Clinical Course of Small Vessel Dementia Patients According to Cholinesterase Inhibitor Treatment

BACKGROUND: Small vessel dementia (SVD) is the most frequent cause of vascular dementia and is regarded a distinct clinical entity. However, the data on the natural course of SVD and drug trials specifically aiming SVD have been sparse. The aim of this study was to answer the following three questions: 1) How does SVD progress? 2) Does cholinesterase inhibitor therapy improves cognitive symptoms and daily activity of life (ADL) in SVD? 3) Is there any clinical difference among the subtypes of SVD? METHODS: According to cholinesterase inhibitor medications, patients with SVD were retrospectively analyzed using Hyoja Dementia registry. In this study, effects of treatment were assessed by comparing the scores of Korea version Mini-Mental State Examination (MMSE), Clinical Dementia Rating scale (CDR), Functional Independence Measure (FIM) at the base line with those at endpoints. RESULTS: After 12 months, the mean MMSE, CDR, FIM scores improved significantly in the cholinesterase inhibitor treatment group, compared with that in no-treatment group. In no-treatment group, annual decline of MMSE was 2.7, compared with 0.3 increment in the treatment group. White matter type of SVD showed worst prognosis compared with other types. CONCLUSIONS: This study suggests that SVD has more benign clinical course than previously reported, and cholinesterase inhibitor improves cognitive and ADL functions in SVD. Among the subtypes of SVD, the white matter type may have poor prognosis.

Treatment with MnTBAP Protects Against Early Nuclear Translocation of Endonuclease G and Reduces Cerebral Infarction after Focal Cerebral Ischemia/Reperfusion in Mice

BACKGROUND: Reactive Oxygen Species (ROS) have been implicated in the pathophysiology of brain injury after ischemia/reperfusion. Recently, it has been reported that endonuclease G (EndoG), a mitochondrial protein, is activated by neuronal excitotoxicity and translocated into nucleus inducing apoptosis. However, it is not elucidated whether ROS are involved in the nuclear translocation of EndoG in focal cerebral ischemia/reperfusion in mice. We investigated whether treatment of manganese tetrakis (4-benzoic acid) porphyrin (MnTBAP) protects against early nuclear translocation of EndoG and reduces cerebral infarction after ischemia/reperfusion in mice METHODS: Adult male mice were subjected to middle cerebral artery occlusion (MCAO) for 60 min, followed by reperfusion. Immunohistochemistry and Western blot analysis for EndoG were performed at various time points after ischemia/reperfusion. Double staining with EndoG and Terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end-labeling (TUNEL) was also performed. MnTBAP was used to determine whether the production of ROS could inhibit translocation of EndoG into the nucleus. RESULTS: Western blot analysis and Immunohistochemistry of EndoG showed that nuclear EndoG was detected as early as 4 hrs after reperfusion, and mitochondrial EndoG was significantly reduced at the same time. Double staining with EndoG and TUNEL showed a spatial relationship between EndoG expression and DNA fragmentation. MnTBAP-treated mice showed that the translocation of EndoG was attenuated in comparison with the vehicle- treated mice and decreased infarction volume after ischemia/reperfusion. CONCLUSIONS: MnTBAP reduced the generation of ROS, and inhibited the early translocation of EndoG, which was followed by the reduction of infarction volume in the ischemic brain after ischemia/reperfusion.

Minocycline Inhibits Caspase-Dependent Cell Death Pathway and is Neuroprotective against Hippocampal Damage after Kainic Acid-Induced Seizure in Mice / 대한간질학회지

PURPOSE: Despite current acceptance of its neuroprotective property, whether the minocycline affords neuroprotection or how it protects neurons against seizures in the animal model of epilepsy is not clear. This prompts us to investigate whether minocycline is neuroprotective against kainic acid (KA)-induced seizure in mice through inhibition of caspase-dependent mitochondrial apoptotic pathways. METHODS: Adult male ICR mice were subjected to seizures by intrahippocampal KA injection with treatment of vehicle or minocycline. For cell death analysis, histological analysis using cresyl-violet staining, TdT-mediated dUTP-biotin nick end labeling (TUNEL), and histone-associated DNA fragmentation analysis were performed. Evaluation of cytochrome c, cleaved caspase-3, and caspase-3 activity were also performed. RESULTS: Hippocampal neuronal death was evident by cresyl violet staining, TUNEL, and cell death assay in vehicle-treated mice after KA injection; however, there was significant reduction of cell death in the minocycline-treated group. Significant decrease of both cytosolic translocation of cytochrome c and subsequent activation of caspase-3 after treatment of minocycline were demonstrated by Western blot analysis, immunohistochemical staining, and caspase-3 activity assay. CONCLUSION: This study suggests that minocycline may be neuroprotective against hippocampal damage after KA-induced seizure through inhibition of caspase-dependent cell death pathways.

