A DIFFICULT CASE
When is ‘idiopathic intracranial hypertension’ no longer idiopathic? Karen Suetterlin,1 Nicholas Borg,2 Harriet Joy,3 Joanna K Lovett,1 Boyd C P Ghosh1 1
Department of Neurology, Wessex Neurological Centre, Southampton General Hospital, Southampton, Hampshire, UK 2 Department of Neurosurgery, Wessex Neurological Centre, Southampton General Hospital, Southampton, Hampshire, UK 3 Department of Neuroradiology, Wessex Neurological Centre, Southampton General Hospital, Southampton, Hampshire, UK Correspondence to Dr Karen Suetterlin, Department of Neurology, Wessex Neurological Centre, Southampton General Hospital, Southampton, Hampshire, SO16 6YD, UK; [email protected] The duties of the senior author were shared between the two authors JKL and BCPG. Published Online First 29 October 2013
To cite: Suetterlin K, Borg N, Joy H, et al. Pract Neurol 2014;14:102–106.
102
HISTORY A 23-year-old woman with idiopathic intracranial hypertension (IIH) presented with a recurrence of headache and visual disturbance. She had presented with similar symptoms 5 years earlier, when the diagnosis of IIH had been made, after magnetic resonance venography (MRV) had excluded cerebral venous sinus thrombosis (VST) (figure 1A,B). She had been asymptomatic for 18 months and had stopped her acetazolamide 6 months earlier. On examination, her visual acuity was 6/ 9 (right) and 6/15 (left). Her left visual field was constricted and there was bilateral papilloedema. Her cerebrospinal fluid (CSF) opening pressure was 80 cmH2O and we drained to a closing pressure of 22 cmH2O, resulting in complete resolution of both headache and visual disturbance. She was started on acetazolamide. Within 48 h, her headaches returned with a new left-sided lower motor neurone seventh nerve palsy. We organised MR imaging with venography and then repeated her lumbar puncture. The opening pressure was now 29 cmH2O and she reported postprocedure improvement in her headache. However, within 24 h, her headache recurred, she developed a right lower motor neurone seventh nerve palsy (figure 2), bilateral sixth nerve palsies, neck stiffness, vomiting and visual disturbance. Magnetic resonance venography (MRV) showed a VST affecting the left transverse and sigmoid sinuses (figure 1C) and we started her on unfractionated heparin. In view of her markedly elevated opening pressure, background of IIH and the need for anticoagulation, we referred for early ventriculoperitoneal shunting. On the evening before her operation she became drowsy and confused. Repeat lumbar puncture gave an opening pressure of 98 cmH2O. All CSF pressures were measured with her lying in the lateral decubitus position.
The following morning she underwent uneventful ventriculoperitoneal shunt insertion and was subsequently reanticoagulated with unfractionated heparin, followed by low molecular weight heparin and eventually warfarin. Her right seventh nerve palsy and bilateral sixth nerve palsies improved during the first postoperative day, consistent with resolution of IIH. Her left seventh nerve palsy (figure 2) gradually improved in the months following discharge. We have not identified any thrombophilia tendency. DISCUSSION Idiopathic intracranial hypertension is a common disorder, classically described in obese young women. Patients experience severe chronic headaches exacerbated by straining, bending forward or lying flat. The historical term, benign intracranial hypertension, has fallen out of favour because of the danger of irreversible visual loss in up to 25% of cases.1 Several conditions causing high intracranial pressure can mimic IIH. However, most of these, such as malignant hypertension, can be excluded by a careful clinical assessment and basic blood tests. In contrast, thrombosis of a venous sinus or jugular vein cannot be excluded without specific imaging. The classical false-localising sign in IIH is a sixth nerve palsy, but seventh nerve palsies have also been reported.2 3 The mechanism leading to these is not fully understood. However, Kuehnen et al4 reported a series of cases of transverse sinus thrombosis causing ipsilateral isolated cranial nerve palsies—in particular sixth, seventh and eighth nerve palsies— without evidence of raised intracranial pressure. They proposed that venous congestion in the veins draining into a thrombosed transverse sinus, such as the petrous vein, cause oedema in the nearby ventral brainstem and upper cranial nerves,
Suetterlin K, et al. Pract Neurol 2014;14:102–106. doi:10.1136/practneurol-2013-000680
A DIFFICULT CASE
Figure 1 Magnetic resonance venography (MRV). (A) MR Venogram at time of diagnosis with IIH in 2007: flow signal is seen in the transverse and sigmoid sinuses bilaterally, although they are asymmetrical, the right side being dominant. (B) MR Venogram 2007. Lack of flow signal in the distal transverse sinuses (arrows) is the characteristic appearance seen in IIH. (C) MR Venogram at time of diagnosis with VST in 2012: there is no flow signal in the left transverse and sigmoid sinuses. (D) MR Venogram 2012. The characteristic IIH appearance remains on the right (arrow).
