Neuroscience LC 7 - Cranial Nerves - Course Outline PDF
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University of Northern Philippines
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This document outlines a neuroscience course on cranial nerves. It contains a breakdown of cranial nerve functions, including somatic-motor, somatic-sensory, and viscero-motor functions. The outline introduces and categorizes 12 pairs of cranial nerves.
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COURSE OUTLINE GLASGOW COMA SCALE TO ASSESS STUDENTS IN CLASSROOM I. INTRODUCTION TO CRANIAL NERVES EYE RESPONSE...
COURSE OUTLINE GLASGOW COMA SCALE TO ASSESS STUDENTS IN CLASSROOM I. INTRODUCTION TO CRANIAL NERVES EYE RESPONSE SCORE II. EXIT FORAMINA III. SOMATIC VS. VISCERAL 4. Maintain eye contact 4 IV. CRANIAL NERVE FUNCTIONS V. SOMATO-MOTOR FUNCTIONS 3. Open eyes, but seems lost 3 A. Corticospinal tract B. Corticobulbar tract 2. Opens eyes only if commotion 2 C. Upper motor neuron (UMN) vs Lower 1.Asleep 1 motor neuron (LMN) VI. SOMATO-SENSORYFUNCTIONS VERBAL RESPONSE VII. VISCERO-MOTOR FUNCTIONS VIII. VISCERO-SENSORY FUNCTIONS 5. Asks relevant questions spontaneously 5 IX. SPECIAL SENSORY FUNCTIONS 4. Answer open question 4 X. PHARYNGEAL ARCH FUNCTIONS XI. PURELY SENSORY CRANIAL NERVES 3. Answer only when directly asked 3 A. CN I B. CN II 2. No response 2 C. CN VIII 1.Asleep 1 XII. PURELY MOTOR CRANIAL NERVES A. CN III MOTOR RESPONSE B. CN IV C. CN VI 6. Raises hand to ask questions 6 D. CN XI E. CN XII 5. Raises hand to respond to questions 5 XIII. MIXED CRANIAL NERVES 4. Sits Straight, but yawns occasionally 4 A. CN V B. CN VII 3. Sits slumped, looking down 3 C. CN IX D. CN X 2. Head-on-hands, on the desk 2 1.Asleep 1 I. INTRODUCTION TO CRANIAL NERVES 12 pairs, Roman numerals I to XII All passes through foramina in base of skull ○ Foramen magnum largest foramina CN XI (Accessory nerve) is the only spinal nerve that enter and exit here Mainly control anatomic structures of head except: ○ CN X: controls thoracic and abdominal cavities ○ CN XI: controls sternocleidomastoid and trapezius muscles Cranial Nerves Nuclei (Nerve Cell Body/Soma Origin) ○ CN I: Basal forebrain ○ CN II: Diencephalon (Thalamus) ○ CN III - XII: Brainstem Figure 1. The Cranial Nerves Figure 3. Cranial Nerves Mnemonics BATCH 2028 1F 1 NEUROSCIENCE LC 7 Other CN Mnemonics: ○ Oh Oh Oh, To Touch And Feel Virgin Girls’ Vaginas And Hymens ○ Oh, Oh, Oh, To Touch And Feel A Guys Vagina, So Homo! ○ Oh Oh Oh, Topless Tiffany And Fat Vicky Got Vaginitis And Herpes Figure 8. The Skull Base Figure 4. Brainstem Posterior View Figure 5. Brainstem Anterior View Figure 9. Internal Cranial Base II. EXIT FORAMINA ANTERIOR FOSSA ○ I - perforations in cribriform plate MIDDLE FOSSA ○ II - optic foramen ○ Superior Orbital Fissure III, IV, VI, & ophthalmic division of V location of cranial nerves that controls Figure 6. Cranial Nerves extraocular muscles Fracture or tumor = difficulty in moving the eyeballs/ paralysis of eye movement, “Frozen Eye” and numbness of forehead due to presence of CN V1 (ophthalmic division); but will not cause blindness because optic nerve traverses the optic canal ○ Maxillary division of V2 – foramen rotundum ○ Mandibular division of V3 – foramen ovale POSTERIOR FOSSA ○ VII and VIII – internal auditory meatus ○ IX, X and XI – jugular foramen ○ XII – hypoglossal foramen Figure 7. Mesencephalon, Pons and Medulla Oblongata ○ Brainstem is located in the posterior fossa BATCH 2028 1F 2 NEUROSCIENCE LC 7 Clinical Correlation: JUGULAR FORAMEN TUMOR GLOMUS JUGULARE TUMOR ○ most common inner ear tumor SIGNS AND SYMPTOMS ○ CN IX & X: Ipsilateral loss of the gag reflex ○ CN IX: Ipsilateral loss of pain, temperature, and taste in the tongue ○ CN X: Ipsilateral paralysis of the soft palate and larynx ○ CN XI: Paralysis of sternocleidomastoid, which results in the inability to turn the head to the opposite side ○ CN XI: Paralysis of trapezius, which causes shoulder droop and inability to shrug the shoulder. CNS involved: CN XI (Accessory nerve), CN X (Vagus nerve), CN IX (Glossopharyngeal nerve) Figure 10. Exit foramina of the 12 cranial nerves EXIT FORAMINA FOR THE CRANIAL NERVES IN THE Anterior I Perforation in fossa cribriform plate II Optic foramen III, IV, VI and Superior orbital ophthalmic fissure division of V Figure 13. Jugular foramen tumor Maxillary division Foramen of V rotundum Clinical Correlation: Mandibular Foramen ovale RIGHT CRIBRIFORM PLATE FRACTURE division of V Posterior VII and VIII Internal auditory Signs and symptoms: ANOSMIA Fossa meatus IX, X, and XI Jugular foramen XII Hypoglossal Figure 11. Summary of CN Exit foramina Signs and Symptoms will depend on what CN enter or exit because they can sensory/ motor Clinical Correlation: INTERNAL AUDITORY MEATUS FRACTURE Figure 14. Right cribriform plate fracture Signs and symptoms: Facial paralysis, Hearing loss III. SOMATIC VS. VISCERAL CN involved: CN VII (Facial nerve) & CN VIII SOMATIC (Vestibulocochlear nerve) ○ Neurons conduct impulses to and from somatic structures skin, skeletal muscles, tendons, joints afferent (sensory) and motor (efferent) VISCERAL ○ Neuron conduct impulses to and from visceral structures smooth muscle, cardiac muscle, glands afferent (sensory) and motor (efferent) Figure 12. Internal auditory meatus fracture ○ Autonomic nervous system BATCH 2028 1F 3 NEUROSCIENCE LC 7 Figure 15. Somatic vs Visceral diagram VISCERO-SENSORY(Visceral Afferent) IV. CRANIAL NERVE FUNCTIONS SPECIAL SENSORY (Special Afferent) SOMATO-MOTOR (Somatic Efferent) ○ smell, sight, taste, hearing, balance SOMATO-SENSORY (Somatic Afferent) VISCERO-MOTOR (Visceral Efferent) Figure 16. Cranial nerve functions BATCH 2028 1F 4 NEUROSCIENCE LC 7 Largest neuron in the CNS V. SOMATO-MOTOR FUNCTIONS 5th layer of the motor cortex (top/medial Part of the pyramidal system homunculus) ○ corticobulbar/ corticonuclear, corticospinal Note: generally, UMN cells are called tract pyramidal cells, excitatory motor neurons, Involved in voluntary control of the skeletal 20-120 um in diameter. These cells are the one muscles firing erratically during epileptic seizures Everything that is voluntary originates from the LMN Body: Ventral horn cells of the spinal cord motor cortex (executive functioning) 2 Neuron System: UMN and LMN ○ Upper Motor Neuron Pyramidal cells in the 5th layer of the motor cortex Control the skeletal muscle, they are the source of seizures - SEIZURES: happens if there is an irritation in the cortex specially the precentral gyrus will pass through the internal capsule -> brain stem -> decussate to the other side -> innervate the skeletal muscles of the head and face (mostly contralateral) ○ Lower Motor Neuron CN nucleus in the brainstem Efferent pathway Figure 18. Corticospinal tract (Motor tract) diagram ○ Away from the CNS towards skeletal muscle As seen in the homunculus, a tumor in the Some cranial nerves have bilateral somatic medial side would result to a lower limb motor control coming from the cortex weakness ○ Example: CN VII (facial expression), CN XI (turning head side to side) Figure 19. Homunculus Most decussate as the lateral