Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032290 (aspiration pneumonia)
 2,291 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A consensus conference on stroke was held on March 22, 1991. Subjects on which consensus was reached were: There are different kinds of cerebral haemorrhage and infarction, which can be differentiated by computerized tomography, and this can have practical consequences. At clinical examination special attention should be paid to cognitive impairment. Angiography is indicated only if carotid surgery or unusual causes are considered. CSF examination and EEG are performed only on special indications. Cardiological consultation is necessary in young patients, or if clinical signs of cardiogenic embolism are present. Coumarin derivatives are prescribed in some of these cardiac causes of stroke, to prevent recurrence. There is as yet no effective medical treatment for cerebral infarction. In lobar and cerebellar haemorrhage surgical treatment may be indicated. In the acute phase of stroke it is always important to prevent aspiration pneumonia, pulmonary embolism and decubitus, and to care for muscles and joints. Advantages and disadvantages of gastric tube and indwelling catheter should be weighed. Treatment of hypertension after the acute phase is indicated to prevent recurrent stroke. After TIA and minor stroke, aspirin is prescribed, which reduces the risk of cerebral and myocardial infarction by 30%. Carotid endarterectomy in symptomatic patients with carotid stenosis of 70% or more, reduces the number of fatal or disabling strokes by 50%, if perioperative complications are less than 4%. Rehabilitation after stroke reduces disability and improves the adaptation of both the patient and his environment. The patient should be stimulated and supported; good information, including the family, is essential. Supplying aids and taking special measures should be done on individual basis, after a period of training.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Consensus cerebrovascular accident]. 174 34

We report a 49-year-old man who presented progressive dysarthria, dysphagia, and left hemiparesis. The patient was well until June 28th of 1993 when he noted 'weakness' in his both legs; despite his weakness, he could play golf on that day. In the beginning of July, he noted difficulty in swallowing solid foods. He was admitted to the neurosurgery service of our hospital on July 15th of 1993 and a neurologic consultation was asked on July 17th. Neurologic examination at that time revealed an alert but somewhat childish man who appeared to have some difficulty in paying attention to questions. He was disoriented to time and showed difficulty in recent memory and calculation. Higher cerebral functions were intact. The optic fundi were normal; pupils were isocoric and reacted to light promptly; ocular movements were intact, however, he showed difficulty in convergence. Facial sensation and facial muscles were intact. He had no deafness. He showed slurred speech and difficulty in swallowing solid foods. The remaining cranial nerves were intact. Motor-wise, he was able to walk normally and no weakness or atrophy was noted. Mild ataxia was noted in the finger-to-nose and the heel-to-knee test on the left. Muscle stretch reflexes were normal and symmetric, however, the plantar response was extensor bilaterally. Sensation was intact and no meningeal signs were noted. General routine laboratory findings were unremarkable. CSF was under a normal pressure containing 1 cell/microliter, 68 mg/dl of protein, and 54 mg/dl of glucose. Cranial CT scan showed low density areas involving the pons, midbrain, left thalamus, and the left parietal cortex. In MRI, these areas presented low signal intensity in T1-weighted images and high signal intensity in T2-weighted in images. The brain stem appeared swollen. Gadolinium enhancement was negative. He was given a course of steroid pulse with 1 g/day of DIV methylprednisolone for three days followed by oral steroid. He showed only temporary improvement in swallowing. In the subsequent course, he showed progressive deterioration in dysarthria and dysphagia. A biopsy was performed on the left parietal lobe lesion. After biopsy, he was treated with steroid and glycerol without improvement. A course of chemotherapy with procarbazine, MCNU, and vincristine was given; he did not respond to chemotherapy. His left hemiparesis deteriorated. He developed aspiration pneumonia from dysphagia and expired on October 22, 1993. The patient was discussed in a neurologic CPC, and the chief discussant arrived at the conclusion that the patient had astrocytoma grade III involving the pons, midbrain, thalamus, and the parietal cortex.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 49-year-old man with progressive dysarthria, dysphagia, and left hemiparesis]. 749 19

