Neurologic Disorders I

Transient monocular visual loss and aphasia are the clinical manifestations of a transient ischemic attack (TIA) in the carotid territory (Denke, 2021, p. 4).

Symptoms of a TIA mimic stroke symptoms, and the specific findings depend on the arterial territory that is involved (Denke, 2021, p. 4).

Choice a is wrong because vertebrobasilar, or brainstem, involvement produces cranial nerve impairments that lead to limb weakness, ataxia, vertigo, and dysphagia rather than isolated monocular visual loss (Denke, 2021, p. 4).

Choice c is wrong because perforating artery disease produces symptoms similar to those of a lacunar stroke, with hemisensory or hemimotor symptoms affecting the face, arm, and leg (Denke, 2021, p. 5).

Choice d is wrong because abnormal oculomotor signs with nystagmus, lateral gaze, and diplopia are manifestations of vertebrobasilar disease rather than isolated monocular visual loss (Denke, 2021, p. 5).

A TIA is an important predictor of stroke, and the 90-day risk of stroke after a TIA is as high as 17% (Denke, 2021, p. 4).

The greatest risk of having a stroke is within the first 2 days after a TIA, with about 50% of strokes occurring within the first year (Denke, 2021, p. 4).

Hypertension greater than 140/90 mm Hg is a risk factor for TIA, and cardiac disease such as arrhythmia, including atrial fibrillation, is also a risk factor (Denke, 2021, p. 4).

Choice a is wrong because migraine is listed as a mimic of stroke or TIA rather than as a risk factor for recurrent stroke after a TIA (Denke, 2021, p. 4).

Choice c is wrong because a glucose of 104 mg/dl is not hypoglycemic, and hypoglycemia less than 60 mg/dl is the value listed as a mimic of TIA or stroke (Denke, 2021, p. 3).

Choice d is wrong because diplopia and vertigo describe vertebrobasilar involvement during the event rather than the 90-day risk of recurrence (Denke, 2021, p. 5).

The middle cerebral artery is the largest vessel branching off the internal carotid artery and is the most common site of occlusion, and a complete middle cerebral artery stroke causes hemiplegia of the contralateral side affecting the lower part of the face, arm, and hand while largely sparing the leg, with contralateral sensory loss in the same areas and contralateral homonymous hemianopia (Denke, 2021, p. 14).

A left, or dominant, hemisphere stroke may also cause aphasia, which is a partial or total loss of the ability to communicate through language (Denke, 2021, p. 14).

Choice a is wrong because the classic signs of an anterior cerebral artery stroke are contralateral leg weakness and sensory loss with leg greater than arm involvement, which is the opposite of this patient's pattern (Denke, 2021, p. 14).

Choice c is wrong because a posterior cerebral artery stroke presents with acute vision loss, usually contralateral homonymous hemianopia, because the posterior cerebral artery feeds the occipital lobe (Denke, 2021, p. 15).

Choice d is wrong because vertebral and basilar artery occlusion affects the cerebellum, brain stem, or both and produces decreased level of consciousness, vertigo, dysphagia, dysarthria, diplopia, and ipsilateral cranial nerve findings rather than the face and arm pattern described here (Denke, 2021, p. 15).

Exclusion criteria for alteplase include a current intracerebral hemorrhage, subarachnoid hemorrhage, active internal bleeding, and recent intracranial or intraspinal surgery or serious head trauma within 3 months (Denke, 2021, p. 19).

Additional exclusion criteria include intracranial conditions that may increase the risk of bleeding, such as some neoplasms, arteriovenous malformations, or aneurysms, as well as bleeding diathesis and current severe uncontrolled hypertension (Denke, 2021, pp. 19–20).

Choice a is wrong because for patients who are candidates for tissue plasminogen activator (tPA), the blood pressure should be lowered to a systolic blood pressure less than 185 mm Hg and a diastolic blood pressure less than 110 mm Hg before tPA is administered, so this value does not exclude her (Denke, 2021, p. 20).

Choice b is wrong because hyperglycemia during the first 24 hr is associated with worse outcomes and should be treated, but this value does not exclude the patient from alteplase (Denke, 2021, p. 23).

Choice c is wrong because treatment with alteplase may also benefit those with mild symptoms, so a low NIHSS score is not an exclusion (Denke, 2021, p. 20).

Before an aneurysm ruptures or bleeds, the patient may have an oculomotor nerve, or CN III, palsy with a dilated pupil, possible ptosis, pain above or behind the eye, a localized headache, and deficits in extraocular movements with CN IV and CN VI involvement (Denke, 2021, p. 40).

