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 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-five patients with occipital lobe seizure origin were retrospectively evaluated to determine clinical seizure characteristics and electroencephalographic manifestations. Certain symptoms and signs served to identify occipital lobe origin in 22 (88%). These included elementary visual hallucinations, ictal amaurosis, eye movement sensations, early forced blinking or eyelid flutter, and visual field deficits. Eye or head deviation, or both, was observed frequently and was contralateral to the side of seizure origin in 13, but 3 patients exhibited ipsilateral deviation in some or all their seizures. After the initial signs and symptoms, clinical seizure characteristics resembled those of seizures originating elsewhere. Seizures typical of temporal lobe origin with loss of contact and various types of automatic, semipurposeful activity occurred in 11 patients. Seizures in 3 patients exhibited asymmetrical tonic or focal clonic motor patterns characteristic of frontal lobe seizures. Eleven of the 25 patients had, on two occasions, two or more distinctly different seizure types. Scalp electroencephalographic findings were seldom helpful for occipital lobe localization and were frequently misleading. Intracranial electroencephalographic recording correctly identified occipital lobe seizure origin in most, but not all, patients who had such studies. Intracranial electroencephalic recording also proved the variability in clinical seizure characteristics was related to different seizure spread patterns, medially or laterally above and below the sylvian fissure, both ipsilateral and contralateral to the occipital lobe of seizure origin. Eighteen patients had occipital lobe lesions detected with computed tomographic or magnetic resonance imaging scans or both. Resection of the lesions in 16 patients produced excellent results in 14 (88%). Five patients had temporal lobectomies, with good results in 3, but poor results in 2. Two patients with unlocalized seizures had complete section of the corpus callosum, 1 with a good result and the other with a poor result.
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PMID:Occipital lobe epilepsy: clinical characteristics, seizure spread patterns, and results of surgery. 154 48

We report 2 cases of corticobasal degeneration (CBD) with reference to the clinical and pathological features and neuroimaging including MRI, positron emission tomography (PET) and single photon emission tomography (SPECT). Case 1 was a 66-year-old right-handed woman. Her spontaneity had been gradually impaired, and she showed a progressive course of naming difficulty, memory disturbance, and right unilateral spatial neglect in addition to the right hemi-parkinsonism and bilateral pyramidal tract signs. Cortical and subcortical atrophy was predominant in the left hemisphere on MRI. As compared with the right side, both cerebral blood flow (CBF) and oxygen metabolism (CMRO2) were decreased in the left hemisphere on the PET which was performed 4 years after onset. She showed further clinical deterioration, and exhibited a bilateral parkinsonism 6 years after the onset. The follow-up SPECT revealed diffusely bilateral hypoperfusion except for the basal ganglia and occipital lobes 6 years after the onset. Case 2 was a 56-year-old right-handed woman. She exhibited a progressive course of bilateral parkinsonism, hallucinations and vertical eye movements disturbance. She died of infection 42 months after the onset of the initial symptoms. Bilateral frontal atrophy was seen on X-ray CT and MRI. PET revealed a diffuse moderate decrease in CBF and CMRO2 particularly in the frontal cortex, central semiovale, paraventricular white matter and cingulate gyrus bilaterally. Pathological examination disclosed a mild frontal atrophy, and there was diffuse neuronal loss, gliosis, and achromasia in the cerebral cortices. There was moderate neuronal cell loss and gliosis in the thalamus, whereas the globus pallidus, striate and substantia nigra were severely affected. Neuronal inclusions termed corticobasal inclusions were present in the substantia nigra, nuclei raphes, and Meynert's nuclei, and none of these regions contained Pick's cell. PET and SPECT studies revealed an asymmetrical decrease in CBF and CMRO2 in the initial stage and diffuse bilateral decrease in the advanced stage in Case 1, whereas Case 2 showed a bilateral decrease in the late stage. This may indicate that the patterns of hypoperfusion and/or hypometabolism differs according to the clinical stages of CBD.
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PMID:[Corticobasal degeneration: a combined clinical, PET and pathological study]. 875 83

