Concussion: Evaluation and Management

Concussion: Evaluation and Management

Concussion results from a traumatic acceleration of the brain that leads to a metabolic mismatch. There is an increased demand for ATP but decreased blood flow to the brain which results to symptoms of headache, dizziness, sleep disturbance, cognitive problems, and emotional difficulties. It affects more than 600/100,000 per year.

Concussion is a common case. The proper identification of its sign and symptoms is of great importance as if these are identified, will guide the physician for the proper management and treatment of the patient.

The Article presents the definition, pathophysiology of concussion and proper identification of sign and symptoms presenting the incidence. It then goes into the detail regarding the various sequela and proper management and treatment of each.

At present concussion is defined as a pathophysiologic process that results from an acceleration or deceleration of the brain secondary to trauma. This causes deformation of axonal membranes and opening of membrane associated Na-K channels which leads to release of excitatory neurotransmitters resulting to neuronal depolarization. The metabolic demand increases utilization of glucose to restore cellular homeostasis and cerebral blood flow decreases. This is termed energy crisis. There is increased demand for ATP and decreased delivery of glucose. This mismatch between energy demand and supply is causes the common signs and symptoms of concussion.

In the history of present illness of the patient, concussion leads to loss of consciousness or a period of confusion with posttraumatic amnesia. Other symptoms are headache, drowsiness, poor balance, and slowed verbal output. In the physical examination a mental status examination is included. For focal neurologic findings consideration of other causes or for a more serious injury, brain imaging is warranted.

Neuroimaging can assess for other etiologies or injuries, such as hemorrhage or contusion. The Canadian CT Head Rule states that CT scan is indicated when a patient fails to reach a Glasgow Coma Scale score of 15 within 2 hours, there is a suspected open skull fracture, there is any sign of basal skull fracture, the patient has 2 or more episodes of vomiting, the patient is 65 or older, the patient has retrograde amnesia for 30 minutes or more, the mechanism of injury was dangerous or the patient fell from 3 feet. The New Orleans Criteria state that CT scan is indicated when a patient has severe headache, vomiting, is age over 60, has drug or alcohol intoxication, deficit in short-term memory, physical evidence of trauma above the clavicle and seizure.

Athletes who participate in contact and collision sports are at higher risk of concussion than the nonathletic population. Therefore, specific assessments of symptoms, balance, oculomotor function, cognitive function, and reaction time have been developed for athletes. Ideally, these measures are taken at baseline.

Treatment depends on the specifics of the injury. The consensus among experts is that patients should undergo a period of physical and cognitive rest. Rest aids recovery but also may have adverse effects such fatigue, diurnal sleep disruption, reactive depression, anxiety, and physiologic deconditioning. Many guidelines recommend physical and cognitive rest until symptoms resolve. As recovery progresses, the somatic symptoms of concussion improve, while emotional symptoms worsen, likely in part due to prolonged rest. A period of rest lasting 3 to 5 days after injury is recommended, followed by a gradual resumption of both physical and cognitive activities as tolerated. The National Collegiate Athletic Association has published an algorithm for a gradual return to sport-specific training. Once aerobic reconditioning produces no symptoms, then noncontact, sport-specific activities are begun, followed by contact activities. Patients are often told to minimize any activities that require attention or concentration. With these interventions, most patients have full resolution of their symptoms and return to preinjury levels of performance.

Posttraumatic headache is the most common sequela of concussion. A prior history of headache, particularly migraine, is a known risk factor for development of posttraumatic headache. Posttraumatic headache is usually further defined by headache type using the International Classification of Headache Disorders criteria. Migraine is the most common type of posttraumatic headache. Tension headache is less common. Analgesics such as NSAIDs are often used initially by patients to treat posttraumatic headache. Treating early with effective therapy is the most important since 80% of those who self-treat have incomplete relief, and almost all of them are using over-the-counter products. In pediatric populations, nonpharmacologic interventions such as rest and sleep hygiene are typically used first, then medications after 4 to 6 weeks if this is ineffective. A number of medications have been studied for prophylactic treatment of posttraumatic headache, including topiramate, amitriptyline, and divalproex sodium, beta-blockers, calcium-channel blockers, selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, and gabapentin. In adults there has been a clinical success with nortriptyline 20 mg or gabapentin 300 mg at night. Gabapentin, amitriptyline, and nortriptyline can produce sedation, which can help those suffering from sleep disturbance. In some patients headache may be related to a cervical strain injury that should be treated with an NSAID or acetaminophen.

