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Year : 2016  |  Volume : 4  |  Issue : 1  |  Page : 25-29

Idiopathic intracranial hypertension: Clinical profile and outcome

1 Department of Ophthalmology, Kasturba Medical College, Mangalore, Karnataka, India
2 Department of Ophthalmology, Sankara Nethralaya, Chennai, Tamil Nadu, India

Date of Submission01-Nov-2014
Date of Acceptance26-Jun-2015
Date of Web Publication19-Jan-2016

Correspondence Address:
Trisha Sharma
Room number 401, KMC PG Ladies Hostel, Lalbagh, Mangalore - 575 003, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2320-3897.174402

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Background: It has been a long standing challenge to clinicians and investigators to explain the pathophysiology of Idiopathic Intracranial Hypertension (IIH).Therefore, the goal of this study is to delineate the clinical course of this disorder. Aim: To delineate the clinical course of Idiopathic Intracranial Hypertension with an emphasis on visual prognosis. Settings and Design: Prospective, observational study of 18 patients. Materials and Methods: Patients with unilateral or bilateral disc oedema; CSF pressure >25 cm H 2 O non- focal neurological examination, and normal CT/MRI/MRV scans were included in the study, while those with concurrent ocular disease were excluded .Ocular examination, visual acuity, fundus photography and visual fields evaluation was done at presentation and during follow up visits for a period of two years. Statistical analysis: Descriptive study. Results: Of the 18 patients, 16 were females. The average age of onset was 31.5 years. Hypertension was the most common systemic comorbidity, seen in 5 patients. Headache was the most common presenting symptom, seen in all 18 patients .Diminution of vision was seen in 16 eyes, out of which 14 improved while 2 showed progressive impairment of vision. Abnormal visual field tests included an enlarged blind spot in 11 out of 36 eyes and peripheral constriction in 14 out of 36 eyes .17 patients had a bilateral and symmetric disc swelling. A CSF opening pressure of more than 40 cm of H 2 O was noted in 6 patients. All the patients were managed medically with diuretics therapy (acetazolamide) and weight reduction. Conclusion: A strong suspicion of Idiopathic Intracranial Hypertension in chronic severe headaches and immediate investigations followed by proper treatment can salvage vision of patients even in cases with established papilledema.

Keywords: Idiopathic Intracranial Hypertension, Pseudotumor cerebri, papilledema, headache

How to cite this article:
Pai SG, Sharma T, Gupta R. Idiopathic intracranial hypertension: Clinical profile and outcome. J Clin Ophthalmol Res 2016;4:25-9

How to cite this URL:
Pai SG, Sharma T, Gupta R. Idiopathic intracranial hypertension: Clinical profile and outcome. J Clin Ophthalmol Res [serial online] 2016 [cited 2022 Jul 4];4:25-9. Available from: https://www.jcor.in/text.asp?2016/4/1/25/174402

It has been a long standing challenge to clinicians and investigators to explain the pathophysiology of the diverse symptoms, collectively termed as idiopathic intracranial hypertension (IIH) or pseudotumor cerebri. It may be associated with serious visual loss. [1],[2] Unfortunately, current knowledge of IIH is limited. Therefore, the goal of this study is to delineate the clinical course of this disorder with an emphasis on visual prognosis.

  Materials and Methods Top

We conducted a prospective study of 18 patients, who presented to the Neurology and Ophthalmology Departments of our hospital over a period of 5 years and were diagnosed as IIH. Approval for this study was obtained from the Institutional Ethics Committee. Written informed consent was obtained from all participants before enrolment in the study. All clinical investigations were conducted according to the principles of Declaration of Helsinki.

The inclusion criteria were unilateral or bilateral disc edema, nonfocal neurological examination, except for isolated abducens nerve palsy, computed tomography (CT)/magnetic resonance venography (MRV) scans and cerebrospinal fluid (CSF) opening pressure ≥25 cm H 2 O. Patients with concurrent ocular diseases were excluded.

All patients underwent a complete medical evaluation including careful history taking, ophthalmic examination, complete blood count, CT scan, MRV scan, and CSF analysis (including opening pressure). Ocular examination consists of visual acuity measurement with Snellen's chart, anterior segment examination using slit lamp biomicroscopy, applanation tonometry, stereoscopic fundus photography and visual fields evaluation using automated perimetry with the Humphrey 30-2 program. The degree of papilledema was graded using Frisen's scheme. [3],[4]

Visual acuity, optic disc changes, and visual field defects were checked in all the patients during follow-up, which was done every 2 weeks for a month, monthly for 3 months, and after that every 6 months for 2 years.

