Scientific papers on hypnosis and brain injury

This is an attempt to make a complete up-to-date list of all literature pertaining to hypnosis and brain injury. I now consider the literature so big and dispersed that I feel quite confident that my list won’t be complete, but hopefully, it can get close. In each section, the most informative paper(s) are highlighted in green font.

This list contains many case-studies so there is likely a strong positive bias. I would advise reading the cases purely for methodological inspiration and look to the more systematic and comprehensive studies for an actual assessment of treatment effects.

I recommend reading the review by Appel (2003) as a start. It is a review on hypnosis for rehabilitation in general (not only brain injury) and is by far the most comprehensive review available so far, citing around half of the papers below.

As a side note, I was completely unaware of the scale of the literature when I undertook this search. The first version of this post contained around 10 papers and I considered it complete. One notable surprise is that the list of researchers now includes Milton Erickson and Aaron T. Beck in addition to John Kihlstrom.


Status (April 2018): Completed.

Summary of the literature: There are (large) positive effects of hypnosis on cognition following acquired brain injury.

  • Cui-ping, L. I. (2011). Influence of hypnosis therapy on recovery of hemorrhagic stroke. Journal of Taishan Medical College, 1, 025. (see my English translation and comments)
    An RCT showing large effects (SMD = 1.0 to 1.7) on Barthel, anxiety, and depression in stroke patients given ten sessions of hypnosis between one and twelve weeks after the injury onset. The study is relatively large with 120 treatment-as-usual patients of which 49 had additional adjunctive hypnosis. It was published in Chinese in a Chinese journal with impact factor 0.1, and it is unclear whether it was peer-reviewed. In general, there are many reasons to be skeptical of the quality of this paper. Nonetheless, everything else being equal, it does increase the probability that hypnosis can improve cognition following acquired brain injury. With the help of Chinese friends, I got hold of the paper and helped reading it. I’ve added a link to my translation in the reference above, containing comments to clarify particular unclear sections and dubious statistics
  • Lindeløv, J. K., Overgaard, R., & Overgaard, M. (2017). Improving working memory performance in brain-injured patients using hypnotic suggestion. Brain, 140(4), 1100–1106.
    Our study, showing a large specific effect on working memory performance of hypnotic suggestions involving the return to pre-injury (or normal) functioning. It’s an RCT with a total of 68 patients stratified to targeted hypnosis, an active control, and a passive control. The effect of four and eight treatment sessions is assessed with long-term follow-up.
  • Milos, R. (1975). Hypnotic exploration of amnesia after cerebral injuries. International Journal of Clinical and Experimental Hypnosis23(2), 103–110.
    This paper is not really on cognitive rehabilitation but it does manage to (temporarily) get retrospective reports of experiences that were otherwise inaccessible due to retrograde or anterograde amnesia during hypnosis in 7 out of 20 cases of severe injury. It was not checked whether these reports were accurate, so this is prone to confabulations or changes in response criterions rather than a true cancellation of amnesia.
  • Sullivan, D. S., Johnson, A., & Bratkovitch, J. (1974). Reduction of behavioral deficit in organic brain damage by use of hypnosis. Journal of Clinical Psychology, 30(1), 96–98.
    Later we discovered this similar study had been carried out by Sullivan et al. (1974). The Sullivan study, however, had an intervention consisting of just seven sentences repeated twice – probably less than two minutes! They obtained a small positive effect on the Picture Completion task from the WAIS battery but not on the Binder-Gestalt test. They had a quite small sample, and the two-page article leaves many details unreported.
  • Vanhaudenhuyse, A., Laureys, S., & Faymonville, M.-E. (2015). The use of hypnosis in severe brain injury rehabilitation: a case report. Acta Neurologica Belgica115(4), 771–772.
    A brief report on a 50-year case with cerebral hemorrhage, who underwent hypnosis when he was deemed chronic with severe symptoms. Hypnosis sparked further improvement. As a side note, the authors write that “To the best of our knowledge, this is the first study reporting on the integration of hypnosis as part of rehabilitation treatment of severe brain injury patients.” Well… 🙂

Motor disorders

Status (April, 2018): Approximately 70% completed. Needs a search for post-2000 literature, references, and citations

With the notable exception of Spankus & Freeman (1962) and Irawan et al. (2018), this literature consists largely of single-case studies, making it very vulnerable to publication bias. Confirming this, most studies report positive findings while Spankus & Freeman (1962) only report positive outcomes for four out of nineteen patients with cerebral palsy. Although somewhat disconcerting, this observation may not generalize to all of the literature given the large variability in the patient characteristics and treatment protocols between papers.

  • Alexander, L. (1966). Hypnosis in primarily organic illness. American Journal of Clinical Hypnosis8(4), 250-253.
  • Appel, P. R. (1990). Clinical Applications of Hypnosis in the Physical Medicine and Rehabilitation Setting: Three Case Reports. American Journal of Clinical Hypnosis, 33(2), 85–93.
    See case number two.
  • Chappell, D. T. (1961a). A Psychological Approach to Traumatic Paraplegia: Use of Hypnosis. The Journal of Nervous and Mental Disease, 132(5), 432.
  • Chappell, D. T. (1961b). The Reduction of Spasticity in Paraplegia with Hypnosis. American Journal of Clinical Hypnosis, 3(4), 213–225.
  • Chappell, D. T. (1964). Hypnosis and Spasticity in Paraplegia. American Journal of Clinical Hypnosis, 7(1), 33–36.
  • Crasilneck, H. B., & Hall, J. A. (1970). The use of hypnosis in the rehabilitation of complicate vascular and post-traumatic neurological patients. International Journal of Clinical and Experimental Hypnosis, 18(3), 145–159.
  • Diamond, S. G., Davis, O. C., Schaechter, J. D., & Howe, R. D. (2006). Hypnosis for rehabilitation after stroke: six case studies. Contemporary Hypnosis, 23(4), 173–180.
  • Holroyd, J., & Hill, A. (1989). Pushing the limits of recovery: Hypnotherapy with a stroke patient. International Journal of Clinical and Experimental Hypnosis, 37(2), 120–128.
    This is an RCT on 2 x 16 stroke patients. Although the descriptive statistics seem convincing, there are some red flags. For example, the journal seems a bit dubious, there are spelling/grammatical mistakes, and half of the citations are non-English. More content-related, the statistics are relatively poor, lacking the test of the crucial 2 (pre/post) x 2 (treatment/control) interaction term, which would be identical to the independent t-test on the change scores in each group. It does look like such a test would come out significant with a test would come out positive given the large improvement in the treatment group (d = 1) as compared to the control group (d = 0.1).
  • Manganiello, A. J. (1986). Hypnotherapy in the rehabilitation of a stroke victim: a case study. The American Journal of Clinical Hypnosis, 29(1), 64–68.
  • Mauersberger, K., Artz, K., Duncan, B., & Gurgevich, S. (2000). Can children with spastic cerebral palsy use self-hypnosis to reduce muscle tone? a preliminary study. Integrative Medicine, 2(2), 93–96.
  • Martin, J. (1983). Hypnosis also useful in rehabilitation therapy. JAMA, 249(12), 1536–1536.
  • Radil, T., Snýdrová, I., Háĉik, L., Pfeiffer, J., & Votava, J. (1988). Attempts to influence movement disorders in hemipareticsScandinavian journal of rehabilitation medicine. Supplement17, 157-161.
  • Safitri, K. H., Irawaty, D., & Masfuri, M. (2018). Effect Hypnotherapy for Increasing Muscle Strength in Stroke Patient with Hemiparesis. International Journal of Nursing, Health and Medicine, 1(1), 7–13. All alarms go off with this paper. An unknown journal, major grammatical errors (bordering on not being comprehensible), and major omissions in the reporting. Still, it’s a controlled study with 44 hemmorrhagic stroke patients, so it has larger weight than many other studies on this list. Says that “No publication of research like this before” which is obviously false, as is apparent from this list.
  • Seder, I. I., & Gelberd, M. B. (1964). Hypnosis as a Relaxant for the Cerebral Palsied Patient. American Journal of Clinical Hypnosis, 6(4), 364–365.
  • Slater, R. C., & Flores, L. S. (1963). Hypnosis in organic symptom removal: A temporary removal of an organic paralysis by hypnosis. American Journal of Clinical Hypnosis5(4), 248-255.
  • Spankus, W. H., & Freeman, L. G. (1962). Hypnosis in cerebral palsy. International Journal of Clinical and Experimental Hypnosis, 10(3), 135–139.
  • Vodovnik, L., Roskar, E., Pajntar, M., & Gros, N. (1979). Modeling the voluntary hypnosis-induced motor performance of hemiparetic patients. IEEE Trans. on Systems, Man, and Cybernetics, SMC-9 (12).
  • Yensen, R. (1963). Hypnosis and Movement Re-Education in Partially Paralysed Subjects. Perceptual and Motor Skills17(1), 211–222.

