Cranial nerves

From Wikipedia, the free encyclopedia

Cranial nerves
Right View of the human brain from below, showing origins of cranial nerves. Left Juxtaposed skull base with foramina in which many nerves exit the skull.
Cranial nerves as they pass through the skull base to the brain.
Details
Identifiers
Latin	nervus cranialis (pl: nervi craniales)
MeSH	D003391
TA	A14.2.01.001 A14.2.00.038
FMA	5865

Cranial nerves
CN 0 – Terminal CN I – Olfactory CN II – Optic CN III – Oculomotor CN IV – Trochlear CN V – Trigeminal CN VI – Abducens CN VII – Facial CN VIII – Vestibulocochlear CN IX – Glossopharyngeal CN X – Vagus CN XI – Accessory CN XII – Hypoglossal

Cranial nerves are the nerves that emerge directly from the brain (including the brainstem), in contrast to spinal nerves (which emerge from segments of the spinal cord).^[1] 10 of 12 of the cranial nerves originate in the brainstem. Cranial nerves relay information between the brain and parts of the body, primarily to and from regions of the head and neck.^[2]

Spinal nerves emerge sequentially from the spinal cord with the spinal nerve closest to the head (C1) emerging in the space above the first cervical vertebra. The cranial nerves, however, emerge from the central nervous system above this level.^[3] Each cranial nerve is paired and is present on both sides. Depending on definition in humans there are twelve or thirteen cranial nerves pairs, which are assigned Roman numerals I–XII, sometimes also including cranial nerve zero. The numbering of the cranial nerves is based on the order in which they emerge from the brain, front to back (brainstem).^[1]

The terminal nerves, olfactory nerves (I) and optic nerves (II) emerge from the cerebrum or forebrain, and the remaining ten pairs arise from the brainstem, which is the lower part of the brain.^[1]

The cranial nerves are considered components of the peripheral nervous system (PNS),^[1] although on a structural level the olfactory, optic and trigeminal nerves are more accurately considered part of the central nervous system (CNS).^[4]

Anatomy

View of the human brain from below showing the cranial nerves on an autopsy specimen

View from below of the brain and brainstem showing the cranial nerves, numbered from olfactory to hypoglossal after the order in which they emerge

The brainstem, with deeper cranial nerve nuclei and tracts inside the brain-stem shaded red.

Most typically, humans are considered to have twelve pairs of cranial nerves (I–XII). They are: the olfactory nerve (I), the optic nerve (II), oculomotor nerve (III), trochlear nerve (IV), trigeminal nerve (V), abducens nerve (VI), facial nerve (VII), vestibulocochlear nerve (VIII), glossopharyngeal nerve (IX), vagus nerve (X), accessory nerve (XI), and hypoglossal nerve (XII). (There may be a thirteenth cranial nerve, the terminal nerve (nerve O or N), which is very small and may or may not be functional in humans^[1][3])

Terminology

Cranial nerves are generally named according to their structure or function. For example, the olfactory nerve (I) supplies smell, and the facial nerve (VII) supplies motor innervation to the face. Because Latin was the lingua franca (common language) of the study of anatomy when the nerves were first documented, recorded, and discussed, many nerves maintain Latin or Greek names, including the trochlear nerve (IV), named according to its structure, as it supplies a muscle that attaches to a pulley (Greek: trochlea). The trigeminal nerve (V) is named in accordance with its three components (Latin: trigeminus meaning triplets),^[5] and the vagus nerve (X) is named for its wandering course (Latin: vagus).^[6]

Cranial nerves are numbered based on their rostral-caudal (front-back) position,^[1] when viewing the brain. If the brain is carefully removed from the skull the nerves are typically visible in their numeric order, with the exception of the last, CN XII, which appears to emerge rostrally to (above) CN XI.^[7]

Cranial nerves have paths within and outside the skull. The paths within the skull are called "intracranial" and the paths outside the skull are called "extracranial". There are many holes in the skull called "foramina" by which the nerves can exit the skull. All cranial nerves are paired, which means that they occur on both the right and left sides of the body. The muscle, skin, or additional function supplied by a nerve on the same side of the body as the side it originates from, is referred to an ipsilateral function. If the function is on the opposite side to the origin of the nerve, this is known as a contralateral function.^[8]

