Neurosurgery

89 questions

Question 81Question →

A 46-year-old male with a history of an uncorrected right-to-left cardiac shunt is evaluated in the neurology unit for a progressively worsening, severe global headache over the past week. This morning, he developed new-onset weakness in his left arm and leg. His temperature is 38.6∘C38.6^\circ\text{C} (101.5∘F101.5^\circ\text{F}), blood pressure is 145/90 mm Hg145/90\text{ mm Hg}, and heart rate is 88/min88\text{/min}. Neurologic examination reveals 3/53/5 motor strength in the left upper and lower extremities and a left homonymous hemianopia. Fundoscopic examination shows bilateral optic disc swelling with blurred margins. A contrast-enhanced MRI of the brain demonstrates a 3.8-cm3.8\text{-cm} solitary ring-enhancing lesion with a necrotic core in the right frontoparietal lobe, surrounded by substantial vasogenic edema and a 7-mm7\text{-mm} midline shift. Which of the following is the most appropriate next step in management?

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Answer: Stereotactic aspiration of the lesion

Answer

Stereotactic aspiration of the lesion
The correct answer is stereotactic aspiration of the lesion. This patient's clinical presentation (fever, headache, focal neurologic deficits) and imaging findings (ring-enhancing lesion with a necrotic core and surrounding edema) in the setting of a right-to-left cardiac shunt are highly characteristic of a bacterial brain abscess. The standard of care for a brain abscess larger than 2.5 cm, or one causing significant mass effect (as evidenced by a 7-mm midline shift), is prompt stereotactic aspiration. This neurosurgical procedure is both diagnostic and therapeutic; it provides a microbial tissue sample to guide targeted antibiotic therapy and immediately relieves intracranial pressure by reducing the volume of the mass.

Step-by-Step Solution

1
Identify the primary diagnosis based on clinical and imaging findings
The patient has a large (3.8 cm) bacterial brain abscess with mass effect and midline shift, likely seeded via his uncorrected right-to-left cardiac shunt.
Establishing the correct pathology (abscess rather than primary tumor) is necessary to determine the appropriate neurosurgical and medical intervention.
2
Evaluate indications for surgical intervention
Brain abscesses larger than 2.5 cm or those causing significant mass effect (e.g., 7-mm midline shift) meet the criteria for surgical drainage.
Medical management alone is insufficient for large lesions and risks progressive neurologic decline and herniation.
3
Select the most appropriate neurosurgical technique
Stereotactic aspiration is chosen as the definitive initial step.
It successfully relieves intracranial pressure, provides a tissue sample for gram stain and culture, and minimizes morbidity compared to open craniotomy.

Key Concept

Management of Brain Abscesses > 2.5 cm
Question 82Question →

Match each patient's clinical presentation and findings with the most appropriate definitive neurosurgical or endovascular intervention.

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Items

A 35-year-old man with severe traumatic brain injury has an intracranial pressure persistently above 30 mmHg despite sedation, hyperosmolar therapy, and cerebrospinal fluid drainage.
A 50-year-old woman treated for a ruptured cerebral aneurysm develops new right-sided hemiparesis on day 7. CT angiography confirms severe localized narrowing of the left middle cerebral artery.
A 65-year-old man on warfarin develops progressive quadriparesis and hyperreflexia over 12 hours. MRI demonstrates a large, hyperacute dorsal fluid collection compressing the cervical spinal cord.
A 42-year-old man presents with sudden bilateral lower extremity weakness, saddle anesthesia, and urinary retention. MRI reveals a massive central disc herniation at L4-L5.

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Answer

Refractory elevated intracranial pressure requires decompressive craniectomy. Symptomatic severe vasospasm is treated with intra-arterial vasodilators. A cervical epidural hematoma necessitates emergent cervical laminectomy and evacuation. Cauda equina syndrome requires emergent lumbar laminectomy and discectomy.
Each clinical scenario describes a distinct neurosurgical emergency with a specific, time-sensitive definitive intervention. Refractory intracranial hypertension requires decompressive craniectomy to increase cranial vault volume. Delayed cerebral ischemia from vasospasm requires endovascular vasodilators to restore perfusion. Compressive spinal lesions, such as an acute epidural hematoma or massive lumbar disc herniation, require emergent surgical decompression appropriate to their specific spinal level to prevent permanent tissue infarction.

