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Peripheral nervous system
Peripheral nervous system
Peripheral nervous system
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Peripheral nervous system
The human nervous system. Sky blue is PNS; yellow is CNS.
Identifiers
AcronymPNS
MeSHD017933
TA98A14.2.00.001
TA26129
FMA9093
Anatomical terms of neuroanatomy

The peripheral nervous system (PNS) is one of two components that make up the nervous system of bilateral animals, with the other part being the central nervous system (CNS). The PNS consists of nerves and ganglia, which lie outside the brain and the spinal cord.[1] The main function of the PNS is to connect the CNS to the limbs and organs, essentially serving as a relay between the brain and spinal cord and the rest of the body.[2] Unlike the CNS, the PNS is not protected by the vertebral column and skull, or by the blood–brain barrier, which leaves it exposed to toxins.[3]

The peripheral nervous system can be divided into a somatic division and an autonomic division. Each of these can further be differentiated into a sensory and a motor sector.[4] In the somatic nervous system, the cranial nerves are part of the PNS with the exceptions of the olfactory nerve and epithelia and the optic nerve (cranial nerve II) along with the retina, which are considered parts of the central nervous system based on developmental origin. The second cranial nerve is not a true peripheral nerve but a tract of the diencephalon.[5] Cranial nerve ganglia, as with all ganglia, are part of the PNS.[6] The autonomic nervous system exerts involuntary control over smooth muscle and glands.[7]

Structure

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The peripheral nervous system can be divided into a somatic and an autonomic division, which are part of the somatic nervous system and the autonomic nervous system, respectively. The somatic nervous system is under voluntary control, and transmits signals from the brain to end organs such as muscles. The sensory nervous system is part of the somatic nervous system and transmits signals from senses such as taste and touch (including fine touch and gross touch) to the spinal cord and brain. The autonomic nervous system is a "self-regulating" system which influences the function of organs outside voluntary control, such as the heart rate, or the functions of the digestive system.

Somatic nervous system

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See also: List of nerves of the human body

The somatic nervous system includes the sensory nervous system (ex. the somatosensory system) and consists of sensory nerves and somatic nerves, and many nerves which hold both functions.

In the head and neck, cranial nerves carry somatosensory data. There are twelve cranial nerves, ten of which originate from the brainstem, and mainly control the functions of the anatomic structures of the head with some exceptions. One unique cranial nerve is the vagus nerve, which receives sensory information from organs in the thorax and abdomen. The other unique cranial nerve is the accessory nerve which is responsible for innervating the sternocleidomastoid and trapezius muscles, neither of which are located exclusively in the head.

For the rest of the body, spinal nerves are responsible for somatosensory information. These arise from the spinal cord. Usually these arise as a web ("plexus") of interconnected nerves roots that arrange to form single nerves. These nerves control the functions of the rest of the body. In humans, there are 31 pairs of spinal nerves: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal. These nerve roots are named according to the spinal vertebrata which they are adjacent to. In the cervical region, the spinal nerve roots come out above the corresponding vertebrae (i.e., nerve root between the skull and 1st cervical vertebrae is called spinal nerve C1). From the thoracic region to the coccygeal region, the spinal nerve roots come out below the corresponding vertebrae. This method creates a problem when naming the spinal nerve root between C7 and T1 (so it is called spinal nerve root C8). In the lumbar and sacral region, the spinal nerve roots travel within the dural sac and they travel below the level of L2 as the cauda equina.

Cervical spinal nerves (C1–C4)

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Further information: Cervical plexus

The first 4 cervical spinal nerves, C1 through C4, split and recombine to produce a variety of nerves that serve the neck and back of head.

Spinal nerve C1 is called the suboccipital nerve, which provides motor innervation to muscles at the base of the skull. C2 and C3 form many of the nerves of the neck, providing both sensory and motor control. These include the greater occipital nerve, which provides sensation to the back of the head, the lesser occipital nerve, which provides sensation to the area behind the ears, the greater auricular nerve and the lesser auricular nerve.

The phrenic nerve is a nerve essential for our survival which arises from nerve roots C3, C4 and C5. It supplies the thoracic diaphragm, enabling breathing. If the spinal cord is transected above C3, then spontaneous breathing is not possible.[citation needed]

Brachial plexus (C5–T1)

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Further information: Brachial plexus

The last four cervical spinal nerves, C5 through C8, and the first thoracic spinal nerve, T1, combine to form the brachial plexus, or plexus brachialis, a tangled array of nerves, splitting, combining and recombining, to form the nerves that subserve the upper-limb and upper back. Although the brachial plexus may appear tangled, it is highly organized and predictable, with little variation between people. See brachial plexus injuries.

Lumbosacral plexus (L1–Co1)

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The anterior divisions of the lumbar nerves, sacral nerves, and coccygeal nerve form the lumbosacral plexus, the first lumbar nerve being frequently joined by a branch from the twelfth thoracic. For descriptive purposes this plexus is usually divided into three parts:

3D Medical Animation still shot of Lumbosacral Plexus
3D Medical Animation still shot of Lumbosacral Plexus

Autonomic nervous system

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The autonomic nervous system (ANS) controls involuntary responses to regulate physiological functions.[8] The brain and spinal cord of the central nervous system are connected with organs that have smooth muscle or cardiac muscle, such as the heart, bladder, and other cardiac, exocrine, and endocrine related organs, by ganglionic neurons.[8] The most notable physiological effects from autonomic activity are pupil constriction and dilation, and salivation of saliva.[8] The autonomic nervous system is always activated, but is either in the sympathetic or parasympathetic state.[8] Depending on the situation, one state can overshadow the other, resulting in a release of different kinds of neurotransmitters.[8]

