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Question 1Basic Neuroscience and Neuropathology of Brain Injury
Which cellular event is the earliest consequence of traumatic axonal stretch injury that ultimately leads to axonal swelling and detachment?
- Retrograde Wallerian degeneration of the neuronal soma
- Loss of dendritic spines at the presynaptic terminal
- Disruption of the axonal cytoskeleton with impaired axonal transport Correct answer.
- Immediate dissolution of the myelin sheath by macrophages
Explanation
Mechanical stretch disrupts the microtubule and neurofilament network, blocking fast axonal transport and causing focal swelling that later detaches as a retraction bulb. Myelin breakdown and macrophage influx occur later, and Wallerian degeneration is anterograde degeneration of the distal stump rather than a primary event.
Question 2Basic Neuroscience and Neuropathology of Brain Injury
A patient with a severe traumatic brain injury develops diabetes insipidus with hypernatremia. Injury to which structure most directly explains this finding?
- Pineal gland at the posterior third ventricle
- Bilateral hippocampal formations
- Posterior pituitary and hypothalamic-hypophyseal axis Correct answer.
- Substantia nigra pars compacta
Explanation
Antidiuretic hormone is synthesized in hypothalamic neurons and released from the posterior pituitary, so injury to this axis produces central diabetes insipidus. The pineal gland, hippocampus, and substantia nigra are not involved in water balance.
Question 3Basic Neuroscience and Neuropathology of Brain Injury
In the Monro-Kellie doctrine applied to a closed skull, which statement best describes the consequence of an expanding intracranial hematoma?
- Total intracranial volume is fixed, so one compartment must decrease to accommodate the mass Correct answer.
- Cerebral blood volume rises to maintain constant total volume
- Intracranial pressure falls initially because the skull can expand
- Cerebrospinal fluid production increases to buffer the added volume
Explanation
Because the skull is a rigid container, an added mass must be offset by displacement of CSF and venous blood, which is the basis of intracranial compliance. Once these buffers are exhausted, intracranial pressure rises steeply.
Question 4Basic Neuroscience and Neuropathology of Brain Injury
Cerebral autoregulation maintains relatively constant cerebral blood flow across which approximate mean arterial pressure range in a healthy adult?
- 50 to 150 mm Hg Correct answer.
- 220 to 280 mm Hg
- 10 to 40 mm Hg
- 160 to 220 mm Hg
Explanation
Autoregulation is classically described as effective between roughly 50 and 150 mm Hg mean arterial pressure, achieved by arteriolar constriction and dilation. Outside this range flow becomes pressure-passive, raising risk of ischemia or hemorrhage.
Question 5Basic Neuroscience and Neuropathology of Brain Injury
A contusion is most likely to be found in which location after a fall directly onto the occiput?
- Cerebellar vermis
- Inferior frontal and anterior temporal poles Correct answer.
- Medial thalamus
- Occipital cortex directly beneath the impact
Explanation
Coup-contrecoup injury produces contusions where the brain impacts the irregular skull base, classically the inferior frontal and anterior temporal regions, even when the blow is occipital. These areas are cushioned poorly and slide over bony ridges.
Question 6Basic Neuroscience and Neuropathology of Brain Injury
Epidural hematoma in adults most commonly results from laceration of which vessel?
- Superior sagittal sinus
- Posterior cerebral artery
- Middle meningeal artery Correct answer.
- Bridging cortical veins
Explanation
Epidural hemorrhage classically follows temporal bone fracture with middle meningeal artery laceration, producing a biconvex collection. Bridging vein tears produce subdural hematoma, and sinus injury is less common.
Question 7Basic Neuroscience and Neuropathology of Brain Injury
Which finding best distinguishes subdural from epidural hematoma on imaging?
- Hypodense lesion within the cerebellar hemisphere
- Hyperdense lesion confined to the ventricular system
- Biconvex collection limited by suture lines
- Crescentic collection that crosses sutures but not dural attachments Correct answer.
Explanation
Subdural blood spreads between the dura and arachnoid, producing a crescent shape that crosses sutures yet is bounded by dural reflections such as the falx. Epidural blood is biconvex because the dura is tethered at sutures.
Question 8Basic Neuroscience and Neuropathology of Brain Injury
Which process underlies secondary brain injury after the primary mechanical trauma?
- Immediate transection of all axons at the moment of impact
- Excitotoxic glutamate release with calcium influx and mitochondrial failure Correct answer.
