We know that there are 12 pairs of cranial nerves and 31 pairs of spinal nerves. Cranial nerves carry information to and from the brain.

Cranial nerves contain 2 types of fibers
1) Sensory fibers – that relay sensory information
2) Motor fibers – that relay motor information
Sensory nerves – carry only sensory information
Eg – olfactory, optic & vestibulocochlear nerve.
Motor nerves – carry only motor information
Eg – hypoglossal & spinal accessory
Mixed nerve – These nerves have both sensory & motor fibres

Attachments
1st and 2nd - forebrain
3rd and 4th – midbrain
5th - pons
6,7,8 - inferior surface of pons.
9-12 - Medulla oblongata
The central sulcus divides the cerebum into two – a portion anterior to it called motor area or motor cortex and a portion posterior to it called sensory cortex.

Motor pathway of cranial nerves
From the motor cortex fibers called the corticonuclear fibres arise and they end in the cranial nerve nuclei. These form the UMN pathway. From the cranial nerve nuclei fibers arise and they end in different parts of body. These form the LMN pathway.

Sensory pathway of cranial nerves
Sensory fibers originates from the sensory organs. They form the first order neurons and their axons terminate in brainstem. From there second order neurons arise and they terminate in thalamus. From there 3rd order neurons arise and their axons end in sensory cortex.

OLFACTORY NERVE
The olfactory mucus membrane in the upper part of the nasal cavity contains olfactory receptors. The central process of these receptors forms the olfactory nerve fibers. These olfactory nerve fibers passes through the cribriform plate to the olfactory bulb, then it forms the olfactory tract. Olfactory tract passes posteriorly and divides into the medial and lateral olfactory straie. Medial olfactory straie gets connected to the olfactory tract of opposite side. The lateral olfactory straie carries the fibers to the primary olfactory cortex in the temporal lobe.

TESTS
Local causes which impair the sense of smell like rhinitis, sinusitis and gross deviation of septum should be looked for and excluded before testing the smell.
Each nostril is tested separately after occluding the other one, by using substances with mild aroma like coffee, powder, peppermint, clove etc.
The patient is asked to close his eyes and mouth and inhale the odour of the test substance and identify it. Ability to perceive the smell and to differentiate one smell from the other is taken as normal even though proper identification may not be sometimes possible. Substance which give pungent smell such as ammonia, chloroform etc should not be used because they stimulate the trigeminal nerve endings and irritate the nose even when the sense of smell is absent.

Disorders of olfaction includes, loss of smell -anosmia, reduction of smell – hyposmia, increased smell – hyperosmia, distortion of smell – parosmia and illusions and hallucinations of smell.

Parosmoia – Head injury or local abnormalities of nose
Hyperosmia – In psychiatric patients
Olfactory hallucinations & delusions – epilepsy, migrane , psychatric patients.

Anosmia – Head injury of cribriform plate
Aneurynsms of circle of Willis
Anterior communicating artery
Ophthalmic artery
Tumors
Olfactory groove meningioma
Pituitary tumors
Frontal lobe glioma
Frontal lobe abscess
Frontal bone osteoma
Increased ICP(rarely)

OPTIC NERVE
Retina is formed by rods and cones, these synapse with the bipolar cells, these in turn synapse with the ganglionic cells. The fibers of the ganglionic cell forms the optic nerve. The optic nerve leaves the orbit through optic foramen, it unites with the other optic nerve at optic chiasma. Only the fibers of the nasal ½ of the retina passes to the other side while the fibers from the temporal half passes straight. Then it forms the optic tract. Optic tract comes to the lateral geniculate body. A few fibers leaves the tract before reaching the lateral geniculate body and pass to the superior colliculus – these fibers are those which are concerned with light reflex. From the lateral geniculate body the fibers get fanned out. This is called optic radiation. In optic radiation fibers which carry information from the lower ½ of visual field passes through the parietal lobe and fibers which passes information through the upper ½ of visual field passes through the temporal lobe. It is important that the ocular system reverses the image. The nasal side of the fundus picks up the temporal image and temporal side of the fundus picks up the nasal image. Damage to nasal side of retina will produce a temporal visual defect and vicevera.

