Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Orthograde and retrograde axoplasmic transport in retinal ganglion-cell axons can be interrupted by axonal ischaemia. This report is believed to be the first to illustrate how this phenomenon can be obserbed clinically in man in cases of retinal vascular disease. The intense retinal "whiteness" of small cottonwool spots and at the periphery of larger areas of retinal ischaemia represents gross localised axonal distension secondary to the cessation axoplasmic flow.
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PMID:Clinical sign of obstructed axoplasmic transport. 5 35

Extensive plexuses of serotonin axons form a supra- and subependymal system in the walls of the ventricles, in the arachnoid sheath around major cerebral blood vessels, and in the pia over the spinal cord. These have been demonstrated by autoradiography after continuous intraventricular perfusions of exogenous [3H]5-HT in rats and monkeys. The axons accumulate 5,6-DHT rendering them electron opaque, but have no uptake systems for [3H]NE. After treatment with MAO inhibitors and [3H]5-HT, the axonal boutons contain large (70nm) variably dense synaptic vesicles, and small (35 nm) vesicles each equipped with a dense dot. The latter vesicles are not seen in untreated controls. Electrical stimulation in the raphe nuclei causes significant increases in axonal [3H]5-HT uptake indicating that the fibers originate in the raphe. Quantitatively, the supraependymal plexus is variable, profuse over the dorsal and ventral aqueductal surfaces, sparse over the lateral aspects. Individual raphe neurons have their specific uptake affinities for [3H]5-HT that are independent of tracer concentration or diffusion gradient. It is suggested that raphe neurons with low 5-HT uptake may utilize other neurotransmitters. Two new functional roles are proposed: (1) the serotonin ventricular and pial axons are probably important modifiers of local cerebrospinal fluid (CSF) composition so that regional CSF variations in 5-HT and its metabolites are highly probable; (2) the subarachnoid plexus around major cerebral vessels may contribute to local vasomotor action, thus affecting the cerebral blood flow. The possible significance of these serotonin systems for an understanding of certain neurological entities such as migraine and hemodynamic regulation in cerebral vascular disease is indicated.
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PMID:Serotonin axons in the supra- and subependymal plexuses and in the leptomeninges; their roles in local alterations of cerebrospinal fluid and vasomotor activity. 81 16

We report the case of a 44-year-old woman presenting with chronic symmetrical, sensitive polyneuropathy on the lower limbs in the course of Chagas' disease. The electrophysiological findings were in keeping with axonal degeneration. The histological data displayed axonal degeneration with perivascular inflammatory mononuclear cells in the epineurium, with some neutrophils and eosinophils. Mononuclear cells surrounding endoneurial vessels were observed. Laboratory data did not suggest neither a mixed connective tissue disease nor a collagen vascular disorder. Hematological disease, malignancies, drug-or medicine-induced neuropathy were ruled out. The polyneuropathy in this case was probably related to Trypanosoma cruzi infection on account of the presence of high levels of anti-T. cruzi antibodies, and an immune mechanism might play a role in the vasculitic process.
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PMID:[Axonal polyneuropathy in Chagas disease]. 176 61

A 41-year-old man with PPP since in 1982 was admitted in May, 1987, because of the progressive asymmetric sensory disturbance in the hands and feet over 4 months, accompanied by an exacerbation of PPP. On admission, eruptions of PPP were observed in the palms and soles. Asymmetric and mildly decreased sensations of touch and pain were present in the distal part of the four extremities as well as in his trunk, accompanied by paresthesia and dysesthesia. Mild to moderate weakness was noted in the hand muscles, and slight muscular atrophy was present in the right lower leg. A work-up for collagen vascular disease was within normal limits. T lymphocyte subset showed a decreased ratio of OKT 4/OKT 8. Left sural nerve biopsy showed axonal degeneration and moderate decrease of myelinated fibers, and the vasculitis was not found. The neurological signs and symptoms as well as the skin eruptions improved with methylprednisolone 40 mg/day. A causal relationship between the multiple mononeuropathy and PPP of our patient was indicated by the almost simultaneous onset of the neuropathy and the exacerbation of PPP as well as the improvement of these two conditions with corticosteroid therapy. Such combination of multiple mononeuropathy and PPP has not so far been reported.
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PMID:[A case of multiple mononeuropathy associated with pustulosis palmaris et plantaris (PPP)]. 176 52

