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Biomedical subjects

M Schmidbauer

Publications and source records attributed to M Schmidbauer.

At least 37 records · Page 2Linked to original sources

[School refusal--a catamnestic study on the diagnostic concept ov "school phobia" and "school anxiety"].

Twenty-six patients diagnosed with school refusal were examined 2.4 years after inpatient treatment. The long-term course of patients with "school phobia" (school refusal unrelated to school) and that of patients with "school anxiety" (school refusal related to school) were compared. In addition, an attempt was made to identify variables predictive of a good outcome. The mean age of the 12 patients with "school phobia" and the 14 patients with "school anxiety" was 12.7 years at the start of inpatient treatment. The assessment of psychiatric disturbances was based on structured interviews for parents and adolescents (MEI and MADEL, 1989) and the dimensional assessment scales of functioning for children and adolescents (MSBF). The variables assessed for predictive value were taken from the patients' records during inpatient treatment and from the hospital documentation system. There was no difference in outcome between the two syndrome groups. There was a tendency to less autonomy in the patients with "school phobia". Girls had a better outcome than boys, as did patients with less absence from school prior to inpatient treatment. Overall there was no difference in the outcome of "school phobia" and "school anxiety". Therefore a new classification should be considered.

Adolescent↗

Chronic relapsing polyradiculoneuropathy in IgG lambda monoclonal gammopathy of undetermined significance (MGUS)--complete remission following carmustine treatment.

A previously healthy 43 year-old female developed IgG lambda monoclonal gammopathy of undetermined significance (MGUS) and ascending sensorimotor polyradiculoneuropathy which relapsed 11 times within 2 years. Marked improvement was noted repeatedly after plasmapheresis. However, on each occasion symptoms and signs of polyradiculoneuropathy recurred almost exactly 3 weeks after plasma-pheresis. Following 6 weeks of treatment with carmustine (70 mg/week), nearly complete recovery was established, which has persisted up to now (82 months after the end of therapy). The close temporal correlation between clinical relapse and recurrence of the IgG paraprotein and its permanent absence in stable clinical remission after carmustine treatment suggest a causal relationship between the paraprotein and the polyradiculoneuropathy. However, further studies are required to confirm this observation, as well as the efficacy of carmustine therapy.

Adult↗

[Reversible changes in brain volume in anorexia nervosa].

Cranial computed tomography (CT) was performed in three different samples of young women with anorexia nervosa before and after treatment. The biggest changes in cerebrospinal fluid volume were observed in the supratentorial and extracerebral-subarachnoid area, with smaller changes in the ventricles. These changes, as assessed by different methods of volumetric and planimetric measurement, were statistically significant and were correlated with the changes in body weight. Two patient groups could be distinguished on the basis of the presence or absence of cerebellar pseudoatrophy in the initial CT, and these groups also showed differences in preclinical and clinical course.

Adolescent↗

Subacute diencephalic angioencephalopathy: an entity similar to angiodysgenetic necrotizing encephalopathy and Foix-Alajouanine disease.

A previously healthy 58-year-old man developed neurological illness with progressive dementia, hallucinations, central motor and vegetative impairment which led to death in 14 weeks. Autopsy revealed lesions in a symmetrical centrencephalic distribution. Inner cerebral veins and arteries were surrounded by extravasation of plasma and perivascular haemorrhage and were thickened by fibrous scarring and muscle fibre proliferation. Necrotized blood vessels were also found. The parenchyma was damaged by incomplete to complete necrosis. The age and sex of the patient, the progressive clinical course, the increase of cerebrospinal fluid protein, and the histopathology of the lesion show some similarities to angiodysgenetic necrotizing encephalopathy and spinal Foix-Alajouanine disease.

Angiodysplasia↗

Presence, distribution and spread of productive varicella zoster virus infection in nervous tissues.

Nervous tissue lesions were retrospectively studied for detection of productive varicella zoster virus (VZV) infection in 33 autopsied cases, including 19 herpes zoster (HZ) (10 trigeminal, nine spinal) and 14 cases of nodular brainstem encephalitis without HZ. Immunocytochemistry for VZV antigens and in situ hybridization with a biotinylated VZV DNA probe were used on formol-fixed paraffin sections. Peripheral and central nervous system, skin and striated muscle were investigated in serial sections; available tissue blocks, however, varied between cases. Varicella zoster virus production (both antigen and DNA) in nervous tissue was found in HZ cases but only of short survival after a rash of up to 7 wks (eight out of 12 patients). Varicella zoster virus was visualized in nerve cells, glial cells, Schwann cells and blood vessels. In the central nervous system (CNS), VZV was detected in trigeminal nuclei (one out of 10 brains) or disseminated nodular brainstem lesions (one out of 10 brains), in subependymal microvessels (one out of 10 brains) or vasculitic arteries (two out of 19 brains or spinal cords). In the peripheral nervous system (PNS), VZV (DNA and antigen) was found in neurons and satellite cells of sensory ganglia (four out of seven cases with sampling of ganglia), and in damaged nerve fibres including a muscle nerve in one case; myositis with VZV in affected muscle fibres was found in the latter case. In nodular brainstem encephalitis, one case contained VZV within nodular lesions. We conclude that (i) VZV neural spread is suggested by detectable virus in ganglia, nerve fibres and CNS target nuclei; (ii) haematogenous spread of VZV is suggested by detection of virus in CNS microvessels and in disseminated brainstem encephalitis; (iii) VZV myositis may occur in zosteric myotomes; and (iv) VZV is a possible agent in nodular brainstem encephalitis.

