The CIWA has also been shortened (now called the CIWA-Ar), while retaining its validity and reliability, to help assess patients more efficiently due to the life-threatening nature of alcohol withdrawal.Other conditions that may present similarly include benzodiazepine withdrawal syndrome (a condition also mainly caused by GABAA receptor adaptation). Treatment
Benzodiazepines  are effective for the management of symptoms as well as the prevention of seizures. Certain vitamins are also an important part of the management of alcohol withdrawal syndrome. In those with severe symptoms inpatient care is often required. In those with lesser symptoms treatment at home may be possible with daily visits with a health care provider. Benzodiazepines
Benzodiazepines are the most commonly used medication for the treatment of alcohol withdrawal and are generally safe and effective in suppressing symptoms of alcohol withdrawal. This class of medication is generally effective in symptoms control, but need to be used carefully. Although benzodiazepines have a long history of successfully treating and preventing withdrawal, there is no consensus on the ideal one to use. The most commonly used agents are long-acting benzodiazepines, such as chlordiazepoxide and diazepam. These are believed to be superior to other benzodiazepines for treatment of delirium and allow for longer periods between doses. However, benzodiazepines with intermediate half-lives like lorazepam may be safer in people with liver problems. Benzodiazepines showed a protective benefit against alcohol withdrawal symptoms, in particular seizure, compared to other common methods of treatment.The primary debate between use of long-acting benzodiazepines and short-acting is that of ease of use.
DPR and NFJS syndromes were specifically found to be differentiated from other syndromes by a mutation of the keratin 14 gene, located on chromosome 17q21.2. This was found when keratin genes KRT14, KRT16, and KRT17 were reassessed in 2006, revealing pathogenic mutations of KRT14 in all patients with NFJS/DPR, displaying a strong correlation and suggesting a potential causation. The type of mutations observed were heterozygous nonsense or frameshift mutations, meaning the function of the gene was completely disrupted (missense is correlated with EBS). The different phenotypic presentations of recessive (EBS-causing) versus dominant (NFJS/DPR-causing) premature truncation mutations in KRT14 are still unclear. The NFJS/DPR mutations were verified using two screening approaches, in which it was found that 17delG was absent from a panel of 100 control individuals, and C18X and Q7X were found to create a novel recognition site for the endonucleases DdeI and BfaI. Because the mutations were found to be heterozygous, the condition was concluded to be autosomal dominant in its inheritance pattern.Interestingly, a study conducted on five families using a two-point linkage analysis of the combined genotyping data for three families across the NFJS/DPR candidate region generated an LOD score of 6.2 at marker D17S800, with a recombination score of 0. Further analysis revealed that NFJS may be caused by an identical founder mutation located within a 6-Mb interval between D17S946 and D17S2180.