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We report a rare case of oculomotor nerve palsy and choroidal tuberculous granuloma associated with tuberculous meningoencephalitis. A 15-year-old male visited our hospital for an acute drop of the left eyelid and diplopia. He has been on anti-tuberculous drugs (isoniazid, rifampin) for 1 year for his tuberculous encephalitis. A neurological examination revealed a conscious clear patient with isolated left oculomotor nerve palsy, which manifested as ptosis, and a fundus examination revealed choroidal tuberculoma. Other anti-tuberculous drugs (pyrazinamide, ethambutol) and a steroid (dexamethasone) were added. After 3 months on this medication, ptosis of the left upper eyelid improved and the choroidal tuberculoma decreasedin size, but a right homonymous visual field defect remained. When a patient with tuberculous meningitis presents with abrupt onset oculomotor nerve palsy, rapid re-diagnosis should be undertaken and proper treatment initiated, because the prognosis is critically dependent on the timing of adequate treatment.
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PMID:A case of oculomotor nerve palsy and choroidal tuberculous granuloma associated with tuberculous meningoencephalitis. 1878 52

We report our findings for a patient with orbital apex syndrome associated with herpes zoster ophthalmicus. Our patient was initially admitted to a neighborhood hospital because of nausea and loss of appetite of 10 days' duration. The day after hospitalization, she developed skin vesicles along the first division of the trigeminal nerve, with severe lid swelling and conjunctival injection. On suspicion of meningoencephalitis caused by varicella zoster virus, antiviral therapy with vidarabine and betamethasone was started. Seventeen days later, complete ptosis and ophthalmoplegia developed in the right eye. The light reflex in the right eye was absent and anisocoria was present, with the right pupil larger than the left. Fat-suppressed enhanced T1-weighted magnetic resonance images showed high intensity areas in the muscle cone, cavernous sinus, and orbital optic nerve sheath. Our patient was diagnosed with orbital apex syndrome, and because of skin vesicles in the first division of the trigeminal nerve, the orbital apex syndrome was considered to be caused by herpes zoster ophthalmicus. After the patient was transferred to our hospital, prednisolone 60 mg and vidarabine antiviral therapy was started, and fever and headaches disappeared five days later. The ophthalmoplegia and optic neuritis, but not the anisocoria, gradually resolved during tapering of oral therapy. From the clinical findings and course, the cause of the orbital apex syndrome was most likely invasion of the orbital apex and cavernous sinus by the herpes virus through the trigeminal nerve ganglia.
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PMID:Orbital apex syndrome associated with herpes zoster ophthalmicus. 2214 Mar 5

Pituitary aspergillosis is a very rare disease, documented in only 12 cases. Although seen in both immunocompetent and immunocompromised patients, serious invasive sequelae, such as meningoencephalitis and death, have been noted in immunocompromised patients. Immunocompromised patients are susceptible and require complex multidisciplinary care to contain the spread of infection and maximize outcomes. This is the first case report, to our knowledge, of pituitary aspergillosis in the setting of an organ transplant. A 68-year-old woman presented with cephalgia, left temporal hemianopsia, and ptosis. Non-contrast magnetic resonance imaging of the head revealed a sellar mass, which was believed to be a benign pituitary adenoma. She underwent trans-sphenoidal resection, and subsequent histopathologic examination showed aspergillosis. She was subsequently started on voriconazole. On postoperative day 3, she developed a left anterior cerebral artery ischemic stroke, likely from Aspergillus angioinvasion and occlusion. Her mental status declined further and she died when care was withdrawn.
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PMID:Pituitary aspergillosis in a kidney transplant recipient and review of the literature. 2409 64

Paranasal mucoceles are benign slow-growing paranasal sinus lesions, which usually develop following the obstruction of the sinus ostiu. They most frequently occur in the frontal sinus. Frontal mucoceles are expansive lesions usually causing visual clinical signs and symptoms such as diminution of vision, visual field defects, diplopia, orbital swelling, retroorbital pain, displacement of eye globe, ptosis, and proptosis. When the frontal mucocele extends intracranially, it can manifest with meningitis, meningoencephalitis, intracranial abscess, seizures, or cerebrospinal fluid fistula. Very rarely it can cause forehead swelling. We report an 80-year-old woman presenting with a forehead skin ulcer and painless subcutaneous forehead induration. Histopathologic examination revealed mucin deposition and inflammation. Computerized tomography (CT) and magnetic resonance imaging (MRI) scans showed a mass originating from the frontal sinus with frontal bony defect and frontocutaneous fistula. Surgical excision of the mass confirmed the mucocele diagnosis. In this article, we present a case of frontocutaneous fistula and skin ulcer, which is an unexpected complication of frontal mucocele. We propose that in the case of a localized non-healing ulcerated forehead skin lesions, mucocele should be considered in the differential diagnosis.
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PMID:Unusual case of frontal mucocele presenting with forehead ulcer. 2541 50

