No abstract

Recent clinical and experimental studies suggest that ischemic strokes may play an important role in the pathogenesis of Alzheimer's disease (AD). Beta amyloid (Abeta), a major component of senile plaque in AD, is known to be derived from ischemic brain or activated platelets. We prospectively enrolled 62 patients with acute ischemic stroke and 27 age-matched controls. The serum Abeta and P-selectin levels were determined using the Sandwich-ELISA. We divided ischemic strokes into subgroups according to the clinical syndrome, pathogenesis, and infarct size, and compared the Abeta level between each subgroup. The Abeta1-40 level was markedly elevated in ischemic stroke patients, as compared to controls (140.2 +/- 54.0 vs 88.44 +/- 34.96 pg/ml, p<0.001). Cardioembolic and larger artery atherosclerotic infarcts had higher Abeta1-40 level than small vessel disease (p = 0.001). Both infarct size and the initial NIHSS score had significantly positive correlations with the serum level of Abeta1-40 (r = 0.539, p<0.001 and r = 0.425, p = 0.001, respectively). However, the P-selectin level was not significantly correlated with serum Abeta1-40. Our data suggest that elevated circulating Abeta1-40 in ischemic stroke patients may be derived from brain as a consequence of ischemic insults.

Cervical dystonia, the most common of the focal dystonia, is characterized by sustained, involuntary contraction of cervical muscles resulting in abnormal head movements or posture [1,2]. Secondary cervical dystonia has been associated with a variety of vascular, traumatic, or infectious conditions affecting the central or peripheral nervous system [3,4]. Here, we describe a patient with a dystonic head tremor associated with a parietal lesion and discuss the possible pathogenesis. PatientA 35-year-old, right-handed man was admitted to our hospital owing to abnormal head posture and tremulous movements of his head. At the age of 23, he sustained a severe closed-head injury in a car accident. He was obtunded for several weeks before recovering slowly over the subsequent few months. At that time, he noted there was a slight weakness of the left extremities. Two years after the initial head injury, he complained of involuntary tremulous movements of the head to the left side. As time passed, these movements were accompanied by an involuntary deviation of the head to the left.On neurological examination at the age of 35, he was alert, attentive, and communicative without cognitive dysfunction. Muscle strength and tendon reflexes were normal without the Babinski sign. He had a slightly spastic gait of the left leg. There were no sensory abnormalities, including joint position sensation, vibration sensation, graphesthesia, and two-point discrimination. There was no evidence of upper limb apraxia, rigidity, or bradykinesia. In the neutral position, his head was rotated 30°to the left side with a b c Figure 1 T2-weighted magnetic resonance imaging reveals cerebromalacia in the right parietal region (arrow, a) with no basal ganglia lesions (b). On brain SPECT, this region shows a discrete perfusion defect (arrow head, c). e32 Ó 2007 EFNS