Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0029089 (ophthalmoplegia)
 3,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a recent case of common adder (Vipera berus) envenoming causing paralytic signs and symptoms. A 12-year-old girl was bitten by the nominate subspecies of the common adder (V. berus berus) in eastern Hungary on May 2, 2012, 22 km away from where the first neurotoxic V. berus berus envenoming was reported in 2008. The patient developed unambiguous cranial nerve disturbances, manifested in bilateral impairment characterized by oculomotor paralysis with partial ptosis, gaze paresis, and diplopia. Drowsiness and photophobia were her additional symptoms; both occurred only during the first day of envenoming. Until now among viper envenomings in Europe, photophobia has only been documented by victims of Vipera aspis. Supportive and symptomatic treatments were administered during 3 days of hospitalization. Although case reports of V. berus berus envenomings are often published, clinical experience with neurotoxicity by this subspecies still remains rare. Population-based and geographic variation of venom composition in V. berus berus seems to include neurotoxic envenomings in certain populations. This second authenticated case provides new clinical evidence for the existence of a possible neurotoxic V. berus berus population in a restricted geographical area in eastern Hungary.
...
PMID:Further clinical evidence for the existence of neurotoxicity in a population of the European adder (Vipera berus berus) in eastern Hungary: second authenticated case. 2407 91

Thirty seven patients with various neuroparalytic manifestations were studied. There were 25 males and 12 females aged 14 to 50 years with majority in 3rd and 4th decades. Their neurological deficits comprised of drowsiness in 12, stupor in 6, coma in 4 and convulsions in 4 patients. Ptosis was found in 22, ophthalmoplegia and pharyngeal paralysis in 12 each, facial paralysis in 9, respiratory paralysis in 8, flaccid limb paralysis in 9, respiratory paralysis in 8, flaccid limb paralysis in 16 and lock jaw in one case. History of snake bite was present in 25 cases and in the remaining 12 cases there was a history of not awakening or inability to come out of the bed in the early morning. These subjects were treated with respiratory support, antivenom serum supplemented with atropine-neostigmine combination. Recovery was dramatic in 25 cases. 6 patients died within 12 hours of hospitalization and remaining 6 patients showed improvement gradually in 2-3 days time. The importance of high index of suspicion in the early diagnosis of elapid bite poisoning as a cause of neuroparalysis has been emphasized.
 ...
PMID:Neuroparalytic syndrome encountered with snake bite poisoning. 2954 92

HistoryA 25-year-old woman with recently diagnosed systemic lupus erythematosus and class IV lupus nephritis confirmed with biopsy and treated with mycophenolate mofetil presented with a 2-day history of progressively worsening edema of her face and lower extremities. She had no antecedent infection or vaccination. She was admitted to the hospital and treated with methylprednisolone, furosemide, and C1 esterase inhibitor. On hospital day 2, she experienced a witnessed generalized tonic-clonic seizure. At that time, she became hypoxic and was intubated for airway protection. Her laboratory study results preceding the seizure were remarkable for hyponatremia, with a blood sodium level of 122 mEq/L (122 mmol/L) (normal range, 135-145 mEq/L [134-145 mmol/L]), which was corrected to 137 mEq/L (137 mmol/L) over 48 hours. Same-day cerebrospinal fluid analysis was unremarkable, and unenhanced head CT findings (not shown) were normal, with no evidence of intracranial hemorrhage or edema.Her subsequent hospital course was complicated by renal failure requiring continuous renal replacement therapy, hypertension (systolic blood pressure ranging from 140 to 190 mm Hg), anemia requiring blood transfusions, thrombocytopenia, and pneumonia. She remained intubated with a limited neurologic examination due to sedative medications until hospital day 10. After extubation, she was noted to have a right gaze preference. She was able to speak in short phrases and follow simple commands. Neurologic examination was notable for drowsiness, right gaze deviation, direction-changing torsional nystagmus, horizontal ophthalmoplegia, and generalized symmetric weakness without upper motor neuron signs. The following day (hospital day 11), unenhanced MRI of the brain was performed along with MR angiography of the brain. Biopsy of the temporal artery was normal, without evidence of inflammation.
 ...
PMID:Case 279: Central-Variant Posterior Reversible Encephalopathy Syndrome. 3253 24

Wernicke's encephalopathy is an acute neurological disorder caused due to thiamine deficiency. It is characterized by a triad of confusion, ataxia, and ophthalmoplegia. Wernicke's encephalopathy can present with atypical clinical manifestations, particularly in setting of nonalcoholic background. Our patient manifested with clinical complaints of acute drowsiness, speech difficulty, and ataxia. Magnetic resonance imaging of the brain revealed T2 hyperintensity in bilateral medial thalami, globus pallidus, periaqueductal gray matter, dorsal pons, and dorsal medulla. The diagnosis of Wernicke's encephalopathy was entertained and he well responded to parental thiamine therapy. The clinician should be aware about atypical presentation of Wernicke's encephalopathy.
 ...
PMID:Wernicke's Encephalopathy: Typical Disease with an Atypical Clinicoradiological Manifestation. 3275 19


<< Previous 1 2 3