Sympathetic nervous system

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The sympathetic system is activated during a "fight or flight" situation in which mental stress or physical danger is encountered.[8] Neurotransmitters such as norepinephrine, and epinephrine are released,[8] which increases heart rate and blood flow in certain areas like muscle, while simultaneously decreasing activities of non-critical functions for survival, like digestion.[9] The systems are independent to each other, which allows activation of certain parts of the body, while others remain rested.[9]

Parasympathetic nervous system

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Primarily using the neurotransmitter acetylcholine (ACh) as a mediator, the parasympathetic system allows the body to function in a "rest and digest" state.[9] Consequently, when the parasympathetic system dominates the body, there are increases in salivation and activities in digestion, while heart rate and other sympathetic response decrease.[9] Unlike the sympathetic system, humans have some voluntary controls in the parasympathetic system. The most prominent examples of this control are urination and defecation.[9]

Enteric nervous system

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There is a lesser known division of the autonomic nervous system known as the enteric nervous system.[9] Located only around the digestive tract, this system allows for local control without input from the sympathetic or the parasympathetic branches, though it can still receive and respond to signals from the rest of the body.[9] The enteric system is responsible for various functions related to gastrointestinal system.[9]

Disease

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Main article: Peripheral neuropathy

Diseases of the peripheral nervous system can be specific to one or more nerves, or affect the system as a whole.

Any peripheral nerve or nerve root can be damaged, called a mononeuropathy. Such injuries can be because of injury or trauma, or compression. Compression of nerves can occur because of a tumour mass or injury. Alternatively, if a nerve is in an area with a fixed size it may be trapped if the other components increase in size, such as carpal tunnel syndrome and tarsal tunnel syndrome. Common symptoms of carpal tunnel syndrome include pain and numbness in the thumb, index and middle finger. In peripheral neuropathy, the function one or more nerves are damaged through a variety of means. Toxic damage may occur because of diabetes (diabetic neuropathy), alcohol, heavy metals or other toxins; some infections; autoimmune and inflammatory conditions such as amyloidosis and sarcoidosis.[8] Peripheral neuropathy is associated with a sensory loss in a "glove and stocking" distribution that begins at the peripheral and slowly progresses upwards, and may also be associated with acute and chronic pain. Peripheral neuropathy is not just limited to the somatosensory nerves, but the autonomic nervous system too (autonomic neuropathy).[8]

See also

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References

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Revisions and contributorsEdit on WikipediaRead on Wikipedia

Peripheral nervous system

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The peripheral nervous system (PNS) is the portion of the vertebrate nervous system that lies outside the brain and , consisting of nerves and ganglia that serve as the primary communication link between the (CNS) and the rest of the body. It transmits sensory (afferent) signals from peripheral receptors to the CNS and motor (efferent) signals from the CNS to muscles, organs, and glands, enabling sensory perception, voluntary movement, and involuntary regulation of bodily functions. The PNS encompasses all neural elements beyond the CNS, including originating from the brain and spinal nerves branching from the , forming an extensive network that extends to every tissue and organ. Structurally, the PNS is composed of bundles of axons known as , supported by , along with clusters of neuronal cell bodies called ganglia located outside the CNS. Functionally, it is divided into the sensory-somatic nervous system, which handles conscious sensations and voluntary , and the , which governs unconscious processes like , , and glandular . The somatic division includes sensory pathways from , muscles, and joints to the CNS, as well as motor pathways to skeletal muscles for precise, voluntary actions. In contrast, the autonomic division operates involuntarily and is further subdivided into the (responsible for "fight-or-flight" responses, increasing and energy mobilization), the (promoting "rest-and-digest" activities, such as slowing and enhancing ), and the (regulating gastrointestinal function semi-independently). This organization allows the PNS to integrate the CNS's processing power with the body's diverse needs, supporting , reflexes, and adaptive behaviors while being vulnerable to conditions like neuropathies due to its exposed, elongated structure. Overall, the PNS's dual sensory-motor architecture ensures bidirectional flow of information, essential for and interaction with the environment.

Overview

Definition and components

The peripheral nervous system (PNS) encompasses all neural structures located outside the brain and spinal cord, which collectively constitute the (CNS). It functions as the primary conduit for communication between the CNS and the body's peripheral tissues, organs, and extremities. Key components of the PNS include 12 pairs of —excluding the optic (II) and olfactory (I) nerves, which are direct extensions of the CNS—and 31 pairs of spinal nerves, totaling 41 pairs of peripheral nerves. These nerves incorporate sensory (afferent) neurons that relay information from sensory receptors toward the CNS and motor (efferent) neurons that transmit commands from the CNS to target effectors like muscles and glands. The PNS also features ganglia, which are aggregations of neuronal cell bodies situated outside the CNS, serving as relay and processing stations for neural signals. The PNS is broadly divided into the , responsible for voluntary control of skeletal muscles and sensory perception from the external environment, and the , which governs involuntary regulation of visceral organs, smooth muscles, and glands. The autonomic division comprises three subsystems: the , which mobilizes the body during stress; the , which promotes conservation and restoration; and the , which manages gastrointestinal functions. This organization facilitates bidirectional connectivity, with afferent pathways delivering sensory data to the CNS and efferent pathways distributing motor instructions to the periphery.