Step-by-Step Solution

1
Evaluate the trauma patient with refractory elevated intracranial pressure.
Identify decompressive craniectomy as the next step.
Maximal medical therapies have failed, leaving surgical decompression as the definitive intervention to relieve pressure.
2
Assess the post-subarachnoid hemorrhage patient with delayed focal deficits.
Identify endovascular intra-arterial vasodilator therapy as the correct intervention.
The timing and imaging are diagnostic for severe vasospasm, which requires endovascular rescue when symptomatic and anatomically localized.
3
Analyze the anticoagulated patient presenting with acute myelopathy and a dorsal fluid collection.
Identify emergent cervical laminectomy and hematoma evacuation.
The findings indicate a spinal epidural hematoma causing critical cord compression, a surgical emergency requiring prompt evacuation.
4
Evaluate the patient with saddle anesthesia, urinary retention, and bilateral leg weakness.
Identify emergent lumbar laminectomy and discectomy.
These are classic signs of cauda equina syndrome due to a massive lumbar disc herniation, requiring immediate surgical decompression of the nerve roots.

Key Concept

Definitive Management of Neurosurgical Emergencies
Estimated Time:1m 30s
Question 83Question →

A 25-year-old male is admitted to the neurosurgical intensive care unit following a severe traumatic brain injury sustained in a motor vehicle collision. He is intubated, mechanically ventilated, and receiving continuous infusions of propofol and fentanyl for sedation and analgesia. An intracranial pressure (ICP) monitor is in place. His ICP acutely rises to 28 mm Hg and remains elevated for 10 minutes despite the current sedation. His vital signs show a blood pressure of 130/80 mm Hg, heart rate of 85/min, and temperature of 37.2°C (99.0°F). Arrange the following interventions in the most appropriate stepwise sequence for managing this patient's elevated intracranial pressure, proceeding from initial, least invasive measures to final salvage therapy.

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Answer

The correct sequence for managing elevated ICP progresses from basic positioning, to osmotic therapy, to temporizing hyperventilation, and finally to salvage surgical decompression.
The management of elevated intracranial pressure (ICP) follows a stepwise algorithm to balance efficacy with the risk of secondary brain injury. First, basic maneuvers such as head-of-bed elevation and neutral neck positioning maximize venous outflow. Second, when basic measures and sedation fail, hyperosmolar therapy (hypertonic saline or mannitol) is administered to osmotically reduce brain volume. Third, if ICP remains refractory, mild hyperventilation can be used to induce cerebral vasoconstriction, though it is delayed due to the risk of causing cerebral ischemia. Finally, decompressive craniectomy is reserved as a surgical salvage therapy for medically refractory intracranial hypertension.

Step-by-Step Solution

1
Implement basic physiological measures.
Head of bed elevated and neck aligned.
Optimizes jugular venous outflow and decreases ICP with minimal risk.
2
Administer hyperosmolar therapy.
Hypertonic saline is given.
Creates an osmotic gradient to reduce cerebral edema; represents the standard first-line medical therapy for elevated ICP.
3
Utilize short-term hyperventilation.
Target PaCO 2_2 reduced to 30-35 mm Hg.
Induces cerebral vasoconstriction for rapid ICP reduction, but used cautiously and later in the algorithm due to the risk of ischemia.
4
Proceed to surgical decompression.
Decompressive craniectomy is performed.
Serves as a definitive salvage therapy for refractory intracranial hypertension.

