By Mayo Clinic staff
Post-concussion syndrome is a complex disorder in which a combination of post-concussion symptoms — such as headaches and dizziness — last for weeks and sometimes months after the injury that caused the concussion.
Concussion is a mild traumatic brain injury, usually occurring after a blow to the head. Loss of consciousness isn't required for a diagnosis of concussion or post-concussion syndrome. In fact, the risk of post-concussion syndrome does not appear to be associated with the severity of the initial injury.
In most people, post-concussion syndrome symptoms occur within the first seven to 10 days and go away within three months, though they can persist for a year or more. Post-concussion syndrome treatments are aimed at easing specific symptoms.
Signs and symptoms
Symptoms can appear immediately, or weeks to months after the initial injury. Their severity lessens progressively over time. The nature of the symptoms tends to change over time: they are most commonly of a physical nature following the injury, but tend to become predominantly psychological later. Signs and symptoms such as noise sensitivity, problems with concentration and memory, irritability, depression, anxiety, fatigue, and poor judgment may be called 'late symptoms' because they generally do not occur immediately after the injury, but rather days or weeks afte.r Nausea and drowsiness commonly occur early after concussion but usually do not last, while headache and dizziness occur immediately after the injury and are long lasting.
The main PCS symptom is headache. While most people have headaches of the same type they experienced before the injury, people with PCS often report more frequent or longer-lasting headaches. Between 30 and 90% of people treated for PCS report having more headaches than they did before the injury, and between 8 and 32% still report them a year after the injury.
Dizziness, the second most common symptom, occurs in about half of people with PCS and is still present in up to a quarter of them a year after the injury. Older people are at especially high risk for dizziness. About 10% of people with PCS develop sensitivity to light or noise, about 5% experience a decreased sense of taste or smell, and about 14% have blurred vision. People may also have double vision or ringing in the ears, also called tinnitus. Loss of hearing occurs in 20% of cases. PCS may cause insomnia, fatigue, sleepiness, or other problems with sleep. Other physical symptoms include nausea and vomiting.
Symptoms have an organic basis.
The fact that these complaints seem to contradict the "negative" medical findings has often generated controversy as to whether post-concussion syndrome has an organic or psychological basis.
However, over the past 30 years evidence for an organic (brain based) aetiology (original cause) of post-concussion syndrome has accumulated through studies of cerebral blood flow, neuropsychological deficits, evoked potential recordings, PET, SPECT, MRI and quantitative EEG or QEEG . The nature of concussive head injury has been extensively discussed and theoretical concepts have been formulated which are supported by QEEG evidence.
The question of the cause or causes of PCS have been heavily debated for many years. It is not known to exactly what degree the symptoms are due to organic factors, such as microscopic damage to the brain, and to other factors, such as psychological ones. The subjectivity of the complaints complicates assessment and makes it difficult to determine whether symptoms are being exaggerated or feigned.
It is possible that some post-concussion symptoms are due to physical causes while others are psychological. One hypothesis holds that physiological factors are responsible for early symptoms that occur after mild head trauma, whereas symptoms that occur later are due to psychological factors.
While the cause of symptoms occurring shortly after head trauma is likely to be physiological nonorganic factors are likely to be involved in symptoms that last longer than three months.
Some experts believe post-concussion symptoms are caused by structural damage to the brain or disruption of neurotransmitter systems, resulting from the impact that caused the concussion. Others believe it is related to psychological factors, especially since the most common symptoms — headache, dizziness and sleep problems — are similar to those often experienced by people diagnosed with depression, anxiety or post-traumatic stress disorder. In many cases, both physiological effects of brain trauma and emotional reactions to these effects play a role in the development of symptoms.
Researchers haven't determined why some people who've had concussions develop persistent post-concussion symptoms while others do not. There has been no proven correlation between the severity of the injury and the likelihood of developing persistent post-concussion symptoms.
Minor Traumatic Brain Injuries
Post-concussion syndrome is the name given to the 10% of people who have a minor closed head injury and experience a range of symptoms such as mood and anger problems, concentration difficulties, headaches and fatigue that may persist for years, sometimes for life. More often than not these people are treated for the symptoms with little if any efficacy.