Distinction from central nervous system

The peripheral nervous system (PNS) is anatomically distinguished from the (CNS) primarily by its location and structural exposure. The CNS, comprising the and , is encased within protective bony structures such as the and vertebral column, which shield it from mechanical trauma. In contrast, the PNS consists of and ganglia that extend beyond these enclosures, branching out to innervate peripheral tissues including muscles, , and organs throughout the body, leaving it more susceptible to external damage. Functionally, the CNS serves as the primary site for information integration and higher-order , where sensory inputs are analyzed and motor outputs are coordinated to generate complex responses. The PNS, however, primarily facilitates the transmission of sensory signals to the CNS and motor commands from the CNS to effectors, enabling direct communication between the central processors and the body's periphery. Additionally, the PNS supports local arcs, such as spinal reflexes, which allow rapid, automatic responses to stimuli without requiring CNS involvement, thereby bypassing the for quicker execution. Protection mechanisms further differentiate the two systems. The CNS is safeguarded by the blood-brain barrier, which selectively regulates substance passage into neural tissue, and by the —a triple-layered envelope that provides cushioning and compartmentalization. The PNS lacks these features but employs its own sheaths for nerve protection: the surrounds individual axons, the bundles axons into fascicles, and the encases entire nerves, collectively forming a blood-nerve barrier analogous to the blood-brain barrier but less impermeable. From an evolutionary perspective, the PNS's decentralized architecture promotes rapid environmental adaptation by distributing control through peripheral reflexes and sensory feedback, allowing organisms to respond efficiently to immediate threats or opportunities without relying solely on centralized CNS processing. This design enhances survival in dynamic habitats, as seen in the modular neural networks that enable adaptive locomotion in and vertebrates alike.

Anatomy

Cranial nerves

The cranial nerves III through XII constitute the peripheral components of the cranial nervous system, originating from the and serving as primary conduits for sensory input and motor output to structures in the . These ten pairs of nerves emerge from distinct regions of the , , and , traversing intracranial and extracranial pathways before exiting the cranium via specific foramina. Their functions encompass pure (e.g., eye and movements), sensory (e.g., sensation and hearing), and mixed modalities, including visceral , thereby facilitating essential activities such as vision, , and . Unlike the olfactory (I) and optic (II) nerves, which are considered extensions, nerves III–XII are unequivocally peripheral, with their cell bodies located outside the brainstem. The (III) arises from the at the level of the , forming a short intracranial course through the interpeduncular cistern before entering the and exiting the via the . Extracranially, it divides into superior and inferior branches that innervate , including the levator palpebrae superioris for eyelid elevation. Primarily motor, it supplies somatic innervation to four (superior rectus, inferior rectus, medial rectus, and inferior oblique) and parasympathetic fibers to the for pupillary constriction and lens accommodation, though the latter integrates briefly with autonomic pathways. The (IV), the smallest cranial nerve, originates from the dorsal to the —the only cranial nerve to emerge posteriorly—and travels a long intracranial path around the , through the , to exit via the . Its extracranial segment is short, directly innervating the of the eye for downward and inward gaze. It is purely motor, with no sensory component. The (V), the largest cranial nerve, emerges from the as a large sensory root and smaller motor root, coursing anteriorly in the to the in Meckel's cave. From there, it divides into three extracranial branches: ophthalmic (exiting via for forehead and eye sensation), maxillary (via for midface sensation), and mandibular (via foramen ovale for lower face sensation and motor to masticatory muscles). It is mixed, providing sensory innervation to the face, mouth, and while motor supply to the . The (VI) originates from the near the pontomedullary junction, traveling a vulnerable intracranial course along the clivus and through the to exit via the . Extracranially, it innervates the for eye abduction. It is purely motor, dedicated to lateral gaze. The (VII) arises from the pontomedullary junction, entering the internal acoustic meatus with the before turning sharply at the geniculum in the of the . It exits the via the stylomastoid , branching extracranially to supply muscles, stapedius for sound attenuation, and anterior tongue via the . Mixed in function, it provides motor innervation to , parasympathetic to salivary and lacrimal glands, and sensory for taste and ear sensation. The (VIII), focusing on its peripheral component, originates from the pontomedullary junction and travels through the internal acoustic meatus alongside VII, with cochlear and vestibular divisions separating extracranially to innervate the for hearing and /otoliths for balance. It is purely sensory, transmitting auditory and vestibular information. The (IX) emerges from the medulla in the postolivary sulcus, joining the and accessory nerves in a sheath to exit via the . Its extracranial path includes tympanic and carotid branches, innervating the , , and . Mixed, it carries general sensation from the posterior and , special taste sensation, and motor/parasympathetic to the and . The (X), the longest cranial nerve, arises from the medulla in the same rootlets as IX, traveling through the and descending through the , , and in the . Extracranially, it branches extensively to innervate the , , heart, lungs, and up to the splenic flexure. Mixed, it provides sensory from thoracic and abdominal viscera, motor to pharyngeal/laryngeal muscles, and extensive parasympathetic control to visceral organs. The (XI) originates from the medulla and upper cervical (C1–C5), with cranial and spinal roots uniting briefly before the cranial root merges with X; the spinal root exits via the and descends in the neck to innervate the sternocleidomastoid and muscles. It is purely motor, controlling head rotation and elevation. The (XII) emerges from the medulla between the and , exiting the via the and traveling extracranially along the to branch into the musculature. It is purely motor, innervating intrinsic and extrinsic muscles for speech, , and mastication.

