PubMed Health⌕ Search

Biomedical subjects

E Wertman

Publications and source records attributed to E Wertman.

At least 19 recordsLinked to original sources
PubMed1992

An association between multiple sclerosis and type I diabetes mellitus.

We report five patients who had multiple sclerosis (MS) associated with type I diabetes mellitus (TODM). Examination of the Israeli National Neurological Disease Register revealed the prevalence of TODM among 334 MS patients under the age of 30 years to be 8.98 per 1,000. This is significantly higher than the prevalence of TODM in the general population of Israel for the same age group, which is 0.095 per 1,000. MS and TODM share clinical, epidemiological and immunological features, and both diseases have a target site that is neuroectodermal in origin. The association between these two putative autoimmune diseases may suggest a similar pathogenetic mechanism.

Adolescent↗
PubMed1992

Iron accumulation in the rat basal ganglia after excitatory amino acid injections--dissociation from neuronal loss.

The current study examines in an animal model the relation of excessive iron accumulation in the basal ganglia to the pathology of Parkinsonism and Hallervoden-Spatz disease. Following a unilateral microinjection of excitatory amino acids, kainate, or quinolinate to the anterior olfactory nucleus/ventral striatal region, an increase in histochemical iron concentration was observed in the ipsilateral ventral pallidum, the islands of calleja, the globus pallidus, the entopeduncular nucleus, the ventral thalamus, and the substantia nigra pars reticulata. The iron was observed both in glia and as intensification of patches in the neuropil. In a second group of rats, after microinjection of ibotenate or quisqualate to the nucleus basalis of Meynert, iron accumulated in the ipsilateral entopeduncular nucleus and pars reticulata of substantia nigra. Increased iron accumulation, compared to that in the contralateral side, was stable for months after a single microinjection. In the basal ganglia distal from the site of EAA injection, no gross morphological changes were associated with the increased iron accumulation. The implications of these findings to the pathology of Parkinson's and Hallervorden-Spatz diseases are discussed.

Animals↗
PubMed1992

Neglect of near peripersonal space. Evidence for multidirectional attentional systems in humans.

Neglect is most commonly observed and studied in the horizontal spatial dimension. Vertical neglect has been described in a few studies. We now report on a patient with near radial space neglect following bilateral posterior parietal lobe lesions. Our patient also had neglect of inferior vertical and left horizontal space. These spatial deficits appear primarily attentional. Our findings compliment other studies that demonstrate neglect may occur in multiple spatial dimensions and provide evidence for a three-dimensional attentional system in humans. Whereas neglect of inferior vertical space may be associated with bilateral parietal lobe lesions, neglect of superior vertical and far radial space has been associated with bilateral inferior temporo-occipital lesions.

Adult↗
PubMed1992

Antibodies from Down's syndrome patients bind to the same cholinergic neurofilament protein recognized by Alzheimer's disease antibodies.

Down's syndrome (DS) patients who survive beyond the third decade develop brain lesions characteristic of Alzheimer's disease (AD). Sera of AD patients contain antibodies that bind specifically to the heavy neurofilament protein (NF-H) of Torpedo cholinergic neurons. In the present report, we examined whether the AD-like pathologic changes in DS are associated with the existence of such antibodies. Our findings show that IgG of older DS patients (greater than 30 years) binds to Torpedo cholinergic NF-H more readily than does that of young DS patients (less than 30 years) and age-matched normal controls. In contrast, the extent of binding of IgG from the young and older DS groups to Torpedo and bovine spinal cords NF-H is similar and equal to that of normal controls. These findings suggest that older DS patients, like AD patients, contain anti-NF-H IgG that binds specifically to epitopes highly enriched in Torpedo cholinergic NF-H.

Adult↗
PubMed1992

Physical and psychosocial benefits of modified judo practice for blind, mentally retarded children: a pilot study.

A modified form of judo training was practiced by a class of 7 blind, mentally retarded children with associated neuropsychiatric disturbances. The biweekly training program lasted for 6 months. Analysis indicated improvements in physical fitness, motor skills, and psychosocial attitude. The authors concluded that a modified form of judo can be used as a therapeutic, educational, and recreational tool for multiply handicapped children.

