HC4_5_Anatomie en fysiologie vh evenwichtsorgaan.pptx

# The vestibular system: anatomy and physiology The vestibular system is crucial for maintaining balance, head stability, and a stable gaze during head movements. ## 1. The vestibular system: anatomy and physiology ### 1.1 Introduction to the vestibular system The vestibular system, also known as the balance system, is anatomically and physiologically related to the auditory system and is located within the inner ear. Its primary function is to gather information about movement and balance, contributing to equilibrium both when stationary and in motion. Dysfunction of this system can lead to balance issues such as dizziness, vertigo, and instability. The vestibular system operates through peripheral input systems, central processing in the brainstem and cerebellum, and subsequent motor output reflexes. These outputs contribute to gaze stabilization, postural stability, head control, autonomic functions, and spatial orientation. ### 1.2 Anatomy of the vestibular organ The peripheral vestibular system consists of the vestibular organ (located in the inner ear) and the vestibular nerve. The vestibular organ is housed within the bony labyrinth, which is a series of cavities and passages within the temporal bone. Inside the bony labyrinth lies the membranous labyrinth, which is suspended and filled with endolymph. The space between the bony and membranous labyrinths contains perilymph. * **Endolymph:** This fluid is rich in potassium ($K^+$) and low in sodium ($Na^+$). It is produced by specific cells within the cochlea and the vestibular part of the labyrinth, and resorbed by the endolymphatic sac. Endolymph movement stimulates the hair cells, generating electrical signals. * **Perilymph:** This fluid has a composition similar to cerebrospinal fluid, being low in potassium ($K^+$) and high in sodium ($Na^+$). It is supplied from the subarachnoid space via the vestibular aqueduct. Perilymph provides a stable environment for the endolymph and helps maintain electrical balance. The membranous labyrinth contains two main structures for balance: * **The Semicircular Canals (SCK):** There are three semicircular canals: * Horizontal semicircular canal (HSCK) * Anterior semicircular canal (ASCK) * Posterior semicircular canal (PSCK) * **The Vestibulum (Otolith Organs):** These include: * The Sacculus * The Utriculus ### 1.3 Physiology of vestibular stimulation The vestibular organ is stimulated by two types of head movements: * **Angular (Rotational) Accelerations:** Detected by the semicircular canals. These movements occur around the head's axes: * Yaw (rotation around the z-axis, e.g., a pirouette) * Roll (rotation around the x-axis, e.g., a cartwheel) * Pitch (rotation around the y-axis, e.g., a somersault) * **Linear Accelerations:** Detected by the otolith organs (utriculus and sacculus). These include translations and head tilts relative to gravity: * Along the z-axis (vertical, e.g., in an elevator) * Along the x-axis (anterior-posterior, e.g., forward/backward motion) * Along the y-axis (inter-aural, e.g., side-to-side motion) * Head position relative to gravity. The actual movement detectors are **hair cells**. Each hair cell has: * A nucleus * 30-200 stereocilia (hair-like projections) of varying lengths * A single kinocilium (the longest stereocilium), which defines the cell's polarization direction. * Nerve endings for afferent and efferent signaling. The bending of stereocilia towards the kinocilium causes **depolarization**, increasing the firing rate of the vestibular nerve. Bending away from the kinocilium causes **hyperpolarization**, decreasing the firing rate. In a resting state, hair cells maintain a moderate spontaneous firing rate (around 70-100 spikes/sec). > **Tip:** The vestibular system is a *mechanical* transducer. Movement of endolymph or the otolithic membrane causes physical bending of stereocilia, which in turn alters ion channel permeability and thus the electrical activity of the hair cell. ### 1.4 The otolith organs: Utriculus and Sacculus The otolith organs are located in the vestibulum of the inner ear and are sensitive to linear accelerations and gravity. * **Anatomy:** * They contain a sensory epithelium called the **macula** (macula sacculi and macula utriculi). * On the macula are hair cells with stereocilia and kinocilia embedded in a gelatinous structure, the **otolith membrane**. * This membrane is covered with heavy calcium carbonate crystals called **otoconia** (otoliths). * The macula sacculi is roughly S-shaped, while the macula utriculi is U-shaped. * The utriculus is oriented primarily in the horizontal plane, and the sacculus in the vertical plane. * **Physiology:** * **Linear Acceleration:** Due to inertia, the otoconia and otolith membrane lag behind head movement during linear acceleration. This relative motion bends the stereocilia. For example, during forward acceleration