Publications by authors named "Aaron de Souza"

25 Publications

  • Page 1 of 1

AstraZeneca COVID-19 vaccine and Guillain- Barré Syndrome in Tasmania: A causal link?

J Neuroimmunol 2021 11 17;360:577719. Epub 2021 Sep 17.

Department of Neurology, Launceston General Hospital, Tasmania, Australia; Faculty of Medicine, University of Tasmania, Launceston, Tasmania, Australia.

The emergence of the coronavirus 2019 (COVID-19) pandemic has presented an unprecedented global challenge. Vaccines against COVID have been developed to date. Covid-19 has been linked with the development of Guillain-Barre Syndrome (GBS), a rare immune-mediated demyelinating neuropathy. We report three cases of Guillain-Barre Syndrome and one case of Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), presenting to a Tasmanian hospital, and review 15 other reported cases and discuss likely immunopathology. Nearly all reported cases of post-COVID-19 vacciation inflammatory demyelinating polyneuropathy are linked to AstraZeneca vaccination and a variant with bifacial weakness is the most reported form of GBS globally.
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http://dx.doi.org/10.1016/j.jneuroim.2021.577719DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8447540PMC
November 2021

New-onset tic disorder following circumscribed brain injury.

Authors:
Aaron de Souza

J Clin Neurosci 2020 May 13;75:234-239. Epub 2020 Mar 13.

Department of Medicine, Launceston General Hospital, 274-280 Charles Street, Launceston, TAS 7250, Australia. Electronic address:

Adult-onset tics represent either a secondary tic disorder ("tourettism") or a late presentation of childhood tics, which may have been previously unrecognised. Head trauma has been recognised as an infrequent cause of adult-onset tic disorder, which exhibits variable temporal relationship to the inciting injury and response to therapy. We present a patient who presented with late-onset tics seven years after a circumscribed brain injury, responding well to antidopaminergic treatment. A review of all the previously reported cases of post-traumatic tic disorder is provided. Our patient is unusual in that the injury presumed to be responsible for the development of tics was of a very focal nature, akin to previously described tic disorder following vascular insults. We discuss the rare occurrence of tourettism after such focal brain lesions and analyse the insights this provides into the anatomical substrates underlying tic disorders.
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http://dx.doi.org/10.1016/j.jocn.2020.03.009DOI Listing
May 2020

Myotonic Dystrophy Type 1 Complicated by Colonic Obstruction Due to a Bezoar.

Ann Indian Acad Neurol 2019 Oct-Dec;22(4):520-523. Epub 2019 Oct 25.

Department of Medicine, Royal Cornwall Hospitals NHS Trust, Treliske, Truro, UK.

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http://dx.doi.org/10.4103/aian.AIAN_529_18DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6839307PMC
October 2019

Parkinsonism and Tremor Complicating Long-term Cinitapride Use.

Ann Indian Acad Neurol 2017 Oct-Dec;20(4):435-436

NeuroCare, Pereira Plaza, Margao - Goa, India.

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http://dx.doi.org/10.4103/aian.AIAN_225_17DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5682757PMC
November 2017

Delayed-onset Reversible Cortical Blindness after Resuscitation from Cardiac Arrest.

J Neurosci Rural Pract 2017 Aug;8(Suppl 1):S133-S135

Department of Neurology, Goa Medical College, Bambolim, Goa, India.

We present a patient who presented with cortical blindness (CB) 1 week after repeated cardiac arrest while undergoing treatment for an acute myocardial infarction. He had been revived within 5 min in each instance and was apparently neurologically normal until presentation. Magnetic resonance imaging showed subtle hyperintensities on fluid-attenuated inversion recovery and diffusion-weighted imaging in both temporooccipital cortices. A rapid recovery over the next 2 weeks was remarkable for the appearance of metamorphopsia. CB may present even days to weeks after hypoxic-ischemic encephalopathy following cardiac arrest, even in patients apparently without immediate neurological sequelae. The pathogenesis of this phenomenon remains to be fully elucidated, but is likely to be due to delayed effects of anoxia on the occipital cortex and may be analogous to the previously described syndrome of delayed posthypoxic leukoencephalopathy. Prognosis for visual recovery appears to be good.
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http://dx.doi.org/10.4103/jnrp.jnrp_63_17DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5602241PMC
August 2017

Choreiform dyskinesias following levodopa treatment of parkinsonism due to osmotic demyelination syndrome.