Lesion of optic nerve
Complete lesion of optic nerve leads to total visual loss. Usually it starts as a central scotoma (area of defective vision) and then progresses to complete loss of vision. Some disease of optic nerve affects some fibers only and spares other fibres. So instead of total blindness there are areas of loss of vision in central and peripheral fields.

Optic nerve is peculiarly liable to Neuritis (Inflammations)
1) Papillitus – inflammation of optic nerve head
2) Retrobulbar neuritis – neuritis of optic nerve just behind the eyeball
3) Optic atrophy – any damage to optic nerve later leads to optic atrophy
4) Optic nerve compression – leads to atrophy
Optic nerve damage starts as scotoma
1) Centro caecal scotoma – When the scotoma extends to involve the blind spot it is called centrocaecal scotoma. It is characteristic of toxic ambylopia, - alcoholism, tobacco
2) Arcuate scotoma – When the scotoma extends from the blind spot and follows the course of the nerve it is called arcuate scotoma seen in glaucoma, choroiditis.

Lesion at optic chiasma
1) Medial compression of optic chiasm interrupts fibers from both nasal ½ of retina this leads to bitemporal visual loss – This is called bitemporal hemianopia. Hemianopia means loss of one half of the visual field. Loss of both temporal ½ or both nasal ½ of visual field is called – heteronymous hemianopia.
2) Lateral compression of optic chiasm – results in interruption of uncrossed nerves. This leads to ipsilateral nasal hemianopia.
3) Pituitary adenoma, nasopharynageal carcinoma, sphenoid sinus mucocele leads to compression of optic chiasma from below it leads to involvement of upper quadrants first & leads to bitemporal quadratopia.
Involvement of lower quadrants indicate compression of optic chiasma from above leads to bitemporal quadrantopia causes: craniophrayngioma or third ventricular tumor.

Lesion of optic tract & lateral geniculate body
Results in loss of vision of nasal half .This is called homonymous hemianopia. Because of relative rotation of nasal & temporal fibers in optic tract the defect will be in congruous.
Lesion in optic radation
Fibers fan out in optic radiation along the temporal and parietal lobes. Fibers of the upper ½ of the visual field pass through the temporal lobe and lesion of optic radiation along temporal lobe leads to upper quadrantanopia. The fibres of lower ½ of visual field passes through the parietal and any lesion of parietal lobe causes lower quadrantopia.

Tubular contraction of visual field
In this condition the visual field is constructed as if the patient looks through a tube. It occurs in frontal lobe lesions, also in hysteria.

Spiral contraction of visual field
When the visual fields are repeatedly tested on one sitting it may be seen to constrict progressively. It is usually a hysterial phenomenon, it can also occur due to fatigue and rarely in frontal lobe lesions.

Testing visual fields
Visual fields can be central and peripheral. Visual field extending up to 30ο from the point of fixation is called central visual field and the rest is called peripheral visual field.

Assessment of peripheral visual field – is by confrontation method. In this method visual field of the patient is compared with the visual field of the examiner. The examiner positions himself face to face in front of the patient in such a way that the eyes of the patient and examiner are almost at the same level. Each eye is tested separately while the other eye is covered. Patient fixes his eyes on the eyes of the examiner. Examiner brings an object from the periphery to the center and asks the patient to say ‘yes’ as he sees the object. Thus the upper nasal, lower nasal upper temporal and lower temporal areas are tested.

If the patient is totally bedridden, uncooperative demented subject, defensive eye blinking brought by moving the examiner’s hand rapidly from periphery towards patients eye can by tested. Absence of expected response should suggest loss of vision in that part of visual field.

Visual inattention is often tested by confrontation test. Here two eyes are kept open and two identical objects (examiners index finger) are presented simultaneously in corresponding positions of both visual fields. If visual inattention is present, the patient appreciates the finger only on one side.

