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July2012 Vol.49 Issue:      3 (Supp.) Table of Contents
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Ophthalmic Manifestations in Idiopathic Intracranial Hypertension

Ashraf A. Aboelsafa1, Usama E. Shalaby2


Departments of Neuropsychiatry1, Ophthalmology2, Tanta University; Egypt



ABSTRACT

Background: Idiopathic intracranial hypertension (IIH) is a headache syndrome affecting vision and can lead to permanent visual loss. Objective: To study the ophthalmological manifestations in patients with IIH. Methods: Thirty two patients were collected in whom the diagnosis of IIH was confirmed. All patients underwent full neurological, ophthalmological and radiological examination. The following ophthalmological assessment was performed for every patient: best-corrected visual acuity, intraocular pressure, ocular motility, slit lamp examination, fundus examination, formal visual field testing and determination of the degree of visual impairment. Results: Most (90.6%) of the patients were females and the mean age at presentation was 28.0±2.4 years. The most common presenting ophthalmic symptom was blurred vision (75.0%). Transient visual obscuration was present in 8 (25%) patients, double vision in 6 (18.8%) patients and ocular pain in 3 (9.4%) patients. In addition to ophthalmic symptoms, headache was the chief complaint, found in 31 patients (96.7%). All patients had papilledema. The visual acuity was less than 20/100 in 3 (9.4%) patients, while moderate visual impairment was found in 21 (65.6%) patients. Sixth nerve palsy was present in 6 (18.75%) patients. Abnormal perimetry was present in 30 (93.8%) patients. Neuroimaging was normal in 29 (90.6%) patients, but revealed slit-like ventricles in 2 patients and one had empty sella. No significant relation was found between the cerebrospinal fluid (CSF) opening pressure and both the duration of symptoms before diagnosis and the visual impairment. Also, no significant relation was found between visual impairment and the duration of symptoms before diagnosis. Repeated withdrawal of CSF by lumbar puncture was done for all patients. It was combined with oral acetazolamide in 29 (90.6%) patients. Twenty four (75%) patients showed complete resolution of their symptoms and signs. Moderate visual impairment persisted in 6 (18.8%) and severe loss of vision persisted in 3 (9.4%) patients. Conclusion: We stress the importance of early diagnosis, prompt intervention and follow up in the management of IIH which is no longer considered benign and is an important cause for visual impairment. [Egypt J Neurol Psychiat Neurosurg.  2012; 49(3): 233-238]

 

Key Words: Idiopathic Intracranial Hypertension, visual loss, papilledema, perimetry

Correspondence to Ashraf A. Aboelsafa, Department of Neurology, Tanta University Egypt.

Tel.: +020106622792       E-mail:draboelsafa@hotmail.com




INTRODUCTION

 

Idiopathic intracranial hypertension (IIH), sometimes called by the older names benign intracranial hypertension (BIH) or pseudotumor cerebri (PTC), is a headache syndrome which affects vision and may result in permanent impairment of vision.1 

It is characterized by increased cerebrospinal fluid (CSF) pressure in the absence of an intracranial mass or ventricular dilatation, with normal findings on neurological examination except for papilledema and occasional 6th nerve palsy, with normal level of consciousness, and normal CSF composition.1

Headache is the most common symptom of IIH. It is characteristically worse in the morning, and throbbing in nature. It is generalized and may be associated with nausea and vomiting. The headache can be made worse by any activity that further increases the intracranial pressure, such as coughing and sneezing. Many have pulsating tinnitus, a whooshing sensation in one or both ears; this sound is synchronous with the pulse.2

The cause of IIH is not known. Different theories have been proposed to explain the pathophysiological mechanisms of IIH. The Monro-Kellie rule states that the intracranial pressure is determined by the amount of brain tissue, CSF and blood inside the bony cranial vault. Three theories therefore exist as to why the pressure might be raised in IIH: an excess of CSF production, increased volume of blood or brain tissue, or obstruction of the veins that drain blood from the brain.2,3

The diagnostic criteria of IIH include the following modified Dandy criteria1,4: (1) Symptoms and/or signs of raised intracranial pressure as headache, nausea, vomiting, transient visual obscuration, or papilledema, (2) No localizing signs with the exception of sixth nerve palsy, (3) The patient is awake and alert, (4) Normal CT/MRI findings without evidence of venous sinus thrombosis, (5) Lumbar puncture (LP) opening pressure of >250 mmH2O and normal biochemical and cytological composition of CSF, and (6) No other explanation for the raised intracranial pressure.

