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Brainstem Lesion (brainstem + lesion)
Selected AbstractsHemicrania Continua Secondary to an Ipsilateral Brainstem LesionHEADACHE, Issue 3 2007Marcelo M. Valença MD We describe a 47-year-old woman with a 3-year history of a continuum mild-moderate right-side headache, with exacerbations, associated with stabbing volleys of pain on right orbit-temporal region (10/10) and right eye ptosis and lacrimation with conjunctival injection. The pain was completely abolished with indomethacin (100 mg per day). The diagnosis of hemicrania continua was made according to the International Headache Society (IHS) criteria. The headache presentation was precipitated by a stroke and a right-side brainstem lesion was present at magnetic resonance imaging. This case report shows anatomoclinical evidence of the involvement of brainstem structures on the pathophysiology of hemicrania continua. [source] Motor aprosodia due to isolated brainstem stroke in a young womanACTA NEUROLOGICA SCANDINAVICA, Issue 3 2005M. Hoffmann A 21 year old woman presented with coma and quadriparesis secondary to bilateral pontine infarction. Three weeks later motor aprosodia was the most notable neurological finding apart from mild asymmetric limb weakness. No other supratentorial lesion was noted on initial and subsequent multimodality magnetic resonance imaging and magnetic resonance perfusion imaging revealed right frontotemporal hypoperfusion. This is the first report of aprosodia with an isolated brainstem lesion. [source] Dystonia Associated with pontomesencephalic lesions,MOVEMENT DISORDERS, Issue 2 2009Thomas J. Loher MD Abstract Secondary dystonia is well known subsequent to lesions of the basal ganglia or the thalamus. There is evidence that brainstem lesions may also be associated with dystonia, but little is known about pathoanatomical correlations. Here, we report on a series of four patients with acquired dystonia following brainstem lesions. There were no basal ganglia or thalamic lesions. Three patients suffered tegmental pontomesencephalic hemorrhage and one patient diffuse axonal injury secondary to severe craniocerebral trauma. Dystonia developed with a delay of 1 to 14 months, at a mean delay of 6 months. The patients' mean age at onset was 33 years (range 4,56 years). All patients presented with hemidystonia combined with cervical dystonia, and two patients had craniofacial dystonia in addition. Three patients had postural or kinetic tremors. Dystonia was persistent in three patients, and improved gradually in one. There was little response to medical treatment. One patient with hemidystonia combined with cervical dystonia improved after thalamotomy. Overall, the phenomenology of secondary dystonia due to pontomesencephalic lesions is similar to that caused by basal ganglia or thalamic lesions. Structures involved include the pontomesencephalic tegmentum and the superior cerebellar peduncles. Such lesions are often associated with fatal outcome. While delayed occurrence of severe brainstem dystonia appears to be rare, it is possible that mild manifestations of dystonia might be ignored or not be emphasized in the presence of other disabling deficits. © 2008 Movement Disorder Society [source] Neurofibrillary tangles and deposition of oxidative products in the brain in cases of myotonic dystrophyNEUROPATHOLOGY, Issue 2 2006Reiko Oyamada Myotonic dystrophy (MyD) is a neuromuscular degenerative disorder that is neuropathologically characterized by minor changes, such as the presence of neurofibrillary tangles (NFT), thalamic inclusions and functional brainstem lesions. In the current study, we conducted an immunohistochemical analysis to examine the distribution of NFT and formation of oxidative products in the brain specimens of 12 patients with MyD. Neurofibrillary tangles were found in the limbic system and/or the brainstem of all the cases examined but there were no senile plaques. The density of distribution of the NFT was not significantly correlated with clinicopathological findings, although cases with fewer NFT in the brain frequently showed sleep disturbances and lack of spontaneity. Nuclear and cytoplasmic immunoreactivities for 8-hydroxy-2,-deoxyguanosine and advanced glycation end products were observed in the glial cells and/or neurons in the brainstem, but not in the cerebral cortex. On the other hand, 10 out of the 12 cases showed cytoplasmic immunoreactivity for 4-hydroxy-2-nonenal-modified protein (4-HNE) in neurons of the temporal cortex and raphe nucleus. Deposition of 4-HNE was also recognized in the hippocampus and mesencephalic central gray matter, but not in the subiculum. The distribution pattern of the immunoreactivity for 4-HNE showed no clear correlation with either the psychological disturbances or the distribution of the NFT. Altered expression of monoaminergic neurons in the brainstem of MyD patients has already been reported, and it is worth noting that most of our cases showed NFT in the brainstem. The selective deposition of 4-HNE in the limbic system and brainstem suggests that lipid peroxidation may be involved in the neurodegenerative process in MyD. Using immunohistochemical analysis to determine the distribution of neurotransmitters in the mesencephalic central gray matter and/or pontine raphe nucleus may help elucidate the relationship between the clinical abnormalities, distribuion of NFT, and 4-HNE deposition in the brain in patients with MyD. [source] | ||||||||||