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PubMed2003

Neurological diseases and accidental falls of the aged.

OBJECTIVE: To assess the influence of central and peripheral neurological diseases on the incidence of accidental falls of the aged. DESIGN: 1. Case-control study with cross-section at two years and 2. prospective study in a follow-up up to seven years thereafter. SETTING: Sample of a population study including all 589 inhabitants older than 70 years in three rural communities. PARTICIPANTS: 44 subjects with recurrent falls during two years' follow-up and 41 age and sex matched controls. MEASURES: Neurological diseases and evaluation, other diseases, and incidence of falls during the seven years' follow-up after the cross-section. RESULTS: Compared with the controls the fallers had more often multiple vascular lesions of the brain, extrapyramidal symptoms and signs as well as lumbar nerve root lesions. In the follow-up, cerebrovascular disease, especially with multiple lesions and residual signs of pyramidal tract lesion, Parkinson's disease, rigidity and hypokinesia were associated with increases risk of falling. In multivariate analysis signs of pyramidal tract lesion, rigidity and prior falls were predictors of falls. An increase in the incidence of falls was also associated with vascular lesion of the cerebellum, cerebral white matter hypodensity and cortical atrophy visible on CT. CONCLUSIONS: High incidence of falls was associated with chronic central nervous system diseases. Lumbar root lesions were more common among the fallers but did not increase the incidence of falls in the follow-up. Neurological diseases and evaluation, other diseases, and incidence of falls during the seven years' follow-up after the cross-section. Compared with the controls the fallers had more often multiple vascular lesions of the brain, extrapyramidal symptoms and signs as well as lumbar nerve root lesions. In the follow-up, cerebrovascular disease, especially with multiple lesions and residual signs of pyramidal tract lesion, Parkinson's disease, rigidity and hypokinesia were associated with increased risk of falling. In multivariate analysis signs of pyramidal tract lesion, rigidity, and prior falls were predictors of falls. An increase in the incidence of falls was also associated with vascular lesion of the cerebellum, cerebral white matter hypodensity and cortical atrophy visible on CT.

Accidental Falls↗
PubMed1995

Developmental effects of dioxins and related endocrine disrupting chemicals.

Alteration of hormones has long been known to affect development. TCDD and related PHAHs modulate the levels of many hormonal systems. Dioxins cause a spectrum of morphological and functional developmental deficits. Fetotoxicity, thymic atrophy, and structural malformations are often noted. Delayed genitourinary tract effects have been observed, and recent studies reported behavioral effects. Highly exposed human offspring have exhibited developmental problems as well. Recently, hormonal and neurological abnormalities have been reported in infants from the general population. The complex alteration of multiple endocrine systems is likely associated with the spectrum of adverse developmental effects caused by dioxin and related compounds.

Abnormalities, Drug-Induced↗
PubMed1988

Immunologic complications of long-term implantation of a total artificial heart.

Bacterial infections are a significant complication of long-term total artificial heart implantation. We evaluated the functional capabilities of host defense mechanisms in two patients sustained long-term by a total artificial heart. Although serum complement and polymorphonuclear leukocyte function remained intact, both patients became B and T lymphopenic and there was an initial decrease in the ratio of helper/inducer to suppressor/cytotoxic cells. Histologic examination of their lymphoidal tissue at autopsy further revealed reduced numbers of germinal centers and atrophy of the T lymphocyte-dependent areas. In addition, the reticuloendothelial system was engorged with degenerate erythrocytes. We hypothesize that blockade of the reticuloendothelial system was induced by multiple blood transfusions necessitated by device-associated hemolysis and coagulopathy. This blockade may have led to a progressive loss of content of the antigen-specific lymphoidal elements and, perhaps, to a reduced ability to ingest microbe-antibody complexes.

Bacterial Infections↗
PubMed2001

Autonomic dysfunction in multiple sclerosis: cervical spinal cord atrophy correlates.

