41: Neurosurgery Flashcards
What happens to the below values in a patient with diabetes insipidus?
- Urine output
- Urine specific gravity
- Serum Na
- Serum osmolarity
- Urine output: Increased
- Urine specific gravity: Decreased
- Serum Na: Increased
- Serum osmolarity: Increased
[UpToDate: In the absence of a glucose-induced osmotic diuresis in uncontrolled diabetes mellitus, there are three major causes of polyuria in the outpatient setting, each of which is due to a defect in water balance leading to the excretion of large volumes of dilute urine (urine osmolality usually below 250 mosmol/kg): primary polydipsia, which is primarily seen in adults and adolescents; central diabetes insipidus (DI); and nephrogenic DI.
Primary polydipsia — Primary polydipsia (sometimes called psychogenic polydipsia) is characterized by a primary increase in water intake. This disorder is most often seen middle-aged women and in patients with psychiatric illnesses, including those taking a phenothiazine which can lead to the sensation of a dry mouth. Primary polydipsia can also be induced by hypothalamic lesions that directly affect the thirst center, as may occur with an infiltrative disease such as sarcoidosis.
Central DI — Central DI (also called neurohypophyseal or neurogenic DI) is associated with deficient secretion of antidiuretic hormone (ADH). This condition is most often idiopathic (possibly due to autoimmune injury to the ADH-producing cells), or can be induced by trauma, pituitary surgery, or hypoxic or ischemic encephalopathy. Rare familial cases have been described.
Nephrogenic DI — Nephrogenic DI is characterized by normal ADH secretion but varying degrees of renal resistance to its water-retaining effect. This problem, in its mild form, is relatively common since most patients who are elderly or who have underlying renal disease have a reduction in maximum concentrating ability. This defect, however, is not severe enough to produce a symptomatic increase in urine output.
Each of the three causes of polyuria – primary polydipsia, central DI, and nephrogenic DI – is associated with an increase in water output and the excretion of a relatively dilute urine. With primary polydipsia, the polyuria is an appropriate response to enhanced water intake; in comparison, the water loss is inappropriate with either form of DI. Measurement of the plasma sodium concentration and the urine osmolality may be helpful in distinguishing between these disorders:
- A low plasma sodium concentration (less than 137 meq/L) with a low urine osmolality (eg, less than one-half the plasma osmolality) is usually indicative of water overload due to primary polydipsia
- A high-normal plasma sodium concentration (greater than 142 meq/L, due to water loss) points toward DI, particularly if the urine osmolality is less than the plasma osmolality.
- A normal plasma sodium concentration is not helpful in diagnosis but, if associated with a urine osmolality more than 600 mosmol/kg, excludes a diagnosis of DI.
In adults with DI and no cognitive impairment, true hypernatremia (plasma sodium concentration greater than 150 meq/L) should not occur because the initial loss of water stimulates thirst, resulting in an increase in intake to match the urinary losses. An exception to this general rule occurs when DI is due to a central lesion that also impairs thirst, thereby causing hypodipsia or adipsia; in this setting, the plasma sodium concentration can exceed 160 meq/L. Adipsic DI is associated with significant morbidity including obesity, sleep apnea, venous thrombosis during episodes of hypernatremia, thermoregulatory dysfunction, seizures, and significant mortality.]
What are the following characteristics of spinal shock?
- 3 main symptoms
- Occurs with injury at what level of spinal cord
- Treatment
- 3 main symptoms: Hypotension, normal or slow heart rate, warm extremities
- Occurs with injury at what level of spinal cord: T5 (loss of sympathetic tone)
- Treatment: Fluids initially, may need phenylephrine drip (alpha agonist)
[UpToDate: Immediately after a spinal cord injury, there may be a physiological loss of all spinal cord function caudal to the level of the injury, with flaccid paralysis, anesthesia, absent bowel and bladder control, and loss of reflex activity. In males, especially those with a cervical cord injury, priapism may develop. There may also be bradycardia and hypotension not due to causes other than the spinal cord injury. This altered physiologic state may last several hours to several weeks and is sometimes referred to as spinal shock.