Key Concept

The stepwise management of elevated intracranial pressure involves a tiered approach, starting with basic physiological optimization, progressing to medical interventions (osmolar therapy, hyperventilation), and ending with salvage surgical procedures.
Question 84Question →

Paramedics transport a patient to the trauma bay after he experienced a sudden loss of consciousness at his workplace. The patient's coworkers state that he abruptly grabbed the back of his head, complained of severe dizziness and nausea, and then collapsed. Medical records indicate he is 62 years old and has a long-standing history of medication nonadherence for essential hypertension. Currently, his blood pressure is 198/115 mmHg, and his heart rate is 54/min. Neurological assessment shows a profoundly lethargic patient who only localizes to painful stimuli and has irregular respirations. Non-contrast cranial computed tomography (CT) demonstrates a 4.2-cm hyperdense collection in the right cerebellar hemisphere, associated with compression of the fourth ventricle and significant dilation of the lateral ventricles. Which of the following is the most appropriate next step in management?

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Answer: Emergent suboccipital craniectomy and hematoma evacuation

Answer

Emergent suboccipital craniectomy and hematoma evacuation
The correct answer is emergent suboccipital craniectomy and hematoma evacuation. This patient presents with an acute spontaneous cerebellar hemorrhage likely secondary to hypertensive emergency. The size of the hematoma (4.2 cm), combined with the effacement of the fourth ventricle, resulting obstructive hydrocephalus, and clinical signs of brainstem compression (bradycardia, irregular respirations, lethargy), constitutes a neurosurgical emergency. The standard of care for cerebellar hemorrhages greater than 3 cm in diameter, or those associated with brainstem compression or hydrocephalus, is immediate surgical evacuation. This prevents fatal cerebellar tonsillar herniation and directly addresses both the primary mass effect and the secondary hydrocephalus.

Step-by-Step Solution

1
Analyze the patient's clinical presentation.
The patient has sudden onset headache, vertigo, and collapse, with profound lethargy, hypertension, bradycardia, and irregular respirations.
These findings are highly suggestive of increased intracranial pressure and impending brainstem herniation (Cushing's triad).
2
Interpret the neuroimaging findings.
CT shows a 4.2-cm cerebellar hemorrhage with fourth ventricle compression and hydrocephalus.
Cerebellar hematomas larger than 3 cm or those causing neurological deterioration require distinct management compared to smaller or supratentorial bleeds.
3
Determine the next best step in management.
The definitive treatment is emergent surgical decompression via suboccipital craniectomy.
Surgical evacuation relieves the mass effect on the brainstem and resolves the obstructive hydrocephalus, preventing fatal tonsillar herniation.

Key Concept

Surgical management of acute cerebellar hemorrhage
Question 85Question →

A 68-year-old man with a known history of metastatic prostate cancer is brought to the emergency department complaining of severe mid-back pain that has steadily worsened over the past two weeks. Over the last 6 hours, he has developed bilateral leg weakness and urinary incontinence. Vital signs are within normal limits. Neurologic examination reveals 3 out of 5 muscle strength in the lower extremities bilaterally, decreased sensation to pinprick below the umbilicus, and absent patellar and Achilles reflexes. Rectal examination demonstrates severely decreased anal sphincter tone. Arrange the following diagnostic and therapeutic steps in the most appropriate chronological order for managing this patient's condition.

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Answer

The correct chronological sequence is to first administer intravenous dexamethasone, followed by obtaining a whole-spine MRI, performing an emergent surgical decompression, and finally initiating adjuvant fractionated radiation therapy.
This patient's presentation of progressively worsening back pain, acute lower extremity weakness, an established sensory level, and bowel/bladder dysfunction in the setting of metastatic prostate cancer is highly suspicious for epidural spinal cord compression (ESCC). ESCC is a true neurologic emergency. The immediate first step in management is the administration of high-dose intravenous glucocorticoids (e.g., dexamethasone) to decrease peritumoral vasogenic edema and relieve pressure on the cord. This empirical step must not be delayed for imaging. Once steroids are given, an urgent MRI of the whole spine is required to confirm the diagnosis and delineate the anatomical extent of the disease. If the MRI confirms epidural compression causing acute neurologic deficits, emergent surgical decompression (such as a laminectomy) is indicated, especially for patients lacking a known diagnosis or those with a reasonable life expectancy who can tolerate surgery. Finally, adjuvant radiation therapy is utilized postoperatively for definitive local disease control.

