Neuroanatomy and Reflexes Review Flashcards

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Schwann cell

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A type of glial cell in the peripheral nervous system that wraps around an axon to form the myelin sheath. It spirals many layers of its membrane around the axon and squeezes out most cytoplasm, leaving fatty myelin that insulates the fiber. Schwann cells enable faster nerve signal conduction via saltatory conduction at nodes of Ranvier.

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Myelin sheath

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A multilayered fatty wrapping formed by glial cells (Schwann cells in PNS, oligodendrocytes in CNS) that insulates axons. It increases the speed of action potential propagation by allowing impulses to jump between nodes of Ranvier. Loss of myelin impairs rapid nerve conduction.

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Nodes of Ranvier

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Regular gaps between successive myelin-wrapping glial cells along a myelinated axon. These nodes expose the axonal membrane and are sites of concentrated voltage-gated sodium channels, enabling saltatory conduction where action potentials jump node to node. They are critical for rapid nerve impulse transmission.

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Astrocytes

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Star-shaped CNS glial cells that support neurons by regulating the extracellular chemical environment, including uptake and buffering of neurotransmitters like glutamate. They contribute to the blood-brain barrier, provide metabolic support, and help maintain ion balance to protect neurons from excitotoxicity. Dysfunction can contribute to neurodegeneration.

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Peripheral neuropathy

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A disorder characterized by damage to peripheral nerves resulting in sensory, motor, or autonomic dysfunction. Causes vary and include infections (e.g., leprosy/Hansen's disease), toxins, metabolic disorders, and trauma. Symptoms can include numbness, weakness, pain, and loss of reflexes in affected areas.

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Leprosy (Hansen)

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An infectious disease caused by Mycobacterium leprae that damages peripheral nerves and skin, commonly affecting fingertips and toes. Nerve damage leads to loss of pain and temperature sensation, predisposing to unnoticed injuries, infections, and deformities. The pathogen can also involve cranial nerve ganglia.

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Local anesthetic

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A drug that decreases sodium permeability in neuronal plasma membranes, preventing sodium influx during depolarization. This blockade stops action potential generation and propagation in sensory neurons, producing loss of pain sensation in the targeted area. The effect is reversible and localized.

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Action potential

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A rapid, transient change in a neuron's membrane potential caused by the opening and closing of voltage-gated ion channels. Depolarization via sodium entry followed by repolarization via potassium exit propagates electrical signals along axons. Blocking sodium channels prevents action potential initiation.

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Hypothalamus

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A brain region that serves as the primary autonomic and endocrine integration center, regulating body temperature, water balance, hunger, thirst, and many homeostatic functions. It links nervous and endocrine systems and controls the pituitary gland. Damage disrupts vital regulatory processes.

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Optic chiasma

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The X-shaped structure where medial (nasal) fibers from each optic nerve cross to the contralateral side. This partial decussation contributes to visual field processing and binocular vision. Lesions here produce characteristic visual field deficits.

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Corpora quadrigemina

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Four collicular structures located on the posterior midbrain that serve as reflex centers for vision and hearing. The superior colliculi mediate visual reflexes and gaze orientation, while the inferior colliculi process auditory information. They coordinate rapid reflexive responses to stimuli.

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Cerebellum

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A posterior brain structure responsible for coordination of complex voluntary movements, maintenance of posture, and motor learning. It integrates sensory input with motor commands to refine timing and precision of muscle activity. Damage leads to ataxia and balance problems.

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Thalamus

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A major diencephalic relay station that receives and processes most afferent sensory information before projecting it to the sensory cortex. It plays key roles in perception, motor functions, and consciousness. Thalamic lesions impair sensory discrimination and cortical processing.

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Medulla oblongata

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The lowest part of the brainstem containing autonomic centers that regulate vital functions such as heart rate, blood pressure, and respiratory rhythm, along with reflex centers for coughing, sneezing, and swallowing. Damage here can be life-threatening by disrupting basic life support functions.

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Corpus callosum

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The large bundle of commissural fibers connecting the left and right cerebral hemispheres, enabling interhemispheric communication. It allows integration of sensory, motor, and cognitive information between hemispheres. Lesions can cause disconnection syndromes.

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Mammillary bodies

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Small paired structures of the diencephalon that act as relay stations in olfactory and limbic pathways. They contribute to memory processing and are part of the Papez circuit. Damage is associated with memory disorders such as Wernicke-Korsakoff syndrome.

