer, additional, Pollard, John D., additional, Ramanathan, Sudarshini, additional, Reddel, Stephen W., additional, Shaw, Cameron, additional, Spies, Judith, additional, Stankovich, James, additional, Sutton, Ian, additional, Vucic, Steve, additional, Walsh, Michael, additional, Wong, Richard C., additional, Yiu, Eppie M., additional, Barnett, Michael H., additional, Kermode, Allan G., additional, Marriott, Mark P., additional, Parratt, John, additional, Slee, Mark, additional, Taylor, Bruce V., additional, Willoughby, Ernest, additional, Brilot, Fabienne, additional, Vincent, Angela, additional, Waters, Patrick, additional, and Broadley, Simon A., additional

Published
2020
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31. Epidemiology of Multiple Sclerosis

Author

O'Gorman, Cullen

Subjects
Multiple sclerosis, Loss of oligodendrocytes, Demyelination of axons, Family recurrence, Segregation analysis, 3. Good health
Abstract

Multiple sclerosis (MS) is a chronic disabling disease of the central nervous system commonly affecting young adults. Pathologically, there are patches of inflammation (plaques) with demyelination of axons and associated loss of oligodendrocytes. Genome-wide association studies have identified over 105 loci of susceptibility, but the total number of possible contributory loci may be considerably higher. Family recurrence risks are available for several northern hemisphere countries, but there are few data for the southern hemisphere and regions at lower latitude such as Australia. The published family data could provide useful recurrence risks if appropriately analysed. Segregation analysis can be used to model the genetic architecture of MS. There is a global latitude gradient in MS prevalence, and the incidence of MS is increasing (particularly in females). These changes suggest a major role for environmental factors in the causation of disease. In the last 20 years there has been increasing evidence for the role of smoking in the aetiology of multiple sclerosis. Cigarette smoking is also associated with increased risk of developing the progressive form of MS. This risk factor has not previously been analysed in Queensland. Furthermore, cigarette smoking represents a possible cause of the changing prevalence of MS over time. Methods The family risks in Australia were measured in three regions at different latitudes. Immediate and extended family pedigrees were collected for three cohorts of MS patients in Queensland, Victoria and Tasmania. Age of onset data from Queensland were utilised to estimate age-adjusted recurrence rates. Meta-analysis of all available family recurrence risk data was performed to define risks to relatives. Standard methods of meta-analysis were combined with novel approaches to age adjustment to provide directly comparable estimates of lifetime risk. Segregation analysis was used to estimate the proportion of the overall genetic risk that can be attributed to identified susceptibility genes. To evaluate risks from smoking in Queensland, a large case-control study was performed, comparing risk of MS (by smoking habit) using regression modelling. The risk of developing progressive disease was measured in a cohort from an MS clinic in Queensland, followed from first clinic attendance until the onset of clinically determined progressive disease. Risk of progression was analysed with gender, age, age of onset, exposure to disease modifying therapy, and smoking status as covariates in a Cox proportional hazards analysis. Finally, a comprehensive meta-analysis was performed of eligible casecontrol and cohort studies that evaluated the risk of MS in smokers and exsmokers. The influence of study design, gender, latitude and year of study were explored with regression modelling. Results Recurrence risks in Australia were significantly lower than in studies from northern hemisphere populations. The age-adjusted risk for siblings across Australia was 2.1% compared with 3.5% for the northern hemisphere. A similar pattern was seen for other relatives. The risks to relatives were proportional to the population risks for each site, and hence the relative risk for siblings (lS) was similar across all sites. From the meta-analysis of family recurrence risks, the overall recurrence risk for monozygotic twins was 18.2% and for siblings 2.7%. The recurrence risk for dizygotic twins was significantly higher than for siblings. The overall estimate of sibling relative risk (lS) was 16.8. Risks for older relatives (parents, siblings, aunts, uncles and cousins) show a latitudinal gradient, in line with population risk. No latitudinal gradient for lS was seen. Segregation analysis supports a multiplicative model of one locus of moderate effect with many loci of small effect. The estimated contribution of the known MS loci is 18–24% of lS. The case-control study in Queensland confirmed an association between increased risk of MS and smoking. The overall adjusted odds ratio was 1.9 (95% confidence interval, CI 1.5–2.5) for ever smokers. There was no statistically significant difference in the risks for males and females. In the progression study, there were significantly higher risks of secondary progressive disease in males (Hazard Ratio, HR 1.83, 95% CI 1.3–2.7) and in ever smokers (HR 1.4, 95% CI 1.0–2.0). Progressive disease occurred approximately 4 years earlier in ever smokers. Smoking did not affect age of onset of primary progressive disease. The meta-analysis of smoking risk included 26 studies representing 8615 cases and 392,352 controls and an additional 792 cases included from a total cohort population of 601,492 individuals, representing more than 9 million person-years. There was a consistent association between smoking and MS with an odds ratio of approximately 1.5, with males at higher risk. This finding was independent of study design. However, latitude and year of study may have unexpected influence. Smoking appeared to confer a greater risk to females living closer to the equator than to females at higher latitudes. Additionally, the effect of cigarette smoke exposure on MS risk may not be fixed over time, but could be increasing. Discussion The familial recurrence risk of MS in Australia is lower than in previously reported studies. This is directly related to the lower population prevalence of MS. The overall genetic susceptibility in Australia as measured by the lS is similar to that seen in the northern hemisphere, suggesting that the difference in population risk is explained largely by environmental factors rather than by genetic admixture. The meta-analysis of family data supports the notion of MS risk being derived from multiple susceptibility genes and environmental factors. Genetic susceptibility appears to be independent of latitude, and the latitudinal gradient of MS prevalence is likely due to environmental factors. The results of the case-control study in Queensland replicate existing work that has shown cigarette smoking increases the risk of MS. Cigarette smoking represents an important modifiable risk factor for the development of MS. Cigarette smoking was also associated with earlier onset of progressive disease in the large clinical cohort studied in Queensland. For patients with relapsing-remitting disease, smoking cessation should be encouraged. The results of the meta-analysis of smoking studies suggest a threshold model of MS risk that includes a fairly constant genetic risk (for Caucasian populations) together with variable environmental risks which are dominated by vitamin D deficiency at higher latitudes and are more significant in women who have an intrinsically lower threshold for development of disease.

