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Background: Empty sella is a commonly described imaging entity in patients with idiopathic intracranial hypertension (IIH). Though menstrual and hormonal disturbances have been associated with IIH, available literature lacks systematic analysis of pituitary hormonal disturbances in IIH. More so, the contribution of empty sella in causing pituitary hormonal abnormalities in patients of IIH has not been described. We carried out this study to systematically assess the pituitary hormonal abnormalities in patients with IIH and its relation to empty sella. Methods: Eighty treatment naïve patients of IIH were recruited as per a predefined criterion. Magnetic resonance imaging (MRI) brain with detailed sella imaging and pituitary hormonal profile were done in all patients. Results: Partial empty sella was seen in 55 patients (68.8%). Hormonal abnormalities were detected in 30 patients (37.5%), reduced cortisol levels in 20%, raised prolactin levels in 13.8%, low thyroid-stimulating hormone (TSH) levels in 3.8%, hypogonadism in 1.25%, and elevated levels of gonadotropins were found in 6.25% of participants. Hormonal disturbances were independent and were not associated with the presence of empty sella (p = 0.493). Conclusion: Hormonal abnormalities were observed in 37.5% patients with IIH. These abnormalities did not correlate with the presence or absence of empty sella. Pituitary dysfunction appears to be subclinical in IIH and responds to intracranial pressure reduction, not requiring specific hormonal therapies.

Tuberculosis (TB) is a global health problem with the major brunt of disease occurring in developing countries. The cornerstone of treatment of TB is anti-tubercular therapy (ATT), which includes rifampicin, isoniazid, pyrazinamide and ethambutol. Because of emerging drug resistance, treatment failures, defaulters and increasing incidence of disseminated and extrapulmonary TB, the guidelines have been modified in some countries. Ethambutol is prescribed for longer times (in some cases8 months) and hence the incidence of ethambutol-induced optic neuropathy (EtON) is expected to rise. The fundamental question which needs explanation is why only a small subset of patients on ethambutol are prone to develop loss of vision. This review focuses on available genetic studies which provide evidence that mitochondria are the likely substrates involved in the final pathway of reactive oxidative damage of the papillo-macular bundle. Genetic analysis of mitochondrial mutations encoding genes involved in oxidative phosphorylation pathways may help in isolating the subset of patients who are genetically susceptible. If the groups having high risk of developing EtON are recognised then prolonged duration of ethambutol treatment can be avoided in these susceptible individuals. A better understanding of the pathophysiology will also pave the way for the development of management strategies in this condition.

There is ongoing debate about whether the oculomotor (III), trochlear (IV), or abducens (VI) nerve paresis in patients with migraine is directly attributable to migraine (ophthalmoplegic migraine [OM]) or is due to an inflammatory neuropathy (recurrent painful ophthalmoplegic neuropathy [RPON]). As migraine is associated with elevated serum calcitonin gene-related peptide (CGRP) levels, we studied serum CGRP levels among patients with OM/RPON to determine whether they are elevated during and between attacks. This is the first study assessing CGRP levels in the serum of patients with OM/RPON.The aim of this case-control study was to assess serum CGRP levels in patients with ophthalmoplegia and a headache consistent with migraine according to ICHD-3 criteria. Serum CGRP levels were measured during the ictal and interictal phases in 15 patients with OM/RPON and compared with age-matched and sex-matched controls without migraine (12 patients).The median serum CGRP levels were significantly elevated (P = 0.021) during the ictal phase (37.2 [36.4, 43.6] ng/L) compared with controls (32.5 [30.1, 37.3] ng/L). Serum CGRP levels during the attack correlated with the total duration of ophthalmoplegia. A CGRP level of 35.5 ng/L in the ictal phase of the attack had a sensitivity of 86.7% and specificity of 75.0% in diagnosing a patient with OM/RPON.Elevated serum CGRP levels during the ictal phase of OM/RPON favor migraine as the underlying cause of episodic headache with ophthalmoplegia.

