Head and Neck Surgery

Posts Tagged ‘Syringobulbia’


Posted by headnecksurgery on September 23, 2008

The diagnosis and management of the numerous and complex neurologic conditions that present in the head and neck are predicated on an understanding of the neuroanatomic and neurophysiologic characteristics of this region (1,2,3 and 4) (Fig. 9.1, Fig. 9.2, Fig. 9.3, Fig. 9.4, Fig. 9.5, Fig. 9.6 and Fig. 9.7), particularly of the cranial nerves (Table 9.1). Many neurologic diseases have manifestations in the head and neck. In diseases such as cerebrovascular accidents and tumors, the location of the lesion determines the manifestations of the disorder. Demyelinating or degenerative diseases also manifest ear, nose, and throat symptoms.
Multiple Sclerosis
Multiple sclerosis is an inflammatory disease involving areas of demyelinization in the central nervous system. This disease primarily affects young adults and is characterized by exacerbations and remissions. The geographic distribution is distinct: the incidence is higher in the higher latitudes and almost nil at the equator. Vertigo is the presenting problem among 7% to 10% of patients and may eventually occur among as many as 30% of patients. Nystagmus occurs among 70% of patients. This is usually horizontal nystagmus, although 33% of patients with nystagmus have vertical nystagmus. Diplopia often is caused by involvement of extraocular muscles from lesions in the medial longitudinal fasciculus, which links the nuclei of cranial nerves VI and III and subserves conjugate lateral gaze. Bilateral internuclear ophthalmoplegia due to a lesion of the medial longitudinal fasciculus strongly indicates the existence of multiple sclerosis. Deafness is rare in multiple sclerosis. The Charcot triad in multiple sclerosis consists of nystagmus, scanning speech, and intention tremor (5). Multiple sclerosis can be diagnosed reliably with appropriate diagnostic studies. The following findings establish the diagnosis: magnetic resonance images that show small, demyelinated foci in the white matter; abnormal brainstem auditory or visual evoked responses, and elevated protein level in the cerebrospinal fluid with the presence of oligoclonal immunoglobulin banding.
Myasthenia Gravis
Myasthenia gravis is caused by impaired transmission across the myoneural junction due to the presence of antibodies to the acetylcholine receptor. Onset occurs at all ages with clustering among young women and older men. This disease is characterized by weakness and abnormal fatigue of striated muscles. Remission and exacerbation are characteristic. Ocular muscles are involved in more than 90% of these patients. There often is weakness of facial, laryngeal, and pharyngeal muscles. The cricopharyngeal muscle often is involved. The weakness is greater after exercise or at the end of the day. Nystagmus and vertigo are rare. Transient neonatal myasthenia gravis occurs among one in seven newborns born to a mother with myasthenia gravis. The infants are unable to suck and swallow. Diagnosis is made from the history and the findings of relief of weakness after administration of neostigmine (6). Myasthenia gravis is associated with thymoma among 10% of patients. The disease is autoimmune in nature and mediated by circulating immunoglobulin G antibodies to the acetylcholine receptor. A positive result for the presence of antiacetylcholine receptor antibody (present in approximately 85% of patients), a positive result of an edrophonium test, and abnormal results of repetitive stimulation electromyography are highly reliable in establishing the diagnosis.
Amyotrophic Lateral Sclerosis
Amyotrophic lateral sclerosis is a degenerative disease of the upper and lower motor neurons of the central nervous system. The disease is characterized by progressive muscular weakness and atrophy along with spasticity. The otolaryngologic manifestations are dysphagia, fasciculation, atrophy of the tongue, dysarthria, and pseudobulbar palsy. Deep tendon reflexes are hyperactive. This disease usually occurs among middle-aged and older persons, mainly men (7).
Syringobulbia is a progressive, degenerative disease that involves cavitation of central parts of the cervical spinal cord (syringomyelia). It extends superiorly into the medulla oblongata and pons and into the area of the descending tract of the trigeminal nerve or other nuclei of bulbar structures. Signs are analgesia and thermoanesthesia of the face, atrophy and weakness of the tongue, palatal paralysis, and vocal cord paralysis. There is usually shoulder and upper extremity involvement (6). Arnold-Chiari type I malformation is frequently associated. This malformation by itself even without syrinx formation can cause Menière-like auditory and vestibular symptoms (8).
