Serum tau protein level serves as a predictive factor for neurological prognosis in neonatal asphyxia

Background: Tau protein is a microtubule-associated protein that is present in axons. Elevated tau protein levels in cerebrospinal fluid or serum are associated with several central nervous system diseases and can indicate neuronal injury. Objective: In the present study, we measured and then compared serum tau protein levels between infants with neonatal asphyxia and control subjects. We examined these data to investigate the correlation between serum tau protein levels and neurological outcomes after neonatal asphyxia. Patients and methods: Serum tau protein levels were determined by an enzyme-linked immunosorbent assay in 19 neonates with neonatal asphyxia. Of these 19 neonates, 3 had severe spastic tetraplegia, and 1 had west syndrome. A group of 19 unaffected neonates was included in the study as a control group. Results: Serum tau protein levels on postnatal day 3 were significantly higher in the poor outcome group than those in the good outcome (p = 0.010) and control groups (p = 0.006). On postnatal day 7, serum tau protein levels again were significantly higher in the poor outcome group than those in the good outcome (p = 0.007) and control groups (p = 0.006). Conclusions: The present findings indicate serum tau protein levels measured on postnatal days 3 and 7 can predict neurological prognosis following neonatal asphyxia.     

Cerebrospinal fluid total tau protein levels in patients with multiple sclerosis

BACKGROUND: Tau protein is present in the microtubules of axons. Markers of various types have been used to demonstrate multiple sclerosis (MS) activity and axonal damage. This study aimed to demonstrate the association between cerebrospinal fluid (CSF) tau protein concentrations and clinical prognosis in MS patients. METHODS: We included 45 patients that were diagnosed according to the McDonald's criteria. The control group was made up of 38 patients that had no signs or symptoms related to the primary central nervous system lesion correlated with the patient group. CSF total tau protein was measured using the ELISA method based on the sandwich method with Innogenetics Innotest hTau antigen kit in pg/ml type. RESULTS: In the patient group, the mean CSF total tau protein level was 238.66 +/- 237.44, whereas it was 93.65 +/- 82.14 in the control group. The mean total tau protein was higher in the three clinical forms when compared with the control group and it was statistically significant (P<0.05). CONCLUSIONS: High tau protein level may be an early marker of axonal damage and this marker may be used for monitoring axon preventing therapies in the follow-up.     

Vasopressin and oxytocin in CSF and plasma of patients with aneurysmal subarachnoid haemorrhage

Objective

Clinicopathological studies on patients succumbing to subarachnoid haemorrhage (SAH) demonstrated hypothalamic lesions. The implication of the hypothalamic neuropeptides arginine-vasopressin (AVP) and oxytocin (OXT) has not been linked to aneurysmal SAH yet. This study investigates AVP and OXT in CSF and plasma of patients with spontaneous aneurysmal SAH and their association with outcome.

Methods

CSF and plasma samples of 12 patients with aneurysmal SAH were prospectively studied for 2 weeks. AVP and OXT were measured by radioimmunoassay. Outcome was assessed on Glasgow-Outcome-Scale. Twenty-nine patients without neuropsychiatric disturbances served as controls. Differences in neuropeptide concentration time courses were assessed by regression models. Group comparisons were performed by Kruskal–Wallis and correlations by Spearman tests.

Results

Regression of CSF levels between patients with poor and good outcome revealed significantly lower levels of AVP in patients with poor outcome (p = 0.012) while OXT showed a trend towards lower levels (p = 0.063). In plasma, no significant differences between outcome groups were found. Group comparisons between poor outcome patients and controls revealed significant differences in CSF for AVP (p = 0.001) and OXT (p = 0.015). In plasma, AVP yielded significantly different results while OXT did not. No differences were found between the good outcome group and controls. Plasma and CSF concentrations showed no significant correlation.

Conclusion

Patients with poor outcome after aneurysmal SAH have lower AVP and OXT levels in CSF than patients with good outcome while neuropeptide levels in plasma failed to reflect differences in outcome. The data indicate hypothalamic damage as an aetiologic factor for outcome after aneurysmal SAH.     

