Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The patient, a 31-year-old married woman, noticed spasticity on walking at the age of 19 accompanied by ataxia, dysarthria and dysphagia. Facial twitching and dystonic movement of extremities have been observed since age 27. A sister of her father showed the similar ataxia and dysarthria, and expired of pneumonia at the age of 45. On admission at the age of 29, neurological examinations revealed nystagmus, marked spasticity with pathological reflexes and clonus, cerebellar ataxia, dysarthria and dysphagia, diffuse muscle wasting, fasciculation in facial musculature, and generalized slow dystonic movement. By neuro-otological studies bilateral MLF syndrome with upward gaze limitation and decreased velocity of saccadic eye movement were detected. Surface EMG at rest showed a dystonic discharges on the extremities. Needle EMG disclosed a systemic neurogenic change with reduced interference and high amplitude potentials. Atrophy of the brainstem was remarkable on the cranial CT and MRI. These abnormal eye movements, especially bilateral MLF syndrome and generalized dystonia seem to be quite unusual in the variety of spinocerebellar degenerations. On reviewing detected clinical descriptions on Joseph disease this case can be probably included.
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PMID:[A case of spinocerebellar degeneration with bilateral MLF syndrome and dystonia]. 274 81

Vertigo is an unpleasant sensation of movement of the subject or of his surroundings. There are many causes of vertigo. Traditionally these are divided into 'central' and 'peripheral'. It is unusual to find it as a symptom of myelopathy. We describe the case of a 67 year-old woman with no significant previous clinical history who complained of the sudden onset of vertigo a few hours previously, which worsened on turning her neck towards the left. On examination, the vertigo recurred on turning her neck to the left after a latent period of a few seconds together with the appearance of ipsilateral conjugated nystagmus, which gradually disappeared. On neurological examination, there was amyotrophy of both arms with weakness, considerably reduced reflexes, except for clonus of the left wrist. There was slight paraparesia with bilateral cutaneoplantar flexion and a level of sensitivity at C2-C3. The sensitivity disorder was more marked in the arms with a bilateral distribution approximately at C5-C7 affecting predominantly thermoanalgesia. Cervical MRI showed a mass consistent with ependymoma. This was removed surgically 2 weeks after admission. The findings of the intraoperative biopsy confirmed the radiological diagnosis. The vertigo improved one week after admission, although the patient died of pneumonia one month after operation. Despite the vertigo was an atypical symptom, it was the clue that led to the diagnosis. Hypotheses about the cause of vertigo are discussed.
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PMID:[Vertigo as an atypical symptom of intraspinal cord tumor]. 868 Nov 75

We report a 70-year-old man with progressive gait disturbance and gaze palsy. The patient was well until summer of 1991 when he was 66-year-old, when he noted a gradual onset of difficulty in gait and looking downward. He was evaluated in our hospital in May, 1994 when he was 69-year-old. On admission, he was alert but markedly demented with disorientation and memory loss. Constructional apraxia and dressing apraxia were noted. He had difficulty in gaze to all directions; he could move his eyes only 20% of the normal range. Oculocephalic response was retained. He had small voice and some dysphagia. Other cranial nerves were unremarkable. He could not walk unsupported. Marked retropulsion was noted in which he would fell down spontaneously upon standing unless supported. Moderate to marked rigidity was noted in the neck, trunk, and in the legs, however, in the upper extremities, rigidity was only mild. No tremor was noted. Deep reflexes were symmetrically exaggerated with ankle clonus bilaterally. Plantar response was flexor. Sensation was intact. Routine laboratory tests were unremarkable, however, his cranial MRI showed moderate to marked fronto-temporal atrophy and moderate midbrain and pontine tegmental atrophy. The third ventricle was markedly dilated. He was discharged for out patient care, however, his dysphagia had become progressively worse, and he suffered from frequent bouts of pneumonia. He was admitted to our service on October 17, 1994. His neurologic examination was essentially similar except that he showed more advanced dementia. He was still able to stand with support. Gastrostomy was placed on October 25. Post-operative course was unremarkable. He was discharged on November 1. His motor disturbance showed gradual deterioration, and by the May of 1995, he became bed-ridden, and was admitted to another hospital on May 30, 1995. He was almost totally unable to move his eyes, but oculocephalic response was still elicited. Marked truncal and limb rigidity were noted. He vomited coffee-ground substance on October 31, 1995, and developed hypotension. The subsequent course was complicated by pneumonia and he expired on November 24. The patient was discussed in a neurological CPC. Majority of the participants thought that the patient had progressive supranuclear palsy, but some participants thought that the patient had corticobasal degeneration because cortical atrophy was so marked. Post mortem examination revealed atrophy of the frontal and parietal lobe. The brain stem was atrophic particularly in the tegmental area including the midbrain. The substantia nigra showed marked neuronal loss and globose type neurofibrillary tangles in the remaining neurons. The neurons in the locus coeruleus was well retained, however neurofibrillary tangles were seen. In addition, the cerebellar dentate nucleus, the inferior olivary nucleus, and the internal globus pallidus showed marked neuronal loss and neurofibrillary degeneration. In the frontal cortex, although macroscopic examination showed some atrophy, microscopic examination failed to show neuronal loss or gliosis. The pathologic findings were consistent with the diagnosis of progressive supranuclear palsy.
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PMID:[A 70-year-old man with a progressive gait disturbance and gaze palsy]. 902 10

