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This is a systematic-prospective study of occipital seizures with elementary visual hallucinations in 18 patients with symptomatic occipital epilepsy. Qualitative and chronological analysis showed that visual seizures usually lasted for seconds to 1-3 minutes. Three patients also had longer visual seizures of 20-150 minutes. Elementary visual hallucinations mainly consisted of coloured and small circular patterns flashing or multiplying in a temporal hemifield. Flashing lights or non-circular patterns were rare. Three patients experienced achromatic flickering lights. None of the patients had the over 4 minute, linear, zigzag, and achromatic or black and white patterns characteristic of migraine visual aura. Blurring of vision could precede visual hallucinations. Visual seizures were usually frequent, often occurring in multiple clusters daily or weekly. They usually occurred alone but they often advanced to other occipital and extra-occipital ictal symptoms. In 7 patients they progressed to temporal lobe seizure manifestations, and in 6 to motor partial seizures or ipsilateral hemiconvulsions. All but 2 had secondary generalised tonic clonic convulsions. Ictal blindness ab initio occurred in 2 and ictal, mainly orbital headache in another 2 patients. One patient had ictal vomiting as an occasional symptom. Postictal headache, often severe and indistinguishable from migraine, occurred in two thirds of the patients, even after brief visual seizures without convulsions. Despite relevant structural lesions in brain imaging, 10 patients had a normal mental and neurological state. In 8 patients, EEG was also normal or nonspecific. Misdiagnosis of visual seizures as visual aura of migraine was common and 3 patients were misdiagnosed as suffering from migraine. The differential diagnosis between migraine and the occipital epilepsies is reviewed. It is concluded that elementary visual hallucinations, blindness or both, alone or followed by headache and vomiting of symptomatic occipital epilepsy are identical to those of idiopathic occipital epilepsy. Progress to temporal lobe structures is different and consistent with symptomatic occipital lobe epilepsy. The clinical diagnosis of visual seizures is easy if individual elements of duration, colour, shape, size, location, movement, speed of development and progress are identified. They are markedly different from visual aura of migraine, although they often trigger migrainous headache, probably by activating trigeminovascular or brain stem mechanisms.
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PMID:Visual phenomena and headache in occipital epilepsy: a review, a systematic study and differentiation from migraine. 1093 55

We describe a 72-year-old woman with a history of acute myeloid leukemia who developed pituitary apoplexy associated with thrombocytopenia secondary to chemotherapy. She presented with new onset severe headache, nausea, vomiting and blurred vision. Initial physical examination was unremarkable. CT scan of the head was initially negative. Upon admission for further work up, She developed a high-grade fever, hypotension and obtundation. Subsequent physical examination revealed bitemporal visual fields defects and decreased visual acuity. Repeat imaging of head revealed a hemorrhagic pituitary mass compressing the optic chiasm. Laboratory results were compatible with the diagnosis of pan-hypopituitary syndrome. She received high dose steroids and was transferred for transnasal sphenoidotomy decompression surgery. The visual defects improved postoperatively. A literature review of Pituitary apoplexy is presented. Pituitary apoplexy secondary to thrombocytopenia has never been reported.
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PMID:Pituitary apoplexy in a patient with acute myeloid leukemia and thrombocytopenia. 1114 94

Androgen was reported to cause cerebral venous thrombosis (CVT) during replacement therapy for aplastic anemia. Oxymetholone, a synthetic androgen analogue, has been widely used in the treatment of aplastic anemia. A 40-year-old woman with aplastic anemia visited our hospital because of severe headache, nausea, vomiting, blurred vision and diplopia for a period of 1 month. She had taken oxymetholone for 2 years. Neurological examination revealed bilateral papilledema and bilateral sixth nerve palsies. Brain magnetic resonance imaging (MRI), performed at the time of admission, demonstrated left-sided tentorial SDH, and focal cerebral thrombosis of the left superficial sylvian vein and sigmoid sinus. MR venography revealed multiple irregularities in the superior sagittal sinus and left transverse sinus. CVT with tentorial subdural hematoma (SDH) caused by oxymetholone was strongly suggested. Oxymetholone was immediately discontinued, and her symptoms and signs disappeared. Because of the thrombocytopenia, anticoagulation was not started. She was discharged and visited the outpatient clinic without neurological symptoms for 6 months. This report supports the cautions given about the risk of CVT with oxymetholone supplementation in aplastic anemia. To the best of our knowledge, this is the first report of CVT associated with tentorial SDH that was probably caused by oxymetholone.
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PMID:Cerebral venous thrombosis associated with tentorial subdural hematoma during oxymetholone therapy. 1126 87

The coincidence of hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome and cortical blindness is an uncommon but very dramatic event. We describe a case of HELLP syndrome complicating with acute cortical blindness before delivery. A 27 year-old woman, gravida 1, para 0, with normal medical history, was referred to our emergency department at the 33th week of gestation due to headache, vomiting, and blurred vision. The ophthalmologic examination showed intact pupillary light reflexes and normal ophthalmoscopic findings, but no light perception in either eye. Brain computed tomography showed normal findings. HELLP syndrome and preeclampsia was diagnosed based on the findings of hypertension and proteinuria as well as laboratory data. Prompt delivery was performed in order to achieve good maternal and neonatal outcomes.
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PMID:Hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome with acute cortical blindness. 1172 Jan 49

