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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Communicating normal pressure hydrocephalus (NPH) is an important remote complication of traumatic brain injury (TBI). The diagnosis of this hydrocephalus depends largely on clinical signs and symptoms, including cognitive deterioration, gait changes and incontinence. However, many of these signs are also seen during post-traumatic amnesia, making early recognition of this syndrome difficult. A case study of one man post-TBI, who presented with new-onset hypertension as a sign of NPH, prompted a retrospective chart review of all patients admitted over a 2-year period with a diagnosis of NPH. Ninety per cent of patients had one or more of the classic triad of NPH and 25% of patients had symptoms suggestive of raised intracranial pressure (unexplained nausea, headache and visual disturbance). Mean systolic and diastolic blood pressures among the 20 subjects for six consecutive days pre-operatively compared with those for days 8-14 and 15-21 post-operatively showed no significant differences; a subgroup of five patients (25%), however, demonstrated a significant change in blood pressure temporally related to shunting. We suggest that demonstration of new-onset systemic hypertension may also be a clinical sign suggestive of NPH useful in the evaluation of the TBI patient.
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PMID:Relationship of new-onset systemic hypertension and normal pressure hydrocephalus. 239 Jun 49

Nausea and vomiting can be induced by a wide variety of stimuli such as pregnancy, space travel, raised intracranial pressure, radiation and cytotoxic drugs. The mechanisms by which all these diverse stimuli culminate in a final common act is unknown. From studies in the 1950s a model of the emetic reflex emerged consisting of a chemoreceptor trigger zone in the area postrema and a vomiting centre in the brain stem. This concept has been reviewed and revised in the light of recent studies. Many discussions of emesis involve detailed descriptions of the gastrointestinal events associated with the act of vomiting only-nausea and retching receiving little attention. Here we have tried to give a broader view by considering the neurophysiology of such events and have included nausea and retching, phenomena that are usually inseparable from vomiting. The possible biological function of these events is also discussed. The involvement of visceral systems (such as the heart, airways and gut) is included, and particular attention is paid to vagal mechanisms underlying the changes in gut motor activity. Emesis has long been thought to be organized by a 'vomiting centre'; the possibility that this vomiting centre could be the parvocellular reticular formation is reviewed, as is the concept that the 'centre' is larger than an anatomically defined single group of cells. The mechanism of action of two clinically relevant emetic stimuli--radiation and cytotoxic drugs-is considered in detail. Recent studies of the antiemetic properties of novel 5-HT-3 receptor antagonists against radiation and cytotoxic drug-induced vomiting are discussed; these studies suggest that important advances will be made in the treatment of emesis induced by these and other related agents.
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PMID:The neurophysiology of vomiting. 328 38

Arachnoid cysts of the middle cranial fossa may manifest themselves in several different ways. Most often they remain asymptomatic and are only diagnosed incidentally on computed tomography or at autopsy. When they are symptomatic, headache, nausea, vomiting and seizures are most common in the patients with increased intracranial pressure. Increased intracranial pressure is caused by the ball-valve mechanism of the cyst's membrane which is in communication with the general subarachnoid space or arachnoid cells which contain specialized membranes and enzymes which have secretory activity. A significant number of middle cranial fossa arachnoid cysts are associated with subdural hematoma which may, in turn, be associated with intracystic hemorrhage. We report an unusual case with posttraumatic, isolated intracystic hemorrhage of the arachnoid cyst in the sylvian area without subdural hematoma.
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PMID:Arachnoid cyst with traumatic intracystic hemorrhage unassociated with subdural hematoma. 783 4

In Part I of this article, we present our data collected over the past 8 years on the clinical evaluations of pediatric brain tumors with an emphasis placed on the more common neoplasms. Our data consists of 385 children ranging in age from newborn to 18 years. The majority of children presented with signs of raised intracranial pressure (including nausea, vomiting, and headaches), seizures or other focal neurologic deficits. Five percent of our children presented to outlying hospitals with symptoms that retrospectively turned out to be due to brain neoplasms but were misdiagnosed as "gastroenteritis," "viral upper respiratory tract infection," or even viral meningitis. These delays in diagnosis can cause serious negative outcomes for these patients and can be avoided through more careful neurologic and ophthalmologic examination at the time of first presentation. Central nervous system neoplasms are not uncommon in children and any child presenting with nausea, vomiting, and headaches should raise the suspicion of a primary brain tumor and should receive both a thorough neurologic exam and screening for papilledema. If papilledema is present, these children should be referred for proper neuroradiologic evaluation (which will be addressed in Part II.
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PMID:The clinical and radiological evaluation of primary brain tumors in children, Part I: Clinical evaluation. 836 34

Intracranial hypertension is not a definitive diagnosis, but rather a syndrome that may result from a number of neurologic and systemic disorders. Intracranial hypertension refers to prolonged elevation of intracranial pressure, generally above 200 mm H2O. This condition may be recognized by the various clinical signs and symptoms that are manifest in most patients, including headache, papilledema, transient visual obscurations, diplopia, ocular motor disorders, tinnitus, nausea, vomiting, and mental irregularities, as well as dysfunctions of the circulatory and respiratory systems. Thorough medical testing as well as a comprehensive ocular evaluation is indicated in these cases. Intracranial hypertension most commonly results from mass lesions, tension hydrocephalus, and pseudotumor cerebri. Other causes include disorders of venous outflow, such as dural sinus thromboses or arteriovenous malformations, and various encephalopathies. Management for intracranial hypertension may involve medical treatment, drug therapy, or surgical intervention. Typically, diuretics are used initially. Corticosteroids may be used as well, although they are not the first choice for treatment. Cerebrospinal fluid shunting procedures may be necessary if medical treatment fails. Optic nerve sheath decompression may also be attempted when chronic papilledema threatens visual function. It is important that the primary care optometrist recognize the manifestations of intracranial hypertension in order to make necessary referrals for management of the underlying etiologies.
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PMID:Intracranial hypertension. 897 12

