1/12. Reversible delayed leukoencephalopathy following intravenous heroin overdose.We present serial neuropsychological, magnetic resonance (MR) imaging and EEG changes in a case of widespread CNS myelinopathy due to intravenous heroin overdose complicated by a period of prolonged unconsciousness. Following recovery from the acute overdose, the subject had the delayed onset of akinetic mutism with urinary incontinence. Sequential formal neuro-psychological assessments over 9 months showed evolution from severe global cerebral dysfunction to moderate disturbance of frontal lobe function. Almost complete resolution of diffuse white matter signal changes, accompanied by the development of a degree of volume loss, was evident on serial MR imaging over the same period, and generalized arrhythmic delta-range slowing on the EEG evolved int o a near normal pattern.- - - - - - - - - - ranking = 1keywords = encephalopathy (Clic here for more details about this article) |
2/12. BIPLEDs in akinetic mutism caused by bilateral anterior cerebral artery infarction.INTRODUCTION: akinetic mutism is described as a result of many disorders. Bilateral infarction of the anterior cerebral artery (ACA) territory is reported rarely, however, often leading to akinetic mutism. CASE REPORT: We report a 70 year-old man with akinetic mutism due to bilateral ACA infarction. electroencephalography, 24h after admission, showed bilateral independent periodic lateralized epileptiform discharges (BIPLEDs) in the frontal region and diffuse theta and polymorphic delta activity. DISCUSSION: Postanoxic encephalopathy, central nervous system infection and chronic seizure disorders are the major causes of BIPLEDs. However, BIPLEDs may occur in bilateral ACA territory infarction.- - - - - - - - - - ranking = 0.25keywords = encephalopathy (Clic here for more details about this article) |
3/12. akinetic mutism caused by bilateral infiltration of the fornix in a patient with astrocytoma.In a 59-year-old female patient, a world health organization (WHO) grade II astrocytoma had been diagnosed 16 years ago, which finally progressed into WHO grade III. Several right frontal neurosurgical resections, local radiation and a local radioimplant had been applied. Despite this long record, she was reported alert with a Karnofsky index of 90% until admission. Within a few weeks she rapidly developed akinetic mutism. Upon admission, computed tomography (CT) scan showed a large cystic right frontal defect and a suggested small tumor recurrence. White matter of the frontal lobe appeared to be translucent and compatible with previous radiation. The severe mental changes were initially attributed to a delayed radiation encephalopathy. Neuropathologically, the white matter of the frontal lobe showed mild elevated cell density consistent with gliosis; however, a tumor recurrence invading the tip of the corpus callosum and invading the entire length both fornices appeared. From the neuropathological findings of massive local tumor recurrence in both fornices, together with the acute clinical onset, it seems unlikely that the sequel of radiotherapy caused akinetic mutism, but the symmetric and severe involvement of the limbic system. We conclude that the rapid progression from a state of alertness to a full clinical picture of akinetic mutism was because of infiltration of both fornices.- - - - - - - - - - ranking = 0.25keywords = encephalopathy (Clic here for more details about this article) |
4/12. OKT3 neurotoxicity presenting as akinetic mutism.BACKGROUND: muromonab-cd3 (OKT3), a mouse monoclonal antibody directed against human T lymphocytes, is a potent immunosuppressive agent used to reverse and more recently to prevent allograft rejection, mostly in cardiac transplant recipients. Neurotoxicity from OKT3 usually manifests itself as a transient aseptic meningitis and remains uncommon. methods: The authors describe a dramatic neurologic syndrome after orthotopic heart transplant characterized by akinetic mutism, blepharospasm, anomic aphasia, and delirium. RESULTS: Magnetic resonance imaging (MRI) showed meningeal enhancement and single-photon emission computed tomography (SPECT) showed markedly reduced tracer uptake. Discontinuation of OKT3 resulted in resolution of this neuropsychiatric syndrome and reversal of abnormalities on neuroimaging that coincided with normalization of CD3 lymphocyte count. CONCLUSIONS: In the initial posttransplant period, it remains difficult to attribute encephalopathic signs to toxicity of immunosuppressive drugs. However, MRI and cerebral perfusion studies may help support the diagnosis. More precise characterization of the prevalence of OKT3-associated encephalopathy could come from prospective SPECT studies.- - - - - - - - - - ranking = 0.25keywords = encephalopathy (Clic here for more details about this article) |