Intracranial course

Nuclei

The cell bodies of many of the neurons of most of the cranial nerves are contained in one or more nuclei in the brainstem. These nuclei are important relative to cranial nerve dysfunction because damage to these nuclei such as from a stroke or trauma can mimic damage to one or more branches of a cranial nerve. In terms of specific cranial nerve nuclei, the midbrain of the brainstem has the nuclei of the oculomotor nerve (III) and trochlear nerve (IV); the pons has the nuclei of the trigeminal nerve (V), abducens nerve (VI), facial nerve (VII) and vestibulocochlear nerve (VIII); and the medulla has the nuclei of the glossopharyngeal nerve (IX), vagus nerve (X), accessory nerve (XI) and hypoglossal nerve (XII). The fibers of these cranial nerves exit the brainstem from these nuclei.^[1]

Ganglia

Some of the cranial nerves have sensory or parasympathetic ganglia (collections of cell bodies) of neurons, which are located outside the brain (but can be inside or outside the skull).^[1]

The sensory ganglia are directly correspondent to dorsal root ganglia of spinal nerves and are known as cranial sensory ganglia.^[7] Sensory ganglia exist for nerves with sensory function: V, VII, VIII, IX, X.^[3] There are also parasympathetic ganglia, which are part of the autonomic nervous system for cranial nerves III, VII, IX and X.

• The trigeminal ganglia of the trigeminal nerve (V) occupies a space in the dura mater called Trigeminal cave. This ganglion contains the cell bodies of the sensory fibers of the three branches of the trigeminal nerve.
• The geniculate ganglion of the facial nerve (VII) is found just after the nerve enters the facial canal; it contains the cell bodies of the sensory fibers of the facial nerve.
• Superior and inferior ganglia of the glossopharyngeal nerve (IX), are located just after the nerve passes through the jugular foramen and contain the cell bodies of the sensory fibers of this nerve.
• inferior ganglion of vagus nerve (nodose ganglion) is located below the jugular foramen and contains the cell bodies of the sensory fibers of the vagus nerve (X).

Exiting the skull and extracranial course

Exits of cranial nerves from the skull.^[1][9]

Location	Nerve
cribriform plate	Olfactory nerve (I)
optic foramen	Optic nerve (II)
superior orbital fissure	Oculomotor (III) Trochlear (IV) Abducens (VI) Trigeminal V1 (ophthalmic)
Foramen rotundum	Trigeminal V2 (maxillary)
Foramen ovale	Trigeminal V3 (mandibular)
internal auditory canal	Facial (VII) Vestibulocochlear (VIII)
jugular foramen	Glossopharyngeal (IX) Vagus (X) Accessory (XI)
hypoglossal canal	Hypoglossal (XII)

After emerging from the brain, the cranial nerves travel within the skull, and some must leave this bony compartment in order to reach their destinations. Often the nerves pass through holes in the skull, called foramina, as they travel to their destinations. Other nerves pass through bony canals, longer pathways enclosed by bone. These foramina and canals may contain more than one cranial nerve, and may also contain blood vessels.^[9]

• The olfactory nerve (I), actually composed of many small separate nerve fibers, passes through perforations in the cribiform plate part of the ethmoid bone. These fibers terminate in the upper part of the nasal cavity and function to convey impulses containing information about odors to the brain.
• The optic nerve (II) passes through the optic foramen in the sphenoid bone as it travels to the eye. It conveys visual information to the brain.
• The oculomotor nerve (III), trochlear nerve (IV), abducens nerve (VI) and the ophthalmic branch of the trigeminal nerve (V1) travel through the cavernous sinus into the superior orbital fissure, passing out of the skull into the orbit. These nerves control the small muscles that move the eye and also provide sensory innervation to the eye and orbit.
• The maxillary division of the trigeminal nerve (V2) passes through foramen rotundum in the sphenoid bone to supply the skin of the middle of the face.
• The mandibular division of the trigeminal nerve (V3) passes through foramen ovale of the sphenoid bone to supply the lower face with sensory innervation. This nerve also sends branches to almost all of the muscles that control chewing.
• The facial nerve (VII) and vestibulocochlear nerve (VIII) both enter the internal auditory canal in the temporal bone. The facial nerve then reaches the side of the face by using the stylomastoid foramen, also in the temporal bone. Its fibers then spread out to reach and control all of the muscles of facial expression. The vestibulocochlear nerve reaches the organs that control balance and hearing in the temporal bone, and therefore does not reach the external surface of the skull.
• The glossopharyngeal (IX), vagus (X) and accessory nerve (XI) all leave the skull via the jugular foramen to enter the neck. The glossopharyngeal nerve provides innervation to the upper throat and the back of the tongue, the vagus provides innervation to the muscles in the voicebox, and continues downward to supply parasympathetic innervation to the chest and abdomen. The accessory nerve controls the trapezius and sternocleidomastoid muscles in the neck and shoulder.
• The hypoglossal nerve (XII) exits the skull using the hypoglossal canal in the occipital bone and reaches the tongue to control almost all of the muscles involved in movements of this organ.^[1]

