TEST 2

Outline for oral and nasal cavity

I. Moutha. Subdivisions of the mouth

i. Vestibule: communicates posterior and directly with the oropharynx. 1. Boundaries

1. Anterior: lips2. Lateral: cheek composed of buccal mucosa and buccinators muscle. Parotid duct pierces the buccinators muscle and

empties into the vestibule opposite the 2nd maxillary molar. 3. Medial: teeth. The interval between the teeth and buccal mucosa contains the free and attached gingival (gums).

ii. Mouth (oral) cavity proper1. The roof of the mouth is positioned superior. The roof of the mouth is the same as the floor of the nasal cavity. The hard and the

soft palate separate the nasal cavity from the oral cavity. 1. Hard palate: formed by the palatine processes of the maxilla and horizontal plates of the palatine bones. 2. Soft palate: formed by five muscles

i. Tensor veli palatine muscle 1. Origin: sphenoid spine2. Insertion: muscle of other side and forms palatine aponeurosis3. Innervated by CN V3 via otic ganglion4. Action: tenses soft palate

ii. Levator veli palatine muscle 1. Origin: temporal bone

2. Insertion: palatine aponeurosis

3. Action: raises soft palateiii. Palatoglossus muscle

1. Origin: soft palate

2. Insertion: side of the tongue (posterior side)

3. Action: pulls roots of tongue upward and backward

4. Innervation: pharyngeal branch of CN X via pharyngeal plexus) iv. Palatopharyngeus muscle

1. Origin: palatine aponeurosis

2. Insertion: lamina of thyroid cartilage

3. Action: elevates wall of pharynx

4. Innervations: pharyngeal plexus (CN X) v. Uvula muscle

1. Origin: hard palate

2. Insertion: mucous membrane of uvula

3. Action: elevates uvula

4. Innervations: pharyngeal plexus (CN X)2. The floor of the mouth:

1. Made by the anterior two-thirds of the tongue (innervated by chorda tympani nerve from facial nerve, which follows the lingual nerve from the mandibular division of the trigeminal) and mucous membrane from sides of the tongue to the mandible. The mucosa has a sublingual fold and underneath the fold is the sublingual gland. It is also the drainage site for the sublingual salivary gland

2. Muscles i. Geniohyoid muscle

1. Origin: mental spine of the mandible2. Insertion: hyoid bone3. Innervation: 1st cervical nerve4. Action: pulls hypoid anterior

ii. Mylohyoid muscle1. Origin: mylohyoid line of mandible2. Insertion: hyoid bone3. Innervations: inferior alveolar nerve4. Action: elevates hyoid and floor of mouth or depresses mandible.

iii. Anterior belly of digastrics muscle1. Origin: mandible body2. Insertion: hyoid bone3. Innervation: inferior alveolar neve4. Action: depresses the mandible.

3. Nerves: i. Lingual nerve branch of CN V3

ii. Hypoglossal nerve (CN XII)3. Posterior: palatoglossal arch. Beneth this is the palatoglossal muscle. 4. Blood supply to the mouth

1. Lips: superior and inferior labile branches of the facial artery2. Cheek: transverse facial artery of the superficial temporal artery and the buccal artery from the maxillary artery3. Teeth: in the maxilla teeth supplied by posterior, middle and anterior superior alveolar arteries from the maxillary

artery. In the mandible teeth are supplied by the inferior alveolar artery. 4. Tongue: lingual and deep lingual arteries.

5. Palate: greater palatine branch of maxillary artery and palatine branches of facial and ascending pharyngeal artery. II. Tongue

a. Sulcusi. Median sulcus (midline groove): a longitudinal furrow that divides the tongue into the right and left halves.

ii. Terminal sulcus: divides the anterior 2/3 of the tongue in the mouth from the posterior 1/3 in the pharynxb. Foramen cecum: embryological remnant of the thyroid gland and a site of upper end of the thyroglossal duct in the embryo. c. Divisions

i. Anterior 2/3 surface:1. Contains filiform (keratinized epithelium) which are the most numerous, fungiform and circumvallate papillae (contains taste

buds and are found just anterior to the sulcus terminalis). 2. Innervated by lingual (CN V3 sensation) and chorda tympani (CN VII taste).

ii. Posterior 1/3 surface1. devoid of papillae, but contains underlying lymph nodules called the lingual tonsils. The lingual tonsils are posterior to the sulcus

terminalis. These are small irregular elevations of the dorsal surface of the tongue. 2. Innervated by the glossopharyngeal nerve (CN IX) does sensation and taste.

iii. Undersurface 1. Lined by non-keratinized stratified squamous epithelium and is smooth. 2. The frenulum attaches to the tongue to the mucosa covering the floor of the oral cavity. 3. Sublingual folds, located at the frenulum, contain salivary openings of the submandibular and sublingual ducts that provide egress

for salivary secretions produced by their respective glands. iv. Root of the tongue

1. Epiglottis is posterior to the root of the tongue. 2. Median and lateral glossoepiglottic folds can be seen. The vallecula is between these folds.

d. Muscles of the tongue: all supplied by the hypoglossal nerve (CN XII) except the palatoglossus muscle (which is innervated by the pharyngeal plexus via the Vagus nerve (CN X).

i. Extrinsic muscles – are attached to the bone or soft palate then to the tongue (four different origins)1. Palatoglossus muscle

1. Origin: soft palate. 2. Action: elevates the tongue.3. Innervation: pharyngeal plexus of CN X

2. Styloglossus muscle 1. Origin: styloid process of the temporal bone2. Action: elevates and retracts the tongue.3. Innervation: CN XII

3. Hyoglossus muscle 1. Origin: hyoid bone.2. Action: depresses and retracts the tongue

3. Innervation: CN XII4. Genioglossus muscle

1. Origin: mandible.2. Action: protrudes and retracts the tongue3. Innervation: CN XII)4. Paralysis of the genioglossus muscle: results in the tongue being shifted posterior. This can cause obstruction of the

airway and can lead to suffocation.ii. Intrinsic muscles – have longitudinal, transverse and vertical skeletal muscle fibers. All muscles of the tongue are supplied by the

hypoglossal nerve (CN XII) except the palatoglossus muscle. e. Nerve damage and reflexes

i. Hypoglossal nerve damage: results in paralysis of one side of the tongue. Tongue shifts to the damaged side during protrusion due to anchoring effect of the inactive side.

ii. Gag reflex: patient will gag when you touch the pharyngeal segment of the tongue. This reflex is promoted via the glossopharyngeal nerve (CN IX), which is important in swallowing and in salivation.

III. Nosea. Bones

i. Two nasal bones that articulate with the frontal bone and the maxilla. b. Cartilages

i. Alar cartilage ii. Septal cartilage

iii. Made up of hylain cartilage. c. Nasal cavity

i. Extends anterior from the nares (vestibule) of the nose to the choanae (posterior). The choanea is at the end of the nasal septum. ii. The roof of the nasal cavity is formed by

1. Nasal bone2. Frontal bone3. Ethmoid bone4. sphenoid bone5. The ethmoid and sphenoid bones form the sphenoethmoid recess.

iii. The floor of the nasal cavity formed by1. Palatine processes of the maxilla 2. Horizontal plates of the palatine bones3. Portion of the soft palate

iv. Lateral wall of the nasal cavity is formed by 1. Nasal bone2. Frontral process of the maxilla

3. Superior and middle conchae of the ethmoid bone. These are also called turbinate because it creates turbulances as air is mixed with the mucosa to warm it.

4. Inferior nasal conchae5. Lacrimal bone

d. Medial nasal septum separates the nasal cavity into two chambersi. Formed by

1. Perpendicular plate of the ethmoid bone2. Septal cartilage of the nose3. Vomer bone: articulates with the sphenoid, ethmoid, septal cartilage, maxilla and the palatine bone.

e. Mucoperiosteum covers all the surfaces of the nasal cavity and lines the paranasal sinuses.f. The area of the lateral wall underlying a respective concha is called a meatus

i. Superior concha (Superior meatus): openings of the posterior ethmoidal air cells. ii. Middle concha (Middle meatus): ethmoidal bulla, hiatus, semilunaris and opening of the infundibulum. The frontal sinus, anterior and

middle ethmoidal cells and maxillary sinus opens to these areas. iii. Inferior concha (Inferior meatus): opening of the nasolacrimal duct

g. Arterial supply of the nasal cavityi. Sphenopalatine artery is derived from the maxillary artery and is the major supply of the nasal cavity. This is a terminal branch of the

maxillary artery. ii. Epistaxis: the nasal mucosa has a rich blood supply and results from anastomosis of five arteries. Bleeding from the nose (epistaxis)

usually occurs from the anterior third of the nose (Kiesselbach’s area) h. Nerve supply to the nasal cavity

i. Olfactory nerve (CN 1) supplies the olfactory mucosa with special sensory supply for olfaction.ii. Maxillary division of the trigeminal nerve (CN V2 – nasopalatine nerve) supplies the medial nasal septum with general sensory

innovation. IV. Paranasal sinuses and the nasolacrimal duct drains into the various meati of the nasal cavity.

a. Function of the sinuses is to make the head lighter and for resonance of the voice when speaking. b. Sinuses

i. Frontal sinuses1. In the frontal bone 2. Mucus from the frontal sinus drains via the frontonasal duct into the infundibulum which in turn drains via the semilunar hiatus

into the middle meatus. 3. Receives blood from the supratrochlear and supraorbital arteries of the ophthalmic artery.

ii. Ethmoidal (aircells) sinuses1. These sinuses are referred to as the ethmoidal cells or the ethmoidal air cells. 2. Three divisions

1. Anterior ethmoidal sinuses drain via the semilunar hiatus into the middle meatus.

2. Middle ethmoidal sinuses drains via an opening in the ethmoidal bulla into the semilunar hiatus ultimately into the middle meatus.

3. Posterior ethmoid sinus drains in the superior meatus. 3. Receives blood from the anterior and posterior ethmoid arteries of the ophthalmic artery anterior and posterior ethmoid artery.

iii. Sphenoid sinus 1. In the sphenoid bone. 2. Drains in the sphenoethmoidal recess. 3. Receives blood from meningeal arteries of maxillary artery and posterior ethmoid artery.

iv. Maxillary sinus1. In the maxilla. This is the largest sinus. 2. Drains via the semilunar hiatus into the middle meatus. 3. Receives blood from the posterior superior alveolar branch from the sphenopalatine artery of maxillary atery and the middle and

anterior superior alveolar arteries of the maxillary artery. v. The nasolacrimal duct that drains the lacrimal sac drains into the inferior nasal meatus.

c. Nerve supply to the paranasal sinusesi. Ophthalmic nerve (CN V1)

ii. Maxillary nerve (CN V2)

V. Regions of the pharynxa. Nasopharynx

i. Lies posterior to the choanea, base of the skull and superior to a plane drawn posterior from the soft palate.

ii. The nasal cavity opens into the nasopharynx. iii. Contains

1. Auditory (Eustachian) tube that enters the area posterior to the inferior meatus demonstrated by eminence called the torus tubarius. Under the mucosa, the tensor veli palatine (descending anteriorly and vertically to the soft palate) and posteriorly the levator veli palatine muscle (passes medially and obliquely to the palate) are seen.

2. Pharyngeal recess Pharyngeal tonsils (adenoids) are located deep to the mucosal surface. 3. Salphingopharyngeal fold overlying the salphingopharyngeal muscle.

b. Oropharynx i. Lies posterior to the palatoglossal arches and situated below the nasopharynx.

ii. Extends inferior to the base of the tongue and epiglottis of the larynx. (elastic cartilage is on the epiglottis) iii. The palatoglossal arch/fold is anterioriv. The palatopharyngeal arch/fold is posteriorv. The palatine tonsils are found between the two arches, which are referred to as a fauces or faucial arches.

1. Palatine Tonsils1. Composed of lymphoid tissue2. Location

i. These tonsils reside in the tonsillar bed between the palatoglossal and palatopharyngeal arches/folds. ii. The floor of the tonsillar bed is formed by the superior pharyngeal constrictor muscle.

iii. The internal carotid arteries are posterior and lateral in close proximity to the tonsillar bed. These could be damaged during a tonsillectomy.

vi. The palatoglossus muscle and palatopharyngeus muscle is beneath the folds, underneath the mucosa. c. Laryngopharynx

i. Region lying inferior to the oropharynx and posterior to the epiglottis of the larynx. Extends inferiorly to the lower border of the cricoids cartilage which is inferior to the thyroid cartilage.

d. Muscles of the pharynxi. Superior, middle and inferior pharyngeal constrictor muscles

1. Insertion: median pharyngeal raphe2. Innervations: pharyngeal plexus primarily from the vagus. 3. Action: propel bolus downward into esophagus.

ii. Salpingopharyngeus muscle1. Origin: cartilage of auditory tube2. Insertion: palatopharyngeus muscle3. Action: elevates pharynx

iii. Palatopharyngeus muscle1. Origin: hard palate and palatine aponeurosis2. Insertion: lamina thyroid cartilage3. Action: elevates the wall of the pharynx

iv. Stylopharyngeus1. Origin: styloid process2. Insertion: thyroid cartilage3. Innervation: CN IX4. Action: elevates larynx during swallowing

e. Nerves i. Pharyngeal plexus of nerves CN IX, CN X and postganglionic sympathetic nerves from the superior cervical ganglion.

ii. Glossapharyngea nerve (CN IX) supplies the stylopharyngeus muscle. f. Blood supply: branches from

i. Ascending pharyngealii. Ascending palatine

iii. Facialiv. Maxillary v. Lingual arteries

VI. Larynxa. Cartilage

i. Larynx consists of hyaline or elastic cartilagesii. Epiglottis is an unpaired, elastic cartilage

iii. Thyroid cartilage is a V shaped, unpaired, hyaline cartilage that forms the laryngeal prominence of Adam’s apple. iv. Cricoid cartilage is a signet ring shaped, unpaired, hyaline cartilagev. Arytenoid cartilages are paired, hyaline cartilages

vi. Corniculate cartilages are paired, elastic cartilages of the aryepiglottic fold that form lateral boundaries of the laryngeal inlet. b. Folds

i. Vestibular folds, or false vocal cords, serve as expiratory sphincter when holding breath.ii. Vocal folds or true vocal cords are free margins containing the vocal ligament.

iii. Rima glottidis is a midline space between the free margins of the vocal folds. Produces the pitch or tone of the voice (free region btwn the two folds.

iv. Vestibule is the interior region of the larynx extending from the laryngeal inlet to the vestibular folds. v. Ventricle is the small indented space between the vestibular fold and the vocal fold.

vi. Supraglottic portion extends from the laryngeal inlet to the vocal fold.vii. Infraglottic portion extends from the vocal fold to the inferior border of the cricoid cartilage and origin of the trachea.

c. Innervationi. The mucosa of the larynx is supplied by the recurrent laryngeal nerve which is a branch of the vagus nerve.

d. Blood supplyi. Superior laryngeal artery, a branch of the superior thyroid artery (from the external caroid) supplies the larynx.

e. Muscles of larynx nerve supply to all intrinsic muscles of larynx is via the recurrent laryngeal branches of the CN X, except the cricothyroid muscle.

i. Oblique arytenoid muscle narrows laryngeal inlet.ii. Thyroepiglottic muscle widens laryngeal inlet.