On average, IIH occurs in about one per 100,000 people, and can occur in children and adults. It occurs predominantly in women of childbearing age2. Overweight and obesity strongly predispose a person to IIH: women who are more than twenty percent over their ideal body weight are nineteen times more likely to develop IIH. In men this relationship also exists, but the increase is only five-fold in those over 20 percent above their ideal body weight.5,6

The aim of this study is to study the ophthalmological manifestations in patients with IIH.

 

SUBJECT AND METHODS

              

This study was carried out in the Neuropsychiatry and ophthalmology Departments, Tanta University Hospitals. Thirty two patients were collected in whom the diagnosis of IIH was confirmed according to the modified Dandy criteria.1 The criteria for diagnosis were the presence of papilledema, elevated CSF opening pressure >250 mmH2O and exclusion of any intracranial pathology by CT scan and/or MRI and CSF analysis. The exclusion criteria included other ocular diseases causing visual loss, systemic conditions or medications that may be associated with intracranial hypertension, and alternative plausible mechanisms of visual loss other than IIH.

               All patients included in the study underwent full neurological, ophthalmological and radiological examination. The following ophthalmological assessment was performed on every patient: best-corrected visual acuity, intraocular pressure, ocular motility, slit lamp examination, fundus examination, and formal visual field testing with static perimetry (Humphrey).

               Visual impairment was determined by the simplified grading system defined by Wall and George which takes into account visual acuity and visual field (field constriction defects involving visual fixation and defects involving the fixation). This system grades visual impairment from grade 0 (normal) to grade 5 (blinding visual loss). Blindness is defined as best visual acuity less than 20/200 (6/60) or visual field less than 20° to the largest Goldmann test object (V4 = 64 mm2).7

               Brain CT scan was done for all patients but MRI was done for patients when cerebral venous sinus thrombosis was suspected as history of oral contraceptive pills, history of thrombotic events in the patient or the family, pregnancy and puerperium.

               The data are presented as means and percentiles. Student-t test was used to compare different groups and to test significance. The X2 test also was used. P<0.05 was considered significant.

         

RESULTS

 

Thirty two patients met the criteria for the diagnosis of IIH. Twenty nine (90.6%) were females and 3 (9.4%) were males. The female: male ratio was 9.6: 1. The age of the studied patients at presentation ranged from 12 to 45 years with a mean of 28.0±2.4 years, as shown in table (1).

               History of oral contraceptive pills intake was present in 18 (56.3%) patients, combined tetracycline and vitamin A intake for treatment of acne in 10 (31.3%) and oral prednisolone in 2 (6.3%) patients. The duration of the presenting symptom (s) before establishing diagnosis was less than one month in 11 (34.4%) patients and more than one month in 21 (65.6%) patents, as shown in table (1).

               Neuroimaging was normal in 29 (90.6%) patients, but 2 patients had slit-like ventricular system and one had empty sella. None of our patients had cerebral venous thrombosis.

               The presenting symptoms were shown in table (2). The most common ophthalmic symptom was blurred vision, present in 24 (75%) patients. Transient visual obscuration (episodes of difficulty seeing that occur in both eyes but not necessarily at the same time) was present in 8 (25%) patients, while double vision was present in 6 (18.8%) patients and ocular pain in 3 (9.4%) patients. In addition to ophthalmic symptoms, 31 patients (96.7%) had headache, and 24 (75.0%) patients had pulsating tinnitus (bilateral in 18 and unilateral in 6 patients). Twelve (37.5%) patients had dizzy spells, 10 (31.3%) had nausea, and 4 (12.5%) had generalized weakness. 

               The ophthalmic signs were shown in table (3). The most common sign was papilledema (100%). All patients had papilledema that was bilateral in 31 (96.9%) patients and unilateral in one (3.1%) patient. In those with bilateral papilledema, 6 had papilledema more pronounced in the right eye, while 5 had papilledema more pronounced in the left eye. Twenty patients had symmetrical papilledema. The visual acuity was less than 20/100 in 3 (9.4%) patients, while moderate visual impairment was found in 24 (75%) patients. A relative afferent pupillary defect was present in 8 (25.0%) patients. Sixth nerve palsy was present in 6 (18.75%) patients. It was bilateral in 4 and unilateral in 2 patients.

               Abnormal perimetry was present in 30 (93.8%) patients; 12 eyes with enlarged blind spot, 12 eyes with generalized constriction, 5 eyes with cecocentral scotomas, and 3 eyes with other defects. The intraocular pressure measured by applanation tonometry was normal (<20 mmHg) in all patients. There were no slit lamp abnormalities. Retinal abnormalities included retinal hemorrhages (2 eyes), macular edema (2 eyes) and retinal exudates (1 eye). Optic atrophy was present in 4 (12.5%) patients.

