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

In proportion to a rapid increase of dialysis patient, death caused by neurological complications is increasing annually among long-term hemodialyzed patients. A case of chronic subdural hematoma during long-term hemodialysis is presented. A 35-year-old male had undergone hemodialysis three times weekly for four years. He had marked changes in body-weight and blood pressure between hemodialysis. In March 1983, he had a headache, vomiting, and left hemiparesis. The CT scan showed a right subdural hematoma. He was admitted to our hospital 10 days later because of progressive hemiparesis and speech disturbance. The neurological examination showed left hemiparesis with sensory deficit and dysarthria. The CT scan showed an increase in the size of the subdural hematoma. Bleeding time was over 10 minutes. A right-sided burr hole was made and altered blood was removed and irrigated. After operation, headache and weakness rapidly subsided, but the next morning, attacks of convulsion occurred. The CT scan showed the rebleeding in the subdural space. After correcting the level of serum potassium by hemodialysis, a right parietal craniotomy was performed. Hematoma of about 100 g was removed and the capsule of the hematoma showed organized tissue histologically. Postoperatively, although attacks of convulsion occurred temporarily, he gradually improved. The levels of serum potassium and BUN were controlled by several treatments of hemodialysis. He was discharged with only mild hemiparesis. Subdural hematoma caused by hemodialysis is a very important complication. Chronic subdural hematoma is sometimes very difficult to differentiate from dysequilibrium syndrome or dialysis dementia. The CT scan is a very valuable examination to rule out subdural hematoma.
 ...
PMID:[A case of chronic subdural hematoma in a hemodialyzed patient]. 372 77

We analyzed 26 cases of primary lymphoma of the central nervous system. There were 14 males and 12 females ranging in age from 5-76 years (median age 51 years, mean age 50.2 years). None had received organ transplantation or immunosuppressive therapy. The most common presenting symptoms were headache, mental changes, nausea, vomiting, and convulsions. The main neurological findings were hemiparesis, papilledema, visual field defects, and cranial nerve palsies. The most common finding in the cerebrospinal fluid (CSF) was high protein content; CSF cytology was positive in only one case. Computerized tomography was done in 14 cases; all showed a contrast-enhancing lesion. Angiography generally revealed an avascular mass. The most common location above tentorium was the frontal lobe; in four cases the tumor was infratentorial (cerebellum, 3 cases). In five cases there was diffuse involvement of the brain; all had severe dementia and diagnosis was not made until the autopsy. Histologically, the most common type was diffuse histiocytic or immunoblastic lymphoma according to Rappaport and the Working Formulation classification respectively. Radiation therapy alone in five patients gave a median survival of 17 months. Five patients received radiation and chemotherapy, and median survival was 16 months. Two patients developed ocular lymphoma 8 and 36 months later that was treated by radiation.
 ...
PMID:Primary lymphoma of the central nervous system: a clinicopathologic analysis of 26 cases. 376 91

Although the occurrence of Wernicke's encephalopathy (WE) in patients on dialysis is frequently alluded to, review of the literature reveals only 3 described cases. We describe 5 patients on dialysis who developed WE in the absence of alcoholism or other predisposing factors. The clinical diagnoses included uremic encephalopathy (2 patients), dysequilibrium syndrome (1), dialysis dementia (1), and brainstem hemorrhage (1). At postmortem examination, classic findings of WE were evident. The rarity of WE in patients on dialysis may in part be explained by studies indicating a genetic defect in transketolase activity. Patients on dialysis are also potentially at risk for thiamine deficiency because of anorexia, vomiting, and intravenous alimentation. Other factors altering thiamine requirements, such as glucose load or infections, may also contribute. Preventable and potentially curable, WE should be suspected in all patients on dialysis who have an unexplained neurological picture.
 ...
PMID:Wernicke's encephalopathy in patients on peritoneal dialysis or hemodialysis. 382 16

We studied a 59-year-old woman with dementia, retinitis pigmentosa, sensorimotor neuropathy, and attacks of vomiting associated with blood pressure lability and loss of consciousness. Abnormalities included CT evidence of cerebral atrophy, low IQ, slow central and peripheral nerve conduction velocities, axonal degeneration in sural nerve biopsy, and elevated levels of catecholamines and slow waves in EEG during attacks. Her sister, two brothers, and daughter also had progressive muscle weakness, visual disturbance, and similar vomiting attacks. The hereditary nervous system disorder does not fit any previously described condition.
 ...
PMID:Familial neuropathy with dementia, retinitis pigmentosa, and dysautonomia. 386 Jul 47