corticospinal tract at the spinomedullary junction to Figure 17. Somato-motor innervation innervate the contralateral limb muscle, some do not decussate as the anterior (ventral) PYRAMIDAL PATHWAYS (General term for corticospinal tract to innervate the trunk MOTOR TRACTS) muscles (chest, back and abdomen) A. CORTICOSPINAL TRACT Movement of muscle of the limbs and trunk with control mostly from opposite side of the brain It has projection fibers TRUNK - anteriorcorticospinal tract(ipsilateral, do not decussate) LIMBS- lateralcorticospinal tract(contralateral, decussate) Direct innervation by the cortical motor neurons (UMN) of the anterior (ventral) horn cell of spinal cord Figure 20. Decussation of pyramidal tract UMN Body: Large pyramidal cells of Betz BATCH 2028 1F 5 NEUROSCIENCE LC 7 CRANIAL NERVE PALSY Clinical Correlation: The Upper Motor Neuron BULBAR PALSY ○ lesion results in an UMN weakness, central palsy Bilateral impairment of function of the lower ○ In the cortex, internal capsule, or brain cranial nerves IX, X, XI and XII, which occurs stem above nucleus due to lower motor neuron lesion either at The Lower Motor Neuron nuclear or fascicular level in the medulla or ○ lesion results in a LMN weakness, from bilateral lesions of the lower cranial nerves peripheral palsy outside the brainstem. ○ In the nucleus in the brain stem (the cell LMN disease: starting from cranial nuclei to bodies from nuclei), or in any lower part of cranial nerve up to the muscles that innervate the cranial nerve. May also involve CN V, VII in some literatures: leads to weak jaw and facial muscles ○ S/S: based on the functions of the above CNs (LMN: IX, X, XI and XII) Figure 21. Cranial Nerve Palsy SOMATOMOTOR FUNCTIONS: PART OF PYRAMIDAL SYSTEM B. CORTICOBULBAR TRACTS Movement of muscles of the head with control mainly from opposite side of brain Some movements of muscle in the head are with control from both cortical sides (bilateral) of the brain (e.g. facial expression, turning head side to side) Direct innervation by the cortical motor neurons Figure 23. Bulbar Palsy (UMN) of cranial nerve nuclei (LMN) in the brainstem UMN Body: Pyramidal Cells 5th layer of the motor cortex (lateral homunculus) LMN Body: CN Nuclei in the brainstem ○ Corticobulbar (motor) tracts that passes thru the cerebral peduncles of the midbrain V3, VII, IX, X, XI, XII A little over 50% decussate CN nuclei innervating skeletal muscles thereby generally receive bilateral first order neuron innervation (i.e. from both left and right cerebral motor cortex). But the dominant control is still Figure 24. (a) LMN lesion. (b) UMN lesion. Most of from contralateral cortex the cranial nerve nuclei are bilaterally innervated (right and left cortices) so a lesion occurring between the cortex and the nuclei (UMN) will not result in paralysis. One exception to that rule is CN VII. In the face, the area above the eyes is bilaterally innervated, so a lesion would result in mild weakness, if anything. However, the area below the eyes is unilaterally innervated, so the same lesion would cause marked weakness or paralysis. Additionally, the unilateral innervation is contralateral, so the effect would be seen on the side of the face opposite to the lesion (lesion right side= paralysis left side) LMN, lower motor Figure 22. Cranial Nerve Motor Function neuron; UMN, upper motor neuron. BATCH 2028 1F 6 NEUROSCIENCE LC 7 Face has mostly contralateral control. But the forehead has bilateral cortical innervation (both sides of the cortex), lower face: controlled only by the contralateral cortex a. Lesion at cranial nerve itself (LMN lesion), everything will be paralyzed b. Lesion in the cortex- weakness or paralysis of lower face but you can still crease your forehead E.g. If you had a viral infection 2 weeks ago and suddenly you had a facial paralysis - it is NOT a stroke but a Bell’s palsy Example of Bilateral Motor Cortex Control: Accessory Nerve ○ The motor cortex sends control to both Figure 27. Differentiation of Bulbar palsy and Pseudobulbar palsy in table form sternocleidomastoid and contralateral trapezius Motor cortex damage will present with C. UPPER MOTOR NEURON weakness to contralateral trapezius and VS LOWER MOTOR NEURON bilateral sternocleidomastoid Example damage to left motor cortex - Weak right shrugging of shoulders (trapezius) - Weak turning of head towards left side (bilateral cortical innervation of sternocleidomastoid), with intact right motor cortex that also contributes to right sternocleidomastoid ○ Damage to the peripheral accessory nerve itself Figure 25. CN XI (Special Visceral Efferent) Trapezius and Sternocleidomastoid BULBAR PALSY VS. PSEUDOBULBAR Figure 28. Corticobulbar tracts: 50% decussate ○ For lower cranial nerves IX, X, XI, XII (contralateral still dominates). Includes V3, VII, IX, X, XI, XII) NOTE: ○ Weakness: more severe in LMN ○ Atrophy- UMN will only atrophy at long term lesions/stroke ○ Fasciculations- rippling effect ○ Tone of muscles- e.g. patient with LMN lesion, arms once raised will immediately drop, hence the decrease in tone. UMN Figure 26. Bulbar palsy vs. Pseudobulbar palsy lesion will have spastic tone, hence the increased in tone BATCH 2028 1F 7 NEUROSCIENCE LC 7 VI. SOMATO-SENSORY FUNCTIONS THE BRAINSTEM SENSORY-MOTOR (AFFERENT) (AKA Cranio-sacral) ○ SENSORY: always contralateral ○ toward the sensorimotor cortex, mostly Ciliary Ganglion: Oculomotor Nerve (II) from the skin ○ controls the ciliary muscle of the eye ○ 3-neuron pathway/ system ○ controls the ciliary muscle that regulates VIA SENSORY GANGLIAS (FIRST ORDER the size or the shape of the legs NEURON) ○ controls also the size of your pupils. ○ ANALOGS OF DORSAL ROOT Pterygo-Palatine Ganglion: Facial Nerve (VII) GANGLION: Submandibular ganglion: Facial Nerve (VII) Otic Ganglion: Glossopharyngeal Nerve(IX) semilunar (trigeminal) ganglion (V) ○ the one that innervates the parotid gland geniculate ganglion (VII) (kaya naglalaway) *Remember: the facial vestibular and cochlear ganglia (VIII) nerve will also contribute to your salivary glossopharyngeal nerve ganglia (IX) glands or the sublingual glands. vagus nerve ganglion (X) Intramural Ganglia: Vagus Nerve (X) SECOND ORDER NEURONS: ○ found in the intestine. Within the target ○ brainstem nuclei organ. THIRD ORDER NEURON ○ thalamus *there is no sensory nuclei in the midbrain VII. VISCERO-MOTOR FUNCTIONS Motor to the viscera (Smooth muscles, cardiac muscles, and glands) ○ Sympathetic - C8-T5 autonomic nerves to the head Note: No sympathetic innervation coming from cranial nerves - There is no function of cranial nerves to the sympathetic: No fight or flight function. ○ Parasympathetic - brainstem (CN: III, VII,IX,X) - these 4 cranial nerves only have viscero-motor functions or parasympathetic functions. 