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At least 361 records · Page 20Linked to original sources
PubMed1991

Brain lesions in chronic granulomatous disease.

In chronic granulomatous disease (CGD) enzyme-deficient neutrophils and mononuclear cells lack the respiratory burst required for biocidal activity. Recurrent infections lead to granulomas in various organs but brain lesions are rare. In the present case, a 23-year-old male with numerous infections since early childhood died of overwhelming pulmonary aspergillosis. He first began to experience neurological deficits at the age of 17. Computerized tomography and magnetic resonance imaging revealed fleeting white matter lesions that were interpreted as multiple sclerosis (MS). At post mortem, three types of brain lesions were found: (1) Pigmented macrophages in perivascular spaces and the leptomeninges similar to those reported previously. They contained fine, golden-brown, lipofuscin-like material whose chemical composition included a sulfur peak by X-ray analysis. (2) Focal, well-demarcated, "burnt out" white matter lesions with loss of both myelin and axons and intense sclerosis. (3) Diffuse areas of mild pallor in the centrum ovale which spared the U fibers. The pigmented macrophages are characteristic of those seen in the periphery in CGD. The origin of the discrete, destructive white matter lesions is unclear. They may have resulted from: (i) earlier activity by CGD macrophages; (ii) previous infections due to sepsis or embolism; or (iii) possibly post-infectious encephalomyelitis. The more diffuse, mild, white matter lesions are attributed to edema. Evidence for MS, progressive multifocal leukoencephalopathy, or human immunodeficiency virus encephalitis was lacking. This case is presented to alert us to look more carefully for brain lesions in CGD, characterize them and to help determine their cause.

Adult↗
PubMed1990

An autopsied case of the Crow-Fukase syndrome: a neuropathological study with emphasis on spinal roots.

An autopsied case of the Crow-Fukase syndrome is reported. Neuropathological findings were as follows: (1) in the sural nerve, there was marked decrease of large and small myelinated fibers. Myelinated fibers showing axonal degeneration and segmental demyelination and remyelination were moderately increased. (2) In the lumbar spinal roots, myelinated fibers showing segmental demyelination and remyelination were frequently observed. The density of myelinated fibers of the ventral root was less at the dural site than the spinal site, while that of the dorsal roots was less at the spinal site than the dural site. (3) In the dorsal root ganglion, there were Nageotte's residual nodules and satelliotosis; (4) in the lumbar and thoracic spinal cord, there was pallor of the dorsal column; and (5) nerve cells showing central chromatolysis were frequently observed in the spinal anterior horn cells. Segmental demyelination and remyelination in the spinal roots and loss of myelinated fibers with axonal degeneration in the sural nerve are main neuropathological features of this syndrome.

Aged↗
PubMed1994

Unusual case of corticobasal degeneration with tau/Gallyas-positive neuronal and glial tangles.

A 74-year-old woman with corticobasal degeneration (CBD) had a 9-year history of progressive loss of strength and rigidity of her right hand and then arm, followed by speech difficulties, dyskinesia, rigidity, spasticity and weakness of the ipsilateral lower limb, ultimately also involving the opposite side. She later developed supranuclear gaze palsy. Her memory remained intact during most of the duration of her disease. Laboratory tests and anti-Parkinsonian medications were not helpful. At autopsy, frontal lobe atrophy, discoloration of putamen (Pt) and pallor of substantia nigra (Sn) were observed. Neuronal loss and gliosis were extensive in motor cortex and milder in frontal cortex, abruptly ending at the central sulcus and junction of cingulate gyrus. "Achromatic" neurons were present. Neuronal loss and gliosis were seen in Pt and Sn and corticobasal inclusions in Sn. Numerous Gallyas/tau-positive, Bielschowsky/ubiquitin-negative coil, sickle, or coma-shaped tangles and thread-like processes were found in affected cortex, Pt and Sn. Some of the tangles were in neurons, but most occurred in astroglia, and their processes. The presence of Gallyas/tau-positive glia in CBD may have the same diagnostic significance as in progressive supranuclear palsy, analogous to the argyrophilic ubiquinated inclusions in oligodendroglia in multisystem atrophy. We suggest that in CBD: (1) cytoskeletal protein metabolism in neurons and glia can simultaneously be perturbed in certain neurodegenerative diseases, and (2) the astrocytosis in CBD may not be simply a reactive process but an integral part of the disease.