We believe that this loss of function may be caused by the loss of potassium within the injured cells in the cord and its accumulation within the extra-cellular space, causing reduced axonal transmission. As the potassium levels normalize within the intracellular and extra-cellular spaces, this spinal shock wears off. Clinical manifestations may normalize, but are more usually replaced by a spastic paresis reflecting more severe morphologic injury to the spinal cord.
A transient paralysis with complete recovery is most often described in younger patients with athletic injuries. These patients should undergo evaluation for underlying spinal disease before returning to play.]
What happens to the below values in a patient with the syndrome of inappropriate antidiuretic hormone secretion (SIADH)?
- Urine output
- Urine concentration
- Serum Na
- Serum osmolarity
- Urine output: Decreased
- Urine concentration: Increased
- Serum Na: Decreased
- Serum osmolarity: Decreased
[Can occur with a head injury]
[UpToDate: SIADH should be suspected in any patient with hyponatremia, hypoosmolality, and a urine osmolality above 100 mosmol/kg. In SIADH, the urine sodium concentration is usually above 40 meq/L, the serum potassium concentration is normal, there is no acid-base disturbance, and the serum uric acid concentration is frequently low.
ADH secretion results in a concentrated urine and therefore a reduced urine volume. In most patients with SIADH, ingestion of water does not adequately suppress ADH, and the urine remains concentrated. This leads to water retention, which increases total body water (TBW). This increase in TBW lowers the plasma sodium concentration by dilution. In addition, the increase in TBW transiently expands the extracellular fluid volume and thereby triggers increased urinary sodium excretion, which both returns the extracellular fluid volume toward normal and further lowers the plasma sodium concentration.]
At what rate do nerves regenerate?
1mm/day
What is antidiuretic hormone (ADH) released in response to?
High plasma osmolarity
[ADH increases water absorption in collecting ducts.]
Which type of intracranial hemorrhage is described by each of the following?
- Caused by torn bridging veins
- Caused by injury to the middle meningeal artery
- Crescent shap on head CT
- Lens shape on head CT
- Classic presentation with LOC -> Lucid interval -> LOC
- Caused by torn bridging veins: Subdural hematoma
- Caused by injury to the middle meningeal artery: Epidural hematoma
- Crescent shap on head CT: Subdural hematoma
- Lens shape on head CT: Epidural hematoma
- Classic presentation with LOC -> Lucid interval -> LOC: Epidural hematoma
[UpToDate: Epidural hematoma (EDH) is caused by bleeding in the potential space between the dura and the skull, usually as a consequence of traumatic injury. Nontraumatic acute EDH is rare. The incidence of EDH is highest among adolescents and young adults. EDH is rare in patients older than 50 to 60 years of age.
The source of blood in EDH is most often arterial, but 15% of cases are due to venous bleeding. The major cause of arterial injury is trauma to the sphenoid bone with associated tearing of the middle meningeal artery, resulting in hemorrhage over the cerebral convexity in the middle cranial fossa.
Clinical manifestations of EDH are highly variable, and include altered consciousness, headache, vomiting, drowsiness, confusion, aphasia, seizures, and hemiparesis. Some patients with acute EDH and transient loss of consciousness have a “lucid interval” with recovery of consciousness, followed by deterioration due to hematoma enlargement. Spinal EDH may present with signs that include local back pain, paraparesis, sensory loss with a discernible level, and bowel or bladder incontinence.
Head CT is a fast and accurate method for the detection of acute intracranial hemorrhage. Epidural blood produces a lens-shaped pattern on head CT. Brain MRI has a higher sensitivity than CT and can be useful when diagnostic uncertainty exists.
The majority of patients have a good recovery after EDH, but mortality in adults and children is approximately 10% and 5%, respectively. Factors associated with prognosis include the severity of neurologic deficits (generally quantified by the Glasgow coma scale score), presence of pupillary abnormalities, hematoma volume, the degree of midline brain shift, and the presence and severity of associated trauma.
Most patients with focal neurologic signs or symptoms attributable to acute EDH require emergent surgical hematoma evacuation to prevent irreversible brain injury or death caused by hematoma expansion, elevated intracranial pressure, and brain herniation. Even in patients who are comatose on admission or have early signs of brain herniation, we recommend urgent surgical hematoma evacuation given the potential for recovery.
