Introduction, SPECT Brain Perfusion Findings in Mild / Moderate Traumatic Brain Injury

SPECT BRAIN PERFUSION FINDINGS IN MILD OR MODERATE TRAUMATIC BRAIN INJURY

INTRODUCTION:

Head trauma is an underestimated cause of chronic disability. It has been called the "silent epidemic" ^(1,2). Under-estimation of the true numbers of head injury victims is attributed to imprecise information gathering, lack of recognition of late developing neurological and endocrinological symptoms, and not recognizing the true range of traumatic brain-injury related dysfunctions⁽³⁾. A meta-analysis of prison inmates indicated that of 1,055 subjects, 489 had head injuries with 31% unattended by a physician and 60% not hospitalized and therefore not part of public health records. It was inferred that the incidence of head injuries should be upwardly adjusted. More permanent effects occurred from unattended and undocumented injuries⁽⁴⁾. A conservative estimate puts the total number of traumatic brain injuries at over 2 million per year, with over 1.5 million in which the injuries are not severe enough to require hospitalization. Young individuals between ages 15-24 have the highest rate of injury. Physical, cognitive, and psycho-social-behavioral-emotional impairment are well known consequences of TBI, with over 25 billion in economic costs⁽⁵⁾. Morbidity from acute and chronic symptoms (headaches, pain, seizures, memory problems, dizziness etc.), has been well recognized post mild TBI^(6,7). The wide range of physiological, neurological, neuropsychological, and emotional symptoms occurring after concussive head injury is associated with diffuse brain damage⁽⁸⁾. The patient is rendered vulnerable to incidents creating further brain injury ⁽⁹⁾.

The pattern of brain injury and its correlation with the patient symptoms has not been traditionally possible because the mechanism of injury rarely involves a pure single force, and because of the unknown contribution of secondary sequella ^(8,9).

It is important to be aware of the following physical and mechanical factors that contribute to brain injury. The brain is vulnerable to trauma because it is deformable, soft and somewhat inelastic. Permanent distortion and tissue destruction occurs locally or in widespread areas due to impact, cutting, absorption of energy, and restricted capacity to recover its original length, shape, or volume, after force is removed. As the brain moves against vessels exiting the skull (including the internal carotid artery), either vessels or brain parenchyma can be torn. Impact and/or rotation occurs in lateral and transaxial planes in the neck and head, creating shearing, stretching, crushing, and torsion within the brain and neck, and between brain and skull, and between cerebral planes at different radial distances from the center of rotation. Brain impact with the flat and sharp surfaces of the skull and dura mater creates lacerations and contusions. Impact and brain acceleration-deceleration causes brain motion-associated positive and negative pressure waves, causing cavitation between the skull and the brain. Rotation in the sagittal plane, unrestrained by the falx, may cause the brain stem to move in and out of the foramen magnum affecting nuclei controlling the vasculature ^(10,11).

Brain trauma is not an event but a process proceeding through time, sometimes many years⁽¹²⁾. Physical forces, as previously mentioned create primary damage. Secondary pathology is consequent to destruction of tissue and hemorrhage, i.e., mass effects and intracellular and vascular changes. The tertiary phase refers to late endocrinological dysfunction. The quaternary phase refers to late development of neurological symptoms (e.g., dystonias, premature dementia, and posttraumatic epilepsy)⁽⁸⁾. This is probably associated with transneuronal degeneration. Neuronal atrophy after initial injury has been reported and is reflected in increased ventricle to brain ratio which may stabilize 9-12 weeks post injury ⁽¹³⁾.

SPECT brain perfusion imaging is highly sensitive for detecting regional cerebral blood flow (rCBF) disturbances in-patients with traumatic brain injury^(1,14-19). Brain SPECT have been playing an ever-increasing important role in evaluating patients complaints following mild TBI, and there is increasing evidence that rCBF SPECT plays an important role in medical, and socio-economic decision making involving mild head injury patients⁽²⁰⁾. Many studies on patients with head injury have already demonstrated that brain perfusion SPECT can depict larger and more numerous lesions than on CT. Most of these studies, however, have addressed rather severe trauma cases^{(14,15,21-24)}. In mild TBI there is increasing literature showing the superiority of SPECT over CT in evaluating the brain ^(1,25,26). The role of CT in mild to moderate trauma is probably limited^(27-29). While SPECT imaging does not replace traditional structural imaging modalities for the identification of major lesions, hematomas, or edema; brain SPECT plays an important role in assessing cortical, basal ganglia, and thalamic perfusion alterations resulting from trauma ⁽³⁰⁾. It is hypothesized that SPECT detected lesions are consequent to the mechanical and physiological effects of an accident upon the neck and head, and the physiological consequences of stress ⁽³¹⁾. All the reports in the literature have several problems such as the small number of patients in each individual report, lack of correlation with neurobehavioral analysis, lack of longitudinal follow-up, the non-specificity of the findings and lack of comparison with normal controls, and comorbidity that interferes with the interpretation of the findings (neurological or psychological diseases; previous history of brain trauma etc.). In addition, there is no standard protocol followed by all investigators for SPECT acquisition, processing and interpretation of the data. There is also lack of quantitation of the regional cerebral perfusion using the current radiopharmaceuticals approved by the FDA.

The objective of this manuscript is to present the SPECT brain perfusion abnormalities in the largest series thus far reported in the literature. In addition, we are presenting other data related to frequency of cause of the accident and patients’ complaints. We are also presenting statistical analysis of the data in order to show the value of early imaging over delayed imaging from the time of the accident and the correlation of the findings with the patients symptoms.