3 NEURON SYSTEM 1. Primary Neuron - Thalamic Nuclei to the brainstem 2. Secondary Neuron (Preganglionic) - Visceromotor brainstem nuclei to a ganglion - found in the brainstem 3. Tertiary Neuron (Post-ganglionic) - Figure 30. Organization and anatomy of parasympathetic Parasympathetic nuclei to the effector organ, found division near or within the target organ (Intramural) Ex: Sectioning your intestines “sometimes” shows Intramural neurons inside. -Bakit kaya nag d-digest? And those are coming ORGANIZATION AND ANATOMY OF from your Vagus Nerve. PARASYMPATHETIC DIVISION (PARASYMPATHETIC OUTFLOW/ CRANIOSACRAL) 4 PARASYMPATHETIC NUCLEI Preganglionic fibers leave the brain via: (PREGANGLIONIC) FOUND IN THE BRAINSTEM CN (III) - To the intrinsic eye muscles, pupil (AKA: Thoraco-Lumbar) (Pupillary sphincter) and lens (Ciliary muscles) CN VII - to the tear (Lacrimal glands and Edinger Westphal Nucleus: Oculomotor Nerve salivary glands) (Submandibular/Sublingual), (III) -located in the midbrain mucosal glands Superior Salivatory Nucleus: Facial nerve (VII) CN IX - to the parotid salivary glands Pons Inferior Salivatory Nucleus: Glossopharyngeal CN X - to the visceral organs of the thoracic nerve (IX) Pons cavity (Heart and Lungs) and abdominal cavity Dorsal Vagal Nucleus: Vagus nerve (X) ○ the vagus nerve will improve the invasions of your heart, lungs, liver, stomach, pancreas as well in intestines (peristalsis)- effect is 4 PARASYMPATHETIC GANGLIONS- OUTSIDE only up to the transverse colon, no more BATCH 2028 1F 8 NEUROSCIENCE LC 7 effect in the sigmoid and rectum (taken cared off by the S2-S4) ○ while the pelvic lower intestines, the large intestines as well as the pelvic organs - urinary bladder, fallopian tube, genitalia are taking care of the s2, s3 and s4. Postganglionic Neurons are near(Terminal) the target organ or within (intramural) the target organ Preganglionic fibers leave the sacral region via: pelvic nerves (to the visceral organs in the inferior portion of the abdominopelvic cavity) Figure 33. Schematic representation of the autonomic nervous system, showing distribution of sympathetic and parasympathetic nerves to the head, trunk, and limbs. HEART VISCEROSENSORY: CN IX ○ Afferent Baroreceptor (BP)/ Chemoreceptor (O2, CO2) transcends info towards respiratory center and affect the level of O2 and CO2, as well as the blood pressure CN IX will send info to the brain if it sensed changes in the BP and O2 and CO2 levels in order for the body to react to the situation Figure 31. Organization of the Parasympathetic Division of the VISCEROSENSORY/VISCEROMOTOR: CN X ANS ○ Afferent Viscerosensory - Sense heart rate EFFERENT VISCEROMOTOR VIII. VISCERO-SENSORY FUNCTIONS ○ Slow heart rate Primary sensory ganglions (1st order) ○ Carotid massage can slow down the heart ○ Glossopharyngeal nerve ganglion (IX) rate ○ Vagus Nerve Ganglion (X) Secondary Nuclei ○ Solitary tract nucleus (Tractus Solitarius) Found in the dorsomedial medulla Assimilate the visceral-sensory information from CN VII (taste) and both CN IX (taste) and CN X (Taste, cardiac, and GI tract) Taste - facial nerve: anterior two-thirds, glossopharyngeal nerve: posterior one-third, cranial nerve 10 (vagus): epiglottis Tertiary Nuclei - Thalamus Figure 34. Extensive Vagus nerve function/innervation IX. SPECIAL SENSORY FUNCTIONS Figure 32. Primary sensory sympathetic afferent fibers (red) SMELL: OLFACTORY NERVE (I) shown in relation to posterior horn tract cells (green) conveying SIGHT/VISION: OPTIC NERVE (II) visceral information to the thalamus and to general visceral TASTE: efferent neurons (blue) ○ FACIAL NERVE (VII). BATCH 2028 1F 9 NEUROSCIENCE LC 7 ○ GLOSSOPHARYNGEAL NERVE (IX) ○ Arch 6: CN X (Recurrent laryngeal branch of ○ VAGUS NERVE (X) the vagus) HEARING: VESTIBULOCOCHLEAR NERVE (VIII) BALANCE:VESTIBULOCOCHLEAR NERVE (VIII) X. PHARYNGEAL ARCHES Pharyngeal arches are paired structures associated with the pharynx that contribute greatly to the formation of the face, jaw, ear and neck Each pharyngeal arch has a cranial nerve associated with it: Figure 35. Summary of pharyngeal arches ○ Arch 1: CN V (trigeminal) ○ Arch 2: CN VII (facial) ○ Arch 3: CN IX (glossopharyngeal) ○ Arch 4: CN X (Superior laryngeal branch of the vagus) PHARYN ARCH ARTERY CRANIAL NERVE SKELETAL ELEMENTS MUSCLES GEAL ARCH 1 Terminal branch of Maxillary and Derived from arch cartilages (originating from neural Muscles of mastication maxillary artery mandibular division crest): (temporalis masseter, and of trigeminal (V) From maxillary cartilages pterygoid), mylohyoid, Alispenoid, Incus anterior belly of digastric, From mandibular tensor tympani, tensor veli Marckel’s cartilage, malleus palatini (originate from cranial somitomere 4) Upper portion of external ear (auricle) is derived from dorsal aspect of 1st pharyngeal arch Derived by direct ossification from arch dermal mesenchyme Maxilla, zygomatic, squamous portion of temporal bone, mandible 2 Stapedius artery Facial Nerve (VII) Stapes, styloid process, stylohyoid ligament, lesser Muscles of facial expression (embryologic) and horns and upper sum of hyoid (derived from the (orbicularis oculi, orbicularis caroticotympanic second arch cartilage, originate from neural crest) oris, auricularis, platysma, artery (adult) fronto-occipitalis, Lower portion of external ear (auricle) is derived from buccinator), posterior belly 2nd pharyngeal arch of digastric, stylohyoid, stapedius (originate from cranial somitomere 6) 3 Common carotid Glossopharyngeal Lower rim and greater horn of hyoid (derived from the Stylopharyngeus (originate artery, most of (IX) third arch cartilage, originate from neural crest cells) from cranial somitomere 7) internal carotid 4 Left: Arch of Aorta Superior Laryngeal Laryngeal cartilages (Derived from the 4th arch Constrictor of pharynx, Right: Right Branch cartilage originate from cricothyroid, Levator veli Subclavian Figure 36. Cranial Nerves function summary BATCH 2028 1F 10 NEUROSCIENCE LC 7 XI. PURELY SENSORY CRANIAL NERVES Damage/lesion/tumor in cribriform plate and/or compression of Olfactory bulb or nerve may lead OLFACTORY (I) - Smell to anosmia (Ipsilateral) OPTIC (II) - Vision - Anosmia: loss of sense of smell VESTIBULOCOCHLEAR (VIII) - Balance and - Anopia: loss of the sense of sight Hearing A. CRANIAL NERVE I: OLFACTORY SHORTEST cranial nerve Origin: Basal forebrain Not considered as Cranial Nerves: CN I and CN II Sense (Afferent) of smell (Odors) Oldest / most primitive sensory, modality - the first sense to develop ○ The "first" CN ○ Derived from the embryonic nasal placode Can provoke the fastest response >5 million receptors with the ability to regenerate because it is a peripheral nerve, it has the ability to regenerate Olfactory hair cells (Cilia) ○ Bipolar Cells (Retinal and Olfactory Epithelium) Figure 39. Olfactory Groove Meningioma The olfactory receptors and bulb are in close Note: Most of the time the frontal lobe is a silent proximity to the cribriform plate of the ethmoid area. A meningioma can grow very large before a bone - trauma or tumor (meningioma) that patient can be symptomatic such as anosmia. compresses the cribriform plate= LOSE YOUR ABILITY TO SMELL OLFACTORY ASCENDING (AFFERENT) PATHWAY Example: Aromatherapy has the ability to affect your mood, the motivational and emotional aspect of smell (Hypothalamus), same goes with the bad odor. Figure 37. The olfactory bulb and receptors Figure 40. Olfactory bulb and Primary Olfactory Cortex Note: The process of Olfaction or smelling begins with