For adult patients with acute EDH who are awake and have no focal neurologic deficits, we suggest management based upon the size of the hematoma and the degree of midline shift (Grade 2C). Patients who have a small (<30 cm^3) hematoma with clot thickness <15 mm and midline shift <5 mm on brain imaging are managed nonoperatively with close observation, while those not meeting these criteria are managed surgically.
Nonoperative management of acute EDH requires close observation and serial brain imaging because of the risk of hematoma enlargement and neurologic deterioration. Thus, we recommend obtaining the first follow-up head CT scan no later than six to eight hours after head injury. For patients with acute EDH who have initially good clinical status but deteriorate with signs of brain herniation or elevated intracranial pressure, we recommend urgent surgical hematoma evacuation within 90 minutes of the onset of deterioration.
Subdural hematoma - The estimated overall mortality rate in patients with acute subdural hematoma (SDH) requiring surgery is 40% to 60%. Age and neurologic status, as assessed with the Glasgow coma scale, are important prognostic indicators. Head CT findings that correlate with poor outcome after SDH (in some but not all studies) include hematoma thickness and volume, the presence and/or degree of midline brain shift and reduced patency of the basal cisterns.
Urgent surgical hematoma evacuation is necessary for patients with acute or chronic SDH and the potential for recovery who are admitted with signs attributable to brain herniation or elevated intracranial pressure, such as asymmetric or fixed and dilated pupils.
For patients with acute SDH, with or without coma, who have evidence of neurologic deterioration since the time of injury and the potential for recovery, we recommend urgent surgical hematoma evacuation (Grade 1C). In addition, we suggest urgent surgical hematoma evacuation rather than nonoperative management for patients with clot thickness ≥10 mm or midline shift ≥5 mm on initial brain scan (Grade 2C). We suggest nonoperative management for patients not meeting these criteria (Grade 2C). Thus, nonoperative management is suggested for patients with acute SDH, including those with coma at presentation, who are clinically stable or improving, have no signs of brain herniation, and have clot thickness <10 mm and midline shift <5 mm on initial head CT.
Patients with acute SDH and diminished consciousness or coma who are managed nonoperatively should be observed in an intensive care unit with intracranial pressure monitoring and serial head CT scans. We suggest that the first follow-up head CT scan should be obtained within six to eight hours of the initial scan for patients with acute traumatic SDH. If a nonoperatively managed patient develops clinical signs of neurologic deterioration, or if intracranial pressure is persistently >20 mmHg, we recommend urgent surgical evacuation within two to four hours of deterioration (Grade 1C).
For patients with chronic SDH and the potential for recovery, we recommend surgical hematoma evacuation if there is evidence of moderate to severe cognitive impairment or progressive neurologic deterioration attributable to the chronic SDH (Grade 1C). In addition, we suggest surgical hematoma evacuation rather than nonoperative management if there is clot thickness ≥10 mm or midline shift ≥5 mm on brain scan (Grade 2C).]
What are the answers to the following questions?
- Name for the region of the brain that is responsible for speech comprehension
- Name for the region of the brain that is responsible for speech motor
- Cervical nerve roots that innervate the diaphragm
- Cells that act as brain macrophages
- Name for the region of the brain that is responsible for speech comprehension: Wernickes’s area
- Name for the region of the brain that is responsible for speech motor: Broca’s area
- Cervical nerve roots that innervate the diaphragm: C3-C5
- Cells that act as brain macrophages: Microglial cells
[UpToDate: The vascular supply of the diaphragm is derived from the phrenic artery below the diaphragm and the pericardiophrenic arteries above the diaphragm. The phrenic nerve originates from the anterior rami of C3, C4, and C5 and traverses the neck and mediastinum before inserting into the diaphragm centrally. The outer rim of the diaphragmatic muscle is innervated laterally from the T7 through T12. The crural group of muscles receives innervation from the vagus nerve.]
What are the following spinal cord tracts responsible for?
- Spinothalamic tract
- Corticospinal tract
- Rubrospinal tract
- Dorsal nerve roots
- Ventral nerve roots
- Spinothalamic tract: Pain and temperature sensation
- Corticospinal tract: Motor
- Rubrospinal tract: Motor
- Dorsal nerve roots: Sensation
- Ventral nerve roots: Motor
Which spinal cord syndrome are characterized by each of the following?
