Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A retrospective examination of lethargic encephalitis finds many parallels with neuroleptic effects. The encephalitis, like the neuroleptics, produced an acute continuum of cognitive disorders from emotional indifference through apathy and onto a rousable stupor. It also produced similar acute dyskinesias, including akinesia, akathisia, dystonia, oculogyric crises, and tremors. The encephalitis also caused similar chronic effects, including dementia and psychosis, and somewhat different persistent dyskinesias. The chronic motor and cognitive disorders, like those associated with the neuroleptics, were often delayed in onset. An acute, severe episode of lethargic encephalitis also finds a parallel in the neuroleptic malignant syndrome. These parallels are probably due to a common site of action in the basal ganglia. They provide a model for understanding many neuroleptic effects and alert us to the probability of persistent cognitive deficits, including dementia, from neuroleptic treatment.
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PMID:Parallels between neuroleptic effects and lethargic encephalitis: the production of dyskinesias and cognitive disorders. 810 24

In 1954, when he was five years old, a patient suffered from encephalitis with a prolonged lethargic state. Following this episode, he presented a severe parkinsonian syndrome which was associated, after a few years, with an axial dystonia and stereotyped involuntary movements of the upper limbs. These abnormal movements were particular by their coordinated appearance, their rhythmicity and their relative slowness. Treatment with L-dopa suppressed all akinetic, dystonic and dyskinetic symptoms. At age of 40 years, all the akinetic, dystonic and dyskinetic symptoms reappeared after drug withdrawal. Cerebral computed tomography, magnetic resonance imaging and fluorodeoxyglucose positron emission tomography were normal. Fluorodopa positron emission tomography revealed a significant bilateral reduction of tracer accumulation in the posterior part of both putamen, similar to that observed in patients with idiopathic Parkinson's disease. In this patient, pharmacological tests revealed that effectiveness of L-dopa was abolished by administration of a D2 antagonist, and was fully reproduced by a D2 agonist. Clinical signs, pharmacological data and past-medical history strongly suggested a limited lesion of the zona compacta of substantia nigra induced by viral agression. This complex and progressive extrapyramidal syndrome had strong similarities with the lethargic encephalitis of Von Economo and its late symptoms. Other diseases associating akinesia and dyskinesia or dystonic phenomena, like dopa-sensitive dystonia and juvenile Parkinson's disease, are very unlikely. Thus, the persistance of sporadic forms of Von Economo's encephalitis could be discussed.
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PMID:[Parkinsonian syndrome and post-encephalitic stereotyped involuntary movements responsive to L-dopa]. 876 55

We report a case of a 19-year-old immunocompetent Malay woman who presented with a worsening psychotic disorder of 1-year duration. She initially presented with social isolation with subsequent mutism and stupor. Physical examination revealed a stuporous, emaciated, dehydrated woman with Glasgow Coma Scale of 11/15 (E4V2M5). She had a blank stare, mutism and akinesia. Motor examination revealed upper motor neuron findings. Neck stiffness was present, however, Kernig's and Brudzinski's signs were negative. There were no other findings on other systems. Brain imaging and EEG were normal. Cerebrospinal fluid investigations revealed positive cerebrospinal fluid Mycobacterium tuberculosis PCR (MTB PCR). The patient was treated with empirical antituberculosis drugs and steroids. On follow-up visit 1 month later, her psychotic symptoms had fully resolved. She was able to ambulate and care for herself; she was unable to recall the symptoms she had experienced before and during admission.
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PMID:Psychosis secondary to tuberculosis meningitis. 2696 52

Regional anaesthesia techniques in ophthalmology are usually utilized for day case surgery. During various procedures, profound akinesia of the eye and anaesthesia of the surgical site are required, both of which are achieved with retrobulbar block. Due to the anatomy of the eye, life-threatening complications are possible. An 82-year-old female with secondary post-herpetic uveitic glaucoma of the right eye presented at the Department of Ophthalmology for an elective trans-scleral laser cyclophotocoagulation. She was given a retrobulbar block to the right eye with 2 mL of 0.5% levobupivacaine and 2 mL of 2% lidocaine. The procedure was technically performed without any issues. 2-3 minutes after the injection she became lethargic and 5 minutes later she lost consciousness and developed severe hypotension with bradycardia and respiratory arrest. She was successfully intubated and resuscitated, using mechanical ventilation, vasoactive medications, fluid therapy and intravenous lipid emulsion. There are three mechanisms for local anaesthetic (LA) to reach the central nervous system after a retrobulbar block: systemic absorption of LA, direct intra-arterial injection and retrograde flow into the cerebral circulation, and injecting LA into the subdural space via puncturing the dural optic nerve sheath, the latter being most common. The clinical picture of our patient was very consistent with subdural anaesthesia after exposure of the pons, midbrain and cranial nerves to LA, i.e. brainstem anaesthesia. Following appropriate life support measures taken in our case, there was a successful outcome. To minimize the chance for brainstem anaesthesia after retrobulbar block, we recommend low volume with low concentration of LA and block performance by an experienced ophthalmologist or anaesthesiologist with proper technique. Patients receiving retrobulbar anaesthesia should be carefully monitored at least 20 minutes after the block. Life support equipment should be available before performing retrobulbar block.
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PMID:Brainstem Anaesthesia after Retrobulbar Block. 3088