1/16. Idiopathic pinealitis. Case report.This 63-year-old man presented with complaints of "having a feeling of falling backward" over a 3-month period. Results of his general physical examination, laboratory studies, and neurological examination were unremarkable. A magnetic resonance image revealed a 1.8 x 1.4 x 1.2-cm enhancing mass in the posterior third ventricle just above the corpora quadrigemina. The pineal gland was found to be diffusely enlarged at operation and separable from the posterior thalamus and was totally resected. The patient had an uneventful postoperative course but continues to be somewhat confused. The lesion consisted of a remarkable chronic inflammatory cell infiltrate permeating the pineal lobules and was composed of T and B lymphocytes, macrophages, eosinophils, and mast cells. Immunoperoxidase studies did not demonstrate langerhans cells, and a search for microorganisms was unrevealing. There was no evidence of neoplasia; results of immunostaining for germ cell markers and other tumor-associated antigens were negative.- - - - - - - - - - ranking = 1keywords = posterior (Clic here for more details about this article) |
2/16. fluorouracil-induced neurotoxicity.OBJECTIVE: To report a case of acute neurologic adverse effects related to fluorouracil administration and to review the neurotoxicity of this agent. CASE SUMMARY: A 73-year-old white man with a history of esophageal carcinoma was treated with fluorouracil 1,500 mg iv daily for four days. After completing treatment, he presented with sudden onset of confusion, cognitive disturbances, a cerebellar syndrome, and repeated seizures. A magnetic resonance image of the brain showed no structural abnormalities, and cerebrospinal fluid examination was normal; none of the other laboratory tests provided an explanation for his symptoms. The patient was treated with anticonvulsants, and the cognitive changes resolved in 72 hours. The cerebellar signs, however, did not resolve completely and persisted when the patient was examined two weeks after discharge. DISCUSSION: fluorouracil can cause both acute and delayed neurotoxicity. Acute neurotoxicity manifests as encephalopathy or as cerebellar syndrome; seizures, as seen in our patient, have rarely been reported. Acute neurotoxicity due to fluorouracil is dose related and generally self-limiting. Various mechanisms for such toxicity have been postulated, and treatment with thiamine has been recommended. Delayed neurotoxicity has been reported when fluorouracil was given in combination with levamisole; this form of subacute multifocal leukoencephalopathy is immune mediated and responds to treatment with corticosteroids. CONCLUSIONS: Clinicians should be aware of the adverse neurologic effects of fluorouracil and should include them in the differential diagnosis when patients receiving the drug present with neurologic problems.- - - - - - - - - - ranking = 48.20674252551keywords = leukoencephalopathy (Clic here for more details about this article) |
3/16. Pure topographic disorientation: A distinctive syndrome with varied localization.Pure topographic disorientation (TD), defined as impaired recall of routes in familiar surroundings, has been attributed to lesions of the right parahippocampus. The authors present three patients encountered consecutively with TD and compare them to previously published cases. Lesions causing TD included a right splenial/cuneus infarct, a right > left medial temporo-occipital infarct, and a left splenial infarct. TD as an isolated symptom may occur from lesion in a variety of posterior medial locations, including the parahippocampus, splenium, and retrosplenial cortex.- - - - - - - - - - ranking = 0.5keywords = posterior (Clic here for more details about this article) |
4/16. Effect of posterior temporal-parietal hematoma on orbital frontal chemistry in relation to a cognitive and anxiety state: a combined 1H-MRS and neuropsychological study of an unusual case as compared with 16 healthy subjects.The authors report the unusual case of a 58-year-old woman (MJP) suffering from left temporal throbbing headache, associated with confusion. magnetic resonance imaging showed a 5 x 3 x 2 cm hematoma at the left posterior temporal--parietal junction (PTPJ). Repeated MRI of MJP's brain performed during a 4-month follow-up period showed decrease in hematoma size (2.3 x 1.5 x 1) with evidence for development of encephalomalacia and resorption of blood products involving the area of hemorrhage. MJP had mild transcortical sensory aphasia characterized by difficulty with reading and processing, with semantic paraphasic errors while speaking and some difficulty with repetition. MJP had remained normotensive and seizure free, on Vasotec therapy and Dilantin prophylaxis. An in vivo proton magnetic resonance spectroscopy (1H-MRS) performed during an 8-month follow-up period showed reduced concentration for N-acetyl aspartate (NAA) by 19.3% (F=4.09, P<0.04), and myo-inositol by 32.0% (F=5.16, P<0.02) in the left orbital frontal cortex (OFC) as compared with 16 healthy subjects (age- and sex-matched). Cognitive tests (the Wechsler abbreviated scale of intelligence (WASI) and the Stroop color--word interference) showed a significant impairment suggesting involvement of higher-order cognitive functioning (memory, learning, and general intelligence) and attentional system. The Spielberger state-trait anxiety inventory (STAI) showed increased anxiety at the moment of the current examination and decreased tendency to be anxious over a long period of time. The Beck anxiety and depression Inventory revealed minimal anxiety and mild to moderate levels of depression. It is hypothesized that the PTPJ hematoma triggered long-distance pathways linking PTPJ area and frontal lobe, including OFC, which resulted in abnormal chemical changes in the left OFC and in cognitive tests impairment, and in long-term anxiety state changes.- - - - - - - - - - ranking = 2.5keywords = posterior (Clic here for more details about this article) |
