Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013362 (dysarthria)
 3,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this paper we report a case of vertebral artery occlusion caused by spontaneous extra-cranial vertebral artery dissection accompanied with cerebellar and thalamic infarctions due to recanalization. Furthermore, after a nine-week time lapse we performed PTA/stenting. A 62-year-old man with vertigo, dysarthria and nuchal pain without injury was admitted to our hospital. Emergent cerebral angiography revealed an occlusion of the right vertebral artery and the right PICA. The patient's symptoms gradually improved owing to local-fibrinolysis with urokinase for the right PICA via the left vertebral artery. Follow-up angiography (2 weeks later) showed re-canalization and dissection of the right vertebral artery. Treatment for spontaneous extra-cranial vertebral artery dissection is chosen, depending on whether there is co-lateral circulation or not. We obtained a good result using PTA/Stenting in this case of spontaneous extra-cranial vertebral artery dissection within nine weeks after onset.
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PMID:[Spontaneous extra-cranial vertebral artery dissection accompanied with multiple cerebral infarctions due to re-canalization]. 1459 46

Episodic ataxia type 2 (EA2) is a dominantly inherited disorder, characterized by spells of ataxia, dysarthria, vertigo, and migraines, associated with mutations in the neuronal calcium-channel gene CACNA1A. Ataxic spells lasting minutes to hours are provoked by stress, exercise, or alcohol. Some patients exhibit nystagmus between spells and some develop progressive ataxia later in life. At least 21 distinct CACNA1A mutations have been identified in EA2. The clinical and genetic complexities of EA2 have offered few insights into the underlying pathogenic mechanisms for this disorder. We identified a novel EA2 kindred in which members had ataxic spells induced by fevers or high environmental temperature. We identified a novel CACNA1A mutation (nucleotides 1253+1 G-->A) that was present in all subjects with febrile spells or ataxia. Moreover, we found that, regardless of age or interictal clinical status, all affected subjects had objective evidence of abnormal saccades, ocular fixation, and postural stability. These findings suggest that early cerebellar dysfunction in EA2 results from the intrinsically abnormal properties of the CACNA1A channel rather than a degenerative process.
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PMID:Novel CACNA1A mutation causes febrile episodic ataxia with interictal cerebellar deficits. 1468 82

The clinical efficacy of gefitinib, a tyrosine kinase inhibitor of epidermal growth factor receptor (EGFR), on brain metastases (BMs) from non-small-cell lung cancer (NSCLC) was evaluated. Fifteen patients with recurrent NSCLC with metastasis to the brain were treated with gefitinib. The objective tumor response rate (60%; 9 of 15 patients) for BM was the same as for primary tumors. The median time to response of BM was 26 days. In 8 of 9 patients who exhibited partial response in the thoracic lesion, BM showed dramatic regression, including 1 complete response. One patient with stable primary tumor also exhibited partial response in BM with this monotherapy. Brain metastasis-related neurologic symptoms such as hemiparesis, dysarthria, dysphagia, and vertigo improved or disappeared with the objective response of BM as confirmed by magnetic resonance imaging. Central nervous system toxicities were not observed during the treatment. Four of the 9 BM responders are still under treatment with neither adverse events nor disease progression. Two discontinued the treatment because of severe hepatic toxicity and 3 died because of acquired resistance in pulmonary lesions, even though partial response was observed in the BMs. Finally, median duration of response of BM was 8.7 months and median overall survival was 8.3 months (range, 1.8 to > 15.7 months). Molecular targeted therapy against EGFR could be an option for the treatment of BM from NSCLC refractory to conventional chemotherapy plus radiation therapy because it has demonstrated a distinct therapeutic potential against BM compared with primary lung tumor and extracranial metastases.
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PMID:Gefitinib in patients with brain metastases from non-small-cell lung cancer: review of 15 clinical cases. 1547 98

Basilar artery occlusion (BAO) is generally associated with a high mortality rate and a poor functional outcome in survivors. Recently, we encountered a patient with BAO, initially manifesting as vertigo and rebound nystagmus, subsequently followed by bilateral sudden deafness and dysarthria and terminating in a coma state within an interval of 6 h. A review of his history showed he had had two episodes of transient vertigo 2 weeks before the major stroke, and the neurological decline of BAO was heralded by the vertiginous symptoms. Restated, patients with BAO often have transient vertiginous attacks preceding fatal stroke. Therefore, those with vertigo and nystagmus may be signaling a forthcoming stroke event, something that should be considered for clinicians seeing vertiginous patients.
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PMID:Vertigo with rebound nystagmus as an initial manifestation in a patient with basilar artery occlusion. 1559 55

The sudden onset of hearing impairment or hearing loss can be a characteristic sign of a vertebrobasilar circulatory disturbance. We report on a 65 year old male patient with an acute left-sided tinnitus followed by hearing loss as an initial symptom of an infarction of the left anterior inferior cerebellar artery (AICA). Successively, additional symptoms with vertigo, nausea, vomiting and a transient dysarthria and ataxia of the left upper extremity occurred. In the course of the illness, the hearing loss, ataxia and dysarthria completely recovered. MRI of the brain showed an infarction in the area of the anterior inferior cerebellar artery; neurosonographic examination of the basilar and vertebral arteries was normal. Therefore, in patients with acute hearing impairment or hearing loss, an AICA-ischemia should be considered and the patient carefully examined for additional brainstem symptoms, since this can be the first sign of an life-threatening basilar artery thrombosis.
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PMID:[Sudden hearing loss as the leading symptom of an infarction of the left anterior inferior cerebellar artery]. 1565 56