Poliomyelitis is a viral illness usually affecting children. It has been almost eliminated in the United States through vaccination. When poliomyelitis does occur, there usually are several cases in a community. The onset of disease is acute and is characterized by fever, muscle weakness, tight neck muscles, decreased deep tendon reflexes, and dysphagia (7). Examination of the cerebrospinal fluid shows acute meningitis.
Guillain-Barré Syndrome
In Guillain-Barré syndrome, an acute postinfectious inflammatory polyneuropathy, the patient has ascending limb weakness and muscle tenderness that in rare instances progresses to dysphagia, respiratory failure, and minimal sensory symptoms. The patient continues to have a fever. Guillain-Barré syndrome usually follows a viral illness or inoculation with vaccine. The Miller-Fisher variant of Guillain-Barré syndrome begins with weakness of facial and neck muscles before limb weakness develops (9). The diagnosis usually is confirmed when there is an elevated level of protein in the cerebrospinal fluid without a cellular response.
Tetanus is caused by a toxin produced by clostridia, usually from infection of puncture wounds or pressure ulcers. The disease is characterized by trismus, rigid abdominal muscles, dysphagia, and perspiration. External stimuli may trigger muscle spasms and even convulsions. Laryngeal spasm may occur. Tetanus can be confined to the head and neck. There usually is a history of injury, but often the trauma was trivial or not reported (10). Tetanus often occurs among elderly persons who have not maintained their immunizations.
Dystonia of the tongue or lips and facial grimacing may be caused by extrapyramidal disease or drug intoxication. Torsion spasm involves excess muscle tone in large muscle groups. This may involve the entire body. Movements are slow, undulant, writhing, and twisting. This disorder may involve only the face, tongue, head, and neck, leading to dysarthria, facial grimacing, and torticollis. Meige syndrome, known as cranial dystonia, presents with focal or segmental dystonia involving the cranial muscles. The most common example is blepharospasm (11). Dystonia musculorum deformans is a rare, progressive, familial disorder manifesting dystonia. Tardive dyskinesia is a dystonia of the lips, tongue, and facial muscles. This is a late side effect of phenothiazines that can occur even after discontinuation of the drug. Spasmodic torticollis involves dystonic movement of the head, neck, and shoulders. Initially, this is intermittent, but it can later develop into persistent muscle contraction with deviation of the head. This condition can be congenital or acquired. Some cases may be psychogenic (6). Spastic dysphonia is considered to be a focal dystonia of the larynx.
Palatal Myoclonus
Palatal myoclonus involves involuntary movement of the pharynx and soft palate. This movement can be suppressed by voluntary effort. Palatal myoclonus is caused by lesions of the olivodentatorubromesencephalic pathway (6).
Cerebrovascular accidents (CVAs) can be caused by hemorrhage, thrombosis, or emboli.
Hemorrhage tends to occur suddenly and during activity, especially among persons with hypertension. Hemorrhage is the most common form of CVA in middle age. Thrombosis is the most common form of CVA. It tends to occur among older patients, often during rest. Thrombosis may be preceded by transient neurologic involvement referred to as transient ischemic attacks. Thrombosis often begins with an intermittent or gradual course. Dural sinus thrombosis occurs most commonly in childhood (3 to 5 years). The longitudinal and straight sinuses are most frequently involved. Among adults, thrombosis often complicates a debilitating disease, hydration, or prolonged labor and delivery. Dural sinus thrombosis may be associated with infection of the ears and paranasal sinuses. Signs of dural sinus thrombosis are edema of the forehead, distention of scalp veins, lower limb spasticity, seizures, and hemiplegia. Persistent convulsions and sudden loss of consciousness are common.
Embolism often is sudden in onset, accounts for about one third of CVAs, and is the most likely form of CVA to resolve. Among 10% of patients who have strokes, atheromatous plaques are found in the proximal arterial system (carotid or vertebral basilar arteries). Atrial fibrillation or flutter and paradoxical emboli are recognized cardiovascular contributing factors. Embolism among younger patients often is associated with valvulitis or acute infection of the throat or teeth. The history includes fever, malaise, weight loss, and joint pain. There often is a sudden onset of lethargy or coma and a cardiac murmur. Petechiae and hematuria may exist.
Subarachnoid Hemorrhage
Subarachnoid hemorrhage usually is caused by rupture of an aneurysm. This is the most common form of CVA among patients between the ages of 17 and 35 years. Signs of subarachnoid hemorrhage are rigidity of the neck, severe nuchal pain, and impairment of consciousness.
