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Intracranial hypertension and intracranial hypotension causing headache in the same patient.

Intracranial hypertension and hypotension can cause headaches; however, it is uncommon for both to cause headache in the same patient since they are on the opposite ends of the intracranial pressure spectrum. We present a patient who had headache due to intracranial hypertension initially, but after spinal tap developed headache due to intracranial hypotension. This situation has been described in only four patients in the literature to our knowledge, all of whom had headaches due to idiopathic intracranial hypertension (IIH).

CASE DESCRIPTION

A 33-year-old man presented with headache and blurring of vision of 2 months' duration. He had known obstructive sleep apnea, for which he had undergone multiple surgeries (tonsillectomy, adenoidectomy, uvulopalatopharyngoplasty). His body mass index was 30.5 kg/[m.sup.2] (height 1.82 m, weight 105 kg). A computed tomography (CT) scan of the head and magnetic resonance imaging (MRI) of the brain were normal. He had bilateral papilledema, worse on the left side than on the right. The cranial nerve and motor and sensory examinations were normal. Lumbar puncture showed elevated opening pressure (440 mm) of cerebrospinal fluid (CSF) (normal, 70-180 mm). Twelve mL of clear colorless fluid was drained for studies, which showed a normal protein, glucose, and cell count and no organisms (Gram stain or culture).

The patient's headache improved temporarily but worsened later. The headache changed in character and was more positional. He felt worse when sitting up or walking and better in a lying-down position, making him bed bound for several days. An MRI with contrast showed pachymeningeal enhancement suggestive of headache due to intracranial hypotension (Figure 1). Conventional analgesics used for intracranial hypotension like caffeine and Excedrin failed to relieve his headache. An epidural blood patch utilizing 20 mL of autologous venous blood immediately relieved his headache. His pain medications were deescalated and he was discharged home the next day. A CT angiogram of the brain revealed chronic occlusion of the right sigmoid sinus collateralizing to an atretic right internal jugular vein (Figure 2). His vitamin A level was normal, and he was not on any medications known to cause intracranial hypertension.

[FIGURE 1 OMITTED]

DISCUSSION

The patient described developed headaches due to both intracranial hypertension and intracranial hypotension within a short span of time. There have been four case reports of a similar presentation in patients (three females and one male) who had headaches due to IIH.

[FIGURE 2 OMITTED]

Since the cranium is a closed compartment, consisting of brain, blood, and CSF, an increase in the volume of any of these components can lead to headache. If the volume of the CSF is low, traction on the meninges can lead to pain as well. IIH is a heterogeneous syndrome characterized by increased intracranial pressure at rest without any apparent explanation. The diagnosis of IIH is based on the modified Dandy criteria. IIH has a prevalence of 1 to 2 per 100,000 people and affects predominantly obese women of childbearing age (15-44 years) (1). More than 80% of patients with IIH are overweight women (2). Repeated lumbar punctures, thereby draining the CSF, have been used as a treatment option for this condition (3). One of the most common adverse effects of lumbar puncture is post-lumbar puncture headache. It is uncommon and paradoxical to have headache due to intracranial hypotension in patients with IIH for which the treatment of choice is drainage of CSF using a shunt.

The mechanism of causation of IIH is not clear; however, it could be due to an imbalance between CSF production and absorption. This is the basis of using procedures like lumboperitoneal shunts (thereby draining CSF and reducing intracranial pressure) in patients with severe symptoms due to IIH. On the other hand, the postlumbar puncture headache is due to intracranial hypotension. The CSF pressure in patients with intracranial hypotension is often less than 60 mm CSF. One of the functions of CSF is to provide buoyancy to the brain. The sagging of the brain causing traction on the pain-sensitive dura in the upright position is the cause of headache (4).