Assessment of central vision
Central visual field can be assessed by red pin test. Since the central portion of retina is rich in rods and cones and is color sensitive, a red pin can be used for confrontation test. A red pin is brought from periphery to the center in all quadrants. Scotomas can be detected by this. If the red pin is of 3mm size at the area of blind spot (place where rods & cons are absent) the pin disappears. Blind spot can be seen.

Field of vision can also be detected by using perimeter. A point of light is moved centrally from the extreme periphery. The position at which the patient observes the target is marked on the chart. Repeated testing from multiple directions provides an accurate record of visual fields.

Visual acuity – Visual acuity tests the central vision. Visual acuity is the resolving power of eye for the central vision. Both the eye is assessed separately. Both near and distant vision is tested.

If there is severe visual impairment v.a can be assessed by asking the patient whether he can appreciate light. If not it is written as no P.L. Ask whether the patient can see hand movement. If not it is written as ‘no H.M.’. Ask if the patient can count fingers if not it is written as ‘no C.F.’.

If the patient can read, near vision and distant vision is tested. Near vision is tested by using an Jaeger type card. It is held 35cm from the patients eye. To exclude the difficulty due to refractory errors a pin hole card can be used. The patient is asked to look through a 1mm size pin hole punched in a card. The pinhole allows the light to fall only on the central part of the retina. If the visual acuity which is originally impaired improves on pin hole test, the visual impairment is due to refractive errors and not due to neurological causes.

Distant vision is tested using the snellen’s chart. Visual acuity is expressed as ‘d/D’. d is the distance of which the patient sits is 6m. ‘D’ no of the line that patient can read.
Optic fundus examination can be done using an ophthalmoscope
Color vision is tested. Ask whether the patient can appreciate colors. Color vision is also tested by using Ishiara’s chart.

OCCULOMOTOR , ABDUCENT AND TROCHLEAR
The occulomotor abducent and trochlear are described together as these three nerves and the muscles innervated by them together participate in the smooth and coordinated movements of the eyes.

COURSE : OCCULOMOTOR NERVE
Occulomotor nerve has got two nuclei , main motor nuclei and Edinger-Westphall nuclei . This nerve arises from the anterior surface of the mid-brain in the interpeduncular fossa . It ends by entering the orbit and all its way supplies leavator palpebra superioris , all ocular muscles except superior oblique and lateral rectus . It also supplies ciliary muscles and constrictor pupillae . Affection of leavator palpabre superioris leads to ptosis . When extra ocular muscles are involved it leads to diplopia, strabismus and defective ocular movements. Involvement of constrictor pupillae and ciliary muscles leads to loss of light reflex.

COURSE : TROCHLEAR NERVE
It is the smallest of all cranial nerves .It arises from the midbrain immediately above pons . It ends by entering the orbit and supplying the superior oblique muscles .

COURSE : ABDUCENT NERVE
This nerve arises from the brain stem at the pontomedullary junction . It has the longest intracranial course and ends by entering the orbit at the superior orbital fissure . It supplies the lateral rectus muscle .

Test for levator palpabrae superioris
Levator palpabrae superioris helps to elevate the upper eye lid. Paralysis of levator palpabrae superioris leads to ptosis
Ask the patient to look at a distant object then ask him to elevate the upper eye lid .
Ptosis can be due to other causes such as sympathetic palsy, myasthenia gravis and partial ptosis due to trachoma and tumors of eyelids .

Test for ocular movements
Steady the patient’s head and ask him to follow an object held at arm’s length .Observe the full range of vertical and horizontal eye movements . The vertical and horizontal eye movements made from the mid position of gaze are called the cardinal movements . Then examine the other directions of gaze .

Upward movement is called elevation- Superior rectus and inferior oblique .
Downward movement is called depression –Inferior rectus and superior oblique .
Lateral movement is abduction – Lateral rectus.
Medial movement is adduction – Medial rectus .

Looking up and out – Superior rectus .
Looking up and in – Inferior oblique .
Looking down and out – Inferior rectus .
Looking down and in – Superior oblique .

