Concussion Assessment

Introduction[edit | edit source]

Assessment and management of concussion is described as a quick onset of short-lived neurologic impairments that resolve spontaneously usually with the first 7-10 days. Loss of consciousness may or may not occur with a concussion.[1] Concussion results in a constellation of physical, cognitive, visual, emotional, and sleep-related disturbances. Signs and symptoms are broad and include headache, dizziness, gait and balance disturbance, nausea, vomiting, photophobia, trouble focusing, and fatigue. A person with concussion may have slowed mental processing, concentratin deficits, memory impairment, irritability, anxiety and depression. [2][3]Amnesia and loss of consciousness are considered the most critical signs indicating the severity of the injury. These factors would indicate the need for further intervention and imaging.[4]

Emotional Assessment[edit | edit source]

An assessment to address emotional stability is beyond the scope of the physiotherapist.The gold standard for the diagnosis of mental disorders remains the structured clinical interview with a neuropsychologist. Self-report measures can play an important role in screening patients in the physiotherapy setting for referral to a Neuropsychologist/neuropsychiatrist. 

Research has shown that concussions can cause new-onset anxiety, and can worsen existing anxiety.[5][6][7] Individuals with a mental health history are at risk for greater depressive and anxiety symptoms post-injury[8] worsening of their pre-existing mental health condition[9], and development of a novel mental health condition.[10] Neurometabolic disturbance secondary to concussion exhibits a similar pattern of brain alterations as individuals diagnosed with clinical depression on advanced neuroimaging.[11] There is evidence of alterations in limbic-frontal circuitry after concussion that resembles the functional alterations seen in major depression.[12]

Other neurochemical changes consistent between mood disorders and concussion are the presence of serotonin disturbance[13] and decreased dopamine in the prefrontal cortex and brainstem.[12][14]Organic brain changes may provide an explanation for mood and anxiety symptoms post-injury in the absence of pre-injury mental health conditions. Anxiety is often triggered by a vestibular event, though maybe maintained by psychosomatic factors.[15] For instance, an athlete with a vestibular disturbance may experience dizziness and anxiety when running sprints at practice, and then begin avoiding any physical activity or movement of their head for fear of re-experiencing the dizziness. When conducting vestibular-oculomotor screening, clinicians should be aware of signs of anxiety given the overlap in the symptoms of anxiety and vestibular dysfunction. If anxiety is not properly identified and addressed, it may interfere with the efficacy of treatment.[16]

Sequencing of Evaluation[edit | edit source]

There is a sequencing of events that physical therapists should go through when evaluating a patient who had a concussive event. Based on the patient's symptoms and probably level of irritability, the PT should plan to strategically sequence or delay assessments as needed. Examinations should begin with tests that are the least irritable progressing to more irritable as tolerated.

It is recommended for PTs to triage first neck pain irritability, followed by dizziness and headache. If the patient has high neck irritability without any pathological cause, the PT should assess cervical and thoracic spine muscular dysfunction and address any issues appropriately. If the patient has dizziness, headache or vertigo, the PT should thoroughly examine for cervical and thoracic dysfunction, oculomotor and vestibular dysfunction, orthostatic dysfunction to determine if any of these issues are contributing to the symptoms.

After triaging headache, dizziness and pain, PTs should complete a comprehensive evaluation of all domains based on clinical judgement.[17]

Cognition: Concussion and Clinical Reaction Time[edit | edit source]

Clinical Reaction Time[edit | edit source]

Impaired reaction time (RT) is one of the most common cognitive sequelae of concussion. It represents one of the most sensitive indices of cognitive change following concussion[18] and has prognostic value in predicting time to recovery.[19] Reaction time deficits occur after injury,[20] with a gradual return to baseline.[21][22] Impaired RT generally parallels the presence of other self-reported concussion symptoms[23][24] but in some athletes RT remains impaired even after the athlete has become asymptomatic.[25][26][24]  RT is an important component of the physiotherapist’s concussion assessment toolkit that can increase the sensitivity of the clinical examination for detecting the effects of concussion.