Blindness↗
PubMed1991

Phonolexical agraphia. Superimposition of acquired lexical agraphia on developmental phonological dysgraphia.

Study of neuropsychological sequelae of a focal acquired brain lesion may bring out and help delineate the features of a compensated developmental language disorder and its anatomical substrate. A left-handed man with a history of phonological developmental dyslexia and dysgraphia learned in early adulthood to read and write using a lexical system. Following a small posterior right parietal infarct when aged 56 yrs he developed a severe agraphia displaying features of phonological dysgraphia with impaired segmentation and features of lexical agraphia. Writing was severely impaired for all classes of word and nonword stimuli but his errors did not resemble those attributable to a deficit in the system responsible for the short-term storage of the graphemic representation of a word (graphemic output buffer). These observations imply that an acquired lexical agraphia has been superimposed on his developmental phonological dysgraphia, resulting in a combined or 'phonolexical' agraphia.

Agraphia↗
PubMed1991

Passive listening and task related P300 measurement for the evaluation of dementia and pseudodementia.

The late evoked potential P300 was tested in three groups of subjects. These consisted of 25 patients suffering from dementia (Group I), 14 patients suffering from pseudodementia due to severe depressive disease (Group II), and 24 age-matched normal controls (Group III). Since patients suffering from dementia frequently have difficulties in counting targets in the "oddball" paradigm, we evaluated the usefulness of a Passive Listening condition. With the classical "oddball" paradigm, 78% of the subjects were correctly related to one of the three groups examined. The "P300-like" wave form produced in the Passive Listening condition was not found to be sensitive enough to allow such a distinction.

Adult↗
PubMed1990

Cortical second messengers after NBM damage: no change in responses to cholinergic agonists.

Damage to the nucleus basalis of Meynert (NBM) decreases acetylcholine (ACh) innervation of cortex. We explored transmission of cholinergic messages in cortex 2-3 weeks after such damage. The NBM damage was unilateral and the ipsilateral denervated cortex was compared to the contralateral nondenervated cortex. The response to carbachol, a muscarinic ACh receptor-agonist, was measured by inhibition of forskolin-induced cAMP accumulation in cortical membranes and by formation of inositol phosphate (IP) in cortical slices. No difference was found in the carbachol effects between ipsi- and contralateral cortices. Thus, we find no evidence of either receptor loss or receptor supersensitivity. There was, however, a significant decrease in K(+)-stimulated IP formation in the cortex ipsilateral to the damage which probably reflected loss of cholinergic terminals. When comparing the cortex contralateral to NBM damage with the cortex contralateral to sham damage in control rats, no difference was found in any of the above parameters. When severe cognitive deficits are observed, 2-3 weeks after NBM damage, loss of presynaptic ACh is the main change in cortical cholinergic transmission.

Acetylcholine↗
PubMed1989

Alzheimer's disease antibodies bind specifically to a neurofilament protein in Torpedo cholinergic neurons.

Alzheimer's disease (AD) is characterized by neurofibrillary tangles and neuritic plaques and by the degeneration of central cholinergic neurons. Recent studies indicated the presence of antibodies in the sera and cerebrospinal fluid of AD patients which react with neuronal tissue and which recognize cholinergic neurons. In order to identify the cholinergic antigens against which the AD antibodies are directed, we have recently used the purely cholinergic electromotor neurons of the electric fish Torpedo which are chemically homogenous and cross-react antigenically with mammalian cholinergic neurons. This study revealed that immunoglobulins (IgG) from sera of AD patients bind specifically to an antigen in Torpedo electromotor neurons with an apparent molecular weight of 200 kDa. In the present report we attempt to characterize this antigen. The similarity in size of this protein to that of the heavy neurofilament subunit (NF-H) and the association of neurofilaments with plaques and tangles prompted us to examine the possibility that it is a neurofilament protein. Our findings show that IgG from sera of AD patients bind to the NF-H protein of Torpedo cholinergic neurons. Comparison of the binding of AD and control IgG to Torpedo cholinergic NF-H revealed that AD IgG bind to this neurofilament protein more readily than do control IgG. In contrast, AD and control IgG bind similarly to NF-H obtained from the chemically heterogenous Torpedo spinal cord and rat brain. These findings suggest that AD sera contain a repertoire of anti-NF-H IgG and that a subpopulation of these antibodies whose levels are significantly elevated in AD binds to epitopes highly enriched in Torpedo cholinergic NF-H.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

Serum antibodies to cholinergic neurons in Alzheimer's disease.

