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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six cases of cocaine-related deaths of infants have covered the spectrum of potentially devastating effects. They include an intrauterine death of a 35-week-old fetus following acute maternal cocaine abuse; anoxic encephalopathy at birth with 3 months' vegetative survival from a similar episode; traumatic compression asphyxia in a 4-month-old; infectious cardiomyopathy with heart failure in a twin at age 21 months following maternal cocaine abuse at birth; malnutrition and dehydration in a 7-week-old during continuing cocaine abuse by the parents; and a teenage sibling's cocaine lacing of a baby milk bottle ingested by his 6-week-old brother. All the cases had positive toxicological screening for cocaine or metabolites or both in the mother at delivery or in the infant at birth, or both. There were no instances of sudden infant death syndrome (SIDS, or "crib death"). Pathologic and toxicologic, as well as birth, developmental, and social data are presented. An integrated medical, public health, law enforcement, and educational policy to prevent or at least ameliorate these tragic cases, now approaching epidemic proportions, has yet to be developed. A careful obstetrical history and examination of the mother, indication on the birth certificate of maternal drug abuse, and notification of health authorities (by birth certificate checking, among other ways) may send an early warning message to providers for intercession. Active ingestion/injection and passive inhalation by older children and teenagers require more intensive monitoring and aggressive interaction by pediatricians, social workers, school authorities, and employers.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cocaine babies: the scourge of the '90s. 200 78

Physicians may have the opportunity to prevent suicide. An awareness of suicide risk factors, such as depression, alcoholism, drug abuse, schizophrenia, and chronic pain or disease, may facilitate suicide prevention. Recognition of acute and chronic suicidal vulnerability occurs through direct questioning. Psychiatric consultation is indicated for patients exhibiting clear self-injury risk, as exemplified by expressed suicide intent, an overt plan for death, or a "gesture." Hospitalization is usually recommended for socially isolated patients presenting with overt suicidal ideation, complicated by injurious self-harm, encephalopathy, or substance abuse. Family involvement and a "no-suicide" contract with the patient, coupled with close outpatient follow-up appointments, should suffice for those exhibiting milder or transient thoughts of suicide without manifest intent to die.
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PMID:A preventive approach to the suicidal patient. 327 11

A. Digital EEG is an established substitute for recording, reviewing, and storing a paper EEG record. It is a clear technical advance over previous paper methods. It is highly recommended. (Class III evidence, Type C recommendation). B. EEG brain mapping and other advanced QEEG techniques should be used only by physicians highly skilled in clinical EEG, and only as an adjunct to and in conjunction with traditional EEG interpretation. These tests may be clinically useful only for patients who have been well selected on the basis of their clinical presentation. C. Certain quantitative EEG techniques are considered established as an addition to digital EEG in: C.1. Epilepsy: For screening for possible epileptic spikes or seizures in long-term EEG monitoring or ambulatory recording to facilitate subsequent expert visual EEG interpretation. (Class I and II evidence, Type A recommendation as a practice guideline). C.2. OR and ICU monitoring: For continuous EEG monitoring by frequency-trending to detect early, acute intracranial complications in the OR or ICU, and for screening for possible epileptic seizures in high-risk ICU patients. (Class II evidence, Type B recommendation as a practice option). D. Certain quantitative EEG techniques are considered possibly useful practice options as an addition to digital EEG in: D.1. Epilepsy: For topographic voltage and dipole analysis in presurgical evaluations. (Class II evidence, Type B recommendation). D.2. Cerebrovascular Disease: Based on Class II and III evidence, QEEG in expert hands may possibly be useful in evaluating certain patients with symptoms of cerebrovascular disease whose neuroimaging and routine EEG studies are not conclusive. (Type B recommendation). D.3. Dementia: Routine EEG has long been an established test used in evaluations of dementia and encephalopathy when the diagnosis remains unresolved after initial clinical evaluation. In occasional clinical evaluations, QEEG frequency analysis may be a useful adjunct to interpretation of the routine EEG when used in expert hands. (Class II and III evidence as a possibly useful test, Type B recommendation). E. On the basis of current clinical literature, opinions of most experts, and proposed rationales for their use, QEEG remains investigational for clinical use in postconcussion syndrome, mild or moderate head injury, learning disability, attention disorders, schizophrenia, depression, alcoholism, and drug abuse. (Class II and III evidence, Type D recommendation). F. On the basis of clinical and scientific evidence, opinions of most experts, and the technical and methodologic shortcomings, QEEG is not recommended for use in civil or criminal judicial proceedings. (Strong Class III evidence, Type E recommendation). G. Because of the very substantial risk of erroneous interpretations, it is unacceptable for any EEG brain mapping or other QEEG techniques to be used clinically by those who are not physicians highly skilled in clinical EEG interpretation. (Strong Class III evidence, Type E recommendation).
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PMID:Assessment of digital EEG, quantitative EEG, and EEG brain mapping: report of the American Academy of Neurology and the American Clinical Neurophysiology Society. 922 9

