Concussion Is Confusing Us All
Concussion Is Confusing Us All
It is commonly assumed that patients with postconcussive symptoms are unlikely to have significant structural brain injury. However, the true pathological situation is often much more uncertain. There are two main mechanisms of acute injury in TBI: direct contact and acceleration/deceleration. An object striking the head or the brain striking the inside of the skull produces a direct injury. Alternatively, rapid acceleration and deceleration imparts shear, and tensile and compressive strains that mainly damage long-distance white matter connections by producing diffuse axonal and vascular injury. Primary injury produces skull fractures, intracranial haematoma and diffuse injuries. In addition, secondary injury results from processes triggered by the initial injury, such as ischaemia, raised intracranial pressure, infection and inflammation. Primary and secondary injuries interact to produce a complex pattern of evolving damage.
In this context, separating concussion as a distinct pathophysiological entity is very problematic (figure 2A). There is no clear pathological definition to distinguish concussion from other types of TBI, and the injuries leading to concussion are biomechanically similar to other types of TBI. Therefore, there is no a priori reason to think that concussion and mild TBI could be distinguished pathologically. It is also unclear how a clinician might decide between mild TBI and concussion, as the symptoms and signs of concussion also follow other types of TBI. For example, headache, cognitive impairment, emotional lability, loss of consciousness and sleep disturbance, each occur to variable extents after all types of TBI. Therefore, it is futile to try to separate concussion as a distinct entity on clinical grounds.
(Enlarge Image)
Figure 2.
Two potential classification systems for traumatic brain injury and concussion.
There are also problems in retaining concussion as a diagnostic label for the constellation of symptoms that are commonly experienced after TBI. Here concussion usually implies a 'benign' set of problems that will eventually resolve spontaneously. However, the assumed transience of 'concussion' symptoms is problematic, as many patients do not recover quickly and it is difficult to predict long-term outcome after TBI. Even apparently trivial injuries can sometimes have long-term effects, with patients reporting similar postconcussive symptoms after TBI of all severities. This can result in a circularity in diagnosis and prognostication. It is easy for the neurologist, who often has limited access to information about the nature of the original injury, to assume that a constellation of 'postconcussive' symptoms is likely to be benign—because of their 'postconcussive' nature. This can obviously result in patients being inappropriately reassured that their symptoms will spontaneously resolve, as well as a lack of investigation and treatment.
Standard investigations also do not particularly help in defining 'concussion'. Many patients with mild TBI do not undergo neuroimaging and are perhaps wrongly reassured about the concussive nature of their problems without any detailed investigation. Even when there is available neuroimaging, it is easy to be falsely reassured by negative neuroimaging findings. Standard neuroimaging will identify large focal contusions or haemorrhage but normal conventional CT and MRI do not exclude diffuse axonal and vascular injury, both major drivers of poor clinical outcome after TBI (see Investigation section). Standard neuroimaging sequences can miss these problems, although more advanced techniques such as susceptibility weighted and diffusion MRI are a more sensitive way of identifying them.
Finally, the term concussion lacks any diagnostic precision and at worst encourages a lazy diagnostic approach. Arriving quickly at the diagnosis of 'postconcussive syndrome' often curtails a detailed assessment of the post-traumatic symptoms. For example, patients with migrainous headaches may be labelled as having concussion, and denied more accurate diagnosis and treatment. This is a type of diagnostic bias where undue emphasis is placed on one aspect of the presentation (the initial injury), which has the effect of obscuring other elements of the diagnostic process. As a result patients with disabling problems often feel that they have not been properly assessed, 'not been listened to' and are 'not getting the services that their injuries deserve'. This type of 'broad-brush' approach to the neurological assessment of patients with TBI is often justified by therapeutic nihilism. We believe such pessimism is inappropriate and that patients with TBI can benefit from the same level of diagnostic precision and careful management that neurologists bring to other areas of their practice.
The Problems With Concussion
It is commonly assumed that patients with postconcussive symptoms are unlikely to have significant structural brain injury. However, the true pathological situation is often much more uncertain. There are two main mechanisms of acute injury in TBI: direct contact and acceleration/deceleration. An object striking the head or the brain striking the inside of the skull produces a direct injury. Alternatively, rapid acceleration and deceleration imparts shear, and tensile and compressive strains that mainly damage long-distance white matter connections by producing diffuse axonal and vascular injury. Primary injury produces skull fractures, intracranial haematoma and diffuse injuries. In addition, secondary injury results from processes triggered by the initial injury, such as ischaemia, raised intracranial pressure, infection and inflammation. Primary and secondary injuries interact to produce a complex pattern of evolving damage.
In this context, separating concussion as a distinct pathophysiological entity is very problematic (figure 2A). There is no clear pathological definition to distinguish concussion from other types of TBI, and the injuries leading to concussion are biomechanically similar to other types of TBI. Therefore, there is no a priori reason to think that concussion and mild TBI could be distinguished pathologically. It is also unclear how a clinician might decide between mild TBI and concussion, as the symptoms and signs of concussion also follow other types of TBI. For example, headache, cognitive impairment, emotional lability, loss of consciousness and sleep disturbance, each occur to variable extents after all types of TBI. Therefore, it is futile to try to separate concussion as a distinct entity on clinical grounds.
(Enlarge Image)
Figure 2.
Two potential classification systems for traumatic brain injury and concussion.
There are also problems in retaining concussion as a diagnostic label for the constellation of symptoms that are commonly experienced after TBI. Here concussion usually implies a 'benign' set of problems that will eventually resolve spontaneously. However, the assumed transience of 'concussion' symptoms is problematic, as many patients do not recover quickly and it is difficult to predict long-term outcome after TBI. Even apparently trivial injuries can sometimes have long-term effects, with patients reporting similar postconcussive symptoms after TBI of all severities. This can result in a circularity in diagnosis and prognostication. It is easy for the neurologist, who often has limited access to information about the nature of the original injury, to assume that a constellation of 'postconcussive' symptoms is likely to be benign—because of their 'postconcussive' nature. This can obviously result in patients being inappropriately reassured that their symptoms will spontaneously resolve, as well as a lack of investigation and treatment.
Standard investigations also do not particularly help in defining 'concussion'. Many patients with mild TBI do not undergo neuroimaging and are perhaps wrongly reassured about the concussive nature of their problems without any detailed investigation. Even when there is available neuroimaging, it is easy to be falsely reassured by negative neuroimaging findings. Standard neuroimaging will identify large focal contusions or haemorrhage but normal conventional CT and MRI do not exclude diffuse axonal and vascular injury, both major drivers of poor clinical outcome after TBI (see Investigation section). Standard neuroimaging sequences can miss these problems, although more advanced techniques such as susceptibility weighted and diffusion MRI are a more sensitive way of identifying them.
Finally, the term concussion lacks any diagnostic precision and at worst encourages a lazy diagnostic approach. Arriving quickly at the diagnosis of 'postconcussive syndrome' often curtails a detailed assessment of the post-traumatic symptoms. For example, patients with migrainous headaches may be labelled as having concussion, and denied more accurate diagnosis and treatment. This is a type of diagnostic bias where undue emphasis is placed on one aspect of the presentation (the initial injury), which has the effect of obscuring other elements of the diagnostic process. As a result patients with disabling problems often feel that they have not been properly assessed, 'not been listened to' and are 'not getting the services that their injuries deserve'. This type of 'broad-brush' approach to the neurological assessment of patients with TBI is often justified by therapeutic nihilism. We believe such pessimism is inappropriate and that patients with TBI can benefit from the same level of diagnostic precision and careful management that neurologists bring to other areas of their practice.