Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histoplasma meningitis (HM) has been reported to occur primarily in association with disseminated histoplasmosis (DH). We report a case of histoplasma meningitis occurring in a patient with common variable hypogammaglobulinemia (CVH) in which no manifestations of DH were observed. L. L., a 66-year-old Caucasian male, clerical worker, developed occasional episodes of dizziness and tinnitus in mid-1971. During 1972, increasing frequency of these episodes and gradually progressive confusion were noted. In January 1973, vomiting, forther confusion, obnubilation, and a left central facial paresis developed and he was hospitalized. Physical examination revealed no pulmonary abnormalities, lymphadenopathy or hepatosplenomegaly. Over the ensuing 6-week evaluation, there was occasional fever to 38.5 degrees C. Chest roentgenogram was normal. Cerebral angiography suggested a mass in the left cerebellar hemisphere. EEG was diffusely slow. Multiple CSF examinations revealed: Glucose 7-18 mg/with a normal blood glucose, protein 109-256 mg/and cells 66-140 (95 + % mononuclear). Histoplasma capsulatum was cultured from CSF but not from sputum, urine, blood or bone marrow. Skin tests for PPD, histoplasmosis, coccidiodomycosis, blastomycosis, mumps, dinitrochlorobenzene and streptokinase-streptodornase were negative then and 6 months later. Histoplasma serum antibody was absent. Immunoglobulin analysis revealed IgG 430 mg %, IgA 46 mg %, and IgM 35 mg %, which with the history and skin test results suggested CVH. Treatment with 2.51 gm of amphotericin B given intravenously over a 3-month period resulted in complete reversal of all neurologic signs and clearing of the confusion. The remission has been maintained for two years. This case represents a primary infection of the CNS by histoplasma. The relationship between the HM and the CVH will be discussed.
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PMID:Histoplasma meningitis with common variable hypogammaglobulinemia. 61 43

We examined potential clinical and pathologic correlates of seizures among the 3,291 children in the Childhood Brain Tumor Consortium database. Fourteen percent had seizures prior to their hospitalization for a brain tumor. Among children who had a supratentorial tumor, seizures occurred in 22% of those less than 14 years of age. The prevalence of seizures increased to 68% of older teenagers. Among children with an infratentorial tumor, the prevalence of seizures was relatively constant at 6% over all age groups. The onset of seizures began more than one year prior to surgical tumor removal in over half of the children aged five or more with supratentorial tumors, significantly longer than for those of the same age with infratentorial tumors. Almost all children (98.9%) with an infratentorial tumor and seizures had at least one other symptom and more than three-fourths of them had at least three. Eighty-nine percent of children with a supratentorial tumor and seizures had at least one other symptom and more than one-half had at least three symptoms. Regardless of whether the tumor was above or below the tentorium, confusion or stupor and coma were more common in children with seizures than in children without seizures. Among children with supratentorial tumors, symptoms of a declining academic performance or an abnormality of personality, speech, walking, or sensation were significantly more frequent in children with seizures, while visual symptoms (other than visual loss or diplopia) and nausea or vomiting were less frequent. Among children with supratentorial tumors, those who had seizures were more likely to have paralysis of an arm, hand, or face, confusion or stupor, or coma and less likely to exhibit irritability, papilledema, optic atrophy, decreased visual acuity, pupillary abnormalities, or abducens paresis. Among children with infratentorial tumors, those with seizures were significantly less likely to have truncal ataxia, but more likely to experience confusion, stupor, or coma. In the supratentorial compartment, astrocytoma (nos), protoplasmic astrocytoma, anaplastic astrocytoma, and ependymoma were more frequently associated with seizures than was craniopharyngioma. No infratentorial tumor type was more or less likely to be associated with seizures. All common tumor types that were represented in both the supratentorial and the infratentorial compartment except astrocytoma (nos) were associated with significantly greater rates of seizures when located in the supratentorial compartment. The tumor location with the highest incidence of seizures was, as expected, the superficial cerebrum. More than 40% of the children with such tumors had seizures.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Epidemiology of seizures in children with brain tumors. The Childhood Brain Tumor Consortium. 154 79