- Congenital malformation of the cortical mantle
- Primary hemorrhage that cannot be modified by any treatment
Explanation
Secondary injury evolves over hours through excitotoxicity, calcium overload, oxidative stress, and mitochondrial dysfunction, which is why neuroprotective management targets these pathways. Primary axonal transection is instantaneous and not modifiable.
Question 9Basic Neuroscience and Neuropathology of Brain Injury
A patient with TBI has a serum sodium of 118 mmol/L with euvolemia and concentrated urine. Which mechanism best explains this?
- Central diabetes insipidus
- Syndrome of inappropriate antidiuretic hormone secretion Correct answer.
- Primary polydipsia
- Cerebral salt wasting with renal sodium loss
Explanation
SIADH produces euvolemic hyponatremia with inappropriately concentrated urine due to excess ADH, a recognized complication of brain injury. Cerebral salt wasting causes hypovolemia, diabetes insipidus causes hypernatremia, and primary polydipsia produces dilute urine.
Question 10Basic Neuroscience and Neuropathology of Brain Injury
Which brain region is most vulnerable to hypoxic-ischemic injury because of its high metabolic demand and watershed location?
- Lateral geniculate body
- Optic nerve head
- Hippocampal CA1 pyramidal neurons Correct answer.
- Deep cerebellar white matter
Explanation
CA1 pyramidal cells of the hippocampus are among the most selectively vulnerable neurons to global ischemia, alongside cerebellar Purkinje cells and neocortical layers 3 and 5. Vulnerability reflects high metabolic demand and glutamate receptor density.
Question 11Basic Neuroscience and Neuropathology of Brain Injury
A patient becomes comatose after a TBI with a fixed dilated pupil on one side. Which process is most likely?
- Central pontine myelinolysis
- Bilateral cortical contusion of the occipital lobes
- Cerebellar tonsillar herniation with pupillary sparing
- Uncal herniation compressing the oculomotor nerve Correct answer.
Explanation
Transtentorial uncal herniation compresses the third nerve, producing a dilated, unreactive pupil on the side of the mass before contralateral signs appear. Tonsillar herniation causes respiratory arrest rather than a unilateral fixed pupil.
Question 12Basic Neuroscience and Neuropathology of Brain Injury
Diffuse axonal injury lesions are most characteristically located in which areas?
- Cerebral cortex exclusively
- Optic chiasm and pituitary stalk
- Gray-white junction, corpus callosum, and dorsolateral brainstem Correct answer.
- Cerebellar cortex and dentate nucleus only
Explanation
Shear strain from angular acceleration concentrates at interfaces of differing density, producing lesions at the gray-white junction, corpus callosum, and rostral brainstem. These sites explain the clinical picture of prolonged coma with relatively normal initial imaging.
Question 13Basic Neuroscience and Neuropathology of Brain Injury
Which immunohistochemical marker is used to identify injured axons in postmortem brain tissue after trauma?
- Myelin basic protein
- Amyloid precursor protein Correct answer.
- Glial fibrillary acidic protein
- Ionized calcium-binding adaptor molecule 1
Explanation
Amyloid precursor protein accumulates at sites of impaired axonal transport and is a sensitive marker of axonal injury within hours. GFAP labels astrocytes, Iba1 labels microglia, and myelin basic protein labels myelin rather than injured axons specifically.
Question 14Basic Neuroscience and Neuropathology of Brain Injury
Which feature best characterizes chronic traumatic encephalopathy at autopsy?
- Amyloid plaques concentrated in the cerebellum
- Spongiform change in the striatum
- Alpha-synuclein inclusions in the substantia nigra
- Perivascular tau deposits at the depths of cortical sulci Correct answer.
Explanation
CTE is defined by perivascular hyperphosphorylated tau aggregates at sulcal depths, a pattern distinct from other tauopathies. Amyloid plaques, Lewy bodies, and prion-like spongiform change are not the defining lesion.
Question 15Basic Neuroscience and Neuropathology of Brain Injury
A blast injury causes a pressure wave that injures the brain without direct head impact. Which mechanism best explains this primary blast injury?
- Rapid pressure changes causing shear and gas embolism at air-fluid interfaces Correct answer.
- Direct cortical laceration by bone fragments
- Ischemic stroke from carotid dissection
- Delayed autoimmune demyelination
Explanation
Primary blast injury results from the shock wave itself, which creates pressure gradients and shear at tissue interfaces and can cause barotrauma-related gas embolism. Bone fragmentation and vascular dissection describe secondary and tertiary mechanisms.