Parkinsonism Relat Disord 2017 10 12;43:120-121. Epub 2017 Jul 12.

NeuroCare, Pereira Plaza, Margao, Goa 403601, India.

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http://dx.doi.org/10.1016/j.parkreldis.2017.07.008DOI Listing
October 2017

Chronic asymmetric tremor and levodopa-responsive parkinsonism due to a vein of Galen aneurysmal malformation.

Parkinsonism Relat Disord 2017 10 12;43:122-123. Epub 2017 Jul 12.

Department of Neurology, Goa Medical College, Bambolim, Goa 403202, India.

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http://dx.doi.org/10.1016/j.parkreldis.2017.07.007DOI Listing
October 2017

T2 relaxometry helps prognosticate seizure outcome in patients with solitary cerebral cysticercosis.

J Neurol Sci 2017 May 27;376:1-6. Epub 2017 Feb 27.

Department of Biostatistics, National Institute of Mental Health and NeuroSciences, Bangalore 560 029, India.

Objective: Correlate serial T2 relaxometry (T2R) values with long term seizure outcome in patients with solitary cerebral cysticercosis (SCC) in order to establish its usefulness as a prognostic marker in these patients.

Methods: Patients with new-onset seizures due to SCC were imaged serially using a pre-determined MRI protocol at enrolment and after 3, 6, 12 and 24months. T2 relaxometry was performed using a dual echo sequence with maps generated manually from the measured image intensities at the level of the lesion. Patients were randomised to receive albendazole plus antiepileptic drugs, or only antiepileptic treatment ("controls"). At each visit, as well as four years after study initiation, patients were reviewed for seizure recurrence. Clinical and radiological outcomes were assessed by physicians blinded to treatment received.

Results: Of 123 patients recruited, 77 had at least four MRIs and >12month follow-up, and were included for analysis. Baseline clinical and demographic parameters as well as antiepileptic treatment were similar between albendazole and control groups. T2 values from the lesion were higher than normal parenchyma initially, and fell to approach normal over six months. Controls had higher T2 values from the lesion centre and wall at six months than those who received albendazole. However no difference was seen in T2 values from perilesional parenchyma between treatment and control groups, indicating lack of modulation of the development of perilesional gliosis by albendazole therapy. Patients with seizures persisting >6months after enrolment had higher perilesional T2 values than those who were seizure-free. A rise in perilesional T2 value at 12months is probably due to gliosis. A later stage of degeneration was associated with a reduced likelihood of seizure relapse.

Significance: T2 relaxometry at three and six months after seizure onset can identify patients likely to have seizures beyond six months after onset. Persistently abnormal T2 values in patients with poorer outcomes reflect the development of perilesional gliosis.
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http://dx.doi.org/10.1016/j.jns.2017.02.052DOI Listing
May 2017

Acute multifocal neuropathy following cocaine inhalation.

J Clin Neurosci 2017 Feb 1;36:134-136. Epub 2016 Nov 1.

NeuroCare, Pereira Plaza, Margao, Goa 403 601, India.

Introduction: We report a young man, not a habitual cocaine user, who developed an acute multifocal neuropathy following a second exposure to inhaled cocaine.

Methods: Case report.

Results: Clinical and electrophysiological findings suggested an acute multiple mononeuropathy following cocaine exposure. Imaging of the shoulder and pelvic girdles revealed multifocal denervation in selected proximal muscles. The patient was empirically treated with intravenous steroids to good effect.

Discussion: Cocaine use, although usually affecting the central nervous system, does produce peripheral nerve disease in rare instances. This unusual pattern of neurological involvement needs to be differentiated from the more common symptoms resulting from affection of the brain.
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http://dx.doi.org/10.1016/j.jocn.2016.10.015DOI Listing
February 2017

Nerve conduction studies in diabetics presymptomatic and symptomatic for diabetic polyneuropathy.

J Diabetes Complications 2015 Aug 21;29(6):811-7. Epub 2015 May 21.

Department of Physiology, Goa Medical College, Bambolim, Goa, 403202, India.

Objective: We performed nerve conduction studies (NCS) on diabetics with and without symptoms of diabetic polyneuropathy (DPN) and evaluated correlations with glycaemic control and clinical features.

