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Radiological Interpretation in Neuro-Ophthalmology
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Chirag Kamal Ahuja, Paramjeet Singh
Trauma forms a major cause of damage to the visual pathway from the level of the eyeball till the occipital lobe visual centers and the intervening pathway constituted by the optic nerve (Figure 22.18), chiasma, tracts, LGN and optic radiation. Blunt or penetrating orbital trauma may lead to open or closed globe injury. The optic nerve may receive contusion or transection resulting from bony fractures (usually at the level of optic canal). There may be entrapment of the muscle belly, commonly seen with inferior rectus resulting in restriction of superior gaze (Figure 22.19). Head injury may lead to contusions or diffuse axonal injury in the occipital lobes as a result of coup/contrecoup injury. CT is an excellent modality to delineate bony fractures. Multiplanar thin-slice reconstructions aid in the identification of even very subtle fractures. Sometimes, it is difficult to delineate soft tissue injury with CT. MRI helps in such cases with detection of signal changes in the components of visual pathways especially the optic nerves, chiasma and occipital lobes for diffuse axonal injury (DAI). High-resolution MR sequences also have a role to play in detection of subtle changes at the level of brainstem CN nuclei as well as actual visualization of the cisternal course of various nerves, especially CN 6, which is prone to injury due to its longest intracranial course (16–18).
Trauma of the Brain and Spinal Cord
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Fernando D. Goldenberg, Ali Mansour
Cerebral contusions (Figure 11.4) are typically hemorrhagic lesions that more commonly involve the basal and anterior portions of the frontal and temporal lobes. They occur when the brain hits against the rough surface of the inner table of the anterior and middle cranial fossa. The classic understanding is that the acceleration and deceleration of the brain within the cranial compartment result in a coup–contrecoup injury pattern, with the coup damage happening directly beneath the site of impact and the contrecoup on the opposite side. Contusions typically begin within the cortex and expand into the subcortical white matter with more severe injury. Pericontusional edema and ischemic changes lead to neuronal cell death in the afflicted areas, with eventual cavitation and reactive gliosis around the perimeter of the injury later on. “Blossoming” of a contusion refers to continued hemorrhagic progression or expansion of a seemingly subtle hemorrhage on initial evaluation. The mechanism of this hemorrhagic progression was classically attributed to coagulopathy. However, more recent literature argues that mechanosensitive endothelial cells are activated in the penumbra of the initial lesion. This penumbra does not experience the destructive forces occurring within the contusional core itself but causes endothelial mechanosensitive activation of transcription factors leading to endothelial necrosis and delayed hemorrhage.5
Biomechanics and Tissue Injuries
Published in Rolland S. Parker, Concussive Brain Trauma, 2016
A compression wave is propagated through molecules within a medium whenever a solid object is struck (e.g., head impact). The medium is cell walls, extracellular fluid, connective tissue, cell membranes and contents, and vessels and contents. The brain’s viscoelastic qualities and varied structure makes it vulnerable to pressure waves that can induce shearing forces. Cerebral damage may occur due to stress wave concentration due to contact forces or acceleration-induced brain damage resulting in tissue-tear hemorrhages (Gennarelli & Graham, 1998). Compression-rarefaction is characterized by a change of volume without a change of internal shape. The skull is an inelastic container that contains three relatively noncompressable substances: brain, CSF, and blood. Since the brain is virtually incompressible, it has a lower tolerance to shear strains than compression strains (Adams et al., 1982). This mechanism may be involved in rotational movement’s creation of coup-contrecoup injury (see contrecoup and cavitation).
Management of migrating intracranial bullet fragments in a 13-year-old female after firearm brain injury: technical and surgical nuances
Published in Brain Injury, 2022
John K. Yue, Diana Chang, Kasey J. Han, Albert S. Wang, Taemin Oh, Peter P. Sun
Primary (e.g. direct) injury to the skull and brain parenchyma is further exacerbated by missile fragmentation, increased missile velocity, ricochet/deviations from a straight path, and coup/contrecoup injury (12). Secondary injuries occur due to sequelae from elevated intracranial pressure (ICP), intracranial hemorrhage (ICH), and cerebral edema similar to blunt TBI, as well as migration. Late complications include bullet migration, seizures, traumatic aneurysms, and infection (13). Pediatric patients are especially vulnerable to missile injuries due to thinner bones of the skull and overlying soft tissue compared to adults (14).
Depressed skull fracture compressing eloquent cortex causing focal neurologic deficits
Published in Brain Injury, 2023
Alexander In, Brittany M. Stopa, Joshua A. Cuoco, Adeolu L. Olasunkanmi, John J. Entwistle
A 40-year-old man presented to the emergency department as a gold alert after falling 12 feet off of a ladder and striking his head. Glasgow Coma Scale was 15 on presentation. Neurologic examination demonstrated a left central facial nerve palsy, left hemiplegia, left hemianesthesia, and fixed right gaze deviation. The patient reported that such symptomatology developed immediately following the fall. There was no evidence of seizure activity witnessed in the field, in transport, or in the trauma bay. The initial CT head demonstrated a right parietal depressed skull fracture with compression of the right precentral gyrus and postcentral gyrus as well as right frontoparietal traumatic subarachnoid hemorrhage and a small right parietal intraparenchymal contusion (Figure 1). Completion films and vascular imaging, including CT angiography of the head and neck, were unrevealing. Anatomically, the neurologic deficits observed were thought to be due to a combination of blunt force trauma to the head (i.e., coup-contrecoup injury) and the depressed fracture fragment compressing the underlying eloquent cortex. Specifically, the left central facial nerve palsy and left hemiplegia were attributed to the depressed fracture fragment compressing the right precentral gyrus. The left hemianesthesia was attributed to the fracture compressing the right postcentral gyrus. The fixed right gaze deviation was difficult to explain based solely on fracture compression, given the topographical location of the frontal eye fields. Additional explanations considered included a coup-contrecoup injury to the right frontal eye field from the initial traumatic event or diffuse axonal injury. Nevertheless, the majority of the observed symptomatology could be plausibly explained by the fracture compressing the underlying eloquent cortex. As such, he was taken emergently to the operating room for right cranioplasty with elevation of the fracture fragment. Postoperative imaging demonstrated fracture reduction without evidence of complications (Figure 2). Immediately post-op, the facial nerve palsy and gaze deviation resolved; however, the hemiplegia and hemianesthesia persisted, prompting extensive physical therapy and inpatient rehabilitation. At his 2-month follow-up, he regained strength on the left with Medical Research Council (MRC) grade 4/5 power throughout and some persistent left hemianesthesia. At 6-month follow-up, he had regained full neurologic function without any residual deficits.