Citations without available abstract or full text below. Notice that the list includes papers on neuromuscular illnesses, even though these typically relate to the peripheral nerve system. But due to my inability to scan these papers, I keep them on the list in case they include cases of brain injury.

  • Baer, R. F. (1962). Hypnosis in the treatment of neuromuscular sequelae of injuries. Industrial medicine & surgery, 31, 315.
  • Kroger, W.S. (1970) Hypnosis therapy in neuromuscular disorders. Osteopathic Physician (1970), pp. 69-70, September.
  • Martin (1983, see above) cites a paper by Korn which I cannot find, saying: “At least Errol R. Korn, MD, can point to definite rehabilitative gains made by “dozens of patients” with stroke and spinal cord injuries in relearning the swallowing reflex, regaining muscle and balance control, and healing decubitus ulcers.”
  • Ortega DF (1978). Relaxation exercise with cerebral palsied adults showing spasticity. J Appl Behav Anal 11(4):447-451
  • E. Roskar, M. Pajntar, L. Vodovnik, and N. Gros (1977) Improvements of motor response in hemiplegic patients by means of hypnosis, in Proc. I st. Mediterranean Conf. on Med. and Biol. Engng., Sorrento, Italy, pp. 1-85-I-88.
  • E. Roskar, M. Pajntar, L. Vodovnik, and N. Gros (1978.) Improved neuromuscular activity of hemiparetic extremity due to hypnosis, Advances in External Control of Human Extremities, Yugoslav Committee for Electronics and Automation, Belgrade, pp. 257-268
  • Secter IL, Gilberd MB (1964). Hypnosis as a relaxant for the cerebral palsied patient. Am J Clin Hypn 6:363-364.
  • Shires EB, Peters JJ, Krout RM (1954) Hypnosis in neuromuscular re-education. U.S. Armed Forces Medical Journal 5: 1519–23.


Status (April 2018): Completed.

  • Kirkner, F. J., Dorcus, R. M., & Seacat, G. (1953). Hypnotic motivation of vocalization in an organic motor aphasic case. Journal of Clinical and Experimental Hypnosis, 1(3), 47–49.
  • Laures, J. S., & Shisler, R. J. (2004). Complementary and alternative medical approaches to treating adult neurogenic communication disorders: a review. Disability and Rehabilitation, 26(6), 315–325.
    Contains a very short section (page 317-318) reviewing Thompson et al. (1986) and Manganielly (1986) (see this list). Finds the results promising but insufficient due to weaknesses from inconsistency in the former and lack of objective outcome measures in the latter.
  • Macfarlane, F. K., & Duckworth, M. (1990). The use of hypnosis in speech therapy: a questionnaire study. British Journal of Disorders of Communication25(2), 227-246.
    This is just a survey on usage frequencies without an assessment of effectiveness. Also covers non-neurological speech problems.
  • Mason, C. F. (1961). Hypnotic motivation of aphasics. International Journal of Clinical and Experimental Hypnosis, 9, 297–301.
  • McKeever, W. F., Larrabee, G. J., Sullivan, K. F., Johnson, H. J., Furguson, S., & Rayport, M. (1981). Unimanual tactile anomia consequent to corpus callosotomy: Reduction of anomic deficit under hypnosis. Neuropsychologia, 19(2), 179–190.
  • Moss, C. S. (1972). Recovery with aphasia: The aftermath of my stroke. Oxford, England: U. Illinois Press.
    This is a self-report (i.e., not a scientific paper) of a clinical neuropsychologist who suffered from aphasia following a cerebral vascular incident. Moss recovered well and reports, among other things, on hypnotherapy in the process.
  • Thompson, C. K., Hall, H. R., & Sison, C. E. (1986). Effects of hypnosis and imagery training on naming behavior in aphasia. Brain and Language, 28(1), 141–153.

   Citations without available abstract or full text:

  • Glazer, M. J. (1964). A comparison of performance of predominantly expressive aphasic patients before, during and after hypnosis: a thesis (Doctoral dissertation, Tulane University).


Status (April, 2018): Approximately 50% completed. Needs a systematic search, reference search, and citation search.

  • Eisenberg, M. G., & Jansen, M. A. (1983). Rehabilitation psychology: State of the art. Annual review of rehabilitation.This review contains a quite extensive section on hypnosis for dementias. Though this is superseded by Appel the (2003) review
  • Duff, S., & Nightingale, D. (2007). Alternative Approaches to Supporting Individuals With Dementia: Enhancing Quality of Life Through Hypnosis. Alzheimer’s Care Today, 8(4), 321. is an RCT with a treatment group, an active control group (discussion groups) and a treatment-as-usual group. The participants were recruited from care homes and had vascular dementia (acquired brain injury) or dementia (unspecified…), and a few Parkinson’s patients. The intervention was quite extensive with 36 weekly sessions of hypnosis or discussion and a 12-month follow-up after that. The outcome was a questionnaire-only assessment of Quality of Life with large effects on all aspects which were all maintained after 12 months, except for relaxation. The small sample size and the subjective nature of the report are reasons to be cautious, but otherwise, it’s some of the most informative data on hypnosis for dementias to date (2018).
  • Palmieri, A., Kleinbub, J. R., Calvo, V., Sorarù, G., Grasso, I., Messina, I., & Sambin, M. (2012). Efficacy of hypnosis-based treatment in amyotrophic lateral sclerosis: a pilot study. Frontiers in psychology3, 465. A small sample of 8 ALS patients was treated using Ericksonian hypnosis during four weekly 45-minute sessions. A CD with the hypnotic induction was offered for daily home use. The effect sizes on (self-reported) depression, anxiety, and quality-of-life was beyond-large (cliff’s delta around 0.75) in general with some larger and some smaller. There were similar effects on relative-reported caregiver burden. While this study is stronger than case studies (eight times stronger?), the lack of control likely means that these effects are likely overestimated.
  • Elkins, G., Sliwinski, J., Bowers, J., & Encarnacion, E. (2013). Feasibility of clinical hypnosis for the treatment of parkinson’s disease: a case study. International Journal of Clinical and Experimental Hypnosis61(2), 172-182. Almost complete removal of tremor in a parkinson patient following three weekly hypnosis sessions. It’s hard to know from this case how well this generalizes, or whether there was something special (read: unrepresentative) about this patient.
  • Stambaugh, E. E. (1977). Hypnotic treatment of depression in the Parkinsonian patient: A case study. American Journal of Clinical Hypnosis19(3), 185-186.