Step-by-Step Solution

1
Administer high-dose intravenous dexamethasone
Reduction of peritumoral vasogenic edema
Empiric administration is critical to prevent irreversible neuronal damage while awaiting definitive imaging.
2
Obtain a magnetic resonance imaging (MRI) scan of the entire spine
Confirmation of epidural spinal cord compression
MRI is required to visualize the exact location and extent of the compression to guide surgical planning.
3
Perform an emergent surgical decompressive laminectomy
Immediate physical relief of spinal cord compression
Surgery is the definitive acute treatment to halt or reverse rapidly progressing neurologic deficits.
4
Initiate adjuvant fractionated radiation therapy
Long-term local tumor control
Radiation prevents local recurrence of the metastatic lesion after the acute surgical emergency is resolved.

Key Concept

Management algorithm for malignant epidural spinal cord compression
Estimated Time:1m 30s
Question 86Question →

A 58-year-old man comes to the physician because of a 5-month history of progressive clumsiness in his hands and an unsteady gait. He frequently drops small objects and has difficulty fastening buttons. He has no history of trauma, fever, or preceding illness. Vital signs are normal. Neurological examination reveals decreased bulk and tone in the intrinsic muscles of both hands. Biceps and brachioradialis reflexes are 1+ bilaterally. In contrast, knee and ankle jerks are 3+ bilaterally, and sustained ankle clonus is present. Babinski sign is present bilaterally. Sensory examination shows decreased vibration and position sense in the toes. Which of the following is the most appropriate next step in management?

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Answer: Magnetic resonance imaging of the cervical spine

Answer

Magnetic resonance imaging of the cervical spine
The patient presents with progressive neurological decline characterized by a distinct combination of lower motor neuron (LMN) signs in the upper extremities and upper motor neuron (UMN) signs in the lower extremities. The LMN signs (muscle atrophy, hyporeflexia in the biceps and brachioradialis) indicate damage at the level of the nerve roots in the cervical spine. The UMN signs (hyperreflexia, clonus, positive Babinski sign) indicate compression of the descending corticospinal tracts. The diminished vibratory and position sense indicates involvement of the ascending dorsal columns. This constellation of findings is classic for cervical spondylotic myelopathy (CSM), the most common cause of non-traumatic spinal cord compression in older adults. The correct diagnostic approach is magnetic resonance imaging of the cervical spine to visualize the extent of cord compression and to plan for appropriate neurosurgical decompression.

Step-by-Step Solution

1
Analyze the neurological physical exam findings.
The patient exhibits lower motor neuron (LMN) signs in the upper extremities (atrophy, hyporeflexia) and upper motor neuron (UMN) signs in the lower extremities (hyperreflexia, clonus, Babinski sign), alongside dorsal column sensory deficits.
Accurate neurological localization is required to identify the site of the lesion.
2
Localize the lesion based on the combination of deficits.
The combination of LMN signs at the level of the lesion and UMN signs below the level of the lesion localizes the pathology to the cervical spinal cord.
Intracranial lesions do not cause bilateral LMN signs in the arms, and peripheral neuropathies do not cause UMN signs in the legs.
3
Determine the diagnostic modality of choice for suspected cervical myelopathy.
Magnetic resonance imaging of the cervical spine is selected to visualize the spinal cord and nerve roots.
MRI is the gold standard for diagnosing structural cervical spinal cord compression and planning subsequent neurosurgical intervention.

Key Concept

Cervical Spondylotic Myelopathy
Question 87Question →

Match each neurosurgical emergency or traumatic brain injury with its characteristic pathophysiologic mechanism and classic neuroimaging findings.

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Items

Epidural hematoma
Subdural hematoma
Subarachnoid hemorrhage
Diffuse axonal injury

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Answer

Epidural hematoma matches middle meningeal artery laceration (biconvex); Subdural hematoma matches bridging vein tearing (crescent-shaped); Subarachnoid hemorrhage matches ruptured saccular aneurysm (basal cisterns); Diffuse axonal injury matches rotational shear forces (punctate lesions).
Each type of intracranial hemorrhage has a distinct pathophysiologic mechanism and radiologic appearance that dictate its appropriate neurosurgical management. Recognizing these classic diagnostic patterns is an essential clinical skill for rapid triage and intervention in neurotrauma and vascular emergencies.