Function

The cranial nerves provide motor and sensory innervation mainly to the structures within the head and neck. The sensory innervation includes both "general" sensation such as temperature and touch, and "special" innervation such as taste, vision, smell, balance and hearing^[1][10]

The vagus nerve (X) provides sensory and autonomic (parasympathetic) motor innervation to structures in the neck and also to most of the organs in the chest and abdomen.^[1][3]

Smell (I)

The olfactory nerve (I) conveys the sense of smell.

Damage to the olfactory nerve (I) can cause an inability to smell (anosmia), a distortion in the sense of smell (parosmia), or a distortion or lack of taste. If there is suspicion of a change in the sense of smell, each nostril is tested with substances of known odors such as coffee or soap. Intensely smelling substances, for example ammonia, may lead to the activation of pain receptors (nociceptors) of the trigeminal nerve that are located in the nasal cavity and this can confound olfactory testing.^[1][11]

Vision (II)

The optic nerve (II) transmits visual information.^[3][10]

Damage to the optic nerve (II) affects specific aspects of vision that depend on the location of the lesion. A person may not be able to see objects on their left or right sides (homonymous hemianopsia), or may have difficulty seeing objects on their outer visual fields (bitemporal hemianopsia) if the optic chiasm is involved.^[12] Vision may be tested by examining the visual field, or by examining the retina with an ophthalmoscope, using a process known as funduscopy. Visual field testing may be used to pin-point structural lesions in the optic nerve, or further along the visual pathways.^[11]

Eye movement (III, IV, VI)

Various deviations of the eyes due to abnormal function of the targets of the cranial nerves

The oculomotor nerve (III), trochlear nerve (IV) and abducens nerve (VI) coordinate eye movement.

Damage to nerves III, IV, or VI may affect the movement of the eyeball (globe). Both or one eye may be affected; in either case double vision (diplopia) will likely occur because the movements of the eyes are no longer synchronized. Nerves III, IV and VI are tested by observing how the eye follows an object in different directions. This object may be a finger or a pin, and may be moved at different directions to test for pursuit velocity.^[11] If the eyes do not work together, the most likely cause is damage to a specific cranial nerve or its nuclei.^[11]

Damage to the oculomotor nerve (III) can cause double vision (diplopia) and inability to coordinate the movements of both eyes (strabismus), also eyelid drooping (ptosis) and pupil dilation (mydriasis).^[12][12] Lesions may also lead to inability to open the eye due to paralysis of the levator palpebrae muscle. Individuals suffering from a lesion to the oculomotor nerve may compensate by tilting their heads to alleviate symptoms due to paralysis of one or more of the eye muscles it controls.^[11]

Damage to the trochlear nerve (IV) can also cause diplopia with the eye adducted and elevated.^[12] The result will be an eye which can not move downwards properly (especially downwards when in an inward position). This is due to impairment in the superior oblique muscle, which is innervated by the trochlear nerve.^[11]

Damage to the abducens nerve (VI) can also result in diplopia.^[12] This is due to impairment in the lateral rectus muscle, which is innervated by the abducens nerve.^[11]

Trigeminal nerve (V)

The trigeminal nerve (V) comprises three distinct parts: The Ophthalmic (V1), the Maxillary (V2), and the Mandibular (V3) nerves. Combined, these nerves provide sensation to the skin of the face and also controls the muscles of mastication (chewing).^[1] Conditions affecting the trigeminal nerve (V) include trigeminal neuralgia,^[1] cluster headache,^[13] and trigeminal zoster.^[1] Trigeminal neuralgia occurs later in life, from middle age onwards, most often after age 60, and is a condition typically associated with very strong pain distributed over the area innervated by the maxillary or mandibular nerve divisions of the trigeminal nerve (V₂ and V₃).^[14]

The facial nerve passes through the petrous temporal bone, internal auditory meatus, facial canal, stylomastoid foramen, and then the parotid gland.

