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Query: UMLS:C0344232 (blurred vision)
 2,072 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report the case of an AIDS patient with rare neurologic manifestations: primary vasculitis of the central nervous system and VIII cranial nerve dysfunction. The authors make a review on the subject, and call special attention for the differential diagnosis. In fact, the patient, a 36 year old woman, with promiscuous life, presented with dizziness, gait ataxia, nausea, headache and hypoacusia. Seven days after the admission, she noted blurred vision in both eyes and soon she became blind. The physical examination showed bilateral optic neuritis and vestibulocochlear dysfunction, stiff neck and fever. No abnormalities were detected on CT scan. CSF showed 40 mononuclear cells/mm3, 79 mg/dl of proteins and normal glucose content. Microbiological research was negative. Serum anti-HIV test was positive. The hypothesis of primary CNS vasculitis was made, and pulse methylprednisolone therapy was introduced with good recovery of neurological syndrome except for persistent amaurosis.
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PMID:[Isolated vasculitis of the central nervous system and involvement of the 8th cranial nerve: rare manifestations of acquired immunodeficiency syndrome]. 130 67

Hypoglycaemia is possibly the most frequent metabolic emergency, in that insulin-induced hypoglycaemia is a common side-effect of treatment of a common disease. The symptoms are partly sympathetic and related to the release of catecholamines. These symptoms include sweating, tremor, palpitations, sensation of hunger, restlessness and anxiety. Other symptoms are caused by an insufficient supply of glucose to the brain, resulting in neuroglucopenia with symptoms like blurred vision, weakness, slurred speech, vertigo and difficulties in concentration. Symptom recognition is the primary and most effective defence against cerebral dysfunction which is the ultimate consequence of hypoglycaemia. Even in insulin-treated diabetic patients symptom failure might occur. Patients who experience severe episodes of hypoglycaemia do not constitute a special subgroup of patients. However, near-normalization of blood glucose levels have resulted in an increase in the incidence of severe hypoglycaemia. Moreover, the threshold for hormonal counter-regulatory responses in adrenaline, growth hormone and cortisol is lowered after a period of strict metabolic control in insulin-dependent diabetic patients. The glucose level at which the patients become subjectively aware of hypoglycaemia is correspondingly reduced. Other reasons for hypoglycaemia to occur are oral hypoglycaemic agents, especially sulfonylureas which may be potentiated by other drugs. Prolonged hypoglycaemia may be seen after first-order sulfonylureas, and may indicate glucose infusion as treatment. Next to insulin and sulfonylurea, ethanol is the most common cause of hypoglycaemia. In non-diabetics, hypoglycaemia will typically develop 6-24 h after a moderate or heavy intake of ethanol by a person who has had an insufficient intake of food for 1 or 2 days. Insulin-producing tumours, insulinomas and non-islet cell tumours may also be reasons for hypoglycaemia in non-diabetics. Treatment of mild episodes of hypoglycaemia is intake of fast-absorbing carbohydrates. Severe episodes can be treated with either i.v. dextrose or glucagon injected i.m. or i.v. The glycaemic response and recovery of a normal level of consciousness is 1-2 min slower after glucagon than after glucose.
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PMID:Endocrine emergencies. Hypoglycaemia. 173 95

A 26-year-old woman, gravida 1, para 0, having episodes of confusion, slurred speech, and blurred vision in pregnancy was documented to have severe hypoglycemia with elevated serum insulin and C-peptide levels. Emergency treatment for hypoglycemia was necessary several times during pregnancy. A healthy female infant was delivered after oxytocin induction of labor. Post partum the patient had numerous episodes of severe hypoglycemia in spite of constant intravenous glucose. Computerized tomographic scan of the pancreas failed to show a lesion, whereas pancreatic arteriography revealed a 2 cm mass in the tail of the pancreas. Partial pancreatectomy was performed 6 days after delivery. Microscopic examination of the tissue confirmed the presence of an insulinoma. Hypercalcemia developed together with elevated parathyroid hormone levels. The presence of an insulinoma, hypercalcemia, and a history of hyperparathyroidism in two relatives indicates that this is a case of multiple endocrine adenomatosis type I first diagnosed during pregnancy.
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PMID:Multiple endocrine adenomatosis type I in pregnancy. 197 95

