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 two cases of reversible brainstem hypertensive encephalopathy (RBHE) with unusual magnetic resonance (MR) findings. Patient 1, an 85-year-old man without a history of hypertension, developed acute severe hypertension and mild consciousness disturbance as the only symptoms. Patient 2, a 46-year-old man with an untreated hypertension, presented with extremely high blood pressure and general fatigue, vertigo, and mild dysarthria as the initial manifestations. In these patients, fluid-attenuated inversion recovery (FLAIR) and T2-weighted MR images revealed diffuse hyperintensities in the brainstem. Diffusion-weighted imaging (DWI) findings were normal, and apparent diffusion coefficient (ADC) values were increased in the brainstem. The supratentorial regions were largely spared, and mildly diffuse hyperintensities were noted in the white matter. There were no accompanying changes in the occipital lobe and cerebellum. The lesions completely resolved after stabilization of blood pressure. The normal DWI findings and high ADC values were consistent with vasogenic edema due to severe hypertension. The characteristics of RBHE are a very high blood pressure, mild clinical and neurologic symptoms, rapidly improved MR findings after initial treatment with the control of hypertension, and a marked clinicoradiologic dissociation.
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PMID:Reversible brainstem hypertensive encephalopathy (RBHE): Clinicoradiologic dissociation. 1867 82

Cavernous angiomas comprise 5-10% of all vascular malformations in the central nervous system, occurring most frequently in the supratentorial region, and 20% of them in the brain stem. According to literature, brain stem cavernous angiomas occur most frequently in the pons (60%), and equally in the mesencephalon (20%) and in medulla oblongata. In clinical evaluation the authors describe the successful removal of a mesencephalic cavernous angioma causing progressive neurological deficits and symptoms. The authors present a case of a 51 year old female, who had developed 1 year prior to her admittance: fatigue, weakness in the right upper limb and fingers, right lower limb ataxia. One month later, her lower right limb developed sensory deficits. The first neurological exploration indicated dysarthria, moderate facial and right hemiparesis, hemihypaesthesia and ataxia. CT and MR imaging indicated multilobulated cavernomas in the mesencephalon. After conservative treatment the patient became almost symptom free, and thus neurosurgical treatment was not discussed. Later on her symptoms fluctuated, but after 6 month she suddenly developed progressive right hemiparesis, right facial weakness, serious dysphasia, and emotional incontinence combined with continuous spastic sobbings. The control MRI showed enlargement of the cavernomas and new extravasation. Surgery was indicated for removing the cavernomas. The left infratentorial, supracerebellar approach revealed a blood engorged cavernoma in the center of the mesencephalon, almost dividing it. The cavernomas and accompanying haematoma was extirpated. The patient's neurological symptoms rapidly improved after surgery, her dysphasia as well as motor weakness have disappeared. Six days after surgery, we discharged a neurologically symptomless and self-supporting patient. The literature and the presented case indicates that the correct timing and proper surgery allows brain stem cavernomas to be safely removed, or significantly bated, which results in the massive regression of neurological symptoms.
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PMID:[Successful surgical removal of a mesencephalic cavernous angioma, which was responsible for progressive neurological deficits]. 1876 80

A 56-year-old man with diabetes mellitus and alcoholic liver cirrhosis was admitted on an emergency basis to our hospital for further examination of headache, general fatigue and dysarthria. He had been treated with antifungal drugs on the suspicion of pulmonary mycosis. Brain MRI revealed multiple cerebellar abscesses with ring enhancement. Due to depression of mental status despite medical treatment, he underwent suboccipital craniotomy and enucleation of the cerebellar abscess, resulting in marked improvement of consciousness level. As the culture of his abscess content yielded Nocardia farcinica, the definite diagnosis of Nocardial cerebellar abscesses and pulmonary Nocardiosis were made. Pulmonary Nocardiosis improved by oral co-trimoxazole treatment. Moreover, no recurrence of cerebellar abscesses was evident. This case indicates that the possibility of Nocardial infection should be considered in the immuno-compromised hosts.
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PMID:[Pulmonary nocardiosis complicated with multiple cerebellar abscess]. 1919 10