We have recently encountered a rare case of fibromuscular dysplasia (FMD) of the vertebral artery (VA) presenting as lateral medullary syndrome. A 39-year-old male was admitted to our hospital due to vertigo, dysarthria and numbness of the left face and the right limbs. A magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) of brain revealed lateral medullary infarction in the territory of the left posterior inferior cerebellar artery (PICA). The angiography of the VA revealed tubular stenosis of the left extracranial VA and a focal vascular kinking as well as web in the right extracranial VA, confirming the diagnosis of FMD. We present this rare case to emphasize that FMD could be one of the risk factors causing lateral medullary syndrome in young people.
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PMID:Fibromuscular dysplasia of the vertebral artery presenting with lateral medullary syndrome: a case report. 1566 96

We reported a 37-year-old man who developed vertigo, dysarthria and left hemiparesis following neck pain. Magnetic resonance imaging (MRI) demonstrated infarct in the right superior cerebellar artery (SCA) territory. Duplex color-flow imaging detected dissection (double lumen) in the right vertebral artery (VA) at the level of the C4-C6 vertebra (V2 segment). Cerebral angiography showed irregular narrowing in the right V2, and occlusion of the right SCA. These findings suggested that dissection in the right V2 caused artery-to-artery embolism in the right SCA. Despite administration of anti-thrombotic agents, he recurrently suffered from transient ischemic attacks. Serial duplex color-flow imaging echography revealed that the dissection of the right VA gradually became more stenotic and extended to the distal site. Coil-embolization of the right VA by endovascular therapy was performed, and thereafter the dissecting lesion of the right VA was completely occluded and ischemic attacks disappeared.
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PMID:[Traumatic extracranial vertebral artery dissection treated with coil embolization--a case report]. 1591 98

Most movement disorders, reflecting degenerative disorders, develop in a slowly progressive fashion. Some movement disorders, however, manifest with an acute onset. We wish to give an overview of the management and therapy of those acute-onset movement disorders.Drug-induced movement disorders are mainly caused by dopamine-receptor blockers (DRB) as used as antipsychotics (neuroleptics) and antiemetics. Acute dystonic reactions usually occur within the first four days of treatment. Typically, cranial pharyngeal and cervical muscles are affected. Anticholinergics produce a prompt relief. Akathisia is characterized by an often exceedingly bothersome feeling of restlessness and the inability to remain still. It is a common side effect of DRB and occurs within few days after their initiation. It subsides when DRB are ceased. Neuroleptic Malignant Syndrome is a rare, but life-threatening adverse reaction to DRB which may occur at any time during DRB application. It is characterised by hyperthermia, rigidity, reduced consciousness and autonomic failure. Therapeutically immediate DRB withdrawal is crucial. Additional dantrolene or bromocriptine application together with symptomatic treatment may be necessary. Paroxysmal dyskinesias are childhood onset disorders characterised by dystonic postures, chorea, athetosis and ballism occurring at irregular intervals. In Paroxysmal Kinesigenic Dyskinesia they are triggered by rapid movements, startle reactions or hyperventilation. They last up to 5 minutes, occur up to 100 times per day and are highly sensitive to anticonvulsants. In Paroxysmal Non-Kinesiogenic Dyskinesia they cannot be triggered, occur less frequently and last longer. Other paroxysmal dyskinesias include hypnogenic paroxysmal dyskinesias, paroxysmal exertional dyskinesia, infantile paroxysmal dystonias, Sandifer's syndrome and symptomatic paroxysmal dyskinesias. In Hereditary Episodic Ataxia Type 1 attacks of ataxia last for up to two minutes, may be accompanied by dysarthria and dystonia and usually respond to phenytoin. In Type 2 they can last for several hours, may be accompanied by vertigo, headache and malaise and usually respond to acetazolamide. Symptomatic episodic ataxias can occur in a number of metabolic disorders, but also in multiple sclerosis and Behcet's disease.
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PMID:Diagnosis and management of acute movement disorders. 1620 29

Basilar-type migraine (BTM) is a type of migraine with aura symptoms resulting from brain stem or bi-hemispheric structures but without motor elements. There are no precise data on the frequency of BTM. The main cohort of the patients includes young people and children with female predomination. The onset of the disease usually occurs before the age of 25. The diagnosis of BTM is based on the finding of two migraine attacks accompanied by a specific aura, with dysarthria, vertigo, tinnitus, impaired hearing, double vision, visual aura elements, ataxia of a cerebellar type, loss of consciousness, and bilateral paresthesias. In the differential diagnosis one should consider the pathology of posterior fossa, diseases with recurrent vertigo, complex epileptic seizures, CADASIL and MELAS syndromes, and alternative hemiplegic migraine with cerebellar symptoms and signs. In the prophylaxis sodium valproate and calcium-entry blockers and, especially in the prophylaxis of vertigo, betahistine chloride are used.
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PMID:[Basilar-type migraine: pathophysiology, symptoms and signs, and treatment]. 1641 73

A 51-year-old man developed sudden vertigo, right hearing loss and dysphagia. Examination revealed right Horner syndrome, spontaneous torsional-horizontal nystagmus, right central type facial palsy, dysarthria, reduced soft palate elevation without gag reflex, left hypesthesia, right dysmetria and imbalance. Audiometry and bithermal caloric tests documented right sensorineural hearing loss and canal paresis. Brain MRI and cerebral angiography documented right lateral medullary infarction from vertebral artery dissection, without involvement of other parts of the brainstem supplied by the anterior inferior cerebellar artery (AICA). This case suggests artery-to-artery embolism as a possible mechanism of isolated vertigo or hearing loss from labyrinthine infarction.
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PMID:Embolic internal auditory artery infarction from vertebral artery dissection. 1658 Jun 95


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