resulting in cranial nerve palsies (figure 3).4 Our patient’s left seventh nerve palsy might also have occurred by this mechanism. It was ipsilateral to the affected transverse sinus, occurred when the opening pressure was relatively low (29 cmH2O) and persisted for several months. In contrast, both sixth nerve palsies and her right seventh nerve palsy appeared when her CSF pressure had risen considerably (98 cmH2O) and resolved within 24 h of ventriculoperitoneal shunt insertion. There are several reports describing VST in patients originally thought to have IIH. This is perhaps not surprising as their presenting symptoms overlap considerably. Both conditions can present with headache and visual disturbance, with raised CSF pressure on lumbar puncture.5 What is more, over one-third of patients with VST can present like IIH without other neurological symptoms or signs6–8 and can have a normal non-contrast brain CT and normal CSF
Suetterlin K, et al. Pract Neurol 2014;14:102–106. doi:10.1136/practneurol-2013-000680
composition.8 Venography can be difficult to interpret, as a significant proportion of the population have a left transverse sinus that is smaller than the right—and in 15%–20%, it may even be hypoplastic or absent.4 We cannot overstate the importance of distinguishing between the two conditions. Treatment is different and while IIH carries the risk of permanent visual loss, VST has a mortality rate of 10%–30%, as well as complications with high morbidity such as seizures and cerebral infarction.9 10 Although VST may complicate spontaneous intracranial hypotension11 and the finding of VST in patients inappropriately labelled as idiopathic intracranial hypertension is well reported, we could not find any papers describing VST being found after an accurate diagnosis of idiopathic intracranial hypertension. However, perhaps this is more common than the literature suggests. Prompted by the experience with our first patient, we made a second diagnosis of VST in a 103
A DIFFICULT CASE
Figure 2
Photographs of cranial nerve palsies.