Dr James Eckner created a test that involves a systematic approach to dropping a weighted stick that is calibrated to reflect speed of reaction for catching it. The athlete holds his or her hand around, but not touching, a rubber puck at the bottom of the stick, then the physiotherapist drops the stick, and the athlete catches it on the way down. The physiotherapist marks where his hand lands, and this becomes a baseline measure of athlete’s reaction time. Theoretically, should a player later be suspected of having sustained a concussion, the physiotherapist could pull out the dowel-puck, repeat the test, and, if the player’s reaction time were slower, conclude that he or she likely was concussed. RT appears sensitive to the effects of concussion and distinguished concussed and non-concussed athletes. The dowel-puck RT test is simple, low cost, and requires minimal time.[27]

Puck and Dowel Test.jpg

Figure 1- Dr. James T. Eckner of the University of Michigan administering the puck-and-dowel ruler test to check for a possible concussion. Credit:Dr. Steven Broglio

Neurocognitive Assessment Tools (NCATs)[edit | edit source]

The assessment of cognitive functioning is an important aspect in the management of concussion. However, the psychometric properties, especially validity, and clinical utility of NCATs have yet to be consistently established.[28] CogState/Axon/CogSport is commonly used in Australian athletics and South African Rugby. CogSport is a computerized neuropsychological test battery that measures psychomotor function, speed of processing, visual attention, vigilance, and verbal and visual learning and memory.[29] The computerised test employs a series of eight “card games” to examine cognitive function including simple reaction time, complex reaction time, and one-back and continuous learning.

Similary, Immediate Post-Concussion Assessment and Cognitive Testing (ImPACT) is another online computerized neuropsychological test battery composed of three general sections:

  1. Part 1- athletes input their demographic and descriptive information (includes sport participation history, history of alcohol and drug use, learning disabilities, attention deficit hyperactive disorders, major neurological disorders, and history of previous concussion).
  2. Part 2- the athletes self-reports any of 22 listed concussion symptoms, which they rate using a 7-point Likert scale.
  3. Part 3- consists of six neuropsychological test modules that evaluate the subject's attention processes, verbal recognition memory, visual working memory, visual processing speed, reaction time, numerical sequencing ability, and learning.

ImPACT is reported to have good sensitivity, specificity and construct validity with standard neuropsychological tests that are sensitive to cognitive functions associated with mTBI[30] however its test-retest reliability has been shown to be somewhat inconsistent. Although neurocognitive tests can contribute to the overall clinical picture, they should not be considered in isolation or favoured over multidimensional clinical assessment approaches. Future research that improves the objective diagnosis of concussion and highlights individual risk factors, as well as patterns of clinical recovery, and the ability of the NCAT to help the clinician with return to play decisions will inform best practice in concussion management programs.[31]

Somatosensory: Postural Control And Concussion[edit | edit source]

Concussion symptoms normally resolve within 7-10 days but vertigo, dizziness and balance dysfunction persist in up to 10-30% of cases causing significant morbidity (Murray et al, 2017) and are the strongest predictors to prolonged recovery following concussion.[32] Deficits in postural control may be evident as early as 24 hours post-concussion and can last for up to six months.[33]

During a concussive event, damage can occur to the vestibulo-ocular system as well as the afferent input from the cervical spine. The altered messages arising from these systems can lead to changes in the efferent input to the somatosensory system and a crescendo of maladaptive patterns may occur.  Previously concussed participants demonstrate a delayed ability to selectively enhance specifically relevant somatosensory information,in comparison with healthy controls.[34] This may lead to further deficits in balance, proprioception and body position, and if unaddressed may leave athletes vulnerable to further concussive and lower extremity musculoskeletal injuries.