Aged↗
PubMed1994

Multicenter study of childhood headache.

This multicenter study reports the results obtained between 1990 and 1991 by the Study Group for Childhood Headache of the Italian Neuropediatric Society. Standardized computerized case sheets were used in order to increase the number of young patients studied and obtain more homogeneous results. A clinical diagnosis of headache was made in 600 patients (314 female and 286 male) between 4 and 12 years of age, in accordance with the classification set down by the International Headache Society. Clinical symptoms and follow-up were more severe in children with migraine as opposed to headache. No sequence of associated neurological and neurovegetative symptoms was observed at onset of headache, and some (phono-photophobia, pallor, drowsiness, abdominal pains) were much more prevalent than others. Because of the patient's age we studied only the treatment of acute attack and did not take account of chronic treatment. In childhood the clinical course of primary headache tends to improve spontaneously, and we believe that prevention of headache attacks should be carried out only in very rare individual cases.

Acute Disease↗
PubMed1991

Brain-stem auditory evoked potentials and blink reflex in Friedreich's ataxia.

The brain-stem involvement in Friedreich's ataxia (FA) was studied by using brain-stem auditory evoked potentials (BAEPs) and the blink reflex. Ten out of 18 patients had abnormal BAEPs, the main abnormality being complete absence of responses and disappearance of wave V. Combined degeneration of the peripheral and central acoustic pathways probably accounts for these findings. The blink reflex was abnormal in 50% of the cases. The outstanding abnormality was bilateral delay of late responses with normal early response, which could be correlated with the known pallor of the descending trigeminal tracts. In contrast with BAEP findings, blink reflex abnormalities did not correlate with either the age of patients or the severity and duration of the disease. These data suggest a difference in susceptibility to degeneration between the auditory system and neuronal system subserving the blink reflex. We conclude that systematic BAEP and blink reflex recording is useful in the electrophysiological evaluation of FA patients.

Adolescent↗
PubMed1989

Decrease in nerve fibres in cerebral white matter in progressive subcortical vascular encephalopathy of Binswanger type. An electron microscopic study.

To study white matter changes in the frontal lobes and to investigate the histopathological basis for the dementia in progressive subcortical vascular encephalopathy (PSVE), the frontal white matter was examined by electron microscopy in seven cases with PSVE, and compared with that in a control group and in cases with senile dementia of Alzheimer's type (SDAT). The number of nerve fibres per unit selected area of the white matter was significantly less in PSVE compared with that in the control group or in SDAT. Nerve fibres in PSVE had a tendency to have thinner myelin sheaths than in the control group or in SDAT, but the difference was not significant. The pallor of the frontal white matter in PSVE is mainly based on the loss of nerve fibres, and may be in part based on the thin myelin sheaths. The dementia in PSVE is probably related to the loss of nerve fibres in the cerebral white matter.

Aged↗
PubMed1986

Cold-induced Raynaud's phenomenon ameliorated by intravenous administration of ketanserin: a double-blind cross-over study.

Fifteen patients suffering from Raynaud's phenomenon (RP) were examined. They were placed in a "climate chamber" (a small room in which the temperature and humidity could be varied). The temperature was gradually decreased, while the humidity was kept constant. After 60-90 min, distinct RP was induced and intravenous medication was administered. The whole trial was performed in a double-blind, cross-over fashion. Every patient participated in two experiments performed 2 days apart. Either ketanserin or placebo was given during the first experiment. In the second experiment, the medication (or placebo) which had not been given was administered. The effects of ketanserin were highly significant: the bluish pallor changed into bright erythema and the skin temperature rose significantly. This was interpreted as a spasmolytic effect. Intravenously administered ketanserin has a place in the clinical treatment of acutely deteriorating RP of diverse etiologies.

Adult↗
PubMed1982

Home monitoring of infants considered at risk for the sudden infant death syndrome. Four years' experience (1977-1981).

