As a result, expansion of the volume of any of the components must be offset by an equal decrease in volume of the others or intracranial pressure will increase. The compensatory capacity within the non-compliant cranium is limited.
The capacity for CSF to displace into the spinal theca and into the venous system via arachnoid granules, and intracranial blood to redistribute peripherally is easily overcome. This usually occurs with mass lesions of about to mls, and when it does intracranial pressure increases linearly. The implication for management of traumatic brain injury is that space is at a premium, and aggressive treatment to control the volume of intracranial contents is essential to prevent raised intracranial pressure which can lead to compression of vital brain structures, impaired blood flow to the brain and ultimately death.
What is cerebral perfusion pressure and how does raised intracranial pressure impair blood flow to the brain? Blood, like any other fluid, tends to flow from high to low pressure. Hence raised intracranial pressure decreases the pressure gradient favouring blood flow to the brain. Hence, CPP is used as a surrogate marker of cerebral blood flow. It also follows that to maintain blood flow to the brain in the presence of raised intracranial pressure, and increased driving pressure i.
How is the concept of cerebral autoregulation relevant to traumatic brain injury? In this normal brain, this is not the case because of cerebral autoregulation.
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In addition to pharmacological treatment, patients with mild TBI who present with cognitive complaints also should be provided with physical rehabilitation and occupational therapy, either in an outpatient or a residential setting. TTH typically presents as bilateral pressure type pain that is mild to moderate in intensity. It can be either episodic or chronic and often occurs daily, especially in the setting of frequent use of products with acetaminophen, ibuprofen, and opioids; it is then referred to as MOH.
Treatment generally is pharmacologic and should include prophylactic and palliative therapies. Among the TCAs, nortriptyline Pamelor, others has the least number of side effects. Tramadol Ultram, others or tizanidine Zanaflex, others may be useful, off-label, to treat these frequent headaches. PTMs typically are episodic headache attacks presenting with or without aura. They generally are described as pulsating and unilateral. Comorbidities, such as nausea, emesis, photophobia, and phonophobia, frequently are present, and symptoms are aggravated by physical activity.
Opioids should be employed only when other medications are ineffective. Prophylactic, or preventive medications for migraine include TCAs, anticonvulsants, calcium channel blockers, beta-blockers, and serotonin norepinephrine reuptake inhibitors. Selective serotonin reuptake inhibitors have not had very good efficacy in general, although they may improve anxiety and depression. MOH, once referred to as rebound headache, is defined by the International Headache Society as headache pain at least 15 days per month, treated pharmacologically for more than 3 months, either developed or worsened during the period of pharmacologic treatment and returned to baseline within 2 months of discontinuing treatment.
Treatment consists of gradual weaning from the overused drug s. Other pain problems associated with mild TBI include neck and back pain, complex regional pain syndrome CRPS , fibromyalgia, and temporomandibular pain. These may be a result of the trauma from the original injury or sequelae of the mild TBI. Treatment for neck, back, and temporomandibular pain should include NSAIDS, acetaminophen, muscle relaxants, and physical therapy followed by a home exercise program.
Both should be treated with a course of physical therapy. Comorbid psychological problems, such as depression and anxiety, arising from mild TBI can complicate both the diagnosis and treatment of headache and other pain conditions after mild TBI.
An elegant overview of post-traumatic epilepsy recently was published, discussing how TBI results in long-term multiple changes in the organization of brain circuits in the cortex and hippocampus that create an imbalance between excitatory and inhibitory neurotransmission, and, therefore, a markedly increased risk for seizures.
Treatment should be aimed at controlling seizure activity with a single medication. In one retrospective study of 30 TBI survivors with active seizure disorders, methylphenidate appeared to decrease seizure rates.
This occurs when there is damage to the semicircular canals, rendering them sensitive to gravity. Treatment by canalith repositioning maneuvers generally is effective in treating this disorder. A less common cause of dizziness after mild TBI is labyrinthine concussion, which occurs when the trauma damages the tissues of the inner ear. It is marked by acute hearing loss and vertigo. In some cases, patients need to be treated with vestibular and balance rehabilitation therapy.
Individuals presenting with complaints of dizziness, balance problems, and hearing loss should be evaluated by electronystagmography, videonystagmography, rotary chair testing, and tilt table testing. Treatment generally involves exercise and therapy.
Patients presenting with persistent complaints of fatigue after mild TBI should undergo a thorough psychological evaluation to rule out other potential causes. Treatment typically consists of physical therapy PT and a home exercise program, combined with education about sleep hygiene. In cases that do not respond to conservative treatment, amantadine or modafinil Provigil, others may be effective.
There also is a large range in the reported number of patients suffering from post-traumatic sleep disorders because sleep disturbances are part of a post-concussional syndrome see Table 1.
Individuals presenting with post-traumatic sleep disorders should undergo a thorough neurological and neuropsychological examination to rule out any neurological or psychological comorbidities. If neurological and neuropsychological studies are negative, patients can be referred for polysomnographic testing. Pharmacological treatments include hypnotic sleep aids such as tizanidine, eszopiclone Lunesta, others and benzodiazepines.
A home exercise program and education in sleep hygiene may also be very useful. Patients with mild TBI who present with post injury vision complaints, including double vision and blurred vision, should be referred to a neuro-ophthalmologist or neuro-optometrist for a thorough examination.
The past 10 to 15 years have seen a renaissance in the diagnosis and treatment of mild TBI. There is a growing acceptance in the existence of both acute and chronic PCD within the medical community.
While the tools to diagnose and treat chronic PCD have improved greatly in recent years, the best treatment is prevention A number of controlled, blinded studies have shown that providing a patient with education about mild TBI, what symptoms to expect, and the general duration of those symptoms in either verbal or written form as well as providing support and treatment in the acute phase significantly lessens the progression of those symptoms to the chronic stage.
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Pain Management in the Elderly: Treatment Considerations. Rationale for Medical Management. Traumatic brain injury TBI , or concussion, can leave a person with lifelong symptoms.
In this segment, specialists in 3 areas discuss TBI-induced cellular damage to the brain and the management of its sequalae. Katz, MD. References Krusz, JC, Treatment of post-traumatic headaches, migraines and sleep disorders. Pract Pain Manage. Traumatic brain injury in the United States: emergency department visits, hospitalizations and deaths — Accessed November 11, Diagnostic and Statistical Manual of Mental Disorders , 5th ed. Saulle M, Greenwald B.
Chronic traumatic encephalopathy: a review. Rehabil Res Pract. Post-concussion symptoms after traumatic brain injury at 3 and 12 months post-injury: a prospective study. Brain Injury. Krusz JC, Robbins L. Traumatic brain injury. Disruptions in the regulation of extracellular glutamate by neurons and glia in the rat striatum two days after diffuse brain injury.
J Neurotrauma. Cereb Cortex. Biologic and plastic effects of experimental traumatic brain injury treatment paradigms and their relevance to clinical rehabilitation, PMR. What are you looking for?
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View Guidelines Publications.Guidelines for the Management of Severe Traumatic Brain Injury, 4th Edition, and the AANS and CNS leadership for their endorsement, which appears on the title page. Funding Source. This material is based in part upon work supported by (1) the U.S. Army Contracting.