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)

The common signs of hypoglycemia include: tachycardia, diaphoresis and vertigo which may be associated to disturbances of the consciousness. Occasionally, focal neurological signs occur with conservation of consciousness which are erroneously interpreted as cerebral vascular disease. An insulin dependent diabetic patient is presented with an initial diagnosis of transient ischemic attack (TIA) with right hemiparesis and dysarthria associated to hypoglycemia (35 mg %) whose remission occurred following the correction of glycemia. The different physiopathogenic mechanisms were also revised postulating (selective neuronal vulnerability, vasospasms and subjacent vascular disease) and the need for considering this diagnosis must be emphasized in those diabetic patients with focal neurological symptoms.
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PMID:[Hypoglycemic hemiparesis]. 161 Jun 4

The central anticholinergic syndrome (CAS) includes central signs (somnolence, confusion, amnesia, agitation, hallucinations, dysarthria, ataxia, delirium, stupor, coma) and peripheral signs (dry mouth, dry skin, tachycardia, visual disturbances and difficulty in micturition). It occurs when central cholinergic sites are occupied by specific drugs and also as a result of an insufficient release of acetylcholine. The CAS can be caused by atropine sulphate, hyoscine (scopolamine), promethazine, benzodiazepines, opioids, halothane, influrane, ketamine. The incidence of CAS during the postoperative period depends on choice and dose of anaesthetic agents, type of surgery, patient's condition and diagnostic criteria. It is close to 10% following general anaesthesia and 4% following regional anaesthesia with sedation. The differential diagnosis of CAS includes an overdose of anaesthetic drugs or an alteration in pharmacokinetics, altered hydratation, electrolyte or acid-base state, hypoglycaemia, hypoxia, hypercapnia, hypocapnia, hyperthermia, hypothermia, hormonal disorders, neurological damage resulting from surgery, embolism, haemorrhage or trauma. The diagnosis of CAS is often determined by a process of exclusion and not actually made until a positive therapeutic response to physostigmine, a centrally active anticholinesterase agent has taken place.
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PMID:[Central anticholinergic syndrome during postoperative period]. 219 41

Neurological involvement occurred in every one of a series of 30 patients with an insulinoma. The episodic nature of the hypoglycaemia caused symptoms and signs to fluctuate and often led to delay in diagnosis (mean length of history was 3 years). The commonest feature at first presentation was confusion (20 instances), but as the illness evolved, coma (16 instances) and convulsions (8 instances) became more frequent. Objective weakness was found in 7 patients, with 3 examples of hemiparesis and 2 each of paraparesis and monoparesis; in all, the weakness resolved over a period of 1 hr to 3 days when normoglycaemia was maintained. Other neurological features included subjective visual disturbances, headache, dysarthria and ataxia. 220 patients with an insulinoma from 7 series in the literature were reviewed. The high incidence of neurological features was confirmed, with confusion (152 cases), coma (82 cases) and convulsions (58 cases) predominating. Visual disturbances were common, though not accurately quantified in some series. Objective evidence of weakness on the other hand was reported in only 6 of the 222 patients. Other less common symptoms included headache (18 instances) and peripheral paraesthesiae (14 instances). In the 7 series reviewed, as in our own, it was found that in any one patient, each episode of hypoglycaemia was accompanied by the same symptom complex. The presence of an insulinoma should be considered in any patient with unusual, or inexplicable neurological features, particularly when they are intermittent. The diagnosis can be confirmed by demonstrating an inappropriately high circulating insulin level, for the ambient blood glucose concentration.
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PMID:Neurological aspects of insulinomas. 609 Oct 78

We present a child with glutaryl CoA-dehydrogenase deficiency (type I glutaric aciduria) who presented with bilateral subdural hydromas, and progressive choreoathetosis and dysarthria. The diagnosis was made when she was investigated for hypoglycaemia at the age of 3.5 years. Temporary adrenocortical insufficiency was also noted. Three years after diagnosis the adrenal insufficiency and hypoglycaemia have resolved and treatment with riboflavin and 'lioresal', a GABA analogue, has prevented any further neurological deterioration.
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PMID:Glutaric aciduria type I presenting with hypoglycaemia. 643 95

The clinical phenotype of multiple acyl-CoA dehydrogenase deficiency in infancy is characterized by recurrent episodes of hypoketotic hypoglycemia and lipid storage myopathy. Brain damage has been described only as a consequence of severe and protracted hypoglycemia. We describe a child who experienced normal physical and psychomotor development until the age of 3 years, who then developed progressive intention tremors, dysarthria, ataxia, and spastic tetraparesis. Episodes of acute metabolic distress were never observed. Magnetic resonance imaging disclosed abnormal signals within the white matter of the brain and cerebellum, suggesting leukodystrophy. Gas chromatography/mass spectrometry analysis revealed abnormally high levels of glutaric acid, dicarboxylic acids, and glycine derivatives in urine. Riboflavin therapy was initiated at 4 years of age, when the patient had already lost control of trunk and head posture. Consistent improvement rapidly occurred after riboflavin supplementation. Glutaric aciduria type II may cause brain damage, in spite of the absence of acute metabolic distress, and should be considered in the differential diagnosis of leukodystrophies.
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PMID:Riboflavin-responsive glutaric aciduria type II presenting as a leukodystrophy. 877 Nov 70

