Case-based MCQ

Correct Answer Is B This patient has recurrent forceful contraction of the eyelid muscles consistent with blepharospasm, a form of focal dystonia.  Blepharospasm is usually bilateral and symmetric.  When associated with spasm of the lower face (eg, jaw, tongue), it is termed Meige syndrome.  Blepharospasm is commonly affected by sensory input; bright lights may trigger the muscle contraction, whereas touching or brushing the skin around the eye may terminate the spasm (“sensory trick”). Blepharospasm can be caused by certain movement disorders (eg, Parkinson disease) or medications (eg, antipsychotics), but most cases are idiopathic (ie, benign essential blepharospasm).  It should be differentiated from simple eyelid twitching, which causes fleeting, minor lid contractions that are unilateral and do not affect vision.  Mild cases may be managed with trigger avoidance, such as wearing dark glasses to block bright lights, but botulinum toxin injection may be needed for more significant symptoms. Acute uveitis is characterized by inflammation of the iris and ciliary body and is a common ocular manifestation of sarcoidosis.  Although it may cause sensitivity to light (with voluntary closure of the lids), it typically presents with ocular pain; examination shows pupillary constriction and redness at the limbus (ciliary flush). Myasthenia gravis is characterized by fluctuating, fatigable muscle weakness that is often worse at the end of the day.  It is occasionally limited to the extraocular muscles, where it presents with diplopia (oculomotor paresis) and ptosis.  Myotonic dystrophy is an autosomal dominant disorder that causes weakness and delayed relaxation of muscle; involvement of the facial muscles may lead to ophthalmoparesis.  Examination in these disorders would show muscular weakness rather than blinking or blepharospasm. Trigeminal neuralgia can cause facial muscle spasm (tic douloureux), but the most prominent feature is paroxysmal, severe, shooting or burning pain in a dermatomal distribution following the trigeminal nerve (cranial nerve V). Blepharospasm is a form of focal dystonia characterized by recurrent forceful contraction of the eyelid muscles.  Bright lights may trigger symptoms, whereas touching or brushing the skin around the eye may terminate the spasm.  Mild cases may be managed with trigger avoidance, but botulinum toxin injection may be needed for more significant symptoms.

A 26-year-old woman comes to the office due to eye problems.  One week ago while driving, her eyes closed spontaneously after she looked at the headlights of an oncoming car.  She briefly could not open her eyes and had to stop driving until the symptoms gradually improved over several minutes.  Since then, she has had 3 similar episodes brought on by bright light exposure.  The patient has had no fever, eye pain or discharge, blurry or double vision, headaches, or extremity weakness or numbness.  She has a history of asymptomatic sarcoidosis and takes no medications.  Vital signs are within normal limits.  On physical examination, there is no facial asymmetry.  Frequent blinking of the eyes is noted, and shining light in the eyes to assess pupillary response causes involuntary tonic closure of the eyelids bilaterally.  The remainder of the examination is normal.  Which of the following is the most likely diagnosis? A. Acute uveitis B. Focal dystonia C. Myasthenia gravis D. Myotonic dystrophy E. Trigeminal neuralgia

Correct Answer Is E This patient’s rapid neurologic deterioration (eg, obtundation, eye deviation) 48 hours after a large ischemic stroke is concerning for malignant hemispheric infarction (MHI), a life-threatening condition that may occur when an ischemic stroke causes massive cerebral edema and/or hemorrhagic transformation: Cerebral edema results from endothelial dysfunction and breakdown of the blood-brain barrier.  The resulting mass effect and increase in intracranial pressure (ICP) can cause brain herniation (eg, herniation of the temporal lobe onto the brainstem). Hemorrhagic transformation occurs when blood extravasates from injured cerebral vessels into the brain parenchyma.  The larger the infarct, the greater the risk of hemorrhagic transformation. Strokes that cause MHI typically are due to occlusion of a large vessel (eg, internal carotid, proximal middle cerebral artery) and initially present with severe deficits (eg, right-sided weakness, hemisensory loss, aphasia) due to the large affected area of the brain.  Deterioration usually occurs in the first 48 hours but can be more gradual (up to a week). Patients with suspected MHI (such as this one) should have a non-contrast CT scan of the head performed emergently to determine the extent of edema and/or hemorrhage and guide further management.  Decompressive hemicraniectomy is often necessary. Although this patient has a fever, the most likely cause is a defect in central thermoregulation (due to extensive stroke or intracerebral hemorrhage) rather than infection (for which blood cultures and antibiotics would be indicated).  Prior to any other testing, a non-contrast CT scan of the head should be performed to assess for life-threatening cerebral edema or hemorrhagic transformation. Osmotic diuretics (eg, intravenous mannitol, hypertonic saline) can decrease cerebral edema (eg, due to stroke) by creating an osmolar gradient that draws water out of edematous brain tissue.  Given the high suspicion for elevated ICP in this patient, administering either agent is reasonable; however, subsequent observation is insufficient.  This patient may require emergency craniectomy, and a CT scan should be obtained emergently to diagnose the extent of cerebral edema and/or hemorrhage and guide management. Although MRI has greater sensitivity for the diagnosis of ischemic stroke, non-contrast CT scan of the head is the preferred modality for detection of cerebral hemorrhage due to its better availability and testing rapidity. Massive cerebral edema and/or hemorrhagic transformation, with rapid neurologic deterioration, can occur following a large, hemispheric ischemic stroke.  Non-contrast CT scan of the head should be performed emergently to determine the extent of edema and/or hemorrhage and guide management.