From 1977 to 1981, 500 infants had been referred to evaluate their risk for the sudden infant death syndrome (SIDS). These included 186 infants who had presented an event (prolonged apnea, hypotonia, pallor or cyanosis) initiated while asleep, 133 siblings and 181 "controls". All-night polygraphic recordings were performed in all infants, and if indicated by the history of the infants, complementary clinical investigations were done. These procedures led to the identification of 50 infants considered at risk for SIDS (10% of all referrals): 30 near-misses for SIDS, 10 siblings and 10 infants with a minor incident during sleep but with abnormal polygraphic recordings. These 50 infants (group I) were monitored at home during sleep with the help of a cardiac and respiratory monitor. Eight infants not considered at risk were monitored similarly at the request of their parents (group II). Forty of the 50 infants in group I presented with repetitive sleep apneas and bradycardias, and required stimulation by their parents to regain normal cardiorespiratory rhythm. Twelve had to be resuscitated at least once for a life-threatening event. None of the infants in group II showed alarms during sleep. Monitoring could be discontinued after a mean length of 7.2 months for the infants in group I, 4.1 months in group II. It is concluded that if identified in time through adequate investigations, some infants may be protected against SIDS through home monitoring. This approach requires expensive and well trained teams, ready, at any time, to cope with the problems that may arise in the homes of the monitored infants.

Ambulatory Care↗
PubMed1988

Spontaneous healing of Langerhans cell histiocytosis (histiocytosis X).

A 3-month-old male infant presented with pallor, hepatomegaly (4.5 cm), splenomegaly (1.5 cm), anaemia (Hb 6 g/dl) and thrombocytopenia (16 X 10(9)/l). A liver biopsy was diagnostic for Langerhans cell histiocytosis (histiocytosis X). The patient's lymphocytes, co-cultured with neonatal lymphocytes, were positive for virus-like particles without reverse transcriptase activity. The hepatomegaly diminished after 6 months and a second liver biopsy showed decreased histiocytic infiltration. A second viral blood culture remained negative. After 14 months, the hepatomegaly had disappeared completely and there were no more abnormal haematological or clinical findings.

Histiocytes↗
PubMed1988

Blood sampling in very low birth weight infants receiving different levels of intensive care.

Sixty very low birth weight infants (birth weight 560-1450 g) were studied during the first 28 days of life. The infants were classified as group A (n = 19 infants who never required ventilator support), group B (n = 20 infants mechanically ventilated for minor respiratory problems), and group C (n = 21 infants ventilated for respiratory distress syndrome). Diagnostic blood sampling was measured, infants were checked for clinical symptoms and laboratory signs of anaemia 24 h before and after the transfusion of packed red cells. A total of 7998 punctures (average: 4.8 per infant per day) were performed, the mean blood loss due to diagnostic sampling was 50.3 ml/kg per 28 days (range 7-142) for all infants. A high correlation (rs = +0.91) was found between the blood volumes sampled and transfused. In group A, the mean blood loss was 24 ml/kg, and a total of 29 blood transfusions were administered. The most frequent symptoms of anaemia were poor weight gain and apnoeic spells. In group B, the mean blood loss was 60 ml/kg and a total of 97 blood transfusions were administered. In group C, the mean blood loss was 67 ml/kg and a total of 116 blood transfusions were administered. In both groups B and C, poor weight gain, pallor and distended abdomen were the most frequent symptoms of anaemia. Following the blood transfusion, haematocrit rose and blood pressure remained unchanged. The symptoms that responded most favourably to the blood transfusion were: poor weight gain, oxygen requirement, and distended abdomen. The results emphasize the need for miniaturizing laboratory techniques and monitoring blood sampling.

Anemia↗
PubMed1987

Motor neuron disease, parkinsonism and dementia. Report of a case with diffuse Lewy body-like intracytoplasmic inclusions.

The clinicopathological findings in a 49-year-old man who presented multisystemic neurological degenerative disease are reported. The patient presented, at the age of 36, distal upper limb amyotrophy and 8 years later pyramidal signs with fasciculations. In his last year of life, he suffered extrapyramidal hypertonus and mental deterioration. Neuropathological examination showed anterior spinal root and cerebral atrophy. Myelin pallor was mild and predominated on posterior cords. Anterior horn neuronal loss was noted in the spinal cord as well as Alzheimer-type changes in the brain. Inclusion bodies consistent with Lewy bodies were diffusely apparent. The peculiar clinical progression in this case and the extension of neuropathological lesions with inclusion bodies mainly in the substantia nigra and cerebral cortex are an interesting subject of discussion.

Brain↗
PubMed1989

Neuropathology of the acquired immune deficiency syndrome (AIDS): a report of 135 consecutive autopsy cases from Switzerland.