in a car, the otoconia lag behind, bending the hair cells backward. When braking, the otoconia move forward relative to the hair cells. * **Head Tilt (Gravity):** The otolith membrane's density causes it to be pulled by gravity when the head is tilted. This gravitational force also bends the stereocilia, allowing the system to detect head position relative to gravity. * **Einstein's Principle:** The vestibular system cannot differentiate between linear acceleration and the force of gravity acting on it. This means that a head tilt is perceived similarly to a linear acceleration. * **Directional Sensitivity:** The stereocilia are arranged in different directions within each macula, with the kinocilium defining the polarization axis. This arrangement allows for optimal detection of movements in various spatial directions. * **Push-Pull Principle:** Within each macula, hair cells are organized such that regions with opposing polarization are separated by a line called the striola. This ensures that for any given linear acceleration or head tilt, some hair cells will depolarize (excite) while others will hyperpolarize (inhibit), creating a sensitive push-pull system. ### 1.5 The semicircular canals (SCK) The three semicircular canals are designed to detect angular accelerations. * **Anatomy:** * Each canal lies in a different plane: horizontal, anterior, and posterior. * The horizontal canals are oriented at approximately 30 degrees relative to the horizontal plane. * The anterior and posterior canals on the same side are nearly perpendicular to each other. * The anterior canal of one side and the posterior canal of the opposite side lie in roughly the same vertical plane. * At one end of each canal is an **ampulla**, a dilated region containing a ridge called the **crista**. * The crista houses the hair cells, whose stereocilia are embedded in a gelatinous structure called the **cupula**. The cupula seals off the ampulla from the utriculus. * **Physiology:** * **Angular Acceleration:** Similar to the otolith organs, the SCK function based on the principle of inertia. When the head rotates, the endolymph within the canals lags behind due to inertia, causing the cupula to bend. This bending of stereocilia in the hair cells initiates a neural signal. * **Inertia and Fluid Dynamics:** During the start of a head rotation, the endolymph lags behind, causing the cupula to bend. When rotation stops abruptly, the endolymph continues to move for a short period, bending the cupula in the opposite direction. * **Constant Velocity:** If rotation is maintained at a constant velocity for a sufficient duration (approximately 20 seconds), friction with the membranous labyrinth and the elasticity of the cupula will cause the endolymph and cupula to return to their neutral positions. Consequently, the system cannot distinguish between standing still and moving at a constant velocity. Only accelerations are detected. * **Directional Sensitivity:** The arrangement of stereocilia within the SCK allows for detection of head movements in any direction. * **Ewald's Laws:** These describe the directional sensitivity of the SCK: * **1st Law:** Stimulation of an SCK elicits eye movements in the plane of that canal and in the direction of endolymph flow. * **2nd Law (Horizontal Canals):** Ampullopetal flow (towards the ampulla) causes stronger excitation than ampullofugal flow (away from the ampulla) in the horizontal semicircular canals. The kinocilium in the HSCK is oriented towards the utriculus. * **3rd Law (Vertical Canals):** Ampullofugal flow causes stronger excitation than ampullopetal flow in the anterior and posterior semicircular canals. The kinocilium in the vertical SCKs is oriented away from the utriculus. * **Push-Pull Principle:** Complementary pairs of SCKs (e.g., left and right horizontal canals, or left anterior with right posterior) work together. When one canal is excited (depolarized), its contralateral synergist is inhibited (hyperpolarized). This principle is fundamental for generating accurate spatial perception of head rotation. ### 1.6 The central vestibular system The central vestibular system processes the input from the peripheral vestibular organs and generates appropriate outputs. * **Vestibular Nuclei:** The vestibular nerve projects to four vestibular nuclei in the brainstem (superior, medial, lateral, and inferior). These nuclei receive input not only from the vestibular labyrinth but also from other sensory modalities, including visual, somatosensory (proprioception), and auditory systems. * **Cerebellum:** The cerebellum plays a significant role in integrating vestibular, proprioceptive, and visual information for gaze stabilization and balance control. The flocculus, a part of the cerebellum, is particularly important for suppressing the vestibulo-ocular reflex (VOR) during visual fixation. * **Connections and Outputs:** From the vestibular nuclei, information is