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)

This report reviews the lateralising and localising signs of epileptic seizures in respect to the differential diagnosis of epilepsy. The lateralising value of epileptic signs and symptoms can frequently be derived from the neuroanatomy. Focal clonic, focal tonic, and versive seizures as well as ictal unilateral dystonia are associated with a seizure onset zone in the contralateral hemisphere. Postictal nose wiping is performed with the hand ipsilateral to the epileptogenic zone. Similarly, unilateral blinking points to an ipsilateral seizure onset. Automatisms with preserved consciousness, ictal speech, and vomiting correlate to an epileptogenic zone in the non-dominant hemisphere, while postictal dysphasia is produced by seizures arising from the dominant hemisphere. Lateralising and localising signs and symptoms of epileptic seizures are of great help in the differential diagnosis of epilepsy from the first diagnosis of epileptic events to presurgical video-EEG monitoring.
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PMID:[Lateralizing and localizing signs and symptoms of epileptic seizures: significance and application in clinical practice]. 1168 74

Headache with neurologic deficits and cerebrospinal fluid lymphocytosis is a benign condition with a transient ischemic attack-like presentation. We present a case of a 22-year-old man with episodes of right-sided weakness, global dysphasia, and right-sided homonymous hemianopsia associated with frequent vomiting. Systemic thrombolytic therapy was considered. A subsequent magnetic resonance image with diffusion-weighted images revealed normal findings. A diagnosis of headache with neurologic deficits and cerebrospinal fluid lymphocytosis was made based mainly on clinical symptoms and cerebrospinal fluid analysis. With the current pressure on "door-to-needle" time for thrombolysis, it is important to keep an open eye to stroke mimics and exclude them if possible. We, therefore, strongly advise considering noninvasive magnetic resonance diffusion-weighted imaging in patients with unusual presentations (e.g., the vomiting in our patient) before thrombolysis.
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PMID:The syndrome of headache with neurologic deficits and cerebrospinal fluid lymphocytosis mimicking acute ischemic stroke. 1858 48

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is caused by mutations in the Notch3 gene on chromosome 19. The condition manifests itself clinically typically in the third to fifth decade with migraine and recurrent episodes of stroke or transient ischaemic attacks. We report the case of an 11-year-old male with CADASIL resulting in stroke with right hemiparesis and dysphasia. Acute magnetic resonance imaging suggested infarction in the left hemisphere; magnetic resonance angiography revealed calibre variation of the intracerebral arteries. The patient suffered from common migraine with five to six attacks per month for 3 years 6 months before the stroke. Attacks occurred early in the morning with severe one-sided headache, photophobia, nausea, and vomiting. Antimigraine medications had no effect. The family history revealed more cases of CADASIL, with an autosomal dominant pattern. The diagnosis of CADASIL was confirmed by the finding of the known mutation of the Notch3 gene running in the family. With treatment in a neurorehabilitation centre the patient recovered most of his functions with only discrete fine-motor and cognitive sequelae. Our case report highlights the need for paediatricians to consider CADASIL in childhood stroke as well as in migraine patients.
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PMID:Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy resulting in stroke in an 11-year-old male. 1920 99

Snakebite is an environmental hazard associated with significant morbidity and mortality. We report a case series of venomous snakebites in a military operational area of north India. Of 33 cases of snake bites presenting to the military hospital, 21 patients were envenomated. The median age of patients was 24 years; all were men. All of the envenomations were neurotoxic in nature. Abdominal pain (91%), headache (86%), dysphagia (86%), ptosis (77%), diplopia (72%), blurred vision (72%), dyspnea (67%), and vomiting (62%) were the predominant clinical presentation. Polyvalent AntiSnakeVenom (ASV) [mean 180 ml; range 90-320 ml] was given to all patients with systemic manifestations, and repeated as needed. Eleven (52%) patients received neostigmine with glycopyrrolate to counter cholinergic effects. Two patients were given ventilatory support. The average time of recovery from envenomation was 16 hours after administration of ASV. All patients recovered without sequelae. Soldiers during military exercise are vulnerable to snakebites. Neurotoxic snakebites predominate in our study and usually present with autonomic features along with headache, abdominal pain, ptosis, diplopia and dysphasia. Preventive measures to minimize snake bites and planned treatment regimens should be emphasized among medical and military personnel deployed in the field operations.
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PMID:Clinical profile of venomous snake bites in north Indian Military Hospital. 1956 85

