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Table of Contents
CASE REPORT
Year : 2015  |  Volume : 18  |  Issue : 4  |  Page : 475-477
 

Clarithromycin Culprit of Benign Intracranial Hypertension


1 Department of Medicine and Cardiovascular Science, Nottingham NHS Trust, Nottingham, United Kingdom
2 Department of Medicine, Cambridge University Hospitals, Cambridge, United Kingdom
3 Department of Medicine, Waterford General Hospital, Waterford, United Kingdom

Date of Submission26-Aug-2014
Date of Decision20-Nov-2014
Date of Acceptance03-Dec-2014
Date of Web Publication17-Nov-2015

Correspondence Address:
Habib Rehman Khan
Nottingham City Hospital, Nottingham
United Kingdom
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0972-2327.165477

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   Abstract 

Benign intracranial hypertension is characterized with increase in CSF opening pressure with no specific etiology. It is predominantly found in women of child bearing age and particularly in individuals with obesity. Visual disturbances or loss and associated headaches are common and can lead to blindness if left untreated. Diagnosis can be achieved once other causes of visual loss, headaches and high opening pressures are excluded. Management consists of serial optic disc assessments although no specific treatment is available despite recent trials using carbonic anhydrase inhibitors. Diet modification and weight management can help in therapy.


Keywords: Benign intracranial hypertension, blurred vision, clarithromycin, headache, psedotumor cerebri


How to cite this article:
Khan HR, Mason C, Mulcahy R. Clarithromycin Culprit of Benign Intracranial Hypertension. Ann Indian Acad Neurol 2015;18:475-7

How to cite this URL:
Khan HR, Mason C, Mulcahy R. Clarithromycin Culprit of Benign Intracranial Hypertension. Ann Indian Acad Neurol [serial online] 2015 [cited 2019 Nov 22];18:475-7. Available from: http://www.annalsofian.org/text.asp?2015/18/4/475/165477



   Introduction Top


A 27-year-old lady presented to the hospital with headache, blurring of vision, and tunnel vision for 4 days. She gave a history of having flu-like illness 3 weeks previously. At the time of the flu-like illness, she did not have a headache, no blurring of vision, no neck stiffness, and no pyrexia She visited her general practitioner and was prescribed Clarithyromycin 500 mg once a day for 1 week. She was never prescribed Clarithromycin previously for any other illness. She noticed the headaches to begin about 5 days after the initiation of Clarithyromycin. The headache was frontal and gradually getting worse over the last 14 days along with visual symptoms. The blurring of vision and constricted field of vision started 2 weeks after the initiation of Clarithyromycin.

Ophthalmologic examination revealed papilloedema bilaterally and haziness of the nasal aspect of the optic nerve [Figure 1] and [Figure 2]. Visual acuity in both eyes was normal and visual field examination was normal []. No focal deficits were noted on detailed neurological examination. Computerized tomography (CT) of the brain was arranged, and no space-occupying lesions or any other cranial causes were located [Figure 3]. A lumbar puncture was performed showing an opening pressure of 42 mmHg and cytology was normal [Table 1]. Blood tests revealed normal full blood count, urea and electrolytes (U&E), and liver function tests (LFT) parameters. Erythrocyte sedimentation rate (ESR) was 11 and C-reactive protein (CRP) was < 10. Systemic examination was normal.
Figure 1: Fundoscopy of right and left eye

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Figure 2: Severe papilloedema (highlighted area)

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Figure 3: Computed tomography of brain

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Table 1: Cerebro-spinal fl uid (CSF) analysis

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The diagnosis was of benign intracranial hypertension (BIH) was suggested and therapeutic lumbar puncture performed. She was commenced on Acetozolamide 250 mg twice a day for 4 weeks. On follow-up 8 weeks from discharge, her ophthalmology examination was normal. She did not have any headaches, or further blurring of vision on further routine follow-up with no medical treatment.


   Discussion Top


BIH direct etiology is currently unknown. In normal patients, the cerebro-spinal fluid (CSF) production is equal to reabsorption rate. CSF is produced by four choroid plexuses located each ventricles of human brain. In patients with BIH, the rate is equal; however, a greater pressure is required against increased resistance at the Arachnoid granulations. The raised intracranial hypertension is transmitted to the optic nerve sheath. The raised pressure alters the flow in the optic nerve resulting in swelling of the nerve with leak of protein, water along with other cellular contents into the extracellular space. There are no race differences, and affects obese females, with highest incidence in child bearing ages [1],[2],[3],[8],[9],[12] .

The initial symptoms are of increased intra-cranial hypertension (ICP) and papilloedema. The symptoms of ICP include headache of various areas, non-specific type and frequency; diplopia due to opthalmoplegia most commonly due to cranial nerve VI (CN VI). Symptoms of papilloedema include transient visual defects mostly orthostatic; progressive loss of peripheral vision in any eye, initially of nasal side; blurring of central vision; and rarely sudden vision loss [4],[5],[6],[7],[8] .

The important examinations are fundoscopy, visual fields, visual acuity, color vision, and ocular movements [1],[2],[3],[4],[5],[6],[7],[8],[9],[10],[11],[12] .

Differential diagnosis would include arteriovenous (AV) malformations, aseptic meningitis, hydrocephalus, intracranial abscess, intracranial hemorrhage, meningioma, Lyme disease, migraine headache, systemic lupus erythematosus (SLE), subarachanoid hemorrhage, malignant hypertension, diabetic papillopathy [9],[12],[13],[14] .