relayed to various parts of the central nervous system to generate motor commands and conscious perceptions related to balance and spatial orientation. ### 1.7 Vestibular output systems The vestibular system generates several crucial output pathways: * **Vestibulo-ocular Reflex (VOR):** * **Function:** Maintains a stable image on the retina during head accelerations, thus stabilizing gaze. * **Mechanism:** When the head moves, the VOR elicits compensatory eye movements in the opposite direction and at the same speed. This reflex involves only three synapses, allowing for a very rapid response (less than 15 milliseconds). * **Types:** * **Angular VOR (aVOR):** Triggered by the semicircular canals, responsible for gaze stabilization during rotational head movements. * **Linear VOR (lVOR):** Triggered by the otolith organs, responsible for gaze stabilization during linear head accelerations and changes in head position relative to gravity. * **Nystagmus:** The VOR output to the extraocular muscles can result in nystagmus, characterized by a combination of a slow, compensatory phase (vestibularly driven) and a fast, reset phase. The direction of nystagmus is named after the fast phase. Physiological nystagmus occurs during head movements, while spontaneous nystagmus (occurring without external stimulation) is typically pathological and can indicate peripheral or central vestibular system dysfunction. * **Vestibulospinal Reflex (VSR):** * **Function:** Maintains postural stability by adjusting muscle tone in the trunk, arms, and legs in response to vestibular input. This reflex is crucial for maintaining an upright posture and balance during movement. * **Vestibulocollc Reflex (VCR):** * **Function:** Stabilizes the head by controlling the muscles of the neck and shoulders. It anticipates head position based on whole-body movements. * **Vestibulovascular and (Sub)cortical Pathways:** * **Autonomic Regulation:** Vestibulovascular pathways influence autonomic functions, such as heart rate and blood pressure, often in response to changes in body posture. * **Spatial Orientation and Cognition:** Projections to the cortex and other central structures contribute to our sense of spatial orientation, navigation, perception of self-motion, attention, memory, concentration, cognition, emotions, and circadian rhythms. ### 1.8 When things go wrong: Vestibular disorders * **Sensory Conflict:** Occurs when conflicting information is received from different sensory systems (vestibular, visual, proprioceptive). For example, feeling stationary in a moving train. This mismatch can lead to dizziness and disorientation. * **Vestibular Complaints:** These can manifest as: * **Vertigo:** A sensation of spinning or movement when there is no external movement, or a distorted sense of movement. * **Dizziness:** A more general sensation of disorientation without a clear sense of movement. * **Vestibulo-visual symptoms:** Such as oscillopsia (visual field appears to move or vibrate with head movements). * **Postural symptoms:** Difficulty maintaining balance while sitting, standing, or walking. * **Central Compensation:** The brain's ability to adapt to vestibular system damage. Following an acute vestibular insult (e.g., unilateral vestibular loss), the brain gradually recalibrates to restore symmetry and reduce symptoms like vertigo and nystagmus through neuroplasticity. However, this compensation may be incomplete, especially for dynamic movements, leading to persistent subtle deficits. Bilateral vestibular loss often results in more severe and persistent symptoms, relying heavily on visual and proprioceptive input. The investigation and diagnosis of vestibular disorders involve detailed history-taking and specific clinical tests aimed at evaluating the function of the peripheral and central vestibular systems. --- # Vestibular output systems and reflexes The vestibular system's output pathways are crucial for maintaining balance, gaze stability, and head control. These outputs manifest as various reflexes that integrate vestibular information with motor commands to ensure appropriate physiological responses to head movements and position. ## 2. Vestibular output systems and reflexes The vestibular system generates essential motor outputs that are vital for maintaining balance, stabilizing gaze, and controlling head movements in response to detected changes in head position and motion. ### 2.1 Overview of vestibular output pathways The vestibular system processes sensory input from the labyrinth and transmits it to central nervous system structures, including the vestibular nuclei in the brainstem and the cerebellum. From these processing centers, various output pathways are activated to control different physiological functions. These pathways mediate reflexes that stabilize gaze, maintain posture, control head position, regulate autonomic functions, and contribute to spatial orientation and cognitive