Facial expression (VII)

Lesions of the facial nerve (VII) may manifest as facial palsy. This is where a person is unable to move the muscles on one or both sides of their face. A very common and generally temporary facial palsy is known as Bell's palsy. Bell's Palsy is the result of an idiopathic (unknown cause), unilateral lower motor neuron lesion of the facial nerve and is characterized by an inability to move the ipsilateral muscles of facial expression, including elevation of the eyebrow and furrowing of the forehead. Patients with Bell's palsy often have a drooping mouth on the affected side and often have trouble chewing because the buccinator muscle is affected.^[1] Bell's palsy occurs very rarely, affecting around 40,000 Americans annually. There are studies in mice and humans suggesting members of the family Herpesviridae are capable of producing Bell's palsy. Facial paralysis may be caused by other conditions including stroke, and similar conditions to Bell's Palsy are occasionally misdiagnosed as Bell's Palsy.^[15] Bell's Palsy is a temporary condition usually lasting 2-6 months, but can have life-changing effects and can reoccur. Strokes typically also affect the seventh cranial nerve by cutting off blood supply to nerves in the brain that signal this nerve and so can present with similar symptoms.

Hearing and balance (VIII)

The vestibulocochlear nerve (VIII) splits into the vestibular and cochlear nerve. The vestibular part is responsible for innervating the vestibules and semicircular canal of the inner ear; this structure transmits information about balance, and is an important component of the vestibuloocular reflex, which keeps the head stable and allows the eyes to track moving objects. The cochlear nerve transmits information from the cochlea, allowing sound to be heard.^[3]

When damaged, the vestibular nerve may give rise to the sensation of spinning and dizziness. Function of the vestibular nerve may be tested by putting cold and warm water in the ears and watching eye movements caloric stimulation.^[1][11] Damage to the vestibulocochlear nerve can also present as repetitive and involuntary eye movements (nystagmus), particularly when looking in a horizontal plane.^[11] Damage to the cochlear nerve will cause partial or complete deafness in the affected ear.^[11]

Oral sensation, taste, and salivation (IX)

Deviating uvula due to cranial nerve IX lesion

The glossopharyngeal nerve (IX) innervates the stylopharyngeus muscle and provides sensory innervation to the oropharynx and back of the tongue.^[1][16] The glossopharyngeal nerve also provides parasympathetic innervation to the parotid gland.^[1] Unilateral absence of a gag reflex suggests a lesion of the glossopharyngeal nerve (IX), and perhaps the vagus nerve (X).^[17]

Vagus nerve (X)

Loss of function of the vagus nerve (X) will lead to a loss of parasympathetic innervation to a very large number of structures. Major effects of damage to the vagus nerve may include a rise in blood pressure and heart rate. Isolated dysfunction of only the vagus nerve is rare, but can be diagnosed by a hoarse voice, due to dysfunction of one of its branches, the recurrent laryngeal nerve.^[1]

Damage to this nerve may result in difficulties swallowing.^[11]

Shoulder elevation and head-turning (XI)

Winged scapula may occur due to lesion of the spinal accessory.

Damage to the accessory nerve (XI) will lead to ipsilateral weakness in the trapezius muscle. This can be tested by asking the subject to raise their shoulders or shrug, upon which the shoulder blade (scapula) will protrude into a winged position.^[1] Additionally, if the nerve is damaged, weakness or an inability to elevate the scapula may be present because the levator scapulae muscle is now solely able to provide this function.^[14] Depending on the location of the lesion there may also be weakness present in the sternocleidomastoid muscle, which acts to turn the head so that the face points to the opposite side.^[1]

Tongue movement (XII)

A damaged hypoglossal nerve will result in an inability to stick the tongue out straight.

A case with unilateral hypoglossal nerve injury in branchial cyst surgery. ^[18]

The hypoglossal nerve (XII) is unique in that it is innervated from the motor cortices of both hemispheres of the brain. Damage to the nerve at lower motor neuron level may lead to fasciculations or atrophy of the muscles of the tongue. The fasciculations of the tongue are sometimes said to look like a "bag of worms". Upper motor neuron damage will not lead to atrophy or fasciculations, but only weakness of the innervated muscles.^[11]

When the nerve is damaged, it will lead to weakness of tongue movement on one side. When damaged and extended, the tongue will move towards the weaker or damaged side, as shown in the image.^[11]

