The evaluation of MRI diffusion values of active demyelinating lesions in multiple sclerosis.

BACKGROUND: Gadolinium (Gd) enhancement of lesions is the main radiologic marker for detection of activity in Multiple Sclerosis (MS). This study compares Diffusion weighted imaging (DWI) characteristics and enhancement to determine whether DWI can be used as an alternative to Gd administration. METHODS: A retrospective study of 72 patients who had MRI with Gd and DWI. Visual assessment and comparison of the Apparent Diffusion Coefficient (ADC) values on Gd+ lesions, all lesions showing restricted diffusion, 2 Gd- lesions and 1 area of normal-appearing white matter (NAWM) in each MRI were performed. RESULTS: DWI values were measured on 275 T2 lesions, 68 Gd+ and 207 Gd- lesions, as well as 104 NAWM. 34 Gd+ lesions showed restricted diffusion. The median ADC-minimum of Gd+ lesions was significantly lower than NAWM and even lower than Gd- lesions. Most DWI restricted lesions were also Gd+(specificity≥94%), however many Gd+ lesions did not show visually detectable restriction in DWI (sensitivity≤34%). The median ADC-minimum of symptomatic lesions was lower than asymptomatic lesions. CONCLUSION: While Gd+ lesions have lower ADC-minimum, visual DWI assessment cannot replace Gd administration for identifying active lesions. Gd+ lesions showing restricted diffusion are clinically important as they are more likely associated with neurological symptoms.

Neurosarcoidosis as an MS Mimic: The trials and tribulations of making a diagnosis.

The clinical presentation of neurosarcoidosis is varied as multiple levels of the neuraxis may be affected. When central nervous system involvement occurs, making an accurate diagnosis of the condition can be challenging, especially given the current definition for definite neurosarcoidosis requires histologic confirmation of the affected tissue (brain biopsy). This article will review our current knowledge and manifestations of neurosarcoidosis, discuss the current diagnostic approach as well as the challenges associated with a condition requiring histologic confirmation, discuss the current treatment approach, and highlight the challenges of this diagnosis with a few real-life clinical cases. We also highlight the selected differential diagnosis of neurosarcoidosis as well as multiple sclerosis which could mimic each other.

Aggressive multiple sclerosis: proposed definition and treatment algorithm.

Multiple sclerosis (MS) is a CNS disorder characterized by inflammation, demyelination and neurodegeneration, and is the most common cause of acquired nontraumatic neurological disability in young adults. The course of the disease varies between individuals: some patients accumulate minimal disability over their lives, whereas others experience a rapidly disabling disease course. This latter subset of patients, whose MS is marked by the rampant progression of disability over a short time period, is often referred to as having 'aggressive' MS. Treatment of patients with aggressive MS is challenging, and optimal strategies have yet to be defined. It is important to identify patients who are at risk of aggressive MS as early as possible and implement an effective treatment strategy. Early intervention might protect patients from irreversible damage and disability, and prevent the development of a secondary progressive course, which thus far lacks effective therapy.

Severe amnesia associated with human herpesvirus 6 encephalitis after bone marrow transplantation.

BACKGROUND: Human herpesvirus 6 (HHV-6) appears to have a predilection for immunocompromised patients and has been implicated as a cause of posttransplant encephalitis. However, the pathogenesis, as well as the appropriate means of diagnosis and treatment of HHV-6 encephalitis is unclear. METHOD: We describe a case of a 20-year-old male university student with anemia who presented with an acute, severe amnesia 1 month after bone marrow transplantation. His illness was subsequently attributed to HHV-6 encephalitis. RESULTS: Cerebrospinal fluid analysis was consistent with encephalitis and polymerase chain reaction confirmed the presence of HHV-6 DNA in both cerebrospinal fluid and serum. No other herpes virus particles were detected. MRI showed bilateral hippocampal involvement. Treatment with acyclovir resulted in a decrease in serum HHV-6 DNA to undetectable levels, coincident with improvement of both memory and lesions on MRI. CONCLUSIONS: This case provides strong clinical and radiological evidence of the reversibility of this disease process and supports the recommendations for empiric treatment of post transplant patients with laboratory evidence of HHV-6 infection, culture or polymerase chain reaction, plus clinical symptoms compatible with HHV-6 infection.