Causes of optic radiation and cortical lesions
The optic radiation (optic radiation) and visual cortex (visual cortex) can be involved in pathological processes due to any adjacent intracranial pathology. Several main groups of causes are distinguished:
- Vascular pathology. The most frequent cause of acute visual deficit is infarction in the posterior cerebral artery (PCA / PCA) basin. If the infarction is bilateral and encompasses the entire primary visual cortex, «cortical blindness» (cortical blindness), also known as Anton–Babinski syndrome (Anton–Babinski syndrome), develops. MRI is the priority method for early diagnosis: diffusion-weighted imaging (DWI) can visualize ischemia and small lesions much earlier than CT, which detects large infarctions only several hours after onset.
- Space-occupying lesions (space-occupying masses). Primary brain tumors, lymphomas, or intracranial metastases cause symptoms through direct infiltration or neural pathway compression. On MRI scans, such lesions (e.g., gliomas or abscesses) are frequently accompanied by marked perifocal edema or ring enhancement.
- Infections and other processes. Abscesses can affect any structures (they are especially important to rule out in immunosuppressed patients). Rarer causes include encephalitides, posterior reversible encephalopathy syndrome (PRES), progressive multifocal leukoencephalopathy (PML), and arteriovenous malformations (AVMs).
Central gaze palsies and internuclear ophthalmoplegia
Gaze control is ensured by the complex interaction of cortical frontal eye fields, the paramedian pontine reticular formation (PPRF), cranial nerve III, IV, and VI nuclei, and vestibulocochlear nuclei.
A special role is played by the medial longitudinal fasciculus (medial longitudinal fasciculus, MLF) — paired white matter tracts running in the dorsomedial part of the pons and midbrain tegmentum (midbrain tegmentum). Their function is to generate conjugate eye movements (conjugate eye movements). Focal lesions of the MLF, most commonly occurring against the background of ischemia or demyelinating diseases, lead to internuclear ophthalmoplegia (internuclear ophthalmoplegia). On MRI (e.g., in FLAIR or DWI sequences), MLF infarction reveals focal signal hyperintensity in the dorsal pons.
Vertical gaze control
Vertical eye movements are controlled by structures in the dorsal rostral midbrain: the interstitial nucleus of Cajal (interstitial nucleus of Cajal) and the rostral interstitial nucleus of the MLF.
Pathologies affecting these zones have a specific neuroimaging and clinical picture:
- Progressive supranuclear palsy (progressive supranuclear palsy). Classically affects the aforementioned nuclei, which manifests on MRI as focal midbrain atrophy.
- Parinaud syndrome (Parinaud syndrome). Impairment of upward gaze due to damage to the dorsal midbrain. A typical cause is compression of the tectal plate (tectal plate) by space-occupying lesions, such as large, partially calcified pineal tumors (pineal tumours).
Chiasmal-sellar region tumors
Neoplasms causing compression of the optic chiasm deserve special attention. A characteristic radiological sign on MRI scans is the optic chiasm appearing stretched or flattened over the suprasellar component of the tumor. Such lesions include:
- Planum sphenoidale meningioma (planum sphenoidale). A calcified tumor with intense contrast enhancement.
- Pituitary macroadenoma.
- Craniopharyngioma.
Other neuro-ophthalmological conditions
Sometimes optic nerve and pathway lesions are not directly related to tumor compression or stroke.
- Idiopathic intracranial hypertension (pseudotumor cerebri). A syndrome of increased intracranial pressure in young obese women, unrelated to cerebral venous sinus thrombosis. MRI findings include: tortuosity and ectasia of the optic nerve sheaths, flattening of the posterior globe, protrusion of the optic disc heads (correlating with clinical papilledema), and an enlarged «empty» sella turcica. The distal transverse venous sinuses are narrowed.
- Recurrent ophthalmoplegic cranial neuropathy. A rare syndrome characterized by attacks of headache and ophthalmoplegia. The oculomotor nerve (cranial nerve III) is most commonly affected, manifesting as ptosis and mydriasis. Contrast-enhanced MRI reveals thickening and pathological contrast enhancement of the third cranial nerve in approximately 75% of cases.
Briefly: answers to topical questions
What types of visual field defects occur in lesions of various parts of the optic radiation?
Lesions of various parts of the optic radiation result in homonymous visual field defects, the nature of which depends on the level of damage.
- Temporal lobe / Meyer's loop (Meyer's loop) or the inferior bundle — results in contralateral superior quadrantanopia.
- Parietal lobe (parietal lobe) or the superior bundle — results in contralateral inferior quadrantanopia.
- Posterior fibers (posterior fibres) or complete radiation lesion — results in complete homonymous hemianopia.
Which arteries supply the primary visual cortex?
The primary visual cortex is supplied predominantly by branches of the posterior cerebral artery, as well as branches of the middle cerebral artery.
- Calcarine artery — the most important branch of the posterior cerebral artery (PCA), which invariably supplies the visual cortex.
- Leptomeningeal branches — branches of the middle cerebral artery (MCA) providing collateral blood supply to the macular area at the posterior pole of the cortex.
Due to dual blood supply, macular vision is spared during PCA occlusion.
Class and exam questions
What is Anton–Babinski syndrome?
This is the development of «cortical blindness» occurring with bilateral infarction in the posterior cerebral artery (PCA) basin with complete involvement of the primary visual cortex.
What are the clinical manifestations of medial longitudinal fasciculus (MLF) damage?
Focal lesion of the medial longitudinal fasciculus leads to impairment of conjugate eye movements — internuclear ophthalmoplegia.
What typical MRI signs are characteristic of idiopathic intracranial hypertension?
These include dilatation and tortuosity of the optic nerve sheaths, flattening of the posterior poles of the globes, protrusion of the optic disc heads, an «empty» sella turcica, and narrowing of the distal transverse venous sinuses.
What pathology causes Parinaud syndrome?
Parinaud syndrome typically occurs due to compression of the dorsal midbrain (tectal plate), most commonly by pineal tumors.
What else to study on this topic
- MRI findings and differential diagnosis of internuclear ophthalmoplegia
- Visualization of chiasmal-sellar region tumors (meningiomas, macroadenomas, craniopharyngiomas)
- Anatomical basis and radiological evaluation of the vestibulo-ocular reflex
- Diffusion-weighted MRI (DWI) in the early diagnosis of visual cortex infarctions
- Radiological features of relapsing ophthalmoplegic cranial neuropathy
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