Ocular manifestations form an important clinical component of several movement disorders. Both hypokinetic and hyperkinetic movement disorders can involve the eye. Ophthalmological manifestations can arise due to dysfunction at the level of retina, optic nerves, oculomotor system, or subcortical or visual cortex. Ophthalmological findings help in differentiating various movement disorders and give a clue about their severity. These follow or may precede the diagnosis of movement disorders. Basal ganglia and its various nuclei especially substantia nigra pars reticulata play an important role in the genesis of eye movements through its connections with the superior colliculus. Eye movement abnormalities using quantitative recording techniques are now being considered as noninvasive biomarkers not only for the diagnosis but also to track the progression of disease as well as to study the effects of therapies in various movement disorders. Moreover, there is ample evidence of presence of retinal degeneration in various neurodegenerative diseases evaluated using optical coherence tomography. Various patterns of retinal thinning have been described in different movement disorders and have been found to have a correlation with the stage and severity of the disorder. In this review, we discuss ophthalmological findings of common hypokinetic and hyperkinetic movement disorders.

Idiopathic intracranial hypertension (IIH) is defined as a syndrome of raised intracranial pressure with normal imaging of the brain and cerebrospinal fluid (CSF) composition. There are many controversies and myths that surround IIH. Although patients of IIH may present "typical" symptoms and signs of raised intracranial pressure, clinical scenarios often vary. A typical clinical and radiological finding poses significant problems in diagnosis and management of patients with IIH. We have tried to resolve these controversies and provide a comprehensive update on different aspects of IIH. In this article, we review the common problems encountered while dealing with patients of IIH.

We prospectively evaluated 22 consecutive patients (24 eyes) suffering from non-arteritic anterior ischaemic optic neuropathy (NAION) at a tertiary care centre in Northern India. The mean age was 51.7 years. Visual loss on awakening was noticed only in three (12.5%) eyes. Six (27.3%) patients had headache while three (9.7%) patients had retro-orbital pain at the onset of visual loss. Peripapillary haemorrhages were seen in two (8.3%) eyes. At follow up, only one eye showed improvement in visual acuity. The results of our study suggest that NAION may not always present with the classic clinical picture. Accordingly, a high index of suspicion remains the key to correct diagnosis.

Acute nontraumatic weakness (ANTW) is defined as acute onset of weakness in any part of the body. The weakness occurs due to interruption at any point along the motor pathway. The motor pathway originates from upper motor neuron cells in the cerebral cortex and traverses through the brainstem till lower motor neurons in the spinal cord. The axon of a lower motor neuron is known as the peripheral motor nerve that synapses with muscle. ANTW is of varied etiology and presentation that may be immediately life-threatening if respiratory muscles or autonomic nervous system is involved. Involvement of respiratory muscles may be associated with respiratory failure that may require mechanical ventilation. The weakness may be localized to one limb or generalized involving several muscle groups. When bulbar muscles are involved, weakness leads to problem in swallowing and coughing that endangers the patient's airway. Similarly, the course of the disease also varies, and these patients may worsen rapidly. Hence, a comprehensive history, systematic evaluation, and a detailed neurological examination are performed to localize the disorder. There are specific clinical features peculiar to the particular location of the lesion in the body. Hence, it is possible to anatomically localize these lesions based on the clinical features. Initial laboratory tests and appropriate neuroimaging should be obtained as indicated by history and examination. The time-sensitive emergencies should be addressed immediately, as the delay in management may lead to either permanent neurological damage or may worsen the overall outcome in such conditions. The initial management should always include care of airway, breathing, and circulation (ABC). The imaging should be obtained only after initial stabilization of ABC. The definitive treatment should be done as per the etiology.

The importance of ovarian teratoma as a cause of opsoclonus myoclonus ataxia syndrome (OMAS) and other paraneoplastic syndromes continues to be underestimated. A strong suspicion and appropriate diagnosis remain keys to successful outcome of paraneoplastic OMAS with ovarian teratoma. We report a 14-year-old girl with paraneoplastic OMAS in association with an ovarian teratoma who improved completely following resection of tumour as well as immunotherapy and review the literature briefly.

