Strokes
Dementia and NMJ Disorders
Trauma
General
General
100

A 37-year-old man is evaluated in the emergency department 12 hours after sudden onset of a global, severe headache with associated neck stiffness. The patient has a 5-year history of migraine treated with sumatriptan. He says that his current headache feels different from previous headaches and did not respond to sumatriptan.


On physical examination, temperature is normal, blood pressure is 148/72 mm Hg, heart rate 86/min and regular, respiration rate is 12/min, and oxygen saturation is 96% with the patient breathing ambient air. The patient has discomfort and appears restless. Funduscopic examination is normal. The left pupil is 2 millimeters larger than the right and poorly reactive to light. Neck stiffness is noted with passive movement.


A CT scan of the head is normal.


What is the next best step?

What is LP? (What would a positive finding show)

Aneurysmal subarachnoid hemorrhage (SAH) is not always evident on CT scans and still needs to be excluded as a diagnosis. 

Sudden onset, nuchal rigidity, and pupillary dilation of the left eye. The latter finding can be seen with a posterior communicating artery aneurysm, as it exerts pressure on the outer portion of the oculomotor nerve (cranial nerve III)


100

A 72‑year‑old woman is brought to the clinic by her daughter because of progressive memory loss and behavioral changes over the past 2 years. Initially, she frequently misplaced objects and repeated questions during conversations. Over the past year, she has become more withdrawn and occasionally accuses family members of stealing her belongings. She needs assistance with paying bills and managing medications but is still independent in basic activities. There is no history of stroke, head trauma, or substance use. Physical examination is normal. Mini‑Mental State Examination reveals impaired immediate and delayed recall, poor orientation to time, and difficulty naming common objects.

MRI of the brain shows generalized cortical atrophy, more pronounced in the medial temporal lobes and parietal regions. Laboratory studies, including vitamin B12, TSH, and CBC, are within normal limits.

What is the most likely diagnosis?

What is Alzheimer's Disease?

100

A 45‑year‑old man is brought to the emergency department after falling off scaffolding. On arrival, his blood pressure is 100/70 mm Hg, heart rate 120 bpm, and oxygen saturation 95% on ambient air. He opens eyes to speech, speaks incoherently, and withdraws to pain (GCS = 10). Pupils are equal and reactive.

After securing the airway and stabilizing blood pressure with normal saline, a noncontrast CT head shows a small left frontal intraparenchymal hemorrhage with mild edema and no midline shift.

What is the best next step in management?

What is administer intravenous tranexamic acid?

Tranexamic acid (TXA) given within 3 hours of injury may reduce intracranial bleeding and mortality in moderate TBI.

Note that post-TBI seizure prophylaxis can also be given for severe TBI w/ a 7-day course of keppra.

100

A 61-year-old woman is admitted to the ICU 1 hour after having a subarachnoid hemorrhage (SAH). An emergent CT scan of the head showed an SAH, and a cerebral angiogram revealed a 6-mm rupture of the anterior communicating artery. The patient has hypertension treated with amlodipine.


On physical examination, vital signs are stable, and oxygen saturation is 96% with the patient breathing ambient air. She is somnolent. Nuchal rigidity is present. Subhyaloid hemorrhages are seen on funduscopic examination. No motor or sensory deficits are present.


Administration of which medication is the most appropriate treatment?

What is Nimodopine? 

The two major complications after SAH are rebleeds and cerebral vasospasm. Rebleeds usually occur within the 1st 24 hours, while there is a risk of vasospasm up to 21 days. Nimodopine is the drug of choice for normotensive patients with SAH to prevent vasospasm.



100

A 78-year-old man is evaluated in the emergency department for a 2-day history of bilateral leg weakness and urinary retention. He has atrial fibrillation and hypertension. Medications are warfarin, lisinopril, and hydrochlorothiazide.


On physical examination, vital signs are normal. Muscle strength is 4/5 in both legs. Decreased sensation in the groin, medial buttocks, and rectal area is noted, as is decreased rectal tone. No spinal sensory level is detected in the abdomen or chest region. Gait is wide based.


