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Internal carotid plexus

The internal carotid plexus is a delicate network of postganglionic sympathetic nerve fibers that surrounds the lateral aspect of the internal carotid artery, extending from the superior cervical ganglion through the carotid canal into the cranial cavity.^[1]^[2] Originating primarily from the internal carotid nerve—a branch of the superior cervical ganglion—this plexus forms a meshwork of neurons that ascends along the artery's surface, distributing fibers to key structures in the head.^[3]^[1] Anatomically, the plexus is divided into segments corresponding to the internal carotid artery's path: the petrous segment (along the ventral petrous portion, approximately 18 mm in length), the lacerum segment (crossing from medial to lateral over 10 mm), and the cavernous sinus segment (ascending 5 mm along the inferior compartment).^[4] It typically presents in a nerve-like morphology (70% of cases, as a single or double trunk) or plexus-like pattern (30%, with net-like transverse and longitudinal branches).^[4] The main named branch is the deep petrosal nerve, which emerges near the foramen lacerum and joins the greater petrosal nerve to form the nerve of the pterygoid canal, ultimately connecting to the pterygopalatine ganglion.^[2]^[1] Additional unnamed fibers distribute via the nasociliary nerve, ophthalmic artery branches, caroticotympanic nerves, and auriculotemporal nerve.^[1] Functionally, the internal carotid plexus delivers sympathetic efferent innervation to vasomotor, sudomotor, and pilomotor structures, including the dilator pupillae muscle (inducing mydriasis) and superior tarsal muscle (Müller's muscle; providing fine control of eyelid elevation).^[5] It also innervates the nasal mucosa, paranasal sinuses, lacrimal and salivary glands, middle ear via the tympanic plexus, and parotid gland.^[1]^[2] It also supplies the internal carotid artery itself and the pterygopalatine artery, while sympathetic connections to the abducens nerve occur in nearly all cases (97.8% from the lateral cavernous wall).^[3]^[6] Disruption of these fibers, as in surgical approaches to the cavernous sinus, can lead to Horner's syndrome, characterized by ptosis, miosis, and anhidrosis.^[2]^[4]

Anatomy

Structure and location

The internal carotid plexus is a network of postganglionic sympathetic nerve fibers that forms a thin, irregular meshwork situated on the lateral aspect of the internal carotid artery (ICA).^[7] This plexus consists primarily of unmyelinated fibers arranged in a loose, anastomosing pattern without forming distinct trunks, adhering loosely to the adventitia of the artery wall.^[8] It typically presents in a nerve-like morphology (70% of cases, as a single or double trunk) or plexus-like pattern (30%, with net-like transverse and longitudinal branches).^[4] It extends along the course of the ICA, beginning at the carotid bifurcation in the neck where sympathetic fibers from the superior cervical ganglion join the artery.^[9] The plexus accompanies the ICA superiorly through the cervical segment within the carotid sheath, enters the skull base via the carotid canal in the petrous temporal bone (petrous segment, approximately 18 mm in length), and passes over the foramen lacerum (lacerum segment, approximately 10 mm in length) before surrounding the artery in the cavernous sinus (cavernous sinus segment, approximately 5 mm in length).^[7]^[4] Intracranially, it continues along the supraclinoid portion of the ICA toward the circle of Willis, maintaining its perivascular position.^[8] In the neck, the plexus lies adjacent to the structures of the carotid sheath, including the common and internal carotid arteries, internal jugular vein, and vagus nerve, without penetrating the arterial wall.^[9] Within the cavernous sinus, it is positioned lateral to the ICA and in close proximity to the intracavernous cranial nerves (III, IV, V1, V2, and VI), which course in the lateral wall; fiber exchanges can occur here, particularly with the abducens nerve (VI) at the carotid portion of its cavernous segment, where the abducens may exhibit variations such as pseudobranching (25%) and duplication (6.7%).^[10] The plexus runs over the foramen lacerum during its petrous transit, between the sphenoid, petrous temporal, and occipital bones.^[7] Variations in plexus density are noted along its course, with denser concentrations of fibers observed in the distal petrous and cavernous segments compared to the sparser arrangement in the cervical segment.^[8]