  Results Top

Of the 18 patients, 16 were females. The average age of onset was 31.5 years (range 9-52 years). Systemic hypertension was observed in 5 patients, all of whom were on medications for the same. Other systemic associations included hyperthyroidism, on treatment, in 1 patient and chronic obstructive pulmonary disease in another [Figure 1]. Headache was the most common presenting symptom seen in all 18 patients, followed by blurring of vision in 8 patients, nausea and vomiting in 7 patients, diplopia in 1 patient, tinnitus in 1 patient and transient obscuration of vision in 1 patient [Figure 2]. Visual acuity ranged from 6/6 to 6/24 at the last visit. Totally, 29 out of 36 eyes had a visual acuity of 6/6 [Table 1]. Only 1 out of 36 eyes had a visual acuity of 6/24. All patients are improved during the course of treatment except for 1 patient whose vision decreased from 6/12 to 6/24 right eye and 6/6-6/18 left eye which was associated with worsening of edema. This patient was initially started on oral acetazolamide 500 mg twice a day. However, the patients showed visual deterioration despite medical therapy and was referred to the neurosurgeon and to consider ventriculoperitoneal (VP) shunt but the patient was not willing for surgery and was lost to follow-up [Figure 3]. While eight subjects was showed no visual field defects, abnormal visual field tests included an enlarged blind spot in 11 out of 36 eyes, peripheral constriction in 14 out of 36 eyes, paracentral scotoma in 1 out of 36 eyes, arcuate scotoma in 1 patient and generalized reduction in sensitivity in 1 patient [Figure 4]. Bilateral and symmetric disc swelling was found in 17 patients [Figure 5]. Neuroimaging like CT scan and MRV were normal for all patients. None of the patients had abnormal ventricular sizes. Lumbar puncture revealed a CSF opening pressure of more than 40 cm of H 2 O in 6 patients, 25-40 cm of H 2 O in 12 patients. CSF composition was normal in all the cases. All the patients were managed medically with acetazolamide, which was started at 500 mg twice a day and monitored for side effects. The dosage was increased up to 2 g/day, depending on the response of patients and any adverse events. In spite of medical treatment, visual function deteriorated in 1 patient, as mentioned above. No recurrences were noted in other patients.
Figure 1: Systemic associations

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Figure 2: Presenting symptoms

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Figure 3: Visual acuity

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Figure 4: Visual field analysis in diagnosed subjects

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Figure 5: Follow-up of papilledema

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Table 1: Comparison of visual acuities of all subjects pre- and post-treatment

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  Discussion Top

IIH is a condition defined by elevated intracranial pressure but no clinical, laboratory, or radiographic evidence of responsible infection, vascular abnormality, space occupying lesion or hydrocephalus. [5] The diagnosis is formally established when the modified Dandy criteria are fulfilled [Table 2]. [6],[7] The pathophysiology of this disorder is unclear. Studies suggest that there exists a relative resistance to the absorption of CSF across the arachnoid villi or through the extracranial lymphatics. [8],[9] Other theories are supported to an abnormality in the cerebral circulation with a resulting increase in brain's water content and this raised intracranial pressure is then transmitted to the optic nerves. Another accepted theory is that elevated intracranial venous pressure, that was found universally in most cases, leads to a rise in CSF and intracranial pressure by resisting CSF absorption. [10],[11],[12],[13],[14],[15] If not treated appropriately, chronic interruption of the axoplasmic flow of the optic nerves with ensuing papilledema may lead to irreversible optic neuropathy. [8]
Table 2: Modified dandy criteria

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The annual incidence of IIH is 0.9/100,000 and 3.5/100,000 in females between 15 and 44 years of age, [16] most being obese. In our study, of the 18 patients, 16 were females (89%) which was found in accordance with the results of previously conducted studies. [17],[18] The average age of onset was 31.5 years (range 9-52 years). A study by Daniels et al. [19] reported that the mean age as 32 years in their subjects.

