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A case of central diabetes insipidus (DI) caused by non-specific chronic inflammation of the hypothalamus was reported. As the central DI was associated with acute posterior multifocal placoid pigment epitheliopathy with an immunogenic predisposition, and human leukocyte antigen class I antigen A2 and class II antigen DR4 were found, it might be a case of autoimmune reaction.
The examination of computertomography (CT) scans of 20 patients suffering from 'cerebral visual disturbance' (CVD) as part of infantile encephalopathy, revealed conspicuous abnormalities, which could be divided into two main groups: (1) lesions of the optic radiations; and (2) lesions of the calcarine cortex. The pathophysiological mechanisms underlying these abnormalities suggest an important role of hypoxia and/or ischaemia in the etiology of CVD.
Changes in regional cerebral blood flow (rCBF) associated with a face-matching task were examined using positron emission tomography (PET) and H2(15)O in 7 patients with mild-moderate dementia of the Alzheimer type (DAT) and in 8 healthy age-matched controls. rCBF was normalized to whole brain flow and pixel-by-pixel difference images were computed by contrasting flow during a control task to flow during face matching. Both patients and controls showed bilateral rCBF increases in occipitotemporal extrastriate cortex during face matching. The magnitude of these increases was not significantly different between the groups. In addition, the patients showed greater rCBF activation in regions of occipital and frontal cortex. These results show that early in the course of DAT, patients utilize extrastriate cortex to perform a visuoperceptual task, as do control subjects but also show rCBF increases in additional cortical areas. Activation of these additional areas of cortex in the patients may reflect an increased attentional load during face matching due to their reduced cognitive capacity.
A 70-year-old man showed Balint's syndrome and other signs of bilateral posterior-hemisphere dysfunction of acute onset without initial unconsciousness. A computerized tomographic scan showed bilateral infarcts in the posterior arterial border-zone areas. Clinical evidence suggests that hypotension at the onset of atrial fibrillation caused these infarcts. There was a marked difference in the time course of recovery between the left and the right infarct which demonstrated that the elements of Balint's syndrome disappeared together with the left-hemisphere symptoms while the right-hemisphere symptoms were still present.
Many articles have discussed the anatomy and pathology of the orbits. Although this area is exquisitely visualized via computed tomography, the bulk of the visual apparatus lies behind the optic canal. A variety of pathologic conditions will manifest themselves by changes in the visual fields. This article demonstrates the normal anatomy of the visual pathways within the brain by CT scanning and correlates various changes that cause visual field defects.
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Two patients with endocrine and visual disturbances had CT evidence of an intra- and suprasellar enhancing mass. Both patients showed clinical improvement following treatment with systemic corticosteroids. In one case, there was no evidence of systemic sarcoidosis; and the exact nature of the juxtasellar lesion was established by surgical biopsy.
Thirteen neurologically impaired children with paroxysmal ocular downward deviation were studied. The eye movement accompanied downward movement of the upper eyelid; there was no coincident paroxysmal discharge on electroencephalography. The ocular abnormality was observed in infancy, predominantly in preterm infants, and spontaneously resolved in many of them. All patients had spastic quadriplegia or diplegia and mental retardation. Many children also had cortical visual impairment. This eye movement abnormality, not reported previously, should be considered to be a neurologic sign in brain-damaged infants with cortical visual impairment.
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Visual evoked potentials (VEPs) to central and lateral half field patterned stimuli of 1, 2 and 4 cycles per degree (cpd) were recorded in a patient with Dorsal Simultanagnosia due to bilateral lesions of parieto-occipital junction. VEPs consisted of the normal N1-P1-N2 components with same spatial frequency sensitivity as in controls. VEPs had similar latencies and amplitudes whether the patient could see or not the patterned stimuli. Event related potentials (ERPs) to visual and acoustic odd-ball paradigm were also recorded in the same patient. Visual ERPs consisted of an early NA-effect, and of N2-P3 components. P3 was recorded only from frontal, central and temporal derivations. The topographical P3 abnormality was, however, the same for visual and acoustic odd-ball paradigms. The amplitude of P3 was smaller when the patient missed visual stimuli. These findings show that severe bilateral lesions at the parieto-occipital junction, inducing Simultanagnosia, do not obliterate VEPs or ERPs components.
PURPOSE: To define the rate of visual field loss in patients with optic nerve head drusen (ONHD). DESIGN: Retrospective chart review. METHODS: Goldmann visual field (GVF) testing from initial visit and last follow-up examination were quantified using the modified Esterman grid technique. The rate of visual field loss was calculated by comparing the initial GVF to the last follow-up GVF. A comparative analysis of GVF and age at initial evaluation was performed on all patients with an initial GVF only. SETTING: Tertiary academic care center. PARTICIPANTS: Inclusion criteria for the rate analysis: (1) diagnosis of ONHD and (2) at least 36 months of follow-up with serial GVF testing. EXCLUSION CRITERIA: (1) patients with glaucoma or glaucoma-suspect; (2) history or examination evidence for other ocular disease; and (3) drusen-related macular causes of visual loss. RESULTS: Thirty-two of 292 charts were included in the rate analysis. The rate of visual field loss was 1.58%. There was no statistically significant difference between men and women (P = .74). One hundred eighty patients were included in the initial visual field analysis. There was a significant negative correlation between age and GVF, with older patients having lower GVF scores with a Spearman correlation of -0.42 (P < 0.0001); 73% of these 180 patients had mild, minimal, or no visual field loss. CONCLUSIONS: The rate of visual field loss for ONHD over a 36-month interval of time was 1.6% per year. Patients with minimal or no visual field loss were younger, and patients with moderate or severe visual loss were older.