Dizziness is also common after concussion. Usually, dizziness is a subjective sense of poor coordination, gait instability, or dysequilibrium. Patients may also complain of associated nausea and motion sensitivity. This may all be secondary to a mechanism in the middle or inner ear or the brain. Patients should be encouraged to begin movement to help the vestibular system accommodate, which it will do with gradual stimulation. It usually resolves spontaneously. There is no established benefit from vestibular suppressants such as meclizine. Referral for a comprehensive balance assessment or to vestibular therapy if there is no recovery from dizziness 4 to 6 weeks after the concussion. Visual symptoms can contribute to dizziness. Convergence spasm or convergence insufficiency can occur after concussion, with some studies estimating that up to 69% of patients have these symptoms. This can interfere with visual tracking and contribute to a feeling of dysequilibrium. Referral to a concussion specialist or vestibular rehabilitation physical therapist can be helpful in treating this issue if it does not resolve spontaneously.

Sleep disturbance is common after concussion. Insomnia, excessive daytime somnolence, and alteration of the sleep-wake cycle are all seen and may themselves affect recovery. Sleep hygiene education should be the first intervention for postconcussive sleep issues. The patient should be encouraged to minimize screen time an hour before going to bed. Screen time pertains to equipment that emit a wavelength of light that suppresses endogenous melatonin release. The patient should go to bed and wake up at the same time each day minimize or avoid caffeine, nicotine, and alcohol. Melatonin is a safe and effective treatment that could be added. In addition, some studies suggest that melatonin may improve recovery from traumatic brain injury. Amitriptyline or nortriptyline may reduce headache frequency and intensity and also help treat insomnia. Trazodone is recommended by some as a first-line agent, but we usually reserve it for protracted insomnia refractory to the above treatments.

Acute-onset anxiety or depression often occurs after concussion. There is abundant evidence that emotional effects of injury may be the most significant factor in recovery. A preinjury history of anxiety may be a prognostic factor. Patients with a history of anxiety or depression are more likely to develop emotional symptoms after a concussion, but emotional problems may develop in any patient after a concussion. The circumstances under which an injury is sustained may be traumatic, leading to an acute stress reaction or disorder and, if untreated, may result in a more chronic condition which is posttraumatic stress disorder. Referral to a therapist trained in skillsbased psychotherapy is advised.

Pharmacologic treatment can be a useful adjunct. Several studies have shown that selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, and tricyclic antidepressants may improve depression after concussion. The prescription of antidepressants, however, is best left to providers with experience in treating anxiety and depression. As with sleep disorders after concussion, benzodiazepines should be avoided, as they can impair cognition.

Cognitive problems are also common after concussion. Patients complain about everyday experiences of forgetfulness, distractibility, loss of concentration, and mental fatigue.

Although patients often subjectively perceive these symptoms as quite limiting, the impairments can be difficult to demonstrate in office testing. A program of gradual increase in mental activity, parallel to recovery of physical capacity, should be undertaken. Most patients make a gradual recovery within a few weeks. When cognitive symptoms cause significant school or vocational problems or become persistent, patients should be referred to a specialty clinic. As with most of the consequences of concussion, there are few established treatments. When cognitive difficulties persist, it is important to consider the complications of concussion which may cause subjective cognitive problems and are treatable. If cognitive symptoms are prolonged despite improvement of other issues like headache and sleep disturbance, a low-dose stimulant medication such as amphetamine salts or methylphenidate may be useful for symptoms of poor attention. They should be only a temporary measure after concussion to carry the patient through a cognitively challenging period, unless there was a history of attention deficit disorder before the injury. A variety of other agents, including amantadine, have been proposed based on limited studies; all are off-label uses. Before considering these types of interventions, referral to a specialist or a specialty program would be appropriate.

Most patients with concussion have a resolution of symptoms and can return to preinjury levels of performance. But some have prolonged symptoms and sequelae. Approximately 10% of athletes have persistent signs and symptoms of concussion beyond 2 weeks. If concussion is not sport-related, most patients recover completely within the first 3 months, but up to 33% may have symptoms beyond that.

Four types of patients have persistent symptoms. Patients who sustained a high-force mechanism of injury. Patients who sustained multiple concussions. Patients with an underlying neurologic condition, recognized prior to injury or not, may have delayed or incomplete recovery. Patients whose symptoms from an apparently single mild concussion do not resolve despite appropriate treatments may have identifiable factors, but intractable pain or significant emotional disturbance or both are common. Once established and persistent, this is difficult to treat. Referral to a specialty practice is appropriate, but even in that setting effective treatment may be elusive.

Ultimately, concussion is a self-limited phenomenon, and reinforcing this is helpful for patients. If concussion is most patients recover completely within 3 months. The next important tenet in patient education is that they should rest for 3 to 5 days, then resume gradual physical and cognitive activities. If resuming activities too soon results in symptoms, then they should rest for a day and gradually resume activity. If their recovery is prolonged, they likely need to be referred to a concussion specialist.

Stillman et al

Cleveland Clinical Journal of Medicine

August 2017

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