Increasing evidence suggests the presence of a lateralizing attentional deficit in schizophrenia. In the present study, 23 unmedicated patients with schizophrenia (mean age = 32.1 years) and 14 age- and sex-matched normal subjects were studied with the Global/Local Task to provide converging evidence for the presence of a left-hemisphere-associated attentional deficit in schizophrenia. This task is sensitive to the integrity of mechanisms involved in discriminating local and global elements of stimuli. Previous research has linked the discrimination of local targets to left hemispheric processes and the discrimination of global targets to right hemispheric processes. As predicted, patients were impaired in the detection of local level targets, consistent with a left hemispheric deficit. The degree of impairment correlated with the patient's level of auditory hallucinations. These results are consistent with previous studies showing an asymmetrical attentional deficit in schizophrenia and left hemispheric dysfunction. The correlation between this deficit and auditory hallucinations is consistent with a hypothesized relationship between this symptom in schizophrenia and left temporal pathology.
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PMID:Perceptual and attentional asymmetries in schizophrenia: further evidence for a left hemisphere deficit. 877 8

A 43-year-old, right-handed woman experienced right hand paresthesias and a visual field abnormality. We attributed her symptoms to psychiatric abnormalities, due to the presence of delusions and auditory hallucinations. Upon photostimulation, she experienced left visual field hallucinations and demonstrated slow waves on the right parieto-occipital regions. The clinical and electro-encephalographic findings suggested that these episodes were epileptic seizures originating from the right occipital region. Ictal fear appeared at the end of the seizure, reflecting the spread of seizure activity to the mesial temporal region. Ictal SPECT images showed hyper-perfusion in the right occipital region and left cerebellar cortex. rCBF in the occipital lobe was significantly asymmetrical. When we encounter an epileptic patient with psychosis who has a visual hallucination, we should consider the possibility of epileptic seizure originating from the occipital lobe.
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PMID:[Ictal visual hallucination intermittent photic stimulation: using evaluation of the clinical findings, ictal EEG, ictal SPECT, and rCBF]. 1051 57

We report the findings of single photon emission computed tomography using 123I-IMP and magnetic resonance image studies of five patients with Charles Bonnet syndrome (CBS) while they were having visual hallucinations. All patients developed complex visual hallucinations after suffering from eye disease. The mean age at onset of CBS was 71.6 years. Single photon emission computed tomography studies in all patients disclosed hyperperfusion areas with some asymmetrical appearances in the lateral temporal cortex, striatum and thalamus. These results suggest that when elderly people suffer from eye disease, subsequent excessive cortical compensation in the lateral temporal cortex, striatum and thalamus may precipitate the development of visual hallucinations.
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PMID:Hyperperfusion in the lateral temporal cortex, the striatum and the thalamus during complex visual hallucinations: single photon emission computed tomography findings in patients with Charles Bonnet syndrome. 1080 9

Auditory--verbal hallucinations (AVH) are a characteristic feature of schizophrenia. Patients with AVHs have been found to differ from non-hallucinating patients in volumes of certain asymmetrical brain structures on MRI, and on certain neuropsychological measures. There is also evidence of corpus callosum (CC) abnormalities in schizophrenia, and it has been proposed that abnormalities of inter-hemispheric transmission may underlie hallucinations and other symptoms. The aim of this study was to examine whether patients with AVHs have smaller corpora callosa than those without AVH, and whether CC size is related to performance on neuropsychological tests of functional cerebral asymmetry. Seventy-one DSM-IV male schizophrenics were recruited on the basis of their hallucination history plus 33 matched normal controls. Twenty-nine patients had no history of AVH, and 42 had a strong history of AVH. The mid-sagittal surface area and longitudinal length of the CC were measured from T(1)-weighted spin echo images. Callosal area was divided into four sections. There were no significant differences in any of the measurements between the two patient groups, or between patients with schizophrenia and controls. There was no association between CC measures and handedness, or performance on dichotic listening or finger tapping tasks. The results of this study do not lend support for there being a major morphological abnormality of the corpus callosum in schizophrenic patients, or for a specific relationship to AVH. However, a significant association between CC area and overall grey and white matter volumes was noted in the hallucinating patients and, to a lesser extent, in the non-hallucinators, which may point to differing influences on brain development or degeneration in such patients compared with normal controls.
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PMID:Corpus callosum area and functioning in schizophrenic patients with auditory--verbal hallucinations. 1137 10