血清、脑脊液中S-100B在颅脑外伤损伤程度中的诊断意义

目的 探讨血清、脑脊液中S-100B与颅脑外伤(traumatic brain injury,TBI)损伤程度的关系.方法 选择45例TBI患者按格拉斯哥昏迷分级(GCS评分)分轻、中、重三组(病例组),采用酶联免疫吸附法(EHSA)测定TBI患者伤后第1、3、5、7天血清及脑脊液S-100B水平,并选择20例与病例组相匹配的疝或静脉曲张手术病人以及健康体检自愿者的血清、脑脊液作为对照组,分析血清及脑脊液S-100B水平与TBI损伤程度的相关性.结果 病例组血清、脑脊液S-100B水平较对照组明显升高(P ＜0.01;P ＜0.01);TBI患者GCS评分与血清及脑脊液S-100B水平比较呈负相关(r=-0.893,P＜0.01;r=-0.947,P＜0.01);血清、脑脊液S-100B在不同程度TBI间比较差异显著(P＜0.01);病例组血清和CSF中S-100B水平比较呈正相关;结论 血清、脑脊液S-100B测定均可作为判断TBI程度的指标,且各有特点.     

Serum and CSF biomarkers in acute pediatric neurological disorders

Background: There have been numerous reports regarding serum or cerebrospinal fluid (CSF) biomarkers in various disorders; however, the validities of such biomarkers for more precise diagnoses and prognosis estimates remain to be determined, especially in pediatric patients with neurological disorders. Methods: Serum/CSF S100B, neuron-specific enolase, and total tau (tTau) were measured in various acute pediatric neurological disorders, and their usefulness for diagnostic and prognostic predictions was validated using receiver operating characteristic curves and area under the curve (AUC) analysis. Results: A total of 336 serum and 200 CSF specimens from 313 patients were examined, and we identified statistically significant differences that were relevant from diagnostic and prognostic viewpoints. CSF and serum tTau levels could be good predictors for diagnosis (CSF tTau; AUC = 0.76) and prognosis (serum tTau; AUC = 0.78). Conclusions: Both CSF and serum tTau levels could be useful for precise diagnostic and prognostic estimations in acute pediatric neurological disorders. Further studies are needed to clarify the clinical significance of such biomarkers.     

Expression of leukemia inhibitory factor in the cerebrospinal fluid of patients with multiple sclerosis

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system, characterized by infiltration of immune cells in the central nervous system, localized myelin destruction and loss of oligodendrocytes. Early detection of MS may be possible via blood and cerebrospinal fluid (CSF) tests based on disease pathology. Leukemia inhibitory factor (LIF), a neurotrophic cytokine, has previously been shown to limit autoimmune demyelination and oligodendrocyte loss in a murine model of MS. Given its potential role in neural cell death and survival, in the present study we measured expression of LIF in serum and CSF from patients with relapsing-remitting MS (n = 46) and control subjects (n = 42). We used western blot analysis and enzyme-linked immunosorbent assays (ELISA), to study LIF expression. Western blot analysis revealed that LIF was present in all CSF samples, and densitometric analysis showed that relative expression was significantly higher in CSF from patients with MS than in controls (p < 0.001). ELISA analysis showed that the concentrations of LIF in both the serum (87.5 ± 11.46 ng/mL) and CSF (56 ± 10.72 ng/mL) of MS patients were significantly higher than those in control subjects (52 ± 8.23 ng/mL, 7.8 ± 3.76 ng/mL, respectively; p < 0.0001 for both serum and CSF), despite there being no significant difference in total protein concentration between the two groups (p = 0.52 for serum, p = 0.2 for CSF). Our data suggest that serum and CSF concentrations of LIF may provide additional useful information during the differential diagnosis of MS. Our findings also indicate that LIF could be significantly involved in the pathophysiology of MS.     

Cerebrospinal fluid analysis in affective and schizophrenic spectrum disorders: Identification of subgroups with immune responses and blood-CSF barrier dysfunction