Nausea and vomiting are both elements of the system that evolved to defend the body against toxins accidentally ingested with the food. When they are induced by an ingested toxin, they are considered to be an appropriate response, but in many clinical settings (eg, anticancer chemotherapy, anesthesia and surgery, raised intracranial pressure) both responses are inappropriate in that the vomiting does not remove the cause and the nausea may lead to aversion to further treatment. Cyclic vomiting syndrome (CVS) is a particularly intense and prolonged example of inappropriate activation of this protective reflex. This review argues that insights into the pattern of emesis in CVS can be gained by examining the basic unit (quantum) of emesis, the emetic episode usually comprising retches followed by a vomit. Two (of several) possible mechanisms for the induction of the intense vomiting in CVS are discussed: (1) defects in intrinsic pathways (eg, opioid neurons) that may modulate the brain-stem emetic mechanisms, and (2) defects in the regulation of cellular mechanisms (eg, cAMP, ion channels) in cells at critical locations in the emetic pathway (eg, nucleus tractus solitarius, area postrema). If it is not possible to identify the causal mechanism of CVS, then will it be possible to treat CVS? This question is discussed in the context of the identification of universal or broad-spectrum antiemetic agents with recent preclinical studies with neurokinin-1 receptor antagonists reviewed to illustrate that such an approach is feasible.
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PMID:Cyclic vomiting syndrome: timing, targets, and treatment--a basic science perspective. 1049 37

Animal models have illustrated that a carbon dioxide (CO(2)) pneumoperitoneum can cause a rise in intracranial pressure (ICP). This study investigated key symptoms and signs of raised ICP in 39 patients after laparoscopic abdominal surgery and compared them with a control group of 33 patients after open operations. The findings show that the incidence of headache and nausea was significantly higher in the laparoscopic group than in the control subjects. End-tidal CO(2) levels were recorded, and no significant difference was found between patients and control subjects. We conclude that these results could be explained by raised intracranial pressure exacerbated by the CO(2) pneumoperitoneum, and that this effect is not mediated by raised expiratory CO(2) levels intraoperatively.
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PMID:Association between laparoscopic abdominal surgery and postoperative symptoms of raised intracranial pressure. 1159 76

Pseudotumor cerebri or benign intracranial hypertension is a syndrome of raised intracranial pressure without obvious explanation. Most patients are obese women at childbearing age. Symptoms and signs usually include headache, nausea, vomiting, edema of the papilla, visual obscurations and rarely palsy of the nervus abducens. The prognosis is generally good, but progressive visual loss and eventual blindness are major risks. We report the case of a 21-year-old non-obese young woman who developed pseudotumor cerebri while taking minocycline for acne therapy. Identical symptoms occurred upon inadvert rechallenge with minocycline for the second time.
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PMID:[Pseudotumor cerebri in minocyline treatment]. 1168 Jan 22

A 50-year-old woman presented with recurrent episodes of headache, nausea and disturbed consciousness that were fully reversible within a few days. Clinical and radiological findings suggested raised intracranial pressure, which on one occasion was confirmed by intracranial pressure monitoring. Magnetic resonance imaging performed in the asymptomatic interval disclosed a diffuse leukoencephalopathy. Brain biopsy surprisingly revealed the typical vascular changes of CADASIL and subtle endothelial alterations. The white matter showed edematous changes and reactive gliosis. Mutational analysis of the Notch3 gene revealed a previously unreported mutation. We suggest that a transient disturbance of the blood-brain barrier related to the underlying vascular pathology may have caused this unusual presentation of CADASIL.
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PMID:Reversible coma with raised intracranial pressure: an unusual clinical manifestation of CADASIL. 1181 Jan 86

Risperidone is an atypical antipsychotic used in the treatment of several psychiatric disorders in both children and adults. We present two patients with hydrocephalus and learning difficulties who were admitted to the neurosurgical unit with a suspected cerebrospinal fluid shunt malfunction and raised intracranial pressure. They had both been commenced on risperidone for the treatment of aggressive outbursts. Twelve days after commencing risperidone, the first patient developed symptoms of headache, nausea, vomiting, drowsiness, lethargy and two episodes of collapse. The second patient presented with similar symptoms 4 days after his risperidone dose was increased. An unnecessary shunt exploration was averted in both cases when it was noted that the side-effect profile of risperidone mimicked exactly those of shunt malfunction. Discontinuation of the drug resulted in complete resolution of all symptoms within 72 h. Many patients with shunted hydrocephalus have associated developmental disorders that may warrant treatment with risperidone. Clinicians should be aware of the potential symptom overlap between shunt malfunction and risperidone side-effects in these patients.
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PMID:Side-effects of risperidone therapy mimicking cerebrospinal fluid shunt malfunction: implications for clinical monitoring and management. 1209 77


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