Autonomic dysfunction has rarely been studied in patients suffering from multiple sclerosis (MS). Some hypotheses have concerned the pathophysiology, especially with regard to a possible spinal cord origin. However, there have been no previous studies on autonomic dysfunction in MS and spinal cord lesions. This study assessed the frequency of autonomic dysfunction (AD) in MS and the correlation to spinal cord magnetic resonance imaging (MRI) findings. We prospectively studied 75 MS patients (25 with relapsing-remitting forms, 25 with secondary progressive forms and 25 with primary progressive forms). We performed sympathetic skin response, R-R interval variability and orthostatic hypotension testing. Spinal cord MRI was performed to detect demyelinating lesions (sagittal and axial plane) or spinal cord atrophy. Clinical and laboratory evidence of AD was found in 84% and 56% of MS patients, respectively. The correlation of the latter with disability was evaluated using the Extended Disability Status Scale. AD was more frequent in primary progressive MS than in the other two forms. AD was correlated with spinal cord cross-sectional area reduction but not with spinal cord hyperintensities. This study confirms that the frequency of AD in MS, especially in primary progressive forms, has until now been underestimated. Furthermore, AD appears to be more closely related to axonal loss, as demonstrated by spinal cord atrophy, than to demyelinating lesions.

Adult↗
PubMed2005

Interferon beta promotes nerve growth factor secretion early in the course of multiple sclerosis.

BACKGROUND: Interferon beta therapy has been shown to reduce the rate of clinical relapse and the frequency of magnetic resonance imaging-defined T2- weighted lesions in patients with multiple sclerosis (MS). When given early, interferon beta also reduces the rate of development of brain atrophy and improves axonal integrity. Nerve growth factor (NGF) can retard the severity and course of experimental allergic encephalomyelitis. OBJECTIVE: To determine whether interferon beta effects on patients with MS could be related to modulation of neurotrophin production within the central nervous system. DESIGN: We studied neurotrophin production by human glial and brain endothelial cells in response to coculture with MS patient-derived lymphocytes, and correlated levels of NGF secretion with clinical and magnetic resonance imaging-defined markers of disease. RESULTS: We demonstrate that production of NGF by human brain microvascular endothelial cells is triggered by interaction with T lymphocytes derived from MS patients. No such response was observed using human adult microglia or human fetal astrocytes. Nerve growth factor production by endothelial cells was potentiated by pretreating lymphocytes with interferon beta in vitro, and by using lymphocytes derived from MS patients treated with interferon beta in vivo. By using this assay, we show that levels of NGF induced by lymphocytes from MS patients inversely correlate with magnetic resonance imaging measures of brain atrophy and axonal injury. CONCLUSION: These findings suggest that interferon beta-mediated production of NGF at the level of the blood-brain barrier, whether acting as an immunomodulator or directly on neural cells, is another potential mechanism contributing to the magnetic resonance imaging-defined effect of interferon beta on brain atrophy when given early in the course of MS.

Adult↗
PubMed1983

Immunoreactive myelin proteolipid, protein-like activity in cerebrospinal fluid and serum of neurologically impaired patients.

Two hundred seventy-eight samples of cerebrospinal fluid and 273 samples of sera from a variety of neurological patients were examined by radioimmunoassay for myelin proteolipid protein-like reactivity as an index of structural damage to myelin. Groups of patients with active central nervous system damage could be distinguished easily, although there was a small percentage of false positive reactions. The reactivity was most marked in the demyelinative, encephalitic, and stroke categories. A radioimmunoassay for proteolipid protein of proper sensitivity and specificity may prove to be a useful objective clinical measure of the presence and degree of disease activity in multiple sclerosis and other diseases.

Brain Damage, Chronic↗
PubMedDate not supplied

MR imaging of white matter lesions in uncomplicated chronic alcoholism.

