Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 30-year-old obese patient with a rapidly progressing chiasmal syndrome presented with acute bitemporal hemianopia, severe bilateral amblyopia, mental confusion, and lethargy. X-ray films of the skull showed a normal sella turcica and computed tomography scan as well as angiography revealed a vascular mass within the chiasmatic cistern. At operation, via left subfrontal approach, an intrachiasmal hematoma was evacuated and biopsies of the hematoma cavity revealed a cavernous hemangioma. Visual symptoms improved markedly postoperatively. This rare association of chiasmal apoplexy and intrachiasmal cavernoma is discussed.
 ...
PMID:Chiasmal apoplexy due to ruptured cavernous hemangioma of the optic chiasm. 406 42

In young and middle age subjects, spontaneous carotid dissection is an increasingly recognized cause of ischemic stroke. Their usual presentation is facial pain with a Horner syndrome and a contra lateral paresis. Blindness has been reported as a presenting symptom in only a few cases. We report a 50 years old man who presented with amblyopia in the left eye, without periocular pain. Fundoscopy showed papilledema and a peripapillar hemorrhage, compatible with an ischemic optic neuropathy. A magnetic resonance angiography confirmed a left carotid dissection.
 ...
PMID:[Blindness caused by an ischemic optic neuropathy by spontaneous carotid dissection. Report of a case]. 1463 92

Reading difficulties caused by hemianopia are well described. We present a study of alexia in a patient (NT) with a milder visual field deficit. The patient had suffered a cerebral haemorrhage causing damage to the left occipital cortex and underlying white matter. NT's text reading was slow and prone to error, but recognition of single letters was preserved. Single word reading was accurate, but slower than normal. On perimetric testing NT initially showed an upper right quadrantanopia, but by attending covertly to this quadrant he could achieve luminance detection except in a small scotoma above the reading line. A whole report experiment showed that letter perception was severely compromised in the quadrant, consistent with cerebral amblyopia. On follow-up testing one and a half year post stroke, a clear spontaneous recovery had occurred, reflected in improved text reading with close to normal eye movements. Still, subtle reading difficulties and oculo-motor abnormalities remained. Overall, the study shows how amblyopia in one quadrant can lead to a characteristic form of alexia.
 ...
PMID:Alexia and quadrant-amblyopia: reading disability after a minor visual field deficit. 1673 22

In 2000, the UK's College of Optometrists commissioned a report to critically evaluate the theory and practice of behavioural optometry. The report which followed Jennings (2000; Behavioural optometry--a critical review. Optom. Pract. 1: 67) concluded that there was a lack of controlled clinical trials to support behavioural management strategies. The purpose of this report was to evaluate the evidence in support of behavioural approaches as it stands in 2008. The available evidence was reviewed under 10 headings, selected because they represent patient groups/conditions that behavioural optometrists are treating, or because they represent approaches to treatment that have been advocated in the behavioural literature. The headings selected were: (1) vision therapy for accommodation/vergence disorders; (2) the underachieving child; (3) prisms for near binocular disorders and for producing postural change; (4) near point stress and low-plus prescriptions; (5) use of low-plus lenses at near to slow the progression of myopia; (6) therapy to reduce myopia; (7) behavioural approaches to the treatment of strabismus and amblyopia; (8) training central and peripheral awareness and syntonics; (9) sports vision therapy; (10) neurological disorders and neuro-rehabilitation after trauma/stroke. There is a continued paucity of controlled trials in the literature to support behavioural optometry approaches. Although there are areas where the available evidence is consistent with claims made by behavioural optometrists (most notably in relation to the treatment of convergence insufficiency, the use of yoked prisms in neurological patients, and in vision rehabilitation after brain disease/injury), a large majority of behavioural management approaches are not evidence-based, and thus cannot be advocated.
 ...
PMID:A critical evaluation of the evidence supporting the practice of behavioural vision therapy. 1915 76

The congenital retinocephalic facial vascular malformation syndrome is characterized by unilateral, nonhereditary retinal and cerebral arteriovenous malformations (AVMs) and is occasionally associated with orbital vascular changes. Typical signs are facial and oral mucosal vascular changes, rarely with changes of the maxilla or mandible. An AVM causes high blood flow because of direct connection (shunting) of major vessels without interposition of capillaries. Ocular complications include retinal and vitreous hemorrhages, edema, venous occlusion (risk of rubeosis iridis and secondary glaucoma). Neuroophthalmological changes comprise optic atrophy, papilledema, proptosis, pupillary changes, hemianopia, gaze paresis, nystagmus, cranial nerve palsies, strabismus, and amblyopia. Neurological complications include headache, subarachnoid hemorrhage, convulsions, cerebral hemorrhages, increased intracranial pressure, hydrocephalus, and stroke with hemiparesis. Threatening oral hemorrhages or epistaxis may rarely occur.
 ...
PMID:[Congenital retinocephalic facial vascular malformation syndrome. Bonnet-Dechaume-Blanc syndrome or Wyburn-Mason syndrome]. 1915 63