Small intermittent leakage of blood may result in neck pain, headache, and nausea and vomiting, and this patient has none of those findings (Denke, 2021, p. 40).

Choice b is wrong because unilateral hearing loss is the most common initial symptom of an acoustic neuroma arising from CN VIII, and it is not a recognized presentation of a cerebral aneurysm (Denke, 2021, p. 58).

Choice c is wrong because unilateral or bilateral sixth nerve palsy with papilledema is a classic assessment finding in hydrocephalus secondary to increased intracranial pressure, not the presenting pattern of an unruptured aneurysm (Denke, 2021, p. 51).

Choice d is wrong because unilateral exophthalmos and anosmia occur with meningioma at the sphenoidal ridge or olfactory groove rather than with a cerebral aneurysm (Denke, 2021, pp. 58–59).

The Hunt and Hess classification is based on clinical assessment, and Grade II is defined as cranial nerve palsy or moderate to severe headache with nuchal rigidity (Denke, 2021, p. 26).

Grading scales provide a standardized way to describe patients with subarachnoid hemorrhage among providers (Denke, 2021, p. 26).

Choice a is wrong because Grade I is defined as asymptomatic or slight headache, and this patient has a severe headache with nuchal rigidity (Denke, 2021, p. 26).

Choice c is wrong because Grade III is defined as a mild focal deficit, lethargy, or confusion, and this patient has none of these findings (Denke, 2021, p. 26).

Choice d is wrong because Grade IV is defined as stupor and/or hemiparesis, which this patient does not demonstrate (Denke, 2021, p. 26).

Myasthenia gravis (MG) is a disorder of the neuromuscular junction resulting in a pure motor syndrome, and it is characterized by weakness that may fluctuate most notably after prolonged muscle use, particularly of the extraocular, pharyngeal, facial, cervical, proximal limb, and respiratory musculature (Durham, 2021, p. 74).

Ocular muscles are affected initially in 40% of patients and eventually in 80%, and ptosis, diplopia, and fatigue after exercise are characteristic, whereas sensory modalities and deep tendon reflexes remain normal (Durham, 2021, p. 75).

Choice a is wrong because symmetric ascending weakness with absent deep tendon reflexes is the classic pattern of Guillain-Barré syndrome (GBS) rather than MG (Durham, 2021, p. 70).

Choice b is wrong because MG affects the extraocular muscles early, and proximal limb weakness occurs in addition to ocular involvement rather than while the ocular muscles are spared (Durham, 2021, pp. 74–75).

Choice d is wrong because unilateral facial paralysis with loss of taste is characteristic of Bell's palsy, which is listed as a mimic of stroke and TIA rather than a presentation of MG (Denke, 2021, p. 4).

Common precipitating factors for myasthenic crisis include infections, stress such as trauma or surgery, rapid introduction, escalation, or tapering of steroids, and withdrawal of cholinesterase inhibitors (Durham, 2021, p. 75).

Myasthenic crisis is defined by respiratory failure, occurs in up to 20% of patients with MG, and requires mechanical ventilation, and patients with muscle-specific kinase (MuSK) antibody positivity are more likely to have a crisis (Durham, 2021, p. 75).

Patients with bulbar weakness, a declining vital capacity, a maximal inspiratory force of negative 30 cm H2O, or a weak and ineffective cough that increases the work of breathing should be admitted to an intensive care unit to monitor for possible intubation and mechanical ventilation (Durham, 2021, p. 79).

Choice b is wrong because pyridostigmine is first-line therapy for the general management of MG, and it is the withdrawal of cholinesterase inhibitors rather than their addition that precipitates crisis (Durham, 2021, pp. 75, 77).

Choice c is wrong because hyperkalemia is not a recognized trigger for myasthenic crisis, and the listed precipitants are infection, stress, steroid changes, and cholinesterase inhibitor withdrawal (Durham, 2021, p. 75).

Choice a is wrong because patients with MG have a greater incidence of thyroid disease rather than hypothyroidism being a trigger for crisis, and thyroid function testing is indicated as part of the evaluation (Durham, 2021, p. 76).

Multiple sclerosis (MS) is a demyelinating disease of the central nervous system that is acquired and immune-mediated, and it is characterized by relapses and remissions (Kuric, 2021, p. 143).

