DOI: 10.1148/radiol.2453050112
(Radiology 2007;245:914-915.)
© RSNA, 2007
The Reversal Sign1
Eoin C. Kavanagh, MRCPI, FFR RCSI
1 From the Division of Neuroradiology, Department of Radiology, Vancouver General Hospital, Vancouver, British Columbia, Canada. Received January 22, 2005; revision requested March 23; revision received March 25; final version accepted June 15.
Address correspondence to the author, Department of Musculoskeletal Radiology, University of Pittsburgh Medical Center, 200 Lothrop St, Pittsburgh, PA 15213 (e-mail: eoinkav{at}yahoo.com).
 |
APPEARANCE
|
|---|
The reversal sign is seen on unenhanced computed tomographic (CT) images of the brain as an inversion of the normal attenuation relationship between gray and white matter; gray matter is of relatively lower attenuation than adjacent white matter (1,2) (Figs 1, 2). Attenuation of the thalami, brainstem, and cerebellum is increased.
View larger version (122K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 1a: Transverse unenhanced CT scans demonstrate reversal sign with decreased attenuation overall and loss of gray-white differentiation. Note relatively increased attenuation of (a) basal ganglia (arrows), (b) thalami (thin arrows), and cerebellum (wide arrows).
|
|
View larger version (118K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 1b: Transverse unenhanced CT scans demonstrate reversal sign with decreased attenuation overall and loss of gray-white differentiation. Note relatively increased attenuation of (a) basal ganglia (arrows), (b) thalami (thin arrows), and cerebellum (wide arrows).
|
|
View larger version (126K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 2: Transverse unenhanced CT scan shows reversal of normal attenuation relationship between gray and white matter. Note relatively increased attenuation of the cerebellum (arrows).
|
|
|
EXPLANATION
|
|---|
Pathogenesis of the reversal sign is complex and not yet fully understood. Mechanical, hemodynamic, chemical, and metabolic factors have been implicated.
One theory is that preservation of central structures is due to transtentorial herniation secondary to acute edema, with pressure partially relieved as the brain herniates through the incisura. The pressure relief is thought to improve tissue perfusion to central structures, thus delaying or preventing necrosis (3). This theory has been questioned by a study (4) that showed that relative sparing of the attenuation of the basal ganglia, thalami, and posterior fossa can occur before transtentorial herniation. The relative preservation of attenuation in the posterior fossa likely reflects preferential maintenance of blood flow in the posterior circulation relative to that in the anterior circulation.
Other researchers (5) have suggested that postischemic hypervascularity may cause the relatively increased attenuation seen in the thalami and basal ganglia. However, administration of intravenous contrast material does not aid in the detection of the reversal sign (2,6).
Autopsies of children whose CT images showed the reversal sign revealed petechial hemorrhages in the brainstem and cerebellum (2). It may be that these petechial hemorrhages contribute to the increased attenuation seen in these areas.
Authors of another study of autopsy findings (7) suggested that the reversed gray-white matter attenuation may be secondary to distention of deep medullary veins caused by partial obstruction of venous outflow due to increased intracranial pressure. The formation of edema is more rapid and severe in the cortex, where high local tissue pressure leads to early occlusion of superficial veins (7,8).
Chemical and metabolic factors, such as hyperglycemia, have also been implicated in the pathophysiology of the reversal sign. One experimental study (9) implicated serum glucose concentrations in the occurrence and distribution of anoxic brain injury.
|
DISCUSSION
|
|---|
The reversal sign indicates diffuse cerebral injury in a patient who has suffered an anoxic insult (1,2,7,8). Causes of the reversal sign include head trauma, hypoxia, birth asphyxia, drowning, status epilepticus, hypothermia, bacterial meningitis, strangulation, nonaccidental trauma, and other causes of global cerebral ischemia (1,2,6,10). When other causes have been excluded, demonstration of intracranial blood in the presence of the reversal sign should be considered an indicator of nontraumatic injury (6). The reversal sign is associated with a poor prognosis and indicates irreversible brain damage (2,6). Mortality rates are high in children whose CT images show the reversal sign (35%), and those who survive have profound neurologic deficits with severe developmental delay (2).
|
FOOTNOTES
|
|---|
Author stated no financial relationship to disclose.
|
References
|
|---|
- Cohen RA, Kaufman RA, Myers PA, Towbin RB. Cranial computed tomography in the abused child with head injury. AJR Am J Roentgenol 1986;146:97–102. [Abstract/Free Full Text]
- Han BK, Towbin RB, De Courten-Myers G, McLaurin RL, Ball WS Jr. Reversal sign on CT: effect of anoxic/ischemic cerebral injury in children. AJNR Am J Neuroradiol 1989;10:1191–1198. [Abstract]
- Myers RE. Experimental models of perinatal brain damage: relevance to human pathology. In Gluck L, ed. Intrauterine asphyxia and the developing brain. Chicago, Ill: Yearbook Medical, 1977; 37–97.
- Chen CJ. Central structure preservation of the reversal sign. Neuroradiology 1999;41:946–948. [CrossRef][Medline]
- Shewmon DA, Fine M, Masdeu JC, Palacios E. Postischemic hypervascularity of infancy: a stage in the evolution of ischemic brain damage with characteristic CT scan. Ann Neurol 1981;9:358–365. [CrossRef][Medline]
- Rao P, Carty H, Pierce A. The acute reversal sign: comparison of medical and non-accidental injury patients. Clin Radiol 1999;54:495–501. [CrossRef][Medline]
- Bird CR, Drayer BP, Gilles FH. Pathophysiology of "reverse" edema in global cerebral ischemia. AJNR Am J Neuroradiol 1989;10:95–98. [Abstract]
- Kjos BO, Brant-Zawadzki M, Young RG. Early CT findings of global central nervous system hypoperfusion. AJR Am J Roentgenol 1983;141:1227–1232. [Abstract/Free Full Text]
- de Courten-Myers GM, Yamaguchi S, Wagner KR, Ting P, Myers RE. Brain injury from marked hypoxia in cats: role of hypotension and hyperglycemia. Stroke 1985;16:1016–1021. [Abstract/Free Full Text]
- Schulman H, Laufer L, Berginer J, et al. CT findings in neonatal hypothermia. Pediatr Radiol 1998;28:414–417. [CrossRef][Medline]
TOP
APPEARANCE
EXPLANATION
