Browsing by Author "Lukande, Robert"

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    Neuroinflammation and Not Tauopathy Is a Predominant Pathological Signature of Nodding Syndrome
    (Journal of Neuropathology & Experimental Neurology, 2019) Hotterbeekx, An; Lammens, Martin; Idro, Richard; Akun, Pamela R.; Lukande, Robert; Akena, Geoffrey; Nath, Avindra; Taylor, Jonee; Olwa, Francis; Kumar-Singh, Samir; Colebunders, Robert
    Nodding syndrome (NS) is an epileptic disorder occurring in chil dren in African onchocerciasis endemic regions. Here, we describe the pathological changes in 9 individuals from northern Uganda who died with NS (n ¼ 5) or other forms of onchocerciasis-associated ep ilepsy (OAE) (n ¼ 4). Postmortem examinations were performed and clinical information was obtained. Formalin-fixed brain samples were stained by hematoxylin and eosin and immunohistochemistry was used to stain astrocytes (GFAP), macrophages (CD68), ubiqui tin, a-synuclein, p62, TDP-43, amyloid b, and tau (AT8). The cere bellum showed atrophy and loss of Purkinje cells with hyperplasia of the Bergmann glia. Gliosis and features of past ventriculitis and/ or meningitis were observed in all but 1 participant. CD68-positive macrophage clusters were observed in all cases in various degrees. Immunohistochemistry for amyloid b, a-synuclein, or TDP-43 was negative. Mild to sparse AT8-positive neurofibrillary tangle-like structures and threads were observed in 4/5 NS and 2/4 OAE cases, preferentially in the frontal and parietal cortex, thalamic- and hypo thalamic regions, mesencephalon and corpus callosum. Persons who died with NS and other forms of OAE presented similar pathological changes but no generalized tauopathy, suggesting that NS and other forms of OAE are different clinical presentations of a same disease with a common etiology. Key Words: Epilepsy, Nodding syndrome, Onchocerciasis, Post-mortem, Uganda.
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    Neuropathological Changes in Nakalanga Syndrome—A Case Report
    (Pathogens, 2021) Hotterbeekx, An; Lammens, Martin; Onzivua, Sylvester; Lukande, Robert; Olwa, Francis; Kumar-Singh, Samir; Van Hees, Stijn; Idro, Richard; Colebunders, Robert
    Nakalanga syndrome is a clinical manifestation of onchocerciasis-associated epilepsy characterized by stunting, delayed or absent secondary sexual development and skeletal deformities, and is often accompanied by epileptic seizures. The pathophysiology of Nakalanga syndrome is unknown. Here, we describe the post-mortem findings of a 17-year-old female who died with Nakalanga syndrome in northern Uganda. Macroscopic and histopathological examination of all major organs (liver, lungs, kidney and heart), including the brain and the pituitary gland, was performed. The suspected cause of death was malaria, and all major organs and pituitary gland appeared normal, except the lungs, which were edematous consistent with the malaria. Neuropathological changes include signs of neuro-inflammation (gliosis and activated microglia), which co-localized with tau-reactive neurofibrillary tangles and threads. The pathology was most abundant in the frontal cortex, thalamic and hypothalamic regions, and mesencephalon. The choroid plexus showed psammoma bodies. These findings indicate accelerated aging, probably due to repeated seizures. The neuropathological findings were similar to other persons who died with onchocerciasis-associated epilepsy. Examination of the pituitary gland did not reveal new information concerning the underlying pathophysiological mechanism of Nakalanga syndrome. Therefore, more post-mortem studies should be performed.