Vasculitis is inflammation of blood vessel walls, which produces dysfunction in both the peripheral and central nervous system (CNS). Cerebral ischemia is the major cause for neurological manifestations of CNS vasculitis. Unfortunately, a universally accepted classification of vasculitis has not emerged. Vasculitis affecting the CNS alone is referred to as primary angiitis of the CNS; secondary vasculitis occurs in association with a variety of conditions, including infections, drug abuse, lymphoproliferative disease and connective tissue diseases. The pathogenesis of vasculitis includes different immunological mechanisms. Recently, anti-neutrophil cytoplasmatic antibody (ANCA) has been demonstrated to play an active role in the immunopathogenesis of the vasculitis. Diagnosis of vasculitis depends on a combination of clinical, radiographic and pathologic features. A wide spectrum of clinical features may occur. The most typical clinical picture of CNS vasculitis is troke, encephalopathy or seizures. Assays for ANCA, serum cytokines, antibodies to endothelial cell antigens have been reported to be useful in diagnosing or monitoring the disease activity. The gold standard in diagnosis is confirmation of vasculitis in a biopsy specimen. Angiography may suggest the diagnosis but no abnormalities are pathognomonic. Ideally, the therapy of each vasculitis would focus on the specific immunologic mechanism causing the disease. Such specific interventions are not yet available. In general the most important approaches induce global immunosuppression. The goal of therapy, however, is to prevent recurrence of disease.
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PMID:Central nervous system vasculitis. 951 75

Drug abuse is associated with a variety of neurological complications. The use of certain recreational drugs shows a marked temporal association with the onset of both haemorrhagic and ischaemic strokes, the majority of which develop within minutes to 1 h after the administration of the index drug. Delayed onset of stroke has also been observed. Acute, severe elevation of blood pressure, cardiac dysrhythmias, cerebral vasospasm, vasculitis, embolization due to infective endocarditis or dilated cardiomyopathy, embolization due to foreign material injected with the diluents under non-sterile conditions and 'street drug' contaminants with cardiovascular effects have been suggested as possible underlying mechanisms. Rupture of aneurysms and arteriovenous malformations have been detected in up to half of the patients with haemorrhagic stroke due to cocaine abuse. The less common findings reported have included a mycotic cerebrovascular aneurysm in a patient with infective endocarditis and haemorrhagic stroke. In addition to stroke, cocaine seems to provoke vascular headache. Seizures precipitated by recreational drug abuse are usually caused by acute intoxication in contrast to the withdrawal seizures encountered in subjects with alcohol abuse. Movement disorders and cerebral atrophy correlating with the duration of abuse have been described. Snorting of organic solvents may cause encephalopathy. Cases of spongiform leukoencephalopathy in heroin addicts have also been reported. Peripheral neuropathy is occasionally precipitated by drug poisoning after intravenous administration. Impurities of the drug, risky administration techniques, and the use of mixtures of various drugs, frequently with simultaneous alcohol drinking, should be taken into account when assessing the background of the adverse event as well as the overall lifestyle of the addicted subjects.
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PMID:Neurological complications of drug abuse: pathophysiological mechanisms. 1113 45