Nerve supply of the muscles .
All the muscles are supplied the occulomotor nerve except the superior oblique which is by trochlear and lateral rectus by abducent.
So in the fourth cranial nerve lesion the patient cannot turn the eyes inwards . Patient will have difficulty in reading and going downstairs, in case of which he will have to tilt his head .
In the sixth cranial nerve palsy the patient will not be able to turn the eyeball to the lateral side . The imposed pull of medial rectus muscle causes the eye to turn inwards thereby producing internal strabismus .

Total paralysis of the 3rd,4th& 6th cranial nerves is known as the internal opthalmoplegia . Paralysis of the extra occular muscles is called the external opthalmoplegia . Paralysis of the intrinsic muscles of the eye ( ciliary muscles and constrictor pupillae) is called the intrinsic opthalmoplegia.

Supranuclear mechanisum of eye movements
1) Pursuit movement – tract –occipito mesencephalic tract .
These are the slow movements accurately tracing a moving object .
2) Saccadic movement - Fronto mesencephalic pathway
These are rapid eye movements on shifting from one point of fixation to other .
3) Convergence mechanism – Ask the patient to look at a distant object then at your finger kept at few centimeters in front of the nose The center for convergence movement is at the occipital cortex. Lesion at occipital cortex leads to impaired convergence mechanism
3) Position maintenance mechanism
Ability of the eyes to fix at a stationary object . tract is the occipito mesencephalic tract . Lesion of this tract leads to impaired fixation .
4) Reflex mechanisum
Occipitocephalic reflex : eye balls reflexively deviate according to the movements of the head.
Doll’s eye movement :
Eyeballs move in a direction opposite to the movements of the head., when the head is passively moved. Presence of doll’s eye movements indicates supra nuclear lesions .
Occulovestibular reflex: Reflex eye movements occur when the external auditory canal is irrigated with warm or cold water .
Absence of reflex movements suggests brain stem lesions . Midbrain and pontine lesions will produce failure of upwards and downward gaze . Impaired vertical movements is common in extra pyramidal diseases.
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DIPLOPIA
Diplopia is said to be present when the patient complains of seeing two images when he looks at an object . This is due to the paralysis of one or a group of extra ocular muscles . When the eyes are fixed on an object the image falls on the macular area in normal eyes and outside macular area in the parietic eye .Thus two images of an object are perceived The image which is seen by the parietic eye is called the false image and by the normal eye is the true image. The patient s asked to look at all directions of gaze and determine in which position maximum separation of true and false images occur. Maximum separation occurs in which direction of gaze , the muscle responsible for gaze in that direction is the parietic one .The abnormal eye can be determined by covering one eye and noting the effect on diplopoia . If this results in disappearance of false image then the paretic muscle belongs to that eye.

SQUINT
Refers to the abnormal deviation of eye. The abnormal deviation of eyes can be divergent , convergent , upwards or downwards . When squinting is noticeable ,if both eyes are open it is called manifest squint . If squinting is noticed on covering one eye , it is called latent squint .

Squinting is due to the paralysis of extra ocular muscles . Abnormality is seen when the eyes are in the resting position but it becomes more obvious when the eyes are turned in the direction of the action of paralysed muscle .The images of the object fail to fall on corresponding points in the retina of both eyes and this also leads to diplopia .In paralysis of medial rectus and superior oblique the squint is divergent due to the unopposed action of lateral rectus .In paralysis of lateral rectus the squint is convergent due to the unopposed action of medial rectus .
We have to differentiate it from the squint that occurs not due to the paralysis of extra ocular muscles

NYSTAGMUS
Nystagmus is defined as the involuntary to and fro movement of the eye in the horizontal ,vertical ,rotatary or mixed direction .Occular posture or tone of extra ocular muscles is normally maintained by the impulses which reach the eye from the retina , labyrinth, cerebellum and midbrain .