Step-by-Step Solution

1
Identify the etiology and imaging for an Epidural hematoma.
Matches with middle meningeal artery laceration and a biconvex (lens-shaped) hyperdensity.
High-pressure arterial bleeding strips the dura from the inner table of the skull, creating a biconvex shape tightly constrained by cranial suture lines where the dura is firmly attached.
2
Identify the etiology and imaging for a Subdural hematoma.
Matches with bridging vein tearing and a crescent-shaped hemorrhage.
Lower-pressure venous bleeding spreads freely between the dura and arachnoid mater, creating a diffuse, crescentic shape that can cross suture lines but is limited by dural reflections (e.g., falx cerebri).
3
Identify the etiology and imaging for a Subarachnoid hemorrhage.
Matches with saccular aneurysm rupture and blood tracking into the basal cisterns and sulci.
Aneurysmal rupture releases arterial blood directly into the subarachnoid space, the normal anatomical compartment for cerebrospinal fluid circulation.
4
Identify the etiology and imaging for Diffuse axonal injury.
Matches with rotational shear forces and punctate lesions at the gray-white matter junction.
Differing physical densities between gray and white matter lead to differential movement and axonal shearing during severe rotational trauma, producing characteristic microhemorrhages.

Key Concept

Distinct pathophysiologic mechanisms and imaging features of intracranial hemorrhages
Question 88Question →

A male patient, aged 45, presents to the emergency room with a 7-day history of escalating mid-thoracic back pain and subjective fevers. He has a known medical history of intravenous substance use disorder. Over the last 24 hours, he noted rapidly progressive weakness in both legs and an inability to void urine. Vital signs show a temperature of 38.9°C (102°F), heart rate of 110/min, and blood pressure of 122/78 mm Hg. Neurologic examination reveals 2/5 motor strength in the bilateral lower extremities, a distinct loss of pain and temperature sensation below the umbilicus, and 3+ patellar reflexes with bilateral Babinski signs. Bladder ultrasound reveals a post-void residual volume of 650 mL. Empiric intravenous vancomycin and ceftriaxone are promptly initiated. Magnetic resonance imaging of the spine demonstrates a peripherally enhancing anterior epidural collection spanning T9-T11, causing severe compression of the spinal cord. Which of the following is the most appropriate next step in management?

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Answer: Urgent surgical laminectomy and debridement

Answer

Urgent surgical laminectomy and debridement
The patient presents with the classic triad of a spinal epidural abscess (SEA): fever, localized back pain, and neurologic deficits. The diagnosis is confirmed by the MRI showing an enhancing anterior epidural collection causing severe spinal cord compression. The neurologic findings, including paraparesis, a sensory level at T10, and bladder dysfunction, indicate acute compromise of the spinal cord. While empiric broad-spectrum antibiotics are initiated immediately, isolated medical therapy is inadequate once neurologic deficits manifest. The definitive treatment for an SEA with active cord compression is emergent surgical decompression (typically via laminectomy) and purulent debridement. Prompt surgical intervention is critical to relieve mechanical pressure and prevent permanent paralysis.

Step-by-Step Solution

1
Identify the clinical syndrome from the patient's presentation.
The patient has the classic triad of a spinal epidural abscess: fever, severe back pain, and neurologic deficits.
Recognizing the syndrome establishes the need for immediate intervention.
2
Localize the neurologic lesion based on physical examination findings.
A sensory level at the umbilicus (T10), bilateral lower extremity weakness, hyperreflexia, and urinary retention indicate an upper motor neuron lesion in the thoracic spinal cord.
Localization correlates with the subsequent imaging findings to confirm the cause of the deficits.
3
Interpret the imaging results provided in the stem.
The MRI confirms a compressive thoracic epidural abscess causing severe central canal stenosis.
Imaging differentiates an epidural abscess from other causes of myelopathy, such as transverse myelitis or malignancy.
4
Determine the therapeutic indication based on the neurologic status.
Because the patient has acute, progressive neurologic deficits (paraparesis and bowel/bladder dysfunction), conservative medical management is insufficient.
Mechanical compression must be relieved immediately to salvage spinal cord function and prevent permanent paralysis.
5
Select the definitive intervention.
Emergent surgical laminectomy and debridement is selected as the next best step.
Open surgical decompression directly relieves the pressure on the spinal cord and allows for source control of the infection.