Background The primary role of neuroimaging in idiopathic intracranial hypertension (IIH) is to exclude secondary causes of raised intracranial pressure. Recently, a few imaging markers have been described which may suggest diagnosis of IIH in atypical cases. We carried out this study to assess the prevalence and accuracy of these neuroimaging signs in predicting the diagnosis of IIH. Methods Eighty treatment-naive patients with IIH and 30 controls were recruited as per a predefined criterion. Magnetic resonance imaging (MRI) brain with detailed sella imaging was done in all patients. Results The most common abnormality noted was optic nerve tortuosity in 82.5% of patients, followed by posterior scleral flattening in 80%, perioptic subarachnoid space (SAS) dilatation in 73.8% and partial empty sella in 68.8% of patients. The presence of optic nerve tortuosity was the most sensitive sign on neuroimaging, though the highest specificity was seen for posterior scleral flattening and perioptic SAS dilatation. The presence of more than three neuroimaging features correlated with severity of vision loss. Conclusion In suggestive clinical scenarios, posterior scleral flattening, perioptic SAS dilatation and optic nerve tortuosity are highly sensitive and specific signs in IIH. This study also highlights the utility of MRI as a valuable tool for prognosis of visual outcome in patients with IIH.

Myoedema is an under-recognised neurological sign that can help the bedside diagnosis of metabolic or endocrine myopathies. Myoedema together with pseudo-hypertrophy make a likely diagnosis of hypothyroid myopathy, and its identification may avoid unnecessary investigations.

Background and purpose The cavernous sinus is a unique region owing to anatomical factors and the pathologies affecting it. The diagnosis of cavernous sinus syndrome (CSS) predominantly relies on clinicoradiological correlation. We studied the utility of computed tomographic (CT) scan versus magnetic resonance imaging (MRI) in the diagnosis of CSS. Methods A prospective observational study was conducted in a tertiary care center in north India. All patients presenting with a clinical syndrome of cavernous sinus involvement with radiologically confirmed lesions were enrolled in the study. MRI and CT scan with cavernous sinus cuts were done and reviewed by experienced neuroradiologists for cavernous sinus lesions and compared with the final diagnosis. Sensitivity and specificity were calculated. Results We included 48 patients in our study. A final diagnosis was achieved in 41 out of 48 (85.6%) patients. Fungal infections (16 (33.3%)) constituted the commonest cause of CSS, followed by neoplastic involvement (13 (27.1%)) and Tolosa–Hunt syndrome (12 (25%)). Vascular involvement was seen in three (6.3%) patients. Other rare causes were seen in four (8.3%) patients. CT scan had an overall sensitivity of 14.6% in achieving a final diagnosis, whereas MRI had an overall sensitivity of 70.7%, with a statistically significant difference ( p Conclusions Although CT scan is a relatively cheap and accessible resource, its role in CSS diagnosis and management is limited because of poor yield. Hence, it is prudent to do an MRI as an initial investigation in cases of CSS.

Background: The pathway underlying ocular convergence is less clear. Convergence weakness is usually a clinical sign of dorsal midbrain pathology. An orbital tumor causing such phenomenon is unknown. We describe its occurrence in patients with proptosis due to orbital tumors. Materials and Methods: Series of six patients with axial proptosis secondary to orbital tumors that demonstrated varying forms of convergence weakness (deficiency to complete failure). Results: Three had weakness of convergence with drifting away of proptosed eyeball on attempted near vision, while the other three had failure. One of these had convergence weakness in nonproptosed eye. MRI excluded a central etiology in all. Conclusions: The article highlights an interesting phenomenon of deficient convergence in the presence of intact medial rectus function in patients with proptosis. The symmetry of orbital contents possibly plays a significant role in the process of convergence.