hair like cilia that line the nasal cavity. This lining is called olfactory epithelium. As air enters the nasal cavity some chemicals in the air bind to and activate nervous system receptors on the cilia. This stimulus sends a signal to the first order neurons connected to the epithelial cells. This signal is carried by these neurons from the nasal cavity through openings of ethmoid bone and then to the olfactory bulbs of the brain. These signals then move Figure 40. Different tracts and central connection from the olfactory bulbs along the olfactory tracts to Note: Olfactory Mucosa also gets branches from the olfactory area of the cerebral cortex. the Trigeminal nerve (CN V1&2) BATCH 2028 1F 11 NEUROSCIENCE LC 7 ○ Reason why some odors have irritating character ○ Explains why even when anosmic, patients can still detect certain irritating substances (eg: Ammonia) ○ Sensory to the olfactory mucosa- CN V1 & 2 IRRITATING SMELL - the sense of irritation (e.g. formalin) you feel is through the trigeminal nerve (CN V1 and V2) but the ability special sense of smell is through the olfactory nerve (CN I) SMELL AND ODORANTS Figure 41. Smell in relation to lacrimation and salivation reflex ○ Qualitative Odor Sensation (e.g. smell of flower/ perfume) - CN I ○ Somatosensory Overtones of Odorants (e.g. - The signal travels from your nasal mucosa warmth, coolness, sharpness and irritation) - towards the brain stem, nucleus solitarius sends CN V (Ophthalmic V1 and Maxillary V2 back the information to the facial nerve towards divisions) the lacrimal gland and nasal palatine gland. - Connection/Relationship between the So when you smell something, you already know olfaction and the facial nerve. The facial what it tastes like because of the connection nerve is associated with the taste and between CN I and CN VII. provides fibers to the anterior two-thirds - There is a connection of the olfactory nerve of your tongue.That is why when you with the lacrimal gland, the taste on the smell something, you begin to salivate. If two-third of the tongue, submandibular and you smell something delicious, it has a sublingual glands. If you smell something your connection with your facial nerve and nasal and palatine glands will send that elicits a reflex action. You begin to information towards the brainstem and will tell remember how the food tastes and your facial nerve to salivate, taste, and tear. sometimes trigger your emotions because - There is also a connection between the there is a complex connection between trigeminal and facial nerves. For example, your taste, your lacrimal gland, and your chopping onions, the irritation of your eyes and sublingual gland. nose is through your trigeminal nerve and the tearing is through your facial nerve OLFACTORY ASCENDING (AFFERENT) PATHWAY B. CN II: OPTIC BATCH 2028 1F 12 NEUROSCIENCE LC 7 Figure 43. CRANIAL NERVE II: Optic Nerve ○ The interconnection of rods and cones forms the receptive fields Sense of sight starts at the rods and cones of the retina, cons will receive the color of light and rods receive the intensity of light. They will form a receptive field, the temporal and nasal retina. Then it will send the information to the optic nerve which runs through the optic canal. From the optic canal it will separate at the optic chiasm where there will be crossing of the nasal fiber. Then to the lateral geniculate body then will go to the optic radiation then finally to visual cortex where in these fusion of your image, color and even the size. Both of your eyes should see only a single image because of the function of your cortex that will fuse the image into a single image. Figure 43. Morphology of the retinal photoreceptors SECONDARY NEURONS ○ Bipolar cells- Links primary neurons to the optic nerve; Interconnects rods and cones to produce receptive fields TERTIARY NEURONS ○ Ends in the lateral geniculate nucleus (LGN) of the thalamus ○ Some do not run into LGN but run the superior colliculus of the midbrain medial to the pretectal region (pretectal nucleus) Connects with the Edinger-Westphal nucleus of Oculomotor nerve (CN III) Controls visual reflex: pupillary light reflex, accommodation reflex (part of the In conjunction with CN III and Edinger Westphal interpretation for brain death) Nucleus: ○ Pupillary Light Reflex ○ Accommodation Reflex PRIMARY NEURON: Receptors in the Retina ○ Converts light into electric potentials ○ The interconnection of rods and cones forms the receptive fields CONES - exclusive to the fovea centralis; interprets color of light waves (red, green and blue); Operate in bright light; responsible for high visual acuity Loss of cones = LEGAL BLINDNESS RODS - Achromatic vision (does not Figure 42. Three dimensional optic nerve pathway interpret color) ;Interpret the intensity of PRIMARY VISUAL CORTEX light; Operate in low light / poor visual ○ Optic radiation: fibers that connect the lateral acuity geniculate nucleus to the primary visual cortex Loss of rods = NIGHT BLINDNESS Responsible for quadrantic vision Transform light into electrical potentials BATCH 2028 1F 13 NEUROSCIENCE LC 7 Superior / parietal fibers (responsible for tract is made up of fibers coming from the the contralateral lower quadrant of ipsilateral temporal retina and contralateral nasal vision) retina. If I ask you, what are the fiber Inferior / temporal fibers (responsible for components of your right optic tract? the contralateral upper quadrant) - temporal retinas of the right eye and nasal Relation with parietal and temporal lobes for retina of the left eye, ‘cause only the nasal image tracing and identification retina will decussate to the other side Relation with motor complex for eye motion through the optic chiasm Optic Tract / Optic Radiation / Visual Cortex Will carry visual information from the: - Ipsilateral temporal retinas (ipsilateral nasal field of vision) - Contralateral nasal retina (Contralateral temporal field of vision) Figure 44. Parts of the visual field BRODMANN'S AREA 17 (PRIMARY VISUAL CORTEX) Within the calcarine sulcus of the occipital lobe Area that “creates” colors, images, and responsible for the fusion of images from both eyes VISUAL FIELDS ○ Nasal retinas: sends info from the temporal FOV ○ Temporal retinas: sends info from the nasal FOV Figure 46. Alternative optic nerve route with field of vision VISUAL FIELDS CONCEPT ○ Right Visual Field: From temporal retina of the left eye plus the nasal retina of the right eye ○ Left Visual Field: From nasal retina of the left eye plus the temporal retina of the right eye. Anopia / Anopsia [Dr. Viado prefers anopia] ○ Sightlessness ○ the state of being blind / lack of sight ○ Unilateral anopia: complete blindness of one eye; damaged optic nerve/ optic canal Optic canal / optic nerve damage (i.e. retinoblastoma) = unilateral anopia ○ Hemianopia / Hemianopsia: loss of vision in half of visual field / one side of vertical midline Homonymous hemianopia (Optic tract / Figure 45. Optic nerve route with field of vision Visual cortex): loss of visual field on the same side of both eyes; damaged on the optic OPTIC CHIASM tract to visual cortex ○ Nasal retinas (Temporal field of