Brain shivers or brain zaps

[mb-909]

" Antidepressant discontinuation syndrome is a common syndrome seen following abrupt termination of treatment with a serotonin reuptake inhibitor.1 It occurs at rates ranging from 17.2% to as high as 78% with venlafaxine.2,3 There is, however, little literature on “brain shivers,”4,5 a common antidepressant-discontinuation symptom described by patients taking venlafaxine, duloxetine, citalopram, and paroxetine. Much of the information comes from Internet blogs and Web sites.6–8 The symptom is described variously as “an electrical shock–like sensation in the brain,” “the sensation of the brain shivering,” “brain zaps,” “brain shocks,” “brain shivers,” “head shocks,” or “cranial zings.” The etiology of the symptom is not known, and there is no known treatment for this distressing symptom.

We describe a case in which “brain shivers” occurred as part of venlafaxine discontinuation syndrome and abated with atomoxetine treatment.

Case report. Mr A, a 34-year-old man, presented with DSM-IV major depressive disorder (MDD) that responded well to venlafaxine (300 mg/d). He achieved remission except for seasonal exacerbations during autumn during the next 4 years. In view of a family history of bipolar disorder, it was decided to add lamotrigine and taper venlafaxine. Mr A maintained remission on venlafaxine (37.5 mg/d) and lamotrigine (200 mg/d) without seasonal exacerbations. Mr A abruptly discontinued venlafaxine 37.5 mg/d. On the second day following discontinuation, he reported feeling an unpleasant sensation of “electricity in the head” that “felt like the brain was shaking inside the skull.” Mr A was also noticed to demonstrate emotional incontinence and complained of anhedonia, anxiety, tinnitus, headache, nausea, and increased sensitivity to noise. Since the “brain shivers” were the most distressing symptom, a trial of atomoxetine 40 mg/d was attempted based on the hypothesis that the symptom was a result of noradrenergic imbalance.9 An immediate improvement in “brain shivers” was reported within 2 or 3 hours of taking the first dose. Over the next 3 days, Mr A reported further improvement in “brain shivers” and anhedonia although emotional incontinence and increased sensitivity to noise persisted. Given the severity of other withdrawal symptoms, venlafaxine (37.5 mg/d) was reinstated and atomoxetine was stopped. All withdrawal symptoms disappeared during the next day.

The case adds to the interesting speculation about the noradrenergic imbalance as the basis of “brain shivers.”9 “Brain shivers,” conceptually related to Lhermitte’s phenomenon,10 have also been reported with the noradrenergic drug 3,4-methylenedioxy-N-methylamphetamine (MDMA). The psychotropic effects of MDMA are mediated via norepinephrine transporter11 and results in an increase in synaptic norepinephrine levels. Venlafaxine’s affinity for norepinephrine transporter (K = 2,984 nM),12 is 103-fold lower than that of atomoxetine (K = 5 nM),13 yet venlafaxine causes an increase (242%)14 in synaptic norepinephrine levels comparable to that by atomoxetine (290% ± 33%).13 Curiously, chronic treatment with venlafaxine does not reduce norepinephrine transporter binding sites.15 These facts point to the possibility that increases in synaptic norepinephrine are due to norepinephrine transporter reversal, akin to dopamine transporter reversal associated with amphetamine.16 Abrupt withdrawal of venlafaxine would hence result in paradoxical increase in synaptic norepinephrine via efflux through norepinephrine transporter channels, which is normalized by atomoxetine’s norepinephrine transporter blockade. This speculation of the noradrenergic basis of “brain shivers” warrants further study."


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3733524/

 

[mb-909]

Brain Zaps, Electrical Shocks, Brain Shivers...


Brain Zaps, Brain Shivers, Brain Shocks. Head Shocks or Electrical shocks are a common side effect and withdrawal symptom from Antidepressants, but they can also occur with Benzodiazepines and Sleeping Pills. The symptoms are described as brief but repeated electric shock-like sensations in the brain and head, or originating in the brain but extending to other parts of the body. Moving one's eyes quickly from side to side has also been shown to trigger Brain Zaps in more rapid frequency. Brain Zaps are often accompanied by disorientation, tinnitus, vertigo and lightheadedness.

In withdrawal from antidepressants, sleeping pills or anxiety medications, these jolts of electricity can worsen and become debilitating, although there is no current evidence that the zaps present any danger to the individual. Currently they are not recognized as a physiological syndrome. So what causes brain zaps?


