Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011551 (depersonalization)
 1,117 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a 76-year-old man who developed blurred vision and dementia. He was apparently well until April 4, 1990 (70-year-old at that time) when he had a sudden onset of bilateral loss of vision. Corrected vision was 0.1 (right) and 0.09 (left). He was admitted to the ophthalmology service of our hospital on April 9, 1990, and neurological consultation was asked on April 11. Neurologic examination revealed alert and oriented man without dementia. Higher cerebral functions were intact. He had bilateral large visual field defects with loss of vision; he was only able to count the digit number with his right eye and to recognize hand movement with his left eye. Otherwise neurologic examination was unremarkable. General physical examination was also unremarkable; he had no hypertension. Cranial CT scan was normal on April 11; lumber spinal fluid contained 1 cell/microliter, 63 mg/dl of sugar, and 97 mg/dl of protein; myelin basic protein was detected, however, oligoclonal bands were absent. He was treated with methylprednisolone pulse therapy and oral steroid, however, no improvement was noted in his vision. He started to show gaze paresis to left, ideomotor apraxia, agnosia of the body, and dementia. Cranial CT scan on June 11 revealed a low density area in the deep left parietal white matter facing the trigonal area of the lateral ventricle. He was discharged on July 2, 1990. Hasegawa dementia scale was 2/32.5 upon discharge. In the subsequent course, he showed improvement in his mental capacity and Hasegawa dementia scale was 22.5/32.5 in 1991, however, no improvement was noted in his vision. In 1994, he started to show mental decline in that he became disoriented, and showed delusional ideation of self persecution and depersonalization with occasional confusional state. He also showed unsteady gait. Cranial MRI on February 13, 1996 revealed a T2-high signal intensity lesion on each side of the parietal deep white matter more on the left and another T2-high signal intensity lesion in the left pons as well as in the right thalamus. He complained of right hypochondrial pain and was admitted to another hospital on April 22, 1996. He was markedly confused and demented. He continued to show bilateral loss of vision, but no motor palsy was noted. Cranial CT scan on April 23, 1996 revealed diffuse cortical atrophy and ventricular dilatation in addition to the low density areas in both parietal deep white matter. He developed jaundice in the middle of May. Abdominal CT scan revealed multiple low-to iso-density areas in the liver and marked iso-to high-density swelling of the right kidney. The patient expired on June 9th, 1996. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had had a carcinomatous limbic encephalitis with optic neuropathy and a choleduct carcinoma. Other opinions entertained included acute disseminated encephalomyelitis with optic neuritis, and granulomatous angiitis of the central nervous system. Some participants thought the primary site of the carcinoma was the right kidney with metastasis to the liver. Post mortem examination revealed a mixed type carcinoma in the right kidney with liver metastases. Neuropathologic examination revealed an incomplete softening in the optic chiasm and the left optic nerve, and in the left parieto-occipital areas. (The right hemisphere was frozen for future biochemical assay.) One of the adjacent cortical arteries had an organized thrombus. Other arteries and arterioles also showed sclerotic changes. Some of the leptomeningeal arteries were positive for Congored staining as well as for beta-amyloid immunostaining. Many senile plaques were seen diffusely in the cerebral cortex and neurofibrillary tangles were seen in the CA1 area and the parahippocampal gylus. No cellular infiltrations or demyelinated foci were seen. The neuropathologic features were consistent with circulatory disturbance based on the amyloid angiopa
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PMID:[A 76-year-old man with loss of vision and dementia]. 928 74

Similarities in the clinical presentation of panic disorder and temporal lobe epilepsy suggest that the two disorders are related and can lead to difficulties in a differential diagnosis. We describe the case of a young girl suffering from paroxysmal anxiety, derealization-depersonalization and autonomic symptoms, lasting from seconds to several minutes; these episodes were very frequent and disabling. The interictal EEGs and MRI were normal. After having diagnosed panic disorder based mainly on the duration of the attacks and the family history, a pharmacological treatment was started.
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PMID:Panic disorder or temporal lobe epilepsy: A diagnostic problem in an adolescent girl. 1055 Jul 6

Recent evidence suggests that borderline personality disorder (BPD) is related to reduced size of the parietal lobe. Dissociative symptoms occur in the majority of individuals with BPD. Structural magnetic resonance imaging (3D-MRI) was used to assess volumes of the superior (precuneus, postcentral gyrus) and inferior parietal cortices in 30 young women with BPD who had been exposed to severe childhood sexual and physical abuse and 25 healthy control subjects. Compared with control subjects, BPD subjects had significantly smaller right-sided precuneus (-9%) volumes. The left postcentral gyrus of BPD subjects with the comorbid diagnosis of dissociative amnesia (DA) or dissociative identity disorder (DID) was significantly increased compared with controls (+13%) and compared with BPD subjects without these disorders (+11%). In BPD subjects, stronger depersonalization was significantly related to larger right precuneus size. Possibly, larger precuneus size in BPD is related to symptoms of depersonalization. Increased postcentral gyrus size in BPD may be related to the development of DA or DID in the presence of severe childhood abuse.
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PMID:Size abnormalities of the superior parietal cortices are related to dissociation in borderline personality disorder. 1782 65

