Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2589_Библиотеки_им_академика_М_И_Перельмана

predispose the eyes to RNFL defects, retinal vas-

cular occlusions, and acute AIONat a young age

visual eld defects or develop choroidal neovas-

Idiopathic intracranial hypertension (IIH) is not an uncommon cause of papilledema due to raised ICPwithout a known cause. Before making this diagnosis, both intracranial space-occupying lesions and non-tumour causes of raised ICP, like central venous thrombosis and meningitis, must be ruled out. It is a progressively blinding disor­der most often seen in obese women. Patients with mild-to-moderate IIH may be asymptom­atic, diagnosed during a routine clinical examina­tion, or symptomatic in severe IIH with headache, diplopia, and pulsatile or non-pulsatile tinnitus. Headaches in IIH may be due to increased ICP with features like early morning worsening, asso­ciation with nausea and vomiting, transient obscuration of vision, and a change in posture or Valsalva precipitates symptoms. Imaging in IIH should include an MRI of the brain and optic nerves with venography. Specic MRI signs of raised ICP include empty(or partially empty) sella turcica, venous sinus stenosis, narrowing of ventricles (slit ventricles), prominence of peri optic nerve sheath, vertical tortuosity of the optic nerves, scleral indentation, and posterior atten­ing of the globe [42]. Other lesser common signs include narrowing Meckel’s cave and cavernous sinuses. Meckel’s cave is a recess in the dura mater containing the CN V and its ganglion. In any case, MRI/CT scans are mandatory to rule out ICSOL.MR or CT venography is required to rule out venous thrombosis (Fig.15.12A and B). Without any secondary cause of raised ICP, CSF opening pressure of 250mm of water on lumbar puncture in adults and 280 mm in children is diagnostic of IIH. Care should be taken while recording CSF pressure, and it should be recorded in a lateral decubitus position with legs relaxed. CSF pressure should not be recorded in isolation, and the patient’s clinical status should be given priority while making the diagnosis. In the pres­ence of at least one of the following criteria, pulse

synchronous tinnitus, bilateral VI nerve paresis,

Friśen grade 2 optic disc edema (Box 15.2), col-

200–250mm of water may be considered posi-

The optic nerve may be affected in the intra­cranial, intraorbital, retrolaminar, laminar, or pre­laminar compartment. It may affect the young <17years, 18–40 or>40. ON is characterized by acute or subacute vision loss, generally described as fading of objects, affecting low-contrast vision more frequently than high-contrast vision. In the optic neuritis treatment trial (ONTT), the pre­senting high contrast visual acuity varied from 6/6 to no light perception (NLP), with only 3% of the patients having NLP [48]. These patients fre­quently complain of the dullness of colour vision (acquired dyschromatopsia) and have retro-

The most important clinical test in the evaluation of ON is the swinging ashlight test to detect the conduction defect in the optic nerve, termed the relative afferent pupil defect (RAPD) in unilat­eral or grossly asymmetric bilateral cases. Briey, in a semi-dark room, bright pen torch light is shone swinging (not more than four times) alter­nately between the eyes. If both eyes are normal, when light is shone on one eye, the pupil con­stricts in both eyes. However, if there is a conduc­tion defect in one eye, on swinging the light from the normal eye (the pupils in both eyes get con­stricted) to the abnormal eye, the pupil of the abnormal eye starts dilating. On fundus examina­tion, there is hyperemia and swelling of the ONH, depending upon the site of inammation (Figs. 15.13 and 15.14). Inammation of the optic nerve posterior to the globe may not show any optic disc swelling or hyperemia. Such patients are often labelled as retrobulbar neuritis.

The introduction of Optical coherence tomogra­phy (OCT) is akin to the profound changes in the practice of medicine brought about by the devel­opment of imaging technologies like ultrasonog­raphy, computerized tomography (CT scan), and magnetic resonance imaging (MRI). It has become an important imaging tool in neurology, neuro-ophthalmology, and ophthalmology clin­ics worldwide. Huang etal. [51] developed OCT technology to examine non-invasively the cros­sectional details of biological tissues. The basic principle of the use of OCT is like the use of ultrasonography. Like the sound waves, the reected light signals are detected as a low-

coherence light beam passes through the retina, which either gets reected or transmitted. The initial time-domain technology has been replaced by spectral-domain (SD) technology. It uses a broad-band near-infrared superluminescent diode as a light source and a spectrometer to detect the Fourier transformation of the reected light from the tissue interfaces. The axial resolution has improved to 1–3μ. There has been a tremendous change in the acquisition time to obtain informa­tion from each point of the retinal structures enabling a 3-D construct of the retina. Apart from the cross-sectional image of the various micro­structures, a layer by retinal layer information is obtained as en-face imaging.

The optic nerve length involvement is predic­tive of the loss of GCIPL thinning at 12months; the longer the optic nerve involvement, the more signicant the loss of GCIPL thickness and vol­ume. There is a compensatory thickening of the INL.The cause of the optic disc edema and the cRNFL thickening in the acute phase of optic neuritis is confusing as the optic disc edema and

The NMO spectrum disorder includes patients with optic neuritis, transverse myelitis (TM), or extensive longitudinal myelitis. Patients with bilateral optic neuritis who are AQP4-positive are also part of the spectrum of the disease. Most often, it affects women at the median age of 39 years. Compared to good visual recovery in MS-ON, visual recovery in patients with AQP4-ON is poor. Thirty percent have ≤6/60 high contrast visual acuity and 70% of patients with a relapsing disease have this level of blind­ness [69].