Methods: Consecutive patients were recruited in three groups: "normals" (nondiabetics without peripheral nerve disease); "presymptomatic diabetics" (diabetes without DPN); and "symptomatic diabetics". Clinical questionnaire and neurological examination were administered, and NCS were performed using standard techniques.

Results: 153 patients were recruited (51 normals, 50 presymptomatic diabetics, 52 symptomatic). Glycosylated haemoglobin and duration of DM were higher in symptomatic diabetics, with symptoms present for 1-60 months (mean 14.5). Alterations in NCS included prolonged latencies, lowered amplitudes and slowed conduction velocities, following a pattern of initially reduced sensory amplitudes and slowed motor velocities, with later reduced motor and sensory amplitudes and prolonged motor latencies. Neuropathic pain, clinical signs and glycosylated haemoglobin correlated with these changes.

Conclusions: Even in asymptomatic patients, NCS show diffuse changes, in a predictable pattern. Electrophysiological parameters correlate with neuropathic pain, physical findings and glycosylated haemoglobin levels.

Significance: We demonstrate that NCS changes in DPN follow a predictable pattern, correlating with clinical features and long-term glycaemic control.
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http://dx.doi.org/10.1016/j.jdiacomp.2015.05.009DOI Listing
August 2015

Quantitative serial T2 relaxometry: a prospective evaluation in solitary cerebral cysticercosis.

Neuroradiol J 2014 Jun 17;27(3):339-49. Epub 2014 Jun 17.

Department of Biostatistics, National Institute of Mental Health and Neurosciences; Bangalore, India.

We describe the evolution of quantitative T2 relaxometry values on serial MRI in patients with a solitary cerebral cysticercal lesion (SCCL), and determine whether albendazole therapy affects T2 relaxation (T2R) values. Patients with new-onset seizures and MRI-confirmed SCCL were randomized to treatment with albendazole and antiepileptics ("treatment group") or antiepileptics only ("controls"). Serial MRI including T2 relaxometry was performed at baseline, three, six, 12, and 24 months. Of 123 patients recruited, 81 had more than three MRI scans (treatment group: 37; controls: 44; 58 patients had five scans). The lesion wall at baseline showed a mean T2R value of 152.3 ms, centre 474.9 and perilesional parenchyma 338.5 ms. These were significantly higher than those from normal parenchyma (114 ms). Over time, most sharply in the initial three months, T2R values fell but even at 24 months, they remained above those from normal parenchyma. A slight increase in T2R values from the lesion centre at six months was thought to represent the initiation of gliosis. In the treatment group, T2R values approached normal at 24 months, while controls had persistently higher T2R values. The decline in T2R values at six months was more prominent in the treatment group. T2R values at baseline and at three months differed significantly depending on the stage of the lesion, being higher in stage 2 SCCL. T2R values from SCCL declined over 24 months, being significantly higher in earlier stages of degeneration. A mild increase after six months may be due to the initiation of gliosis. T2R values appear to decline faster in patients who receive albendazole.
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http://dx.doi.org/10.15274/NRJ-2014-10054DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4202884PMC
June 2014

Involuntary movements due to vitamin B12 deficiency.

Neurol Res 2014 Dec 22;36(12):1121-8. Epub 2014 May 22.

Deficiency of vitamin B12 produces protean effects on the nervous system, most commonly neuropathy, myelopathy, cognitive and behavioural symptoms, and optic atrophy. Involuntary movements comprise a relatively rare manifestation of this readily treatable disorder. Both adults and infants deficient in vitamin B12 may present with chorea, tremor, myoclonus, Parkinsonism, dystonia, or a combination of these, which may precede diagnosis or become apparent only a few days after parenteral replacement therapy has begun. The pathogenesis of these movement disorders shows interesting parallels to certain neurodegenerative conditions. The clinical syndrome responds well to vitamin B12 supplementation in most cases, and an early diagnosis is essential to reverse the haematological and neurological dysfunction characteristic of this disorder. In this article, we elucidate the association of vitamin B12 deficiency with movement disorders in adults and in infants, discuss the pathogenesis of this association, review previously reported cases, and present a young adult male with severe generalized chorea that showed a salutary response to vitamin B12 supplementation.
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http://dx.doi.org/10.1179/1743132814Y.0000000396DOI Listing
December 2014

Survival from rabies encephalitis.