When the head receives a sharp blow, the difference in the movement between the brain and the skull produces forces that result in traumatic brain injuries (TBIs). Although maximum injury is suffered at the point of impact, the frontal and temporal regions have been shown to be consistently vulnerable to contusions regardless of the direction or the point of impact due to percussion and shearing forces on delicate brain tissue. A "contre-coup" due to a percussion wave travelling through the brain matter and impacting the skull diagonally opposite can cause further contusion, and shear forces at the boundary between white and grey matter can result in axonal shearing.
The term Post-concussion syndrome or post-concussional disorder has been used to describe the range of residual symptoms that persist 12 months and beyond, sometimes years after the injury. Although minor head injuries are generally considered benign, a significant number of people report persistent symptoms for weeks or months and some for years after injury despite a lack of evidence of brain abnormalities on MRI and CT scans. The core deficits of post-concussion syndrome overlap with those of Attention Deficit Disorder, Adjustment disorder and Mood Disorders. In addition, sufferers often report memory and socialization problems, frequent headaches and personality changes.
The cluster of symptoms reported by these patients is referred to as the Post-concussion syndrome. The following are amongst the most commonly reported symptoms of post-concussion syndrome:
Often despite several of these chronic symptoms, there is no evidence of brain abnormality from conventional structural neuroimaging tests, such as CT scans and MRIs. Consequently the person can be labelled a "hot head" with a "short fuse" or as having either a mood disorder or anger problem, or as having a personality or psychological disorder.
Psychological and behavioral
Psychological symptoms, which are present in about half of people with PCS, may include irritability, anxiety, depression, and a change in personality. Other emotional and behavioral symptoms include restlessness, aggression, mood swings, anger, decreased libido, impulsiveness, loss of social judgment, and lack of ability to tolerate stress or alcohol . People with PCS may also display a lack of emotion, emotional liability or mood swings. Another common symptom—apathy, or lack of motivation—may result directly from the syndrome or be secondary to depression.
Higher mental functions
Cognitive or mental symptoms can include confusion or impaired cognition, problems with attention, impaired judgment, and amnesia or other problems with memory, especially short-term memory. Problems with memory and attention are the longest-lasting cognitive symptoms. one in four people with PCS still suffer from memory problems a year after the injury. PCS may cause slowed information processing and reactions to stimuli or difficulty with abstract thinking] or problem solving. People may also experience a decrease in abilities related to work performance or social interaction. While cognitive symptoms usually resolve within a few months of injury, physical and emotional symptoms can last longer.] Most cognitive symptoms clear within half a year of the injury, and the longest-lasting ones, such as memory, attention and language problems, usually resolve within a year.
Post-concussion syndrome is usually not treated, though specific symptoms can be addressed; for example, people can take pain relievers for headaches and medicine to relieve depression, dizziness, or nausea. Rest is advised, but is only somewhat effective. Physical and behavioral therapy may also be prescribed for problems such as loss of balance and difficulties with attention, respectively.
Treatment of Post-Concussion Syndrome
A review paper in the October 2004 issue of Clinical EEG and Neuroscience concluded that QEEG was the most sensitive neuroimaging tool for the assessment of post-concussion syndrome and that Neurotherapy had been shown to be the most promising treatment to date for post-concussion syndrome.
Medication, Counseling and Cognitive Rehabilitaton
Medication may provide temporary relief from pain and counselling may help some persons understand the need to control their impulses and anger. However, there is no evidence in the literature that medication or cognitive rehabilitation can effectively restore cognitive deficits or concentration in post-concussion syndrome.
Though no pharmacological treatments exist especially for PCS, if necessary, doctors may prescribe medications used for symptoms that also occur in other conditions; for example, anti-depressants are used for the depression that frequently follows TBI. Side effects of medications (pharmaceuticals) may affect people suffering the consequences of TBI more severely than they do others, and thus it is recommended that medications be avoided if possible; there may be a benefit to avoiding narcotic medications. In addition, headache medications may cause rebound headaches when they are discontinued.
Basically there is not much in the way of help to be had. Medical marijuana may be the only logical alternative treatment for symptoms.
Jeffrey Hergenrather, MD " In my opinion, there is no better drug for the treatment of anxiety disorders, brain trauma and post concussion syndrome."