Neuropathological changes were studied in a consecutive autopsy series of 135 cases, comprising 73% of all patients who died of AIDS in Switzerland between April 1981 and December 1987. Central nervous system involvement was found in 119 patients (88%), 19 of which had multiple concomitant intracerebral lesions. Among the non-viral opportunistic infections, encephalitis due to Toxoplasma gondii was most frequent and occurred in 35 patients (26%), followed by central nervous system infection with Cryptococcus neoformans, which was found in five patients (4%). Cytomegalovirus (CMV) encephalitis was present in 14 patients (10%). Disseminated microglial nodules without morphological or immunocytochemical evidence of CMV was encountered in 18 patients (13%). However, in all but two of these patients there was evidence of extracerebral CMV infection, suggesting that CMV was responsible for these nodular encephalitides. Nine patients (7%) had progressive multifocal leukoencephalopathy (PML); in five of these, demyelination was associated with extensive tissue destruction and cyst formation. HIV-associated encephalopathy was observed in 21 patients (16%) and showed two characteristic morphological patterns: progressive diffuse leukoencephalopathy (PDL) and multifocal giant cell encephalitis (MGCE). PDL was observed in 13 cases and characterized by diffuse pallor and gliosis of the cerebral and cerebellar white matter with scattered multinucleated giant cells, but without significant inflammatory response. MGCE was found in eight patients and characterized by clusters of numerous multinucleated giant cells, rod cells, macrophages, lymphocytic infiltrates and occasional necroses. In our view, PDL and MGCE represent the two opposite variants of HIV-induced encephalopathies, with overlapping intermediate manifestations.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Early axonal lesion and preserved microvasculature in epilepsy-induced hypermetabolic necrosis of the substantia nigra.

The time course of structural change in epilepsy-induced necrosis of the substantia nigra was studied by light and electron microscopy, and was correlated with previous metabolic studies. By light microscopy, tinctorial pallor appeared early, followed by pan-necrosis and macrophage infiltration. Mild lesions showed neuropil vacuolation but sparing of neurons, rather than a selective neuronal vulnerability. Electron microscopy of the evolving necrosis revealed an orderly sequence of structural damage involving first axons, then dendrites, neurons, and glia. No necrotic endothelial cells could be found, even in areas of apparent pan-necrosis by light microscopy. Pericytes near the vascular lumen were spared, whereas those in outer locations were necrotic. Edema, measured densitometrically, was absent. Previous metabolic studies of this lesion have demonstrated a pronounced focal lactic acidosis due to anaerobic hypermetabolism. Although the lesions resemble infarcts, hypermia rather than ischemia has been shown to accompany their development. Structural preservation of endothelial cells and inner pericytes likely stems from proximity to the moving blood stream, away from the site of lactic acid production in the neuropil. The findings indicate that the perfusion of necrotic tissue occurs via a persisting, intact microcirculation. The relative neuronal sparing and the early axonal rather than dendritic lesion show a clear distinction from excitotoxic pathology.

Animals↗
PubMed1980

Cerebral lesions in rats with streptozotocin-induced diabetes.

We studied cerebral lesions in the streptozotocin-diabetic rat, an established model of diabetic retinopathy. A group of diabetic rats all had cerebral lesions, but showed no gross abnormalities of the brain or signs of effects on the central nervous system. Light and electron microscopy of horizontal brain sections stained by a variety of methods showed focal accumulation of collagen fibrils in the basement membranes of arteriole and capillary walls, slight degeneration of random neuronic cells (mainly in the brain stem), and no evidence of perivascular myelin pallor plaques. A marked tendency toward platelet aggregation, which leads to thrombosis, was also seen. There was no difference between results from rats killed 9 and 12 months after streptozotocin injection. The brain lesions bore a close resemblance to those seen in a nutritional encephalopathy known to be induced by a diet deficient in tocopherol and rich in oxidized oil, but differed from that encephalopathy in that the peculiar hypertrophic cerebral astroglia associated with diabetes resembled Alzheimer Type II astroglia. The differences between these cerebral astroglia and the retinal Müller cells may account for the difference in degree between the effects of diabetes on the brain and the retina.

Animals↗
PubMed1980

The AB-variant of GM2-gangliosidosis. Clinical, biochemical, and pathological studies of two patients.