Transient Ischemic Attacks
Narrowing of the internal carotid artery or middle cerebral artery can be associated with contralateral transient muscle weakness or sensory disturbances referred to as transient ischemic attacks. If the left or dominant hemisphere is involved, there may be a speech disturbance. Intermittent blindness can occur in the ipsilateral eye (amaurosis fugax). If the internal carotid artery is involved, a bruit may be heard in the neck.
Posterior Inferior Cerebellar Artery Thrombosis
Posterior inferior cerebellar artery thrombosis (Wallenberg syndrome) is characterized by vertigo, dysphagia, ipsilateral facial paresthesia and hypesthesia, ipsilateral Horner syndrome, and ipsilateral incoordination. There may be hypalgesia of the contralateral trunk and limbs along with ipsilateral hypesthesia.
Basilar Artery Insufficiency
Basilar artery insufficiency is associated with recurrent vertigo, transient decrease in vision, dysphagia, dysarthria, and diplopia. There may be hemiparesis, which may shift from side to side. The patient may have episodes of confusion or loss of consciousness.
Thrombosis of the Anterior Spinal Artery
Thrombosis of the anterior spinal artery affects the pyramids and emerging hypoglossal fibers. It is associated with hemianesthetic hemiplegia or with hypoglossal hemiplegia. There is a contralateral loss of proprioception and a decrease in tactile sensation. This may spare the hypoglossal nerve. Another result of anterior spinal artery thrombosis is hemiplegia cruciata, a lesion of the decussation of the pyramid. The patient has contralateral and ipsilateral spastic paresis of the lower extremities, may have ipsilateral flaccid paresis and atrophy of the sternocleidomastoid and trapezius muscles, and may have ipsilateral paresis of the tongue.
Anterior Inferior Cerebellar Artery Thrombosis
Anterior inferior cerebellar artery thrombosis involves the tegmentum of the upper medulla, lower pons, restiform body, the lower part of the cerebellar peduncle, and the inferior surface of the cerebellar peduncle. The deficits include ipsilateral loss of facial pain, light touch and temperature sensations, ipsilateral Horner syndrome, ipsilateral deafness, vertigo, and ipsilateral facial palsy. The patient has ipsilateral cerebellar ataxia and a contralateral decrease in pain and temperature sensation in the limbs and trunk. This lesion may follow excision of acoustic neuroma.
Superior Cerebellar Artery Thrombosis
Superior cerebellar artery thrombosis causes choreiform or choreoathetoid involuntary movement and contralateral loss of pain and temperature sensation in the face and body. The patient has ipsilateral cerebellar ataxia with hypotonia, nausea and vomiting, and slurred speech. There may be a central facial palsy, ipsilateral Horner syndrome, and partial deafness. This lesion involves the lateral tegmentum of the pons and midbrain, superior cerebellar peduncle, superior surface of the cerebellum, and cerebellar peduncle.
Thrombosis of the Vertebral Artery
Thrombosis of the vertebral artery (Avellis syndrome) involves the spinothalamic tract, nucleus ambiguus, and usually the bulbar nucleus of the accessory nerve. The patient has ipsilateral paralysis of the soft palate and larynx, ipsilateral anesthesia of the pharynx and larynx, and ipsilateral loss of taste. There is contralateral loss of pain and temperature sensation in the trunk and extremities. Ipsilateral Horner syndrome occasionally results.
Cestan-Chenais Syndrome
Cestan-Chenais syndrome is occlusion of the vertebral artery inferior to the origin of the posteroinferior cerebellar artery. This lesion involves the nucleus ambiguus, restiform body, and descending sympathetic pathways. The syndrome is characterized by paralysis of the soft palate, pharynx, and larynx, Horner syndrome, and ipsilateral cerebellar ataxia, contralateral hemiplegia, and decreased proprioception and tactile sensation. Possible involvement of cranial nerves XI and XII may cause ipsilateral paralysis of the sternocleidomastoid and trapezius muscles and the tongue. The descending tract of the trigeminal nerve may be involved. The result is ipsilateral loss of temperature and pain sensation in the face.
Babinski-Nageotte Syndrome
Babinski-Nageotte syndrome involves scattered lesions in the distribution of the vertebral artery. This causes ipsilateral paralysis of the soft palate, larynx, pharynx, and tongue, ipsilateral decrease in taste sensation on the posterior third of the tongue, diminished pain and temperature sensation on the face, and Horner syndrome. There is a contralateral spastic hemiplegia and loss of proprioception and touch. There may be decreased pain and temperature sensation in the trunk and limbs.