A 67-year-old man is brought to the emergency department due to right-sided weakness, numbness, and slurred speech.  The patient was in his usual state of health last night but awoke this morning with these symptoms.  He has a history of hypertension, hyperlipidemia, type 2 diabetes mellitus, and peripheral arterial disease.  The patient does not drink alcohol regularly but has a 45-pack-year history.  Physical examination shows an awake and alert patient with right-sided weakness, hemisensory loss, homonymous hemianopsia, and aphasia.  CT scan of the head reveals a large left hemispheric infarction due to an occluded middle cerebral artery.  The patient is hospitalized but is not treated with fibrinolytic therapy or mechanical thrombectomy due to ineligibility.  Forty-eight hours later, he becomes obtunded.  Temperature is 38.3 C, blood pressure is 154/86 mm Hg, and pulse is 64/min.  Physical examination now shows complete right hemiplegia and deviation of the eyes to the left.  Which of the following is the best next step in management of this patient? A. Blood cultures and empiric antibiotics B. Intravenous hypertonic saline and observation C. Intravenous mannitol and observation D. MRI of the head E. Repeat CT scan of the head

Correct Answer Is E One of important points to consider in dealing with patients who have presented with motor neurological deficits, such as this patient, is the possible origin(s) of such presentation. Distinguishing lower motor neuron lesions from those of upper motor neuron is of paramount importance. Upper motor neurons (UMNs) neurons originate from the primary motor cortex of the cerebrum (precentral gyrus). These neurons have long axons that form corticospinal and corticobulbar tracts. Lesions of UMN presents with: Stiffness (spasticity) Brisk tendon refiexes (hyperreflexia) Presence of abnormal reflexes (e.g., Babinski, Chaddock, or Hoffman signs) Loss of dexterity in the presence of normal strength Muscle spasms Lower motor neuron (LMNs), on the other hand, originate from the brainstem (cranial nerve [CN] motor nuclei) and spinal cord (anterior horn cells) and directly innervate skeletal muscles. Findings consistent with LMNs lesions include: Fasciculations (twitching muscles) Reduction of muscle bulk (atrophy) Decreased muscle strength Depressed deep tendon reflexes While the weakness of muscles responsible for weak ankle flexion and dorsiflexion indicates a LMN lesion, the increased ankle tendon reflexes on the same side reflects an UMN impairment. This patient therefore has both LMN and UMN disorders at the same time. Additionally, he has no sensory impairment. This constellation of findings makes a motor neuron disease (MND), more specifically, amyotrophic lateral sclerosis, the most likely diagnosis. Of the given options, only lesions of cerebral cortex can give rise to this scenario. Injuries to the common peroneal nerve can weaken the ankle dorslflexion and disturbed sensation over the anterolateral aspect of the leg and lateral aspect of the foot. However, such lesions are associated with a depressed ankle reflex. Moreover, with such Injuries, sensation of the lateral aspect of the lower leg and foot that are innervated by the superficial branch of this nerve would be expected. Lesions of the L5/S1 nerve root can cause weak ankle dorsifiexion and drop foot (L5) and decreased plantar flexion(S1). Atrophy of muscles innervated by these nerve roots is another feature, but since the lesions are of lower motor origin, decreased reflexes would be expected. This patient has also features consistent with UMN deficits making this diagnosis unlikely. Cervical spine lesions caused by conditions such as multiple sclerosis (MS), or spinal canal stenosis/compression can cause signs and symptoms consistent with UMN lesions. But with cervical spine involvement,neurological deficits are expected to be more pronounced in upper extremities than the lower extremities. Normal neurologic exam findings in the face and arms make cervical spine lesions a less likely diagnosis. UMN lesions of the brainstem origin is almost an unlikely diagnosis in this scenario due to lack of signs and symptoms suggestive of bulbar involvement such slurred speech, oropharyngeal dysphagia, especially for liquids or facial involvement.