Question 16Basic Neuroscience and Neuropathology of Brain Injury
Which neurotransmitter system is the principal target of excitotoxic injury after traumatic brain injury?
- Dopaminergic transmission via D2 receptors
- Cholinergic transmission via muscarinic receptors
- Glutamatergic transmission via NMDA and AMPA receptors Correct answer.
- Serotonergic transmission via 5-HT1A receptors
Explanation
Massive glutamate release activates NMDA and AMPA receptors, allowing calcium and sodium influx that triggers proteolysis and cell death. Other transmitter systems are not the primary excitotoxic pathway.
Question 17Basic Neuroscience and Neuropathology of Brain Injury
Which statement about cerebral edema after severe TBI is most accurate?
- Cytotoxic edema results from blood-brain barrier breakdown
- Cytotoxic edema results from cellular swelling due to failure of ion pumps Correct answer.
- Vasogenic edema resolves before cytotoxic edema begins
- Vasogenic edema is caused by intracellular water accumulation in neurons
Explanation
Cytotoxic edema reflects energy failure and ion pump dysfunction with water shifting intracellularly, whereas vasogenic edema follows blood-brain barrier disruption with protein-rich fluid in the extracellular space. The two often coexist and evolve over different time courses.
Question 18Basic Neuroscience and Neuropathology of Brain Injury
Which vascular structure is most commonly injured in traumatic subarachnoid hemorrhage?
- Pial vessels traversing the subarachnoid space Correct answer.
- Deep perforating lenticulostriate arteries
- Internal carotid artery in the cavernous sinus
- Basilar artery at the pontomedullary junction
Explanation
Traumatic subarachnoid hemorrhage typically arises from rupture of small pial and cortical vessels over the brain surface, often in the basal cisterns. Deep perforators and large named arteries are less typical sources.
Question 19Basic Neuroscience and Neuropathology of Brain Injury
A patient with a TBI develops a focal seizure in the first 24 hours. Which factor most strongly predicts early posttraumatic seizures?
- Mild concussion without loss of consciousness
- Penetrating injury or cortical contusion with hemorrhage Correct answer.
- Isolated whiplash injury of the neck
- Remote history of migraine
Explanation
Early seizure risk rises with cortical injury, particularly penetrating trauma, contusions, and intracranial hemorrhage that expose cortex to blood products. Mild concussion and isolated cervical injury carry low risk.
Question 20Basic Neuroscience and Neuropathology of Brain Injury
Which cranial nerve is most vulnerable to injury from a fracture of the petrous temporal bone?
- Hypoglossal nerve
- Optic nerve
- Facial nerve Correct answer.
- Olfactory nerve
Explanation
The facial nerve traverses the temporal bone through the internal acoustic meatus and facial canal, making it vulnerable to petrous fractures. The olfactory, optic, and hypoglossal nerves are located elsewhere.
Question 21Basic Neuroscience and Neuropathology of Brain Injury
Which feature distinguishes a diffuse axonal injury grade III lesion from grade II on pathology?
- Involvement of the dorsolateral rostral brainstem in addition to the corpus callosum Correct answer.
- Hemorrhage confined to the subarachnoid space
- Presence of cortical contusions only
- Isolated white matter lesion in the frontal lobe
Explanation
DAI grades progress from white matter lesions (I) to corpus callosum involvement (II) to additional dorsolateral brainstem lesions (III). Cortical contusions and isolated subarachnoid blood are not part of the DAI grading scheme.
Question 22Basic Neuroscience and Neuropathology of Brain Injury
Which mechanism explains the increased risk of intracranial hemorrhage after even minor head trauma in a patient taking warfarin?
- Warfarin causes cerebral vasospasm
- Warfarin directly dissolves the skull's inner table
- Anticoagulation accelerates neuronal apoptosis
- Impaired coagulation prolongs bleeding from injured microvessels Correct answer.
Explanation
Anticoagulation prevents effective hemostasis at torn vessels, allowing small hemorrhages to expand and causing delayed deterioration. The drug does not affect bone or directly cause vasospasm.
Question 23Basic Neuroscience and Neuropathology of Brain Injury
Which structure is most likely injured in a patient with a TBI who develops a carotid-cavernous fistula with pulsatile exophthalmos?
- Cavernous segment of the internal carotid artery Correct answer.