patient with an established diagnosis of IIH a few months later. In this case, as before, repeat imaging was prompted by refractory symptoms and greater CSF pressures than found during previous IIH episodes. Again, careful review of all available imaging showed that there was no VST at the original diagnosis. There could be a link between a diagnosis of IIH and VST. VST is more common in young patients who are on the oral contraceptive pill or in pregnancy or puerperium. IIH, by comparison, is more common in obese young women, and oral contraceptive use is listed as a potential cause. There will therefore be a subset of patients with IIH who are independently at risk of developing thrombosis because they share some of the same risk factors. However, perhaps finding a VST in a patient with IIH could be due to more than a coincidence of risk factors and may also be attributable to pathological synergy centred on the tapering of the lateral sinuses in IIH. The lateral sinuses are well recognised sometimes to taper in patients with a confirmed diagnosis of IIH 104
(figure 1). This has been attributed to functional compression of the sinus secondary to high pressure, although others have postulated that high pressure could be secondary to a narrowed sinus, leading to the more recent treatment modality of venous stenting.12 13 However, could the tapering of the sinus and ensuing flow changes within that region predispose to thrombosis? Iliac vein stenosis is an independent risk factor for developing deep vein thrombosis in young women—for every 1% increase in stenosis there is a small but significant rise in risk.14 Subjects with >70% stenosis of the iliac vein, who were also on the combined oral contraceptive pill, had an OR of 17 for the development of a deep vein thrombosis.14 If the same is true for venous sinus stenosis: patients with IIH are likely to be at a higher risk of VST. Whatever the link between VST and IIH, we suggest that clinicians keep an open mind when reviewing patients with an established diagnosis of IIH. Red flags that should alert physicians include the return of symptoms after a long period of quiescence, the absence of a
Suetterlin K, et al. Pract Neurol 2014;14:102–106. doi:10.1136/practneurol-2013-000680
A DIFFICULT CASE
Figure 3 Cranial nerve topography in relation to venous drainage of the ventral aspect of the posterior fossa (modified and complemented from A. Berenstein and P. Lasjaunas). CN III–XII 5 cranial nerve roots III–XII; tr.s, transverse sinus; sig.s., sigmoid sinus; sup.petr.s., superior petrosal sinus; pt.v., petrous vein; a.m.v., anterior medullary vein; l.m.v., lateral medullary vein; p.m.v., pontomedullary vein; a.m.p.v., anterior medial pontine vein; tr.p.v., transverse pontine vein. Taken with permission from Oxford University Press, Kuehnen J, et al.4
clear trigger such as weight gain, symptoms resistant to treatment, exceptionally high CSF pressures and aggressive disease in patients who had a previously benign course. The presence of any of the above should prompt consideration of imaging to exclude VST.
images and the radiology figure legend. Joanna Lovett was the consultant in charge of the case management with input from Ashwin Pinto. Boyd Ghosh and Joanna Lovett are the guarantors. Competing interests None. Patient consent Obtained. Provenance and Peer Review Not commissioned. Externally peer reviewed. This paper was reviewed by Luke Bennetto, Bristol.
PRACTICAL POINTS ▸ This case highlights the importance of keeping an open mind in the management of patients with existing diagnostic labels. ▸ Clinicians should consider magnetic resonance venography or CT venography to look for venous sinus thrombosis (VST), even in patients with an established diagnosis of IIH, especially if the patient has a very high opening CSF pressure, drowsiness or focal neurology. ▸ False localising signs of raised CSF pressure in VST and IIH can include sixth and seventh nerve palsies. ▸ Cranial nerve palsies can be the presenting feature of VST, even without raised CSF pressure. ▸ Consider CSF shunting procedures in patients with VST and/or IIH with significantly elevated CSF pressures that remain high despite sequential lumbar punctures, especially if anticoagulation is required. Acknowledgements Our thanks are given to the patient for allowing publication of this material. We would also like to thank Ashwin Pinto, Jonathan Frankel and Sean Slaght for useful discussions concerning this case. Contributors The idea for the article came from discussions between Ashwin Pinto, Sean Slaght, Jonathan Frankel, Joanna Lovett and Boyd Ghosh. Literature search was performed by Karen Suetterlin and Nicholas Borg. The article was written by Karen Suetterlin with contribution from Nicholas Borg. Joanna Lovett and Boyd Ghosh edited the article. Harriet Joy provided radiology
Suetterlin K, et al. Pract Neurol 2014;14:102–106. doi:10.1136/practneurol-2013-000680
REFERENCES 1 Digre KB. Idiopathic intracranial hypertension headache. Curr Pain Headache Rep 2002;6:217–25. 2 Larner AJ. False localising signs. J Neurol Neurosurg Psychiatry 2003;74:415–18. 3 Davie C, Kennedy P, Katifi HA. Seventh nerve palsy as a false localising sign. J Neurol Neurosurg Psychiatry 1992;55:510–11. 4 Kuehnen J, Schwartz A, Neff W, et al. Cranial nerve syndrome in thrombosis of the transverse/sigmoid sinuses. Brain 1998;121:381–8. 5 Burger BM, Chavis PS, Purvin V. A weed by any other name. Surv Ophthalmol 2013;58:176–83. 6 Friedman DI, Jacobson DM. Diagnostic criteria for idiopathic intracranial hypertension. Neurology 2002;59:1492–5. 7 Friedman DI, Rausch EA. Headache diagnoses in patients with treated idiopathic intracranial hypertension. Neurology 2002;58:1551–3. 8 Sylaja PN, Ahsan Moosa NV, Radhakrishnan K, et al. Differential diagnosis of patients with intracranial sinus venous thrombosis related isolated intracranial hypertension from those with idiopathic intracranial hypertension. J Neurol Sci 2003;215:9–12. 9 Diaz JM, Schiffman JS, Urban ES, et al. Superior sagittal sinus thrombosis and pulmonary embolism: a syndrome rediscovered. Acta Neurol Scand 1992;86:390–6. 10 Jacobs K, Moulin T, Bogousslavsky J, et al. The stroke syndrome of cortical vein thrombosis. Neurology 1996;47:376–82.