iii. Cricothryoid muscle tenses vocal fold supplied by the external laryngeal nerve, a branch of the superior laryngeal branch of the vagus nerve.

iv. Posterior cricoarytenoid muscle abducts vocal fold opens up.v. Lateral cricoarytenoid muscle adducts vocal fold closes it up.

vi. Transverse arytenoid muscle adducts vocal foldvii. Thyroarytenoid and vocalis muscles relaxes vocal cord.

f. Nerve injury i. Injury to the recurrent laryngeal nerve results in paralysis of a vocal fold. Paralysis of one vocal fold results in hoarseness. If both nerves

are damaged, the voice is almost completely diminished because the folds can’t be adducted to produce a tone. VII. Trachea

a. Extends from the cricoids cartilage of the larynx to its bifurcation at the carina into the two main bronchi. Ends at T4-T5 at the carina. Forms the left and right mainstream bronchi. Composed of the cartilaginous rings.

b. The trachea is composed of 16-20 C-shaped hyaline cartilages closed posterior by the trachealis muscle. c. The mucosa that lines the lumen is well vascularized, it contains glands, and is supplied by the vagus and postganglionic sympathetic nerves.d. Tracheotomy

i. An emergency tracheotomy is performed if the airway is blocked. ii. An incision is usually made 1 cm below the cricoid cartilage between the 2nd and 3rd cartilaginous rings.

iii. At this site, the isthmus of the thyroid gland is caudal to the first two tracheal rings. VIII. Deep neck: the root of the neck is the area of neck immediately above the inlet to the thorax.

a. Muscles i. Anterior scalene muscles—nerve coming over the anterior scalene is the phrenic nerve

1. Origin: transverse process of C3-6 vertebrae2. Insertion: first rib. Muscles that attach to the ribs play a role in respiration. 3. Function: laterally flexes and rotates the cervical part of the vertebral column and elevates the first rib 4. Nerve supply: anterior rami of C4-6.

ii. Middle scalene muscles—this is the posterior border of the brachial plexus. 1. Origin - transverse processes of C1-7 vertebrae 2. Insertion - first rib 3. Function - acts as anterior scalene muscle.4. Nerve supply - anterior rami of cervical nerves.

iii. Posterior scalene muscles 1. Origin - transverse processes of lower cervical vertebrae 2. Insertion - second rib3. Function - lateral flexes the vertebral column and elevates the second rib.4. Nerve supply - anterior rami of cervical nerves.

iv. Longus capitis muscle 1. Action - flexes head anterior2. Nerve supply - C1-3 spinal nerves

v. Longus colli muscle 1. Action - flexes neck anterior and slightly rotates cervical vertebral column 2. Nerve supply - C2-7 spinal nerves

b. Nerves i. Glossopharyngeal nerve (CN IX) exits jugular foramen and supplies the stylopharyngeus muscle and sensory supply to the uvula and

posterior third of tongue.ii. Vagus nerve (CN X) exits the cranial vault via the jugular foramen.

iii. Accessory nerve (CN XI) 1. This nerve exits cranial vault via the jugular foramen.2. The spinal part supplies the trapezius and sternocleidomastoid muscles.3. Cranial part has fibers which merge with CN X.

iv. Hypoglossal nerve (CN XII) 1. This nerve exits cranial vault via hypoglossal canal.2. This nerve supplies intrinsic and extrinsic muscles of the tongue, except for the palatoglossus muscle.

v. Recurrent laryngeal nerves1. Right recurrent laryngeal nerve loops under the first part of the subclavian artery.2. Left recurrent laryngeal nerve loops under the arch of the aorta.3. The recurrent laryngeal nerves supply muscles of the larynx except the cricothyroid muscle.

vi. Superior laryngeal nerve 1. Internal laryngeal nerve supplies the mucous membrane of larynx down to vocal folds.2. External laryngeal nerve supplies the cricothyroid muscle.

vii. Trunks of the brachial plexus are formed by anterior rami of C5-8 and T1 spinal nerves.viii. Superior cervical ganglion is one of three ganglia in the cervical part of the sympathetic trunk.

ix. Phrenic nerve originates from the cervical plexus which is formed by the anterior rami of 3-5 cervical nerves. c. Arteries

i. Common carotid arteryii. Internal carotid artery

iii. External carotid artery1. Superior thyroid artery

1. Superior laryngeal artery: passes through foramen in thyrohyoid membrane with internal laryngeal nerve. 2. Facial artery3. Lingual artery

iv. Brachiocephalic trunk is found only on right side and is derived from the arch of the aorta.

v. The left common carotid artery branches from the arch of the aorta, while the right common carotid artery branches from the brachiocephalic trunk.

vi. The left subclavian artery is derived from the arch of the aorta, while the right subclavian artery from the brachiocephalic trunk.vii. Branches from the first part of the subclavian artery include

1. vertebral artery 2. internal thoracic artery (also known as mammilary art.

viii. Branches from the second part of the subclavian artery include the following.1. Thyrocervical trunk

1. Transverse cervical artery2. Suprascapular artery3. Inferior thyroid artery

ix. Branches from the third part of the subclavian artery1. Costocervical trunk

1. Deep cervical artery2. Supreme intercostal artery

d. Veins i. Subclavian veins drain blood from the arm.

ii. External jugular vein drains into subclavian vein. iii. Right and left brachiocephalic veins are formed by the union of the subclavian and internal jugular veins.

IX. Thyroid glanda. The thyroid gland is an endocrine organ.b. It is derived from the foramen cecum of the tongue.c. The thryoid is bi-lobed and interconnected by an isthmus.d. Arterial supply

i. Superior thyroid artery branches from external carotid artery. ii. Inferior thyroid artery branches from thyrocervical trunk.

e. Veins draining the thyroid gland includei. superior thyroid vein to the internal jugular vein.

ii. middle thyroid vein to the internal jugular vein.iii. inferior thyroid vein to the brachiocephalic vein.

f. Thyroid hormonesi. Thyroxin (tetra-iodothyronine, T4)

ii. Tri-iodothyronine (T3)iii. Calcitonin -lowers blood calcium levels

X. The parathyroid glands are endocrine organs.a. Superior parathyroids are derived from 4th pharyngeal pouch.b. Inferior parathyroids are derived from the 3rd pharyngeal pouch.

c. Blood supply and venous drainage is the same as for the thyroid gland.d. Parathyroid hormone

i. Parathyroid hormone (PTH) raises blood calcium levels by causing bone resorption e. Thyroidectomy

i. The parathyroid glands can be damaged or removed during a complete thyroidectomy.ii. An incomplete thyroidectomy saves the posterior thyroid gland, thus the parathyroid glands.

iii. If the parathyroid glands are removed, the patient will suffer tetany due to reduced blood calcium levels.

Outline for Brainstem physiology

I. Brainstema. Function

i. Control of respirationii. Control of cardiac function

iii. Partial control of gastrointestinal function (CN X)iv. Control of equilibrium (CN VIII)v. Control of eye movements ( CN III, IV & VI)

vi. Control of many stereotyped movements (medial and lateral tracts)b. Tracts

i. Descending brainstem medial tracts1. Vestibulospinal

a. Extends from the vestibule to the spin. b. Controls paraveterbral extensors and proximal limb extensors (important for posture and balance).

2. Reticulospinala. Controls the gamma motor neurons to maintain posture and modulate muscle tone.

3. Tectospinala. Extends from the tectum to the spineb. Controls head movements for orienting reactions.

ii. Descending brainstem lateral tract1. Lateral rubospinal tract: goal directed movements. In humans with a corticospinal lesion, it provides the remaining function

a. Extends from the red nucleus to the spineb. Controls motor neurons

i. Through interneurons in the dorsolateral gray, it controls distal limb musclesii. Innervates proximal limb flexors of the upper limb

II. Lesionsa. Decorticate Rigidity

i. Results in flexion of the upper limb and extension of the lower limbs. ii. Section through neural axis rostal to superior colliculus

iii. Results in unchecked rubrospinal drive which overexcites flexor motor neurons (in humans, this is limited to upper limb)b. Decerebrate Rigidity

i. May occur in patients with trauma, vascular disease or tumors. ii. Section through the neural axis between the colliculi, resulting in decerebrate rigidity.

iii. Results in tonic over activity which is due to the influence of sensory stimuli from reticulospinal tract (gamma rigidity—leads to a disrupt in the sensory afferent from spindals which inhibits alha motor neurons. Gamma motor neurons stimulate the spindle, but the path of 1a and 2 is disrupted.) and vestibulospinal tract.

III. Eyea. Movements that rotate the eye around the orbit

i. Abduction: rotates the eye away from the nose.ii. Adduction: rotates the eye toward the nose

b. Musclesi. Superior rectus (CN III): elevates and intorts

ii. Inferior rectus (CN III): depresses and extortsiii. Medial rectus (CN III): adductsiv. Lateral rectus (CN VI): abductsv. Inferior oblique (CN III): elevates and extorts

vi. Superior oblique (CN IV): depresses and intortsc. Nerves

i. Occulomotor (CN III)1. Innervates the med, inf and sup retus, inf oblique and levator palpebrae.2. Controls the sphincter papillae muscle of the iris and the ciliary muscle3. Location: in the midbain at the level of the superior colliculus4. Palsy:

a. Lateral strabismus caused by unopposed action of the lateral rectus muscle. b. Inability to direct the eye medially or vertically. c. Drooping of the upper eyelid (ptosis due to levator palpebrae palsyd. Dilation of the pupil, enhanced by unopposed action of the dilator papillae muscle in the irise. The ciliary muscle does not contract to allow the lens to increase in thickness for focusing on near objects

ii. Trochlear (CN IV)1. Controls superior oblique2. Midbrain (caudal to CN III)3. Palsy:

a. Vertical diplopia which is maximal when the eye is directed downward and inwardb. Patients experience difficulty walking downstairsc. This is a rare palsy. It can occur due to diabetes mellitus as an isolated lesion of the trochlear nerve (peripheral

neuropathy). It can also occur due to complication in head injury.d. Patient tilts head to eliminate diplopia.

iii. Abduncens (CN VI)1. Controls lateral rectus.2. Pathway: located beneath the facial colliculus in the floor of the 4th ventricle and passes through the pons in a ventrocaudal

direction, emerging from the pontomedullary junction. 3. Susceptible to the increased intracranial pressure because of the very short distance between the egress point at the junction. 4. Palsy:

a. Causes medial squint and an inability to direct the eye laterally. b. If the abducens nucleus is destructed, it can lead to paralysis on the contralateral medial rectus. The patient will be unable

to direct the gaze toward the side of lesion. Nuclear lesion can also involve a nearby nucleus or axons of the facial nerve, which can cause paralysis of the ipsilateral facial muscle.

c. CT scans will show a demyelination of the pons at the left CN VI (if it’s a left lesion)IV. Neuronal systems

a. Three neuronal systems: keep the fovea on a visual target in the environmenti. Saccade: rapid, ballistic movements which shift the fovea rapidly to visual target. Moves the eyes conjugate (both eyes move in the same

direction by contracting and relaxing different muscles)ii. Smooth pursuit: keeps image of moving target on the fovea. Moves the eyes conjugate (both eyes move in the same direction by

contracting and relaxing different muscles)iii. Vergence: moves the eyes in opposite directions so that the image is positioned on both foveas. Produces disconjugate eye movement. The

eyes move toward each other when the object is near converge. Eyes move away from each other when the object is far away diverge)

b. Two neuronal systems: stabilize the eye during head movementi. Vestibulo-ocular reflex (VOR): movements hold images still on the fovea during head movements.

ii. Optokinetic movements: hold images during sustained head movement and supplements VOR.c. Visual fixation: holds the eye still during intent gaze

i. Fixation zone (neural center): most rostal portion of the superior colliculusii. Fixation requires active suppression of eye movements

iii. Neurons in the fixation zone inhibit saccades.

Frontal Eye Field

Cranial nerves

Cranial Nerve Type and Location FunctionOlfactory (I) nerve

Sensory: Arises in the olfactory mucosa, passes through the olfactory bulb then the olfactory tract, which extends to the primary olfactory area of the cerebral cortex.

Sensory function: smell.

Optic (II) nerve Sensory: Arises in the retina of the eye, forms the optic chiasm and then the optic tracts, and terminates in the primary visual area of the cerebral cortex.

Sensory function: vision.

Oculomotor (III) nerve

Sensory: consist of axons from the proprioceptors in the extrinsic eyeball muscles that terminate in the midbrain.

Motor: originates in the midbrain. Axons of somatic motor neurons innervate the muscle of the upper eyelid and four extrinsic eyeball muscles. Parasympathetic axons innervate intrinsic eyeball muscles.

Sensory function: proprioception.

Somatic motor function: movement of the upper eyelid and eyeball.

Autonomic motor function (parasympathetic): alters lens for near vision and constricts pupils.

Trochlear (IV) nerve

Sensory: consists of axons from proprioceptors in an extrinsic eyeball muscle, which terminates in the midbrain.

Motor: originates in the midbrain and innervates an extrinsic eyeball muscle.

Sensory function: proprioception.

Somatic motor function: movement of the eyeball.

Trigeminal (V) nerve

Sensory: consist of three branches which end in the pons

1. Opthalmic nerve (V1): contains axons from the scalp, forehead, upper eyelid, eyeball, lacrimal glands and nose

2. Maxillary nerve (V2): contains axons from the lower eyelid, mucosa of the nose, upper mouth and pharynx

3. Mandibular nerve (V3): contains axons from the cheek, tongue, lower mouth, mandible, side of head and lower side of face.

Motor: originates in the pons and innervates muscles of mastication.

Sensory function: conveys impulses for touch, pain, and temperature sensation and proprioception.

Somatic motor function: chewing,

Abduncens (VI) nerve

Sensory: consist of axons from proprioceptors in an extrinsic eyeball muscle that ends in the pons.

Motor: originates in the pons and innervates an extrinsic eyeball muscle.

Sensory function: proprioception.

Somatic motor function:

movement of eyeballs.

Facial (VII) nerve

Sensory: arises from taste buds on the tongue, enters the pons, then passes to the primary gustatory area of the cerebral cortex. Also contains axons from the proprioceptors in muscles of the face and scalp.

Motor: originates in the pons. Axons of somatic motor neurons innervate facial, scalp and neck muscles. Parasympathetic axons innervate lacrimal, and salivary glands.

Sensory function: taste and proprioception.

Somatic motor function: facial expression.

Autonomic motor function (parasympathetic): secretion of tears and saliva.

Vestibulocochlear (VIII) nerve

Sensory1. Vestibular nerve arises in the organs of equilibrium and ends in the pons and cerebellum2. Cochlear nerve arises in the organ of hearing, passes through the medulla oblongata, then relays

impulses to the primary auditory area of the cerebral cortex

Vestibular branch function: conveys impulses related to equilibrium.

Cochlear branch function: conveys impulses for hearing.

Glossopharyngeal (IX) nerve

Sensory: consists of axons from taste buds and somatic sensory receptors on the tongue, from proprioceptors in swallowing muscles, and from receptors in carotid sinus and carotid body. Axons end in the medulla oblongata.

Motor: originates in the medulla oblongata. Axons of somatic motor neurons innervate a muscle of the pharynx used in swallowing. Parasympathetic axons innervate the parotid (salivary) gland.