Key Concept

Management of a spinal epidural abscess complicated by neurologic deficits requires emergent surgical decompression via laminectomy in addition to broad-spectrum antibiotics.
Question 89Question →

A 28-year-old man is brought to the emergency department after a high-speed motorcycle collision. In the field, his Glasgow Coma Scale (GCS) score was 6, and he was immediately intubated. On arrival, his blood pressure is 170/100 mm Hg, and his heart rate is 50/min. His right pupil is 7 mm and nonreactive to light, while his left pupil is 3 mm and briskly reactive. Extensor posturing is noted on the left side in response to painful stimuli. A stat non-contrast head CT reveals a large right-sided acute subdural hematoma with a 15-mm midline shift. Arrange the following interventions in the most appropriate chronological sequence for managing this patient's condition, from the most immediate initial bedside action to definitive ongoing care.

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Answer

The correct sequence of actions is: 1) Elevate the head of the bed and ensure neutral neck alignment, 2) Administer intravenous hyperosmolar therapy, 3) Transfer for emergent craniotomy, 4) Admit for ICU monitoring.
In a patient presenting with severe traumatic brain injury and signs of uncal herniation (ipsilateral fixed and dilated pupil, contralateral extensor posturing, and Cushing reflex), management must follow a logical, stepwise approach prioritizing speed and availability. First, mechanical interventions such as elevating the head of the bed to 30 degrees and ensuring neutral neck alignment should be performed instantly to maximize jugular venous outflow. Second, hyperosmolar agents (hypertonic saline or mannitol) should be administered to medically reduce cerebral edema and intracranial pressure. These initial steps serve as a critical bridge to the third step: definitive surgical decompression via craniotomy and hematoma evacuation. Finally, following surgery, the patient requires ongoing postoperative monitoring in the intensive care unit to manage potential secondary brain injury and ensure adequate cerebral perfusion pressure.

Step-by-Step Solution

1
Recognize signs of increased intracranial pressure (ICP) and impending herniation.
The patient has Cushing reflex (hypertension, bradycardia) and a dilated, unreactive right pupil indicating right uncal herniation.
Identifying uncal herniation dictates the need for immediate, stepwise ICP reduction and emergent surgical decompression.
2
Prioritize immediate bedside interventions that do not require medication preparation.
Elevate the head of the bed to 30 degrees and maintain a neutral neck position.
This physical maneuver immediately optimizes jugular venous outflow, quickly decreasing ICP while pharmacologic agents are being prepared.
3
Initiate temporizing medical management.
Administer hyperosmolar therapy (mannitol or hypertonic saline).
Hyperosmolar agents create an osmotic gradient to pull fluid from the brain parenchyma into the intravascular space, rapidly lowering ICP as a bridge to surgery.
4
Perform definitive treatment.
Transfer the patient to the operating room for a craniotomy and evacuation of the subdural hematoma.
Surgical decompression is the definitive lifesaving treatment to reverse brainstem compression caused by the expanding hematoma.
5
Plan for postoperative care.
Admit the patient to the neurosurgical intensive care unit (NICU) with continuous ICP monitoring.
After severe traumatic brain injury and surgery, close monitoring in the ICU is required to optimize cerebral perfusion pressure and prevent secondary insults.

Key Concept

The stepwise management of acute traumatic brain injury with impending herniation prioritizes immediate physical bedside maneuvers to reduce intracranial pressure, followed by medical temporizing measures (hyperosmolar therapy), definitive surgical decompression, and subsequent intensive care monitoring.
Estimated Time:1m 30s
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