EXTENSIVE NEUROSARCOIDOSIS AND OPTIC NERVE COMPLICATIONS

inflammatory disease that can affects almost any organ and many parts of the body. This disease is termed neurosarcoidosis when the nervous system is involved. Although sarcoidosis is well described in literature, however, the cause of the disease is still not understood. Neurosarcoidosis may be asymptomatic or present debilitating chronic condition such as headache, cranial nerve palsy, seizures, paresis and paresthesias. The prevalence of neurosarcoidosis is estimated to be one-fourth of the systemic sarcoidosis patients that have histological evidence of central nervous system involvement. Herein, we report the MR findings of a 35-year-old patient with neuro sarcoidosis. The lesions were characterized by pachyand lepto meningeal lesions complicated by optic nerve compression and cervical spinal cord damage.


Case report
A 35-year-old patient, who had complaints of nasal obstruction and headache for 3 years was hospitalized for a recent decline and progressive loss vision of the right eye. Clinical examination showed a grasping and behavioral disorder of frontal lobe type, afferent pupillary deficit and inferior altitudinal hemianopsia right. Lumbar puncture showed slight increase of protein and glucose concentration, and oligoclonal bands identical to those of serum. Biology showed high levels of converting enzyme angiotensin.
In the year 2006, he underwent resection of cervical lymphadenopathy with the diagnosis of sarcoidosis. MR images showed thick, tions are highly polymorphic, depending on the location, size of lesions and their evolution (1,3,6).
The finding on the imaging examinations are however nonspecific. The differential diagnosis with other diseases such as tuberculosis, Wegener's granulomatosis, fungal meningitis, lymphoma, and meningeal carcinomatosis can be difficult. In neurosarcoidosis, the clinical presentation is often of low expression or even asymptomatic, in discrepancy with the major radiolog-nodular pachymeningeal lesion and leptomeningeal extension in frontal ( Fig. 1, 2) and right temporal area ( Fig. 3) associated to meningeal enhancement in the hypothalamopituitary area (Fig. 2).
Right optic nerve was compressed and stretched by pachymeningitis. He also had multifocal leptomeningeal enhancement of the spinal cord and cervico-dorsal myelitis. Biopsy of the sphenoid sinus lesions showed epithelioid granulomas without caseous necrosis.

EXTENSIVE NEUROSARCOIDOSIS AND OPTIC NERVE COMPLICATIONS
In one third of cases, there is cranial nerve damages (4.8) often symptomatic, sometimes with a wide predilection for the facial and the optic nerve (3)(4)(8)(9). In our case there was an excellent correlation between radiological observation and clinical symptoms. Oculomotor nerve damage is very rare and is mainly secondary to intracranial hypertension (3,6). These lesions were observed frequently in women (4). Optic nerve damage may be primary (unilateral or bilateral) or secondary to chiasmatic lesions (6,8). Nerve damages are of 2 types: either by perivascular lymphocytic infiltration (3) or more often, as observed in our case, compression by granulomatous pachymeningitis (Fig. 4).
Involvement of the brain parenchyma himself is rarely observed. If so, lesions are caused by the extension of sarcoid granulomas from the meninges into the spaces of Virchow-Robin and present as nodular or pseudo-tumor lesions enhancing after intravenous gadolinium (1, 3-6).
These tumor-like lesions, however, are the most clinically symptomatic (4). It may also present as white matter lesions, of high signal intensity on T2, and non enhancing after gadolinium injection (Fig. 3). They are either gliotic scars of deep inflammatory lesions or lesions secondary to microangiopathy sarcoidosis (10).
Moreover, acute ischemic injury in a young person without known etiology must evocate the diagnosis of neurosarcoidosis (11). Lesions of cerebral white matter are considered irreversible (2), have no clinical correlation, and do not always regress under immunosuppressive therapy (4,9). A spine cord myelo-meningtis is classic but not systematic in a neurosarcoïodosis. It has the same radiological and histopathological features as brain damage and affects most of the entire cervical spine (3.4).
A normal MRI does not exclude the diagnosis of neurosarcoidosis, especially in patients with only cranial neuropathy (3,6) or in patients previously treated with corticosteroids (1).
The imaging can assess the response to immunosuppressive therapy (3,4). The regression of lesions on MRI is often delayed compared with clinical improvement (3,6).

Conclusion
Our patient is diagnosed with neuro sarcoidosis, presenting as lesions of the pachy-and leptomeninges of brain and cervical spine. Our report confirms other similar observations already described in literature by Authors using MRI. Thus, our observations support the usefulness of MRI as a powerful tool for diagnosing and monitoring symptomatic neurosarcoidosis.