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)

We report a case of a 22-year-old male who was transferred to our hospital in a comatose state following successive seizures. Low blood glucose had been detected upon his arrival at the previous hospital. He became responsive 12 days after the onset of coma. Upon regaining consciousness he exhibited severe dysarthria and several interhemispheric disconnection signs such as intermanual conflict, left-hand dysgraphia, left hemispatial neglect confined to the right hand, impaired interhemispheric transfer, and unilateral constructional apraxia of the right hand. Brain MRI disclosed T2-weighted and diffusion-weighted hyperintense lesions with reduced apparent diffusion coefficients in the bilateral centrum semiovale, splenium of the corpus callosum, right posterior limb of the internal capsule, and bilateral middle cerebellar peduncles. As the MRI findings vanished, his interhemispheric disconnection signs gradually resolved. Abdominal imaging studies revealed a pancreatic tumor, which was later endocrinologically diagnosed as an insulinoma. This is an extremely rare report of interhemispheric disconnection signs due to hypoglycemic encephalopathy. The lesions in the bilateral centrum semiovale likely contributed to the interhemispheric disconnection signs.
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PMID:Transient interhemispheric disconnection in a case of insulinoma-induced hypoglycemic encephalopathy. 2413 56

Encephalopathy caused by manganese compounds used for illicit production of ephedrone (methcathinone) is described. The onset of disease could be observed after some months of regular intravenous use of ephedrone contaminated with manganese. In clinical picture dominate neurological signs and symptoms, mainly extrapyramidal syndromes: parkinsonism, tremor, muscle distonia, pro- and retropulsion. Some other symptoms may be observed: hypophonia or dysarthria, gain disturbances, impairment of precise movement, and micrographia. In cranial NMR often appears bilaterally an increase of an intensity of T1 signal in globus pallidus and in some other brain structures. Elimination of manganese with the use of chelating therapy as well as symptomatic treatment, mainly with the antyparkinsonic drugs, seems to be ineffective.
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PMID:[Encephalopathy caused by intravenous potassium permanganate used for illegal production of methcathinone (ephedrone) from medicines containing pseudoephedrine]. 2446 4

We report the case of a 75-year-old ex-professional boxer who developed diplopia and eye movement abnormalities in his 60's followed by memory impairment, low mood and recurrent falls. Examination shortly before death revealed hypomimia, dysarthria, vertical supranuclear gaze palsy and impaired postural reflexes. Pathological examination demonstrated 4-repeat tau neuronal and glial lesions, including tufted astrocytes, consistent with a diagnosis of progressive supranuclear palsy. In addition, neurofibrillary tangles composed of mixed 3-repeat and 4-repeat tau and astrocytic tangles in a distribution highly suggestive of chronic traumatic encephalopathy were observed together with limbic TDP-43 pathology. Possible mechanisms for the co-occurrence of these two tau pathologies are discussed.
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PMID:Concomitant progressive supranuclear palsy and chronic traumatic encephalopathy in a boxer. 2455 32

This is the case of a 24-year-old woman with relapsed acute undifferentiated leukemia who developed subacute encephalopathy with hemiparesis and dysarthria after treatment with high dose and intrathecal methotrexate, clofarabine, and cytarabine that resolved rapidly and completely after the administration of corticosteroids. We hypothesize that clofarabine might predispose to methotrexate-induced central nervous system toxicity by increasing endothelial permeability (capillary leak syndrome) and suggest that corticosteroids are effective in the treatment of this type of encephalopathy.
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PMID:A Case of Subacute Encephalopathy Developing After Treatment With Clofarabine and Methotrexate That Resolved With Corticosteroids. 2498 45

Hashimoto's encephalopathy (HE) is an acute encephalopathy associated with Hashimoto's thyroiditis. The majority of reported cases have been associated with hypothyroidism, while cases with hyperthyroidism are rare. The current study reported on a 56-year old female patient with HE, who was found to have progressively aggregated dysarthria, gait disturbance, somniloquy and delirium. Thyroid function tests revealed that the patient had hyperthyroidism, with high levels of anti-thyroid antibodies. Following treatment with corticosteroids, the neurological/psychiatric symptoms of the patient were relieved quickly. The one-year follow-up investigation indicated that there was no recurrence of the disease, demonstrating that the treatment administered for this rare case was effective.
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PMID:Hashimoto encephalopathy associated with hyperthyroidism: A case report. 2500 11

Reversible focal lesions on the splenium of the corpus callosum (SCC) have been reported in patients with mild encephalitis/encephalopathy caused by various infectious agents, such as influenza, mumps, adenovirus, Varicella zoster, Escherichia coli, Legionella pneumophila, and Staphylococcus aureus. We report a case of a reversible SCC lesion causing reversible encephalopathy in nonfulminant hepatitis A. A 30-year-old healthy male with dysarthria and fever was admitted to our hospital. After admission his mental status became confused, and so we performed electroencephalography (EEG) and magnetic resonance imaging (MRI) of the brain, which revealed an intensified signal on diffusion-weighted imaging (DWI) at the SCC. His mental status improved 5 days after admission, and the SCC lesion had completely disappeared 15 days after admission.
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PMID:Reversible splenial lesion on the corpus callosum in nonfulminant hepatitis A presenting as encephalopathy. 2554 47

