BACKGROUND: Ten randomly selected adult cadaveric specimens were dissected to analyse the anatomy of the vertebral artery during its course from the C3 transverse process to its entry into the spinal dural canal at the level of C1. In addition, 10 dry cadaveric C1-C2 bones were studied. The course of the artery and the parameters relevant during surgery in the region are evaluated. METHODS: Ten adult cadaveric specimens and 10 adult dry cadaveric C1 and C2 bones were studied. In five cadaveric specimens, the arteries and veins were injected with coloured silicon. The artery during its course from the transverse process of C3 to the transverse process of C2 was labelled as V1 segment, the artery during its course from the C2 transverse process to the C1 transverse process was labelled as V2 segment and the segment of the artery after its exit from the transverse foramen of C1 to the point of its dural entry was labelled as V3 segment. The relationship of the artery to the C1-2 joint and facets, distance of the location of the artery from the midline, from the C2 ganglion and from the other surgery related landmarks were evaluated. The extent of occupancy of the artery into the vertebral artery groove on the inferior surface of the superior facet of the C2 vertebra, and over the posterior arch of the atlas was studied. RESULTS: The V1 segment of the vertebral artery takes a varying degree of loop inside the vertebral artery foramen on the inferior aspect of the superior facet of the C2 vertebra. The loop extends towards the midline and was at an average distance of 14.6 mm from the midline of the vertebral body. The V2 segment of the artery takes an initial lateral loop after its exit from the transverse process of the C2 vertebra. The average distance of the artery from the lateral end of the C2 ganglion was 7.2 mm and from the dural tube was 15.3 mm. The vertebral artery groove in the superior facet of C2 and the groove over the posterior arch of the atlas were completely occupied by the vertebral artery only in six sides and in none respectively, suggesting the possibility of the dynamic nature of the relationship of the artery to the bone. CONCLUSIONS: The vertebral artery adopts a serpentine course in relationship to the C2 vertebra, making it susceptible to injury during the surgical procedures in the region. The multiple loops of the artery and a buffer space within the vertebral artery groove on the inferior surface of the superior facet of the C2 vertebra and over the posterior arch of atlas provide the artery an extra length and space, probably essential to avoid any stretch during neck movements.

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Eighty-five women with epilepsy were followed up for reproductive functions under the registry of epilepsy and pregnancy. 32 of them had completed the pregnancy. Their mean age was 26 years and mean seizure frequency was 0.7 during current pregnancy. Nineteen of them (59.4%) had generalized epilepsy. Nine of them were not on any anti epileptic drugs (AED), 23 women were on various AEDs, 19 being on monotherapy. Only 40% of the women were taking folic acid during pregnancy. Pregnancy ended as spontaneous abortion in one patient. Nearly one third required cesarean section. Majority (87.5%) had term babies. Three (10.7%) babies had birth asphyxia. Six babies (21.4%) had low birth weight. Congenital malformations were detected in four cases (12.5%). Malformations included neural tube defects, talipes equinovarus and other minor anomalies. These babies were exposed to sodium valproate, carbamazepine or phenobarbitone. The risk of malformation was significantly greater (p<0.05) when the mother had generalized epilepsy. The odds ratio for risk of malformation was much higher with sodium valproate (6) than that with carbamazepine (1.2) or phenobarbitone (0.8). Majority of women with epilepsy had safe pregnancy and childbirth without any aggravation of epilepsy.

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The study was carried out to determine the safe site of entry and the appropriate trajectory of the screw implantation in the lateral masses of atlas (Cl) and axis (C2) during their fixation using the plate and screw technique. Fifty dried specimens of atlas and axis vertebrae were studied. Various dimensions of the lateral masses were quantitatively measured, laying stress on their relationship with the vertebral artery foramen. As the vertebral artery foramen was present entirely in the transverse process in all specimens, screw implantation in the facet of atlas was relatively safe. Best direction of screw implantation in the facet of atlas was observed to be 15 degrees medial to sagittal plane and 15 degrees superior to axial plane. It should be implanted from the middle of the posterior surface of facet. Vertebral artery foramen formed a deep groove in the undersurface of a majority of superior facets of axis. In 15% facets, vertebral artery foramen occupied the entire undersurface of the superior facet. Safe angle for screw implantation in the facet of axis through its pedicle was seen to be 40 degrees medial to sagittal plane and 20 degrees superior to axial plane. Safe site of screw entry in the axis was superior and medial third of the posterior surface of the pedicle. Quality of cancellous bone in the lateral masses in the proposed trajectory of screw in Cl and C2 was good, providing an excellent purchase of the screw.

