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)

Thrombocytosis may appear in rheumatoid arthritis, nevertheless, thromboembolic phenomena have rarely been recorded. This case describes a 71-year old patient suffering from long-standing seropositive and nodular rheumatoid arthritis with severe pulmonary involvement. During an exacerbation of her disease and following the appearance of thrombocytosis, several episodes of transient ischemic attacks occurred. The neurological manifestations were right facial nerve paralysis, paraesthesia of the right cheek and dysarthria. The patient was treated successfully by antiaggregants, anticoagulants and busulfan.
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PMID:Recurrent transient ischemic attacks associated with thrombocytosis in rheumatoid arthritis. 718 35

Cerebellar infarcts have been neglected for a long time and are now shown well by CT and especially MRI. Some infarcts involve the full territory supplied by a cerebellar artery. They are frequently complicated by edema with brain stem compression and supratentorial hydrocephalus, requiring at times emergency surgery, and are often accompanied by other medullary, medial pontine, mesencephalic, thalamic and occipital infarcts. On the other hand, partial territory infarcts are usually confined to the cerebellum and have a benign outcome with total recovery or minimal disability. They are more common than full territory infarcts. However, clinical presentations are similar to those full territory infarcts, differing mainly by the lack of drowsiness or unconsciousness. The main symptoms are vertigo, headache, vomiting, unsteadiness of gait and dysarthria. Signs include ipsilateral limb dysmetria, ipsilateral axial lateropulsion, ataxia and dysarthria. Vertigo is more severe and rotary in posterior inferior cerebellar artery territory infarcts, whereas dysarthria and ataxia are prominent in superior cerebellar artery territory infarcts. A few brain stem signs are sometimes added. In these territorial cerebellar infarcts, cardioembolism is the most common cause. Atherosclerotic occlusion comes next, involving the intracranial part of the vertebral artery and, less frequently, the lower basilar artery, both locations inaccessible to surgery. Other causes are artery to artery embolism from a vertebral artery origin stenosis, or the aortic arch, in situ intracranial branch atherosclerotic occlusion, and vertebral artery dissection. Border zone cerebellar infarcts occur in one third of the cases. They are small cortical or deep infarcts. They have the same symptoms and signs as territorial infarcts except for more frequent postural symptoms occurring over days, weeks or months after the ischemic event. The infarcts mainly have a thromboembolic mechanism, and sometimes have a hemodynamic mechanism: 1) focal cerebellar hypoperfusion due to large artery occlusive disease in more than half the cases, 2) small or end (pial) artery disease due to hypercoagulable state (thrombocythemia, polycythemia, hypereosinophilia, disseminated intravascular coagulation), arteritis or intracranial atheroma, and 3) rarely systemic hypotension due to cardiac arrest.
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PMID:[Cerebellar infarctions and their mechanisms]. 809 Oct 85

We report the presenting neurologic and visual symptoms in 17 patients with primary thrombocythemia. Poorly localizing symptoms occurred in 14 patients: transient unsteadiness in 13, dysarthria in eight, and scintillating scotomata in four. Nine patients had focal symptoms: transient monocular blindness in two patients, transient mono- or hemiparesis in six, and both of these in one patient. The attacks all had a sudden onset, occurred sequentially rather than simultaneously, lasted for a few seconds to several minutes, and were usually associated with a dull or pulsatile headache. A causal platelet-mediated arterial thrombosis was evident in 15 patients. There were no recurrences of thrombotic or ischemic events during long-term treatment of 12 patients with aspirin and during cytostatic reduction of platelet count to normal in seven patients. We conclude that low-dose aspirin and reduction of platelet count to normal are effective, but coumarin is ineffective, in the treatment and prevention of arterial thrombosis in thrombocythemia.
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PMID:Transient neurologic and ocular manifestations in primary thrombocythemia. 817 May 52

We report the details of an accidental overdosage of haloperidol in 24 children in one hospital in Kyushu, Japan. Evidence of acute toxicity included disturbances in consciousness (24/24), tremors in the extremities (16/24), an oculogyric or similar crisis (14/24), dysarthria (9/17), drooling (8/24), akathisia (6/20), hyperreflexia (6/24) and opisthotonos (3/24). Laboratory examinations revealed late-onset transient thrombocytosis (5/24), elevated AST and GPT (1/24) and abnormal ECG with prolonged QT interval in 2 of 8 children. We detected haloperidol in 11 of 18 children whose blood was specifically examined within four days after the final haloperidol administration. The maximum serum haloperidol level was 28.9 ng/ml. The mean half-life of haloperidol in the serum of five children (age range 2-10 years) was 18.6 +/- 12.2 h (mean +/- SD) (range 9.1-39.4 h).
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PMID:Acute accidental overdosage of haloperidol in children. 824 51

