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Abstract

The internet is rapidly becoming a first-line source for clinicians and patients alike, and it is increasingly necessary that clinicians maintain an open dialogue with their patients about their information sources. In this paper, I look at the emergence of ‘brain shivers' as a side-effect that appears to have emerged online, in the context of antidepressant side-effects and withdrawal. I discuss possible biological explanations for this strange, possibly new, complaint, as well as the emergence of particular symptoms as a sociological phenomenon aided by new technology.
special articles
Psychiatric Bulletin (2005), 29,219^221
DAVIDM.B.CHRISTMAS
‘Brain shivers’: from chat room to clinic
The internet is rapidly becoming a first-line source for
clinicians and patients alike, and it is increasingly neces-
sary that clinicians maintain an open dialogue with their
patients about their information sources. In this paper, I
look at the emer gence of ‘brain s hivers’ as a side -effect
that appears to have emerged online, in the context of
antidepressant side-effects and withdrawal. I discuss
possible biological explanations for this strange, possibly
new, complaint, as well as the emergence of particular
symptoms as a sociological phenomenon aided by new
technology.
Psychiatrists frequently ask their patients about the
presence of adverse effects caused by antidepressants.
We often ask about dizziness and postural hypotension,
for example, but may not enquire about variations upon
common adverse effects, and unless our patients volun-
teer a specific side-effect, we run the risk of being
unaware of it.
We need to be aware of our patients’ use of the
internet, since those who are computer literate may be
beginning to shift their first port of call on health matters
away from their general practitioner or specialist to the
World Wide Web. Half of all households in the UK in 20 03
had internet access (Office of Telecommunications, 20 03).
The e asy accessibilit y, ‘always on’ nature and rapid
respons e of this ‘fountain’ of information ser ve t o re mind
us of what many of our patients actually want from
health information services.
In this paper I should like to suggest that an example
of the emergence of ‘new drug effects may be ‘brain
shivers’. It is difficult to establish when the term first
came into existence, but web pages from 1999 refer to
‘brain shivers’ in relation to antidepressants (Tamburini,
1999). Online, the term seems to occur most commonly
in the context of both use and discontinuation of venla-
faxine, although it has also been associated with most
selective serotonin reuptake inhibitors (SSRIs).
Medline returns no reference to ‘brain shivers’
relating to antidepressant use. In contrast, the search
engine Google returned 3100 ‘hits’ for the term ‘brain
shivers’ on 1 November 20 04 (http://w ww.google.com).
There is even a weblog (‘blog’) devoted to discussion of
venlafaxine (Brainzaps, 20 04). While t he m edical literature
is silent, online there is active discussion about ‘brain
shivers’. In contrast to this online community of people
discussing a particular side-effect, psychiatrists appear to
be unfamiliar with these patient-led terms. Of a small
sample of psychiatrists sampled by the author, none had
come across the term ‘brain shivers’ before.
Descriptions of the same phenomenon
A number of different descriptions are in use for what
appears to be a similar phenomenon. Other terms
include: ‘watermelon he ad’ and ‘electric brain thingies’
(Anonymous, 2004),‘brain zaps’ (‘dde’, 2003) and ‘brain
flips’ (Mangan, 200 0). There are cross-cultural variants
such as ‘svimmelhed’, from Denmark, which means ‘dizzy
in English.
Brain shivers
Descriptions
It is difficult to draw clear conclusions about the sensa-
tions described by the terms in question. Different people
tend to describe different sensations, but there are core
features in common, primarily a combination of dizziness
and electrical sensations. A selection is given below:
...dizziness, my skin feels as though it is crawling . . .
(‘Amanda’, 2004).
‘Brain shivers can run your whole body right out to the tips of
your fingers and toes. A nd back again’ (Anonymous, 20 04).
‘I feel like my he ad has a const ant electric ‘‘whirr’’insid e of it
that won’t stop . . .’ (‘JJohnson, 2004).
...myheadwasdoing this w eird, pulsing, samba-like thing
that some [venlafaxine] users desc ribe as ‘‘brain shivers’’, but
that I find similar to how one feels under a strobe light’
(Pears on, 2002).
‘[Brain shivers ] which are similar to ele ctric shock s pulsing
rapidly through your brain ever y 2
-
5 second s’ (‘Claire’, 20 04).
What are brain shivers?
From some of the above extracts, this term could be
describing a multiplicity of phenomena, from tinnitus to
migraine. An awareness of it being experienced as
elec trical’ seems relevant, and it is undoubtedly similar
Christmas ‘Brain shivers’
219
to dizziness since this is one of the most common
synonyms.
