Colour doppler imaging for diagnosis of intracranial hypotension

doi:10.1016/S0140-6736(99)80013-0

The Lancet

Volume 354, Issue 9181, 4 September 1999, Pages 826-829

https://doi.org/10.1016/S0140-6736(99)80013-0 Get rights and content

Summary

Background

Measurement of CSF pressure is the only known way to confirm the diagnosis of intracranial hypotension. We aimed to assess colour doppler flow imaging (CDFI) for measurement of blood flow of the superior ophthalmic vein for the diagnosis of intracranial hypotension.

Methods

We enrolled 25 consecutive patients with orthostatic headache who had clinical features of intracranial hypotension. We defined low-pressure headache as cerebrospinal-fluid pressure below 60 mm H₂O. We used CDFI to measure the diameter and maximum flow velocity of the superior ophthalmic vein in all patients. Magnetic resonance imaging of the brain and lumbar puncture with measurement of cerebrospinal-fluid pressure within 24 h were also done after sonographic examination. The control group comprised 13 healthy individuals of a similar age; in addition, those patients who had orthostatic headache without low pressure served as a control group for the patients.

Findings

Of the 25 patients recruited for this study, 13 satisfied the criteria for low-pressure headache. The remaining 12 patients with normal cerebrospinal-fluid pressure had transformed migraine (five patients) or chronic tension-type headache (seven patients), and therefore served as the control group for the patients. The mean diameter of the superior ophthalmic vein was substantially larger in the patients with intracranial hypotension (3·9 [SD 0·2] mm) than in the healthy controls (2·6 [0·4] mm) and the controls from the patients' group (2·7 [0·2] mm) (p < 0·0001). The mean maximum flow velocity was significantly higher in the intracranial-hypotension group (17·0 [SD 3·4] cm/s) than in the healthy controls (7·9 [1·1] cm/s) and the other patients (7·3 [1·7] cm/s) (p < 0·0001). Seven patients with intracranial hypotension were reassessed after treatment with epidural blood patch. After this treatment the clinical symptoms were relieved and there was a striking reversal of the superior ophthalmic vein flow.

Interpretation

CDFI to measure blood flow of the superior ophthalmic vein provides a practical, simple, and non-invasive diagnostic method for suspected intracranial hypotension.

Introduction

Intracranial hypotension has diverse causes1, 2 and is characterised by orthostatic headaches. Such headaches result from decreased cerebrospinal-fluid pressure, volume of cerebrospinal fluid, or both that commonly occur after a diagnostic lumbar puncture or spinal anesthesia.³ Nevertheless, a syndrome called spontaneous intracranial hypotension has been reported in patients with headache.2, 4, 5, 6, 7 The exact pathophysiology of the syndrome is uncertain, but one hypothesis is that the underlying mechanism is related to leakage of cerebrospinal fluid from the spinal meningeal diverticula, which is usually located in the cervicothoracic junction or in the thoracic spine.5, 6, 8

The only currently available way to confirm the diagnosis of orthostatic headache—ie, intracranial hypotension—is lumbar puncture.2, 6, 7, 8 Several reports described non-specific findings of diffuse meningeal enhancement on magnetic resonance imaging (MRI) with gadolinium, which is a complementary test; however, this finding has been noted in only some patients.2, 4, 6, 7, 8, 9 Most investigators suggest that these nonspecific MRI findings might be a result of engorgement of dural bridging veins secondary to decreased cerebrospinal-fluid pressure and volume.2, 4, 5, 6, 7, 8, 9 Venous drainage from the orbit is mainly done through the superior ophthalmic vein.10, 11 Since the blood-flow direction and volume of the superior ophthalmic vein can change during various disorders (eg, valsalva manoeuvre, cerebral oedema, and hyperthermia),11, 12, 13, 14 we postulated that a low cerebrospinal-fluid pressure and volume in patients with headache should reflect their blood flow in the superior ophthalmic vein. On the basis of the relation between intracranial pressure and volume, we further postulated that the venous flow in the superior ophthalmic vein would be increased in patients with intracranial hypotension.1, 15 Thus, we designed a study to measure blood flow in the superior ophthalmic vein by means of transorbital colour doppler flow imaging (CDFI) in patients with intracranial hypotension to explore the intracranial haemodynamics and to test the validity of this diagnostic method in clinical diagnosis and monitoring.