Human status epilepticus (SE) is consistently associated with cognitive problems, and with widespread neuronal necrosis in hippocampus and other brain regions. In animal models, convulsive SE causes extensive neuronal necrosis. Nonconvulsive SE in adult animals also leads to widespread neuronal necrosis in vulnerable regions, although lesions develop more slowly than they would in the presence of convulsions or anoxia. In very young rats, nonconvulsive normoxic SE spares hippocampal pyramidal cells, but other types of neurons may not show the same resistance, and inhibition of brain growth, DNA and protein synthesis, and of myelin formation and of synaptogenesis may lead to altered brain development. Lesions induced by SE may be epileptogenic by leading to misdirected regeneration. In SE, glutamate, aspartate, and acetylcholine play major roles as excitatory neurotransmitters, and GABA is the dominant inhibitory neurotransmitter. GABA metabolism in substantia nigra (SN) plays a key role in seizure arrest. When seizures stop, a major increase in GABA synthesis is seen in SN postictally. GABA synthesis in SN may fail in SE. Extrasynaptic factors may also play an important role in seizure spread and in maintaining SE. Glial immaturity, increased electronic coupling, and SN immaturity facilitate SE development in the immature brain. Major increases in cerebral blood flow (CBF) protect the brain in early SE, but CBF falls in late SE as blood pressure falters. At the same time, large increases in cerebral metabolic rate for glucose and oxygen continue throughout SE. Adenosine triphosphate (ATP) depletion and lactate accumulation are associated with hypermetabolic neuronal necrosis. Excitotoxic mechanisms mediated by both N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors open ionic channels permeable to calcium and play a major role in neuronal injury from SE. Hypoxia, systemic lactic acidosis, CO2 narcosis, hyperkalemia, hypoglycemia, shock, cardiac arrhythmias, pulmonary edema, acute renal tubular necrosis, high output failure, aspiration pneumonia, hyperpyrexia, blood leukocytosis and CSF pleocytosis are common and potentially serious complications of SE. Our improved understanding of the pathophysiology of brain damage in SE should lead to further improvement in treatment and outcome.
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PMID:Pathophysiological mechanisms of brain damage from status epilepticus. 838 2

Granulomatous meningitis attributable to Coccidioides immitis was diagnosed on postmortem examination in a 4-year-old Border Collie. Clinical signs included CNS disease, aspiration pneumonia secondary to a megaesophagus, and otitis externa. Central nervous system signs included central vestibular and cranial nerve dysfunction. Cerebellar and medullary infiltrates seen on histologic examination affected cranial nerves VIII, IX, and X. Despite extensive diagnostics, diagnosis was not made antemortem. Analysis of CSF suggested suppurative meningitis, but bacteriologic culture results were negative. Coccidioides endospores were identified on reexamination of brain tissue. The clinical course of disease and rate of Coccidioides immitis infection is variable. Causative agents of granulomatous or inflammatory CNS disease may include fungal infection more often than is currently suspected.
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PMID:Granulomatous meningitis caused by Coccidioides immitis in a dog. 953 Apr 20

We report a 64-year-old Japanese woman who died one year after the onset of progressive gait disturbance and dementia. She noted a difficulty in holding a glass and hand tremor in June of 1996 when she was 63 years old. In July of 1996, she tended to lean toward left when she walked. She also noted truncal titubation. In November of 1996, she started to have visual hallucination and delusion in which she said "I see something is flying on the wall.", "Somebody has come into my room", and things like that. She was admitted to our service on November 22, 1996. On admission, she was alert and general physical examination was unremarkable. Neurologic examination revealed disturbance in recent memory. Hasegawa's dementia rating scale was 22/30. She showed vivid visual hallucination with colors in which she saw faces of dwarfs and angels, a space ship, and others. Higher cerebral functions were normal. She showed left oculomotor palsy which was a sequel of an aneurysm and subarachnoid hemorrhage nine years before. Otherwise cranial nerves were unremarkable. She showed ataxic gait, limb ataxia, truncal titubation, and postural hand tremor. She had no weakness and no muscle atrophy. Deep tendon reflexes were within normal limits. Plantar response was flexor. Sensation was intact. Laboratory examination was also unremarkable. Complete survey for occult malignancy was negative. CSF was under a normal pressure and cell count was 1/microliter, total protein 27 mg/dl, and sugar 68 mg/dl. Cranial CT scan was unremarkable. MRI was not obtained because of the presence of an aneurysm clip in the left internal carotid-posterior communication artery junction. She showed progressive deterioration in her mental function. By January 1997, she became unable to stand or walk with marked dementia. Repeated CSF exams and cranial CT scans were unremarkable. She suffered from several episodes of aspiration pneumonia. A trial of three days methylprednisolone pulse therapy was given starting on March 7, 1997, which was of no effect on her neurologic status. On March 28, 1997, she was intubated because of acute respiratory distress syndrome. In April 2, her body temperature rose to 38 degrees C. On April 9, 1997, her blood pressure dropped and resuscitation was unsuccessful. She was pronounced dead on the same day. The patient was discussed in a neurologic CPC and the chief discussant arrived at the conclusion that the patient had primary leptomeningeal lymphoma. Other possibilities entertained among the audience included brain stem encephalitis of unknown type, carcinomatous cerebellar degeneration plus limbic encephalitis, Creutzfeldt-Jakob disease, thalamic degeneration, and progressive multifocal leukoencephalopathy. Post-mortem examination revealed thickening and clouding of the leptomeninges; Gram-positive diplococci were found in the leptomeninges. This meningitis appeared to have been an complication in the terminal stage of her illness. Microscopic examination revealed astrocytosis in the midbrain tegmentum. Cerebral cortices showed only mild astrtocytosis. No cerebellar atrophy was seen and Purkinje cells were retained which excluded paraneoplastic cerebellar degeneration. Neuropathologic diagnosis was bacterial meningitis, however, the presence of brain stem encephalitis prior to the onset of bacterial meningitis could not be excluded. It is interesting to note that the diagnosis of the primary neurologic disease of this patient was not easy even after autopsy. As autopsy permission was obtained only for the brain, it was not clear whether or not this patient had an occult malignancy somewhere in her body, however, there was no evidence to indicate paraneoplastic degeneration of the central nervous system. As the patient did not have meningeal signs until one month before her death, it is difficult to ascribe her entire neurologic problems to her meningitis. Finally, her visual hallucination was vivid and colorful; we thought this might have been
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PMID:[A 64-year-old woman with progressive gait disturbance and dementia for one year]. 978 11