Although the symptom may be simple dizziness, it is
one that has been elaborated upon by fervent online
discussion. The web offers ample opportunity for creative
interpretations, which take on a life of their own.
Membership of a group, even one only united by side-
effects, is often important to many people who frequent
online message boards. Some people might be more
willing to admit to sharing a symptom or side-effect if it
conferred membership of a particular group.
The most constructive way of viewing the phenom-
enon of ‘brain shivers’ is probably to see it as a 21st-
century creation. Antidepressant discontinuation is an
important and highly relevant condition that results in a
number of unpleasant experiences for those concerned.
Some of these experiences may be novel for the indivi-
dual, and may be difficult to describe. As people’s use of
the web increases, they go online to find information, and
come across others’descriptions of similar experiences
which have been labelled ‘brain shivers’. Their identifica-
tion of similar symptoms results in their own adoption of
the label, and so it is perpetuated. The availability of
almost instantaneous communication means that such
concepts can be widely disseminated very quickly.
Could brain shivers have a biological basis?
There may be more biological explanations of ‘brain
shivers’. Venlafaxine is a drug that acts on both ser otonin
and noradrenaline pathways. It can also reduce the
release of noradrenaline in response to benzodiazepine
receptor inverse agonists, which are anxiogenic in
nature (Dazzi
et al
, 2002). This suggests a link with g-
aminobutyric acid (GABA) neuromodulation.
Benzodiazepines are effective treatments for vertigo
and associated disorders such as Me
¤nie
're’s disease (Hain
& Uddin, 2003).They act centrally by suppressing vestib-
ular output. Therefore, it is possible that venlafaxine
might have effects on GABA neurotransmission. Acute
discontinuation of venlafaxine might have the unwanted
effect of upregulation of receptors in these pathways, in
a similar mechanism to acute alcohol withdrawal.
Adverse effects of venlafaxine
A number of adverse effects were repor ted during the
premarketing evaluation of venlafaxine by Wyeth in the
USA. These include ‘feeling drunk’, ver tigo and nystagmus
(Wyeth, 2003). Wyeth also rep ort a number of similar
adverse effects during venlafaxine discontinuation,
including dizziness, sensory disturbances (including
shock-like electrical sensations) and vertigo (Wyeth,
2003). Again, these phenomena (singly or in combination)
could all account for the users experience of ‘brain
shivers’.
Is there a treatment?
Given that the aetiology of the experience is uncertain (it
may represent a hypotensive phenomenon or simple
dizziness), it is difficult to postulate an effective treat-
ment. There are a number of personal accounts of people
using alprazolam, a short-acting benzodiazepine, to treat
the withdrawal symptoms of venlafaxine and SSRIs
(‘Kerry ’, 199 9). It is possible, however, that discontinua-
tion symptoms were remitting at the time that other
drugs were started. There are also repor ts of venlafaxine
withdrawal being treated with fluoxetine (Giakas & Davis,
1997).
Assuming that abrupt discontinuation of some SSRIs
and venlafaxine is responsible, gradual reduction of
dosage is undoubtedly the preferred option. The manu-
facturers of venlafaxine recommend dose tapering over at
least a 2-week period, but also state that ‘individualiza-
tion of tapering may be necessary’ (Wyeth, 2003).
Regular monitoring of our patients and open discussion
of adverse effects is needed.
Conclusions
Although the aetiolog y of ‘brain shiver s’ and other as so-
ciated descriptions remains uncertain, it serves as an
introduction to the web as being an indicator of many
patients’ ex periences of the drugs that we pre scribe. We
will undoubtedly see an increase in the amount of infor-
mation being provided to our patients in this way without
our control. We have to underst and the implications of
this, especially in relation to a group of people who,
frequently feeling dise mpowere d by ‘the sy stem’ and by
their illnesses, find solidarity online.
Declaration of interest
None.
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(e-mail:d.m.christmas@dundee.ac.uk)
221
... [1][2][3][4] To fill this gap, over the last 25 years, patients have developed a robust Internet-based subculture of volunteer peer support for tapering off psychiatric drugs and recovering from withdrawal syndrome. [5][6][7][8][9][10][11][12] Since 2011, under the pseudonym Altostrata, I have operated one of those online communities, SurvivingAntidepressants.org. It is frequently mentioned in articles, books, papers, and websites about psychiatric drug withdrawal, [13][14][15][16][17] even in continuing medical information about psychiatric deprescribing. ...
