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The anatomical basis of cognitive dysfunction and other non-motor symptoms in multiple sclerosis (MS) is poorly understood. In MS patients, transcranial sonography (TCS) shows neurodegenerative disease-like lesions of the substantia nigra (SN) and basal ganglia, thought to reflect iron accumulation. The present study deals with the question of whether sonographic changes of SN, brainstem raphe, lenticular nucleus (LN) or caudate nucleus are related to non-motor symptoms of MS. We used TCS to investigate 54 MS patients and 54 age- and sex-matched healthy subjects. Degree of cognitive (executive) dysfunction, fatigue, depression, and urinary urge incontinence in MS patients was assessed using the Paced Auditory Serial Addition Test, the Faces Symbol Test, the Modified Fatigue Impact Scale, the Beck Depression Inventory, and the Urinary Distress Inventory. Abnormal TCS findings of SN, brainstem raphe, LN, and caudate nucleus were found in 13, 7, 11, and 6% of the healthy subjects, but in 54, 43, 62, and 41% (each, p < 0.001) of the MS patients, with similar frequency in relapsing-remitting and primary or secondary progressive MS patients. Sonographic alteration of the LN correlated with cognitive dysfunction. Combined alteration of both, LN and SN, was clearly associated with cognitive dysfunction and cognitive fatigue. The combined sonographic alteration of SN and brainstem raphe indicated severe urinary urge incontinence irrespective of the presence of spinal MS lesions. No relation was found between depression and any of the TCS findings. These findings suggest that neurodegenerative processes affecting deep brain structures contribute to cognitive and autonomic dysfunction in MS. [ABSTRACT FROM AUTHOR]

Callosal dysfunction is known to be evident in a variety of neurodegenerative and inflammatory diseases of the central nervous system. Cerebral microangiopathy (CMA) may also affect callosal pathways by chronic demyelination. The aim of the present study was to investigate callosal function with respect to the extent of CMA. Callosal function was tested by a bimanual tapping task and by analysis of the ipsilateral silent period (iSP) and the transcallosal conduction time (TCT) using transcranial magnetic stimulation. Results were correlated to the extent of CMA measured by cranial magnetic resonance imaging (cMRI) in 44 patients with CMA compared to 10 control subjects. The extent of CMA was quantified by a cMRI score. Additionally, callosal atrophy was quantified by cMRI morphometry. Frequency of pathological iSP findings or disturbed bimanual tapping was significantly correlated to a higher CMA score. Moreover, the extent of CMA was significantly correlated to the degree of callosal atrophy. It is concluded that CMA considerably affects callosal pathways, possibly by chronic demyelination of callosal fibres. As the extent of CMA and atrophy of the corpus callosum is correlated to callosal dysfunction, analysis of the iSP can be used to assess the clinical impact of CMA detected by cMRI. [ABSTRACT FROM AUTHOR]