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)

We report a new case of non-familial dysautonomia. The patient was a boy with no known Jewish ancestry in whom psychomotor retardation in early infancy failed to lead to specialized evaluation. Regressive episodes of ataxia developed at the age of three and infrequent generalized seizures occurred between four and seven. Diagnosis was first considered at the age of seven after neuroparalytic keratitis developed and rapidly became bilateral. This case has remained highly unusual throughout the course since none of the commonly reported complications (swallowing disorders, aspiration pneumonia, and dysautonomic "attacks") has occurred. No life-threatening manifestations have developed. Peripheral nerve biopsy specimens showed that myelinated fibers, especially of large diameters, were abnormally scarce, and that the histogram failed to exhibit the normal bimodal aspect. Ultrastructural studies also disclosed a marked reduction in the caliber of unmyelinated fibers, whose axons were flattened or occasionally missing. No evidence of regeneration was found. The atypical clinical features in our patient are discussed.
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PMID:[Dysautonomia. A clinical study of a case, ultrastructural data]. 236 47

We reported a 71-year-old male with lateral medullary syndrome presented acute respiratory arrest after ataxic respiration. The patient had experienced transient diplopia repeatedly for about 2 weeks and then the developed persistent diplopia and vertigo. On the third day he was admitted to our hospital because of neurological deterioration and aspiration pneumonia. He showed left Horner's sign and double vision. And he had sensory disturbances of pain and temperature in the left face and the right side of the body, left limb ataxia and truncal ataxia. He showed dysarthria, severe dysphagia and left mild central facial paresis, but no hemiparesis. This case was clinically considered to be a typical case of left lateral medullary syndrome. When he was admitted to our hospital, he showed hypoxia with hypercapnea in spite of no history of chronic obstructive pulmonary disease. This condition was considered to be a central alveolar hypoventilation. He had two episodes of sudden-onset respiratory arrest following ataxic respiration on the 4th and 5th days, but no cardiac arrest. He was supported his respiration by mechanical ventilation until he was able to breathe spontaneously on the 29th day. The 22nd day MRI disclosed high intensity area in the left lateral and dorso-medial medulla in T2-weighted image, and this lesion was 1.5 cm in length. Therefore this case was diagnosed medullary infarction. This case developed ipsilateral facial pain in chronic stage. Pain existed around the eye and in the cheek, and pain was like toothache and unbearable like thalamic pain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of medullary infarction presented lateral medullary syndrome and respiratory arrest after ataxic respiration]. 268 32

Progressive supranuclear palsy (PSP) is an uncommon, but debilitating, neurological disease. Characterized by paralysis of eye movements, difficulty talking and swallowing, body trunk rigidity, gait ataxia, and dementia, the disease progresses rapidly over a 6-8 year time span. Death usually occurs from aspiration pneumonia. To provide meaningful care for the PSP patient and his/her family, the neuroscience nurse must first understand the disease pathophysiology, then the appropriate care interventions.
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PMID:Progressive supranuclear palsy: nursing care implications. 297 88

The anticonvulsant activity of nitrazepam (Mogadon) was studied in 31 children with various seizure patterns. Dosage ranged from 0.3 to 2.2 mg. per kg. body weight daily.Eleven of 15 children with minor motor seizures showed improvement and six obtained complete relief. Nine of 16 with miscellaneous seizures were improved, but only one was completely relieved and the other eight responded to a variable extent. In cases with more than one type of seizure, the myoclonic elements were those most often diminished, but sometimes this effect was only temporary. Side effects were transient and usually mild, consisting of drowsiness, ataxia, slurred speech and excessive secretion of mucus and saliva. However, three cases of aspiration pneumonia were encountered and may have been at least partly due to the side effects. No hematological or biochemical abnormalities were observed.The results indicate that nitrazepam is a relatively safe and effective drug in the treatment of minor motor seizures, particularly infantile spasms, and is even more useful than ACTH in this serious form of epilepsy. In older children its value is chiefly for myoclonic seizures, but the degree and duration of its effectiveness appear to be more limited.
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PMID:Nitrazepam in the treatmet of epilepsy in childhood. 555 May 46

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

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

A 2 day old foal was presented with central nervous depression (coma) after moxidectin overdose. Moxidectin belongs to the milbemycin anthelmintics which elicit their working mechanism through a GABA (gamma-aminobutyric acid)-stimulatory mode of action. The foal developed profound hypothermia, bradycardia and hypoventilation. Absence of urine voiding and mild abdominal distension suggested a ruptured bladder, which was confirmed by transabdominal ultrasound and clinical-pathologic parameters. Repeat auscultation of the ventral lung parts and the occurrence of gastric reflux were suggestive of an aspiration pneumonia. The foal underwent surgical bladder repair, however, did succumb due to mixed acidosis and early signs of sepsis postoperatively. The findings in this foal are suggestive for moxidectin overdosing. The GABAergic working mechanism of moxidectin does explain the development of profound central nervous depression and its sequels hypothermia, bradycardia, hypoventilation and paralytic ileus. Dyssynergia was unexpected, however, has to be related to a central nervous problem, rather than a peripheral nervous problem.
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PMID:[Moxidectin poisoning in a foal?]. 1041 82