vision) - ex. Left homonymous hemianopia (patients - fibers cross the optic chiasm= perspective) *CONTRALATERAL Quadrantanopia / Quadrantanopia: loss of ○ Temporal retinas (Nasal field of vision) a quarter of the visual field; damaged optic - fibers DO NOT cross at the optic radiation (parietal or temporal) or even the chiasm; IPSILATERAL visual cortex - ex. Right superior homonymous Only the nasal retina will cross at the optic Quadrantanopia (patients perspective) chiasm and the temporal retina will remain ipsilateral. When talking about optic tract, Optic Quadrantic vision function of optic radiation BATCH 2028 1F 14 NEUROSCIENCE LC 7 - The parietal lobe is responsible for the lower quadrant division and the temporal lobe is responsible for your upper quadrant division. - Example: walang makita sa taas then that means the damage is on the left temporal lobe Pituitary tumor compresses the optic chiasm from below = damages nasal retinas of both eyes = bitemporal Hemianopia Optic tract lesion = contralateral homonymous hemianopia Ex. Damaged right optic tract = Left homonymous hemianopia (damage to temporal retina of the right eye; nasal retina of the left eye) Figure 49. Alternative anopia guide C. CRANIAL NERVE VIII: VESTIBULOCOCHLEAR Transmits afferent signals for sound (cochlear nerve division) and equilibrium (vestibular nerve division) from the inner ear to the brain. CN VIII Anatomy: Nuclei emerges from the pontomedullary junction at the cerebellopontine angle, consists mostly of bipolar neurons (involves CN V, VII, VIII) Exits thru the internal acoustic meatus (with CN VII) Vestibular apparatus and semicircular Figure 47. Anopia guide canals: afferent signals associated with balance; Cochlea: afferent signals associated with sound Figure 48. Anopia guide with correlation to optic nerve damage (Ex. Cut 6 in the right temporal lobe = left superior homonymous quadrantanopia; Cut 5 in the right parietal lobe = left inferior homonymous quadrantanopia) Left parietal lobe damage = complete right inferior homonymous quadrantanopia Figure 50. Cochlear innervation Temporal lobe damage = complete right superior homonymous quadrantanopia 3-ORDER NEURON BATCH 2028 1F 15 NEUROSCIENCE LC 7 Primary neuron: Vestibular nerve (balance) ○ Vestibular ganglia: nuclei consists of bipolar neurons ○ Five sensory organs (Vestibular labyrinth): 3 Cristae / semicircular canals (rotational acceleration); 2 otolith organs: maculae of the saccule (for vertical acceleration) & maculae of the utricle (horizontal acceleration) ○ Fluid filled with endolymph which move the ampulla and trigger the stereocilia to generate electric signals ○ There are four vestibular nuclei in the brainstem: lateral, superior, medial, and inferior which all connect to the cerebellum ○ Intimately related to the Cerebellum which is the center for balance and coordination Second order neuron: Superior olivary nucleus (info from both ears are compared to localize the sound source); Inferior colliculus Third order neuron: medial geniculate nucleus in the thalamus Temporal gyrus/ cortex: processes auditory info ○ Low frequency sound: anterolateral temporal cortex ○ High frequency sound: posteromedial temporal cortex Associative auditory cortex: comparison with Primary neuron: Cochlear nerve (hearing) former experience of sound ○ Spiral ganglia: nuclei consists mostly of ○ Brocka’s & Wernicke’s areas (in the left bipolar neuron lobe): integration of speech ○ Organ of Corti as the sensory organ (primary neuron) ○ Right temporal lobe: integration of music Has inner hair cells (stereocilia) which vibrate with sound waves and generate electrical signals Stereocilia distribution: base spiral of cochlea: detects high pitch sounds; near the top spiral: lower pitch sounds; top of spiral: lowest pitch sounds Housed in the spiral ganglion Detects soundwaves that vibrate the eardrums Figure 52. Cochlear nerve pathway Figure 51. Cochlear morphology, focused on the organ of Corti BATCH 2028 1F 16 NEUROSCIENCE LC 7 CNIII, CNIV, CNVI Figure 53. Vestibular nerve pathway. There are four vestibular nuclei in the brainstem: lateral, medial, superior, and inferior Damage to CN VIII (i.e otitis media) leads to Figure 54. Pathway of Oculomotor Nerve Ipsilateral effects to: ○ Sensorineural Hearing loss (cannot hear Function summary soundwaves thru both air conduction or bone ○ Moves the eyeball in all directions conduction) ○ Adduction is the most important action ○ Others effects: Vertigo, false sense of motion, ○ Rises eyelid loss of balance even in the dark, nystagmus, ○ Constricts pupils motion sickness, gaze-evoked tinnitus ○ Accommodates eye XII. PURELY MOTOR CRANIAL NERVES Oculomotor (III) ○ Moves eyeball in all directions except pure abduction ○ Adduction (inward) is most important action ○ Elevates eyelid (Levator palpebrae superioris) ○ Constricts pupils (pupillary constrictor - short ciliary nerve branch) ○ Accommodates the eye (ciliary muscle - short ciliary nerve branch) Trochlear (IV) - Motor to superior oblique muscle Figure 55. Oculomotor Nerve Abducens (VI) - Motor to lateral rectus muscle; abducts eye (outward) Accessory (XI) - Motor to sternocleidomastoid and trapezius Hypoglossal (XII) - Motor to muscles of the tongue *Oculomotor, trochlear, and abducens nerves will supply the extraocular muscles A. CRANIAL NERVE III: OCULOMOTOR Originates at the mesencephalon or the midbrain Figure 56. Superior Orbital Fissure Responsible for eye movements in all directions except lateral and abduction movements. Before CN III enters the midbrain it will run to the Responsible for adduction movements which are lateral wall of the Cavernous Sinus and exit through more important, like elevates the eyelid, Superior orbital fissure and enter the orbit. constricting the pupil; and accommodates the Somatic Motor Neurons eye. All of these are the parasympathetic ○ It innervates the extra ocular muscles functions to the ciliary ganglion, ciliary muscle ○ Via oculomotor neurons which change the diameter of the eye lens and - somatic motor nucleus constrictor pupillae muscles Preganglionic Parasympathetic Neurons *CN that enter the superior orbital fissure: BATCH 2028 1F 17 NEUROSCIENCE LC 7 ○ CN III (Oculomotor), VII (Facial), IX Ciliary Ganglion (Glossopharyngeal), X (Vagus): has ○ Short Ciliary Nerve parasympathetic functions - Ciliary Muscle ○ Pupillary constriction and accommodation - The shape of the lens will change. ○ Via Edinger-Westphal nucleus (accessory - Makes your lens rounder or to focus on oculomotor nucleus) objects which is the power of ○ Superior cranial nerve III fibers: innervates the Accommodation. (e.g. myopia) extraocular muscle ○ Constrictor Pupils (Pupillary sphincter) - Decreases the diameter of the pupil or pupillary constriction also known as Miosis CNIII has the only power for Miosis * Pupillary dilation is Mydriasis opposite of Miosis Figure 57. Nucleus oculomotorius and Edinger-Westphal (accessorius) Figure 60. Ciliary Muscle Both the actions, contraction in ciliary muscle as well as the constriction of pupils contribute to the regulation of eyeball pressure (measured by tonometer, used by an ophthalmologist) Figure 