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Tolosa-Hunt syndrome

Tolosa-Hunt syndrome
Literature review current through: Jan 2024.
This topic last updated: Apr 09, 2021.

INTRODUCTION — The Tolosa-Hunt syndrome is a rare syndrome with an estimated annual incidence of one case per million per year [1]. It is characterized by painful ophthalmoplegia (weakness of the eye muscles) and is caused by an idiopathic granulomatous inflammation of the cavernous sinus. This syndrome was first described in 1954, and its exquisite responsiveness to glucocorticoid treatment was recognized a few years later [2-4].

While considered a benign condition, permanent neurologic deficits can occur, and relapses are common, often requiring prolonged immunosuppressive therapy. Tolosa-Hunt syndrome must be carefully differentiated from more malignant diagnoses, a mandate challenged by the lack of a specific diagnostic test abnormality.

PATHOGENESIS — The Tolosa-Hunt syndrome is caused by an inflammatory process of unknown etiology. On histopathology, there is a nonspecific inflammation of the septa and wall of the cavernous sinus, with a lymphocyte and plasma cell infiltration, giant cell granulomas, and proliferation of fibroblasts [2,3]. The inflammation produces pressure and secondary dysfunction of the structures within the cavernous sinus, including cranial nerves III, IV, and VI, as well as the superior divisions of cranial nerve V.

While reports of intracranial extension of the inflammation exist [1], there are no reports of systemic involvement. Cases of Tolosa-Hunt syndrome have been reported in patients with other inflammatory disorders, such as systemic lupus erythematosus, but this may simply represent an association of the two autoimmune conditions [5]. Cases of orbital inflammation may be the initial presentation of systemic inflammatory disorders such as sarcoidosis and granulomatosis with polyangiitis (table 1). (See "Neurologic sarcoidosis" and "Granulomatosis with polyangiitis and microscopic polyangiitis: Clinical manifestations and diagnosis".)

CLINICAL FEATURES — Tolosa-Hunt syndrome is described as "episodic orbital pain associated with paralysis of one or more of the third, fourth, and/or sixth cranial nerves, which usually resolves spontaneously but tends to relapse and remit."

Patients may present at any age, from the first through the eighth decade of life [6,7]. Men and women are affected at the same frequency.

Patients report a constant pain behind the eye that may begin several days (up to 30 days) prior to the ophthalmoplegia; in one series the median time interval between onset of pain and cranial nerve palsy was two days [6,8]. The pain is characteristically described as a steady gnawing or boring pain.

Tolosa-Hunt syndrome is typically unilateral; bilateral symptoms occur in 4 to 5 percent of cases [8-10].

Diplopia results from cranial mono- or polyneuropathy. Involvement of cranial nerve III is reported most frequently (85 percent), followed by cranial nerve VI (70 percent), the ophthalmic division of cranial nerve V (30 percent), and cranial nerve IV (29 percent) [9]. Involvement of periarterial sympathetic fibers causes a third order Horner syndrome in approximately 20 percent of patients [10,11]. (See "Horner syndrome".)

In conjunction with ophthalmoplegia, the maxillary and mandibular divisions of the fifth nerve, the optic nerve, and the facial nerve have also been affected in individual cases, suggesting that inflammation extends beyond the cavernous sinus in rare cases [3,4,9,12-15]. Involvement of the optic nerve occurs at the orbital apex and may cause optic disc edema or pallor [6]. Loss of visual acuity is uncommon but may occur unpredictably and may be permanent.

Left untreated, symptoms of Tolosa-Hunt syndrome may resolve spontaneously after an average of approximately eight weeks [3,6].

DIFFERENTIAL DIAGNOSIS — Most patients (greater than 75 percent) who present with painful ophthalmoplegia will not have Tolosa-Hunt syndrome [16,17].

The syndrome of painful ophthalmoplegia may be caused by any process exerting a mass effect on the cavernous sinus (table 1). These include a primary intracranial tumor, lymphoma or other local or distant metastatic tumors, aneurysm, carotid-cavernous fistula, carotid dissection, cavernous sinus thrombosis, infection, vasculitis, and sarcoidosis [6,8,18]. Of these conditions, tumors and vascular conditions are the most common. Many of these conditions can be identified by magnetic resonance imaging (MRI), although in some cases serial imaging is required.