Results of laboratory studies show an INR level of 5.3.


What is the most appropriate management?

What is MRI of the lumbosacral spine?

In a patient with suspected compression of the lower spinal cord, emergent MRI of the lumbosacral spine is the most appropriate test both to localize the injury and to determine its cause.

Given the elevated INR, the most likely diagnosis is a spinal epidural hematoma compressing the lumbosacral spine

200

A 48-year-old man is hospitalized with new-onset right hemiparesis and difficulty speaking. He was well when last seen 20 hours earlier.


On physical examination, blood pressure is 138/76 mm Hg, pulse rate is 72 and regular, and respiration rate is 12/min. The patient has aphasia. A right visual field deficit and right facial, arm, and leg weakness are noted. Decreased pinprick sensation is present on the right. Reflexes also are decreased on the right; a right plantar extensor response is noted.


An electrocardiogram shows sinus rhythm. A CT scan of the head shows a hypodensity in the left frontal and parietal lobes, and a CT angiogram of the head and neck shows patent internal carotid arteries and 80% stenosis of the left middle cerebral artery.


Results of laboratory studies include a serum LDL cholesterol level of 108 mg/dL (2.80 mmol/L) and a hemoglobin A1c value of 6.8%.


The patient is given aspirin.


What is the next best step in treatment?

What is give the patient a statin?

In ischemic stroke due to intracranial atherosclerosis, the use of high-intensity atorvastatin therapy for secondary stroke prevention is associated with a reduced long-term risk of ischemic stroke

Use of atorvastatin for secondary stroke prevention is associated with a reduced long-term risk of ischemic stroke, regardless of the baseline LDL cholesterol level.




200

A 75‑year‑old woman is brought to the clinic by her son because of worsening forgetfulness over the past three months. She says, “I can’t remember anything anymore—I think I’m losing my mind.” She has lost interest in gardening and church activities, has difficulty falling asleep, and reports decreased appetite with a 5‑kg weight loss. She appears tearful and anxious during the interview. Her son says she constantly worries about being a burden since her husband passed away six months ago. She states that she feels “hopeless.”

On examination, she is oriented to person, place, and time. She gives short answers such as “I don’t know” to several cognitive test questions. She recalls none of three objects after five minutes but remembers them when prompted with clues. Neurological examination is normal.

Mini‑Mental State Examination: 25/30.
Laboratory studies: Normal TSH, vitamin B12, CBC, and metabolic panel.

What is the most likely diagnosis?

What is depression-related cognitive impairment?

This patient’s rapid onset of cognitive complaints, depressed mood, and complaints of memory loss disproportionate to testing results suggest cognitive impairment secondary to depression, commonly called pseudodementia.

200

A 25‑year‑old man is brought to the emergency department after being hit in the temple by a baseball bat. He briefly lost consciousness but was alert and oriented on arrival. Thirty minutes later, he becomes progressively somnolent and develops right‑sided pupillary dilation. His blood pressure is 160/80 mm Hg, heart rate 52 bpm, and respirations 10/min. Neurological examination reveals weakness of the left upper and lower extremities.

A noncontrast CT scan of the head is obtained and shows a hyperdense, biconvex, lens‑shaped collection over the right temporal region that does not cross the suture lines.

Which of the following best describes the underlying cause of this patient’s condition?

What is laceration of the middle meningeal artery?

200

A 28‑year‑old woman with obesity presents with daily headaches worse in the morning, transient blurry vision, and pulsatile tinnitus for 2 months. Fundoscopic examination shows bilateral papilledema, and MRI of the brain is normal. Lumbar puncture reveals an opening pressure of 32 cm H₂O with normal CSF composition.

What is the most appropriate initial pharmacologic treatment for this patient’s condition?

What is begin acetazolemide?

Acetazolemide inhibits carbonic anhydrase, leading to decreased CSF production and lower intracranial pressure.