processes. The primary output pathways include: * **Vestibulo-ocular pathways:** Responsible for gaze stabilization. * **Vestibulospinal pathways:** Crucial for postural stability. * **Vestibulocollic pathways:** Involved in head control. * **Vestibulospinal pathways:** Influence autonomic functions. * **Vestibulocortical pathways:** Contribute to spatial orientation and cognitive functions. ### 2.2 The vestibulo-ocular reflex (VOR) The vestibulo-ocular reflex (VOR) is a primary vestibular reflex responsible for stabilizing vision during head movements. Its main goal is to ensure that the image of an object remains stable on the retina, even when the head is moving rapidly. #### 2.2.1 Function and types of VOR * **Function:** The VOR stabilizes gaze during head accelerations by generating compensatory eye movements in the opposite direction of the head movement, with equal speed. This reflex is essential for maintaining clear vision during dynamic activities such as walking, running, or sudden head turns. * **Types of VOR:** * **Angular VOR (aVOR):** Triggered by angular accelerations (rotations) detected by the semicircular canals (SCK). This reflex is crucial for stabilizing gaze during head turns. * **Linear VOR (lVOR):** Triggered by linear accelerations (translations) detected by the otolith organs (utriculus and sacculus). * **Translational lVOR:** Compensates for linear movements of the head, such as moving forward in a car. * **Tilt lVOR:** Compensates for changes in head position relative to gravity, such as tilting the head forward or backward. #### 2.2.2 Mechanism of VOR action The VOR is a rapid reflex, typically involving only three synaptic connections, leading to a response time of less than 15 milliseconds. 1. **Input:** Vestibular hair cells in the SCK and otolith organs detect head movements and position. Bending of stereocilia towards the kinocilium causes depolarization and increased firing rate, while bending away from the kinocilium causes hyperpolarization and decreased firing rate. 2. **Processing:** Vestibular nuclei in the brainstem receive this information. The SCK operates on a push-pull principle, where excitation in one canal corresponds to inhibition in its contralateral counterpart. For example, a head turn to the left excites the left horizontal SCK and inhibits the right horizontal SCK. 3. **Output:** The vestibular nuclei project to the motor nuclei of cranial nerves III (oculomotorius), IV (trochlearis), and VI (abducens). These nerves innervate the extraocular muscles (musculus rectus medialis, lateralis, superior, inferior, and obliquus superior, inferior). The coordinated contraction and relaxation of these muscles generate compensatory eye movements. #### 2.2.3 Nystagmus and VOR When the VOR elicits eye movements, it often results in nystagmus, which is characterized by a combination of a slow, compensatory phase and a fast, reset phase. * **Slow phase:** This is the vestibularly induced compensatory eye movement that tracks the target to maintain gaze stability. Its direction is opposite to the head movement. * **Fast phase (nystagmus):** This is a rapid flick of the eyes back to the primary position. The nystagmus is named after the direction of its fast phase. * **Physiological nystagmus:** Occurs during head acceleration or deceleration. For instance, during a head turn to the right, the slow phase of the eye movement is to the left, and the fast phase (nystagmus) is to the right. * **Spontaneous nystagmus:** Occurs in the absence of external stimuli or head movement, indicating a pathological condition affecting the peripheral or central vestibular system. * **Peripheral nystagmus:** Arises from issues in the inner ear or vestibular nerve (e.g., vestibular neuritis, Ménière's disease, BPPV). It typically decreases with visual fixation. * **Central nystagmus:** Stems from problems in the brainstem or cerebellum (e.g., stroke, tumors). It does not usually decrease with fixation. * **VOR and nystagmus direction:** The direction of nystagmus evoked by stimulating specific semicircular canals is predictable. For example, stimulation of the horizontal semicircular canals leads to horizontal nystagmus. Stimulation of the anterior and posterior semicircular canals leads to vertical or torsional nystagmus. > **Tip:** The direction of the fast phase of nystagmus is generally towards the side with higher vestibular nerve firing rate. In cases of unilateral vestibular loss, the nystagmus beats towards the intact side. ### 2.3 The vestibulo-spinal reflex (VSR) The vestibulo-spinal reflex (VSR) is crucial for maintaining postural stability and balance, particularly in upright stance and during movement. * **Input:** Vestibular information from the otolith organs and semicircular canals. * **Output:** Projections from vestibular nuclei to motor neurons in the spinal cord, influencing the tone of postural muscles in the trunk, arms, and