Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The outcomes of infarctions of the cerebellar arteries may range from self-limited neuro-ophthalmic symptoms to sudden death. Identification of the affected territory may assist in clinical management because the vascular syndromes, as well as vascular mechanisms of cerebellar infarcts, are different according to the involved cerebellar arteries. However, it is usually difficult to tell the exact vascular territories using only transaxial imagings. Magnetic resonance imaging is a good tool for obtaining parasagittal and coronal images of the cerebellum, which are better for showing the vascular territories. To illustrate this point we report a 61-year-old woman and bilateral cerebellar infarcts (right posterior inferior cerebellar artery and left superior cerebellar artery who had vertigo, vomiting, headache, intermittent vertical diplopia, and difficulty walking. The clinical value of parasagittal imaging of the cerebellum in this case is discussed.
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PMID:Value of parasagittal magnetic resonance images in visualizing the vascular territories of the cerebellum. 760 63

Lamotrigine is a novel antiepileptic that, although its mechanism is not completely understood, appears to affect voltage-activated sodium channels, resulting in inhibition of the presynaptic release of the excitatory neurotransmitter glutamate. It is well absorbed after oral administration. Its route of elimination is hepatic glucuronidation, which is susceptible to both hepatic microsomal enzyme-inducing and -inhibiting agents. In clinical trials lamotrigine was effective as add-on therapy for refractory partial seizures in adults. Small trials suggest the feasibility of monotherapy, but further controlled trials are warranted to support this practice. Additional data indicate the utility of lamotrigine for generalized seizures. Reported side effects are rash, nausea, vomiting, blurred vision, diplopia, and vision abnormalities. Lamotrigine appears to be an attractive alternative to currently available antiepileptics.
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PMID:Lamotrigine. 762 59

Felbamate is currently being developed as an antiepileptic agent. Although its mechanism of action has yet to be fully elucidated, felbamate appears to inhibit both the spread of seizures and increase seizure threshold in animal models. Data available in the clinical setting provide evidence that, at doses of up to 3600 mg/day as an adjunct to existing antiepileptic therapy or as monotherapy following substitution for other medications, the drug reduces the frequency of partial onset seizures in adult patients refractory to conventional antiepileptic treatments. Felbamate is also effective in the treatment of Lennox-Gastaut syndrome in children, a severe epilepsy which is usually refractory to antiepileptic agents. The effect of felbamate in the treatment of generalised tonic-clonic seizures in adults with partial onset seizures which are secondarily generalised is promising but requires clarification in large-scale trials. The most common adverse effects occurring during administration of felbamate are mild to moderate gastrointestinal (nausea, vomiting and anorexia) and central nervous system (headache, somnolence, diplopia, dizziness and insomnia) disturbances. Drug interactions with other antiepileptic agents may prove problematic in terms of adverse effects. Thus, at this stage of its development, the antiepileptic efficacy of felbamate in treatment-refractory patients with partial onset seizures and Lennox-Gastaut syndrome has been proven but efficacy in generalised tonic-clonic seizures requires further substantiation in large well controlled and well designed clinical trials. In addition, a more comprehensive base of comparative clinical trials data is necessary to further clarify issues of relative efficacy and tolerability compared with other antiepileptic agents. The clinical implications of the drug interactions associated with felbamate also require more detailed investigation. These data will be awaited with interest and when available will help to place felbamate in perspective in the management of epilepsy.
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PMID:Felbamate. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy in epilepsy. 769 93

A 66-year-old man suddenly developed bilateral ptosis after awaking from a nap. He did not experience nausea, vomiting or headache. In the emergency room, high blood pressure was noted. On examination, his consciousness was clear. Ptosis was present bilaterally and worse on the right side. The pupils promptly constricted to light. He could fully adduct his eyes during conjugate gaze movements, but convergence was impaired in the right eye. There was no diplopia or nystagmus. The assessment of the motor and sensory systems revealed no significant findings. Computed tomographic scanning and magnetic resonance imaging of the brain showed a small hematoma in the midbrain. Six months later, ptosis improved; however, the convergence deficit remained.
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PMID:Midbrain hemorrhage presenting as bilateral ptosis without hemiplegia: a case report. 775 61

Reported is one case of cerebral cryptococcosis in a 12-year-old girl. The diagnosis was confirmed by the detection of Cryptococcus neoformans with both India ink preparation of the cerebrospinal fluid and Sabouraud's media culture. Clinical presentation included progressive severe headache, vomiting, left eye pain, diplopia, dizziness and unstable gait. Fever was absent as a symptom. Initial brain magnetic resonance imaging revealed a focal lesion over the right cerebellar hemisphere with better demonstration than contrast-enhanced computed tomography. The patient was treated with amphotericin B and 5-flucytosine with good final outcome. Early diagnosis and proper therapy are necessary in order to decrease the motality of cerebral cryptococcosis.
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PMID:Cerebral cryptococcosis in a child. 779 79

