Background: Mastitis is a problem of dairy animals including buffaloes. Treatment failure has become a common problem and the most cited reason is antibiotic resistance. The paper presents the scenario of antibiotic resistance with special reference to multi drug resistance pattern. Methods: Microbiological assay of mastitis affected 48 milk samples was carried out using standard protocols to establish the prevalence of mastitis caused by E. coli and S. aureus. Antibiotic sensitivity test was carried out against these organisms and the whole milk culture for commonly used antibiotics. The drug resistance pattern was established. Result: The overall prevalence of mastitis was 20%. The prevalence of E. coli and S. aureus was 29.17% and 54.17% respectively. The antibiotic sensitivity revealed that E.coli isolates were 100% susceptible to tetracycline, gentamicin, enrofloxacin and streptopenicillin followed by Ceftriaxone and sulbactum combination and streptomycin (92.86%) and ceftriaxone and methicillin (85.71%). The isolates of S. aureus were 100% sensitive to only two antibiotics gentamicin and streptopenicillin. The antibiogram of whole milk culture revealed maximum susceptibility to enrofloxacin, gentamicin and streptopeniciliin (95.83% each). Multiple drug resistance has been observed in this study.

Background Longitudinally extensive transverse myelitis (LETM) is a severe inflammatory spinal cord disorder. It is commonly associated with neuromyelitis optica spectrum disorders and other autoimmune conditions like Sjögren syndrome, infectious and idiopathic aetiologies. Interleukin-6 (IL-6) is one of the key pro-inflammatory cytokines implicated in neuroinflammation and may serve as an important biomarker of disease activity.Objective To evaluate the correlation between cerebrospinal fluid (CSF) IL-6 levels and disease activity in patients with LETM and to assess its prognostic value for short-term functional outcomes.Methods In this prospective follow-up study conducted over 18 months, 41 patients with LETM and 21 controls with non-inflammatory neurological conditions were enrolled. Disease severity was assessed using the Expanded Disability Status Scale (EDSS) at admission and at 3-month follow-up. CSF IL-6 levels were analysed and correlated with clinical and radiological variables using Spearman correlation, receiver operating characteristic (ROC) analysis and multivariate regression.Results Median CSF IL-6 levels were significantly higher in LETM patients than controls (11.26 vs 5.02 pg/mL; p<0.001). CSF IL-6 showed a moderate positive correlation with EDSS at admission (ρ=0.34, p=0.027) and follow-up (ρ=0.51, p<0.001). ROC analysis demonstrated fair predictive accuracy for severe disease (AUC=0.70), with a cut-off of approximately 7 pg/mL. Multivariate analysis identified CSF IL-6 as an independent predictor of disease severity.Conclusions CSF IL-6 correlates with disease activity and disability in LETM and may serve as a useful biomarker for prognostication and treatment planning.