58. Muscles that help in the movement of the eye Oblique muscles are hinged. Superior oblique- looking downwards Only two muscles are not innervated by oculomotor nerve: the superior oblique which is innervated by cranial nerve IV or trochlear nerve and the lateral rectus which is innervated by cranial nerve VI or abducens nerve and the rest are under CNIII. Figure 61. Simple Illustration of Oculomotor Nerve Damage In the paralysis of the oculomotor nerve, the patient can no longer open the eyelid. The pupils will be dilated. With the weakening of the medial and superior rectus, the lateral rectus muscle will dominate, moving the eye towards the side. Difficulty in opening the eye against resistance- damage in the CNII - Difficulty in closing the eye: damage in the Facial Nerve - Dilation of the pupil: mydriasis, opposite of constricting pupils *CNIII damage of one eye will cause “down and out” Figure 59. Ciliary Ganglion deviation, because CNIV and CNVI will now dominate and CNIII lose its power. CN III: PARASYMPATHETIC FIBERS Damage presentation: Ptosis (eyelid fell down) >> (VISCEROMOTOR FUNCTION) Pupil Dilation >> Eye Deviation >> Down and Out BATCH 2028 1F 18 NEUROSCIENCE LC 7 R R (optic) X X CRANIAL NERVE II AND III REFLEX EXAM R R (oculomotor) X ✔ THE PUPILLARY LIGHT REACTION: (DIRECT R L (optic) ✔ ✔ AND CONSENSUAL) R L (oculomotor) ✔ X ○ Consensual light reflex: If you shine a light on one eye that will result in constriction of pupil Damage in the optic nerve: no direct and consensual not only on the lighted eye but also on the other light reflex. The eyes will not react because there is eye. no sensory information going towards the brainstem. Nasal retina will move towards the optic chiasm and the temporal retina will move Damage in the oculomotor nerve: no direct light towards the pretectal nucleus. reflex, but there is consensual light reflex. The ○ Direct light reflex: The direct constriction of information will only be sent towards the other eye. the lighted eye. No signal going to the ciliary ganglion. The eye will ○ Afferent: Optic Nerve CN II not constrict from the site of the stimulus. ○ Efferent: Parasympathetic (Visceral Efferent) Component of the CN III on both sides When the optic nerve on the opposite side is (Bilaterally) damaged, there is direct and consensual light reflex. ACCOMMODATION REACTION When the oculomotor nerve on the left is damaged, ○ Afferent: Optic Nerve CN II there is direct light reflex, but no consensual light ○ Efferent: Parasympathetic (Visceral reflex. Efferent) Component of the CN III on both sides Figure 63. Pathway of the Pupillary light reflex Figure 62. Pupillary Light Reflex 1. If you shine a light on one eye Figure 64. Pupillary reactions in coma 2. the conduction of impulses will travel to the optic nerve, which has two fibers: temporal fibers and nasal fibers 3. Nasal fiber will cross over at the optic chiasm so both conduction will proceed towards the pretectal nuclei at the back. 4. Pretectal nucleus of the body (pre-tectum and tectum) 5. From the Edinger Westphal nucleus it will send that information towards the oculomotor nerves 6. Via the oculomotor nerves it will travel through the towards the ciliary ganglia on both sides and goes towards the ciliary nerve to innervate your pupillary constrictor muscle to affect an action 7. There will be constriction of the pupils on both eyes that is known as concept direct reflex and a consensual reflex on the other eye LIGHT DAMAGE DIRECT CONSENSUAL BATCH 2028 1F 19 NEUROSCIENCE LC 7 In coma patients, pupils will become small and Three responses of Accommodation Reflex: reactive. Pupillary Constriction, Lens Shape of the Ciliary The damage in the diencephalon will cause small Muscle, and Convergence by Contraction of the reactive pupils. Left and Right Medial Rectus muscle In metabolic cases (e.g. hypoglycemic), pupils will Convergence of the two eyes – this is to make sure the object is focused on the fovea of each be small and reactive. retina. Failure of doing so – for example, when the If both sides of mesencephalon/midbrain are eye muscles are weak – would result in double damaged, both eyes will dilate. vision. This is because the object is focused on During uncal herniation (only one side that is different parts of the two retinas and the brain sees enlarging and compressing on the midbrain, two images. compressing on the oculomotor nerve), that pupil Constriction of pupil – this is to reduce spherical on the side will dilate - Anisocoria - one side of aberration. Spherical aberration occurs when light the eye will dilate while the other side will react to rays hit the edge of a lens and produce blurriness. light. Constricted pupil allows light rays to enter the lens When the whole midbrain is damaged (affecting only at the center where they are best refracted. the superior colliculus that functions for vision, you Accommodation of the lens – ciliary muscles will have a large fixed pupils) contract to make the shape of the lens more When herniation reaches the pons, pupils will convex. become pinpoint. This increases the optical power of the lens. It now When the patient is brain dead (medulla is can converge the divergent light rays onto the affected), pupils will be non reactive and fully retina. dilated - absence of pupillary light reflex. Presbyopia − is a very common age-associated condition in which the eye loses the ability to ACCOMMODATION REFLEX adjust to near vision. In presbyopia, the lens loses its flexibility with age and becomes stiff. It can no The “near response” of the eye longer change its shape to accommodate near Reflex action of the eye in response to focusing on vision. near object (constricting), then looking at distant objects Coordinated changes in: ○ Convergence – both eyes will converge to focus on the object ○ Lens shape – changes in shape of lens ○ Pupillary size – changes in pupillary size (pupillary constriction) Controlled by the parasympathetic nervous system (via Edinger-Westphal nucleus) Figure 67. Muscles controlling the eyelid If we draw an object near our eyes, both eyes will converge through the left and right medial rectus. Corrected with convex lenses that converge the light rays slightly before they enter the eye. Presbyopia is not to be confused with hyperopia, a condition in which the eyeball is too short. When you look up, why does the upper eyelid also retract upward? The reason is because of the levator palpebrae superioris which is innervated by CN III Figure 65. Longitudinal section of the eye Figure 68. Ptosis defect of CN III Damage to CN III- Ptosis B. CRANIAL NERVE IV TROCHLEAR Innervates the superior oblique muscle Figure 66. Convergence Eye Test CN IV action: Moves the eyes downward and laterally The afferent component is the optic nerve. The Moves eye inferiorly when adducted oculomotor nerve will move the eyelid and constrict the pupil through the ciliary ganglion and Internally rotates when abducted the shape of the lens. Aids more in abduction BATCH 2028 1F 20 NEUROSCIENCE LC 7 Extraocular Muscle Movements: - Oculomotor palsy- ptosis on left eye and Superior oblique: moves the eyeball down