Formation and components

The internal carotid plexus arises primarily from postganglionic sympathetic fibers of the superior cervical ganglion, which form the internal carotid nerve that ascends alongside the artery. These postganglionic fibers receive preganglionic input from neurons in the intermediolateral cell column of spinal cord segments T1 to T3, conveyed through the cervical sympathetic trunk.^[2]^[1]^[11] The plexus comprises mainly unmyelinated postganglionic sympathetic fibers that are noradrenergic, providing vasomotor control, along with occasional parasympathetic fibers communicating via the pterygopalatine ganglion and minor sensory contributions from trigeminal connections; it contains no motor or somatic fibers.^[12]^[13] Assembly occurs as these postganglionic fibers travel superiorly along the internal carotid artery after leaving the superior cervical ganglion, intertwining to create a loose network without a distinct connective tissue sheath, while branches diverge at key arterial segments including the cervical, petrous, cavernous, and cerebral portions.^[15]^[16] Historical anatomical descriptions, such as those by Jacques-Bénigne Winslow in 1732, first identified the structure as a sympathetic network surrounding the internal carotid artery within the cavernous sinus region.^[17]

Function

Sympathetic innervation

The internal carotid plexus delivers postganglionic sympathetic fibers originating from the superior cervical ganglion, forming a network that ascends along the internal carotid artery to innervate key structures in the head. These fibers constitute the primary sympathetic supply to select cranial targets, emphasizing vasomotor control and pupillary responses.^[3] The main trunk, known as the internal carotid nerve, gives rise to branches that target the dilator pupillae muscle of the eye via the long and short ciliary nerves, enabling pupillary dilation in response to low light levels or sympathetic activation. Additional targets encompass the smooth muscle of cerebral and dural blood vessels, where fibers regulate vasoconstriction to modulate blood flow, and the nasopharyngeal mucosa, providing vasomotor innervation to regulate blood flow and support glandular function. It also supplies sympathetic innervation to the lacrimal gland, paranasal sinuses, salivary glands including the parotid, and middle ear via the tympanic plexus.^[18]^[19]^[2] Pathways from the plexus extend intracranially through the cavernous sinus, where sympathetic fibers contribute to the cavernous plexus and often hitchhike along the abducens nerve for distribution. Further anastomoses occur with the ophthalmic plexus, facilitating targeted supply to ocular structures via branches of the trigeminal nerve.^[20]^[6]^[21] The constituent fibers are primarily noradrenergic, releasing norepinephrine to mediate vasoconstriction in cerebral vessels and contraction of the dilator pupillae, though cerebral vasodilation involves coordinated input from minor non-adrenergic components within the broader autonomic network. The plexus maintains bilateral symmetry, with independent right and left distributions coordinated centrally via hypothalamic and brainstem sympathetic nuclei.^[18]^[22]

Physiological roles

The internal carotid plexus, through its sympathetic postganglionic fibers originating from the superior cervical ganglion, plays a key role in vasomotor control by innervating the smooth muscle of cerebral arteries, inducing vasoconstriction via norepinephrine release to regulate cerebral blood flow in response to systemic hypertension or hypoxia, thereby preventing cerebral hyperperfusion.^[23] This mechanism helps maintain autoregulation of blood flow during physiological stressors, although under normal conditions, the sympathetic influence on cerebral vessels is minimal compared to local metabolic factors. For instance, activation of these fibers during acute hypertensive episodes constricts the internal carotid artery and its branches, reducing flow to protect against excessive pressure transmission to downstream cerebral tissues.^[24] In ocular physiology, the plexus mediates pupillary dilation (mydriasis) by innervating the dilator pupillae muscle of the iris, facilitating increased light entry and visual acuity during sympathetic arousal, such as in fight-or-flight responses.^[25] Additionally, these fibers supply the superior tarsal muscle (Müller's muscle), contributing to sustained eyelid elevation and tone to support continuous eye opening without skeletal muscle fatigue.^[26] The plexus also supports thermoregulatory and secretory functions in the head region via minor branches that innervate sweat glands on the medial forehead and central face, promoting sudomotor activity to dissipate heat during elevated body temperature.^[27] Furthermore, sympathetic input from the plexus modulates vascular tone in the nasal and pharyngeal mucosa, indirectly influencing glandular secretion by controlling blood flow to these tissues, which aids in maintaining mucosal hydration and minor thermoregulatory adjustments. It similarly modulates secretion in lacrimal, paranasal sinus, and salivary glands via vasomotor effects.^[28]^[2] Regarding integration with the baroreflex, the sympathetic fibers of the internal carotid plexus contribute to modulating vascular tone in the internal carotid artery wall, providing an efferent component that adjusts vasoconstriction in response to baroreceptor signals from the carotid sinus, although the primary afferent pathway involves the glossopharyngeal nerve via the carotid sinus nerve.^[29] This efferent role helps fine-tune arterial compliance and pressure buffering during fluctuations in systemic blood pressure.^[30]

