Multiple sclerosis and Parkinson's disease: the two faces of neurodegeneration. Report of the first Greek case and review of the literature.

There is still an open debate whether multiple sclerosis (MS) lesions can cause parkinsonian symptoms, or the coexistence of both diseases in the same patient is accidental. Moreover, α-synuclein (α Syn), the hallmark of Parkinson's disease (PD) seems also to play a crucial role in MS. So far, 42 cases of co-occurrence of parkinsonism and MS have been reported, but CSF α Syn measurement is lacking. To our knowledge, we report the first case with concomitant MS and PD diagnosis based on both clinico-radiological and CSF α Syn findings and review of literature.

Age-dependent variation of female preponderance across different phenotypes of multiple sclerosis: A retrospective cross-sectional study.

INTRODUCTION: Multiple sclerosis (MS) is an autoimmune disease of the CNS, which predominantly affects women. Studies investigating the sex distribution in MS are sparse. We aim to analyze the female-to-male ratio (F/M ratio) in different MS phenotypes in association with age at diagnosis and year of birth. METHODS: We performed a retrospective cross-sectional analysis by cumulating data (sex, year of birth, age at diagnosis, and MS phenotypes) from unpublished and published studies of the participating centers. RESULTS: Datasets of 945 patients were collected. The overall F/M ratio was 1.9:1.0 and female preponderance was present in all phenotypes except for primary progressive MS (PPMS), in which men were predominantly affected (F/M ratio: 0.5:1.0). Female preponderance declined with increasing age at diagnosis and was no longer present in relapsing-remitting MS (RRMS) patients > 58 years of age. CONCLUSION: Our data demonstrate an age dependency of female preponderance in MS except for PPMS. This could be influenced by the lifecycle of sex hormone secretion in women. In PPMS, a male preponderance was observed in all age-groups, which might point to pathophysiological mechanisms being less influenced by sex hormones.

Immune reconstitution inflammatory syndrome mimicking progressive multifocal leucoencephalopathy in a multiple sclerosis patient treated with natalizumab: a case report and review of the literature.

Natalizumab (NTM) represents an effective drug for the treatment of relapsing-remitting multiple sclerosis (RRMS). Progressive multifocal leucoencephalopathy (PML) is a potential life-threatening complication of NTM treatment. A close follow-up and MRI monitoring of patients under NTM are required to avoid such devastating complications. The case of a 47-year-old woman with RRMS (EDSS 1.5) treated with NTM for 44 months is reported. The patient had a relapse with mild cerebellar symptomatology and visual complaints. MRI revealed a new area of abnormal signal intensity in the subcortical white matter of the right parietal lobe with mild peripheral enhancement. Visual fields showed scotomata mostly of the left eye. NTM was discontinued. JC virus (JCV) polymerase chain reaction (PCR) in cerebrospinal fluid was negative. The patient received IV corticosteroids for 5 days and then monthly for 2 months with subsequent clinical and MRI improvement. On month 4, she presented with a new relapse with severe ataxia, mild behavioral change, increase of cerebellar symptoms and internuclear opthalmoplegia (EDSS 3.5). MRI showed reappearance of the right parietal lobe lesion, with decreased size and less pronounced contrast enhancement. A new 2-cm lesion was noted in the left cerebellar hemisphere with a speckled pattern of contrast enhancement. JCV PCR was negative and the patient was treated with IV corticosteroids. On month 12, she demonstrated clinical and MRI improvement. Although initially PML was highly suspected in this patient, the clinical and MRI findings were supportive of the presence of immune reconstitution inflammatory syndrome (IRIS).

Unusual association of multiple sclerosis with monoclonal gammopathy of undetermined significance (MGUS): two case reports.

We present two patients with demyelinating disease meeting the diagnostic criteria for multiple sclerosis. Both patients had IgG lambda monoclonal gammopathy in serum and cerebrospinal fluid associated with intrathecal antibody synthesis. This association is very unusual and it is not certain whether the co-occurrence of these disorders might be the result of a causal link between multiple sclerosis and monoclonal gammopathy or a fortuitous phenomenon.