Force of impact has been shown to be reduced by 67% when the head is aligned with the torso.[35] Adequate proprioception of cervical and lumbar trunk muscles helps to minimise injury by enhancing the player’s ability to pre-set the head in an optimal position.[36]. These muscle groups are largely modulated by the vestibulo-spinal system where alteration in input can lead to changes in the deep cervical and trunk muscles. For this reason, we need to look at testing trunk and cervical proprioception. Understanding the effects of concussion on the postural control system is imperative to complete a physiotherapy assessment.

Assess the Cervical Spine[edit | edit source]

Normalisation of range and a decrease in pain symptoms is imperative for concussion patients. As part of the manual therapy assessment, you need to assess for the following:

  • Whiplash associated disorder
  • Cervicogenic headaches
  • Cervicogenic dizziness
  • Temporomandibular dysfunction
  • Assess for Deep neck extensor and flexor motor control dysfunction
  • Assess cervical strength and endurance

Proprioception or Cervical Joint Position Error (JPE)[edit | edit source]

This test is considered a primary measure of mismatched cervical afferent input leading to abnormalities with sensorimotor control.The test is positive in whiplash patients[37]

Laser mounted on head test[38]

  • Laser point fixed to a headband, sitting 90 -100 cm away from a wall with the patient’s head in neutral. Align the laser with the centre of the bull's eye target on the wall.
  • Patient closes eyes and then rotates their head and then returns to neutral (i.e. as close to the centre of the bull's eye target as possible).
  • Patient now opens their eyes to see where the laser has stopped. We now measure the average difference between the start and end position after 3 tries to each side.
  • A difference of more than 6.5 cm shows a dysfunction (positive test) - normal is approximately 3-5 cm from the centre of the target.
  • Patients with poor proprioception may have jerky movements, or “search” for the right position, or overshoot (sign of altered cervicocollic reflex), some patients may complain of feelings of dizziness or unsteadiness during the test.

Smooth Pursuit Neck Torsion (SPNT) Test[edit | edit source]

Part 1 of the test-Tests for eye movement control with the head and trunk in neutral. Then it is compared with part 2 of the test when the trunk is rotated[38] . The head sits in neutral over the trunk. The patient is asked to follow a pen with their eyes in a figure of 8 pattern.

Symptoms include:

  • Quick saccadic eye movements - it looks like the eye is trying to catch up with the object, especially in mid-range
  • Reproduction of patient’s symptoms like dizziness or blurry vision

Part 2 of the test-This test detects eye movement changes due to changes in the cervical afferent input.[38] The head remains in neutral while the trunk is rotated 45 degrees[37] in either direction.[38] With a positive test:

  • There is a change in eye movement control when the trunk is rotated[37]or an increase in saccadic eye movements
  • It’s usually seen in patients with neck pain due to whiplash.[38]

Test outcome:

Sensorimotor impairment- Change in eye movements when trunk is rotated (Part 2 of the test) but normal eye movements/ no symptoms with head and trunk in neutral (Part 1 of the test)

If the patient has poor performance with the head and trunk in neutral (Part 1 of the test) and the performance remains the same with the trunk rotated (Part 2 of the test) then it is most likely a CNS disorder and not sensorimotor impairment.[38]

Assessment Of Vestibulospinal System[edit | edit source]

The vestibulospinal system is responsible for postural control. Balance is commonly disrupted[39][40], especially within the first few days after a concussion.[40][41] Balance impairments alone as a measure of a vestibular system injury may be limited because objective clinical balance impairments recover for the majority of athletes within 3 to 5 days after the injury.[41][42]

The Balance Error Scoring System (BESS) or the Sensory Organization Test (SOT) is commonly used to assess static vestibular impairments after concussion. However these tests only represent the vestibulospinal aspect of the vestibular system. These tests do not address dynamic aspects of the vestibular system or vestibulo-ocular control. 

