Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case associated with multiple cerebral vascular anomalies, which consisted of fenestration of the middle cerebral artery, arteriovenous malformation and aneurysm of the anterior communicating artery, was reported. A 48 year-old male has been suffering from the left paralysis and mental disorder after the initial attack of subarachnoid hemorrhage, and the second attack resulted in the deterioration of the symptoms. He was admitted to our clinic on October 28, 1974. On neurological examination, mental disorders, such as disorientation, emotional incontinence, amnesia and acalculia, hemiplegia on the left and meningeal irritation signs were observed in admission period. Physical examination was negative. Cerebral angiographic findings were as follows: 1) Moderate vasospasm of the right internal carotid artery at the terminal segment, mild bowing of the anterior cerebral artery and stretching of the frontparietal opercular branches of the middle cerebral artery were observed. 2) Right frontpolar arteriovenous malformation fed by the frontobasal artery and the frontopolar artery, and drained via the aberrant cortical vein into the superior sagittal sinus. 3) Aneurysm of the anterior communicating artery was opacified by left carotid angiography. 4) An abnormal vessel derived from the terminal segment of the right internal carotid artery and terminated at the portion of the sphenoidal segment of the middle cerebral artery. Complete loop was formed between genuine middle cerebral artery and this abnormal artery. He was operated with dissecting microscope on November 11, 1974. The arteriovenous malformation at right frontopolar region was totally removed and aneurysm of the anterior communicating artery was clipped. According to the operative findings, the arachnoid membrane over the right frontopolar region was turbid and adhered to the adjacent tissues. On the contrary, no abnormal findings suggestive of previous subarachnoid hemorrhage were observed around the region of the anterior communicating artery aneurysm. These findings showed that subarachnoidal bleeding was caused by rupture of the arteriovenous malformation of right frontopolar region, but not by the aneurysm on the anterior communicating artery. The postoperative course was uneventful and during the hospitalization the patient starts on rehabilitation therapy. The authors discussed the genesis of fenestration of the middle cerebral artery and relation among these combined vascular anomalies. We inferred that fenestration of the middle cerebral artery arose from the in complete fusion of procursor vascular network in embryonic stage. Additionally, we emphasized that it was necessary to make a distinction between these two terms "fenestration" and "duplication".
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PMID:[A case of multiple anomalies of cerebral vessels--fenestration of the middle cerebral artery aneurysm of the anterior communicating artery and arteriovenous malformation on the frontopolar region (author's transl)]. 55 79

Multiple sclerosis (MS) is usually diagnosed on the basis of the typical clinical course, with remission and exacerbation in multiple parts of the central nervous system (CNS). Recently, magnetic resonance imaging (MRI) has made a large contribution to the diagnosis of patients with MS. But it is difficult to make a definite diagnosis due to clinical variability of the disease and variable MRI findings. We report the case of a 26-year-old woman who developed progressive left hemiplegia, mental dysfunction, and had extensive bilateral cerebral white matter lesions diagnosed by brain MRI. Complete recovery from the left hemiplegia followed the use of corticosteroid, and her brain MRI findings also improved after medication. Early in the clinical course it was difficult to differentiate between multiple sclerosis and granulomatous angiitis of the CNS. After recovery from the first episode of left hemiplegia and mental dysfunction, she developed acute visual disturbance five months after her first admission. Readmission followed and her retrobulbar neuritis was successfully treated by methylpredonisolone pulse therapy. In summary, she experienced two episodes of neurological deficit, had left hemiplegia and mental dysfunction associated with multiple lesions in bilateral cerebral white matter in brain MRI, and the left retrobulbar neuritis with delay of P100 by visual evoked potential study. Due to these two episodes we concluded that she had multiple sclerosis. Though the initial diagnosis was difficult, prompt treatment and close follow-up was important, since multiple sclerosis and granulomatous angiitis of the CNS can both recur.
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PMID:Multiple sclerosis with extensive lesions left hemiplegia, mental dysfunction and retrobulbar neuritis. 1049 30

