Encephalopathy contrast

Cerebrovascular Carotid spasm Compromise of ECA ostium Hyperfusion syndrome Contrast encephalopathy Transient symptomatic cerebral ischemia Global Focal Carotid dissection Carotid perforation Hyperperfusion syndrome Acute stent thrombosis Major ischemic stroke Cerebral hemorrhage... 

It remains remarkable that, after the discovery of chronic Al encephalopathy and numerous reports of patients suffering from this syndrome, fourteen years passed before the first publication on acute Al neurotoxicity appeared [62], Acute Al encephalopathy is a devastating, often fatal disease that is the result of iatrogenic exposure to Al. Unfortunately, in spite of efforts to avoid Al exposure as much as possible, recently new sources of serious exposure have been added to the growing list of sources of Al exposure. In contrast to a fascinating history and abundant literature, many uncertainties about Al toxicity still exist. Clinical data in humans on acute Al neurotoxicity are very limited and we will, therefore, compare our experience in one of the two documented outbreaks in dialysis centers, with that of the literature. 

Slow, relatively low exposure accumulation of Al over a period of years can lead to a number of clinical manifestations, some of which seem to be bypassed in acute Al encephalopathy due to extremely high exposure to Al. Al encephalopathy is a clinical syndrome and, as can be seen in Table 5, there are similarities and differences in the neurological symptoms of acute and chronic Al encephalopathy. In chronic Al encephalopathy microcytic anemia [41, 93, 95—98] and EEG changes [99-104] can precede clinical symptoms [105]. It is unknown if these symptoms can also precede the clinical symptoms of acute encephalopathy. In contrast to acute Al encephalopathy, where speech disturbances are absent, speech disorders are an important presenting clinical sign of neurotoxicity in chronic Al encephalopathy. The neurological basis of the speech apraxia is obscure but it appears to have elements of dysarthria and dysphasia [33, 73], The initial... 

Almost all patients with acute or chronic Al encephalopathy showed EEG alterations. These were characterized by multifocal bursts of slow (delta) and spike activity. Background rhythms between bursts were relatively normal in patients with chronic Al encephalopathy, in contrast to uremia and other metabolic encephalopathies where there is general slowing of the rhythmic cycle [33, 99-102, 105, 118]. 

Transient contrast encephalopathy has been reported after carotid artery stenting (88). 

Dangas G, Monsein LH, Laureno R, Peterson MA, Laird JR Jr, Sailer LF, Mehran R, Leon MB. Transient contrast encephalopathy after carotid artery stenting. J Endovasc Ther 2001 8(2) 111-13. 

The 1994 report of the Institute of Medicine concluded that the evidence was inadequate to accept or reject a causal relation between MMR and encephalopathy, and it is known that the incidence of encephalitis after measles immunization of healthy children tends to be lower than the observed incidence of encephalitis of unknown cause. Two large studies have been negative. In a study analogous to the British Childhood Encephalopathy Study there were no increased risks of either encephalopathy or neurological sequelae after measles immunization (19). A retrospective case-control study through the CDC Vaccine Safety DataUnk assessing the risk for 300 000 doses of MMR found not a single case of encephalitis/ encephalopathy within 30 days of the administration of MMR (20). In contrast, the review mentioned above (18) reported an association between measles vaccine and encephalopathy. However, the conclusion of the report of the Institute of Medicine is still valid, namely that evidence is stiU inadequate to accept or reject a causal relation between measles vaccine and these diseases. 

Table 37-8 describes the treatment goals for patients with HE and contrasts the differences between acnte and chronic HE. The general approach to the management of HE is to first identify and treat any precipitating factors, which often results in prompt resolution of the encephalopathy. The development of mental status changes in cirrhosis is associated with increased morbidity and mortality. However, universal treatment of patients with suhclinical HE is not recommended because the consequences of motor and attention deficits are considered minor, and prevention of progression to more severe HE has not been studied. ... 

Dick F, Semple S, Chen R, et al Neurological deficits in solvent-exposed painters a syndrome including impaired colour vision, cognitive defects, tremor and loss of vibration sensation. QJM 93 655-661, 2000 Donoghue AM, Dryson EW, Wynn-Williams G Contrast sensitivity in organic-solvent-induced chronic toxic encephalopathy. J Occup Environ Med 37 1357-1363, 1995... 

A study, undertaken to confirm the involvement of the cytochrome P450 isoenzyme CYT2D6 in the metabolism of trazodone, found that when 11 depressed patients were given trazodone 150 to 300 mg at bedtime for 18 weeks, and then with thioridazine 20 mg twice daily for one week, the plasma levels of the trazodone and its active metabolite, /w-chlorophenyl-piperazine, rose by 36% and 54%, respectively. No adverse reactions were described. In contrast, a case of fatal hepatic necrosis with cholestasis has been attributed to the concurrent use of trazodone and phenothiazines. A 72-year-old woman taking trifluoperazine, trazodone and lithium carbonate developed an elevated alanine aminotransferase level. Trifluoperazine was replaced with thioridazine, but 9 weeks later she became jaundiced and developed hepatic encephalopathy, and died 6 weeks after the onset of jaundice. The authors consider that the combination of the phenothiazines and trazodone were the cause of her hepatic necrosis both phenothiazines and trazodone have been reported to individually cause hepatic adverse effects. ... 