Immune and inflammatory mechanisms are detected in a subgroup of treatment resistant hospitalized affective and schizophrenic spectrum disorder patients. We analysed albumin, IgG, IgA, IgM, oligoclonal IgG and specific antibodies in paired cerebrospinal fluid (CSF) and serum samples. Numerical and graphical interpretation of CSF protein data was performed by Reibergrams with a new CSF statistics tool for nonlinear group analysis with reference to a large control group (n = 4100). In 41% of the psychiatric patients (n = 63) we observed CSF pathologies: 14% displayed intrathecal humoral immune responses, 10% slightly increased CSF cell counts (5-8/μL) and 29% had moderate blood-CSF barrier dysfunctions, in 24% as the only pathological sign with normal IgG, IgA and IgM concentrations in CSF (p = 0.9 testing the null hypothesis for intrathecal synthesis with reference to Qmean of the reference group). In the group of affective (n = 24) spectrum disorders 20% displayed a systemic immune reaction as detected by oligoclonal IgG. CSF analysis and interdisciplinary clinical approach revealed 6% of psychiatric patients likely to represent a virusspecific, bacterial or autoimmune associated disorder with CNS involvement. Elevated CSF neopterin concentration in 34% of the patients was interpreted as an increased release from astrocytes or from other glia cells. The low level immune response and barrier dysfunctions are discussed on the base of a mild encephalitis pathomechanism in subgroups of psychiatric patients. CSF analysis is shown to be a useful diagnostic tool for differential diagnosis in psychiatric diseases.     

Cognitive impairment and optic nerve axonal loss in patients with clinically isolated syndrome

Objective

To investigate cognitive impairment, to assess optical nerve axonal loss, and to determinate whether there is correlation between optical nerve axonal loss and cognition impairment in Clinically Isolated Syndrome (CIS).

Methods

Fifteen CIS patients and 15 controls were submitted to Wechsler memory scale, Rey Auditory Verbal Learning, Rey Complex Figure, Paced Auditory Serial Addition, Digit Span, verbal fluency, stroop color, D2, and Digit Symbol tests. CIS patients were evaluated by optical coherence tomography (OCT) (23 eyes).

Results

CIS patients had worse performance in Paced Auditory Serial Addition Test (PASAT) 2 seconds (P = 0.009) and fluency tests (P = 0.0038). Optical nerve axonal loss was found more frequently in eyes with previous optic neuritis (ON) (85.7%) than in those without previous ON (21.7%) (P = 0.0146). There were no significant correlations between optical nerve axonal loss and cognitive findings.

Conclusions

CIS patients had worse cognitive performance than controls. OCT can detect axonal loss resulting from optical neuritis and subclinical axonal loss in eyes without previous optical neuritis. Optical nerve axonal loss was not correlated with cognition.     

Immune responses to Helicobacter pylori infection in children with intellectual disabilities

Infection with Helicobacter pylori was assessed through serum H. pylori IgG antibody in children with intellectual disabilities (ID). The sero-status of cytotoxin-associated gene A (CagA) was determined as a risk determinant for severe H. pylori-associated diseases. In total, 210 children with ID were included who were permanent resident of three institutes in Tehran. Medical history and demographic data were collected by reviewing the medical file records. The anti H. pylori IgG antibody was detected in serum of 74.8% of children using ELISA. Significant correlations were found between the rate of infection and age (P = 0.001) and duration of institutionalization (P = 0.018). The likelihood of H. pylori IgG positive response increased with age with the highest response in 15-18 years age group (OR = 6.66, 95% CI: 2.14-20.17; P = 0.001). Similarly, the average titers of H. pylori IgG antibody were increased with age. The institutionalization duration of more than 49 months affected the likelihood of H. pylori IgG positive response (OR = 2.437, 95% CI: 1.12-5.26; P = 0.023). Anti-CagA titers were higher than 5 arbU/ml in 92 (58.6%) children, indicating a positive response against CagA protein. The titer of H. pylori IgG was significantly higher in CagA-positive (mean ± SE = 51.04 ± 3.41) than in CagA-negative children (38.07 ± 4.18; P = 0.017). In contrast to total H. pylori IgG titers, anti-CagA antibody had non-regular trend of alterations with age. The seropositivity rate of H. pylori infection in ID children was higher than other reports in healthy children from various regions of the country. The risk of H. pylori infection is increased with age and duration of institutionalization. The serostatus of CagA in children with IDs has not been reported so far. The regular monitoring of the CagA-positive carriers is recommended; since CagA positive cases carry the risk of progression of infection toward severe H. pylori associated sequels such as gastric cancer and duodenal ulcers.     