Basilar Artery Thrombosis
Basilar artery thrombosis causes a disorder in superficial and deep sensation in the extremities, trunk, and sometimes the face. The pupils usually are miotic. The patient usually has decerebrate rigidity, profound coma, and respiratory and circulatory difficulties. This can affect bilateral cranial nerves and long tracts. There is bilateral supranuclear fiber involvement to the bulbar nuclei.
Thrombosis of the Medial Pontine Branches
Thrombosis of the medial pontine branches involves the nuclei of cranial nerves VI and VII, the medial longitudinal fasciculus, medial lemniscus, and pyramidal tract. The patient has ipsilateral facial paralysis and paralysis of the lateral rectus muscle or of lateral conjugate gaze. There is a contralateral lateral hemiplegia, loss of proprioception, and decrease in sensation of light touch.
Thrombosis of Lateral Pontine Branches
Thrombosis of lateral pontine branches involves the middle cerebellar peduncle, the superior olivary body, the facial nucleus, the vestibular and cochlear nuclei, and a portion of the motor and sensory nuclei of the trigeminal nerve. The deficit involves ipsilateral cranial nerves V, VII, and VIII and ipsilateral cerebellar ataxia. The patient frequently has contralateral diminution of pain, temperature, proprioception, and tactile sensation on the trunk and limbs.
Thrombosis of the Upper Pontine Branches
Thrombosis of the upper pontine branches of the basilar artery affects the pyramidal tract, medial lemniscus, spinothalamic tract, and the ventral and dorsal secondary ascending tract of the trigeminal nerve. This causes contralateral hemiplegia that includes the face and tongue. There is also a loss of proprioception, pain, and temperature sensation of the face, extremities, and trunk.
Thrombosis of the Internal Auditory Artery
Thrombosis of the internal auditory artery causes ipsilateral deafness and loss of vestibular function.
Jackson Vagus-Accessory-Hypoglossal Paralysis
Jackson vagus-accessory-hypoglossal paralysis is a nuclear or radicular lesion of cranial nerves X, XI, and XII. The patient has ipsilateral flaccid paralysis of the soft palate, pharynx, and larynx. Flaccid weakness and atrophy of the sternocleidomastoid and trapezius muscles and the tongue also occurs.
Vagus-Accessory Syndrome
Schmidt (vagus-accessory) syndrome is a lesion of the nucleus ambiguus and the bulbar and spinal nuclei of cranial nerve XI. It results in ipsilateral paralysis of the soft palate, pharynx, and larynx and in flaccid weakness and atrophy of the sternocleidomastoid and trapezius muscles. Ipsilateral paralysis of the soft palate, pharynx, and larynx and paralysis and atrophy of the tongue are caused by Tapia syndrome (vagohypoglossal syndrome), a tegmental lesion in the lower third of the medulla that involves the nucleus ambiguus and the hypoglossal nerve.
Vernet Syndrome
Vernet syndrome, a lesion at the jugular foramen, can be a result of a vascular lesion, a tumor, aneurysm of the internal carotid artery, thrombosis of the jugular bulb, tuberculosis, or syphilis. The most common cause, however, is basilar skull fracture, which produces ipsilateral paralysis of cranial nerves IX, X, and XI. Villaret syndrome is a lesion of the retropharyngeal or retroparotid space that causes ipsilateral paralysis of cranial nerves IX, X, and XI and of cervical sympathetic fibers, producing Horner syndrome.
Collet-Sicard Syndrome
Collet-Sicard syndrome is similar to Villaret syndrome, but there is no Horner syndrome. Glossolaryngoscapulopharyngeal hemiplegia is caused by a complete lesion of cranial nerves IX through XII.
Garel-Gignoix Syndrome
Garel-Gignoix syndrome involves the vagus and accessory nerves below the jugular foramen (9,10).
Otolaryngologic symptoms can be caused by tumor involvement of nerves of the head and neck region.
Two percent of gliomas among children are pinealoma. The patient has extraocular muscle involvement, ptosis, restriction of upward gaze, and bilateral hyperacusis. Some patients have sexual changes and macrogenitosomia praecox. Central nervous system tumors among adults usually are supratentorial.
Meningioma constitutes 15% of intracranial tumors. These usually slow-growing tumors originate in the sagittal sinus, the sphenoid ridge, or the olfactory groove. If the tumor arises on the sphenoid ridge, there may be unilateral exophthalmos and oculomotor nerve involvement with subsequent diplopia and vision loss. Signs of olfactory groove involvement are unilateral or bilateral anosmia and mental or personality changes. There may be optic atrophy late in the course.