Balance Error Scoring System (BESS)[edit | edit source]

The BESS is an objective measure of assessing static postural stability or balance (designed for the mild head injury population, to assist in return to sports play decisions).  It consists of six stances, three on a firm surface and the same three stances on an unstable (Airex foam) surface.[41][42]The athlete  stands with eye closed and hands on iliac crests for 20 seconds in 3 stances: feet together, single-leg stance on the person's non-dominant leg and tandem stance (standing heel to toe with non-dominant foot at the back) .[41][42]

For every error made (lifting hands off the iliac crests, opening the eyes, stepping, stumbling, or falling, moving the hip into more than a 30 degree of flexion or abduction, lifting the forefoot or heel), one point is given. If the patient remains out of the testing position for more than 5 seconds, the highest possible score of 10 is given,The higher the score, the worse the athlete has performed. The maximum total number of errors for any single condition is 10.

The BESS test has very good test-retest reliability[42] , low to moderate sensitivity, with high specificity [43]. The BESS has only been found to be useful within the first 2 days following injury[43][22]

BESS Test.JPG  

Figure 2- The testing conditions for the BESS test

Sensory Organization Test (SOT)[edit | edit source]

Postural stability is the ability to control the centre of mass (COM) in relation to a person's base of support and can be affected by both musculoskeletal injury and traumatic brain injury. The NeuroCom SOT can be used to objectively quantify impairments to postural stability. This test has the ability to predict injury, and can be used as an acute injury-evaluation tool in the screening and rehabilitation process.

The SOT uses a force plate to create six sensory conditions to objectively test for any abnormalities in the patient's use of somatosensory, visual, and vestibular systems to maintain postural control. The test conditions systematically eliminate useful visual and proprioceptive information in order to assess the patient's vestibular balance control and adaptive responses of the central nervous system.[44] The SOT has limitations as it is impractical for sideline use and the equipment is costly. It is reported to have a low sensitivity but high specificity.[43]

Sensory Organisation Test.JPG

Figure 3- The Six conditions of the Sensory Organisation Test

CONCUSSION AND BENIGN POSITIONAL PAROXYSMAL VERTIGO (BPPV)[edit | edit source]

Dizziness is an extremely common symptom after head trauma and is frequently dismissed as post-concussion syndrome. With concussion patients who complain of dizziness, it is hugely important to be able to differentiate dizziness from vertigo. Dizziness is a feeling of unsteadiness or light-headedness, whereas with vertigo, the world keeps moving even when a person is still, and is often in response to a change in head movement.

When symptoms occur in episodes of brief duration and are related to movement of the head, clinicians should consider a diagnosis of benign paroxysmal positional vertigo (BPPV). Specific neurological examination can diagnose this condition and importantly vestibular manoeuvres exist that can correct this disabling and under-recognised disorder.[45]

The Dix Hallpike Manoeuvre[edit | edit source]

The Dix-Hallpike manoeuvre is the gold standard for to identifying BPPV. This disease process is thought to be caused by dislodging of calcium carbonate crystals (otoconia) from the otolithic membrane within one of the semi-circular canals of the inner ear. This dislodgment physically displaces hair cells on movement and creates persistent action potentials until the response is fatigued, generally within 30 to 60 seconds. This results in the sensation of movement and nystagmus characteristic of vertigo in brief paroxysms with positional changes of the head.

The posterior semi-circular canal is affected 90% of the time in BPPV, and lateral canal pathology causes approximately 8% of cases. The patient is positioned recumbent with the head back and rotated toward the affected ear. Typically, after a five to 20-second delay, this will cause vertigo and rotary or up-beating nystagmus, which will resolve within 60 seconds.[46][47]

The Dix Hallpikemanuever.JPG

Figure 4- Demonstration of the Dix Hallpike manoeuvre

References[edit | edit source]