We described the major diagnostic difficulties encountered in the case of a 25-year-old man with the pathological diagnosis of a germinoma. The patient initially developed an eating disorder at the end of 2003 and a character change ensued since the beginning of 2004. On admission in August 2004, his cardinal symptoms and signs included marked apathy, depersonalization, generalized muscle wasting, and decreased tendon reflexes. Brain T2-weighted (T2-WI) MR and FLAIR images showed high signal intensities in the suprasellar region and at the genu of the corpus callosum that extended along the sub-pia mater of the right anterior horn. These lesions showed mild enhancement on gadolinium-enhanced T1-WI. CSF examination revealed a mildly elevated level of protein and increased cell counts but did not show any malignant cells on repeated spinal tap. The patient's status remained practically unchanged till December 2004 when he developed diabetes insipidus. Soon afterward, the patient collapsed into akinetic mutism and developed corresponding new lesions at the tegmentum of the midbrain. These new lesions disappeared spontaneously and akinetic mutism regressed without any specific therapy. We tentatively diagnosed of neurosarcoidosis based on a characteristic progressive-regressive clinical course, CSF data, and radiological findings. Clinical symptoms and the enhanced masses on MRI were highly responsive to steroid therapy after which the patient was able to return home. However, disturbances in consciousness and tenacious vomiting recurred in September. Brain MRI revealed a markedly re-enlarged and easily enhanced mass at the right anterior horn, which extended into the cerebral aqueduct and resulted in obstructive hydrocephalus. On surgery, histopathological investigation revealed germinoma. This case highlights the need for careful discrimination between a slow growing germinoma and chronic granulomatous diseases of the brain such as neurosarcoidosis. Early histological investigation may be warranted in patients who present difficulties during differential diagnoses.
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PMID:[Germinoma presenting with personality and socio-behavioral abnormalities may challenge differential diagnoses]. 1871 99

The mirror-gazing task (MGT) experimentally induces illusions, ranging from simple color changes in the specular image of oneself, to depersonalization-like anomalous self-experiences (ASE) as in experiencing one's specular image as someone else. The objective was to characterize how connectivity in resting-state networks (RSNs) differed in adolescents reporting such depersonalization-like ASEs during the MGT, in a cross-sectional (Y1) and in a longitudinal manner (a year after). 75 adolescents were recruited; for the cross-sectional analysis, participants were split into 2 groups: those who reported depersonalization-like ASEs on the MGT (ASE), and those who did not (NoASE). For the longitudinal analysis, participants were split into 3 groups whether they experienced MGT depersonalization-like ASEs: only at Y1 (Remitters), both times (Persisters), or never (Controls). Participants also filled out self-reports assessing schizotypal personality (Schizotypal Personality Questionnaire [SPQ]), and underwent resting-state functional MRI procedure (rs-fMRI). A group level Independent Component Analysis (ICA) was conducted and voxel-wise inter-group differences within RSNs were examined. The rs-fMRI analysis revealed lower connectivity of specific visual areas within the primary visual network (PVN), and higher connectivity of regions within the Default Mode Network (DMN) when contrasting the ASE and NoASE groups. The areas that were atypically connected within the PVN further presented differential pattern of connectivity in the longitudinal analysis. Atypical connectivity of visual area within the DMN at Y1 was associated with higher scores on the disorganized dimension of schizotypy at the second evaluation. The present study uncovers a subtle signature in the RSNs of non-clinical adolescents who experienced task-induced ASEs.
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PMID:Resting-State Networks of Adolescents Experiencing Depersonalization-Like Illusions: Cross-sectional and Longitudinal Findings. 2956 27

Background: Alice in Wonderland syndrome (AIWS) is a rare neurological disorder characterized by distortions of visual perception (metamorphopsias), the body image, and the experience of time, along with derealization and depersonalization. Some 85% of patients present with perceptual distortions in a single sensory modality, e.g., only visual or only somesthetic in nature. Moreover, the majority experience only a single type of distortion, e.g., only micropsia or only macropsia. AIWS has many different etiologies, and hence an extensive differential diagnosis. Its amenability to treatment depends on the underlying pathological process, which in children is mostly encephalitis, and in adults, migraine. In the literature, no more than 180 "clinical" cases of AIWS have been described (i.e., cases in need of medical attention). Of them, some 50% showed a favorable prognosis. However, non-clinical cases (i.e., fleeting, transient cases of AIWS for which no professional help is needed) have been described in up to 30% of the general population. This indicates that AIWS is perhaps not as rare as traditionally assumed, and has led some authors to conclude that, prognostically, AIWS is usually harmless. Methods: From our own clinical practice, we describe the first known case of Creutzfeldt-Jakob Disease (CJD, Heidenhain variant) that presented with symptoms of AIWS. Results: In our patient, disease onset was sudden and rapidly progressive, starting with isolated visual symptoms. Symptoms of AIWS comprised akinetopsia, chloropsia, micropsia, macropsia, zoom vision, and time distortions (quick-motion phenomenon and protracted duration). Soon, these were complicated by paraesthesias, gait instability, aphasia, expressive amusia, cognitive decline, and behavioral changes in the form of agitation and emotional lability. The diagnosis of probable sporadic CJD was confirmed with the aid of a head MRI and cerebrospinal fluid (14-3-3 protein). In the absence of any treatment options, our patient was discharged home and died within 2 months after his visual symptoms had begun. Autopsy consent was not obtained. Conclusion: We conclude that AIWS is not always as harmless as sometimes suggested, and that CJD, although extremely rare, must be part of its extensive differential diagnosis, notably in the presence of rapid cognitive decline.
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PMID:Alice in Wonderland Syndrome as a Presenting Manifestation of Creutzfeldt-Jakob Disease. 3114 56