- Vertebral artery at the foramen magnum
- Superior cerebellar artery
- Anterior cerebral artery at the genu of the corpus callosum
Explanation
A carotid-cavernous fistula results from a tear in the cavernous internal carotid artery communicating with the cavernous sinus, producing proptosis and orbital bruit. The other vessels are anatomically distant from the cavernous sinus.
Question 24Basic Neuroscience and Neuropathology of Brain Injury
Which microscopic change represents a retraction bulb in an injured axon?
- Swollen axon terminal containing accumulated organelles and cytoskeleton Correct answer.
- Loss of myelin with relative axonal preservation
- Astrocytic scar with dense collagen deposition
- Microglial nodule surrounding a neuron
Explanation
A retraction bulb is a swollen, disconnected axonal ending packed with organelles and cytoskeletal elements after transport failure. Demyelination, collagenous scarring, and microglial nodules describe other processes.
Question 25Basic Neuroscience and Neuropathology of Brain Injury
Which cerebral blood flow threshold is most closely associated with the ischemic penumbra in acute brain injury?
- Flow increased above normal resting levels
- Complete absence of flow for several hours
- Flow that is normal but with increased oxygen extraction only
- A modestly reduced flow where electrical function fails but membrane integrity is preserved Correct answer.
Explanation
The penumbra is tissue with reduced but not absent perfusion, where neurons stop functioning but remain viable and potentially salvageable. Complete absence of flow defines the infarct core, and increased flow is not ischemic.
Question 26Basic Neuroscience and Neuropathology of Brain Injury
Which cell type is the principal component of the blood-brain barrier?
- Pericytes
- Astrocytes
- Microglia
- Endothelial cells Correct answer.
Explanation
The blood-brain barrier is formed by tight junctions between endothelial cells of the cerebral capillaries, which restrict paracellular movement of solutes. Astrocytes and pericytes provide inductive and structural support but are not the principal barrier component.
Question 27Basic Neuroscience and Neuropathology of Brain Injury
In the Monro-Kellie doctrine, which component is initially displaced to compensate for an expanding intracranial mass?
- Venous blood
- Brain parenchyma
- Cerebrospinal fluid Correct answer.
- Arterial blood
Explanation
The Monro-Kellie doctrine states that the skull is a rigid container with fixed volumes of brain, blood, and cerebrospinal fluid (CSF). When a mass expands, CSF is displaced first into the spinal subarachnoid space, followed by venous blood; brain tissue is not displaced until later.
Question 28Basic Neuroscience and Neuropathology of Brain Injury
A 45-year-old man sustains a severe TBI and develops diabetes insipidus with polyuria and hypernatremia. Which structure is most likely injured?
- Posterior pituitary Correct answer.
- Adrenal medulla
- Hypothalamus
- Pineal gland
Explanation
Diabetes insipidus after TBI results from damage to the neurohypophysis (posterior pituitary) or its stalk, impairing antidiuretic hormone (ADH) release. The hypothalamus synthesizes ADH, but the posterior pituitary is the release site most vulnerable to traumatic injury.
Question 29Basic Neuroscience and Neuropathology of Brain Injury
Which process best explains the development of cerebral edema after traumatic brain injury?
- Increased cerebrospinal fluid production
- Disruption of the blood-brain barrier Correct answer.
- Obstruction of arachnoid granulations
- Vasodilation of cerebral arteries
Explanation
Cerebral edema after TBI is primarily cytotoxic and vasogenic; vasogenic edema results from blood-brain barrier disruption, allowing fluid to leak into the extracellular space. This leads to increased brain water content and swelling.
Question 30Basic Neuroscience and Neuropathology of Brain Injury
A 30-year-old woman has a mild TBI and later develops syndrome of inappropriate antidiuretic hormone secretion (SIADH). Which laboratory pattern is most consistent with this diagnosis?
- Low serum osmolality, high urine osmolality, euvolemia Correct answer.
- Low serum osmolality, low urine osmolality, hypervolemia
- High serum osmolality, low urine osmolality, hypovolemia
- High serum osmolality, high urine osmolality, euvolemia
Explanation
SIADH is characterized by euvolemic hypotonic hyponatremia: low serum osmolality with inappropriately concentrated urine (high urine osmolality) due to excess ADH. Volume status is typically normal, helping distinguish it from hypovolemic or hypervolemic causes of hyponatremia.
Question 31Epidemiology, Prevention, and Mechanisms of Brain Injury
Which age group has the highest incidence of traumatic brain injury in the United States?
- Adults aged 65 years and older
- Adolescents and young adults aged 15 to 24 years Correct answer.