Clinical significance

Examination

Physicians, neurologists, and other medical professionals may conduct a cranial nerve examination as part of a neurological examination to examine the functionality of the cranial nerves. This is a highly formalized series of tests that assess the status of each nerve.^[19] A cranial nerve exam begins with observation of the patient because some cranial nerve lesions may affect the symmetry of the eyes or face. The visual fields are tested for nerve lesions or nystagmus via an analysis of specific eye movements. The sensation of the face is tested, and patients are asked to perform different facial movements, such as puffing out of the cheeks. Hearing is checked by voice and tuning forks. The position of the patient's uvula is examined because asymmetry in the position could indicate a lesion of the glossopharyngeal nerve. After the ability of the patient to use their shoulder to assess the accessory nerve (XI), and the patient's tongue function is assessed by observing various tongue movements.^[1][19]

Damage

Compression

Nerves may be compressed because of increased intracranial pressure, a mass effect of an intracerebral haemorrhage, or tumour that presses against the nerves and interferes with the transmission of impulses along the nerve.^[20] A loss of functionality of a single cranial nerve may sometimes be the first symptom of an intracranial or skull base cancer.^[21]

An increase in intracranial pressure may lead to impairment of the optic nerves (II) due to compression of the surrounding veins and capillaries, causing swelling of the eyeball (papilloedema).^[22] A cancer, such as an optic glioma, may also impact the optic nerve (II). A pituitary tumour may compress the optic tracts or the optic chiasm of the optic nerve (II), leading to visual field loss. A pituitary tumour may also extend into the cavernous sinus, compressing the oculuomotor nerve (III), trochlear nerve (IV) and abducens nerve (VI), leading to double-vision and strabismus. These nerves may also be affected by herniation of the temporal lobes of the brain through the falx cerebri.^[20]

The cause of trigeminal neuralgia, in which one side of the face is exquisitely painful, is thought to be compression of the nerve by an artery as the nerve emerges from the brain stem.^[20] An acoustic neuroma, particularly at the junction between the pons and medulla, may compress the facial nerve (VII) and vestibulocochlear nerve (VIII), leading to hearing and sensory loss on the affected side.^[20][23]

Stroke

Occlusion of blood vessels that supply the nerves or their nuclei, an ischemic stroke, may cause specific signs and symptoms that can localise where the occlusion occurred. A clot in a blood vessel draining the cavernous sinus (cavernous sinus thrombosis) affects the oculomotor (III), trochlear (IV), opthalamic branch of the trigeminal nerve (V1) and the abducens nerve (VI).^[23]

Inflammation

Inflammation resulting from infection may impair the function of any of the cranial nerves. Inflammation of the facial nerve (VII) may result in Bell's palsy.^[24]

Multiple sclerosis, an inflammatory process that may produce a loss of the myelin sheathes which surround the cranial nerves, may cause a variety of shifting symptoms affecting multiple cranial nerves.^[24]

Other

Trauma to the skull, disease of bone such as Paget's disease, and injury to nerves during neurosurgery (such as tumor removal) are other possible causes of cranial nerve damage.^[23]

History

The Graeco-Roman anatomist Galen (AD 129–210) named seven pairs of cranial nerves.^[25] Much later, in 1664, English anatomist Sir Thomas Willis suggested that there were actually 9 pairs of nerves. Finally, in 1778, German anatomist Samuel Soemmering named the 12 pairs of nerves that are generally accepted today.^[25] However, because many of the nerves emerge from the brain stem as rootlets, there is continual debate as to how many nerves there actually are, and how they should be grouped.^[25] There is reason to consider both the olfactory (I) and Optic (II) nerves to be brain tracts, rather than cranial nerves.^[25] Further, the very small terminal nerve (nerve N or O) exists in humans but may not be functional. In other animals, it appears to be important to sexual receptivity based on perceptions of phermones^[1][26]

Other animals

Dog-fish brain in two projections.
top; ventral bottom; lateral
The accessory nerve (XI) and hypoglossal nerve (XII) cannot be seen, as they are not always present in all vertebrates.

Cranial nerves are also present in other vertebrates. Other amniotes (non-amphibian tetrapods) have cranial nerves similar to those of humans. In anamniotes (fishes and amphibians), the accessory nerve (XI) and hypoglossal nerve (XII) do not exist, with the accessory nerve (XI) being an integral part of the vagus nerve (X); the hypoglossal nerve (XII) is represented by a variable number of spinal nerves emerging from vertebral segments fused into the occiput. These two nerves only became discrete nerves in the ancestors of amniotes (non-amphibian tetrapods).^[27]

• 

  Diagrammatic view of the cranial nerves of the horse.
• 

  Ventral view of the sheep's brain. The exits of the various cranial nerves are marked with red.