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Although psychiatric drug withdrawal syndromes have been recognized since the 1950s – recent studies confirm antidepressant withdrawal syndrome incidence upwards of 40% – medical information about how to safely go off the drugs has been lacking. To fill this gap, over the last 25 years, patients have developed a robust Internet-based subculture of peer support for tapering off psychiatric drugs and recovering from withdrawal syndrome. This account from the founder of such an online community covers lessons learned from thousands of patients regarding common experiences with medical providers, identification of adverse drug reactions, risk factors for withdrawal, tapering techniques, withdrawal symptoms, protracted withdrawal syndrome, and strategies to cope with symptoms, in the context of the existing scientific literature. Keywords: antidepressant, deprescribing, discontinuation syndrome, iatrogenic, kindling, post-acute withdrawal, polypharmacy, psychotropic, tapering, withdrawal syndrome
... [1][2][3][4] To fill this gap, over the last 25 years, patients have developed a robust Internet-based subculture of volunteer peer support for tapering off psychiatric drugs and recovering from withdrawal syndrome. [5][6][7][8][9][10][11][12] Since 2011, under the pseudonym Altostrata, I have operated one of those online communities, SurvivingAntidepressants.org. It is frequently mentioned in articles, books, papers, and websites about psychiatric drug withdrawal, [13][14][15][16][17] even in continuing medical information about psychiatric deprescribing. ...
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Although psychiatric drug withdrawal syndromes have been recognized since the 1950s – recent studies confirm antidepressant withdrawal syndrome incidence upwards of 40% – medical information about how to safely go off the drugs has been lacking. To fill this gap, over the last 25 years, patients have developed a robust Internet-based subculture of peer support for tapering off psychiatric drugs and recovering from withdrawal syndrome. This account from the founder of such an online community covers lessons learned from thousands of patients regarding common experiences with medical providers, identification of adverse drug reactions, risk factors for withdrawal, tapering techniques, withdrawal symptoms, protracted withdrawal syndrome, and strategies to cope with symptoms, in the context of the existing scientific literature.
... He noted the possibility that as the name (he used "brain shivers") became increasingly widely known on the internet, people with vaguely similar experiences simply adopted it for their own symptoms, hence the appearance of a regularly occurring phenomenon. 11 In 2012, Nielsen et al 12 compared symptoms resulting from the discontinuation of benzodiazepines versus SSRIs in a study reviewing 76 articles. They identified 42 symptoms associated with discontinuation, 37 of which were shared by both groups. ...
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Article
Objective: To describe the characteristics of the electrical phenomena of antidepressant discontinuation syndrome known as brain zaps and their effect on quality of life. Methods: We examined 595 unsolicited posts made by individuals frequenting a popular lay mental health website. The site was accessed between December 13, 2014, and December 12, 2016, and its content was saved in a text document. The posts had been accumulating on the site since December 2014. These posts were analyzed and separated into 648 separate statements regarding antidepressant intake. Of the statements, 378 contained reference to symptoms experienced in the context of antidepressant discontinuation. These posts were further analyzed for specifics of the medications involved, temporal characteristics of the medication intake, associated symptoms, specifics of the "zap" experience itself, and effect of the zaps on quality of life. As this was a convenience sample, only qualitative analysis was performed. Results: Venlafaxine and paroxetine were reported more frequently, and fluoxetine less frequently, in the sample compared to their frequency of prescription in clinical practice. This finding mirrors the frequency distribution of all withdrawal effects versus antidepressant prescriptions written as reported in the literature. The most likely cause of brain zaps was abrupt discontinuation of the medication, but gradual tapering had only a partial mitigating effect. An unexpected finding was the frequent association of brain zaps with lateral eye movements. The presence of brain zaps was typically transitory, but in a small number of cases it caused significant disability lasting for months or years with no treatment available. Patients' inability to obtain effective help from prescribers and the perceived lack of interest in this symptom on the part of the medical profession risks fueling antipsychiatry attitudes among patients. Conclusions: Brain zaps are a poorly understood symptom of antidepressant discontinuation, which require further study for both better prevention and treatment. The apparent association of brain zaps with lateral eye movements may open avenues for investigation of this process.
... Minerva recently drew the attention of readers of the BMJ to a report of a symptom that patients have described as "brain shivers"-attributed to venlafaxine and other antidepressants and also after venlafaxine withdrawal. 1 Other terms that have been used to describe this symptom are "electric brain thingies," "brain zaps," and "brain flips." ...