Surgical options (CSF shunt or optic nerve sheath fenestration) are indicated for rapid or progressive vision loss resistant to medication.

What drugs increase the risk of this condition?

What is this patient most at risk for?

200

A 58-year-old man is evaluated in the emergency department for a 3-week history of worsening pain in the middle back and a 2-day history of increasing leg weakness that has made ambulation difficult. He has metastatic prostate cancer treated with leuprolide.


On physical examination, vital signs are normal. Muscle strength testing shows 4/5 weakness in the hip flexors. Reflexes are 3+ in both legs.


An MRI of the thoracic spine shows a contrast-enhancing mass originating in the T8 vertebral body with invasion into the epidural space that causes moderate cord compression.



After administration of high-dose glucocorticoids, what is the most appropriate next step in management?

    


What is decompressive surgery with radiation    

Spinal cord compression from metastatic disease requires emergent use of high-dose glucocorticoids followed by maintenance glucocorticoids and urgent surgical decompression followed by radiation.

300

A 71-year-old woman is evaluated in the emergency department 1 hour after acute onset of a severe headache and left-sided weakness. The patient had a myocardial infarction 3 years ago that was treated with a bare metal stent in the right coronary artery. She also has hypertension. Medications are carvedilol, atorvastatin, and aspirin.


On physical examination, blood pressure is 200/110 mm Hg, pulse rate 78/min, respiration rate is 20/min, and oxygen saturation is 98% with the patient breathing ambient air. The patient is awake and attentive to both sides and has normal language function. Funduscopic examination shows no papilledema or hemorrhage. Pupils are both 3 millimeters in size and reactive. Left facial weakness, dysarthria, and flaccid paralysis in the left arm and leg with loss of sensation are noted.


An emergent noncontrast CT scan shows an acute intracerebral hemorrhage, 1 centimeter in diameter, in the right basal ganglia without intraventricular hemorrhage or midline shift.


Which of the following is the most appropriate treatment?


A Hematoma evacuation

B Intravenous nicardipine

C Intravenous nitroprusside

D Platelet transfusion

What is intravenous nicardipine


BP is greater than 180 mm Hg; this means she is at high risk for hematoma expansion.

Patients who have intracerebral hemorrhage without elevated intracranial pressure whose systolic blood pressure is greater than 180 mm Hg should be treated with an intravenous antihypertensive agent, such as nicardipine, to a target blood pressure of 140 mm Hg.

300

A 55‑year‑old man presents with 3 days of progressive difficulty walking and swallowing. He has noticed dry mouth and constipation. He denies diplopia. He has a 40‑pack‑year smoking history. On examination, he has symmetric proximal muscle weakness in the arms and legs and depressed reflexes. Strength improves after several repeated contractions. Cranial nerves are intact.

Serologic testing is positive for antibodies to P/Q‑type voltage‑gated calcium channels.

What best explains the underlying pathophysiology of this patient’s symptoms?

What is autoimmune destruction of voltage‑gated calcium channels at presynaptic terminals?

Remember, the key difference between this and myasthenia gravis is that the weakness improves with use and you are more likely to see bulbar symptoms. 

Note that LE syndrome can be treated with Amifampridine or by treating the underlying cancer.

300

A 62‑year‑old man undergoes open repair of an abdominal aortic aneurysm. Six hours after surgery, he develops sudden-onset weakness in both legs and loss of pain and temperature sensation below the umbilicus. Vibration and position sense are preserved.

On physical examination, tone and reflexes in the lower extremities are decreased. There is urinary retention, but the upper extremities and cranial nerves are normal.

Which of the following best explains this patient's findings?

What is occlusion of the anterior spinal artery?

This is classic anterior cord syndrome, which is commonly caused by aortic surgeries, vertebral burst fractures, and hemorrhage. 

In anterior cord syndrome, the spinothalamic tract and motor tracts are damaged, while the dorsal column is left intact. Note that there is a major watershed area between T3 and T8 where there is a risk of infarct due to hypoperfusion.