Section snippets

Study participants

Between October, 1997, and May, 1998, all consecutive patients with profound orthostatic headache with a clinical feature of intracranial hypotension1, 2, 7 were enrolled in the study. We excluded patients who had evidence of focal neurological deficits, had previously had lumbar puncture, and who had a history of other neurological disorders or any cardiovascular disease. We defined low-pressure headache as cerebrospinal-fluid pressure below 60 mm H₂O. All study participants underwent brain

Results

We enrolled 25 patients with orthostatic headache. 13 of the patients (one man, 12 women; mean age 36·5 [range 18–74] years) satisfied the criteria for a diagnosis of low-pressure headache2, 7 with an opening cerebrospinal-fluid pressure of less than 60 mm H₂O (mean 23·2 [SD 19·2, range 0–55] mm H₂O).1, 8 The remaining 12 patients who had normal cerebrospinal-fluid pressures (110·3 [16·9, 94–146] mm H₂O) comprised the patients' control group (four men, eight women, mean age 42·6 [27–77] years).

Discussion

With transorbital CDFI we were able to show the presence of the bilaterally engorged superior ophthalmic vein that carried antegrade high-velocity blood flow in all our patients with intracranial hypotension. We clearly showed that among patients with low cerebrospinal-fluid pressure, all (26/26) of their bilateral superior ophthalmic veins had a diameter that exceeded the upper limit (figure 2) and the maximum flow velocities were significantly higher than the normal range in all patients. The