Kennedy Syndrome
Kennedy syndrome is associated with a tumor in the olfactory groove. Findings are optic atrophy on the side of the tumor and papilledema on the opposite side.
Acoustic Neuroma
Acoustic neuroma originates along the vestibular nerve. Two percent of intracranial tumors are acoustic neuroma. Vertigo with or without tinnitus usually is the first symptom, and recurrent episodes presumed to be benign can occur. The patient later has hearing loss, ipsilateral corneal hypesthesia, and incoordination of cerebellar origin. Late in the course of acoustic neuroma, ipsilateral facial paresis develops. Because the tumors are most frequently on the vestibular portion of cranial nerve VIII, canal paresis with caloric testing is an early finding.
Nasopharyngeal Carcinoma
Nasopharyngeal carcinoma can include extension of central nervous system tumors into the nasopharynx and sinuses. Tumors in this region can impair hearing. Extension of nasopharyngeal tumors can cause Garcin syndrome, which is paralysis of cranial nerves III through X. The effects usually are unilateral but can be bilateral. This condition is caused by lesions in the retropharyngeal space, usually produced by infection in this area but also caused by granuloma or metastasis or extension from the nasopharynx.
Epidermoid Tumor
Epidermoid tumors are the third most common primary mass lesion of the cerebellopontine angle. The patient may have multiple cranial nerve palsies with or without brainstem involvement. Hearing loss generally appears late in the course of the tumor.
Metastatic Tumor
Metastatic tumors tend to have a rapid course, and evidence of neoplasia elsewhere usually can be obtained. Multiple upper and lower cranial nerve palsies usually evolve. Glioma from the brainstem or cerebellum also can invade the cerebellopontine angle, producing symptoms of a cerebellopontine angle mass lesion. Aneurysms also may appear in the cerebellopontine angle.
Tumor of the Glomus Jugulare
Tumor of the glomus jugulare involves cranial nerves IX, X, and XI at the jugular foramen. There often is evidence of dysfunction of cranial nerves VII and VIII.
Pituitary Adenoma
Pituitary adenoma can be classified as functional (secreting) or nonfunctional (nonsecreting). Prolactinoma is the most common pituitary tumor and occurs most frequently among young women. Symptoms are galactorrhea with or without amenorrhea. Most patients respond to medical treatment with bromocriptine. Growth hormone adenoma causes gigantism among children before closure of the epiphyses of the long bones. Adults have acromegaly and enlargement of the jaw, hands, and feet. Other signs are hyperhidrosis, hypertrichosis, diabetes, cardiac disease, and paresthesia, such as carpal tunnel syndrome.
Corticotropin-secreting tumors manifest as Cushing disease, which is characterized by truncal obesity, moon facies, buffalo hump, pigmented stretch marks, hypertension, and hirsutism. The lesions usually manifest as microadenomas. Nelson syndrome, hyperpigmentation, and increasing sellar size can occur after bilateral adrenalectomy for corticotropin-secreting tumors. In these patients, the tumors are large and aggressive.
Nonfunctional pituitary tumors manifest as decreased hormonal function or without endocrine deficiencies. Patients often have panhypopituitarism with visual symptoms. The patient may have increased intracranial pressure or extraocular muscle palsy. The visual symptoms are caused by suprasellar extension of the adenoma, which affects the optic chiasm. This causes bitemporal hemianopia and progressive loss of visual acuity. Extraocular muscle palsy is caused by lateral extension of the tumor toward the cavernous sinus (6,9).
Sinusitis is a common cause of facial pain and headache. Trigeminal neuralgia, usually induced by palpation of a trigger zone, causes severe pain. Sphenopalatine neuralgia (Sluder syndrome) is localized facial pain associated with vasomotor abnormality, such as lacrimation, rhinorrhea, and salivation. The pain involves the eye, nose, palate, maxillary teeth, ear, and temple. Glossopharyngeal neuralgia involves unilateral throat pain associated with ipsilateral rhinorrhea, salivation, coughing, and facial burning. Postherpetic neuralgia is similar to trigeminal neuralgia. It occurs after attacks of herpes zoster. Trotter syndrome involves pain in the mandibular division of cranial nerve V, unilateral deafness, ipsilateral palate hypomotility, and trismus. Ramsay Hunt syndrome is caused by herpes zoster infection of the geniculate ganglion. Signs are vesicles on the ear, oral mucosa, tonsils, pharyngeal mucosa, and posterior third of the tongue; facial palsy; loss of taste; decreased salivation; palatal paralysis; and pain. Eagle syndrome is caused by elongation and calcification of the styloid process along with calcification of the stylohyoid ligament. Symptoms are parapharyngeal pain, dysphagia, odynophagia, trismus, headache, and facial pain. Vail syndrome, vidian nerve neuralgia, causes unilateral pain of the nose, eye, face, neck, and shoulder.