Headache is a common complaint. In most patients, it is usually a problem of migrainous or tension-type headache. It is crucial that a physician is able to differentiate sinister causes of headache from the more benign ones. Six cases are presented to illustrate the fact that there are clues in the history to suggest a sinister cause of headache even though there are minimal or no neurological deficits on physical examination. At some point of time, these cases were examined by a senior physician but they were diagnosed as migrainous or tension-type headaches. The first case is a 41-year-old labourer with cryptococcal meningitis. He presented with severe headaches at a relatively late age. A 20-year-old female complained of the worst headache she ever had and this was due to a subarachnoid haemorrhage. The third case was a young woman with a large parietal meningioma. Her headaches had recently assumed a different character. The fourth case involved an investment manager who developed headaches with transient diplopia and projectile vomiting and investigations revealed an ependymoma. A shipyard worker complained of a constant headache which disturbed his sleep. Two weeks after medical consultation, the character of his headache changed and he developed diplopia in all directions of gaze. He succumbed to pituitary apoplexy. The final case is a 28-year-old woman who had a complicated migraine. CT scan of the brain showed a large arterio-venous malformation.
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PMID:Warning symptoms of sinister headache. 799 8

Seventy-two patients (69 women and 3 men) with benign intracranial hypertension were examined. Besides general clinical signs, such as headache in 71, giddiness in 29, vomiting in 19, poor health in general in 18, painful movements of the eyeballs in 11, unsteady walking in 10, ringing in the ears in 9, noise in the head in 3, all the patients developed changes in the organ of vision. Congestive optic disks were detected in all the cases. Obnubilations were detected in 34 (47.2%) patients, diplopia in 5 (6.9%). Vision acuity was reduced in 33 (45.8%) patients, visual field was limited in 23 (31.9%). Forty-three patients completely recovered, negligible residual symptoms of benign intracranial hypertension persisted in 16, and all symptoms of the condition were virtually unchanged in 13 patients. Vision acuity remained reduced in 10 (13.9%) patients, and one female patient developed amaurosis of both eyes.
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PMID:[Visual functional disorders in benign intracranial hypertension]. 807 84

The activation of oncogenes and the inactivation of tumor suppressor genes within neoplastic cells lead to transformation and loss of growth control. The key clinical feature that should arouse suspicion of a primary brain tumor and lead to a prompt evaluation is the progressive nature of the signs and symptoms, which include headaches, nausea and emesis, double vision, change in personality or cognition, speech difficulty, seizures and weakness. Neuroimaging with contrast-enhanced computed tomography or magnetic resonance imaging is the best method of confirming the presence of a primary brain tumor. Initial treatment in most patients is biopsy or surgical resection. For malignant and selected benign primary brain tumors, further treatment is necessary and may include radiation therapy, chemotherapy or experimental protocols.
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PMID:Primary brain tumors: review of etiology, diagnosis and treatment. 794 21

A case of lymphocytic hypophysitis is described in a patient presenting with panhypopituitarism 8 years after her last childbirth. The patient developed headache, vomiting, and diplopia (due to palsy of the right lateral rectus muscle) 7 months after delivery of her last baby. The diplopia disappeared after a few days with symptomatic treatment, and the headache and vomiting decreased in intensity with analgesic therapy. Eight years later the patient developed symptoms suggestive of hypoadrenalism, hypothyroidism, and amenorrhea. Investigations revealed panhypopituitarism with a pituitary mass lesion. Repeat evaluation 1 year later demonstrated no change in the size of the pituitary gland. The patient underwent transsphenoidal surgery with a provisional diagnosis of pituitary adenoma. Histological examination of the resected gland revealed evidence of lymphocytic hypophysitis. Symptoms suggestive of a pituitary mass lesion were noted during the peripartum period, but features of hypopituitarism developed much later. Such a long latent period has not been reported before. This report also highlights the fact that glandular enlargement may persist for many years after the onset of lymphocytic hypophysitis.
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PMID:Lymphocytic hypophysitis. Case report. 816 36

A 67-year-old woman experienced a severe headache and vomiting. A computed tomographic (CT) scan showed a mild subarachnoid hemorrhage. Cerebral angiography revealed a saccular aneurysm at the apex of the basilar artery. Several days later, she noticed mild hemiparesis of the left extremities. She underwent a clipping operation on the aneurysm by approaching from the right temporal love. Postoperatively, she developed diplopia and dilatation of the left pupil. Cerebral angiography revealed an occlusion of the left posterior cerebral artery. She was admitted to another hospital in order to continue rehabilitation. General physical examination was normal. Neurological examination revealed paralysis of the left medial and left inferior rectus muscles and palsy of the left inferior oblique muscle. The pupil of the left eye was dilated, measuring 5 mm in diameter, and it did not constrict to any stimuli. The left superior rectus and levator palpebrae superioris functioned normally. Visual acuity and visual fields were normal except for the influence of a senile cataract. She had a mild left hemiparesis, slight left ataxia and slurred speech. She had numbness of the left half of the body. A CT scan showed small low density areas in the right thalamus and left cerebellar hemisphere. Her ophthalmologic findings were compatible with the inferior branch palsy of the oculomotor nerve. The ophthalmoplegia of this case seems to be due to partial damage of the oculomotor nerve induced by ischemia of vascular supply. It is supposed to be caused by a vasospasm of the left posterior cerebral artery following a clipping operation of the basilar apex aneurysm.
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PMID:[Inferior branch palsy of the oculomotor nerve following clipping of basilar apex aneurysm]. 831 94


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