A 58-year-old man presents with complaint of progressive difficulty in walking for the past few months. He denies any pain or pins and needles. On examinations, he drags his left foot while walking. On the left side, ankle tendon reflexes are exaggerated, the strength of plantar flexion and dorsifiexion are decreased and are 4/5. Sensation is intact. The right foot is completely normal. Plantar reflexes are equivocal bilaterally. The rest of physical examination including neurologic exam of the face and upper extremities are unremarkable. Lesions of which one of the following parts could be the mostly likely cause to this presentation? A. Common peroneal nerve B. LS/51 nerve root C. Cervical spine D. Brainstem E. Cerebral cortex

Correct Answer Is D This patient with bilateral lower extremity weakness associated with upper motor neuron signs (UMNS) (ie, increased deep tendon reflexes, extensor plantar response), urinary incontinence, and sensory deficit below the umbilicus likely has acute transverse myelitis.  Transverse myelitis is an immune-mediated disorder characterized by the infiltration of inflammatory cells into a segment of the spinal cord, leading to neuron and oligodendrocyte cell death and demyelination.  Most cases follow a recent infection (eg, gastroenteritis, upper respiratory infection), although the condition is also associated with multiple sclerosis and systemic disease (eg, sarcoidosis).  The incidence of transverse myelitis has a bimodal peak, with most cases occurring in teens and in those age 30-40. Inflammation localizes to ≥1 contiguous spinal cord segments (usually in the thoracic cord) leading to a rapidly progressive myelopathy characterized by: motor weakness that progresses from flaccid to spastic paraparesis with UMNS. autonomic dysfunction including bowel/bladder incontinence or retention and sexual dysfunction. sensory dysfunction including pain, paresthesia, or numbness with a distinct sensory level (ie, lowest spinal cord level with intact sensation). MRI demonstrates enhancement of the affected cord segments without evidence of compression, whereas lumbar puncture typically reveals cerebrospinal fluid pleocytosis and elevated IgG.  Management includes high-dose intravenous glucocorticoids, often with plasmapheresis. Guillain-Barré syndrome causes rapidly progressive, ascending weakness.  Upper extremity and respiratory muscle involvement is expected to develop, and a distinct sensory level would be atypical.  In addition, patients develop flaccid (rather than spastic) paralysis. Spinal cord compression would cause similar myelopathic symptoms; however, cauda equina syndrome is usually associated with severe back pain and sensory loss that involves the thighs and buttocks.  This patient has sensory loss below the umbilicus (provided by the T10 spinal nerve), indicating involvement of the thoracic cord. Anterior spinal artery syndrome is characterized by motor weakness and loss of pain and temperature sensation below the lesion; however, proprioception and vibratory sensation are spared (unlike in this patient). Subacute combined degeneration (due to vitamin B12 deficiency) causes sensory ataxia with progressive spastic paraparesis and incontinence.  However, it occurs over a prolonged period (years) and is often associated with neuropsychiatric changes. Transverse myelitis is an immune-mediated disorder characterized by the infiltration of inflammatory cells into a segment of the spinal cord.  Inflammation localizes to ≥1 contiguous spinal cord segments, leading to a rapidly progressive myelopathy characterized by motor weakness, autonomic dysfunction (eg, bowel/bladder dysfunction), and sensory deficits with a distinct sensory level.