5/16. Diffuse metabolic abnormalities in reversible posterior leukoencephalopathy syndrome.Two cases of reversible posterior leukoencephalopathy syndrome were examined with proton MR spectroscopic imaging. Widespread metabolic abnormalities, consisting of increased choline and creatine levels and mildly decreased N-acetylaspartate, occurred in regions with both normal and abnormal MR imaging appearances. In one case for which proton MR spectroscopic imaging follow-up was available, all metabolite levels had returned to normal by 2 months. Proton MR spectroscopic imaging may be helpful for the diagnosis and investigation of the underlying pathophysiology of reversible posterior leukoencephalopathy syndrome.- - - - - - - - - - ranking = 1754.5717848433keywords = posterior leukoencephalopathy, leukoencephalopathy, posterior (Clic here for more details about this article) |
6/16. Posterior leukoencephalopathy in a girl with acute haemorrhagic leukoencephalitis.In children, posterior leukoencephalopathy is frequently associated with hypertensive encephalopathy, anticancer chemotherapy, treatment with immunosuppressive drugs in patients with organ transplantation, transfusion or human immunodeficiency virus infection. Posterior leukoencephalopathy in these children appears as a complicating illness and resolves once precipitating factor (e.g. cancer chemotherapy) is removed. Here we are reporting a fatal case of acute haemorrhatic leukoencephalitis in a 13 year old girl, imaging abnormalities are also suggestive of posterior leukoencephalopathy. Posterior leukoencephalopathy in our patient possibly, is a part of post-infectious haemorrhagic leukoencephalitis, rather than because of ischaemia or cerebral oedema secondary either to abrupt increase in blood pressure or following administration of immunosuppressive drugs.- - - - - - - - - - ranking = 874.09771676748keywords = posterior leukoencephalopathy, leukoencephalopathy, posterior (Clic here for more details about this article) |
7/16. limbic encephalitis presenting with topographical disorientation and amnesia.A case of paraneoplastic limbic encephalitis presenting with topographical disorientation is reported. A 70 year old woman became unable to identify familiar buildings and landscapes and could not recall the way to destinations she had known very well for years. She also showed attentional disturbance and severe anterograde amnesia. Her retrograde amnesia extended for one year at most. No other neuropsychological deficits were noted. Thus her topographical disorientation was of the primary form. Specific tests related to topographical disorientation showed that her two main symptoms seem to fall into the categories of landscape agnosia and heading disorientation. T2 weighted magnetic resonance imaging revealed high intensity signals in the anteromedial temporal lobes bilaterally, in the right posterior parahippocampal gyrus, in the right retrosplenial region, and in the right inferior precuneus. Anti-Hu antibody was found in the serum. This case shows that topographical disorientation can be a primary symptom of limbic encephalitis.- - - - - - - - - - ranking = 0.5keywords = posterior (Clic here for more details about this article) |
8/16. survival with serum sodium level of 180 mEq/L: permanent disorientation to place and time.A 41-year-old woman who had undergone transfrontal craniotomy for a pituitary tumor 4 months before presentation was admitted with confusion and orientation only to self. She had a fever of 40 degrees C. serum sodium and chloride levels on admission were 180 and 139 mEq/L, respectively. Measured serum osmolality was 380 mOsmol/L with a urine osmolality of 360 mOsmol/L. magnetic resonance imaging revealed a 1.5-cm mass in the sella turcica, which was nonfunctioning on endocrine evaluation. The "bright spot" of a normal posterior pituitary was absent. Central diabetes insipidus was confirmed by a 300% increase in urine osmolality with desmopressin. The patient survived her severe hypernatremia, which has 70% mortality with a serum sodium level of 160 mEq/L or above. However, she developed permanent (6 months) disorientation to time and place even when hypernatremia was corrected, which has not been described previously.- - - - - - - - - - ranking = 0.5keywords = posterior (Clic here for more details about this article) |
9/16. Pure topographical disorientation--the anatomical basis of landmark agnosia.We used MRI studies of four patients to investigate the lesions responsible for landmark agnosia. A detailed investigation of the relationship between the symptoms and the lesions suggests that the right posterior part of the parahippocampal gyrus is critical for the acquisition of novel information about buildings and landscapes, and that the same region plus the anterior half of the lingual gyrus and the adjacent fusiform gyrus play an important role in the identification of familiar buildings and landscapes. Furthermore, the lesion responsible for prosopagnosia, which frequently occurs with landmark agnosia, seems to involve the posterior half of the lingual and fusiform gyri. This suggests that the lesions responsible for landmark agnosia and prosopagnosia are close to each other, but distinct.- - - - - - - - - - ranking = 1keywords = posterior (Clic here for more details about this article) |
10/16. confusion and memory loss from capsular genu infarction: a thalamocortical disconnection syndrome?We examined six patients with an abrupt change in behavior after infarction involving the inferior genu of the internal capsule. The acute syndrome featured fluctuating alertness, inattention, memory loss, apathy, abulia, and psychomotor retardation, suggesting frontal lobe dysfunction. Contralateral hemiparesis and dysarthria were generally mild, except when the infarct extended into the posterior limb. Neuropsychological testing in five patients with left-sided infarcts revealed severe verbal memory loss. Additional cognitive deficits consistent with dementia occurred in four patients. A right-sided infarct caused transient impairment in visuospatial memory. Functional brain imaging in three patients showed a focal reduction in hemispheric perfusion most prominent in the ipsilateral inferior and medial frontal cortex. We infer that the capsular genu infarct interrupted the inferior and anterior thalamic peduncles, resulting in functional deactivation of the ipsilateral frontal cortex. These observations suggest that one mechanism for cognitive deterioration from a lacunar infarct is thalamocortical disconnection of white-matter tracts, in some instances leading to "strategic-infarct dementia."- - - - - - - - - - ranking = 0.5keywords = posterior (Clic here for more details about this article) |
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