What happens if there is damage to the visual pathway? Different visual problems will occur depending on where the damage is. The black bars labeled 1 through 5 indicate where damage may occur and the chart to the right of the pathway indicates the resulting "blind" area gray shading of the visual field. Damage at site 1: this would be like losing sight in the left eye. The entire left optic nerve would be cut and there would be a total loss of vision from the left eye.
Damage at site 2: partial damage to the left optic nerve. Here, information from the nasal visual field of the left eye temporal part of the left retina is lost. Damage at site 3: the optic chiasm would be damaged. Most patients complain of mild eye pain, which often feels worse with eye movements [ 3 , 8 ].
Visual field analysis shows bitemporal hemianophia in a patient with pituitary adenoma. Optic neuropathy describes abnormalities of the optic nerve [ 8 ]. This may occur as a result of ischaemia, vascular and blood pressure abnormalities, toxins, compression, infiltrations and trauma [ 9 , 10 ].
Optic neuropathy is divided into anterior and posterior types: anterior optic neuropathy, which causes a pale oedema of the optic disc; and posterior, in which the optic disc is not swollen and the abnormality occurs between the globe and the optic chiasm [ 3 , 4 , 8 ]. Optic disc oedema is the swelling and elevation of the disc. It can be caused by a number of conditions. Papilloedema relates more specifically to optic nerve head swelling secondary to raised intracranial pressure Table 1.
Disc swelling is distinct from disc atrophy which refers to a loss of nerve fibres at the optic nerve head [ 2 , 3 , 11 ]. There are various signs visible during fundoscopic evaluation.
These are: optic disc swelling, unclearness around the margin of the disc, optic disc hyperaemia, venous dilatation, peripapillary haemorrhages, disc exuda or exuda in peripapillar area and cotton wood spots [ 11 ]. The pathogenesis of optic disc oedema is mostly related to inhibition of axoplasmic flow.
Although histopathological and ophthalmoscopic findings are similar, it is important for treatment approaches to find the causes of optic disc swelling. Often, the cause remains obscure despite undergoing a thorough evaluation [ 3 - 11 ]. Papilloedema is swelling of the optic nerve head, secondary to raised intracranial pressure. There may be diplopia if there is a VI cranial nerve palsy [ 3 ]. In papilloedema, disc swelling is nearly always bilateral it may be asymmetrical in the early phase and may be hyperaemic; dilatation of veins and loss of spontaneous venous pulsation are the findings of fundoscopic examination.
All other causes of disc oedema in the absence of raised intracranial pressure are referred to as disc swelling. But not all patients who have raised intracranial pressure will necessarily develop papilloedema [ 3 ]. Visual acuity VA is normal in the early stage and will be reduced in the late stage.
Colour vision is impaired and there may have a relative afferent pupillary defect RAPD. Transient obscurations are frequently seen. VI cranial nerve palsy and diplopia are the others clinical features of raised intracranial pressure.
In some cases chronic papilloedema can progress to chronic atrophic papilloedema and in this situation visual loss develops [ 3 , 8 ]. Papilloedema is a neurological emergency. The underlying cause needs to be investigated. Papilloedema in early phase is seen. The boundaries of the optic disc are not seen clearly. We do not observe vascular tortuousity With the permission of Marmara University Dept. Ischemic optic neuropathy is the most commonly seen neuropathy in elderly.
Ischemic neuropathy is divided into two parts: 1 Anterior and 2 Posterior. Both of them are also divided arteritic and non-arteritic forms. Non-arteritic anterior ischemic optic neuropathy is the most common form of ischemic optic neuropathy. The underlying mechanism of anterior ischemic optic neuropathy is the interruption of the blood flow in the short posterior ciliary arteries that supply the optic nerve head.
It generally occurs between the ages of 55 and 70 years old. The non-arteritic type involves mainly vascular occlusive disease or disorders that reduce the circulation of blood in the short posterior ciliary arteries. Predisposing systemic conditions include hypertension, diabetes mellitus, hypercholesterolaemia and collagen vascular disease Table 2. Visual loss may be sudden or occur over several days.
Most of the patients complain of painless monocular visual loss. Impairment of visual acuity in ischemic optic neuropathy may vary from moderate to severe with no light perception. Fundoscopic examination shows a pale, swollen optic disk, with peripapillary haemorrhages noticeable Figure 3.
Inferior altitudinal visual field defects are typical findings but other defects may also be seen. An afferent pupillary defect is present [ 3 , 8 , 12 , 13 ].