300

A 32-year-old woman presents with right eye pain and decreased vision for 3 days. She reports intermittent numbness and tingling in her legs over the past year, which resolved spontaneously. Neurological examination shows decreased visual acuity, pain with eye movement, and a right afferent pupillary defect. MRI of the brain reveals multiple periventricular white-matter lesions.


She receives high-dose IV methylprednisolone 1 g/day for 5 days, with improvement in vision. Two months later, she returns requesting long-term therapy to reduce relapse risk.

What is the best next step in management?

What is start patient on natalizumab, glatiramer, or interferon-beta?

It is critical to know the difference in acute t/x and long-term management for MS. For acute flares, treat with IV methylprenisone. Long-term management is accomplished with the above medications.

Additionally, what is the black box warning for natalizumab?

300

A 46-year-old woman presents with fever, headache, and confusion for 2 days. Her husband reports that she began speaking incoherently and had a tonic-clonic seizure earlier today. On examination, she is drowsy, with right facial droop and expressive aphasia.

MRI of the brain reveals hyperintense lesions in the left temporal lobe. A lumbar puncture is performed and shows:

Test Result 

Opening pressure18 cm H₂O 

WBC count 65/mm³ (85% lymphocytes) 

RBC count 250/mm³ 

Protein 80 mg/dL 

Glucose 65 mg/dL (serum 100 mg/dL) 

What is the most likely diagnosis?

What is HSV-1 encephalitis?


HSV-1 encephalitis classically presents with acute febrile encephalopathy, focal temporal lobe findings(aphasia, personality change), and CSF abnormalities showing:

  • Lymphocytic pleocytosis,
  • Normal glucose,
  • Mild protein elevation, and
  • RBCs from necrotizing hemorrhagic inflammation in the temporal lobes.

Diagnosis is confirmed with CSF PCR for HSV DNA, which is highly sensitive and specific.


Empiric IV acyclovir should be started immediately and continued while awaiting PCR confirmation since early treatment improves prognosis

400

A 72-year-old woman is evaluated in the emergency department. She has been having hoarseness, nausea, vertigo, and difficulty swallowing. On physical exam, her R pupil is 1 mm with ptosis. She also has L-sided sensory loss to pain and temp.


What artery is most likely affected?

What is the posterior inferior cerebellar artery?

The key to knowing this vs an anterior inferior cerebellar artery infarct is the dysphagia and hoarseness. In lateral medullary syndrome, the nucleus ambiguus is impacted, leading to CN IX and X palsies.

Lateral pontine syndrome will have a CN VII palsy along with hearing difficulties.

400

A 46‑year‑old woman with a PMH of generalized myasthenia gravis presents to the emergency department with increasing shortness of breath and difficulty speaking for the past six hours. She was recently started on a high‑dose prednisone taper two weeks ago for worsening diplopia.

On examination, she is alert but anxious, speaking in short sentences. Temperature is 38.2°C (100.8°F), respiratory rate 24/min, and oxygen saturation 90% on room air. She has mild ptosis and fatigable limb weakness. Breath sounds are clear without wheezing or rales.

What is the next best step in treatment?

What is intubation?

This patient is presenting with myasthenic crisis, which is a life-threatening complication of MG. Given the risk of respiratory failure, it is critical to intubate these patients swiftly.

Additionally, myasthenic crisis is treated w/ IV corticosteroids (to suppress autoimmune activity) and either plasma exchange transfusion or IVIG (to remove anti-ACH receptor antibodies).

400

A 28‑year‑old man is brought to the emergency department after his car struck a tree at high speed. His Glasgow Coma Scale is 5 (E1, V1, M3). Pupils are equal and reactive. There is no evidence of external trauma or skull fracture. Vital signs are stable, and blood glucose is normal. A noncontrast head CT shows scattered, tiny punctate hemorrhages at the gray–white matter junction and corpus callosum.

Over the next 24 hours, he remains comatose with minimal response to painful stimuli, but repeat imaging shows no large hematoma or mass effect.

Which of the following best explains this patient’s neurologic findings?