  1. Katz M, Lenoski S, Ali H, Craton N. Concussion office based rehabilitation assessment: a novel clinical tool for concussion assessment and management. Brain sciences. 2020 Aug 27;10(9):593.
  2. Kushner D. Mild traumatic brain injury: toward understanding manifestations and treatment. Arch Intern Med. 1998 Aug 10-24;158(15):1617-24.
  3. Alexander MP. In the pursuit of proof of brain damage after whiplash injury.Neurology Editorials 1998: 51 (2) DOI: https://doi.org/10.1212/WNL.51.2.336
  4. Jabali MM, Alhakami AM, Qasheesh MA, Uddin S. Efficacy of physical therapy intervention in sports-related concussion among young individuals age-group–A narrative review. Saudi Journal of Sports Medicine. 2020 May 1;20(2):31.
  5. Broshek DK, De Marco AP, Freeman JR. A review of post-concussion syndrome and psychological factors associated with concussion. Brain Inj. 2015;29(2):228-37. doi: 10.3109/02699052.2014.974674. Epub 2014 Nov 10.
  6. Clement D, Granquist MD, Arvinen-Barrow MM. Psychosocial aspects of athletic injuries as perceived by athletic trainers. J Athl Train. 2013 Jul-Aug;48(4):512-21. doi: 10.4085/1062-6050-48.3.21. Epub 2013 May 31.
  7. Sandel N, Reynolds E, Cohen PE, Gillie BL, Kontos AP. Anxiety and Mood Clinical Profile following Sport-related Concussion: From Risk Factors to Treatment. Sport Exerc Perform Psychol. 2017;6(3):304-23.
  8. McCauley SR, Wilde EA, Miller ER, Frisby ML, Garza HM, Varghese R, McCarthy JJ (2013). Preinjury resilience and mood as predictors of early outcome following mild traumatic brain injury. Journal of neurotrauma. 30(8):642–652.
  9. Bombardier CH, Fann JR, Temkin NR, Esselman PC, Barber J, Dikmen SS. Rates of major depressive disorder and clinical outcomes following traumatic brain injury.2010 Jama 303(19):1938–1945.
  10. Ellis MJ, Ritchie LJ, Koltek M, Hosain S, Cordingley D, Chu S, Russell K (2015b). Psychiatric outcomes after pediatric sports-related concussion. Journal of Neurosurgery: Pediatrics16(6):709–718.
  11. Barkhoudarian G, Hovda DA, Giza CC (2011). The molecular pathophysiology of concussive brain injury. Clinics in sports medicine 30(1):33–48.
  12. 12.0 12.1 Chen J-K, Johnston KM, Petrides M, Ptito A. Neural substrates of symptoms of depression following concussion in male athletes with persisting postconcussion symptoms. Archives of General Psychiatry. 2008:65(1):81–89.
  13. Smyth K, Sandhu SS, Crawford S, Dewey D, Parboosingh J, Barlow KM (2014). The role of serotonin receptor alleles and environmental stressors in the development of post‐concussive symptoms after pediatric mild traumatic brain injury. Developmental Medicine & Child Neurology. 56(1):73–77. 
  14. Venzala E, Garcia-Garcia A, Elizalde N, Tordera R. Social vs. environmental stress models of depression from a behavioural and neurochemical approach. EuropeanNeuropsychopharmacology. 2013:23(7):697–708.
  15. Edelman S, Mahoney AEJ, Cremer PD,Cognitive behavior therapy for chronic subjective dizziness: a randomized, controlled trial.American Journal of Otolaryngology. 2012; 33(4): 395-401
  16. Kontos AP. Deitrick JM, Reynolds E, Mental health implications and consequences following sport-related concussion. Br J Sports Med 2016; 50(3): 139-40
