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\title{A case of Foster Kennedy Syndrome (FKS) with Increase Intracranial Pressure (ICP) Attributed to Cerebral Venous Sinus Thrombosis (CVST)}
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\begin{document}

             \author[1]{Madihah  ALhubayshia}

             \affil[1]{  King AbdulAziz Medical city, Jeddah, Saudi Arabia}

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\date{\small \em Received: 10 December 2012 Accepted: 1 January 2013 Published: 15 January 2013}

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\begin{abstract}
        


Foster Kennedy syndrome (FKS) is a very rare neurological syndrome with a unique ophthalmological manifestation described in 1911 by Robert Foster Kennedy attributed to anterior fossa mass lesion and raised intracranial pressure (ICP) caused by the tumor's mass effect. Meningioma is the most common cause of the syndrome. Rarely vascular lesions and tuberculous meningitis had been reported as a cause of FKS.Here we present a case of Foster Kennedy-like syndrome, in which meningioma compressed one optic nerve and cerebral venous sinus thrombosis impair cerebral venous drainage inducing intracranial hypertension, and papilledema in the other eye. This case emphasis the importance of considering of CVST as underlying pathogenesis of raised ICP in absence of cerebral edema or obstructed hydrocephalus.

\end{abstract}


\keywords{foster kennedy syndrome (FKS), raised intracranial (pressure (ICP), cerebral venous sinus thrombosis CVST).}