J Neurol Sci 2014 Apr 20;339(1-2):8-14. Epub 2014 Feb 20.

Department of Neurovirology, National Institute of Mental Health and Neuro Sciences, Bangalore 560029, India.

Rabies is a major public health problem in Asia and Africa, with nearly 60,000 deaths every year, and represents a substantial economic burden. Neurologists frequently encounter atypical cases, and need to make informed decisions regarding diagnosis and management. No therapy has been shown to unequivocally improve survival in rabies till date. Despite the overwhelmingly fatal nature of this disease, a small number of patients have been reported to survive acute rabies encephalitis with varying degrees of neurological sequelae. This paper presents the eleventh documented case of survival from rabies, which developed after being bitten by a stray dog, albeit with severe neurological residua. Similar to patients in previous reports, this man demonstrated a robust immune response as indicated by peripheral viral clearance and very high serum and cerebrospinal fluid antibody titres. Immunologically-mediated virus clearance therefore appears to be a prerequisite for survival. A detailed review of previously reported survivors, as well as descriptions of the host response and viral clearance in human rabies, current therapy for this disease and future directions in improving the currently dismal prognosis are provided.
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http://dx.doi.org/10.1016/j.jns.2014.02.013DOI Listing
April 2014

Solitary cerebral parenchymal cysticercosis: a prospective comparative study with computed tomography and magnetic resonance imaging.

Neurol India 2013 Nov-Dec;61(6):639-43

Department of Neurology, National Institute of Mental Health and Neuro Sciences, Bangalore, Karnataka, India.

Aim: To present a prospective series of 86 patients with solitary cerebral cysticerci who underwent both contrast computed tomography (CT) and contrast magnetic resonance imaging (MRI), and to correlate and compare the imaging findings using these two modalities.

Materials And Methods: Lesion characteristics, staging of the cyst and perilesional hypodensity on CT and hyperintensity on MRI were analyzed, and the lesion was described with regard to the appearance of the scolex, cyst fluid, cyst wall and the perilesional area.

Results: Patients were largely children and adolescents (mean age 17.4 years, range 6-52) with 52.3% males. MRI was performed, on average, 10.7 days after CT. MRI was more sensitive than plain CT scan in detecting cysticercal lesions (P = 0.003), but there was no statistically significant difference between contrast CT and MRI. None of the patients were detected with an alternative disease on serial MRI. No cyst showed significant mass effect. Non-contrast CT was less sensitive than either contrast CT or MRI in detecting the scolex (P = 0.011), but no difference was seen between the latter two modalities. Qualitative imaging characteristics of the cysticercus on MRI and CT scan are described. All cysts were round in shape, with an average diameter of <10 mm, and maximum diameter of 19 mm.

Conclusion: In the present prospective series, contrast CT was nearly as sensitive as MRI in detecting solitary cerebral cysticerci. Thus, in highly resource-limited settings contrast CT may be sufficient for the diagnosis and management of neurocysticercosis.
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http://dx.doi.org/10.4103/0028-3886.125272DOI Listing
March 2014

The neurological effects of methyl bromide intoxication.

J Neurol Sci 2013 Dec 20;335(1-2):36-41. Epub 2013 Sep 20.

Department of Neurology, Goa Medical College, Bambolim, Goa 403 202 India. Electronic address:

Used primarily as a fumigant or as a substrate in chemical processes, methyl bromide is a highly toxic gas. The gas is usually absorbed by inhalation and effects on the lungs, gastrointestinal tract, skin, and brain are seen. Numerous instances of acute and chronic neurologic injury have been reported: acute poisoning results in seizures, myoclonus, ataxia or cerebral oedema beginning as early as 30 min after exposure while subacute or chronic intoxication presents with diverse slowly progressive neurological and neurobehavioral symptoms. Serum bromide levels may be elevated, but often return rapidly to normal. Electroencephalography may show frontally-predominant slow waves or polyspikes with following slow wave, and MRI reveals characteristic involvement in the dentate nucleus of the cerebellum, the brainstem, and the splenium of the corpus callosum. Symmetric and selective lesions in characteristic sites are observed on imaging and on histopathological examination. These are likely produced by methylation of intracellular lipids, protein and glutathione; production of toxic metabolites; defective neurotransmitter function; and abnormal oxidative phosphorylation. This article reviews the toxic effects of this gas, the pathophysiology and symptoms of its effects on the nervous system, and characteristic findings on MRI; and presents an illustrative case of methyl bromide intoxication due to exposure at a factory producing the compound commercially.
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http://dx.doi.org/10.1016/j.jns.2013.09.022DOI Listing
December 2013

Movement disorders and the osmotic demyelination syndrome.