Spinal nerves and plexuses

The peripheral nervous system's spinal nerves consist of 31 pairs that emerge from the , providing motor and sensory innervation to the body trunk and limbs. These nerves are organized segmentally: eight cervical pairs (C1–C8), twelve thoracic pairs (T1–T12), five pairs (L1–L5), five sacral pairs (S1–S5), and one coccygeal pair (Co1). Each forms by the union of a dorsal root, which carries sensory (afferent) fibers from the periphery to the , and a ventral root, which conveys motor (efferent) fibers from the to the periphery. The dorsal root contains a housing the cell bodies of sensory neurons, while the ventral root lacks such a structure. Immediately after exiting the , each divides into four primary branches: the dorsal ramus, , meningeal ramus, and communicating rami. The dorsal ramus supplies the intrinsic muscles and skin of the back, while the innervates the anterior and lateral trunk as well as the limbs. The meningeal ramus re-enters the vertebral canal to provide sensory and innervation to the and blood vessels, and the communicating rami connect the to the sympathetic chain ganglia for autonomic functions. In regions requiring complex innervation, the ventral rami of adjacent spinal nerves interconnect to form plexuses, allowing for distributed nerve supply to specific body areas. The , derived from the ventral rami of C1–C4, primarily innervates the neck muscles and skin of the neck, head, and upper shoulder. The , formed by C5–T1, supplies the upper limbs and includes major branches such as the (extensor muscles and posterior skin of the arm and forearm), (flexor muscles of the forearm and ), and (intrinsic hand muscles and medial forearm). The arises from L1–L4 ventral rami and innervates the lower abdominal wall, anterior thigh, and medial leg, giving rise to nerves like the femoral and obturator. The , contributed by L4–S4, provides innervation to the , , , and lower limbs, originating nerves such as the sciatic and pudendal. The coccygeal plexus, a small network from Co1 and contributions from S4–S5, supplies the skin around the and perianal region.

Ganglia

Ganglia are discrete clusters of cell bodies located outside the , serving as key organizational units within the peripheral nervous system. They house the somata of peripheral s, enabling the transmission and, in certain cases, modulation of neural signals between the and peripheral tissues. Unlike nuclei in the , ganglia lack extensive synaptic integration in sensory types but facilitate relay functions in autonomic varieties. Peripheral ganglia are broadly classified into sensory, autonomic, and enteric types, each with distinct roles in signal handling. Sensory ganglia primarily contain cell bodies of afferent neurons that convey sensory information from peripheral receptors to the central nervous system. These include the dorsal root ganglia, paired swellings located adjacent to the spinal cord near the dorsal roots of spinal nerves, and the trigeminal ganglion associated with cranial nerve V, positioned in the middle cranial fossa within Meckel's cave. The neurons in sensory ganglia are pseudounipolar, featuring a single axonal process that splits into a peripheral branch extending to sensory endings and a central branch projecting to the spinal cord or brainstem; notably, these ganglia lack synapses, serving solely as waystations for unprocessed sensory input. Dorsal root ganglia, for example, are closely linked to spinal nerves, containing cell bodies for somatic and visceral sensory fibers. Autonomic ganglia encompass those of the sympathetic and parasympathetic divisions, where postganglionic cell bodies receive preganglionic inputs to signals to visceral effectors. form the paravertebral chain—a bilateral series of 22-23 interconnected masses running parallel to the vertebral column from the cervical to sacral regions—with examples including the superior, middle, and inferior . Prevertebral sympathetic ganglia, such as the celiac and superior mesenteric, lie anterior to the in the . are typically terminal, situated close to or embedded within target organs; the , for instance, resides in the posterior to the eye, between the and , to innervate intraocular structures. Neurons in autonomic ganglia are multipolar, with multiple dendrites receiving synapses from preganglionic fibers, allowing for signal without extensive central processing. Enteric ganglia constitute the intrinsic nervous system of the , embedded within the gut wall to coordinate local neural circuits. They form two main plexuses: the , located between the longitudinal and circular layers along the entire digestive tract, and the , situated in the submucosal primarily in the small and large intestines. These ganglia contain multipolar neurons interconnected by fibers, forming integrative networks capable of autonomous processing. In all peripheral ganglia, the primary function is to provide a peripheral locus for neuron cell bodies, protecting them from central vulnerabilities while facilitating efficient axonal distribution. Sensory ganglia emphasize passive conduction of afferent signals, whereas autonomic and enteric ganglia support local integration through synaptic relays, enabling decentralized control of peripheral targets.

Somatic nervous system

Structure

The comprises two primary components: afferent (sensory) fibers that transmit signals from sensory receptors in the skin, muscles, and joints to the (CNS), and efferent (motor) fibers that carry signals from the CNS to skeletal muscles via alpha motor neurons, enabling voluntary movement. These afferent fibers originate from specialized receptors such as mechanoreceptors in the skin for touch and proprioceptors in muscles and joints for position sense, relaying information directly to the or . Efferent fibers, in contrast, are lower motor neurons whose cell bodies reside in the ventral horn of the or cranial nerve nuclei, synapsing directly at neuromuscular junctions without intermediary structures. The pathways of the somatic nervous system travel through the cranial and spinal nerves, providing direct innervation to peripheral targets. There are 12 pairs of cranial nerves (primarily the oculomotor (III), trochlear (IV), abducens (VI), trigeminal (V), facial (VII), accessory (XI), and hypoglossal (XII) for somatic motor functions) that connect the brainstem to head and neck structures, while 31 pairs of spinal nerves emerge from the spinal cord to supply the rest of the body. Unlike the autonomic nervous system, somatic efferent pathways lack intervening ganglia, allowing for rapid, voluntary control of skeletal muscles. The somatic nervous system is organized somatotopically, with sensory and motor innervation segmented according to spinal cord levels, forming dermatomes and myotomes. Dermatomes represent specific areas of skin innervated by a single spinal nerve root, such as the C6 dermatome covering the thumb and lateral forearm, allowing clinicians to localize spinal lesions based on sensory deficits. Myotomes, the motor counterparts, are groups of muscles supplied by one spinal nerve root, for example, the C5 myotome including the deltoid and biceps for shoulder and elbow flexion. This segmental arrangement arises from embryonic development and ensures precise mapping of the body's periphery to CNS levels. Nerve fibers in the somatic nervous system are classified by diameter, myelination, and conduction velocity, with types A-alpha and A-beta being prominent. A-alpha fibers, with diameters of 12-20 μm and heavy myelination, conduct at 70-120 m/s and primarily serve motor functions to or via muscle spindles. A-beta fibers, smaller at 5-12 μm with moderate myelination, transmit touch and pressure sensations at 30-70 m/s from cutaneous mechanoreceptors. These classifications, based on Erlanger-Gasser grouping, highlight how fiber properties optimize signal speed for somatic functions.
Fiber TypeDiameter (μm)Conduction Velocity (m/s)MyelinationPrimary Function in Somatic System
A-alpha12-2070-120HeavyMotor to ;
A-beta5-1230-70ModerateTouch and pressure from