Grade
I - Nystagmus is present only when the eyes are deviated to one side .
II – Nystagmus produced in mid position and also when the eyes are deviated to one side.
III - Nystagmus present in all direction of gaze .

Nystagmus can be pendular – eyes found to drift in one direction giving rise to a slow phase as a corrective phenomenon they are quickly brought back into the neutral position - Quick phase
.Nystagmus can be of eqnal amplitude to both sides

1) Retinal nystagmus : Vision is defective & fixation is impaired rapid pendular nystagmus occurs
2) Vestibular nystagmus:- Any damage to labrinth or veatibular nerve leads to vestibular nystasgmus .Slow phase towards side of lesion and quick phase to normal side .
3) Labrynthine disease – Nystagmus occurs when the patient assumes certain postures . This is known as positional nystagmus .To elicit this suddenly reposition the patient . After several seconds nystagmus develops and on repeated testing it disappears .
4) Posterior fossa lesion – In posterior fossa lesions positional nystagmus occurs .
5) Cerebellar damage – In cerebellar damage nystagmus occurs with fast phase towards the side of lesion .
6) Vestibular nuclei or brainstem lesion- Here the fast phase of nystagmus occurs towards the direction of gaze .
7) Medial longitudinal fasiculus – A lesion in medial longitudinal fasiculus leads to dissociate nystagmus .Nystagmus is present in one eye and not in other eye .( A lesion in MLF leads to internuclear ophtalmoplegia . MLF are a bundle of fibers which connect some of the cranial nerve nuclei together viz. 3,4 5 , 6. 8., 11, and 12th cranial nerves.These bundles have connections also with brainstem and motor nuclei of the upper cervical nerves ).

7) Lesion in cervico medullary junction - Downbeat nystagmus.
8) Lesion in upper midbrain – Convergence nystagmus.
9) Lesion in sellar & para sellar region – See-saw nystagmus .

Occular bobbing ( up & down motion of the eye )
is seen in large pontine lesions . Opsoclonus ( rapid jerky movements of the
eyes ) is seen in brain stem lesions.

Test for pupils
1) Size of pupil – Normally both pupils are equal in size . Difference in
the size of the pupil is called anisocoria .
2)Shape - Normally both pupils are circular in shape .
3) Light reflex –When the light is shown in one eye the pupil of that eye constricts .This is the direct light reflex. When the opposite pupil also constricts it is the indirect light reflex.

Pathway
A stimuli such as bright light shone in one eye will send an afferent impulse along the optic nerve and the efferent impulse pass to the eye through the occulomotor nerve .

1) In optic nerve lesions – Direct light reflex will be abolished ,
2) Occulomotor nerve lesion - No direct light reflex but consensual reflex is present in the affected eye . In normal eye direct light reflex is present but consensual light reflex absent .

Accomodation reflex
This reflex occurs when the patient immediately focuses his vision on a near object.
Test - The patient is asked to fix his eyes on the examiners index finger kept at a meter away and rapidly brought near the patient’s nose.

The 3 “ C” of accommodation
1) Convergence of eye .
2) Contraction of ciliary muscle .
3) Constriction of pupil.

Ciliospinal reflex
When the skin over the neck is pinched , pupil on the same side dilate reflexively . This results from the stimulation of the sympathetic nerves which supply the dialator pupillae muscles . Ciliospinal reflex is abolished in lesions of cervical sympathetic nerves , affection of upper cervical and thoracic segments and medulla oblongata .

Other abnormalities of pupillary reflex
1) Argyll Robertson’s pupil
Pupils are small , irregular in shape , they do not react to light but react to accommodation reflex. This is characteristic of tabes dorsalis & GPI .
This response can also occur in midbrain lesions which are neoplastic, inflammatory , vascular & demylinative .
2)Marcus Gunn pupil
Seen in optic nerve lesions .Light is swung from one eye to another as it falls on affected eye it dialates and on unaffected eye it constricts .
3) Hippus
Rhythmic alternating constriction and dialatation of pupils . It is usually normal but is marked in retrobulbar neuritis and encephaalities .

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