The results of clinical, neuropsychological and MRI study of 21 patients with "ephedron" encephalopathy caused by intake of methcatinon ("ephedron"), a surrogate drug obtained from phenylpropanolamine-containing compounds by adding potassium permanganate, are presented. Signs of brain lesions emerged 3-14 (mean 6.8 +/- 4.9) months after the beginning of the regular drug intake. Neurological disturbances were measured using the Scale of clinical assessment of ephedron encephalopathy. In the acute stage of the disease, most patients had the combination of extrapyramidal disorders (parkinsonism, muscular dystonia, tremor, myoclonia) with pronounced postural instability, pseudobulbar syndrome, autonomic, cognitive and affective personality abnormalities of subcortical and frontal types. In 18 (86%) patients, MRI revealed a bilateral symmetric elevation of the signal from the basal ganglia on T1-weighted images, mostly from the medial segment of globus pallidus and the reticular part of substantia nigra that reflected magnesium accumulation. The spread of hyperintensive MRI changes negatively correlated with the disease duration (r = -0.6; p < 0.01), but did not depend on the drug abuse duration or its approximate total dosage, and also did not correspond to the disease severity. In follow-up, a tendency to spontaneous regress of symptoms was observed in 29% of the cases, and in 33% patients symptoms have been regressing even 4 years after stopping of methcatinon intake. The main mechanisms of "ephedron" encephalopathy development are probably related to the manganese accumulation in the brain that might trigger secondary pathogenetic mechanisms, such as mitochondrial dysfunction, oxidative stress, etc. The induction courses of calcium and sodium EDTA that accelerates manganese excretion decrease a probability of the further disease progress, though do not contribute significantly to symptoms regress. The data on possibilities of symptomatic therapy of movement and affective disturbances is presented.
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PMID:["Ephedron" encephalopathy]. 1611 41

There is a lack of awareness of acutely presenting inborn errors of metabolism in adults, of which the X-linked urea cycle defect ornithine transcarbamylase (OTC) deficiency is an example, many comparatively mild mutations having been identified. In male hemizygotes clinical manifestations and age at presentation vary and depend on the mutation. In female heterozygotes the clinical spectrum depends on the extent to which the abnormal gene is expressed. Milder versions of the defect may not cause clear clinical symptoms and may remain unrecognized until the person is subjected to an unusually high nitrogen load when they develop severe hyperammonaemia. During acute episodes liver enzymes may be normal or only slightly elevated and occasionally accompanied by coagulopathy, but the key finding is hyperammonaemia. Boys with these milder forms may exhibit abnormal behaviour and be diagnosed with attention deficit hyperactivity disorder. This case illustrates how late presentation of OTC deficiency in a non-specialist centre can be difficult to differentiate from drug abuse, psychiatric illness or encephalopathy. Failure to measure blood ammonia in adults with unexplained key symptoms - particularly prolonged vomiting without diarrhoea and altered mental state/hallucinations, or to recognize the significance of elevated blood ammonia without evidence of liver decompensation can lead to delayed or missed diagnosis.
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PMID:Fatal ammonia toxicity in an adult due to an undiagnosed urea cycle defect: under-recognition of ornithine transcarbamylase deficiency. 2040 75