Authors:
Aaron de Souza

Parkinsonism Relat Disord 2013 Aug 7;19(8):709-16. Epub 2013 May 7.

Department of Neurology, Goa Medical College, Bambolim, Goa 403 202, India.

With the advent of MRI, osmotic demyelination syndromes (ODS) are increasingly recognised to affect varied sites in the brain in addition to the classical central pontine lesion. Striatal involvement is seen in a large proportion of cases and results in a wide variety of movement disorders. Movement disorders and cognitive problems resulting from ODS affecting the basal ganglia may occur early in the course of the illness, or may present as delayed manifestations after the patient survives the acute phase. Such delayed symptoms may evolve over time, and may even progress despite treatment. Improved survival of patients in the last few decades due to better intensive care has led to an increase in the incidence of such delayed manifestations of ODS. While the outcome of ODS is not as dismal as hitherto believed - with the acute akinetic-rigid syndrome associated with striatal myelinolysis often responding to dopaminergic therapy - the delayed symptoms often prove refractory to medical therapy. This article presents a review of the epidemiology, pathophysiology, clinical features, imaging, and therapy of movement disorders associated with involvement of the basal ganglia in ODS. A comprehensive review of 54 previously published cases of movement disorders due to ODS, and a video recording depicting the spectrum of delayed movement disorders seen after recovery from ODS are also presented.
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http://dx.doi.org/10.1016/j.parkreldis.2013.04.005DOI Listing
August 2013

Adult lead encephalopathy.

Neurol Res 2013 Jan;35(1):54-8

Department of Neurology, Goa Medical College, Bambolim, Goa, India.

The neurotoxicity of lead to the adult brain is less well-known than that seen in children. It may present as acute severe encephalopathy or as chronic cognitive and behavioural symptoms, either in isolation or with systemic features of lead intoxication. Magnetic resonance imaging findings in lead encephalopathy vary. The pathogenesis of lead encephalopathy and its effects on cognition both during development and in the adult are discussed. That encephalopathic symptoms do not correlate with blood lead levels and that they may persist after chelation are highlighted. As an illustration, we describe a patient with chronic cumulative lead intoxication, who presented with peripheral neuropathy, anaemia, and a 'lead line' on the gingiva. She had cognitive dysfunction with extensive subcortical and cerebellar white matter lesions on magnetic resonance imaging. An area of restricted diffusion in both frontal regions is likely to be due to active ongoing demyelinating at the 'leading edge' of the lesion. Although systemic features and the peripheral neuropathy improved with chelation, the encephalopathy showed only marginal change, with later appearance of a symmetric akinetic-rigid state.
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http://dx.doi.org/10.1179/1743132812Y.0000000115DOI Listing
January 2013

Delayed chorea after recovery from a symmetric parkinsonian syndrome due to striatal myelinolysis.

J Clin Neurosci 2012 Aug 7;19(8):1165-7. Epub 2012 Jun 7.

Department of Neurology, Goa Medical College, Bambolim, Goa 403 202, India.

Extrapontine myelinolysis (EPM) is rare and usually results from osmotic stress due to inappropriate correction of electrolyte disturbances. Parkinsonism is a relatively common manifestation of EPM, seen in 60% of patients. Dopaminergic therapy leads to good recovery in many patients. Delayed extrapyramidal manifestations, including hyperkinetic movement disorders such as chorea or dystonia, are postulated to result from aberrant neuronal regeneration or denervation supersensitivity following the initial osmotic insult. We present a patient with a symmetric parkinsonian syndrome due to EPM involving the striatum who made a good recovery with levodopa therapy, only to develop chorea five months later. The possible mechanisms underlying the genesis of these movement disorders in EPM is discussed.
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http://dx.doi.org/10.1016/j.jocn.2011.11.024DOI Listing
August 2012

More often striatal myelinolysis than pontine? A consecutive series of patients with osmotic demyelination syndrome.