Non-neurological surgery and cerebrospinal fluid biomarkers for neuronal and astroglial integrity

Non-neurological surgery has both acute and long-term effects on the brain. Markers for Alzheimer pathology may be used to study surgically induced neurological changes relevant for postoperative confusion, asthenia or cognitive decline. Inflammatory biomarkers, total tau (T-tau) and phosphorylated tau (P-tau) were recently shown to increase progressively in the cerebrospinal fluid (CSF) during surgery for nasal CSF leak, suggesting a neuroinflammatory response with signs of neuronal damage. We used a study group of 35 patients, undergoing knee arthroplasty with a spinal blockade and propofol sedation, to replicate this finding. Five CSF biomarkers were analyzed before, 3 h after and on the morning after the interventions: T-tau and P-tau for cortical axonal integrity and tangle pathology, respectively, the 42 amino acids form of amyloid β (Aβ42) for plaque formation, neurofilament light (NFL) for the integrity of large-caliber myelinated axons and glial fibrillary acidic protein (GFAp) for astroglial cell integrity. CSF T-tau concentrations increased significantly during and after surgery (p = 0.028) and were significantly correlated with the administered doses of bupivacaine. P-tau, Aβ42 and NFL remained unchanged, while the mean GFAp concentration increased with a large standard deviation. CSF T-tau and P-tau correlated significantly with the CSF/serum albumin ratios as an indicator of blood–brain barrier permeability. Findings from earlier studies showing a significant increase in biomarkers for Alzheimer’s pathology during surgery were partly replicated, as neurochemical signs of impaired cortical axonal integrity during non-neurological surgery were detected. Bupivacaine may be involved in these reactions.     

Tau protein and 14-3-3 are elevated in the cerebrospinal fluid of patients with multiple sclerosis and correlate with intrathecal synthesis of IgG

Abstract. Recently it has been shown that axonal damage occurs in all stages of multiple sclerosis (MS) and can be detected very early in the course of the disease. Axonal pathology has been related to the inflammatory demyelinating environment, but its dependence on inflammation is still unknown. We measured tau protein and 14-3-3, two intracellular proteins expressed in neurons and glial cells, in the cerebrospinal fluid (CSF) of 114 patients with MS, in 79 patients with other inflammatory neurological diseases (IND) and in the CSF of 60 patients with non-inflammatory neurological diseases (NIND) as controls. Concentrations of tau protein and 14-3-3 were measured by enzymelinked immunoassay and were correlated to the following immune parameters in the CSF: leukocyte cell count, total protein, albumin CSF/serum ratio as a marker of disruption of the blood-brain barrier, immunoglobulin (IgG concentrations and IgG index as an indicator for intrathecal synthesis of IgG in the CSF). Both in MS and IND tau protein levels were significantly higher than in NIND (p < 0.05). In MS patients levels of tau protein were positively correlated with the IgG index (p < 0.05) and this association was present in both relapsing remitting MS (RRMS) (p < 0.05) and progressive MS (p < 0.05). Tau and 14-3-3 were also correlated with the IgG index in patients with IND (p < 0.05). These findings strengthen the hypothesis that inflammation may be at least in part responsible for the axonal damage observed in MS patients.     

Inverse association of cortisol serum levels with T-tau,P-tau 181 and P-tau 231 peptide levels and T-tau/Aβ 1–42 ratios in CSF in patients with mild Alzheimer’s disease dementia

Hypercortisolemia and increased levels of hyperphosphorylated tau proteins in cerebrospinal fluid (CSF) are common features with pathogenic relevance in Alzheimer`s disease (AD). Experimental studies point to an influence of cortisol on Aβ and tau pathology in AD. Association of both parameters have not yet been described in a sample of AD patients. In the present study, serum levels of cortisol were determined in 26 patients with mild AD dementia and 20 age-matched healthy elderly controls by ELISA. In addition, we measured in AD patients CSF levels of cortisol, total tau (T-tau), tau phosphorylated at threonine 181 (P-tau 181), tau protein phosphorylated at threonine 231 (P-tau 231) and beta-Amyloid (Aβ) 1–42 and determined T-tau/Aβ 1–42 ratios in CSF. We found in AD patients significantly increased cortisol serum levels (551.4 ± 146.1 nmol/l; P = 0.002) as compared to healthy controls (435.3 ± 83.9 nmol/l). In AD patients, cortisol serum levels were significantly inversely correlated with T-tau (r = −0.496; P = 0.01), P-tau 181 (r = −0.558; P = 0.003) and P-tau 231 (−0.500; P = 0.009) protein levels and T-tau/Aβ 1–42 ratios (r = −0.450; P = 0.021) in CSF. In addition, cortisol serum levels showed a trend of positive correlation with Aβ 1–42 CSF levels (r = 0.386; P = 0.052). However, no significant correlations of cortisol serum with CSF levels as well as cortisol CSF levels with CSF biomarkers could be detected in AD patients. In conclusion, our results show that increased cortisol serum but not CSF levels are associated with minor signs of AD pathology in CSF, indicating a putative neuroprotective effect of moderately elevated cortisol serum levels in patients with mild AD dementia.     