Erasmus Darwin was the founder of evolutionary biology, a renown poet, an inventor, and a general medical practitioner. Erasmus Darwin wrote specifically about the evolutionary and phylogenetic development of the nervous system, neuroembryology, psychiatric illness (including delusions and depression), and electrical therapy for childhood hemiplegia. He conducted experiments in neuro-ophthalmology and wrote about color vision, afterimages, the blind spot, and visual memory.
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PMID:Erasmus Darwin (1731-1802): neurologist. 1742 Apr 18

We report on the case of a 36-year-old Hispanic woman with a spinal cord infarct, who was subsequently diagnosed with methylmalonic aciduria and homocystinuria, cblC type (cblC). Mutation analysis revealed c.271dupA and c.482G > A mutations in the MMACHC gene. The patient had a past medical history significant for joint hypermobility, arthritis, bilateral cataracts, unilateral hearing loss, anemia, frequent urinary tract infections, and mental illness. There was no significant past history of mental retardation, failure to thrive, or seizure disorder as reported in classic cases of cblC. Prior to the thrombotic incident, the patient experienced increased paresthesia in the lower extremities, myelopathy, and impaired gait. Given her previous psychiatric history, she was misdiagnosed with malingering until hemiplegia and incontinence became apparent. The authors would like to emphasize the recognition of a neuropsychiatric presentation in late onset cblC. Ten other reported late onset cases with similar presentations are also reviewed.
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PMID:Late-onset combined homocystinuria and methylmalonic aciduria (cblC) and neuropsychiatric disturbance. 1785 53

Progressive multifocal leukoencephalopathy (PML) is a central nervous system infection caused by John Cunningham (JC) virus reactivation in an immunocompromised patient. PML has various neurologic symptoms and has very poor prognosis. A 36-year-old man developed transverse myelitis and had a psychiatric disorder at the age of 26. He was diagnosed with systemic lupus erythematosus (SLE) and neuropsychiatric SLE (NPSLE), on the basis of leukopenia and presence of anti-DNA and anti-nuclear antibodies. Treatment with glucocorticoid (GC) was started, and remission was introduced. Six months before PML onset, his condition was complicated with hemophagocytic lymphohistiocytosis (HLH) due to exacerbation of SLE. Remission re-induction therapy by GC, cyclosporine-A, intravenous cyclophosphamide, and rituximab (RTX) was initiated and HLH improved. However, interleukin-6 levels of the cerebrospinal fluid (CSF) continued to rise. We thought that the disease activity of NPSLE worsened; thus, we introduced mycophenolate mofetil (MMF) 4 months before the PML onset. He developed progressive dysarthria and right hemiplegia. He was diagnosed with PML via magnetic resonance imaging and JC virus polymerase chain reaction in CSF. Considering that immunosuppressants, including RTX and MMF, are precipitating factors of PML, we discussed the RTX removal using plasma exchange (PEx), but we did not introduce PEx, because it was expected that the concentration of RTX was already lowered when he was diagnosed with PML. Treatment for PML with mefloquine and mirtazapine saved his life, but severe residual disabilities remained. This is the first report of a patient who developed PML during combination therapy with RTX and MMF.
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PMID:A case of developing progressive multifocal leukoencephalopathy while using rituximab and mycophenolate mofetil in refractory systemic lupus erythematosus. 2998 69