5/12. adult "failure-to-thrive" syndrome.The analogy between the "failure-to-thrive" syndrome of childhood and a symptom complex seen in adult neurology is described. Adults presenting with a variety of central nervous system diseases occasionally seem to follow an unusual stereotyped course resulting in intractable weight loss, wide variations in temperature, and a tendency to intractable decubitus ulcerations in a setting of decreased levels of consciousness. Sudden death occurs unexpectedly. This syndrome can be observed following cerebral thrombosis, traumatic encephalopathy, degenerative central nervous system disorders, and encephalitis. The pathophysiology is thought to result from the random aggregate of lesions rather than a verifiable discrete hypothalamic deficit.- - - - - - - - - - ranking = 0.25keywords = encephalopathy (Clic here for more details about this article) |
6/12. Posterior encephalopathy subsequent to cyclosporin A presenting as irreversible abulia.A case of cyclosporin A (Cys A)-induced posterior encephalopathy developed into persistent abulia despite rapid and marked improvement of abnormal T2- and FLAIR MRI hyperintense regions. diffusion-weighted MRI signal intensity was also high at the onset. This change is atypical in Cys A-induced encephalopathy and was thought to predict poor recovery from the encephalopathy. Persistent abulia was probably due to marked hypoperfusion in the whole cortex including bilateral frontal lobes and basal ganglia as detected by SPECT. Apart from the breakdown of the blood-brain barrier, direct toxicity of Cys A to the brain may play a role in the pathogenesis of chronic, irreversible encephalopathy.- - - - - - - - - - ranking = 2keywords = encephalopathy (Clic here for more details about this article) |
7/12. Leukoencephalopathy induced by tegafur: serial studies of somatosensory evoked potentials and cerebrospinal fluid.A case of leukoencephalopathy induced by tegafur, an antineoplastic derivative of 5-FU, is reported. The patient received 600 mg of tegafur p.o. for 16 days before excision of rectal cancer. After the operation, gait disturbance and mental abnormalities appeared. He became akinetic and mute within a few days following readministration of tegafur. Serial studies of brain CT, somatosensory evoked potentials (SEP) were made, and myelin basic proteins (MBP) in the cerebrospinal fluid were measured. The level of MBP was about twice the normal value and the central conduction time (CCT) of SEP was prolonged at admission. The value of MBP and CCT improved with recovery from akinetic mutism.- - - - - - - - - - ranking = 1.25keywords = encephalopathy (Clic here for more details about this article) |
8/12. akinetic mutism in bilateral necrotizing leucoencephalopathy after radiation and chemotherapy: electrophysiological and autopsy findings.In a patient with akinetic mutism, extensive circumscribed bilateral lesions in the precentral part of the centrum semiovale, due to delayed necrotizing leucoencephalopathy after combined intravenous polychemotherapy and radiation, were found at autopsy. CT and somatosensory evoked potentials were normal and a slow alpha rhythm was present, but there was a lack of EEG desynchronization. akinetic mutism and the loss of desynchronization in this case are thought to result from interrupted thalamofrontal and extrathalamic reticulofrontal projections and the disconnection of the anterior limbic cortex.- - - - - - - - - - ranking = 1.25keywords = encephalopathy (Clic here for more details about this article) |
9/12. Unsuccessful intraventricular pentosan polysulphate treatment of variant Creutzfeldt-Jakob disease.Pentosan polysulphate, delivered by chronic intraventricular infusion, has been proposed as a potential therapy for human prion disease. The first treated patient is still alive several years after treatment started. Here we describe in detail a case of variant Creutzfeldt-Jakob disease in which this treatment was started at a relatively early stage but had no definite clinical benefit. The patient died from disease progression 16 months after diagnosis and 5 months after pentosan polysulphate treatment was commenced.- - - - - - - - - - ranking = 0.0037352086624519keywords = variant (Clic here for more details about this article) |
10/12. Bithalamic lesions of butane encephalopathy.Butane inhalation can cause serious medical complications and is particularly toxic to the nervous system. This is a report of an acutely encephalopathic youth with prominent abulia. MRI revealed severe bithalamic injury attributed to butane toxicity. Clinical issues, including particular radiologic findings, related to butane inhalation are reviewed.- - - - - - - - - - ranking = 1keywords = encephalopathy (Clic here for more details about this article) |
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