We like to think that our homes are a safe haven. However, in recent years we have been discovering that certain products, designs, and even the siting of our homes can create health risks. When families moved into a new development in Waynesville, NC, called "Barber Orchard," they were ecstatic about their new surroundings--the fresh air, mountain views, and clean water. When one of the new residents had his well water tested, their dream homes took on a different character. The water was reflective of the years of pesticide use on the former orchard on which their homes were sited; it contained DDT, DDE, and benzene hydrochlorides (Manual, 2000). The soil was contaminated with lead and arsenic, also the result of pesticide applications. The Environmental Protection Agency (EPA) sent in an emergency response team, removed toposil, and advised residents to install carbon filters on their water systems. Sometimes, we unintentionally bring pollution into our homes. In the homes of middle-income families with small children, vacuum dust was found to have pesticide concentrations 10-100 times greater than those found in the surface soils surrounding their houses (Lewis et al, 1994). In the agricultural area of Washington State, 47 of 48 farm homes had chlorpyrifos (an organophosphate pesticide) measured in the house dust. The human health risks associated with chlorpyrifos are substantial (including headaches, dizziness, muscle twitching, vomiting, and blurred vision); hence, in 2000, the EPA eliminated the widely used pesticide for nearly all-household purposes. The purpose of this independent study module (ISM) is to introduce the reader to basic concepts and issues associated with environmental health risks to children in homes and communities. In this ISM, some of the key hazardous exposures occurring in the home will be discussed. Indoor air quality, drinking water, lead, mercury, pesticides, radon, and UV radiation have been selected as topics of focus. A resource section provides a brief listing of resources; many of them are Web sites, which, in turn will link the reader to additional resources. The EPA's Web site is particularly helpful. The University of Maryland School of Nursing has a new Web site, http://enviRN.umaryland.edu, with links to all of the Web sites noted in this ISM.
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PMID:Environmentally healthy homes and communities. Children's special vulnerabilities. 1178 92

Syncope is defined as a temporary interruption of cerebral perfusion with a sudden and transient loss of consciousness and spontaneous recovery. Approximately one third of the population experiences syncope at least once during a lifetime. Presyncopal signs and symptoms, including weakness, headache, blurred vision, diaphoresis, nausea, and vomiting are sometimes present for seconds or minutes prior to loss of consciousness. After syncope, the patients may present with persisting drowsiness, headache, dizziness, nausea, but not usually confusion. Causes of syncope have been categorized as cardiovascular, non-cardiovascular, and unexplained. Cardiovascular causes can be subdivided into structural heart disease, coronary heart disease, and arrhythmia. Non-cardiovascular causes include neurological, metabolic, psychiatric and other disorders.Orthostatic hypotension - one of the most frequent causes of syncope - has manifold etiologies comprising various neurological and internal diseases. Orthostatic hypotension usually can be attributed to an impairment of peripheral vasoconstriction or to a reduction of the intravascular volume. Signs and symptoms, including the above prodromi are often present just after rising from a supine or sitting position. Frequently, blood pressure decreases significantly without an increase in heart rate. Autonomic cardiovascular modulation is often reduced. Many of the patients with "unexplained" syncope experience neurally mediated (i. e. neurocardiogenic or vasovagal) syncope. In these patients, cardiovascular control may be stable for an extended period of time during orthostatic stress, then there is a sudden decrease in blood pressure and heart rate. Neurocardiogenic or neurally mediated syncope can be associated with painful or emotionally stressful situations such as anxiety or fear, with prolonged standing or specific trigger situations such as micturition, defecation, coughing or sneezing, visceral or carotid sinus stimulation, or with trigeminal or glossopharyngeal neuralgia. So far, the mechanisms of neurocardiogenic syncope are not completely understood. The passive 60 degrees to 70 degrees head-up tilt test is useful for the diagnosis of orthostatic and neurally mediated syncope. The sensitivity of the test can be improved by additional pharmacological provocation, e. g. by isoproterenol, or by increased orthostatic stress using lower body negative pressure stimulation. For the treatment of syncope one should first consider non-pharmacological options. Patients with orthostatic hypotension should avoid rapid changes of the body position from supine to standing, as well as high room temperature or other situations inducing peripheral vasodilatation. An increased intake of sodium and fluids, mild physical exercise or so-called postural counter-maneuvers can improve orthostatic tolerance. Among the drugs recommended for pharmacologic treatment are mineralocorticoids (e. g. fludrocortisone), vasoconstrictor agents (e. g. ephedrine, midodrine), adenosine receptor blockers (theophylline) and beta2-blockers (propanolol), anticholinergic agents, e. g. scopolamine or disopyramide, and negative cardiac inotropes, e. g. beta1-adrenergic blockers or disopyramide. Serotonin reuptake inhibitors (e. g. fluoxetine, sertraline), alpha2-adrenergic agonists (clonidine), central nervous system stimulants such as methylphenidate or phentermine are thought to be beneficial in specific cases. Cardiac pacemakers often seem to be recommended without adequate indication. The antidiuretic, V2-receptor specific, vasopressin analogue desmopressin increases the intravascular volume. Erythropoietin improves anemia and red blood cell decrease and augments blood pressure and cerebral oxygenation. In postprandial hypotension, octreotide, a somatostatin analogue, prostaglandin inhibitors such as indomethacin or ibuprofen, as well as metoclopramide or two cups of coffee per day might be beneficial.
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PMID:[Syncope - a systematic overview of classification, pathogenesis, diagnosis and management]. 1182 26