Sensory function: taste and somatic sensations (touch, pain, temperature) from posterior third of tongue; proprioception in swallowing muscles; monitoring of blood pressure; monitoring of oxygen and carbon dioxide in blood for regulation of breathing.

Somatic motor function: elevates the pharynx during swallowing and speech.

Autonomic motor function (parasympathetic): stimulates secretion of saliva.

Vagus (X) nerve

Sensory: consists of axons from the external ear, taste buds in the epiglottis and pharynx, proprioceptors in muscles of the neck and throat, receptors in the carotid sinus, carotid body, aortic body and thoracic and abdominal cavity organs. Axons end in the medulla oblongata and pons.

Motor: originates in medulla oblongata. Axons of somatic motor neurons innervate skeletal muscle sin the throat and neck. Parasympathetic axons innervate the lungs, heart, esophagus, stomach, small intestine, large intestine, gallbladder, and glands of gastrointestinal (GI) tract.

Sensory function: taste and somatic sensations (touch, pain, temperature, and proprioception) from epiglottis and pharynx; monitoring of oxygen and carbon dioxide in blood for regulation of breathing; sensations from visceral organs in thorax and abdomen.

Somatic motor function: swallowing, coughing, and voice production.

Autonomic motor function (parasympathetic): muscle contraction and relaxation in organs of the GI tract; slowing of the heart rate; secretion of digestive fluids.

Accessory (XI) nerve

Sensory: consists of axons from proprioceptors in muscles of the pharynx, larynx, and soft palate and ends in the medulla oblongata.

Motor: supplies muscle soft the pharynx, larynx, soft palate and the sternocleidomastoid and trapezius muscle.

Sensory function: proprioception.

Somatic motor function: swallowing and movement of head and shoulders.

Hypoglossal (XII) nerve

Sensory: consists of axons from proprioceptors in tongue muscles and ends in the medulla oblongata.

Motor: originates in the medulla oblongata and supplies muscles of the tongue.

Sensory function: proprioception.

Motor function: movement of tongue during speech and swallowing.

RMR: BRAINSTEM SEGMENTS ASSOCIATED WITH THE CRANIAL NERVES:

Midbrain – CN 3,4

Pons- CN: 5, 6, 7 and parts of 8.

Medulla- CN: 8, 9, 10, 11, 12

Outline for visual system

I. Visual systema. Relays information from the external environment to the brain. The information is processed by the visual cortex to make a “map” of the visual

worldb. Damage to the brain will most likely result in visual dysfunction because a majority of the fibers carry visual information. c. Visual system is made up of:

i. Eyeballii. Retina

iii. Optic nerveiv. Visual pathways in the brain

II. Anatomy of the eyea. Cornea: transparent layer for the optical structures of the eye. Laterally, it is continuous with the conjunctiva (a mucous membrane that lines the

sclera inside the eyelid. It provides the cornea with moisture.) The central segment of the cornea is non-vascularized. b. Anterior chamber: filled with aqueous humor (produced by the epithelium of the ciliary body). Behind the cornea. Bounded posteriorly by the iris

and the pupilc. Posterior chamber: bounded by the iris anterior and the lens posterior. Filled with aqueous humor. The aqueous humor is secreted into the

posterior chamber, it goes into the anterior chamber. Drains in the tubercular meshwork. Then it goes into the canal of schlem d. Vitreous body: lies posterior of the lens and anterior to the retina.

i. Made of 99% water, with a viscosity that is 2-4 times higher, thus it has a gelatinous consistency. It has a refractive index of 1.336. It is resilient (if you press on the eye, it will return to its shape) and it maintains more than 80% of the volume of the eyeball.

ii. The vitreous body strongly adheres to the retina and can lead to retinal detachment by pulling on the retina and causing fluid to be filled between the RPE and the sensory retina. If this happens and the surgeon does not fix it soon, the photoreceptor cells will die and patient lose vision in the area of the detachment.

iii. Components: salts, sugars, collagen fibers and halocytes (these serve to remove debris in the visual field and are derived cells of the bone marrow)

III. Retinaa. Transparent so that the light reaches the photoreceptors without any interference. b. Contains 6 types of neurons.

i. Glial and astrycyte cells in the innermost layer surrounding the blood vessels. ii. Mullerian glial cells extend from the inner limiting membrane to the outer limiting membrane. Primary function is structural and trophic

support of the retinal cells. c. Retina has 10 layers

i. Photoreceptor cell outer segments (outermost)ii. Photoreceptor cell inner segmentsiii. Outer limiting membraneiv. Outer nuclear layerv. Outer plexiform layervi. Inner nuclear layervii. Inner plexiform layerviii.Ganglion cell layerix. Nuclear fiber layerx. Inner limiting membrane (innermost)

d. RPE (retinal pigment epithelium):i. Not a part of the sensory retina. ii. Flat layer of cuboidal cellsiii. Supports the photoreceptor cells and secretes growth factors. iv. Interconnected by tight and gap junctionsv. Located between the sensory retina and the choroid, which contains melanin granules. vi. Important in the development and maintainence of the sensory retina (especially the photoreceptors) vii. Forms an important structural relationship with Bruch’s membrane and allows the transport to and from the choriocapillaries. viii.Involved in phagocytosis of the outer segment of the photoreceptors which is critical to maintain the life of the cone and the rods. This

occurs everyday. If RPE fail to phagocytize, there will be an accumulation of debris between the RPE and the photoreceptors leading to death of the cells and eventually blindness.

ix. Recycles retinoids. e. Fovea centralis: area with the highest number of cones, no rods. Thin compared to other areas of the retina so there is less resistance/interference.

This area is useful for fine and color vision. f. Photoreceptor cells:

i. Detection of light1. Rods and cones detect light in the retinal image and convert light energy into chemical energy phototrasnduction. 2. Light is transduced in the outer segment which is enveloped by apical processes of the RPE. 3. The cilium connects the OS to the inner segment. 4. Inner segment has the mitochondria inorder to synthesize outer segment membrane proteins and energy. 5. The nucleus of all the photoreceptors are found in the outer nuclear layer. 6. Axons of the rods and cones synapse with the dendrites of the bipoarl neurons in the outer plexiform layer. (synapse between the

bipolar and ganglion cells occur in the inner plexiform layer.)ii. Rods

1. Appear as membrane bound cylinders and have many stacked membraneous disks. These disks are shed off daily in order to renew the rods. The new discs move from the basal to the distal surface to maintain the length of the rod OS. Rod OS is renewed every 10 days.

2. The outer segments of the rods are involved in transduction. 3. Within these OS disks membrane is the rhodopsin which consist of opsin and chromophore proteins. Opsin (a 7 TM component)

and 11 cis retinal (which responds to light and undergoes a conformational change), resulting in hyperpolarization. Glutamate is released as the major NT.

4. Rods are very sensitive to light. When stimulated, these result in low visual acuity because many rods synapse with the dendrites of a single bipolar neuron.

5. Rods are located throughout the retina, but are absent in the fovea. Number of rods is highest near the fovea but decrease toward the periphery.

6. Important for dark vision. Respond to wavelengths around 500 nm. iii. Cones

1. Cell body is in the outer nuclear layer. 2. Outer segment (OS) consists of membranous stacks which are conic in shape. It is not enclosed with a second membrane; it is open

to the extracellular space adjacent to the RPE. Continuous membrane. 3. Important for fine vision and color vision. Many cones, especially in the fovea, synapse one on one with the bipolar neuron which

synapses with only one ganglion cell, resulting in fine vision information. 4. Highest concentration of cones is in the fovea and cones are very tightly packed here. This is important for visual acuity. The

concentration decreases toward the periphery. The diameter of the cones increase toward the periphery but is very small in the fovea.

5. There are 3 cone opsins that absorb light and undergo a conformational change resulting in hyperpolarization. 6. Hyperpolarization is propagated to the cynaptic end (cone pedicle) in the outer plexiform layer. . 7. Do not signal color. These send a signal to the brain about the presence of light in the visual field. The brain interoperates color by

taking in all the information from the entire population to determine what the color of the object is. This allows trichromatic color vision in humans.

8. Three types of cones: respond to wavelengths between 400-800 nm. Stimulation of the eye by the entire range of wavelengths produces white light.

a. Red cones (L cones) are sensitive to long wavelengths (560 nm)b. Green cones (M cones) are sensitive to medium wavelength (530 nm)c. Blue cones (S cones) are sensitive to short wavelengths (430 nm)

9. The colors are interoperated based on the combination of the responses in these three cones10. Color blindness

a. If any of the cone types are absent, the person will confuse the colors color blindness which is a lack of sensitivity to a particular color. Absolute color blindness is rare.

b. Red/green color blindness: most common. Red and green opsins are located in the X chromosome so it is more common in males.

i. Protanopia: red receptors are lost. Sex linked associated with the Y chromosomeii. Deuteranopia: green receptors are lost. Sex linked.

c. Yellow/blue color blindness: second most common, but rare. i. Tritanopia: rare and hereditary. Blue receptors are lost. Form of dichromacy. Can’t perceive the differences

between red, orange, yellow and green. Colors appear similar. d. Monochromacy: total color blindness. Lacks the ability to distinguish color because 2 cone receptors are defective or lost.

Black and white vision. e. Trichromacy: one of the cone 3 pigments is altered in spectral sensitivity resulting in imparement, but not a loss of

trichromacy. IV. Macula lutea and fovea centralis:

a. Macula lutea: yellow appearing region that is at the posterior pole of the eye. The yellow color is produced by xanthophylls pigments in the outer plexiform layer centered on the fovea.

b. Fovea is at the center of the macula. ONLY cones are in the fovea, no rods. The inner retinal layer becomes thinner and disappears. Only the ONL, IS and OS are present with some of the plexiform layer. This is to allow maximum light to reach the OS of the cones. BV form a network of capillaries that are found at the periphery of the fovea, but not within it. Most of the visual input to the brain comes from the fovea.

c. Rods and cones are found in the macula lutea. Rods become more prevalent going toward the periphery. Cones are most dense in the fovea and decrease as you go to the periphery.

V. Cellsa. Bipolar neurons

i. Soma in the INLii. Interneuron that connects the photoreceptor with the ganglion cells

iii. Bipolar neurons of rods are different than cones based on synaptic inputs. iv. Can have multiple internactions (20-50 photoreceptor cells)

b. Horizontal cellsi. Body in the INL

ii. Receive glutaminergic input from photoreceptorsiii. Dendrites and axons course parallel to the plane of the retina to a nearby and distant photoreceptorsiv. Sharpen the edge of a receptive field by inhibiting surrounding photoreceptor cells.

c. Amacrine cells: i. Body in the INL

ii. Do not have an obvious axon but have highly branched dendrites that extend over a large distance. iii. Appear to modulate signals from rods and cones.

d. Ganglion cellsi. Output cells of the retina.

ii. Soma is within the ganglion cell layer and axons extend into the nuclear fiber layer. iii. Axons are unmeylinated as they exit the retina in the optic nerve head (a weak region in the posterior pole of the eye) which is surrounded

by the lamina provosa. This lamina gives strength to the optic nerve head. When pressure is increase,d the lamina gets older and axons become damaged, leading to blindness (glaucoma)

VI. Optic nerve head: a. Axons of the ganglion cells become myelinated with the optic nerve by oligodendrocytes. b. BV exit or enter the retina at the optic nerve head and axons of the ganglion cells exit the retina. Vein is larger than the artery. c. Optic nerve is a CNS nerve not a peripheral nerve. d. Referred to as the blind spot because there are no photoreceptors in this region.

VII. Visual fielda. Total area in which an object can be seen in the periphery but is focused in the center. b. Perimetry tests may indicate retinal disease or disorders of the CNS (tumors) which damage the area of the brain involved in vision. Diabetes,

hyperthyroidism, hypertension, disease of the pituitary gland and MS also affect vision.VIII. Adaptation

a. Dark adaptation: eye adjusts in reduced illumination in which the sensitivity to light is increased or the light threshold is greatly reduced. Moving from a bright environment to a dark environment.

i. Retina becomes more sensitive to light as the person becomes accustomed to the darkii. Maximal response time is 30 minutes because the rods are bleached during the day, so it takes time to synthesize them.

b. Light adaptation: eye moves from dim environment to bright environment. i. Light is intense and uncomfortable until the eye adapts.

ii. Occurs in less than one minute. IX. Accomodation

a. Unaccommodated: normal eye looking at a distance. Object is focused on the fovea. b. Emmetropia: focal length of the optics and the distance from the cornea to the retina are matched. c. Accommodation: brings closer objects to focus. Eye increases its refractive pathway by accomadation. d. Ability to do so decreases with age as the lens loses its elastiticity. e. Prysbyopia: loss of accommodation for 50 year olds.

X. Diseasesa. Myopia: nearsightness. Refracting system (cornea, lens) is too powerful. Image is focused in front of the retina (fovea) instead of at the retina.

Correct it by biconcave lens.

b. Hyperopia: farsightness. Refrating system is too weak. Causes the image to appear at the fovea of the retina before it focuses (focuses behind the fovea). Correct by a biconvex lens.

c. Astigmatism: occurs when the curvature of the lens or cornea is greater in one axis. If the refracting power is greater in its vertical axis, than its horizontal axis, vertical rays will be more refracted than the horizontal rays producing a source of light that looks like an ellipse. Cornea is oval instead of spherical. Results in blurred vision. Usually occurs after myopia or hyperopia.

d. Age related macular degeneration (ARMD): patient suffering from central vision loss (cones). This is found in the aging population and involves a dysfunctional RPE. This is a leading cause of vision loss in the US> There is no therapy to restore vision, but progression can be slowed. Transplantation of RPE has been attempted but was unsuccessful. Patients have a hard time reading or recognizing faces because central vision is lost. Peripheral vision is present. ARMD can occur as in a dry form (loss of pigment and formation of drusen) and wet (new vessel formation in the photoreceptor cells. The RPE loses pigment granules and detaches from the Bruch’s membrane.

e. Stargardt’s disease: autosomal recessive hereditary disease. Form of macular dystrophy that beings early in life. Most common form in juvenile macular degeneration. Characterized by yellow flecks around the macula called fundus flavimaculatus. Cones are lost in the fovea, so both eyes lose central vision. No cure.

f. Retinitis pigmentosa (RP): patients suffer from peripheral vision loss due to a defective rod photoreceptors resulting from a dysfunctional or mutated protein (opsin, peripherin-rods/peripherin). 39 gene loci identified, but half of RPs have no cause. Initially the rods are lost, so patient has trouble seeing in the dark. Night blindness is the earliest and most frequent symptom of RP. Cones can be involved later, leading to central visual loss and color perception loss.

g. Glucoma: send leading cause of blindness. It is an ocular condition that contributes to the loss of axons of retinal ganglion cells with a corresponding loss of vision (optic neuropathy). This is a disease of the optic nerve, which transmits signals from the retina to the brain. Intraocular pressure (IOP) is high due to a blockage of aqueous humor outflow through the trabecular meshwork from the anterior chamber or an overproduction of aqueous humor by the ciliary bodies. This leads to a damage of the lamina provosa, which damages the optic nerve. Cupping of the optic nerve head is seen. Treat the IOP by increasing outflow or decreasing the production of the aqueous humor.

h. Diabetic retinopathy: most common diabetic eye disorder and is the leading cause of blindness in adults. It is caused by changes in and proliferation of retinal blood vessels. Blood vessels swell and leak fluid (edema). New vessels can also grow on the surface of the retina. Blood vessels are leaky because they don’t have tight junctions. over time, there is vision loss in both eyes. Blood vessels have a corkscrew appearance, and leak into the center of the eye leading to blurred vision (this occurs in the advanced stage of diabetic retinopathy) fluid leaks into the macula. This makes the macula swell and leads to blurred vision (macular edema). Occurs at any stage of the retinopathy, but is progressive.

i. Detached retina: occurs when the retina is pulled away from the RPE. This is a serious problem and if left untreated, it can lead to blindness in the area of detachment. Fluid from the vitreous can accumulate between the retina and the RPE.

j. Scotomas: blind spots in the visual field. In a central scotomas, loss of macular vision is see nin the optic neuritis or retrobulbar neuritis (without swelling of the optic disc). These conditions are inflammation of the topic nerve either close to or behind the eye. Color vision, reading and other high visual acuity functions are affected. No known treatment.

k. Papilledema: chocked disc. Observed as swelling of the optic nerve head. Bilateral condition. Nerve head is elevated and swollen but the papillary response is normal. Vision is not affected initially, but permanent visual loss can occur if the primary cause of the papilledema is left untreated. Visual acuity not affected, but optic disc can get enlarged. This occurs due to intracranial pressure. The optic nerve is surrounded by meninges and if the intracranial pressure is high, it can impact the optic nerve, thus impacting vision. The increased pressure is transmitted to the optic disc

through the extension of the subarachnoid space around the optic nerve. Swelling of the optic disc is characterized by hyperemia (increased blood), blurring of disk margins, microhemorrhages and engorgement of the retinal veins. Chronic papilledema can cause optic atrophy and vision loss.