"Marijuana is the only thing that helps me, physically and mentally as I started using almost on a daily basis now early this summer ....I've used on occasion through out highschool but a few times a year....I truly believe it has helped save my life and/or get my life back together and am starting to enjoy life again, as I was severly depressed given my life was gone at 20 years old. It takes my nausea away, makes me relax and stop dwelling on my symptoms and future."
"Cannabis has been shown to reactivate brain cells as well as regenerate new growth."
Recommendation: Whole plant extract (Indica x Sativa hybrid), tincture, edibles, vaporize, spray.
. Thatcher, R.W., EEG operant conditioning (biofeedback) and traumatic brain injury. Clin Electroencephalography, 2000. 31(1): p. 38-44.
2. Hugenholtz, H., et al., How long does it take to recover from a mild concussion? Neurosurgery, 1988. 22(5): p. 853-8.
3. Slagle, D.A., Psychiatric disorders following closed head injury: an overview of biopsychosocial factors in their etiology and management. Int J Psychiatry Med, 1990. 20(1): p. 1-35.
4. Fenton, G.W., The postconcussional syndrome reappraised. Clin Electroencephalogr, 1996. 27(4): p. 174-82.
5. Ponsford, J. and G. Kinsella, Attentional deficits following closed-head injury. J Clin Exp Neuropsychol, 1992. 14(5): p. 822-38.
6. Ponsford, J., S. Sloan, and P. Snow, Traumatic Brain Injury: Rehabilitation for everyday adaptive living. 1995, Hillsdale (USA): Lawrence Erlbaum Associates.
7. Zwil, A.S., M.E. Sandel, and E. Kim, Organic and psychological sequelae of traumatic brain injury: the postconcussional syndrome in clinical practice. New Dir Ment Health Serv, 1993(57): p. 109-15.
8. Stevens, M.M., Post concussion syndrome. J Neurosurg Nurs, 1982. 14(5): p. 239-44.
9. Elkind, A.H., Headache and facial pain associated with head injury. Otolaryngol Clin North Am, 1989. 22(6): p. 1251-71.
10. Fann, J.R., et al., Psychiatric disorders and functional disability in outpatients with traumatic brain injuries. Am J Psychiatry, 1995. 152(10): p. 1493-9.
11. Munoz-Cespedes, J.M., et al., [The nature, diagnosis and treatment of post-concussion syndrome]. Rev Neurol, 1998. 27(159): p. 844-53.
12. Pelczar, M. and B. Politynska, [Pathogenesis and psychosocial consequences of post-concussion syndrome]. Neurol Neurochir Pol, 1997. 31(5): p. 989-98.
13. Harrington, D.E., et al., Current perceptions of rehabilitation professionals towards mild traumatic brain injury. Arch Phys Med Rehabil, 1993. 74(6): p. 579-86.
14. Binder, L.M., Persisting symptoms after mild head injury: a review of the postconcussive syndrome. J Clin Exp Neuropsychol, 1986. 8(4): p. 323-46.
15. Hilton, G., Behavioral and cognitive sequelae of head trauma. Orthop Nurs, 1994. 13(4): p. 25-32.
16. Hillier, S.L., M.H. Sharpe, and J. Metzer, Outcomes 5 years post-traumatic brain injury (with further reference to neurophysical impairment and disability). Brain Inj, 1997. 11(9): p. 661-75.
17. Millis, S.R., et al., Long-term neuropsychological outcome after traumatic brain injury. J Head Trauma Rehabil, 2001. 16(4): p. 343-55.
18. Hillier, S.L. and J. Metzer, Awareness and perceptions of outcomes after traumatic brain injury. Brain Inj, 1997. 11(7): p. 525-36.
19. Johansson, E., M. Ronnkvist, and A.R. Fugl-Meyer, Traumatic brain injury in northern Sweden. Incidence and prevalence of long-standing impairments and disabilities. Scand J Rehabil Med, 1991. 23(4): p. 179-85.
20. Malia, K., G. Powell, and S. Torode, Personality and psychosocial function after brain injury. Brain Inj, 1995. 9(7): p. 697-712.
21. Max, J.E., B.A. Robertson, and A.E. Lansing, The phenomenology of personality change due to traumatic brain injury in children and adolescents. J Neuropsychiatry Clin Neurosci, 2001. 13(2): p. 161-70.