Cerebrospinal fluid biomarkers of white matter lesions – cross‐sectional results from the LADIS study

Background and purpose: White matter lesions (WMLs) caused by small vessel disease are common in elderly people and contribute to cognitive impairment. There are no established biochemical markers for WMLs. We aimed to study the relation between degree of WMLs rated on magnetic resonance imaging of the brain and cerebrospinal fluid (CSF) levels of structural biomarkers associated with Alzheimer’s disease (AD) and subcortical vascular dementia. Methods: Fifty‐three non‐demented elderly individuals with WMLs were subjected to lumbar puncture. Degree of WMLs was rated using the Fazekas scale. Volumetric assessment of WMLs was performed. CSF samples were analyzed for the 40 and 42 amino acid fragments of amyloid β, α‐ and β‐cleaved soluble amyloid precursor protein, total tau (T‐tau), hyperphosphorylated tau (P‐tau₁₈₁), neurofilament light protein (NFL), sulfatide and CSF/Serum‐albumin ratio. Results: Fifteen subjects had mild, 23 had moderate and 15 had severe degree of WMLs. CSF‐NFL levels differed between the groups (P < 0.001) and correlated with the volume of WMLs (r = 0.477, P < 0.001). CSF sulfatide concentration displayed similar changes but less strongly. T‐tau, P‐tau₁₈₁ and the different amyloid markers as well as CSF/S‐albumin ratio did not differ significantly between the groups. Conclusions: The association of increased CSF‐NFL levels with increasing severity of WMLs in non‐demented subjects suggests that NFL is a marker for axonal damage in response to small vessel disease in the brain. This manifestation may be distinct from or earlier than the neurodegenerative process seen in AD, as reflected by the lack of association between WMLs and AD biomarkers.     

Quantitative T2 mapping as a potential marker for the initial assessment of the severity of damage after traumatic brain injury in rat

Severity of traumatic brain injury (TBI) positively correlates with the risk of post-traumatic epilepsy (PTE). Studies on post-traumatic epileptogenesis would greatly benefit from markers that at acute phase would reliably predict the extent and severity of histologic brain damage caused by TBI in individual subjects. Currently in experimental models, severity of TBI is determined by the pressure of applied load that does not directly reflect the extent of inflicted brain injury, mortality within experimental population, or impairment in behavioral tests that are laborious to perform. We aimed to compare MRI markers measured at acute post-injury phase to previously used indicators of injury severity in the ability to predict the extent of histologically determined post-traumatic tissue damage. We used lateral fluid-percussion injury model in rat that is a clinically relevant model of closed head injury in humans, and results in PTE in severe cases. Rats (48 injured, 12 controls) were divided into moderate (mTBI) and severe (sTBI) groups according to impact strength. MRI data (T2, T2*, lesion volume) were acquired 3 days post-injury. Motor deficits were analysed using neuroscore (NS) and beam balance (BB) tests 2 and 3 days post-injury, respectively. Histological evaluation of lesion volume (Fluoro-Jade B) was used as the reference outcome measure, and was performed 2 weeks after TBI. From MRI parameters studied, quantitative T2 values of cortical lesion not only correlated with histologic lesion volume (P < 0.001, r = 0.6, N = 34), as well as NS (P < 0.01, r = − 0.5, N = 34) and BB (P < 0.01, r = − 0.5, N = 34) results, but also successfully differentiated animals with mTBI from those with sTBI 70.6 ± 6.2 6.2 ms vs. 75.9 ± 2.6 ms, P < 0.001). Quantitative T2 of the lesion early after TBI can serve as an indicator of the severity of post-traumatic cortical damage and neuro-motor impairment, and has a potential as a clinical marker for identification of individuals with elevated risk of PTE.     

