Slowing of voluntary movement, reduced speech, aboulia, increased prompt dependency and obsessive-compulsive symptoms are frequently seen; negativism, (auto-)aggressive behaviors and ill-defined hallucinations have also been reported. Both the causes of this disorder as well as its prognosis appear to be heterogenous, with most patients showing partial recovery upon treatment. It seems to be related to chronic stress as a result of life transitions, loss of external time structuring, sensory sensitivities and/or traumatic experiences, co-morbid mental disorders, or other unknown causes. Since clinical catatonia can not always be diagnosed, this condition has also been renamed to the more general term "late regression". Complications
Patients may experience several complications from being in a catatonic state. The nature of these complications will depend on the type of catatonia being experienced by the patient. For example, patients presenting with retarded catatonia may have refusal to eat which will in turn lead to malnutrition and dehydration. Furthermore, if immobility is a symptom the patient is presenting with, then they may develop pressure ulcers, muscle contractions, and are at risk of developing deep vein thrombosis (DVT) and pulmonary embolus (PE). Patients with excited catatonia may be aggressive and violent, and physical trauma may result from this. Catatonia may progress to the malignant type which will present with autonomic instability and may be life-threatening. Other complications also include the development of pneumonia and neuroleptic malignant syndrome. Causes
Catatonia is almost always secondary to another underlying illness, often a psychiatric disorder.
in several papers the involvement of the cranial nerve nuclei and central gray matter on MRI, is very specific to WE in the appropriate clinical setting. Non-recovery upon supplementation with thiamine is inconclusive.The sensitivity of MR was 53% and the specificity was 93%. The reversible cytotoxic edema was considered the most characteristic lesion of WE. The location of the lesions were more frequently atypical among people who drank appropriate amounts of alcohol, while typical contrast enhancement in the thalamus and the mammillary bodies was observed frequently associated with alcohol misuse. These abnormalities may include:
Dorsomedial thalami, periaqueductal gray matter, mamillary bodies, tectal plate and brainstem nuclei are commonly affected. Involvement is always bilateral and symmetric. Value of DWI in the diagnosis of WE is minimal. Axial FLAIR MRI images represent the best diagnostic MRI sequence. Contrast material may highlight involvement of the mamillary bodies.There appears to be very little value for CT scans.Thiamine can be measured using an erythrocyte transketolase activity assay, or by activation by measurement of in vitro thiamine diphosphate levels. Normal thiamine levels do not necessarily rule out the presence of WE, as this may be a patient with difficulties in intracellular transport. Prevention
There are hospital protocols for prevention, supplementing with thiamine in the presence of: history of alcohol misuse or related seizures, requirement for IV glucose, signs of malnutrition, poor diet, recent diarrhea or vomiting, peripheral neuropathy, intercurrent illness, delirium tremens or treatment for DTs, and others.