Diagnosis is by performing opthalmological examination, exclusion of differential diagnosis by neuroimaging, and lumbar puncture. Magnetic resonance imaging (MRI) is the neuroimaging modality of choice [14],[15],[16],[17],[18],[19] .

Treatment of benign intracranial hypertension is to remove any causative or associated factor. If no obvious cause is found, then pharmacological strategies have shown some benefit. In acute settings, particularly with visual disturbances, therapeutic lumbar puncture tap of about 20 ml improves acute symptoms. Pharmacological therapy consists of reduction in CSF production by carbonic anhydrase inhibitors, reduced salt intake, and sometimes diuretics are effective. Carbonic anhydrase inhibitors block bicarbonate (HCO3 - ) formation by the enzyme carbonic anhydrase and reduce CSF production. Corticosteroids are effective but the mechanism is unknown [16],[17],[18],[19] . Lumboperitoneal shunting is recommended if patients do not respond to pharmacological therapy. Regular follow-up is recommended with opthalmological examinations. Complication of most importance is optic atrophy if not cured at early presentation.

 
   References Top

1.
Minckler DS, Tso MO, Zimmerman LE. A light microscopic, autoradiographic study of axoplasmic transport in the optic nerve head during ocular hypotony, increased intraocular pressure, and papilledema. Am J Ophthalmol 1976;82:741-57.  Back to cited text no. 1
    
2.
Tso MO, Hayreh SS. Optic disc edema in raised intracranial pressure. IV. Axoplasmic transport in experimental papilledema. Arch Ophthalmol 1977;95:1458-62.  Back to cited text no. 2
    
3.
Vaphiades MS. The disk edema dilemma. Surv Ophthalmol 2002;47:183-8.  Back to cited text no. 3
    
4.
Alder JB, Fraunfelder FT, Edwards R. Levonorgestrel implants and intracranial hypertension. N Engl J Med 1995;332:1720-1.  Back to cited text no. 4
    
5.
Burgett RA, Purvin VA, Kawasaki A. Lumboperitoneal shunting for pseudotumor cerebri. Neurology 1997;49:734-9.  Back to cited text no. 5
    
6.
Farb RI, Vanek I, Scott JN, Mikulis DJ, Willinsky RA, Tomlinson G, et al. Idiopathic intracranial hypertension: The prevalence and morphology of sinovenous stenosis. Neurology 2003;60:1418-24.  Back to cited text no. 6
    
7.
Roberts I, Yates D, Sandercock P, Farrell B, Wasserberg J, Lomas G, et al., CRASH trial collaborators. Effect of intravenous corticosteroids on death within 14 days in 10,008 adults with clinically significant head injury (MRC CRASH trial): Randomised placebo-controlled trial. Lancet 2004;364:1321-8.  Back to cited text no. 7
    
8.
Cinefro RJ, Frenkel M. Systemic lupus erythematosus presenting as optic neuritis. Ann Ophthalmol 1978;10:559-63.  Back to cited text no. 8
    
9.
Orcutt JC, Page NG, Sanders MD. Factors affecting visual loss in benign intracranial hypertension. Ophthalmology 1984;91:1303-12.  Back to cited text no. 9
    
10.
Cruz OA, Fogg SG, Roper-Hall G. Pseudotumor cerebri associated with cyclosporine use. Am J Ophthalmol 1996;122:436-7.  Back to cited text no. 10
    
11.
Goh KY, Schatz NJ, Glaser JS. Optic nerve sheath fenestration for pseudotumor cerebri. J Neuroophthalmol 1997;17:86-91.  Back to cited text no. 11
    
12.
Durcan FJ, Corbett JJ, Wall M. The incidence of pseudotumor cerebri. Population studies in Iowa and Louisiana. Arch Neurol 1988;45:875-7.  Back to cited text no. 12
    
13.
Giuseffi V, Wall M, Siegel PZ, Rojas PB. Symptoms and disease associations in idiopathic intracranial hypertension (pseudotumor cerebri): A case-control study. Neurology 1991;41:239-44.  Back to cited text no. 13
    
14.
Gucer G, Viernstein L. Long-term intracranial pressure recording in the management of pseudotumor cerebri. J Neurosurg 1978;49:256-63.  Back to cited text no. 14
    
15.
Digre KB, Varner MW, Corbett JJ. Pseudotumor cerebri and pregnancy. Neurology 1984;34:721-9.  Back to cited text no. 15
    
16.
Rowe FJ, Sarkies NJ. Assessment of visual function in idiopathic intracranial hypertension: A prospective study. Eye (Lond) 1998;12:111-8.  Back to cited text no. 16
    
17.
Wall M, McDermott MP, Kieburtz KD, Corbett JJ, Feldon SE, Friedman DI, et al. NORDIC Idiopathic Intracranial Hypertension Study Group Writing Committee. Effect of acetazolamide on visual function in patients with idiopathic intracranial hypertension and mild visual loss: The idiopathic intracranial hypertension treatment trial. JAMA 2014;311:1641-51.  Back to cited text no. 17
    
18.
Vogh BP, Godman DR, Maren TH. The effect of AlCl 3 and other acids on cerebrospinal fluid production: A correction. J Pharmacol Exp Ther 1987;243:35-9.  Back to cited text no. 18
    
19.
Cowan F, Whitelaw A. Acute effects of acetazolamide on cerebral blood flow velocity and pCO 2 in the newborn infant. Acta Pediatr Scand 1991;80:22-7.  Back to cited text no. 19
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1]



 

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