Headache is the most frequently reported symptom in IIH [18],[20] and was the presenting complaint of all the subjects in our study. It was reportedly seen in 78% of IIH patients by Ozer et al. [21] and in more than 90% cases by Binder et al. [22] It is usually severe and of throbbing type, generalized, continuous, and associated with neck pain. [23] It worsens in the morning and is increased by Valsalva manoeuvre. [24] However, it may conspicuously be absent in some cases. It was observed in all our patients as opposed to 76% reported by a previous Indian study. [25] Diminution of vision was the second most common presenting symptom in our study, seen in 16 eyes as the presenting symptom, in correspondence with the results of a study done by Ambika et al. [25] Out of these, 14 eyes showed improvement while both eyes of a single patient showed progressive impairment of vision. Other studies reported that the progressive, permanent worsening of visual acuity in up to 25% of cases. [26],[27],[28] While transient visual obscurations were reported in high numbers in previous studies, they were noted in just 10 patients. They are said to occur due to deficient maintenance of perfusion of swollen optic nerve head even with slight changes in blood pressure. [26],[29]

Pulsatile intracranial noises/pulse-synchronous tinnitus that is, described as hearing a swishing heartbeat in one/both ears, is ascribed to flow disturbances in the cerebral venous system. [30] While, it was reported by a single patient in our study, Schlosser et al. [31] report it to be a presenting symptom in 45% of patients. Another symptom encountered is diplopia, mainly horizontal, owing to unilateral or bilateral abducens nerve paresis. Vertical diplopia rarely occurs due to trochlear or oculomotor nerve palsies [32],[33] or skew deviation. Diplopia was seen in just 1 patient in our study while it was reported to be present in about 8% of patients as per another Indian study [25] and as high as 60% by Binder et al. [22]

Important concerns in the patient's history include medications taken over the previous year (oral contraceptive pills, corticosteroids), history of systemic disorders (such as anemia, chronic respiratory insufficiency, sarcoidosis, systemic lupus erythematosus and thrombocytopenic purpura), history of weight gain or weight loss and previous head trauma or any intracranial surgeries. Although steroid withdrawal and Addison's disease are clearly associated with IIH, [34],[35],[36] the role of other endocrine abnormalities as risk factors remain unproven. Our study investigated these associated risk factors and found that eight cases demonstrated systemic risk factors, the most common one being hypertension. This is supported by a study conducted by Bruce et al. [37]

Bilateral and symmetrical papilledema was seen in 17 patients. Similar results were reported in studies by Ambika et al[25] It is also worth noting that though papilledema is a cardinal feature of this condition, there have been case reports suggesting occurrence without papilledema [38],[39] or pseudopapilledema. [40] The most important entities to address in differential diagnosis of papilledema include brain tumors, ventricular system obstruction, and dural sinus thrombosis, thus warranting neuroimaging with CT scan and MRV. It was found normal for all patients in our study.

In IIH, enlarged blind spots and peripheral field defects are early visual losses. [41],[42] A careful evaluation and monitoring of visual field defects are required using quantitative perimetry. Out of 36 eyes, 11 showed blind spot enlargement while 14 showed peripheral constriction. Blind spot enlargement was also reported by Suh and Kim. [43]

Lumbar puncture revealed a CSF opening pressure of more than 40 cm of H 2 O in 6 patients and between 25 and 40 cm of H 2 O in 12 patients. The Median CSF opening pressure was found to be 35 cm H 2 O in a study by Riggeal et al. [44] CSF composition was normal in all cases.

IIH patients with persistent signs and symptoms can be treated either medically or surgically. Carbonic anhydrase inhibitors, such as, acetazolamide along with weight reduction was the initial line of treatment for our all subjects. Indications for surgery include progressive visual loss despite medical therapy, severe or rapid visual loss, and severe papilledema causing macular edema or exudates. [12],[45],[46] Accordingly, 1 patient was referred for surgery but was lost to follow-up. The procedures include optic nerve sheath decompression and CSF diversion procedures [11],[26],[27],[28],[29],[30],[47] like lumbo-peritoneal shunting [48] and wVP shunting. [49],[50],[51] Though these procedures are deemed to be effective treatment options, they do not actually treat the problem so much as just reduce the chances of complication till there is spontaneous resolution. [52]

Limitations in our study were small sample size and no documentation of body mass index which is one of the contributing factors as per research. However, all patients were advised weight loss along with medical therapy.

  Conclusion Top

The diagnosis of IIH is made on identifying the typical symptoms of the disease along with documentation of papilledema, high CSF pressure, normal neuroimaging and neurologic examination, except occasional abducens nerve palsy. The best way to prevent visual loss is to test visual acuity regularly as well as assess visual fields. The course of IIH may be short, benign or may progress to a more aggressive form that ultimately results in blindness over a short period of time. [53] Follow-up of the patients forms an integral part of patient care in IIH as there have been several reports of delayed worsening, recurrences, and late occurrence of raised intracranial tension, some even after several years of initial presentation, [8],[18] A strong suspicion of IIH in chronic severe headaches and immediate investigations followed by proper treatment can salvage vision of patients even in established papilledema.

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]

  [Table 1], [Table 2]

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