Clinical, neuropathological, and biochemical studies are reported in two children with the AB-variant of GM2-gangliosidosis. One patient had become symptomatic by 1--1.5 years, initially showing cerebellar signs, and then progressive psychomotor retardation, with hypotonia, spasticity, dementia, and macular cherry red spots, until death at the age of 4.5 years. The second patient showed an earlier onset of retardation and a more rapidly progressive course. At postmortem, the brains were of normal or near normal weights and displayed grossly only mild cerebral cortical and cerebellar atrophy, and mild pallor or attenuation of the white matter. Neuronal storage was widespread throughout the CNS, and both neurons and glia contained a variety of abnormal, membranous inclusions. Visceral organs were not involved. Ganglioside sialic acid was increased several fold in gray matter, with GM2 the predominant ganglioside species. N-acetyl-beta-glucosaminidase activities in serum, leukocytes, fibroblasts, and postmortem gray matter, assayed with an artificial, fluorogenic substrate, were normal, as were activities of other lysosomal hydrolases.

Atrophy↗
PubMed1992

Acute tubulointerstitial nephritis with uveitis syndrome presenting as multiple tubular dysfunction including Fanconi's syndrome.

We describe an 11-year-old male patient with acute tubulointerstitial nephritis with uveitis (TINU) syndrome. He presented with easy fatigability, pallor, nocturia and weight loss. Laboratory examination disclosed anaemia, polyclonal hypergammaglobulinaemia, low molecular weight proteinuria, glycosuria, aminoaciduria, proximal and distal renal tubular acidosis, a urine concentration defect and decreased creatinine clearance. The multiple renal tubular dysfunction and slight glomerular dysfunction subsided spontaneously. Bilateral anterior uveitis was manifested 7 months after the onset of the disease. This is the first reported case of TINU syndrome with multiple proximal and distal tubular dysfunction including a complete type of Fanconi's syndrome.

Acidosis, Renal Tubular↗
PubMed1992

Intra- and inter-observer variation of optic nerve head measurements in glaucoma suspects using disc-data.

The aim of this study was to determine the intra- and inter-observer variation in the use of a system designed for exact measurements from standard optic nerve head photographs. The commercially available system consisted of a colour CCD Videocamera, a dedicated frame grabber and customized software run on a IBM AT compatible computer. Masked measurements were made 3 times by 2 observers, from stereophotographs of the optic nerve head of 56 eyes from 30 glaucoma suspects. The cup was defined on the basis of contour, not pallor and the disc area was defined as the area inside Elschnig's ring. Intra-observer variances were 0.001 +/- 0.001 mm2 for cup area (mean +/- SD), 0.002 +/- 0.002 mm2 for disc area and 0.002 +/- 0.003 mm2 for rim area. These values for intra-observer variance were comparable with the results obtained using manual planimetric techniques. Intra-observer variance for disc area was significantly larger for the less trained of the two experienced observers. Inter-observer variances were 0.004 +/- 0.009 mm2 for cup area, 0.008 +/- 0.013 mm2 for disc area and 0.009 +/- 0.014 mm2 for rim area. These inter-observer variances were significantly larger than those previously reported for manual planimetry. The absolute differences between the two observers ranged from -0.35 to +0.20 mm2 (-0.08 +/- 0.11 mm2) for cup area, from -0.38 to +0.15 mm2 (-0.08 +/- 0.11 mm2) for disc area and from -0.29 to +0.34 mm2 (-0.06 +/- 0.12 mm2) for rim area.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Severe combined immune deficiency presenting with cyclic hematopoiesis.

At age 2 months a male infant presented with a cyclic clinical syndrome every 14-21 days that included pharyngeal aphthous ulcers, high fever, lymphadenopathy, pallor, and malaise. Serial blood studies indicated cycling of all blood cell elements, compatible with a diagnosis of cyclic hematopoiesis (CH). He also manifested a progressively severe immune deficiency, not described before in human CH. When first studied at age 5 months, he was hypogammaglobulinaemic with normal B lymphocyte numbers. By 6.5 months, he was agammaglobulinaemic. At age 8 months, he developed severe pneumocystis carinii pneumonia, and studies showed a state of severe combined immune deficiency. The patient received a bone marrow transplant from his HLA-identical sister with no preconditioning therapy. Subsequently, normal immune function developed and the cyclic hematopoiesis resolved. The majority of lymphocytes is of donor origin. Persistence of erythrocytes and neutrophils of recipient origin suggests that the hematopoietic stem cells were not abnormal. We speculate that this patient had a primary deficiency of a differentiation factor affecting maturation of lymphoid and myeloid progenitor cells.

Blood Cell Count↗