Vascular dementia, with special reference to its vascular and immunological events.

Vascular dementia (VaD) is an poorly defined entity; it relates to different vascular mechanisms and different changes in the brain and has different clinical manifestations with different etiologies. From the pathogenetic and therapeutic point of view, we tried to find some practical events that could help identify VaD. We combined critical review with our own clinical and laboratory experience and found that some vascular, nonvascular, and immunological components are involved in the pathogenesis and treatment of VaD. We concluded that although the definition, etiology, clinical manifestation, laboratory data, and treatment are still controversial, it is useful to find some common, key points in the pathogenesis and treatment of VaD.

Clinical neuroimmunology.

Clinical research has focused on autoimmune disease (AID) for a couple of decades. More sensitive and specific methods have been developed for neuroimmunological research. Gamma fraction bands (bands separated by electrophoresis and visualized by amino black staining) and IgG fraction bands (bands separated by iso-electric focusing and visualized by immunostaining) are used instead of oligoclonal bands. Myasthenia gravis (MG) mainly involves acetylcholine receptors of the postsynaptic membrane at the neuromuscular junction. Myasthenia gravis has been considered to be a generalized AID, because 7% of patients with myasthenia gravis associate with other AIDs and more than one autoimmune antibody is detected in 52.5% patients with myasthenia gravis. Pyramidal signs in myasthenia gravis patients are described; the possible mechanism may at least be partly due to the acetylcholine receptor antibody. P2 protein and its antibody are studied in patients with acute and chronic inflammatory demyelinating polyneuropathy.