UNIVERSITY OF JORDAN FACULTY OF MEDICINE DEPARTMENT OF PHYSIOLOGY & BIOCHEMISTRY NEUROPHYSIOLOGY (MEDICAL) Spring, 2014

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UNIVERSITY OF JORDAN FACULTY OF MEDICINE DEPARTMENT OF PHYSIOLOGY & BIOCHEMISTRY NEUROPHYSIOLOGY (MEDICAL) Spring, 2014 Textbook of Medical Physiology by: Guyton & Hall, 12 th edition 2011 Eman

Anencephaly is the best model to study brain stem functions. Anencephaly is one of the most severe forms of a neural tube defect (NTD) and is typically not compatible with life.

1 UNIVERSITY OF JORDAN FACULTY OF MEDICINE DEPARTMENT OF PHYSIOLOGY & BIOCHEMISTRY NEUROPHYSIOLOGY (MEDICAL) Spring, 2014 Textbook of Medical Physiology by: Guyton & Hall, 12 th edition 2011 Eman Al-Khateeb, Professor of Neurophysiology No.7 The Brain Stem, Balance & Equilibrium The Brain Stem consists of Medulla Oblongata, Pons, Midbrain. Anencephaly is the best model to study brain stem functions. Anencephaly is one of the most severe forms of a neural tube defect (NTD) and is typically not compatible with life. NTDs in general are one of the most common birth defects, occurring in approximately 1 in 1,000 live births in the United States. Anencephaly occurs when the cephalic portion, of the neural tube does not close properly during fetal development. This results in a partial or complete absence of the brain and skull. It is strongly suspected that anencephaly and other NTDs are due to a combination of multiple genetic and environmental factors. Those babies are capable to suckle, cry, and follow objects with eye movement & perform all the other stereotyped, subconscious functions of the brain stem. Functions of Brainstem: 1. Motor & sensory functions for the face & the head regions in the same way the SC perform its function from the neck downward. 2. Control of Respiration. 3. Control of Cardiovascular system 4. Partial control of the gastrointestinal functions. 5. Control of many stereotyped movements of the body 6. Control of Equilibrium 7. Control of Eye movements 8. Serves as a station for command signals from higher centers. Role of Brain Stem in Equilibrium: Function of Vestibular & Reticular Nuclei: I. The Reticular Nucleus:They are divided into two major groups: 1. Pontine Reticular System: they transmit excitatory signals to anterior motor neurons that control the axial muscles of the body (muscles of the vertebral column& the extensors of the limbs) through the Pontine Reticulospinal tract in the anterior

column of the SC. These nuclei have high degree of natural excitability, besides they receive excitatory signals from vestibular nuclei & deep nuclei of cerebellum. 2.

SC. The medullary reticular system receives from the Corticospinal tract & the Rubrospinal tract.

2 column of the SC. These nuclei have high degree of natural excitability, besides they receive excitatory signals from vestibular nuclei & deep nuclei of cerebellum. 2. Medullary Reticular System: they transmit inhibitory signals to the same anterior motor neurons that control the axial muscles through the Medullary Reticulospinal tract in the lateral column of the SC. The medullary reticular system receives from the Corticospinal tract & the Rubrospinal tract. The excitatory & the inhibitory reticular nuclei presents a controllable system that is manipulated by the cerebral cortex & other motor control centers to provide neccessary background muscle contractions for standing against gravity & to inhibit the approprate groups of muscles as needed. II. The Vestibular Nuclei: They transmit strong excitatory signals to the antigravity muscles through the Lateral & Medial Vestibulospinal tracts in the anterior column of the SC, in doing so this system supports the function of the pontine reticular system in exciting the axial antigravity muscles. Vestibular System;