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Current philosophy of treatment of brain abscess includes aspiration, appropriate antibiotics, treatment of sequelae and eradication of the primary source. Early clinical suspicion and diagnosis with CT is crucial. Small abscesses (<3 cm) in cerebritis or capsular stage located deep in clinically stable, poor surgical risk patients with diagnosis firmly supported by CT, may be treated with medical treatment only. Biweekly CT scan must be done to monitor the treatment response. CT or ultrasound guided aspiration should be performed in the event of clinical deterioration, failure of reduction in size or enlargement of abscesses. Encapsulated abscess (>3 cm), presence of significant neurological deficit or mass effect, doubt in the diagnosis and presumed resistant organisms are best treated with aspiration. Excision is required in large superficial abscesses resistant to multiple aspirations, post-traumatic abscess with a foreign body or fistula and multiloculated abscess of nocardial or actinomycotic aetiology. Results are directly related to the sensorium at the time of presentation. Stereotactic aspiration of all the loculi of multiloculated abscess in single or staged aspiration, and more completed drainage and lavage with endoscopic stereotactic evacuation may cut down indications of excision of brain abscess in future. It is concluded that, with diagnostic and technical advancements, a trend of adequate drainage of brain abscess via minimally invasive surgery is emerging. Confirmation of diagnosis and monitoring of treatment response with magnetic resonance spectroscopy may allow greater number of patients in future to be managed with medical treatment only.

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Organophosphorous compounds, the anticholinesterases, produce significant morbidity and mortality in India. Although exact estimates are not available, hospital based statistics suggest that nearly half of the admissions to emergency with acute poisoning are due to organophosphates. Following accidental or suicidal exposure, these anticholinesterases lead to three well defined neurological syndromes i.e. initial life threatening acute cholinergic crisis which often requires management in intensive care unit, intermediate syndrome in which cranial nerve palsies, proximal muscle weakness and respiratory muscle weakness are common and patients often require respiratory support and delayed organophosphate induced polyneuropathy. In addition to these three classical neurological syndromes following acute exposure and in some following low dose chronic exposure, several neurobehavioural changes have been observed and these have been termed together as 'chronic organophosphate induced neuropsychiatric disorders' (COPIND). Organo-phosphate compounds produce significant pesticide related illness in developing countries. There is, thus, a need to determine exact extent of the problem and to develop appropriate strategies to manage these cases with available resources in these countries.

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Moyamoya is probably an inherited vasocclusive disease first described in Japan and now reported from all over the world. Genetic linkage studies and study of the factors possibly involved in its pathogenesis have shed new light on this disease. There is some suggestion that the pathogenesis may vary between races. A number of revascularization procedures have been devised. There is still controversy regarding the timing and the type of surgery. Functional MRI and PET scanning may provide more objective criterion on the outcome of these procedures. Neuropsychological studies may also be of use in judging the benefits of surgery. In this review, some of the recent advances in the study of the genetics and pathogenesis of the disease are reviewed and the clinical manifestation and the role of surgery are discussed. Relative lack of literature from outside Japan and the Korean peninsula has hampered the understanding of the disease in other countries.

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Background: Intracerebral hemorrhage (ICH) results in secondary brain edema and injury that may lead to death and disability. ICH also causes inflammation. It is unclear whether inflammation contributes to brain edema and neuron injury or functions in repairing the brain tissue. Aims: To understand the effect of inflammation in ICH, we have carried out an investigation on the various aspects and the dynamic changes of inflammation. Settings and Design: An ICH model was generated by injecting 50 ml autologous tail artery blood stereotactically into the right caudate nucleus of 30 rats, which were randomly divided into five ICH groups. Similarly, five Sham control groups were generated by inserting the needle to the right caudate nucleus of rats. Materials and Methods: Rat behavior was evaluated over the time course (6 h, 24 h, 48 h, 72 h and 7 d) in each group. The rats were then killed by administering an overdose of pentobarbital. Following the euthanasia, the brain water content, neuronal loss, glia proliferation, inflammatory infiltration and brain morphology of the rats were measured. Additionally, the expression of TNF-a,IL-6, ICAM-1, VEGF, NF-kB, C3 and CR2 was analyzed by immunohistochemistry. Statistical Analysis: The data were analyzed by student's t test. Results: Rat brain water content increased progressively over the time course and reached its peak at 48h followed ICH. The maximum of inflammatory infiltrate (especially neutrophils) and immunopositive cells of TNF-a, IL-6 and NF-kB, were at 48h. The expression of C3 and CR2 reached their peaks at 48-72h, while the expression ICAM-1 and VEGF were at maximum at 72h followed ICH. Conclusions: The results suggested that the inflammatory cytokines, complement system and VEGF may have a function in the development of the brain edema and neuron injury followed ICH.