Function

The somatic nervous system's sensory function primarily involves the transmission of tactile sensations, , and information from peripheral receptors to the via primary afferent neurons. These pseudounipolar neurons, with cell bodies located in dorsal root ganglia for spinal nerves or sensory ganglia for , detect stimuli through specialized endings such as mechanoreceptors for touch, nociceptors for , and muscle spindles or Golgi organs for . Action potentials generated in these afferents travel along peripheral processes through dorsal roots into the or via to the , where they with second-order neurons to relay signals for conscious perception in the . In its motor role, the somatic nervous system facilitates voluntary control of skeletal muscles through a hierarchical organization of upper and lower motor neurons. Upper motor neurons originate in the motor cortex and brainstem, descending via corticospinal or other tracts to influence lower motor neurons in the ventral horn of the spinal cord or cranial nerve nuclei; these lower motor neurons extend axons through peripheral nerves to form excitatory neuromuscular junctions on skeletal muscle fibers. At the neuromuscular junction, acetylcholine release from the motor neuron terminal binds to nicotinic receptors, triggering depolarization and contraction, while inhibitory inputs from interneurons or descending pathways modulate activity to prevent excessive excitation. Reflex arcs represent an integral aspect of somatic function, enabling rapid, automatic responses to maintain posture and protect the body. The monosynaptic , exemplified by the knee-jerk response, occurs when sudden muscle stretch activates intrafusal fibers in muscle spindles, prompting Ia afferent fibers to monosynaptically excite alpha motor neurons in the , resulting in reflexive to resist the stretch. In contrast, the polysynaptic coordinates a more complex evasion from noxious stimuli, such as heat or pressure, where sensory afferents with spinal interneurons that activate flexor motor neurons ipsilaterally while inhibiting extensors, often involving contralateral extension for balance. Somatic integration occurs through local spinal circuits that process sensory inputs and generate immediate motor outputs for reflexes, independent of higher centers, ensuring swift responses critical for survival. However, voluntary actions arise from descending CNS signals that override or modulate these circuits, allowing conscious initiation, coordination, and inhibition of movements via pathways like the . This dual mechanism balances reflexive stability with adaptive voluntary behavior.

Autonomic nervous system

Sympathetic division

The sympathetic division of the autonomic nervous system, also known as the thoracolumbar division, originates from preganglionic neurons located in the intermediolateral cell column of the from segments T1 to L2. These neurons provide the outflow for the "fight-or-flight" response, mobilizing the body during stress by increasing energy availability and alertness. Postganglionic neurons are situated in paravertebral ganglia, which form the sympathetic chain along the vertebral column, or in prevertebral ganglia such as the celiac, superior mesenteric, and inferior mesenteric ganglia. This two-neuron chain allows for widespread innervation throughout the body, contrasting with the more localized parasympathetic division. Preganglionic fibers are relatively short and myelinated, exiting the spinal cord via ventral roots and entering the sympathetic chain through white rami communicantes. Within the chain, some fibers synapse immediately, while others ascend or descend to distant ganglia or pass through without synapsing to reach prevertebral ganglia via splanchnic nerves, such as the greater, lesser, and least splanchnic nerves that innervate abdominal organs. Postganglionic fibers are longer and unmyelinated, extending from the ganglia to target effectors, enabling diffuse activation across multiple organs simultaneously. The primary neurotransmitter at preganglionic synapses is (ACh), which binds to nicotinic receptors on postganglionic neurons. Most postganglionic neurons release norepinephrine (NE), acting on adrenergic receptors (α and β subtypes) to mediate excitatory effects, though sympathetic innervation to sweat glands uses ACh on muscarinic receptors. This noradrenergic transmission predominates, facilitating rapid physiological adjustments. Key targets include the heart, where postganglionic fibers via cardiac nerves increase heart rate and contractility through β1-adrenergic stimulation. In the lungs, sympathetic innervation causes bronchodilation via β2-adrenergic receptors to enhance airflow. The adrenal medulla receives direct preganglionic input, triggering release of epinephrine and norepinephrine into the bloodstream for amplified systemic effects. For the skin, sympathetic fibers innervate sweat glands to promote perspiration (cholinergic) and arrector pili muscles to induce piloerection (noradrenergic), aiding thermoregulation and defense responses.

Parasympathetic division

The parasympathetic division of the promotes "rest and digest" activities, facilitating energy conservation, , and restorative processes during periods of low stress. It originates from the craniosacral outflow, with preganglionic neurons located in nuclei associated with III (oculomotor), VII (), IX (glossopharyngeal), and X (vagus), as well as in the intermediolateral cell column of the sacral segments S2–S4. Postganglionic neurons near or within target organs, enabling localized control unlike the more diffuse sympathetic innervation. Preganglionic fibers in the parasympathetic system are long and myelinated, traveling significant distances to reach terminal ganglia, while postganglionic fibers are short and unmyelinated, providing precise innervation to effector tissues. Both preganglionic and postganglionic neurons release as the primary , acting on muscarinic receptors in target organs. The (CN X) accounts for approximately 75–80% of parasympathetic outflow, innervating thoracic and abdominal viscera including the heart, lungs, and up to the splenic flexure. Key targets of the parasympathetic division include the heart, where vagal stimulation induces bradycardia by slowing sinoatrial node firing; the gastrointestinal tract, where it enhances peristalsis and secretory activity to promote digestion; the pupils, causing miosis via constriction of the iris sphincter muscle through oculomotor nerve fibers; and salivary glands, stimulating watery secretion via facial and glossopharyngeal nerve pathways. Parasympathetic ganglia are primarily terminal structures located close to or embedded within target organs, such as the otic ganglion for glossopharyngeal (CN IX) innervation of the parotid gland, and intramural ganglia within the walls of viscera like the heart and intestines for fine-tuned local responses. This arrangement supports organ-specific effects, contrasting with the sympathetic division's chain-linked ganglia.