Introduction: Healthcare-associated infections (HAIs) are a significant cause of morbidity and mortality. HAIs become crucial in patients with neurological illnesses, as they need invasive procedures and extended care, prolonging the hospital stay in most cases. In this study, we report the type, microbial etiology, and outcome of patients with HAIs in a Neurology Intensive Care Unit setting. Methods: In this prospective study, 213 neurologically ill patients were recruited. Patient demographics, primary diagnosis, comorbidities, invasive interventions, device specific data, and length of hospital stay were recorded. Data collected for each episode of HAI included- site of infection, causative organisms, and susceptibility. Site specific infections were categorised as per CDC/NHSN definitions for HAIs. Results: The median age of patients was 60 years (range 15-88) and 66.70 % were male. HAIs were observed in 135 (63.38 %) patients. Majority of the patients had stroke (ischemic/haemorrhagic) [n = 142;66.66 %] followed by neuromuscular [n = 18; 8.45%] and seizure disorder [n = 14; 6.57 %]. Most prevalent site of HAIs was urinary tract infections (UTI) (n = 80;37.55 %) followed by pneumonia (n = 74;34.74 %) and blood stream infections (n = 53;24.88 %). 209 patients (98.12 %) underwent urinary catheterization, 90 (42.3 %) required intubation and mechanical ventilation, and 70 (32.86 %) central venous catheterisations. Amongst various HAIs, commonly isolated bacterial pathogens in UTI were Escherichia coli [18/48;37.59 %], Enterococcus [10/48;20.83 %] while Candida species [35/40;87.50 %] was the most common amongst fungal pathogens. Causative organisms in Pneumonia were Klebsiella pneumoniae (27/104;25.96 %), Acinetobacter baumannii (n = 25/104;24.03 %), and Pseudomonas aeruginosa [14/104;13.46 %]. Among the blood stream infections, Staphylococcus species were the most common [39/161;24.22 %] followed by candida species [5/161;3.10 %]. Out of 55 patients who died, HAI was observed in 39 patients (70.90 %). Mean length of hospital stay was 17.56 +/- 13.17 days. Presence of coronary artery disease, pulmonary site infection, low Glasgow Coma Scale, central venous catheterization, mechanical ventilation, abnormal chest x-ray, and multiple site infections were significantly associated with high mortality (p < 0.05). Conclusion: In our study 63.38% of neurological patients had HAIs. The most common sites were urinary, pulmonary, and blood stream infections. Device associated infections were common and significantly associated with poor outcome. Considering the high incidence of HAIs early recognition and treatment of site-specific pathogens may improve the outcome in these patients.

Abstract Objective Only a few studies have compared the different classification systems of psychogenic nonepileptic seizures (PNESs). A universally acceptable classification system for PNES will aid in the early diagnosis and may lead to better standardization for future studies. This study aimed to describe the clinical semiology and provide comparative analysis of PNES classification systems described by Hubsch et al, Wadwekar et al, Dhiman et al, and Asadi-Pooya. Methods Prospectively, patients provisionally diagnosed clinically as PNES were confirmed on video electroencephalography and their semiology was classified according to the classification systems mentioned earlier. Patients were additionally evaluated for coexisting anxiety or depression using Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition criteria and its severity assessed using Hamilton's depression/anxiety rating scales. Results A total of 104 PNES patients were included in the study. Mean age at presentation was 24.5 ± 10.4 years with females as the predominant proportion (76.9%). Whole body flaccidity was the commonest clinical presentation of PNES seen in 60.58% cases. All PNES cases could be classified using the Asadi-Pooya's classification, while 8.7, 47.1, and 53.8% PNES events remained unclassified, respectively, using the classification system as described by Dhiman et al, Wadwekar et al, and Hubsch et al; 33(31.73%) PNES patients had depression and 8 (7.7%) had generalized anxiety disorder in our study. Conclusion Nonmotor manifestations were the most frequent semiology in our cohort. Of the PNES classification systems studied, Asadi-Pooya's classification was easier to apply and could classify all the patients in the study.

Early diagnosis and treatment of tubercular meningitis (TBM) is one of the best predictors of survival. The smear testing of the cerebrospinal fluid (CSF) has a low sensitivity and cultures, though having higher sensitivity, take a long time in TBM diagnosis. The present study was done to evaluate the proportion of positive Gene Xpert test, a rapid nucleic acid amplification test, in clinically suspected patients with TBM. The results of Gene Xpert tests were then compared with the culture results. One hundred and fifty prospective patients with a clinical suspicion of TBM were classified as probable or possible TBM and underwent CSF examination for culture and Gene Xpert assay. Out of 124 patients available for statistical evaluation, 52 were in the probable and 72 in possible TBM group. The proportion of patients with Gene Xpert positivity were significantly more in probable compared to possible TBM (63.15% vs 36.85%, p<0.001). Twenty-eight patients had a positive culture result. The sensitivity of Gene Xpert relative to culture testing was 68.42%, specificity of 97.61%, a positive predictive value of 92.85% and a negative predictive value of 87.23%. Gene Xpert testing provided a rapid diagnosis in patients suspected with TBM. The high sensitivity and specificity of this test relative to culture testing is a strong indication that it should be included as one of the gold standard tests in patients with suspected TBM.