Investigations: Fasting lipid profile and blood glucose, serological analysis, vasculitis markers, investigations of the carotid artery [ 3 ]. Treatment: There is no definite treatment to reverse the damage. Aspirin treatment is effective in reducing systemic vascular events but it does not appear to prevent the involvement of the other eye [ 3 ].
That study and a natural history study on NAION [ 15 ] showed that visual acuity can improve for up to six months. To minimize the risk of further visual loss in the other eye or the same eye, it is essential to reduce the risk factors. Prognosis: In most patients, there is no further loss of vision but vision loss continues for six weeks in a small percentage of patients. Bilateral visual loss may be seen in non-arteritic anterior ischemic optic neuropathy and it usually occurs sequentially instead of simultaneously [ 16 ].
Non-arteritic anterior ischemic optic neuropathy: FFA shows hypofluorescence area caused by diffuse haemorrhage; diffuse microaneurysms, ischemic hypofluorescence area related to peripheric capillary blockages right eye ; crowded optic disc; oedema especially on the upper side; and boundaries on the nasal and temporal side show haemorrhages left eye diffuse haemorrhages, exudates and microvascular abnormalities in intraretinal segments With the permission of Bezmialem University Dept.
It is also known as giant cell arteritis. Therapy is immediate intervention with systemic steroids, especially to protect against vision loss in the other eye [ 17 - 19 ]. The visual loss is sudden and unilateral, but if the treatment is delayed, bilateral visual loss may be seen. Patients with arteritic anterior ischemic optic neuropathy AION often have symptoms other than visual loss, such as malaise, weight loss, headache, scalp tenderness and loss of pulsation of one or both temporal arteries, jaw pain on mastication jaw claudication , generalized muscle aches and swelling.
Temporal artery biopsy is the gold standard for diagnosis and should be performed within seven days of starting treatment. But the treatment should never be delayed while waiting for biopsy. The treatment regime continues by tapering the oral doses. Prognosis: The course of the illness results in poor prognosis. Visual loss is generally permanent; partial visual recovery can be achieved by steroid therapy [ 3 ].
Posterior ischemic optic neuropathy is a rare type of neuropathy and diagnosis depends largely upon exclusion of other causes, such as stroke and brain tumour. Decreased visual acuity and altitudinal visual field defects are present. Decreased blood flow in the pial capillary plexus supplying the nerve, connective tissue disorders, diabetes mellitus, trauma and radiotherapy to the orbit have all been described as causes.
It is also divided into two types; arteritic and non-arteritic [ 3 , 12 ] Table 2. The dysfunction of the optic nerve due to inflammation is called optic neuritis. The acute demyelinating optic neuropathy is the most common type of inflammatory optic neuropathy.
Systemic or local inflammations and infections can cause inflammatory optic neuropathy other than acute optic neurolopathy [ 21 ]. Symptoms are usually unilateral, with eye pain and partial or complete vision loss. Diagnosis is primarily clinical. Treatment is directed at the underlying condition; most cases resolve spontaneously [ 3 , 8 ].
The ages of the patients are generally between 18 and 40 years. Symptoms develop over a few to several days, reaching maximum severity within two weeks. Fundoscopic examination shows that the appearance of optic disc is normal because the illness enhances the optic nerves of the retrobulber type. Ninety-five percent of patients demonstrate an optic nerve enhancement in Gadolinium-enhanced magnetic resonance imaging MRI. Patients typically present with subacute, monocular visual loss.
The patients complain of pain in or around the eye which increases with ocular movement. Characteristic findings other than visual loss include a visual field deficit usually central scotoma type , disturbed colour vision, an afferent pupillary defect, diminished light brightness and impairment contrast sensitivity. The Optic disc is normal in about two thirds of patients inflammation is entirely retrobulbar.
The rest show disc hyperaemia, oedema in or around the disk and vessel engorgement. A few exudates and haemorrhages may be present. Visual recovery is common and often complete; most patients achieve better vision over months [ 3 ]. Despite the return of visual acuity, colour vision, contrast sensitivity and light brightness often remain abnormal [ 3 ].
Recurrent attacks may cause optic atrophy. The Optic Neuritis Study Group published their findings in [ 22 ]. The aim of the study was to identify the factors associated with a high and low risk of developing multiple sclerosis after an initial episode of optic neuritis. Three hundred and eighty-eight patients who had acute optic neuritis were included the study and were followed up for the development of multiple sclerosis after an initial episode of acute optic neuritis for a 10 year risk.
