Browsing by Author "Espay, Alberto J."

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    Rapidly progressive atypical parkinsonism associated with frontotemporal lobar degeneration and motor neuron disease
    (BMJ Publishing Group Ltd., 2011) Espay, Alberto J.; Spina, Salvatore; Houghton, David J.; Murrell, Jill R.; de Courten-Myers, Gabrielle M.; Ghetti, Bernardino; Litvan, Irene; Department of Pathology & Laboratory Medicine, IU School of Medicine
    Objective To report the rare but distinct clinical and neuropathological phenotype of non-familial, rapidly progressive parkinsonism and dementia associated with frontotemporal lobar degeneration with motor neuron disease (FTLD-MND). Methods Subjects included two 70-year-old women presenting with rapidly progressive severe postural instability, axial-predominant parkinsonism, oculomotor dysfunction and frontal-predominant dementia with language impairment and pseudobulbar palsy. One had diffuse weakness without signs of lower motor neuron disease. Post-mortem evaluations included immunohistochemistry with antiphospho-TAR DNA-binding protein 43 (TDP-43) and genetic analysis of the TARDBP and PGRN genes. Results Subjects died within 14 months from symptom onset. TDP-43-positive neuronal intracytoplasmic inclusions were prominent in the primary motor cortex, granule cell layer of the hippocampus, and several cranial and spinal cord nuclei. TDP-43 globular glial inclusions (GGI) were identified in one case. There were no mutations in PGRN or TARDBP genes. Conclusions FTLD-MND due to TDP-43-proteinopathy should be considered in patients with rapidly progressive parkinsonism and dementia phenotype, especially when aphasia and/or weakness are also present.
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    Should neurologists diagnose and manage functional neurologic disorders? It is complicated
    (American Academy of Neurology, 2019-04) Perez, David L.; Haller, Andrea L.; Espay, Alberto J.; Neurology, School of Medicine
    Whereas only neurologists can "rule in" functional neurologic disorders (FNDs)-using physical signs and semiologic features-their role in follow-up care remains debated. We outlined the arguments for and against a neurologist's primary role in both assessing and managing FNDs. Favorable arguments include the following: (1) FND presents neurologically, and thus, only neurologists can ascertain the etiology of new neurologic deficits appearing on follow-up, and (2) neurologic encounters facilitate acceptance of diagnosis and enhance treatment engagement. Counter arguments include the following: (1) FND is a Diagnostic and Statistical Manual of Mental Disorders, 5th Edition codified psychiatric disorder with largely psychiatric treatments, and (2) neurologists can reassess patients if new neurologic symptoms develop without playing a primary follow-up role. Although more research is needed to clarify optimal approaches, neurologic expertise could be leveraged for diagnostic and coordinating roles if the pool of neurologists, psychiatrists, psychotherapists, physical and occupational therapists, and other allied clinicians trained in the interdisciplinary care of FNDs is substantially increased.