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Fungal infections of the central nervous system (CNS) are rare in the general population and are invariably secondary to primary focus elsewhere, usually in the lung or intestine. Except for people with longstanding diabetes, they are most frequently encountered in immunocompromised patients such as those with acquired immunodeficiency syndrome or after organ transplantation. Due to the lack of inflammatory response, neuroradiological findings are often nonspecific and are frequently mistaken for tuberculous meningitis, pyogenic abscess or brain tumor. Intracranial fungal infections are being identified more frequently due to the increased incidence of AIDS patients, better radiological investigations, more sensitive microbiological techniques and better critical care of moribund patients. Although almost any fungus may cause encephalitis, cryptococcal meningoencephalitis is most frequently seen, followed by aspergillosis and candidiasis. The biology, epidemiology and imaging features of the common fungal infections of the CNS will be reviewed. The radiographic appearance alone is often not specific, but the combination of the appropriate clinical setting along with computed tomography or magnetic resonance may help to suggest the correct diagnosis.

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Thrombolytic therapy for acute ischaemic stroke has recently become available in India but its success depends on initiating the treatment in the narrow therapeutic time window. There is commonly a delay of several hours before patients with acute stroke seek medical attention. A prospective study was conducted to assess the factors influencing this delay in admission of acute stroke cases. 110 cases (71 males, 39 females) of acute stroke that arrived within 72 hours at our hospital casualty were recruited. A standardized structured questionnaire was given to patients or their attendants. The median time to casualty arrival was 7.66 hours with 25% cases arriving within 3 hours and 49 % cases within 6 hours. Distance from hospital, contact with a local doctor and low threat perception of symptoms of stroke were independent factors associated with delay in arrival. Living in city, presence of family history and older age were associated with early arrival. There was no correlation with patients' or attendants' sex, educational status, history of previous stroke or transient ischaemic attack, subtype or severity of stroke, time of stroke and availability of transport. Adequate measures need to be taken to improve the public awareness of stroke and the role of local doctors.

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A prospective study was conducted to look for various factors that could predict the risk of recurrence of a single unprovoked idiopathic seizure. Seventy six patients with a history of single episode of seizure ultimately completed the study and the data regarding age, sex, duration of seizure, time of occurrence of the ictus, interval between onset and referral, family history of seizure and alcohol consumption were analysed. All patients of symptomatic epilepsy and those with an abnormal scan were excluded. The patients were randomized into two groups, one of which received anti epileptic medication and the other did not. All patients underwent electroencephalography (EEG). Twenty two (M=16, F=6) of the 76 patients (M=56, F=20) had a recurrence of seizure. The duration of seizure at initial presentation was 10.1 +/- 5.2 min. in the recurrence group and 6.5 +/- 4.1 min. in the non-recurrence group. Twelve of the 16 patients with an abnormal EEG had a recurrence whereas only 10 of the 60 patients with a normal EEG had a recurrence (p <0.001). Of the treated cases (n=36), only 4 had a recurrence compared to 18 of the untreated cases (n=40) (p <0.002). Eighteen of the 22 cases having a recurrence did so within three months. Six of the cases with family history of seizure (n=10) had a recurrence, whereas only 16 of the cases without family history of seizure (n=16) had a recurrence (p <0.05). Patients of a single unprovoked idiopathic seizure with a normal CT scan are less likely to have a recurrence if the duration of seizure at presentation is short, EEG is normal, more than 3 months have passed since the first seizure and if treatment has been started. Family history of seizures does have a moderately significant bearing, but alcohol intake does not increase the chances of seizure.