In addition to these structural compressive lesions, painful ophthalmoplegia can also be caused by ophthalmoplegic migraine, giant cell arteritis, or a diabetic cranial nerve palsy [8].

Orbital pseudotumor is a related condition of idiopathic inflammation involving the orbit [19]. Some patients with immunoglobulin G4 (IgG4) related disease develop a similar condition. Patients with orbital pseudotumor present with painful ophthalmoplegia and orbital signs (proptosis, conjunctival injection, and chemosis). This condition, which is also glucocorticoid responsive, may be identical to Tolosa-Hunt syndrome, distinguished only by a different anatomic localization. Therefore, distinguishing between this syndrome and Tolosa-Hunt syndrome is less important than excluding other causes of painful ophthalmoplegia (table 1).

In general, it is difficult to exclude alternative diagnoses by clinical features alone [8]. Neuroimaging and other diagnostic tests are generally required. Authors note that either a sudden or a gradual onset of symptoms can be observed in patients with aneurysm, tumor, as well as Tolosa-Hunt syndrome [6]. Other clinical signs may be suggestive but are not completely reliable. Signs of orbital congestion (proptosis, conjunctival injection, and chemosis) usually accompany cavernous sinus thrombosis and diseases involving the orbit. Diabetic ophthalmoplegia usually results from a mononeuropathy rather than a polyneuropathy. Fever suggests infection but may not be present in patients with more indolent pathogens. Another report emphasized that other clinical features atypical for Tolosa-Hunt syndrome suggest alternative diagnoses. Such atypical features included ophthalmoplegia preceding the onset of pain, bilateral symptoms, and hemicranial rather than orbital pain [20].

DIAGNOSTIC EVALUATION — The diagnosis of Tolosa-Hunt syndrome is based upon the clinical presentation in conjunction with neuroimaging results and a clinical response to corticosteroids. Laboratory tests and lumbar puncture are also recommended. Direct tissue biopsy is rarely performed due to the technically difficult and potentially harmful approach to the cavernous sinus.

Diagnostic criteria — The specific diagnostic criteria recommended by the International Headache Society are summarized [21]:

Unilateral headache, and

Granulomatous inflammation of the cavernous sinus, superior orbital fissure or orbit, demonstrated by magnetic resonance imaging (MRI) or biopsy, and

Paresis of one or more of the ipsilateral third, fourth, and/or sixth cranial nerves, and

Evidence of causation demonstrated by both of the following:

Headache has preceded oculomotor paresis by ≤2 weeks or developed with it

Headache is ipsilateral to the granulomatous inflammation

Symptoms not better accounted for by an alternative diagnosis

These combined clinical and radiologic criteria have a high sensitivity (95 to 100 percent) in the diagnosis of Tolosa-Hunt syndrome [20]. However, the specificity is low (50 percent in one series), unless atypical clinical and radiologic findings are used to exclude the diagnosis. Thus, it is important to monitor these patients for development of any atypical findings and to reconsider the broad differential diagnosis. (See 'Differential diagnosis' above.)

Experts have debated the continued utility of the term "Tolosa-Hunt syndrome" [22], while others have suggested broadening the definition of Tolosa-Hunt syndrome under the current International Classification of Headache Disorders guidelines [23].

Magnetic resonance imaging — A contrast-enhanced MRI is essential to the diagnostic evaluation of a patient with painful ophthalmoplegia, primarily to exclude other causes of painful ophthalmoplegia [8,16,20]. In patients with Tolosa-Hunt syndrome, MRI findings can include [11,24-27]:

Enlargement of the cavernous sinus with abnormal tissue that is usually isointense to gray matter on T1 and iso- or hypointense on T2, and strongly enhances with gadolinium

Abnormal convexity of the wall of the cavernous sinus

Focal narrowing of the intracavernous internal carotid artery

In rare cases of Tolosa-Hunt syndrome, the MRI is normal [28,29], and some have suggested that the required diagnostic criterion of granulomatous inflammation demonstrated by MRI or biopsy may be too restrictive [23]. In one series, these patients tended to improve more rapidly than others with Tolosa-Hunt syndrome [18].

Computed tomography (CT) may also show cavernous sinus signal changes in Tolosa-Hunt syndrome, but is less sensitive than MRI [11,24,30,31].