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Epidural blood patch: A narrative review
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This increase in CSF and intracranial pressure is likely the dominant determinant of the immediate effect of the EBP by increasing CSF pressures and normalizing cerebral blood flow. Boezaart has shown in a swine model that an EBP immediately decreases cerebral blood flow [24]; these experimental intracranial hemodynamics changes are in accordance with Doppler measurements performed in humans after an EBP [25–27]. Clot formation is the critically important second effect of the EBP; it is considered that it is the clot that ultimately seals the dural defect and restores CSF pressure [5,28,29].
The epidural blood patch (EBP) is one of the most effective treatments for intracranial hypotension. Anesthesiologists are familiar with performing EBPs for the treatment of dural puncture-associated intracranial hypotension following spinal anesthesia, complicated epidural analgesia, and diagnostic lumbar puncture. Increasingly, EBPs are used to treat patients with spontaneous intracranial hypotension. However, the treatment of these non-iatrogenic conditions presents new therapeutic challenges. The purpose of this narrative review is to discuss both procedural and diagnostic considerations of EBP for the various presentations of intracranial hypotension and allow the clinician to tailor treatment for the patient, especially in the setting of diagnostic dilemmas. After discussing EBP history and relevant anatomy, we review mechanisms of action and clinical indications for this intervention. The contraindications, complications, and treatment alternatives to the blood patch are examined in detail. Finally, objective methods to evaluate the effectiveness of the EBP, such as MRI or Doppler ultrasound, are presented as novel methods that may improve future diagnostic accuracy and treatment success.
Delayed recurrence of spontaneous intracranial hypotension syndrome mimicking a Chiari I malformation: Case report with a review of the literature
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However, it has reported that the prevalence of some brain MRI features, such as the dural enhancement, may decrease with time especially in chronic CSF leakages [58]. Promising surrogate for intracranial pressure in SIH have been described such as: collapsed superior ophthalmic veins, high blood flow velocities in greatly engorged superior ophtalmic veins, significantly reduced optic nerve sheath diameter (ONSD) and thickness [59–64]. Other indirect signs of SIH on MRI images may occurs such as: subdural hematoma often bilateral, chronic cerebellar hemorrhage [65], dural sinus thrombosis and brain swelling [36,37,66].
Cerebellar tonsils descent seen on brain MRI is, along with other findings, a recognized radiological sign of possible spontaneous intracranial hypotension (SIH). The short-term outcome of SIH is usually favorable with symptoms improvement and reversibility of the low-lying tonsils. Nevertheless, data on the long-term outcome are lacking or inconsistent.
A 32-year-old woman presented to her general practitioner with a six months history of non-specific headaches. An MRI brain with gadolinium showed a 12mm tonsillar descent with no other remarkable findings. Headaches were initially managed conservatively as migraines. Following the onset of progressive upper back and shoulder pain at rest, nausea, photophobia and fogging in her vision, the patient was referred to our Department with a suspicion of symptomatic Chiari I malformation. After an in-depth anamnesis, it emerged a previous history of SIH, 14 years earlier, successfully treated conservatively in another center. A whole spine MRI confirmed the suspicion of recurrent SIH showing an anterior cervico-thoracic epidural fluid collection. The patient underwent an epidural blood patch with complete resolution of the symptoms and radiological signs.
To our knowledge, this case is the first report of delayed recurrence of a SIH successfully treated conservatively over 10 years earlier. The etiopathogenesis and management of this rarity with literature review is discussed.
An isolated cerebellar tonsil descent with no other remarkable findings on brain MRI and a previous history of SIH should always alert the clinician of a possible late recurrence of a CSF leak and avoid unnecessary Chiari I malformation surgical procedures.
Spine Surgery Complicated by an Engorged Lumbar Epidural Venous Plexus from Cerebrospinal Fluid Overshunting: A Case Report and Review of the Literature
2018, World Neurosurgery
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On T1-weighted MRI sequences with gadolinium, diffuse dural enhancement is often seen secondary to dura mater venous plexus dilation.14,15 Furthermore, dilation of the superior ophthalmic, cortical, and medullary veins along with the anterior falx artery has been described.3-6 The increase in intracranial venous volume can be explained by the Monro-Kellie doctrine, which establishes an inverse relationship between CSF volume and intracranial blood volume.14
Overshunting of cerebrospinal fluid may lead to intracranial hypotension and dilation of spinal epidural veins. Radiculopathy may rarely occur secondary to engorged spinal epidural veins. In addition, the cause of radiculopathy may be obscured by concomitant spinal degenerative changes. We present a case and review the pathogenesis as well as the current clinical literature.
A 29-year-old woman presented with positional headaches from intracranial hypotension in the setting of cerebrospinal fluid overshunting. The patient also had back pain and lumbar radiculopathy, which became more severe after lumboperitoneal shunt placement. On radiographic work-up, there was evidence of right L5 nerve root impingement secondary to a disc bulge and an engorged lumbar epidural venous plexus secondary to overshunting. The patient underwent surgery for a planned L4-5 decompression with a transforaminal lumbar interbody fusion. The operation was complicated by rapid blood loss originating from the epidural venous plexus, and we were unable to safely place the interbody graft.
Spinal surgeons need to be aware of the rare diagnosis of radiculopathy secondary to epidural venous plexus engorgement, as it may change the treatment approach or lead to deleterious intraoperative consequences, such as hemorrhage.
Post-dural puncture headache and blood-patch: Theorical and practical approach