Published
2018
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33. Psychiatric management of anti-NMDAR encephalitis: a cohort analysis.

Author

Warren, Nicola, O'Gorman, Cullen, McKeon, Gemma, Swayne, Andrew, Blum, Stefan, and Siskind, Dan

Subjects
*ACQUISITION of data methodology, *RETROSPECTIVE studies, *TREATMENT effectiveness, *ANTI-NMDA receptor encephalitis, *MEDICAL records, *IMMUNOLOGICAL adjuvants, *ADVERSE health care events, *CEREBROSPINAL fluid, *PSYCHIATRIC treatment, *IMMUNOTHERAPY, *LONGITUDINAL method, *ANTIPSYCHOTIC agents
Abstract

Background: Anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis is an immune-mediated disorder which requires multi-disciplinary treatment including immunomodulation therapy. First presentation is most commonly to psychiatric services and continuing psychiatric care is required to treat disabling symptoms, such as behaviour disturbance, psychosis and catatonia. There is minimal available evidence to guide symptomatic treatment and concern for increased sensitivity to antipsychotics complicates traditional approaches. Methods: All cases of cerebrospinal fluid positive anti-NMDAR encephalitis tested in Queensland, Australia were identified. Demographic, clinical and therapeutic data were collected and reviewed by two independent clinicians. Pre-specified variables reflecting possible treatment side effects were compared. Results: The majority of the 30 cases (83%) had early psychiatric symptoms and were treated with antipsychotics (67%), average daily olanzapine equivalence dose of 11.5 mg, prior to immunomodulation therapy. Although there was an 88% reduction in cases with aggression, there was little improvement in psychosis, affective symptoms or catatonia with antipsychotics alone. In the cases with psychiatric symptoms, there was no significant difference in the rate of occurrence of neurological and autonomic symptoms between cases prescribed and not prescribed antipsychotics. Conclusions: Psychiatric input is imperative for both acute and longer-term management of anti-NMDAR encephalitis. Primary symptomatic treatment should remain immunotherapy and surgery. Antipsychotic medications have particular value in managing agitation and aggression. Potential side effects from antipsychotic treatment are difficult to differentiate from progression of anti-NMDAR encephalitis but there was no evidence in this cohort of increased antipsychotic sensitivity. Treatment with psychotropic medication should be individualised and adjusted during the course of the illness. [ABSTRACT FROM AUTHOR]

Published
2021
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37. 058 ANTI-CASPR2-ANTIBODY associated encephalitis in a 63-year old male with chronic lymphocytic leukaemia

Author

Lilley, Kate, primary, Swayne, Andrew, additional, Watson, Emily, additional, Kee, Rachel, additional, Wong, David, additional, Lehn, Alexander, additional, Brown, Helen, additional, O’Gorman, Cullen, additional, Sheikh, Nabeel, additional, Bird, Robert, additional, Prain, Kerri, additional, Gillis, David, additional, Wong, Richard C, additional, and Blum, Stefan, additional