Leber hereditary optic neuropathy (LHON) is a maternally inherited disease resulting in irreversible visual loss usually in patients belonging to the age group of 15-35 years. Clinically, the patients present with sequential or bilateral, painless, progressive visual loss with central (or ceco-central) scotomas. Although the three mutations, namely, G11778A, T14484C, and G3460A contribute to95% of LHON cases globally, the relative frequency of each mutation varies.We aimed to assess the clinical and genetic profile of patients with mutation-positive LHON at a north Indian tertiary care center.One hundred sixty-one patients (61 prospective and 100 retrospective) presenting with the clinical diagnosis of LHON were screened for the three known mitochondrial mutations (G1178A, G3460A, T14448C). Patients were assessed for detailed clinical, ophthalmological, and neurological examinations. Five milliliter of blood sample was taken to assess the three known mutations using DNA isolation and Sanger sequencing.Clinical profile of 83 patients with both positive and negative mutations was analyzed. Twenty-three out of 161 patients (14.3%) tested positive for either of the three mutations. The majority of the patients harbored G11778A mutation (56.52%) followed by T14484C (34.78%) and G3460A (8.69%). No statistical difference could be noted between the clinical profiles of mutation-negative and -positive patients.

Despite the potential of Idiopathic Intracranial Hypertension (IIH) to cause visual morbidity, limited literature is available focussing on predictors of visual outcome in IIH. This study was planned to assess visual morbidity in patients of IIH in terms of clinical and neuro-ophthalmo- logical parameters. In this prospective study of 40 patients of IIH, neuro-ophthalmological parameters were noted in the form of visual acuity, visual field, contrast sensitivity, Retinal Nerve Fibre Layer thickness, and visual evoked potential. Visual outcome was defined in using specific criteria. Final visual outcome of patients was compared with clinical and neuro-ophthalmologic para- meters to determine any correlation. The most common presenting clinical symptoms were headache (85%) and Transient visual obscurations (TVOs) (52.5%). In univariate analysis severity of visual loss, Cerebro Spinal Fluid (CSF) pressures and abnormal Visual evoked potential (VEP) were associated with worse visual outcome or need of aggressive management. When adjusted for severity of visual loss no independent clinical/neuroophthalmic predictor could be established. High CSF opening pressure, worsening vision/papilledema, greater Retinal Nerve Fiber Layer (RNFL) thickness and abnormal VEPs may be some of the alarming signs for physicians, but none of these parameters can be used as an independent predictor for visual outcome in isolation. Visual loss at presentation is probably the most important predictor of the final visual outcome in these patients. This may also suggest that patients presenting in an advanced disease course (with worse visual status) fair badly despite best medical/surgical management. Early diagnosis and prompt management is the cornerstone of management.

The predictors of poor outcome in tuberculous meningitis (TBM) remain to be delineated. We determined role of various clinical, radiological and cerebrospinal fluid (CSF) parameters in prediction of outcome in TBM.Current study was a prospective observational study including 209 patients of TBM. All patients underwent detailed evaluation including Gadolinium enhanced Magnetic resonance imaging (GdMRI) of brain as well as tests to detect evidence of tuberculosis elsewhere in body. They also underwent GdMRI at three and nine month follow up. All patients received treatment as per standard guidelines.Mean age was 30.4±13.8years. 139 (66.5%) patients had definite TBM while 70 (34.5%) had highly probable TBM. 53 (25.4%) patients died. On univariate analysis, longer duration of illness, altered sensorium, stage III TBM, hydrocephalus and exudates correlated with poor outcome. On multivariate analysis presence of hydrocephalus (p=0.003; OR=3.2; 95% CI=1.5-6.7) and stage III TBM (p0.0001; OR=8.7; 95% CI=3.7-20.2) correlated with higher risk of mortality. In addition, there was significant positive association between presence of hydrocephalus (p=0.05; OR=2.2; 95% CI=0.97-5.1), stage III TBM (p0.0001; OR=28; 95% CI=4.9-158) and presence of altered sensorium (p=0.05; OR=22; 95% CI=0.99-4.8) with either death or survival with severe disability.It is possible to prognosticate TBM using a combination of clinical and radiological. The duration of illness (65.9±92days) before diagnosis of TBM continues to be unacceptably long and this stresses on need to educate primary care physicians about TBM. Future studies where intensity and duration of treatment is guided by these cues may help in sorting out some of the most difficult questions in TBM, namely duration of antitubercular therapy as well as dose and duration of steroid therapy etc.

