The cranial nerves


This sensory nerve arises from olfactory (smell) receptors in the nasal mucosa. Branches pierce the cribriform plate and synapse in the olfactory bulb. The olfactory tract then passes to the olfactory cortex in the anteromedial surface of the temporal lobe.
Loss of the sense of smell (anosmia) occurs with head injury andtumours of the olfactory groove (e.g. meningioma, frontal glioma).
The sense of smell is often lost, sometimes permanently, after upper respiratory viral infections. It is diminished in nasal obstruction.


The optic nerve carries axons from the ganglion cells of the retina to the lateral geniculate bodies. The visual pathway is shown in Fig. 18.4. It should be noted that the lens causes the image on the retina to be inverted. Thus, an object in the lower part of the visual field is projected to the upper retina and an object in the temporal half of the visual field is projected to the nasal half of the retina. At the optic chiasm, fibres travelling in the nasal portions of the optic nerves cross to the opposite sides, where they join uncrossed temporal fibres from the lateral portion of each optic nerve. One optic tract thus carries fibres from the temporal side of the ipsilateral retina and the nasal side of the contralateral retina.
From the lateral geniculate body, fibres pass in the optic radiation to the visual cortex of the occipital lobe. The visual field projected to each optic tract, radiation and cortex is called ‘homonymous’, to indicate the different (i.e. bilateral) origins of each pathway. (A homonym is the same word used to denote different things.) Field defects are ‘hemianopic’ when half the field is affected, and ‘quadrantanopic’ when a quadrant is affected. ‘Congruous’ denotes symmetry and ‘incongruous’ lack of symmetry.

The visual pathway
The visual pathway

Visual acuity

This should be tested with a Snellen test chart and corrected for refractive errors with lenses or a pinhole. The corrected visual acuity should be recorded. The normal acuity should be 6/6 to 6/9 in both eyes. Blindness can be due to:
• Ocular causes, e.g. glaucoma, macular degeneration or diabetes
• Central (neurological) causes, e.g. optic nerve lesions, chiasmal compression

Visual field defects

These should be charted by confrontation with white and red headed pins and, if abnormal or in doubt, recorded in detail with a Goldmann (or similar) screen. The common defects.

Retinal and local eye lesions

Lesions of the retina produce either scotomata (small areas of visual loss) or peripheral visual loss (tunnel vision). Common causes are diabetic retinal vascular disease, glaucoma and retinitis pigmentosa.
Local lesions of the eye (e.g. cataract) can also cause visual loss.

Optic nerve lesions

Unilateral visual loss, commencing as a central or paracentral scotoma, is characteristic of optic nerve lesions. Complete lesions of the optic nerve produce total unilateral visual loss with loss of pupillary light reflex (direct and consensual) when the blind eye is illuminated. The causes of optic nerve lesions. The principal pathological appearances of the visible part of the nerve (the disc) seen on fundoscopy are:
• Disc swelling (papilloedema)
• Pallor (optic atrophy)
PAPILLOEDEMA (TABLE 18.10). This means swelling of the papilla-the optic disc. The earliest ophthalmoscopic signs are redness of the disc followed by blurring and heaping up of its margins (the nasal margin first). There is loss of the normal, visible, spontaneous pulsation of the retinal veins. The physiological cup becomes obliterated and the disc engorged, with dilatation of its vessels and the retinal veins. Small haemorrhages surround the disc.
True disc oedema should be distinguished from various conditions that simulate it. Marked hypermetropic (longsighted) refractive errors make the disc appear pink, distant and ill-defined. Opaque (myelinated) nerve fibres near the disc and hyaline bodies (drusen) can be mistaken for disc swelling.
In difficult cases fluorescein angiography is diagnostic . In papilloedema, fluorescein injected intravenously leaks from the disc capillaries and may be seen and photographed. Early papilloedema from causes other than optic neuritis (see below) often produces few visual symptoms, the  patient’s complaints being those of the underlying disease.
As disc oedema develops there is enlargement of the blind spot and blurring of the vision. As the disc becomes engorged its arterial blood flow is reduced and, in severe papilloedema, infarction of the nerve occurs, often suddenly, with resulting blindness.
OPT IC NEURITI s. Optic neuritis is swelling of the optic disc due to inflammation of the optic nerve. The commonest cause is demyelination (e.g. multiple sclerosis). Disc swelling due to optic neuritis is distinguished from other causes of disc oedema by the occurrence of early  and severe visual loss.
The term retrobulbar neuritis implies that the inflammatory process is ‘behind the bulb’ (i.e. the eye), so that no abnormality may be seen with the ophthalmoscope in spite of visual impairment. OPTIC ATROPHY. Disc pallor (optic atrophy) may fol- Iowa variety of pathological processes, including infarction of the nerve, demyelinating optic neuritis (in MS), optic nerve compression, syphilis, vitamin BI2 deficiency and toxins (e.g. quinine and methyl alcohol). Optic atrophy is described as consecutive or secondary when it follows papilloedema. The degree of visual loss depends upon the underlying pathology.

Lesions of the optic chiasm

Bi-temporal hemianopic field defects occur when a lesion compresses the central part of the chiasm. Common causes are:
• Pituitary neoplasm
• Craniopharyngioma
• Secondary neoplasm

Lesions of the optic tract and optic radiation. Homonymous hemianopia or quadrantanopia are the typical field defects caused by unilateral compression or infarction of these structures. Optic tract lesions are rare. Temporal lobe lesions (due to tumour or infarction) cause upper quadrantanopic defects; parietal lobe lesions cause lower quadrantanopic defects. Lesions of the occipital cortex. Homonymous hemianopic defects are caused by unilateral posterior cerebral artery infarction. The macular region (at the occipital pole) is spared because it has a separate blood supply from the middle cerebral artery. Damage to one occipital pole causes a small, congruous, scotomatous, homonymous hemianopia (site 8). Widespread bilateral occipital lobe damage by tumour, trauma or infarction causes the syndrome of ‘cortical blindness’ (Anton’s syndrome). The patient is blind but characteristically lacks insight into the degree of visual loss and may deny it. The pupillary responses are normal .

Optic and retrobulbar neuritis

Optic nerve compression (e.g. tumour or aneurysm) Toxic optic neuropathy (e.g. tobacco, ethambutol, methyl alcohol, quinine)


Ischaemic optic neuropathy (e.g. in giant-cell arteritis) Hereditary optic neuropathies.

Severe anaemia

Vitamin B’2 deficiency
tnfective=spread of paranasal sinus infection or orbital cellulitis
Causes of papilloedema

Intracranial mass lesions

Brain oedema, e.g. encephalitis, trauma Subarachnoid haemorrhage
Benign intracranial hypertension Metabolic causes, e.g. CO2 retention, chronic anoxia, hypocalcaemia.

Accelerated hypertension
Optic neuritis
Disc infiltration, e.g. leukaemia
Ischaemic optic neuropathy
Retinal venous obstruction (thrombosis, orbital lesions

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