Intracranial hypotension syndrome as a complication of diagnostic lumbar puncture is a rarely observed entity. Intracranial hypotension syndrome is characterized by postural headache, neck pain/stiffness, blurred vision, nausea, vomiting, clouding of consciousness, dizziness and vertigo. The majority of cases resolve spontaneously with conservative treatment. Rarely, epidural blood patch is required. We report a 41-year-old man with multiple sclerosis, who developed intracranial hypotension syndrome after diagnostic lumbar puncture and who did not respond to conservative treatment. A subdural hematoma was subsequently found, when the patient showed considerable worsening of clinical conditions with life-threatening symptoms. Surgical evacuation of the subdural hematoma was not sufficient to improve significantly the patient's conditions, while complete symptoms remission was achieved 12 hours after epidural blood patch. We stress the need for epidural blood patch in any case of post-diagnostic lumbar puncture postural headache which does not resolve with conservative therapy.
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PMID:Life-threatening intracranial hypotension after diagnostic lumbar puncture. 1191 83

A needs assessment of 274 women admitted for delivery to the Maternity Hospital in Kathmandu, Nepal, in a 1-week period in 1994 revealed an alarming incidence (94.1%) of maternal morbidity during pregnancy and delivery. 90.9% of women were under 30 years of age and 47.2% were primiparous; 75.5% were urban residents and 49.6% had no formal education. 89.4% of women reported at least one problem during pregnancy and, of these, 82.0% experienced multiple morbidities. These illnesses included dizziness (60.9%), excessive vomiting (56.2%), swelling of the hands and feet (36.9%), fever exceeding 3 days' duration (26.3%), blurred vision (24.1%), and urinary problems (19.7%). 62.0% of women sought medical care, primarily from a government hospital, for at least 1 pregnancy-related illness. Delivery-related problems included labor exceeding 18 hours (17.6%), heavy bleeding (25.2%), and fainting (10.9%). Among the 136 women who had at least 1 delivery prior to the index pregnancy, 16.9% experienced urinary canal damage or infection, 38.2% had uterine pain, and 33.1% reported breast pain. Although most of the problems recorded in this study were not life-threatening, it is reasonable to assume that so large a morbidity burden affected the pregnant women's productivity and the well-being of their families. A larger, more comprehensive study of the nature and magnitude of maternal morbidity in Nepal is planned.
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PMID:Maternal morbidity among women admitted for delivery at a public hospital in Kathmandu. 1215 44

Pseudotumor cerebri (PC) is a syndrome characterized by intracranial hypertension in the absence of any space-occupying lesion, hydrocephalus, cerebral sinus thrombosis and biochemical or cytological abnormalities in the CSF. PC has ben associated with several factors such as systemic conditions or drugs. We report here the case of a patient who presented with headache, vomiting and blurred vision accompanied by bilateral papilledema and had been diagnosed with systemic lupus erythematosus (SLE) seven years before. Treatment was started with high-dose corticosteroids with rapid resolution of the clinical symptoms and papilledema of the patient.
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PMID:[Pseudotumor cerebri and systemic lupus erythematosus]. 1260 79

Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome has various presentations. We report on a case of MELAS in which alternate-sided homonymous hemianopia was the main symptom of recurrent neurological defects. A 19-year-old woman suffered from blurred vision, headaches, vomiting, and fever that subsided within days. The ophthalmic examination demonstrated right homonymous hemianopia. One month later a similar episode occurred again. Computed tomography (CT) and magnetic resonance imaging (MRI) of her brain revealed an infarct in the left temporo-occipital lobes. Exercise tests showed lactic acidosis, and a muscle biopsy confirmed the diagnosis of mitochondrial myopathy. Half a month later, a third episode occurred. Visual field examination demonstrated left homonymous hemianopia and partial recovery of the right visual field. The infarct in the brain, as revealed by CT and MRI, was compatible with the visual field changes. MELAS should be ruled out in young patients who present with homonymous hemianopia accompanied by recurrent headaches or other recurrent symptoms.
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PMID:Alternate-sided homonymous hemianopia as the solitary presentation of mitochondrial encephalomyopathy, lactic acidosis, stroke-like episodes syndrome. 1279 Feb 25


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