Thalamus

From Wikipedia, the free encyclopedia

 

Thalamus
thalamus marked (MRI cross-section)
anterolateral view
Details
Part of	Diencephalon
Parts	See List of thalamic nuclei
Artery	Posterior cerebral artery and branches
Identifiers
Latin	thalamus dorsalis
MeSH	D013788
NeuroNames	300
NeuroLex ID	birnlex_954
TA	A14.1.08.101 A14.1.08.601
TE	E5.14.3.4.2.1.8
FMA	62007
Anatomical terms of neuroanatomy [edit on Wikidata]

The thalamus (from Greek θάλαμος, "chamber")^[1] is the large mass of gray matter in the dorsal part of the diencephalon of the brain with several functions such as relaying of sensory signals, including motor signals, to the cerebral cortex,^{[2][3][page needed]} and the regulation of consciousness, sleep, and alertness.^[4]

It is a midline symmetrical structure of two halves, within the vertebrate brain, situated between the cerebral cortex and the midbrain.

It is the main product of the embryonic diencephalon, as first assigned by Wilhelm His, Sr. in 1893.^[5]

Anatomy

The thalamus in a 360° rotation

The thalamus is located in the forebrain which is superior to the midbrain, near the center of the brain, with nerve fibers projecting out to the cerebral cortex in all directions. The medial surface of the thalamus constitutes the upper part of the lateral wall of the third ventricle, and is connected to the corresponding surface of the opposite thalamus by a flattened gray band, the interthalamic adhesion.

Blood supply

The thalamus derives its blood supply from a number of arteries: the polar artery (posterior communicating artery), paramedian thalamic-subthalamic arteries, inferolateral (thalamogeniculate) arteries, and posterior (medial and lateral) choroidal arteries.^[6] These are all branches of the posterior cerebral artery.^[7]

Some people have the artery of Percheron, which is a rare anatomic variation in which a single arterial trunk arises from the posterior cerebral artery to supply both parts of the thalamus.

Thalamic nuclei

Nuclei of the thalamus

The thalamus is part of a nuclear complex structured of four parts, the hypothalamus, epithalamus, prethalamus (formerly called ventral thalamus), and dorsal thalamus.^{[8][need quotation to verify]}

Derivatives of the diencephalon also include the dorsally-located epithalamus (essentially the habenula and annexes) and the perithalamus (prethalamus) containing the zona incerta and the thalamic reticular nucleus. Due to their different ontogenetic origins, the epithalamus and the perithalamus are formally distinguished from the thalamus proper.

The thalamus comprises a system of lamellae (made up of myelinated fibers) separating different thalamic subparts. Other areas are defined by distinct clusters of neurons, such as the periventricular nucleus, the intralaminar elements, the "nucleus limitans", and others.^[9] These latter structures, different in structure from the major part of the thalamus, have been grouped together into the allothalamus as opposed to the isothalamus.^[10] This distinction simplifies the global description of the thalamus.

Connections

The thalamus is connected to the spinal cord via the spinothalamic tract.

The thalamus is manifoldly connected to the hippocampus via the mammillo-thalamic tract, this tract comprises the mammillary bodies and fornix.^[11]

The thalamus is connected to the cerebral cortex via the thalamocortical radiations.^[12]

The spinothalamic tract is a sensory pathway originating in the spinal cord. It transmits information to the thalamus about pain, temperature, itch and crude touch. There are two main parts: the lateral spinothalamic tract, which transmits pain and temperature, and the anterior (or ventral) spinothalamic tract, which transmits crude touch and pressure.

Function

The thalamus has multiple functions, generally believed to act as a relay station, or hub, relaying information between different subcortical areas and the cerebral cortex.^[13] In particular, every sensory system (with the exception of the olfactory system) includes a thalamic nucleus that receives sensory signals and sends them to the associated primary cortical area.^{[citation needed]} For the visual system, for example, inputs from the retina are sent to the lateral geniculate nucleus of the thalamus, which in turn projects to the visual cortex in the occipital lobe.^{[citation needed]} The thalamus is believed to both process sensory information as well as relay it—each of the primary sensory relay areas receives strong feedback connections from the cerebral cortex.^{[citation needed]} Similarly the medial geniculate nucleus acts as a key auditory relay between the inferior colliculus of the midbrain and the primary auditory cortex.^{[citation needed]} The ventral posterior nucleus is a key somatosensory relay, which sends touch and proprioceptive information to the primary somatosensory cortex.^{[citation needed]}

