What is the only paired circumventricular organ?

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The American Association of Neurological Surgeons has a great new YouTube channel hosting videos on surgical anatomy, including some Rhoton lectures. Even some videos in 3D if you have a computer capable of playing such. I hope they keep updating it but it’s a great resource as is.

List the segments of the facial nerve.

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The trochlear nerve, along with the abducens nerve, are perhaps the simplest of the cranial nerves in their function. Yet, the trochlear has a couple of unique properties and certainly some clinical correlates for the neurosurgeon.

The nerve carries somatic efferent fibers which do but a single job, innervate the superior oblique muscle. The nucleus trochlear nerve is located near the midline, just inferior to the motor nucleus of the occluomotor nerve and at the level of the inferior colliculus. The axons of the fourth cranial nerve leave the nucleus and actually decussates in the superior medullary velum. This is the only cranial nerve to decussate prior to exiting the brainstem. The significance is obvious that the right superior oblique muscle is controlled by neuronal cell bodies in the left midbrain.

The trochlear nerve exits dorsally from the midbrain. Again, this is unique amongst cranial nerves.

It travels along the medial, free edge of the tentorium cerebelli through which the brainstem is passing. It pierces the dura just posterior to the posterior clinoid process and enters the cavernous sinus where runs just medial and posterior to the occulomotor nerve before entering the orbit through the superior orbital fissure.

Since the superior oblique muscle acts to rotate the eye down and medially a palsy of the trochlear nerve leaves the affected eye rotated “down” and “out”

Attempts to compensate lead to the patient tilting their head to the contralateral side.

Amongst cranial nerve palsies a trochlear injury is the second most common manifestation of raised intracranial pressure, only the abducens more likely. It is the longest nerve and the smallest in diameter and particularly prone to the effects of raised ICP due to its lengthy free course starting dorsally and then extending through the anterior cisterns.

Compressive injuries can also occur uniquely with posterior cerebral artery as early in its course the trochlear passes between the superior cerebellar and posterior cerebral arteries. Obviously pathology in the cavernous sinus can affect the trochlear, as it can the occulomotor or abducens or the first branch of the trigeminal.

A more unique consideration for the neurosurgeon is the trochlears path along the medial edge of the tentorium. Transtentorial surgical approaches to the lower brainstem or the proximal cranial nerves located there, must be careful when incising the tentorium not to incur sharp damage to the trochlear or to overstretch it with retraction.

To date in my little series I’ve dealt with the first of the twelve paired cranial nerves. Both of these serve exclusively special afferent functions. The third cranial nerve, the occulomotor nerve, dishes out parasympathetics and motor fibers.

The third cranial nerve arises from two nuclei at the level of the superior colliculus anterior in the midbrain. The motor nucleus of the third nerve give rise to fibers which innervate four of the six extraoccular muscles responsible for movement of the eye:

In addition it innervates the superior levator palpebrae which assists in opening the lid.

The Nucleus of Edinger-Westphal is the second nucleus involved in the occulomotor nerve. It sits just superior to the motor nucleus. Its fibers run congruent with the motor fibers of the third nerve and run along the outside of the nerve. It exits the brain stem centrally and ventrally, essentially initially parallel to but inferior to the optic tracts. In the basil cisterns anteriorly it is easily compressed by an encrounching herniated uncus.

Just lateral to the posterior clinoid process the nerve pierces the dura and enters the cavernous sinus.

In the sinus it is the most superior cranial nerve and pushed more medially.

It exits through the superior orbital fissure where the parasympathetic fibers almost immediately synapse with the ciliary ganglion. The motor fibers go on to innervate the superior rectus, medial rectus, inferior rectus, inferior oblique and levator palpebrae.

Post ganglionic parasympathetic fibers from the ciliary ganglion go on to innervate the sphincter pupillae which causes miosis and the cilliary muscle which, on contraction, causes the lens to relax and accomidate for near vision.

Clinically occulomotor nerve palsies are at times associated with diabetes. Classically the palsy associated with diabetes spares the pupillary light reflex. This is felt to be because the blood supply to the nerve run supperficially along it, supplying the pre ganglionic fibers the easiest and the ischemic neuropathy associated with diabetes is thus more likely to affect the motor fibers along the watershed zone.

The relationship of the motor and pre ganglionic fibers also explains why in uncal herniation syndrome the first sign of a compressive occluomotor nerve palsy is a dilated pupil as the pre ganglionic fibers are the first to be compressed and this leads to unopposed sympathetic action causing mydriasis.

There is a unique syndrome called Adie syndrome which leads to essentially isolated loss of ciliary ganglion nerve bodies and thus a tonic, chronically dilated pupil.

It’s fair to say that vision is the most important sensation, the one from which we draw the most information.

The first order neurons of the visual pathway are the rods and cones lying deep in the retina.