XI. Optic nervea. Orbital portion of the optic nerve is invested by sheaths derived from the meninges (dura mater, arachnoid and pia mater.) all three layers fuse and

become continuous with the sclera at the lamina cribosa. Dura extends into the cranial cavity, arachnoid and the pia goes to the optic canal. b. Optic atrophy:

i. Occurs when the optic nerves do not develop properly. ii. Results from inflammation of the optic nerve or from glaucoma because of high IOP.

iii. Results from (unusual) poisions, vitamine deficiencies or tumors. iv. Some causes are unknown. v. Symptoms

1. Blurred vision2. Abnormal peripheral vision3. Abnormal color vision4. Poor constriction of the pupil in light 5. Decreased brightness in one eye relative to the other.

vi. Characteristics: color of the optic disc changes to pink, white or grayvii. Primary optic atrophy caused by multiple sclerosis or neurosyphilis, and is associated with degeneration of the optic nerve, but does not

produce papilledema. viii. Degeneration and atrophy is IRREVERSIBLE because the optic nerve is in the CNS. It is myelinated by oligodendrocytes.

ix. Secondary optic atrophy is associated with papilledema due to neuritis, glaucoma or increased intracranial pressure. XII. Physiology of vision

a. Phototransduction: process by which light captured by a visual pigment in a photoreceptor cell outer segment, generates an electrical response. b. Process:

i. Inside the photoreceptor cells, normal levels of cGMP keep the Na channels open, so that in resting state, the cell is depolarized. ii. Photoexcited rhodopsin (R*) and G protein transducin (T) diffuse on the disk membrane, these collide and bind.

iii. R* catalyzes the exchange of a GDP for a GTP on the Talpha subunit. Activated Talpha is released.iv. This process repeats many times and results in amplification. v. Talpha diffuses along the membrane surface and activates a single cGMP phosphodiesterase (PDE) subunit.

vi. Hydrolysis of cGMP by Talpha activated PDE converts cGMP into GMP, so cGMP decreases and cannot bind to Na channels. Na channesl close and the cell becomes hyperpolarized.

vii. This causes a reduction in positive charges in the outer segment, so the membrane potential is more negative. The cell is hyperpolarized. viii. Because of this imbalance in the OS, positive ions are drawn from the terminals of the photoreceptors making it more netative.

ix. Hyperpolarization of the photoreceptor terminals reduces the rate of glutamate release. Glutamate is released at its highest, in the dark. So when a photon hits, glutamate is not released.

x. In reverse, cGMP is synthesized from GTP by guanylate cyclase (GC) which results in reopening of the Na channels.

c. Rhodopsin: i. 7 TM helicies that surrounds the protoreactive chromophroe, 11 cis retinal.

ii. Retinal is derived from vitamin A. iii. Light causes isomerization of 11 cis retinal into all trans retinal. This leads to a conformational change in opsin that activates the

associated G protein and triggers a second messenger cascade leading to an action potential at the level of the ganglion cell. The ultimate goal is to close the channel by decreasing the intracellular concentration of cGMP.

d. Role of RPE i. Phagocytosis of the OS of the photoreceptor cells.

ii. Involved in vitamin A cycle. It isomerizes all trans retinol into 11 cis retinal.1. All trans retinol is carried from the OS to the RPE by interstitial retinol-binding protein (IRBP). 2. It is converted in the RPE by lecithin retinol acetyltransferase to all trans retinyl ester. 3. This is converted to 11 cis retinol by RPE65. 4. 11 cis retinol is converted to 11 cis retinal by 11 cis retinol dehydrogenasse.

5. 11 cis retinal is carried to OS by IRBP.

XIII. Visual pathwaysa. Axons course along the inner retina and pass through the lamina cribrosa of the sclear to form the optic nerve. b. The axons continue through the optic canal to form the optic chiasm. c. Fibers of the nasal half of the retina cross (are contralateral) at the optic chiasm, while the temporal fibers remain ipsilateral. d. Axons from the temporal half of the left retina and the nasal half of the right retina project centrally behind the chiasm within the left optic tract.

These two halves of the left and right retina receive visual information from the right sided half of the visual environment (right hemisphere). e. The left hemisphere receives information from the contralateral half of the visual friend (from the right side) f. After passing the optic chiasm, axons pass centrally in the optic tract and to the lateral geniculate nucleus (LGN) and superior collicullus. g. The LGN and medial geniculate nucleus are important relay nuclei within the thalamus. From each LGN, axons pass ipsilateral via the optic

radiation to the calcarine cortex (primary visual cortex) in the occipital lobe. XIV. Optic radiation (geniculocalcarine tract)

a. Collection of axons from the relay neurons in the LGN that carry visual information to the visual cortex (striated cortex) along the calcarine fissure. All of the axons that go to the visual cortex combine as the optic radiation.

b. This is on each side of the brain and it splits into two parts on each side. XV. Meyer’s loop (Archambault’s loop)

a. Axons from the inferior retina that consists of geniculocalcarine fibers that curves around the inferior horn of the lateral ventricle. The axons carry back and go around the lateral ventricle.

b. Fibers reach forward into the temporal lobe before passing to the calcarine cortex. c. This loop carries optic radiation fibers representing the superior quadrant of the contralateral visual field. d. The left Meyer’s loop receives information from the nasal left and temporal right. e. Lesion of the temporal lobe can damage the Meyer’s loop and cause a loss of vision in the superior quadrant. There is a loss of the nasal left and

the temporal right only on the superior quadrant. f. Axons from the superior retina travel straight back to the occipital lobe in the retrolenticular limb of the internal capsule to the visual cortex. These

carry information from the inferior part of the visual field and take the short path. These are less susceptible to damage.

XVI. Superior colliculus: axons of the retinal ganglion cells in the optic tract terminate here, forming a retinotrophic map. This area receives fibers from the visual cortex and it sends fibers to the spinal cord via the tectospinal tract. This tract controls the reflex movements of the head, neck and eye in response to the visual stimuli.

XVII. Lesions:

a. Impaired vision in one eye due to a disorder involving the eye, retina, optic nerve, tract or radiationb. Lesion at the optic nerve head (1) affecting the central region will result in vision loss at the macula. c. Lesion of the complete optic nerve (2) results in complete loss of vision of that eye.d. Lesion of the optic chiasm (3) leads to a loss of the decussating axons. Patient loses nasal vision of both eyes bitemporal hemianopsia.

Blindness in the temporal half of the visual fields for each eye. Loss of peripheral vision on both eyes. This can be caused by pituitary tumors because the pituitary lies just under the optic chiasm.

e. Lesion of the optic tract (5) results in loss of vision from the ipsilateral nasal field and contralateral temporal field homonymous hemianopsia. . Lesion at 5 will result in a right homonymous heminopsia because both eyes are blind to anything on the right side of the world.

f. Lesion in the Meyer’s loop leads to loss of vision from the superior quadrant of the ipsilateral nasal and contralateral temporal superior quadrantanopsia.

g. Lesion in the parietal portion of the optic radiation (7) affects the inferior vision in the right hemifield. h. Lesion of the cortex (9) results in macular sparing. Macula is ok but vision is lost from the right hemifield.

XVIII. Effects of vessel occlusiona. Occlusion of the ophthalmic artery can cause blindness in the respective eye

b. Occlusion of the posterior cerebral artery causes homonymous hemianopsia. The LGN is supplied by a branch of the posterior cerebral artery, thalamogeniculate artery.

XIX. Oculomotor nervea. Supplies all the muscles controlling the movement of the eye except lateral rectus (CN VI) and superior oblique (CN IV), so it controls all

movements of the eye except lateral rotation and looking down when the pupil is adducted. b. Supplies parasympathetics to the eye to maintain the elevation of the eyelid (levator palpebrae superioris muscle), constrict the pupil (sphincter

papillae muscle ) and allow the broadening of the lens (ciliary muscle) c. Edinger Westphal nucleus sends parasympathetic neurons within the occulomotor nerve to terminate in the ciliary ganglion. Postganglionic

neurons in the ciliary ganglion project to the iris sphincter muscle. These neurons are responsible for papillary light reflex which results in constriction of the pupil in response to light. So when light is shined on the retina of one eye, it causes constriction of both pupils

XX. Horner’s syndromea. Interruption of the oculosympathetic nerve pathway between its origin in the hypothalamus and the eye. b. No predilection for age, race, gender, or geographic location. Horner's syndrome of congenital origin is typically around the age of two years with

heterochromia and absence of a horizontal eyelid fold or crease in the ptotic eye.c. Iris pigmentation (which is under sympathetic control during development) is completed by the age of two, making heterochromia an uncommon

finding in Horner's syndromes acquired later in life. d. Pupillary size differences may arise from lesions in the path of the pupillary light reflex.e. Horner’s syndrome, which is characterized by one pupil being small (miotic), results from dysfunction of the sympathetic supply to the pupil or

orbit.f. Post-ganglionic Horner's syndromes tend to be benign and are typically vascular in origin.g. Damage giving rise to these symptoms include

i. Strokeii. tumor in the upper part of the lung and low cervical spinal cord

iii. cluster headachesiv. injury to a carotid artery in the neck.

h. Characteristicsi. Ptosis drooping of the upper eyelid

ii. Papillary miosis constricted pupilsiii. Enophthalmos sunken eyeiv. Facial anhidrosis decreased sweating. v. Increased amplitude of accommodation

vi. heterochromia of the irisvii. paradoxical contralateral eyelid retraction

viii. transcient decrease in IOPix. changes in tear viscosity

Outline for cerebrovascular system

I. Introductiona. Brain needs glucose and oxygen to function properly

i. Uses 20% cardiac output and extracts 18% of total oxygen requirement. ii. Rate of perfusion of blood through the brain is relatively high.

b. Brain is susceptible to ischemiai. A flow rate of <25 ml/100 gm/min induce ischemia.

ii. At rates of <12 ml/100 gm/min infraction occurs. c. Cerebrovascular disease is the 3rd leading cause of death.

i. Affects people above age 50ii. Hypertension is closely associated factor. If hypertension is untreated, patient will have a higher risk for developing stroke. Other factors

are women smoking and eating birth control pills. iii. Classifications

1. Arteriosclerosis: atherosclerotic plaque formation. Arteriosclerosis is the sub intimal layer of vessels leads to consequences in the heart and the brain.

2. Formation of thrombi (clot) or emboli (air bubble or plaque that breaks off and gets into circulation) a. TIA (transcient ischemic attacks)—have fibrinolysis with lack of vision and then it goes away in 24 hours. The clot lyses

after time. This is a medical emergency because a stroke is pending. Usually a stroke will occur in 30 days of TIA. b. RIND (Reversible Ischemic Neurological Deficit)—clears in 72 ours.

3. Aneurysmsa. Berry aneurysm: silent diseases. Occurs in the anterior portion of the circle of Willis, especially the internal carotid,

anterior cerebral and anterior communicating, where the middle cerebral branches from the internal carotid. 4. Arteriovenous malformations: anastamosis of arterial and venous and shunting blood away from the brain. Some are inaccessible

to surgery and these patients are at a greater risk of strokes. This takes away oxygen and glucose from tissues at high rate. 5. Strokes/brain attacks—etiologies

a. Hemorrhagic: lenticolo striate arteries are very small and these penetrate the internal capsule and lenticular complex of the basal ganglia. If there is a hemorrhage, patient will die (hypertensive disease).

b. Thrombolic/embolic: due to hematologic disorders like sickle cell, polycythemia vera, develop thrombus and can plug major vessels.

i. Hematologic disordersii. Atherosclerosis

iii. Myocardial infarction: After an MI, there may be a plaque in the coronary circulation. Deep structures may not be getting enough O2 and nutrients. The squamous epithelium (endocarium) lets loose and a plaque may get into the vessel. It may go into the brain and lead to a stroke.

II. Source of blood supply to the cerebrum and brainstem. Brain and kidneys are the last organs to give up their blood supply. a. Right side

i. Heartii. Arch of the aorta

iii. Brachiocephalic trunk: divides into common carotid and subclavian. iv. Common carotid artery: at C3 (at the level of the superior thyroid cartilage) the common carotid branches into internal and external

carotid. v. Internal carotid artery branches after the petrous portion. Goes through the cavernous sinus into the subarachnoid space and gives off 5

branches. vi. Subclavian artery

vii. Vertebral artery: from the first part of the subclavian artery. It goes through the upper 6 foramen transversari of the Cervical vertebra, pierce the AO membrane, dural sac at the foramen magnum and arachnpid. Joins the vertebral artery from the other side to form the basilary artery. Then it bifurcates into posterior cerebral arteries in the posterior cranial fossa this is the main supply to the visual cortex. It ascends through the tentorial notch and penetrates to supply the temporal and occipital lobes. When a patient complains of turning their head and loosing vision for a moment, this is caused by stretching of the artery over the tentorium. NOTE: Amaurosis fugax (Transient monocular blindness) is sometimes associated with occlusive disease involving these vessels. Plaque formation in the internal or common carotid, if the piece breaks off, patient may experience a loss of vision.

b. Left sidei. Heart

ii. Arch of the aortaiii. Common carotid arteryiv. Internal carotid arteryv. Subclavian artery

vi. Vertebral arteryc. Clinical

i. Subclavian steal syndrome: subclavian artery takes away all the blood. Blood goes up the common carotid and the subclavian to the vertebral artery (in the posterior cranial fossa). If there is blockage between the common carotid and the subclavian, there will be orthograde perfusion to the brain and retrograde perfusion through the posterior cerebral and basillary arteries.

1. Orthograde perfusion via ICA circle of Willis2. Retrograe perfusion via posterior cerebral artery basilary artery vertebral artery subclavian artery.

ii. This occurs due to occlusion of the aorta between the origins of the left common carotid artery and left subclavian artery by atherous plaque formation.