22. Gerring, J., et al., Neuroimaging variables related to development of Secondary Attention Deficit Hyperactivity Disorder after closed head injury in children and adolescents. Brain Inj, 2000. 14(3): p. 205-18.
23. Voller, B., et al., Neuropsychological, MRI and EEG findings after very mild traumatic brain injury. Brain Inj, 1999. 13(10): p. 821-7.
24. Jansen, H.M., et al., Cobalt-55 positron emission tomography in traumatic brain injury: a pilot study. J Neurol Neurosurg Psychiatry, 1996. 60(2): p. 221-4.
25. Rudolf, J., et al., Cerebral glucose metabolism in acute and persistent vegetative state. J Neurosurg Anesthesiol, 1999. 11(1): p. 17-24.
26. Bergsneider, M., et al., Cerebral hyperglycolysis following severe traumatic brain injury in humans: a positron emission tomography study. J Neurosurg, 1997. 86(2): p. 241-51.
27. Matz, P.G. and L. Pitts, Monitoring in traumatic brain injury. Clin Neurosurg, 1997. 44: p. 267-94.
28. Thatcher, R.W., et al., Biophysical Linkage between MRI and EEG Amplitude in Closed Head Injury. Neuroimage, 1998. 7(4): p. 352-367.
29. Thatcher, R.W., et al., Biophysical linkage between MRI and EEG coherence in closed head injury. Neuroimage, 1998. 8(4): p. 307-26.
30. Thatcher, R.W., et al., Quantitative MRI of the gray-white matter distribution in traumatic brain injury. J Neurotrauma, 1997. 14(1): p. 1-14.
31. Shaw, N.A., The neurophysiology of concussion. Prog Neurobiol, 2002. 67(4): p. 281-344.
32. Montgomery, E.A., et al., The psychobiology of minor head injury. Psychol Med, 1991. 21(2): p. 375-84.
33. Duff, J., The usefulness of Quantitative EEG (QEEG) and Neurotherapy in the Assessment, and Treatment of Post-Concussion Syndrome. Clinical EEG and Neuroscience, 2004. 35(4): p. 1-12.
34. Hughes, J.R. and E.R. John, Conventional and quantitative electroencephalography in psychiatry. Journal of Neuropsychiatry and Clinical Neurosciences, 1999. 11(2): p. 190-208.
35. Thatcher, R.W., et al., EEG discriminant analyses of mild head trauma. Electroencephalogr Clin Neurophysiol, 1989. 73(2): p. 94-106.
36. Thatcher, R.W., et al., QEEG and traumatic brain injury: rebuttal of the American Academy of Neurology 1997 report by the EEG and Clinical Neuroscience Society. Clin Electroencephalogr, 1999. 30(3): p. 94-8.
37. Gordon, E., Integrative neuroscience in psychiatry: the role of a standardized database. Australasian Psychiatry, 2003. 11(2): p. 156-163.
38. Lubar, J.F., Discourse on the development of EEG diagnostics and biofeedback for attention-deficit/hyperactivity disorders. Biofeedback and Self Regulation, 1991. 16(3): p. 201-225.
39. Sterman, M.B., Sensorimotor EEG operant conditioning: Experimental and clinical effects. Pavlovian Journal of Biological Science, 1977. 12(2): p. 63-92.
40. Sterman, M.B., EEG biofeedback: physiological behavior modification. Neurosci Biobehav Rev, 1981. 5(3): p. 405-12.
41. Thompson, L. and M. Thompson, Neurofeedback combined with training in metacognitive strategies: Effectiveness in students with ADD. Applied Psychophysiology and Biofeedback, 1998. 23(4): p. 243-263.
42. Thatcher, R.W., Normative EEG databases and EEG biofeedback. Journal of Neurotherapy, 1998. 2(4): p. 8-39.
43. Thatcher, R.W., EEG database guided neurotherapy, in Introduction to Quantitative EEG and Neurofeedback, A. Abarbanel, Editor. 1999, Academic Press: San Diego.
44. Sterman, M.B., Physiological origins and functional correlates of EEG rhythmic activities: Implications for self-regulation. Biofeedback and Self Regulation, 1996. 21(1): p. 3-33.