Chronic alcoholics may have CNS lesions, such as microvasculitis or glial, neural, and myelin degeneration, as documented in postmortem studies on subjects who had Wernicke encephalopathy, corpus callosum degeneration, or central pontine myelinolysis. One may also expect the presence of early white matter disease in patients who do not have neurologic complications of alcoholism. Thirty-five chronic alcoholics (Diagnostic and Statistical Manual III criteria) and 35 normal control subjects were studied by means of magnetic resonance (MR) imaging. Subjects greater than 60 years old, or those with CNS involvement, or clinically evident systemic disorders were excluded. Of the remaining asymptomatic alcoholics, MR detected multiple round hyperintense areas in the white matter of 14 patients, in addition to aspecific corticosubcortical and cerebellar atrophies. None of the normal control subjects showed such a finding. These results suggest an early involvement of the brain in asymptomatic alcoholic patients.

Adult↗
PubMed1987

Ocular findings in linear sebaceous naevus syndrome.

The case of a 5-month-old black female child with a linear sebaceous naevus syndrome and multiple congenital anomalies is presented. Ocular malformations consisted of colobomatous changes of the lid and retina, dermoid of the conjunctiva, chorioretinal changes, and peripapillary atrophy of the optic nerve. Systemic findings included midline cleft of the secondary palate with involvement by the naevus, bilateral hearing loss, asymmetrical skull bones, ventricular septal defect, epidermal inclusion cyst, and developmental delay without seizures.

Basal Cell Nevus Syndrome↗
PubMed1976

Studies on the lymphoid system of mice with lethal acute toxoplasmosis.

Acute toxoplasmosis was induced in CFLP mice by infecting them intraperitoneally with the 25 x 10(3) multiplicity of the virulent RH strain of Toxoplasma gondii. The lymphoid system of mice succumbing to acute toxoplasmosis showed characteristic changes. Significant spleen hypertrophy (spleen index: 1.76), severe thymus atrophy (thymus index: 0.27) and a striking decrease of the lymphocyte count in blood (86%) was found as compared with the uninfected controls.

Acute Disease↗
PubMed1992

Inadvertent intrathecal injection of daunorubicin with fatal outcome.

We report the first known case of daunorubicin administered directly into the human central nervous system. A 3 1/2-year-old female with pneumonia and otitis media was diagnosed with acute lymphoblastic leukemia and was admitted for antibiotics and chemotherapy. On the first day she inadvertently received a 17 mg intrathecal (IT) injection of daunorubicin. When the error was recognized about 1 hour later, her cerebrospinal fluid (CSF) was exchanged with sterile saline by barbotage, IT hydrocortisone was given, a subarachnoid catheter was inserted, and the CSF was allowed to drain for 36 hours. Only 5.6 mg (33%) of the dose was recovered from CSF, 2.7 mg as daunorubicin and 2.9 mg as the metabolite, daunorubicinol. Initially she was asymptomatic and induction therapy continued with vincristine, 1-asparaginase, prednisone, and IT methotrexate. One week after the daunorubicin injection she developed headache and irritability; CSF protein was 3.2 gm/dl. On the 12th day, she developed fungal sepsis and worsening pneumonia. On the 15th day, she became comatose with a flacid paraparesis, areflexia, and an ascending progressive bulbar palsy. A series of computerized tomography scans over 6 weeks showed increasing diffuse cerebral atrophy. Nerve conduction velocity studies were consistent with an axonal neuropathy. Despite her multiple concurrent medical problems, the timing and characteristics of neurologic damage suggest that IT daunorubicin caused progressive destruction of the nervous system.

Central Nervous System Diseases↗
PubMedDate not supplied

[Multiple sclerosis associated with biological symptoms of systemic lupus erythematosus. A case with anatomical study].

A clinical history typical of multisclerosis began in a 20-year old man with transient, then permanent manifestations involving the optic tract and the pyramidal, extrapyramidal and cerebellar systems. The patient died at the age of 62, at the end-stage of a complex clinical situation which included paraplegia, bilateral cerebellar syndrome, optic nerve atrophy, epileptic seizures and dementia. When the patient was 54 years old, laboratory findings suggestive of systemic lupus erythematosus (SLE) were discovered, namely: antinuclear, native anti-DNA, anti-Sm antibodies, circulating anticoagulant, cryoglobulinaemia and low complement level. These abnormalities persisted up to the patient's death, 8 years later, without any non-neurological sign of SLE. Post-mortem examination showed lesions of focal demyelination characteristic of multiple sclerosis, but no evidence of cerebral or extracerebral SLE. This case raises the problem of borderlines or associations between systemic lupus erythematosus and multiple sclerosis. In our case, as in other cases of "lupoid sclerosis" reported in the literature, there was a frank and isolated elevation of serum IgM levels.