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Erythrocyte lipid peroxidation, oxidative hemolysis, erythrocyte antioxidant enzymes, viz. superoxide dismutase, glutathione reductase, glutathione peroxidase, catalase and plasma antioxidants, viz. vitamin A, vitamin E, vitamin C and ceruloplasmin have been determined by spectrophotometric methods in 15 patients with Parkinson’s disease (PD) and in 50 controls. Lipid peroxidation, oxidative hemolysis and plasma ceruloplasmin were significantly higher in PD patients as compared to normals. Erythrocyte antioxidants in PD patients were not significantly different from the controls. However, plasma vitamin C in PD patients was significantly lower than the controls. It is concluded that these patients are under oxidative stress which points to a possible involvement of free radicals in PD.

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Background: Tissue thromboplastin (TTP) is an integral membrane protein contributing to coagulopathy after trauma of brain, which is a rich source of TTP. Aims: A study was undertaken to establish the TTP content of various areas of normal brain and estimate the changes in TTP activity of brain in response to varying degrees of trauma. Materials and Methods: Samples from different areas of brain of ten cadavers were used as controls and they were compared with contused brain tissue obtained after surgery in 25 head injury (HI) patients of varying severity. Results: In the study group, the TTP activity of the frontal, parietal, and temporal lobes after HI was significantly raised in contrast to that of the control group. The TTP activity was also significantly higher in the severe HI patients than those having moderate HI. The mode of injury and the time lapse after HI had no significant bearing on the TTP activity. Subjects above 40 years of age demonstrated a higher mean TTP activity after HI, though it was not statistically significant. Conclusion: The study provides quantitative data on TTP activity of normal brain and highlights the role of TTP in coagulopathy following HI through its increased activity after HI, more so in the severe HI group.

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Background: Given the constraints of resources, thrombolysis for acute ischemic stroke (AIS) is under evaluation in developing countries. Prothrombin time (PT), platelet count and activated partial thromboplastin time (aPTT) may not be feasible within the time window. Aim: To evaluate the safety and efficacy of thrombolysis in selected patients without the coagulation profile. Design: Open, nonrandomized, observational study. Materials and Methods: Fifty-four stroke patients were classified using TOAST criteria (large artery atherosclerotic = 13; cardioembolic = 12; small vessel occlusion = 22; other determined etiology =three; undetermined etiology = four). The mean time to reach emergency was 2.4h (1.15-3.4), the mean door to CT, 24 min (10-47) and the door to recombinant tissue plasminogen activator (r-tPA) injection, 26.8 min (25-67). The NIHSS scores ranged from 11 to 22 (mean = 15.5 ± 2.7). Patients with history of liver or renal disease or those on anticoagulants were excluded. The PT, aPTT and platelet count were not done. Recombinant tissue plasminogen activator was administered at a dosage of 0.9 mg/Kg. Results: Thirty-five patients (65%) significantly improved on NIHSS at 48h (³4 points) (mean change = 10; range= 4-17). At one month, 43 (79%) improved on Barthel Index (mean change = 45%). One each developed small frontal lobe hemorrhage and recurrent stroke; one died of aspiration; and eight showed no improvement. Conclusions: Hyperacute thrombolysis was found useful and safe in selected patients with AIS even without the coagulation studies.

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Acute disseminated encephalomyelitis (ADEM) is an uncommon inflammatory demyelinating disease of the central nervous system. The true incidence of the disease in India is undetermined and is likely to be more frequent than reported, as the common antecedent events, exanthematous fevers and Semple antirabies vaccination, which predispose to ADEM, are still prevalent. The existing evidence suggests that ADEM results from a transient autoimmune response towards myelin or other self-antigens, possibly via molecular mimicry, or by non-specific activation of auto-reactive T cell clones. ADEM is a monophasic illness with favourable long-term outcome. Involvement of neuroaxis is variable and can be diffuse or multifocal and site restricted. Magnetic resonance imaging (MRI) is highly sensitive in detecting white matter lesions and the lesions described are rather extensive and subcortical in location. Involvement of the deep gray matter, particularly basal ganglia, is more frequent. Oligoclonal bands in CSF are usually absent. No therapy has been established by controlled trials in ADEM. Use of high-dose methylprednisolone, plasma exchange, and IVIG are based on the analogy of the pathogenesis of ADEM with that of multiple sclerosis (MS). Differentiation of ADEM from the first attack of MS is important from prognostic as well as therapeutic point of view. However, in the absence of biological marker, at times differentiation of ADEM from the initial presentation of MS may not be possible even by combination of clinical, CSF analysis, and MRI. This differentiation is more relevant to India where the incidence of MS is low.