Not properly vetted for this list yet (copy-pasted from Appel (2003)):

  • H.J. Wain, D. Amen, B. Jabbari The effects of hypnosis on a Parkinsonian tremor: Case report with polygraph/EEG recordings.
    Am J Clin Hypn, 33 (1990), pp. 94-98
  • F.A. Buell, J.P. Biehl The influence of hypnosis on the tremor of Parkinson’s disease
    Journal of Disorders of the Nervous System, 10 (1949), pp. 20-23
  • H.W. Bird Varying hypnotizability in a case of Parkinsonism
    Bull Menninger Clin, 12 (1948), pp. 210-217
  • M. Witz, S. Kahn Hypnosis and the treatment of Huntington’s Disease
    Am J Clin Hypn, 34 (1991), pp. 79-90
  • R. Moldawsky Hypnosis as an adjunctive treatment in Huntington’s disease
    Am J Clin Hypn, 26 (1984), pp. 229-231
  • V. Stein Hypnotherapy of involuntary movements in an 82-year-old man
    Am J Clin Hypn, 23 (1980), pp. 128-131
  • D. Vann Successful hypnotherapy for anxiety neuroses in Huntingtonı́s chorea
    Med J Aust, 2 (1971), p. 166
  • G. Ambrose Multiple sclerosis and treatment by hypnotherapy
    Am J Clin Hypn, 3 (1955), pp. 203-209
  • R.F. Baer Hypnosis, An adjunct in the treatment of neuromuscular disease
    Arch Phys Med Rehabil, 41 (1960), pp. 514-515
  • J.T. Brunn Hypnosis and neurological disease: A case report
    Am J Clin Hypn, 8 (1966), pp. 312-313 (Link)
  • J.R. Dane Hypnosis for pain and neuromuscular rehabilitation with multiple sclerosis: Case summary, literature review, and analysis of outcomes
    Int J Clin Exp Hypn, 44 (1996), pp. 208-231
  • H. McCord Hypnotically hallucinated physical therapy with a multiple sclerosis patient
    Am J Clin Hypn, 5 (1963), p. 168
  • H. McCord Hypnosis and multiple sclerosis: A brief case report
    Am J Clin Hypn, 8 (1966), pp. 313-314
  • D.Y. Medd The use of hypnosis in multiple sclerosis: Four case studies
    Contemp Hypn, 9 (1) (1992), pp. 62-66
  • B. Strauss, S. Billie Hypnosis with cerebral palsy patients, and how may it be applied
    ASCH Newsletter, 26 (6) (1985), p. 2
  • R.F. Baer Hypnosis applied to bowel and bladder control in multiple sclerosis, syringomelia and traumatic transverse myelitis
    Am J Clin Hypn, 4 (1961), pp. 22-23
  • Also check out other papers by Duff. For example, is this a fulltext? Are they merely reporting the same results as Duff (2007) at earlier stages? 

Pain, vertigo, anxiety (in progress)

Status (April, 2018): Approximately 40% completed. Needs a systematic search, reference search, and citation search.

This is a catch-all category for directly unpleasant sequelae following acquired brain injury. Sullivan et al. (1974) hypothesized that they relieved anxiety. But they never directly assessed anxiety, so I presented it on the list for cognitive rehabilitation. Fromm (1964) and Gruenewald & Fromm (1967) tried to induce catastrophic anxiety in healthy subjects.

  • Cedercreutz, C., Lähteenmäki, R., & Tulikoura, J. (1976). Hypnotic treatment of headache and vertigo in skull injured patients. International Journal of Clinical and Experimental Hypnosis, 24(3–4), 195–201.
    This paper summarizes clinical results of 155 patients with pain and/or vertigo sequelae. So this is a large portion of evidence as compared to the rest of this list. As with the other case studies, it may be prone to experimenter bias. The reported effects are quite impressive in a median of three-to-four sessions to achieve complete symptom relief in more than half of the patients.
  • Laclave, L. J., & Blix, S. (1989). Hypnosis in the management of symptoms in a young girl with malignant astrocytoma: A challenge to the therapist. International journal of clinical and experimental hypnosis37(1), 6-14.
    A single-case study on a 6½-year old girl predominantly focused on nausea following chemotherapy. I still include it on this list because of the neurogenic nature of the disease.
  • Moss, D. (2018). I hurt so: hypnotic interventions and palliative care for traumatic brain injury. Annals of Palliative Medicine, 7(1), 151–158.
    Case study with a TBI patient. Hypnosis for pain and anxiety.
  • Sapp, M. (1992). Relaxation and hypnosis in reducing anxiety and stress. Australian Journal of Clinical Hypnotherapy and Hypnosis, 13(2), 39-55. Stuff
  • Bertoni, F., Bonardi, A., Magno, L., Mandracchia, S., Martinelli, L., Terraneo, F., & Tonoli, S. (1999). Hypnosis instead of general anaesthesia in paediatric radiotherapy: report of three cases. Radiotherapy and oncology52(2), 185-190.
    Two cases of child patients with resected cerebellar tumors undergoing hypnotically induced general anesthesia.
  • Nolan, M. (2008). Hypnosis to enhance time limited cognitive-behaviour therapy for anxiety. Australian Journal of Clinical and Experimental Hypnosis36(1), 30-40.
    I was in doubt whether to include this on the list. It is the case of hypnosis with a client who self-reports transient ischemic attacks and fears a full-blown stroke, but there no direct evidence is reported for either. She did have high blood pressure and was subjected to bypass and other treatments.


Status (April 2018): Completed.

Take-home: Brain injured patients are as suggestible/hypnotizable as the general population

  • Laidlaw, T. M. (1993). Hypnosis and Attention Deficits After Closed Head Injury. International Journal of Clinical and Experimental Hypnosis, 41(2), 97–111.
    No difference in suggestibility on the HGSHS:A for young concussion patients relative to healthy controls.
  • Lindeløv, J. K., Overgaard, R., & Overgaard, M. (2017). Improving working memory performance in brain-injured patients using hypnotic suggestion. Brain, 140(4), 1100–1106.
    Our study tested 49 brain-injured patients on SHSS:C but did not compare them directly to healthy controls. However, looking at SHSS:C norms from other countries, the suggestibility of the patients seemed normal.
  • Kihlstrom, J. F., Glisky, M. L., McGovern, S., Rapcsak, S. Z., & Mennemeier, M. S. (2013). Hypnosis in the right hemisphere. Cortex, 49(2), 393–399.
    No difference in suggestibility between middle-aged stroke patients relative to young controls on AMSH.