Radiation-induced ocular injury secondary to treatment of nasal cancer occurs in humans and animals. Dogs with nasal carcinomas were randomized to receive 36 to 67.5 Gy in fractionated doses given in 4 weeks using a 6 MV linear accelerator. Ophthalmic examinations were performed according to a predetermined protocol and eyes were removed for histologic examination when dogs were euthanatized. The eye in the radiation field exhibited greater injury than the contralateral eye with nasal areas of the globe having more severe lesions than temporal areas. Lesions occurred in all dogs and at all doses. At 1 month or less postirradiation treatment, all dogs had blepharitis, keratoconjunctivitis and corneal epithelial atrophy. Surface lesions persisted in all eyes, becoming less severe and more chronic with time. At 3-6 months postirradiation treatment, degenerative angiopathy of retinal vessels appeared with multifocal retinal hemorrhage and mild diffuse retinal degeneration which affected outer layers first and progressed inwardly with time. At 6 months postirradiation treatment, there were cataracts, fibrosis of retinal vessel walls with loss of vascular smooth muscle, retinal hemorrhage, and mild to moderate retinal degeneration. At 1 year postirradiation treatment, retinal vessels remained sclerotic, retinal hemorrhage was less frequent, and there was moderate retinal degeneration with swelling and loss of ganglion cells. By 2 years or more postirradiation treatment, optic nerve axonal degeneration secondary to retinal changes had appeared. Tapetal and choroidal atrophy were inconsistently seen. Thus, ocular lesions at the doses received developed along a relatively predictable time course and recovery was not seen. Structures of the canine eye appear sufficiently sensitive that even relatively low total doses given in small doses per fraction cause significant long-term injury.
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PMID:Radiation-induced ocular injury in the dog: a histological study. 239 11

Computed tomography is often insensitive to such lesions as atrophic demyelination, enlarged perivascular spaces and infarction in the periventricular white matter. In attempt to better understand the discrepancy between the pathologic and X-CT findings, the author correlated areas that had focal, patchy on X-CT and brains with gross and microscopic findings. Patients with cerebral strokes had larger volume infarcts characterized centrally by necrosis, axonal loss, and demyelination. The progressive subcortical vascular encephalopathy (Binswanger's disease) is characterized by ischemic demyelinization of white matter provoked by hypertensive vascular changes in small vessels and is usually accompanied by multiple lacunar infarcts in a periventricular area and the basal ganglia. Small, deep hemispheric infarcts may be of no clinical significance unless a sufficient aggregate of these occurs. It should be pointed out that many small infarcts are clinically silent, and chronic multifocal ischemia may be responsible for observed senescent changes in cerebral tissue. The extension of the infarcted area might be most important in the development of cerebrovascular dementia. Mixed forms of degenerative dementia and any type of cerebral vascular disease are common and account for 10-20% of all dementias.
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PMID:[Cerebrovascular dementia; correlation of computed and histopathologic findings]. 260 Oct 93

On the basis of a large material of organic dementia, accumulated during a 20 year long prospective study, certain basic structural changes in dementia, mainly of Alzheimer's type (DAT) viz. the topography of lesions, the amyloid angiopathy and white matter changes are discussed with respect to their relevance for modern etiologic and pathogenetic theories and implications for the clinical picture and treatment in DAT. The topographic pattern and its evolution appears to be a relevant basis for the symptomatology and the picture shown by PET and regional cerebral blood flow studies. It lends some support to theories implicating the spread of a causative agent via olfactory pathways. The amyloid depositions, particularly those in the vessels present, both with regard to amount and topography, features which to some extent validate the modern etiological gene theories but which in other respects lend little or no support to the etiologic or pathogenetic importance ascribed to amyloid. The white matter changes, common in DAT and of an incomplete infarction type, may blur the DAT clinic and also serve to block axonal transport through the white matter and cause dysfunction or death of neurons dependent upon routes involved. It might thus influence therapeutic measures such as administration of transmitter substitutes or their precursors and the outgrowth or efficacy of transplanted cholinergic replacement neurons.
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PMID:Structural changes in ageing and dementia of Alzheimer's type with special reference to recent etiologic and therapeutic theories. 269 Jan 4