This study presents particular clinical manifestations in 7 patients with autoiMmune diseases: rheumatoid purpura with right crural nerve paresis (1 case), Stevens-Johnson syndrome with encephalomyeloradicular syndrome (1 case) and left Wallenberg syndrome (1 case), rheumatoid arthritis with right parieto-occipital syndrome (1 case) and Gowers local panatrophy (1 case), systemic lupus erythematosus with confusional state and meningeal syndrome (1 case) and left ictal hemiplegia (1 case). The importance of neurological clinical manifestations at the onset or during the evolution of the autoimmune diseases is emphasized.
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PMID:Particular neurological aspects in vascular autoimmune diseases. I. Rheumatoid purpura, Stevens-Johnson syndrome, rheumatoid arthritis and systemic lupus erythematosus. 260 78

Migraine in children is diagnosed in presence of paroxystic episodes of headache which recur with free intervals, provided intracranial diseases are excluded. Pathogenesis of this disorder is unclear; migraine with and migraine without aura may be different entities. Many factors can precipitate a migraine attack. In school age, psychologic stress is the commonest factor. Main characteristics of attacks in children are headache, which may be hemicranial; nausea and vomiting, abdominal pain, paraesthesiae. Scotomata are not very common in the pediatric age. In some cases, migraine attacks are complicated by sensory or motor symptoms (paraesthesiae, paresis), usually at one hemisoma. In the basilar artery migraine syndrome, features of brain-stem dysfunction predominate. In a few patients a migraine attack presents itself as an acute confusional state. In migraine, EEG abnormalities are frequent (predominance of diffuse or focal slowing). In some cases a CSF pleocytosis is found after an attack of complex migraine. Prognosis is good. Preventive treatment is necessary if the attacks are severe and if they cannot be relieved by rest or sleep. Symptomatic headaches may be produced by a variety of causes. Rarely, it is secondary to increased intracranial pressure. In the great majority of cases recurrent headache is due to migraine. Usually, clinical data are sufficient for diagnosis, though in some cases the diagnosis is difficult and it is necessary to perform laboratory examinations in order to exclude symptomatic headache.
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PMID:Headache in childhood. 266 55

The term "top of the basilar" has been used in reference to a group of signs and symptoms of midbrain, diencephalic, and posteroinferior hemispheric dysfunction. It has been attributed to ischemia in the territory of second- and third-order vessels that arise from the uppermost portion of the basilar artery. We report our experience with four patients who had alteration of consciousness, confusion, and vertical gaze paresis accompanied by other physical abnormalities. Extensive evaluation did not help in documenting the lesions or in understanding their pathogenesis. The top of the basilar syndrome is a not uncommon form of stroke and carries a variable prognosis. Treatment by anticoagulation may prevent further infarction in selected patients who are seen early.
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PMID:Altered sensorium, confusion, and vertical gaze paresis: the top of the basilar syndrome. 339 40

A patient developed weakness in the upper limbs, eventually causing brachial diplegia with only slight paresis of the legs after rapid correction of severe hyponatraemia. Pseudobulbar palsy, mental confusion and urinary incontinence were also present. CT scan showed a zone of lucency in the pons. Clinical recovery occurred and the zone of lucency had disappeared 12 months after the appearance of the neurological signs.
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PMID:Brachial diplegia in central pontine myelinolysis. 397 43

We observed 24 patients with symptomatic neurosyphilis. Of these 24 patients, nine had clinical manifestations of general paresis, seven tabetic neurosyphilis, five meningovascular neurosyphilis, one taboparetic, one tabomeningovascular, and one spinal neurosyphilis. Confusion, disorientation, lancinating pain, impaired memory, and bizarre behavior were the most prevalent symptoms. Sensitivity of the CSF FTA-ABS test was higher (96%) than that of the CSF VDRL test (79%). CSF cell count and total protein determination may be inadequate for assessing activity of neurosyphilis.
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PMID:Symptomatic neurosyphilis. 666 3

A patient is described who was diagnosed in an outpatient department as having paranoid psychosis and later chronic schizophrenia, which was treated with chlorpromazine. Two years later, the patient was admitted to hospital because of increasing confusion, disorganization, and numerous manic symptoms. Physical examination and serologic examination of blood and CSF confirmed the diagnosis of general paresis. Correct treatment led to the eventual discontinuation of neuroleptics and the cessation of paranoid and manic symptoms.
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PMID:Reversible neurosyphilis presenting as chronic mania. 709 76

