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Query: UMLS:C0011206 (
delirium
)
5,996
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Reye syndrome (RS) is an acute
encephalopathy
in childhood, and is very rare in adulthood. Here we report a 21-year-old woman with RS. Because of her dysmenorrhea, she took 3 tablets of diclofenac sodium (25 mg) per day in 3 divided doses for two days. Two days after the last intake of the medicine, she developed high fever, nausea, vomiting, and disturbance of consciousness with
delirium
, i.e., acute
encephalopathy
. She did not have seizure, hemiplegia, or other focal neurological manifestations. The serum GOT level was normal at onset, but in 12 hours dramatically increased up to 8,632 IU/L. The serum bilirubin level was normal. The cerebrospinal fluid revealed normal cell count, and protein. Although the liver biopsy was not performed because of thrombocytopenia, we diagnosed her as an adult case of RS according to the clinical criteria of the Center for Disease Control. In addition to treatment for the brain edema, plasma exchange was performed once treat the
encephalopathy
at the onset. The next day, her consciousness level and serum GOT level markedly improved. She completely recovered from acute
encephalopathy
in a week after her admission. In conclusion, diclofenac sodium, as well as aspirin, should be considered as a possible causal agent for RS, and early plasma exchange may be beneficial.
...
PMID:[An adult case of Reye syndrome induced by diclofenac sodium, and recovered by plasma exchange]. 974 77
In patients with AIDS, cerebral infection due to cytomegalovirus (CMV) results in two distinct neuropathological patterns: microglial nodular encephalitis (MGNE) and ventriculoencephalitis (VE). In order to identify clinical features to facilitate the differential diagnosis of these two forms of CMV
encephalopathy
in living patients, we retrospectively reviewed the clinical records of 18 patients with MGNE or VE diagnosed at autopsy. We identified the following clinical features as distinguishing the two encephalopathies: (1) MGNE manifests earlier than VE; (2) the onset of MGNE is acute, whereas the onset of VE is insidious; (3) the onset of MGNE is marked by confusion and
delirium
, which do not occur in VE; (4) VE is frequently associated with radiculopathy, which is absent in MGNE; and (5) VE is associated with more marked alterations in cerebrospinal fluid (high protein levels and pleocytosis). The early neurological manifestations of MGNE should prompt a search for systemic CMV infection, which may lead to earlier treatment.
...
PMID:Microglial nodular encephalitis and ventriculoencephalitis due to cytomegalovirus infection in patients with AIDS: two distinct clinical patterns. 977 Jan 48
We report the case of a bipolar patient developing severe
delirium
and extrapyramidal signs shortly after initiation of a lithium-neuroleptic combination therapy. Clinical presentation, EEG changes and lithium plasma levels showed a close correlation. The
delirium
was reversible when all drugs were stopped; however, dyskinesia was found to be persistent after a period of 6 months. This rare syndrome is difficult to differentiate from lithium intoxication and neuroleptic malignant syndrome. Given the additional use of valproate and biperiden in this patient, valproate
encephalopathy
and anticholinergic
delirium
are further differential diagnoses. To avoid this serious pharmacodynamic drug interaction, patients should be closely monitored when lithium-neuroleptic comedication is started.
...
