• The Journal of Korean Medicine
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• v.18 no.1
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• pp.385-398
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• 1997

The location and local arrangement of motor, sensory neurons within brain stem, nodose ganglia, spinal ganglia and sympathetic ganglia projecting to rat's kidney and meridian point BL 23, GB 25 were investigated by HRP immunohistochemical methods following injection of 5% WGA-HRP into left kidney and meridian point BL 23, GB 25. Following injection of WGA-HRP into left kidney, anterogradely labelled sensory neurons were founded within either nodose ganglia and spinal ganglia. The sensory neurons innervating rat's left kidney were observed within spinal ganglia $T_{7}{\sim}L_3$. Sympathetic motor neurons innervating rat's left kidney were labelled within left suprarenal ganglia, either celiac ganglia, superior mesenteric ganglia, and sympathetic chain ganglia $T_{1}{\sim}L_3$. Sympathetic chain ganglia were concentrated in $T_{12}{\sim}L_1$. The sensory neurons innervating rat's meridian point BL 23 were founded within spinal ganglia $T_{2}{\sim}L_2$. They were numerous in spinal in ganglia $T_{10}{\sim}T_{12}$. Sympathetic motor neurons innervating rat's meridian point BL 23 were observed in suprarenal ganglia and greater splanchnic trunk, sympathetic chain ganglia from $T_1$ to $L_3$. They were concentrated in $T_{12}{\sim}L_3$. The sensory neurons innervating rat's meridian point GB 25 were labelled within spinal ganglia $T_{6}{\sim}T_{13}$. They were numerous in from T10 to $T_{12}$. Sympathetic motor neurons innervating rat's meridian point GB 25 were labelled within greater splanchnic trunk and sympathetic chain ganglia $T_{12}{\sim}L_3$. They were concentrated in $T_{13}{\sim}L_1$. This results neuroanatomically imply that the location of rat's motor and sensory neurons innervating meridian point BL 23 and GB 25 were closely related that of innervating kidney.

• Applied Microscopy
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• v.26 no.2
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• pp.137-155
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• 1996

The development of the ganglia of the trachea was studied by electron microscopy in human fetuses ranging from 40 mm to 260 mm crown rump length. At 40 mm fetus, the tracheal ganglia was observed in the submucosa of the trachea. The primitive ganglia consisted of neuroblasts, undifferentiated cells, and unmyelinated nerve fibers. At 50 mm fetus, the neuroblast and their processes in the tracheal ganglia ware ensheathed by the bodies or processes of satellite cells. The cytoplasm of the neuroblast contained rough endoplasmic reticulum, mitochondria, Golgi complex, and ribosomes. At 70 mm fetus, cholinergic and adrenergic axon terminals were observed. Cholinergic axon terminals with agranular vesicles were abundant in the tracheal ganglia with increasing age. During next prenatal stage from 100 mm fetus, the ganglion cells and its processes were completely covered by a thin processes of the satellite cells. Unmyelinated nerve fibers were also completely ensheathed by processes of Schwann cell. Synaptic contacts between the cholinergic axon and dendrite of ganglion cells and a few dendrodendritic synapses were first observed at 100 mm fetus. The granule-containing cells were first identified in the tracheal ganglia at 200 mm fetus. These findings indicate that tracheal ganglia of human fetus resembles other parasympathetic and sympathetic ganglia, but not the enteric ganglia.

• The Korean Journal of Pain
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• v.35 no.3
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• pp.250-260
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• 2022

Background: Cranial nerve ganglia, which are prone to viral infections and tumors, are located deep in the head, so their detailed anatomy is difficult to understand using conventional cadaver dissection. For locating the small ganglia in medical images, their sectional anatomy should be learned by medical students and doctors. The purpose of this study is to elucidate cranial ganglia anatomy using sectioned images and three-dimensional (3D) models of a cadaver. Methods: One thousand two hundred and forty-six sectioned images of a male cadaver were examined to identify the cranial nerve ganglia. Using the real color sectioned images, real color volume model having a voxel size of 0.4 × 0.4 × 0.4 mm was produced. Results: The sectioned images and 3D models can be downloaded for free from a webpage, anatomy.dongguk.ac.kr/ganglia. On the images and model, all the cranial nerve ganglia and their whole course were identified. In case of the facial nerve, the geniculate, pterygopalatine, and submandibular ganglia were clearly identified. In case of the glossopharyngeal nerve, the superior, inferior, and otic ganglia were found. Thanks to the high resolution and real color of the sectioned images and volume models, detailed observation of the ganglia was possible. Since the volume models can be cut both in orthogonal planes and oblique planes, advanced sectional anatomy of the ganglia can be explained concretely. Conclusions: The sectioned images and 3D models will be helpful resources for understanding cranial nerve ganglia anatomy, for performing related surgical procedures.