- Bilateral loss of motor, pain, and temperature with preservation of position-vibratory sensation and light touch
- Loss of ipsilateral motor and contralateral pain/temperature
- Bilateral loss of motor, pain, and temperature in upper extremities with sparing of lower extremities
- Pain and weakness in lower extremities due to compression of lumbar nerve roots
- Bilateral loss of motor, pain, and temperature with preservation of position-vibratory sensation and light touch: Anterior spinal artery syndrome
- Loss of ipsilateral motor and contralateral pain/temperature: Brown-Sequard syndrome
- Bilateral loss of motor, pain, and temperature in upper extremities with sparing of lower extremities: Central cord syndrome
- Pain and weakness in lower extremities due to compression of lumbar nerve roots: Cauda equina syndrome
What do the following terms mean?
- Neuropraxia
- Axonotmesis
- Neurotmesis
- Neuropraxia: Temporary loss of function as in when foot falls asleep (No axonal injury:
- Axonotmesis: Disruption of axon with preservation of axon sheath (will improve with time)
- Neurotmesis: Disruption of axon and axon sheath (whole nervie is disrupted and may require surgery for recovery)
What are the following characteristics of subarachnoid hemorrhage?
- Usual causes
- Symptoms
- Treatment
- Usual causes: Cerebral aneurysms (50% middle cerebral artery), AVMs, and trauma
- Symptoms: Stiff neck (nuchal rigidity), severe headache, photophobia, neurologic defects
- Treatment: Clipping vascular supply of aneurysm (Goal is to isolate aneurysm from systemic circulation), Maximize cerebral perfusion to overcome vasospasm (use hypervolemia and calcium channel blockers to overcome vasospasm)
[Go to OR only if neurological defecits are present.]
[UpToDate: The primary symptom of aneurysmal SAH is a sudden, severe headache (97% of cases) classically described as the “worst headache of my life”. The headache is lateralized in 30% of patients, predominantly to the side of the aneurysm. Consistent with the rapid spread of blood, the symptoms of SAH typically begin abruptly.
The onset of the headache may or may not be associated with a brief loss of consciousness, nausea or vomiting, and meningismus In one series, these occurred in 53%, 77%, and 35% of patients respectively. Meningismus and often lower back pain may not develop until several hours after the bleed since it is caused by the breakdown of blood products within the CSF, which lead to an aseptic meningitis. While many patients have an altered level of consciousness, coma is unusual. Seizures occur during the first 24 hours in less than 10% of patients, but are a predictor of poor outcome. SAH may also present as sudden death; at least 10% to 15% of patients die before reaching the hospital.
The complaint of the sudden onset of severe headache is sufficiently characteristic that a SAH should always be considered. In a prospective study of 148 patients presenting with sudden and severe headache, for example, SAH was present in 25% overall and in 12% of those in whom headache was the only symptom. Similar findings were noted in another report in which 20 of 107 patients with the “worst headache of my life” had an SAH.
An estimated 15% to 20% of patients with subarachnoid hemorrhage (SAH) are nonaneurysmal. The causes of nonaneurysmal SAH (NASAH) are potentially diverse, and the mechanism of bleeding in these cases is often not identified.
Patients with aneurysmal SAH are admitted to an intensive care setting for continuous hemodynamic and neurologic monitoring. Initial management includes bedrest, analgesia, pneumatic compression stockings, and discontinuation of antithrombotics. Hypoxemia, metabolic acidosis, hyperglycemia, cardiovascular instability are common complications, worsen outcome and should be prevented and promptly treated.
A ventriculostomy is placed in patients with elevated intracranial pressure (ICP) with acute hydrocephalus and allows measurement and treatment of elevated ICP.
The optimal therapy of hypertension in SAH is not clear. While lowering blood pressure may decrease the risk of rebleeding, this benefit may be offset by an increased risk of infarction. A decrease in systolic blood pressure to <160 mm Hg in the setting of an unsecured aneurysm is reasonable. Agents such as labetalol, nicardipine, and enalapril are preferred.