Orbital apex syndrome is a rare manifestation of Herpes Zoster (HZ). HZ Mmeningoencephalitis are also rare in immunocompetent persons. We report a rare case that was considered to be HZ meningoencephalitis with orbital apex syndrome in an immunocompetent female. The patient initially manifested with HZ skin lesions and lose of her left sight, diplopia, ptosis, followed by headache, neck pain, and fever, dizziness. Cerebrospinal fluid analysis showed elevation of lymphocytes and protein. A MRI abnormality was remarkable for the presence of a left cerebellum, occipital lobe as well as dura lesion. Head computed tomography and Magnetic resonance venography was normal. Corticosteroid therapy and antiviral therapy was effective to decrease the headache and skin pain. Symptoms were markedly improved after corticosteroid therapy. Three months later, we called the patient to follow up. Her meningoencephalitis symptom recovered. Her follow up brain MRI was normal. But left blindness and external ophthalmoplegia was persistent. This case suggested HZ could affect central nervous system and peripheral nervous system at the same time.
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PMID:Orbital apex syndrome and meningoencephalitis: a rare complication of herpes zoster. 2655 Apr 8

Meningitis or meningoencephalitis is a known complication of scrub typhus. Focal neurological deficits are rarely reported including hemiparesis, quadriparesis and isolated cranial nerve palsies. Here we are reporting a 24 years female who presented with fever, headache, ptosis, diplopia, facial deviation and unsteadiness of gait due to scrub typhus. Scrub typhus can present as acute or subacute meningitis complicated by multiple cranial palsies and cerebellitis. Hence it needs to be differentiated from acute bacterial meningitis and tubercular meningitis as delay in diagnosis and treatment will affect the morbidity and mortality.
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PMID:Scrub Meningitis Complicated by Multiple Cranial Nerve Palsies and Cerebellitis. 3157 66

Chronic enteroviral meningoencephalitis is a well-known complication in patients with X-linked agammaglobulinemia (XLA). However, progressive neurodegenerative disorders or chronic neuroinflammatory diseases with no causative microorganisms have been recognized as rare central nervous system (CNS) complications in XLA. We herein report a family in which two of three members with XLA had developed progressive meningoencephalitis with an unknown etiology. A 15-month-old male infant presented with left-sided ptosis. Initially, the family denied any family history of inherited diseases, but later disclosed a family history of agammaglobulinemia previously diagnosed in two family members. In the early 1980s, one of the elder brothers of the index patient's mother who had been treated with intramuscular immunoglobulin [or later intravenous immunoglobulin (IVIG)] for agammaglobulinemia deceased at 10 years of age after showing progressive neurological deterioration during the last several years of his life. The index patient was diagnosed with XLA caused by Bruton tyrosine kinase deficiency (654delG; Val219Leufs*9), and chronic meningoencephalitis with an unknown infectious etiology. Magnetic resonance imaging of the brain demonstrated inflammatory changes in the basal ganglia, hypothalamus, midbrain, and pons, with multiple nodular lesions with ring enhancement, which showed impressive amelioration after the initiation of IVIG replacement therapy. Pleocytosis, which was characterized by an increase in CD4-positive and CD8-positive T cells expressing an activation marker and an elevation in inflammatory cytokines in the cerebrospinal fluid, was identified. No microorganism was identified as a cause of CNS complications. He thereafter developed brain infarction at 19 months of age and fatal status epilepticus at 5 years of age, despite regular IVIG with high trough levels and regular intraventricular immunoglobulin administration. The etiology of this rare CNS complication in XLA is currently unknown. Previous studies have suggested a possible association of IVIG, which was clearly denied in our index case because of the demonstration of his neurological disorder at presentation. In the future, extensive and unbiased molecular methods to detect causative microorganisms, as well as to investigate the possible role of autoimmunity are needed to clarify the etiology of CNS complications.
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PMID:Fatal Progressive Meningoencephalitis Diagnosed in Two Members of a Family With X-Linked Agammaglobulinemia. 3304 21