A 30-year-old woman comes to the emergency department due to worsening, bilateral lower extremity weakness and numbness for the past 4 days.  She has had no fever, headache, or back pain, but she had an incident of urinary incontinence today.  The patient has no other medical conditions and takes no medications.  She does not use tobacco, alcohol, or illicit drugs.  Temperature is 37 C (98.6 F), blood pressure is 110/60 mm Hg, pulse is 72/min, and respirations are 16/min.  On physical examination, the patient is alert and oriented with normal comprehension and speech.  The pupils are equal and reactive, and there is no facial weakness.  Upper extremity muscle strength is normal with normal reflexes, but both legs are diffusely weak.  Bilateral lower extremity deep tendon reflexes are increased with extensor plantar response.  Sensation to pinprick is decreased below the level of the umbilicus, and vibratory sensation is absent in the toes.  Which of the following is the most likely cause of this patient’s current symptoms? A. Autoimmune demyelination of peripheral nerves B. Compression of cauda equina nerve roots C. Embolic occlusion of the anterior spinal artery D. Segmental inflammation of the spinal cord E. Vitamin B12 nutritional deficiency

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Correct Answer Is D Clear, unilateral rhinorrhea that increases at times of relatively increased intracranial pressure (eg, bending over, bowel movements) is suspicious for cerebrospinal fluid (CSF) rhinorrhea.  Patients also often report a salty or metallic taste.  Most cases occur after head trauma, especially with fracture of the skull base (eg, cribriform plate, temporal bone).  CSF rhinorrhea can be evident immediately after the trauma or may have a delayed presentation (days to months) in which rhinorrhea is noted after acute edema resolves. Testing the nasal discharge for CSF-specific proteins (eg, beta-2 transferrin, beta-trace protein) is diagnostic.  Imaging or endoscopic nasal examination can be used to localize the precise site of the defect.  Patients typically require inpatient management for bed rest, head-of-bed elevation, and frequent neurologic evaluation because they are at risk for meningitis due to nasal flora contamination of the CSF.  If the CSF rhinorrhea does not resolve with these measures, further interventions (eg, lumbar drain, operative repair) are necessary. A personal or family history of atopy may suggest allergic rhinitis, which would present with bilateral (rather than unilateral) rhinorrhea and pale or bluish, boggy, edematous turbinates.  Accompanying symptoms of sneezing, itching, and watery eyes are also typically present. Intranasal cocaine and nasal decongestants cause vasoconstriction.  Overuse can result in bilateral (rather than unilateral) rhinorrhea and severe “rebound” nasal congestion (eg, rhinitis medicamentosa).  Examination often shows swollen, erythematous turbinates.  Tissue destruction from vasoconstriction caused by intranasal cocaine typically occurs at the septum (resulting in septal perforations) rather than at the skull base. Clear, unilateral rhinorrhea that increases at times of relatively increased intracranial pressure (eg, bending over, bowel movements) is suspicious for cerebrospinal fluid rhinorrhea, which is most often caused by head trauma and can result in meningitis

A 35-year-old woman comes to the office due to persistent rhinorrhea.  The patient has clear drainage from the right side of her nose that increases when she has a bowel movement or bends over to pick something off the floor.  On examination, the external nose appears normal, the turbinates are pink, and the septum is straight.  There is a small amount of clear fluid from her right nostril.  The remainder of the examination is normal.  Which of the following additional history is most important for establishing a diagnosis in this patient? A. Family history B. Illicit drug use C. Prior seasonal allergies D. Recent head trauma E. Use of decongestant sprays

Correct Answer Is C Epiglottitis is a rare, potentially fatal infection that presents with acute onset of fever, sore throat, and signs of upper airway obstruction (eg, stridor, drooling).  Symptoms often develop over hours without a notable prodrome, as seen in this patient.  Impending signs of respiratory failure include anxiety, worsening stridor, and a muffled/hoarse, “hot potato” voice.  Patients may display tripod positioning (leaning forward, neck hyperextension) to maximize airway diameter.  The anterior neck near the hyoid bone may be tender, and oropharyngeal examination is typically normal other than pooled oral secretions. X-ray is not required for diagnosis if clinical suspicion is high, but lateral view shows an enlarged epiglottis, suggestive of edema.  Diagnosis is confirmed via direct visualization of an edematous epiglottis.  However, detailed oropharyngeal examination is often deferred in children due to risk of laryngospasm from provoked aggravation.  Direct laryngoscopy during intubation (a controlled setting to secure the airway) is often preferred for diagnosis and management. Bacterial tracheitis presents with fever, stridor, and respiratory distress.  Croup presents with a “barky” cough, hoarseness, stridor, and fever.  In both conditions, onset is gradual (over days), and neck x-ray (posterioanterior view) reveals subglottic narrowing (eg, steeple sign) and a normal epiglottis.  This patient has a thickened epiglottis on x-ray, a finding consistent only with epiglottitis. Foreign body aspiration most commonly presents with acute onset of wheezing, stridor, and/or respiratory distress without fever.  X-ray may reveal a foreign body if the object is radiopaque (eg, coin).  Examination typically shows unilateral wheezing or asymmetric breath sounds, neither of which are found in this case. Peritonsillar abscess is most common in older children and adolescents; it presents with gradual onset of fever, muffled voice, and unilateral tonsillar swelling with uvular deviation.  This patient’s age, normal oropharyngeal examination, and acute symptom onset make this diagnosis unlikely. Epiglottitis is a rare but potentially fatal infection that presents with acute onset of fever, sore throat, and signs of upper airway obstruction (eg, stridor, drooling).  Plain x-rays may help confirm the diagnosis by revealing an enlarged epiglottis (thumb sign).