legs. * **Function:** The VSR helps to adjust muscle activity to counteract the effects of gravity and maintain an upright posture. It also contributes to balance during dynamic activities by anticipating and responding to head movements. ### 2.4 The vestibulocollic reflex (VCR) The vestibulocollic reflex (VCR) is responsible for stabilizing the head and controlling neck muscles. * **Input:** Vestibular signals, primarily from the otolith organs. * **Output:** Projections to motor neurons controlling the neck and shoulder muscles (e.g., sternocleidomastoid). * **Function:** The VCR helps to maintain a stable head position relative to the body and anticipates changes in head posture in response to whole-body movements. ### 2.5 Vestibular influence on autonomic and cortical functions Beyond motor reflexes, vestibular pathways also influence other systems: * **Vestibulospinal pathways (Autonomic):** These pathways interact with the sympathetic nervous system to regulate autonomic functions. For example, heart rate and blood pressure can increase in response to postural changes detected by the vestibular system (e.g., standing up). * **Vestibulocortical pathways:** Projections from vestibular nuclei extend to the cerebral cortex (including areas like the thalamus). These pathways contribute to: * **Spatial orientation and navigation:** Creating a sense of where the body is in space. * **Perception of self-motion:** Understanding one's own movements. * **Cognitive functions:** Influencing attention, memory, concentration, cognition, and emotion. * **Circadian rhythms:** Playing a role in regulating daily and nightly cycles. ### 2.6 Consequences of vestibular system dysfunction When the vestibular system is compromised, it can lead to a variety of symptoms due to sensory conflict and impaired reflex function. * **Sensory conflict:** Occurs when vestibular input is inadequate or contradictory to information from visual and somatosensory systems. This mismatch can cause disorientation and dizziness. * **Vestibular complaints:** * **Vertigo:** A sensation of spinning or movement when no such movement is occurring, or a distorted sensation of movement during normal head motion. * **Dizziness:** A general feeling of spatial disorientation without a specific sensation of movement. * **Vestibulo-visual symptoms:** Visual disturbances such as oscillopsia (the perceived movement of the visual environment when the head moves) resulting from vestibular dysfunction. * **Postural symptoms:** Difficulty maintaining balance while sitting, standing, or walking, leading to instability and an increased risk of falls. * **Central compensation:** The brain can adapt to vestibular system damage through neuroplasticity, aiming to restore symmetry and function. This process involves re-establishing tonic activity between vestibular nuclei and relies on input from other sensory systems (vision, proprioception). While compensation can alleviate symptoms like spontaneous nystagmus and vertigo, limitations in dynamic compensation may persist, particularly during rapid head movements. Bilateral vestibular loss severely impairs compensation, leading to significant challenges in balance and visual stability. --- # Vestibular dysfunction and central compensation This section delves into the consequences of vestibular system malfunctions, the resulting sensory conflicts and common symptoms, and the brain's adaptive mechanism known as central compensation. ## 3. Vestibular dysfunction and central compensation When the vestibular system, responsible for balance and spatial orientation, malfunctions, it can lead to a variety of symptoms and challenges. The brain's ability to compensate for these issues is crucial for recovery and maintaining function. ### 3.1 Sensory conflict Sensory conflict arises when the brain receives contradictory information from different sensory systems that contribute to balance and spatial awareness. Normally, the vestibular system, the visual system (eyes), and the somatosensory system (proprioception and touch) work in harmony to provide a coherent sense of the body's position and movement in space. * **Mechanism:** When there is a loss of information from one system or conflicting signals from multiple systems, the brain struggles to integrate this data. * **Examples:** * **Train Illusion:** Sitting in a stationary train and observing the train next to you start to move can create a sensory conflict. Your eyes perceive movement, but your vestibular system registers that you are stationary, leading to a feeling of disorientation or dizziness. * **Motion Sickness:** This is a common manifestation of sensory conflict, particularly when visual input suggests motion that is not matched by vestibular input, or vice versa. ### 3.2 Vestibular complaints Dysfunction of the vestibular system can manifest in a range of symptoms, impacting a person's quality of life significantly. These can be