Infection of the central nervous system with Nocardia sp. usually manifests as supratentorial abscesses. Supratentorial and cerebellar abscesses from infection with Nocardia sp. following immunosuppression with long-term corticosteroids for idiopathic thrombocytopenia (ITP) have not been reported. An 83 years-old, human immunodeficiency virus (HIV)-negative, polymorbid male with ITP for which he required corticosteroids since age 53 years developed tiredness, dyspnoea, hemoptysis, abdominal pain, and progressive gait disturbance. Imaging studies of the lung revealed an enhancing tumour in the right upper lobe with central and peripheral necrosis, multiple irregularly contoured hyperdensities over both lungs, and right-sided pleural effusions. Sputum culture grew Nocardia sp. Neurological diagnostic work-up revealed dysarthria, dysphagia, ptosis, hypoacusis, tremor, dysdiadochokinesia, proximal weakness of the lower limbs, diffuse wasting, and stocking-type sensory disturbances. The neurological deficits were attributed to an abscess in the upper cerebellar vermis, myopathy from corticosteroids, and polyneuropathy. Meropenem for 37 days and trimethoprime-sulfamethoxazole for 3 months resulted in a reduction of the pulmonary, but not the cerebral lesions. Therefore, sultamicillin was begun, but without success. Long-term therapy with corticosteroids for ITP may induce not only steroid myopathy but also immune-incompetence with the development of pulmonary and cerebral nocardiosis. Cerebral nocardiosis may not sufficiently respond to long-term antibiotic therapy why switching to alternative antibiotics or surgery may be necessary.
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PMID:Cerebellar nocardiosis and myopathy from long-term corticosteroids for idiopathic thrombocytopenia. 2004 27

Bulbar weakness and fatigue resulting in dysphagia and dysarthria is common in myasthenia gravis. In chronic MG it is often assumed that these symptoms herald an exacerbation of the patient's disease and doses of cholinergic agents and immunomodulatory therapies may be increased, along with initiation of plasma exchange. A case is presented in which dysphagia was refractory to standard MG therapy, leading to the subsequent discovery of cricopharyngeal sphincter achalasia as the primary cause of the patient's symptoms rather than an assumed myasthenia gravis exacerbation. The patient's dysphagia resolved after esophageal dilatation. Cricopharyngeal sphincter achalasia is a common disorder producing dysphagia in the elderly and needs to be considered in the evaluation of a myasthenic patient with worsening dysphagia when standard myasthenia gravis therapy fails. Discussion of myasthenia gravis, cholinergic therapy and cricopharyngeal sphincter achalasia is undertaken. Clinicians are encouraged to consider non-neurologic causes of worsening dysphagia in the myasthenic patient.
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PMID:Reversible oropharyngeal dysphagia secondary to cricopharyngeal sphincter achalasia in a patient with myasthenia gravis: a case report. 2018 78

A 72-year-old woman was admitted to a local hospital with general fatigue, ptosis and dysarthria. Her anti-AchR antibody titer was high, so myasthenia gravis was diagnosed. She was given a cholinesterase inhibitor, but her symptoms did not improve. CT and MRI scans revealed a mass in the anterior mediastinum infiltrating the superior vena cava (SVC) and the right atrium (RA) . The diagnosis was an invasive thymoma extending into the SVC and the RA. Moreover, there was a mass in the right middle lobe of her lung, which was suspected to be the result of metastasis of the thymoma. She was transferred to our hospital for medication and surgery for the invasive thymoma. Urgent surgery was performed without preoperative therapy, because the tumor was nearly obstructing her tricuspid valve. An expanded thymomectomy and a right middle lobectomy were performed. As the tumor had infiltrated into the SVC, the SVC was replaced with an artificial graft. The clinicopathological diagnosis of thymoma (Masaoka Stage IVb) was given. The patient had a myasthenic crisis for several weeks after surgery, so her breathing was controlled by an artificial respirator. Her symptoms improved after treatment with steroids, tacrolimus and a cholinesterase inhibitor. Although major surgery was required to prevent tumor embolism, the patient survived. Careful observation is necessary to detect signs of relapse of invasive thymoma.
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PMID:[A case of myasthenia gravis with an invasive thymoma infiltrating the superior vena cava and right atrium and causing lung metastasis]. 2047 80