Encephalopathy is evidenced as an altered mental state with various neurological symptoms, such as memory and cognitive problems. The type of a substance-evoked encephalopathy will depend on the drug, substance, or combination being abused. The categories into which we could place the various abused substances could be tentatively divided into stimulants, amphetamines, hallucinogens, narcotics, inhalants, anesthetics, anabolic steroids, and antipsychotics/antidepressants. Other factors that may underlie encephalopathy, such as infectious agents, environmental, and other factors have also to be taken into account. Drugs of abuse can be highly toxic to the CNS following acute, but more so in chronic exposure, and can produce significant damage to other organs, such as the heart, lungs, liver, and kidneys. The damage to these organs may be at least partially reversible when drug abuse is stopped but CNS damage from repeated or prolonged abuse is often irreversible. The major pathways for the organ and CNS toxicity could be related to ischemic events as well as increased cell damage due to metabolic or mitochondrial dysfunction resulting in increased excitotoxicity, reduced energy production, and lowered antioxidant potential. These susceptibilities could be strengthened by the use of antioxidants to combat free radicals (e.g., vitamin E, lipoic acid); trying to improve energy generation by using mitochondriotropic/metabolic compounds (e.g., thiamine, coenzyme Q10, carnitine, riboflavin); by reducing excitotoxicity (e.g., glutamate antagonists) and other possible strategies, such as robust gene response, need to be investigated further. The drug-abuse-evoked encephalopathy still needs to be studied further to enable better preventative and protective strategies.
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PMID:Neuroprotective strategies in drug abuse-evoked encephalopathy. 2063 9

We report two patients manifesting with involvement of central and peripheral nervous system with brain magnetic resonance imaging (MRI) changes and pathological features of neuropathy possibly due to harmful and chronic use of various nitroimidazole group of medications for recurrent diarrheal illness. Patient 1, a 21-year-old man with obsessive-compulsive disorder, impulsive behavior and harmful use of substance (tinidazole), had developed encephalopathy and biopsy-proven neuropathy with partial remission. The MRI of brain showed involvement of bilateral caudate, lentiform and dentate nuclei, and splenium, with contrast enhancement of the caudate and putaminal lesions and restricted diffusion of the splenial lesion. Patient 2 was a 50-year-old woman with irritable bowel syndrome and was on harmful use of tinidazole and metronidazole. She manifested with encephalopathy, ataxia, and neuropathy. Her MRI of brain revealed involvement of bilateral putamen, dentate nuclei and periventricular white matter with restricted diffusion. Sural nerve biopsy revealed evidence of vasculitic neuropathy. At follow-up, there was definite, though incomplete, recovery in both the patients. The MRI alterations improved completely in patient 2 and substantially in patient 1. Increasing awareness among the physicians may enable early recognition of potentially reversible neurotoxicity and avoid unwarranted prescription of such medications.
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PMID:Clinical, neuroimaging and pathological features of 5-nitroimidazole-induced encephalo-neuropathy in two patients: Insights into possible pathogenesis. 2201 62

Drug abuse is a substantial problem in society today and is associated with significant morbidity and mortality. Various drugs are associated with serious complications affecting the brain, and it is critical to recognize the imaging findings of these complications to provide prompt medical management. The central nervous system (CNS) is a target organ for drugs of abuse as well as specific prescribed medications. Drugs of abuse affecting the CNS include cocaine, heroin, alcohol, amphetamines, toluene, and cannabis. Prescribed medications or medical therapies that can affect the CNS include immunosuppressants, antiepileptics, nitrous oxide, and total parenteral nutrition. The CNS complications of these drugs include neurovascular complications, encephalopathy, atrophy, infection, changes in the corpus callosum, and other miscellaneous changes. Imaging abnormalities indicative of these complications can be appreciated at both magnetic resonance (MR) imaging and computed tomography (CT). It is critical for radiologists to recognize complications related to drugs of abuse as well as iatrogenic effects of various medications. Therefore, diagnostic imaging modalities such as MR imaging and CT can play a pivotal role in the recognition and timely management of drug-related complications in the CNS.
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PMID:Your brain on drugs: imaging of drug-related changes in the central nervous system. 2258 55


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