The Role of MMP-9 on the Hippocampal Neuronal Cell Death and Mossy Fiber Sprouting due to Pilocarpine-Induced Status Epilepticus in Mice / 대한간질학회지

PURPOSE: Matrix metalloproteinases (MMPs) have been known to participate in various pathologic situations by modulating extracellular matrix. Although MMP-9 upregulation has been reported in some experimental seizure models, the exact role of MMP-9 in hippocampal cell death during epileptogenesis and subsequent mossy fiber sprouting (MFS) is not clear. Here, we investigated the role of MMP-9 on hippocampal cell death and MFS after pilocarpine-induced status epilepticus (SE) in mice, using highly specific hydroxamic MMP-9 inhibitor. METHODS: SE was induced by intraperitoneal pilocarpine administration in adult male C57BL/6 mice. MMP-9 specific inhibitor was administered intracerebroventrically 3 h after pilocarpine-induced SE. Expression and activation of MMP-9 were assessed by zymography and Western blot analysis. TdT-mediated UTP-biotin nick end labeling (TUNEL) and caspase-3 activity assay were also performed. MFS was investigated using Timm staining. RESULTS: Increased expression and activation of MMP-9 after pilocarpine-induced SE were observed in zymography and Western blot analysis. MMP-9 specific inhibitor decreased MMP-9 activity in in situ zymography and hippocampal cell death in cresyl violet staining. DNA fragmentation and caspase-3 activity were also attenuated by MMP-9 specific inhibitor. Four months after pilocarpine-induced SE, MFS was evident in vehicle-treated mice; in contrast, MFS was barely observed in MMP-9 specific inhibitor-treated mice. CONCLUSIONS: This study suggests MMP-9 is associated with hippocampal cell death and MFS after pilocarpine-induced SE. Furthermore, the findings that MMP-9 specific inhibitor ameliorates cell death and MFS offers the possibility of MMP-9 specific hydroxamic inhibitor as novel therapeutic strategy to reduce hippocampal damage and epileptogenesis.

Expression of Apurinic/apyrimidinic Endonuclease and Neuronal Apoptosis in the Striatum after Treatment of 3-Nitropropionic Acid in Mice

BACKGROUND: 3-Nitroporpionic acid (3-NP) is an irreVersible inhibitor of succinate dehydrogenase in mitochondria and can induce apoptosis-like cell death in the striatum. It has been reported that oxidative stress plays a role in the 3-NP induced neuronal damage. 3-NP induced striatal damage is implicated in the pathogenesis of several neurological diseases, such as chronic neurodegenerative diseases and stroke. The DNA repair enzyme, apurinic/apyrimidinic endonuclease (APE), is a multifunctional protein in the DNA base excision repair (BER) pathway. To clarify the relationship between APE and neuronal cell death associated with the apoptosis in the striatum was induced by 3-NP in vivo. METHODS: After intra-striatal injection of 3-NP, expression of the APE protein and mRNA were evaluated by Western blot, immunohistochemistry, RT-PCR and DNA fragmentation patterns. Oxidative DNA damage was investigated by detection of oxidized DNA, AP site and superoxide. RESULTS: Expression levels of APE was rapidly reduced as early as 1hr after injection of 3-NP. DNA fragmentation was observed 24 hours after 3-NP treatment but not 4 hours. APE gene expression was increased to 1hr after 3-NP treatment. The number of AP sites were reduced and the reduction of APE proteins were blocked by a superoxide scavenger, MnTBAP-treatment. CONCLUSIONS: These results suggest that the reduction of APE is the preceding event of DNA fragmentation that causes apoptosis and a decrease of APE may be induced by ROS after 3-NP treatment.