III. Arterial supply to the braina. Divisions

i. Anterior circulation provided by branches derived from the internal carotid artery. Perfusions provided by branches of the ICA. 1. Cervical portion of ICA no branches. Supplies the CNs in the cavernous sinus (trigeminal ganglion, CNs III, IV and VI).

Vessels emerging from here and tentorium cerebellum attaches to sphenoid bone. Supraclinoid parts of the artery relate to

branches that are in the subarachnoid space above the cavernous sinus. The first artery given off is ophthalmic that accompanies optic nerve through optic canal. Supraclinoid portion of the ICA terminates by dividing into five branches

a. Opthalmic artery: first major branch given off intracranially. The ophthalmic artery accompanies the optic nerve in the optic canal and gives rise to these vessels:

i. Central artery of the retina branches into the temporal and nasal branches. Supplies the retinal surface that faces vitreous.

ii. Anterior and posterior ciliary arteries1. Anterior ciliary artery: supplies the sphincter papillary muscle and the iris2. Posterior ciliary artery: encircles the optic nerve as it tries to exit the posterior aspect of the eyeball

through the lamina crisbosa. Effected by lesions or clots and will lead to blindness in the entire eye. iii. Branches to the muscles and structures of the orbitiv. The supratrochlear branch anastomoses with the angular branch of the facial artery.

2. Petrous portion of ICA (in the carotid canal of the temporal bone) caroticotympanic artery and artery of the pterygoid canal (at the base of the pterygoid fossa).

ii. Posterior circulation provided by branches derived from the vertebral-basilar arteryb. Circle of Willis

i. Internal carotid artery branch into1. Anterior cerebral artery has A1 and A2 segments. Supplies the medial surfaces of the cerebral hemisphere (motor cortex for the

leg) up to the parieto-occipital fissure. a. A1: proximal segment of this vessel from its origin from the ICA to the anterior communicating artery

i. Branches: Medial striate artery (lenticulostriate artery)—very important vessel. A rupture here is the leading cause of intracerebral (intraparenchymal) hemorrhage. Chance of survival is less than 10%.

b. A 2: portion of the vessel from the anterior communicating artery distally to the cortex. i. Branches these terminate at the parito-occipital fissure.

1. Recurrent artery of Hubner2. Frontopolar branch3. Callosomarginal branch4. Pericallosal branch

2. Anterior communicating artery extends to the medial surface of the brain. Formed by connecting the two anterior cerebral artery. This artery has a high incidence of berry aneurysms. Optic chiasm is right below. If there is a mass pushing on the artery, the lower field of vision will be affected.

3. Posterior communicating artery anastomosis with the posterior cerebral artery. ii. Posterior cerebral artery: terminal branch of the basilar

NOTE: these vessels may be symmetrical and well developed or hypoplastic and sometimes completely absent due to agenesis. NOTE: ICA also branches into middle cerebral which supplies the lateral aspect. This artery is the common vessel of cardiovascular disease.

iii. Middle cerebral artery: ARTERY OF CEREBROVASCULAR DISEASE

1. Supplies the superiolateral surface of the cerebral hemisphere and many deep brain structures (internal capsule and optic radiations)

a. M1: proximal segment is the arterial portion from the ICA to the trifurcation of the vessels in the lateral fissurei. Branches: Lateral striate (lenticulostriate) arteries these vascularize the thalamus, basal ganglion. So if this

artery is damaged, the ventricles and other areas will fill with blood. These are hairlike, so it does not take much to damage them.

b. M2: thie portion from the trifurcation of the artery distally to the margin of the cortexi. Branches

1. Temporopolar arterypolar region2. Precentral (Rolandic) branches in the central sulcus3. Postcentral (Rolandic) branches in the central sulcus4. Angular branches weirnickes area found posterior to the superior ramus of the lateral fissure. Find the

angular gyrus and these arteries are right there. 5. Posterior temporal branches supplies the occipital cortex. if there is a problem with the posterior

cerebral artery, total blindness is expected, but parts of the macular vision is spared because of these arteries. Occasionally these are from the temporal polar branch of the middle cerebral.

iv. Anterior choroidal artery: supples the optic tract, choroid plexus in the inferior horn of the lateral ventricle and some of the thalamic nuclei psoteriorly. NOT A PART OF THE CIRCLE OF WILLIS

v. Posterior communicating artery: establishes anastomosis between the anterior and posterior brain circulations. Supplies the base of the brain, especially the hypothalamus and adjacent structures.

c. Posterior circulation: profusion provided by branches derived from the vertebral and basilar arteriesi. Vertebral arteries

1. Origin: arise from the internal segment of the subclavian arteries2. Associated with the upper six cervical vertebrae (foramina transversaria) and enter the posterior cranial fossa via the foramen

magnum. 3. Joints the basilar artery at the pontomedullary junction, at the base of the brainstem. Basilar artery turns into the posterior

cerebrals. The tentorium cerebella is here, so the artery must cross the tentorial notch to get to the supratentorial. Supplies medial and lateral occipital and basal portion of the temporal lobe.

4. Branchesa. Posterior spinal artery supplies the Cervical spinal cord dorsal columnsb. Posterior inferior cerebellar artery supplies the posterior lateral medulla (Wallenberg’s syndrome), 4th ventricle, the

choroid plexus and the posterior inferior cerebellum. c. Anterior spinal artery the medullary pyramids, medial leminiscus, tectospinal tract, medial longitudinal fasiculus (MLF),

hypoglossal nerve (CN XII-Dejerine’s syndrome). 5. Supplies

a. Spinal cord includes the gray matter, the lateral and anterior funiculi. Anterior spinal artery supplies 2/3 of the cord. Part of the dorsal gray column is supplied by the posterior spinal artery but the rest is the anterior spinal artery.

ii. Basillar artery1. Branches

a. Anterior inferior cerebellar artery (a.i.c.a.)b. Labyrinthine (internal auditory) arteryc. Paramedian(pontine) arteriesd. Long and short circumferential arteriese. Superior cerebellar artery supplies the superior cerebellum including its deep nuclei.f. Posterior cerebral artery P1,P2 and P3 segments supply respectively, the hypothalamus, post. lat. thalamus

(thalamogeniculate br.), choroid plexus (post. choroidal br.), midbrain peduncles, tectum (quadigeminal brs.), basal surface of the temporal lobe (ant. and post. temporal brs.) and all of the occipital lobe of the brain, and especially the visual cortex. (calcarine br.). This artery must leave the infratentorial posterior cranial fossa to cross the tentorium cerebelli in order to supply the structures of the cerebrum. This makes the vessel vulnerable to injury as it can be stretched and compressed by the free edge of the tentorium in passage. As it ascends to the temporal lobe and occipital lobe, it touches the Thalamus.

2. Suppliesa. The basilar artery supplies all brainstem structures through its many branches. b. Vascular insufficiencies result in the syndromes of Weber, Benedickt’s, Parinaud, Millard-Gubler and Foville depending

on level of involvement. IV. Venous drainage

a. Deep (internal) cerebral veinsi. Tributaries

1. Thalamostriate vein2. Caudate vein3. Septal vein

b. Great Vein of Galeni. Tributaries

1. Deep (internal) cerebral veinsc. Straight sinus (dural sinus)

i. Tributaries1. Great vein of Galen2. Basal vein of Rosenthal3. Inferior sagittal sinus4. Superior cerebellar veins

d. Confluence of the sinusesi. Tributaries

1. Superior sagittal sinus2. Straight sinus

3. Occipital sinuse. Transverse (lateral) sinus f. Sigmoid sinus

i. Superior petrosal sinusg. Internal jugular vein

i. Inferior petrosal sinus drains the cavernous sinus.h. Cavernous Sinus

i. Tributaries1. Sphenoparietal sinus2. Intercavernous sinus3. Circular sinus4. Superior and Inferior ophthalmic veins5. Pterygoid plexus of veins

ii. The cavernous sinus is drained by the inferior petrosal sinus.i. Superficial Cortical Veins

i. Middle cerebral veinii. Bridging veins - associated with subdural hematoma

iii. Large (Superior) anastomotic Vein of Trolard drains to the superior sagittal sinus. It is usually observed in the postcentral sulcus of the brain.

iv. Small (Inferior) Anastomotic vein of Labbe’ drains to the transverse (lateral ) dural sinus from the lateral fissure.

Outline for somatosensory system

I. Somatosensory receptorsa. Structures specialized to respond to stimuli (pain, temperature, proprioception, vibration) b. Activation of the sensory receptors results in depolarization that triggers impulses to the CNS. c. The realization of these stimuli, sensation and preceptor occur in the brain. d. Classified as simple or complex.

i. Most receptors are simple and include encapsulated and unencapsulated varieties. These have three major gateways ligand receptors, voltage gated receptors and mechanoereceptors.

ii. Complex receptors are special sense organse. Associations

i. Free nerve endings of sensory neuron thermoreceptors are associated with the spinothalamic tract. ii. Pacinian corpuslces (lamellated corpuscles) are associated with the DCML

iii. Muscle spindles, Golgi tendon organs and joint kinesthetic receptors are associated with the spinocerebellar and DCML tracts. f. Classes of receptors based on location

i. Exteroceptors:1. Found near the body surface2. Respond to stimuli arising outside the body3. Sensitive to touch, pressure, pain and temperature4. Includes the special sense organs

ii. Interoceptors1. Found in internal viscera and blood vessels2. Respond to stimuli arising within the body3. Sensitive to chemical changes, stretch, temperature changes

iii. Proprioceptors associated with the DCML pathways1. Located in skeletal muscles, tendons, joints, ligaments, connective tissue coverings of bones and muscles. 2. Respond to degree of stretch of organs they occupy3. Constantly advice the brain of one’s movements

g. Class of receptors based on stimulus typei. Mechanoreceptors respond to touch, pressure, vibration, stretch and itch

ii. Thermoreceptors ensitive to changes in temperature. Associated with the spinothalamic tractiii. Photoreceptors respond to light energy (retina). Associated with the DCML tractiv. Chemoreceptors respond to chemicals (smell, taste, changes in blood chemistry)v. Nociceptor sensitive to pain causing stimuli

II. General organization: thee neuron chaina. DCML and spinothalamic tracts have 1st, 2nd and 3rd order neurons. The receptor is associated with the 1st order neuron. b. Cell body of the 1st order neuron is found in the DRG for spinothalamic and DCML trattsc. 1st order neurons can be found in the DRG or trigeminal ganglion. Trigeminal is sensory. Its 1st order is found in the trigeminal gangliond. 2nd order neuron is found in the medulla or spinal cord. e. The VPL is coming up from the limbs and the VPM from the trigeminal tracts. f. After the thalamus, the neuron synapses on the postcentral gyri on areas 3, 2, 1g. Spinothalamic tract: First order neurons synapse with second order neurons in the dorsal hornh. Rexed lamina II substantia gelatinosai. Rexed lamina VII dorsal nucleus of Clarke (ANS)j. Lateral funiculus dorsal spinocerebellar, ventral spinocerebellar and lateral spinothalamick. Anterior anterior spinothalamic

III. Major ascending pathwaysa. Ventrolateral pathway conscious sensory information

i. Lateral spinothalamic tract pain and temperatureii. Ventral spinothalamic tract light touch and pressure

b. Dorsal column-medial leminiscal pathway conscious sensory informationi. Pressure

ii. Discriminative touch1. Stereognosis (feeling something with eyes closed02. 2 point discrimination3. Complex tactile discrimination

iii. Vibratory senseiv. Proprioception

c. Spinocerebellar pathway unconscious sensory infomationi. Dorsal spinocerebellar tract carries sensations from the trunk and upper and lower limb proprioceptors for maintenance of posture and

coordination of limb movements. ii. Ventral spinocerebellar tract carries sensation from trunk and upper and lower limb proprioceptors for maintenance of posture and

coordination of limb movements.

IV. DCML and spinothalamic: fibers for touch are bigger than for pain, so they get to the brain faster.

V. Cranial nerve V- trigeminal: 1st order synapses in the trigeminal ganglia with the 2nd order (in the principal sensory trigeminal nucleus). 2nd order rises and goes to VPM to synapse with 3rd order. 3rd order neuron goes to the inferior part of the precentral gyri (to the area associated with sensory of the face.

VI. Spinal cord compositea. Spinothalamic tracts b. Gracili and Cuneate Fasiculi c. Spinocerebellar tracts in the thoracic level

VII. Composition in the brainstema. Gracile and Cuneate Nuclei: Dorsal column made up by the axons of the first order neurons with the cell bodies in the DRG. The 1st order neurons

synapse with 2nd order neuron whose cell bodies are found in these nuclei. b. Internal arcuate fibers and Medial lemniscus: fibers start to cross at the internal arcuate fibers which make the Medial Leminicus. The connection

between the DC and ML is the internal aruate, which is made up of the 2nd order axons. The medial leminiscus is in the entire length of the brainstem. These axons will end in the VPL of the thalamus.

VIII. Thalamus encloses the 3rd ventricle.

IX. Postcentral gyusa. Legs terminate high and hands are lower. b. Anterior cerebral artery supplies higher up while the middle cerebral artery supplies lower. To lose sensation to the face, for example, the middle

cerebral artery must have been blown out. Loss of sensation to the feet will be due to anterior cerebral artery, because the feet are anterior.

c. Ventrolateral pathway: d. DCMLi. lateral spinothalamic tract

ii. ventral spinothalamic tract

d. Spinocerebellar unconscious proprioceptive stimuli synapse in the cerebellar cortex on the same side as the original stimuli. Have only 2 neurons. The nucleus of Clarke doesn’t transcend the length of the entire spinal cord. It is present only in C8-L2. Spinal cerebellar tracts from the

sciatic nerve come in and climb through the sacral portion in the lower lumbar to synapse with Nucleus of Clarke at L1/L2. In higher cervical regions, axons will come down and synapse with the Nucleus of Clarke at C8.

i. Dorsal spinocerebellar: 1st order neuron is in the DRG. It synapses with the 2nrd order neuron in the Nucleus of Clarke. The 2nd order neuron ascends, remains uncrossed and goes into the inferior or superior cerebellar peduncle.

ii. Ventral spinocerebellar tract: axons cross to the opposite side in the spinal cord and ascent to the cerebellum, and recross within the cerebellum.