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\let\tabcellsep& 	 	 		 
\section[{Introduction}]{Introduction}\par
he Foster Kennedy syndrome consists of optic disc pallor in one eye, optic disc edema in the other eye, and reduced olfaction caused by spaceoccupying lesion. \hyperref[b0]{(1,}\hyperref[b1]{2)} Classically, The ophthalmological sign of Foster Kennedy syndrome (FKS) produced by direct compression of the ipsilateral optic nerve by basal frontal lobe, olfactory groove or sphenoid wing meningioma leading to optic atrophy with concomitant contralateral optic disc swelling secondary to raised (ICP) caused by the mass effect of the tumor. \hyperref[b0]{(1)}\hyperref[b1]{(2)}\hyperref[b2]{(3)}\hyperref[b3]{(4)}\hyperref[b4]{(5)}\hyperref[b5]{(6)} Anosmia results from direct compression of the olfactory nerve. \hyperref[b0]{(1,}\hyperref[b1]{2)} We describe a case report regarding the different pathogenic mechanisms, for which increased intracranial pressure (ICP) resulting from CVST. This is to suggest that not all FKS cases have the same underlying pathogenesis.\par
Our aim is to document this unique association and to draw attention on the importance of its presence. This is because the management in such situation advocates the use of anticoagulation. There was left 6 th cranial nerve palsy. Humphrey perimeter of the left eye revealed a superior nerve fiber bundle defect (fig.  {\ref 2.}). The rest examination was normal.   The patient was treated with enoxoparine 1mg/kg subcutaneous BID, acetazolamid 500mg BID. 
\section[{II.}]{II.} 
\section[{Case Study}]{Case Study}\par
As vision of the left eye continued to deteriorate, the decision was taken to relief the pressure surgically and the patient underwent lumboperitoneal shunt, CSF examination done intra operatively showed opening pressure of 450 mm with normal compositions and negative cultures for bacterial and fungal infections, there was no evidence of malignant cell.\par
Other diagnostic tests including complete blood count, complete metabolic panel, erythrocyte sedimentation rate, c-reactive protein, and were unremarkable.\par
Post operatively, The patient received warfarin with therapeutic INR (2-3).\par
One month later the papilledema and visual field had improved on the left eye, and visual acuity was stable.\par
After 5 years, the patient vision stabilized and developed no shunt complication. 
\section[{III.}]{III.} 
\section[{Discussion}]{Discussion}\par
The mechanism and underlying pathology of ophthalmic feature of the FKS is variable. The classical pattern is caused by unilateral direct compression of the optic nerve fiber by meningioma and secondary increased intracranial pressure (ICP) causing papilledema of the contralateral eye. \hyperref[b0]{(1,}\hyperref[b1]{2,}\hyperref[b3]{4)} Other mechanism have been suggested to explain the underlying pathology due to bilateral direct optic nerve fiber compression with normal ICP while atrophic changes resulting from asymmetrical compression of both optic nerve by tumor. \hyperref[b6]{(7)} It may also results from chronic increased ICP which initially gives bilateral papelledema, with one optic disc subsequently developing pallor as a result of axonal death while the other optic disc remains swollen. \hyperref[b6]{(7)} This case of FKS meningioma cause direct compression of the right optic nerve, and presence of CVST impair cerebral venous drainage that round the other optic nerve by thrombus in which CSF is at a higher pressure than normal and which becomes responsible for papilloedema on the opposite side.\par
The treatment of visual loss due to Papilledem depends largely on the underlying pathology hence it is important to look for CVST when obvious brain edema and obstructed hydrocephalus are lacking, Prompt use of anticoagulation and cerebrospinal fluid diversion is critical in prevented visual loss in our case.\par
There is a previous report a patient with FKS in which meningiomas compressed the superior sagittal sinus to block cerebral venous drainage causes increased intracranial pressure, and papilledema in the other eye. \hyperref[b7]{(8)} Our case differ from this patient by having CVST.\par
We may postulate that some of the previous cases of FKS may have CVST as a cause of ophthalmic feature of this syndrome rather than a direct compression and/or an intracranial hypertension while MRI, MRV were lacking it emphasizes the importance of looking for this association as adding anticoagulation among other measures.\begin{figure}[htbp]
\noindent\textbf{}\includegraphics[]{image-2.png}
\caption{\label{fig_0}}\end{figure}
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\noindent\textbf{1}\includegraphics[]{image-3.png}
\caption{\label{fig_1}Figure 1 .}\end{figure}
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\noindent\textbf{234}\includegraphics[]{image-4.png}
\caption{\label{fig_2}Figure 2 :Figure 3 :Figure 4 :}\end{figure}
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\noindent\textbf{56}\includegraphics[]{image-5.png}
\caption{\label{fig_3}Figure 5 :Figure 6 :}\end{figure}
 			\footnote{© 2013 Global Journals Inc. (US)} 			\footnote{A case of Foster Kennedy Syndrome (FKS) with Increase Intracranial Pressure (ICP) Attributed to Cerebral Venous Sinus Thrombosis (CVST)} 		 		\backmatter  			  				\begin{bibitemlist}{1}
\bibitem[Lee et al. (2012)]{b7}\label{b7} 	 		\textit{},  		 			A G Lee 		,  		 			M Wall 		,  		 			Papilledema 		.  	 	 		\textit{Curr Neurol Neurosci Rep}  		2012 Jun. 12  (3)  p. .  	 
\bibitem[Walia et al. ()]{b2}\label{b2} 	 		\textit{An aggressive sphenoid wing meningioma causing foster kennedy syndrome. Case Rep Ophthalmol Med},  		 			H S Walia 		,  		 			F L Grumbine 		,  		 			G K Sawhney 		,  		 			D S Risner 		,  		 			N V Palejwala 		,  		 			M E Emanuel 		.  		2012. 2012 p. 102365.  	 
\bibitem[Liang and Ozanne (2010)]{b0}\label{b0} 	 		‘An atypical case of Foster Kennedy Syndrome’.  		 			F Liang 		,  		 			A Ozanne 		.  	 	 		\textit{Interv Neuroradiol}  		2010 December. 16  (4)  p. .  	 
\bibitem[Watnick and Trobe ()]{b6}\label{b6} 	 		‘Bilateral optic nerve compression as a mechanism for the Foster Kennedy Syndrome’.  		 			R L Watnick 		,  		 			J D Trobe 		.  	 	 		\textit{Ophthalmology}  		1989. 96  (12)  p. .  	 
\bibitem[Jarus and Feldon ()]{b4}\label{b4} 	 		‘Clinical and computed tomographic findings in the Foster Kennedy Syndrome’.  		 			G D Jarus 		,  		 			S E Feldon 		.  	 	 		\textit{Am J Ophthal}  		1982. 93 p. .  	 
\bibitem[Massey and Schoenberg ()]{b5}\label{b5} 	 		‘Foster Kennedy Syndrome’.  		 			E W Massey 		,  		 			B Schoenberg 		.  	 	 		\textit{Arch Neurol}  		1984. 41 p. .  	 
\bibitem[Neville et al. ()]{b3}\label{b3} 	 		‘Foster Kennedy Syndrome and an optociliary vein in a patient with a falx meningioma’.  		 			R G Neville 		,  		 			S H Greenblatt 		,  		 			C R Kollarits 		.  	 	 		\textit{J Clin Neuroophthalmol}  		1984. 4 p. .  	 
\bibitem[Acebes et al. (2009)]{b1}\label{b1} 	 		‘Intracranial meningiomatosis causing foster kennedy syndrome by unilateral optic nerve compression and blockage of the superior sagittal sinus’.  		 			X Acebes 		,  		 			J Arruga 		,  		 			J J Acebes 		,  		 			C Majos 		,  		 			S Muñoz 		,  		 			I A Valero 		.  	 	 		\textit{J Neuroophthalmol}  		2009 Jun. 29  (2)  p. .  	 
\end{bibitemlist}
 			 		 	 
\end{document}