What is the optimal dose of acetazolamide in the treatment of idiopathic intracranial hypertension

@#Objective: Acetazolamide is preferred as the first-line drug for the medical treatment of idiopathic intracranial hypertension. In this study, the efficacy of different doses of the drug on visual functions; visual acuity, optic disc appearance- papilledema grade and visual field-mean deviation (VF-MD) were evaluated. Methods: The medical records of 73 patients diagnosed as idiopathic intracranial hypertension based on Modified Dandy Criteria and treated with acetazolamide who were on follow-up between 2010 and 2017 at the Neuro-ophthalmology Unit of Ege University Medical School, Department of Neurology were analyzed. Improvement in the visual functions at the end of the sixth month in three groups taking different doses of the drug; low (500, 750, 1000 mg/day), moderate (1500, 1750, 2000 mg/day) and high (3000, 4000 mg/day) were compared. Results: Improvement in visual acuity (p: 0.784), was not affected from different doses of the drug whereas papilledema grade (p: 0.014) and VF-MD (p<0.001) were affected. Binary comparisons revealed significant improvement in the high dose group when compared with the moderate and low dose groups both for the papilledema grade (lowhigh: p: 0.003, moderate-high: p: 0.024 ) and VF-MD (low-high: p<0.001, moderate-high: p: 0.001) Conclusion: Treatment with high doses of acetazolamide is associated with improvement in visual field defects and regression of optic disc edema in idiopathic intracranial hypertension.

Rebound intracranial hypertension after noninvasive treatment of intracranial hypotension: Case report and literature review

@#Intracranial hypotension is a clinical syndrome characterized by orthostatic headache and low cerebrospinal fluid pressure. Noninvasive management is the usual first line treatment. Epidural blood patch is the treatment of choice if noninvasive treatments are ineffective. Cases with rebound intracranial hypertension after epidural blood patch treatment have been reported in the medical literature previously. We report here three patients with rebound intracranial hypertension who were treated noninvasively for intracranial hypotension. This phenomenon has not been reported previously. The underlying cause of intracranial hypotension was epidural anesthesia in the first, lumbar disc surgery in the second patient, and idiopathic in the third patient. They had been treated either with bed rest or with medical treatment not requiring epidural blood patch. After a short remission the patients were seen with a different headache pattern. They all had papilledema on examination. Automated perimetry revealed bilateral blind spot enlargement in Patient 1 and peripheral constriction in Patient 2. Cranial MRI and MRV in all three patients were normal. All the patients recovered very quickly with acetazolamide 1.5 or 2gm/day. In conclusion, rebound intracranial hypertension should be kept in mind in patients with intracranial hypotension who developed changes in the headache pattern, had new symptoms of nausea, vomiting, blurred or double vision during follow-up. Rebound intracranial hypertension can develop after conservative treatment of intracranial hypotension.

Evaluation of posterior reversible encephalopathy syndrome from different aspects: What is the role of serum LDH and albumin level in pathogenesis?

Background: Posterior reversible encephalopathy syndrome (PRES), is characterized by headache, lethargy, visual complaints and epileptic seizures. Brain imaging findings include abnormalities of the white matter and the grey matter.The diagnosis currently relies on clinical manifestations and typical neuroimaging findings. Different pathophysiological factors can play role in the disease process. The purpose of this study is to review causes, clinical aspects, imaging-laboratory findings and prognosis in patients diagnosed with PRES. Method: Patients who showed clinical and magnetic resonance imaging (MRI) findings consistent with PRES between January 2011 and December 2014 were included in the study. Patient data were collected retrospectively from hospital records. Results:Total number of patients was 22 (18 female, 4 male). Median age was 28 years (range 18-84). Comorbid conditions included eclampsia (n=10, 45%), pre-eclampsia (n=1, 4.5%), HELLP (hemolysis, elevated liver enzymes, low platelet count) syndrome (n=1), primary kidney disease (n=3, 13%). Acute elevation of blood pressure was found in 9 patients (40%). Five patients (22%) were using steroids or immunosupressive drugs. Typical PRES imaging pattern with bilateral parieto-occipital involvement was present in 15/22 patients (68%) and occipital involvement was present in 3/22 patients (14%). Atypical neuroimaging features included frontal involvement in 10 patients (45%), basal ganglia gray matter lesion in 1 patient (4%) and the cerebellum was involved in 3 patients (14%). Serum LDH level was high in 13 patients (59%). Hypoalbuminemia was detected in 12 patients (54%). Conclusion: Although hypertension is thoughtto be the main pathologic factor in the disease process, endothelial dysfunction seems to be equally important.

Neuro-Behçet’s disease mimicking cerebral abscesscomplicated by metronidazole-induced encephalopathy

This is the report of a 32-year-old man with Behçet’s disease described dizziness, double vision and headache. The cranial MRI demonstrated a ring enhancing nodular lesion in left medial occipital lobe, and T2 hyperintense lesion in diencephalon mimicking abscesses. A stereotactic biopsy was performed. The histology showed features of neuro-Behçet’s disease and an abscess was ruled out. During the procedure till the histopathologic results were gathered he was given ceftriaxone and metronidazole when cerebellar signs appeared. Cranial MRI showed additional symmetrical hyperintensities in bilateral cerebellar dentate nuclei which was attributed to metronidazole toxicity. Repeat MRI performed forty days later showed complete resolution of both dentate hyperintensities and diencephalic and occipital ring enhancing lesions. This is the first case of neuro-Behcet’s disease complicated by metronidazoleinduced encephalopathy. This case also showed that nodular ring enhancing lesions can be seen in neuro-Behçet’s disease and can lead to difficulties in diagnosis and management.