Article
BACKGROUND: Patients with depression who are treated in primary care practices may receive antidepressants for prolonged periods. Data are limited on the effects of maintaining or discontinuing antidepressant therapy in this setting. METHODS: We conducted a randomized, double-blind trial involving adults who were being treated in 150 general practices in the United Kingdom. All the patients had a history of at least two depressive episodes or had been taking antidepressants for 2 years or longer and felt well enough to consider stopping antidepressants. Patients who had received citalopram, fluoxetine, sertraline, or mirtazapine were randomly assigned in a 1:1 ratio to maintain their current antidepressant therapy (maintenance group) or to taper and discontinue such therapy with the use of matching placebo (discontinuation group). The primary outcome was the first relapse of depression during the 52-week trial period, as evaluated in a time-to-event analysis. Secondary outcomes were depressive and anxiety symptoms, physical and withdrawal symptoms, quality of life, time to stopping an antidepressant or placebo, and global mood ratings. RESULTS: A total of 1466 patients underwent screening. Of these patients, 478 were enrolled in the trial (238 in the maintenance group and 240 in the discontinuation group). The average age of the patients was 54 years; 73% were women. Adherence to the trial assignment was 70% in the maintenance group and 52% in the discontinuation group. By 52 weeks, relapse occurred in 92 of 238 patients (39%) in the maintenance group and in 135 of 240 (56%) in the discontinuation group (hazard ratio, 2.06; 95% confidence interval, 1.56 to 2.70; P<0.001). Secondary outcomes were generally in the same direction as the primary outcome. Patients in the discontinuation group had more symptoms of depression, anxiety, and withdrawal than those in the maintenance group. CONCLUSIONS: Among patients in primary care practices who felt well enough to discontinue antidepressant therapy, those who were assigned to stop their medication had a higher risk of relapse of depression by 52 weeks than those who were assigned to maintain their current therapy. (Funded by the National Institute for Health Research; ANTLER ISRCTN number, ISRCTN15969819.).
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Objective: To build on the findings of our prior study of spontaneous posts made about brain zaps on a popular lay mental health website using questions specifically targeting brain zaps in a web-based questionnaire. Methods: 3,141 responses were examined from an online questionnaire made available between June 2016 and February 2018. The questions probed the specifics of the medications taken, the temporal characteristics of medication taken, the symptoms associated with the brain zaps, the specifics of the "zap" experience itself, and their effect on quality of life. Special attention was paid to gathering data regarding the triggers of brain zaps, because in our previous study, eye movements triggering brain zaps emerged as an unexpected finding. As this was a convenience sample, qualitative analysis was primarily performed, except regarding the interaction between the half-life of antidepressants and the time to the onset of the first brain zaps, for which the numerical data appeared to be specific enough to allow such analyses. Results: The data from the targeted questionnaire showed a pattern of responses that was very similar to that obtained from analysis of the spontaneous posts. These data include the types of medications taken, the length of time these medications were taken before the onset of the zaps, the length of the zaps, the feeling quality of the zaps, and the effect of gradual versus sudden discontinuation on their onset and presence. Lateral eye movement as a trigger emerged with even more clarity than in the previous study. The positive correlation between the time from onset of the brain zaps and the half-life of the drugs strongly suggests that brain zaps are indeed associated with antidepressant discontinuation. Conclusions: Brain zaps remain a barely examined and poorly understood symptom of antidepressant discontinuation. Further studies are needed from both a prevention and treatment perspective. There is now an even stronger indication that brain zaps are typically triggered by lateral eye movements, which may open avenues for investigating this process.
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Venlafaxine is an antidepressant drug that inhibits the reuptake of serotonin and norepinephrine with different efficacies. The effects of repeated administration of this drug on the increase in the extracellular concentration of norepinephrine in the prefrontal cortex, induced by stress or by the anxiogenic drug FG 7142, were studied in freely moving rats. Exposure to foot-shock stress induced a marked increase (+120%) in the extracellular norepinephrine concentration in the prefrontal cortex of control rats. Long-term administration of venlafaxine (10 mg/kg i.p., once a day for 21 days) reduced the effect of stress on norepinephrine output by 75%. This effect of venlafaxine persisted for at least 5 days after discontinuation of drug treatment. Acute administration of FG 7142 (20 mg/kg i.p.), a benzodiazepine receptor inverse agonist, increased norepinephrine output (+90%) in control rats. Chronic treatment with venlafaxine prevented the effect of FG 7142. In contrast, the acute administration of this antidepressant had no effect on the stress- or FG 7142-induced increase in norepinephrine output. These plastic changes in the sensitivity of norepinephrine neurones to foot-shock stress and to an anxiogenic drug may reveal an important neuronal mechanism for the physiological regulation of emotional state. Furthermore, this mechanism might be relevant to the anxiolytic and antidepressant effects of venlafaxine.