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Cerebral aqueduct

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A narrow channel in the midbrain that connects the third and fourth ventricles, allowing cerebrospinal fluid (CSF) flow. Obstruction can lead to hydrocephalus and increased intracranial pressure. It traverses the central part of the midbrain.

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Midbrain

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The superior portion of the brainstem that contains cerebral peduncles, nuclei (including those in the corpora quadrigemina), and pathways for motor and sensory information. It houses reflex centers for vision and hearing and contributes to motor control. Lesions affect eye movement and sensorimotor integration.

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Cranial nerves

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Twelve paired peripheral nerves that arise from the brain and brainstem, carrying sensory, motor, or mixed fibers to head, neck, and visceral structures. Each nerve has specific functions tested clinically (e.g., smell for I, vision for II, facial expression for VII). Mnemonics help recall their names and types.

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Olfactory I

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Cranial nerve I is purely sensory and mediates the sense of smell. Clinical testing involves identifying odors (e.g., coffee). Lesions cause anosmia on the affected side.

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Optic II

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Cranial nerve II transmits visual information from the retina to the brain and mediates visual acuity, visual fields, and pupillary light reflexes. Visual field defects localize lesions along the visual pathway. Testing includes acuity and confrontation fields.

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Oculomotor III

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Cranial nerve III controls most extraocular muscles, eyelid elevation, and pupil constriction via parasympathetic fibers. Clinical signs include ptosis, abnormal eye movements, and pupillary abnormalities. Tests include pupil reaction and eye movement assessment.

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Trochlear IV

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Cranial nerve IV is a motor nerve that innervates the superior oblique muscle to mediate downward and inward eye movement. Lesions cause difficulty looking down, especially when descending stairs. It is the smallest cranial nerve by axon count.

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Trigeminal V

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Cranial nerve V has both sensory and motor components; it provides facial sensation and motor innervation for mastication. Clinical testing includes facial sensation and jaw clench. Trigeminal neuralgia causes severe facial pain.

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Abducens VI

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Cranial nerve VI is a motor nerve that innervates the lateral rectus muscle to abduct the eye. Lesions cause inability to move the eye laterally and horizontal diplopia. Testing checks lateral gaze.

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Facial VII

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Cranial nerve VII carries motor fibers for facial expression, parasympathetic fibers to salivary glands, and taste from the anterior two-thirds of the tongue. Lesions cause Bell's palsy with facial paralysis, loss of taste, and decreased salivation. Clinical tests include smiling, frowning, and puffing cheeks.

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Vestibulocochlear VIII

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Cranial nerve VIII is sensory for hearing and balance, with cochlear and vestibular components. Tests include hearing assessments (Weber and Rinne) and balance exams. Lesions cause hearing loss, tinnitus, vertigo, and imbalance.

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Glossopharyngeal IX

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Cranial nerve IX has sensory, motor, and parasympathetic functions including taste and sensation from the posterior third of the tongue and contributing to the gag reflex. It innervates the parotid gland and helps regulate swallowing. Testing includes gag reflex and taste.

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Vagus X

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Cranial nerve X is mixed and provides parasympathetic innervation to thoracic and abdominal organs, plus motor fibers for pharynx and larynx. It influences heart rate, digestion, and voice quality. Clinical tests include saying “ah” and assessing voice.

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Accessory XI

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Cranial nerve XI is a motor nerve that innervates the sternocleidomastoid and trapezius muscles to control head turning and shoulder elevation. Clinical testing includes shoulder shrug and head rotation. Lesions cause weakness in these movements.

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Hypoglossal XII

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Cranial nerve XII is a motor nerve controlling tongue movements important for speech and swallowing. Testing involves protruding the tongue and observing deviation toward the weak side. Lesions impair articulation and swallowing.

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Internal capsule hemorrhage

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Bleeding in the internal capsule typically produces contralateral motor deficits because corticospinal fibers have crossed or will cross to supply the opposite side. A right internal capsule hemorrhage causes left-sided paralysis. This reflects the decussation of motor pathways.

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Brainstem trauma

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Injury to the brainstem is especially dangerous because it contains centers that control respiration, cardiovascular function, and consciousness. Damage can disrupt these essential life-sustaining processes and quickly lead to coma or death. Frontal lobe injury is usually less immediately life-threatening.

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Reticular activating system

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The ascending reticular activating system is a brainstem network that regulates arousal and transmits signals to the cerebral cortex to support awareness. Damage to this system can impair signal transmission to the cortex and contribute to unresponsive wakefulness or coma. It mediates wakefulness despite intact primary sensory pathways.