Alzheimer's disease (AD) is associated with degenerative changes in nuclei of the basal forebrain which provide most of the cholinergic innervation of the cortex and hippocampus. Although the etiology and pathogenesis of AD are not known, several reports indicate the involvement of immunological mechanisms. In the present work we examined the existence of antibodies in sera of AD patients which bind specifically to cholinergic neurons. As antigen we employed the purely cholinergic electromotor neurons of the electric fish Torpedo which are chemically homogeneous and cross react antigenically with human and other mammalian cholinergic neurons. Our findings show that immunoglobulins (IgG) from sera of AD patients bind to the heavy neurofilament subunit (NF-H) of these neurons. Comparison of the binding of AD and control IgG to Torpedo cholinergic NF-H revealed that AD IgG bind to this neurofilament protein more than control IgG. In contrast, AD and control IgG bind similarly to NF-H obtained from the chemically heterogeneous Torpedo spinal cord and from rat brain. These findings suggest that AD sera contain a repertoire of anti NF-H IgG and that a subpopulation of these antibodies, whose levels are significantly elevated in AD, binds to epitopes highly enriched in Torpedo cholinergic NF-H. The diagnostic potential of these AD antibodies is discussed.

Alzheimer Disease↗
PubMed1988

Antibodies to ganglioside GM1 in patients with Alzheimer's disease.

Gangliosides are thought to have a role in neuronal development and regeneration while anti-ganglioside antibodies have been shown to impair these processes. In the present work we examined whether the neuronal degeneration in Alzheimer's disease is associated with the presence of anti-ganglioside antibodies. A significant level of antibodies specific to ganglioside GM1 but not to other gangliosides (GD1a, GD1b, GT1b and GQ1b) was found in patients with Alzheimer's disease as compared to normal age matched controls. A high level of antibodies to GM1 was also found in patients with multi-infarct dementia and Parkinson's disease with dementia but not in non-demented patients with other neurodegenerative diseases. These results may reflect a specific change in ganglioside metabolism which is associated with the neurodegenerative processes underlying Alzheimer's disease and other causes of dementia.

Adult↗
PubMed1988

Antibodies to cholinergic neurons in Alzheimer's disease.

Alzheimer's disease (AD) is associated with degenerative changes in nuclei of the basal forebrain which provide most of the cholinergic input to the cortex and hippocampus and with a reduction in presynaptic cholinergic parameters in these areas. Although the etiology and pathogenesis of AD are not known, several reports indicate the involvement of immunological mechanisms. In the present work we examined the existence of antibodies in sera of AD patients that bind specifically to cholinergic neurons. As antigens we employed the purely cholinergic electromotor neurons of the electric fish Torpedo which are chemically homogeneous and cross-react antigenically with human and other mammalian cholinergic neurons. Our findings show that immunoglobulins from sera of AD patients bind to a specific antigen (molecular mass 200 kilodaltons) in the cell bodies and axons of Torpedo electromotor neurons and that the levels of such antibodies are significantly higher in AD patients than in controls. The possible role of these antibodies in the cholinergic dysfunction in AD and their diagnostic potential are discussed.

Aged↗
PubMed1988

Chronic inflammatory demyelinating polyradiculoneuropathy: features and prognostic factors with corticosteroid therapy.