Clinical observations of 17 goat kids inoculated with 100-1000 infective larvae of Elaphostrongylus rangiferi and autopsied 21-154 days post inoculation (p.i.) are reported. Pruritus was common in the period 4-10 weeks p.i. Six animals displayed neurological signs starting 35 to 94 days p.i. The most frequent sign was posterior paresis. Other signs included cranial nerve paresis, ataxia, lameness, scoliosis, reduced vision, abnormal behaviour, depression and mental confusion. Recoveries were recorded. An apparent dose-response related eosinophilia was observed at days 14 and 32 p.i. None of the experimentally infected kids shed E. rangiferi first-stage larvae in the faeces, indicating that the nematode will not complete its life-cycle in goats.
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PMID:Experimental cerebrospinal elaphostrongylosis (Elaphostrongylus rangiferi) in goats: I. Clinical observations. 832 46

We report a 76-year-old man who developed blurred vision and dementia. He was apparently well until April 4, 1990 (70-year-old at that time) when he had a sudden onset of bilateral loss of vision. Corrected vision was 0.1 (right) and 0.09 (left). He was admitted to the ophthalmology service of our hospital on April 9, 1990, and neurological consultation was asked on April 11. Neurologic examination revealed alert and oriented man without dementia. Higher cerebral functions were intact. He had bilateral large visual field defects with loss of vision; he was only able to count the digit number with his right eye and to recognize hand movement with his left eye. Otherwise neurologic examination was unremarkable. General physical examination was also unremarkable; he had no hypertension. Cranial CT scan was normal on April 11; lumber spinal fluid contained 1 cell/microliter, 63 mg/dl of sugar, and 97 mg/dl of protein; myelin basic protein was detected, however, oligoclonal bands were absent. He was treated with methylprednisolone pulse therapy and oral steroid, however, no improvement was noted in his vision. He started to show gaze paresis to left, ideomotor apraxia, agnosia of the body, and dementia. Cranial CT scan on June 11 revealed a low density area in the deep left parietal white matter facing the trigonal area of the lateral ventricle. He was discharged on July 2, 1990. Hasegawa dementia scale was 2/32.5 upon discharge. In the subsequent course, he showed improvement in his mental capacity and Hasegawa dementia scale was 22.5/32.5 in 1991, however, no improvement was noted in his vision. In 1994, he started to show mental decline in that he became disoriented, and showed delusional ideation of self persecution and depersonalization with occasional confusional state. He also showed unsteady gait. Cranial MRI on February 13, 1996 revealed a T2-high signal intensity lesion on each side of the parietal deep white matter more on the left and another T2-high signal intensity lesion in the left pons as well as in the right thalamus. He complained of right hypochondrial pain and was admitted to another hospital on April 22, 1996. He was markedly confused and demented. He continued to show bilateral loss of vision, but no motor palsy was noted. Cranial CT scan on April 23, 1996 revealed diffuse cortical atrophy and ventricular dilatation in addition to the low density areas in both parietal deep white matter. He developed jaundice in the middle of May. Abdominal CT scan revealed multiple low-to iso-density areas in the liver and marked iso-to high-density swelling of the right kidney. The patient expired on June 9th, 1996. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had had a carcinomatous limbic encephalitis with optic neuropathy and a choleduct carcinoma. Other opinions entertained included acute disseminated encephalomyelitis with optic neuritis, and granulomatous angiitis of the central nervous system. Some participants thought the primary site of the carcinoma was the right kidney with metastasis to the liver. Post mortem examination revealed a mixed type carcinoma in the right kidney with liver metastases. Neuropathologic examination revealed an incomplete softening in the optic chiasm and the left optic nerve, and in the left parieto-occipital areas. (The right hemisphere was frozen for future biochemical assay.) One of the adjacent cortical arteries had an organized thrombus. Other arteries and arterioles also showed sclerotic changes. Some of the leptomeningeal arteries were positive for Congored staining as well as for beta-amyloid immunostaining. Many senile plaques were seen diffusely in the cerebral cortex and neurofibrillary tangles were seen in the CA1 area and the parahippocampal gylus. No cellular infiltrations or demyelinated foci were seen. The neuropathologic features were consistent with circulatory disturbance based on the amyloid angiopa
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PMID:[A 76-year-old man with loss of vision and dementia]. 928 74


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