Dear Sir, 21-year-old male (Bachelor of Arts student) born out of full-term normal delivery of non-consanguineous parentage, with normal developmental milestones in all four domains, presented to the neurology outpatient (OPD) for the evaluation of a gait abnormality that had been noticed by his relatives since the age of 6 years. It was insidious in onset and gradually progressive, starting simultaneously in both lower limbs. While walking, he used to cross over to either side, which was associated with stiffness, and he used to drag both feet while walking. After 4 years of these symptoms, he also developed swaying to either side while walking without any aggravating or relieving factors, but there were no falls while walking initially. After about 10 years, the patient also developed intermittent tripping in both feet while walking. It was not associated with any sensory symptoms. His difficulty was gradually progressive, such that since last 1 year, the patient has noticed that he is unable to run and has frequent falls while running, though he is still able to walk independently. There was no history of any change in the voice or cranial nerve involvement. He had no tremors when reaching out for objects and had no symptoms referring to bowel or bladder functions. There was no history suggestive of any cognitive decline or behavioral abnormalities. Family history was negative for neurologic disease, diabetes mellitus, or sudden cardiac death. On general examination, he had pes cavus, hammer toes, a Swan neck deformity, and a Z deformity of the fingers [Figure 1]. There were no telangiectasias or tendon xanthomas. His higher mental functions were normal. The fundus examination was normal. He had normal visual acuity in both eyes. He had gaze-evoked nystagmus, saccadic pursuits, and hypermetric saccades. A power examination showed weakness of the shoulder abductors, elbow and wrist extensors, hip and knee flexors, and ankle dorsiflexors. There was spasticity in both upper and lower limbs. Sensory examination showed impaired joint position sense, vibration, and fine touch up to both ankle joints. Deep tendon reflexes were exaggerated with an absent ankle reflex, and the planters were bilaterally extensor. Cerebellar examination showed impaired finger-to-finger nose, and heel-shin tests. His tandem gait was impaired.Figure 1: Pes cavus, hammer toes, swan neck deformity of fingers, and Z deformity of thumbThe differential diagnoses considered were Friedrich’s ataxia, Autosomal Recessive Spastic Ataxia of Charlevoix Saguenay (ARSACS), complicated hereditary spastic paraplegia, cerebrotendinuous xanthomatosis, Refsum’s disease, Spinocerebellar ataxias, and X-linked adrenomyeloneuropathy. A detailed biochemical workup for ataxia and neuropathy was negative. In the nerve conduction study (NCS), demyelinating motor polyneuropathy was present while sensory nerves were not recordable. Demyelinating neuropathy helped narrow down the differentials to ARSACS, CTX, and Refusum’s disease. The very slow progression and distal limb deformities were favoring the possibility of ARSACS. Magnetic resonance imaging (MRI) of the brain showed significant superior vermian atrophy, linear hypointensities in the pons on T2/FLAIR sequences (striped pons), called the tigroid pattern of the pons, along with thinning of the thoracic spinal cord, all pointing towards the diagnosis of ARSAC [Figure 2].Figure 2: (a) MRI Brain T2 FLAIR image showing the striped appearance of the pons (Tigroid pons); (b) MRI Brain T2W image showing superior vermian atrophy (red arrow) and thoracic spinal cord atrophy (green arrow)Clinical exome sequencing was performed, which showed a heterozygous frame shift variant c. 6114_6117dupAGAA in Exon 10 of the SACS gene that results in the amino acid substitution p.Ala2040fs*10. Another heterozygous frame shift variant, c. 2215_2216dupAA, that results in the amino acid substitution p.Asn739fs*13, was also detected in the same exon. Whole-family genetic studies are more helpful with negative family histories, but due to financial constraints, we could not perform the genetic testing of parents and siblings. ARSACS is a rare early-onset neurodegenerative disease with a distinctive phenotype characterized by cerebellar ataxia, spasticity, polyneuropathy, nystagmus, and retinal changes.[1] ARSACS typically starts at the age of 1–2 years and results in a bed-bound stage at the age of 40 (range 17–58) years, with death usually around 50 (range 21–72) years.[2] ARSACS is due to deletions or point mutations in a large, single-exon gene encoding sacsin (SACS gene). Sacsin contains a heat shock domain, which suggests that it serves a chaperone function. The SACS gene is located on chromosome 13q12.12 and encodes the large protein sacsin.[13] ARSACS was first described in the French-Canadian population in the regions of Charlevoix and Saguenay-Lac-St-Jean in Quebec, Canada.[1] Later, it was detected in several other countries, suggesting a worldwide distribution. However, only a few genetically proven cases of ARSACS have been reported from India.[4-7] The worldwide incidence of ARSACS is unknown, though it is thought to be underdiagnosed. In this clinical case report, we describe the case of an ARSACS from North India, highlighting the clinical presentation, neurological imaging, and genetic analysis involved in the diagnosis. ARSACS is mainly characterized by progressive cerebellar ataxia, spasticity, and peripheral neuropathy. Other symptoms and signs include dysarthria, nystagmus, and hypermyelination of the retinal fibers.[1] Ataxia is progressive, and additional cerebellar features like dysarthria and nystagmus typically appear in late childhood. Clinical signs of neuropathy tend to appear later. In many patients, the neuropathy only becomes clinically obvious in the late teenage years.[8] Additional atypical cases include patients with epilepsy, a CMT-like phenotype, or hearing loss.[9] In our patient, all these findings except for the retinal changes and dysarthria were present. The onset of the illness and slow progression were also indicators toward ARSACS. Axonal neuropathy with demyelinating features on NCS with or without myelinated retinal fibers is highly suggestive of ARSACS.[78] This feature helps in narrowing down the differential diagnosis, as seen in the NCS of our patient as well. Brain MRI features include early and progressive superior vermis atrophy and linear hypointensities on T2-weighted images in the pons near the pyramidal tracts. Recent studies also found T2-hyperintensities of the lateral pons when merging into the middle cerebellar peduncles that appear thickened, probably related to abnormally large transverse ponto-cerebellar fibers, along with a frequent association with posterior fossa arachnoid cysts. Furthermore, bilateral parietal atrophy, short-stretchedness and thinning of the posterior mid-body of the corpus callousum were also demonstrated in ARSACS patients. Other useful imaging features include the T2 hyperintense rim around the thalami (known as bithalamic stripes) and thinning of the cervical spinal cord.[10] Our patient also had linear pontine hyperintensities and superior vermian atrophy. However, the thinning of the thoracic spinal cord in our case was in contrast to the thinning of the cervical spinal cord reported in the literature. The founder mutations in the SACS gene discovered in Quebec were a single-base deletion at position 6594 (6594delT) and a nonsense mutation 5254C > T17. The causal mutations vary between individuals. The presence of the novel mutation can explain minor changes in the phenotype in our case. Table 1 shows other novel gene mutations detected in other parts of the country.Table 1: Comparison of genetic variants in the SACS gene in studies previously reported from IndiaCONCLUSION The early diagnosis of hereditary ataxias is difficult because of evolving phenotypes and overlapping features. However, a good clinical evaluation and carefully selected ancillary tests can narrow down the differential diagnosis. ARSACS must be suspected in patients with early-onset spastic cerebellar ataxia and peripheral neuropathy with the typical imaging findings. The diagnosis can be confirmed by genetic analysis. Physical therapy and oral medications such as baclofen to control spasticity in the early phase of the disease may prevent tendon shortening and joint contractures, and hence, may help to postpone major functional disabilities. Carrier testing for at-risk family members and prenatal testing for pregnancies at increased risk can be done, if both pathogenic variants have been identified in an affected family member. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