Seven cases of lobar cerebral haemorrhage due to amyloid angiopathy were found among 60 necropsy cases of intracerebral haemorrhage. Clinically five patients were demented and two had hypertension. Immediately after the onset of stroke there was a high incidence of headache and vomiting, followed by nuchal rigidity. Amyloid angiopathy was most prominent in the cerebral cortex and the leptomeninges. Senile plaques were noted in all cases. One should suspect that a haemorrhage may be due to amyloid angiopathy, when lobar cerebral haemorrhage occurs in an aged, normotensive patient with or without dementia. Surgical evacuation of the haematoma is inadvisable, because of the diffuse nature of amyloid angiopathy, high recurrence rate and less tendency to cause brain stem compression.
 ...
PMID:Amyloid angiopathy and lobar cerebral haemorrhage. 650 78

We report a 78-year old woman with 30 years history of rheumatoid arthritis and nephrotic syndrome, who developed right hemiparesis and renal failure recently. The patient was diagnosed as having rheumatoid arthritis in 1965, and had been treated with gold -sol, steroid hormone, and non-steroidal anti-inflammatory drugs intermittently. Later on her clinical course was complicated by nephrotic syndrome, however, her renal function was well compensated. Otherwise, she was apparently doing well until October of 1988 when she had an onset of anomic aphasia; she was 73-year-old at that time. She was admitted to our hospital; a cranial CT scan at that time revealed a low density area in the left temporal region, and she was diagnosed as suffered from an atherothrombotic infarction involving the left middle cerebral artery territory. She recovered soon and was discharged for out patient follow up with ticlopidine 100 mg/day. She was doing well until December 15, 1990, when she had an acute onset of nausea, vomiting, and speech disturbance; she was admitted to our hospital for the second time. On admission, she was alert, but she had motor aphasia, right hemiparesis, and dysarthria. A cranial CT scan revealed a low density area in the left temporal region extending into adjacent frontal and parietal areas including the angular gyrus; in addition, leukoaraiosis, cortical atrophy, and ventricular dilatation were noted (Fig. 1A, B). She was treated supportively, and she showed improvement in her aphasia, however, moderate weakness remained in her right upper and lower extremities. She was discharged for out patient follow up. She was doing well until May 21, 1993, when she developed difficulty in swallowing and speech. She became unable to take foods orally and she was admitted again on May 31. On admission, she was afebrile and BP was 120/80 mmHg. General physical examination was unremarkable except for pitting edema and multiple contracture of her joints. On neurologic examination, she was alert but appeared to have aphasia and dementia; she could utter only a few simple words, and was able to understand only simple questions.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:[A 78-year-old woman with rheumatoid arthritis, right hemiparesis, and renal failure]. 789 38

A 65-year-old woman had suffered from slowly progressive hearing loss for one year. She had neither repeated episodes of headache or vomiting nor a past history of neurosurgical operation. Neurologic examination revealed moderate diminution in hearing, pyramidal tract sign and cerebellar ataxia without dementia. CSF was under normal pressure, clear and colorless, with total protein 35 mg/dl, glucose 59 mg/dl and a cell count of 2 WBC/mm3. T2-weighted images (TR200/TE80) of high-field MRI demonstrated marginal hypointensity of the brainstem, the Sylvian fissures and the entire spinal cord. Angiography of the cerebral vessels failed to identify the source of bleeding. To our knowledge, this is the first report of superficial hemosiderosis of the central nervous system with normal CSF findings and an unknown source of bleeding confirmed by MRI.
 ...
PMID:[A case of superficial hemosiderosis of the central nervous system with normal CSF findings and unknown source of bleeding]. 820 Jan 46

A 17-year old girl presented with recurrent seizures, strokes, fatigue, vomiting, cerebellar ataxia, dementia and hypertrichosis. Further examinations showed jerking left-sided arm reflexes, partial internal deafness and myopathy. CT and MR of the skull revealed radiolucencies within the cerebral matter of the cortex and the medulla. Laboratory tests showed increased levels of lactate and pyruvate in serum and cerebro-spinal fluid. Microscopic examination of muscular tissue showed "ragged red fibers". Electron microscopy yielded crystal inclusions in mitochondria. The symptoms represented the complete picture of the so-called MELAS/MERRF-complex, which can be easily misdiagnosed as strokes and seizures of unknown cause.
 ...
PMID:[Stroke, epilepsy and abdominal pain as leading symptoms in a case of mitochondrial encephalomyopathy]. 844 77