A case of familial juvenile Alzheimer's disease with apallic state at the relatively early stage and various neurological features was reported. A 33-year-old woman showed a progressive dementia followed by apallic state at the relatively early stage, and died of cardiac failure at the age of 45. Neurological examination disclosed chorea, myoclonus, rigidity, pyramidal sign, and generalized convulsion. Neuropathologically, extensive senile changes such as senile plaques, neurofibrillary tangles, and granurovascular degenerations were observed in the brain, chiefly in the cerebral cortex and limbic system. The present case was characterized by a severe neuronal loss in the subcortical gray matter such as the caudate nucleus, dentate nucleus, substantia nigra, and thalamus as well as a marked myelin loss and axonal damages in the cerebral white matter. This case suggested a combination of multisystemic degeneration and a primary degeneration of the cerebral white matter. The additional peculiar aspects in this case were the senile plaques and amyloid angiopathy in the cerebellar cortex, and the senile plaques and grumose degeneration in the cerebellar dentate nucleus. In the clinicopathological standpoint, the apallic state in this case could be attributed to a severe degeneration of the cerebral white matter in addition to the cerebral cortical deterioration. Furthermore, the occurrence of chorea and myclonus might be contributed to the severe degeneration of the caudate nucleus and to the degeneration of the dentate nucleus, particularly to the grumose degeneration, respectively.
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PMID:[A case of familial juvenile Alzheimer's disease with apallic state at the relatively early stage and various neurological features--a clinicopathological study]. 279 15

We report the quantitative and qualitative, light and electron microscopic studies, including teased fiber preparations of nerve biopsies obtained from eight patients, treated with almitrine, presenting with the characteristic association of a sensory peripheral neuropathy with a recent body weight loss. The data were consistent with an axonal damage affecting myelinated fibers, predominantly large ones and to a lesser degree unmyelinated fibers, some degree of segmental demyelination. Marked axonal regeneration was observed when the nerve biopsy was delayed after withdrawal of the drug, Micro-angiopathy secondary to the formation of concentric lamellae from the basement membrane was observed in five patients suffering from chronic hypoxemia. Almitrine is an agonist of the chemoreceptors. The pathogenesis of the toxic neuropathy induced by this compound remains obscure. Clinical features do not fit with a purely hypoxic mechanism at the origin of the neuropathy.
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PMID:Almitrine neuropathy. A nerve biopsy study of 8 cases. 303 44

A quantitative ultrastructural study has been made of the innervation of 461 arterioles in 114 skeletal muscle biopsies of patients with or without neuromuscular disease excluding diabetes and autonomic neuropathy. In 18 controls the number of nerves and Schwann cells around each vessel was related to the size of the vessel, whether the vessel was within a muscle fascicle or between muscle fascicles. The innervation of arterioles increased with increased diastolic blood pressure. There was no statistically significant change in innervation with increased systolic blood pressure or with age, from 4 to 85 years. In 96 cases of neuromuscular disease and especially in motor neurone disease, axonal varicosities in cross section tended to be larger, more often contained no vesicles or only a few and had altered satellite cell cover depending on the location of the arteriole. Whilst the numerical density of Schwann cells did not change with disease, fewer varicosities were identified within Schwann cells in motor neurone disease, metabolic myopathy and neuropathy and myopathy due to toxins or vascular disease. Preterminal axons in nerve fascicles adjacent to arterioles were lost in polymyositis and muscle disease due to toxins or vascular disease. In polymyositis, metabolic myopathy and motor neurone disease there was some evidence of compensatory nerve sprouting, either in the nerve fascicles or in the adventitia of the arterioles. These structural changes may be related to the changes in blood flow or vascular reactivity described by others in motor neurone disease, polymyositis and metabolic myopathy. It is concluded that the ultrastructure of the vascular innervation of human skeletal muscle is similar to that in other mammals and is changed more with increased diastolic blood pressure and neuromuscular disease than with age.
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PMID:Vascular innervation in human skeletal muscle with and without neuromuscular disease. A quantitative ultrastructural study with references to the effects of age and different blood pressure. 318 43


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