The thalamus also plays an important role in regulating states of sleep and wakefulness.^[14] Thalamic nuclei have strong reciprocal connections with the cerebral cortex, forming thalamo-cortico-thalamic circuits that are believed to be involved with consciousness.^{[citation needed]} The thalamus plays a major role in regulating arousal, the level of awareness, and activity. Damage to the thalamus can lead to permanent coma.^{[citation needed]}

The role of the thalamus in the more anterior pallidal and nigral territories in the basal ganglia system disturbances is recognized but still poorly understood. The contribution of the thalamus to vestibular or to tectal functions is almost ignored. The thalamus has been thought of as a "relay" that simply forwards signals to the cerebral cortex. Newer research suggests that thalamic function is more selective.^[15] Many different functions are linked to various regions of the thalamus. This is the case for many of the sensory systems (except for the olfactory system), such as the auditory, somatic, visceral, gustatory and visual systems where localized lesions provoke specific sensory deficits. A major role of the thalamus is support of motor and language systems, and much of the circuitry implicated for these systems is shared. The thalamus is functionally connected to the hippocampus^[16] as part of the extended hippocampal system at the thalamic anterior nuclei^[17] with respect to spatial memory and spatial sensory datum they are crucial for human episodic memory and rodent event memory.^[18][19] There is support for the hypothesis that thalamic regions connection to particular parts of the mesio-temporal lobe provide differentiation of the functioning of recollective and familiarity memory.^[11]

The neuronal information processes necessary for motor control were proposed as a network involving the thalamus as a subcortical motor center.^[20] Through investigations of the anatomy of the brains of primates^[21] the nature of the interconnected tissues of the cerebellum to the multiple motor cortices suggested that the thalamus fulfills a key function in providing the specific channels from the basal ganglia and cerebellum to the cortical motor areas.^[22][23] In an investigation of the saccade and antisaccade^[24] motor response in three monkeys, the thalamic regions were found to be involved in the generation of antisaccade eye-movement (that is, the ability to inhibit the reflexive jerking movement of the eyes in the direction of a presented stimulus].^[25]

Recent research suggests that the mediodorsal thalamus may play a broader role in cognition. Specifically, the mediodorsal thalamus may "amplify the connectivity (signaling strength) of just the circuits in the cortex appropriate for the current context and thereby contribute to the flexibility (of the mammalian brain) to make complex decisions by wiring the many associations on which decisions depend into weakly connected cortical circuits."^[26] Researchers founds that "enhancing MD activity magnified the ability of mice to “think,”^[26] driving down by more than 25 percent their error rate in deciding which conflicting sensory stimuli to follow to find the reward." ^[27]

Development

The thalamic complex is composed of the perithalamus (or prethalamus, previously also known as ventral thalamus), the mid-diencephalic organiser (which forms later the zona limitans intrathalamica (ZLI) ) and the thalamus (dorsal thalamus).^[28][29] The development of the thalamus can be subdivided into three steps.^[30] The thalamus is the largest structure deriving from the embryonic diencephalon, the posterior part of the forebrain situated between the midbrain and the cerebrum.

Early brain development

After neurulation the anlage of the prethalamus and the thalamus is induced within the neural tube. Data from different vertebrate model organisms support a model in which the interaction between two transcription factors, Fez and Otx, are of decisive importance. Fez is expressed in the prethalamus, and functional experiments show that Fez is required for prethalamus formation.^[31][32] Posteriorly, Otx1 and Otx2 abut the expression domain of Fez and are required for proper development of the thalamus.^[33][34]

Formation of progenitor domains

Early in thalamic development two progenitor domains form, a caudal domain (TH-C) and a rostral domain (TH-R). The caudal domain gives rise to all of the glutamatergic neurons in the adult thalamus while the rostral domain gives rise to all of the GABAergic neurons in the adult thalamus.^[35]

The formation of the mid-diencephalic organiser (MDO)

At the interface between the expression domains of Fez and Otx, the mid-diencephalic organizer (MDO, also called the ZLI organiser) is induced within the thalamic anlage. The MDO is the central signalling organizer in the thalamus. A lack of the organizer leads to the absence of the thalamus. The MDO matures from ventral to dorsal during development. Members of the SHH family and of the Wnt family are the main principal signals emitted by the MDO.