Optic disc edema may be caused by a number of conditions. A commonly ignored but important aspect is the presence of “infiltration” of disc; that may closely mimic disc edema. Disc edema, optic nerve dysfunction and a normal appearing disc in any combination may occur in infiltrative optic neuropathies. Identifying disc infiltration can aid in diagnosis of many sinister pathologies even in the absence of other specific clinical features. We describe two patients presenting with optic nerve dysfunction and infiltrated disc appearance, which on investigations were found to have underlying malignancies thereby underscoring the importance of detecting infiltrative optic neurpathies.

A young male with acute blurring of vision (6/9) complained of an inferior altitudinal field defect in right eye. Clinical ophthalmological examination was normal. Magnetic resonance imaging (MRI) of the brain revealed the expansion and mucosal thickening of right posterior ethmoid and sphenoid sinuses and opacified right maxillary sinus. Surgical intervention (transethmoidal sphenoidotomy) and histopathological examination revealed chronic invasive granulomatous fungal sinusitis. Anti-fungal therapy led to resolution of visual complaints and restoration of visual field defects.

Tuberculosis never stops fascinating physicians. The burden of tuberculosis is a major cause of disability. While drugs are often blamed when patients develop new focal deficits on treatment, the deterioration in these patients can have a myriad of causes including the development of new tuberculomas. Recognizing the critically located tuberculomas as potential causes of vision loss is indispensable. Here, we report two patients with strategic tuberculomas leading to vision loss. In one patient, the cause of visual morbidity was compression of the optic pathways; in the other patient, cortical vision loss was noted due to strategic location of tuberculomas.

Brain metastases are known to be present with a history of increased intra-cranial pressure headache, seizures or altered sensorium. Corresponding to the clinical brain metastases are the most feared complication of a systemic cancer. Classically, brain metastases are associated with significant morbidity and are known to present with a history of increased intracranial pressure headache, seizures or altered sensorium. Neuroimaging is usually suggestive of massive peri-lesional edema and mass effect surrounding the space occupying lesions. This, however it is not a universal rule. We report a 50-year-old gentleman who presented with rapidly progressive forgetfulness. Interestingly, the patient’s neuroimaging discretely showed disproportionate involvement with regards to the clinical picture. The lesions were finally recognized as metastases underscoring the importance of an avid search for a primary systemic malignancy if similar findings are noted on radiology.

Purpose To review recurrent NAION as a cause for PFK syndrome. Methods In an observational study patients presenting with sudden loss of vision were evaluated. We reviewed patients presenting with disc edema on one side and optic atrophy in contralateral eye on fundus examination. Their visual field defects and fundus fluorescein angiography was assessed. Results Of the 7 patients evaluated 4 (57.1%) were females. Mean age at presentation was 53.7 ± 11.9 years. Mean duration between the two episodes was 12.7 months (range: 2–30). The visual acuity of presenting eye ranged from 6/9 to worse counting fingers close to face. Conclusions The diagnosis in a PFK presentation is essentially one of exclusion. Patients with NAION are at risk for recurrence in fellow eye, thereby presenting as PFK syndrome. NAION should be considered as a differential especially when imaging and other laboratory investigations are not suggestive of any compressive lesion.

Paraneoplastic neurological syndromes (PNS) are well established entities associated with onconeural antibodies. Paraneoplastic parkinsonism is a highly under narrated presentation of PNS. Rapid progression of typical or atypical parkinsonism with red flags like multiaxial involvement, complete gaze palsy and a clinico-radiological mismatch should prompt a clinician to suspect secondary etiologies like infection, metabolic, vascular, metastatic and paraneoplastic causes. We describe a patient with rapidly progressive parkinsonism. Diagnosis of Breast carcinoma associated ANNA-2/ Anti Ri mediated PSP like phenotype was made in this patient based upon clinical examination and investigations. We also present a review of literature on paraneoplastic parkinsonism in this manuscript.