Nimodipine (60 mg by mouth or nasogastric tube every four hours) has been demonstrated to improve neurologic outcomes in SAH. Treatment is started within four days of onset and is continued for 21 days. The mechanism of benefit of nimodipine in SAH is unknown.
Prophylactic antiepileptic drug (AED) therapy is not required in all patients, but may be considered in some with unsecured aneurysms and large concentrations of blood at the cortex. Seizures should be treated promptly. Continuation of AED therapy may not be necessary in patients without acute seizures after the aneurysm is secured. AEDs are usually continued for approximately six months in patients who have experienced an acute seizure (within seven days) following SAH.
Aneurysmal rebleeding is associated with a very high mortality. Surgical clipping and endovascular coiling are effective in preventing rebleeding and generally should be performed early. Short-term use of antifibrinolytic agents to prevent rebleeding can be considered in those whose aneurysm treatment is unavoidably delayed.
Clinically significant vasospasm complicates 20% to 30% of aneurysmal SAH and is associated with delayed cerebral ischemia and worse neurologic outcome:
Hypovolemia is a risk factor for ischemic complications and should be avoided.
- There is limited data to suggest that hyperdynamic therapy is of value in the prevention of symptomatic vasospasm but may be used to ameliorate documented vasospasm in a patient with a secured aneurysm. Hyperdynamic therapy employs maintenance of euvolemia with induced hypertension with pressor agents.
- Clinical vasospasm that persists despite hyperdynamic therapy may be treated by percutaneous intraarterial angioplasty or intraarterial administration of vasodilators. There is limited data suggesting that their use improves clinical outcomes.
- Limited data suggests that statin therapy (pravastatin 40 mg daily or simvastatin 80 mg daily) may reduce the incidence of vasospasm, delayed ischemic deficits and mortality.
Hydrocephalus is a common complication of SAH. Placement of a ventricular drain should be considered in patients with impaired level of consciousness and progressive or not improving hydrocephalus. Some patients may require placement of a permanent shunt.
Hyponatremia is common after SAH usually due to SIADH.
Mortality within the first 30 days after SAH approaches 50% and is attributed largely to the effects of initial and recurrent bleeding. The most important predictive factors for acute prognosis after SAH include: level of consciousness and neurologic grade on admission, patient age, amount of blood on initial CT scan.]
What are the following characteristics of spine tumors?
- Most common tumor
- Intradural tumors are more likely what (benign or malignant)
- Extradural tumors are more likely what (benign or malignant)
- Most common tumor: Neurofibroma
- Intradural tumors are more likely what (benign or malignant): More likely benign
- Extradural tumors are more likely what (benign or malignant): More likely malignant
What are the following characteristics of central cord syndrome?
- Most common cause
- Neurological deficits
- Preserved neurological function
- Most common cause: Hyperflexion of cervical spine
- Neurological deficits: Bilateral loss of motor, pain, and temperature in upper extremities
- Preserved neurological function: Lower extremities spared
What is the treatment for syndrome of inappropriate antidiuretic hormone secretion (SIADH)?
Fluids followed by diuresis
[UpToDate: Fluid restriction is the mainstay of the treatment of most patients with SIADH, with a suggested goal intake of less than 800 mL/day; patients with subarachnoid hemorrhage are an exception since fluid restriction may promote cerebral vasospasm.
In addition to fluid restriction, the therapy of SIADH-associated hyponatremia often requires the administration of sodium chloride, either as oral salt tablets or intravenous saline. When using intravenous saline, the electrolyte concentration of the administered fluid must be greater than the electrolyte concentration of the urine. This usually requires the use of hypertonic saline. Isotonic saline is infrequently effective and often leads to further lowering of the serum sodium.
Among patients with a urine osmolality more than twice the plasma osmolality (which typically means a urine osmolality above 500 mosmol/kg), a loop diuretic may be used to reduce urinary concentration, thereby increasing water excretion.