  17. Quatman-Yates CC, Hunter-Giordano A, Shimamura KK, Landel R, Alsalaheen BA, Hanke TA, McCulloch KL, Altman RD, Beattie P, Berz KE, Bley B. Physical therapy evaluation and treatment after concussion/mild traumatic brain injury: clinical practice guidelines linked to the international classification of functioning, disability and health from the academy of orthopaedic physical therapy, American Academy of sports physical therapy, academy of neurologic physical therapy, and academy of pediatric physical therapy of the American Physical therapy association. Journal of Orthopaedic & Sports Physical Therapy. 2020 Apr;50(4):CPG1-73.
  18. Erlanger D, Feldman D, Kutner K, Kaushik T, Kroger H, Festa J, Barth J, Freeman J, Broshek D. Development and validation of a web-based neuropsychological test protocol for sports-related return-to-play decision-making. Archives of Clinical Neuropsychology. 2003;18(3):293–316.
  19. Lau B, Lovell MR, Collins MW, Pardini J,Neurocognitive and symptom predictors of recovery in high school athletes. Clin J Sport Med 2009; 19(3):216-21
  20. Lempke LB, Howell DR, Eckner JT, Lynall RC. Examination of Reaction Time Deficits Following Concussion: A Systematic Review and Meta-analysis. Sports Med. 2020;50(7):1341-59.
  21. Collie A, McCrory P, Makdissi M, Does history of concussion affect current cognitive status? Br J Sports Med. 2006; 40(6): 550–1.
  22. 22.0 22.1 McCrea M, Guskiewicz KM, Marshall SW, Barr W, Randolph C, Cantu RC, Onate JA, Yang J, Kelly JP. Acute effects and recovery time following concussion in collegiate football players: the NCAA Concussion Study. JAMA. 2003.19;290(19):2556-63.
  23. Collins M, Lovell MR, Iverson GL, Ide T, Maroon J.Examining concussion rates and return to play in high school football players wearing newer helmet technology: a three-year prospective cohort study.Neurosurgery. 2006; 58(2):275-86; discussion 275-86.
  24. 24.0 24.1 Broglio SP, Ferrara MS, Macciocchi SN, Baumgartner TA, Elliott R. Testretest reliability of computerized concussion assessment programs. Journal of Athletic Training. 2007;42(4):509–514.
  25. Warden DL, Bleiberg J, Cameron KL, et al (2001). Persistent prolongation of simple reaction time in sports concussion. Neurology. 57(3):524–526.
  26. Makdissi M, Darby D, Maruff P, Ugoni A, Brukner P, McCrory PR. Natural history of concussion in sport: Markers of severity and implications for management. American Journal of Sports Medicine. 2010;38(3):464–471.
  27. Eckner JT, Kutcher JS, Richardson JK. Effect of concussion on clinically measured reaction time in nine NCAA Division I collegiate athletes: A preliminary study. PM & R. 2011b;3(3):212–218.
  28. Arrieux JP, Cole WR, Ahrens AP. A review of the validity of computerized neurocognitive assessment tools in mild traumatic brain injury assessment. Concussion. 2017 Jan 30;2(1):CNC31
  29. Falleti MG, Maruff P, Collie A, Darby DG. Practice effects associated with the repeated assessment of cognitive function using the CogState battery at 10-minute, one week and one month test-retest intervals. Journal of Clinical and Experimental Neuropsychology. 2006;28(7):1095–1112.
  30. Maerlender A, Flashman L, Kessler A, Kumbhani S, Greenwald R, Tosteson T, McAllister T. Examination of the construct validity of ImPACT™ computerized test, traditional, and experimental neuropsychological measures. Clinical Neuropsychologist 2010;24(8):1309–1325. 
  31. Nelson LD ,LaRoche AA , Pfaller AY ,Lerner EB ,Hammeke TA,  Randolph C, Barr WB, Guskiewicz  and McCrea MA. Prospective, Head-to-Head Study of Three Computerized Neurocognitive Assessment Tools (CNTs): Reliability and Validity for the Assessment of Sport-Related Concussion. Journal of the International Neuropsychological Society. 2016; 22: 24–37.