categorized as follows: * **Vertigo:** The distinct sensation of movement (spinning, tilting, or swaying) when no external movement is occurring, or a distorted sense of movement during normal head turns. * **Dizziness:** A broader term encompassing a sense of spatial disorientation without a clear perception of movement. Individuals may feel "off-balance" or "ungrounded." * **Vestibulo-visual symptoms:** These are visual disturbances resulting from vestibular disorders or the interaction between the visual and vestibular systems. * **Oscillopsia:** The perception that the surrounding environment is moving or oscillating, particularly noticeable when the head is moved. This is a hallmark symptom of impaired gaze stabilization. * **Postural symptoms:** Difficulties in maintaining a stable posture when sitting, standing, or walking. This can include a loss of balance and an increased risk of falls. #### 3.2.1 Common vestibular disorders While a detailed discussion of specific disorders falls under pathology and diagnostic sections, some of the most frequent causes of vestibular complaints include: * Benign Paroxysmal Positional Vertigo (BPPV) * Vestibular Migraine * Vestibular Neuritis (inflammation of the vestibular nerve) * Ménière's Disease #### 3.2.2 Impact on quality of life Vestibular disorders can have a profound negative impact on an individual's quality of life, affecting: * Daily activities * Work efficiency and absenteeism * Social relationships * Travel * Mood (anxiety and depression) * Cognition (e.g., "brain fog," attention deficits) * Increased risk of falls ### 3.3 Central compensation Central compensation is the brain's remarkable ability to adapt to and overcome vestibular disturbances, particularly those originating from the peripheral vestibular system (the inner ear organs and vestibular nerve). This process involves neuroplasticity, allowing the central nervous system to recalibrate and restore balance and gaze stability. #### 3.3.1 Mechanism of central compensation When there is a sudden loss of input from one vestibular organ (e.g., due to unilateral vestibular loss), a temporary imbalance occurs, leading to symptoms like vertigo, nausea, and nystagmus. 1. **Acute phase (Harmonie vestibulaire):** * **Asymmetry:** The immediate cessation of vestibular input from one side creates a significant asymmetry in the signals sent to the brainstem's vestibular nuclei. * **Symptoms:** This asymmetry results in acute, severe vertigo, nausea, vomiting, nystagmus (involuntary eye movements, typically beating towards the healthy side), and a tendency to fall towards the affected side. 2. **Compensation phase:** * **Brain's Recognition:** The brain recognizes this imbalance and initiates compensatory mechanisms. * **Neuroplasticity:** This involves the rewiring and recalibration of neural pathways within the vestibular nuclei and other central structures. New neural connections can form, and existing ones can be strengthened or weakened. * **Restoration of Symmetry:** Over time, the brain works to restore tonic symmetry between the vestibular nuclei on both sides. This process is facilitated by: * **Movement:** Actively moving the head and body is crucial for stimulating these adaptive processes. * **Other Sensory Inputs:** The visual and somatosensory systems play an increasing role in providing compensatory information. * **Vestibular Rehabilitation:** Specific exercises and therapies are designed to expedite and optimize this compensation. #### 3.3.2 Outcomes of central compensation * **Resolution of Acute Symptoms:** With successful central compensation, acute symptoms like spontaneous vertigo, nausea, and spontaneous nystagmus typically resolve within days to weeks. * **Static vs. Dynamic Compensation:** * **Static Compensation:** The ability to maintain balance while stationary or during slow movements is usually well-restored. Many standard vestibular tests may appear normal. * **Dynamic Compensation:** The ability to maintain balance and gaze stability during rapid head movements may remain compromised. This can lead to persistent, though often subtler, issues. * **Persistent Deficits:** Despite good central compensation, some individuals may still experience limitations, especially in demanding situations requiring rapid head movements or in challenging sensory environments (e.g., darkness, uneven surfaces). #### 3.3.3 Bilateral vestibular loss Bilateral vestibular loss (loss of function in both vestibular organs) presents a more challenging scenario for central compensation. * **Mechanism:** When both vestibular systems are compromised, the brain cannot rely on the crucial information from these organs. Compensation must then heavily depend on other sensory systems, primarily vision and proprioception. * **Symptoms:** * **Severe Oscillopsia:** The visual world will appear to move significantly with head movements, making tasks like reading or focusing