Clinical significance

Associated disorders

The internal carotid plexus, a network of postganglionic sympathetic fibers surrounding the internal carotid artery, can be disrupted in various pathological conditions, leading to oculosympathetic denervation and associated symptoms. Horner's syndrome represents the most common disorder linked to plexus dysfunction, characterized by ipsilateral ptosis, miosis, and anhidrosis due to interruption of the sympathetic pathway to the eye. This syndrome arises from causes such as internal carotid artery (ICA) dissection, which damages the periarterial sympathetic fibers; apical lung tumors like Pancoast tumors that compress preganglionic fibers or the plexus; and brainstem lesions that interrupt preganglionic sympathetic outflow. In ICA dissection, the mechanical injury to the arterial wall directly affects the overlying plexus, resulting in acute painful Horner's syndrome, often confirmed as the most frequent identifiable etiology in isolated cases.^[31]^[32]^[33]^[34]^[35]^[36] Cluster headache and other autonomic cephalgias involve hyperexcitability of the internal carotid plexus, contributing to trigeminovascular activation and sympathetic imbalance. In these primary headache disorders, parasympathetic overactivity may dilate the ICA, compressing the sympathetic periarterial plexus and exacerbating vasomotor symptoms such as lacrimation and nasal congestion. Sympathetic dysfunction in the plexus has been implicated in the autonomic features of cluster headache, with studies showing altered noradrenergic transmission along these fibers during attacks. ICA dissection can also mimic cluster headache presentations due to similar irritation of the plexus, highlighting the overlap in pathophysiology.^[37]^[38]^[39]^[40]^[41] Rare cases of isolated plexopathy, without full Horner's syndrome, may occur from direct trauma or inflammation affecting the internal carotid sympathetic plexus. Traumatic injuries, such as those from blunt neck trauma or arterial dissection, can selectively damage plexus fibers, leading to transient miosis or other partial oculosympathetic symptoms due to denervation or aberrant sympathetic reinnervation. Post-viral inflammation, including after COVID-19 infection, has been reported to cause isolated postganglionic sympathetic disruption. These presentations are uncommon and often resolve spontaneously, distinguishing them from more systemic sympathetic lesions.^[42]^[43]^[44] Diagnostic approaches for disorders involving the internal carotid plexus focus on confirming sympathetic dysfunction and identifying underlying pathology. Pharmacological testing with cocaine or apraclonidine eye drops confirms Horner's syndrome by demonstrating failure of pupil dilation (cocaine) or reversal of anisocoria (apraclonidine), localizing postganglionic lesions to the ICA plexus. Hydroxyamphetamine drops can further distinguish postganglionic from preganglionic sites by assessing residual norepinephrine release. Imaging with MRI and magnetic resonance angiography (MRA) is essential to detect ICA dissection or tumors compressing the plexus, with high sensitivity for vascular abnormalities. These methods, combined with clinical evaluation, guide targeted management while referencing the sympathetic innervation pathway to the eye.^[45]^[46]^[47]^[48]^[34]^[49]

Surgical considerations

In carotid endarterectomy (CEA), the internal carotid plexus is vulnerable to injury during atheromatous plaque removal, as the sympathetic fibers lie along the adventitia of the internal carotid artery (ICA), potentially resulting in postoperative Horner's syndrome. The incidence of Horner's syndrome persisting at hospital discharge after CEA is approximately 3.7%, though it is typically transient and resolves in the majority of cases.^[50] Preservation techniques emphasize subadventitial dissection to maintain the integrity of the media and adventitia, thereby minimizing damage to the plexus and reducing the risk of sympathetic denervation.^[51] During endoscopic endonasal approaches for pituitary tumors, the internal carotid plexus becomes visible within the cavernous sinus, where tumor resection carries risks of sympathetic denervation that may affect adjacent cranial nerves and lead to Horner's syndrome or oculosympathetic palsy. Surgical mapping of the plexus anatomy during these procedures helps mitigate injury risks by guiding precise dissection around the ICA wall.^[4] Intraoperative neuromonitoring, including electromyography and evoked potentials, is employed in skull base surgeries to safeguard neural structures, though specific sympathetic monitoring remains investigational.^[52] In skull base surgeries such as acoustic neuroma resection, the plexus adheres closely to the petrous and cavernous segments of the ICA, necessitating meticulous microdissection to prevent vasospasm or autonomic instability from fiber disruption.^[53] Postoperative management of plexus-related injuries focuses on addressing vasomotor imbalance, with prophylactic beta-blockers used to stabilize hemodynamics and reduce hypertension risks following ICA manipulation. Long-term outcomes indicate resolution of transient symptoms, such as those in Horner's syndrome, in most cases.^[54]^[55]

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