• Journal of Korean Neurosurgical Society
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• v.40 no.3
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• pp.196-198
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• 2006

Familial idiopathic basal ganglia calcification[FIBGC] is an inheritable neurological condition characterized by calcium deposits in the basal ganglia and extra-basal ganglia areas. The condition manifests as parkinsonism and other variable neuropsychiatric symptoms. FIBGC is a rare condition, and its pathophysiology has not yet been fully elucidated. Here we report the results of a clinical study of two related patients diagnosed with FIBGC.

• The Journal of Korean Medicine
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• v.18 no.1
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• pp.58-71
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• 1997

In order to the location and local arrangement of nerve cell bodies and nerve fibers projecting to the meridian points related to facial nerve paralysis in the rat using the neural tracers, CTB and WGA-HRP, labeled neurons the were investigated by immunohistochemical and HRP histochemical methods following injection of 2.5% WGA-HRP and 1% CTB into Hyopko$(S_6)$. Chichang$(S_4)$, Sugu$(GV_{26})$, Sajukkong$(TE_{23})$ and Yangbaek$(G_{14})$. Following injection of Hyopko$(S_6)$, Chichang$(S_4)$, labeled motor neurons were founded in facial nucleus, trigeminal motor nucleus, reticular nucleus and hypoglossal nucleus. labeled sensory neurons were founded in trigeminal ganglia and $C_{1-2}$ spinal ganglia. sympathetic motor neurons were found in superior cervical ganglia. Sensory fibers labeled in brainstem were found in mesencephalic trigeminal tract, sensory root of trigeminal nerve, oral, interpolar and caudal part of trigeminal nucleus, area postrema, nucleus tractus solitarius, lateral reticular nucleus and $C_{1-2}$ spinal ganglia. Following injection of Sugu$(GV_{26})$, labeled motor neurons were founded in facial nucleus. Labeled sensory neurons were founded in trigeminal ganglia and $C_{1-2}$ spinal ganglia. Sympathetic motor neurons were found in superior cervical ganglia. Sensory fibers labeled in brainstem were found in spinal trigeminal tract, trigeminal motor nucleus, mesencephalic trigeminal tract, oral. interpolar and caudal parts of trigeminal nucleus, area postrema, nucleus tractus solitarius, lateral reticular nucleus, dorsal part of reticular part and $C_{1-2}$ spinal ganglia. Following injection of Sajukkong$(TE_{23})$ and Yangbaek$(G_{14})$, labeled motor neurons were founded in facial nucleus, trigeminal motor nucleus. Labeled sensory neurons were founded in trigeminal ganglia and $C_{1-2}$ spinal ganglia. sympathetic motor neurons were found in superior cervical ganglia. Sensory fibers labeled in brainstem were found in oral, interpolar and caudal parts of trigeminal nucleus, area postrema, nucleus tractus solitarius, inferior olovary nucleus, medullary reticular field and lamina I-IV of $C_{1-2}$ spinal cord. Location of nerve cell body and nerve fibers projecting to the meridian points related to the facial nerve paralysis in the rats were found in facial nucleus and trigeminal motor nucleus. Sensory neurone were found in trigeminal ganglia and $C_{1-2}$ spinal ganglia. Sympathetic motor neurons were found in superior cervical ganglia. Sensory fibers labeled in brainstem were found in mesencephalic trigeminal tract, oral, interpolar and caudal parts of trigeminal nucleus, area postrema, nucleus tractus solitarius. lateral reticular nucleus, medullary reticular field.

• Journal of Biomedical Engineering Research
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• v.28 no.1
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• pp.24-28
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• 2007

Presuming that firing neurons have motions inside the MRI magnet due to the interaction between the neuronal magnetic field and the main magnetic field, we applied motion encoding gradients to dissected snail ganglia to observe faster responding MRI signal than the BOLD signal. To activate the snail ganglia in synchronization with the MRI pulse sequence, we used electrical stimulation with the frequency of 30 Hz and the pulse width of 2s. To observe the fast responding signal, we used the volume selected MRI sequence. The magnetic resonance signal intensity, measured with 8 ms long motion encoding gradient with a 20mT/m gradient strength, decreased about $3.46{\pm}1.48%$ when the ganglia were activated by the electrical stimulation.

