Neurological sequelae

Himnan DJ Tolerance and reverse tolerance to toluene inhalation effects on open-field behavior. Pharmacol Biochem Behav 21 625-631, 1984 Hinman DJ Biphasic dose-response relationship for effects of toluene inhalation on locomotor activity. Pharmacol Biochem Behav 26 65-69, 1987 Hormes JT, Filley CM, Rosenberg NL Neurologic sequelae of chronic solvent vapor abuse. Neurology 36 698—702, 1986... 

Muller, D.P.R. and Lloyd, J.K. (1982). Effect of large oral doses of vitamin E on the neurological sequelae of patients with abetalipoproteinaemia. Ann. N.York Acad. Sci. 339, 133-144. 

Surgery plays a key role in the management of patients with brain metastases, particularly patients whose systemic disease is well controlled and in those with solitary lesions. Surgery also may benefit patients with multiple metastatic sites who have a single dominant lesion with current or impending neurologic sequelae. 

Matsuo F, Cummins JW, Anderson RE. 1979. Fetters to the editor—neurological sequelae of massive hydrogen sulfide inhalation. Arch Neurol 36 451-452. 

Snyder JW, Safir EF, Summerville GP, et al. 1995. Occupational fatality and persistent neurological sequelae after mass exposure to hydrogen sulfide. Am J Emerg Medl3 199-203. 

Signs and Symptoms Range from mild fever and headache to high fever, headache, stupor, disorientation, tremors, meningoencephalitis, convulsions, spastic paralysis, and coma. There is a high incidence of neurologic sequelae. 

The goals of treatment include eradication of infection with amelioration of signs and symptoms, and prevention of neurologic sequelae, such as seizures, deafness, coma, and death. 

The use of glucocorticoids for tuberculous meningitis remains controversial. The administration of steroids such as oral prednisone, 60 to 80 mg/ day (1 to 2 mg/kg/day in children), or 0.2 mg/kg/day of IV dexametha-sone, tapered over 4 to 8 weeks, improves neurologic sequelae and survival in adults and decrease mortality, long-term neurologic complications, and permanent sequelae in children. 

The goals of treatment are (1) terminate clinical and electrical seizure activity, (2) minimize side effects, (3) prevent recurrent seizures, and (4) avoid pharmacoresistent epilepsy and/or neurologic sequelae. 

Vitamin 6 2 deficiency is known to manifest as dementia along with other neurological sequelae, as subacute combined degeneration (SCD). A study done on choline-deficient mice fed with vitamin B12 showed... 

Neurologic sequelae with vinblastine are much less common than those seen with vincristine and vindesine. Nonetheless, a causal relationship has been established for seizures, psychotic episodes, and confusional episodes. As common with other vinca agents, absence of reflexes and peripheral neuropathy are well described 23,24). 

A frequent cause of vitamin B12 deficiency is atrophic gastritis leading to a lack of intrinsic factor. Besides megaloblastic anemia, damage to mucosal linings and degeneration of myelin sheaths with neurological sequelae will occur (pernicious anemia). 

Mitoxantrone must not be given by intrathecal injection. Neuropathy and neurotoxicity have been reported. These reports have included seizures leading to coma and severe neurologic sequelae, and paralysis with bowel and bladder dysfunction. 

Deficiencies of thiamine and B vitamins arising from poor nutrition and malabsorption are usually the basis for these neurological sequelae. 

Abnormalities of liver function tests are occasionally seen, as is a varying degree of anemia due to reduced erythropoietin production by damaged renal tubular cells. After intrathecal therapy with amphotericin, seizures and a chemical arachnoiditis may develop, often with serious neurologic sequelae. 

Individuals affected with porphyria present with acute attacks, skin lesions, or both. The onset of these attacks rarely occurs before puberty. An attack usually consists of severe abdominal pain and often neurological sequelae. During and after such attacks, excessive amounts of aminolevulinic acid and PBG are excreted in the urine. The most common porphyria is PBG deaminase deficiency (acute intermittent porphyria), which primarily affects liver function. A positive result coupled with a clinical indication of hepatosplenomegaly suggests that evaluation for tyrosine metabolites in the urine should be pursued (using the nitrosonaphthol test). 

W. Colangelo and D.G. Jones, The fetal alcohol syndrome A review and assessment of the syndrome and its neurological sequelae, Progr. 

Blood-brain barrier Treatment of central nervous system infections, such as meningitis, depends on the ability of a drug to penetrate into the cerebrospinal fluid (CSF). The blood-brain barrier (see p. 8) ordinarily excludes many antibiotics. However, inflammation facilitates penetration and allows sufficient levels of many (but not all) antibiotics to enter the CSF. [Note For cure of meningitis, it is important that a bactericidal rather than a bacteriostatic effect is achieved in the CSF. Yet, this is not without its problems, since rapid bacteriolysis in the infected CSF will liberate high concentrations of bacterial cell walls and lipopolysaccharide that can exacerbate the inflammation. This has led to the use of adjunctive (simultaneous administration of) corticosteroids, which diminish the inflammatory process and neurologic sequelae.]... 

Swartz and Jones (1994) reviewed the literature and presented three cases concerning severe and often persistent adverse reactions to the abrupt withdrawal of lithium in patients suffering from elevated serum levels during routine treatment. One of the patients became severely demented. In their review of 50 cases obtained from the Lithium Information Center of the University of Wisconsin, they found that many patients became demented or otherwise deteriorated severely when abruptly withdrawn from lithium. Patients subjected to kidney dialysis for lithium toxicity often deteriorated mentally with a rapid drop in lithium levels. Neurologic sequelae persisted in 30% of the 50 patients. The authors found substantial neurotoxic risks in rapidly withdrawing patients from high lithium levels. 

Choi, I.S. 1983. Delayed neurologic sequelae in carbon monoxide intoxication. Arch. Neurol. 40 (7) 433-435. 

Chronic neurological sequelae of intoxication included two patients with a persistent cerebellar syndrome and severe cerebellar atrophy (175), one with subcortical dementia (176), and one with a diffuse sensorimotor peripheral neuropathy (177). 

Roy M, Stip E, Black DN, Lew V, Langlois R. Sequelles neurologiques secondaires a une intoxication aigue au lithium. [Neurologic sequelae secondary to acute lithium poisoning.] Can J Psychiatry 1999 44(7) 671-9. 

---