Rapid Loss of Apurinic/Apyrimidinic Endonuclease and Subsequent Apoptosis in Kainate-Induced Seizure Model / 대한간질학회지

PURPOSE: The DNA repair enzyme, apurinic/apyrimidinic endonuclease (APE) plays a role in base excision repair pathway involved in repairing apurinic/apyrimidinic (AP) site after oxidative stress. To reveal the relationship between APE and neuronal apoptosis associated with oxidative stress after kainate treatment, the temporal change of APE expression was investigated in kainate-induced seizure model. METHODS: Status epilepticus was induced by unilateral intrahippocampal injection of kainate. Superoxide anion radical production and DNA oxidation were evaluated by in situ detection of oxidized hydroethidine and 8-hydroxyguanine (8-OHG) immunore activity. APE expression was examined by Western blot and immunohistochemical analysis. DNA fragmentation was visualized with terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end labeling (TUNEL) staining. RESULTS: Cell loss occurred at 24 hr in CA1, CA2, and CA3 after kainate-injection. 8-OHG immunoreactivity and oxidized hydroethidine were increased comparing with control after kainate-injection. APE immunoreactivity was decreased 4 and 24 hours in the hippocampus after kainate-injection. TUNEL-positive cells were observed 24 hours but not 4 hours in hippocampus after kainate-injection. In double labeling with APE and TUNEL, TUNEL-positive cells did not show APE immunoreactivity. These data showed that cellular oxidative stress was increased, thereby APE was decreased in the hippocampus after kainate-injection. Also, it was shown that the reduction of APE preceded DNA fragmentation. CONCLUSION: This study suggests that rapid loss of APE may produce the failure of DNA repair-machinary and then induce neuronal apoptosis following kainate-injection.

Presentation Time to Hospital and Recognition of Stroke in Patients with Ischemic Stroke

BACKGROUND: Recent advances in stroke therapies require patients to be treated very early after the onset of symptoms. To reduce the delay in time upon stroke and arriving at the hospital, we assessed the time delay, stroke recognition, and awareness before and after a public education program designed to increase recognition and awareness. METHODS: Prospective standardized and structured interviews were performed in 155 patients with ischemic stroke who were admitted to the Severance hospital before and after the public education program. The educational program included local newspaper articles, distribution of pamphlets, and lectures to 119 emergency care teams. Time delay, variable factors, stroke recognition, and stroke awareness of patients were then assessed (75 pre-education and 80 post-education groups). RESULTS: 52% of the pre-education group and 52.5% of the post-education group arrived at the hospital within 24 hours. Those who arrived within 3 hours were only 21.3% and 15% respectively. A direct visit to the hospital and a cardioembolic infarction appeared to be associated with a shorter time delay. About half of the patients recognized their symptoms as a stroke before a diagnosis was made by a doctor. Most of them had known that a stroke should be treated urgently. However, the stroke recognition and awareness was not associated with an early arrival, which suggests that their knowledge was not solid. The efforts to inform the public using local newspaper articles and pamphlets geared towards the local residents for the limited time period was not effective in shortening arrival times. CONCLUSIONS: Many of the stroke patients did not arrive within the therapeutic time window. Our findings suggest that extensive and multi-directional campaigns should be performed to reduce the time delay. Our findings also suggest that educational aims should include the need for the rapid treatment of stroke and a therapeutic time window as well as stroke recognition.

The Mechanism of Striatal Damage in Mice after Intraperitoneal Injection of 3-nitropropionic Acid

BACKGROUND: A newly-found mitochondrial toxin, 3-nitropropionic acid (3-NP), has been proved to induce apoptosis in the striatum. Although striatal lesions produced by 3-NP could develop through an excitotoxic mechanism, the exact relationship between apoptosis induction and excitotoxicity after 3-NP treatment is still not clear. We investigated the role of excitotoxicity and oxidative stress on apoptosis induction within the striatum following intra-peritoneal injection of 3-NP. METHODS: 3-NP was injected for 5 days intra-peritoneally in three month-old mice. One day after the last injection, animals were decapitated. To confirm the presence of apoptosis, we performed in-situ detection of DNA fragmentation by using TUNEL technique and agarose gel elctrophoresis after DNA extraction from striatum. To examine the effect of frontal cortex removal on 3-NP-indeced apoptosis, we removed left frontal cortex by aspiration. For excitotoxicity, NMDA-receptor antagonist-MK 801, non-NMDA antagonist-NBQX, and saline were injected intraperitoneally before 3-NP treatment To detect superoxide, we administered hydroethidium (HEt: 200 ul; 1mg/ml) into the jugular vein 2 days after 3-NP, and the density of oxidized HEt in samples were examined under flouscent microscope. We performed caspase staining to test immunoreactivity of caspase 3 in samples. RESULTS: The TUNEL positive cells were not observed in the striatum ipsilateral to the frontal cortex-removed side, but found in the contralateral striatum. Superoxide radicals measured by using HEt and caspase immunoreactivity were also significantly weaker in the striatum ipsilateral to the frontal cortex-removed side than the contralateral striatum. TUNEL staining revealed less apoptotic changes in the striatum of MK801-treated group than NBQX-or saline-treated groups. DNA laddering on agarose gel electrophoresis was observed in the striatum of NBQX- or saline-treated mice, but not found in MK 801-treated group. CONCLUSION: We demonstrated that removal of the corticostriatal glutamate pathway reduced superoxide production as well as apoptosis induced by 3-NP and NMDA receptor antogonist, but not non-NMDA antagonist, prevented 3-NP-induced apoptosis in the striatum. These results suggest that NMDA-mediated glutamatergic excitotokicity plays an important role in 3-NP related striatal damage.