PMID:Delirium and persistent dyskinesia induced by a lithium-neuroleptic interaction. 983 53
Renal failure is relatively common, but except in association with spina bifida or paraplegia it is unlikely to occur as a result of disease of the CNS. Renal failure, however, commonly affects the nervous system. The effects of kidney failure on the nervous system are more pronounced when failure is acute. In addition to the important problems related to renal failure there are both acquired and genetically determined diseases which may affect the kidney and the brain. Those acquired diseases include the vasculitides, the paraproteinaemias, and various granulomatous conditions (considered in other chapters of Neurology and Medicine). In two of the most commonly encountered genetically determined diseases, Von Hippel-Lindau disease and polycystic kidney disease, location of pathogenic mutations will provide improved screening programmes and, possibly, allow therapeutic intervention. Uraemia may affect both the central and peripheral nervous systems. Whereas the clinical features of uraemia are well documented, the pathophysiology is less well understood and probably multifactorial. Uraemic encephalopathy, which classically fluctuates, is associated with problems in cognition and memory and may progress to
delirium
, convulsions, and coma. The
encephalopathy
may initially worsen with periods of dialysis and almost certainly relates to altered metabolic states in association with ionic changes and possibly impaired synaptic function. Renal failure may affect the peripheral nervous system, resulting in a neuropathy which shows a predilection for large diameter axons. This may be reversed by dialysis and transplantation. The myopathy seen in renal failure, often associated with bone pain and tenderness, is similar to that encountered in primary hyperparathyroidism and osteomalacia. Dialysis itself is associated with neurological syndromes including the dysequilibrium syndrome, subdural haematoma, and Wernicke's encephalopathy. Dialysis dementia, which was prevalent during the 1970s, has reduced in frequency with the use of aluminium free dialysate. With the introduction of transplantation and the concomitant use of powerful immunosuppressive drugs, the pattern of neurological problems encountered in renal replacement therapy has shifted. Five per cent of patients develop nerve injuries during renal transplantation, and up to 40% of patients experience neurological side effects from cyclosporine. Furthermore, CNS infections, often fungal in type, have been reported in up to 45% of transplant patients coming to postmortem. The nature of the involvement of neurologists with their nephrology colleagues is therefore evolving.
...
PMID:Neurology and the kidney. 985 55
This preliminary report deals with a polyetiological and pathophysiologically multifacted
encephalopathy
that is fairly common and yet in need of identification as a clinical (but not nosological) entity: Mixed-Type
Encephalopathy
(MTE). MTE is a mostly acute condition, characterized by change of mentation (confusion,
delirium
, etc.) with little or no neurological deficit but with impressive diffuse EEG slowing. A variety of medical conditions lead to MTE, especially at an age above 50 years, but status-post-surgery (leaving aside cranial neurosurgery, but also cardiac surgery in view of common embolic cerebral pathology) may also result in MTE, especially with the use of general anesthesia. An attempt is made to analyze the plethora of contributory factors and underlying pathophysiological mechanisms. All types of classical brain pathology such as strokes, meningitis-encephalitis and typical metabolic encephalopathies (hepatic, renal, etc.) and others must be excluded from the diagnosis of MTE. Special emphasis is being placed on behavioral and EEG criteria in the early state of impaired consciousness with subdivision into 4 types: obtundation, somnolence, morbid lethargy and
delirium
. Cases of MTE are best picked up by an interdepartmental consultation (liaison) service making use of neurological consultations and EEG assessment. The value of the latter cannot be overestimated in these cases, especially in view of the very limited contributions of neuroimaging methods. The prognosis tends to be good. Severe and fatal developments are usually due to intervening cerebral hypoxia or anoxia. In such a development, epileptic manifestations, which are usually absent or mild in MTE, can become quite prominent. A thorough multi-institutional and international study of MTE is already in the planning stage. It is hoped that preventive measures can minimize the cerebral complications.
...
PMID:Mixed-type encephalopathies: preliminary considerations. 989 Nov 86
The purpose of this article is to review current knowledge regarding potential neural mechanisms of
delirium
. A MEDLINE search for relevant English language articles was undertaken using various combinations of
delirium
(including cognitive disorders,
encephalopathy
, and confusion) with pathogenesis and pathophysiology. These articles were scanned for content related to hypotheses concerning the neurobiology of
delirium
. Additional references were obtained from a manual search of the bibliography of these articles. A secondary MEDLINE search of
delirium
with the mechanism in question (i.e., serotonin, acetylcholine, etc.) was then undertaken. Literature review was last updated as of April 1998. Despite being a common problem among elderly patients, the mechanisms of
delirium
are poorly understood.
Delirium
is a syndrome that may occur as the result of multiple complex interacting neurotransmitter systems and pathologic processes. The neurotransmitters acetylcholine and serotonin may play particularly important roles in common medical and surgical
delirium
. Other neurotransmitters such as dopamine and gamma-aminobutyric acid each may be involved in the development of
delirium
under special conditions. Other neurobiologic factors such as cytokines, cortisol abnormalities, and oxygen free radicals will require further study to define their role in
delirium
. Distinct neuropathologic processes leading to
delirium
are beginning to be defined. Such mechanisms may differ in various clinical settings. There is probably no final common pathway to
delirium
, but rather,
delirium
is the final common symptom of multiple neurotransmitter abnormalities. Further situation-specific studies of
delirium
pathophysiology should lead to more effective prevention and treatment strategies.
