PCS From The Neuro-Otology Experience
Post-concussion syndrome (PCS) commonly involves the vestibular system, which is essential to normal movement and balance. The most persistent symptoms reported following PCS include vertigo deficits, neck spasms, exercise intolerances and memory problems.1 Vestibular symptoms of vertigo, imbalance and visual motion intolerances can last for 6 months or greater.2
The level of neuraxis impacted by concussion can range from the distal peripheral vestibular apparatus of the inner ear to the proximal brain processing centers of the central nervous system. Inner ear peripheral vestibular dysfunctions associated with PCS include labyrinthine concussion (jarring to the inner ear peripheral bony and membranous labyrinths), vestibular nerve or receptor injury resulting in vestibular hypofunction, injury to the labyrinthine artery, and otolithic displacement. Due to the head trauma, the central mechanisms of the vestibular system of brainstem vestibular nuclei and vestibulocerebellum can also be damaged and can often result in a combined peripheral and central vestibular dysfunction.
Pathophysiology
What is a labyrinthine concussion? This is a trauma (blast, direct blow, jarring of the head or whiplash) to the inner ear peripheral vestibular system’s labyrinths, resulting in vertigo, nausea, disequilibrium, blurred vision (due to nystagmus), occasional hearing loss and often tinnitus.3
Labyrinthine concussion occurs when impact forces from a head trauma or jarring to the head/neck are not absorbed and the vestibular receptors are injured or concussed, usually resulting in four specific vestibular pathologies: 1) otolithic displacement (benign paroxysmal positional vertigo (BPPV); 2) damage to the vestibulocochlear nerve or receptors (vestibular hypofunction as measured by diagnostic calorics); 3) imbalance in the endolymphatic fluid (post-traumatic Meniere’s disease); and/or 4) physical damage of superior semicircular canal dehiscence due to bony trauma resulting in the creation of a third window.
Evaluation
History, physical examination and diagnostic tests of videonystagmography (VNG), audiogram, plus calorics, vestibular evoked myogenic potential (VEMP), video head impulse testing (vHITs) are used to determine vestibular involvement associated with PCS. These detailed inner ear tests can help identify the level of organelle in the vestibular apparatus. Once the diagnosis has been determined, appropriate medical management is initiated.
Otolithic displacement, resulting in BPPV, is a common result of PCS and has been seen in more than 90 percent of the patients with PCS treated in our practice.4 BPPV in this population can be typical, as seen in unilateral poste- rior semicircular canal, or atypical that may present with multiple canal involvement or bilateral. The utricle that houses the otoliths may be jarred in PCS patients and cause a cascade of otolithic crystal displacement resulting in these atypical manifestations. Full assessment of a PCS patient should include Dix-Hallpike testing to determine BPPV.
Repositioning techniques are effective for peripheral BPPV. The Epley maneuver5 is reported as the most effective treatment for posterior semicircular canal BPPV; however, there are other positioning techniques for horizontal and anterior semicircular canal BPPV.
It is important to recognize the different positioning nystagmus patterns (type, direction, latency and duration) specific to each semicircular canal involvement during assessments of Dix-Hallpike to determine the appropriate repositioning maneuver. Posterior canal BPPV presents with geotropic upbeating torsional nystagmus. Anterior canal BPPV presents with ageotropic downbeating torsional nystagmus, and horizontal canal BPPV presents with horizontal geotropic or ageotropic nystagmus patterns.
Timing strategies for repositioning techniques are based upon the latency and duration of nystagmus/symptoms. Cupulolithiasis (dislodged otolithic material that may be stuck on the cupula at the base of the semicircular canal) manifests when there is no latency of nystagmus upon Dix- Hallpike testing, and nystagmus may be intermittent for several minutes.
Canalithiasis manifests with a latent reaction of nystagmus to allow the dislodged otolithic material or canaliths that are free-floating in the canal to begin movement, resulting in nystagmus. The latency may be 5-30 seconds, and the positioning nystagmus is typically of 60 seconds duration or less and should fatigue with repetitions. There are specific repositioning techniques based upon the timing strategies of latency and duration of nystagmus demonstrated during Dix-Hallpike testing.
In patients with positional symptoms but nystagmus is atypical for BPPV, central positional vertigo or nystagmus (CPV or CPN) should be considered and is common in PCS.