3 Sensory Receptore; The vestibular system contains two kinds of sensory receptors, one kind in the Utricle and the Saccule and the other in the Semicircular ducts. The Utricle and the Saccule are two large sacs, each containing a patch of hair cells in a macula. Each macula responds to linear acceleration and detects positional changes in the head relative to gravity. Within the macula there are thousands of hair cells, having their hair projections embedded within a gelatinous material contains calcium carbonate crystals called "Statoconia". The bases of hair cells synapse with sensory endings of the vestibular nerve. Each hair cell has cilia called "Stereocilia" plus one large "Kinocilium". Minute attachments connects the tips of stereocilia to the next longer stereocilia& then to the kinocilium. Bending of the cilia towards the kinocilium opens ion channels leading to receptor potential depolarization while bending towards the other side lead to hyperpolarization. There are continuous nerve impulses at a rate of 100 / sec. in resting condition & bending of cilia towards the kinocilium increase the rate of discharge while movement of cilia in the opposite direction decrease the rate of discharge. There are groups of hair cells within the macula that gets stimulated when the head is at a given orientation. There are three semicircular ducts in the inner ear, each lying in a bony semicircular canal. Each semicircular duct contains an ampullary crest "Crista ampullaris" of hair cells that detects changes in angular acceleration resulting from circular movements of the head. The cilia or hair projections are embedded in gelatinous material called "Cupula".The three semicircular ducts, superior, posterior, and horizontal, are oriented such that they lie in three planes of space. Circular movements of the head in any plane will depolarize hair cells in a semicircular duct in one labyrinth and hyperpolarize hair cells in the corresponding duct in the opposite labyrinth. When the head suddenly rotates the semicircular ducts turns while the endolymph within the semicircular ducts remain stationary because of the inertia, the hair cells bend & the discharge rate increase greatly for a very short time then the discharge rate decrease to its resting level after few seconds this is because the endolymph now rotates as rapid as the semicircular ducts & the cupula slowly returns to resting position. When rotation suddenly stops the endolymph continue to rotate while semicircular ducts stops. This time the cupula bends in the opposite direction leading to stop the discharge completely. After few seconds the endolymph stops moving & the cupula back to resting condition & the discharge rate to its resting tonic level of 100 / sec. The semicircular ducts predicts that dysequilibrium is going to occur & signal the equilibrium centers to make proper adjustments before falling "Predictive function of the semicircular ducts"

Primary vestibular fibers terminate in the vestibular nuclei and the flocculonodular lobe of the cerebellum.

4 Vestibular nuclei; There are four vestibular nuclei located in the rostral medulla and caudal pons. The vestibular nuclei receive afferents from the vestibular nerve, which innervates receptors located in the semicircular ducts, utricle, and saccule. Primary vestibular fibers terminate in the vestibular nuclei and the flocculonodular lobe of the cerebellum. Vestibular fibers Secondary vestibular fibers, originating in the vestibular nuclei, join the Medial longitudinal fasciculus (MLF) and supply the motor nuclei of CN III, IV, and VI. These fibers are involved in the production of conjugate eye movements. These compensatory eye movements represent the efferent limb of the vestibule-ocular reflex, which enables the eye to remain focused on a stationary target during movement of head or neck. When the head turns horizontally to the right, both eyes will move to the left using the following vestibule-ocular structures. Head turning to the right stimulates hair cells in the right semicircular ducts. The right eighth nerve increases its firing rate to the right vestibular nuclei. These nuclei then send axons by way of the MLF to the right oculomotor nucleus and the left abducens nucleus. The right oculomotor nerve to the right medial rectus adducts the right eye, and the left abducens nerve to the lateral rectus abducts the left eye. The net effect of stimulating these nuclei is that both eyes will look to the left.

5 Vertigo Vestibular dysfunction may result from either peripheral or central lesions. Vertigo may result from a lesion of either the peripheral (end organ, nerve) or central (cerebellopontine angle, brainstem, cerebellum, or rarely the supranuclear connections) vestibular structures. Vertigo refers to the perception of rotation, which may involve either the subject or the external space. Often there is accompanying nausea and vomiting. The vertigo is usually severe in peripheral disease and mild in brain stem disease. Chronic vertigo (i.e. persisting longer than 2-3 weeks strongly suggests a central lesion. 1. Vertigo may be caused by a variety of drugs, including anticonvulsants, aspirin, alcohol, and certain sedatives and antibiotics. 2. brain stem vertigo is associated with ipsilateral cranial nerve palsies and contralateral pyramidal limb weakness. 3. cerebellar vertigo is associated with other cerebellar dysfunction (to be discussed later). 4. Vertigo may be the sole symptom of peripheral vestibular dysfunction. Meniere disease is characterized by abrupt, recurrent attacks of vertigo lasting minutes to hours accompanied by tinnitus or deafness and usually involving only one ear. Nausea and vomiting and a sensation of fullness or pressure in the ear also are common during the acute episode. The attacks often severe and the patient may be