X. Clinical correlationsa. DCML Lesions

i. Inability to identify the position of a limb in space with the eyes closed. These patients are unable to tell whether a joint is in a position of flexion or one of extension.

ii. Inability to identify objects placed in the hands, such as keys and coins, from their shape, size, and texture with the eyes closed.iii. Loss of two-point discrimination. These patients are unable to recognize two stimuli simultaneously applied to the skin when the stimuli

are seperated by the minimal necessary distance for their proper identification as two stimuli.iv. Inability to perceive vibration when a vibrating tuning fork is applied to a bony promience.v. Inability to maintain a steady standing posture when the eyes are closed and the feet are placed close together. These patients begin to

sway and may fall when they close their eyes, eliminating visual compensation.b. Spinocerebellar lesion

i. Result in incoordinate movement.ii. Tend to walk with a wide base, stagger, and frequently fall.

c. Spinothalamic lesionsi. Diminution or loss of pain & thermal sense CONTRA lateral to the lesion.

ii. When the tract is affected in the spinal cord, the sensory deficit begins one or two segments below the level of the lesion.iii. The spinothalmic tract may be sectioned surgically (cordotomy) to relieve intractable pain.

d. Corticospinal lesioni. Lower Motor Lesion (found in muscles supplied by the affected spinal cord segment)

1. Muscle paralysis2. Muscle atrophy3. Loss of myotatic reflexes4. Fibrillations & fasciculations 5. Hypotonia

ii. Upper Motor Lesion (occur at & below the level of the hemisection)

1. Muscle paralysis2. Spasticity3. Hyperactive myotatic reflexes4. Babinski sign5. Clonus

e. Somatosensory systemi. involves dorsal or sensory root of spinal nerve

ii. causes: local tumors, infections, injuries, herniated disciii. manifestations (ipsilateral and at level of lesion only)

1. pain & paresthesias 2. hypotonia & loss of deep tendon reflexes3. intact muscle strength4. no muscle atrophy5. deterioration of coordination

iv. Syringomyeliaprogressive tissue destruction with cavitation around central canal of spinal cord1. Cause: unknown2. Lesion is at the white commissure3. Manifestations (both sides and at level of lesion only).

i. loss of pain and temperature and light touch & pressure sensations (“band” of anesthesia or “cape-like” anesthesia

v. Hemisection of spinal cord. Brown Sequard syndrome1. Causes: trauma, vascular injury2. Manifestations below the lesion

ii. ipsilateral loss of discriminative touch, vibratory sense, proprioception iii. contralateral loss of pain & temperature sense and light touch & pressure coming down one to two levels. iv. ipsilateral spastic paralysis. v. Ipsilateral loss of motor and tactile sensation.

Outline for diencephalon

I. Topography of the braina. Divisions of the brain

i. Prosencephalon (forebrain)1. Telencephalon: anterior division of the prosencephalon. Develops into the olfactory lobe, cortex of the cerebral hemisphere (6

lobes), subcortical telencephalic nuclei, basal nuclei (striatum and amygdale. 2. Diencephalon: the caudal part o the prosencephalon composed of dorsal thalamus, epithalamus, subthalamus and hypothalamus.

ii. Midbrain (Mesencephalon)iii. Hindbrain (Rhombencephalon)

II. Lobes in the telencephalona. Frontal lobe

i. Extends from the frontal pole to the central sulcus and the lateral fissureii. Cognition and memory.

iii. Prefrontal area involved in the ability to concentrate, attention, and elaboration of thought. Involved in judgment, inhibition, personality and emotional traits.

iv. Primary Motor Area (Brodmann area 4) primary motor in the precentral gyri. 1. Axonal fibers from large pyramidal neurons (Betz’s cells) and small neurons descend to form the corticospinal tract. Correspond

to a motor homunculus feet anterior and face posterior. 2. involved with voluntary motor activity

v. Premotor (Cortex) Area (Brodmann 6)

1. Involved in the storage of motor patterns and voluntary activities.vi. Frontal Eye Field (Brodmann 8)

1. Concerned with eye movements. Sends projections to lateral gaze center (paramedium pontine reticular formation).vii. Broca’s Area (Brodmann 44 & 45)

1. Located anterior to the motor cortex controlling the lips and tongue. Involved in the motor production of speech. Projects to Wernicke’s area via arcuate fasciculus.

viii. Damage to this lobe may result in impairment of recent memory, inattentiveness, inability to concentrate, behavior disorders, difficulty in learning new information, inappropriate social and/or sexual behavior, emotional liability and/or flat affect, contralaeral plegia/paresis, expressive/motor aphasia.

b. Parietal lobei. Bounded in front by the central sulcus and below by the lateral sulcus before it turns upwards to the line that forms the posterior boundary

of the lobeii. Processing of sensory input, sensory discrimination

iii. Body orientation iv. DCML and spinothalamic tracts come up and terminate here. If the parietal lobe is damaged, patient will lose sensation. v. Primary zones: Exp. Postcentral gyrus / Primary Sensory Cortex (Brodmann areas 1,2, & 3)

1. Primarily concerned with perception or gnosis2. Commonly termed primary projection areas3. Possess high modal specificity, i.e. each particular area responds to highly differentiated properties of visual, auditory, or body

sense information4. Made up largely of cells that respond only to a specific sense modality5. Primarily concerned with sensation.6. Somatotypically represented, in a sensory homonculus, in the postcetral gyrus. Involved in somatosensory interpretation.7. Receives somatosensory input from the VPL (ventro posterolateral) and VPM (ventro posteromedial) nuclei.

vi. Secondary zones: Exp. Parietal lobe / Sensory Assoc Area (Brodmann 5 & 7) 1. Adjacent to the primary projection areas where the modality-specific information becomes integrated into meaningful wholes 2. Primary is sensing something and secondary involved in knowing what you sensed.

vii. Tertiary zones: Parietal lobe / Assoc. Areas (Brodmann 40 & 39) 1. Integrate information across sense modalities. They lie at the borders of the parietal, temporal, and occipital secondary zones. 2. Takes visual and sensory information and puts it all together

viii. Damage to the primary/secondary somatic area results in an inability to discriminate between sensory stimuli. Inability to locate and recognize parts of the body (“neglect”). Severe injury may result in inability to recognize self. Disorientation of environment space. Inability to write.

c. Occipital lobei. Lies posterior to the vertical boundary line on the convex surface. On the medial aspect to the parieto-occipital sulcus and a line joining

the junction of the parieto-occipital sulcus with the pre occipital notch.ii. Primary Sensory Cortex (Brodmann Area 17): Process of visual stimuli. Input from lateral geniculate, and projects to areas 18 & 19.

iii. Visual Association Cortex (Brodmann Area 18, 19): Allows for visual interpretation. Input from area 171. Damage to the primary visual cortex results in loss of vision in the contralateral visual field.2. Damage to the association cortex results in a loss of the ability to recognize objects seen in the contralateral field of vision, may

experience “flash of lights,” “stars.” d. Temporal lobe

i. Bounded by the lateral sulcus and the artificial line of demarcation. ii. Primary Auditory Cortex (Broadmann area 41): Process of auditory stimuli. Input from medial geniculate

iii. Associative Auditory Cortex (Broadmann area 42): Assist in the processing of auditory stimuli.iv. Wernicke’s Area (Broadmann area 22) receptive speech, language comprehension. Input from auditory association cortex, visual

association cortex, Broca’s area (Brodmann’s Area 44 &45) (via arcuate fasciculus).v. Expressed behavior.

vi. Memory: information retrieval.1. Damage results in hearing deficits, agitation, irritability, childish behavior.2. Receptive/sensory aphasia.

e. Insular lobei. Sunken portion of the cerebral cortex. Lies deep within the lateral cerebral fissure and can be exposed by separating the upper and lower

lips (opercula) of the lateral fissure. The insula is bound by the circular sulcus.f. Limbic System Components

i. The cortical components of the limbic system include the amygdaloid (almond) body, Limbic Lobe (made up of 3 gyri): cingulate (girdle or belt) gyrus, parahippocampal gyrus, and dentate gyrus. These gyri conceal the hippocampus (sea horse). These components form a ring of cortex that forms a border (limbus) between the diencephalon and more lateral cerebral hemisphere.

III. Broadmanns areasa. Motor: 4b. Somatosensory: 3, 1, 2c. Speaking: 44-45. Can’t speak if this area is damaged. UMN going to the larynx are damaged. Can’t say anything but can write it. d. Auditory: 41, 42. If 42 are knocked out, patients will have a word deafness. Patient knows people are taking but won’t understand what people are

saying. e. Visual: 17. If this area is lost, patient will go blind. f. 18g. Frontal eye gaze: 8

IV. White matter of the Cerebrum

a. Made up of millions of fiber processes or axons of nerve cells. b. Association fibers (intracerebral fibers) connect various regions within one hemisphere. These may join areas that are close together or the fibers

may be very long. i. Definition: connect gyri, lobes or widely separated areas within each cerebral hemisphere.

ii. U fibers - short fibers lie beneath the cortex and arch around the bottom of the sulci to connect adjacent gyri.iii. Long fibers lie more deeply and may be gathered into rather indefinite bundles or tracts, which connect the different lobes

1. Superior longitudinal fasciculus courses backwards from the frontal lobe to the occipital lobe and this tract sends fibers to the posterior part of the temporal lobe.

2. Fibers at the bottom of the superior longitudinal fasciculus sweep around the region of the insula connecting the superior and middle frontal gyri with parts of the temporal lobe. These fibers, known as the arcuate fasciculus, are important for an anatomical understanding of the aphasias.

3. inferior longitudinal fasciculus runs from the occipital to the temporal poles4. The uncinate fasciculus connects the anterior and the inferior parts of the frontal lobe with parts of the temporal lobe by a bundle,

which is fan shaped at either end and drawn together in a compact bundle as it arches sharply around the stem of the lateral sulcus.5. The cingulum is the principal association tract of the medial aspect. It lies within the cingulate gyrus and runs an arched course

over the corpus callosum beginning below the rostrum and terminating in the uncus.

c. Projection fibers convey impulses from deeper structures to the cortex or from the cortex to deeper structuresi. Two types

1. Afferent fibers convey impulses to the cortex.2. Efferent fibers carry impulses away from the cortex.

ii. Examples1. Corona radiate: fan out to all parts of the cortex dorsally, intersecting the commissural fibers of the corpus callosum. Ventrally,

they converge upon the striatum (caudate and putamen) and once they begin to funnel down between these nuclei, the fibers are referred to as the internal capsule. Many fibers of the internal capsule continue down to the brainstem in the crus cerebri and on into the spinal cord; some terminate in the thalamus and basal ganglia.

2. Thalamic radiations: The visual pathway can be followed from the stump of the optic nerves through the chiasm and optic tract to the lateral geniculate nucleus and then through the optic radiations to the primary visual cortex in the occipital lobe. Thalamic radiations also contain reciprocal connections from the cortex to the thalamus.

d. Commissural fibers (intercerebral fibers) unite homologous or equivalent areas of structures in the two cerebral hemispheres. i. The corpus callosum is the largest mass of connecting fibers in the nervous system. It joins corresponding areas in the neocortex of the

two cerebral hemispheres. Although most of the fibers in the corpus callosum unite corresponding or homologous areas, there are a small number of non-homologous fibers. Agenesis of the corpus callosum partially forms or does not form at all. Results in partial or complete separation of the two hemispheres except in the region of the anterior commissure and lamina terminalis. This anomaly may be associated with seizures, mental retardation or hydrocephalus. Gyral pattersl on the medial surface may also be abnormal while occipital lobe may appear normal. CAUSED BY FETAL ALCOHOL SYNDROME.

ii. The anterior commissure is a rounded, compact bundle of fibers, which crosses the midline just anterior to the anterior column of the fornix and just below the interventricular foramen. Its main part connects regions of the inferior and middle temporal gyri while a smaller portion interconnects olfactory regions on the two sides.

(A) Short fibers connect one gyrus to another nearby gyrus (intergyral or short association fibers). (B) Superior longitudinal fasciculus interconnects temporal, parietal, occipital and frontal lobes (a part of it is the arcuate fasciculus associated with language). (C) Superior occipitofrontal fasciculus interconnects occipital, parietal and frontal lobes. (D) Cingulum interconnects the cingulate and parahippocampal gyri. (E) Inferior longitudinal fasciculus interconnects occipital and temporal cortex. (F) Inferior occipitofrontal fasciculus interconnects occipital and frontal lobes. The arcuate fasciculus, a part of the superior longitudinal fasciculus, interconnects Wernicke's area (the posterior part of the superior temporal gyrus that is involved in the interpretation of spoken language) with Broca's area (the "motor speech" area in the posterior part of the inferior frontal gyrus, the opercular and triangular regions). The arcuate fasciculus is thus essential for normal speech and language function. Note also the optic radiation: the bundle labeled here probably includes fibers of the inferior longitudinal fasciculus, an association fiber bundle that interconnects the superior, middle, and inferior temporal gyri with the occipital lobe; the optic radiation fibers are between it and the lateral ventricle.

iii. The hippocampal commissure is composed of transverse fibers, which join the posterior columns of the fornix.V. Diseases

a. Parkinson’s disease – characterized by tremor, rigidity, and akinesis (poverty of voluntary movement). There are often accompanying abnormalities of equilibrium, posture, and autonomic function. Characteristic signs include slow, monotonous speech; diminutive writing (micrographia); and loss of facial expression (masked face), often without impairment of mental capacity. Associated with loss of pigmented neurons in the substantia nigra which send neurons to the BG, which then become overactive.

b. Huntington’s Disease – inherited disease involved with the destruction of ACh-secreting and GABA-secreting neurons in the Basal Ganglia. Leads to massive destruction of the BG and later of the cerebral cortex. Initial symptoms in many are wild, jerky, almost continuous “flapping” movements called chorea [Gk.. dance]. Opposite of PD, usually treated with drugs that block, rather than enhance, dopamine effects.

c. Alzheimer’s Disease – progressive degenerative disease of the brain that ultimately results in dementia (mental deterioration). Patients exhibit memory loss, shortened attention span, disorientation, and eventual language loss. Beta amyloid plaques and neurofibrillary tangles (protein called Tau)

d. Concussion – alteration in brain function, following a blow to the head.e. Contusion – a serious concussion causing bruising of the brain.f. CVA (cerebral vascular accident) / Stroke – blood circulation to a brain area is blocked and brain tissue dies.g. TIA (transient ischemic attack) – temporary episodes of reversible cerebral ischemia. Last 5 to 50 minutes, and are characterized by temporary

numbness, paralysis, or impaired speech.VI. Diencephalon: main processing center for information destined to reach cerebral cortex from all ascending sensory pathways (except olfaction) and

other subcortical cell groups. a. Thalamus

i. Gateway to cerebral cortexii. Primarily related to somatic functions

iii. Collection of neuronal cell groups1. Sensory: Lateral geniculate, medial geniculate, ventral posterolateral, ventral posteromedial 2. Motor: Ventral anterior, ventral lateral3. Limbic: Anterior, dorsomedial 4. Multimodal: Pulvinar, lateral posterior (posterolateral), lateral dorsal (dorsolateral)5. Intralaminar: Reticular, centrum medianum, intralaminar

iv. Thalamic organization1. Thalamocortical and corticothalamic axons2. Relay & association nuclei3. Specific or nonspecific

v. Nuclei of the thalamus1. Anterior Group: Part of the limbic system2. Medial Group: Integrates sensory information for projection to the frontal lobes.3. Ventral Group: Projects sensory information to the primary sensory cortex; relays information from cerebellum and basal nuclei

to the motor area of the cerebral cortex.

4. Posterior Groupa. Pulvinar – Integrates sensory information for projection to association areas of cerebral cortexb. Lateral geniculate nuclei – Project visual information to the visual cortexc. Medial geniculate nuclei – Project auditory information to the auditory cortex.