Influence of circadian and activity patterns in onset of cerebral infarction

BACKGROUND AND OBJECTIVES: Stroke onset is known to vary by several factors. Although it has been known that stroke may develop most frequently in the morning, its association with the type of activity has quite rarely been described. METHODS: We prospectively investigated by interview the time of and the activity during or before the onset of stroke in patients with acute cerebral infarction from Aug. 1995 to Mar. 1996. The activities were subdivided into basal metabolic rate state, sedentary, light, moderate, and heavy movements based on the caloric expenditure. RESULTS: One hundred-twenty five patients were enrolled. The time of day when ischemic stroke most frequently occurred was from 8:00 AM to noon. The type of activity was significantly associated with stroke onset in that it developed most commonly during and just after sleep or resting. The relationship between the onset of stroke and such patterns of onset time and the activity was found only in the atherothrombotic infarction, but not in the other stroke types. CONCLUSION: We demonstrated that stroke has clear diurnal variation. Our observations also suggested that the activity may be significantly associated with stroke onset. These findings may be useful for better understanding of the pathogenesis and prevention of ischemic stroke.

Vertigo of cerebrovascular origin proven by CT scan or MRI: pitfalls in clinical differentiation from vertigo of aural origin

To get a better insight into the clinical differentiation between vertigo of cerebrovascular origin and of aural origin, we investigated radiologically proven stroke patients who presented with vertigo as an initial clinical manifestation. Of 154 stroke patients, 30 patients with vertigo (20%) had the relevant lesion, demonstrated with the initial computerized tomographic scan (13 patients) or the follow-up magnetic resonance imaging (MRI) study (17 patients) of the brain. Every lesion was in the vertebrobasilar arterial territory; 19 in the cerebellum, 8 in the pons, and 3 in the medulla oblongata. Although 12 of the 30 patients (40%) presented with vertigo in isolation at the onset of stroke, eight patients (27%) developed additional neurologic abnormalities from four hours to seven days later. Patients with isolated vertigo (13%) had the small lesion exclusively in the cerebellum of the PICA medial branch territory. The most frequent accompanying neurological sign was swaying in the cerebellar and medullary lesion, and dysarthria in the pontine lesion. The direction of nystagmus or swaying did not match the lesion side in some patients. Our findings suggest that cerebellar stroke may commonly manifest isolated vertigo or vertigo with swaying mimicking labyrinthine disorder, particularly at the onset of the disease. MRI study and tests for truncal ataxia and lateropulsion may be crucial for the detection of vertigo of cerebrovascular origin.

The Prognostic Significance of Infection in Acute Stroke: Preliminary study

BACKGROUND & OBJECTIVE: Infection is one of the common complications of acute stoke. However, it's characteristics and prognostic significance have not yet been sufficiently studied. METHOD: We prospectively investigated the frequency of infection and the conditions prone to develop it, and the influence of infection on patients prognosis in acute stroke. We assessed each patient with modified National Institute of Health (NIH) stroke scale immediately after the admission(NIH-0), at the hospital day 1(NIH-1), 3(NIH-3), 7(NIH-7), at the discharge(NIH-d). The degree of improvement was evaluated by improvement ratio([NIH-0-NIH-d]/NIH-0). RESULT: One hundred and twenty five patients were enrolled. Twenty-eight patients (22.4%) were infected during admission. Pneumonia(23), UTI(10), sepsis(4), URI(2), aseptic meningitis(1) and FUO(1) were developed in that order of frequency. Using indwelling instruments and poor initial neurological status were factors prone to develop infection. Mean NIH-0 score was 26.50 in patients with infection, and 8.13 in those without infection(p<0.05). There were significant differences in the improvement ratio between infected and non-infected patients both at the 7th hospital day(-0.64 vs. 0.28) and at the discharge (-0.016 vs. 0.27). CONCLUSION: About one fifth of acute stroke patients were infected during their admissions. Infection, especially pneumonia, was significantly correlated with the poor prognosis. The prevention and the appropriate control of infection may improve neurologic outcomes in stroke patients.