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In cross-sectional studies, low levels of folate and B12 have been shown to be associated with cognitive decline and dementia Evidence for the putative role of folate, vitamin B12 in neurocognitive and other neurological functions comes from reported cases of severe vitamin deficiencies, particularly pernicious anemia, and homozygous defects in genes that encode for enzymes of one-carbon metabolism. The neurological alterations seen in these cases allow for a biological role of vitamins in neurophysiology. Results are quite controversial and there is an open debate in literature, considering that the potential and differential role of folate and B12 vitamin in memory acquisition and cognitive development is not completely understood or accepted. What is not clear is the fact that vitamin B12 and folate deficiency deteriorate a pre-existing not overt pathological situation or can be dangerous even in normal subjects. Even more intriguing is the interaction between B12 and folate, and their role in developing hyperhomocysteinemia. The approach to the rehabilitation of the deficiency with adequate vitamin supplementation is very confusing. Some authors suggest it, even in chronic situations, others deny any possible role. Starting from these quite confusing perspectives, the aim of this review is to report and categorize the data obtained from the literature. Despite the plausible biochemical mechanism, further studies, based on clinical, neuropsychological, laboratory and (lastly) pathological features will be necessary to better understand this fascinating biochemical riddle.

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CONTEXT: Careful evaluation of pharmacotherapy, seizure control and quality of life (QOL) are helpful in improving epilepsy care but such data are relatively meager from developing countries. AIMS: To audit pharmacotherapy, seizure control and QOL in persons with epilepsy and to identify factors associated with impaired QOL. SETTINGS AND DESIGN AND MATERIALS AND METHODS: The study was carried out using a cross-sectional design in the setting of a tertiary care epilepsy center in India. Persons with epilepsy with >12 months follow-up at this Center and aged >16 years were eligible for enrollment. Persons with other disabilities or pregnancy were excluded. Subjects were interviewed with a standard questionnaire and an adapted version of Quality of Life in Epilepsy - 31 (QOLIE-31). Data pertaining to treatment at the time of referral to this center was extracted from medical records. STATISTICAL ANALYSIS USED: Chi-square test, analysis of variance and multiple regression analysis were carried out for statistical significance. RESULTS: One hundred and twelve patients with epilepsy (59 males, mean age 31.2±10.7 years) were included. Forty-seven (42%) persons had Generalized Epilepsy (GE) and 65 persons (58%) had Localization-Related Epilepsy (LRE). At entry 24 persons (21.4%) were not on treatment and 59 persons (64.8%) had frequent seizures. At last follow-up 64 persons (57.1%) were seizure-free, 83 persons (74.1%) were on monotherapy and 29 were (25.9%) on polytherapy. Cost of drug at entry was INR 2276 (monotherapy) and INR 3629 (polytherapy) (45 INR = 1 USD). At the time of last follow-up, it was 1898 and 4929 respectively. QOLIE-31 Total Score (TQOL) ranged from 22.6 to 94.4 (mean 68.0 ± 15.8). Multiple regression analysis showed significant correlation between low TQOL score and polytherapy (P=0.002) and occurrence of one or more seizures per month (P=0.001). CONCLUSIONS: Frequent seizures and polytherapy are associated with lower QOL in persons with epilepsy.

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Glioblastoma multiforme (GBM) Patients generally have a dismal prognosis, with median survival of 10-12 months. GBM with long-term survival (LTS) of ³ 5 years is rare, and no definite markers indicating better prognosis have been identified till date. The present study was undertaken to evaluate GBMs with LTS in order to identify additional correlates associated with favourable outcome. The cases were evaluated for relevant clinicopathological data, proliferation index and expression of tumortumour suppressor gene ( p53 ), cyclin-dependant kinase-inhibitors ( p27 and p16 ) and epidermal growth factor receptor (EGFR) proteins. Six cases of GBM with LTS with an average survival of 9 years (range 5-15 years) were identified. All were young patients with mean age of 27 years (range 8-45 years). Histology of three cases was consistent with conventional GBM, while two showed prominent oligodendroglial component admixed with GBM areas. One was a giant cell GBM, which progressed to gliosarcoma on recurrence. The mean MIB-1LI was 12% (range 6-20%). p53 was immunopositive in 4 out of 5 cases. EGFR and p27 were immunonegative in all, whereas p16 was immunonegative in 3 out of 5 cases. Currently, in the absence of specific molecular and genetic markers, GBM in young patients should be meticulously evaluated for foci of oligodendroglial component and/or giant cell elements, in addition to proliferative index and p53 expression, since these probably have prognostic connotations, as evident in this study. The role of p16 and p27 however needs better definition with study of more number of cases.