PURPOSE: To describe the outcome of a patient with visual loss and optic nerve edema that resulted from osteopetrosis who underwent an optic nerve sheath fenestration (ONSF). DESIGN: Interventional case report. METHODS: A 33-year-old man with osteopetrosis had bilateral visual field loss and optic nerve edema. Computed tomography and magnetic resonance imaging demonstrated open optic canals. Although a lumbar puncture showed a normal opening pressure, there were other findings that were suggestive of increased intracranial pressure. The patient elected to undergo a unilateral optic nerve sheath fenestration. RESULTS: After ONSF, the patient experienced markedly improved visual acuity, visual field, and optic nerve appearance. CONCLUSION: Individuals with visual loss and optic disk edema that is associated with osteopetrosis may benefit from ONSF if the optic canals appear to be open and the optic nerve edema is thought to be related to increased intracranial pressure.
A case of sphenoid sinusitis and internal carotid aneurysm presenting with multiple cranial nerve palsy is reported. A 46-year-old man with high fever and neck rigidity developed progressive visual loss and ophthalmoplegia on both sides, and ptosis, mydriasis and facial numbness on the right side. CT scan and MRI revealed abnormal shadow of the sphenoid sinus and the cavernous sinus. Sphenoidectomy and antibiotic therapy improved left visual acuity, but the right visual disturbance remained. Cerebral angiography performed 20 days after the operation, showed an aneurysm of the cavernous portion of the right internal carotid artery. This aneurysm could be called "bacterial aneurysm" due to sphenoid sinusitis and cavernous sinusitis. However, there is another possibility that the enlargement of an idiopathic and asymptomatic intracavernous aneurysm due to rapid and severe parasinusitis induced bilateral cavernous sinus syndrome with the right side dominance. After endovascular coil placement, his right visual disturbance partially recovered.
The Onodi cell is a large pneumatized posterior ethmoid cell and closely related to optic nerve. We present an extremely rare case of retrobulbar optic neuropathy caused by mucocele in an Onodi cell. A 79-year-old man complained of headaches and simultaneous bilateral visual disturbance. A computed tomography (CT) scan demonstrated a mucocele in an Onodi cell, which involved bilateral optic nerves. The surgical treatment with a transnasal endoscopic approach was performed, resulting in the improving of visual acuity. The bilateral optic nerves were identified along each lateral wall into an Onodi cell accompanied with bone defect. In an Onodi cell, even if the lesion is isolated and/or small, it may be closely related to ocular symptoms. Imaging studies should be considered for the differential diagnosis because early diagnosis and prompt surgical treatment for mucocele are needed for recovery of visual impairment.
The most important ability of the human vision is object recognition, yet it is exactly the less understood aspect of the vision system. Computational models have been helpful in progressing towards an explanation of this obscure cognitive ability, and today it is possible to conceive more refined models, thanks to the new availability of neuroscientific data about the human visual cortex. This work proposes a model of the development of the object recognition capability, under a different perspective with respect to the most common approaches, with a precise theoretical epistemology. It is assumed that the main processing functions involved in recognition are not genetically determined and hardwired in the neural circuits, but are the result of interactions between epigenetic influences and the basic neural plasticity mechanisms. The model is organized in modules related with the main visual biological areas, and is implemented mainly using the LISSOM architecture, a recent self-organizing algorithm closely reflecting the essential behavior of cortical circuits.
Increased intracranial pressure is rarely seen in association with spinal tumors. We describe a young, non-obese man who presented with increased intracranial pressure, papilledema and visual obscuration. Multiple cerebrospinal fluid (CSF) examinations with normal or minimally elevated CSF protein lead to the initial diagnosis of idiopathic intracranial hypertension. After a lumboperitoneal shunt placement a progressive thoracic myelopathy developed 7 months after onset of symptoms. The spinal MRI showed a low cervical-upper thoracic intramedullary tumor. Open biopsy confirmed a grade 3 fibrillary astrocytoma. The suspected mechanisms of spinal tumors causing increased intracranial pressure are reviewed as well as three other cases of spinal astrocytomas previously reported in the literature that presented with papilledema and increased intracranial pressure without hydrocephalus. This case illustrates that increased intracranial pressure may in exceptional cases of spinal tumors precede the more typical myelopathic presentation by months and mimic idiopathic intracranial hypertension.