Chronic granulomatous disease (CGD) is an uncommon genetic immunodeficiency disorder affecting neutrophil function, characterized by recurrent bacterial and fungal infections. X-linked carriers of CGD have an increased risk of autoimmune disorders, in particular lupus like disorders. We describe the case of a 37 years old female carrier of X-linked CGD, who presented with clinical features and serology consistent with a definite diagnosis of Systemic lupus erythematosus (SLE), with rare immune mediated neurological manifestations including secondary central nervous system (CNS) vasculitis and Longitudinally extensive transverse myelitis (LETM), responsive to immunomodulation. These neurological manifestations have not been described previously in carriers of CGD. We recommend early diagnosis of these immune mechanisms, especially in X-linked carriers of CGD, and appropriate immunomodulation in order to improve life expectancy and improve neurological outcome.

Background: Although first described more than two decades ago, posterior reversible encephalopathy syndrome (PRES) continues to be enigmatic. We prospectively followed consecutive patients of PRES both clinically and radiologically for a better understanding of natural history, symptomatology, and prognosis of this not so uncommon entity. Patients and Methods: The current study included 22 consecutive patients of PRES who were followed both clinically as well as radiologically at a tertiary care institute in Northern India from December 2014 to June 2016. Results: Mean age was 30.68 ± 12.68 years. The most common symptoms included altered sensorium (77.3%), headache (72.7%), seizures (63.6%), vomiting (36.4%), and visual disturbances (22.7%). About 94.5% of patients had parieto-occipital signal changes on neuroimaging. Magnetic resonance imaging (MRI) (n = 20) revealed involvement of sites considered atypical for PRES in 95% (frontal [55%], temporal [40%], cerebellum [40%], basal ganglia [15%], deep white matter [10%] and brainstem [10%]). Diffusion restriction, haemorrhage, and contrast enhancement were seen in 30%, 22.2%, and 25% of patients. At 3 months follow-up, modified Rankin scale was 0 in 19 patients and 1 in 1 patient. Two (9.1%) patients died. Eight (36.4%) patients had eclampsia, 5 (22.7%) each had chronic kidney disease and essential hypertension whereas 2 (9.1%) each had immune-mediated disorders and drug-induced PRES. None of the clinical or imaging features predicted outcome in PRES. Conclusion: Atypical MRI presentations of PRES are common, and there is a need to keep a strong index of suspicion for the diagnosis of PRES. The prognosis of PRES is good, and most cases show excellent recovery, particularly if underlying etiology can be treated satisfactorily.

Acute comitant esotropia in a child has a mixed set of differentials and we present a report of three cases in children who presented with acute onset diplopia. On careful history taking, all the kids reported an excessive use of the smart phone in the preceding month. We hypothesise that excessive use of the smart phone at near leads to excessive stimulation of ciliary muscle, hence accommodative spasm in these children. This is the first case series to report an association of smart phones and accommodative spasm.

Introduction: Ishikawa and Jefferson are the two most commonly used systems used for the classification of cavernous sinus syndrome (CSS). However, relative utilities of these two classification systems have not been evaluated in detail in developing countries. In this study, we compared relative utilities of these two classification schemes in the evaluation of CSS. Objective: To compare the utility of Jefferson and Ishikawa classifications in the evaluation of CSS. Patients and Methods: A total of 73 consecutive patients of CSS were prospectively classified using either Ishikawa or Jefferson classification and relative utility of these two classification schemes in determining etiology of CSS was compared. Results: While only 46.6% of patients could be classified using Jefferson classification, 95.5% of patients could be classified using Ishikawa scheme. CSS was classified as anterior, middle, and posterior in 17.8%, 21.9%, and 8.2% of patients, respectively, as per the Jefferson classification. As per the Ishikawa classification, 37% of patients each showed anterior and posterior CSS, 16.4% showed middle CSS, whereas 4.1% had whole CSS. Middle CSS was significantly associated with the presence of fungal infections (P = 0.045) as per Jefferson classifications, and anterior CSS was significantly associated with a vascular etiology (P = 0.005) as per Ishikawa classification. Overall, inflammatory causes were the most common cause for anterior CSS, while tumors accounted for maximum cases of posterior CSS. Conclusion: Although more number of patients could be classified using Ishikawa classification, there was no advantage of Ishikawa classification over Jefferson with regard to determination of etiology of CSS.