The vasopressin receptor antagonists produce a selective water diuresis without affecting sodium and potassium excretion. Intravenous conivaptan (which is used in hospitalized patients) and oral tolvaptan are available and approved for use in patients with hyponatremia due to SIADH. The utility of tolvaptan therapy is limited by concerns about hepatotoxicity, excessive thirst, prohibitive cost (at least in the United States), and the potential for overly rapid correction of the hyponatremia which has led to the necessity for hospitalization for the initiation of therapy. Because of potential hepatotoxicity, tolvaptan should not be used for longer than 30 days and should not be given to patients with liver disease (including cirrhosis).
The maximum rate of correction of chronic hyponatremia should be less than 10 meq/L at 24 hours and less than 18 meq/L at 48 hours. The serum sodium concentration should be checked at two to three hours initially and then every three to four hours until the patient is stable. In selected patients with severe hyponatremia who are correcting too rapidly, prevention of further short-term elevation in serum sodium or even relowering of the serum sodium may be warranted.]
What are the following characteristics of cerebral aneurysms?
- Common age at presentation
- Presenting signs/symptoms
- Most common vessel involved
- Treatment
- Common age at presentation: >40 years old
- Presenting signs/symptoms: Bleeding, mass effect, seizures, infarcts
- Most common vessel involved: Middle cerebral artery (occur at branch points)
- Treatment: Place coils before clipping and resecting aneurysm
[UpToDate: The prevalence of intracranial saccular aneurysms by radiographic and autopsy series is estimated to be 3.2% in a population without comorbidity, a mean age of 50 years, and a 1:1 gender ratio,. Of patients with cerebral aneurysms, 20% to 30% have multiple aneurysms. Aneurysmal SAH occurs at an estimated rate of 6 to 16 per 100,000 population. In North America, this translates into approximately 30,000 affected persons per year. Thus, most aneurysms, particularly small aneurysms, do not rupture.
Rupture of an intracranial aneurysm is believed to account for 0.4% to 0.6% of all deaths. Approximately 10% of patients die prior to reaching the hospital, and only one-third has a “good result” after treatment.
Most intracranial aneurysms (approximately 85%) are located in the anterior circulation, predominantly on the circle of Willis. Common sites include the junction of the anterior communicating artery with the anterior cerebral artery, the junction of the posterior communicating artery with the internal carotid artery, and the bifurcation of the middle cerebral artery. Posterior circulation sites often include the top of the basilar artery, the junction of the basilar artery and the superior or anterior inferior cerebellar arteries, and the junction of the vertebral artery and the posterior inferior cerebellar artery.
There is a female preponderance for aneurysms ranging from 54% to 61%. In populations older than 50 years, the increased prevalence in women may approach a 2 to 1 ratio or greater.
Surgical clipping and endovascular coiling are the most commonly used techniques for aneurysm treatment. In many cases, anatomic considerations, such as size, location, other morphological features determine which treatment is most appropriate for the patient.
Patients with ruptured cerebral aneurysms present with aneurysmal subarachnoid hemorrhage (SAH). Patients have a high risk of rebleeding in the first days and hours after SAH, and this complication is associated with increased mortality and morbidity.
Decisions regarding the timing and choice of therapy for a ruptured intracranial aneurysms are ideally made by a team of experienced clinicians who consider the neurologic grade and clinical status of the patient, the availability of expertise in surgical and endovascular techniques, as well as the anatomic characteristics of the aneurysm.
- For patients with good grade aSAH (Hunt and Hess grades I to III) (table 1), we suggest early aneurysm repair (within 24 to 72 hours) (Grade 2C). In centers with available expertise and in patients with endovascularly-accessible lesions, short term outcomes appear to be improved with endovascular coiling as compared to surgical clipping.
- The optimal timing and choice of therapy in patients with more severe aSAH (Hunt and Hess grades IV and V) is uncertain. There overall prognosis is poor, particularly for older patients. Treatment decisions need to be individualized in consultation with family members.
Asymptomatic aneurysms ≥7 to 10 mm in diameter warrant strong consideration for treatment, taking into account patient age, existing medical and neurologic conditions, and relative risks for treatment. This is discussed separately
Patients with aneurysmal SAH are at enduring risk of recurrent SAH despite aneurysm treatment and may require follow-up evaluations.]
Which region of the brain controls the release of antidiuretic hormone (ADH)?