PURPOSE:Cranial autonomic symptoms are typically associated with the trigeminal autonomic cephalalgias and also present in substantial cases of migraine. Autonomic nervous system dysfunctions are also been reported in headache disorders and postulated to promote headache attacks. This study was aimed to evaluate the parasympathetic and sympathetic autonomic functions tests in patients with a episodic primary headache and to investigate, if any, electrophysiological abnormalities in the blink reflex test and sympathetic skin response test in these patients.METHODS:In this cross-sectional study, a total of 100 patients, 50 patients each of migraine and tension-type headache attending the neurology OPD and fulfilling the diagnostic criteria of headache disorders were enrolled. Autonomic functions tests were performed in the Department of Physiology, whereas electrophysiological tests were powered by the Editorial Manager and ProduXion Manager from Aries Systems Corporation performed in the Department of Neurology.RESULTS:Significant association ( P < 0.05) was observed in "blood pressure response to sustained handgrip" (sympathetic activity) and "heart rate response to Valsalva maneuver" (parasympathetic activity) among patients with migraine. Although the mean sympathetic skin response latency of patients with migraine was within the normal range, it was significantly prolonged in comparison with the control group. "Blood pressure response to sustained handgrip" and "heart rate variability" were found to be significantly ( P < 0.05) different in patients with a tension-type headache. The blink reflex test was observed to be normal in all patients with a headache. Patients with migraine showed a significant dysautonomia in category three of the Ewing battery for autonomic functional disability.CONCLUSIONS:Autonomic functional abnormality, both sympathetic and parasympathetic, does exist in patients with a primary episodic headache.