Enteric nervous system

The (ENS) is a complex, semi-autonomous network of neurons embedded within the walls of the , often referred to as the "second brain" due to its ability to control digestive processes independently of the . It extends continuously from the to the , forming intricate plexuses between the layers of the gut wall. The ENS comprises approximately 400-600 million neurons, containing a similar number to the and enabling sophisticated local regulation of gut function. The ENS is organized into two primary plexuses: the myenteric (Auerbach's) plexus and the submucosal (Meissner's) plexus. The is located between the longitudinal and circular muscle layers of the muscularis externa, primarily coordinating gastrointestinal through motor neurons that innervate . In contrast, the resides in the layer beneath the mucosa, regulating glandular , mucosal blood flow, and absorption via sensory and secretory neurons. These plexuses contain diverse neuron types, including sensory, , and motor neurons, which form local circuits for reflex activity. Although the ENS receives modulatory inputs from the sympathetic and parasympathetic divisions of the —such as vagal parasympathetic fibers for excitatory effects—it operates largely autonomously through intrinsic neural pathways. This independence allows for reflexive responses without central input, exemplified by the peristaltic reflex, where local circuits detect luminal distension and coordinate propulsion. Sympathetic inputs generally inhibit , while parasympathetic enhance it, but the ENS can sustain basic functions even if these extrinsic connections are severed. Key functions of the ENS include the coordination of , for propulsion of contents, and segmentation for mixing, all mediated by integrated sensory-motor networks. Sensory neurons within the plexuses detect mechanical stretch, chemical nutrients, and changes in the gut lumen, relaying this information to trigger appropriate motor and secretory responses. These capabilities ensure efficient and nutrient handling across the .

Physiology

Sensory functions

The peripheral nervous system (PNS) plays a crucial role in sensory functions by transmitting information from peripheral receptors to the (CNS) via afferent pathways. These pathways enable the detection and relay of various stimuli, including touch, , , and body position, ensuring environmental awareness and internal monitoring. Sensory neurons in the PNS originate from cell bodies in dorsal root ganglia or cranial nerve ganglia, with axons extending to peripheral receptors and centrally to the or . Sensory receptors in the PNS are specialized structures that convert environmental stimuli into electrical signals, classified primarily by the type of stimulus they detect. Mechanoreceptors respond to mechanical deformation, such as touch and pressure; examples include Meissner's corpuscles for light touch and Pacinian corpuscles for vibration and deep pressure. Nociceptors detect potentially harmful stimuli like extreme heat, cold, or mechanical injury, initiating pain signals. Thermoreceptors sense temperature changes, with separate populations for warmth and cold. Proprioceptors, located in muscles, tendons, and joints, provide information on body position and movement, exemplified by muscle spindles and Golgi tendon organs. Afferent pathways in the PNS carry these signals from receptors to the CNS through primary afferent neurons, entering via dorsal roots of spinal nerves or . These pathways are categorized by fiber type based on myelination and conduction speed: fast-conducting myelinated A-fibers (including Aα for , Aβ for touch, and Aδ for sharp pain) transmit signals rapidly, while slow-conducting unmyelinated C-fibers mediate dull pain, , and with lower velocity. Conduction speeds vary from 0.5–2 m/s in C-fibers to 12–30 m/s in Aδ-fibers and up to 120 m/s in Aα-fibers, allowing for differentiated sensory experiences. Sensory modalities in the PNS are divided into somatic and visceral types, each serving distinct purposes. Somatic sensations arise from skin, muscles, and joints, encompassing fine touch, , and localized . Visceral sensations, from internal organs, detect stretch, ischemia, or chemical changes, often perceived as diffuse discomfort rather than precise localization. occurs when visceral afferents converge with somatic afferents in the , causing pain from an organ to be felt in a distant somatic region, such as cardiac ischemia referred to the left arm due to shared T1–T5 segments. Initial sensory processing in the PNS culminates at the first central synapse, where afferent terminals contact second-order neurons. For spinal inputs, this occurs in the dorsal horn of the , with mechanoreceptive and proprioceptive fibers synapsing in laminae III–VI, nociceptive Aδ-fibers in lamina I and V, and C-fibers in lamina II (substantia gelatinosa). Cranial nerve afferents synapse in brainstem nuclei, such as the trigeminal nucleus for facial sensations or the for visceral inputs from the head and neck. This synaptic organization allows for local modulation before ascending to higher CNS centers.