General reviews

Status (April 2018): Completed.

  • Appel, P. R. (2003). Clinical hypnosis in rehabilitation. Seminars in Integrative Medicine, 1(2), 90–105.
    This is an impressive review of the field. For brain injury and neurological conditions, pages 96-97 are particularly relevant.
  • Appel, P. R. (2003) Clinical Hypnosis. In S. Wainapel, & A. Fast (Eds.) Alternative Medicine and Rehabilitation: A guide for practitioners. NY: Demos
    This is basically a shortened version of the excellent other Appel (2003) review. Pages 224-227 are especially relevant for neurological cases.
  • Wainapel, S. E., & Fast, A. (2002). Alternative Medicine and Rehabilitation: A Guide for Practitioners (1 edition). New York: Demos Medical.
    There is a short review on hypnosis for rehabilitation of motor dysfunction, aphasia, etc. on page 225-227. Most, if not all, of the cited literature by Weinapel is on the present list.

Citations without available abstract or full texts:

  • Wright, M. E. (1960) Hypnosis and rehabilitation. Rehabilit. Lia, 21(1), 2-12.
  • LaScolla, R. (1975). Hypnosis in stroke rehabilitation. In Scientific Proceedings of the 22nd Annual Meeting of the Am Society of Clinical Hypnosis.
  • Feher, T.L. (1987) Hypnosis in clinical neurology. In W. Wester (Ed.), Clinical Hypnosis: A Case Management Approach, Behavioral Science Center Inc. Publications, Cincinnati, OH
  • Celinski, M.J. (1992) Hypnosis in neurological rehabilitation. In W. Bongartz (Ed.), Hypnosis: 175 years after Mesmer-Recent developments in theory and application, Universitaetsverlag, Konstanz, Germany, pp. 357-362
  • Halama, P. (1993). Hypnotherapy for stroke patients. Hypnos20(3), 154-162.
  • Spellacy, F. (1992). Hypnotherapy following traumatic brain injuries. Hypnos19(1), 34-39.

Papers not fitting into the above categories

  • Gravitz, M. A. (1981). Non-verbal hypnotic techniques in a centrally deaf brain-damaged patient. International Journal of Clinical and Experimental Hypnosis29(2), 110-116.
  • Erickson, M. H. (1963). Hypnotically Oriented Psychotherapy in Organic Brain Damage. American Journal of Clinical Hypnosis, 6(2), 92–112.
    A case of hemiparesis, aphasia, and hyperalgesia following some vascular anomalities. This is Milton Erickson! After 11-months of no progress, Erickson takes on therapy in (at least) five months. There was great progress in this time, though it is not self-evident that this can be attributed to the intervention given the extensive duration of the intervention. His strategy relies heavily on frustrating the patient including lying, overruling, deceiving, etc. in front of others. I personally find his approach appalling. There is very little formal hypnosis in this paper.
  • Beck, A. T., & Guthrie, T. (1956). Psychological Significance of Visual Auras: Study of Three Cases with Brain Damage and Seizures. Psychosomatic Medicine, 18(2), 133–142. (link to PDF)
    Epilepsy following acquired brain injury. Hypnosis was employed in two cases to reveal painful emotional memories connected to the aura. Yes, Aaron T. Beck, the father of cognitive behavioral therapy (CBT) did a study on hypnosis and acquired brain injury!
  • Mittenberg, W., & Burton, D. B. (1994). A survey of treatments for post-concussion syndrome. Brain Injury, 8(5), 429–437.
    Simply shows the result of a survey, that 5.1 % (around 7 out of 165) of therapists use hypnotherapy for post-concussion patients. This is the only mention of hypnosis in the article.

Brain injury “models” in non-injured humans

Status (April 2018): Probably completed. But needs systematic search, reference search, citation search.

Take-home: healthy subjects can be hypnotized to play the role of brain-injured patients, but they are probably not realistic brain-injury models.

  • Fromm, E., Sawyer, J., & Rosenthal, V. (1964). Hypnotic simulation of organic brain damage. The Journal of Abnormal and Social Psychology, 69(5), 482.
    Hypnotized subjects (n=9) to believed that they had sustained an organic brain injury. After “hypnotic brain injury,” the subjects who experienced being in deep hypnosis were judged to be more “organic” by blinded neuropsychologists than under “hysterical” and no-hypnosis conditions, in which they were judged to be non-injured. The results from this study failed to replicate in a methodologically superior follow-up in Gruenwald & Fromm (1967).
  • Gruenewald, D., & Fromm, E. (1967). Hypnosis, simulation, and brain damage. Journal of Abnormal Psychology, 72(2), 191–192. 
    Replication of Fromm et al. (1964) with an improved method, controlling for more potential confounders. There were no difference between the hypnosis and control group judgment, actual score, or subjective experience.
  • Wagstaff, M., Parkes, M., & Hanley, J. R. (2001). A comparison of posthypnotic amnesia and the simulation of amnesia through brain injury. International Journal of Psychology and Psychological Therapy, 1(1), 67–78.
    Like Fromm (1964), but adds malingering-detection tests to the test battery, showing that “hypnotically brain injured” healthy subjects indeed do act as malingerers, not as real brain-injured patients.

Search strategy and current status of this list

Google Scholar was searched using the term “hypnosis OR “hypnotic suggestion” brain-injury OR brain-damage OR stroke OR hemiplegia OR paraplegia OR “traumatic brain” OR “diffuse axonal” OR hemorrhage”. The reference list of all hits for which I had access to full texts were scanned. For some papers, the list of papers citing that paper were scanned too, using Google Scholar.

Next steps (my to do):

  • Read Appel (2003) thoroughly again for more keywords to search on.
  • Make a histogram of publication years relative to general science publication volume.
  • Do searches on post-concussion syndrome?
  • Dementias? start with this Duff search.

Identified papers that I need to screen/comment:

  • Look into Apparently contains something on hypnosis and brain injury
  • Appel PR: Performance enhancement in physical medicine and rehabilitation. Am J Clin Hypn 35:11-19, 1992

Highlight these as best-quality (not necessarily “very good”!) publications in their field:

  • Lindeløv
  • Irawan
  • Duff
  • Cedercreutz
  • Laidlaw
  • Appel (2003)
  • Wagstaff

Hypnosis and brain injury: where to find stuff

This post is a continually updated list of important communications on research following our paper in Brain entitled “Improving working memory performance in brain-injured patients using hypnotic suggestion.”

Scientific reports

All my/our articles have associated free data and analysis. I encourage everyone to scrutinize this, e.g., with alternative analyses, and let me know what you conclude. Please notice that a pre-print is the author’s manuscript before peer-review. So it may have weaknesses that will be corrected through peer-review. Sometimes, peer review also obscures it a bit, so there are pros and cons.