Besides its importance as signalling center, the organizer matures into the morphological structure of the zona limitans intrathalamica (ZLI).

Maturation and parcellation of the thalamus

After its induction, the MDO starts to orchestrate the development of the thalamic anlage by release of signalling molecules such as SHH.^[36] In mice, the function of signaling at the MDO has not been addressed directly due to a complete absence of the diencephalon in SHH mutants.^[37]

Studies in chicks have shown that SHH is both necessary and sufficient for thalamic gene induction.^[38] In zebrafish, it was shown that the expression of two SHH genes, SHH-a and SHH-b (formerly described as twhh) mark the MDO territory, and that SHH signaling is sufficient for the molecular differentiation of both the prethalamus and the thalamus but is not required for their maintenance and SHH signaling from the MDO/alar plate is sufficient for the maturation of prethalamic and thalamic territory while ventral Shh signals are dispensable.^[39]

The exposure to SHH leads to differentiation of thalamic neurons. SHH signaling from the MDO induces a posterior-to-anterior wave of expression the proneural gene Neurogenin1 in the major (caudal) part of the thalamus, and Ascl1 (formerly Mash1) in the remaining narrow stripe of rostral thalamic cells immediately adjacent to the MDO, and in the prethalamus.^[40][41]

This zonation of proneural gene expression leads to the differentiation of glutamatergic relay neurons from the Neurogenin1+ precursors and of GABAergic inhibitory neurons from the Ascl1+ precursors. In fish, selection of these alternative neurotransmitter fates is controlled by the dynamic expression of Her6 the homolog of HES1. Expression of this hairy-like bHLH transcription factor, which represses Neurogenin but is required for Ascl1, is progressively lost from the caudal thalamus but maintained in the prethalamus and in the stripe of rostral thalamic cells. In addition, studies on chick and mice have shown that blocking the Shh pathway leads to absence of the rostral thalamus and substantial decrease of the caudal thalamus. The rostral thalamus will give rise to the reticular nucleus mainly whereby the caudal thalamus will form the relay thalamus and will be further subdivided in the thalamic nuclei.^[30]

In humans, a common genetic variation in the promotor region of the serotonin transporter (the SERT-long and -short allele: 5-HTTLPR) has been shown to affect the development of several regions of the thalamus in adults. People who inherit two short alleles (SERT-ss) have more neurons and a larger volume in the pulvinar and possibly the limbic regions of the thalamus. Enlargement of the thalamus provides an anatomical basis for why people who inherit two SERT-ss alleles are more vulnerable to major depression, posttraumatic stress disorder, and suicide.^[42]

Clinical significance

A cerebrovascular accident (stroke) can lead to the thalamic syndrome,^[43] which involves a one-sided burning or aching sensation often accompanied by mood swings. Bilateral ischemia of the area supplied by the paramedian artery can cause serious problems including akinetic mutism, and be accompanied by oculomotor problems. A related concept is thalamocortical dysrhythmia. The occlusion of the artery of Percheron can lead to a bilateral thalamus infarction.

Korsakoff's syndrome stems from damage to the mammillary body, the mammillothalamic fasciculus or the thalamus.

Fatal familial insomnia is a hereditary prion disease in which degeneration of the thalamus occurs, causing the patient to gradually lose his ability to sleep and progressing to a state of total insomnia, which invariably leads to death. In contrast, damage to the thalamus can result in coma.

Additional images

Drawings are by Gray and Carter (1858).^[44]

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  The left optic nerve and the optic tracts.
  
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  Coronal section of lateral and 3rd ventricles.
  
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  Dissection showing the ventricles of the brain.
  
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  Section of brain showing upper surface of temporal lobe.
  
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  Horizontal section of right cerebral hemisphere.
  
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  Mesal aspect of a brain sectioned in the median sagittal plane.
  
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  Schematic representation of the chief ganglionic categories (I to V).
  
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  Scheme showing the course of the fibers of the lemniscus; medial lemniscus in blue, lateral in red.
  
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  Deep dissection of brain-stem. Lateral view.
  
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  Deep dissection of brain-stem. Ventral view.
  
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  Coronal section of brain immediately in front of pons.
  
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  Coronal section of brain through intermediate mass of third ventricle.
  
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  Human brain frontal (coronal) section
  
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  Thalamus
  
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  Ventricles of brain and basal ganglia. Superior view. Horizontal section. Deep dissection
  
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  Ventricles of brain and basal ganglia. Superior view. Horizontal section. Deep dissection