Motor functions

The motor functions of the peripheral nervous system (PNS) encompass the efferent pathways that transmit signals from the to effectors, enabling voluntary movement and involuntary regulation of internal organs. These functions are divided into somatic and autonomic components, with the somatic system controlling skeletal muscles for locomotion and posture, while the autonomic system modulates smooth muscles, , and glands for . In the somatic motor system, efferent signals originate from alpha motor neurons in the or , which extend unbranched axons directly to fibers. These neurons release as the at the , where it binds to nicotinic acetylcholine receptors on the muscle endplate, triggering and contraction. Action potentials propagate along the myelinated axons of these motor neurons at speeds up to 120 m/s, ensuring rapid transmission, and synaptic release at the involves calcium influx leading to quantized vesicle fusion. Coordination in somatic motor output often involves , where activation of muscles inhibits antagonists via inhibitory in spinal reflex circuits, such as the Ia inhibitory pathway, to facilitate smooth, antagonistic movements without co-contraction. The autonomic motor system employs a two-neuron chain for efferent output: preganglionic neurons release onto nicotinic receptors in autonomic ganglia, while postganglionic neurons innervate visceral effectors. Sympathetic postganglionic neurons primarily release norepinephrine, which acts on adrenergic receptors (alpha and beta subtypes) to excite or inhibit smooth and , whereas parasympathetic postganglionic neurons release onto muscarinic receptors for similar modulatory effects on glands and viscera. occurs via action potentials along preganglionic (myelinated) and postganglionic (mostly unmyelinated) axons, with synaptic transmission at neuroeffector junctions involving diffuse varicosities that release neurotransmitters onto a broader effector area compared to the focal . Coordination in the autonomic system features divergent and convergent wiring, where a single preganglionic can synapse with numerous postganglionic neurons across ganglia levels, enabling mass activation of multiple organs during stress responses. Visceral motor functions highlight the antagonistic roles of sympathetic and parasympathetic divisions: the sympathetic system promotes mobilization by increasing , dilating bronchi, and redirecting blood flow to muscles via norepinephrine-mediated excitation, preparing the body for "fight-or-flight" scenarios. In contrast, the parasympathetic system supports conservation and restoration by slowing , enhancing , and promoting glandular secretion through at muscarinic receptors, aligning with "rest-and-digest" activities.

Development

Embryological origins

The peripheral nervous system (PNS) originates during early embryogenesis from three primary sources: the , , and ectodermal placodes, which collectively contribute to its sensory, motor, and autonomic components. These origins occur through a coordinated process of cell specification, migration, and differentiation, beginning with the formation of the around the third week of human gestation. The , formed by the process of , primarily contributes efferent components to the PNS. Specifically, somatic motor neurons arise from progenitor cells in the ventral ventricular zone of the developing and migrate to form the ventral horn, where they extend axons peripherally to innervate skeletal muscles. Similarly, preganglionic autonomic neurons originate from the intermediolateral column (lateral horn) of the thoracic and lumbar , providing sympathetic outflow, while parasympathetic preganglionic neurons emerge from nuclei and the sacral cord. These central origins ensure direct neural control over peripheral effectors. Neural crest cells, induced at the dorsal border during the third to fourth weeks, delaminate and undergo epithelial-to-mesenchymal transition before migrating extensively to populate peripheral sites. These multipotent cells differentiate into sensory neurons of the ganglia, which relay somatosensory to the ; postganglionic autonomic neurons forming the sympathetic chain ganglia and ; adrenal chromaffin cells involved in catecholamine production; and Schwann cells, which provide myelination to peripheral axons. Neural crest migration in humans commences around the fourth week, with cells reaching target locations such as the sympathetic chain by the sixth to seventh weeks. Ectodermal placodes, thickenings of the non-neural head adjacent to the , contribute to the cranial sensory components of the PNS. These neurogenic placodes give rise to sensory neurons in cranial ganglia, including the (from the trigeminal placode), which handles facial sensation, as well as contributions to the geniculate, petrosal, and nodose ganglia associated with VII, IX, and X. Placode-derived neuroblasts migrate inward to join contributions, forming mixed ganglia by the fifth to eighth weeks. By the eighth week, initial peripheral nerve outgrowth from these embryonic sources establishes the basic PNS framework.

Postnatal maturation

The postnatal maturation of the peripheral nervous system (PNS) involves progressive myelination by Schwann cells, which begins around the 15th week of and is largely complete by birth, though additional myelination and maturation occur postnatally as the body grows, continuing into to optimize conduction along elongating axons. This process is essential for optimizing , as sheaths insulate axons and enable , dramatically increasing signal transmission speed from the slower unmyelinated state in infancy to efficient propagation in . Schwann cells, derived from precursors, wrap multiple layers of around larger-diameter axons during this period, with the majority of motor and sensory fibers achieving full myelination by toddlerhood, supporting refined and sensory discrimination. Axonal elongation accompanies overall body growth throughout childhood and , allowing peripheral to extend in length to match somatic expansion, particularly in limbs and spinal . This growth is coupled with synapse in sensory and motor pathways, where excess axonal branches and polyinnervated synapses—common in early infancy—are selectively eliminated to refine connectivity and enhance precision. For instance, at neuromuscular junctions, competitive interactions between motor axons lead to the withdrawal of superfluous terminals, reducing from multiple to single innervation per muscle fiber by late childhood, thereby streamlining motor function and preventing inefficient signaling. The PNS exhibits notable plasticity postnatally, including a robust capacity for regeneration that contrasts sharply with the limited repair potential in the (CNS), primarily due to supportive roles of s in clearing debris and guiding axonal regrowth. such as (NGF) play a critical role in maintaining neuronal survival, promoting axonal branching, and sustaining plasticity throughout life by binding to TrkA receptors on sensory and sympathetic neurons. In aging, however, the PNS undergoes demyelination and axonal , leading to slowed conduction velocities and increased vulnerability to injury, as sheaths thin and Schwann cell efficiency wanes.