My blogs with further info

  • A list of published scientific literature on hypnosis and brain injury. Three papers support the positive effect of hypnosis on cognitive sequelae following acquired brain injury. Many more have been published on motor rehabilitation, aphasia, pain, dementia, etc.
  • An anti-hype blog post: Anticipates some potential overinterpretations by the general public (particularly journalists, therapists, and patients) and counter them.
  • Answers to frequently answered questions by patients, relatives and rehabilitation professions: English and Danish.

Press and public dissemination

  • Spot on Danish national television, including a case with a 19-year old man who had sustained a traumatic brain injury in a high-speed car crash two years before enrollment in the experiment. The spot is accompanied by two articles and a radio spot (also Danish). Our impression is that this case is in the top 30% on real-life improvement, i.e. not too unrepresentative.
  • Oxford University Blog: A summary for the general public. It includes a back-of-the-envelope estimation of how much you should update your belief based on this study alone.
  • This study has been featured in multiple Danish papers, but this contains no new information that isn’t contained in the above. See my press appearances here.

Can I get the manuscript / are new studies ongoing?

We plan to make the hypnosis scripts available to everybody eventually. On the other hand, we want to avoid putting it “out in the wild” if it somehow turns out to be a fluke. So for now, we pursue a strategy where we only make non-published details about the intervention and the hypnosis scripts available to institutions/companies who can and will evaluate the effectiveness of the scripts systematically.

If you’re such an institution, we’d be eager to set up a collaboration. For example, Tryg Foundation just funded an RCT at Jobkompagniet Silkeborg which will include 90 patients. The first results are expected to be published around January 2021 with an additional report in the summer of 2022. The design and outcome measures simultaneously satisfy research purposes and Jobkompagniet’s core mission.

We expect to stick to this institution-and-evaluation-only strategy for 2-4 years until enough evidence has accumulated that we feel confident about the clinical effectiveness of hypnosis following acquired brain injury. If you’re a private therapist, if you have suffered an acquired brain injury, or if you’re a relative, we will ask you to wait until we have this evidence. Also, see FAQ and answers in the previous section.

What our paper on hypnosis following brain injury does not show

We just published a paper in Brain entitled “Improving working memory performance in brain-injured patients using hypnotic suggestion.” We argue that for patients with acquired brain injury, hypnotic suggestion which asks the patient to recover an ability to concentrate and remember improves working memory performance. I also reported the study and the results at the Oxford University Press blog, including an estimate of how skeptical you should be. We expect quite some publicity – and perhaps even hype – around the results of this paper.

Hype and overinterpretation work for advertising but not for science. In this post, I will try to counter some potential misunderstandings. We are incredibly excited about our findings. We just want to make sure that the public is excited for the right reasons and at the right level. As I argued on the OUP blog post, the appropriate state of belief is probably that of a “pessimist turned hopeful” who awaits further data to decide whether to leave the pessimistic stance or keep it. Given that brain injury constitutes the second- and third-largest health-related cost in the world, even a small hope is quite substantial.

Before I continue, I want to highlight that this research was a joint effort by Professor Morten Overgaard, hypnotist Rikke Overgaard, and me. The project was funded by the European Research Council and the Karen Elise Jensen Foundation and organized under Cognitive Neuroscience Research Unit at Center for Functionally Integrative Neuroscience and Aalborg University. The following reflect the views of all authors.

This study does not show that subjects were “cured”

The participants in our study improved to the population average in measures of working memory, which is an important but not all-encompassing cognitive function. We did not assess other domains such as psychological trauma, physical impairment, etc. because we did not target the hypnosis at these domains and therefore it was not part of the research question. Therefore, we cannot make any data-based claims about the effect of hypnosis on those domains.

Hypnosis does not involve anything “mystic” or otherwise “out of this world”

On the gray market of hypnotists, it is all too common to see the same persons offering regression to previous lives, contact with the dead, healing auras, etc. As a scientist, I reject this. In our experiment, the hypnotist sat in a chair and read aloud from a piece of paper. The patient sat in another chair and listened. There’s only a vibrating vocal chord, sound moving through the air, hitting the eardrums of the patient, and then sensory transduction to action potentials in the brain. From there, we strongly expect that the mechanism underlying the effect will eventually be identified among the on-shelf phenomena in psychology and neuroscience, e.g. neural plasticity working bottom-up, unlearning learned non-use, using a different strategy/realization of the same surface behavior, etc. The only novelness of our findings, if they replicate, would then be that these mechanisms apply to brain injury with a large effect size. There’s a long and serious research history on hypnosis in the top neuroscience journals by top researchers. See e.g. this 2013-paper in Nature Reviews Neuroscience by Oakley & Halligan. This is the line of research we are continuing, and it is very different from the current public perception of what hypnosis is.

The cognitive consequences following acquired brain injury are not unreal or hypocrisy

Some may say “if it’s that easy to recover, then it wasn’t a real problem” and perhaps even put the patient at fault. I hope you would agree with me that such a claim would be straight up ridiculous. First, such a claim would entail a psychology-only understanding of brain injury, and since we do now know the mechanism of why hypnotic suggestion works, this remains an open question. Second, even if it turns out that the cognitive impairment following acquired brain injury somehow can be described in purely psychological terms, this does not change the seriousness of the condition. PTSD is not less severe or hypocrisy because it has a psychogenic origin.

No direct evidence of clinical effectiveness (yet)

Neuropsychological test have surprisingly low predictive value for the ability to participate in society, e.g. returning to work, living independently, etc. which is often the primary criterion of clinical success in rehabilitation (sorry, psychologists!) We did not assess the latter directly, but we plan to this in an in-progress follow-up experiment. However, we do have anecdotal evidence that targeted hypnotic suggestion could be effective for participation. Many of the patients returned to us with reports of getting jobs, beginning or finishing education, not getting exhausted from grocery shopping and family parties, etc. This effect was immediate for some and slower for others. I recall one case where the patient only realized that there had been an improvement when the spouse pointed to very tangible evidence such as no more bruises from inattentively walking into stuff. Similarly, an independent psychologist was inspired by our findings and used hypnosis on two brain injured clients with excellent clinical results. But these reports are prone to selection bias (only the positive cases report back) and neglecting base-rate improvements (some would have improved anyway). We need direct evidence on clinical effectiveness, and we don’t have that now.

No direct evidence that hypnosis drives the effect (yet)

In casual talk, it’ll be easy to say that “hypnosis improved working memory.” We even do this ourselves. However, it does not follow directly from our design since both the targeted suggestion procedure and our non-targeted (intended as placebo) suggestion procedure was administered under hypnosis. We did not deliver the same treatment in a non-hypnotic setting (the so-called London-Fuhrer design). So it remains possible that hypnosis is not necessary. From the empirical literature, however, it is generally found that hypnosis boosts the effect of suggestion (though it’s disputed why; some of it is just that the Gandhi-Oakley finding that the word “hypnosis” increases suggestibility in and of itself). My best guess is that hypnosis adds considerably to the effect given that, if not, the effect of suggestion on working memory performance would have been discovered a long time ago in studies of psychotherapeutic treatment following acquired brain injury.


$$\sqrt{2}$$ is superior to Bessel’s correction

… for the estimation of the population standard deviation. That is, if you substitute $$n – 1$$ with $$n – \sqrt{2}$$, you get a much less biased estimate of the population SD. I just stumbled upon this when I desperately (!) looked to frequentist methods because of convergence problems with my bayesian model. The details can be seen in my post on Cross Validated about this curious finding as well as some excellent answers/elaborations.

