We describe an unusual case of Hallervorden-Spatz disease (HSD). After presenting with limb rigidospasticity at the age of 9 years, our patient developed progressive dementia, spastic tetraparesis and myoclonic movements, leading to akinetic mutism. He died of pneumonia at the age of 39 years. Autopsy revealed a severely atrophic brain, weighing 510 g. Histologically, there were iron deposits in the globus pallidus and substantia nigra pars reticulata, and numerous axonal spheroids throughout the brain and spinal cord. Neurofibrillary tangles were abundant in the hippocampus, cerebral neocortex, basal ganglia and brain stem. Neuritic plaques and amyloid deposits were absent. Lewy bodies and Lewy neurites, which were immunolabeled by anti-alpha-synuclein, were found in the brain stem, cerebral cortex and spinal gray matter. Sarkosyl-insoluble tau extracted from the temporal cortex resolved on immunoblots into three major bands of 60, 64 and 68 kDa and a minor band of 72 kDa, as reported for Alzheimer's disease. The present case, together with a few similar cases reported previously, may represent a particular subset of neuroaxonal dystrophy, i.e., HSD associated with extensive accumulation of both tau and alpha-synuclein.
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http://dx.doi.org/10.1007/s004010050049 | DOI Listing |
ACS Chem Neurosci
December 2024
Neuroscience Group of Antioquia (GNA) and Molecular Genetics Group (GENMOL), University of Antioquia, Medellín 050010, Colombia.
Neurogenetics
December 2024
Department of Medical Genetics, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Orphanet J Rare Dis
November 2024
Andalusian Centre for Developmental Biology-CSIC-Pablo de Olavide University, 41013, Seville, Spain.
Neurocase
August 2024
Department of Psychiatry, Istanbul University-Cerrahpasa Cerrahpasa Faculty of Medicine, Istanbul, Turkey.
Neurodegeneration with brain iron accumulation (NBIA) is a genetic disorder characterized by iron accumulation in the basal ganglia. Patients may develop behavioral abnormalities, dementia, movement disorders, and neuropsychiatric symptoms such as emotional lability, depression, anxiety, hallucinations, impulsivity, obsessions, and hyperactivity. In this case, a 46-year-old male patient with a C19orf12 mutation experienced depressive complaints before movement disorders, followed by cognitive deficits and psychotic symptoms as the disease progressed.
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