Supraoptic nucleus of hypothalamus
[UpToDate: Unlike the anterior pituitary, which does not have nerve terminals, the posterior pituitary contains the axons and nerve terminals of larger neurons that originate in the paraventricular and supraoptic nuclei of the hypothalamus. The posterior pituitary is supplied by the inferior hypophyseal artery and drains into the inferior hypophyseal veins where its products, vasopressin and oxytocin, are released directly into the systemic circulation.]
What are the following characteristics of Brown-Sequard syndrome?
- Most common cause
- Neurological deficits
- Percent that recover to ambulation
- Most common cause: Penetrating injury (Incomplete cord transection)
- Neurological deficits: Loss of ipsilateral motor and contralateral pain/temperature below level of lesion
- Percent that recover to ambulation: 90%
What is the difference between a meningocele and a myelomeningocele?
Myelomeningocele is a herniation of spinal cord and nerve roots through a defect in the vertebra, most commonly occuring in ght lumbar region.
[Meningocele is just herniation of the meninges.]
What are the following characteristics of arteriovenous malformations?
- Common age at presentation
- Percent that present with hemorrhage
- Treatment
- Common age at presentation: <30 years old (sudden headache and loss of consciousness)
- Percent that present with hemorrhage: 50%
- Treatment: Resection if symptomatic (can coil embolize prior to resection)
[UpToDate: Brain arteriovenous malformations (AVMs) are considered to be sporadic congenital developmental vascular lesions. They occur in about 0.1% of the population. These are usually single, supratentorial lesions; their size can vary widely.
The angioarchitecture of brain AVMs is direct arterial to venous connections without an intervening capillary network. Aneurysms arise in 20% to 25% of lesions.
Brain AVMs usually present between the ages of 10 and 40 years with either intracranial hemorrhage, seizure, headache, and focal neurologic deficit. Hemorrhage is the most common presentation, particularly in children.
Overall, annual hemorrhage rates from brain AVMs are between 3%. After an initial hemorrhage, annual hemorrhage rates are approximately 5%.
Brain AVMs can be detected on computed tomography or magnetic resonance imaging (MRI). MRI is more sensitive, particularly in the setting of an acute intracerebral hemorrhage. Angiography is the gold standard for the diagnosis, treatment planning, and follow-up after treatment of brain AVMs.
A number of variables are factored into the decision to treat AVMs and the therapy chosen. Surgery is the mainstay of treatment; radiosurgery is a useful option in lesions deemed at high risk for surgical therapy, and endovascular embolization has become a useful adjunct to these techniques. Important considerations in the choice of treatment are the patient’s age, lesion size and location, and prior history of intracerebral hemorrhage.]
What are the following characteristics of anterior spinal artery syndrome?
- Most common cause
- Neurological deficits
- Preserved neurological function
- Percent that recover to ambulation
- Most common cause: Acutely ruptured cervical disc
- Neurological deficits: Bilateral loss of motor, pain, and temperature below the level of the lesion
- Preserved neurological function: Preservation of position-vibratory sensation and light touch
- Percent that recover to ambulation: 10%
[UpToDate: The most common clinical presentation of a spinal cord infarction is anterior spinal artery (ASA) syndrome. Consistent with its functional neuroanatomy, an ASA infarct typically presents as loss of motor function and pain/temperature sensation, with relative sparing of proprioception and vibratory sense below the level of the lesion. The acute stages are characterized by flaccidity and loss of deep tendon reflexes; spasticity and hyperreflexia develop over ensuing days and weeks. Autonomic dysfunction may be present and can manifest as hypotension (either orthostatic or frank hypotension), sexual dysfunction, and/or bowel and bladder dysfunction. Chest pain with ECG changes has been reported in a patient with C7 to T1 spinal cord infarction. In the acute evaluation of patients, it is important to recognize that hypotension may be both a cause as well as a manifestation of spinal cord ischemia. If the lesion is in the rostral cervical cord, respiration is compromised.
While bilateral presentations are more common, unilateral ASA deficits are frequently reported. This occurs either because of occlusion of a unilateral sulcal artery, or because incomplete collateralization with the PSA maintains perfusion on one side of the cord. Very rostral ASA infarctions produce sensory loss in all modalities because of involvement of the medial lemniscus in the medulla.]
