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)

A 38-year-old man gradually developed gait instability, dysarthria, and dysphagia over two months associated with an elevated blood pressure after starting hemodialysis therapy for diabetic nephropathy. Brain MRI studies indicated vasogenic edema in the brainstem, extending from the lower midbrain to the upper medulla oblongata. The patient's high blood pressure was refractory to treatment, and his neurological disabilities and MRI abnormalities progressed. FDG-PET, MR spectroscopy, and cerebrospinal fluid studies did not suggest neoplastic pathologies. The patient was diagnosed with a brainstem variant of reversible posterior leukoencephalopathy syndrome, and received three courses of steroid pulse therapy. After the pulse therapy, the clinical manifestations and MR findings improved. By maintaining strict management of blood pressure and body water balance during hemodialysis, he did not experience any further clinical exacerbation, and the lesion on MR images continued to regress. Ten months after the pulse therapy, T1-weighted images showed slightly hyperintense signal. This case suggests that reversible posterior leukoencephalopathy syndrome (RPLS) may take a chronic clinical course without acute onset.
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PMID:[Brainstem variant of reversible posterior leukoencephalopathy syndrome with a prolonged clinical course: a case report]. 1908 30

Antemortem diagnosis of isolated inner ear infarction remains a diagnostic challenge since current imaging techniques do not permit differentiation of isolated labyrinthine infarction from other more benign disorders involving the inner ear. An 81-year-old woman with diabetes, hypertension and hypercholesterolemia presented with vertigo and hearing loss. Initial examination revealed findings of left cochleovestibular labyrinthitis without brainstem or cerebellar signs. MRIs including the diffusion-weighted images were normal. Five days later, however, she developed dysarthria, and decreased facial sensation, subtle facial palsy, and dysmetria in the left side. Follow-up MRI was consistent with acute infarctions in the territory of anterior inferior cerebellar artery (AICA), involving the left lateral pons, left middle cerebellar peduncle, and inferolateral cerebellum. AICA infarction should be considered in acute audiovestibular syndrome, especially in aged patients with vascular risk factors, even though the classic brainstem or cerebellar signs are absent.
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PMID:Progression of acute cochleovestibulopathy into anterior inferior cerebellar artery infarction. 1910 52

Lacunar infarcts or small subcortical infarcts result from occlusion of a single penetrating artery and account for one quarter of cerebral infarctions. Patients with a lacunar infarct usually present with a classical lacunar syndrome (pure motor hemiparesis, pure sensory syndrome, sensorimotor stroke, ataxic hemiparesis or dysarthria-clumsy hand) and, less frequently, an atypical lacunar syndrome. Hypertension and diabetes mellitus are major risk factors for lacunar stroke. Lacunar infarcts show a paradoxical clinical course with a favorable prognosis in the short term, characterized by a low early mortality and reduced functional disability on hospital discharge, but with an increased risk of death, stroke recurrence and dementia in the mid- and long term. Asymptomatic progression of small-vessel disease is a typical feature of the lacunar infarcts. For this reason, lacunar infarction should be regarded as a potentially severe condition rather than a relatively benign disorder and, therefore, lacunar stroke patients require adequate and rigorous management and follow-up. Antiplatelet drugs, careful blood pressure control, the use of statins and modification of lifestyle risk factors are key elements in secondary prevention after lacunar stroke.
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PMID:Lacunar stroke. 1921 Jan 94

A 39-year-old man who presented with unilateral proptosis and periocular pain rapidly developed reduced consciousness, facial numbness, dysarthria, and gait ataxia from a direct carotid-cavernous fistula (CCF) with drainage into posterior fossa veins. Brain MRI revealed abnormal signal throughout the brainstem, indicative of venous hypertension and edema. Closure of the fistula by detachable balloon eliminated the clinical and imaging abnormalities. This is the fifth reported case of brainstem complications of a direct CCF. It highlights potentially serious complications of this condition and their reversibility with prompt treatment.
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PMID:Direct carotid-cavernous fistula causing brainstem venous congestion. 1945 71