I’m re-posting the simulation results here, just because they’re pretty and I want some content on this blog.

TL: no correction. TR: Bessel’s correction. BL: $$\sqrt{2}$$ correction (superior). BR: 1.5. Red: real population sd. Blue: estimated sd (corrected). Gray lines indicate different sample size with 3000 simulations per sample size. Click on the image to view the script.

Naturally, $$\sqrt{2}$$ doesn’t outperform the analytically correct solution but it is a surprisingly good approximation. For larger sample sizes (n > 10), $$n – 1.5$$ becomes superior. In any case, it’s a nice reminder that Bessel’s correction does NOT magically make the sample SD into a population SD as is currently taught in many statistics classes.

I’m considering adding this fun-fact to the Wikipedia page on unbiased estimation of the standard deviation, where you can read more about the issue of bias in frequentist estimation.


This PNAS paper could be the go-to example of how not to interpret statistics

A few days ago, a science reporter asked me to evaluate a PNAS paper titled Gender differences in the structural connectome of the human brain. As it turns out, this paper is awful. On the positive side, it’s an excellent opportunity to highlight common mistakes in psychology/neuroscience and how to do it (more) properly.

1. Minute effect sizes do not allow for bold generalizations

From abstract:

In all supratentorial regions, males had greater within-hemispheric connectivity, as well as enhanced modularity and transitivity, whereas between-hemispheric connectivity and cross-module participation predominates in females.

The paper generalizes it’s significant findings of structural brain differences between males and females to ALL males and females. Let’s evaluate how wrong you’d be to take the author’s conclusion for granted (using Common Language effect size): If you guess that a randomly picked female has got more between-hemispheric connections than a randomly picked male, you’d be wrong more than 41 % of the time. And for their second major conclusion: If you do the same tests, guessing male superiority with respect to within-hemispheric connections, you’d be wrong at least 37 % of the time. It is outright frightening to think of the possibility that policy makers could be influenced by this paper!

2. Don’t do reverse inference when you can do forward inference

From abstract:

“Overall, the results suggest that male brains are structured to facilitate connectivity between perception and coordinated action, whereas female brains are designed to facilitate communication between analytical and intuitive processing modes”.

The authors say that the (minute) structural differences explain behavioral differences between genders. This is reverse inference which can be very uninformative when applied to macrostructures such as lobes or hemispheres (read: small effect size). Therefore the same critique applies as above.

It is particularly strange that the authors did collect gender-relevant behavioral data on all subjects (see page 4, right column) but they do not statistically test them against the structural connectivity of said subjects. This is more than obvious to do if they wanted to claim that the structural differences underlie behavioral gender differences, and it could shut down critics like me if it showed a convincing relationship. The fact that they didn’t explicitly test to what extent the relationship between individual’s connectivity and behavior is modulated by gender makes me worry that it does not.

3. Interaction is required to claim developmental differences

From abstract:

“Analysis of these changes developmentally demonstrated differences in trajectory between males and females, mainly in adolescence and adulthood”.

… but the age x sex interaction is non-significant (page 3, right column). Thus it is invalid to conclude that sexes develop differently as a major part of this difference might be present at the outset. This is an all too common error in neuroscience.

4. Keep conclusions close to what’s actually tested

From abstract:

between-hemispheric connectivity and cross-module participation predominates in females.

and from significance-section:

”female brains are optimized for interhemispheric connections.

… yet they only statistical test it on connections between frontal lobes. It’s a quite violent generalization to equate a frontal lobe with a hemisphere. Figure 2 clearly indicates that almost only connections between frontal lobes are significant in females. E.g. there are no parietal-parietal or temporal-frontal connections. It seems very post-hoc (only report significant findings), and it’s certainly not a valid generalization.


If we remove the invalid parts of the abstract (and the study motivation), here’s what’s left:

“In this work, we modeled the structural connectome using diffusion tensor imaging in a sample of 949 youths (aged 8–22 y, 428 males and 521 females). Connection-wise statistical analysis, as well as analysis of regional and global network measures, presented a comprehensive description of network characteristics.”

… which is just a description of what they did without any interpretations. This is exactly the part that I like about the paper. The design is good, the data set is very impressive, and the modeling of connections between regions seems valid. I’d love to see these data in the hands of other researchers.

The fact that this paper got published in its current form is frankly discouraging for PNAS, for peer-review and the reputation of neuroscience. Let’s hope that cases like this only generalizes to the same extent as the conclusions of this paper do.


Renaming Brain Vision Recorder EEG recordings

Renaiming Brain Vision Recorder files is a pain. Here’s a python script that makes it (more of) a breeze.

The problem

Brain Vision Recorder is a widely used software for EEG-recordings. Every EEG-recording is saved as three files:

  1. One .eeg file, containing all the data
  2. One .vmrk/.amrk/.bmrk file, containing markers and a reference to the .eeg file
  3. One .vhdr/.ahdr/.bhdr file, containing header information and references to the marker file and data file. This is the file that represents the recording and opened by analysis software

Because of these internal references between the files, it is quite laborious (and risky) to rename a recording. I often rename my recordings before analysis. I use the Python script below for this purpose.

The script

import os, fileinput

# Specify folder with .eeg and meta-files
folder = '/home/jonas/Desktop/test/'

# Loop through all files
for filename in sorted(os.listdir(folder)):
    filebase, filetype = os.path.splitext(filename)

    # Only operate on selected file extensions
    if filetype in ('.eeg', '.bhdr', '.vhdr','.ahdr','.bmrk','.amrk','.vmrk'):
        print 'processing '+filename+'...'

        # Generate new name
        newname = 'XXXX' + filename

        # Actually rename file

        # Updates header and marker files to match actual filenames
        filebase, filetype = os.path.splitext(newname)
        if filetype != '.eeg':
            for line in fileinput.FileInput(folder +newname, inplace=1):
                # For header-files and marker-files
                if 'DataFile=' in line: line = 'DataFile='+filebase+'.eeg'

                # For header-files
                elif 'MarkerFile=' in line:
                    tmp_str = 'MarkerFile='+filebase
                    if filetype == '.bhdr': tmp_str +='.bmrk'
                    if filetype == '.ahdr': tmp_str +='.amrk'
                    if filetype == '.vhdr': tmp_str +='.vmrk'
                    line = tmp_str
                print line.replace('\n','')

How to modify the script

The important part is just below the “#Generate new name”. You can use this in two ways. First, you can rename your files in the browser and type in

newname = filename

This will simply update the header information in the header- and marker-files. Secondly, you can use all sorts of generative filename generation. E.g. this takes a subject ID from the middle of the filename and adds it to the front after a paradigm-name:

newname = 'aud-oddball, subject ' +filename[6:10] + filename[:6] + filename[10:]

I hope this helps someone out there.