Background During the global H1N1 pandemic, neurological complications were reported in approximately 6–10% of children suffering from H1N1 infection, but only rarely in adults. Generalized convulsive status epilepticus (GCSE) as a presenting manifestation of H1N1 infection in an adult is exceedingly rare and has not been reported in literature. We report a patient who presented to us with GCSE as a presenting manifestation of H1N1 infection who improved following appropriate antiviral treatment. Methods and results This 20-year-old gentleman presented to us with history of fever followed by GCSE of 24 h duration. He was treated symptomatically and was evaluated in detail. He was diagnosed to be suffering from H1N1 infection based on appropriate serological tests. After start of antiviral therapy, he improved and is doing well at 4 months follow up. Conclusion This case report further expands the spectrum of clinical findings associated with sporadic H1N1 infection. A possibility of H1N1 infection should be considered in all patients who present with GCSE without any obvious cause so that appropriate diagnostic tests and treatment can be carried out at the earliest.

A 38 year lady had recurrent generalized and myoclonic seizures since 6 years of age. On examination she had facial adenoma sebaceum and periungal fibromas, cutaneous angiofibromas on the back. Contrast enhanced magnetic Resonance Imaging of brain was suggestive of multiple cortical tubers with sub ependymal nodules consistent with the diagnosis of Tuberous sclerosis. Focal hypertrophy of the skin of the dorsal aspect of the left hand with focal gigantism was noted.

Dear Editor, Posterior-circulation stroke is of grave concern to any physician versed with the mortality and morbidity associated with the condition. Various nonvascular neurological and nonneurological conditions may mimic posterior-circulation stroke. We report a 29-year-old male with no prior comorbidities who presented to the emergency room of a tertiary-care hospital in northern India with sudden-onset alteration in consciousness following severe vertigo with multiple episodes of vomiting and gait imbalance. Detailed history-taking revealed the presence of pain in the nape of the neck and low-grade fever for the previous 10 days and a history of chiropractic neck manipulation for the previous 7 days. The possibility of acute posterior-circulation stroke following vertebral artery dissection was considered, and a computed tomography (CT) scan of the head was performed on an emergency basis. The CT scan revealed a large hypodensity in the midbrain, pons, and cerebellum (Fig. 1A). However, CT angiography of the neck and the intracranial vessels did not show any evidence of vertebral artery dissection. Routine hemogram, biochemistry, and chest X-ray findings were normal. The possibility of an alternative diagnosis was considered, based specifically on the history of preceding fever and the normal CT angiography findings. Magnetic resonance imaging (MRI) of the brain revealed multiple ring enhanced lesions in the cerebellum with significant surrounding perilesional edema (Fig. 1B and C). Cerebral spinal fluid (CSF) analysis showed a total count of 250 cells/mm3, predominantly lymphocytes, with proteins 90 at mg/dL and sugar at 35 mg/dL. Cryptococcal antigen, acid fast bacilli stain, and fungal smear findings were negative in the CSF. The blood sugar level was 121 mg/dL. The possibility of multiple infratentorial tuberculomas was considered, and the patient was started on antitubercular therapy with steroids. The patient was completely asymptomatic after 6 months of treatment. Fig. 1 A: Contrast enhanced CT head showing hypodensity of pons and cerebellum. B and C: Shows multiple ring enhancing lesions in cerebellum on contrast enhanced, T1 weighted MRI brain. Posterior-circulation stroke is associated with grave mortality and morbidity statistics.1 A population-based case-control study2 found that chiropractic manipulation was positively correlated with vertebrobasilar accidents, specifically in subjects aged

An 18-year-old woman presented with headache, right focal seizures, and diminished vision in the left eye for 20 days. Fundus examination revealed bilateral papilledema with large premacular sub–internal limiting membrane and subhyaloid bleeding in the left eye (figure 1A). MRI brain showed hemorrhagic infarct in the left temporal lobe (figure 2, A and B). Magnetic resonance venography showed left transverse and sigmoid sinus thrombosis (figure 2C). A diagnosis of Terson syndrome1 (vitreous hemorrhage) was made. Procoagulant workup was negative and the patient improved with conservative management2 (figure 1B). Even though Terson syndrome has been reported with subarachnoid hemorrhage, its occurrence with cortical venous sinus thrombosis is rare.