Achromatic visual function in primates is distributed between two pathways from retina to cortex, the parvocellular and the magnocellular. The relative contribution of these to human achromatic vision is controversial and largely unknown. Here, we use an optic neuritis (ON) model to investigate the effects of a severe loss of parvocellular function on human contrast sensitivity. In our first experiment, we use Gabor stimuli (0.5 cpd, 2 Hz) to show that, compared to normal control eyes, ON causes selective deficits in the two chromatic, cone opponent pathways, with L/M cone opponency affected more than S cone opponency, and a relative sparing of achromatic function. Since L/M cone opponency is carried exclusively by the midget ganglion cells of the parvocellular pathway, this demonstrates a selective deficit of parvocellular function. In a second experiment, we report on two subjects who have lost all L/M cone opponent response in both eyes, indicating a severe loss of parvocellular function. We measure the spatial and temporal contrast sensitivity functions of their remaining achromatic vision, compared with a normal control group, to determine the selectivity of the visual deficit caused by the differential parvocellular loss, and assess the relative contributions of the parvocellular and magnocellular pathways to achromatic contrast sensitivity. We find that parvocellular function contributes selectively at mid- to high spatial frequencies (at low temporal frequencies), whereas magnocellular function determines contrast sensitivity over a very broad temporal frequency range (at low spatial frequencies). Our data bear a striking resemblance to results obtained from primate parvocellular lesions.
684Cerebral venous thrombosis (CVT) is an uncommon form of cerebrovascular disease, with an incidence of three to four cases per million persons. Although acute-onset headache is the most consistent presentation, CVT may also manifest as seizures, intracranial hypertension, and focal sensorimotor deficits 1 . Here, we report the unusual development of subacute parkinsonism secondary to multiple cerebral sinus thromboses. CASE REPORTA 57-year-old right-handed woman with a three year history of diffuse, intermittent headaches presented to the Jewish General Hospital (Montreal) with worsening non-pulsatile headache and progressive hypophonia, micrographia, bradyphrenia and gait unsteadiness over a three week period. There were no complaints of hyposmia, sleep disturbances, constipation or other pre-motor symptoms of idiopathic Parkinson disease. Her past medical history was unremarkable and her medication list included vitamin D and calcium supplements only. Physical examination revealed normal vital signs with no evidence of postural hypotension, normal level of consciousness, orientation, attention, language, affect, judgment and insight. There was facial hypomimia but the rest of the cranial nerve exam, including bilateral olfactory nerve testing, was normal. There was marked hypophonia and micrographia and moderate bradykinesia and cogwheel rigidity. Muscle power was normal and tremor was absent. The gait was narrow-based, small-steppage and unsteady. There was severe retropulsion on pull-testing. Sensory, cerebellar and reflex testing was unremarkable save for prominent glabellar tap and palmomental signs.A computed tomogram (CT) scan of the head (Figure) showed small, scattered hyperdensities in bilateral frontal, temporal and parietal lobes and in the region of the interpeduncular cistern. The white matter appeared abnormally hypodense consistent with generalized edema (a1-a2). Magnetic resonance imaging axial FLAIR sequences showed heterogeneous hyperintense signal of the transverse sinuses (left, arrow) and congested peripheral veins (b1-b2). Axial FLAIR and T2 sequences showed diffuse, hyperintense signal of the periventricular and subcortical white matter and mild sulcal effacement (c1-c2). Magnetic resonance venography (MRV) demonstrated occlusion of the transverse sinuses and distal internal cerebral veins, minimal flow within the vein of Galen, and severely congested cortical and subcortical veins and straight sinus (d1-d2).Routine hematology, erythrocyte sedimentation rate and Despite intravenous heparin and a therapeutic partial thromboplastin time, there was abrupt clinical deterioration characterized by confusion, worsening gait and double incontinence. A repeat CT of the head was unchanged. A trial of intra-jugular tPA and mechanical venous sinus thrombectomy were unsuccessful due to "rock-hard" clot consolidation. The patient was started on warfarin and dexamethasone with gradual improvement of neurological status to near-admission levels. She was discharged to a rehabilitation hospital on warfa...
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