Takayasu's arteritis is a chronic inflammatory disease, and neurological symptoms occur in 50% of cases, most commonly including headache, dizziness, visual disturbances, convulsive crisis, transient ischemic attack, stroke and posterior reversible encephalopathy syndrome. The aim of this study was to report the case of a young Brazilian female with a focal neurological deficit. She presented with asymmetry of brachial and radial pulses, aphasia, dysarthria and right hemiplegia. Stroke was investigated extensively in this young patient. Only nonspecific inflammatory markers such as velocity of hemosedimentation and C-reactive protein were elevated. During hospitalization, clinical treatment was performed with pulse therapy showing improvement in neurological recuperation on subsequent days. In the chronic phase, the patient was submitted to medicated angioplasty of the brachiocephalic trunk with paclitaxel, with significant improvement of the stenosis. At the 6-month follow-up, the neurological exam presented mild dysarthria, faciobrachial predominant disproportionate hemiparesis, an NIHSS score of 4 and a modified Rankin Scale score of 3 (moderate incapacity). In conclusion, Takayasu's arteritis must be recognized as a potential cause of ischemic stroke in young females.
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PMID:Stroke as the First Clinical Manifestation of Takayasu's Arteritis. 2556 58

The long-term consequences of repetitive head impacts have been described since the early 20th century. Terms such as punch drunk and dementia pugilistica were first used to describe the clinical syndromes experienced by boxers. A more generic designation, chronic traumatic encephalopathy (CTE), has been employed since the mid-1900s and has been used in recent years to describe a neurodegenerative disease found not just in boxers but in American football players, other contact sport athletes, military veterans, and others with histories of repetitive brain trauma, including concussions and subconcussive trauma. This article reviews the literature of the clinical manifestations of CTE from 202 published cases. The clinical features include impairments in mood (for example, depression and hopelessness), behavior (for example, explosivity and violence), cognition (for example, impaired memory, executive functioning, attention, and dementia), and, less commonly, motor functioning (for example, parkinsonism, ataxia, and dysarthria). We present proposed research criteria for traumatic encephalopathy syndrome (TES) which consist of four variants or subtypes (TES behavioral/mood variant, TES cognitive variant, TES mixed variant, and TES dementia) as well as classifications of 'probable CTE' and 'possible CTE'. These proposed criteria are expected to be modified and updated as new research findings become available. They are not meant to be used for a clinical diagnosis. Rather, they should be viewed as research criteria that can be employed in studies of the underlying causes, risk factors, differential diagnosis, prevention, and treatment of CTE and related disorders.
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PMID:Clinical subtypes of chronic traumatic encephalopathy: literature review and proposed research diagnostic criteria for traumatic encephalopathy syndrome. 2558 Jan 60

Recently, mutations in FARS2, which encodes for mitochondrial phenylalanyl-tRNA synthetase, have been implicated in autosomal recessive combined oxidative phosphorylation deficiency 14. Associated clinical features in three previously reported patients with confirmed FARS2 mutations include infantile onset epilepsy, and a fatal Alpers-like encephalopathy. Herein, we report on two siblings with global developmental delay, dysarthria and tremor and compound heterozygous FARS2 abnormalities. They have a heterozygous missense mutation, c.1255C>T which predicts p.Arg419Cys in exon 7 of FARS2, inherited from their father and uncovered on exome sequencing, and an interstitial deletion of chromosome 6p25.1 inherited from their mother and uncovered on SNP array. This interstitial deletion includes all of exon 6 and parts of introns 5 and 6 of FARS2. Biochemical studies were also consistent with a mitochondrial disorder. While these siblings had considerable developmental difficulties, they are making consistent developmental progress and appear to be considerably less severely affected than the other patients reported in the literature with FARS2 associated mitochondrial disease. Thus, this study expands the phenotypic spectrum of FARS2 related disease and emphasizes intragenic deletion in the list of causative mutations.
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PMID:Mutations in FARS2 and non-fatal mitochondrial dysfunction in two siblings. 2585 14

A 52-year-old female presented with stroke-like symptoms after high-dose methotrexate (HDMTX) therapy and MTX intrathecal injection (IT-MTX) as central nervous system (CNS) prophylaxis for intravascular large B-cell lymphoma (IVLBCL). She had been diagnosed as having IVLBCL without CNS involvement 5 months earlier and had received 6 courses of R-CHOP and 2 courses of HDMTX combined with IT-MTX. She experienced acute-onset right hemiparesis involving the face and arm, along with dysarthria, 7 days after the second HDMTX infusion. Brain magnetic resonance imaging (MRI) and cerebrospinal fluid results were normal and suggested neither stroke nor CNS infiltration. Her symptoms gradually resolved within 4 days and follow-up neurologic examination showed no abnormalities. MRI on day 2 (after the onset) showed an area of hyper-intensity on diffusion weighted imaging (DWI). Follow-up MRI performed on day 38 showed resolution of the DWI intensity, while the T2 and FLAIR signals became more evident. Based on her clinical course and these MRI findings, she was diagnosed as having MTX-induced subacute encephalopathy. This syndrome has been reported mainly in children with ALL after HDMTX or IT-MTX, but there have been few reports of adult patients. MTX-induced subacute encephalopathy should be taken into account as a possible cause of neurologic manifestations because early differentiation from stroke and CNS infiltration is essential to successful management.
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PMID:[Subacute encephalopathy after high-dose methotrexate as prophylaxis for central nervous system relapse in a patient with intravascular large B-cell lymphoma]. 2587 88


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