Treatment
Treatment in PCS is varied and depends upon the specific diagnoses identified. Post-concussion BPPV is treated with repositioning techniques, and vestibular hypofunction is treated with adaptation exercises to aid in central compensation.
Post-traumatic Meniere’s disease is treated with vestibular suppressants, diuretics, a low-salt diet and antiemetic medications. If severe impairing symptoms develop, ablative intratympanic gentamicin intervention may be necessary. Hearing aids and tinnitus habituation treatments are included if the patient has resultant hearing loss and/or tinnitus. Superior canal dehiscence is usually monitored, and surgery for this condition is complicated and presents with risks. Headache management is typically coordinated with the treating neurologist.
It is not unusual to see patients with vestibular dysfunction associated with PCS present with more than one diagnosis. For example, a patient with PCS may have BPPV and post-traumatic Meniere’s disease. We had a case recently of a lady with post-traumatic BPPV, headache, Meniere’s disease and superior canal dehiscence.
Vestibular rehabilitation of movements to promote central nervous system adaptation, habituation or compensation; oculomotor retraining; balance and gait retraining; neck stretches; and canalith repositioning/dispersement techniques are all also effective for treating vestibular dysfunction seen with PCS. Vestibular assessments are quite detailed and include videonystagmography, posturography, clinical balance tests, dynamic gait index, sensory organization tests, vestibular ocular reflex testing (dynamic acuity, eye-head, head shaking, head thrust and gaze stability), vestibulospinal reflex testing, and Dix-Hallpike/positioning testing. Traditional therapy may not be effective due to the central nervous system involvement and low tolerance of motion demonstrated by patients with PCS, and the vestibular rehabilitation program must be customized, monitored and individualized consistently based upon the patient’s tolerances and other PCS symptoms, such as headache and neck/vascular injuries.
Other potential rehabilitation considerations with this patient population include recognizing CNS vestibular adaptation may take up to 6 months or greater, and that patient’s anxiety, memory, agitation, fatigue, sleep disturbances and emotions have to be factored into program development and monitoring.
Other possible complicating histories may include migraine headaches, comorbidity, seizures, medication side effects, cervical injuries, other visual disturbances such as diplopia, and mood disorders, making it extremely important to coordinate with other healthcare professionals involved in the treatment of these patients. Medical management of post-traumatic migraines, epilepsy, cognitive disorders and mood disorders may be necessary for better participation and results from vestibular therapy interventions.
Vestibular dysfunction in PCS is a common manifestation and should be medically and therapeutically recognized. Appropriate assessments, re-assessments (serial monitoring) and interventions should also be initiated for improved patient outcomes. This population is best served by multiple healthcare disciplines addressing the multiple symptoms and manifestations of PCS.
References
1. Vidal J, Goodman A, Colin A, et al. Rehabilitation strategies of prolonged recov- ery in pediatric and adolescent concussion. Peditri Ann 2012; 41:1-7.
2. Akin F, Murnan O. Head injury and blast exposure: vestibular consequences. Otolaryngol Clin N Am 2011; 44:323-334.
3. Tangeman P, Wheeler J. Inner ear concussion: vestibular implications and physical therapy. Acute Care Trauma Rehabil 1986; 1:72-83.
4. Steenerson R, Cronin G, et al. Effectiveness of treatment techniques in 923 cases of benign paroxysmal positional vertigo. Laryngoscope 2005; 115:226-231. 5. Fife T, Iverson T, et al. Practice parameter: therapies for BPPV (an evidenced based review) report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2007: 70:2067-2074.
Gaye W. Cronin, OTD, OTR
Dr. Gaye Cronin, director of the Vestibular Rehabilitation and Facial Retraining Programs at the Atlanta Ear Clinic received her BS and Masters from the Medical College of Georgia and Doctorate from the University of St. Augustine. Dr. Cronin is associate professor at MCG and University of St. Augustine, has published extensively in medical and therapy journals and texts, conducted numerous national and international educational courses and received several professional accolades.
Ronald Leif Steenerson, M.D.
Dr. Ronald Leif Steenerson, neurotologist at the Atlanta Ear Clinic graduated from Purdue University and Indiana University School of Medicine followed by prestigious experiences in major medical centers. He served as a flight surgeon in the Air Force, and then into private practices. Further training included fellowships in Otology and Neurotology. He has conducted multiple medical educational courses and published in numerous medical journals and texts. Dr. Steenerson has received distinguished medical awards.