It has become increasingly apparent, especially with the advent of MRI brain scanning, that a large number of patients develop signal intensity changes in the subcortical white matter and periventricular region as they age. This appears to be accelerated by risk factors for small vessel cerebrovascular disease such as hypertension, smoking, diabetes mellitus and hyperlipidemia. The major question becomes when such changes become clinically significant. It is obvious that subcortical lacunar-type infarction can be identified by the clinical presentation. For example, typical examples of so-called "lacunar syndrome" include pure motor hemiparesis, pure sensory stroke, sensorimotor stroke, clumsy hand-dysarthria, and hemiataxia-hemiparesis. The issue becomes a measure of impact on functional ability. This is influenced by several factors. Baseline IQ and educational level, as well as expectations of age, certainly play a role. A person who develops cognitive impairment and long tract signs in their 50s or 60s is certainly going to be recognized as more impaired than an 80 year old individual who is retired and primarily is engaged in recreational activity. It would be expected that a person born with limited intellectual capacity and/or limited educational opportunity would be less likely to be identified as impaired than a person who has achieved substantial economic achievement through their innate talents. The concept of tissue loss or lesion load becomes important when determining how pronounced the ischemic cerebrovascular changes translate into functional impairment. Correlative pathology may include cortical atrophy and ventricular dilatation. Loss of either cortical or subcortical tissue function is expected to be related to functional compromise. In addition, there are potential features such as the coexistence of small vessel cerebrovascular disease and Alzheimer's disease. Small vessel cerebrovascular disease might also play a contributing factor in patients susceptible to Dementia with Lewy Bodies or patients susceptible to fronto-temporal dementia or any other dementing process. Thus, the concept of tissue loss or lesion burden of disease becomes increasingly important as we recognize the potential for multifactorial issues, including genetic factors, to contribute to the phenotypic expression. The relationships between cognitive impairment, dementia and subcortical vascular lesions are poorly understood. There have been several papers on the different aspects of cerebral insults and their impact on cognition, the various kinds of dementia and different methods of analyzing the impact of the various insults to the brain. This chapter is an attempt to review all pertinent information currently available on the poorly understood condition of "subcortical ischemic cerebrovascular dementia."
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PMID:Subcortical ischemic cerebrovascular dementia. 1950 11

A 77-year old man who consulted due to left arm weakness and dysarthria. He reported having been diagnosed of high blood pressure and that he was taking enalapril/hydrochlorothiazide without adequate blood pressure control. He had smoked 2 packs of cigarettes a day and continues to smoke at present. He was admitted to the emergency service about 90 min after the onset of his symptoms. He did not report headache, nausea or vomiting. His BP was 182/104 mmHg, with irregular pulse at 88 beats per minute. The neurological examination revealed dysarthria, left homonymous hemianopsia, muscle weakness and hypoesthesia of the left limbs. How should this patient be evaluated and treated?
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PMID:[Cardioembolic stroke]. 2016 14

Toxic leukoencephalopathy has been more thoroughly investigated during the last decade because of the advance of magnetic resonance imaging (MRI) techniques. We analyzed fludarabine (Flu)-associated hematopoietic cell transplantation (HCT), resulting in severe leukoencephalopathy (n = 39/1596, 2.4%), and describe 3 clinical syndromes with unique clinical and radiographic characteristics. Posterior reversible encephalopathy syndrome (PRES) presents predominantly with seizures, persistent headache, and vision changes, along with variable mental status alterations. PRES is likely to be reversible, particularly after withholding cyclosporine (CsA). Acute toxic leukoencephalopathy (ATL) presents with cognitive dysfunction, decreased levels of consciousness, and vision changes. Other leukoencephalopathy (OLE) includes patients who behave similar to the ATL group, but with less prominent deep white matter changes on MRI. ATL and OLE are less likely to be reversible. The neurologic syndromes correlate with different MRI patterns. In PRES, subcortical and cortical involvement on MRI is associated with seizure, blurred vision, and dysarthria versus ATL and OLE, which involve deep white matter and cause mainly cognitive dysfunction. The different syndromes also carry different prognoses. All patients with Flu-associated encephalopathy had a median overall survival of only 169 days. Those with ATL had shorter overall survival (median 66 days) than patients with PRES (median 208 days). Potential risk factors for Flu-associated encephalopathy were older age, poor renal function, Flu dose, previously treated central nervous system (CNS) disease, or previous Flu-based transplant conditioning. Additional risk factors for PRES CNS toxicity are CsA use and acute hypertension. Flu pharmacokinetic studies may be useful to reduce life-threatening Flu-associated risks of neurotoxicity.
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PMID:Toxic leukoencephalopathy following fludarabine-associated hematopoietic cell transplantation. 2039 78