We report a case of a 40-year-old man presenting with relapsing encephalopathy 4 years post-intestinal transplantation. Each episode was preceded by symptoms suggestive of subacute intestinal obstruction, marked dehydration, and, on one occasion, grade 4 encephalopathy. Physical examination revealed hypertonia, clonus, and hyperreflexia. Biochemistry was consistent with renal impairment, metabolic alkalosis, hyperammonaemia, and normal liver function. Plain radiographs and abdominal computed tomography revealed dilated proximal small bowel loops, and barium radiography demonstrated a strictured distal anastomosis. Hydrogen breath testing indicated bacterial overgrowth. Following rehydration and antibiotic therapy, the patient recovered fully between episodes. Further episodes of encephalopathy did not recur following resection of the distal anastomotic stricture and resolution of bacterial overgrowth. Unfortunately, one year later the patient died of pneumonia. To the best of our knowledge, encephalopathy secondary to intestinal transplant related porto-caval shunt and bacterial overgrowth in strictured bowel has not been previously reported but might have implications for the management of future patients.
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PMID:Relapsing encephalopathy following small bowel transplantation. 1282 21

BACKGROUND Serotonin syndrome is a life-threatening condition that involves overstimulation serotonin receptors, which can be caused by medication overdose, drug-drug interactions, and regular doses of medications. It is often an overlooked diagnosis due to the presenting symptoms. CASE REPORT Our patient was a 79-year-old man with a past medical history significant for coronary artery disease status after coronary bypass surgery who presented to the Emergency Department with altered mental status. Vital signs were significant for hyperthermia. On initial assessment, he was only oriented to person and demonstrated shaking rigors. Lab test results were significant for leukocytosis, with troponins 2.94. A chest X-ray revealed left lower-lobe opacification. He was initially treated for community-acquired pneumonia and his elevated troponin required further work up. He was moved to the Intensive Care Unit (ICU) due to worsening respiratory distress, shaking tremors, and confusion. His troponins remained elevated. On his third day of hospitalization, his rigors had improved, but clonus was present. A medication review revealed the patient was on sertraline. He was started on cyproheptadine. The next morning, his mental status had improved to alert and oriented, and his condition returned to baseline. Upon discharge to a rehab facility, sertraline was discontinued. CONCLUSIONS Serotonin syndrome is a condition that is often not initially recognized. Our patient had multiple health problems and presented with altered mental status and tremors, and serotonin syndrome was not recognized until a full neurological exam and medication review had been done. It is important for physicians to be aware of serotonin syndrome as a differential diagnosis, as the symptoms can be masked by other presenting symptoms.
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PMID:Underlying Serotonin Syndrome, Masked by Community-Acquired Pneumonia and Myocardial Ischemia. 3250 63