Kyung-Seok Park

HER2 status in pure ductal carcinoma in situ and in the intraductal and invasive components of invasive ductal carcinoma determined by fluorescence in situ hybridization and immunohistochemistry

Aim : To determine the HER2 status of ductal carcinoma in situ (DCIS) and invasive ductal carcinoma (IDC) of the breast. The increased prevalence of HER2 amplification and overexpression in DCIS is considered to be maintained in the intraductal component of IDC; however, HER2 amplification and overexpression are detected much less in IDC.

Nervous System Involvement by Pancreatic Cancer

From 1,229 consecutive patients with pancreatic cancer, seven patients who developed nervous system metastasis were evaluated retrospectively. Nervous system metastasis frequently antedated the diagnosis of the primary cancer (five out of seven patients). Four patients had cerebral metastasis. Brain computed tomography or magnetic resonance imaging revealed single or multiple cyst-like lesions with ring enhancement in half of these patients. Three patients had spinal metastasis which caused myelopathy in two. The metastatic lesions were localized to the thoracic level. Radiation therapy directed to the metastatic sites could not change the clinical course.

Interdigital nerve conduction study of the foot for an early detection of diabetic sensory polyneuropathy

OBJECTIVE To report on the value of interdigital nerve (IDN) conduction study (NCS) of the foot for the recognition of diabetic sensory polyneuropathy with normal routine NCS and the nature of electrophysiological abnormality in early diabetic sensory polyneuropathy. METHODS The sensory nerve conductions in the two digital and 4 IDNs of the foot were obtained orthodromically using the near-nerve needle and signal averaging technique. RESULTS In 21 patients with diabetic sensory polyneuropathy with normal routine NCS, a definite neuropathy pattern (abnormalities in more than 3 of 6 tested nerves) was observed in 12 patients (57.1%). The most common abnormalities that were found were a low amplitude in the sensory compound nerve action potential and an absent potential, indicating that early diabetic sensory polyneuropathy is due to axonal degeneration. CONCLUSIONS Interdigital NCS of the foot using near-nerve needle technique can identify neuropathy in diabetic sensory polyneuropathy with normal routine NCS. This technique offers a useful means of detecting nerve conduction abnormalities in the early stage of diabetic polyneuropathy.

Acute symptomatic seizures in CNS infection

To determine the frequency and aetiology of acute symptomatic seizures in central nervous system (CNS) infections and to assess the clinical factors predicting the occurrence of the seizures, we retrospectively reviewed the medical records of patients diagnosed with CNS infections from 2000 to 2005. One hundred and forty‐seven patients were included in the study. The clinical variables between those with and without acute symptomatic seizures were compared. Of the 147 patients, 23% (34/147) had acute symptomatic seizures. A significant relation between clinical variables and the occurrence of acute symptomatic seizures was found: encephalitis as the aetiology of the CNS infection, Glasgow Coma Scale (GCS) ≤12, and neurological deficits. By multiple logistic regression analysis, age of onset >42 years, encephalitis, and GCS ≤12 were found to be independently significant clinical variables for predicting the occurrence of acute symptomatic seizures. Encephalitis and GCS ≤12 are significant clinical variables for predicting the occurrence of acute symptomatic seizures in CNS infection, suggesting that patients with a greater extent of parenchymal damage are more vulnerable to acute symptomatic seizures.

Diffusion tensor tractography-based analysis of the pyramidal tract in patients with amyotrophic lateral sclerosis.

We attempted to measure DTI parameters of the brainstem pyramidal tract using two approaches, ie, simple ROI and tract‐specific analyses. Results obtained for healthy subjects and ALS patients were compared.

Defective neurite outgrowth in aphidicolin/cAMP-induced motor neurons expressing mutant Cu/Zn superoxide dismutase.

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder characterized by motor neuron involvement. Mutations in the human Cu/Zn superoxide dismutase (SOD1) gene are found in some cases of familial ALS. Many studies have reported SOD1 mutation‐related neurodegeneration. However, whether or not a mutant SOD1 affects neural development has not been demonstrated. We developed motor neuron‐neuroblastoma hybrid cells that expressed a mutant (G93A) or the wild type (WT) SOD1. Cells were differentiated by dibutyryl cAMP and aphidicolin. The mutant showed a defect in neurite outgrowth and had decreased viability. Cytochrome c released and nuclear fragmentation were observed. Western blot analysis showed that the amount of neurofilament and microtubule associated proteins‐2 (MAP‐2) decreased during differentiation. These results suggest that the defect in neurite outgrowth of mutant SOD1 cells is a cytoskeletal defect and is associated with neuronal death.

Cerebral glucose metabolism in Fisher syndrome

Background: Fisher syndrome (FS) is characterised by a triad of ophthalmoplegia, ataxia and areflexia. The lesion sites responsible for ataxia and ophthalmoplegia in FS require further exploration. The aim of this study was to determine the involvement of the central nervous system in FS using 18F-fluorodeoxyglucose-positron emission tomography (FDG-PET). Methods: Cerebral glucose metabolism in 10 patients with FS was compared with that of 60 age and sex matched normal controls using PET. For individual analyses, 15 age and sex matched controls were selected from the control group. Patients also underwent MRI of the brain and measurement of serum anti-GQ1b antibody. Results: Group analyses revealed increased metabolism in the cerebellar vermis and hemispheres, pontine tegmentum, midbrain tectum, left thalamus and right inferior frontal cortex (p<0.001, uncorrected). In contrast, the visual association cortices (Brodmann areas 18 and 19) showed decreased metabolism bilaterally. Individual analyses disclosed hypermetabolism in the cerebellar vermis or hemispheres (n = 7), inferior frontal cortex (n = 5) and brainstem (n = 4, p<0.005, uncorrected). A negative correlation between the cerebellar hypermetabolism and the interval from symptom onset to PET (r = −0.745, p = 0.013) was also found. Hypermetabolism was normalised on follow-up PET with an improvement in ophthalmoplegia and ataxia in one patient. Conclusions: These findings indicate involvement of the central nervous system in FS, and the hypermetabolism in the cerebellum and brainstem suggests an antibody associated acute inflammatory process as a mechanism of this autoimmune disorder.

Brain morphology in juvenile myoclonic epilepsy and absence seizures

We evaluated the differences in brain morphology among patients with juvenile myoclonic epilepsy according to the occurrence of absence seizures.

Cerebral hemodynamics in orthostatic intolerance with normal head-up tilt test

Orthostatic hypotension (OH) and postural orthostatic tachycardia syndrome (POTS) are well‐known causes of orthostatic intolerance (OI). In addition, there are OI patients who are characterized by the symptoms of OI and lack of abnormal findings in head‐up tilt (HUT) test. The aim of this study was to determine the cerebral hemodynamic changes in HUT test of OI patients with normal HUT (OINH).

Effective connectivity in temporal lobe epilepsy with hippocampal sclerosis

We hypothesized that temporal lobe epilepsy (TLE) patients with and without hippocampal sclerosis (HS) showed differences in their limbic networks. This study aimed to evaluate the role of the thalamus in TLE patients with HS.