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)

Neurocysticercosis is the most frequent parasitosis of central nervous system in the world. Neurological manifestations are in relation with locations number and topography, inflammatory reactions level and state of development of the parasite. Epilepsy is the main revealing symptom. Among other neurological manifestations, chronic headache, focal neurological signs, ataxia, language and behaviour disorder are the most anecdotal. The authors report a case of neurocysticercosis in a 71-year-old man with dysarthria and memory problems. Suspected by computed tomography, diagnosis was confirmed by immunoserologic assays such as enzyme-linked immunosorbent assay (ELISA) or enzyme-linked immunoelectrotransfer blot assay (EITB). This later emphasized on active form of the cyst. Specific treatment used albendazole as antihelminthic drug. Clinical evolution was good: neuroimaging and immunoserology results were normal respectively 2 and 6 months after the drug therapy.
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PMID:[Diagnosis of neurocysticercosis: a case report]. 1247 50

Neuropsychiatric complications after liver transplantation are common and have an incidence ranging from 0.5% to 47% in several international reports. They are due to different causes (coagulation, haemodynamic or electrolyte disorders, infections, immunosuppressive drugs). In patients receiving cyclosporin and tacrolimus, headache, tremors, dysarthria, seizures and delirium are the most common disorders and are not always related to toxic drug concentrations or overdosage. We report the case of a liver transplant patient receiving cyclosporin who presented a state of lucid delirium with a mystic persecutory content. in the first few postoperative days. Cyclosporin was withdrawn and the patient switched to tacrolimus, initially combined with chlorpromazine and later with clotiapine. She rapidly improved and recovered completely within a few days. At follow-up the patient is doing well and can remember the episode of delirium perfectly well. Psychiatric evaluation preoperatively and during follow-up is important to recognize and treat these complications, which can prevent the full recovery of transplanted patients and also increase the cost of this procedure.
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PMID:[State of lucid delirium after orthotopic liver transplantation. Clinical case]. 1261 41

A 38-year-old man was admitted to our hospital with headache, dysarthria and paraparesis. Brain CT and diffusion MRI disclosed cerebral infarction at bilateral anterior cerebral artery (ACA) territories. His symptoms and signs deteriorated in several days despite intensive antithrombotic therapy, resulting in right hemiparesis, akinetic mutism, memory disturbance, change of personality, urinary incontinence, forced grasping, and starting delay of speech and motion. Cerebral angiography demonstrated occlusion with contrast pooling at the right ACA A2 portion. Stenosis and dilatation were found at left ACA A2 portion. An intimal flap was also demonstrated on serial angiography. This case was diagnosed as cerebral infarction caused by dissection of bilateral ACA. Although no definite primary arteriopathy was demonstrated, bilateral dissection could be occurred simultaneously.
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PMID:[A case of juvenile cerebral infarction caused by bilateral anterior cerebral artery dissection]. 1266 Nov 8

A 41-year-old woman presented with tinnitus in the left ear and headache, followed by diplopia and pain in the left cheek. Angiography showed a left high-flow direct carotid-cavernous fistula (CCF), causing steal of the blood flow from the internal carotid artery into the cavernous sinus. A few days later, she rapidly developed right hemiparesis, dysarthria, and ocular conjugate deviation to the right, and became somnolent. Angiography at that time revealed occlusion of the superior petrosal sinus, causing engorgement of the veins in the surrounding brainstem. The CCF was completely embolized with interlocking detachable coils. Her consciousness disturbance and ophthalmoparesis dramatically improved within a few days, and the right hemiparesis and dysarthria gradually resolved. Magnetic resonance (MR) imaging after the treatment showed small pontine hemorrhage and perifocal edema but no ischemic lesions in the cerebral hemisphere. Re-evaluation of the MR imaging with gadolinium taken on admission demonstrated engorged veins in the brainstem parenchyma, which corresponded to the hemorrhagic lesion in the brainstem. Brainstem congestion caused by direct CCF is very rare, but it can be life-threatening. Good outcome can be expected if the CCF is completely occluded before congestive hemorrhage occurs.
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PMID:Brainstem congestion caused by direct carotid-cavernous fistula--case report. 1279 Feb 86

Although there have been attempts to make clinical-MRI correlation in patients with lateral medullary infarction (LMI), studies with a large number of patients are unavailable. In this study, clinical features, MRI findings and angiogram results of 130 acute, consecutive patients with pure LMI were studied and correlated. MRI-identified lesions were classified rostro-caudally as rostral, middle and caudal, and horizontally as typical, ventral, large, lateral and dorsal. The distribution of horizontal subtypes was significantly different (P <0.001) among three rostro-caudal lesions in that rostral lesions tend to be ventral types and caudal lesions are lateral types. Patients with rostrally located lesions had dysphagia, facial paresis (P < 0.01, each) and dysarthria (P < 0.05) significantly more often, and severe gait ataxia and headache (P < 0.05, each) less often than those with caudal lesions. The frequencies of dysphagia (P < 0.01), dysarthria (P < 0.01) and bilateral trigeminal sensory pattern (P < 0.05) were significantly different among horizontal subtypes in that these symptoms were frequent in patients with "large type" as compared with those with lateral type lesions. Angiograms performed in 123 patients showed vertebral artery (VA) disease in 67% and posterior inferior cerebellar artery (PICA) disease in 10%. The presumed pathogenetic mechanisms included large vessel infarction in 50%, arterial dissection in 15%, small vessel infarction in 13% and cardiac embolism in 5%. Dissection occurred more often in patients with caudal (versus rostral) lesions (P < 0.01), whereas dorsal type infarcts (versus other types) were related more often to cardiogenic embolism and normal angiogram findings (P < 0.05, each). Patients with isolated PICA disease (versus those with VA disease) more often had cardiogenic embolism (P < 0.05) and less often had dissection (P < 0.01). It is concluded that rostro-caudal and horizontal classification of MRI helps us to understand the clinical and, partly, the aetiopathogenetic aspect of the heterogeneous LMI syndrome.
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PMID:Pure lateral medullary infarction: clinical-radiological correlation of 130 acute, consecutive patients. 1280 95