Calculating d’, beta, c and Ad’ in Python and PHP

About d’

A central component of Signal Detection Theory is d’ – a measure of the ability to discriminate a signal from noise. The d’ is flanked by the parameters “beta” and c, which are measures of the criterion that the observer uses to discriminate between the two.

These measures can be calculated in every experiment where there is a signal (e.g. target trials) and noise (e.g. nontarget trials), and the observer (e.g. subject) is to indicate whether the signal was present or not. d’, beta and c are statistical measures in a model where noise and noise+signal are regarded as two “probability-of-detection” distributions on a “threshold-of-detection” continuum. d’ is basically a Z-score on how well the observer discriminates the two distributions, i.e. the number of standard deviations between the probability-of-response distributions for signal and noise for this given subject. c (the criterion) is the number of standard deviations from the midpoint between these two distributions, i.e. a measure on a continuum from “conservative” to “liberal”.

Every trial is scored as one of four possibilities:

  • noise + signal + response: HIT
  • noise + signal + no response: MISS
  • noise + response: FALSE ALARM (FA)
  • noise + no response: CORRECT REJECTION (CR)

It is often analyzed in terms of rates:

  • HIT RATE = HIT/SIGNALS (ratio of signals detected as signals)
  • FA RATE = FA/NON-SIGNALS (ratio of noise detected as signals)

You want to have a high hit rate and a low fa rate (hitrate > farate). Say you have conducted an experiment on a subject and calculated hitrate and farate. A signal-detection account of the subjects signal-detection-abilities can be one of the following

  • If hitrate=1 and farate=0, d’ is infinite, meaning that you signals and noise are totally separated, i.e. the distributions are non-overlapping. In that case, you have effectively discriminated signal from noise.
  • If hitrate > farate, d’ is positive, meaning that you are more likely to detect the information as signal when signal is present than when it is absent.
  • If hitrate=farate, d’=0, meaning that you are just as likely to detect signals and noise as signals, i.e. you were unable to discriminate the signal and noise and hence the probability-of-detection distributions overlap perfectly. This occurs when responses are perfectly random.
  • If hitrate < farate, d’ is negative, meaning that you have a wierd bias of primarily detecting noise as signals while ignoring the actual signals.
  • If hitrate = 0 and farate = 1, d’ is negatively infinite, meaning that you have completely confused noise and signal.

For a a more thorough introduction and guide to calculating d’/beta, “Calculation of signal detection theory measures” by Stanislaw & Todorov.

Calculating d’, beta, c and Ad’ in Python

Using the Percentile Point Function (ppf) from scipy:

from scipy.stats import norm
import math
Z = norm.ppf

def SDT(hits, misses, fas, crs):
    """ returns a dict with d-prime measures given hits, misses, false alarms, and correct rejections"""
    # Floors an ceilings are replaced by half hits and half FA's
    half_hit = 0.5 / (hits + misses)
    half_fa = 0.5 / (fas + crs)
    # Calculate hit_rate and avoid d' infinity
    hit_rate = hits / (hits + misses)
    if hit_rate == 1: 
        hit_rate = 1 - half_hit
    if hit_rate == 0: 
        hit_rate = half_hit
    # Calculate false alarm rate and avoid d' infinity
    fa_rate = fas / (fas + crs)
    if fa_rate == 1: 
        fa_rate = 1 - half_fa
    if fa_rate == 0: 
        fa_rate = half_fa
    # Return d', beta, c and Ad'
    out = {}
    out['d'] = Z(hit_rate) - Z(fa_rate)
    out['beta'] = math.exp((Z(fa_rate)**2 - Z(hit_rate)**2) / 2)
    out['c'] = -(Z(hit_rate) + Z(fa_rate)) / 2
    out['Ad'] = norm.cdf(out['d'] / math.sqrt(2))

Note the adjustment of rate=0 and rate=1, to prevent infinite values.

Calculating d’, beta, c and Ad’ in PHP

// Percentile Point Function from
function Z($p){
	$a1 = -39.6968302866538; $a2 = 220.946098424521; $a3 = -275.928510446969;
	$a4 = 138.357751867269; $a5 = -30.6647980661472; $a6 = 2.50662827745924;
	$b1 = -54.4760987982241; $b2 = 161.585836858041; $b3 = -155.698979859887;
	$b4 = 66.8013118877197; $b5 = -13.2806815528857; $c1 = -7.78489400243029E-03;
	$c2 = -0.322396458041136; $c3 = -2.40075827716184; $c4 = -2.54973253934373;
	$c5 = 4.37466414146497; $c6 = 2.93816398269878; $d1 = 7.78469570904146E-03;
	$d2 = 0.32246712907004; $d3 = 2.445134137143; $d4 = 3.75440866190742;
	$p_low = 0.02425; $p_high = 1 - $p_low;
	$q = 0.0; $r = 0.0;
	if($p < 0 || $p > 1) throw new Exception("NormSInv: Argument out of range.");
	else if($p < $p_low){
		$q = pow(-2 * log($p), 2);
		$ppf = ((((($c1 * $q + $c2) * $q + $c3) * $q + $c4) * $q + $c5) * $q + $c6) / (((($d1 * $q + $d2) * $q + $d3) * $q + $d4) * $q + 1);
	else if($p <= $p_high){
		$q = $p - 0.5; $r = $q * $q;
		$ppf = ((((($a1 * $r + $a2) * $r + $a3) * $r + $a4) * $r + $a5) * $r + $a6) * $q / ((((($b1 * $r + $b2) * $r + $b3) * $r + $b4) * $r + $b5) * $r + 1);
	else {
		$q = pow(-2 * log(1 - $p), 2);
		$ppf = -((((($c1 * $q + $c2) * $q + $c3) * $q + $c4) * $q + $c5) * $q + $c6) / (((($d1 * $q + $d2) * $q + $d3) * $q + $d4) * $q + 1);
	return $ppf;
// Credit to comment on
function erf($x) { 
        $pi = 3.1415927; 
        $a = (8*($pi - 3))/(3*$pi*(4 - $pi)); 
        $x2 = $x * $x; 
        $ax2 = $a * $x2; 
        $num = (4/$pi) + $ax2; 
        $denom = 1 + $ax2; 
        $inner = (-$x2)*$num/$denom; 
        $erf2 = 1 - exp($inner); 
        return sqrt($erf2); 
function cdf($n) { 
        if($n < 0) return (1 - erf($n / sqrt(2)))/2; 
        else return (1 + erf($n / sqrt(2)))/2; 
// Calculate d' and avoid infinity
function dPrime($hits, $misses, $fas, $crs) {
	$half_miss = 0.5/($hits+$misses);
	$half_fa = 0.5/($fas+$crs);
	$hitrate = $hits/($hits+$misses);
	$farate = $fas/($fas+$crs);
	// Avoid d' negative infinity
	if($hitrate < 0.025) {
		if($hitrate+$half_miss < 0.025) $hitrate = 0.025;
		else $hitrate = $half_miss;
	if($farate < 0.025) {
		if($farate+$half_fa < 0.025) $farate = 0.025;
		else $farate = $half_fa;
	// Avoid d' infinity
	if($hitrate > 0.975) {
		if($hitrate-$half_miss > 0.975) $hitrate = 0.975;
		else $hitrate = 1-$half_miss;
	if($farate > 0.975) {
		if($farate-$half_fa > 0.975) $farate = 0.975;
		else $farate = 1-$half_fa;
	// Calculate d' using Percentile Point function
	$out = new stdClass;
	$out->d = Z($hitrate)-Z($farate);
	$out->beta = exp((pow(Z($farate),2) - pow(Z($hitrate),2))/2);
	$out->c = -(Z($hitrate)+Z($farate))/2;
	$out->Ad = cdf($out->d/sqrt(2));
	return $out;

Note that a rate-threshold of 0.025 is used because the PHP-ppf function above is only an estimation which fails violently if this threshold is exceeded.