and slightly deviated down and out. Cannot look the outward: downward abduction left eye to the medial side, can abduct, but ○ ABduction: moving the eye laterally cannot adduct. ○ ADduction: moving the eye medially - Medial longitudinal vasiculus- controls the Ex: When we look to the right, we are impulses coming from CN III adducting our left eye, and aBducting our ○ An elderly patient is unable to abduct, adduct, and look up & down using her right eye = right eye; we are using 2 CNs (CN VI on “frozen eye” the right, CN III on the left) All the cranial nerves in the right eye are Lateral rectus: purely abduction; moves damaged the eye laterally Damage is either at the cavernous sinus Left and right eye have varying eye or the superior orbital fissure movements: conjugate eye movement (they should move at the same time, but If a patient was in an accident, the most probable each eye has a different action) cause for a frozen eye is a superior orbital fracture, Both eyes can only adduct at the same which might possibly signify aneurysm. time (when we converge our eyes) Cavernous Sinus Thrombosis - double vision, because the medial rectus is innervated numbness, frozen eye, facial pain can also only by the CN III manifest. - Has the same course as CN III (towards the Third nerve palsy- right eye deviated upward and superior orbital fissure); they both originate at the outward, lateral rectus will dominate back of the midbrain Fourth - superior oblique muscle is affected - Has the longest intracranial course among all the Sixth- cannot abduct, opposite eye will always CNs dominate (medial rectus) Conjugate Eye Movements - the eyes will always move in the same direction - eye movement from one direction to another C. CRANIAL NERVE VI: ABDUCENS Draw the eye toward the side of the head Supply and innervate the lateral rectus muscle (turning the eye laterally) Enter the orbit through superior orbital fissure Abducts the eye Abducens nucleus: ○ Located in the pons. Figure 70. Six cardinal positions of gaze ○ The small motor nucleus is situated beneath Gaze deviations the floor of the upper part of the fourth ○ MEDIAL SIDE/ADDUCTION: Medial rectus ventricle, close to the midline and beneath the (CNIII) colliculus facialis. ○ LATERAL SIDE/ABDUCTION:Lateral rectus Receives afferent corticonuclear fibers from both (CN VI) cerebral hemispheres. ○ UP AND IN: Superior rectus (CN III) It receives the tectobulbar tract from the superior ○ DOWN and IN: Inferior rectus (CN III) colliculus, by which the visual cortex is connected ○ UP and OUT: Inferior oblique (CN III) to the nucleus. ○ DOWN and OUT: Superior oblique (CN IV) It also receives fibers from the medial longitudinal fasciculus, by which it is connected to the nuclei Brain death: Midline, no deviations of the third, fourth, and eighth cranial nerves - When we look up, we are contracting BOTH the Course of the Abducens Nerve Superior rectus and Inferior oblique; when we ○ The fibers of the abducens nerve pass look down, we are contracting BOTH the anteriorly through the pons and emerge in the Inferior rectus and Superior oblique. groove between the lower border of the pons - Essentially, when we look up, we are using the and the medulla oblongata. CN III; when we look down we use both the CN ○ It passes forward through the cavernous sinus, III and CN IV lying below and lateral to the internal carotid artery. CLINICAL CASES: Extraocular Muscle Movements ○ A young patient with a right eye ocular gaze ○ CN III: Oculomotor abnormality (patient is able to adduct but unable to abduct their eye) = Lateral rectus Superior (in & up), Inferior (in & down) and palsy on the right eye; CN VI (Abducens) Medial (in-adduction) rectus Inferior damage - can be caused by trauma. oblique: UP and OUT (upward abduction) Ciliary muscle (Accommodation) BATCH 2028 1F 21 NEUROSCIENCE LC 7 Levator Palpebrae Superioris(Eyelid Reflex movement that stabilizes the images elevation) on the retina during the head movement ○ CN IV: Trochlear Nerve CN III, VI, VIII (Vestibular) Stabilization occurs by producing an eye Superior Oblique movement in the direction opposite to the DOWN and OUT (downward abduction) head movement thus preserving the image ○ CN VI: Abducens on the center of the vision field. Lateral rectus *Absence of doll’s eye indicates brain death OUTWARDS (Direct abduction) Figure 71. Conjugate eye movement TABLE 1. TYPES OF EYE MOVEMENT AND THEIR SITES OF CONTROL 4 TYPES OF EYE SITE OF CONTROL MOVEMENT Saccadic Cortical: Frontal lobe (command) (frontal eye fields) Subcortical: superior colliculus of the midbrain + basal ganglia and thalamus Pursuit Occipital lobe ○ Convergence: the movement that maintain fixation as an object is brought close the Vestibular - Cerebellar Vestibular nuclei face;Midbrain positional ○ Conjugate Eye deviation in Stroke (vestibulo-ocular 81% if right sided stroke has eye deviation reflex) to the right Convergence Midbrain: Oculomotor nuclei 59% of left sided stroke has eye deviation to the left Generally, the eye will deviate towards the CONJUGATE EYE MOVEMENT lesion. ○ Motor coordination of the eyes that allows for Saccadic eye movement– Rapid bilateral fixation on a single object. movement from one fixation to another is ○ Movement of both eyes to maintain disrupted binocular gaze - Frontal lobe ○ “Yoked” eye movement - Frontal eye field (Brodmann 8) ○ Saccadic (command): rapid movement from one fixation to another ○ Pursuit: the slow eye movement used to maintain fixation to a moving object. ○ Vestibulo-positional (Vestibulo-ocular reflex/Occulocephalic reflex ): eye movement that compensates for movement of the head to maintain fixation (Doll’s eye - SIGN THAT YOU’RE STILL ALIVE) ***Oculocephalic reflex/Vestibulo-ocular reflex (Doll’s eye) BATCH 2028 1F 22 NEUROSCIENCE LC 7 Figure 74. Site of lesions and their corresponding gaze deviations. Exercises: Figure 72. Saccadic System Figure 73. Gaze deviation in different clinical cases - In brain dead patients, eyes will remain midline with no deviations. - Lesion on the brain stem (eg. pons), eyes will deviate away from the lesion. - In a patient will an epileptic seizure (eg. eyes were deviated on the left side), the possible lesion is on the right side (contralateral). - Left III nerve palsy: with dilation Hypoglossal nerve - if the lesion is on the left, vision is towards the left Tongue Innervation BATCH 2028 1F 23 NEUROSCIENCE LC 7 Medial Longitudinal Fasciculus- only if at rest, (+) diplopia when looking medially ○ DOUBLE VISION: EXTRANUCLEAR LESION/NERVE LESION (Outside brainstem): problem on the either on CN III, IV, VI Both eyes – Squint (may be corrected by covering one eye/eyepatch) Nerve (Multiple Sclerosis / Guilan Barre / Diabetes) Neuromuscular Junction Muscle (Myasthenia gravis / Graves disease) One eye (not resolved by covering the - Anterior ⅔ of the tongue is the trigeminal nerve. unaffected eye) - Posterior ⅓ is the glossopharyngeal nerve. Cornea (Keratoconus) and - Epiglottic area: vagus nerve. Lens (cataract) ○ You can feel the sweetness of the sugar, hot Astigmatism temperature of the drink, and the pain when a Dry eye fishbone is stuck at