Classification There are several different forms of<unk> , which can be distinguished by the age of onset, as well as the types and severity of symptoms. All forms of<unk>  present with only neurological symptoms, including intellectual disability (IQ scores below 20 are common), hypotonia, apneic seizures, and brain malformations. With the classical, or neonatal presentation of<unk> , the infant is born after an unremarkable pregnancy, but presents with lethargy, hypotonia, apneic seizures and myoclonic jerks, which can progress to apnea requiring artificial ventilation, and often death. Apneic patients can regain spontaneous respiration in their second to third week of life. After recovery from the initial episode, patients have intractable seizures and profound intellectual disability, remaining developmentally delayed. Some mothers comment retrospectively that they noticed fetal rhythmic "hiccuping" episodes during pregnancy, most likely reflecting seizure episodes in utero. Patients with the infantile form of<unk>  do not show lethargy and coma in the neonatal period, but often have a history of hypotonia. They often have seizures, which can range in severity and responsiveness to treatment, and they are typically developmentally delayed.<unk>  can also present as a milder form with episodic seizures, ataxia, movement disorders, and gaze palsy during febrile illness. These patients are also developmentally delayed, to varying degrees. In the later onset form, patients typically have normal intellectual function, but present with spastic diplegia and optic atrophy. The mild form of the disorder corresponds to greatly reduced but not fully absent GCS activity. Transient neonatal hyperglycinemia has been described in a very small number of cases. Initially, these patients present with the same symptoms and laboratory results that are seen in the classical presentation. However, levels of<unk>  in plasma and cerebrospinal fluid typically normalize within eight weeks, and in five of six cases there were no neurological issues detected at follow-up times up to thirteen years. A single patient was severely retarded at nine months. The suspected cause of transient neonatal hyperglicinemia is attributed to low activity of the<unk>  cleavage system in the immature brain and liver of the neonate.
Glycine encephalopathy
Toxic encephalopathy
Ethylmalonic encephalopathy
Wernicke encephalopathy
Post-encephalitic parkinsonism
Early myoclonic encephalopathy
Carbamate poisoning
Viral encephalitis