6 unable to stand. The disease usually occurs in middle age and results from distention of the fluid spaces in the cochlear and vestibular parts of the labyrinth. Nystagmus; Nystagmus refers to rhythmic oscillations of the eyes slowly to one side followed by a rapid reflex movement in the opposite direction. Nystagmus is defined by the direction of the rapid reflex movement or the fast phase. It is usually horizontal, although rotatory or vertical nystagmus may also occur. Unilateral vestibular nerve or vestibular nucleus lesions may result in a vestibular nystagmus. In a pathologic vestibular nystagmus, the initial slow phase is the response to the pathology, and the fast phase is the correction attempt made by the cortex in response to the pathology. So if the left vestibular nerve or nuclei are lesioned, because of the loss of balance between the two sides, the right vestibular nuclei are unopposed and act as if they have been stimulated, causing both eyes to look slowly to the left. This is the slow phase of a pathologic vestibular nystagmus. Because the head did not move, the cortex responds by moving both eyes quickly back to the right, the direction of the Fast phase of the nystagmus. The integrity of the vestibule-ocular reflex can be an indicator of brain stem integrity in comatose patients. To test this reflex, a vestibular nystagmus is indicated by performing a caloric test in which an examiner introduces warm or cool water into an external auditory meatus. The caloric test : With the patient lying supine, his head is raised 30 from horizontal so that the horizontal canals are vertical. Each external meatus is irrigated for 30 seconds with water, first at 30 C, and then, about 5 minutes later at 44 C. Warm water introduced into the external ear stimulates the horizontal semicircular duct and causes the eyes to move slowly in the opposite direction. Because the head did not turn, the eyes are moved quickly back by the cortex (if intact) toward the same ear where the warm water was introduced, producing a fast phase of nystagmus to the same side. Introduction of cool water into the external ear mimics a lesion; the horizontal duct activity is inhibited on the cool water side, and the opposite vestibular complex moves the eyes slowly toward the cool water ear. The corrective or fast phase of the nystagmus moves the eyes quickly away from the ear where the cool water was introduced. A mnemonic which summarizes the direction of the fast phase

7 of vestibular nystagmus in a caloric test toward the warm water side and away from the cool water side is COWS; Cool, Opposite, Warm, Same Positional test: When patients indicate that vertigo occurs with a change in position, the Dix- Hallpike maneuver is used to try to reproduce the precipitating circumstance. The head, turned to the right, is rapidly lowered 30 degrees below horizontal while the gaze is maintained to the right. This process is repeated with the head and eyes turned first to the left and then straight ahead. The eyes are observed for Nystagmus, and the patient is asked to note the onset, severity and cessation of vertigo. The Doll's head (Oculocephalic) maneuver : When the head is suddenly rotated, signals from semicircular ducts cause the eyes to rotate in a direction equal & opposite to the rotation of the head, this results from reflex transmitted through the vestibular nuclei & the medial longitudinal fasciculus to the oculomotor nuclei. the absence of the doll s eye sign is an indicator of brain stem dysfunction, The eyes remain fixed in midposition, instead of the normal response of moving laterally toward side opposite the direction the head is turned. The absence of doll s eye sign indicates injury to the midbrain or pons, involving cranial nerves III and VI. It typically accompanies a coma caused by lesions of the cerebellum and brain stem. This sign usually can t be relied upon in a conscious patient because he can control eye movements voluntarily. Absent doll s eye sign is necessary for a diagnosis of brain death. Horizontal conjugate gaze; The ocular muscles function to move and position both eyes as a unit so that an image falls on a corresponding spot on the retina of each eye. For both eyes to look to the right in horizontal gaze, the right abducens nerve and the right lateral rectus muscle must be active to abduct the right eye, and the left oculomotor nerve and the left medial rectus muscle must be active to adduct the left eye. It is the fibers in the MLF

that permit conjugate gaze, either when the target moves or when the head moves, through their interconnections to gaze centers and the vestibular system.

8 that permit conjugate gaze, either when the target moves or when the head moves, through their interconnections to gaze centers and the vestibular system. Horizontal gaze is controlled by two interconnected gaze centers; 1. The Frontal eye field (Broamann area 8). This area acts as a center for contralateral horizontal gaze. 2. The Pontine gaze center (PPRF) (the paramedical pontine reticular formation). This is a center for ipsilateral horizontal gaze. The net effect of stimulation of the left frontal eye field is activation of the right pontine gaze center and a saccadic horizontal eye movement of both eyes to the right. Horizontal gaze to the right results from activation of the right abducens nucleus and left oculomotor nucleus by fibers in the MLF. Lesions in the MLF result in an internuclearophthalmoplegia in which there is an inability to adduct one eye on attempted gaze to the opposite side. For example, a lesion in the right MLF results in an inability to adduct the right eye on an attempt to gaze to the left. The left eye abducts normally but exhibits a nystagmus. If the MLF is lesioned bilaterally (in Multiple sclerosis), neither eye adducts on attempted gaze and the abducting eye exhibits nystagmus. Brain death Brain death is the cessation and irreversibility of all brain function, including brain stem. Historical Aspects; In 1564, Versalius a famous anatomist is said to have conducted an autopsy in Madrid on a nobleman who had been his patient. This autopsy was carried out in front of a large crowd of citizens and when the thorax of the body was