Delayed traumatic intracranial hemorrhage (DTICH) is seen mostly in trauma to the occipitoparietal region by countercoup mechanism. It is most encountered within the first posttraumatic 10 days, particularly in the first 3. Herein, two cases of delayed traumatic intracerebral hemorrhage were discussed, first one presented with headache and vomiting who had been asymptomatic for 168 days after head trauma and the other presented with dysarthria and hyperkynesias after 92 days of asymptomatic interval, either being longer than that of the previous cases reported in the literature. Despite a long time elapse, DTICH should be considered in the differential diagnosis in the patients with history of head trauma that manifests at later stages with intracranial pressure elevation symptoms such as headache, vomiting.
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PMID:Asymptomatic interval in delayed traumatic intracerebral hemorrhage: report of two cases. 1286 May 5

A patient with Schmidt's syndrome and atypical symptoms of Addison's disease is presented. Autoimmune thyroiditis was diagnosed at the age of 12 years and then at 15 years; a diagnosis of migraine was made following 10 days of headache, visual field defects and dysarthria. One week later the patient was admitted to hospital in critical condition. Addison's disease was diagnosed and replacement therapy was introduced which brought about a rapid clinical improvement. Positive adrenal autoantibodies confirmed the diagnosis. We suggest that patients with organ-specific autoimmune disease undergo annual screening for adrenal activity, and in the event of abnormal results, adrenal autoantibody evaluation should be carried out, to avoid a life-threatening crisis caused by Addison's disease, which is often difficult to recognize due to atypical clinical presentation, as in the patient reported here.
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PMID:Unusual presentation of Addison's disease in Schmidt's syndrome. 1288 Jan 29

Long-term exposure to carbon disulfide (CS(2)) may induce diffuse encephalopathy with parkinsonism, pyramidal signs, cerebellar ataxia, and cognitive impairments, as well as axonal polyneuropathy. The pathogenic mechanisms of diffuse encephalopathy are unclear, although vasculopathy and toxic demyelination have been proposed. Recently, we have encountered a patient who developed headache, limb tremors, gait disturbance, dysarthria, memory impairment, and emotional lability after long-term exposure to CS(2). The brain magnetic resonance images (MRI) showed diffuse hyperintensity lesions in T(2)-weighted images in the subcortical white matter, basal ganglia, and brain stem. The brain computed tomography perfusion study revealed a diffusely decreased regional cerebral blood flow and prolonged regional mean transit time in the subcortical white matter and basal ganglion. To our knowledge, there have been few reports demonstrating diffuse white matter lesions in chronic CS(2) encephalopathy using brain MRI. In addition, the (99m)Tc-TRODAT-1 single photon emission computed tomography showed a normal uptake of the dopamine transporter, indicating a normal presynaptic dopaminergic pathway. We conclude that diffuse white matter lesions may develop after chronic exposure to CS(2), possibly through microangiopathy. In addition, CS(2) poisoning can be considered as one of the causes of chronic leukoencephalopathy.
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PMID:Diffuse white matter lesions in carbon disulfide intoxication: microangiopathy or demyelination. 1463 66

The baroreflex maintains blood pressure through the glossopharyngeal (IX) cranial nerve. We report a 54-year-old man who developed a left sided headache, hoarseness, dysarthria, dysphagia, and sustained hypertension from a left internal carotid artery dissection. We hypothesise that interruption of the left IX nerve caused hypertension in this patient.
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PMID:Left internal carotid artery dissection presenting with headache, Collet-Sicard syndrome and sustained hypertension. 1464 21

Bruxism characterized by clenching and grinding of teeth can lead to toothwear, headaches and depression. While bruxism has been associated with a number of neurological diseases, it has not been highlighted following cerebral infarction. An elderly man presented with an acute onset of tooth grinding and jaw clenching associated with dysarthria. His bruxism was worse during the day and resolved during sleep. He had frequent jaw aches, headaches and swallowing difficulty. Examination demonstrated the presence of dysarthria with jaw clenching and tooth grinding, producing persistent high pitch and loud squeaky sounds. A magnetic resonance imaging and angiography examination revealed a recent infarct in the right thalamus. In addition, chronic lacunar infarcts were present in the bilateral caudate nuclei with severe basilar artery stenosis. He was successfully treated with botulinum toxin. We discuss the pathophysiologic mechanisms of bruxism associated with basal ganglia infarcts. Dysfunction of the efferent and/or afferent thalamic or striatopallidal tracts may play a role in bruxism. Early recognition of bruxism following stroke could reduce unnecessary suffering since the condition can be effectively treated.
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PMID:Severe bruxism following basal ganglia infarcts: insights into pathophysiology. 1470 29


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