To define glycemic thresholds for activation of counterregulatory hormone secretion, initiation of symptoms (autonomic and neuroglycopenic), and onset of deterioration of cognitive function, we measured indexes of these responses during glycemic plateaus of 90, 78, 66, 54, and 42 mg/dl in 10 normal volunteers, with the use of the hyperinsulinemic glucose clamp technique. Activation of glucagon, epinephrine, norepinephrine, and growth hormone secretion began at arterialized venous plasma glucose concentrations of 68 +/- 1, 68 +/- 1, 65 +/- 1, and 67 +/- 2 (SE) mg/dl, respectively. Autonomic symptoms (anxiety, palpitations, sweating, irritability, and tremor) began at 58 +/- 2 mg/dl, which was significantly (P = 0.0001) lower. Neuroglycopenic symptoms (hunger, dizziness, tingling, blurred vision, difficulty thinking, and faintness) and deterioration in cognitive function tests began at 51 +/- 3 and 49 +/- 2 mg/dl, respectively, values that were both significantly (P = 0.018 and 0.004, respectively) lower than that for initiation of autonomic symptoms. We therefore conclude that there is a distinct hierarchy of responses to decrements in plasma glucose, such that the threshold for activation of counterregulatory hormone secretion occurs at higher plasma glucose levels than that for initiation of autonomic warning symptoms, which in turn occurs at higher plasma glucose levels than that for onset of neuroglycopenic symptoms and deterioration in cerebral function. Such a hierarchy would maximize the opportunity to avoid incapacitating hypoglycemia.
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PMID:Hierarchy of glycemic thresholds for counterregulatory hormone secretion, symptoms, and cerebral dysfunction. 198 94

A 24-year-old female was admitted to our hospital on Aug. 20 in 1986 because of blurred vision and right pupillary dilatation. She had sometimes noticed headache later than 1976, and blurred vision without headache several times a year later than 1983. She had been told her right pupil dilated when she had complained of blurred vision. Neurological examination revealed abnormal findings as follows; diminished sense of smell in the right side, anisocoria (R 8 mm, L 5 mm), bilateral hippus, hypesthesioalgesia in her right face, left trunk and left arm. The pupils were round and contracted promptly to light. Accommodation reflex and ciliospinal reflexes were normal. Neither blepharoptosis nor external ocular muscle paresis were observed. Deep tendon reflexes were normal. Planter responses were flexor. There was no meningeal irritative sign. No abnormal findings were obtained in blood and urine, chest X-p, brain enhanced CT scan, EEG, and cerebral angiography except for slight degree of anemia. Serum TPHA was negative. However, the cell count of cerebrospinal fluid (CSF) was 18/mm3 (Ly 100%) and decreased to 9/mm3 (Ly 100%) in nine days. Protein content and glucose level of CSF were normal. Pupils were not constricted by 0.125% pilocarpine instillation. Loss of smell and sensory disturbance disappeared within three days and her pupils became isocoric by five days after admission. The patients of episodic unilateral mydriasis without apparent cause had relatively same clinical features as "unilateral springing pupil" proposed by Hallett et al. (1970). Except for mydriasis, they had no abnormal findings of neurological and laboratory examinations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Recurrent episodic unilateral mydriasis with pleocytosis in the cerebrospinal fluid--a case report]. 259 48

Visual improvement following octreotide for growth hormone secreting pituitary macroadenomas is uncommon without tumour shrinkage. A 45-year old lady presented with blurred vision for 12 months. Visual assessment revealed a bitemporal hemianopia and CT scan demonstrated a large pituitary tumour with lateral and suprasellar extension. Acromegaly was confirmed by 75 g glucose tolerance testing. Primary transsphenoidal surgery was performed with normalisation of visual acuity and fields of vision. Post-operatively she had anterior pituitary hormone deficiency. As GH and IGF-1 levels remained elevated she underwent external pituitary irradiation. CT scanning demonstrated tumour shrinkage associated with a modest fall in GH levels. IGF-1 levels remained elevated falling to the age-related upper limit of normal after 5 years. At regular review she had stable visual acuity and fields of vision. She presented as an emergency 7 years from presentation with reduced vision and recurrence of bitemporal hemianopia. An MRI demonstrated a large pituitary adenoma. We therefore undertook a carefully monitored trial of octreotide with great caution with daily reassessment of acuity and fields. A decision was made to proceed to surgery in the event of deterioration or lack of improvement after a short trial over 5-7 days. We observed normalisation of visual acuity and perimetry within 3 days. She then commenced long-acting octreotide (Sandostatin LAR) 20 mg every 28 days. MRI after 1 week showed shrinkage of the tumour by a few millimetres. Five months later repeat MRI failed to show any further improvement in tumour size. However she remains well 29 months from treatment with normal vision and is being monitored carefully as her chosen form of therapy. Somatostatin analogues may be effective as therapy in a selected group of patients with acromegaly and visual loss who are not suitable for pituitary surgery. If used in this way the drug must be given cautiously with frequent detailed ongoing visual assessments. In this present case there has been a restoration of vision but the long-term outlook remains guarded without significant tumor shrinkage.
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PMID:Sustained improvement in vision in a recurrent growth hormone secreting macroadenoma during treatment with octreotide in the absence of marked tumour shrinkage. 1523 32