Clinical significance

Disorders

Disorders of the peripheral nervous system (PNS) encompass a range of conditions that impair nerve function outside the , leading to sensory, motor, or autonomic deficits. These disorders often arise from damage to axons, sheaths, or supporting structures, resulting in symptoms such as , numbness, weakness, or organ dysfunction. Common etiologies include metabolic disturbances, infections, toxins, trauma, genetic mutations, and autoimmune processes. Unlike pathologies, PNS disorders typically present with distal symmetrical involvement and can be classified as mononeuropathies, polyneuropathies, or autonomic neuropathies based on the extent and pattern of nerve involvement. Peripheral neuropathies represent a major category of PNS disorders, characterized by damage to multiple peripheral nerves and often manifesting as progressive sensory loss, paresthesias, and motor weakness starting in the extremities. Causes include diabetes mellitus, which affects up to 50% of long-term patients through hyperglycemia-induced microvascular damage and oxidative stress; exposure to toxins like chemotherapy agents or heavy metals; and traumatic injuries such as nerve compression or laceration. Symptoms typically involve numbness, tingling, burning pain, and muscle weakness, with severity correlating to the underlying etiology. Neuropathies are broadly classified as axonal, where the nerve fiber degenerates primarily, or demyelinating, involving loss of the myelin insulation that speeds conduction; the latter often progresses more rapidly and may respond better to immunomodulatory therapies. Guillain-Barré syndrome exemplifies an acute demyelinating polyneuropathy, triggered post-infection by molecular mimicry leading to autoimmune attack on myelin, causing ascending weakness and potential respiratory failure within days to weeks. Autonomic disorders disrupt the involuntary control of visceral functions mediated by the sympathetic, parasympathetic, and enteric divisions of the PNS, often resulting in with symptoms like , gastrointestinal dysmotility, or abnormal sweating. , a rare neurodegenerative condition, primarily affects postganglionic sympathetic neurons, leading to severe —defined as a systolic drop of at least 20 mmHg upon standing—due to impaired and norepinephrine release. In the , arises from congenital failure of cell migration during embryogenesis, causing aganglionosis (absence of enteric ganglia) in segments of the colon, which results in tonic contraction, functional obstruction, and severe or intestinal in neonates. These enteric defects highlight the PNS's role in gut motility, with aganglionic regions exhibiting absent due to lack of inhibitory neurons. Disorders affecting specific cranial or spinal nerves often present as focal mononeuropathies with localized symptoms. involves acute inflammation or ischemia of the (cranial nerve VII), leading to unilateral weakness, drooping of the mouth, and inability to close the eye, typically resolving spontaneously but with risk of in 15-30% of cases. , affecting the (cranial nerve V), causes paroxysmal, electric-shock-like in the face due to vascular compression of the or demyelination, triggered by light touch and severely impacting . Spinal nerve involvement, such as in radiculopathies from disc herniation, can mimic but is distinguished by dermatomal and loss. Genetic and rare PNS disorders include hereditary conditions like Charcot-Marie-Tooth (CMT) disease, the most common inherited neuropathy, caused by mutations in genes such as PMP22 leading to demyelination or axonal degeneration, resulting in progressive distal , foot deformities (), and sensory loss starting in adolescence. Chronic inflammatory demyelinating polyneuropathy (CIDP), an acquired autoimmune disorder, features relapsing or progressive symmetrical weakness and sensory deficits over months, with nerve conduction studies showing slowed velocities due to macrophage-mediated demyelination and remyelination cycles. These rare entities underscore the PNS's vulnerability to both inherited structural defects and chronic immune dysregulation, often requiring specialized diagnostic confirmation.

Diagnosis and treatment

Diagnosis of peripheral nervous system (PNS) disorders typically begins with a comprehensive clinical examination to evaluate sensory, motor, and reflex functions. Reflex testing assesses deep tendon reflexes, such as the patellar or Achilles reflex, to identify or indicative of nerve dysfunction. Sensory mapping involves testing light touch, pinprick, vibration, and across dermatomes to localize affected nerves. Cranial nerve assessments, particularly for nerves , VII, IX, X, and XII, evaluate sensation, motor function, and autonomic responses relevant to PNS involvement. Advanced diagnostic techniques provide objective measures of PNS integrity. Electromyography (EMG) and nerve conduction studies (NCS) evaluate muscle electrical activity and nerve signal speed, respectively, with NCS measuring conduction velocity to distinguish axonal from demyelinating neuropathies. Nerve biopsy, obtained via sural or superficial peroneal nerve sampling, allows histopathological analysis for inflammatory, degenerative, or infiltrative processes, though it is reserved for cases where non-invasive tests are inconclusive. Magnetic resonance imaging (MRI), including neurography sequences, visualizes nerve plexuses and entrapments, such as in brachial plexopathy, by highlighting signal abnormalities in affected nerves. Autonomic testing, including tilt-table testing for orthostatic hypotension and quantitative sudomotor axon reflex testing (QSART) for sweat gland function, assesses sympathetic and parasympathetic PNS components. Treatment strategies for PNS disorders aim to alleviate symptoms, address underlying causes, and promote recovery, tailored to the specific condition such as neuropathy or . Pharmacological interventions include anticonvulsants like for , which modulate calcium channels to reduce neuronal excitability. Surgical options encompass decompression to relieve , as in , and direct nerve repair via microsuturing for traumatic injuries to restore continuity. Supportive therapies, such as , focus on improving strength, balance, and mobility through targeted exercises to mitigate . , including intravenous immunoglobulin (IVIG) or plasma exchange, is employed for inflammatory conditions like Guillain-Barré to modulate autoimmune responses. Emerging therapies hold promise for enhancing PNS regeneration, particularly in hereditary or severe injuries. Gene therapy targets mutations in inherited neuropathies, such as Charcot-Marie-Tooth disease, using adeno-associated viral vectors to deliver corrective genes and improve nerve function. approaches, involving mesenchymal stem cells, promote axonal regrowth and remyelination by providing neurotrophic support and in nerve grafts or conduits.

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