These MRI findings are not specific to Tolosa-Hunt syndrome. Similar findings are seen with other etiologies, such as lymphoma, sarcoidosis, and meningioma [6]. MRI findings in some of these disorders may also respond to glucocorticoid therapy.

When MRI suggests a vascular anomaly, an angiographic study (magnetic resonance angiography, CT angiography, digital subtraction angiography) is usually required [20].

Blood and CSF evaluation — When the MRI is normal or shows changes consistent with cavernous sinus inflammation, further evaluation should include blood and cerebrospinal fluid (CSF) testing to exclude other possible causes of orbital inflammation [6]. Recommended blood testing includes:

Complete blood count

Electrolytes

Glucose and hemoglobin A1C

Renal and liver function tests

Angiotensin converting enzyme

Antinuclear antibody

Anti-dsDNA antibody

Anti-Sm antibody

Antineutrophil cytoplasmic antibody

Fluorescent treponemal antibody test

Lyme serologies

Serum protein electrophoresis

Erythrocyte sedimentation rate (ESR)

C reactive protein

In patients with Tolosa-Hunt syndrome, these results are generally normal [10]. Although case reports of elevated ESR, mild leukocytosis, and antinuclear antibody concentrations have been reported in Tolosa-Hunt syndrome, these should suggest an underlying connective tissue disorder.

CSF should also be evaluated for protein, glucose, cell count with differential, cytology, Lyme and syphilis serology, angiotensin converting enzyme (for sarcoidosis), and cultures for bacteria, fungi, and mycobacteria. The expected findings in Tolosa-Hunt syndrome are normal. Mildly raised protein and/or mild pleocytosis have been reported, but if found, these should suggest alternative diagnoses (neoplasm, inflammatory or infectious meningitis).

Response to glucocorticoids and further investigation — Glucocorticoid administration has diagnostic as well as therapeutic utility. Rapid resolution of pain (within 24 to 72 hours) helps to confirm suspected Tolosa-Hunt syndrome [4,7,8,32]. Improvement of cranial nerve deficits and regression of MRI abnormalities over the next two to eight weeks provide further confirmation of the diagnosis [10,33]. However, an initial clinical or MRI response to steroids is not diagnostic; other entities, such as lymphoma and vasculitis, may also respond clinically and radiographically to glucocorticoid therapy [15].

The clinician needs to be vigilant regarding the continued possibility of misdiagnosis of Tolosa-Hunt syndrome (see 'Follow-up' below). More aggressive testing, including repeat CSF evaluation and consideration of surgical biopsy, is recommended if symptoms do not respond promptly to steroids, or if glucocorticoid efficacy is lost after an initial response.

Even with careful adherence to clinical criteria and diagnostic evaluation, misdiagnosis still occurs. As an example, a case of painful ophthalmoplegia with characteristic clinical and MRI findings, both initially glucocorticoid responsive, was subsequently demonstrated to be caused by actinomycosis infection [34]. An underlying neoplasm was finally diagnosed in other patients who either failed to respond to initial glucocorticoid therapy or did not maintain a clinical response [10,35-37].

TREATMENT

Glucocorticoids — Glucocorticoids have been the recommended treatment for Tolosa-Hunt syndrome since the 1960s [3,4]. However, there are few data other than case series to determine the most effective dose, route and schedule of administration, or length of glucocorticoid therapy [6]. While glucocorticoids clearly hasten the resolution of orbital pain, there is no definitive evidence that the cranial neuropathies recover any faster with or without treatment [32]. Little consideration has been given to alternative therapies, probably due to the typical rapid response to glucocorticoids.

Specific glucocorticoid regimens reported for treatment of Tolosa-Hunt syndrome vary, but in general they include initial high-dose glucocorticoids for two to four weeks followed by a gradual taper over a period of at least four to six weeks and up to several months [10,38,39]. Prompt administration of intravenous glucocorticoids is often recommended, but oral prednisone is also effective. The rate of the taper should be guided by clinical symptoms, but persistent magnetic resonance imaging (MRI) findings should not deter dose reductions as long as the findings are regressing.

A suggested glucocorticoid regimen is:

Prednisone 80 to 100 mg daily for three days.

If the pain has resolved, taper to 60 mg daily, then 40 mg, then 20 mg, then 10 mg every two weeks.