Adult↗

Morphological spectrum, distribution and clinical correlation of white matter lesions in AIDS brains.

This paper analyses the histopathological characteristics and the topographical distribution of 'pure' HIV-associated white matter lesions of the brain in 18 AIDS patients at autopsy; it includes a time-controlled correlation of neuropathology to clinical staging of the AIDS dementia complex. Three distinct lesion types can be delineated: 1 Vacuolar myelin damage (n = 15) in the hemispheric and interhemispheric white matter, in projection fibre tracts, and in intracerebral segments of cranial nerves III, VII, and VIII; 2 Angiocentric foci (n = 14), disseminated randomly in the white matter; 3 HIV leukoencephalopathy (n = 14), as previously defined, seen predominantly in the hemispheric white matter. As a sole lesion type, HIV leukoencephalopathy is found in two cases, while vacuolar myelin damage and angiocentric foci always occur in combination with one or both other types of pathology. Patients with advanced AIDS-dementia complex consistently show severe and combined white matter pathologies at autopsy. We conclude that, in addition to the previously defined features of diffuse HIV leukoencephalopathy, vacuolar myelin damage and angiocentric foci are significant and frequent components of white matter pathology in AIDS autopsies. This reflects the multitude of pathogenetic factors which co-operate in damaging the brain in AIDS. The advanced AIDS dementia complex correlates with the combined and severe white matter lesions.

Acquired Immunodeficiency Syndrome↗

Atypical vertebral artery in a patient with an intra-and extraspinal cervical neurenteric cyst.

A 15 year old girl experienced Horner's syndrome on the right side, paraesthesia of the right arm and meningitis. CT and MRI showed a cystic lesion on the right side of the cervical spine at C3/C4 which descended with an extraspinal portion down to C6. Histology revealed a complex neurenteric cyst. The ipsilateral vertebral artery showed an atypical course. This abnormal artery besides a partial fusion of the vertebrae C2/C3/C4 suggest a complex malformation at the site of the cyst. Disturbed developmental relationships in this case indicate that pathological blood vessels may represent a risk factor in the surgical treatment of neurenteric cysts.

Adolescent↗

Progressive multifocal leukoencephalopathy (PML) in AIDS and in the pre-AIDS era. A neuropathological comparison using immunocytochemistry and in situ DNA hybridization for virus detection.

Twenty-five brains with definite, and three brains with possible, progressive multifocal leukoencephalopathy (PML), including six brains of AIDS patients, were studied with special regard to the detection of papovaviruses. Formalin-fixed serial paraffin sections were immunostained with monospecific anti-JC virus (JCV) and genus-specific anti-simian virus (SV) 40 antisera, and hybridized in situ with DNA probes for JCV and SV 40, respectively. Immunocytochemistry (ICC) and in situ hybridization (ISH) were similarly sensitive in detecting virus in classical PML lesions. In all but one definite PML cases at least one method detected virus (96%). Possible PML tissue was never labeled. Labeling patterns were generally similar in ICC and ISH: mainly oligodendroglia and, less frequently, astroglia harbored virus, whereas labeling of neurons and endothelia was absent. Bizarre giant astrocytes were occasionally labeled by ICC and ISH. Burnt-out lesions harbored JCV DNA but not virus antigens. SV 40 DNA was never detectable. PML morphology in AIDS cases did not usually differ from the disease process seen in the pre-AIDS era. However, two AIDS brains presented extremely extended and, in one case, unusually necrotizing PML damage; in the latter case, PML lesions contained large amounts not only of JCV, but also of human immunodeficiency virus (HIV) antigens. We conclude that ICC and ISH are methods of comparable sensitivity for detection of papovavirus in fluorishing PML lesions. In burnt-out PML lesions only ISH may detect virus. The possibility of an exceptional non-JCV (e.g., SV 40) etiology of PML could be neither confirmed nor disproved. In AIDS, massive coinfection by HIV of PML lesions may increase damage to tissue, resulting in unusually extended and necrotizing PML.

