Following extended sobriety, the volume of the lateral and third ventricles was decreased, and abstainers showed an improvement in working memory and balance. Finally, evidence for the recovery of brain volume with continued sobriety is supported by the improvement in neuropsychological performance. Compared to the control participants, abstinent alcoholic patients scored significantly better on tests measuring cognitive, sensory, and motor functions including abstract reasoning, memory, visuospatial ability, and gait and balance. That being said, while short-term abstinence suffices to produce structural and functional recovery, some alcohol-induced brain changes may persist even after long-term sobriety. See also
Cerebral atherosclerosis
Neurodegeneration
Traumatic brain injury
Neuroimmunology
Neuroendocrinology
Comorbidity
Migraine


== References ==
Adverse effects
The most common adverse reactions experienced by patients who received ivacaftor in the pooled placebo-controlled Phase III studies were abdominal pain (15.6% versus 12.5% on placebo), diarrhoea (12.8% versus 9.6% on placebo), dizziness (9.2% versus 1.0% on placebo), rash (12.8% versus 6.7% on placebo), upper respiratory tract reactions (including upper respiratory tract infection, nasal congestion, pharyngeal erythema, oropharyngeal pain, rhinitis, sinus congestion, and nasopharyngitis) (63.3% versus 50.0% on placebo), headache (23.9% versus 16.3% on placebo) and bacteria in sputum (7.3% versus 3.8% on placebo). One patient in the ivacaftor group reported a serious adverse reaction: abdominal pain. Pharmacology
Pharmacodynamics
Ivacaftor is a "potentiator" of CFTR, meaning it increases the probability that the defective channel will be open and allow chloride ions pass through the channel pore. Pharmacokinetics
Distribution
Ivacaftor is approximately 99% bound to plasma proteins, primarily to alpha 1-acid glycoprotein and albumin. Ivacaftor does not bind to human red blood cells. Biotransformation
Ivacaftor is extensively metabolised in humans. In vitro and in vivo data indicate that ivacaftor is primarily metabolised by CYP3A. M1 and M6 are the two major metabolites of ivacaftor in humans. M1 has approximately one-sixth the potency of ivacaftor and is considered pharmacologically active. M6 has less than one-fiftieth the potency of ivacaftor and is not considered pharmacologically active. Elimination
Following oral administration, the majority of ivacaftor (87.8%) is eliminated in the faeces after metabolic conversion. The major metabolites M1 and M6 accounted for approximately 65% of total dose eliminated with 22% as M1 and 43% as M6.