Patterns of retinal nerve fiber layer loss in multiple sclerosis patients with or without optic neuritis and glaucoma patients

Objective

Optical coherence tomography (OCT) has gained increasing attention in multiple sclerosis (MS) research and has been suggested as outcome measure for neuroprotective therapies. However, to date it is not clear whether patterns of retinal nerve fiber layer thickness (RNFLT) loss are different in MS compared to other diseases such as glaucoma and data on RNFLT loss in MS patients with or without optic neuritis (ON/NON) have remained inconsistent or even contradictory.

Methods

In this large cross-sectional study we analyzed the patterns of axonal loss of retinal ganglion cells in MS eyes (n = 262) with and without history of ON (MS/ON: 73 eyes; MS/NON: 189 eyes) and patients eyes with glaucomatous optic disc atrophy (GA: n = 22; 39 eyes) in comparison to healthy control eyes (HC: n = 406 eyes).

Results

We found that significant average and quadrant RNFLT loss is detectable by OCT in both MS and GA patients compared to healthy controls (p < 0.01). The age- and gender adjusted average and quadrant RNFLT did not differ significantly between MS and GA patients (p > 0.05). Average (p < 0.0001) and quadrant (p < 0.05) RNFL thinning is significantly more severe in MS/ON versus MS/NON eyes, and the extent of RNFL thinning varies across quadrants in MS/ON eyes with the highest degree of RNFLT loss in the temporal quadrant (p < 0.001).

Conclusion

RNFLT reduction across all four quadrants in MS patients as a whole as well as in MS/NON eyes argues for a diffuse neurodegenerative process. Superimposed inflammatory attacks to the optic nerve may cause additional axonal damage with a temporal preponderance. Future studies are necessary to further evaluate the capacity of OCT to depict disease specific damage patterns.     

Progressive axonal dysfunction and clinical impairment in amyotrophic lateral sclerosis

Objective

To elucidate longitudinal changes in axonal function in amyotrophic lateral sclerosis (ALS) patients, and to relate such changes with motor unit loss and functional impairment.

Methods

37 ALS patients (age, 53.7 ± 1.7 years; 22 males) were studied using axonal excitability techniques at baseline and 12 weeks follow-up.

Results

Longitudinal measurements across excitability parameters suggested increasing K⁺ channel dysfunction, with further increases in depolarising threshold electrotonus (90–100 ms, baseline, 46.8 ± 1.0%; follow-up, 48.7 ± 0.8%; P = 0.02) and superexcitability (baseline, −24.0 ± 1.2%; 12 weeks, −26.0 ± 1.2%; P = 0.04). Patients with preserved compound muscle action potential (CMAP) amplitude at follow-up developed more severe changes in axonal excitability than those in whom CMAP decreased from baseline, suggesting that the most pronounced disease effects were on motor axons immediately prior to axonal loss in ALS patients. Fine motor decline was associated with more severe changes in axonal excitability, suggesting that functional impairment was related to axonal dysfunction.

Conclusions

Longitudinal changes in axonal excitability in ALS patients suggest increasing K⁺ channel dysfunction in motor axons.

Significance

Axonal excitability studies enable investigation of longitudinal changes in axonal ion channel dysfunction, and thereby the processes that potentially contribute to axonal degeneration in ALS.     

Factors predicting the development of new onset post-operative Hydrocephalus following trans-sphenoidal surgery for pituitary adenoma

Background

The aim of this retrospective study was to identify the factors which can predict the development of new onset post-operative Hydrocephalus following transsphenoidal surgery for pituitary adenomas.

Methods

A total of 224 patients with the diagnosis of pituitary adenoma and without preoperative Hydrocephalus were identified from 1995 to 2012. Age, gender, tumor volumes, prior craniotomy and irradiation, outcome, hospital stay, CSF leak, infection and functional status of the tumor were included in the model for analysis.

Results

A total of 13 patients (5.8%) developed new onset post-operative Hydrocephalus. Intraoperative and post-operative CSF leaks were noted in 19 (8.5%) and 17 (7.6%) patients respectively. CSF infection was seen in only 7 (3.1%) patients. Age of the patient (p = 0.010), length of hospital stay (p = 0.012), intraoperative CSF leak (p = 0.000), post-operative CSF leak (p = 0.000) and CSF infection (p = 0.000) had shown significant correlation with the de novo onset of postoperative HC. The independent predictors of post-operative HC were post-operative CSF leak [p = 0.002, OR 27.898, 95% CI 3.350–232.311] and intra-operative CSF leak [p = 0.050, OR 7.687, 95% CI 1.003–58.924].