A 3-year-old boy is brought to the emergency department due to a sore throat.  The boy woke up with the sore throat this morning and has refused to eat.  His mother gave him acetaminophen, but it did not relieve his pain.  Temperature is 38.7 C and respirations are 28/min.  The patient is sitting still on his mother’s lap and appears scared.  He has a hoarse voice, rhinorrhea, and mild stridor.  Tympanic membranes are clear bilaterally.  Examination of the posterior pharynx shows no erythema or tonsillar exudate.  The anterior neck is tender to palpation.  Lung examination reveals transmitted upper airway sounds that are equal bilaterally without crackles or wheezes.  Lateral neck x-ray is shown below. Which of the following is the most likely diagnosis in this patient? A. Bacterial tracheitis B. Croup C. Epiglottitis D. Foreign body aspiration E. Peritonsillar abscess

Correct Answer Is A This clinical finding is known as external auditory exostosis (EAE) or ‘Surfer’s ear’ and is a common condition among both professional and recreational surfers. The exact cause of the condition is unknown, but it is thought that exposure to cold water and wind may stimulate osteoblasts in the temporal bone to produce bony growths that project into the ear canal. Surfer’s ear is a benign but irreversible condition and is often asymptomatic in the early stages. Patients are recommended to avoid cold and windy conditions, and the use of ear plugs and a protective hood may also be helpful as a preventative measure. Ear plugs, however, will not resolve exostoses that are already present. Surgical treatment is reserved for patients with severe and symptomatic external auditory exostosis. Referral is indicated for large lesions, progressive hearing loss, and recurrent ear infections

A 25 year old male patient who attends with right-sided ear discomfort. He tells you that he has had discomfort for a few months and has a feeling like his ear is ‘blocked’. He is a keen early morning surfer and thinks that the blocked feeling might just be some trapped water in his ears. He has not noticed any ear discharge. He has no fevers and feels systemically well. However, the aching sensation is getting progressively worse in his right ear and he is keen to know if there is any problem. You perform an otoscopic examination of his ears and note the following finding on both left and right sides: What is the most appropriate advice to provide to him today about his ear complaint? A. Advise him that he has an increased risk of developing otitis externa and conductive hearing loss B. Advise him that he will require oral flucloxacillin 500mg 6 hourly for five days C. Advise him that the condition is aggravated by sand in the auditory canals D. Advise him that wearing ear plugs while surfing will assist with resolution of the condition. E. Advise him that he will require an urgent review with an Ear Nose Throat (ENT) surgeon due to the malignant potential of this condition