The Chiari malformations are a group of central nervous system defects that involve the posterior cranial fossa. The clinical complaints range from headache, sensory changes, vertigo, ataxia, and imbalance to hearing loss. In patients with Chiari malformation, only those with type I malformation were born grossly normal, the neurological dysfunction developing gradually as they grew up, which spurred our interest. From August 1990 to September 1998, seven patients received surgical intervention at Kaohsiung Medical College Hospital under the impression of Chiari malformations. There were 4 males and 3 females, with age ranging from 7 years to 41 years. All these patients were diagnosed via magnetic resonance imaging and surgical findings revealed a hypoplasic vermis. Among them, 4(57%) were cranial nerve plasy, 2(29%) nystagmus, 6(100%) syringomyelia, 7(100%) scoliosis and one (14%) with hydrocephalus. Cerebellar ataxia and upper limbs weakness was noted in 5(71%) patients. Our surgical interventions included suboccipital craniectomy and dural opening(7/7), C1 posterior arch decompression (7/7), C4,5 laminectomy (1/7), and syringostomy(4/7). There was one mortality in a 41 y/o male with progressively lower cranial nerve(V, VII, IX) impairment as well as poor lung compliance. Other patients improved in their symptoms after follow-up periods of 6 months to 6 years. Our study shows that 1) surgical decompression was indicated in all patients with brain stem and lower cranial nerve dysfunction as well as central cord syndrome caused by syringomyelia; 2) a better result was achieved in those patients who received adequate nervous system decompression; and 3) much attention should be payed to cases with lower cranial nerves XI, X, XII impairment, because complications such as choking and aspiration pneumonia can happen.
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PMID:Surgical outcome of Chiari I malformations--an experience sharing and literature review. 1063 63

A 65-year old man was admitted with severe dysphagia, ataxia and aspiration pneumonia. Dysphagia and ataxia were caused by lateral medullary infarction (Wallenberg's syndrome). The swallowing abnormality was assessed by videofluorography and we attempted the balloon dilatation method for cricopharyngeal dysphagia. Three months after initiation of swallowing training, videofluorography (VF) showed that the magnitude of aspiration to the trachea had decreased and the patient began taking food by mouth. The balloon dilatation method is successful for chronic stage cricopharyngeal dysphagia and the VF test is useful for quantitative assessment of dysphagia and for deciding when to start oral intake in elderly patients.
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PMID:[Swallowing rehabilitation using balloon catheter treatment evaluated by videofluorography in an elderly patient with Wallenberg's syndrome]. 1099 32

Neuroaxonal dystrophy (NAD) was examined in two Papillon dogs and a mix breed dog between Papillon and Chihuahua. In addition, cerebellar cortical abiotrophy (CCA) in a Papillon dog, which had similar clinical and magnetic resonance imaging (MRI) features to those of NAD, was also investigated. The common clinical symptoms of all dogs affected with NAD and CCA, were pelvic limb ataxia and cerebellar ataxia including intention tremor, head tremor, and hypermetria in the early onset. These clinical signs were progressed rapidly, and two dogs with NAD were euthanized by owner's request and the other two died by aspiration pneumonia. MRI examinations and gross observations at necropsy revealed moderate to severe cerebellar atrophy in all cases of NAD and CCA. The most typical histological change of NAD was severe axonal degeneration with marked spheroid-formation in the dorsal horn of the spinal cords, the nuclei gracilis, cuneatus, olivalis and its circumference in the medulla oblongata. The spheroids were characterized as large eosinophilic or granular globes within the enlarged myelin sheaths, sometimes accompanied by moderate accumulation of microglias and/or macrophages. In contrast, such spheroid formation was minimal in the brain of CCA. In the cerebellum, mild to moderate loss of the Purkinje and granular cells were recognized in three dogs with NAD, whereas these changes were more prominent in a dog with CCA. Although the clinical signs and MRI findings relatively resembled between NAD and CCA, the histopathological features considered to be quite differ, suggesting distinct pathogenesis and etiology. Since both NAD and CCA are proposed as the autosomal recessive hereditary disorders, careful considerations might be needed for the breeding of Papillon and Chihuahua dogs.
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PMID:Clinicopathological features of canine neuroaxonal dystrophy and cerebellar cortical abiotrophy in Papillon and Papillon-related dogs. 1798 92


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