               The CSF opening pressure ranged from 260 to 560 mmH2O with a mean of 340±67 mmH2O. No significant relation was found between the CSF opening pressure and both the visual impairment and the duration of symptoms before diagnosis, as shown in table (4). Also, no significant relation was found between visual impairment and the duration of symptoms before diagnosis, as shown in table 5. The CSF composition was nearly normal.    

               Repeated withdrawal of CSF by lumbar puncture was done for all patients as the treatment of choice. It was combined with oral acetazolamide 500 to 750 mg daily in 29 (90.6%) patients. Complete resolution of symptoms and signs occurred in 15 (46.9%) patients. Moderate visual impairment (20/40-20/100) persisted in 6 (18.8%) patients and severe loss of vision (<20/100) persisted in 3 (9.4%) patients, 2 of them underwent lumboperitoneal shunt operation.


 

Table 1. Demographic data of the studied patients (n=32).

 

Data

Number of patients (%)

Sex

Females

29 (90.6%)

Males

3 (9.4%)

Female: Male ratio

9.6 : 1

Age at presentation (in years)

Range

12 - 45

Mean±SD

28.0 ± 2.4

Oral contraceptive pills

18 (56.3%)

Combined tetracycline and vitamin A

10 (31.3%)

Oral prednisolone

(6.3%)

Duration of symptoms before diagnosis

Less than one month

11 (34.4%)

More than one month

21 (65.6%)

 

Table 2. The presenting symptoms of IIH in the studied patients (n=32).

 

Symptoms

Number of patients (%)

Ophthalmic

Blurred vision

24 (75.0%)

Transient visual obscuration

8 (25.0%)

Double vision

6 (18.8%)

Ocular pain

3 (9.4%)

Non-ophthalmic

Headache

31 (96.7%)

Tinnitus

24 (75.0%)

Dizzy spells

12 (37.5%)

Nausea

10 (31.3%)

Generalized weakness

4 (12.5%)

 

Table 3. Ophthalmic signs of idiopathic intracranial hypertension in the studied patients (n=32).

 

Sign

Number of patients (%)

Papilledema

32 (100%)*

Abnormal perimetry

30 (93.8%)

Relative afferent papillary defect

8 (25.0%)

Sixth nerve palsy

6 (18.75%)

Optic atrophy

4 (12.5%)

Severe visual loss

3 (9.4%)

* Bilateral = 31, unilateral = 1

Bilateral = 4, unilateral = 2

 

Table 4. Relation between CSF opening pressure and both visual impairment and the duration of symptoms before diagnosis.

 

 

CSF opening pressure

(Mean±SD)

t-test

P-value

Vision

Impaired (n=24)

341±68

0.279 

0.782

Normal (n=8)

334±64

Duration of symptoms before diagnosis

Less than one month (n=11)

332±66

0.452

0.654

More than one month (n=21)

344±69

Table 5. Relation between vision and duration of symptoms before diagnosis.

 

 

Duration of symptoms before diagnosis

X2

P-value

Less than one month

(n=11)

More than one month

(n=21)

Normal vision (n=8)

2 (18.18%)

6 (28.57%)

1.794

0.408

Moderate impairment (n=21)

8 (72.73%)

13 (61.91%)

Severe visual loss (n=3)

1 (0.09%)

2 (9.52%)

 

 


DISCUSSION

              

Idiopathic intracranial hypertension is an uncommon headache syndrome8,9, more frequently encountered in women, especially obese women of childbearing age. Children of both sexes and adult men are occasionally affected.5 Atypical patients include men, slim women, pre-pubertal children, and patients older than 45 years.9,10 In the present study, the female to male ratio was 9.6: 1 that is going with previous observations, as was our mean age of 28.0±2.4 years.2,5,9

Pathogenesis of pseudotumor cerebri is unclear11, but decreased CSF absorption by the arachnoid villi is the most commonly suggested explanation. Elevated intracranial venous pressure causes delayed absorption of the CSF. Obesity causes raised intra-abdominal pressure that results in increased pleural and cardiac filling pressure, leading to raised intracranial venous pressure and ultimately, increased CSF pressure.12,13     

Proper and early diagnosis of IIH is important as timely intervention may provide relief of symptoms and help prevent irreversible loss of vision, which has been shown in the present study and others.7,14,15 Long-term untreated papilledema leads to visual loss, initially in the periphery but progressively towards the center of vision.2,3 The diagnosis is established by the presence of papilledema, increased CSF opening pressure, normal CSF composition and normal radiographic studies4, with the occasional exception of enlarged sella turcica and/or slit-like ventricular system.(1,2,5) All of our patients had papilledema and increased CSF opening pressure. Two patients had slit-like ventricular system and one had empty sella.