difficult. * **Increased Fall Risk:** Particularly in low-light conditions or on uneven terrain. * **Fatigue:** Constant attentional effort is required to maintain balance. * **Disorientation:** Especially in environments like water. * **Congenital vs. Acquired Loss:** Individuals born with bilateral vestibular loss often adapt better from an early age due to the brain's inherent plasticity and its development without vestibular input. Those who acquire bilateral loss later in life may experience more severe and persistent symptoms. > **Tip:** Active engagement in vestibular rehabilitation and maintaining an active lifestyle are critical for promoting effective central compensation after vestibular injury. Sedation and prolonged immobility can hinder this process. --- ## Common mistakes to avoid - Review all topics thoroughly before exams - Pay attention to formulas and key definitions - Practice with examples provided in each section - Don't memorize without understanding the underlying concepts

| Term | Definition | |---|---| | Vestibular system | The sensory system responsible for providing the brain with information about spatial orientation, head position, and motion, crucial for balance and gaze stabilization. | | Otolith organs | A pair of organs in the inner ear (utriculus and sacculus) that detect linear acceleration and the pull of gravity, providing information about head tilt and linear movements. | | Semicircular canals (SCK) | Three fluid-filled loops in the inner ear that detect angular (rotational) accelerations of the head, oriented in different planes to provide three-dimensional sensing of head rotation. | | Hair cell | Sensory receptor cells within the vestibular organs that possess cilia (stereocilia and a kinocilium) which, when bent by fluid movement, generate electrical signals that are transmitted to the brain. | | Stereocilia | Hair-like projections on hair cells, arranged in order of increasing length, which are mechanically sensitive to fluid motion and play a role in signal transduction. | | Kinocilium | The longest cilium on a hair cell, which defines the polarization direction; bending towards the kinocilium causes depolarization, while bending away causes hyperpolarization. | | Endolymph | The fluid filling the membranous labyrinth of the inner ear; its movement, stimulated by head motion, bends the cilia of hair cells, initiating neural signals. | | Perilymph | The fluid found in the bony labyrinth of the inner ear, surrounding the membranous labyrinth; it is similar in composition to cerebrospinal fluid and plays a protective role. | | Vestibulo-ocular reflex (VOR) | A reflex eye movement that stabilizes vision during head movement by producing an eye movement in the opposite direction to the head movement, with the same velocity, ensuring that the image remains focused on the retina. | | Nystagmus | An involuntary, rapid, and repetitive eye movement characterized by a slow, compensatory phase and a fast, reset phase, often observed in response to vestibular stimulation or as a pathological sign. | | Sensory conflict | A situation where the brain receives contradictory information from different sensory systems (e.g., visual, vestibular, proprioceptive), leading to symptoms like dizziness or disorientation. | | Central compensation | The brain's ability to adapt and recalibrate its responses to restore balance and stability following damage or dysfunction in the peripheral vestibular system, utilizing neuroplasticity and other sensory inputs. | | Macula | The sensory epithelium within the utriculus and sacculus containing hair cells embedded in an otolith membrane, which is sensitive to linear acceleration and gravity. | | Ampulla | A dilated portion of a semicircular canal that houses the crista, which contains the hair cells responsible for detecting angular acceleration. | | Cupula | A gelatinous structure in the ampulla of the semicircular canals that moves with the endolymph and bends the cilia of the hair cells when the head rotates, thus detecting angular acceleration. | | Push-pull principle | A concept in sensory systems where complementary receptors, located in opposite orientations, work together; excitation of one receptor is paired with inhibition of the other, enhancing sensitivity and precision of detection. | | Velocity storage | A phenomenon where the vestibular system retains information about head rotation for a period after the actual movement has stopped, contributing to sensations of continued movement and post-rotatory nystagmus. | | Postural stability | The ability to maintain an upright body position against gravity, both when stationary and during movement, which relies heavily on input from the vestibular system, proprioception, and vision. | | Oscillation | A rhythmic movement or variation, often used in the context of vestibular complaints to describe the perception of a moving or shaking visual environment. |