Conclusion

Age of the patient, intra-operative and post-operative CSF leak, CSF infection and duration of hospital stay were correlated with the development of HC. Post-operative and intra-operative CSF leaks were the independent predictors of new onset HC.     

Cerebrospinal fluid tau as a marker of neuronal damage after epileptic seizure

PurposeWhether repeated brief seizures can cause neuronal damage is controversial. Cerebrospinal fluid (CSF) total tau (T-tau) and phosphorylated tau (P-tau) measurements have been suggested for the diagnosis of Alzheimer's disease, and T-tau may also be a marker of axonal damage and neuronal degeneration. We studied T-tau and P-tau levels and P-tau/T-tau ratio in CSF after epileptic seizures in order to determine whether they are increased after seizures.MethodsA total of 54 patients with tonic–clonic or partial secondarily generalized seizures due to various etiologies were studied and CSF obtained within 48 h after the seizure.ResultsThere were no statistical differences in the levels of T-tau (p = 0.09, ANOVA) or P-tau (p = 0.60) between different etiologic groups or controls. No patients with epilepsy of unknown origin had abnormal CSF T-tau whereas 11 patients with acute or remote symptomatic seizures had abnormal T-tau levels and the P-tau/T-tau ratio showed significant differences between the groups and controls (p = 0.003).ConclusionsEpileptic seizures with unknown etiology did not increase CSF tau levels. Abnormal tau levels were associated with either acute or remote symptomatic seizures with known etiology. The presence of elevated CSF tau increases the probability of symptomatic cause in a patient with a seizure.     

Increased cerebrospinal fluid protein tau concentration in neuro-AIDS

OBJECTIVES: Assessment of cerebrospinal fluid (CSF) levels of protein tau in human immunodeficiency virus type 1 (HIV-1) infection. MATERIAL AND METHODS: CSF tau levels were analyzed in 52 HIV-1-infected patients, 37 of whom had no neurological symptoms, eight had aquired immunodeficiency syndrome (AIDS) dementia complex (ADC), and seven had AIDS with other neurological complications. RESULTS: A significantly higher mean CSF tau concentration was found in patients with ADC (380 pg/ml) compared with patients with neuroasymptomatic HIV-1 infection (120 pg/ml, P<0.01) and HIV-negative controls (150 pg/ml, P<0.05). No difference in CSF tau levels was found between patients with ADC and patients with AIDS with other neurological complications. CONCLUSION: CSF tau might be used as a biochemical marker for axonal degeneration and might be of use to identify HIV-1-infected patients with ADC and other neurological complications, but it cannot discriminate between ADC and other neurological complications in HIV-1-infection.     

Assessment of white matter integrity of autistic preschool children with diffusion weighted MR imaging

The purpose was to assess white matter integrity of autistic preschool children with diffusion weighted MR imaging. Prospective study was carried on 19 autistic children (mean age 55.2 ms, IQ of 86.5) and 10 sex, age and IQ matched control (mean age 53.2 ms, IQ 84.5). The childhood Autism Rating Scale (CARS), social age and language age were calculated. Patients and controls underwent diffusion weighted MR imaging of the brain with b factor of 0, 500 and 1000 s/mm². The apparent diffusion coefficient (ADC) value at different regions of the white matter were calculated and correlated with CARS, social age and language age. There were significant differences at the ADC value of the white matter between autistic and control children at genu (P = 0.043), splenium (P = 0.003) of the corpus callosum, frontal white matter (P = 0.015) and temporal white matter (P = 0.020). There was positive correlation of CARS score with ADC value of the genu (r = 0.63, P = 0.001), splenium (r = 0.59, P = 0.005), frontal white matter (r = 0.81, P = 0.001) and temporal white matter (r = 0.74, P = 0.001). The social age well correlated with ADC value of the frontal white matter (r = 0.81, P = 0.001) and language age well correlated with ADC value of the temporal white matter (r = 0.78, P = 0.001). We concluded that ADC value can be helpful in assessment of integrity of the white matter in autistic preschool children and well correlated with CARS score, social age and language age.