Lhermitte's sign, described as electrical sensations in the limbs, is a subjective manifestation of MS, and optic neuritis may be the initial symptom in 25% of patients, with MRI demonstrating T2-weighted lesions in the periventricular white matter of the brain and spinal cord (Kuric, 2021, pp. 145–146).

Choice a is wrong because MG produces fluctuating weakness of the extraocular, pharyngeal, facial, cervical, proximal limb, and respiratory musculature without the sensory and visual findings described here (Durham, 2021, p. 74).

Choice b is wrong because GBS is an acute inflammatory demyelinating radiculoneuropathy of the peripheral nervous system with ascending weakness and areflexia, and it does not produce optic neuritis or periventricular white matter lesions (Durham, 2021, pp. 69–70).

Choice d is wrong because migraine is listed as a mimic of stroke and TIA, and it does not produce the demyelinating lesions or Lhermitte's sign seen in this patient (Denke, 2021, p. 4).

Relapsing-remitting MS is characterized by clear and defined episodes of relapses and recovery, with recovery that can be full or leave some residual deficit and no clinical progression between the relapse episodes, and it is the usual initial presentation in 85% to 90% of patients with MS (Kuric, 2021, p. 144).

Choice a is wrong because primary progressive MS involves continued disease progression from the initial neurologic episode and most commonly occurs in patients with onset after 40 years of age (Kuric, 2021, p. 144).

Choice b is wrong because secondary progressive MS usually begins as relapsing-remitting MS and is followed by deterioration or progression of the disease, with clinical progression noted between relapsing episodes, whereas this patient has no progression between episodes (Kuric, 2021, p. 144).

Choice d is wrong because progressive relapsing MS involves progressive disease from the onset with clear relapses after onset and continued progression between relapses, which does not match this patient's course (Kuric, 2021, p. 144).

Acute intervention for a relapse of MS is glucocorticoids given orally or intravenously, with high-dose therapy of 500 to 1000 mg/day usually given as intravenous methylprednisolone, and the duration depends on the clinical response (Kuric, 2021, p. 147).

Glucocorticoids are thought to promote early recovery from an exacerbation but do not have any long-term effect, and short-term pulse therapy is preferred to prevent long-term steroid effects (Kuric, 2021, p. 147).

Mild acute exacerbations that do not produce functional decline may not require treatment at all (Kuric, 2021, p. 147).

Choice b is wrong because low-dose oral prednisone is not the recommended regimen for an acute relapse, and high-dose therapy is used to promote early recovery (Kuric, 2021, p. 147).

Choice c is wrong because IVIG at 0.4 g/kg/day for 5 days is the treatment regimen for GBS rather than for an acute MS relapse (Durham, 2021, p. 73).

Choice d is wrong because plasma exchange five times every other day is first-line therapy for severe GBS and for myasthenic crisis, not for an MS relapse (Durham, 2021, pp. 72, 79).

GBS is an acute, usually rapidly progressive, form of inflammatory demyelinating radiculoneuropathy that typically affects motor neurons more than sensory neurons, and the classic pattern is symmetric, rapidly progressive distal muscle weakness and paresthesia beginning in the legs and ascending rapidly to the arms, face, and oropharynx (Durham, 2021, pp. 69–70).

Deep tendon reflexes are often significantly reduced or absent on presentation, although this may take days to develop, and autonomic dysfunction often presents as a hyper-sympathetic state with unexplained tachycardia (Durham, 2021, pp. 70–71).

Choice a is wrong because descending paralysis with eye muscle involvement describes the Miller Fisher variant, which is a primary axonopathy that accounts for approximately 5% of cases (Durham, 2021, p. 70).

Choice c is wrong because unilateral weakness with ipsilateral sensory loss below a level describes Brown-Séquard syndrome in spinal cord trauma rather than GBS (Yeager & Livesay, 2021, p. 95).

Choice b is wrong because weakness that worsens with repetitive use and improves with rest is characteristic of MG, and GBS produces progressive rather than fatigable weakness (Durham, 2021, p. 74).

The CSF finding in GBS is albuminocytologic dissociation, which is an elevation in CSF protein, especially IgG, without pleocytosis, or a lack of nucleated cells (Durham, 2021, p. 71).

Normal CSF values may be seen on presentation, and CSF protein elevation may not occur until the second week of illness, so a repeat lumbar puncture may be indicated if the diagnosis is strongly suspected (Durham, 2021, p. 71).

Choice b is wrong because an elevated white blood cell count with normal protein suggests an infectious or inflammatory process of the central nervous system rather than the albuminocytologic dissociation of GBS (Durham, 2021, p. 71).