UNDERSTANDING THE BRAIN

In the late 1700s, an Italian anatomist named Luigi Galvani discovered evidence of a bioelectric force within living tissues. Since his discovery, other scientists have proposed theories about how electricity is conducted in the human body. One prevailing theory states that electrical impulses in the central and peripheral nervous system are transmitted from one nerve to another with the help of electrically charged salts passing through ion channels. And nowhere in the body are nerve cells as prevalent as in the brain.

Grasping the brain's complexity isn't easy. This organ gives us the capacity for art, language, rational thought and moral judgments. It is responsible for our memories, movements, personality and the way we sense the world. Basically it governs everything that comprises the human experience.

The brain is a 3-pound (1.4 kilogram) mass of fat and protein that has the appearance of a small cauliflower. As one of the body's biggest organs, it consists of 100 billion nerve cells that regulate our conscious and unconscious body processes, including digestion and breathing. To put this into perspective, consider the fact that there are as many nerve cells in the human brain as there are stars in our galaxy.

To compound the intricacy, each of these 100 billion nerve cells make 10,000 connections with other nerve cells, so ensuring these nerves remain in balance is critical.

Each brain cell depends on a regulated stability to function properly. Excess sugar, salt, fat, and caffeine can cause imbalances in the brain's normal chemistry. This is especially true with medications that target specific neurotransmitters. Fifty neurotransmitters have been discovered to date, with about six associated with addiction by causing feelings of euphoria. Medications that target Serotonin (antidepressants) appear to be linked to Brain Zaps, as do anxiety medications and sleeping pills that target GABA.

SSRIs (Selective Serotonin Reuptake Inhibitors) work by forcing the level of Serotonin higher in the brain by blocking the natural recycling process to other nerves. But Serotonin is both a hormone and a neurotransmitter that is required to have communication between nerve cells. Serotonin can either excite or restrain. So pushing the levels artificially high in the brain also starves other areas. This could account for the extensive list of side effects related to antidepressants and also the mysterious side effect of Brain Zaps.

The average adult human possesses only 5 to 10 mg of serotonin, 90% of which is in the gut region, with only 2% reaching the central nervous system. The remainder is in the blood platelets and the brain. No physiological substance known possesses such diverse actions in the body as serotonin.

The small amount of Serotonin in the CNS attaches to receptors that lie along the brain stem from the midbrain to the medulla (lower half of the brainstem). Most antidepressant medications work by holding serotonin for longer periods in the synaptic spaces of the nervous system, and it is this space between nerve cells that has an electrical current. Since Serotonin transmits currents, it is highly possible that holding the Serotonin longer than nature intended could cause a misfiring of electrical current resulting in a Brain Zap.

Benzodiazepines and Sleeping pills work on GABA (Gamma-Aminobutric Acid), which is the neurotransmitter that prevents over-stimulation of the central nervous system. Continual use of anxiety medications and sleeping pills 'down regulate' the GABA receptors and reduce their ability to ease an over-excited state. This could explain the Brain Zaps that occur while on medications or in the withdrawal process for drugs that affect GABA. Rather than inhibiting the electrical activity in the brain, tolerance and withdrawal symptoms over-stimulate, allowing more electrical impulses to go unchecked.

OXIDATIVE STRESS AND THE BRAIN


Free radicals are highly reactive molecules that modify, disrupt and impair the stable structure within our brain and body. Excitotoxicity is the process by which nerve cells are damaged by toxins. Both an inflammatory response and excitotoxicty are known to play important roles in all neurodegenerative diseases, and may also play a significant role in Brain Zaps.

The brain makes up only 2% of the total body weight but consumes 25% of the energy for the entire body. The oxygen we breathe helps to burn sugar and fat inside our body cells to produce energy. But about 2% of the converted oxygen remains as free radicals. Oxidative Stress in the brain can result from poor diet, the extended use of medications or environmental toxins. If these reactive elements are not neutralized, oxidative stress on the brain occurs.

According to Dr. Jimmy Gutman, the brain is particularly susceptible to free radical attack because it generates more oxidative by-products per gram of tissue than any other organ. It could be this increase in oxidative stress that worsens Brain Zaps.