The case for PsychoPy

Most researchers in cognitive neuroscience have to program an experiment in a stimulus-delivery environment at some time in their career. Everyone have heard about Presentation and E-prime but much fewer have heard about PsychoPy – a free cross-platform stimulus delivery environment.

PsychoPy logo

Advantages over Presentation and E-Prime:

  1. Free and open source, meaning no license problems!
  2. Cross-platform. You can develop on Windows, Mac or Linux and run your experiment on Windows, Mac and Linux!
  3. Limitless functionality. Psychopy is a Python module, which means that it can be heavily extended with other Python modules for e.g. Matlab-level matrix operations (numpy), image and audio manipulations, advanced statistics etc.
  4. Flexible stimulus-handling: “Online” stimulus-generation, e.g. random-noise masks or moving Gaussian gratings. Also, you can define stimuli-sizes in degrees relative to the subject’s eyes, rather than having to do the trigonometry yourself.


It compares to E-Prime and Presentation on timing. I’ve tested it on our stimulus-facilities using a photosensitive diode and comparing the timing of stimuli-appearance on the monitor to the triggers sent on a parallel port. It is reliably below 0,1 ms.

In PsychoPy you can (optionally) define durations of stimuli in monitor-frames rather than milliseconds, which ensures that timing is very well-controlled.


  1. PsychoPy’s timing of audio stimuli is still not perfect. I’ve found a ~10ms jitter in audio onset (I’ve seen much worse in some C-compiled experiments…). If you need very precise audio timing, go for something else.
  2. The serious experimenter still needs to script all of his experiment. Although a very nice graphical interface is in development, it is still not thoroughly tested and tried. In my oppinion programming in Python is much cleaner and easier than E-Prime and Presentation.

Getting started:

Good introduction to Python syntax: Learn Python in 10 minutes
Download PsychoPy at and read documentation here.

Computing half-area latency in matlab/EEGLAB

In EEG research the latency of a component (hidden in the ERP) is conventionally measured as the time when the ERP is most extreme. However, this method is not well warranted, as should be clear to anyone who have read Steven Lucks excellent chapters on ERP analysis in “An Introduction to the Event Related Potential Technique”. Instead he proposes a 50% area latency method: the latency is the point in time where the area under the curve is equal on both sides. It yields the same latencies as peak-measures on symmetrical ERPs and more correct latencies on non-symmetrical ERPs, where peak-measures fails.

A first solution

If you have your ERP as an array in MATLAB, you can compute the 50% area in this way:

erp = [1,2,3,4,5,6,7,8,9,7,4,2,-2,3]; #ERP data, one point for each sample.
[~,latency_index] = min(abs(cumsum(erp)-sum(erp)/2)); #Index in array that best divides it into 50-percent area

To use it with EEGLAB (assuming you have your epoched EEG structure) you might implement it in this way:

#Get the ERP waveform as erp_data. Insert the channel-number, e.g. 5 for Fz.
[~,~,~,~,~,erp] = pop_erpimage(EEG,1, channel, [], [], 1, 1, {}, [], '', 'erp','on','noshow','on');

#Only use the part of the ERP that represents the component you're analyzing, e.g.
samples = 100:200;
erp = erp(samples);

#Get the index in the ERP, as above.
[~,latency_index] = min(abs(cumsum(erp)-sum(erp)/2))

#Get the index in milliseconds from stimulus onset.
latency_ms = (EEG.xmin + (samples(1)+latency_index)/EEG.srate)*1000;

How it works

Let’s have a look at how this works. Remember that we want to find the sample where the area is equal on both sides. It consists of the following steps:

  1. Transform the erp array into an array of cumulative sums, i.e. every element is the sum of all previous elements. E.g. the array erp=[1,3,4,0] becomes erp_cumsum = [1,4,8,8]. (try to imagine this ERP to ease your understanding). Each element then corresponds to the area that precede it in the ERP. The last element corresponds the total area of the ERP.
  2. Now the job is simply to find the midmost value in erp_cumsum, i.e. the value that separates the area into two equal parts. To do this, we subtract the half area from every element in erp_cumsum. Continuing the example from above, sum(erp)/2 = 4. The subtraction giveserp_reduced = erp_cumsum-sum(erp)/2 = [-3,0,5,5].
  3. The midmost value in erp_cumsum is now the element closest to zero (we can already see that this is sample number 2). Finding it in matlab is done by taking the absolute value, which gives erp_abs = abs(erp_reduced) = [3,0,5,5], and finding the index of the minimum value. This is simply [~,index] = min(erp_abs).

Correction: defining the direction of the component

This method is not fool-proof but things can be done to prevent some errors. Consider a positive ERP (e.g. P300) that starts and ends at negative values, .e.g erp = [-3,0,5,2,-1,-4]. This is a very nice peak and visually you would consider it all to be part of the P300. However, using cumulative sums, the start and end would be “negative area”, which doesn’t make sense when we’re trying to find a latency.

The solution starts off by defining whether you’re looking for the latency of a positive or a negative peak. Then you adjust your ERP to only contain positive or negative values by raising or lowering the whole ERP so that all elements have the same sign. In this example, we’re looking for a positive component and then we raise the ERP by 4. If we were looking for a negative component, we’d lower the ERP by 5. So:

# For positive components:
erp_adjusted = erp-min(erp) = [1,4,9,6,3,0]; 

# For negative components:
erp_adjusted = erp-max(erp) = [-8,-5,-3,0,-6,-9];

Extending it to multiple ERPs

Say you’re dealing with multiple ERPs and want to calculate 50% latencies on all of them. You want to put in e.g. 50 ERPs and get 50 latencies as output. This is practical if you want to calculate latencies on individual trials to investigate variability or on multiple subjects at the same time. This is where Matlab’s excellent matrix operations get to work. I don’t want to go into details on this one. I’m just going to give you the code for positive-going components in single-trial ERPs:

samples = 100:200;
erp_matrix = pop_erpimage(EEG,1, channel, [], [], 1, 1, {}, [], '','noshow','on');
erp_adjusted = bsxfun(@minus,erp_matrix(samples,:),min(erp_matrix(samples,:)));
[~,latency_indicies] = min(abs(bsxfun(@minus,cumsum(erp_adjusted),sum(erp_adjusted)/2)));
latencies = (EEG.xmin + (samples(1)+latency_indicies)/EEG.srate)*1000;