• Journal of Korean Neurosurgical Society
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• v.41 no.4
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• pp.272-274
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• 2007

Bilateral traumatic hemorrhage of the basal ganglia is an extremely rare neuropathologic entity. This report describes a 50year-old man with bilateral basal ganglia hemorrhage with occipital fracture of the skull after head trauma. The mechanism of development of traumatic hemorrhage of the basal ganglia has been not clear. But, it is presumed to be secondary to rupture of the lenticulostriate or anterior choroidal artery by shearing as a result of acceleration/deceleration forces. We briefly summarize our uncommon case and discuss its possible mechanisms.

• Korean Journal of Biological Psychiatry
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• v.13 no.1
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• pp.38-42
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• 2006

The case of a 66- year-old woman with coexisting idiopathic basal ganglia calcification(IBGC) and dementia was presented. The calcification was detected in bilateral basal ganglia, dentate nucleus, and thalamus by brain imaging. Serum calcium and phosphorus levels were normal. The underlying diseases of calcification of basal ganglia such as parathyroid dysfunction and other infectious, toxic, or metabolic illness were excluded. The patient had memory impairment and frontal executive dysfunction without aphasia, agnosia, apraxia, and visuospatial impairment in neuropsychological test. It suggested that the cognitive impairment might be due to the dysfunction of frontal-subcortical circuit.

• Molecules and Cells
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• v.38 no.6
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• pp.540-547
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• 2015

Attention deficit/hyperactivity disorder (ADHD) is one of the most common neurodevelopmental disorders, affecting approximately 5% of children. However, the neural mechanisms underlying its development and treatment are yet to be elucidated. In this study, we report that an ADHD mouse model, which harbors a deletion in the Git1 locus, exhibits severe astrocytosis in the globus pallidus (GP) and thalamic reticular nucleus (TRN), which send modulatory GABAergic inputs to the thalamus. A moderate level of astrocytosis was displayed in other regions of the basal ganglia pathway, including the ventrobasal thalamus and cortex, but not in other brain regions, such as the caudate putamen, basolateral amygdala, and hippocampal CA1. This basal ganglia circuit-selective astrocytosis was detected in both in adult (2-3 months old) and juvenile (4 weeks old) $Git1^{\check{s}/\check{s}}$ mice, suggesting a developmental origin. Astrocytes play an active role in the developing synaptic circuit; therefore, we performed an immunohistochemical analysis of synaptic markers. We detected increased and decreased levels of GABA and parvalbumin (PV), respectively, in the GP. This suggests that astrocytosis may alter synaptic transmission in the basal ganglia. Intriguingly, increased GABA expression colocalized with the astrocyte marker, GFAP, indicative of an astrocytic origin. Collectively, these results suggest that defects in basal ganglia circuitry, leading to impaired inhibitory modulation of the thalamus, are neural correlates for the ADHD-associated behavioral manifestations in $Git1^{\check{s}/\check{s}}$ mice.

• Journal of Korean Neurosurgical Society
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• v.61 no.1
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• pp.120-126
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• 2018

Intraparenchymal meningiomas without dural attachment are extremely rare, especially when they occur in basal ganglia region in child. An 8-year-old boy was admitted at our hospital, complaining of recurrent headache and vomiting for 3 months. Neurological examination showed impaired vision and mild paresis of the left extremities. Magnetic resonance imaging demonstrated a lesion located in the right basal ganglia region extending to superasellar cistern with solid, multiple cystic and necrotic components. Computed tomography revealed calcification within the mass. Due to the anterior cerebral artery involvement, a subtotal resection was achieved and postoperative radiotherapy was recommended. Histopathological examination indicated that the lesion was an atypical meningioma. The postoperative rehabilitation was uneventful. Mildly impaired vision and motor weakness of left extremities improved significantly and the patient returned to normal life after surgery. To our knowledge, intraparenchymal atypical meningioma in basal ganglia extending to superasellar cistern was never reported. The significance in differential diagnosis of lesions in basal ganglia should be emphasized.