Background: Cryptococcal meningitis is considered to affect HIV patients and those with impaired immune systems. Early identification and treatment are the keys to decreasing morbidity and mortality related to CM. Using 1H NMR spectroscopy, a prospective case–control study will assess the metabolic profile of adults' serum, urine, and CSF. Methodology: The present multicentric study was conducted at Lucknow. The study included 150 participants, out of which there were 31 cryptococcal meningitis cases, 34 positive meningitis controls, and the rest, 85, were disease controls. Result: The discriminant function analysis (DFA) of the three biofluids was used to find significant metabolites between the cases and the control group collectively. A group categorization between control group and the cases in serum, urine, and CSF samples was also made possible by the NMR spectral bin-based orthogonal signal correction and principal component analysis score plots of important metabolites produced from DFA. The cases group had a higher proportion of patients with higher CSF protein levels than the positive control group (BM and TM). Acetone was found among urine samples in both control samples, i.e., positive and negative. Conclusion: This is the first study to explore biomarkers in serum, urine, and CSF in addition to radiological features and clinical symptoms. Hence, a quick, non-invasive prognosis and diagnosis of cryptococcal meningitis in adults can be made using clinical and microbiological investigation, as well as metabolomic analysis of urine samples. This study shows that urine can be used as a biofluid to differentiate between Cryptococcus meningitis in adults. However, when compared to the negative control, our sample size was significantly smaller, necessitating further confirmation on a larger sample size.