Published
2018
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42. Incidence and prevalence of NMOSD in Australia and New Zealand

Author

Bukhari, Wajih, primary, Prain, Kerri M, additional, Waters, Patrick, additional, Woodhall, Mark, additional, O‘Gorman, Cullen M, additional, Clarke, Laura, additional, Silvestrini, Roger A, additional, Bundell, Christine S, additional, Abernethy, David, additional, Bhuta, Sandeep, additional, Blum, Stefan, additional, Boggild, Mike, additional, Boundy, Karyn, additional, Brew, Bruce J, additional, Brown, Matthew, additional, Brownlee, Wallace J, additional, Butzkueven, Helmut, additional, Carroll, William M, additional, Chen, Celia, additional, Coulthard, Alan, additional, Dale, Russell C, additional, Das, Chandi, additional, Dear, Keith, additional, Fabis-Pedrini, Marzena J, additional, Fulcher, David, additional, Gillis, David, additional, Hawke, Simon, additional, Heard, Robert, additional, Henderson, Andrew P D, additional, Heshmat, Saman, additional, Hodgkinson, Suzanne, additional, Jimenez-Sanchez, Sofia, additional, Killpatrick, Trevor, additional, King, John, additional, Kneebone, Christopher, additional, Kornberg, Andrew J, additional, Lechner-Scott, Jeannette, additional, Lin, Ming-Wei, additional, Lynch, Christpher, additional, Macdonell, Richard, additional, Mason, Deborah F, additional, McCombe, Pamela A, additional, Pender, Michael P, additional, Pereira, Jennifer A, additional, Pollard, John D, additional, Reddel, Stephen W, additional, Shaw, Cameron, additional, Spies, Judith, additional, Stankovich, James, additional, Sutton, Ian, additional, Vucic, Steve, additional, Walsh, Michael, additional, Wong, Richard C, additional, Yiu, Eppie M, additional, Barnett, Michael H, additional, Kermode, Allan G, additional, Marriott, Mark P, additional, Parratt, John D E, additional, Slee, Mark, additional, Taylor, Bruce V, additional, Willoughby, Ernest, additional, Wilson, Robert J, additional, Vincent, Angela, additional, and Broadley, Simon A, additional

Published
2017
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47. A case of immune-mediated encephalitis related to daclizumab therapy.

Author

Devlin, Michael, Swayne, Andrew, Newman, Martin, O'Gorman, Cullen, Brown, Helen, Ong, Benjamin, Robertson, Thomas, Airey, Caroline, and Blum, Stefan

Subjects
ENCEPHALITIS, CENTRAL nervous system, CEREBROSPINAL fluid, MULTIPLE sclerosis, MONOCLONAL antibodies
Abstract

This report will detail a case of immune-mediated encephalitis in the context of daclizumab therapy. Daclizumab is a humanised monoclonal antibody which, prior to its recent worldwide withdrawal due to safety concerns, was utilised as a disease-modifying therapy in relapsing-remitting multiple sclerosis. The withdrawal of this therapy was prompted by concerns over 12 cases of serious immune-mediated adverse reactions in the central nervous system. We report an additional case, including clinical data and results of neuroimaging, cerebrospinal fluid (CSF) examination and brain biopsy. [ABSTRACT FROM AUTHOR]

Published
2019
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48. Status epilepticus from GABABR antibody positive encephalitis due to de novo mixed small cell and adenocarcinoma of the prostate.

Author

Kwan, Christopher, Sia, Aaron, and O’Gorman, Cullen

Abstract

We present a case study of a 67-year-old man who presented with a new onset of recurrent tonic-clonic seizures. He had tested positive to gamma-aminobutyric acid B receptor antibodies in his blood and cerebrospinal fluid, and subsequent CT imaging and transrectal biopsy confirmed the presence of a locally advanced mixed small cell and Gleason 9 adenocarcinoma of the prostate. His seizures remained resistant to treatment with multiple antiepileptic drugs, including sodium valproate, clobazam, topiramate, carbamazepine, phenytoin and lacosamide. He progressed to status epilepticus, which required intravenous immunoglobulin and steroids, followed by plasma exchange 1 week later. The status epilepticus was refractory and required multiple admissions to the intensive care unit. [ABSTRACT FROM AUTHOR]

Published
2020
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50. A tardy tongue palsy

Author

O'Gorman, Cullen M., primary, Lindell, E. Paul, additional, Van Gompel, Jamie J., additional, and Klaas, James P., additional

Published
2015
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