105
A DIFFICULT CASE 11 Rice CM, Renowden SA, Sandeman DR, et al. Spontaneous intracranial hypotension and venous sinus thrombosis. Pract Neurol 2013;13:120–4. 12 Corbett JJ, Digre K. Idiopathic intracranial hypertension: an answer to, “the chicken or the egg?”. Neurology 2002;58: 5–6.
106
13 Higgins JN, Cousins C, Owler BK, et al. Idiopathic intracranial hypertension: 12 cases treated by venous sinus stenting. J Neurol Neurosurg Psychiatry 2003;74:1662–6. 14 Chan KT, Tye GA, Popat RA, et al. Common iliac vein stenosis: a risk factor for oral contraceptive-induced deep vein thrombosis. Am J Obstet Gynecol 2011;205:537 e1–6.
Suetterlin K, et al. Pract Neurol 2014;14:102–106. doi:10.1136/practneurol-2013-000680
When is ‘idiopathic intracranial hypertension’ no longer idiopathic? Karen Suetterlin,1 Nicholas Borg,2 Harriet Joy,3 Joanna K Lovett,1 Boyd C P Ghosh1 1
Department of Neurology, Wessex Neurological Centre, Southampton General Hospital, Southampton, Hampshire, UK 2 Department of Neurosurgery, Wessex Neurological Centre, Southampton General Hospital, Southampton, Hampshire, UK 3 Department of Neuroradiology, Wessex Neurological Centre, Southampton General Hospital, Southampton, Hampshire, UK Correspondence to Dr Karen Suetterlin, Department of Neurology, Wessex Neurological Centre, Southampton General Hospital, Southampton, Hampshire, SO16 6YD, UK; [email protected] The duties of the senior author were shared between the two authors JKL and BCPG. Published Online First 29 October 2013
To cite: Suetterlin K, Borg N, Joy H, et al. Pract Neurol 2014;14:102–106.
102
HISTORY A 23-year-old woman with idiopathic intracranial hypertension (IIH) presented with a recurrence of headache and visual disturbance. She had presented with similar symptoms 5 years earlier, when the diagnosis of IIH had been made, after magnetic resonance venography (MRV) had excluded cerebral venous sinus thrombosis (VST) (figure 1A,B). She had been asymptomatic for 18 months and had stopped her acetazolamide 6 months earlier. On examination, her visual acuity was 6/ 9 (right) and 6/15 (left). Her left visual field was constricted and there was bilateral papilloedema. Her cerebrospinal fluid (CSF) opening pressure was 80 cmH2O and we drained to a closing pressure of 22 cmH2O, resulting in complete resolution of both headache and visual disturbance. She was started on acetazolamide. Within 48 h, her headaches returned with a new left-sided lower motor neurone seventh nerve palsy. We organised MR imaging with venography and then repeated her lumbar puncture. The opening pressure was now 29 cmH2O and she reported postprocedure improvement in her headache. However, within 24 h, her headache recurred, she developed a right lower motor neurone seventh nerve palsy (figure 2), bilateral sixth nerve palsies, neck stiffness, vomiting and visual disturbance. Magnetic resonance venography (MRV) showed a VST affecting the left transverse and sigmoid sinuses (figure 1C) and we started her on unfractionated heparin. In view of her markedly elevated opening pressure, background of IIH and the need for anticoagulation, we referred for early ventriculoperitoneal shunting. On the evening before her operation she became drowsy and confused. Repeat lumbar puncture gave an opening pressure of 98 cmH2O. All CSF pressures were measured with her lying in the lateral decubitus position.
