Heroin-induced leukoencephalopathy has had three stages described. The first stage features soft (pseudobulbar) speech, cerebellar ataxia, motor restlessness, and apathy/bradyphrenia. The intermediate stage includes pyramidal tract and pseudobulbar signs, spastic paresis, myoclonic jerks, and choreoathetoid movements. The final or terminal stage is characterized by stretching spasms, akinetic mutism, hypotonic paresis, central pyrexia, and death. Similarly, leukoencephalopathy induced by orally administered methotrexate for arthritis patients presents similar symptoms including ataxia, dysarthria, and seizures; however, long-term cognitive effects remain unknown. Symptoms of leukoencephalopathy caused by overdose of metronidazole medication include dysarthria, gait disturbance, weakness of extremities, and mental confusion. Despite the pharmacological agent or source of toxicity, some patients completely recover from toxic leukoencephalopathy. Related disorders
Posterior reversible encephalopathy syndrome (PRES) can also result from medication toxicity. Symptoms similar to those of leukoencephalopathy patients have been seen in PRES patients. However, the prognosis of toxic leukoencephalopathy is typically slightly worse than that of PRES because toxic leukoencephalopathy is more likely to lead to ataxia, dementia, or coma.Hypoglycemic encephalopathy is often seen in diabetics as a result to accidental overdose with the long-acting sulfonylurea drug group. Brain regions affected by toxic leukoencephalopathy have been seen to be affected by this disease as well; however, hypoglycaemic encephalopathy has been known to involve both white and grey matter abnormalities. Causes
Various pharmacological agents have been known to cause toxic leukoencephalopathy. The most common causes are substance use and chemotherapy; however, the disease has also occurred on the rare occasion as a side effect of certain medications and environmental toxins.
Full trisomy 9 is a lethal chromosomal disorder caused by having three copies (trisomy) of chromosome number 9. It can be a viable condition if trisomy affects only part of the cells of the body (mosaicism) or in cases of partial trisomy (trisomy 9p) in which cells have a normal set of two entire chromosomes 9 plus part of a third copy, usually of the short arm of the chromosome (arm p). Presentation
Symptoms vary, but usually result in dysmorphisms in the skull, nervous system problems, and developmental delay. Dysmorphisms in the heart, kidneys, and musculoskeletal system may also occur. An infant with complete trisomy 9 surviving 20 days after birth showed clinical features including a small face, wide fontanelle, prominent occiput, micrognathia, low set ears, upslanting palpebral fissures, high-arched palate, short sternum, overlapping fingers, limited hip abduction, rocker bottom feet, heart murmurs and a webbed neck.Trisomy 9p is one of the most frequent autosomal anomalies compatible with long survival rate. A study of five cases showed an association with Coffin–Siris syndrome, as well as a wide gap between the first and second toes in all five, while three had brain malformations including dilated ventricles with hypogenesis of the corpus callosum and Dandy-Walker malformation. Diagnosis
Trisomy 9 can be detected prenatally with chorionic villus sampling and cordocentesis, and can be suggested by obstetric ultrasonography.Because trisomy 9 may appear with mosaicism, it is suggested that doctors take samples from multiple tissues when karyotyping for diagnosis.