Diagnosis: Optic neuritis is suspected in patients with characteristic pain and vision loss. Gadolinium-enhanced orbital MRI may show an enlarged, enhanced optic nerve. Prognosis : Prognosis depends on the underlying condition. Treatment: Corticosteroids are an option, especially if multiple sclerosis is suspected. Final visual outcomes are not influenced by treatment, but recovery can be reached quickly by intravenous methylprednisolone.
Oral prednisone therapy alone is contraindicated because it is associated with a significantly higher recurrence rate. Patients at high risk for multiple sclerosis, assessed on the basis of MRI, may benefit from immunomodulatory therapy [ 3 ]. Corpus callosum involvement is noted on the sagittal T2WI. TON refers to the direct or indirect injury of the optic nerve secondary to trauma.
The optic nerve runs in the optic canal and can be affected indirectly from blunt head trauma. The visual loss may be partial or complete and generally causes severe and permanent visual defects. The incidence of traumatic optic neuropathy in a closed traumatic head injury ranges from 0. The most common causes were motor vehicle and bicycle accidents, followed by falls and assaults. The diagnosis of TON is difficult and can be delayed when life-threatening systemic symptoms are present.
Direct optic nerve injury is generally rare because of the protecting effect of the orbital bones. It is caused by trauma to the head or orbit. In direct trauma, the anatomy and function of the optic nerve are disrupted. Penetrating injury to the orbit and bony fragments in the optic canal or orbit can result in optic nerve piercing. Orbital haemorrhage and optic nerve sheath haematoma can also cause TON by direct compression.
The diagnosis of TON depends on the clinical signs. The cases of TON are generally of monocular involvement. Visual acuity is generally below 0. Visual defect is often seen in the acute phase. The diagnosis of it is important because of the possibility of surgical intervention. Colour vision dysfunction, visual field defect and visual evoked potential are established.
Indirect injuries transmit force to the optic nerve without transgressing tissue planes. This type of injury is most common in the intracanalicular portion of the nerve. Direct optic nerve injuries crosses normal tissue planes and disrupts the anatomy and function of the optic nerve; e.
Indirect injuries, like blunt trauma to the forehead during a motor vehicle accident, transmit force to the optic nerve without transgressing tissue planes. This type of force causes the optic nerve to absorb excess energy at the time of impact.
The most common site of injury is the intracanalicular portion of the nerve. Optic neuropathy is most commonly seen in patients in an unconsciousness state associated with a fall [ 3 , 8 , 24 , 25 ]. CON is the result of compression of the optic nerve. The optic nerve can be pressed in the orbit, the optic canal and the intracranial levels.
But it is much more strongly related to orbital pathologies. The optic nerve is most vulnerable to injury by a compressive force in the orbital apex or optic canal [ 26 ]. The optic nerve is resistant to force in other parts of the orbita and intracranial level. The most common causes of compressive optic neuropathy in the orbit are inflammatory disease thyroid orbitopathy, pseudotumour orbita, orbiata cellulitis , tumours and orbital traumas.
A variety of tumours can produce optic nerve compression. Sellar and parasellar masses craniopharyngioma, meningioma, or pituitary adenoma , optic nerve sheath meningiomas and metastatic lesions are included in the differential diagnosis. The other causes related to intracranial pathologies include hypophysis tumours, meningiomas, craniopharyngiomas and aneurisms [ 3 , 8 , 27 ].
Tumours can also infiltrate the optic nerve, particularly optic nerve gliomas in neurofibromatosis , also lymphoma and other hematologic malignancies.
Furthermore, the optic nerve is also a part of the central nervous system. Therefore, it is also called a cranial nerve. Optic tract is a continuation of the optic nerve. Therefore, it is a part of the visual system of the brain.
The optical tract has two individual components; namely, the right optical tract and left optical tract. Left optical tract carries information from the right visual field whereas the right optical tract carries the information from the left visual field. Both optical tracts terminate at the lateral geniculate nucleus in the thalamus. The optic tract consists of fibres that come from the ipsilateral temporal hemiretina and contralateral nasal hemiretina.
The optical nerve is the nerve which connects your eye to the brain while the optical tract is the continuation of the optical nerve. Therefore, the optical tract is a part of the visual system of the brain. This is the key difference between optic nerve and optic tract. Moreover, the optical nerve is located in the back of the eye while the optical tract is located in the brain. Optical nerve and optical tract are two important structures of the visual system. The optical nerve is located at the back of the eye, and it continues to the optical tract in the brain.
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