Microsurgical removal of acoustic neurinoma is still one of the challenging topics in neurosurgery in spite of the development of Gamma-knife or radiosurgery, with which small and moderate sized tumors can be treated. Surgical technique necessitates more expertise in dealing with larger tumors. In this report ongoing microsurgical standard technique for removal of acoustic neurinomas of approx. 3 cm (extrameatal) in diameter is presented along with its historical backgrounds and literature review with reported techniques used by experienced neurosurgeons. 1) Standard sitting position with head turned (30) and flexed (20) head, and not semisitting position. 2) retromastoid retrosigmoid osteoplastic craniotomy following a linear incision. Special mention is made on how to manage the air embolism inherent to the sitting position in which the use of fibrin glue to seal the air entrance is presented along with early detection. 3) Intracapsular enucleation after the dural incision and retraction of the biventer lobule with special emphasis on the infrequent anatomical course of the facial and vestibulocochlear nerves on the posterior wall of neurinomas. 4) Localizing the facial nerve and vestibulocochlear nerve at the pontine side, so that decision of preserving or sacrificing the latter in the course of surgery can be made from the viewpoint of hearing preservation and concentrate on facial nerve function. 5) Drilling away of the posterior meatal lip in which sufficient drilling away should be performed to minimize opening of the posterior semicircular canal and that of mastoid cells. Complete sealing of either is necessary to prevent hearing loss or CSF rhinorrhoe. 6) Reduction of remaining tumor-capsule volume by sharp dissection or bipolar cutting, using intraoperative EMG-stimulation which identifies the presence of flattened facial nerve fibers on the capsule. Presence tiny remnant of the tumor capsule attached to the nerve bundles just before the entrance of internal acoustic porus (macroscopical "radical" resection) is considered to be acceptable for better postoperative quality of life. 7) Water tight dural closure and secure sealing of mastoid cells is necessary to prevent CSF rhinorrhoe. 8) Facial muscle EMG monitoring and AEP monitoring are mandaroty to accomplish surgery which enables postoperative good quality of life. 9) Results of 88 cases during last 10 years are: good function (HB I and II) of the facial nerve 90.5% at the time of two years follow-up, 11.5% hearing preservation, 1 mortality due to aspiration pneumonia. CSF rhinorrhoe 10%.
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PMID:[Operative neurosurgery: personal view and historical backgrounds (2) acoustic neurinoma]. 1715 74

Germinal matrix hemorrhages (GMHs) are typically seen in preterm neonates during the first 4 days of life. The authors encountered 2 children with late-onset GMH subsequent to ventriculoperitoneal (VP) shunt insertion for congenital hydrocephalus. Both children were delivered at full term with normal body weight, although they were compromised with the preceding hypoxic events prior to shunt insertion. The first case involved a female infant with severe craniofacial deformities. Because of aspiration pneumonia related to the comorbid upper airway stenosis, endotracheal intubation with intermittent mechanical ventilation was necessary. The associated congenital hydrocephalus was treated with VP shunt insertion when she was 35 days of age, and GMH was confirmed 1 week after shunt placement. During a period of conservative observation, the hemorrhage resolved without any neurological deterioration. The second case involved a male infant with a large intraparenchymal cyst on the left parietal portion. He was intubated for pneumonia at 1 month of age. He had associated congenital hydrocephalus that was progressive, and he was treated with VP shunting at 69 days of age, after his pneumonia had resolved. Postoperative GMH was confirmed, although hydrocephalus was well controlled by VP shunt insertion. Observed conservatively, he fared well and the GMH resolved. These 2 cases had unique features in common; both had congenital anomalies in the CNS and respiratory problems before shunting. The hypoxic insults on the residual germinal matrix layer and sudden decrease in CSF pressure may relate to the occurrence of these late-onset GMHs.
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PMID:Delayed germinal matrix hemorrhage induced by ventriculoperitoneal shunt insertion for congenital hydrocephalus. 2364 62