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Spinal reflex arc

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The basic pathway for a spinal reflex includes a receptor, sensory (afferent) neuron, integration center (often interneurons in the spinal cord), motor (efferent) neuron, and effector (muscle or gland). Reflexes allow rapid, automatic responses without cortical involvement. Testing reflex arcs helps localize neurological lesions.

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Patellar reflex

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A stretch reflex where tapping the patellar tendon stretches the quadriceps femoris and elicits knee extension via L2–L4 spinal segments. It tests integrity of the femoral nerve and the corresponding spinal cord segments. Abnormal responses indicate peripheral or central nervous system dysfunction.

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Calcaneal reflex

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Also called the ankle-jerk reflex, it is elicited by tapping the Achilles tendon, stretching the gastrocnemius and soleus and causing plantarflexion. It tests S1–S2 spinal function. Diminished or absent reflexes suggest peripheral neuropathy or spinal lesion at those levels.

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Crossed-extensor reflex

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A protective spinal reflex in which withdrawal of a limb from a painful stimulus is accompanied by extension of the contralateral limb to maintain balance. It coordinates bilateral limb responses during injury and involves interneuronal circuits across spinal segments. It stabilizes posture during reflexive withdrawal.

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Plantar reflex

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A sole-of-foot stimulation producing toe plantarflexion in normal adults, mediated by corticospinal pathways. An abnormal Babinski sign (upward big toe and fanning toes) indicates corticospinal tract damage or central motor pathway dysfunction. It is used clinically to assess pyramidal tract integrity.

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Corneal reflex

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A protective blink reflex triggered by corneal stimulation, with sensory input via the ophthalmic branch of CN V and motor output via CN VII causing orbicularis oculi contraction. It protects the cornea from injury. Absence suggests lesions in the trigeminal or facial pathways or brainstem.

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Gag reflex

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A protective reflex that prevents foreign objects from entering the throat, with sensory input from CN IX and motor output via CN X causing pharyngeal muscle contraction. It helps protect the airway during swallowing. Loss or asymmetry indicates cranial nerve or brainstem dysfunction.

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Ciliospinal reflex

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An autonomic sympathetic reflex where painful stimulation of the neck, face, or upper trunk causes ipsilateral pupil dilation (mydriasis) via sympathetic pathways from C8–T2. It tests integrity of sympathetic innervation to the eye. Absence may indicate sympathetic pathway lesions.

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Salivary reflex

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An autonomic reflex controlling saliva production triggered by taste, smell, or even thought of food. Sensory input travels via CN VII (anterior 2/3 tongue) and CN IX (posterior 1/3), with parasympathetic output stimulating salivary glands and secretion. It aids digestion and oral health.

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Hyporeflexia

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A condition in which normal reflexes are weak but present, which can result from muscle damage, sensory neuron impairment (reduced afferent signaling), or motor neuron lesion (weak efferent output). Localization of the lesion requires clinical correlation and other tests. It contrasts with areflexia (absent reflexes).

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Tetanus toxin

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A neurotoxin that blocks inhibitory neurotransmitter release in the spinal cord, removing inhibition of motor neurons. This causes simultaneous contraction of agonist and antagonist muscles, producing rigidity and spasms (e.g., lockjaw). It disrupts normal regulation of stretch reflexes and motor control.

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Varicella-zoster virus

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The virus that causes chickenpox and then can remain dormant in dorsal root or cranial nerve ganglia, reactivating later to produce shingles along a sensory dermatome. Because the virus persists lifelong, recurrent reactivation and multiple episodes of shingles are possible. Reactivation produces painful vesicular rashes and neuralgia.

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Radial nerve

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A major peripheral nerve of the upper limb that innervates wrist and finger extensor muscles and provides sensory innervation to part of the hand. Injury to the radial nerve causes wrist drop due to loss of wrist extensors. It commonly is injured in humeral shaft fractures or compression.

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Two-point threshold

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A measure of tactile spatial resolution indicating the minimum distance at which two simultaneous touches are perceived as distinct. It reflects receptor density and cortical representation in different skin areas. Low thresholds indicate high tactile acuity (e.g., fingertips).

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Tactile localization

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The ability to accurately identify the location of a tactile stimulus on the skin. It depends on receptor distribution and cortical sensory mapping. Clinical testing evaluates sensory discrimination and cortical function.

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Sensory adaptation

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The process by which sensory receptors reduce their response to a constant, unchanging stimulus over time, allowing the nervous system to focus on new or changing stimuli. Examples include touch receptor and temperature receptor adaptation. Adaptation improves perceptual efficiency.