By recalling gustatory memories, it is possible to generate vivid gustatory perceptions in the absence of gustatory inputs. This gustatory image influences our gustatory processing. However, the mechanism of the "top-down" modulation of gustatory perception in the human is still unclear. Our findings propose a new perspective on the neural basis of gustatory processing. Although gustatory imagery and gustatory perception shared common parts of neural substrates, there was an asymmetrical topography of activation in the insula: the left insula was predominantly activated by gustatory imagery tasks. In addition, the middle and superior frontal gyri were not activated by gustatory perception but they participated in the generation of gustatory hallucinations. These regions in the frontal cortex may mediate the "top-down" control of retrieving gustatory information from the storage of long-term memories.
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PMID:Functional imaging of gustatory perception and imagery: "top-down" processing of gustatory signals. 1558 92

Bipedal locomotion and fine motility of hand and larynx of humans introduced musculoskeletal adaptations, new pyramidal, corticostriatal, corticobulbar, nigrostriatal, and cerebellar pathways and expansions of prefrontal, cingular, parieto-temporal and occipital cortices with derived new brain capabilities. All selectively degenerate in aged homo sapiens following 16 syndromic presentations: (1) Parkinsonism: nigrostriatal control for fast automatic movements of hand, larynx, bipedal posture and gait ("simian gait and hand"). (2) Frontal (highest level) gait disorders (lower body parkinsonism, gait apraxia, retropulsion): prefrontostriatal executive control of bipedal locomotion. (3) ataxia: new synergistic coordination of bipedal gait and fine motility. (4) Dyskinesias (chorea, dystonia, tremor...): intrusions of simian basal ganglia motor subroutines. (5) motoneuron diseases: new proximo-distal and bulbar motoneurones, preserving older ones (oculomotor, abdominal...). (6) Archaic reflexes: prefrontal disinhibition of old mother/tree-climbing-oriented reflexes (sucking, grasping, Babinski/triple retraction, gegenhalten), group alarms (laughter, crying, yawning, grunting...) or grooming (tremor=scratching). (7) Dysautonomia: contextual regulation (orthostatism...). (8) REM sleep disorders of new cortical functions. (9) Corticobasal syndrome: melokinetic control of hand prehension-manipulation and language (retrocession to simian patterns). (10) Frontal/temporal lobe degeneration: medial-orbitofrontal behavioural variant: self monitoring of internal needs and social context: apathy, loss of personal hygiene, stereotypia, disinhibition, loss of concern for consequences of acts, social rules, danger and empathy; dorsolateral executive variant: inadequacy to the context of action (goal, environmental changes...); progressive non-fluent aphasia: executive and praxic processing of speech; temporal variant: abstract concepts for speech, gestures and vision (semantic dementia, progressive nonfluent aphasia) (11) Temporomesial-limbic-paralimbic-associative cortical dementias (Alzheimer's disease, Lewy body, progressive amnesia): processing of explicit cognition: amnesic syndrome, processing of hand, larynx and eye: disorientation, ideomotor apraxia, agnosia, visuospatial processing, transcortical aphasia. (12) Focal posterior atrophy (Benson, progressive apraxia): visuomotor processing of what and where. (13) Macular degeneration: retinal "spot" for explicit symbols. (14) "Psychiatric syndromes": metacognition, self monitoring and regulation of hierarchical processing of metacognition: hallucinations, delusions, magic and mystic logic, delusions, confabulations; drive: impulsivity, obsessive-compulsive disorders, mental automatisms; social interactions: theory of mind, autism, Asperger. (15) Mood disorders: control on emotions: anxio-depressive and bipolar disorders, moria, emotional lability. (16) Musculoskeletal: inclusion body myositis: muscles for bipedal gait and fine motility. Paget's disease: bones for bipedal gait and cranium. Understanding of the genetic mechanisms underlying the evolution of these recent human brain regions and paleoneurology my be the key to the focal, asymmetrical or systemic character of neurodegeneration, the pathologic heterogeneity/overlap of syndromic presentations associating gait, hand, language, cognition, mood and behaviour disorders.
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PMID:Paleoneurology: neurodegenerative diseases are age-related diseases of specific brain regions recently developed by Homo sapiens. 1870 90