- Adults aged 45 to 54 years
- Children younger than 5 years
Explanation
TBI incidence peaks in two groups: adolescents/young adults (15-24) and older adults (75 and older). The 15-24 peak reflects high-risk behavior and motor vehicle crashes, while the older-adult peak reflects falls.
Question 32Epidemiology, Prevention, and Mechanisms of Brain Injury
Falls are the leading cause of traumatic brain injury in which population?
- College athletes
- Motorcyclists
- Adults aged 65 years and older Correct answer.
- Military personnel in combat
Explanation
Falls are the most common mechanism of TBI among older adults, and this group also has the highest rates of TBI-related hospitalization and death.
Question 33Epidemiology, Prevention, and Mechanisms of Brain Injury
Which mechanism most commonly produces diffuse axonal injury?
- Rotational acceleration-deceleration forces Correct answer.
- Penetrating missile injury
- Hypoxic-ischemic insult
- Direct blunt impact without head movement
Explanation
Diffuse axonal injury results from shear-strain forces generated by rotational and angular acceleration of the head, which stretch axons at tissue interfaces.
Question 34Epidemiology, Prevention, and Mechanisms of Brain Injury
A patient struck by a vehicle develops a lucid interval followed by rapid neurologic decline. Which injury is most likely?
- Diffuse axonal injury
- Chronic subdural hematoma
- Epidural hematoma Correct answer.
- Traumatic subarachnoid hemorrhage
Explanation
Epidural hematoma classically follows middle meningeal artery disruption and presents with a brief loss of consciousness, a lucid interval, then deterioration from expanding hematoma.
Question 35Epidemiology, Prevention, and Mechanisms of Brain Injury
Which type of cerebral edema develops hours to days after injury due to blood-brain barrier disruption?
- Vasogenic edema Correct answer.
- Interstitial edema
- Osmotic edema
- Cytotoxic edema
Explanation
Vasogenic edema results from blood-brain barrier breakdown with protein-rich fluid leaking into the extracellular space, typically developing hours to days after trauma.
Question 36Epidemiology, Prevention, and Mechanisms of Brain Injury
Which finding best characterizes a concussion on standard neuroimaging?
- No visible abnormality on CT or MRI Correct answer.
- Midline shift on CT
- Large contusion on CT
- Ring-enhancing lesion on MRI
Explanation
Concussion is a functional disturbance without gross structural injury, so conventional CT and MRI are typically normal. Advanced sequences may detect subtle changes but are not used for routine diagnosis.
Question 37Epidemiology, Prevention, and Mechanisms of Brain Injury
Which factor most strongly predicts mortality after severe traumatic brain injury?
- Initial Glasgow Coma Scale score Correct answer.
- Handedness
- Patient sex
- Season of injury
Explanation
The initial Glasgow Coma Scale score is a strong independent predictor of outcome after severe TBI, with lower scores associated with higher mortality.
Question 38Epidemiology, Prevention, and Mechanisms of Brain Injury
A helmet designed to reduce linear acceleration primarily protects against which injury type?
- Chronic traumatic encephalopathy
- Focal skull fracture and contusion Correct answer.
- Rotational diffuse axonal injury
- Hypoxic-ischemic injury
Explanation
Helmets reduce linear acceleration and impact forces, lowering the risk of skull fracture and focal contusion. They are less effective against rotational forces that cause diffuse axonal injury.
Question 39Epidemiology, Prevention, and Mechanisms of Brain Injury
Which prevention strategy has the strongest evidence for reducing traumatic brain injury from motor vehicle crashes?
- Promoting helmet use for drivers
- Seat belt and child restraint use Correct answer.
- Reducing street lighting
- Increasing speed limits
Explanation
Seat belts and age-appropriate child restraints reduce ejection and occupant impact, and are among the most effective population-level TBI prevention measures for vehicle occupants.
Question 40Epidemiology, Prevention, and Mechanisms of Brain Injury
Which secondary injury mechanism after TBI results from excessive glutamate release?
- Apoptosis of oligodendrocytes
- Excitotoxicity Correct answer.
- Demyelination
- Vasospasm
Explanation
Excess glutamate overactivates NMDA and AMPA receptors, causing calcium influx and excitotoxic neuronal injury after TBI.
Question 41Epidemiology, Prevention, and Mechanisms of Brain Injury
A patient with a mild TBI has a normal head CT but persistent symptoms at one month. Which term best describes this presentation?
- Persistent post-concussive symptoms Correct answer.