Also in contrast to cirrhotics and patients with porto-systemic bypass without hepato-cellular disease, altered mental status in patients with acute liver failure may be due to the presence of seizure activity or hypoglycemia. A status of complex partial seizures may be misinterpreted as bizarre behaviour in the course of acute hepatic encephalopathy. Seizures may even continue under neuroleptanalgesia, and then cannot be detected by clinical observation. 

Rare complications of liver cirrhosis are chronic persistent hepatic encephalopathy and hepatic myelopathy. Both occur in less than 1% of the patients, and both are accompanied by extensive porto-systemic shunts. Chronic persistent hepatic encephalopathy is also known as acquired hepato-lenticular degeneration (Victor, Adams and Cole, 1965). In contrast to the nsnal cirrhotic patient with HE, these patients show obvions neuronal alterations a patchy, spongy degeneration most consistently observed in the deep layers of the cerebral cortex and subcortical white matter, particularly in the parieto-occipital cortex, basal ganglia and cerebellum. 

Ammonia metabolism within the muscle may be improved by the administration of L-omithine-L- aspartate (LOLA). Controlled trials suggest that enteral and parenteral formulations of ornithine aspartate significantly reduce blood ammonia levels and have useful therapeutic effects in patients with cirrhosis and encephalopathy (Kircheis et al., 1997 Stauch et al., 1998). Poo et al. (2006) recently showed in a randomized, lactulose-controlled study of oral ornithine-aspartate in 20 patients with clinically overt HE that LOLA in contrast to lactulose significantly improved parameters of mental status, number connection test scores, asterixis scores and EEG. Both lactulose and LOLA reduced serum ammonia levels and improved quaUty of life scores. Since only 20 patients were included in this study the results cannot be considered proof for the superiority of LOLA compared to lactulose, while the data underscore the effect of both agents. Ornithine aspartate is well tolerated in general. From a theoretical point of view the combination of disaccharides and ornithine aspartate may be useful in patients with insufficient efficacy of only one of the two drugs. 

Perhaps the most likely mechanism of low thiamine-induced brain injury has revolved around impairment of the Krebs cycle and deficit in available ATP (Desjardins and Butterworth, 2005). This could readily lead to apoptosis and necrosis of neurons, as has been described in such patients (Vorhees et al, 1977). In this context, the data on pyruvate dehydrogenase are somewhat difficult to interpret. Postmortem brain from patients with Wernicke s encephalopathy did show a major decrease in pyruvate dehydrogenase, albeit in only a few specimens (Butterworth et al, 1993). However, this was not corroborated in experimental models of this syndrome (Desjardins and Butterworth, 2005 Butterworth et al., 1993). By contrast a major decrease in brain a-ketoglutarate dehydrogenase was seen in every type of thiamine deficiency (Desjardins and Butterworth, 2005 Butterworth et al., 1993). Moreover, an impairment in this enzyme could readily explain an increase in brain lactate, due to anaerobic metabolism, and this has been observed uniformly, even... 

Mascalchi, M., Simonelli, P., Tessa, C., Giangaspero, F., Petruzzi, P., Bosincu, L., Conti, M., Sechi, G., and Salvi, F. (1999). Do acute lesions of Wernicke s encephalopathy show contrast enhancement Report of three cases and review of the literature. Neuroradiology 41 249-254. 

Uses Rifaximin is a non-systemic, gut-selective antibiotic and has been approved in the USA for reducing the risk of recurrence of hepatic encephalopathy in adults. The effects of rifaximin 400-1200 mg/day have been assessed in a retrospective study after treatment with lactulose 20-120 g/day in improving hospitalization outcomes in 65 patients with hepatic encephalopathy [17 ]. Rifaximin reduced the risk, number, and duration of hospitalizations for hepatic encephalopathy compared with lactulose. Fewer patients had evidence of spontaneous bacterial peritonitis while taking rifaximin. Lactulose was associated with many adverse events, including abdominal cramps (n = 2l), bloating ( = 8), pain ( = 19), and excessive diarrhea ( = 54) in contrast, there was only one case of abdominal pain in those who took rifaximin. 

Nervous system Cases of encephalopathy have been reported in patients who have been given contrast media. 

A transient encephalopathy has been reported after the use of an iodinated contrast medium in a neurointerventional procedure with development of psychomotor agitation, disorientation, and progressive left faciobrachial hemiparesis 30 minutes after successful treatment of a right carotid-ophthalmic fusiform aneurysm [6 ]. A CT scan showed marked cortical enhancement and edema in the right cerebral hemisphere, thought to be due to contrast extravasation after disruption of the blood-brain barrier. Treatment with dexa-methasone and maimitol produced complete recovery. 

Guimaraens L, Vivas E, Fonnegra A, Sola T, Soler L, Balaguer E. Transient encephalopathy from angiographic contrast a rare complication in neurointerventional procedures. Cardiovasc Intervent Radiol 2010 33 383-8. 

Ozelsancak R, Erken E, Yildiz I, Giray S, Yildirim T, Micozkadioglu H. A very rare case of encephalopathy in a patient with end-stage renal disease contrast agent ioversol. Ren Fail 2010 32 1128-30. 

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