There is now general agreement that lack of insight is not merely a fundamental aspect of delusions and hallucinations, or just a symptom of psychotic disorders but rather a multi-dimensional construct. Several different components of insight have been proposed and empirically examined during the last three decades, such as the ability to recognize that one has a mental illness, the capacity to relabel unusual mental events as pathological, the specific attribution of one's symptoms to having a mental illness, awareness of illness' consequences, and compliance with treatment.1 Insight impairment is an important prognostic factor in schizophrenia, impacting negatively on medication adherence, treatment outcome, and social functioning.2 Although largely investigated in schizophrenia and other psychoses, insight impairments are observed in many, if not all, mental disorders. Varying levels of awareness of mental illness and/or of specific symptoms are expected in patients with bipolar disorders, Alzheimer disease and other neurocognitive disorders, obsessive-compulsive (OCD) and related disorders.1,3 While in DSM-5 an "insight" specifier was incorporated for OCD, body dysmorphic and hoarding disorder, patients' insight has been found ranging from good to absent in other disorders, such as depressive disorders,4 eating disorders,5 and even specific6 and social7 phobias. Moreover, impaired insight is a common reason that many people with clinical depression or anxiety disorders never seek appropriate treatment and most of the people with addictions and personality disorders fail to recognize and address their problems even when the consequences are devastating: personal suffering, broken relationships, and physical health problems. Depending on the disorder and reflecting different conceptual approaches, many different terms are used to describe lack of insight, such as poor self-awareness, denial, anosognosia (mainly in neurological deficits, e.g. hemiplegia), ego-syntonic symptoms, or even self-deception. At any rate, as an aspect of self-knowledge, insight has psychological (defense mechanisms, coping strategies), social and cultural facets. On the other hand, the attitudes and behaviours towards one's illness are products of inference processes and therefore can be influenced by cognitive dysfunctions. Previous research in schizophrenia showed correlations between neurocognitive functions and insight measures but the strength of this association is rather weak.8 Social cognition may be a crucial cognitive determinant of impaired insight in schizophrenia. The correct attitude toward morbid change in oneself relies on the capacity to reflect upon self from the perspective of the other (i.e., "to see ourselves as others see us"). This capacity is clearly linked to the ability to understand mental states (e.g., beliefs, knowledge, and intentions) of others, that is, theory of mind or mentalizing. Recent research has shown that mentalizing deficits may substantially contribute to insight impairment in schizophrenia.9 This effect could be further examined in the broader context of patient's failures in metacognition, i.e. the general ability to think about thinking, and their relationships with insight impairment in schizophrenia. Mentalizing and introspection are closely related developmentally and it is yet unclear which one is the primary ability: we are able to understand others and then apply this understanding to ourselves or we are able to reflect on ourselves and then apply this reflection to others. A recent line of research in schizophrenia is based on the distinction introduced by Beck et al10 between clinical insight (i.e., awareness of illness) and cognitive insight, which describes a metacognitive ability, specifically patients' flexibility towards their beliefs, judgements and experiences. The self-report Beck Cognitive Insight Scale (BCIS) examines two subcomponents: self-certainty, assessing overconfidence about being right (e.g. "I know better than anyone else what mycomponents: self-certainty, assessing overconfidence about being right (e.g. "I know better than anyone else what my problems are"), and self-reflectiveness, assessing willingness to accept external feedback and recognition of dysfunctionalreasoning style (e.g. "Some of the ideas I was certain were true turned out to be false"). Cognitive insight in thisform describes two related but distinct aspects of metacognition in patients with psychosis, differentially associated withclinical insight, symptoms, treatment outcomes, and functioning.11 Another method for assessment of similar metacognitiveskills also used in schizophrenia is a scale (Metacognition Assessment Scale - Abbreviated, MAS-A) that is administeredthrough a specific interview and examines the capacities of self-reflectivity, understanding of the other individuals'mental states, and using metacognitive knowledge to respond to psychosocial challenges. Lysaker and colleaguesfound recently that metacognitive deficits assessed with MAS-A predict impaired insight in schizophrenia independentof symptoms.12 It is questionable whether BCIS and other methods used so far to assess self-reflection in psychoses arevalid and useful for patients with non-psychotic disorders.11 However, the metacognitive conceptualization of insightmight contribute to a new research framework for insight impairments across mental disorders. According to this approach, poor insight is in part a failure of self-reflection, i.e. the process by which we synthesizeand comprehend ideas about ourselves. This may be due to general deficits in metacognitive abilities (self-reflectivity,mentalizing) or may represent limited, domain-specific, or transient dysfunctions in metacognitive processes. Insight hasto be thought of as a relational concept, that is insight into something: insight into illness, current syndrome, specificsymptoms, pathological personality traits, social difficulties etc.1,3 In an integrated model of insight across mental disorders,aspects of metacognition interacting with multiple other (clinical, neurocognitive, emotional, and social) factorsdetermine patient's ability to correctly process information into self-awareness. The identification of these factors andtheir interactions may be a fruitful field in the research of insight.
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PMID:Insight across mental disorders: A multifaceted metacognitive phenomenon. 3111 49