1/7. Adverse effects of subthalamic nucleus DBS in a patient with multiple system atrophy.A 59-year-old woman with levodopa-responsive parkinsonism complicated by motor fluctuations and generalized levodopa dyskinesia underwent bilateral subthalamic deep brain stimulation (STN DBS) 7 years after symptom onset. DBS improved levodopa-responsive upper extremity bradykinesia but aggravated speech, swallowing, and gait. Motor fluctuations were not improved and levodopa dose remained unchanged. pulse generators were turned off. Clinical features and brain MRI in this case were indicative of multiple system atrophy (MSA). STN DBS is not recommended for patients with MSA.- - - - - - - - - - ranking = 1keywords = subthalamic nucleus, subthalamic, nucleus (Clic here for more details about this article) |
2/7. Bilateral subthalamic nucleus deep brain stimulation in a patient with cervical dystonia and essential tremor.The role of subthalamic nucleus (STN) deep brain stimulation (DBS) is well established in Parkinson's disease, but experience with STN DBS in other movement disorders is limited. We report on a patient with medically refractory cervical dystonia and essential tremor resulting in dystonic head tremor and action tremor of the hands who obtained complete tremor suppression and near resolution of her cervical dystonia with bilateral STN stimulation. The results in this case demonstrate that STN DBS can dramatically improve dystonia and tremor in nonparkinsonian movement disorders.- - - - - - - - - - ranking = 1.1825474199658keywords = subthalamic nucleus, subthalamic, nucleus (Clic here for more details about this article) |
3/7. Corticobasal syndrome with novel argyrophilic glial inclusions.A 42-year-old, left-handed woman first noted impaired dexterity of the dominant hand, soon followed by dysarthria and cognitive decline. Over a 4-year period, she developed severe left-sided apraxia with eventual neglect of the left arm and progressive extrapyramidal signs. Cognitive testing showed progressive executive, visuospatial, fluency, and naming impairment with relative preservation of memory. Single-photon emission computed tomography demonstrated asymmetric right posterior frontal and superior parietal hypoperfusion. The clinical impression was corticobasal degeneration. At autopsy, severe atrophy was seen in the perirolandic and frontal regions. There was marked neuronal loss and gliosis in the posterior frontal and precentral regions and less severe pathology in prefrontal, temporal, and parietal areas. Mild to moderate gliosis and neuronal loss were also seen in the putamen, globus pallidus, subthalamic, and dentate nuclei. Gallyas silver stain revealed numerous inclusions adjacent to oligodendrocyte nuclei in white and gray matter of affected cortical and subcortical regions. The gracile inclusions were wavy, slender, and stained positively with antibodies to ubiquitin and alphaB-crystallin but not to microtubule-associated proteins (tau, MAP1B, MAP2), tubulin, neurofilaments, glial fibrillary acidic protein, or alpha-synuclein. The argyrophilic inclusions identified in this case are distinct from those previously described in neurodegenerative diseases.- - - - - - - - - - ranking = 0.053962064027349keywords = subthalamic (Clic here for more details about this article) |
4/7. Changes induced by levodopa and subthalamic nucleus stimulation on parkinsonian speech.levodopa (L-dopa) and subthalamic nucleus (STN) stimulation treatments have been associated with both improvement and exacerbation of dysarthria in Parkinson's disease (PD). We report four cases illustrating variant responses of dysarthria to dopaminergic and STN stimulation therapies. patients' motor disability and dysarthria were perceptually rated by the Unified Parkinson's Disease Rating Scale (UPDRS) in four conditions according to medication and STN stimulation. Dedicated software packages allowed acquisition and analysis of acoustic recordings. Case 1, who had a severe off period aphonia, experienced improvement of speech induced by both levodopa and STN stimulation. In Case 2, both treatments worsened speech due to the appearance of dyskinesias. Case 3 had a dysarthria exacerbation induced by STN stimulation with parameters above optimal levels, interpreted as current diffusion from the STN to corticobulbar fibers. In Case 4, dysarthria exacerbation occurred with stimulation at an electrode contact located caudally to the target, also arguing for current diffusion as a potential mechanism of speech worsening. The presented cases demonstrated variant effects in relation to L-dopa and STN stimulation on speech. It seems that motor speech subcomponents can be improved like other limb motor aspect, but that complex coordination of all speech anatomical substrates is not responsive to STN stimulation. These hypotheses may be helpful for better understanding and management of STN stimulation effects on motor speech and skeleton-motor subsystems.