Medical literature contains various, and sometimes conflicting, recommendations regarding the minimum CSF opening pressure required for diagnosing IIH. In general, however, a CSF pressure above 250 mmH2O is consistent with a diagnosis of IIH, below 200 mmH2O is considered normal, and 201-249 mmH2O is considered to be nondiagnostic. Contrary to popular belief, there is no evidence that body weight influences these cutoff values.12

Headache is reported to be the most common and the most constant initial symptom of IIH, which occurs in almost all (92–94%) cases2. This was borne out by most of our patients (96.7%) complaining of headache. Most of these patients obtained headache relief from repeat LP and/or oral acetazolamide. Pulsating tinnitus was present in 75% of patients of the present study. This is going with that shown in other studies2,6, that reported the presence of pulsating tinnitus (unilateral or bilateral) in almost 64–87% of patients with IIH. This form of tinnitus is caused by high intracranial pressure compressing blood vessels. It can be the presenting symptom of the disorder and is recognized as part of the diagnostic criteria for chronic IIH.6

However, an ophthalmologist may receive patients complaining of blurred vision7, transient visual obscuration2,3, and diplopia14, with or without headache.14 As demonstrated in this study, many of these patients would have moderate or severe loss of vision, relative afferent pupillary defect, visual field defects and 6th nerve palsy. In most patients the prognosis for vision is excellent, but loss of vision, the only serious complication, can occur either early or late in the course of the disease.16

Previous studies have suggested that up to 96% of patients would have visual abnormalities at some time during the course of IIH7. The natural history of IIH is largely unknown, although several researchers have highlighted the potential risk of permanent visual impairment in a small, but significant, proportion of patients with IIH.(7,16) An early hospital-based study that followed up 57 patients for 5 to 41 years found that 24% of them developed blindness or severe visual impairment.17 Another study reported severe visual loss in 9% cases over 3 years (16). In contrast, a community-based epidemiological study reported a lower rate of severe visual loss of 6% (14). In the current study, the visual impairment was moderate in 24 (75%) patients and severe in 3 (9.4%) patients. These differences could be due to differences in study methodology, referral bias, different management options and variable follow-up periods. However, variable degrees of visual impairment and visual outcome in patients with IIH are present.

We did not find any significant association between CSF opening pressure and both visual impairment and the duration of symptoms before diagnosis, which is similar to previous literature.16,18 Also, we did not find any significant association between visual impairment and the duration of symptoms before diagnosis.

The characteristic visual field abnormalities in IIH are disc related. These include enlarged blind spot19,20, inferior nasal defects16, arcuate defects16, generalized constrictions16, and cecocentral scotomas16. All of which were seen in our study. An enlarged blind spot is the classic defect in IIH and is attributed to displacement of peri-papillary retinal percipient elements by the swollen disc. However, since these are usually relative rather than absolute scotomas, retinal disorganization probably accounts for most blind spot enlargements.(16) 

Rowe and Sarkies (16) studied 35 IIH patients prospectively and found that visual field assessment was the most sensitive indicator of visual loss with a statistically greater sensitivity than visual acuity or contrast sensitivity testing.

Sixth cranial nerve palsy was the only accepted neurological abnormality in diagnosing IIH until recently.21 It was encountered in 6 (18.75%) patients in the present study that is going with other published data reporting 6th cranial nerve palsy in 12% of adults, but it continues to be more common among children with IIH, occurring in 9% to 48%.21,22 Other cranial nerve palsies, including the 3rd, 4th, 7th, 9th, and 12th cranial nerves, have been reported in children.(22) Ophthalmoparesis in IIH may be related directly to very elevated CSF pressure and may be secondary to altered CSF flow in the posterior fossa.23  

Lumbar punctures are useful to relieve increased intracranial pressure of idiopathic pseudotumor cerebri. The rationale behind the procedure is uncertain. Repeated LPs are specifically useful in patients with symptom exacerbations and during pregnancy. Some clinicians prefer ‘high volume’ LP removing 20 ml of CSF or more but others prefer to lower the pressure into the normal range (target range for closing pressure 140-180 mm water), which generally affords relief while lessening the likelihood of post-LP headache.24

We attribute the relatively low rate of permanent disability in our study to early diagnosis, prompt medical intervention and meticulous follow up for at least six months after remission. Only 3 (9.4%) patients showed severe visual loss and 2 (6.3%) of them required neurosurgical intervention, a rate similar to other series.(16) IIH is etiologically related to obesity, nutritional preferences, and consumption of certain medicines and drugs. Hence, it is possible that IIH may have different natural history and long-term outcome in different geographic locations. We stress the importance of early diagnosis, prompt intervention and diligent possible long term follow up in the management of IIH which is no longer considered benign and is an important cause for visual impairment.