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Soft stabilization has an important role in the treatment of the degenerative lumbar spine. Fusion of one or two motion segments may not make a big difference in the total range of motion of the lumbar spine, but preserving flexibility of a motion segment may prevent adjacent segment disease and may permit disc replacement, even when facet joints need to be excised. A favourable environment is created in the motion segment by unloading the disc and permitting near normal motion, the disc may be able to repair itself or may supplement reparative potential of gene therapy.

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Background and Aims: In view of the prevailing controversy about the role of Methylenetetrahydrofolate reductase (MTHFR) C677T mutation in stroke and paucity of studies from India, this study has been undertaken to evaluate MTHFR C677T gene polymorphism in consecutive ischemic stroke patients and correlate these with folic acid, homocysteine (Hcy) and conventional risk factors. Settings and Design: Ischemic stroke patients prospectively evaluated in a tertiary care teaching hospital. Materials and Methods: Computerized tomography proven ischemic stroke patients were prospectively evaluated including clinical, family history of stroke, dietary habits and addictions. Their fasting and postprandial blood sugar, lipid profile, vitamin B12, folic acid and MTHFR gene analysis were done. Statistical Analysis: MTHFR gene polymorphism was correlated with serum folic acid, Vitamin B12 and Hcy levels; family history of stroke in first-degree relatives; and dietary habits; employing Chi-square test. Results: There were 58 patients with ischemic stroke, whose mean age was 50 (4-79) years; among them, 10 were females. MTHFR gene polymorphism was present in 19 (32.8%) patients, 3 were homozygous and 16 were heterozygous. Both serum folate and B12 levels were low in 29 (50%) patients and Hcy in 48 (83%). Hypertension was present in 28 (48%) patients, diabetes in 12 (21%), hyperlipidemia in 52 (90%), smoking in 17 (29%), obesity in 1 (1.7%) and family history of stroke in first-degree relatives in 13 (22.4%). There was no significant relationship of MTHFR gene polymorphism with folic acid, B12, Hcy levels, dietary habits and number of risk factors. Vitamin B12 level was low in vegetarians ( P <0.003). In 3 patients with MTHFR TT alleles, Hcy was elevated in all 3, low folic acid in 2 and family history of stroke in 1 patient. Conclusion: MTHFR gene polymorphism was found in one-third of patients with ischemic stroke and was insignificantly associated with higher frequency of elevated Hcy.

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Cryptococcal meningitis has emerged as a leading cause of infectious morbidity and mortality in patients with AIDS. Among the human immunodeficiency virus (HIV)-seropositive subjects, cryptococcal meningitis is the second most common cause of opportunistic neuro-infection. Current trends are changing due to the marked improvement of quality and length of life produced by highly active antiretroviral therapy (HAART). The introduction of generic HAART in India has resulted in an increase in the number of individuals getting treatment for HIV infection, as the cost of highly active antiretroviral therapy (HAART) has decreased 20- fold. Cryptococcal meningitis occurs in non-HIV patients who are immunodeficient due to diabetes, cancer, solid organ transplants, chemotherapeutic drugs, hematological malignancies etc and rarely in healthy individuals with no obvious predisposing factors. Diagnosis of cryptococcal meningitis is fairly straightforward once the diagnosis is considered in the differential diagnosis of chronic meningitis. Treatment of a patient with cryptococcal infection is a challenge for both the physician and the patient, but rewarding, as many would recover with timely and adequate antifungal therapy.