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This review discusses the physiology and pharmacological treatment of vertigo and related disorders. Classes of medications useful in the treatment of vertigo include anticholinergics, antihistamines, benzodiazepines, calcium channel antagonists and dopamine receptor antagonists. These medications often have multiple actions. They may modify the intensity of symptoms (e.g. vestibular suppressants) or they may affect the underlying disease process (e.g. calcium channel antagonists in the case of vestibular migraine). Most of these agents, particularly those that are sedating, also have a potential to modulate the rate of compensation for vestibular damage. This consideration has become more relevant in recent years, as vestibular rehabilitation physical therapy is now often recommended in an attempt to promote compensation. Accordingly, therapy of vertigo is optimised when the prescriber has detailed knowledge of the pharmacology of medications being administered as well as the precise actions being sought. There are four broad causes of vertigo, for which specific regimens of drug therapy can be tailored. Otological vertigo includes disorders of the inner ear such as Ménière’s disease, vestibular neuritis, benign paroxysmal positional vertigo (BPPV) and bilateral vestibular paresis. In both Ménière’s disease and vestibular neuritis, vestibular suppressants such as anticholinergics and benzodiazepines are used. In Ménière’s disease, salt restriction and diuretics are used in an attempt to prevent flare-ups. In vestibular neuritis, only brief use of vestibular suppressants is now recommended. Drug treatments are not presently recommended for BPPV and bilateral vestibular paresis, but physical therapy treatment can be very useful in both. Central vertigo includes entities such as vertigo associated with migraine and certain strokes. Prophylactic agents (L-channel calcium channel antagonists, tricyclic antidepressants, β-blockers) are the mainstay of treatment for migraine-associated vertigo. In individuals with stroke or other structural lesions of the brainstem or cerebellum, an eclectic approach incorporating trials of vestibular suppressants and physical therapy is recommended. Psychogenic vertigo occurs in association with disorders such as panic disorder, anxiety disorder and agoraphobia. Benzodiazepines are the most useful agents here. Undetermined and illdefined causes of vertigo make up a large remainder of diagnoses. An empirical approach to these patients incorporating trials of medications of general utility, such as benzodiazepines, as well as trials of medication withdrawal when appropriate, physical therapy and psychiatric consultation is suggested.
Unprepared for the horrendous withdrawal from Effexor. International Coalition for Drug Awareness.Website. Last updated:1July Accessed: 5 http:// www.drugawareness.org/Archives/ Survivors/record 0198.html OFFICE OF TELECOMMUNICATIONS (2003) Consumers' Use of Internet - Oftel Residential Survey
  • Mangan Articles
articles MANGAN, L. (2000) Unprepared for the horrendous withdrawal from Effexor. International Coalition for Drug Awareness.Website. Last updated:1July 2000. Accessed: 5 November 2004. http:// www.drugawareness.org/Archives/ Survivors/record 0198.html OFFICE OF TELECOMMUNICATIONS (2003) Consumers' Use of Internet - Oftel Residential Survey. Q14 August 2003. London: Oftel (http:// www.ofcom.org.uk/static/archive/ oftel/publications/research/2003/ q14intres1003.pdf)
Christmas Lecturer in Psychiatry
  • M B David
David M. B. Christmas Lecturer in Psychiatry, University of Dundee, Ninewells Hospital and Medical School, Dundee DD1 9SY (e-mail: d.m.christmas@dundee.ac.uk)
Brain shivers.The Dr. Bob Home PageWebsite accessed1March http://dr-bob.securesites.com/ babble Intractable withdrawal from venlafaxine treated with fluoxetine
  • W J Davis
'DDE' (2003) Brain shivers.The Dr. Bob Home Page.Website accessed1March 2004. http://dr-bob.securesites.com/ babble/20030520/msgs/ 227974.html GIAKAS,W. J. & DAVIS, J. M. (1997) Intractable withdrawal from venlafaxine treated with fluoxetine. Psychiatric Annals, 27, 85-92.
Unprepared for the horrendous withdrawal from Effexor. International Coalition for Drug Awareness.Website. Last updated:1July Accessed: 5 Consumers' Use of Internet - Oftel Residential Survey
  • Mangan Christmas
Christmas 'Brain shivers' special articles articles MANGAN, L. (2000) Unprepared for the horrendous withdrawal from Effexor. International Coalition for Drug Awareness.Website. Last updated:1July 2000. Accessed: 5 November 2004. http:// www.drugawareness.org/Archives/ Survivors/record 0198.html OFFICE OF TELECOMMUNICATIONS (2003) Consumers' Use of Internet - Oftel Residential Survey. Q14 August 2003. London: Oftel (http:// www.ofcom.org.uk/static/archive/ oftel/publications/research/2003/ q14intres1003.pdf)
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