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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sequential computerized tomography (CT) was performed on a patient with seizures and an organic mental syndrome. Cerebral sarcoidosis was subsequently diagnosed on the basis of noncaseating granulomas in three organ systems. Cranial nerve palsies, hypothalamic dysfunction, and widespread disease were absent. An unusual neuroradiologic sequence of events indicated focal and asymmetric hydrocephalus, mass effect, ependymitis, diffuse breakdown of the blood-brain barrier, and periventricular white matter destruction. These findings have not been previously described together in a patient with sarcoid. With the advent of noninvasive CT, it is possible to perform serial investigations of encephalopathies of obscure origin. Findings similar to those in the present case should prompt a thorough search for subclinical systemic involvement by sarcoid.
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PMID:Sarcoid encephalopathy with diffuse inflammation and focal hydrocephalus shown by sequential CT. 57 4

Intracranial sarcoidosis is rare. Usually it involves the cranial nerves and presents with symptoms of meningeal irritation, convulsive seizures, hydrocephalus, hemiparesis, mental changes and hypothalamic dysfunction. A case in which the condition simulated a subdural hematoma is reported.
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PMID:Intracranial sarcoidosis presenting angiographically as a sub-dural hematoma. 63 62

A rare case of neurosarcoidosis presenting with psychomotor seizure is reported. A 35-year-old woman was admitted to our ward for further evaluation of syncopal attacks and suspected sarcoidosis. The patient had a history of syncopal attacks for about 15 years prior to admission; however, the pathogenesis was not clarified in spite of various examinations. Three months prior to admission, left peripheral facial nerve palsy, bilateral hypopion and bilateral hilar lymphadenopathy on plain chest film were noted at the departments of neurosurgery and ophthalmology of our hospital. She was referred and admitted to our ward. The diagnosis of sarcoidosis was made by scalene node biopsy. The syncopal attacks could not be controlled by several anticonvulsant agents. Although no significant findings were observed on brain CT and cerebral angiography, spike wave was revealed on electroencephalography (EEG) in the parieto-temporal lead. The syncopal attacks were diagnosed psychomotor seizures from both the clinical features and the EEG findings. We concluded that syncope was caused by neurosarcoidosis. The patient was prescribed steroid with much improvement of these symptoms.
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PMID:[A case of central nervous system sarcoidosis, presenting with psychomotor seizure]. 148 41

A 50-year-old black man with steroid-dependent stage IV sarcoidosis and a prior seizure attributed to neurosarcoidosis had progressive disorientation, ataxia, cranial neuropathies, and increased dyspnea. Neuroradiologic evaluation showed a ring-enhancing lesion in the left basal ganglion causing a mass effect. Craniotomy yielded purulent material that grew a pure culture of Listeria monocytogenes. He responded well to antibiotic therapy.
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PMID:Listerial brain abscess in long-standing sarcoidosis. 158 11

Seizures are a recognized manifestation of neurosarcoidosis, but their clinical relevance is not well established. We reviewed the characteristics, clinical correlations, and prognosis of seizures in 79 patients with neurosarcoidosis. Thirteen (15%) of the 79 patients had seizures, and in eight patients (10%) a seizure was the first manifestation of neurosarcoidosis. These seizures were generalized tonic-clonic seizures in 12 patients (92%) and partial seizures in four patients (31%). The patients with neurosarcoidosis with seizures were more likely to have a progressive or relapsing clinical course and intracranial mass lesions (four patients [31%]), encephalopathy or vasculopathy (eight patients [62%]), or hydrocephalus (five patients [38%]). These central nervous system disorders, rather than the seizures per se, were responsible for most of the serious morbidity and the two deaths (15%) among our patients with seizures. Indeed seizure control was good in 11 (85%) of 13 patients treated with combinations of steroids and antiepileptic medications. Seizures are an important sign in neurosarcoidosis because they are associated with more severe and progressive or relapsing forms of central nervous system sarcoidosis and may be an early manifestation of such disorders.
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PMID:Clinical implications of seizures in neurosarcoidosis. 189 59

Observation of neurosarcoidosis in a thirty-year-old black female characterised predominantly by bilateral facial nerve paralysis gave rise to a review of literature since 1978 and also to a comparison with an early study in 1963. As described 1963 the clinical picture is characterized by increased protein content of the CSF (33.8%), facial nerve paresis (25.5%), pleocytosis (23%), diabetes insipidus (21%), hemiparesis (17.2%), organic psychosis (16.9%), papilloedema (15.5%), ataxia (13%), convulsive seizures (12.5%), optic atrophy (12.5%), loss of hearing (12.2%), nystagmus (8.6%) and numerous other symptoms more rarely found. This corresponds to the symptoms of chronic basal meningitis with an infiltration in the neighbouring structures of brain and less frequently the spinal cord. In only 58.7% of the cases (presumably at the onset of sarcoidosis) was the bronchial tract (or the lungs) affected, in 11.5% the skin or the eyes. Although the clinical picture is clear enough the etiology has yet to be determined. Evidence of a pathogen or a pathogenic agent (analogous to berylliosis) has never been established to date. On the other hand there are some indications of a disturbance in the immune system, perhaps of a particular genetic foundation since sarcoidosis strikes black patients with conspicuous frequency. There exist more cases in one family. Exceeding expected random distribution, many patients have the HLA-Factor B 8 (on the chromosome 6) and DR 3. The Kveim-Test was in 71 cases positive, in 12 cases negative. The possibilities of carrying out studies of CSF - analogous to the studies of bronchial lavage - in the most cases of neurosarcoidosis have not been exhausted as to determine the activity of the T-lymphocytes, the interleucines, the angiotensin-converting enzyme while the Gallium 67 scintigraphy and other methods to determine the non-specific activity of the inflammation. The efficiency of the treatment with corticosteroids (Prednison or Triamcinolonacetonid) depends of the phase of the inflammatory process. 12% of the registered cases died.
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PMID:[Neurosarcoidosis. Comparative analysis of the clinical profile based on 537 cases from the world literature up to 1963 and from 1976-1988]. 240 26