We report a 32-year-old man who developed cerebellar ataxia and a posterior fossa mass 12 years after the radiation therapy for a cerebellar arteriovenous malformation (AVM). The patient was well until 19 years of the age when he had an acute onset of vertigo and vomiting. A spinal tap was performed and the CSF was bloody. He was admitted to another hospital where an arteriovenous malformation was found in the cerebellum by angiography. Four years after the onset, he developed tingling sensation in the distribution of the second division of the right trigeminal nerve. He was admitted to the neurosurgery service of our hospital where the cerebellar AVM was confirmed. He was transferred to University of California where Bragg peak stereotaxic radiotherapy was successfully performed; this utilizes high energy alpha-ray produced by a cyclotron. Three years after the radiotherapy, marked reduction in the size of the AVM was confirmed by angiography. Twelve years after the onset of his initial symptom, he noted unsteadiness of gait. He was readmitted to our neurosurgery service where obstructive hydrocephalus was found. He was treated by ventriculoperitoneal shunting and placement of a Ommaya reservoir. After these therapy, he noted marked improvement in his gait and ataxia. However, in 1993, his unsteadiness of gait recurred, and he was again admitted to our neurosurgery service on June 20, 1993. On admission, T1-weighted MRI revealed a slightly low signal intensity mass lesion in the right cerebellar hemisphere compressing the brain stem; a spotty high signal intensity lesion and another small low intensity lesion were seen within the mass. Vertebro-basilar angiograms revealed upward displacement of the superior cerebellar arteries. No arteriovenous nidus was visualized. On July, 3rd, the cyst was surgically drained and the Ommaya reservoir was removed. Post-operative course was uneventful, however, he developed head tremor after the surgery. Neurologic examination on July 20, 1993 revealed an alert and well oriented man in no acute distress. General physical examination was unremarkable. Neurologic examination revealed no dementia; higher cerebral functions appeared intact. The optic discs were flat, and visual fields were intact. Ocular movements were full but convergence was restricted. Horizontal gaze nystagmus was noted more in the right lateral gaze. Pupils were intact. Facial sensation and facial muscles were intact. Hearing was normal. His voice was of nasal quality. Pharyngeal reflex was diminished. The tongue showed deviation to the left without atrophy. Head tremor at 5 c/s was noted. He was able to stand with support but was unable to walk. No muscle atrophy or weakness was noted. The finger-to-nose and the heel-to-knee tests showed dysmetria and decomposition more on the right. Rapid alternating movements were ataxic on the right. Muscle tone was diminished on the right. Muscle stretch reflexes were normally elicited and were symmetric. The plantar response was flexor bilaterally. Sensation was intact. On July 21, a posterior fossa exploration was performed. After the surgery, he was treated with 30 mg/day of alotinolol which showed no effect on his head tremor. He was then treated with gradually increasing doses of clonazepam; when he received 8 mg/day of clonazepam, his tremor showed marked improvement. He was discussed in a neurologic CPC on the nature of the posterior fossa lesion and his tremor. Opinions were divided between delayed radiation necrosis and a radiation-induced brain tumor. The chief discussant arrived at the conclusion that the patient had delayed radiation necrosis compressing the brain stem and cerebellar hemispheres. Regarding the nature of his tremor, he thought that his head tremor was of cerebellar type of postural tremor. Histologic examination of the biopsied specimen revealed accumulation of relatively fresh blood constituents in the deep area of the cerebellum forming a mass. Most of the
 ...
PMID:[A 32-year-old man who developed a posterior fossa mass 12 years after the radiation therapy for cerebellar arteriovenous malformation]. 867 25

Cigarette smoking is an established risk factor for cancer and cardiovascular disease, and is the leading cause of avoidable disease in most industrialized countries. Less well-known are possible beneficial effects, which are briefly considered in this survey. Preliminary data suggest that there may be inverse associations of smoking with uterine fibroids and endometriosis, and protective effects on hypertensive disorders and vomiting of pregnancy are likely. Smoking has consistently been found to be inversely related to the risk of endometrial cancer, but cancers of the breast and colon seem unrelated to smoking. Inverse associations with venous thrombosis and fatality after myocardial infarction are probably not causal, but indications of benefits with regard to recurrent aphthous ulcers, ulcerative colitis, and control of body weight may well reflect a genuine benefit. Evidence is growing that cigarette smoking and nicotine may prevent or ameliorate Parkinson's disease, and could do so in Alzheimer's dementia. A variety of mechanisms for potentially beneficial effects of smoking have been proposed, but three predominate: the 'anti-estrogenic effect' of smoking; alterations in prostaglandin production; and stimulation of nicotinic cholinergic receptors in the central nervous system. Even established inverse associations cannot be used as a rationale for cigarette smoking. These data can be used, however, to clarify mechanisms of disease, and point to productive treatment or preventive options with more narrowly-acting interventions.
 ...
PMID:Beneficial effects of nicotine and cigarette smoking: the real, the possible and the spurious. 874 97


<< Previous 1 2 3 4 5 6 7 Next >>