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Background: In May 2006, there was a large Chikungunya virus infection (CHIKV) outbreak in the Nagpur district of Maharashtra, a province in western India. Usually, CHIKV is a self-limiting febrile illness. However, neurological complications have been described infrequently. Aim: To study the clinical characteristics of various neurological complications associated with CHIKV infections. Materials and Methods: Patients with neurological complications following CHIKV infection during the outbreak were the subjects of the study. On the basis of clinical features and investigative findings, patients were grouped into various neurological syndromes: Encephalitis, myelopathy, peripheral neuropathy, myeloneuropathy, and myopathy. Cerebrospinal fluid (CSF) samples were also collected for biochemical and serological studies. Results: Of the 300 patients with CHIKV infection seen during the study period, June-December 2006, 49 (16.3%) [M : F: 42:7] had neurological complications. The neurological complications included: Encephalitis (27, 55%), myelopathy (7, 14% ), peripheral neuropathy (7, 14%), myeloneuropathy (7, 14%), and myopathy (1, 2%). Reverse Transcriptase polymerase chain reaction (RT-PCR) and real-time PCR was positive in the CSF in 16% and 18%, respectively. Conclusion: Recent CHIKV infection was associated with various neurological complications, suggesting neurotropic nature of the virus. The outcome of the neurological complications is likely to be good.

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Catabolism of tryptophan and tyrosine in relation to the isoprenoid pathway was studied in neurological and psychiatric disorders. The concentration of trytophan, quinolinic acid, kynurenic acid, serotonin and 5-hydroxyindoleacetic acid was found to be higher in the plasma of patients with all these disorders; while that of tyrosine, dopamine, epinephrine and norepinephrine was lower. There was increase in free fatty acids and decrease in albumin (factors modulating tryptophan transport) in the plasma of these patients. Concentration of digoxin, a modulator of amino acid transport, and the activity of HMG CoA reductase, which synthesizes digoxin, were higher in these patients; while RBC membrane Na+-K+ ATPase activity showed a decrease. Concentration of plasma ubiquinone (part of which is synthesised from tyrosine) and magnesium was also lower in these patients. No morphine could be detected in the plasma of these patients except in MS. On the other hand, strychnine and nicotine were detectable. These results indicate hypercatabolism of tryptophan and hypocatabolism of tyrosine in these disorders, which could be a consequence of the modulating effect of hypothalamic digoxin on amino acid transport.

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AIMS AND OBJECTIVES: To study the clinical and laboratory features of patients admitted with vitamin B12 deficiency-related (B12def) neurological syndromes. SETTINGS AND DESIGN: A hospital-based retrospective and prospective study conducted at a referral teaching hospital. MATERIALS AND METHODS: Consecutive patients admitted with vitamin B12 deficiency-related neurological disorders during a three-year period from June 2000 to May 2003 were included. Data regarding clinical and laboratory features were obtained. Follow-up was done at least six months following treatment with parenteral vitamin B12. Chi-square test was used for statistical analysis. RESULTS: A total of 63 patients (52 males) with a mean age of 46.2 years were studied. The mean duration of symptoms at presentation was 10.3 months. Myeloneuropathy (54%) was the commonest neurological manifestation, followed by myeloneuropathy with cognitive dysfunction (34%), and peripheral neuropathy (9%). Neuropsychiatric manifestations and dementia were observed in 38% and 19% of patients respectively. All the patients had megaloblastic changes in the bone marrow smear. Eleven (17.5%) patients had both hemoglobin and the mean corpuscular volume (MCV) within the normal range. Follow-up after at least six months of therapy with parenteral B12 showed improvement in 54% patients. CONCLUSIONS: A high index of suspicion of B12def is required in patients presenting with myelopathy, cognitive decline, or neuropathy. A normal hemoglobin or MCV does not exclude B12def; therefore, other tests such as bone marrow smear and serum vitamin B12 assay are essential, as the condition is often reversible with treatment.

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Hyperammonemic encephalopathy with normal liver function is an uncommon serious adverse effect of valproate therapy. We retrospectively analyzed the case records of 5 patients of epilepsy on valproate with hyperammonemic encephalopathy. Of the 5 patients, 3 were on monotherapy. The mean valproate dose was 1250 mg/day and the duration of therapy ranged between 4 and 90 days. Alteration in the sensorium was the presenting clinical feature. The risk factors included high initial dose (2), long-term valproate therapy (1), and long-term valproate therapy with concomitant topiramate (1). There was good correlation between the fall in serum ammonia levels and clinical improvement. Hyperammonemic encephalopathy should be suspected in patients on valproate with altered sensorium. Response to treatment is rewarding.

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Over the past century, steady advances have been made in fixating an unstable atlantoaxial complex. Current options for fixation of the atlantoaxial complex include posterior clamps, posterior wiring techniques, C1-C2 transarticular screw fixation, posterior C1 lateral mass screw with C2 pars or pedicle screw fixation, and anterior transoral C1 lateral mass to C2 vertebral body fixation.

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