Choice c is wrong because decreased glucose with an elevated white blood cell count is characteristic of bacterial meningitis rather than GBS (Denke, 2021, p. 54).

Choice d is wrong because elevated IgG with oligoclonal bands in the CSF but not the serum is consistent with MS and is not the CSF pattern of GBS (Kuric, 2021, p. 146).

A score of 8 is considered comatose, and intubation should be considered if the GCS score is less than 8 or if airway protection is a concern (Yeager & Livesay, 2021, pp. 83–84).

The GCS assesses and grades the best response of eye opening, verbal response, and motor response, with a range of 3 to 15, where 3 is the worst and 15 is the best (Yeager & Livesay, 2021, p. 84).

Choice a is wrong because a GCS score of 12 reflects a mild injury and does not in itself indicate the need for intubation (Yeager & Livesay, 2021, pp. 83–84).

Choice b is wrong because a GCS score of 10 is above the threshold at which intubation is considered for airway protection (Yeager & Livesay, 2021, p. 83).

Choice c is wrong because although a GCS score of 5 is well below the threshold and would warrant intubation, the threshold itself is 8 (Yeager & Livesay, 2021, p. 83).

An epidural hematoma is bleeding into the epidural space between the skull and the dura mater, is most commonly seen in the temporal or parietal region, is associated with a skull fracture that frequently results in middle meningeal arterial, diploic vein, or venous sinus injury, and produces a lenticular shape that does not cross suture lines on CT because the blood rests on top of the dura (Yeager & Livesay, 2021, p. 87).

An epidural hematoma generally causes a brief loss of consciousness with a lucid interval in which the patient is initially unconscious, wakes up without an obvious deficit, and subsequently deteriorates, and the deterioration may be rapid (Yeager & Livesay, 2021, p. 87).

Choice a is wrong because a subdural hematoma is most commonly caused by tearing of bridging veins, is the most frequently seen type of intracranial bleeding at 12% to 29%, and occurs between the dura mater and the arachnoid or pial layers rather than in a lenticular shape that respects suture lines (Yeager & Livesay, 2021, p. 87).

Choice b is wrong because traumatic subarachnoid hemorrhage is an accumulation of blood between the arachnoid and pial surface that is generally located over the cerebral convexities and produces headache, a reduced level of consciousness, nuchal rigidity, hemiplegia, and ipsilateral pupillary abnormalities (Yeager & Livesay, 2021, p. 88).

Choice c is wrong because diffuse axonal injury is immediate structural damage to the axial elements that affects the junction between cortex and white matter, the corpus callosum, the brainstem, and the corona radiata, and it is associated with depressed consciousness out of proportion to the findings on head CT (Yeager & Livesay, 2021, p. 88).

Cerebral perfusion pressure is calculated as the mean arterial pressure minus the intracranial pressure, and the CPP should ideally be maintained at a minimum of 60 mm Hg because it is an indirect indication of the adequacy of cerebral perfusion (Yeager & Livesay, 2021, p. 92).

If the intracranial pressure is greater than 22 mm Hg for more than 5 min, treatment should be initiated to lower the intracranial pressure, and monitoring of the intracranial pressure allows the practitioner to calculate the cerebral perfusion pressure (Yeager & Livesay, 2021, p. 92).

Choice b is wrong because a cerebral perfusion pressure minimum of 40 mm Hg is below the threshold required to maintain adequate cerebral perfusion (Yeager & Livesay, 2021, p. 92).

Choice c is wrong because a minimum of 50 mm Hg does not meet the recommended cerebral perfusion pressure goal (Yeager & Livesay, 2021, p. 92).

Choice d is wrong because the recommended minimum is 60 mm Hg, and a goal of 80 mm Hg is higher than the recommended target (Yeager & Livesay, 2021, p. 92).

After rupture or bleeding from an aneurysm, the patient may have nuchal rigidity due to meningeal irritation, cranial nerve II, IV, and VI deficits, stroke-like symptoms such as hemiparesis, hemiplegia, aphasia, and cognitive deficits, numbness of one side of the face, seizure, hypertension with bradycardia and widening pulse pressure due to increased intracranial pressure, and confusion or loss of consciousness (Denke, 2021, p. 40).

A subarachnoid hemorrhage presents with a sudden headache of intense severity that radiates into the posterior neck region and is worsened by neck and head movements, often described as a thunderclap headache or the worst headache of the patient's life (Denke, 2021, p. 25).

