The subthalamic nucleus (STN) is a small, ovoid structure, and an important site of deep brain stimulation (DBS) for the treatment of Parkinson’s disease. Although the STN is a clinically important structure, there are many unresolved issues with regard to it. These issues are especially related to the anatomical subdivision, neuronal phenotype, neuronal composition, and spatial distribution. In this study, we have examined the expression pattern of 8 neuronal markers [nNOS, NeuN, parvalbumin (PV), calbindin (CB), calretinin (CR), FOXP2, NKX2.1, and PAX6] in the adult human STN. All of the examined markers, except CB, were present in the STN. To determine the neuronal density, we have performed stereological analysis on Nissl-stained and immunohistochemical slides of positive markers. The stereology data were also used to develop a three-dimensional map of the spatial distribution of neurons within the STN. The nNOS population exhibited the largest neuronal density. The estimated total number of nNOS STN neurons is 281,308 ± 38,967 (± 13.85%). The STN neuronal subpopulations can be divided into two groups: one with a neuronal density of approximately 3,300 neurons/mm3 and the other with a neuronal density of approximately 2,200 neurons/mm3. The largest density of STN neurons was observed along the ventromedial border of the STN and the density gradually decreased toward the dorsolateral border. In this study, we have demonstrated the presence of 7 neuronal markers in the STN, three of which were not previously described in the human STN. The human STN is a collection of diverse, intermixed neuronal subpopulations, and our data, as far as the cytoarchitectonics is concerned, did not support the tripartite STN subdivision.
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The subthalamic nucleus (STN) is a small, excitatory nucleus that regulates the output of basal ganglia motor circuits. The functions of the STN and its role in the pathophysiology of Parkinson’s disease are now well established. However, some basic characteristics like the developmental origin and molecular phenotype of neuronal subpopulations are still being debated. The classical model of forebrain development attributed the origin of STN within the diencephalon. Recent studies of gene expression patterns exposed shortcomings of the classical model. To accommodate these findings, the prosomeric model was developed. In this concept, STN develops within the hypothalamic primordium, which is no longer a part of the diencephalic primordium. This concept is further supported by the expression patterns of many transcription factors. It is interesting to note that many transcription factors involved in the development of the STN are also involved in the pathogenesis of neurodevelopmental disorders. Thus, the study of neurodevelopmental disorders could provide us with valuable information on the roles of these transcription factors in the development and maintenance of STN phenotype. In this review, we summarize historical theories about the developmental origin of the STN and interpret the gene expression data within the prosomeric conceptual framework. Finally, we discuss the importance of neurodevelopmental disorders for the development of the STN and its potential role in the pathophysiology of neurodevelopmental disorders.
Hashimoto's encephalopathy is a rare condition, classifiable as an autoimmune non-paraneoplastic encephalopathy. Euthyroid patients can also suffer from this disease. It shows no response to thyroid replacement therapy, but immunosuppressive therapy has proved to be very efficient in treating this disease. Two types of clinical presentation may be observed, the first being characterized by acute onset with focal neurological deficits and epileptic seizures, and the second by non-specific, subacute symptoms such as cognitive impairment, psychiatric disorders, myocloni, and tremor. This paper reports the case of a 63-year old woman referred to a neurologist after being diagnosed with instability while walking, forgetfulness, hand tremor, and headache. Routine laboratory tests and CSF examination showed no abnormalities. Infectious etiology, neurodegenerative and systemic connective tissue diseases were excluded. Paraneoplastic and tumour markers were negative. After eight days, the patient experienced cognitive deterioration, motor dysphasia, ideomotor apraxia, myoclonic jerks of hands with a grand mal epileptic seizure. Antiepileptic treatment was started. Laboratory tests showed normal levels of T3, T4 and TSH with increased levels of anti-TPO and anti-hTG antibodies. Based on these results and AST screening tests (Apraxia Screen of Tulia), the patient was diagnosed with Hashimoto's encephalopathy. Daily treatment was started, with 5 plasmapheresis procedures and corticosteroid therapy. Due to good clinical response, the patient was soon discharged. After two months, due to relapse and the development of tremor, ataxia, dysmetria, and myoclonic jerks, pulse corticosteroid therapy was applied. The patient was discharged home with Medrol oral therapy from which she developed Cushingoid appearance without diabetes or osteoporosis. 18 months later, she developed hypothyroidism and was recommended levothyroxine treatment by an endocrinologist. Presently, neurological assessment is normal. The patient regularly checks up with a neurologist and an endocrinologist. This case report seeks to emphasize consideration of Hashimoto's encephalopathy as a part of differential diagnosis in patients who exhibit atypical neuropsychiatric symptoms, while infectious, paraneoplastic or immune causes of encephalopathy are excluded. Due to the etiology of the disease and side effects of therapy, a multidisciplinary approach in diagnosis and treatment is needed.
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