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1/3. Brain imaging in a patient with hemimicropsia.

    Hemimicropsia is an isolated misperception of the size of objects in one hemifield (objects appear smaller) which is, as a phenomenon of central origin, very infrequently reported in literature. We present a case of hemimicropsia as a selective deficit of size and distance perception in the left hemifield without hemianopsia caused by a cavernous angioma with hemorrhage in the right occipitotemporal area. The symptom occurred only intermittently and was considered the consequence of a local irritation by the hemorrhage. Imaging data including a volume-rendering MR data set of the patient's brain were transformed to the 3-D stereotactic grid system by Talairach and warped to a novel digital 3-D brain atlas. Imaging analysis included functional MRI (fMRI) to analyse the patient's visual cortex areas (mainly V5) in relation to the localization of the hemangioma to establish physiological landmarks with respect to visual stimulation. The lesion was localized in the peripheral visual association cortex, Brodmann area (BA) 19, adjacent to BA 37, both of which are part of the occipitotemporal visual pathway. Additional psychophysical measurements revealed an elevated threshold for perceiving coherent motion, which we relate to a partial loss of function in V5, a region adjacent to the cavernoma. In our study, we localized for the first time a cerebral lesion causing micropsia by digital mapping in Talairach space using a 3-D brain atlas and topologically related it to fMRI data for visual motion. The localization of the brain lesion affecting BA 19 and the occipitotemporal visual pathway is discussed with respect to experimental and case report findings about the neural basis of object size perception.
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2/3. Cognitive dysfunction after isolated brain stem insult. An underdiagnosed cause of long term morbidity.

    Cognitive dysfunction adversely influences long term outcome after cerebral insult, but the potential for brain stem lesions to produce cognitive as well as physical impairments is not widely recognised. This report describes a series of seven consecutive patients referred to a neurological rehabilitation unit with lesions limited to brain stem structures, all of whom were shown to exhibit deficits in at least one domain of cognition. The practical importance of recognising cognitive dysfunction in this group of patients, and the theoretical significance of the disruption of specific cognitive domains by lesions to distributed neural circuits, are discussed.
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3/3. Frontal ataxia in childhood.

    Frontal ataxia may be the result of a unilateral frontal lesion. In this report three cases are presented with ataxia due to right frontal lesions. One case concerns a boy presenting with an unsteady gait and titubation of the trunk, mimicking developmental disequilibrium and with complex partial seizures. It proved to be caused by a small right-sided cavernoma in the middle frontal gyrus. After surgical intervention the symptoms and the seizures disappeared. Two subsequent cases concern teenage patients presenting with headache after an ENT infection and on physical examination mild dysmetric function of the upper limbs and slight disequilibrium, due to right-sided frontal lobe abscesses. After neurosurgical and antibiotic therapy the symptoms were relieved. The frontal origin of ataxia should be considered in children presenting with a "cerebellar syndrome". Frontal gait disorders consist of a clinical pattern of different gait disorders. The syndrome has been mentioned in the literature under different names. Our patients show signs compatible with the term frontal disequilibrium, a clinical pattern of frontal gait disorder. This assumes walking problems characterized by loss of control of motor planning, leading to imbalance. Remarkably, frontal ataxia may mimic developmental delay as demonstrated in the first case and may be the leading mild symptom in extensive frontal lobe damage as demonstrated by the two other cases. We suppose that frontal ataxia is the result of a disturbance in the cerebellar-frontal circuitries and an impairment of executive and planning functions of the basal ganglia-frontal lobe circuitry.
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