Acquired Immunodeficiency Syndrome↗

Multifocal vacuolar leucoencephalopathy: a distinct HIV-associated lesion of the brain.

A 20-year-old male AIDS patient developed rapidly progressive dementia for more than 3 months prior to death. Autopsy showed, in addition to adrenal cytomegalovirus (CMV) infection and focal cerebral necrosis due to toxoplasmosis, multifocal subcortical white matter lesions of the brain which were strikingly similar to the histopathology of vacuolar myelopathy in AIDS. These distinct lesions contained macrophages which were rarely multinucleated and expressed HIV antigens by immunocytochemistry. The distribution of lesions mimics extrapontine myelinolysis and progressive multifocal leucoencephalopathy (PML); PML was excluded by the absence of papovaviruses by immunocytochemistry and by in situ DNA hybridization. Tissue damage in multifocal vacuolar leucoencephalopathy is different from hitherto characterized HIV-specific neuropathology such as HIV encephalitis and HIV leucoencephalopathy, and should be included in the list of conditions with damage of the brain white matter in AIDS.

AIDS Dementia Complex↗

[Stereotaxic biopsy of intracranial processes: validity of histologic diagnosis].

The diagnostic validity of stereotactic intracranial biopsies was investigated in 70 patients retrospectively. In 56 cases (80%) the presence of a neoplastic lesion as well as its grade of malignancy was proved by cytological, histological and immunohistochemical techniques. An inflammatory or vascular lesion was found in 8 patients (11.4%). In 6 patients (8.6%) the nature of the lesion remained unclear because of nonspecific histological findings. In 27 cases a correlation was found between the biopsy specimens and corresponding material obtained during open surgery or autopsy. 24 concordant results were found (88.9%). In one case a malignant tumour was classified only according to the findings obtained at operation. In two cases subsequently diagnosed as glioblastoma biopsy reported a higher differentiated astrocytoma and a non-neoplastic lesion, respectively. These results confirm stereotactic biopsy of intracranial lesions as a method with low complication rate and high diagnostic validity.

Astrocytoma↗

Cytomegalovirus (CMV) disease of the brain in AIDS and connatal infection: a comparative study by histology, immunocytochemistry and in situ DNA hybridization.

Brain tissues from 45 patients with AIDS and two brains with connatal cytomegalic inclusion body disease were investigated for a cytomegalovirus (CMV) etiology of encephalitic lesions. Nineteen brains showed evidence of CMV infection by histology, immunocytochemistry (ICC) using two different antibodies (mono- and polyclonal), and in situ hybridization (ISH). Fourteen cases with typical cytomegalic cells in conventional histology [eight with focally necrotizing encephalitis/ventriculitis including the two connatal infections and six with nodular encephalitis (NE)] revealed CMV with any method. In 5 of 15 AIDS cases of NE without cytomegalic cells, CMV infection was established by ISH, whereas ICC remained negative in these cases. Typical lesions of human immunodeficiency virus (HIV)-induced multi-focal giant cell encephalitis (HIV encephalitis) in 13 brains were never labeled for CMV. In necrotizing encephalitis/ventriculitis, cell types which labeled for CMV, with and without cytomegalic change, comprised neurons, astrocytes, oligodendrocytes, ependyma, choroid plexus, endothelia, and cells in peri- and endoneurium, and in leptomeninges. Both ISH and ICC were able to detect widespread non-cytomegalic CMV-infected cells in normal parenchyma, well beyond the necrotizing lesions, in two AIDS cases. Labeling patterns of nuclei versus cytoplasms varied between the three methods for CMV detection. We conclude that in CNS tissues with cytomegalic cells, ICC and ISH are of comparable sensitivity; however, a diagnosis of CMV disease is possible in such cases by conventional histology. For an in situ diagnosis of CMV infection in NE without cytomegalic cells in AIDS, ISH is the method of choice. A selective vulnerability to CMV infection of any specific cell type of the human CNS is absent.(ABSTRACT TRUNCATED AT 250 WORDS)

Acquired Immunodeficiency Syndrome↗

Intestinal neuronal degeneration in a patient with chronic idiopathic intestinal pseudoobstruction.

Neuropathological examination of the gut in a patient with chronic idiopathic intestinal pseudoobstruction and temporal lobe epilepsy showed a degeneration of Auerbach's and of Meissner's plexus. The extent of generative changes increased in an aboral to oral direction. Neuronal degeneration was characterized by ballooning of the cytoplasm of the ganglial cells, by a hyperargyrophilia, a shortening and dilation of cell processes, and a progressive fragmentation and loss of axons. In rectal biopsies, a PAS-positive granular material was detected in the cytoplasm of ballooned ganglial cells. A severe peripheral neuropathy with fiber degeneration in the posterior columns and axonal lesions within ventral nerve roots and a more recent fiber degeneration in the lateral columns corresponding to the picture of subacute combined degeneration of the spinal cord and a symmetrical Ammon's horn sclerosis was present. This case of progressive intestinal neuronal degeneration of unknown origin is a newly described condition leading to chronic idiopathic intestinal pseudoobstruction.

