As of the year 2012, nobody in the scientific community has really been able to answer this question with research. Although the brain itself does not possess sensory innervation, the outer covering of the brain, called the meninges, does. These meninges can sense pain through the meningeal branches of the trigeminal nerve. This is the reason why people can sense pain when they have meningitis and this is probably the reason why people can feel the electrical sensations that most on the internet have described as "brain zaps," "brain shivers," or "battery head."

Brain zaps are usually associated with taking or withdrawing from certain anti-depressants, such as SSRIs, but they can also be caused by taking or withdrawing from other drugs, such as benzodiazapines. Some may go as far as even claiming that they can have psychogenic origins, such as with anxiety or panic attacks.

It appears to be a form of post-acute withdrawal syndrome and some might argue that it falls under the purview of SSRI discontinuation syndrome. Whatever it is, one thing is certain: it is extremely uncomfortable, it is extremely irritating, and it must be scientifically investigated.

Theoretically, these symptoms could last anywhere from months, years, to a lifetime. These symptoms could be permanent, there is little known about how to best treat them, and it is not known whether or not these have any unforeseen long-term health consequences, such as predisposing an individual to early dementia. Nevertheless, anecdotal evidence exists on the internet regarding the use of GABA agonists and NMDA antagonists to treat this disease, such as acaprosate, memantine, magnesium, ketamine, dextromethorphan, and phencyclidine.

Genetics, GABA receptor downregulation, and NMDA upregulation must play a large role in the pathogenesis of these symptoms. It seems to be a phenomenon of cerebral neuroexcitability sensed via the meningeal branches of the trigeminal nerve.

It is entirely possible that coconsumption of GABA agonists while taking SSRIs may precipitate this symptom in the genetically susceptible. For example, studies have shown that the chronic administration of GABA agonists can cause hyperexcitability (Begleiter 1977) and binge drinking and depression are associated with serontonin receptor mutations (Herman et al 2003). Many people take benzodiazapines and/or drink alcohol while on SSRIs, so it is possible that they are causing permanent downregulation of the GABA receptors allowing for a hyperexcitable cerebral cortex--i.e. "battery head."

What seems to be the most disconcerting about this symptom, however, is the fact that Alzheimer's disease is associated with a hyperexcitable cerebral cortical cortex as well. Thus, in will interesting to see how many legal complaints will be filed against pharmaceutical companies if it turns out that there is an association between taking SSRIs and dementia in the near future.

Begleiter, H., & Porjesz, B. (1977). Persistence of brain hyperexcitability following chronic alcohol exposure in rats. Advances in experimental medicine and biology, 85B, 209-222.

Herman AI et.al. (2003). Serotonin Transporter Promoter Polymorphism and Differences in Alcohol Consumption Behavior in a College Student Population. Alcohol and Alcoholism 38: 446-449.

Glutamate-mediated excitotoxicity and neurodegeneration in Alzheimer's disease.

Matthew R. Hynd, Heather L. Scott, Peter R. Dodd

Neurochem Int. 2004 October; 45(5): 583-595. doi: 10.1016/j.neuint.2004.03.007