the back of your tongue because of this nerve. ○ DOUBLE VISION RULES: Double vision is maximal in the direction of the gaze of the affected muscle. Example: If your right eye is affected, if I look towards the right, the right side will have double vision. False image is the outer image. Fale image arises in the affected eye. ○ MEDIAL LONGITUDINAL FASCICULUS Paired, highly specialized, and heavily myelinated nerve bundle responsible for extraocular muscle movements Figure 75. Clinical presentation: Mass effect on Cavernous sinus Facilitates the conjugate eye movement: Oculomotor reflex Saccadic eye movement CAVERNOUS SINUS Pursuit ○ CN (III, IV, V1, V2, VI): Ptosis, diplopia, “Frozen Vestibulo-ocular reflex eye”, Ophthalmoplegia, facial pain ○ Occlusion of C5 (venous outflow Heavily myelinated tract that allows conjugate eye blockage): Proptosis (exophthalmos), chemosis movement by connecting the Paramedian ○ Carotid artery encasement: Stroke Pontine Reticular Formation (PPRF)- Abducens Nucleus complex of the contralateral side of the Oculomotor Nucleus of the ipsilateral side. Figure 76. Three types of eye movements and their origins Diplopia – Double vision ○ NO DOUBLE VISION (GENERALLY) Figure 77. Schematic representation of Median longitudinal Supranuclear - above the nuclei fissure (MLF) and associated structures. Internuclear - connections between nuclei: BATCH 2028 1F 24 NEUROSCIENCE LC 7 INTERNAL/INTERNUCLEAR The nucleus receives corticonuclear fibers from OPHTHALMOPLEGIA both cerebral hemispheres Disorder of conjugate lateral gaze The efferent fibers of the nucleus emerge from Injury to medial longitudinal fasciculus the anterior surface of the medulla oblongata Eyes do not move together with markedly slowed Between the olive and the inferior cerebellar adduction and with nystagmus (oscillation) in the peduncle. The nerve runs laterally in the posterior cranial abducting eye. fossa and joins the spinal root. The two roots Generally, no diplopia but horizontal diplopia may unite and leave the skull through the jugular occur (affected eye tries to adduct) foramen. Convergence is preserved. The nerve fibers emerge from the spinal cord midway between the anterior and posterior nerve roots of the cervical spinal nerves. The fibers form a nerve trunk that ascends into the skull through the foramen magnum. Nucleus is innervated from cortex to the contralateral side (decussation at the medullary pyramids) Face and neck is on the lateral side. Bilateral cortical control to the sternocleidomastoid muscle Figure 78. Right median longitudinal fissure (MLF) Lesion Generally if patients do not move eye (at rest), no diplopia is noted Diplopia occurs when affected eye looks medially (affected eye fails to ADDUCT) Impaired adduction of the ipsilateral eye (affected eye) with nystagmus of the abducting eye (normal eye). CLINICAL CORRELATION: Figure 81. Spinal Nucleus of the Accessory Nerve Cranial nerves that enter the jugular foramen are CN IX, X, & XI Figure 79. Leading eye nystagmus Where is the lesion? - Left eye fails to adduct and nystagmus of the right eye - Lesion is located at the left medial longitudinal fasciculus D. CN XI: ACCESSORY NERVE Another way to localize lesion is through the accessory nerve Other name: SPINAL ACCESSORY because it Figure 80. Function Summary of the Accessory Nerve has continuation from the spinal radices C1 to C6 The only cranial nerve that enters and exits the foramen magnum because it has the spinal When you have a jugular foramen tumor/glomus radices C1 to C6. jugular tumor, the manifestation is on CN IX, X, Purely motor: the only somato-motor that and XI innervates the trapezius and sternocleidomastoid All of the cranial nerves can innervate a single muscles - not on the face rather on the neck muscle or single part of your face or neck. Arises from medulla Localization: Localizing a certain problem can Leaves the skull through the jugular foramen be done by knowing the function of the particular It has a nucleus known as nucleus ambiguus. cranial nerve. BATCH 2028 1F 25 NEUROSCIENCE LC 7 Cerebellopontine angle tumor/CP angle tumor: characterized by hearing loss, facial numbness, incorporated with facial paralysis Cranial nerves on CP angle: CN V, VII, and VIII CN XI: SOMATOMOTOR Somatomotor to the Sternocleidomastoid and Trapezius muscles ○ STERNOCLEIDOMASTOID Tilt, flexion and rotate the head Figure 83. Flexion, Tilt, and Rotate the Head Contraction turns the head to opposite side ○ TRAPEZIUS CN XI DAMAGE Shrug the shoulder Ipsilateral contraction: If you're shrugging your right shoulder, it contracts the right DAMAGE TO RIGHT MOTOR CORTEX/UMN trapezius, and vice versa. Somatomotor to the Sternocleidomastoid and An acute damage to the UMN (corticobulbar Trapezius muscles tract) will cause predominantly contralateral Note: Cerebral motor cortex (UMN) supplies the hemiplegia/ paresis of sternocleidomastoid and contralateral trapezius and sternocleidomastoid trapezius. plus ipsilateral sternocleidomastoid muscle thus, Ex. Right side of stroke weakness on the left a single UMN lesion can give rise to signs of both sternocleidomastoid and trapezius. If you have sides. But the dominant cortex will still be the a weak shoulder shrug on the left, you cannot contralateral cortex tilt your head on the left. The right cerebral cortex will still be the dominant NOTE: Contraction of sternocleidomastoid will control for the left sternocleidomastoid and turn/rotate the head to the opposite side, tilt trapezius muscle and vice versa, thus the head to the ipsilateral side. dominant weakness will still be on the Weak left sternocleidomastoid and trapezius contralateral side. Head tilted towards right/side of UMN lesion (strong side, which is the right sternocleidomastoid will dominate - supplied by the intact left motor cortex) Weak shrug on the left side (contralateral cortical innervation of trapezius) Right UMN: Left Weak - left sternocleidomastoid ( you're not able to rotate your head towards the right and you'll have weakness tilting your head ipsilateral) What will happen when your head turns towards the right because the right sternocleidomastoid will now dominate, your head will tilt towards the right. DAMAGE TO RIGHTACCESSORY NERVE Figure 82. Trapezius m. and Sternocleidomastoid m. (PERIPHERAL NERVE) / LMN CN XI: Sternocleidomastoid: Flexion, Tilt, and Rotate the head So the weak or paralysis will be an ipsilateral ○ Flexion: contract both sternocleidomastoid weakness. Ex: You have damage on your right accessory nerve, you cannot rotate towards the Flexing neck left. ○ Tilt: Tilting the head in one side will contract the ipsilateral sternocleidomastoid Weak/paralysis turning/rotating head to left side (contraction of sternocleidomastoid turns the Ex: Right head tilt will contract right head to the opposite side) sternocleidomastoid - Tilting head towards Head tilted towards left (opposite intact the right, you're using your right accessory nerve will dominate, cannot tilt head sternocleidomastoid towards right or side of LMN lesion) Ex: Looking towards the left - contract left Weak/paralysis of shoulder shrug right sternocleidomastoid