Delirium may present with hyperactive, hypoactive or mixed clinical pictures. The signs of hypoactive delirium are lethargy, confusion, apathy, hypersomnia, muttering, difficulty in maintaining attention, and difficulty in understanding and performing commands. Valproate is commonly used for the treatment of epilepsy and bipolar disorders. It is also used for the management of alcohol withdrawal delirium and agitative-aggressive deliriums. However, few reports are available about the valproate-induced delirium. In this report, we present a 46 years-old woman with bipolar disorder for 14 years. During her last two hospital admissions, she had been diagnosed with manic episode with psychotic features and she had received valproate. She experienced three hypoactive delirium episodes lasting 2-3 days throughout the treatment period of first week. The patient predominantly had the following signs; vomiting, hypersalivation, confusion, drowsiness, dysphasia, and hypoactivity. At the first day of delirium episode, serum valproate level was found to be within the therapeutic range (98.4, 117.1, and 65.6 mug/ml; respectively). In addition, she had normal results of cranial MRI, complete blood count, urine analysis, electrocardiogram, ALT, AST, albumin, bilirubin, BUN, creatinine and electrolytes. The serum ammonia level of the patient could not been measured due to limitations of laboratory facilities. The patient's consciousness improved dramatically 2-3 days after cessation of valproate. In conclusion, valproate can induce delirium at therapeutic blood levels in some patients via various mechanisms and this side effect has to be considered during valproate use.
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PMID:[Valproate induced hypoactive delirium in a bipolar disorder patient with psychotic features]. 2020 7

Swift diagnosis and treatment are critical for good outcomes in patients with nontraumatic subarachnoid hemorrhage, which is usually caused by a ruptured aneurysm. This type of stroke often results in death or disability. Rates of misdiagnosis and treatment delays for subarachnoid hemorrhage have improved over the years, but these are still common occurrences. Subarachnoid hemorrhage can be more easily diagnosed in patients who present with severe symptoms, unconsciousness, or with thunderclap headache, which is often accompanied by vomiting. The diagnosis is more elusive in patients who present in good condition, yet these patients have the best chance for good outcome if they are correctly diagnosed at the time of presentation. Physicians should be alert for warning headaches, which are often severe, and headaches that feel different to the patient. Other symptoms may include nausea, vomiting, impaired consciousness, nuchal rigidity, orbital pain, focal neurologic deficits, dysphasia, lightheadedness, and dizziness. The most important risk factors for subarachnoid hemorrhage include cigarette smoking, hypertension, heavy alcohol use, and personal or family history of aneurysm or hemorrhagic stroke. The first step in the diagnostic workup is noncontrast computed tomography of the head. If computed tomography is negative or equivocal, a lumbar puncture should be performed. Subsequent imaging may include computed tomographic angiography, catheter angiography, and magnetic resonance angiography.
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PMID:Recognition and evaluation of nontraumatic subarachnoid hemorrhage and ruptured cerebral aneurysm. 2413 85

Between January 2005 and August 2011 141 victims of krait bite poisoning were admitted to the general hospital at Mahad. Clinical signs and symptoms preceding the development of neuroparalysis were analyzed. Fifty-six percent of patients were male. A total of 140 victims reported between midnight and 05:00. Patients awoke in the night due to abdominal colic (85%) and chest pain (72%). Patients gave a history of vomiting (42%), sweating (17%) and excessive salivation (35%). On arrival at hospital, 78% cases had dysphasia with pooling of saliva, 89% had heaviness in both eyelids and ptosis; 12.5% of patients died on the way to hospital while 13.47% died during treatment. In total, 74.46% recovered, and of these 48% needed artificial ventilation. The sudden onset of abdominal colic and vomiting in a person sleeping on the floor without a mosquito net led to neuroparalysis due to krait bite poisoning.
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PMID:Premonitory signs and symptoms of envenoming by common krait (Bungarus caeruleus). 2454 31


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