What is a shearing injury to white matter tracts due to diffuse axonal injury?

400

A 61-year-old man is brought to the emergency department with rapidly worsening confusion and involuntary muscle jerks. His wife reports a 6-week history of memory loss, ataxia, and mood changes.
Physical examination reveals startle-induced myoclonus and ataxic gait. MRI of the brain demonstrates hyperintensity in the caudate and putamen on diffusion-weighted imaging. EEG shows periodic sharp wave complexes at 1–2 Hz.

What will be seen on CSF analysis for this patient?

What is 14-3-3 protein?

Rapidly progressive dementia with myoclonus, characteristic EEG, and basal ganglia hyperintensities suggest Creutzfeldt-Jakob disease.


Definitive diagnosis requires detection of misfolded prion protein (PrPSc) via real-time quaking-induced conversion (RT-QuIC), or elevated 14-3-3 and tau proteins in CSF.

400

A 40-year-old man with AIDS (CD4 count 35/μL) and poor adherence to antiretroviral therapy presents with headaches, left-sided weakness, and intermittent confusion for 2 weeks.

MRI brain with contrast shows two ring-enhancing lesions in the right basal ganglia and thalamus with extensive surrounding edema. CSF PCR is negative for Toxoplasma, positive for EBV DNA. Serum is positive for Toxoplasma IgG.

He is initially started on pyrimethamine/sulfadiazine/leucovorin but shows no clinical or radiographic improvement after 2 weeks.

Which of the following next steps most accurately differentiates the potential underlying cause of his CNS lesions?

What is perform stereotactic brain biopsy to confirm diagnosis?

In HIV/AIDS patients with CNS ring-enhancing lesions, the top differentials are cerebral toxoplasmosis and primary CNS lymphoma (PCNSL) 

Features favoring toxoplasmosis: multiple lesions, basal ganglia involvement, T. gondii IgG positivity, and clinical improvement after empiric anti-toxoplasma therapy.

Features favoring PCNSL: solitary or periventricular lesion, EBV PCR-positive CSF, and lack of response to anti-toxoplasma therapy.

500

A 49-year-old-man is evaluated 1 day after having an episode of right arm weakness without pain that lasted 5 minutes. He is now asymptomatic. The patient has type 2 diabetes mellitus and dyslipidemia. Medications are aspirin, metformin, and atorvastatin.


On physical examination, blood pressure is 126/68 mm Hg, pulse rate is 86/min and regular, and respiration rate is 12/min. No carotid bruits or cardiac murmurs are heard on cardiac auscultation. All other physical examination findings are normal.


An electrocardiogram shows normal sinus rhythm with no ST-segment or T-wave changes.


Which of the following is the most appropriate initial imaging test?


    

A    Carotid duplex ultrasonography


B    CT angiography of the neck


C    MRI of the brain


D    Transesophageal echocardiography

A    Carotid duplex ultrasonography

Initial test of choice for evaluating ICA stenosis is duplex ultrasonography because of its wide availability, low cost, and low risk; readily available, and noninvasive imaging modality for identifying high-grade stenosis and the possible need for surgery.

500

A 68‑year‑old man is brought by his wife because of repeated falls over the past six months. His speech has become slurred, and he has trouble looking down when reading. On examination, his facial expression is fixed, and he intermittently laughs and cries inappropriately. There is symmetric rigidity of the neck and trunk, mild bradykinesia, and impaired voluntary vertical gaze with preserved vestibulo‑ocular reflexes.

MRI of the brain shows midbrain atrophy with relative preservation of the pons.

What is the most likely diagnosis?

What is Progressive Supranuclear Palsy?