Neurol Res 2012 Apr 5;34(3):262-71. Epub 2012 Mar 5.

Department of Neurology, Goa Medical College, India.

Introduction: Osmotic demyelination syndrome (ODS) is increasingly recognized to involve extrapontine locations in addition to the better-known central pontine myelinolysis.

Aims: This study describes clinical and radiological features of consecutive patients with ODS detected over 1 year.

Methods: Patients fulfilling clinical and radiological criteria for ODS were prospectively enrolled and were followed with serial assessments during hospital stay and up to 253 days after discharge.

Results: Eight patients (five females) aged 24-89 years were enrolled, comprising 0·06% of all admissions to the general medical and neurology services. All had preceding hyponatraemia and hypokalaemia of various aetiologies. One patient developed ODS after postpartum pituitary haemorrhage, which has been reported only rarely. Sodium levels were corrected at maximal rates exceeding 8 mmol/l/day. Neurological symptoms attributed to ODS began 3-15 days after clinical improvement following sodium correction in four patients; the remainder did not show any intervening lucent interval. Fifty per cent were stuporous at admission, 50% had seizures, 62·5% had symmetric parkinsonism, and 75% had prominent primitive reflexes. Stretch reflexes were absent in 25% and normal or brisk in the remainder. Magnetic resonance imaging (MRI) showed symmetric striatal lesions in all patients, with concomitant pontine involvement in only 25%. Four patients had poor outcomes (modified Rankin score >3), with prognosis dependent on the presence of severe systemic illness, liver dysfunction, encephalopathy, seizures, and degree of disability upon discharge from hospital. Patients with parkinsonism responded to dopaminergic therapy, with chorea, dystonia, and depression as later developments. This series is remarkable for the high incidence of extrapontine lesions, much more common than pontine involvement.
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http://dx.doi.org/10.1179/1743132812Y.0000000009DOI Listing
April 2012

Perilesional gliosis around solitary cerebral parenchymal cysticerci and long-term seizure outcome: a prospective study using serial magnetization transfer imaging.

Epilepsia 2011 Oct 21;52(10):1918-27. Epub 2011 Jul 21.

Department of Neurology, National Institute of Mental Health and NeuroSciences, Bangalore, India.

Purpose: Epilepsy following solitary cerebral cysticercosis (SCC) is possibly caused by perilesional gliosis, best visualized on magnetization transfer imaging (MTI).This study aims to describe development of gliosis around SCC by prospective serial MTI and to correlate this gliosis with long-term seizure outcome.

Methods: We randomized 123 patients with SCC and new-onset seizures to treatment with albendazole plus antiepileptics (treatment), or antiepileptics only (control), and performed magnetic resonance imaging (MRI) scans at 0, 3, 6, 12, and 24 months. Prospective follow-up data regarding seizure outcome up to 5 years later were collected. MRI studies were analyzed for lesion characteristics and perilesional magnetization transfer (MT) hyperintensity.

Key Findings: Clinical and radiologic data of 77 patients were analyzed. Demographic and seizure characteristics were similar in treatment and control groups. Clinical data were available up to 64 months after enrollment. At 12 months, 89.5% patients were seizure-free. MTI is more sensitive than routine imaging for detection of perilesional gliosis. Albendazole treatment did not affect imaging or clinical outcome, including development of gliosis. Independent of duration of follow-up, gliosis was associated with more seizures, and with seizure recurrence at 12 months; duration of seizures and antiepileptic therapy was longer. Gliosis was not dependent on seizure type or stage of degeneration at enrollment or persistence/calcification of the lesion.

Significance: Perilesional gliosis around SCC helps prognosticate seizure outcome. Poorer outcome in patients with persistent lesions is likely to be related to mechanisms other than gliosis. The lack of effect of albendazole on seizure outcome may be due to its inability to decrease formation of gliosis.
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http://dx.doi.org/10.1111/j.1528-1167.2011.03189.xDOI Listing
October 2011

Akinetic-rigid syndrome due to extrapontine and pontine myelinolysis following appropriate correction of hyponatraemia.