We report a case of branch atheromatous disease (BAD) presenting capsular warning syndrome, who subsequently showed a complete recovery by the combination therapy as described below. A 54-year-old man with untreated hypertension was admitted to our hospital because of dysarthria and right hemiplegia. The NIHSS on admission was 12 points, but his symptoms soon completely disappeared during examination. After admission administration of aspirin, heparin, atorvastatin and t-PA were started, but stereotyped episodes of dysarthria and the right hemiplegia occurred repeatedly. We added plasma expander, and he thereafter revealed no further ischemic episodes at 22 hours from admission. Over all, he had 15 times of transient ischemic attack with no lasting deficit. The DWI scan obtained 5 hours after the onset demonstrated a high-intensity region in the left putamen to corona radiata. MRA showed no significant abnormalities. He had been diagnosed as having branch atheromatous disease with capsular warning syndrome. The present case suggests that combination therapy including t-PA and plasma expander may be effective to BAD presenting capsular warning syndrome.
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PMID:[Case of branch atheromatous disease presenting capsular warning syndrome]. 2053 81

A 34-year-old Thai woman developed acute left hemiparesis with dysarthria from subcortical infarction of the right MCA territory eighteen months after being diagnosed with Noonan syndrome, diabetes mellitus, dyslipidaemia, and hypertension. Further investigations suggested atherosclerosis as a cause. Modifying her risk factors was difficult, partly because of limited adherence. Three years later, she had another attack of ischaemic stroke in the same area. Unlike the three previously reported cases, the causation of strokes in this patient appeared to be a more 'complex' interaction between genetic defect and environment including possible subtle arterial abnormalities, metabolic risk factors, and mental insufficiency.
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PMID:Noonan syndrome, metabolic syndrome and stroke-in-the-young: coincidence, causal or contribution? 2087 82

We present a case of tacrolimus-induced encephalopathy after successful kidney transplantation. An 11-year-old girl presented with sudden onset of neurologic symptoms, hypertension, and psychiatric symptoms, with normal kidney function, after kidney transplantation. The symptoms improved after cessation of tacrolimus. Magnetic resonance imaging (MRI) showed acute infarction of the middle cerebral artery (MCA) territory in the right frontal lobe. Three days later, she had normal mental function and maintained normal blood pressure with left hemiparesis. Follow-up MRI was performed on D19, showing new infarct lesions at both cerebral hemispheres. Ten days later, MRI showed further improvement, but brain single photon emission computed tomography (SPECT) showed mild reduction of uptake in both the anterior cingulate gyrus and the left thalamus. One month after onset of symptoms, angiography showed complete resolution of stenosis. However, presenting as a mild fine motor disability of both hands and mild dysarthria, what had been atrophy at both centrum semiovale at 4 months now showed progression to encephalomalacia. There are two points of interest in this case. First, encephalopathy occurred after administration of tacrolimus and improved after discontinuation of the drug. Second, the development of right-side hemiplegia could not be explained by conventional MRI; but through diffusion tensor imaging (DTI) and diffusion tensor tractography (DTT) of white matter tract, visualization was possible.
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PMID:A case of tacrolimus-induced encephalopathy after kidney transplantation. 2135 60


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