Objective:Our aim was to observe frequency of cranial autonomic symptoms (CAS) in migraineurs (primary) and its relation with laterality of headache or other factors, if any.Background:Migraine episodes have headaches with or without aura, and sometimes associated with systemic autonomic nervous system symptoms. Primarily presence of cranial autonomic symptoms suggests diagnosis of TACs. But many studies reported cranial autonomic symptoms (CAS) ranging from 26% to 80% in migraine patients.Material and Methods:Consecutive patients of migraine attending our headache clinic were included in our study. Presence of CAS was recorded with respect to ocular, nasal, facial and aural symptoms along with headache characteristics and laterality information. Detailed clinical examination was performed. We used ICHD 3 (beta version) criteria.Results:Our study cohort comprised of 200 patients having mean (± SD) age 31.12 (± 10.67) years. There were 157 (78.5%), females. Out of 200 patients, 148 (74%) were having at least one CAS, of which 70% were having 2 or more CAS. Frequency of CAS was lacrimation (45.5%), conjunctival injection (34.5%), eyelid edema (34%), aural fullness (27.5%), facial sweating (25%), facial flushing (17.5%), nasal congestion (9%), rhinorrhea (5%) and ptosis (4%). Bilateral CAS was present in 129 (87%) and unilateral CAS in 19 (13%) (OR 35.31; 95% CI 9.19 to 135.7), (P < 0.0001). Sunlight as a trigger was present in all 148 (100%) patients.Conclusion:Our study showed that CASs in migraine is common and bilateral. Sunlight triggers headache in almost all CAS positive patients.

Introduction  Stroke is a major cause of death and disability around the globe. The development of depression following a stroke further increases the disability and impairs functional recovery. In recent decades, despite the advancement in structural and nuclear medicine imaging, the pathophysiologic basis of poststroke depression (PSD) is not well understood. Etiopathogenesis of PSD is multifactorial and afflictions of the frontal lobe, hippocampus, limbic region, and basal ganglia projections are implicated. Aim  The aim of this study was to assess the regional cerebral blood flow (rCBF) using 99m Tc-ethyl cysteinate dimer single-photon emission computed tomography (SPECT) in patients with (PSD + ) or without PSD (PSD–). Materials and Methods  To evaluate the hemispheric asymmetry, the percentage of asymmetry index (AI) was calculated for frontal, temporal, parietal, occipital, putamen, caudate, and thalamic regions of brain and compared between PSD+ and PSD–. The correlation between AIs over the different brain regions was also established in patients of PSD+ and PSD–. Our study cohort included 122 patients between 6 weeks and 1 year of stroke. Depression was present in 52 (42.6%) patients, assessed by hospital anxiety and depression scale (HADS) and general health questionnaire-28 items (GHQ-28) scale. The 28 patients with PSD+ and 18 PSD– gave consent for SPECT study. Results  Our results are based on 46 patients who underwent SPECT study. In patients with PSD+ and PSD–, the HADS and GHQ-28 scores were 8.93 ± 2.77 vs. 3.94 ± 2.15 ( p  = 0.001) and 40.96 ± 9.48 vs. 17.72 ± 5.38 ( p  = 0.001), respectively. A significant difference in rCBF AI was found in the temporal lobe ( p  = 0.03) between patients of PSD+ and PSD–. On logistic regression analysis, the odds ratio of rCBF AI for temporal lobe was 0.89 (95% confidence interval [CI]: 0.80–0.99; p  = 0.04) and caudate nucleus was 0.85 (95% CI: 0.73–0.98; p  = 0.03), which were statistically significant. PSD correlated with AI in temporal region ( r  = –0.03; p  = 0.03) but did not show significant correlation with other regions of brain between PSD+ and PSD–. Conclusion  The presence of temporal lobe rCBF AI on SPECT is significantly associated with PSD. This may reflect the dysfunction of the limbic system and contribute to the occurrence of PSD.