Authors:
Aaron de Souza

J Clin Neurosci 2011 Apr 26;18(4):587-9. Epub 2011 Jan 26.

Department of Neurology, Goa Medical College, Bambolim, Goa 403 202, India.

Extrapontine myelinolysis in association with the more common central pontine variety is increasingly reported. Although typically associated with rapid correction of hyponatraemia, myelinolysis is also seen when sodium correction occurs at recommended rates. We present a 60-year-old man who developed hyponatraemia and hypokalaemia due to repeated vomiting. An acute symmetric akinetic-rigid syndrome followed correction of hyponatraemia, performed in line with current guidelines. There were no clinical features of pontine involvement even though a typical lesion was seen on MRI. Bilateral putaminal and caudate lesions were seen. He recovered well with only symptomatic treatment. Myelinolysis can present with features of extrapontine involvement with the pontine lesions remaining asymptomatic. Current guidelines for the correction of hyponatraemia do not prevent development of myelinolysis in all instances. In contrast to the generally expected poor outcome in this condition, patients do make a good recovery with symptomatic treatment and good nursing care.
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http://dx.doi.org/10.1016/j.jocn.2010.08.001DOI Listing
April 2011

Bilateral thalamic necrosis following ingestion of ridge gourd infested with coelomycete fungi (Diplodia).

J Neurol Sci 2010 Aug 18;295(1-2):104-6. Epub 2010 Jun 18.

Department of Neurology, Goa Medical College, Goa 403 202, India.

Bilateral thalamic lesions detected on magnetic resonance imaging have a wide differential diagnosis. This report describes a previously healthy young man who developed bilateral thalamic necrosis with seizures, vomiting, hepatitis, neutrophilic leukocytosis and metabolic acidosis following consumption of raw dried fruits of the ridge gourd plant (Luffa acutangula) prescribed by a traditional medicine practitioner. These fruits were subsequently shown to be infested with spores and conidiomata of Diplodia, a coelomycete fungus known to cause neurotoxicity in farm animals. The patient made a partial recovery with supportive care, and has persistent deficits consistent with bilateral medial thalamic damage. This is the first report of neurological toxicity attributable to Diplodia in humans, and this entity should be considered in the differential diagnosis of bilateral thalamic lesions in the appropriate clinical setting.
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http://dx.doi.org/10.1016/j.jns.2010.05.021DOI Listing
August 2010

Randomized controlled trial of albendazole in new onset epilepsy and MRI confirmed solitary cerebral cysticercal lesion: effect on long-term seizure outcome.

J Neurol Sci 2009 Jan 11;276(1-2):108-14. Epub 2008 Oct 11.

Department of Neurology, National Institute of Mental Health and Neurosciences, Bangalore, India.

No trials to date have focused on long-term seizure outcome in solitary cerebral cysticercal lesion (SCCL), which is believed to produce a relatively benign form of epilepsy. This is a prospective randomized controlled study to evaluate the effect of Albendazole on long-term seizure outcome in patients with MRI-confirmed solitary cerebral cysticercal lesion (SCCL). One hundred and twenty-three patients with new-onset seizures and SCCL on contrast MRI were randomized to treatment with albendazole and followed for up to five years with serial MRI and clinical evaluation. At final analysis 103 patients (M-54, F-49) with a mean age of 18.6+/-10.7 years and follow-up period more than 12 months were included. The mean follow-up duration was 31.4+/-14.8 months (12-64). At one month follow-up more patients receiving albendazole were seizure-free (62% versus 49% for controls). Subsequently there was no significant difference in overall seizure outcome between the two groups. There was no correlation between seizure semiology, albendazole therapy and long-term seizure outcome. Baseline MRI showed active lesions in all; 23% remained active at 12 months with no difference between the albendazole and control groups. Patients whose lesions resolved at 12 months showed better seizure outcome. Reduction in mean cyst area was greater in the albendazole group as compared to the controls and the difference at six months was significant (p<0.05). At three months follow-up perilesional edema also resolved faster in albendazole group (p<0.05). Thus, albendazole did not alter the long-term seizure outcome in patients with SCCL and epilepsy. However, albendazole hastened resolution of SCCL on MRI, but interestingly 23% of lesions were still active 12 months after treatment.
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http://dx.doi.org/10.1016/j.jns.2008.09.010DOI Listing
January 2009
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