The following morning she underwent uneventful ventriculoperitoneal shunt insertion and was subsequently reanticoagulated with unfractionated heparin, followed by low molecular weight heparin and eventually warfarin. Her right seventh nerve palsy and bilateral sixth nerve palsies improved during the first postoperative day, consistent with resolution of IIH. Her left seventh nerve palsy (figure 2) gradually improved in the months following discharge. We have not identified any thrombophilia tendency. DISCUSSION Idiopathic intracranial hypertension is a common disorder, classically described in obese young women. Patients experience severe chronic headaches exacerbated by straining, bending forward or lying flat. The historical term, benign intracranial hypertension, has fallen out of favour because of the danger of irreversible visual loss in up to 25% of cases.1 Several conditions causing high intracranial pressure can mimic IIH. However, most of these, such as malignant hypertension, can be excluded by a careful clinical assessment and basic blood tests. In contrast, thrombosis of a venous sinus or jugular vein cannot be excluded without specific imaging. The classical false-localising sign in IIH is a sixth nerve palsy, but seventh nerve palsies have also been reported.2 3 The mechanism leading to these is not fully understood. However, Kuehnen et al4 reported a series of cases of transverse sinus thrombosis causing ipsilateral isolated cranial nerve palsies—in particular sixth, seventh and eighth nerve palsies— without evidence of raised intracranial pressure. They proposed that venous congestion in the veins draining into a thrombosed transverse sinus, such as the petrous vein, cause oedema in the nearby ventral brainstem and upper cranial nerves,
Suetterlin K, et al. Pract Neurol 2014;14:102–106. doi:10.1136/practneurol-2013-000680
A DIFFICULT CASE
Figure 1 Magnetic resonance venography (MRV). (A) MR Venogram at time of diagnosis with IIH in 2007: flow signal is seen in the transverse and sigmoid sinuses bilaterally, although they are asymmetrical, the right side being dominant. (B) MR Venogram 2007. Lack of flow signal in the distal transverse sinuses (arrows) is the characteristic appearance seen in IIH. (C) MR Venogram at time of diagnosis with VST in 2012: there is no flow signal in the left transverse and sigmoid sinuses. (D) MR Venogram 2012. The characteristic IIH appearance remains on the right (arrow).
resulting in cranial nerve palsies (figure 3).4 Our patient’s left seventh nerve palsy might also have occurred by this mechanism. It was ipsilateral to the affected transverse sinus, occurred when the opening pressure was relatively low (29 cmH2O) and persisted for several months. In contrast, both sixth nerve palsies and her right seventh nerve palsy appeared when her CSF pressure had risen considerably (98 cmH2O) and resolved within 24 h of ventriculoperitoneal shunt insertion. There are several reports describing VST in patients originally thought to have IIH. This is perhaps not surprising as their presenting symptoms overlap considerably. Both conditions can present with headache and visual disturbance, with raised CSF pressure on lumbar puncture.5 What is more, over one-third of patients with VST can present like IIH without other neurological symptoms or signs6–8 and can have a normal non-contrast brain CT and normal CSF
Suetterlin K, et al. Pract Neurol 2014;14:102–106. doi:10.1136/practneurol-2013-000680
composition.8 Venography can be difficult to interpret, as a significant proportion of the population have a left transverse sinus that is smaller than the right—and in 15%–20%, it may even be hypoplastic or absent.4 We cannot overstate the importance of distinguishing between the two conditions. Treatment is different and while IIH carries the risk of permanent visual loss, VST has a mortality rate of 10%–30%, as well as complications with high morbidity such as seizures and cerebral infarction.9 10 Although VST may complicate spontaneous intracranial hypotension11 and the finding of VST in patients inappropriately labelled as idiopathic intracranial hypertension is well reported, we could not find any papers describing VST being found after an accurate diagnosis of idiopathic intracranial hypertension. However, perhaps this is more common than the literature suggests. Prompted by the experience with our first patient, we made a second diagnosis of VST in a 103
A DIFFICULT CASE
Figure 2
Photographs of cranial nerve palsies.