 

[Disclosure: Authors report no conflict of interest]

REFERENCES

 

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17.    Corbett JJ, Savino PJ, Thompson HS, Kansu T, Schatz NJ, Orr LS, et al. Visual loss in pseudotumor cerebri. Follow-up of 57 patients from five to 41 years and a profile of 14 patients with permanent severe visual loss. Arch Neurol. 1982; 39: 461-74.

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الملخص العربى

 

المظاهر البصرية لارتفاع الضغط الدماغى مجهول السبب

 

يعتبر مرض ارتفاع الضغط الدماغى مجهول السبب من الأمراض النادرة لكنه ومع هذا من الممكن أن يؤدى مباشرة إلى فقدان البصر دون رجعة، ولا يزال السبب الرئيسى والمسبب له غير محدد. يهدف هذا البحث إلى تقييم بعض الأعراض الأولية والى يشكو منها المرضى وبخاصة الأعراض البصرية وكذا العلامات الإكلينيكية المصاحبة لها. وقد تم إجراء هذه الدراسة بقسم الأمراض العصبية والنفسية وقسم الرمد بكلية الطب جامعة طنطا على 32 مريض بهذا المرض حيث تم تقييم الأعراض وفحص العين من خلال قياس حدة الأبصار، فحص قاع العين بدقة، قياس ضغط العين، حركة عضلات العين الخارجية، وقياس محيط الرؤية، كما تم عمل فحص بالأشعة المقطعية على المخ بالكمبيوتر لكل المرضى وأشعة بالرنين المغناطيسى على المخ لمن كانوا قد تناولوا أقراص منع الحمل في وقت ما. كما تم قياس الضغط الأنفتاحى للسائل النخاعي في كل المرضى وكذا تحليل السائل النخاعي تحليلا معمليا. تبين من هذه الدراسة  أن أغلب المرضى من النساء (93.7%)، وكان متوسط أعمار المرضى هو 28±2.4 عاما. كان أكثر الأعراض البصرية شيوعا لدى المرضى هو غشاوة الرؤية (75%)، يليه نوبات الإظلام البصرى العابر (25%) ثم ازدواج الرؤية (18.8%) وألم بالعين (9.4%). أما الأعراض الغير بصرية فقد كان الصداع أكثرها شيوعا (96.7%) ثم طنين الأذنين (75%) ثم نوبات الدوخة (37.5%) و الغثيان (31.3%) و الضعف العام (12.5%). وقد كان ارتشاح العصب البصرى موجودا في كل المرضى لكنه كان على الناحيتين في 31 (96.9%) مريضا وعلى ناحية واحدة في المريض المتبقي (3.1%) وقد كانت حدة الأبصار أقل من 20/100 في 3 (9.4%) مرضى، بينما كان هناك اختلالا بصريا متوسطا فى 24 (75%) مريضا، وكان هناك اعتلال بمحيط الرؤية لدى (93.8%) من المرضى. كان متوسط الضغط الأنفتاحى للسائل النخاعي لدى المرضى 340±67 مليميتر ماء والذى لم يكن له علاقة ذات دلالة مع كل من اختلال البصر و الفترة الزمنية للأعراض قبل التشخيص. كما لم تكن هناك أيضا علاقة ذات دلالة بين اختلال البصر والفترة الزمنية للأعراض قبل التشخيص. وقد تم عمل بذل للسائل النخاعي كأجراء علاجي لكل المرضى وقد تمت إضافة العلاج بعقار أسيتازولامايد أقراص في 29 (90.6%) مريضا، لوحظ التحسن الكامل مع زوال الأعراض والعلامات الإكلينيكية في 24 (75%) مريضا وقد استمر اختلال النظر المتوسط في 6 (18.8%) والشديد في 3 (9.4%) من المرضى. ولهذا فنحن نؤكد على أهمية التشخيص المبكر والتدخل العلاجي السريع والمناسب مع أهمية المتابعة المستمرة والتي قد تكون طويلة المدى لمرضى ارتفاع الضغط الدماغى مجهول السبب والذى لم يعد يعتبره البعض حميدا كما كان سابقا حيث يعد الآن سببا مهما من أسباب فقدان البصر.    

 

 



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