Horner syndrome is caused by interruption of sympathetic pathways in the medulla, spinal cord, and sympathetic trunk. This syndrome is characterized by constriction of pupils, enophthalmos, ptosis, and decreased sweating of the ipsilateral face. The gustatory lacrimal reflex (crocodile tears) is ipsilateral tearing when spicy foods are placed on the tongue. This is caused by faulty regeneration of nerves responsible for salivation with those responsible for lacrimation. Frey syndrome (auriculotemporal syndrome) causes flushing, a sensation of heat, and excessive perspiration over the cheek and pinna after ingestion of spicy food. This is caused by misdirected regeneration of secretomotor fibers, often after injury to the auriculotemporal nerve (4).
Osteomyelitis occurs through extension of infection from the paranasal and mastoid sinuses. This usually involves the temporal, frontal, and parietal bones. Facial nerve palsy and vertigo can be caused by osteomyelitis of the temporal bone. If it erupts into the epidural space, the infection causes an epidural abscess. The patient has fever, malaise, tenderness, and pain. Nuchal rigidity is rare.
Subdural Empyema
Extension of infection through the dura can cause subdural empyema. This disorder is characterized by localized headache and can mimic mastoid or sinus infection. The patient has fever, malaise, and decreased consciousness. Seizures, nuchal rigidity, and other neurologic deficits follow.
Meningitis is the most common intracranial infection. The pia mater and arachnoid are infected. Headache, lethargy, and irritability are early signs. Other signs of meningitis are nuchal rigidity, limited flexion of the legs, altered mental status, and fever. Diagnosis is made by means of analysis of cerebrospinal fluid, which shows pleocytosis (more than 1,000, mostly polymorphonuclear, leukocytes), elevated protein level, and decreased glucose level. Antibiotic therapy should be guided by the cerebrospinal fluid culture results.
Brain Abscess
Brain abscess forms by means of direct extension, hematogenous spread from septic thrombophlebitis, and extension through congenital defects, traumatic fistulae, or tumors. Brain abscess begins as localized cerebritis consisting of leukocytic infiltration and microscopic necrosis. At this stage, it is difficult to diagnose. In 7 to 10 days, a capsule forms, and the abscess enlarges and causes edema in adjacent tissues, producing neurologic symptoms. Between 40% and 50% of brain abscesses are of otogenic origin. Sinus infection accounts for about 10%. General symptoms are lethargy, headache, and fever. Focal signs depend on the location of the abscesses. Frontal lobe abscesses, almost exclusively the result of paranasal sinus infection, rarely have localizing symptoms. Increased intracranial pressure, stupor, and papilledema are signs of abscesses in this area. Brain abscesses can cause brainstem herniation and can rupture into the ventricular system.
Orbital Cellulitis
Extension of paranasal sinusitis into the orbit can cause orbital cellulitis, which causes chemosis, exophthalmos, diplopia, and immobility of the globe. Orbital cellulitis can advance to orbital abscess with ophthalmoplegia, proptosis, and visual loss. Optic neuritis characterized by acute loss of vision, decreased pupillary response, and pain with eye movement can be caused by extension of posterior ethmoidal or sphenoidal sinusitis. Fungal involvement with mucormycosis is a life-threatening infection associated with diabetes mellitus and immunosuppression.
Superior Orbital Fissure Syndrome
Superior orbital fissure syndrome usually is a complication of sphenoid sinusitis. The abducent nerve is paretic, and there may be involvement of cranial nerves III, IV, and V. The patient has diplopia, exophthalmos, ophthalmoplegia, and decreased sensation over the forehead.
Cavernous Sinus Thrombosis
Cavernous sinus thrombosis is the result of phlebitis spreading from the ethmoid and sphenoid sinuses. The eye becomes proptotic and chemotic, and the eyelid is edematous. Involvement of cranial nerves III, IV, and VI causes ophthalmoplegia (9).


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