  32. Hides JA & Stanton WR. Predicting football injuries using size and ratio of the multifidus and quadratus lumborum muscles. Scandinavian journal of medicine and science in sports. 2012
  33. Murray NG, Szekely B, Moran R, Ryan G, Powell D, Munkasy BA et al. Concussion history associated with increased postural control deficits after subsequent injury. Physiol Meas. 2019;40(2):024001.
  34. Tennant JR (2018). A thesis: Investigating the long-term effects of concussion on sensory gating. https://pdfs.semanticscholar.org/d854/e78f27429f005072b3a2bd460ce83a94fd40.pdf (accessed 23/8/2019)
  35. Viano DC, Casson IR, Pellman EJ, Zhang L, King AI, Yang KH. Concussion in professional football: brain responses by finite element analysis: part 9. Neurosurgery. 2005 Nov;57(5):891-916; discussion 891-916.
  36. Pinsault N, Anxionnaz M, Vuillerme. Cervical joint position sense in rugby players versus non-rugby players. Physical Therapy in Sport 2010; 1-5
  37. 37.0 37.1 37.2 Treleaven J, LowChoy N, Darnell R, Panizza B, Brown-Rothwell D, Jull G. Comparison of sensorimotor disturbance between subjects with persistent whiplash-associated disorder and subjects with vestibular pathology associated with acoustic neuroma. Archives of physical medicine and rehabilitation. 2008 Mar 1;89(3):522-30.
  38. 38.0 38.1 38.2 38.3 38.4 38.5 Kristjansson E, Treleaven J. Sensorimotor function and dizziness in neck pain: implications for assessment and management. JOSPT. 2009; 39(5):364-77.
  39. Alsalaheen BA, Mucha A, Morris LO, Whitney SL, Furman JM, Camiolo-Reddy CE, Collins MW, Lovell MR, Sparto PJ. Vestibular rehabilitation for dizziness and balance disorders after concussion. J Neurol Phys Ther. 2010 Jun;34(2):87-93.
  40. 40.0 40.1 Covassin T, Elbin RJ, Harris W, Parker T, Kontos A. The role of age and sex in symptoms, neurocognitive performance, and postural stability in athletes after concussion. Am J Sports Med. 2010;40(6):1303-12.
  41. 41.0 41.1 41.2 41.3 Guskiewicz KM, Ross SE, Marshall SW. Postural stability and neuropsychological deficits after concussion in collegiate athletes. J Athl Train. 2001;36(3):263-273.
  42. 42.0 42.1 42.2 42.3 Riemann BL, Guskiewicz KM. Effects of mild head injury on postural stability as measured through clinical balance testing. J Athl Train. 2000;35(1):19-25.
  43. 43.0 43.1 43.2 Giza CD, Kutcher JS, Ashwal, Barth J, Getchius TSD, Gioia GA, Gronseth GS, Guskiewicz K,  Mandel S, Manley G, McKeag DB, Thurman DJ, and Zafonte R. Summary of evidence-based guideline update: Evaluation and management of concussion in sports. Report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology 2013;11; 80(24): 2250–2257.
  44. NeuroCom. Sensory Organizing Test. 2013. [August 23, 2013]. http://www.resourcesonbalance.com/neurocom/protocols/sensoryImpairment/SOT.aspx.
  45. Dubrey SW and Rakowicz W. Post-traumatic dizziness. Reminder of important clinical lesson. BMJ Case Rep. 2010 doi: 10.1136/bcr.10.2009.2380
  46. Bhattacharyya N, Gubbels SP, Schwartz SR, Edlow JA, El-Kashlan H, Fife T, Holmberg JM, Mahoney K, Hollingsworth DB, Roberts R, Seidman MD, Steiner RW, Do BT, Voelker CC, Waguespack RW, Corrigan MD. Clinical Practice Guideline: Benign Paroxysmal Positional Vertigo (Update). Otolaryngol Head Neck Surg. Mar 2017;156 (3 suppl):S1-S47.
  47. Scocco DH, García IE, Barreiro MA. Sitting Up Vertigo. Proposed Variant of Posterior Canal Benign Paroxysmal Positional Vertigo. OtolNeurotol. 2019 Apr;40(4):497-503.