Follow-up — Close clinical follow-up with repeat MRI every one to two months is necessary to be sure the glucocorticoid treatment remains effective and no evidence of another etiology develops [40]. Radiographic improvement often lags several weeks behind clinical improvement [1,7]. In uncomplicated patients, MRI scans to monitor improvement and maintenance of improvement on and then off treatment should be performed every one to two months until findings normalize [1]. This should be followed by MRI scans every six months for a period of two years following the diagnosis [15].

If symptoms recur, MRI and other diagnostic testing including blood and cerebrospinal fluid (CSF) studies should be performed promptly to confirm that there is no alternative diagnosis.

Second-line treatments — A small group of patients will require other immunosuppressive medications either to limit the complications of corticosteroid use or to keep the disorder in remission. Typically, such patients will have biopsy confirmation of the diagnosis.

Cyclosporine, azathioprine, methotrexate, mycophenolate mofetil, and infliximab have been used in this setting [15,41-44].

A few case reports have described long-term remittance of symptoms with radiotherapy after a history of relapsing Tolosa-Hunt syndrome and corticosteroid dependence [41,45], or as primary treatment when corticosteroids are contraindicated [46].

PROGNOSIS — Glucocorticoids drastically hasten the resolution of symptoms, with pain often resolving within 24 to 72 hours after initiating treatment [4]. In one series, 40 percent of patients experienced pain relief within 72 hours and 78 percent experienced relief within a week [8]. Cranial neuropathies tend to recover more slowly over two to eight weeks even with glucocorticoid therapy [4,8,10,32,33,47]. In unusual cases, residual deficits remain [3,6].

Recurrences occur in approximately one-half of reported patients over an interval of months to years [3,6] and appear to be more likely in patients who are younger [32]. Ipsilateral, contralateral, and bilateral relapses have been reported. Relapses require repeated investigations to rule out inflammatory and neoplastic disorders such as sarcoid, granulomatosis with polyangiitis, and lymphoma [15,45]. (See 'Diagnostic evaluation' above.)

There is no evidence that corticosteroid therapy alters the prognosis with regard to the frequency of relapses or persistent ophthalmoplegia. It is unlikely that this information will be forthcoming given the relative rarity of the disorder and the widespread use of glucocorticoids.

SUMMARY AND RECOMMENDATIONS

Pathogenesis – The Tolosa-Hunt syndrome is caused by an inflammation in the cavernous sinus or superior orbital fissure of unknown etiology. (See 'Pathogenesis' above.)

Clinical features – Cardinal features include retroorbital pain and ophthalmoplegia affecting the third, fourth, and/or sixth cranial nerves. All age groups may be affected. (See 'Clinical features' above.)

Differential diagnosis – The differential diagnosis is broad and includes malignancies and infections, as well as vascular and other inflammatory etiologies (table 1). (See 'Differential diagnosis' above.)

Evaluation and diagnosis Contrast-enhanced magnetic resonance imaging (MRI), blood, and cerebrospinal fluid (CSF) evaluation are required to exclude other conditions. (See 'Diagnostic evaluation' above.)

The diagnosis of Tolosa-Hunt syndrome requires the presence of a unilateral headache that occurs in close temporal association with ipsilateral oculomotor paresis along with neuroimaging that reveals ipsilateral inflammation involving the cavernous sinus, superior orbital fissure or orbit. In addition, neuroimaging and CSF evaluation do not suggest an alternative etiology. (See 'Diagnostic criteria' above.)

Treatment – For patients who meet clinical and diagnostic criteria for Tolosa-Hunt syndrome, we recommend treatment with glucocorticoids (Grade 1B). We use prednisone 80 to 100 mg daily for three days. If pain has resolved, we then taper prednisone to 60 mg, then to 40 mg, 20 mg, and 10 mg in two-week intervals. (See 'Treatment' above.)

Response to treatment provides further support for but does not definitively confirm the diagnosis. (See 'Response to glucocorticoids and further investigation' above.)

Follow-up – Close clinical and MRI follow-up is essential. We recommend repeating diagnostic investigations and considering a surgical biopsy for patients who fail to respond clinically or radiographically to treatment, or who relapse on treatment. (See 'Response to glucocorticoids and further investigation' above.)

Prognosis – The prognosis for most patients is favorable. However, some patients follow a relapsing-remitting course requiring prolonged corticosteroid or other immunosuppressive therapy, and a few have permanent cranial nerve deficits. (See 'Prognosis' above.)

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