Glycogen storage disease type Ib (GSD Ib, OMIM 232220) is an inborn disorder of glucose metabolism, caused by mutations in the G6PT gene, encoding a glucose 6-phosphate transporter (G6PT). GSD Ib is mainly associated with fasting hypoglycaemia and hepatomegaly. Most GSD Ib patients also show neutropenia and neutrophil dysfunction and therefore are at risk of developing severe infections and inflammatory bowel disease (IBD). An increased risk for autoimmune disorders, such as thyroid autoimmunity and Crohn-like disease, has also been demonstrated, but no systematic study on the prevalence of autoimmune disorders in GSD Ib patients has ever been performed. We describe a 25-year-old patient affected by GSD Ib who developed 'seronegative' myasthenia gravis (MG), presenting with bilateral eyelid ptosis, diplopia, dysarthria, severe dysphagia, dyspnoea and fatigue. The repetitive stimulation of peripheral nerves test showed signs of exhaustion of neuromuscular transmission, particularly evident in the cranial area. Even in the absence of identifiable anti-acetylcholine receptor antibodies, seronegative MG is considered an autoimmune disorder and may be related to the disturbed immune function observed in GSD Ib patients.
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PMID:Myasthenia gravis in a patient affected by glycogen storage disease type Ib: a further manifestation of an increased risk for autoimmune disorders? 1843 26

The patient suffered loss of consciousness, dysarthria and right sided hemiparesis. The CT scan and MRI scans were negative. These findings are more in keeping with a diagnosis of Transient Ischemic Attack (TIA) or mild CVA. Hypoglycemia per se does not usually cause hemiparesis. The blood glucose level was low but I am not sure if one can conclude that hypoglycemia caused the above noted neurological signs and symptoms. The authors do not present any data to prove that this patient had "hypoglycemic coma".
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PMID:Solitary fibrous pleural tumor associated with loss of consciousness due to hypoglycemia. 1877 52

Hypoglycemic hemiparesis is rare and can be misdiagnosed as cerebral infarction or transient ischemic attack. Early diagnosis of these two disorders is critical because, if not treated with prompt glucose administration, hypoglycemia may lead to a fatal clinical course. We reported two cases of hypoglycemic hemiparesis with a reversible splenial lesion on MRI. The first case was a 69-year-old woman presenting with dysarthria and right hemiparesis. The second case was a 60-year-old man presenting with right hemiparesis. Plasma glucose level was 39 mg/d/ and 32 mg/d/, respectively. In both cases, initial diffusion-weighted imaging (DWI) showed hyperintensity lesions with decreased apparent diffusion coefficient (ADC) values in the splenium of the corpus callosum. Following appropriate correction of hypoglycemia, repeat DWI showed complete resolution of hyperintensity lesions with normalized ADC values. These findings can provide complementary information in the differential diagnosis of hypoglycemic hemiparesis and stroke, though underlying pathophysiological mechanisms are still elusive. We emphasize that checking plasma glucose level is necessary even in cases with hemiparesis. Furthermore, we should be aware that not every hyperintensity lesion on DWI is due to ischemia. There are times when it could be due to hypoglycemia.
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PMID:[Reversible splenial lesion of the corpus callosum on diffusion-weighted magnetic resonance imaging in hypoglycemic hemiparesis: report of two cases]. 1943 96

An 89-year-old man with diabetes treated with metformin 500 mg/day and glimepiride 4 mg/day was hospitalized because of hypoglycemic right hemiparesis and dysarthria (casual glucose value 1.8 mmol/L), which resolved quickly following administration of 40 mL of 40% dextrose. Hemiparesis is a rare symptom (4.2%) of hypoglycemia. There are about 200 case reports of hypoglycemic hemiparesis. The average glucose level at which hemiparesis developed was 1.8 mmol/L. Right-sided hemiparesis predominated (R 66%; L 34%). On imaging studies, abnormal findings were frequently observed in the internal capsule or splenium of the corpus callosum. The mechanism of hemiparesis is not fully understood. The existence of cases in which hypoglycemia cannot be distinguished from stroke on imaging studies suggests the importance of measurement of the blood glucose level when the symptoms of stroke are first recognized.
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PMID:A case of hypoglycemic hemiparesis and literature review. 2224 79

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


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