5. Lateral group: Integrates sensory information and influences emotional states.vi. Location/landmarks

1. Large, ovoid, gray mass of nuclei2. Its broad posterior end, pulvinar, extends over the medial and lateral geniculate bodies.3. The narrower rostral end of the thalamus contains the anterior thalamic tubercle.4. In many individuals there is an interthalamic adhesion (massa intermedia) between the thalami, across the narrow third ventricle.

b. Dorsal thalamusc. Internal capsuled. Hypothalamus

i. Receives sensory input regarding internal environmentii. Regulates and modifies internal environment through motor systems

iii. Principal modulator of ANSiv. Viscerosensory transducerv. Regulates anterior pituitary

vi. Performs endocrine functionvii. Functions

1. The subconscious control of skeletal muscle contraction2. The control of autonomic function (heart rate, blood pressure, respiration, and digestive functions)3. The coordination of activities of the nervous and endocrine systems (regulatory hormones: TRH)4. The secretion of two hormones – ADH & oxytocin 5. The production of emotions and behavioral drives6. Coordination between voluntary and autonomic functions7. Regulation of body temperature8. Control of circadian rhythms

viii. Components1. Mammillary bodies – control feeding reflexes (licking, swallowing, etc.)2. Autonomic centers – control medullary nuclei that regulate heart rate and blood pressure3. Tuberal nuclei – release hormones that control endocrine cells of the anterior pituitary gland (TRH)4. Supraoptic nucleus – secretes ADH, restricting water loss at the kidneys5. Paraventricular nucleus – secretes oxytocin 6. Preoptic areas – regulates body temperature7. Suprachiasmatic nucleus – coordinates day-night cycles of activity

ix. Landmarks

1. Lies between and in front of the thalamus2. Forms the floor and lower walls of the third ventricle3. External landmarks

a. Optic chiasmb. Tuber cinereum (tuber: a localized swelling or knob)– a prominence of the base of the hypothalamus with its

infundibulum extending to the posterior lobe of the posterior pituitary gland (hypophysis)c. Mammillary bodies – lying between the cerebral peduncles

e. Ventral thalamusf. Epithalamus

i. Consists of the habenular trigones (small triangular area in front of the superior collicus containing the habenular nuclei) of each side of the third ventricle, the pineal body, and the habenular commissure.

ii. FUNCTION: regulation of circadian rhythms; linking of olfactory system to brainstem. Other functions still unknown.iii. Pineal gland

1. Produce melatonin from serotonin2. Melatonin helps regulates circadian rhythms

Outline for neuroanatomy and functions of the cerebellum

I. Cerebelluma. If there is a unilateral lesion, the clinical sign is ipsilateral to the damage. b. Somatotrophy of the cerebellum reflects a body

i. Central portion vermis and intermediate zone: subserves the midline body (trunk). Control coordination of muscle tone of the trunk. These areas have the spinocerebellar tracts.

1. Lesion along the midline will result in symptoms such as gait problems (ataxia) due to issues with posture. With the exception of the flocculus and nodules, the midline portions of the cerebellum project to the midline deep cerebellular nuclei.

ii. Lateral portions hemispheres: subserves the extremities (limbs).controls muscle coordination and tone on the ipsilateral side of the body. These areas have the cerebrocerebellum tracts.

1. Lesions along the lateral result in symptoms involving the distal extremities (dysmetria or dysidadochokinesia). The lateral portions tend to project to their correspondingly more lateral deep cerebellular nuclei.

iii. Flocculus and nodules: coordinate equilibrium and eye movement. Have the vestibulocerebellum tract. c. The primary output (purkinje cell efferent) from the cerebellum is through the superior cerebellular peduncle. The primary input into the

cerebellum (climbing fiber, mossy fiber and aminergic fiber afferents) is through the middle and inferior cerebellular peduncles. d. Granule cells are the only excitatory cells in the cerebellular cortex. All other cell types are inhibitory.

II. Landmarks of the cerebellum

a. The cerebellum is located at the dorsal aspect of the pons and medulla. It forms the roof of the 4th ventricle. The choroid plexus makes and filters the CSF.

i. Clinical implications: 1. Mass lesions, swelling (edema following an infact) or compression can lead to obstructive hydrocephalus since the cerebellum is

directly above the 4th ventricle. The cerebellum can obstruct the flow of CSF from the 4th ventricle leading to hydrocephalus. If it is in a child, the child’s head swells and gets larger. If it is in an adult, it is more serious because it can result in a big increase in pressure. A shunt is usually required.

2. Examples: tumors (esp. astrocytomas) hypertensive hemorrhage, cerebellular infarct and chiari malformation (genetic narrowing of the area)

b. The superior cerebellular peduncle is the major outlet of the cerebellum.c. The tentorium is a fold of the dura mater that separates the cerebellum from the occipital lobe. The cerebellum fills most of the posterior fossa,

which is the caudal portion of the skull cavity. d. The vermis is in the midline. e. The intermediate zone is paravermal. f. Lateral hemispheresg. Flocculonodular lobes-near the pons (which is in the ventral aspect)

III. Cerebellum consists of:a. Cerebellular cortex: cell bodies (gray matter)b. Cerebellular fiber tracts (white matter)c. Deep cerebellular nuclei located amongst the white matter. These are also known as roof nuclei because they are located near the roof of the fourth

ventricle.d. Projections from the cerebellular cortex to the deep brain nuclei

Deep cerebellular nucleus Projections from cerebellular portions of1. Fastigial Vermis2. Globose Intermediate zone (medial part of the hemisphere) 3. Emboliform Intermediate zone (medial part of the hemisphere)4. Dentate Lateral hemisphere

Note: Globose and Emboliform nuclei are collectively referred to as interpositus (from intermediate zone). Note: the floccular-nodular lobe projects upon the vestibular nuclei (in the medulla)

IV. Cerebellar pedunclesa. Attach cerebellum to the brainstem. b. Located above and around the 4th ventricle. c. Three pairs: the primary output (efferent) from the cerebellum is through the Superior Cerebellular Peduncle, whilte the primary input (afferents)

to the cerebellum is through the Inferior and Middle Cerebellular Peduncles. i. Inferior: carry input fibers (afferent connections)

1. Ipsilateral Dorsal Spinocerebellular Tract (proprioceptive inputs from the body)2. Ipsilateral Cuneocerebellar Tract3. Contralateral Olivocerebellular (Brainstem) Tracts (proprioceptive input from the whole body via the inferior olive) 4. Vestibulocerebellular (from vestibular nuclei) 5. Some afferent (ventral spinocerebellular and tectocerebellular (audio/visual inputs from the colliculi) and reciprocal efferents

travel back to the vestibular nuclei through the inferior cerebellular peduncle. ii. Middle: carry input fibers. Largest.

1. Contralateral Pontocerebellular (from Pontine Nuclei which receive input from many areas of the cortex)iii. Superior: carry output fibers

1. Contralateral Dentatorubrothalamocortical tract (terminates in VL nucleus of thalamus (some indirectly via red nucleus),l then relayed to the cortex)

d. Contain afferent (incoming) and efferent (outgoing) fiber tracts. V. Types of afferent fibers to the cerebellum

a. Climbing fibers:

i. Originate in inferior oliveii. Synapse as Purkinje cells

iii. Send collaterals to deep nuclei b. Mossy fibers:

i. Originate from a variety of tracts (spinal cord, vestibular and pontine nuclei) ii. Synapse on granule cells (excitatory)

iii. Send collaterals to deep nuclei. c. Aminergic fibers

i. Locus ceruelus (noradrenergic) ii. Raphe nucleus (serotonergic)

Note: Both climbing and mossy fibers provide excitatory input. The aminergic inputs modulate cerebellular activity. (Aminergics are biological amines like dopamine, norepinepherine, etc).

VI. Primary neuronal cell types in the cerebellular cortex and their inputs and outputs

Input from Input synapses on cell type (located in the cerebellum)

Cell type activity and projects to

Excitatory climbing fibers Purkinje Inhibit deep nucleiExcitatory mossy fibers Granule Excite Purkinje cellsExcitatory granule cell parallel fibers Basket Inhibit Purkinje cellsExcitatory granule cell parallel fibers Stellate Inhibit Purkinje cellsExcitatory granule cell parallel fibers and mossy fibers

Golgi Inhibit Granule

Note:

1. Glutamate: major excitatory NT in the brain2. GABA: major inhibitory NT in the brain.3. Glycine: plays inhibitory factors in the spinal cord. 4. Interneurons: connects two neurons. The synapse is localized in one area. 5. Basket, stellate, and golgi cells are interneruons. 6. Granule cells are the only excitatory (glutamatergic) neurons in the cerebellular cortex. 7. Purkinje cells provide primary inhibitory (GABAergic) output of the cerebellular cortex by projecting to their ipsilateral deep nuclei (esp.

dentate nuclei which projects to the lateral hemisphere) VII. Layers of the cerebellular cortex (gray matter): outer to inner

a. Molecular layer

i. Stellate cellsii. Basket cells

iii. Dendrites from Purkinje cellsiv. Bifurcated (T-shaped) parallel fibers from granule cells (synapse on Purkinje cell dendrites)v. Dendrites of golgi cells

b. Purkinje cell layeri. Purkinje cells (cell bodies) output

ii. Basket cell projectionsc. Granule cell layer

i. Granule cellsii. Golgi cells (cell bodies)

iii. Mossy fiber (glomeruli) synaptic connections inputiv. Climbing cell fibers input

VIII. Functions of the cerebelluma. Coordination of voluntary motor activity by influencing muscle activity

i. Fine skilled movements (writing, painting, typing)ii. Gross propulsive movements (walking, aerobics)

b. Maintanence of posture and balance (equilibrium) via connections with the vestibular system. If the vestibular nuclei is damaged, patient will experience a loss of balance.

c. Maintainence of muscle tone via connections to the spinal cord (gamma motor neurons)d. Motor learning and memory (stereotyped movement), like walking and running (these are learned tasks, don’t want to think about it but it takes a

long time to learn.)

IX. Clinical correlations signs of cerebellular dysfunctions

X. Divisions of the cerebellum and their associated cerebellular cortex areas and functions

Outline for neuroanatomy and functions of the basal ganglia

I. Movement disordersa. Akinesia – greatly diminished or lack of movementb. Bradykinesia - abnormal slowness of movement, sluggishness. c. Some Dyskinesias :

i. Athetosis - ceaseless occurrence of slow , sinuous writhing movements preformed involuntarily and especially severe in the hands.ii. Chorea - ceaseless occurrence of a wide variety of rapid, highly complex, and jerky movements that appear to be well coordinated but are

involuntary.iii. Tremor - rhythmic oscillating movements.iv. Ataxia – unsteady movements, inability to coordinate voluntary muscle movements.

v. Asynergy – loss of coordinationd. Dystonia - disorder tonicity of muscles. Contortions of the muscles of the truck and extremities. Usually relates to posture.

II. Overview of Basal Gangliaa. The basal ganglia influence movement indirectly. They do not project directly to motor neurons in the spinal cord or brainstem. They influence the

output of the cortical neurons through a series of parallel loops.b. Circuit:

i. Widespread areas of the cortex project to the stratum. ii. The striatum projects to the globus pallidus.

iii. The globus pallidus sends inhibitory projects to the thalamus. iv. The thalamus sends excitatory projections to the cortex

c. Basal ganglia are masses of gray matter deep within the cerebral hemispherei. Major nuclei

1. Caudate nuclei: major site of input 2. Putamen: major site of input 3. Globus pallidus

i. GPeii. GPi

The caudate and putamen are collectively referred to as the striatum (striped) The putamen and golbus pallidus are collectively referred to as the lenticular (lens shaped nuclei) All three are collectively referred to as the corpus (body) striatum (striped)

ii. Basal ganglia anatomy1. All basal ganglia nuclei are bilaterally symmetrical in the sagittal axis2. The caudate nucleus forms a long tapering loop. It has a larger portion called the head and a thinner portion called the tail. The

loop follows along the anterior horn of the lateral ventricle to the (even more lateral) temporal horn of this ventricle. In some cross sections, the head and the tail of the caudate can be seen. The tail is more lateral than the head, near the occipital lobe.

3. The globus pallidus is split by a medullary lamina into interior and exterior portions called GPi and GPe. III. Internal capsule

a. Sheets of white colored myelinated fiber tracts that pass between the head of the caudate and lenticular nucleus. It gives a striped (striatal) appearance. This is not a part of the basal ganglia

b. Three portions that form an obtuse V shapei. Anterior limb

1. Separates the head of the caudate and lenticular nucleus2. Contains the following fiber tracts

i. Thalamocortical and corticothalamicii. Frontopontine

iii. Transverse fibers from the caudate to putamenii. Genu (knee)

iii. Posterior limb1. Separates the lenticular nucleus and the thalamus2. Contains the following fiber tracts (anterior portion)

i. Anterior portiona. Corticospinal

b. Corticobulbar

c. Cortiborubralii. Posterior portion

a. sensory fibers from PL nucleus of thalamus to postcentral gyrus3. In both portions, there is a somatotopy (Face Arms Legs) so lacunar (small) infarcts pf the penetrating artery branches with the

internal capsule can produce selective motor or sensory deficits. (Example: a lacunar infarct in the anterior portion of the posterior limb will produce a “pure motor” stroke)

IV. Extrapyramidal system (outside of the pyramids) is comprised of:a. Basal ganglia nuclei

i. caudate – major site of input (from cortex and SNc)ii. putamen – major site of input (from cortex and especially SNc)

iii. globus pallidus (GPi) – major source of output (to thalamus)b. (Other) midbrain nuclei

i. subthalamic nucleus (STN)ii. substantia nigra (SN)

V. Basal ganglia connections/circuits

VI. Diseases involving the basal ganglia or other extrapyramidal nuclei

a. Parkinson’s disease: bilateral degeneration of dopaminergic neurons in the substantia nigra (pars compacta) that project to the striatum nigrostriatal pathway

i. Progressive, idiopathic neurodegenerative movement disorder of the basal ganglion. ii. Onset between 50-65 years old. Can have an early onset but this is rare, usually due to family history and is more severe

iii. Due to loss of darkly pigmented dopaminergic neurons in the substantia nigra (SNc) nigrostriatal pathway. Darkly pigmented dopamine (black because dopamine is oxidized) cells in the substantia nigra die off in Parkinson’s.

iv. Clinical signs1. Tremors (pill-rolling)2. Rididity (cog wheel)3. Akinesia4. Often abnormal posture, equilibrium and autonomic function5. Masked (expressionless) face6. Slow, monotonous speech7. Micrographia (small handwriting)8. Often there will be no loss of mental capacity, especially in the early stage.

v. Problem: loss of dopaminergic input into the striatum results in enhanced inhibition of the thalamus (1) which underexcites the motor cortex (2).

vi. Surgical treatment strategies1. Pallidotomy: lesioning of the GPi (reduces excessive inhibition of the thalamus by this nucleus in PD, which results in enhanced

stimulation of the cortex)2. Lesioning of the subthalamic nucleus.

Black: inhibitory. White: excitatory. Blocking output from the STN or GPi relieves the symptoms of PD. vii. Drug treatment

X

1. Muscarinic anticholinergics (useful in early stages): inhibitory dopaminergic control of cholinergic interneurons in striatum is lost in PD and blocking muscarinic receptors prevents the over activity of the cholinergic interneurons.

2. Levodopa (L-DOPA): a domaine precursor that restores the lost dopamine. L DOPA can cross the blood brain barrier easily because transporters take it up thinking its an AA. (shouldn’t have L DOPA right after a high protein meal, because the AA in the proteins will compete with L DOPA). This drug is given in combination with carbidopa (a peripheral AAAD inhibitor) to prevent L DOPA from being converted to Dopamine in the periphery.