...
PMID:Neural mechanisms of delirium: current hypotheses and evolving concepts. 1041 Oct 9
A case of acute
encephalopathy
with selective bilateral symmetrical striatal lesions is reported. The patient was a previously healthy 4-year-old boy who became obtunded after a febrile illness and fell into a state of
delirium
with severe pain in the feet. He showed abnormal postures: hyperextension of the neck and upper limbs and extreme flexion of both lower limbs, and abnormal involuntary movements of the limbs: tremor, athetotic movement and right hemiballismus. Analysis of serum antibody titres suggested recent primary infection of herpes simplex type 1 (HSV-1). Cranial T2-weighted magnetic resonance imaging (MRI) demonstrated areas of high-signal intensity involving the whole basal ganglia bilaterally. He showed rapid clinical improvement after the initiation of corticosteroid therapy; complete clinical recovery was noted 3 months after the onset. Serial MRI studies demonstrated a rapid reduction of the lesions, resulting in only slight T2-hyperintense areas in both caudate nuclei. The pathogenesis of the disorder remains unknown, though an autoimmune mechanism has been speculated. The clinical and laboratory findings in this case suggested a possible role of HSV-1 in the pathomechanism of the disorder and a beneficial effect of early corticosteroid therapy.
...
PMID:Acute encephalopathy with bilateral striatal necrosis: favourable response to corticosteroid therapy. 1072 92
Symptomatic arsenic poisoning is not often seen in occupational exposure settings. Attempted homicide and deliberate long-term poisoning have resulted in chronic toxicity. Skin pigmentation changes, palmar and plantar hyperkeratoses, gastrointestinal symptoms, anemia, and liver disease are common. Noncirrhotic portal hypertension with bleeding esophageal varices, splenomegaly, and hypersplenism may occur. A metallic taste, gastrointestinal disturbances, and Mee's lines may be seen. Bone marrow depression is common. 'Blackfoot disease' has been associated with arsenic-contaminated drinking water in Taiwan; Raynaud's phenomenon and acrocyanosis also may occur. Large numbers of persons in areas of India, Pakistan, and several other countries have been chronically poisoned from naturally occurring arsenic in ground water. Toxic
delirium
and
encephalopathy
can be present. CCA-treated wood (chromated copper arsenate) is not a health risk unless burned in fireplaces or woodstoves. Peripheral neuropathy may also occur. Workplace exposure or chronic ingestion of arsenic-contaminated water or arsenical medications is associated with development of skin, lung, and other cancers. Treatment may incklude the use of chelating agents such as dimercaprol (BAL), dimercaptosuccinic acid (DMSA), and dimercaptopanesulfonic acid (DMPS).
...
PMID:Chronic arsenic poisoning. 1186 18
We performed a retrospective review of 5 years of experience with electroconvulsive therapy (ECT) in patients with organic brain lesions. On 26 of 27 occasions, patients with organic brain disease and a concurrent depressive disorder obtained a good affective response to a course of ECT. Patients with diffuse or multifocal brain disease were vulnerable to ECT-induced
delirium
; however, this was severe enough to compel discontinuation of ECT on only one occasion. We conclude that ECT is an effective treatment for depression in patients with concurrent neurological disease, although patients with degenerative brain disease or diffuse
encephalopathy
may be especially prone to ECT-induced
delirium
.
...
PMID:Safety and Efficacy of ECT in Depressed Patients with Organic Brain Disease: Review of a Clinical Experience. 1194 Nov 55
Delirium
has been recognized for the last 3 millennia and is the most common complication found in hospitalized patients aged 65 and older in the United States. However, critical basic science and clinical research did not progress until the DSM III criteria clearly defined
delirium
20 years ago. The term
delirium
then replaced many nonspecific entities, such as acute confusion state, acute brain syndrome, metabolic
encephalopathy
, and toxic psychosis. This review discusses the epidemiology, risk factors, interventions, causes, management, and outcomes of
delirium
. The pathophysiology of
delirium
has the potential to radically alter our management of
delirium
and is a controversial area of research.
...
PMID:Southwestern Internal Medicine Conference. Etiology and management of delirium. 1254 81
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