- - - - - - - - - - ranking = 1.1825474199658keywords = subthalamic nucleus, subthalamic, nucleus (Clic here for more details about this article) |
5/7. Primary lateral sclerosis: a case report.The syndrome of primary lateral sclerosis (PLS) has been reported clinically on many occasions. Pathologic confirmation in the modern era, however, has generally been lacking. In a recently reported case of PLS, the disorder was complicated by a pontine infarct. We describe a 65-year-old woman whose illness began with spastic dysarthria, which gradually worsened to the point that 18 months later she could barely utter a sound. Meanwhile, dysphagia, brisk reflexes, and a pseudobulbar affect had developed. Three years after onset she had a spastic contractured right-sided hemiplegia and walked with short shuffling steps. The spasticity slowly progressed, and she died of aspiration pneumonia 3.5 years after the onset of dysarthria. Neuropathologic examination showed bilateral atrophy of the precentral gyri, which microscopically showed a paucity of Betz cells. There was loss of myelin throughout the corticospinal system, yet the anterior-horn cells of the spinal cord and hypoglossal nuclei were well preserved. Intracytoplasmic eosinophilic inclusion bodies, of unknown cause and significance, were observed in occasional motor neurons, one in the hypoglossal nucleus and two in spinal cord anterior horns. Clinically and pathologically, this case meets the criteria for PLS.- - - - - - - - - - ranking = 0.0017500564507467keywords = nucleus (Clic here for more details about this article) |
6/7. Pretectal eyelid retraction and lag.We report 2 patients who had eyelid retraction and eyelid lag with minimal impairment of vertical gaze. In both patients, magnetic resonance imaging demonstrated a circumscribed unilateral lesion immediately rostral and dorsal to the red nucleus involving the lateral periaqueductal gray area. Our clinical and radiological findings support the existence of a premotor eyelid control center in the region of the nucleus of the posterior commissure.- - - - - - - - - - ranking = 0.0035001129014934keywords = nucleus (Clic here for more details about this article) |
7/7. speech dysfunction due to trazodone--fluoxetine combination in traumatic brain injury.New serotonin reuptake inhibitors are available for the treatment of affective disorders and sleep dysfunction in traumatic brain injury (TBI) patients. Commonly reported serotonergic side-effects include nausea, headache, dizziness, nervousness and orthostatic hypotension. trazodone, a non-selective serotonin reuptake inhibitor, is often used in conjunction with fluoxetine, a selective serotonin reuptake inhibitor, in order to combat the insomnia associated with fluoxetine. Successful use of this combination is generally limited by the cumulative serotonergic side-effects of the two medications. This paper describes the first reported case of speech dysfunction as a complication of combined trazodone and fluoxetine use. A 43-year-old male suffered bilateral wrist fractures and a moderate TBI during a fall. Within 1 week of adding fluoxetine to trazodone the patient developed new-onset dysarthria and speech blocking. Upon discontinuation of fluoxetine, speech returned to normal. Possible mechanisms include inhibition of hepatic metabolism, unmasking of caudate nucleus injury, increased noradrenergic activity or previously unreported serotonergic effects. This case illustrates the importance of monitoring drug combinations for unexpected side-effects in the TBI population.- - - - - - - - - - ranking = 0.0017500564507467keywords = nucleus (Clic here for more details about this article) |