Benign intracranial hypertension (BIH) in children is recognized as elevated intracranial pressure without hydrocephalus or intracranial mass. It manifests differently in adults, with no apparent predilection for sex or weight. Headache, papilledema, and possibly sixth nerve palsy with visual field defects are the typical symptoms of this syndrome. Vitamin A toxicity is a rare cause of BIH. We report the case of a previously healthy 13-year-old girl presenting with photophobia, a frontal headache, and vomiting. She had bilateral papilledema discovered by fundoscopy. Both magnetic resonance imaging and brain CT were normal. At admission, a lumbar puncture (LP) revealed an opening pressure of 26 cm H2O with normal cerebrospinal fluid (CSF) analysis. The diagnosis of BIH was established, and treatment with acetazolamide was started, with good clinical results. Regular eye evaluations showed a regression of papilledema. Elevated serum vitamin A levels were the only positive findings. Within two weeks, the patient was discharged without any symptoms. This study aims to attract the attention of clinicians to the importance of evaluating vitamin A toxicity in the context of papilledema and oculomotor problems in a child who has undergone normal neuroradiological investigations.

The dynamics of increased intracranial pressure (ICP) and sixth cranial nerve palsy has undergone a paradigm shift, with emphasis shifting from a length hypothesis to a theory based on novel anatomic findings pertaining to the geometry of Dorello\'s canal. In particular, the sixth cranial nerve resides in a transfixed coaxial cylinder within the canal. The cisternal portion of the nerve is intradural and the rest of the nerve is extradural; therefore, with increased ICP, the former is stretched, thereby pulling on the rest of the nerve, which is anchored in Dorello\'s canal. We present a case of pseudotumor cerebri secondary to minocycline presenting with an isolated sixth nerve palsy. This case is used as a platform to segue into the recent findings outlined above, in particular, the evolutionary transformation of Dorello\'s canal from a circular outline with a bony roof to an elliptic profile with a fibro-osseus roof during hominid basocranial expansion. The fibro-osseus roof, being elastic, is particularly susceptible to the influence of raised ICP, thereby narrowing the canal and injuring the sixth cranial nerve.

Primary Spinal tumors presenting as increased intracranial pressure is a rare and intradural extramedullary (IDEM) spinal schwannoma with unique presentation of pseudotumour cerebri (PTC) is extremely rare. Here, we describe a case of 48 years old male patient who presented to us with six months\' history of headache and visual disturbances and was found to have bilateral papilledema. CT scan of brain was normal and CSF opening pressure on Lumbar puncture (LP) was 30 cm of H2O with raised protein level. His headache and visual symptoms settled down after LP (Lumbo-peritoneal) shunt was performed. Three days postoperatively, patient complained of hypoesthesia and weakness of left leg that became an established complain after 2 weeks. A Lumbosacral MRI was performed with concerns of any postoperative complications of LP Shunt, which revealed IDEM spinal tumour at D11-D12 level. Patient underwent second surgery for excision of tumor. We reviewed the relevant literatures and discuss the possible mechanism of such atypical presentation of spinal tumors.

To investigate whether conditions causing inflammatory activation are associated with increased risk of idiopathic intracranial hypertension.
All newly diagnosed idiopathic intracranial hypertension patients (cases) in Sweden between 2000-2016 were identified using pre-determined algorithms (n = 902) and matched with five controls from the general population and five individuals with an obesity diagnosis (n = 4510) for age, sex, region, and vital status. National health registers provided information on infections, inflammatory disorders and dispensed medications. Conditional logistic regression was used to estimate odds ratios and 95% confidence intervals.
Compared to general population controls, the cases had fourfold increased odds of having an infection (odds ratio = 4.3, 95% confidence interval 3.3-5.6), and threefold increased odds of an inflammatory disorder the year prior to idiopathic intracranial hypertension diagnosis (odds ratio = 3.2, 95% confidence interval 2.4-4.3). Organ specific analyses showed that odds were increased for the study diseases in the respiratory organ, kidney organ and gastrointestinal tract, but not for female genital infections. Similar results were found when comparing idiopathic intracranial hypertension with obese controls though the odds ratios were of lower magnitude. Sub-analyses on exposure to anti-infectious and anti-inflammatory drugs confirmed the increased odds ratios for idiopathic intracranial hypertension patients.
These findings suggest that major inflammatory activation may be a risk factor in idiopathic intracranial hypertension development.