Multiple sclerosis (MS) is the most frequent demyelinating disease of the central nervous system, with versatile manifestations--relapsing-remitting or progressive--and an unpredictable course, with prognoses ranging from minimal neurological impairment to severely disabled. Disease modifying agents can minimize relapse rate and slow disease progression. Yet most patients suffer relapses and progression despite use of these agents. Several of the manifestations of MS may cause overall decrease in the performance of the aviator. These include cognitive impairment, fatigue, and depression. Episodes of spasms, dysarthria, ataxia, parasthesias, diplopia, and hemiplegia, as well as drug side effects may also affect flight. Seizures and episodes of vertigo may occur suddenly and result in in-flight incapacitation. We present our experience with two aviators with definite MS and a navigator with probable MS. The various manifestations of MS are specifically addressed with an emphasis on the aeromedical implications.
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PMID:Return to flight with multiple sclerosis: aeromedical considerations. 2123 9

Symptoms management in multiple sclerosis is an integral part of its care. Accurate assessment and addressing the different symptoms provides increased quality of life among patients with multiple sclerosis. Multiple sclerosis symptoms may be identified as primary, secondary, or tertiary symptoms. Primary symptoms, such as weakness, sensory loss, and ataxia, are directly related to demyelination and axonal loss. Secondary symptoms, such as urinary tract infections as a result of urinary retention, are a result of the primary symptoms. Tertiary symptoms, such as reactive depression or social isolation, are a result of the social and psychological consequences of the disease. Common multiple sclerosis symptoms include fatigue and weakness; decreased balance, spasticity and gait problems; depression and cognitive issues; bladder, bowel, and sexual deficits; visual and sensory loss; and neuropathic pain. Less-common symptoms include dysarthria and dysphagia, vertigo, and tremors. Rare symptoms in multiple sclerosis include seizures, hearing loss, and paralysis. Symptom management includes nonpharmacological methods, such as rehabilitation and psychosocial support, and pharmacological methods, ie, medications and surgical procedures. The keys to symptom management are awareness, knowledge, and coordination of care. Symptoms have to be recognized and management needs to be individualized. Multiple sclerosis therapeutics include nonpharmacological strategies that consist of lifestyle modifications, rehabilitation, social support, counseling, and pharmacological agents or surgical procedures. The goal is vigilant management to improve quality of life and promote realistic expectations and hope.
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PMID:Therapeutics for multiple sclerosis symptoms. 2142 63

Soporific acute hyperammonemic hepatic encephalopathy (aHE) can induce considerable changes in cerebral white and gray matter. This report describes a patient in the subacute phase of aHE grade I without disturbed consciousness and with reversible fine laminar cortical involvement on magnetic resonance imaging (MRI). The 59-year-old patient had esophageal varices bleeding due to primary biliary cirrhosis (ammonium blood level: 140 mmoL/L) and presented with sensory Jacksonian seizures, dysarthria, and increased drowsiness and fatigue. MRI revealed patchy hyperintense (T2-weighted, T2w) white-matter lesions and bilateral signal intensities in the striatum (T1w). During a rise of ammonium blood level to 220 mmoL/L, the patient had increased drowsiness, persistent dysarthria and mild temporary hemiparesis without loss of consciousness. Two weeks later, the patient was asymptomatic and blood ammonium level had reverted to normal value. MRI at that time revealed bihemispheric fine laminar subcortical hyperintensities on T2w and fluid-attenuated inversion recovery (FLAIR) imaging, and partially on T1w sequences, with no swelling or restricted diffusion; the hyperintensities were fully reversible a month later. Such a distinct cortical signal increase not only on T2w images, but also on T1w, in a patient after a mild form of aHE is a new MR finding.
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PMID:Reversible laminar signal intensity in deep cortical gray matter in T1-weighted images and FLAIR after mild acute hyperammonemic hepatic encephalopathy. 2265 36

Environmental contamination has exposed humans to various metal agents, including mercury. This exposure is more common than expected, and the health consequences of such exposure remain unclear. For many years, mercury was used in a wide variety of human activities, and now, exposure to this metal from both natural and artificial sources is significantly increasing. Many studies show that high exposure to mercury induces changes in the central nervous system, potentially resulting in irritability, fatigue, behavioral changes, tremors, headaches, hearing and cognitive loss, dysarthria, incoordination, hallucinations, and death. In the cardiovascular system, mercury induces hypertension in humans and animals that has wide-ranging consequences, including alterations in endothelial function. The results described in this paper indicate that mercury exposure, even at low doses, affects endothelial and cardiovascular function. As a result, the reference values defining the limits for the absence of danger should be reduced.
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PMID:Toxic effects of mercury on the cardiovascular and central nervous systems. 2281


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