Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013421 (dystonia)
 8,418 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 68 year-old man developed progressive hemidystonia and chorea 8 months after a contralateral thalamic stroke. The neurological examination also showed a right pyramidal syndrome without hemiparesis, a right horizontal sectoranopia, and a right hemihypesthesia for all sensory modalities. The MRI revealed infarctions in the left medial temporo-occipital lobes and left posterolateral thalamus, corresponding to the vascular territories of both the thalamo-geniculate and posterolateral choroidal arterial pedicles. The thalamic lesion involved the pulvinar, the lateral geniculate body, and the ventro-postero-lateral, dorso-lateral, posterolateral, and dorso-medial nuclei, but apparently did not extent to the ventrolateral thalamic nucleus, and the subthalamic and midbrain regions. Thalamic and striatopallidal dystonia have not a common pathophysiological mechanism. The involvement of the pulvinar nucleus and of the strategic crossing of proprioceptive, cerebellar, pyramidal, and subthalamic pathways may play a role in the genesis of the posterolateral thalamic dystonia.
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PMID:Delayed-onset hemidystonia and chorea following contralateral infarction of the posterolateral thalamus. A case report. 900 80

Sleep bruxism refers to a nocturnal parafunctional activity including the clenching, grinding or gnashing of teeth. While most of the nocturnal bruxism cases seen in the general population are apparently idiopathic, it has been reported to be associated with a range of neurological diseases such as Huntington's disease, cranio-cervical dystonia and post-anoxic brain damage, but not multiple sclerosis (MS). We describe three cases of MS patients who have had moderate to severe complaints of bruxism in the two weeks following their relevant MS attacks. None of the three patients had a diagnosis of bruxism prior to her attack. The diagnosis was confirmed in one out of three by a polysomnography. One patient did not have any complaints related to bruxism previous to her attack, whereas two had mild and infrequent complaints. The symptoms of the relevant attacks were left hemihypesthesia in all and hemiparesis in two. None of the patients had spasticity that could result in severe teeth clenching. All three patients presented with morning headaches and jaw pain or tightness and were treated successfully with botulinum toxin (Btx) injections applied to their masseter and temporalis muscles. The cause of bruxism is controversial but lesions of the cortico-basalganglia-thalamo-cotrical loops are thought to be most likely. However, acute or chronic lesions in those pathways were not demonstrated in the 3 patients. It is feasible that they had normal appearing white matter interruptions in their cortico-basalganglia-thalamocortical loops along with their relevant attack.
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PMID:Sleep bruxism possibly triggered by multiple sclerosis attacks and treated successfully with botulinum toxin: Report of three cases. 2634 87

A 33 year-old male presented with right upper limb rest tremor that disappeared on action, posture associated with bradykinesia, and rigidity of right upper and lower limbs (Video S1). Patient also presented right-sided pyramidal weakness (grade 4), hyperreflexia, extensor plantar response, and hemihypesthesia. Skull X-ray and computed tomography (CT) of the brain showed several metal pellets producing multiple artifacts (Fig. 1A,B). Only one pellet settled in brain parenchyma (left midbrain), while other pellets settled in the skull bone (Fig. 1A). Transcranial sonography (TCS) was performed, confirming that the midbrain pellet was placed within the left substantia nigra (Fig. 1C). Levodopa challenge test was conducted, showing no improvement (pre- and post-l-dopa motor UPDRS were 21 and 20, respectively). A further chronic trial of l-dopa (for 3 months) also proved negative. Biperiden and propranolol were also tried with negative results. Figure 1Computed tomography (CT) of the brain and X-ray skull showed several pellets that produced multiple streak artifacts (Fig. 1A,B). Only one pellet rested in the brain parenchyma, the left (contralateral) midbrain as detected by CT (Fig. 1A), and transcranial sonography (Esaote MyLab Five, Providian, Italy) via temporal window (Fig. 1C). Abbreviations: SN, substantia nigra.Hemiparkinsonism has been previously reported secondary to midbrain lesions.1, 2 To the best of our knowledge, movement disorders (secondary to brain injuries) related to bullet fragments have been scantly reported. In one reported case, hemiparkinsonism and dystonia were the result of a bullet in midbrain,2 and in another, dystonia was caused by a bullet in internal capsule.3.
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PMID:Patient with Hemiparkinsonism Secondary to a Gun Pellet in the Contralateral Substantia Nigra. 3086