Ten years after a diagnosis of sarcoidosis, a 33-year-old woman presented with a severe headache of 5 days' duration. Neuroradiologic evaluation revealed a large cystic lesion of the left temporal lobe, causing a mass effect. An exploratory operation proved the lesion to be a loculated portion of the temporal horn of the lateral ventricle. Drainage of the loculated ventricle relieved the patient's cephalgia. Within 2 months, however, pain in the head recurred and an unsteady, broad-based gait appeared. Reevaluation disclosed hydrocephalus for which a ventriculoperitoneal shunt was inserted. After this procedure, the patient did well neurologically for 1 year, after which seizures, personality changes, incontinence, and disturbance of gait developed. Death occurred after revision of the shunt, and widespread granulomatous disease was found at autopsy. Neurosarcoidosis, with emphasis on intracranial mass lesions in sarcoidosis, is discussed; the role of surgical treatment in some of these lesions, and in hydrocephalus, is stressed.
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PMID:Neurosarcoidosis causing ventricular loculation, hydrocephalus, and death. 371 3

Four teenagers with partial epileptic seizures presented focal cortical enhanced CT scan images. Angiographies were normal. Stereotactic biopsies revealed astrocytic proliferation. CT scan abnormalities diminished or vanished in some months. On long-term follow-up seizures were either less frequent or disappeared. None of the possible aetiologic hypotheses (astrocytoma, encephalitis, sarcoidosis, multiple sclerosis, vascular malformation) was fully satisfying. Nevertheless, a regressive evolution observed in these four patients demonstrates that acquired epileptogenic lesions during adolescence are not always of poor prognosis.
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PMID:[Partial epilepsies of adolescence with computer tomography abnormalities, localized astrocytic reaction and spontaneously remitting course]. 642 75

In a retrospective study of 4,294 consecutive postmortem cases, there were 15 with histologically proved sarcoidosis, including 4 with CNS involvement. Whereas in previously reported autopsy series the prevalence of neurosarcoidosis was 15%, it is 27% in this review. Five cases with incidental, clinically inapparent sarcoidosis died at a mean age of 54.6 years; those six with systemic sarcoidosis, not involving the CNS, died at a mean age of 47.0 years; while those four with a variety of neurologic manifestations in addition to systemic sarcoidosis died at a mean age of 38.2 years. Thus, it appears that at one end of the spectrum of morbidity, sarcoidosis may cause no or only trivial symptoms and permit prolonged survival. At the other extreme, sarcoidosis may affect a younger population more severely. CNS involvement occurs relatively early in the course and its rather rapidly progressive, accounting for the poor prognosis, despite appropriate medical and neurosurgical management. In its turn, neurosarcoidosis may present with a variety of signs and symptoms, depending on the site of involvement along the craniospinal axis. This feature is illustrated by the manifestations of compression myelopathy, hydrocephalus with dementia, hydrocephalus with seizures and ataxia, and anosmia, blindness, seizures, and diabetes insipidus. In addition, one patient developed a Nocardia brain abscess as a complication of the altered immune system in sarcoidosis.
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PMID:Pathobiology of neurosarcoidosis and clinicopathologic correlation. 683 29

Infections caused by Actinomyces organisms have been demonstrated to occur in association with IUD use. Uterine actinomycosis infection is usually superficial, but it is potentially invasive. It may prove fatal. When Actinomyces is detected in a vaginal Papanicolaou smear, establishment of the correct diagnosis followed by IUD removal and appropriate antibiotic therapy are recommended. A case history is presented of a 28 year old woman who had been using an IUD and who had systemic Actinomyces infection and a brain abscess develop several years after removal of her uterus and fallopian tubes. The woman was referred to the Johns Hopkins Hospital in Baltimore in 1977 for evaluation of headaches and grand mal seizures. 4 years earlier, in 1973, she had been seen at another hospital with a recent weight loss of 18 kg. She was found to have a tubo-ovarian abscess, for which she underwent a hysterectomy, bilateral salpingectomy, and unilateral oophorectomy. At the time of surgery, an IUD was in place. A histopathological diagnosis of botryomycosis tubo-ovarian abscess was made on submitted tissues. She received no antibiotic therapy. In 1975, pulmonary infiltrates developed that were attributed to bronchopneumonia. She was treated with a short course of tetracycline hydrochloride. Later that year she was thought to have sarcoidosis and was treated for 1 year with several doses of prednisone. Clinically, her condition remained stable until March 1977, when a pyogenic subcostal abscess was drained. In July 1977, she had headache, dizziness, generalized seizures, and an incomplete right homonymous hemianopsia develop. A craniotomy for excision and drainage of an abscess was performed. The presence of Actinomyces israelii in brain tissue was confirmed by direct immunoflourescence using specific antiserum. It was confirmed that Actinomyces had been present at the time of her 1st surgical procedure. She was treated with high doses of intravenous penicillin G potassium for the first 4 weeks, followed by lower doses of oral penicillin V potassium for an additional 15 months. She recovered completely, except for a persistent right homonymous hemianopsia. The case illustrates that systemic dissemination and potentially life threatening complications of uterine actinomycosis can occur if the infection is unrecognized and/or inadequately treated.
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PMID:Systemic Actinomyces infection. A potential complication of intrauterine contraceptive devices. 712 Jun 9


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