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Referred pain

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Pain perceived at a location distant from the site of the actual pathology because visceral and somatic afferents converge on the same spinal neurons. A classic example is left shoulder or arm pain during cardiac ischemia. Recognizing referred pain is important for correct diagnosis.

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Visual field defects

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Areas of lost vision that localize lesions along the visual pathway from the retina through the optic nerves, chiasm, tracts, and visual cortex. For example, a right optic tract lesion causes loss of left visual fields in both eyes. Systematic testing helps determine lesion site.

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Macular degeneration

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Degeneration of the macula lutea, the central high-acuity area of the retina, leading to loss of central detailed vision while sparing peripheral vision. Because the macula mediates fine detail and color, its deterioration disproportionately impairs tasks like reading and facial recognition compared with peripheral retinal damage.

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Near triad

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Three coordinated reflexes required for near vision: lens accommodation (increased curvature), pupillary constriction to increase depth of focus, and convergence of the eyeballs. These responses allow clear, binocular focus on close objects. Dysfunction of any component impairs near vision.

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Strabismus

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A misalignment of the eyes in which one or both eyes fail to converge or point in the same direction, often causing double vision. It primarily affects extrinsic extraocular muscles (commonly the medial rectus). Clinical issues include impaired convergence and potential amblyopia in children.

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Blind spot

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The retinal area where the optic nerve exits the eye (optic disc), which lacks photoreceptors and therefore produces an insensible spot in the visual field. Demonstrations show that a dot falling on this area is not seen, revealing that visual fields have natural gaps. Binocular vision typically compensates for blind spots.

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Near point

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The closest distance at which the eye can maintain focus on an object, indicating accommodative ability. Measuring near point helps evaluate presbyopia and other refractive or accommodative disorders. It guides corrective lens prescriptions for near tasks.

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Visual acuity

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A measure of the clarity or sharpness of vision, typically assessed with a Snellen chart. It quantifies how well a person can resolve fine spatial detail at a standardized distance. Reduced acuity can result from refractive errors, retinal disease, or optic pathway lesions.

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Astigmatism

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A refractive error caused by an irregular curvature of the cornea or lens, which prevents light from focusing evenly on the retina and produces blurred or distorted vision at all distances. Testing identifies uneven curvature so corrective lenses or surgery may be prescribed. It commonly coexists with other refractive errors.

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Color blindness

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A condition in which a person has difficulty distinguishing certain colors, often due to genetic defects in retinal cone photopigments. Common forms involve red-green discrimination problems. Clinical testing identifies specific deficits to guide counseling and adaptation strategies.

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Binocular vision

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The coordinated use of both eyes to produce a single, three-dimensional image with depth perception. It relies on proper alignment and cortical processing in the primary visual cortex. Disruption (e.g., strabismus) impairs stereopsis and depth judgments.

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Acute labyrinthitis

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Sudden inflammation of the membranous labyrinth structures of the inner ear, including the cochlea, vestibule, and semicircular canals, and the endolymphatic system. Symptoms include vertigo, imbalance, nausea, hearing changes, and abnormal eye movements. It transiently impairs auditory and vestibular reception.

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Weber test

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A simple hearing test using a vibrating tuning fork placed on the skull midline to determine if sound is perceived equally by both ears. It helps differentiate conductive hearing loss (sound louder in affected ear) from sensorineural loss (sound louder in normal ear). It complements the Rinne test.

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Rinne test

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A hearing test comparing bone conduction (via skull vibrations) to air conduction (via ear canal) using a tuning fork. Normally air conduction is greater than bone conduction; if bone conduction exceeds air, conductive hearing loss is suggested. It helps classify the type of hearing impairment.

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Balance tests

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Clinical assessments (e.g., Romberg, Barany, balance test) that evaluate the vestibular system, proprioception, and cerebellar function. Findings like nystagmus or inability to maintain posture indicate vestibular or neurological dysfunction. They help localize causes of dizziness and imbalance.

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Nystagmus

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An involuntary, rapid, repetitive movement of the eyes often seen with vestibular dysfunction, cerebellar disorders, or intoxication. It can be horizontal, vertical, or rotary and sometimes accompanies vertigo. Observation of nystagmus aids diagnosis of balance and neurological conditions.

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Vertigo

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A false sensation of spinning or movement caused by dysfunction of the vestibular apparatus, vestibular nerve, or central pathways. It is often accompanied by nausea, imbalance, and nystagmus. Identifying vertigo's peripheral versus central origin is key to management.