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Category : Brain & Nerves
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Jul01
Natural History of Solitary Cerebral Cysticercosis on Serial Magnetic Resonance Imaging and the Effect of Albendazole Therapy on its Evolution
Authors: Dr Aaron de Souza,
Dr Atchayaram Nalini, Dr Jerry M. E. Kovoor, Dr Gangappa Yeshraj, Dr Hanumanthaiah S. Siddalingaiah, and Dr Kandavel Thennarasu

Type of study: Original Research, prospective randomized controlled trial studying imaging parameters

Journal: Journal of the Neurological Sciences 288 (2010) 135Ė141.
[official journal of the World Federation of Neurology]


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Jul01
Prospective Quantitative Imaging Using Magnetisation Transfer in Solitary Cerebral Cysticercal Lesion
Authors: Dr Aaron de Souza,
Dr Atchayaram Nalini, Dr Jerry M. E. Kovoor, Dr Gangappa Yeshraj, Dr Hanumanthaiah S. Siddalingaiah, and Dr Kandavel Thennarasu

Type of Study: Original Research. Prospective randomised controlled trial studying imaging parameters.

Journal: The Neuroradiology Journal 23(5) 2010:574-589.
[official journal of the Italian Association for Neuroradiology]


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Jul01
Prospective quantitative imaging study for appearance of perilesional gliosis in solitary cerebral parenchymal cysticercal lesion by magnetisation transfer
Authors: Dr Aaron de Souza,
Dr Atchayaram Nalini, Dr Jerry M. E. Kovoor, Dr Gangappa Yeshraj, Dr Hanumanthaiah S. Siddalingaiah, and Dr Kandavel Thennarasu

Type of Article: Original Research, prospective randomised controlled study of imaging parameters.

Journal: Journal of the Neurological Sciences 285:S1 (2009).
[official journal of the World Federation of Neurology]


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Jul01
Natural history of solitary cerebral cysticercosis on serial magnetic resonance imaging and the effect of albendazole therapy on its evolution.
Authors: Dr Aaron de Souza,
Dr Atchayaram Nalini, Dr Jerry M. E. Kovoor, Dr Gangappa Yeshraj, Dr Hanumanthaiah S. Siddalingaiah, and Dr Kandavel Thennarasu

Type of Article: Prospective randomised controlled study of imaging parameters

Journal: Journal of the Neurological Sciences 285:S1 (2009)
[official journal of the World Federation of Neurology]


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Jul01
Randomised Controlled Trial of Albendazole in Solitary Cerebral Cysticercal Lesion: Effect on Long-Term Seizure Outcome.
Authors: Dr Aaron de Souza,
Dr Atchayaram Nalini, Dr Jerry M. E. Kovoor, Dr Gangappa Yeshraj, , and Dr Kandavel Thennarasu

Type of Article: Randomised controlled prospective trial.

Journal: Journal of the Neurological Sciences 276 (2009) 108Ė114.
[official journal of the World Federation of Neurology]


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Jul01
Prospective Quantitative Imaging Using Magnetisation Transfer in Solitary Cerebral Cysticercal Lesion
Authors: Dr Aaron de Souza,
Dr A Nalini, Dr H S Siddhalingaiah, Dr J M E Kovoor, Dr G Yeshraj, Dr K Thennarasu

Type of Study: Prospective Randomised Controlled Study of Imaging parameters

Journal: Annals of Indian Academy of Neurology 2008.
[official journal of the Indian Academy of Neurology]


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Jul01
Solitary Cerebral Cysticercal Lesion: A Comparative Study by Computed Tomography and Magnetic Resonance Imaging
Authors: Dr Aaron de Souza, Dr A Nalini, Dr S G Srikanth, Dr G Yeshraj.

Type of Study: Prospective, Comparison of Imaging modalities

Journal: Annals of the Indian Academy of Neurology 2006.
[official journal of the Indian Academy of Neurology]


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Jul01
Current Trends in the Management of Epilepsy
Author: Dr Aaron de Souza
Type of Article: Invited Review
Published in: Souvenir of the Goa Conference of the Indian Medical Association (GIMACON), 2009


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Jul01
ďGuillain-Barrť Syndrome in Goa: A Prospective AnalysisĒ
Author: Dr Aaron de Souza.
Category: Original Research, prospective descriptive study.
Journal: Archives of Goa Medical College, 2005.


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May25
Smells Like Parkinsonís Disease
Parkinsonís disease has always been primarily seen as a movement disorder resulting in symptoms of shaking, tremors, rigidity, and trouble walking. Interestingly, however, at least 90% of patients with Parkinsonís experience either loss or decreases in the sense of smell. Studies have shown that problems with olfaction actually generally precede the onset of other motor symptoms. Most people are not personally aware of changes in their olfactory acuity, but the increasing range and prevalence of smell tests offer a quick, easy, cheap, and non-invasive diagnostic test, as well as a measure of disease progression. In addition, the shift of focus for researchers from Parkinsonís as a motor disorder to a more global neurodegenerative disorder allows consideration of new paradigms about the causes and disease progression.
The cellular basis of olfactory dysfunction in Parkinsonís remains an enigma. Post-mortem studies have confirmed shrinkage of the olfactory bulb, but this fails to shed light onto the root causes as it only demonstrates the end effect. Experimental models of Parkinsonís have demonstrated various results such as protein aggregation in the olfactory bulb, changes in levels of neurotransmitters, microglial activation, and loss of cells in the olfactory bulb. However, as all of these effects are inter-related, none of these clarify the actual initial cause of damage.
Many of the hypotheses as to why olfactory dysfunction occurs and precedes other symptoms remain grounded in the long-held paradigm of Parkinsonís as a motor disease caused by the loss of dopaminergic neurons in the substantia nigra. For example, in some experimental models an increase in dopamine was found in the olfactory bulb. The researchers suggested this occurs as a compensatory mechanism in response to the loss of dopamine in the substantia nigra. As it has also been shown that sense of smell is particularly vulnerable to changes in dopamine, excess dopamine in the olfactory bulb would, thus, lead to olfactory dysfunction.
However, a number of other theories have been proposed suggesting that perhaps the olfactory bulb is the first brain structure to exhibit signs of damage because Parkinsonís could be caused by respiratory viruses or inhaled toxins that enter the brain through the nose. The cause of Parkinsonís has not been conclusively determined. And while a genetic component has been uncovered, the causes are clearly much more complex with various environmental factors involved. A number of studies have been performed demonstrating Parkinsonís-like symptoms following exposure to viruses, heavy metals, and pesticides in experimental models. Epidemiological studies have also linked pesticides exposure to an increased risk of Parkinsonís. It is certainly an interesting hypothesis that inhaled toxins could cross the blood brain barrier, and that the damage in Parkinsonís could begin first in the olfactory bulb and then spread from there to the substantia nigra. In addition, as the olfactory bulb is heavily involved in adult neurogenesis, any damage to this structure could severely limit the brainís ability to repair itself by replenishing damaged neurons with new ones. Perhaps, then, Parkinsonís disease does not depend on a single source of damage, but rather multiple insults occurring. For example, genetically induced damage to the dopaminergic neurons in the substantia nigra combined with inhaled toxins damaging the olfactory bulb could, together, cause Parkinsonís, while one or the other would be insufficient.


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