The DREAM Study
Following traumatic brain injury (TBI), patients can experience significant problems with concentration, attention, and memory (so called 'cognitive impairments'). These cognitive impairments can drastically impact on a patient's well-being, and can lead to significant economic and social consequences. Roughly a quarter of TBI patients improve but an equal number deteriorate over time. We know little about why patients vary so much in how they recover. Crucially, we have no treatments to improve brain functioning or recovery after TBI.
Trials investigating ways of protecting the brain just after injury have been disappointing. An alternative strategy, however, is to improve the function of brain regions that remain intact, but that function inefficiently after TBI. We know that dopamine (a chemical in the brain) is known to influence many brain functions and we know that dopamine pathways are affected by TBI.
Animal models demonstrate that TBI can produce dopamine deficiency, which can be treated by using drugs such as methylphenidate that increase dopamine levels. In humans, dopamine increasing drugs are sometimes used to enhance cognitive function after TBI, but the response to treatment can be highly variable between patients. Therefore, what is needed in the clinic is a way to target the use of these drugs to patients who are likely to respond.
In this study we are using SPECT (Single Photon Emission Computed Tomography) imaging to measure dopamine levels in the brain. MRI (Magnetic Resonance Imaging) scans are also used to assess brain structure and function. We are testing whether treatment with methylphenidate improves cognitive functions in TBI patients who have ongoing cognitive problems, whether the mechanism involves a normalisation of brain functioning and whether brain dopamine levels can predict the magnitude of any improvement in symptoms.
Following traumatic brain injury (TBI), patients can experience significant problems with concentration, attention, and memory (so called 'cognitive impairments'). These cognitive impairments can drastically impact on a patient's well-being, and can lead to significant economic and social consequences. Roughly a quarter of TBI patients improve but an equal number deteriorate over time. We know little about why patients vary so much in how they recover. Crucially, we have no treatments to improve brain functioning or recovery after TBI.
Trials investigating ways of protecting the brain just after injury have been disappointing. An alternative strategy, however, is to improve the function of brain regions that remain intact, but that function inefficiently after TBI. We know that dopamine (a chemical in the brain) is known to influence many brain functions and we know that dopamine pathways are affected by TBI.
Animal models demonstrate that TBI can produce dopamine deficiency, which can be treated by using drugs such as methylphenidate that increase dopamine levels. In humans, dopamine increasing drugs are sometimes used to enhance cognitive function after TBI, but the response to treatment can be highly variable between patients. Therefore, what is needed in the clinic is a way to target the use of these drugs to patients who are likely to respond.
In this study we are using SPECT (Single Photon Emission Computed Tomography) imaging to measure dopamine levels in the brain. MRI (Magnetic Resonance Imaging) scans are also used to assess brain structure and function. We are testing whether treatment with methylphenidate improves cognitive functions in TBI patients who have ongoing cognitive problems, whether the mechanism involves a normalisation of brain functioning and whether brain dopamine levels can predict the magnitude of any improvement in symptoms.