INTRACRANIAL HYPOTENSION CAUSING RECURRENT SUBDURAL HAEMATOMAS: A CASE REPORT

Dr. Ali Al Balushi, Dr. Mahmood Al Hattali, Dr. Mohammad Al Tamimi, Dr. Aziz Haris, Dr. Chandrasekhar B. V. K. Yandrapati, Dr. Ramsha Nisar, Dr. Waad Ahmed Saleh Al-Farsi, Dr. Rawan Nuaaman Mohammed Al Mandhari and Dr. Neeraj Salhotra*

ABSTRACT

Spontaneous intracranial hypotension, as the name implies, is caused by low CSF pressure, usually secondary to an occult leak. A CSF leak occurs in weak areas around the dura mater and nerve root sheaths and around small defects due to small traumas, a fall, severe exercise, or a cough that tears the dura or arachnoid. Some studies have reported that connective tissue disorders such as Marfan syndrome, Ehlers-Danlos syndrome type 2, and autosomal dominant polycystic kidney disease play a significant role in causing SIH. While the pathophysiology of SDH in patients with SIH remains unknown, studies have proposed several mechanisms. Downward displacement of the brain due to low CSF pressure may produce tears in the bridging veins of the dural border cell layer, causing these veins to rupture. Alternatively, as subdural CSF collections gradually enlarge the subdural space, the bridging veins may stretch and rupture in some cases. Although the most common presenting symptom in SIH is orthostatic headaches, the exact mechanism of orthostatic headaches in CSF leak is unknown. The total volume of the brain, CSF, and the intracranial blood remains constant inside the rigid skull. Therefore, a decrease in one of these components should cause a reciprocal increase in either or both of the remaining two. The intracranial venous structures are pain-sensitive, and their dilatation in turn may lead to headaches.MR imaging represents the method of choice to depict intracranial manifestations; the neuroimaging features include diffuse meningeal enhancement, acquired Chiari malformation, and subdural fluid collections. The Monro-Kellie hypothesis is the mechanism frequently used to explain MRI findings with aforementioned conditions. A reduction in the volume of the CSF requires an increase in volume of one or both of the other components. The most reliably demonstrated area of increased volume on imaging is the pachymeninges, which show diffuse thickening and enhancement with gadolinium-enhanced MRI due to lack of a blood-brain barrier and an increase in the volume of venous blood in this compartment. In cases of SIH, the site of the CSF leak rests predominantly in the cervical or thoracic region, and the diagnosis is typically established by CT myelography or radionuclide imaging. Although supportive measures and medical therapy such as hydration, bed rest, caffeine, steroid and parenteral fluid may provide temporary relief, a more durable treatment is to seal the site of the leak. The mainstay of the treatment is the injection of autologous blood (10-20 mL) into the spinal epidural space. Relief of symptoms is often dramatic after EBP. If EBP fails the first time, it can be repeated. Complications of cervical EBP include spinal cord and nerve root compression, chemical meningitis, intrathecal injection of blood, seizures, and stiffness of the neck. Cases of large subdural hemorrhage require surgical drainage and treatment of the underlying cause of SIH. With the current technology, we can perform imaging-guided procedures in the spine with relative safety and minimal discomfort to the patient. In cases of cervical leaks, it is reasonable to offer a cervical blood patch as the initial treatment. In our patient first middle menineal artery embolisation, later we performed EBP and later patient required burr hole evacuation of subdural haeamtomas in view of neurodetrioration.

Keywords: Intracranial hypotension.