Choice b is wrong because CN III, VII, and XII are not the group affected after aneurysm rupture, and CN III palsy occurs before rupture rather than as part of the post-rupture pattern (Denke, 2021, p. 40).

Choice c is wrong because CN I, V, and XI are not the cranial nerves affected by aneurysm rupture, and anosmia with optic nerve compression is associated with meningioma at the olfactory groove (Denke, 2021, p. 59).

Choice d is wrong because CN VIII, IX, and X involvement is associated with acoustic neuroma and Chiari malformation rather than aneurysm rupture (Denke, 2021, pp. 51, 58).

Cerebral vasospasms occur in approximately 30% of patients, most frequently between days 7 and 10 after aneurysm rupture and/or coiling, and usually resolve after 21 days, and they may be associated with the presence of a thick clot in the subarachnoid space (Denke, 2021, p. 29).

Calcium channel blockers such as nimodipine 60 mg orally or by nasogastric tube every 4 hr for 21 days may be used to treat cerebral blood vessel spasm after subarachnoid hemorrhage from a ruptured aneurysm or after clipping (Denke, 2021, p. 30).

Vasospasm symptoms include confusion, decreased level of consciousness, localizing neurologic deficits, and headache, and cerebral infarction can occur with severe vasospasm (Denke, 2021, p. 30).

Choice a is wrong because rebleeding is unpredictable but often occurs between days 2 and 19 after the initial rupture, and 40% of patients rebleed with approximately half of those rebleeds being fatal, so it is not the complication most specific to days 7 to 10 (Denke, 2021, p. 30).

Choice b is wrong because hydrocephalus is seen in up to 20% of patients and is usually managed by the placement of an external ventricular drain or lumbar drain rather than being the peak complication at days 7 to 10 (Denke, 2021, p. 46).

Choice d is wrong because cerebral salt wasting produces hyponatremia after aneurysmal subarachnoid hemorrhage through excessive secretion of natriuretic peptides, making it a metabolic complication rather than the vascular complication seen at days 7 to 10 (Denke, 2021, p. 30).

Central cord syndrome results from hyperextension injuries with stretching of the cord and subsequent hemorrhaging in the center of the cord, occurs almost exclusively in the cervical spine, and produces greater motor loss and sensation loss in the upper extremities than in the lower extremities because the upper extremities are controlled by the central portion of the cord (Yeager & Livesay, 2021, p. 95).

Choice a is wrong because anterior cord syndrome results from disruption of blood flow through the anterior spinal artery from hyperflexion injuries and produces weakness or paralysis with loss of the sense of pain and temperature while proprioception and vibration remain intact (Yeager & Livesay, 2021, p. 95).

Choice b is wrong because posterior cord syndrome is a rare injury resulting from disruption of the posterior column that decreases touch, proprioception, and vibration below the level of injury while motor, pain, and light touch sensation are preserved (Yeager & Livesay, 2021, p. 95).

Choice d is wrong because Brown-Séquard syndrome results from damage to one side of the spinal cord from stab wounds, gunshot wounds, fractures of the vertebral process, or spinal cord tumors, and it produces ipsilateral motor loss with contralateral loss of pain and temperature sensation (Yeager & Livesay, 2021, p. 95).

Neurogenic shock results from loss of sympathetic innervation, produces hypotension, bradycardia, and warm and dry skin, and requires that other sources of shock symptoms be ruled out (Yeager & Livesay, 2021, p. 96).

Management of neurogenic shock includes monitoring with rapid identification of indicators, fluid and vasopressor support, and normotonic fluid, because the loss of sympathetic innervation results in loss of peripheral vasoconstriction, loss of cardiac compensation including tachycardia, and loss of increased stroke volume and cardiac output (Yeager & Livesay, 2021, p. 100).

Choice a is wrong because high-dose methylprednisolone has not shown benefit in several clinical trials, may be associated with multiple complications, and is generally not supported by multiple professional societies and guidelines (Yeager & Livesay, 2021, p. 100).

Choice c is wrong because bradycardia and hypotension result from sympathetic blockade with unopposed parasympathetic innervation, and the priority is fluid and vasopressor support rather than atropine (Yeager & Livesay, 2021, p. 96).

Choice d is wrong because aggressive diuresis would worsen the hypotension, and hemodynamic support in spinal cord injury focuses on fluid resuscitation, avoidance of hypotension, and blood pressure augmentation (Yeager & Livesay, 2021, p. 99).