The Reference Values and Influencing Factors of TCD Measurements in 200 Normal Korean Adults

The clinical utility of transcranial doppler ultrasonography (TCD) in cerebrovascular disease has been extended recently. Although number of studies have been performed to define normal reference values of TCD measurements, they have some limitations to be used as reference values which include relatively small number of subjects, lack of data about some cerebral vessels and/or parameters. This study was aimed to obtain clinically useful reference values of TCD measurements with consideration of the influence of age and sex in Korean adults, particularly who are in stroke-prone age group. We measured flow velocities, pulsatility indecies, side-to-side differences and vasomotor reactivities of all intra-and extracranial cerebral arteries using TCD in 209 normal Korean adults (age, 23-78 years; 94 men and 115 women), and analyzed the influence of age and sex on those measurements. With advancing age, subjects showed significant reduction in velocity measurements and increase in pulsatility indecies of most examined arteries. Females showed hight velocities of middle cerebral, internal carotid, vertebral and basilar artery and lower pulsatility indecies of middle cerebral arteries compared with males. Asymmetry measurements including side-to-side differences and asymmetry index, and ,breath holding index testing vasomotor reactivity were also measured and the normal range of those parameters were calculated. Since present study included large number of subjects, and checked paramenters of TCD in both extra- as well as intracranial cerebral arteries, we are convinced that these results can be used as a reference data of TCD measurements in Korean adults.

P300 Cognitive Evoked-potential and Pattern of Learning Impairments in Idiopathic Parkinson's Disease

To evaluate P300 cognitive evoked-potential, the pattern of learning impairment and their possible relationship in patients with idiopathic Parkinson's disease, we performed P300 cognitive potential test and neuropsychologic tests evaluating learning ability-Gollin's incomplete drawing test (GIDT) , the tower of Hanoi Puzzle (TOHP), and recall the name of pictures in Gollin's incomplete drawing test (GIDT recall), on 37 patients with idiopathic Parkinson's disease (19 never-medicated and 18 with levodopa therapy for more than 6 months) and age- and sex-matched normal healthy controls. Compared with controls, patients showed significant delay in P300 latency and significant impairment in TOHP and GIDT recall, but not in GIDT. The revodopa-treated patients showed significantly shorter P300 latency and better performance in TOHP than never-medicated patients, although they still showed impairments in both tests compared with controls. Although all neuropsychologic tests used in present study significantly correlated to the P300 latency in patients, the most significant correlation was found in TOHP. These results suggest, first, the P300 latency significantly delayed in parkinsonian patients which is partially improved by levodopa therapy ; second, visuomotor procedural learning but not visuoperceptual procedural learning is impaired in parkinsonian patients which is also partially responsive to levodopa therapy third, although visuoperceptual procedural learning is not impaired, the transformation process of procedural learning into declarative learning is probably impaired in Parkinson's disease ; fourth, the dopaminergic lesion in Parkinson's desease may have a role in producing both P300 abnormality and impairments in visuomotor procedural learning.

Relationship between the auditory P300 and the procedural memory function in drug-naive patients with Parkinson's disease

We evaluated and compared procedural memory and auditory P300 event-related potential in age-matched normal controls (n = 15) and drug-naive patients with Parkinson's disease (n = 16). We used Gollin's incomplete picture test for visual procedural memory function and Tower of Hanoi puzzle for visuomotor procedural memory function. The mean latency of P300 was significantly prolonged in the Parkinsonian group than in the controls. In the neuropsychology test, the patients group revealed selective impairment of visuomotor procedural memory against preserved visual procedural memory. In the patients group, the latency of P300 was inversely correlated with performance of visuomotor procedural memory. These results suggest that prolonged auditory P300 event-related potential show the dysfunction of visuomotor procedural memory in the basal ganglia, which appears to be more selectively impaired than visual procedural memory in drug-naive patients with Parkinson's disease.