A study in The Journal of Neuroscience in December 2000 indicated that Tricyclic antidepressants and SSRIs (Selective Serotonin Reuptake Inhibitors) were shown to cause oxidative stress in a nerve cell line due to a reduction of intracellular Glutathione (master antioxidant of the body) levels.

http://www.pointofreturn.com/brain_zaps.html

 

[mb-909]

"Cymbalta® Withdrawal Brain Zaps

Cymbalta Withdrawal and “Brain Zaps”

In his book, The Antidepressant Solution, Joseph Glenmullen, M.D., of Harvard Medical School, describes a common symptom of withdrawal from SSRI and SNRI antidepressants, referred to by many as “brain zaps.”

“These are lightening-like jolts inside the head that make patients feel as if they are having a dangerous neurological event, such as a stroke…. In some patients … bending the neck brings on waves of electric shock-like sensations down the spine, arms, and legs.”


Brain zaps and other symptoms of withdrawing from Cymbalta therefore can be seen as the brain’s reaction to suddenly being removed from the abnormal environment to which it has adapted.


Dr. Glenmullen gives a detailed report of a patient who experienced shooting electric shock sensations, accompanied by severe shaking and trembling. An electrocardiograph (“EEG”) provided evidence the woman was having seizures and she was put on anticonvulsants.

In 2007, two British psychiatrists wrote an article describing "sensory symptoms (e.g. sensations resembling electric shocks) or symptoms of disequilibrium (e.g. dizziness) in brief bursts when they move their head or eyes. Such symptoms are highly characteristic of primary discontinuation syndrome” (emphasis added).

What Is a Brain Zap From an Antidepressant?

The exact cause of brain zaps and other withdrawal effects of Cymbalta are unknown, but they are thought to be related to changes that occur in the brain when exposed to antidepressants.

Nerve signals are transmitted from one cell to another through the release of a chemical messenger, called a neurotransmitter, into the space between the sending and receiving cells. The receiving cell has receptors into which the neurotransmitter fits like a key in a lock, triggering complex reactions in the cell. Antidepressants like Cymbalta increase the neurotransmitters serotonin and norepinephrine (similar to adrenaline) in the gap between nerve cells. The cells have multiple reactions to this increase. The sending cell becomes “desensitized” – it doesn’t fire as much – and the receiving cells decrease the number of receptors.

In 1996, Steven Hyman, former director of the National Institute of Mental Health, described these adjustments in a paper published in the American Journal of Psychiatry. Chronic administration of antidepressants and antipsychotics, he explained, creates changes in the normal functioning of the brain that “likely exceed the strength or time course of almost any natural stimulus.” The cells, responding to what Hyman called the “significant environmental challenges” of the drugs, try to adjust, leading to “substantial and long-lasting alterations in neural function.” Antidepressants produce their effects, wrote Hyman, by “altering the functional activity of critical neural circuits in the brain,” producing a state “which may be qualitatively as well as quantitatively different from the normal state.” In short, after chronic administration of antidepressants, the brain is functioning abnormally.

Cymbalta Treatment and Brain Zaps

Brain zaps and other symptoms of withdrawing from Cymbalta therefore can be seen as the brain’s reaction to suddenly being removed from the abnormal environment to which it has adapted, like a deep sea diver who returns to the surface too quickly. The authors of a 2003 paper in the journal Psychopharmacology suggested that paresthesia (sensations of pricking, tingling, or creeping on the skin, including electric shock sensation in the brain) resulting from antidepressant withdrawal may be connected to the role that serotonin plays in controlling muscle movement and sensory function, noting that shock sensations often intensify with movement. “Significant alteration of neuronal activity may occur during treatment, possibly increasing with higher dosages or longer duration of treatment,” they wrote.

How Long do Cymbalta Brain Zaps Last?

Other investigators have theorized that brain zaps are connected to antidepressants’ effect on norepinephrine (also called noradrenaline), arguing that brain zaps are “similar to pre-seizure symptoms in epilepsy, and there is now evidence of the relevant role of the noradrenergic system in modulating seizures.” They also offer evidence that the withdrawal symptoms may not be dose dependent. The persistence of withdrawal effects, which can continue for over a year, indicates that Cymbalta and similar drugs may cause alterations in the brain that have a degree of permanence that is not easily reversed.
- See more at: http://www.baumhedlundlaw.com/cymbalta/ ... S8xrC.dpuf"

http://www.baumhedlundlaw.com/cymbalta/ ... n-zaps.php

 

[BlueBull]

This is interesting information. Thanks for taking the time to compile it!