3. Selegiline: a monoamine oxidase B (MAOB) inhibitor that prolongs the actiosn of dopamine, but preventing its degradation. 4. Amantadine: an antiviral agent that also acts as a weak antiglutamatergic (reduces cortical glutamatergic excitation)

b. Huntington’s disease: bilateral degeneration of GABAergic neurons in the striatum that project to the substantia nigra (pars inteculata) striatonigral pathway

i. Genetic neurodegenerative movement, cognitive and mental disorder of the basal ganglia1. Autosomal dominant2. Mutation of Huntington gene (on chromosome 4) whose function is unknown. 3. An expanded CAG trinulceotide repeat disease.

ii. Onset usually between 35-45 years old. Childhood form can occur earlier and is more severe.iii. Due to loss of striatal GABAergic (and some cholinergic) neurons in the caudate and putamen (striatonigrial pathway) iv. Signs include

1. Choreaform movements (rigidity if early onset) due to loss of GABAergic neurons2. Cognitive dysfunction3. Psychiatric dysfunction (often depression)

c. Hemiballism: contralateral damage to subthalamic nucleusi. Due to lesion of contralateral subthalamic nucleus (usually due to infarct) in a normal person. In PD, lesioning the subthalamic nucleus

bilaterally is a treatment and does not result in hemiballism. ii. Signs include

1. Involuntary and violent (large) flailing movements of one extremity (arm or leg) on one side2. Often spontaneously resolves after several weeks.

Outline for neuroanatomy of motor control

Medical neuroanatomy of motor control

I. Introductiona. Efferent: exit. Leaving where you are going to somewhere distant output. b. Afferent: arriving from some distant place to where you are inputc. Lower motor neuron: from the motor neuron in the brainstem as a cranial motor neuron or fibers from the motor neuron out to the muscle. d. Upper motor neuron: all things before you get to the motor neurone. Cerebellular signs are due to ipsilatearl lesions. Motor signs are due to contralateral lesions. f. In the basal ganglia, the direct pathways refer to the monosynaptic connection between the putamen and the GPi. The indirect pathway refers to

the polysynaptic connections between the putamen and the GPi (goes from the putamen to GPe to STN then to GPi). These pathways go through the striatum.

g. The pyramidal neurons in the cerebral cortex become the pyramidal tracts (coticospinal and some of the corticobulbar tracts). That is fiber tracts of pyramidal neurons become part of the internal capsule, while becomes a part of the cerebral peduncles, which pass through the pons and become the pyramids.

II. Overviewa. Cerebral Cortex/Cortical (gray matter)b. Subcortex/Subcortical (gray matter) basal ganglion (below the cortex) c. (Descending) Motor Fiber Tracts (white matter) myelinated

i. corticobulbar – face & cranial nuclei—synapse on the cranial nerve nuclei. Motor neurons in the brainstemii. corticospinal – body –in the spinal cord.

iii. corticopontine – (cerebellum) - equilibrium/posture/gait iv. rubrospinal – (red nucleus) to the spinal cordv. reticulospinal – (reticular (biogenic amine) nuclei) project to spinal cord

vi. vestibulospinal – (vestibular system) balancevii. tectospinal – (visual/auditory) – sight and sound (sensory) cues

d. gray matter of spinal cord (motor neurons) e. efferent nerve (of spinal cord)f. Cerebellum (cerebellar cortex and deep cerebellar nuclei)g. Basal ganglia and Extrapyramidal nuclei

III. Divisions of motor system on the basis of generalized function

Type of movement Example Controlled byReflexes Extensor plantar (Babinski) Spinal (L3-5, S1)Reflexes (Visceral reflex) Light Higher levels (CN 2, midbrain)Sterotypic repetitious movements Walking Spinal cord, brain stem,

cerebellumSpecific, goal-directed movements

Writing or reaching for a piece of cake

Cerebral Cortex

Note: in higher animals transaction of upper brainstem produces spontaneous walking movements due to release from inhibitory cortical control. Reflexive movements are automatic, instinctive and unleamed movements that involve neurotransmission from sensory receptor afferent nerve through a ganglion cell to motor neurons then the muscle

IV. Corticospinal tract fibers Ia. A direct pathway from the motor cortex to motor neurons of the spinal cord exist only for muscles of the distal extremities. b. Arises from sensorimotor cortex

i. 55% motor/premotor areas 4, 6 (frontal lobe)ii. 35% sensory 3,1,2 (postcentral gyrus of parietal lobe)

iii. 10% other cortical areasiv. Only 5% specifically from large pyramidal (Betz cells) from layer V of area 4

c. Tracts originating from the frontal lobes subserve motor function, while those from the parietal lobe modulate ascending (sensory) inputs.d. These fiber tracts terminate or send collaterals to

i. Thalmus (VL nucleus)ii. Brainstem (reticular formation, pontine and cranial nuclei)

iii. Spinal cord (motor neurons in anterior horn and interneurons)

e. Also contains fibers that modulate the function of ascending systemsi. Thalamus (VP nuclei)

ii. Brainstem (dorsal column nuclei)iii. Spinal cord (dorsal horn laminas)

f. The fibers passes through the pyramids of the medullai. 87% of the fibers decussate in pyramids descend in the lateral column of the spinal cord

ii. 3% do not cross and descend in the lateral column of the spinal cord– these ipsilateral fibers control muscles of the trunk and proximal limbs; they are involved inmaintaining an upright posture and gross position of the limbs.

iii. ~10% descend in the anterior column of the spinal cord and decussate at lower cord levels close to their destination.g. There is somatic organization of the pyramidal tracts.

V. Corticobulbar tract fibersa. Also known as corticonuclear b. Arises from the portion of the sensorimotor cortex that subserves the face (big portion)c. Tracts pass through posterior limb of internal capsule and middle part of crus cerebri (cerebral peduncles)d. These fiber tracts terminate in brain stem nuclei

i. somatic efferent nuclei ii. brachial efferent nuclei

e. The nerves subserve muscular functions related to swallowing, chewing, coughing, breathing and speakingNote: corticobulbar fibers subserving the hypoglossal and lower portion of the facial nuclei are from the contralateral cortex only, while all other corticobulbar projects are bilaterally crossed.

VI. Extrapyramidal system motor systema. a set of subcortical circuits and pathways (outside of the pyramidal tracts) includes

i. basal ganglia nuclei (corpus striatum) – caudate, putamen & globus pallidus ii. midbrain nuclei/formations –subthalamic nucleus, substantia nigra, red nucleus, reticular formation

Note: sometimes the non-corticospinal tracts (e.g.,rubrospinal, reticulospinal, vestibulospinal, tectospinal) are considered part of the extrapyramidal system.

b. Many of the large number of interconnections between cortical and subcortical motor systems cross through the basal ganglia.VII. Basal ganglia motor system

a. Major site of INPUT is striatumb. Major site of OUTPUT is GPi c. GPi sends its inhibitory output to thalamic nuclei in fiber tracts (known as the ansa lenticularis, and lenticular fasciculus a.k.a. H2 fields of Forel)

that run through or around the internal capsuled. None of the Corpus Striatum projects directly to the spinal cord . However, the GP projects to the red nucleus, which then projects via the

rubrospinal tract to the spinal cord where it modulates flexor muscle tone. VIII. Cortico-basal ganglia loops: this happens to be what is know as the “direct pathway”, because it is monosynaptic from the striatum to the output

nucleus GPi. The only difference between the first and the second pathway is the nuclei in the middle and sometimes for convenience they are grouped together.a. Cortex > striatum > GPi > thalamus > Cortexb. Cortex > striatum > SNr > thalamus > Cortex

{terminate in brain stem nuclei

http://content.answers.com/main/content/wp/en-commons/thumb/1/12/200px-Gray764.png

{Originate in facial

region

IX. Cortico-subthalamic loopa. Cortex > Striatum > GPe > STN > GPi > thalamus > Cortexb. Cortex > STN > GPi > thalamus > Cortex

Pathway 1 happens to be what is know as the “indirect pathway”, because it goes from the striatum to the GPi via the GPe and STN. There are also projections (pathway 2) from the cerebral cortex directly to the STN.

X. Striato striatal loop (striatonigral-GABAergic) striatum > SNr then SNc > striatum (nigrostriatal –DAergic)XI. Subcortical descending systems/pathways

a. Rubrospinal (red nucleus to spinal cord) - modulates flexor muscle tone (coordinates with corticospinal to control hand and finger movement). Synapses on interneurons.

b. Vestibulospinal (brain stem vestibular nucleus to spinal cord) – modulates equilibrium/balance. Most synapses are on interneurons, which then project to alpha and gamma motor neurons, some synapses are directly onto extensor muscle motor neurons.

c. Tectospinal (midbrain tectum to spinal cord) – controls reflex movements of the upper trunk, neck and eyes in response to visual stimuli. Synapses on interneurons at the cervical levels.

d. Reticulospinal (reticular formation to spinal cord). Synapse on interneurons and gamma motor neurons. Note that vestibulo- , tecto-, and reticulospinal pathways have a very limited role on the control of extremities, and instead control

muscular of the trunk.XII. Clinical correlations

a. Decerebrate rigidity:i. A purely unilateral lesion of the corticospinal tract may result in only minor weakness, but movements of distal extremities (like a finger)

is often impaired. ii. Decerebrate rigidity occurs when the posterior portion of brain stem is severed by injury to the superior border of the pons. This results in

increased extensor tone in all muscles (trunk, limbs and neck), because cortical and basal ganglia inhibitory influence to the spinal cord are

blocked, but the vestibulospinal and reticulospinal excitatory influences remain intact. The end result is increased activity to extensor muscles (due mostly to increased gamma motor neuron activity which increases the activity of alpha motor neurons resulting in muscle extension)

XIII. Motor disturbance signsa. Four signs

i. Paresis (weakness)ii. Paralysis (can’t move)

iii. Abnormal reflexesiv. Abnormal movements

b. General categories i. Muscular or Neuromuscular Disturbance – damage to muscle or neuromuscular junction

ii. “Lower Motor” Neuron Lesions – damage to motor neuron cell body or fibers. Can be in the brainstem as well (corticobulbar) “Lower Motor” Neuron Lesions – damage to motor neuron cell body (in the spinal cord or brain stem) or fibers

a. poliomyelitis – viral disorder that kills motor neuronsb. spinal musclar atropy - a degenerative motor neuron disease of varying time of onset and severity

i. infantile form (Werdnig-Hoffman disease) - deathii. juvenile form (Kugelberg-Welander disease) - disability

c. Spinal cord tumor (mass lesion effect)d. Herniated disk

iii. “Upper Motor” Neuron Lesions – damage to anything rostral to motor neuron. In the internal capsulre, cerebral peduncle, “Upper Motor” Neuron Lesions – damage to anything rostral to the motor neuron. Often due to stroke

a. Lesions of portions of corticospinal tracts which synapse on motor neurons in the spinal cord. A purely unilateral lesion of the corticospinal tract may result in only minor weakness, but movements of distal extremities (like a finger) is often impaired. How can this be true? Long tracts

b. Lesions of corticobulbar which synapse on brain stem cranial nuclei which then innervate striated muscles. Note: Affected neurons are those that control voluntary (but not necessarily reflex) activation of lower motor neurons. Cerebral

palsy is technically an UMN disorder due to damage to cerebral cortex in utero. Characterized by spastic paralysis, BUT a variety of other signs may be present including rigidity, tremor, ataxia, athetosis, speech disorders and sometimes mental retardation.

Pons

iv. Basal Ganglia Related (includes extrapyramidal) – damage to corpus striatum, substantia nigra or subthamalic nucleusv. Cerebellular – damage to cerebrocerebellular, vestibulocerebellular or spinocerebellar structures or fibers

XIV. Muscular or neuromuscular junction disturbancesa. Disorder/Damage to

i. the musclesii. components of the neuromuscular junction (on the muscle side)

b. Examples includei. myasthenia gravis - autoantibodies to AChR characterized by fatigue, weakness and inability to sustain muscle contraction (esp. eyes and

mouth) and that resolves after rest.ii. myotonia - a group of hereditary neuromuscular disorders (caused by mutations in the chloride, sodium or potassium channels that affect

the muscle membrane) and characterized by slow relaxation of muscles after a contraction. Described as “stiffness” (e.g., difficulty releasing ones grip like after a handshake).

Table and Figure from Waxman et al.25th ed., 2003

DSA: taste and olfaction

I. List the four elementary taste qualities. (W: Fig 8-17)a. Sweetb. Saltc. Sourd. Bitter

II. Describe the sensory innervation of the tongue.a. CN VII (Facial): innervates anterior 2/3 of tongueb. CN IX (Glossopharyngeal): innervates posterior 1/3 of tonguec. CN X (Vagus): innervates epiglottis

III. i. (Note: all 3 of these taste sensory components of these nerves synapse in the solitary nucleus)

IV. Describe central taste pathwaysa. All taste sensory components (CN VII, IX, X) synapse in the IPSILATERAL solitary nucleus VPM part of thalamus cortex (insula and

postcentral gyrus)V. Describe olfactory receptors

a. Specialized neurons located in the olfactory mucous membrane (a portion of the nasal mucosa)b. Highly sensitive and respond with depolarization when confronted with odor-producing molecules that dissolve in the mucous layerc. Contain specialized odorant receptors that are coupled to G-protein molecules, which link these receptors to adenylate cyclased. When a specific odoriferous molecule binds to the appropriate olfactory receptor, it activates the G-protien molecule via adenylate cyclase,

generates a depolarization in the olfactory receptorVI. Describe the central pathways involved in olfaction.

a. The axons of the olfactory receptors travel within 10-15 olfactory nerves to convey the sensation of smell from the upper nasal mucosa through the cribriform plate to the olfactory bulb and olfactory tract (peduncle) lie in the olfactory sulcus on the orbital surface of the frontal lobe

b. The tract divides into the lateral and medial olfactory straie

c. Within the olfactory bulb, they olfactory receptor axons terminate in specialized synaptic arrangements (glomeruli) on the dendrites of mitral cellsd. Mitral cells of the olfactory bulb send their axons posteriorly via the olfactory tracts (medial and lateral olfactory stria) to the olfactory projection

area in the cortexi. The lateral stria is the projection bundle of fibers that passes laterally along the floor of the lateral fissue and enters the olfactory projection

area near the uncus in the temporal lob1. Olfactory projection area: pyriform and entorhinal cortex and parts of the amygdale

a. The pryiform projects via the thalamus to the frontal lobe, where conscious discrimination of odors presumably occurs ii. The small medial olfactory stria passes medially and up toward the subcallosal gyrus near the inferior part of the corpus callosum

1. Carries the axons of some mitral cells to the anterior olfactory nucleus, which sends its axons back to the olfactory bulbs on both sides, presumably as part of a feedback circuit that modulates the sensitivity of olfactory sensation

2. Other fibers reach the anterior perforated substance, a thin layer of gray matter with many openings that permit the small lenticulostriate arteries to enter the brain

a. It extends from the olfactory straie to the optic tract3. These fibers and the medial stria serve olfactory reflex reactions

VII. List potential causes of anosmiaa. Nasal infection = most common cause (common cold)b. Damage to cribiform plate due to head trauma damage to olfactory nerves, bulbs, or tractsc. Tumors in the dura lining above the cribiform plates (near the base of the frontal lobe – olfactory groove meningiomas) can lead to

compression/invasion injuries of the olfactory bulbs or tractsd. GOES UNREPORTED UNLESS BILATERAL!