On the diagram light would enter from the left, pass through the cornea, lens, vitreus humor and multiple layers of the retina to reach the first order neurons in the pathway. Rod cells are peripherally located cells with a low activation threshold, some responding to single photons. They are primarily associated with “night vision” and peripheral vision. Many rod cells may converse on a single second order neuron. This convergance of data means that the acuity of rod cells is not nearly as great as the more centrally located cone cells which converge nearly one to one on second order bipolar and amacrine cells.

The physiology of the activation of rod and cone cells is complex but here is a good very basic summary.

The short bipolar and amacrine cells in the retina relay the signal to the third order ganglion cells. The long axons of the ganglion cells converge to form the actual optic nerve.

The axons converge at the disc and form the optic nerve which exits posteriorly where it becomes myelinated and takes up the dural covering of the brain. The nerve exits the orbit at the optic canal. The tracts within the optic nerve are grossly somatically organized.

Generally the temporal fields of both retina travel laterally in the nerve and the nasal fields from both retina travel medially. Even this gross simplification takes some thinking about. Essentially objects of focus in the right visual field project onto the nasal fields of the right eye and the temporal fields of the left eye.

This is something to think about as the optic nerves come to the optic chiasm. At the chiasm approximately half of the ganglion cell axons will decussate. Primarily the axons carrying information from the nasal fields decussate. Functionally what you end up with is information from the right visual fields(temporal fields of the left eye and nasal fields of the left eye) in the left optic tract and information from vision to the right (temporal fields of the right eye and nasal fields of the left eye) in the optic tract on the right.

However, because the lens inverts the image prior to it reaching the retina, things you see to your left actually end up as information traveling through the left optic tract and vice/versa.

The first branches from the optic tracts travel to the superior colliculi and the pretectal area. These represent the afferent limb of the pupillary light reflex. They will synapse on the pretectal nuclei which will send axons to the accessory nucleus of the third nerve, then on to the cillary ganglion, then on to the sphinter pupillae muscle causing narrowing of the pupil.

The majority of the axons in the optic tracts however continue on the lateral geniculate bodies in the thalami.

The above image sourced here.

The neurons in the lateral geniculate body send axons which make up the optic radiations which run posteriorly around the temporal and occipital horns of the lateral ventricles to the occipital lobe, particularly the medial surface, Brodmann Area 17.

The primary clinical considerations are understanding how lesions along the pathway might manifest in terms of visual field deficits.

The sense of smell is a special afferent skill facilitated by the first numbered cranial nerve, the olfactory nerve.

The first order neurons of the olfactory nerve are the olfactory sensory neurons. These are bipolar cells whose dendrites project g-coupled olfactory receptors into the olfactory mucosa. Dissolved molecules within the mucosa act as ligands at these receptors and trigger an action potential which travels ‘up’ the bipolar olfactory sensory neurons. The axons of these cells colasce into processes which head through the cribiform plate. These processes truly represent the olfactory ‘nerve’.

The processes which make up this short nerve end as they synapse on the second order neurons at intracranial olfactory bulb. The olfactory bulb is complexly organized however the primary secondary neurons are the mitral and tufted cells. The axons of these secondary neurons make up the olfactory tract. Of note, a very small number of these mitral and tuft cells will synapse onto the neurons of the anterior olfactory nucleus, just at the junction of the olfactory bulb and tract. The role of the anterior olfactory nucleus is extremely poorly understood.

The majority of the second order neurons however continue through the olfactory tract and just anterior to the anterior perforating substance the tract splits into striae, primarily lateral and medial striae, however many texts also list an intermediate striae.

The lateral striae ends in the primary olfactory area where the second order neurons synapse on third order neurons of the pyriform area; primarily in the cortex of the amygdala and entorhinal area in the temporal lobe. These third order neurons provide the primary projections from the olfactory system to the rest of the brain. Meanwhile the third order neurons found at the end of the axons of the medial striae are found in nuclei of the subcollasal and preseptal areas. We should note that some fibers from the medial striae cross at the anterior commisure to synapse in the contralateral subcollasal regions.

Projections from the primary olfactory area, the termination for the second order neurons of the lateral striae, include Brodmann Area 28.

From subcallosal nuclei projections extend through the medial forebrain bundle to the hypothalamus. Other projections carry through the retroflex fasciculus to the habenular nucleus. From the habenular nucleus and the hypothalamus projections go the reticular formation, superior salivatory nucleus, inferior salivatory nucleus, dorsal vagal nucleus and elsewhere.

Beyond fractures through the ethmoid bone which may lead to transection of the olfactory nerve and anosmia, the primary clinical consideration (at least as far as the Board Exam goes) is likely Foster-Kennedy Syndrome [PDF]. Here you get a collection of typical symptoms:

• Anosmia
• Optic Atrophy
• Papilledema
• Unilateral central scotoma
• Sometimes frontal lobe injury signs such as emotional lability or personality changes

This related to a large anterior skull base mass causing, typically unilateral, olfatory tract compression.