The post-traumatic syndrome (PTS), previously called post-concussion syndrome, is a pattern of symptoms that can follow mild to moderate head injury (actual cranial impact). It is also seen after flexion-extension trauma (whiplash) in which no actual cranial contact has occurred.

The primary symptoms of PTS may include one or more of the following: head, neck, and shoulder pain; headache; sleep disturbance; cognitive abnormalities; mood and personality changes; and dizziness, with or without vertigo.

The prevailing view of most knowledgeable authorities is that the condition is a neurologic disorder that may arise even if frank unconsciousness has not occurred. Some patients who experience momentary loss of consciousness are not aware of it and fail to report it in emergency departments.

Headache is present in as many as 88% of patients who have mild head injury, persisting for more than 2 months in 60% of patients, even those who have apparently minor trauma. The symptoms do not correlate with the presence or duration of unconsciousness, amnesia, or any identifiable finding. Actually, an inverse relation may exist between the severity of head injury, as determined by the duration of posttraumatic amnesia, and the incidence of headache.

The prevailing view is that posttraumatic headache probably reflects a set of pathophysiologic factors that produce the wide-ranging set of symptoms and that cognitive, psychological, behavioral disturbances, and pain reflect the sequelae of brain tissue injury. Moreover, direct or indirect injury to the neck, jaw, or tissues of the scalp may similarly play a role in the development of many of the headache and other painful symptoms.

These acute or new changes, which may produce pain in the immediate posttraumatic period, may be followed by delayed and chronic disturbances centrally that involve pain modulation. Peripherally, painful injury can induce central pain phenomena (such as windup and sensitization) that include wide dynamic-range neurons and other recently recognized central nervous system factors involved in pain. Moreover, the kindling phenomenon, seen in experimental epilepsy, could influence the evolution from peripheral injury to chronic, centrally maintained pain, possibly producing a daily persistent headache that evolves later.

The pain and headache symptoms may arise from both central or peripheral factors. Persistent pain, particularly neck ache, may arise from traumatic injury to cervical facet joints or the third cervical nerve, estimated to be involved in 58% of patients whose major complaint after whiplash is headache.

Moreover, entrapment or trauma to the third occipital nerves by osteophytes of C2-3 or traumatic arthritis of C2-3 is relevant and often overlooked, as are instances of occipital neuralgia and facet joint disturbances. Jaw injury, styloid process trauma, and other peripheral causes of pain are likewise frequently overlooked.

The neurocognitive impairment results in reduced concentration, an inability to process information at a normal pace, and memory impairment. These have been well delineated in the literature. Neuropsychiatric and behavioral phenomena are likewise noted. Recently, in a well-controlled study, noted amelioration of psychological disturbances in patients who had head and neck pain when pain control was established.

A variety of spells or seizure-like events is also reported in patients who have PTS. Although true epilepsy or syncope rarely occurs, a variety of nonspecific, periodic, paroxysmal events is noted, including narcolepsy or cataplexylike phenomena. These events should not be discounted simply because of the absence of true epilepsy features or because they represent variations from classical presentations.

Diagnostically, no diagnostic study can confirm the diagnosis; conversely, neither do they refute it. Neurocognitive tests are the most sensitive practical studies to assess cerebral dysfunction. MRI or CT imaging rules in or rules out serious alterations in brain, which are either related or unrelated to the trauma.

The neurologist must rule out organic disturbances that might mimic PTS or cause persistent head or neck ache. Some of these may be the direct result of the trauma itself. These include subdural or epidural hematomas, CSF hypotension (from traumatic leak), cerebral vein thrombosis, cerebral hemorrhage, true seizures, posttraumatic hydrocephalus, vertebral (facet joint)/cervical root/cervical nerve/suboccipital injury, temporomandibular disorders, or styloid ligament or process damage.

In a review of the available literature after 1 month 31% to 90% of patients still had headache. At 2 to 3 months postinjury, 32% to 78% of patients still had headache. One year after injury, 8% to 35% of patients still had headache.

Between 2 and 4 years after injury, as many as 20% to 24% of patients have persistent headache. Neurocognitive, dizziness, and mood symptoms may persist for years.

The legitimacy of this condition and the believability of patients reporting largely subjective complaints have been challenged because of long-standing assumptions regarding the influence of litigation dynamics on the presence and persistence of symptoms. However, the premise that protracted cases result primarily from litigation-related motives or other nonphysiologic circumstances is not currently supported by the data.

PTS should no longer be arbitrarily denied its physiologic legitimacy, particularly with such compelling clinical support and growing physiologic data. There is yet much more to learn than is currently known. The absence of objective markers does not prove the absence of legitimacy.

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