The biomarkers are a group of chemical compounds pro-duced in body fl uid owing to various biological phenomenon in health and disease. The U.S. National Institutes of Health (NIH) working group de fi ned a biomarker as: “ a characteris-tic that is objectively measured and evaluated as an indicator of normal biological processes, pathogenic processes, or pharmacologic responses to a therapeutic intervention. ” 1 Stroke is still among the leading causes of death and disability across the globe despite recent therapeutic advan-ces in the past few decades. 2 After acute cessation of blood supply to brain which eventually leads to dead ischemic core with surrounding salvageable penumbra, the latter can be saved either spontaneously or by intravenous tissue plas-minogen activator (tPA) and endovascular therapy. 2 Timely diagnosis of acute stroke is very important in emergency room as the success of treatment is time dependent. How-ever, only computed tomography (CT) and magnetic reso-nance imaging (MRI) reliably aid in diagnosis of stroke and able to differentiate between ischemia and hemorrhage as treatment for both differs. Apart from high cost of tPA, lack of infrastructure for CT and MRI, fi nancial issue, and contraindications to neuroimaging are also leading barriers in acute stroke management. 3 After acute ischemia, there is a series of biological events leading to neuronal injury and death in time-dependent manner, if untreated. Every step in this cascade is character-ized by speci fi c biochemical process and release of biomarkers which can be utilized for early diagnosis. At this juncture, the role of biomarkers of stroke come into play. If available, the ideal biomarker should readily identify the stroke type, severity, and help in prognostication and potentially capable to exclude the stroke mimics. As the brain is affected by various pathological

Introduction: The presence of cranial autonomic symptoms (CAS) is a hallmark of trigeminal autonomic cephalalgia like cluster headache but their presence in migraine is also not uncommon. Like in trigeminal autonomic cephalalgias, the activation of the trigeminal autonomic reflex pathway is thought to be the possible explanation of the presence of cranial autonomic symptoms in migraine also. Previous studies suggested that around half of the patients of migraine suffer from these symptoms. The aim of our study was to observe the frequency of cranial autonomic symptoms in episodic migraine patients along with their clinical and autonomic characteristics.Methods and Materials: Fifty patients of episodic migraine attending the headache clinic of Dr. RMLIMS, Lucknow and fulfilling the diagnostic criteria of International classification of headache disorder third edition beta were randomly selected and enrolled in the study. The detailed interview regarding presence of cranial autonomic symptoms was recorded along with the clinical characteristics, demographic features and autonomic profile of the migraine patients.Results: About three-fourth (72%) of the patients were females. The mean age of study participants was 27.7±8.3 years. A considerable number of patients (54%) had a long duration (5-10 years) of illness and 70% of patients had severe headaches. Photophobia was the most common (88%) associated clinical symptoms while lacrimation was the most common (56%) cranial autonomic symptom in migraine patients. Among 50 patients of migraine 74% of patients were having at least one cranial autonomic symptoms.Conclusion: Cranial autonomic symptoms are common in patients of episodic migraine. More severe headache is more likely to be associated with the development of cranial autonomic symptoms.

Varicella zoster virus (VZV) is well known for its neurotropism, primary infection and reactivation after variable latency periods. After reactivation from spinal or cranial nerve ganglia, viruses can affect the central nervous system and cranial vasculature via transaxonal migration followed by transmural spread from the adventitial layer to the intima. Stroke can occur following primary infection by VZV (varicella) or after reactivation (zoster). These infectious vasculitides by VZV can lead to unifocal or multifocal ischemic and hemorrhagic stroke either after cranial nerve or spinal dermatomal zoster. Usual difference between immunocompetent versus immunocompromised individuals is involvement of unifocal large vessel vasculopathy in the former while multifocal small vessel in later. This vasculopathy in some cases may be progressive leading to recurrent stroke even after antiviral treatment. Diagnosis becomes challenging and needs a high degree of suspicion in immunocompetent, younger individuals, in absence of rash and when there are comorbidities. We report a case of elderly immunocompetent women, who developed multifocal infarcts followed by ventricular and subarachnoid haemorrhage after thoracic varicella zoster. Diagnosis was confirmed by the presence of anti-VZV IgG antibodies in the cerebrospinal fluid. In view of the diverse clinic-radiological spectrum of VZV vasculopathy, early recognition of this clinical entity is warranted for improved outcome.