Cerebral venous sinus narrowing has been reported in up to 90% of patients with IIH in recent studies (1). Repeat studies after normalization of the intracranial pressure demonstrated normalization of this finding (1). The cerebral sinus narrowing might be a consequence of the increased intracranial pressure. However, venous sinus narrowing/thrombosis could cause increased intracranial pressure as well. This situation could represent the chicken or egg debate as to which occurs first. Our patient had features of chronic occlusion of the sigmoid sinus on the right side, which could have caused his intracranial hypertension; however, a chronic narrowing of his sinus by IIH could have caused a secondary thrombosis in it as well. There is no clear answer to this question.

Analgesics and sumatriptan have been known to be ineffective in patients with headache due to intracranial hypotension. Caffeine is reported to be effective in this condition. An epidural blood patch is the treatment of choice for headache due to postlumbar puncture leak of CSF when conservative methods fail (5, 6). This treatment is believed to relieve the headache by closing the dural leaks in CSF. Displacement of CSF from the spinal canal as a result of the epidural blood patch has also been thought to be a mechanism of relief of headache due to CSF leaks. However, there is a concern that an epidural blood patch might lead to worsening of intracranial pressure (which can be symptomatic or asymptomatic), as reported in multiple case reports of patients with baseline intracranial hypotension/normal intracranial pressure (7).

In our patient, an epidural blood patch helped relieve his headache without rebound intracranial hypertension. Multiple mechanisms are proposed for causation of intracranial hypertension after epidural blood patch. Mokri et al reported that rebound increase in intracranial pressure could be due to either an increased CSF production in response to CSF fluid depletion or a disturbed mechanism of CSF resorption due to a prolonged leak of CSF (7). The closure of the leak in CSF leads to increased production without continuous CSF loss. The choroid plexus might adjust ultimately to this situation and gradually result in abatement of this condition. However, our patient tolerated this procedure well and did not have a headache after the procedure. He was discharged the next day, without analgesics.

(1.) Shaw GY, Million SK. Benign intracranial hypertension: a diagnostic dilemma. Case Rep Otolaryngol 2012; 2012: 814696.

(2.) Safavi-Abbasi S, Di Rocco F, Nakaji P, Feigl GC, Gharabaghi A, Samii M, Valavanis A, Samii A. Thrombophilia due to factor V and factor II mutations and formation of a dural arteriovenous fistula: case report and review of a rare entity. Skull Base 2008; 18(2): 135-143.

(3.) Corbett JJ, Thompson HS. The rational management of idiopathic intracranial hypertension. Arch Neurol 1989; 46(10): 1049-1051.

(4.) Binder DK, Sarkissian V, Dillon WP, Weinstein PR. Spontaneous intracranial hypotension associated with transdural thoracic osteophyte reversed by primary dural repair. Case report. J Neurosurg Spine 2005; 2(5): 614-618.

(5.) Duffy PJ, Crosby ET. The epidural blood patch. Resolving the controversies. Can J Anaesth 1999; 46(9): 878-886.

(6.) Turnbull DK, Shepherd DB. Post-dural puncture headache: pathogenesis, prevention and treatment. Br J Anaesth 2003; 91(5): 718-729.

(7.) Mokri B. Intracranial hypertension after treatment of spontaneous cerebrospinal fluid leaks. Mayo Clin Proc 2002; 77(11):1241-1246.

Ragesh Panikkath, MD, John Welker, MD, Robert Johnston, MD, and Joaquin Lado-Abeal, MD

From the Departments of Internal Medicine (Panikkath, Lado-Abeal) and Anesthesiology (Welker, Johnston), Texas Tech University Health Sciences Center, Lubbock, Texas.

Corresponding author: Ragesh Panikkath, MD, Department of Internal Medicine, Texas Tech University Health Sciences Center, 3601 4th Street, Lubbock, TX 79430 (e-mail: ragesh.panikkath@ttuhsc.edu; drrageshp@gmail.com).
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Author:Panikkath, Ragesh; Welker, John; Johnston, Robert; Lado-Abeal, Joaquin
Publication:Baylor University Medical Center Proceedings
Article Type:Clinical report
Date:Jul 1, 2014
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