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Volume 3, No 2 - Spring 2006

Volume 3, No 2 - Spring 2006

Table of Contents

The Natural History of Optic Neuritis Diagnosis and Management Update
Optic neuritis is a common cause of visual loss in young patients, typically presenting with painful monocular visual loss and decreased color vision. Visual function generally spontaneously improves over weeks, and 95% of patients return to visual acuity of at least 20/40 within 12 months. The initial magnetic resonance imaging (MRI) helps stratify the risk of multiple sclerosis (MS) in patients with acute isolated optic neuritis. In the Optic Neuritis Treatment Trial, the 10-year risk of MS in the group of patients with at least one MRI T2 lesion was 56%, whereas the 10-year risk with a normal baseline MRI was 22%. A normal MRI in concert with painless optic neuritis, severe optic nerve head edema, peripapillary hemorrhages, or a macular star defines a very low MS risk subgroup. High-dose steroids hasten the rate, but not the final extent, of visual recovery in optic neuritis, and the decision to use this therapy is individualized. Interferon beta-1a therapy should be considered in selected high-risk patients. [Rev Neurol Dis. 2006;3(2):45-56]
Initial Management of Acute Bacterial Meningitis in Adults: Summary of IDSA Guidelines Management Update
The management of acute, community-acquired bacterial meningitis is a neurologic and infectious disease emergency. Early recognition and prompt diagnostic evaluation and treatment are essential to the successful treatment of patients with this condition. Recommendations from the Infectious Disease Society of America practice guidelines for the diagnosis and treatment of bacterial meningitis are presented and discussed. The importance of a thorough understanding of the appropriate initial management is explained. [Rev Neurol Dis. 2006;3(2):57-60]
Restless Legs Syndrome and Periodic Limb Movements Clinical Update
The history, clinical aspects, and treatment of restless legs syndrome (RLS), a heterogeneous, distressing sensorimotor disorder, and periodic limb movements (PLMs) that are the typical motor accompaniment of the syndrome, are described. A positive family history, a positive response to dopaminergic treatment, and the presence of PLM while awake or asleep are supportive criteria for the diagnosis of the disorder. RLS and PLM occur more frequently at the beginning of night and exponentially decline across sleep cycles, suggesting circadian influences. Altered circadian rhythmicity in dopamine metabolism and enhanced circadian variations in dopaminergic functions have been reported in the disorder. Dysfunction or atrophy of A11 cells from the diencephalic-spinal dopamine A11 system has been suggested to explain the efficacy of dopaminergic drugs in relieving RLS symptoms and the circadian rhythmicity of RLS. Studies support the hypothesis that the A11 dopaminergic neurons and spinal pathways may be more involved in the pathophysiology of RLS than the nigrostriatal system. Neurophysiological evidence indicates that the involuntary movements in RLS may be of spinal or propriospinal origin. Despite these findings, however, the pathogenic mechanisms underlying the peculiar sensory and motor manifestations of RLS remain unexplained. Among the current treatment options offered for the treatment of RLS, dopaminergic agents have provided the best evidence for efficacy in symptom relief. [Rev Neurol Dis. 2006;3(2):61-70]
A Unique International Event—Bringing the Parkinson’s Community Together Meeting Review
Highlights of the First World Parkinson’s Congress Washington DC February 22-26, 2006
Advances in Neuroimaging Technology Meeting Review
Highlights of the 29th Annual Meeting of the American Society of Neuroimaging March 2-5, 2006 San Diego, CA
Chronic Peripheral Neuropathy Responsive to Rituximab Case Review
A 73-year-old man was referred for evaluation of unsteady gait and numbness of the feet. His symptoms had progressed over the previous 3 years from numbness and tingling in his left lateral thigh to a gait imbalance severe enough to necessitate crutches for ambulation. After a thorough neurological work-up, including an electromyogram that was markedly abnormal, and extensive testing for anti-nerve antibodies, a diagnosis of neuropathy, secondary to monoclonal IgM antibodies against myelin-associated glycoprotein, was made. Aggressive treatment was deemed necessary; however, none of the standard options, including intravenous immunoglobulin, prednisone, and cytotoxic drugs, seemed suitable given his underlying health and the severity of his deficit. A course of rituximab 375 mg/m2 weekly for 4 weeks was recommended for the patient. Shortly after the treatment was completed, he began to notice a slow and steady improvement. Within 3 months his gait had improved to the point where he no longer required crutches or a cane and he was able to return to work. [Rev Neurol Dis. 2006;3(2):78-81]
Guillain-Barré Syndrome in an Immunocompromised Patient and Coccidioidomycosis Infection Case Review
A 70-year-old man was referred for evaluation of a 2-week history of numbness and progressive weakness in his lower and upper extremities and subsequently diagnosed with Guillain-Barré syndrome. The patient had been taking mycophenolate mofetil 500 mg twice daily and tacrolimus 6 mg daily for immunosuppression following a kidney transplant 2 years earlier. However, 5 weeks prior to presentation he had been diagnosed with pneumonia due to coccidioidomycosis and his tacrolimus dose was reduced to 1 mg daily to prevent a drug interaction with fluconazole, which was prescribed to treat the coccidioidomycosis infection. The authors surmise that the reduced tacrolimus dose, coupled with a relatively low maintenance dose of mycophenolate mofetil, left the patient less immunosuppressed and therefore able to mount an immune response to the coccidioidomycosis infection, resulting in Guillain-Barré syndrome. This is the first known report of an association between coccidioidomycosis infection and Guillain-Barré syndrome. [Rev Neurol Dis. 2006;3(2):82-84]