patient with an established diagnosis of IIH a few months later. In this case, as before, repeat imaging was prompted by refractory symptoms and greater CSF pressures than found during previous IIH episodes. Again, careful review of all available imaging showed that there was no VST at the original diagnosis. There could be a link between a diagnosis of IIH and VST. VST is more common in young patients who are on the oral contraceptive pill or in pregnancy or puerperium. IIH, by comparison, is more common in obese young women, and oral contraceptive use is listed as a potential cause. There will therefore be a subset of patients with IIH who are independently at risk of developing thrombosis because they share some of the same risk factors. However, perhaps finding a VST in a patient with IIH could be due to more than a coincidence of risk factors and may also be attributable to pathological synergy centred on the tapering of the lateral sinuses in IIH. The lateral sinuses are well recognised sometimes to taper in patients with a confirmed diagnosis of IIH 104
(figure 1). This has been attributed to functional compression of the sinus secondary to high pressure, although others have postulated that high pressure could be secondary to a narrowed sinus, leading to the more recent treatment modality of venous stenting.12 13 However, could the tapering of the sinus and ensuing flow changes within that region predispose to thrombosis? Iliac vein stenosis is an independent risk factor for developing deep vein thrombosis in young women—for every 1% increase in stenosis there is a small but significant rise in risk.14 Subjects with >70% stenosis of the iliac vein, who were also on the combined oral contraceptive pill, had an OR of 17 for the development of a deep vein thrombosis.14 If the same is true for venous sinus stenosis: patients with IIH are likely to be at a higher risk of VST. Whatever the link between VST and IIH, we suggest that clinicians keep an open mind when reviewing patients with an established diagnosis of IIH. Red flags that should alert physicians include the return of symptoms after a long period of quiescence, the absence of a
Suetterlin K, et al. Pract Neurol 2014;14:102–106. doi:10.1136/practneurol-2013-000680
A DIFFICULT CASE
Figure 3 Cranial nerve topography in relation to venous drainage of the ventral aspect of the posterior fossa (modified and complemented from A. Berenstein and P. Lasjaunas). CN III–XII 5 cranial nerve roots III–XII; tr.s, transverse sinus; sig.s., sigmoid sinus; sup.petr.s., superior petrosal sinus; pt.v., petrous vein; a.m.v., anterior medullary vein; l.m.v., lateral medullary vein; p.m.v., pontomedullary vein; a.m.p.v., anterior medial pontine vein; tr.p.v., transverse pontine vein. Taken with permission from Oxford University Press, Kuehnen J, et al.4
clear trigger such as weight gain, symptoms resistant to treatment, exceptionally high CSF pressures and aggressive disease in patients who had a previously benign course. The presence of any of the above should prompt consideration of imaging to exclude VST.
images and the radiology figure legend. Joanna Lovett was the consultant in charge of the case management with input from Ashwin Pinto. Boyd Ghosh and Joanna Lovett are the guarantors. Competing interests None. Patient consent Obtained. Provenance and Peer Review Not commissioned. Externally peer reviewed. This paper was reviewed by Luke Bennetto, Bristol.