Adolescent↗

Herpes simplex virus (HSV) DNA in microglial nodular brainstem encephalitis.

Thirty-four brains with microglial nodular brain stem encephalitis were retrospectively investigated for herpes simplex virus (HSV) and cytomegalovirus (CMV) by in situ hybridization (ISH) with biotinylated cDNA probes, and by immunocytochemistry with polyclonal and monoclonal antibodies on formalin fixed paraffin embedded serial tissue sections. In 16 cases (47%), HSV DNA was found by ISH in the nuclei of neurons in microglial nodules or in the adjacent parenchyma of the brainstem, and more rarely at various cerebellar and telencephalic sites. None of the 34 cases was labeled for CMV DNA and none revealed HSV or CMV antigens. Ten control brains without microglial nodules were not labeled. This study suggests an HSV etiology for many cases with microglial nodular brainstem encephalitis.

Brain↗

Diffuse cerebrospinal gliomatosis presenting as motor neuron disease for two years.

A patient with symptoms and signs of motor neuron disease for 2 years finally developed sensory disturbances and increased intracranial pressure. MRI and CT showed enlargement of the right side of the cerebellum, the brainstem and parts of the cerebral hemisphere with focal hyperperfusion demonstrated by SPECT. Necropsy revealed a diffuse cerebrospinal gliomatosis with loss of spinal motor neurons in tumour infiltration of the anterior horns. This type of spinal cord involvement is considered responsible for the unusual clinical presentation of the neoplasm.

Adult↗

[Immunologic hormone detection in hypophyseal adenomas: correlation of serum hormone findings with immunocytochemical hormone levels in tumor tissue].

Forty-four out of 82 patients with neurosurgically removed pituitary adenomas showed preoperatively elevated plasma hormone levels of prolactin (PRL; 22 patients), of human growth hormone (hGH; 15 patients), and of adrenocorticotropic hormone (ACTH; 7 patients). Immunocytochemical detection of the hypersecreted hormone in paraffin sections of tumour tissue, was possible in all 7 patients (100%) with Cushing's disease, in 20 patients (90%) with hyperprolactinaemia, and in 10 patients (66%) with acromegaly. In a further 3 cases beta-TSH, in one case beta-LH, and in 8 cases alpha-HCG were demonstrated in sections of tumour tissue. No clinical evidence of endocrine disturbance was found in any of these latter cases. More than one anterior pituitary hormone was detected in sections of tumour tissue in 7 cases. An overall qualitative correlation of 85% was found between the elevated plasma hormone level and immunocytochemical hormone detection in tumour tissue sections. Since there is no correlation between conventional histological staining modalities (acidophilic, basophilic, chromophobic) on the one hand, and the level of plasma hormones or immunological hormone detection in tumour tissue on the other hand, modern histological diagnosis of a pituitary adenoma should include assessment of the functional state as found by immunocytochemical hormone determination.

Adenoma↗

Comparison of in situ DNA hybridization (ISH) and immunocytochemistry for diagnosis of herpes simplex virus (HSV) encephalitis in tissue.

Formol-fixed and paraffin-embedded brain tissue of 33 cases of human necrotizing encephalitis was investigated for Herpes simplex virus (HSV) by immunocytochemistry with a polyclonal antiserum, and by in situ hybridization (ISH) with a biotinylated cDNA probe. HSV antigens (VA) were found in various types of cells in the cytoplasm, cellular processes and nuclei. Labelling by ISH was mostly restricted to nuclei and intranuclear inclusions but otherwise matched the distribution of VA. Eighteen of 25 acute cases had HSV antigen detectable by immunocytochemistry, and 18 of the acute cases contained HSV DNA detectable by our ISH technique. However, results differed somewhat between the techniques: three brains negative for VA showed hybridization, and other 3 VA-positive cases remained negative by ISH. Thus 21 brains with acute necrotizing encephalitis were labelled with one or both techniques. In 8 cases with a subacute course (duration of disease was longer than 1 month), HSV antigens were never detectable although 4 brains showed hybridization. All brains labelled by one or both techniques contained nuclear inclusions bodies. Only one case, of subacute course, with inclusion bodies remained unlabelled. Brain tissue of 11 controls, including cytomegalic inclusion body disease, was never labelled. These results demonstrate that immunocytochemistry and ISH are techniques of comparable sensitivity (72%) for detection of HSV in paraffin sections of acute necrotizing encephalitis brains; their combined use enhanced sensitivity, in our hands, to 84%. In cases with a disease course longer than one month, ISH seems to be the method of choice to demonstrate HSV in situ.

Acute Disease↗