Neurological symptoms of transient unsteadiness, dysarthria, dysphasia, dysbasia, transient monoor hemiparesis, hemiparesis, scintillating scotomas, amaurosis fugax, vertigo, dizziness, migraine accompaniments, syncope and seizures were the presenting manifestations of thrombocythemia in various myeloproliferative disorders. Erythromelalgia preceded or followed the neurologic ischemic attacks. The neurologic and ocular attacks usually had a sudden onset, lasted for a few seconds to several minutes and occurred independently or sequentially rather than simultaneously. This clinical syndrome is caused by platelet-mediated ischemic and thrombotic processes in the end-arterial microvasculature and reflects the existence of a platelet dependent and aspirin responsive arterial thrombophilia in thrombocythemia as novel disease entity, which confirms and elucidates Mitchell's hypothesis.
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PMID:Atypical transient ischemic attacks in thrombocythemia of various myeloproliferative disorders. 895 74

In 2004, diabetes insipidus was the first clinical sign of Erdheim-Chester disease in our patient. Following introduction of substitution therapy with adiuretin, the patient had no further health complaints for four years until 2008 when he gradually developed dysarthria and, consequently, movement disorder in the form of mild right hemiparesis. The first CNS CT scan (2004) did not reveal any pathology. The first pathological MRI of the brain in 2006 - thickening of pituitary stalk by pathological infiltration to 4-5 mm. During the following year, further infiltrates were detected in the CNS. The number and size of CNS infiltrates increased gradually on MRIs performed repeatedly up to 2008. Erdheim-Chester disease has become suspected based on PET-CT examination at the end of 2008. CT showed irregular structure of the skeleton with noticeable sclerotic foci in otherwise osteoporotic bone structure; changes were the most evident in the long bones of lower limbs, in the pelvic bones, skull and arms, while only one vertebra was affected from within the entire spine. Finding ofthickened aortic wall (up to 8 mm) as another pathological circumstance was consistent with the Erdheim-Chester disease-associated changes described as coated aorta. CT scan revealed clear fibrotic changes in the area of retroperitoneum. Applied fluorodeoxyglucose has accumulated in the bone foci described on CTscans as well as in the thickened wall ofthe thoracic and abdominal aorta (SUV 3.6). Tc-pyrophosphonate skeleton scintigraphy showed the same bone foci as PET-CT. Full body MRI showed pathological signal from the bone marrow of the above mentioned locations, particularly during STIR imagining, where there was clear abnormal signal corresponding to accumulated histiocytes, the higher signal of which was well-differentiated from the normal bone marrow. Measurement of bone mineral density with DEXA confirmed reduced density in lumbar vertebrae to the average value of - 2.7 SD (the lowest value was -3.1SD). The disease is associated with elevated inflammatory parameters: leucocytosis, thrombocytosis, elevated CRP and fibrinogen levels. Diagnosis was verified following histological assessment ofiliac bone marrow, where focal infiltrations with foamy histiocytes of typical immunophenotype (CD68+, CD1a-, S100-) were confirmed. Treatment was initiated with chemotherapy consisting of 2g/m2 of cyclophosphamide on day 1 and 200 mg/m2 of etoposide IV infusion on days 1-3, and followed by administration of 5 microg/kg of G-CSF and collection of haematopoietic peripheral blood stem cells (PBSC). PBSC collection was followed by 5-day administration of 5 mg/m2/day of 2-chlorodeoxyadenosine (Litac) administered to the patient at monthly intervals.
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PMID:[Diabetes insipidus followed, after 4 years, with dysarthria and mild right-sided hemiparesis--the first clinical signs of Erdheim-Chester disease. Description and depiction of a case with a review of information on the disease]. 2007 34

A 47-year-old female with a prior history of POEMS (polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes) syndrome was admitted with transient ischemic attacks complicated by dysarthria and right-sided hemiparesis. A blood survey indicated thrombocytosis and hyperfibrinogenemia while imaging of intracranial vasculature showed occlusion of the bilateral middle cerebral arteries. POEMS syndrome, of which arterial thromboses have been mentioned as a manifestation, is rarely accompanied by transient ischemic attacks. The pathophysiologic mechanism is yet unclear and needs further investigation.
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PMID:Recurrent Transient Ischemic Attacks in a Patient with POEMS Syndrome. 2471 13