Hemiataxia-hypesthesia in Thalamic Stroke

Hemintaxia-hypesthesia in thalamic stroke has been rarely reported. We experienced six patients who has hemiataxia-hypesthesia with or without transientweakness due to thalamic stroke. Upon reviewing the pattern of sensory deficits and the presence of weakness m our cases and those in previously reported thalamic stroke patients with hemiataxiahypesthesia with or without transient weakness, hemiataxia-hypesthesia has a localizing value of the thalamic lesion, particularly in case of presenting with pain sensory loss and of no weakness.

RETT's syndrome in Korea: report of two cases

Rett's syndrome(RS) is a progressive neurodegenerative disorder characterized by exclusive occurrence in females, autistic behavior, dementia, gait ataxia, loss of purposeful use of the hands with stereotypic hand movement, and seizures. Initially RS was considered to be very rare; however, recent reports suggest that the prevalence is considerably higher and occurrence is world-wide. Because the pathophysiological process remains unknown, the diagnosis of RS is based mainly on its characteristic clinical features and course. We experienced two cases of RS which, to our knowledge, are the first reported in Korea. It is quite possible that many patients with RS not yet being diagnosed in Korea.

Two cases of mitochondrial myopathy with predominant respiratory dysfunction

Although it is well known that the respiratory failure is a major cause of death in most patients with chronic neuromuscular disease, predominant respiratory dysfunction without severe involvement of limb muscles is an unusual complication of mitochondrial myopathy in adult age. We experienced two cases of mitochondrial myopathy with severe involvement of respiratory function and only mild involvement of limb muscles. One is a 16 year old female and another is a 22 year old male. The diagnosis is based on morphologic characteristics of "ragged red fibers" under the light microscope and abnormal mitochondrias on the electron microscope in the muscle biopsy.

A Case of True Myoclonic Epilepsy of Childhood

The myoclonic epilepsies of infancy and early childhood pose the most difficult problems in the diagnosis and classification of epilepsies because they are often confused with the Lennox-Gastaut syndrome sharing a number of common features. However, their correct differentiation is easily justifiable because some of the myoclonic epilepsies of early childhood have better prognosis than the Lennox-Gastaut syndrome. We experienced and treated a 4-year-old boy who had normal intellectual function but frequent myoclonic and generalized clinic-tonic-clinic seizures, which were successfully controlled by anti-epileptic drugs. Hence we report a case with brief review of literatures.

Diagnostic Values of Serum and CSF CRP in Tuberculous Meningits

C-reactive protein(CRP) of the serurn and CSF vras quantitatively measured in patients who were diagnosed as tuberculous meningitis(19 cases), aseptic meningitis(44 cases) and control group(23 cases) in order to evaluate the diagnostic value and the possible dynarnics of CRP between serum and CSF. Following results were obtained. 1. Significant difference(p<0.005) OF CRP was observed in the initial CSF of the patients with tuberculous meningitis and aseptic meningitis. When the CRP of CSF was set above 0.4rng /dl, a sensitivity of 0 79 apd a specificity of 0.90 were obtained. 2. When the CRP in the initial serurn as compared, significant difference(p<0.0210) was also observed between the patients with tuberculous rneningitis and aseptic meningitis. However, serurn CRP were not diagnostic because of significant overlap between the tuberculous and the aseptic meningitis. 3. On follow up measurement of CRP, patients with tuberculous meningitis showed signihcant decrease in both serurn and CSF while patients with aseptic meningitis showed significant decrease only in the serum. 4. In both groups of patients with tuberculous meningitis and aseptic meningitis, CRP values in the CSF were closely correlated to those of the serum(Pearson's r=0.25326 p<0. 035, Pearson's r=0.4520 p<0.0000 respectively) Considering that the content of protein was also significantly(p<0.000) elevated in the patients with tuberculous meningitis and that the CRP ratio(Qcrp) was also significantly(p<0.0035) elevated in comparison to the controls, the increased CRP in the CSF of tuberculous meningitis is probably due to an increased simple diffusion through the blood-CSF barrier resulted from increased serurn CRP and through impairrnent of blood-CSF barrier.

A Case of Carotidynia

A carotidynia is a syndrome of vascular neck pain or tenderness arising from one or both carotid artery which is frequently associated with various forms of extracranial vascular headache, Carotidynia is a common but infrequently recognized syndrome. Careful history taking, physical examination and appropreate Lab(ex: CT scan of neck) may be indicated for accurate diagnosis and adequate management. We experienced a case of carotidynia which was believed to be related to a carotid arteritis evidenced by elevated ESR, abnormalities of neck CT, angiogram, and good response to steroid.