- Chronic subdural hematoma
- Severe traumatic brain injury
- Second impact syndrome
Explanation
Persistent symptoms beyond the expected recovery window after mild TBI are termed persistent post-concussive symptoms. Normal imaging does not exclude this functional syndrome.
Question 42Epidemiology, Prevention, and Mechanisms of Brain Injury
Which population has the highest rate of traumatic brain injury-related emergency department visits in recent US surveillance?
- Children aged 0 to 4 years
- Adults aged 75 years and older Correct answer.
- Adults aged 35 to 44 years
- Adolescents aged 15 to 19 years
Explanation
Recent surveillance shows the highest rates of TBI-related emergency department visits and hospitalizations among adults aged 75 and older, driven largely by falls.
Question 43Epidemiology, Prevention, and Mechanisms of Brain Injury
Which statement about sex differences in traumatic brain injury epidemiology is most accurate?
- Rates are equal across sexes at all ages
- Females dominate TBI from sports and recreation
- Females have consistently higher TBI rates at all ages
- Males have higher TBI rates overall, with the gap largest in young adulthood Correct answer.
Explanation
Males experience higher TBI rates overall, and the male predominance is most pronounced in adolescence and young adulthood, largely due to risk-taking and sports or vehicle crashes.
Question 44Epidemiology, Prevention, and Mechanisms of Brain Injury
Which injury pattern is most characteristic of a blast-related traumatic brain injury?
- Penetrating fragment tract
- Isolated skull fracture
- Diffuse axonal injury with vestibular and auditory involvement Correct answer.
- Focal cortical contusion only
Explanation
Blast injury combines primary blast wave effects with acceleration and impact, commonly producing diffuse axonal injury along with vestibular and auditory dysfunction.
Question 45Epidemiology, Prevention, and Mechanisms of Brain Injury
Which secondary injury process after TBI is most directly addressed by avoiding hypotension?
- Free radical generation
- Cerebral ischemia from impaired perfusion Correct answer.
- Neuroinflammation
- Excitotoxicity from glutamate release
Explanation
Hypotension reduces cerebral perfusion pressure and worsens secondary ischemic injury, so maintaining adequate blood pressure is a core neurocritical care target.
Question 46Epidemiology, Prevention, and Mechanisms of Brain Injury
Which statement best describes the relationship between repetitive head impacts and chronic traumatic encephalopathy?
- CTE occurs only in boxers
- CTE is caused by a single severe TBI
- CTE is associated with repetitive head impacts and has been described pathologically in contact-sport athletes Correct answer.
- CTE is a purely clinical diagnosis confirmed by MRI
Explanation
CTE is a neurodegenerative tauopathy associated with repetitive head impacts and has been described pathologically in athletes in contact sports and others with exposure. Diagnosis currently requires postmortem tissue examination.
Question 47Epidemiology, Prevention, and Mechanisms of Brain Injury
Which measure is most effective for preventing TBI in older adults?
- Daily high-intensity exercise without supervision
- Routine helmet use indoors
- Fall risk assessment and home hazard modification Correct answer.
- Restricting driving after age 70
Explanation
Falls are the leading cause of TBI in older adults, so multifactorial fall risk assessment with home hazard modification and strength and balance training reduces risk.
Question 48Epidemiology, Prevention, and Mechanisms of Brain Injury
Which finding on CT most strongly suggests a poor prognosis after severe TBI?
- Isolated linear skull fracture
- Small cortical contusion
- Compressed basal cisterns with midline shift Correct answer.
- Small subarachnoid hemorrhage
Explanation
Compressed or absent basal cisterns and midline shift indicate mass effect and raised intracranial pressure, which are associated with worse outcomes.
Question 49Epidemiology, Prevention, and Mechanisms of Brain Injury
Which mechanism best explains cerebral contusions occurring at the frontal and temporal poles?
- Hypoxic injury
- Contrecoup injury from brain movement within the skull Correct answer.
- Coup injury from direct impact
- Infectious process
Explanation
Contrecoup contusions occur when the brain strikes the opposite inner skull surface after impact, commonly affecting the frontal and temporal poles because of the irregular skull base.
Question 50Epidemiology, Prevention, and Mechanisms of Brain Injury
Which factor is most associated with increased risk of TBI from intimate partner violence?
- Advanced maternal age
- Rural residence only
- Higher education level
- Female sex and history of prior head injury Correct answer.
Explanation
Intimate partner violence-related TBI disproportionately affects women, and prior head injury increases vulnerability to further injury.