9 opened the heart was beating. After that Versalius was compelled to leave Spain. This and others episodes probably have made it necessary to have physicians pronounce the death of patients. The Need of the Determination of Brain Death; Nowadays, modern resuscitative devices and techniques can maintain the function of the heart, lungs and visceral organs for a period of time(hours or days) after the life-maintaining centers of the brain stem tissue have stopped function, which results in a medical dilemma of a dead brain in a otherwise living body. In the other hand, the development of transplant surgery and the need of viable organs have focused ethical and legal attention on the desirability of agreeing on the medical criteria of brain death. Criteria for Diagnosis of Brain Death;In 1981, the President's Commission for the Study of Ethical Problems in Medicine and Biomedical and Behavioral Research (USA) developed standards for the determination of brain death which with some modifications are accepted worldwide. Some steps are important to be followed: Unresponsiveness The patient is completely unresponsive to external visual, auditory, and tactile stimuli and is incapable of communication in any manner. Absence of cerebral and brain stem function o Pupillary responses are absent, and eye movements cannot be elicited by the vestibuloocular reflex or by irrigating the ears with cold water. o The corneal and gag reflex are absent, and there is no facial or tongue movement. o The limbs are flaccid, and there is no movement, although primitive withdrawal movements in response to local painful stimuli, mediated at a spinal cord level, can occur. o Apnea Test: An apnea test should be performed to ascertain that no respirations occur at a PCO2 level of at least 60 mmhg. The patient oxygenation should be maintained with giving 100% oxygen by a cannula inserted into endotracheal tube as the PCO2 rises. The inability to develop respiration is consistent with medullary failure. Some causes must be ruled out ; Body temperature must be above 32 C to rule out hypothermia, No chance of drug intoxication or neuromuscular blockade and Patient is not in shock. Confirmatory tests (are not necessary to diagnose brain death) o EEG with no physiologic brain activity o No cerebral circulation present on angiographic examination( is the principal legal sign in many European countries) o Brain stem-evoked responses with absent function in vital brain stem structures Classic brain stem syndromes; *Lateral medullary syndrome (Wallenberg syndrome);this is the commonest of the brain stem strokes, results from occlusion of the PICA. Involvement of the spinothalamic tract results in contralateral loss of pain and temperature sensation below the neck. Involvement of the descending nucleus and tract of V results in loss of pain and temperature sensation on the face ipsilateral to the lesion. Involvement of descending autonomic fibers results in an ipsilateral Horner's syndrome (ptosis, meiosis, and anhidrosis). Involvement of the nucleus ambiguous causes palatal weakness and dysphagia. Involvement of the inferior cerebellar peduncle (restiform

10 body) causes ipsilateral ataxia. *The locked in syndrome (infarction of the base of the pons); Corticospinal and corticobulbar tracts in the basis pontis are interrupted, causing quadriplegia and paralysis of all cranial nerve muscles except for those controlling eye movements. If the lesion extends into the tegmentum of the caudal pons, horizontal eye movements may also be affected (so only vertical eye movements are possible), and sensation can be affected. The critical feature of these lesions is that they spare the reticular formation above the caudal pons, and therefore the patients remain awake. The only way to communicate with these unfortunate patients is to ask them to move their eyes in response to questions. *Pontine hemorrhage; Hemorrhage into the pons (usually the result of hypertensive vascular disease) results in coma (from involvement of the reticular formation), decerebrate posturing (lesion between red nucleus and vestibular nucleus), and small (Pin point) pupils due to (involvement of descending sympathetic fibers). Parinaud syndrome; Parinaud syndrome usually occurs as a result of a pineal tumor compressing the superior colliculi. The most common sign is paralysis of upward or vertical gaze, combined with bilateral pupillary abnormalities (e.g. slightly dilated pupils, which may show an impaired light or accommodation reaction) and signs of elevated intracranial pressure. Compression of cerebral aqueduct can result in noncommunicating hydrocephalus

THE VESTIBULAR APPRATUS AND PATHWAY

THE VESTIBULAR APPRATUS AND PATHWAY Dental Neuroanatomy February 23, 2012 Suzanne Stensaas, Ph.D. Reading: Waxman Chapter 17 Also pp 105-108 on control of eye movments Computer Resources: HyperBrain Ch. 8 Vestibulospinal Pathway Quiz http://library.med.utah.edu/kw/animations/hyperbrain/pathways/