Adult↗
PubMed1992

[Histopathologic features of opportunistic infections of the small intestine in acquired immunodeficiency syndrome].

The frequency of the opportunistic infections of the duodenum in AIDS patients was determined by way of histologic study in 207 patients between January 1987 and June 1991. All cases had serial paraffin sections, run through HES, PAS, Giemsa, Brown-Brenn, and Zieh-Neelsen stains, and 20 cases had in addition cytologic and electron microscopic study. 63 patients had opportunistic infections (10 cryptosporidiosis and 2 isosporiasis; 12 mycobacterial enteritis; 15 CMV enteritis; 7 candidosis; 7 intestinal microsporidiosis confirmed by electron microscopic examination; 12 Giardiasis; 3 duodenal leishmaniasis; 1 intestinal cryptococcosis). Multiple concurrent infections were noted in 6 cases. A mild to severe villous atrophy was observed in 28 cases, associated with opportunistic infection. A patchy distribution of pathogen agent was noted in 34 cases, and 37 cases were associated with oesophagal candidosis. This study points out the value of histologic examination of intestinal biopsy for the diagnosis of systemic infections as well as of unusual parasitosis, and the necessity for multiple endoscopic biopsies because of the frequent patchy distribution of pathogens.

AIDS-Related Opportunistic Infections↗
PubMed1993

[The use of NMR tomography for the dynamic observation of patients with disseminated sclerosis].

NMR-tomography data and clinical topographic parallels were followed up in 27 multiple sclerosis patients on treatment. Primary NMR tomography identified disseminated foci of more intensive signal in the brain and spinal cord of 78% of the patients. In 6 patients the diagnosis was not confirmed, in 21 patients there was tomographic evidence of various disorders: foci of hyperintensity associated with ventricular system enlargement, cerebral atrophy, hyperintensity zones. The number of more intensive signal foci correlated with the disease severity. Hemispheric foci of hyperintensity were clinically most important. Most of the foci were localized in periventricular region. Changes in the above parameters were observed only 1-2 years after the treatment. It is inferred that NMR tomography is both diagnostic and follow-up tool in multiple sclerosis.

Adult↗
PubMed1985

[Epidermal nevus syndrome (of Solomon, Fretzin and Dewald)].

Epidermal naevus syndrome is an entity which has been well established by Solomon, Fretzin and Dewald since 1968, presenting cutaneous, visceral, ocular, osseous and neurological malformations. We report a case with multiple osseous manifestations affecting the entire skeleton, but mainly the skull (osteolysis with absence of frontal bone), the vertebral column (scoliosis with triple deviation), the upper right limb (demineralisation and multiple pathological fractures) and lower members (fractures of the right and left femur) with enlargement of the entire ventricular system and well marked scissures, signs of an cortico-subcortical atrophy shown by scanogram.

Adolescent↗
PubMed1997

[Cerebral positron emission tomographic study in systemic lupus erythematosus].

The cerebral glucose metabolism in eight patients with systemic lupus erythematosus (SLE) and in five healthy controls were examined by positron emission tomography (PET) using 18-F-labeled deoxy-glucose (FDG) as tracer. One of the eight patients had no abnormality by magnetic resonance imaging (MRI), three of them had cerebral atrophy and four patients had multiple white matter hyperintensities and vascular infarcts in the striatum as assessed by MRI. With FDG-PET, inhomogeneous multifocal cerebral glucose hypometabolism was detected, more frequently in the temporal lobe of right hemisphere. The PET findings did not correlate always with the neurological symptoms. Abnormalities in brain metabolism can be detected more frequently by PET, than morphological changes by MRI, indicating the involvement of the central nervous system.

Adult↗