Frontotemporal lobar degeneration is currently associated with three syndromic variants. Disorders of speech and language figure prominently in two of the three variants, and are associated with left-sided frontotemporal atrophy. The detailed characterization of these syndromes contrasts with the relative paucity of information relating to frontotemporal lobar degeneration primarily affecting the right cerebral hemisphere. The objective of this study was to identify the clinical profile associated with asymmetrical, predominantly right-sided, temporal lobe atrophy. Twenty patients with predominant right temporal lobe atrophy were identified on the basis of blinded visual assessment of the MRI scans. The severity of right temporal lobe atrophy was quantified using volumetric analysis of the whole temporal lobes, the amygdala and the hippocampus. Profiles of cognitive function, behavioural and personality changes were obtained on each patient. The pattern of atrophy and the clinical features were compared with those observed in a group of patients with semantic dementia and predominant left-sided temporal lobe atrophy. The mean right temporal lobe volume in the right temporal lobe atrophy group was reduced by 37%, with the mean left temporal lobe volume reduced by 19%. There was marked atrophy of the right hippocampus and right amygdala, with mean volumes reduced by 41 and 51%, respectively (left hippocampus and amygdala volumes were reduced by 18 and 33%, respectively). The most prominent cognitive deficits were impairment of episodic memory and getting lost. Prosopagnosia was a symptom in right temporal lobe atrophy patients. These patients also exhibited a variety of behavioural symptoms including social disinhibition, depression and aggressive behaviour. Nearly all behavioural disorders were more prevalent in the right temporal lobe atrophy patient group than the semantic dementia group. Symptoms particular to the right temporal lobe atrophy patient group included hyper-religiosity, visual hallucinations and cross-modal sensory experiences. The combination of clinical features associated with predominant right temporal lobe atrophy differs significantly from those associated with the other syndromes associated with focal degeneration of the frontal and temporal lobes and it is, therefore, proposed that this right temporal variant should be considered a separate syndromic variant of frontotemporal lobar degeneration.
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PMID:The clinical profile of right temporal lobe atrophy. 1929 6

Clinical features and results of neuroimagings of an 86 year old woman with the Charles Bonnet syndrome are reported. She had become completely blind bilaterally due to cataracts and glaucoma. Shortly after an operation for cataracts, she developed visual hallucinations which lasted for 22 years. She had no deterioration of intelligence. Computed tomography (CT) and magnetic resonance imaging (MRI) showed moderate generalized atrophy, particularly of the temporal lobes. A serial single photon emission computed tomography (SPECT) study during visual hallucinations demonstrated hyperperfusion in the left temporal region and the basal ganglia and hypoperfusion in the right temporal region. These findings suggest that asymmetrical blood flow, particularly in the temporal regions, may be correlated with visual hallucination in the Charles Bonnet syndrome.
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PMID:Asymmetrical blood flow in the temporal lobe in the Charles Bonnet syndrome: serial neuroimaging study. 2448 95


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