Classic features of this condition include:

  • Early postural instability and falls, particularly backward.
  • Vertical (especially downward) gaze palsy with preserved vestibulo‑ocular reflexes.
  • Frontal cognitive and behavioral changes, such as apathy, pseudobulbar affect, and impaired reasoning.
  • Poor response to levodopa therapy, differentiating it from idiopathic Parkinson disease.
  • Neuroimaging revealing the Hummingbird sign—midbrain atrophy with preserved pontine volume.
500

A 32‑year‑old man presents after being stabbed in the neck with a screwdriver. He has weakness in the right leg and difficulty walking. Neurological examination reveals the following:

  • Right leg: spastic weakness, hyperreflexia, and an upgoing plantar response.
  • Left leg: loss of pain and temperature sensation below the umbilicus.
  • Bilateral upper extremities: normal strength and sensation.
  • Pupils: right‑sided miosis and mild ptosis.

What is the most likely diagnosis?

What is Brown-Sequard Syndrome?

This patient exhibits the classic pattern of Brown‑Séquard syndrome:

  • Ipsilateral motor weakness and UMN signs below the lesion → damage to the lateral corticospinal tract.
  • Ipsilateral loss of vibration and proprioception (not shown in this vignette) → damage to dorsal columns.
  • Contralateral loss of pain and temperature sensation one or two levels below lesion → interruption of the spinothalamic tract, which crosses within the spinal cord about 1–2 segments above its entry point 1.
  • Ipsilateral Horner syndrome (ptosis, miosis, anhidrosis) → disruption of descending sympathetic fibers in lesions above T1 12.
500

A 65-year-old man is evaluated in the ICU for a 24-hour history of altered mental status with a fluctuating level of consciousness. He was admitted to the hospital 5 days ago for urosepsis and acute kidney injury and developed acute respiratory distress syndrome on hospital day 3. The patient is currently intubated, mechanically ventilated, and receiving continuous hemodialysis. Medications are cefepime, norepinephrine, and fentanyl.


On physical examination, temperature is 38.4 °C (101.1 °F), blood pressure is 105/71 mm Hg, pulse rate is 108/min, and respiration rate is 12/min; FIO 2 is 0.9. The patient opens his eyes to voice but does not fixate on the examiner or follow commands. Pupils are reactive, and gag and corneal reflexes are present. All limbs move intermittently but not on command. The patient withdraws from painful stimuli in all four limbs. Intermittent twitching of the shoulders and eyelids is noted.


Results of laboratory studies show a serum creatinine level of 5.4 mg/dL (477 µmol/L). Glucose, calcium, and electrolyte levels are within normal limits.


A 20-minute electroencephalogram shows generalized slow activity, a nonspecific finding compatible with encephalopathy, but no evidence of seizure activity.


A head CT scan is normal.



Which of the following is the most appropriate next step in management?


A    Continuous (24-hour) electroencephalography

B    Intravenous fosphenytoin

C    Intravenous lorazepam

D    No treatment

A    Continuous (24-hour) electroencephalography



-Nonconvulsive status epilepticus should be suspected in patients with critical illness who develop altered mental status; the diagnosis is confirmed with continuous (24-hour) electroencephalography. At least 24 hours of monitoring is recommended in non-comatose patients, and at least 48 hours is recommended in comatose patients.

500

A 33-year-old woman from Guatemala presents with persistent headache, vomiting, and low-grade feversfor 4 weeks. She reports night sweats and weight loss. On examination, she has mild nuchal rigidity and a right sixth cranial nerve palsy. MRI brain shows basilar meningeal enhancement and mild communicating hydrocephalus.

CSF studies are as follows:

Opening pressure 25 cm H₂O 

WBC 250/mm³ (90% lymphocytes) 

Protein 200 mg/dL 

Glucose 28 mg/dL (serum glucose 90 mg/dL) 

What do you expect to find on CSF analysis?

What is elevated adenosine deaminase?

The subacute presentation, cranial nerve palsy, and characteristic CSF profile—lymphocytic pleocytosis, high protein, and low glucose—indicate tuberculous meningitis.

Adenosine deaminase (ADA) levels are elevated in TB meningitis because of T-cell and macrophage activation during granulomatous inflammation

Elevated ADA helps differentiate TB meningitis from viral or cryptococcal meningitis, which have normal or minimally increased ADA levels

M
e
n
u