PRACTICAL POINTS ▸ This case highlights the importance of keeping an open mind in the management of patients with existing diagnostic labels. ▸ Clinicians should consider magnetic resonance venography or CT venography to look for venous sinus thrombosis (VST), even in patients with an established diagnosis of IIH, especially if the patient has a very high opening CSF pressure, drowsiness or focal neurology. ▸ False localising signs of raised CSF pressure in VST and IIH can include sixth and seventh nerve palsies. ▸ Cranial nerve palsies can be the presenting feature of VST, even without raised CSF pressure. ▸ Consider CSF shunting procedures in patients with VST and/or IIH with significantly elevated CSF pressures that remain high despite sequential lumbar punctures, especially if anticoagulation is required. Acknowledgements Our thanks are given to the patient for allowing publication of this material. We would also like to thank Ashwin Pinto, Jonathan Frankel and Sean Slaght for useful discussions concerning this case. Contributors The idea for the article came from discussions between Ashwin Pinto, Sean Slaght, Jonathan Frankel, Joanna Lovett and Boyd Ghosh. Literature search was performed by Karen Suetterlin and Nicholas Borg. The article was written by Karen Suetterlin with contribution from Nicholas Borg. Joanna Lovett and Boyd Ghosh edited the article. Harriet Joy provided radiology
Suetterlin K, et al. Pract Neurol 2014;14:102–106. doi:10.1136/practneurol-2013-000680
REFERENCES 1 Digre KB. Idiopathic intracranial hypertension headache. Curr Pain Headache Rep 2002;6:217–25. 2 Larner AJ. False localising signs. J Neurol Neurosurg Psychiatry 2003;74:415–18. 3 Davie C, Kennedy P, Katifi HA. Seventh nerve palsy as a false localising sign. J Neurol Neurosurg Psychiatry 1992;55:510–11. 4 Kuehnen J, Schwartz A, Neff W, et al. Cranial nerve syndrome in thrombosis of the transverse/sigmoid sinuses. Brain 1998;121:381–8. 5 Burger BM, Chavis PS, Purvin V. A weed by any other name. Surv Ophthalmol 2013;58:176–83. 6 Friedman DI, Jacobson DM. Diagnostic criteria for idiopathic intracranial hypertension. Neurology 2002;59:1492–5. 7 Friedman DI, Rausch EA. Headache diagnoses in patients with treated idiopathic intracranial hypertension. Neurology 2002;58:1551–3. 8 Sylaja PN, Ahsan Moosa NV, Radhakrishnan K, et al. Differential diagnosis of patients with intracranial sinus venous thrombosis related isolated intracranial hypertension from those with idiopathic intracranial hypertension. J Neurol Sci 2003;215:9–12. 9 Diaz JM, Schiffman JS, Urban ES, et al. Superior sagittal sinus thrombosis and pulmonary embolism: a syndrome rediscovered. Acta Neurol Scand 1992;86:390–6. 10 Jacobs K, Moulin T, Bogousslavsky J, et al. The stroke syndrome of cortical vein thrombosis. Neurology 1996;47:376–82.
105
A DIFFICULT CASE 11 Rice CM, Renowden SA, Sandeman DR, et al. Spontaneous intracranial hypotension and venous sinus thrombosis. Pract Neurol 2013;13:120–4. 12 Corbett JJ, Digre K. Idiopathic intracranial hypertension: an answer to, “the chicken or the egg?”. Neurology 2002;58: 5–6.
106
13 Higgins JN, Cousins C, Owler BK, et al. Idiopathic intracranial hypertension: 12 cases treated by venous sinus stenting. J Neurol Neurosurg Psychiatry 2003;74:1662–6. 14 Chan KT, Tye GA, Popat RA, et al. Common iliac vein stenosis: a risk factor for oral contraceptive-induced deep vein thrombosis. Am J Obstet Gynecol 2011;205:537 e1–6.
Suetterlin K, et al. Pract Neurol 2014;14:102–106. doi:10.1136/practneurol-2013-000680
