This pattern of comorbidities poses a significant challenge to those who claim that SPD is an identifiably specific disorder, rather than simply a term given to a set of symptoms common to other disorders.Two studies have provided preliminary evidence suggesting that there may be measurable neurological differences between children diagnosed with SPD and control children classified as neurotypical or children diagnosed with autism. Despite this evidence, that SPD researchers have yet to agree on a proven, standardized diagnostic tool undermines researchers ability to define the boundaries of the disorder and makes correlational studies, like those on structural brain abnormalities, less convincing. Causes
The exact cause of SPD is not known. However, it is known that the midbrain and brainstem regions of the central nervous system are early centers in the processing pathway for multisensory integration; these brain regions are involved in processes including coordination, attention, arousal, and autonomic function. After sensory information passes through these centers, it is then routed to brain regions responsible for emotions, memory, and higher level cognitive functions. Damage in any part of the brain involved in multisensory processing can cause difficulties in adequately processing stimuli in a functional way. Mechanism
Research in sensory processing in 2007, is focused on finding the genetic and neurological causes of SPD. Electroencephalography (EEG), measuring event-related potential (ERP) and magnetoencephalography (MEG) are traditionally used to explore the causes behind the behaviors observed in SPD. Differences in tactile and auditory over-responsivity show moderate genetic influences, with tactile over-responsivity demonstrating greater heritability.
Calcium channel blocker toxicity is the taking of too much of the medications known as calcium channel blockers (CCBs), either by accident or on purpose. This often causes a slow heart rate and low blood pressure. This can progress to the heart stopping altogether. Some CCBs can also cause a fast heart rate as a result of the low blood pressure. Other symptoms may include nausea, vomiting, sleepiness, and shortness of breath. Symptoms usually occur in the first six hours but with some forms of the medication may not start until 24 after hours.There are a number of treatments that may be useful. These include efforts to reduce absorption of the drug including: activated charcoal taken by mouth if given shortly after the ingestion or whole bowel irrigation if an extended release formula was taken. Efforts to bring about vomiting are not recommended. Medications to treat the toxic effects include: intravenous fluids, calcium gluconate, glucagon, high dose insulin, vasopressors and lipid emulsion. Extracorporeal membrane oxygenation may also be an option.More than ten thousand cases of calcium channel blocker toxicity were reported in the United States in 2010. Along with beta blockers and digoxin calcium channel blockers have one of the highest rates of death in overdose. These medications first became available in the 1970s and 1980s. They are one of the few types of medication in which one pill can result in the death of a child.