A 6-year-old girl complained of diplopia and headache over a 2-week period after sustaining a minor head injury. Her neurological examinations were normal, but visual examination identified bilateral papilledema. Magnetic resonance imaging of the brain revealed a protruding nodular lesion causing compression within the anterior superior sagittal sinus in the midline, showing high signal intensity on T2-weighted imaging (T2WI) and low signal intensity on T1WI, similar to that of cerebrospinal fluid. Enhanced T1WI showed irregular narrowing of the anterior superior sagittal sinus adjacent to this lesion. The cortical vein drained to the frontal pole of the arachnoid granulation lesion and into the superior sagittal sinus. No other parenchymal abnormality was noted. A lumbar puncture showed increased opening pressure (30 mmHg), and the laboratory findings were normal. Based on the imaging and clinical findings, benign intracranial venous hypertension with giant arachnoid granulation was diagnosed. The patient\'s symptoms were reduced satisfactorily following daily treatment with 750 mg acetazolamide.
We report a case of giant arachnoid granulation involving the anterior superior sagittal sinus in a 6-year-old girl who presented with benign intracranial hypertension. Clinicians should be aware of this rare anatomic variant to avoid unnecessary invasive procedures or examinations in children with benign intracranial hypertension.

A 4-year-old boy with kaposiform lymphangiomatosis (KLA) developed progressive headaches and papilloedema and was diagnosed with pseudotumor cerebri initially treated with acetazolamide. Clinical deterioration prompted placement of a ventriculoperitoneal shunt. After the surgery, the child\'s condition has markedly improved.
A network of intracranial lymphatics is presently being investigated. Neuroimaging excluded KLA infiltration of the skull and/or meninges, leaving as the most plausible explanation for the child\'s pseudotumor cerebri the existence of an increase in intracranial venous pressure by venous compression at the thorax. To our knowledge, our case constitutes the first report of pseudotumor cerebri occurring in the context of KLA.

Elevation of a depressed skull fracture (DSF) overlying a venous sinus is generally avoided due to risk of sinus injury. Rarely, the sinus may be compressed by the fractured segment, causing intracranial hypertension (IH) or encephalopathy and can only be diagnosed with cerebral angiography or MR imaging techniques. The posterior third of the superior sagittal sinus (SSS) was found involved in all the reported cases. There is no consensus on its management, but most patients did not have any sinus thrombosis and improved after elevation of the compressing DSF alone. There are isolated reports of improvement with serial lumbar punctures or ventriculoperitoneal shunt.We report for the first time, a single session lumboperitoneal shunt and DSF elevation for a patient with thrombosis of the posterior part of SSS due to an overlying DSF, causing florid papilledema and impending blindness. Elevation of the DSF alone would not have achieved patency of the thrombosed sinus immediately to save his vision. Hence a lumboperitoneal shunt was done for immediate relief of IH. This CSF diversion alone was insufficient to achieve patency of the thrombosed sinus in the presence of significant external compression by the DSF; even if anticoagulants were used. Hence we elevated the DSF after craniotomy using a technical modification; by making a wide gutter circumferentially around the DSF with a high speed drill, to avoid sinus injury; prior to its elevation. The patient\'s vision improved in 48 hours and anticoagulants were used till 2 months when sinuses were found normal on MRI. Serial CT &MR images showing progression to thrombosis and recovery after decompression are presented. Both CSF diversion and DSF elevation are necessary when vision is threatened by IH due to sinus thrombosis with an overlying DSF.

BACKGROUND: Spontaneous cerebrospinal fluid (CSF) rhinorrhea is a rare entity. The accurate preoperative localization of the leak point is essential for planning surgical treatment, but is sometimes difficult. To localize the leak point, magnetic resonance cisternography (MRC) is the method of choice, but its effectiveness remains unclear.
METHODS: A 34-year-old mildly obese female experienced spontaneous CSF rhinorrhea after an attack of bronchial asthma. High-resolution computed tomography (CT) failed to reveal the leak point, while MRC demonstrated an arachnoid herniation at the olfactory cleft. The patient underwent endoscopic endonasal repair of the CSF leak with success. There has been no recurrence of CSF rhinorrhea for 14 months after surgery followed by the administration of acetazolamide.
CONCLUSIONS: We report a rare case of spontaneous CSF rhinorrhea associated with benign intracranial hypertension, in which the leak point was successfully detected by MRC. The CSF leak was completely repaired by minimally invasive endoscopic endonasal surgery. MRC may be a reliable method for detecting CSF leak points.