The purpose of this study was to determine whether the perception of hypoglycemia is reduced during acute stress. In Session I each of our 40 healthy male volunteers received a bolus injection of human insulin (0.05 IU/kg) resulting in plasma glucose nadirs of below 2.8 mmo/L. In Session 2 participants received insulin or saline, with half of each group being stressed by having to prepare and give a speech. Data collection at 5- to 25-min intervals included a symptom checklist, blood pressure, heart rate, and blood sampling for measurement of plasma glucose and counterregulatory hormones. Individuals in the stress + insulin group were less sure of having received insulin and ate fewer cookies compared with controls. They reported lower intensity of the hypoglycemic symptoms of palpitations, tremor, dizziness, and blurred vision, in contrast to the reduced subjective and behavioral reactions, they showed the strongest hormonal counterregulation. We conclude that acute stress during hypoglycemia reduces symptom awareness and the ability to detect hypoglycemia.
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PMID:Acute stress modulates symptom awareness and hormonal counterregulation during insulin-induced hypoglycemia in healthy individuals. 1625 Jul 6

Corneal clouding is uncommon in infants and children but when present in this age group, it is often associated with mucopolysaccharidoses or Fabry disease. This report describes the case of an 11-year-old male who demonstrated poor weight gain, short stature, segmental myoclonus, and learning problems from 5 years of age followed by general weakness and extremely poor balance. Corneal clouding was evident as a result of a blurred vision complaint at 9 years of age. Both urine metabolic screening for mucopolysaccharidoses and analysis of lysosomal enzymes displayed negative findings. Clinical conditions worsened, including ptosis, progressive weakness, and positive Gowers' sign. Oral glucose lactate stimulation test was positive, therefore a muscle biopsy was performed at 11 years of age. Light microscopy of muscle biopsy disclosed abundant ragged red fibers; electron microscopy revealed abnormal mitochondria in terms of tubular cristae, concentrated cristae, stacking cristae, and round granular patterns of inclusion bodies in the matrix. Thus mitochondrial disease was diagnosed. We conclude that mitochondrial disease should be added to the list of differential diagnosis of corneal clouding in children, especially in cases with normal urine metabolic screening for mucopolysaccharidoses or when assays of lysosomal enzymes appear normal.
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PMID:Corneal clouding: An infrequent ophthalmic manifestation of mitochondrial disease. 1676 25

Diabetes mellitus develops in about 10% of acromegalic patients, usually secondary to insulin resistance caused by growth hormone excess. Diabetic ketoacidosis is a result of relative insulin deficiency and is a rare feature of acromegaly. Here, we present one case of this disorder. A 57-year-old man came to the emergency room due to 2 weeks of dizziness. He also had polyuria, polydipsia, nausea, diplopia, blurred vision and dysarthria. His plasma glucose level was 32.06 mmol/L, plasma osmolarity was 322 mOsm/L, arterial pH was 7.30, level of bicarbonates was 18 mmol/L, urine ketones was 4+, and HbA1c was 14.1%. No specific cause for the development of this metabolic derangement could be found. He displayed clinical features of acromegaly during admission, which was confirmed by an elevated growth hormone level and pituitary macroadenoma shown on magnetic resonance imaging. The patient underwent total transsphenoid tumor removal 2 weeks later; plasma glucose levels became normal thereafter.
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PMID:Diabetic ketoacidosis in a patient with acromegaly. 1790 70

Blurred vision and cognitive difficulties are prominent symptoms during acute insulin-induced hypoglycemia. Our hypothesis was that changes in cerebral activity reflect these symptoms. Positron emission tomography (PET) with oxygen-15-labelled water was used to measure relative changes in regional cerebral blood flow (rCBF) as a marker of cerebral activity. Hypoglycemia was induced by intravenous insulin infusion in 19 healthy men performing two different cognitive tasks of varying complexity. The hypoglycemic stimulus [plasma glucose 2.2 mmol/liter (0.4)] produced a significant hormonal counterregulatory response. During the low cognitive load, rCBF decreased in response to hypoglycemia in a large bilateral area in the posterior part of the temporal lobe, and rCBF increased bilaterally in the anterior cingulate gyrus, the right frontal gyrus, the fusiform gyrus, thalamus, and the left inferior part of the frontal gyrus. During the high cognitive load, rCBF decreased bilaterally in a large region in the posterior part of the temporal gyrus and increased in the left and right anterior cingulate gyrus, left and right frontal gyrus, right parahippocampal and lingual gyrus, and left superior temporal gyrus. Visual impairment during hypoglycemia was associated with deactivation in the ventral visual stream. The anterior cingulate gyrus was activated during hypoglycemia in a load-dependent manner. Areas on the frontal convexity were differentially activated in response to the cognitive load during hypoglycemia. Our findings suggest that hypoglycemia induces changes in sensory processing in a cognition-independent manner, whereas activation of areas of higher order functions is influenced by cognitive load as well as hypoglycemia.
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PMID:Changes of cognition and regional cerebral activity during acute hypoglycemia in normal subjects: A H2 15O positron emission tomographic study. 1917 Jan 63


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