Japanese encephalitis is an important cause of encephalitis in Southeast Asia. Survivors may suffer from various movement disorders leading to disability, presumed to be due to involvement of basal ganglia and thalamus. Oromandibular dystonia is a rare complication of Japanese encephalitis and treatment is unsatisfactory in severe cases. We report a child with JE who developed markedly severe oromandibular dystonia in subacute phase of illness. His Magnetic Resonance Imaging revealed involvement of basal ganglia and thalami. Oral antidystonic medications were used without much avail. In view of severe disabling oromandibular dystonia he was treated with botulinum toxin without adverse effects and had improved quality of life. Botulinum toxin may be considered as a therapeutic option in severe oromandibular dystonia following Japanese encephalitis.

Pathological and experimental studies indicate the existence of a "penumbra" of progressive tissue damage and edema in regions immediately surrounding a hematoma in patients of intracerebral hemorrhage (ICH). This zone of oligemia surrounding ICH has a potential for perfusion recovery. Improved understanding of the pathophysiology of perilesional blood flow changes and brain injury after ICH may result in improved treatment strategies. The aim was to study perilesional blood flow changes in ICH by perfusion deficit (PD) measured by single-photon emission computed tomography (SPECT) and to correlate it with the severity of ICH and outcome. Forty-four patients of computed tomography (CT) documented nonlobar deep ICH suggestive of hypertensive hematoma of <7 days duration were subjected to99mTc-ethylene diacetate SPECT scans of the brain. Patients with significant midline shift (0.5 cm) or global blood flow reduction were excluded from the analysis. SPECT scan of the brain was analyzed by segmental analysis, a semi-quantitative method of cerebral blood flow. A difference of radiotracer uptake of >10% between the region of interest of ICH cases and the ratio between the two ROI below 0.9 was taken as a significant PD. A correlation of PD was analyzed with that of various parameters such as the severity of stroke, duration from onset of ictus, and imaging including CT scan of the brain and SPECT scan. A statistically significant difference in the percentage of radiotracer uptake on comparison of ipsilateral and contralateral to ICH (P < 0.001) was observed, suggesting a significant hypoperfusion in the perilesional area in patients with ICH. A statistically significant correlation was noted between the severity of stroke and PD indicated by various parameters such as the National Institutes of Health Stroke Scale (NIHSS) score at admission (r = 0.328, P = 0.016), Glasgow Coma Scale (GCS) score at admission (r = -0.388, P = 0.005), and ICH score at admission (r = 0.314, P = 0.020). This study demonstrated more severe hypoperfusion in clinically severe ICH which is a possible explanation of poor outcomes in severe ICH cases. We observed hypoperfusion on SPECT study in 25 of 34 (73.5%) patients with subacute ICH and 5 of 10 patients (50%) with acute ICH. The mean time from the onset of ictus to SPECT scan done was 5.04 1.75 days with a range of 1-7 days, suggesting the persistence of hypoperfusion in subacute stages too. This finding may be of clinical importance for identifying the salvageable area surrounding ICH for any possible intervention in future to improve the outcome. This study demonstrates that perilesional PD occurs in acute and subacute cases of ICH. This hypoperfusion is possibly time related and appears to be more severe in patients having major ICH with poor clinical and imaging parameters. This area of hypoperfusion or ischemic penumbra is a potential site for perfusion recovery to improve clinical outcomes and to reduce long-term neurological deficits.

Herpes zoster oticus or Ramsay Hunt syndrome is an uncommon neurological manifestation of herpes virus infection causing external ear rash with otalgia and facial nerve palsy. Rarely herpetic infection may present with multiple cranial nerves palsies involving VII, VIII, IX and X cranial nerves. Here we report a case of herpes zoster oticus with multiple cranial nerve palsy. This case study will help in understanding the dermatomal distribution of cranial nerves with cranial polyneuropathy due to reactivation of neurotropic herpes virus. Some interesting case reports regarding different cranial nerve involvement in herpetic infection are discussed in the table which helps in understanding the neurotropism of herpes virus.