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Le syndrome de post-ponction lombaire (SPPL) est défini par l’International Headache Society comme des céphalées attribuées à des troubles moteurs intracrâniens non vasculaires en rapport avec une hypotension du LCR. Responsable de céphalées typiquement positionnelles, le tableau clinique s’accompagne également de troubles digestifs (nausées, vomissements), de troubles visuels ou auditifs dus à l’atteinte de nerfs crâniens voire de radiculalgies liées à l’étirement des nerfs rachidiens cervicaux. Le mécanisme physiopathologique est lié à une hypotension intracrânienne de LCR, consécutive à la brèche méningée. Les modifications de l’hémodynamique cérébrale (vasodilatation) et le déplacement rostro-caudal des principales structures intracrâniennes sont les principales conséquences de la fuite de LCR dont le débit n’est pas corrélé à l’intensité des céphalées. Divers traitements symptomatiques adjuvants (antalgiques, alitement, vasoconstricteurs…) sont proposés dans le cadre d’une attitude conservatrice purement médicale, mais leur efficacité semble très modeste. En rétablissant la pression intracrânienne du LCR par « contre-pression » dans l’espace péridural, l’injection de sang autologue ou « blood-patch » (BP) s’impose comme le traitement de référence du SPPL. De réalisation simple dans des conditions stériles, le BP présente un taux de succès supérieur à 80 % avec un amendement rapide des céphalées. Certaines modalités sur la procédure (délai de réalisation, volume à injecter, type de solutés…) doivent encore faire l’objet de recommandations scientifiques.
To review the current research and formulate a rational approach to the physiopathology, cause and treatment of post-dural puncture headache (PDPH).
Articles published to December 2011 were obtained through a search of Medline for the MeSh terms “epidural blood-patch” and “post-dural puncture headache”.
Six hundred and eighty-two pertinent studies were included and 200 were analysed.
Resulting of a dural tap after spinal anaesthesia or diagnostic lumbar puncture or as a complication of epidural anaesthesia, PDPH occurs when an excessive leak of cerebrospinal fluid leads to intracranial hypotension associated to a resultant cerebral vasodilatation. Reduction in cerebrospinal fluid volume in upright position may cause traction of the intracranial structure and stretching of vessels. Typically postural, headache may be associated to nausea, photophobia, tinnitus or arm pain and changes in hearing acuity. In severe cases, there may be cranial nerve dysfunction and nerve palsies secondary to traction on those nerves. The Epidural Blood-Patch (EBP) is considered as the “gold standard” in the treatment of PDHP because it induces a prolonged elevation of subarachnoid and epidural pressures, whereas such elevation is transient with saline or dextran. EBP should be performed within 24–48 hours of onset of headache; the optimum volume of epidural blood appears to be 15–20 mL. Severe complications following EBP are exceptional. The use of echography may be safety puncture. The optimum timing of epidural blood-patch, the resort of repeating procedure if the symptomatology does not disappear, the alternative to the conventional medical treatment need to be determined by future clinical trial.
Hemodynamics of the Internal Jugular Vein: An Ultrasonographic Study
2009, Tzu Chi Medical Journal
To establish a simple classification of internal jugular venous flow using ultrasonography.
We retrospectively analyzed the sonographic findings of 1600 consecutive patients who were referred to the neurosono-graphic laboratory. Abnormal jugular venous flow was classified into five groups: (A) markedly decreased flow velocity; (B) stasis and/or thrombus formation; (C) reversed flow; (D) increased turbulent flow; and (E) pulsa-tile turbulent flow. Groups A to C were categorized as slow flow groups and groups D and E as high flow groups.
Abnormal jugular venous flow was found in 182 (11%) patients. A slow flow pattern (73%) comprised the majority of abnormalities. Eightynine percent of patients in the slow flow groups had abnormalities in the left internal jugular vein (IJV) and 92% of those in the high flow groups had abnormalities in the bilateral IJV. Incompetence of the jugular valve was the most common cause of slow flow in the IJV. Most of the increased turbulent flow was found in patients with hyperthyroidism and in pregnant women. Arteriovenous malformation and carotid-cavernous fistula were the causes of pulsatile turbulent jugular venous flow. Associated clinical symptoms occurred in only two (1.5%) patients (with a concomitant left IJV and left subclavian vein thrombosis) in the slow flow groups, and in 34 (68%) patients in the high flow groups.
Most of the abnormally decreased jugular venous flow occurred on the left side. Decreased venous flow or even thrombosis of one side of the IJV was usually asymptomatic. Increased jugular flow was associated with a physiological hyperemic state in cerebral hemodynamics. Increased awareness and angiographic studies are indicated in patients with pulsatile turbulent jugular venous flow because of a high correlation with intracranial arteriovenous shunting.
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2004, EMC - Neurologie
L'hypotension intracrânienne spontanée est une cause rare de céphalée secondaire due à une hypovolémie du liquide cérébrospinal, survenant en l'absence de brèche durale connue. L'association d'une présentation clinique simple, d'une céphalée orthostatique et d'une imagerie par résonance magnétique caractéristique a permis ces dernières années d'en faire plus facilement et beaucoup plus fréquemment le diagnostic. La sémiologie jusqu'alors rigoureusement stéréotypée s'enrichit d'année en année de formes atypiques trompeuses. En revanche l'attitude thérapeutique, qui repose sur l'emploi du « blood-patch » épidural, commence à être mieux codifiée.
Spontaneous intracranial hypotension is an infrequent cause of secondary headache due to a CSF hypovolemia, that occurs in the absence of known dural tear. Associated simple clinical presentation, orthostatic headache, and characteristic MRI findings have resulted these last years in an improved recognition of this syndrome. The spectrum of clinical presentation has increasingly broadened, with numerous ambiguous atypical presentations. The management - based on epidural blood patch - is getting better codified.

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Early ReportColour doppler imaging for diagnosis of intracranial hypotension

Summary

Background

Methods

Findings

Interpretation

Introduction

Section snippets

Study participants

Results

Discussion

Mayo Clin Proc

Br J Anaesth

Opthalmol

Intracranial pressure: physiology and pathophysiology

Dural enhancement and cerebral displacement secondary to intracranial hypotension

Neurology

Meningeal biopsy in intracranial hypotension: meningeal enhancement on MRI

Neurology

Spontaneous spinal cerebrospinal fluid leaks and intracranial hypotension

J Neurosurg

Spontaneous intracranial hypotension: clinical and magnetic resonance imaging characteristics

Clin Neurol Neurosurg

Orthostatic headache caused by CSF leak but with normal CSF pressure

Neurology

Lumbar and thoracic epidural blood injections to treat spontaneous intracranial hypotension

Anesthesiology

Early Report
Colour doppler imaging for diagnosis of intracranial hypotension