Of a series of 16 cases with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) 14 patients were treated with high-dose steroid therapy (HDST, 1.0-1.5 mg/kg/day of prednisone). The average functional disability score (FDS) before treatment was 3.06 +/- 0.11 (maximum FDS = 4). There was a significant improvement under this treatment (FDS = 1.43 +/- 1.12, p less than 0.001). Maximal improvement appeared in 10 patients after 4 weeks of HDST. Following improvement, repeated attempts were made to taper off HDST in 9 patients, 8 of them developed 26 relapses. In most of the patients medium-dose steroid therapy (MDST) with 0.5-0.75 mg/kg/day of prednisone was continued, sometimes with addition of other immunosuppressive medication. The duration of HDST + MDST was between 0.5 and 6.0 years (average 2.6). The following factors were found to correlate with better response to HDST: shorter duration of CIDP, milder neurological deficit, milder decrease of nerve conduction velocity, younger age and being female. Global distribution of weakness, muscle atrophy and a positive Babinski sign were predictive of poor prognosis. Involvement of cranial nerves and level of protein in the cerebrospinal fluid did not correlate with the results of HDST. The risk of relapse was higher with shorter periods of HDST and with more rapid tapering off of HDST. The results indicate that treatment with HDST should be initiated as early as possible, a period of stability of remission is needed before tapering off, and lowering of HDST must be very gradual.

Action Potentials↗
PubMed1988

Post-partum psychosis in adult GM2 gangliosidosis. A case report.

Adult hexosaminidase A deficiency is a form of GM2 gangliosidosis with autosomal recessive inheritance. Only 35 cases (mostly among Ashkenazic Jews) have been reported worldwide. Symptoms include, in a third of the cases, psychosis. A 27-year-old sufferer with no prior psychiatric history, developed a post-partum psychosis, with affective and hebephrenic components, 3 days following her first delivery. She responded to lithium within 10 days of initiating treatment; the full episode lasted 1 month. We conclude that lithium is the preferred treatment for psychosis in such adult patients, especially in light of possible long-term neurological deterioration caused by phenothiazines. Ashkenazic Jews with atypical neurological syndromes presenting with psychosis should be tested for hexosaminidase A deficiency.

Adult↗
PubMed1987

Regional cerebral blood flow in Down's syndrome.

Regional cerebral blood flow was measured in 14 patients with Down's syndrome, in 46 patients with Alzheimer's disease and senile dementia of the Alzheimer type, and in 114 age-matched controls, using the xenon 133 inhalation technique. Cerebral blood flow was reduced in 13 of 14 Down's patients by a mean of 16.8 +/- 2.5% from expected age-matched normal values. Degrees of regional cerebral blood flow reduction did not differ among the frontal, temporal, parietal, and occipital regions in both cerebral hemispheres. The regional cerebral blood flow decreases were similar in magnitude and pattern to those in Alzheimer patients. These findings constitute an additional similarity between the two disorders.

Adolescent↗
PubMed1987

Effect of hypothalamic lesions on experimental autoimmune diseases in rats.

The development of experimental autoimmune encephalomyelitis (EAE) was prevented in rats immunized with encephalitogenic antigen two weeks, but not twelve weeks, after stereotaxic electrolytic destruction of the anterior hypothalamus. Serum antibody level to the antigen myelin basic protein was decreased, and in vitro lymphocyte transformation response to a mitogen was increased. On the other hand, incidence and intensity of chronic experimental autoimmune myasthenia gravis (EAMG) induced by acetylcholine receptor immunization were higher in rats with anterior hypothalamic lesion. In addition, expression of EAE in rats was inhibited when dopamine and norepinephrine in brain were depleted due to intraventricular injection of 6-hydroxydopamine or subcutaneous injection of reserpine. The study indicates hypothalamic modulatory effects on autoimmune response as well as possible involvement of neurotransmitters in this kind of neuroimmunomodulation.

Animals↗
PubMed1985

Prevention of experimental allergic encephalomyelitis by anterior hypothalamic lesion in rats.

Bilateral electrical lesions were performed in the anterior hypothalamus (AH) and hippocampus (HC) of female Lewis rats. AH but not HC lesions were found to inhibit the appearance of clinical signs typical of experimental allergic encephalomyelitis (EAE). The incidence of EAE was 17.2% and the duration was 1.33 +/- 0.07 days after AH lesions compared with an incidence of 85% and duration of 4.81 +/- 0.6 days in the controls. Destruction of the AH was followed by decreased levels of antibodies to myelin basic protein and increased reactivity of splenic lymphocytes to concanavalin A, but did not affect the extent of mononuclear cell infiltration within the brain and spinal cord.

Animals↗