Vision loss after retinal or cerebral visual injury (CVI) was long considered to be irreversible. However, there is considerable potential for vision restoration and recovery even in adulthood. Here, we propose the "residual vision activation theory" of how visual functions can be reactivated and restored. CVI is usually not complete, but some structures are typically spared by the damage. They include (i) areas of partial damage at the visual field border, (ii) "islands" of surviving tissue inside the blind field, (iii) extrastriate pathways unaffected by the damage, and (iv) downstream, higher-level neuronal networks. However, residual structures have a triple handicap to be fully functional: (i) fewer neurons, (ii) lack of sufficient attentional resources because of the dominant intact hemisphere caused by excitation/inhibition dysbalance, and (iii) disturbance in their temporal processing. Because of this resulting activation loss, residual structures are unable to contribute much to everyday vision, and their "non-use" further impairs synaptic strength. However, residual structures can be reactivated by engaging them in repetitive stimulation by different means: (i) visual experience, (ii) visual training, or (iii) noninvasive electrical brain current stimulation. These methods lead to strengthening of synaptic transmission and synchronization of partially damaged structures (within-systems plasticity) and downstream neuronal networks (network plasticity). Just as in normal perceptual learning, synaptic plasticity can improve vision and lead to vision restoration. This can be induced at any time after the lesion, at all ages and in all types of visual field impairments after retinal or brain damage (stroke, neurotrauma, glaucoma, amblyopia, age-related macular degeneration). If and to what extent vision restoration can be achieved is a function of the amount of residual tissue and its activation state. However, sustained improvements require repetitive stimulation which, depending on the method, may take days (noninvasive brain stimulation) or months (behavioral training). By becoming again engaged in everyday vision, (re)activation of areas of residual vision outlasts the stimulation period, thus contributing to lasting vision restoration and improvements in quality of life.
 ...
PMID:Vision restoration after brain and retina damage: the "residual vision activation theory". 2176 27

Long-term potentiation and long-term depression are enduring changes in synaptic strength, induced by specific patterns of synaptic activity, that have received much attention as cellular models of information storage in the central nervous system. Work in a number of brain regions, from the spinal cord to the cerebral cortex, and in many animal species, ranging from invertebrates to humans, has demonstrated a reliable capacity for chemical synapses to undergo lasting changes in efficacy in response to a variety of induction protocols. In addition to their physiological relevance, long-term potentiation and depression may have important clinical applications. A growing insight into the molecular mechanisms underlying these processes, and technological advances in non-invasive manipulation of brain activity, now puts us at the threshold of harnessing long-term potentiation and depression and other forms of synaptic, cellular and circuit plasticity to manipulate synaptic strength in the human nervous system. Drugs may be used to erase or treat pathological synaptic states and non-invasive stimulation devices may be used to artificially induce synaptic plasticity to ameliorate conditions arising from disrupted synaptic drive. These approaches hold promise for the treatment of a variety of neurological conditions, including neuropathic pain, epilepsy, depression, amblyopia, tinnitus and stroke.
 ...
PMID:Long-term potentiation and long-term depression: a clinical perspective. 2177 18

In this introductory article, we summarize the evidence from humans and animal models on the shaping of postnatal visual development by focused binocular input. When balanced input is missing during a sensitive period, deficits emerge, including seemingly permanent impairments in visual acuity that are labeled amblyopia. Rodent models have identified neurochemical changes that control the onset of such sensitive periods and molecular and structural brakes that lead to the diminution of the plasticity thereafter. Both animal and human studies of amblyopia have recently identified exciting ways to remediate vision in adulthood that bear some similarity to the interventions that have proved successful in promoting recovery from stroke.
 ...
PMID:Amblyopia: background to the special issue on stroke recovery. 2241 12

Noninvasive brain stimulation is a technique for inducing changes in the excitability of discrete neural populations in the human brain. A current model of the underlying pathological processes contributing to the loss of motor function after stroke has motivated a number of research groups to investigate the potential therapeutic application of brain stimulation to stroke rehabilitation. The loss of motor function is modeled as resulting from a combination of reduced excitability in the lesioned motor cortex and an increased inhibitory drive from the nonlesioned hemisphere over the lesioned hemisphere. This combination of impaired neural function and pathological suppression resonates with current views on the cause of the visual impairment in amblyopia. Here, we discuss how the rationale for using noninvasive brain stimulation in stroke rehabilitation can be applied to amblyopia, review a proof-of-principle study demonstrating that brain stimulation can temporarily improve amblyopic eye function, and propose future research avenues.
 ...
PMID:From motor cortex to visual cortex: the application of noninvasive brain stimulation to amblyopia. 2241 15

The human brain possesses a remarkable ability to adapt in response to changing anatomical (e.g., aging) or environmental modifications. This form of neuroplasticity is important at all stages of life but is critical in neurological disorders such as amblyopia and stroke. This review focuses upon our new understanding of possible mechanisms underlying functional deficits evidenced after adult-onset stroke. We review the functional interactions between different brain regions that may contribute to motor disability after stroke and, based on this information, possible interventional approaches to motor stroke disability. New information now points to the involvement of non-primary motor areas and their interaction with the primary motor cortex as areas of interest. The emergence of this new information is likely to impact new efforts to develop more effective neurorehabilitative interventions using transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (tDCS) that may be relevant to other neurological disorders such as amblyopia.
 ...
PMID:Recovery of motor function after stroke. 2241 14


1 2 3 Next >>