Correct Answer Is A Of the options, labyrinthitis, Meniere’s disease and lateral medullary syndrome can cause acute onset vertigo, tinnitus and hearing loss. Ataxia can be a presentation in patients with cerebellar or vestibular disease. Of these three and given the inconclusive neurological examination, labyrinthitis is the most likely diagnosis. Another hint that pointed towards labyrinthitis is that the vertigo provoked with changes in head position as stated in the context. Acute labyrinthitis presents with acute vertigo often followed by nausea and vomiting, tinnitus and  hearing loss. A history of preceding viral upper respiratory tract infection is present in up to 50% of patients. Change in head position provokes vertigo. Each episode of vertigo lasts from few seconds to minutes. Meniere’s disease also presents with episodes of acute onset vertigo, tinnitus and hearing loss. However, patients with Meniere’s disease often complain of ear fullness because the pathophysiology is excess endolymph in the labyrinth. Patients are usually middle-aged women with a positive family history for the condition. Finally, Meniere’s disease is much less common compared to labyrinthitis. Given these, Meniere’s disease in this patient is a less likely diagnosis compared to labyrinthitis. Vestibular neuronitis is the inflammation of the vestibular nerve often by a viral infection. Patients usually have a preceding viral upper respiratory infection or herpes zoster. Vertigo and imbalance are the prominent features of vestibular neuronitis and there is no hearing loss or tinnitus. Loss of balance is more prominent in vestibular neuronitis compared to other causes of vertigo and patient commonly present with vertigo and falls. Symptoms in vestibular neuronitis are aggravated by change in the position of the head. Neurological examination in patients with vestibular neuronitis is otherwise normal. Acoustic neuromas are intracranial tumors that arise from the Schwann cell sheath of either the vestibular or cochlear nerve. As acoustic neuromas increase in size, they eventually occupy a large portion of the cerebellopontine angle. Although 5-15% of patients with acoustic neuroma present with acute onset of unilateral hearing loss, deafness has an insidious onset in this condition, making it a less likely diagnosis. Gradual hearing loss is overwhelmingly the most common presenting symptom of patients with acoustic neuroma . Imbalance and vertigo is not a prominent feature because as the tumor growth disrupts the vestibular nerve function slowly, there is enough time for compensation. Other features that may be present in patients with acoustic neuroma are headache and facial sensory impairment. Lateral medullary syndrome, also known as Wallenberg syndrome or posterior inferior cerebellar artery (PICA) syndrome has other clinical features in addition to vertigo, hearing loss,and tinnitus. Such features include cross-body sensory impairment (sensory impairment of the face on the affected side and that of the body on the other side), Horner’ssyndrome, and signs and symptoms indicative of the involvement of cranial nerves or their nucleus. Such signs and symptoms may include dysphagia(due to involvement of nucleus ambiguus that supplies the vagus and glossopharyngeal nerves),dysarthria, dysphonia, disrupted temperature and pain sensation, palatal clonus and heart rate and blood pressure dysregulation (due to involvement of the vagus nerve)

A 54-year-old woman presents to the emergency department with complaints of sudden onset vertigo, nausea, vomiting and hearing loss in her left  ear. Vertigo provoked with changes in head position. On examination, her vitals are within the normal  range. Hearing is decreased on the left side on whisper test. Rinne and Weber tests establish sensori neural deafness of the left ear. She has also nystagmus with the rapid eye to the left side. The rest of the examination is inconclusive.Which one of the following could be the most likely diagnosis? A. Labyrinthitis B. Vestibular neuronitis C. Acoustic neuroma D. Meniere's disease E. Lateral medullary syndrome

Correct Answer Is E The inner ear contains the endolymphatic fluid-filled semicircular canals (which convey movement and position of the head) and the cochlea (which is the sensory organ of hearing).  Conditions that cause disruption of endolymph flow can present with vertigo (semicircular canals) and/or sensorineural hearing loss (cochlea). Perilymphatic fistulas are a rare, but debilitating, complication of head injury or barotrauma.  They cause leakage of endolymph from the semicircular canals and cochlea into surrounding tissues, resulting in characteristic clinical features: Progressive sensorineural hearing loss caused by damage to cochlear hair cells from loss of endolymph. Episodic vertigo with nystagmus triggered by pressure changes in the inner ear (eg, Valsalva maneuver, elevation changes [eg, riding in elevator]) due to acutely increased endolymph leakage.  This can be demonstrated clinically by performing a loud clap (ie, pressure change due to sound conduction through the ossicles) near the patient’s ear and observing for nystagmus (Tullio phenomenon). Patients are advised to limit activities that increase inner ear pressure; they also require ENT referral for further management. Benign paroxysmal positional vertigo is caused by debris (otoliths) that temporarily alters endolymph flow through the semicircular canals.  Therefore, patients typically have sudden, brief (<1-min) episodes of vertigo triggered by head movement. Eustachian tube dysfunction can result in fluid in the middle ear space (not the inner ear vestibular system) and can cause ear popping, cracking, and hearing loss in response to changes in pressure.  However, it also causes a sense of ear fullness or pain, not episodic vertigo with nystagmus. Ménière disease is caused by increased endolymphatic fluid volume or pressure in the vestibular system.  It also causes episodic vertigo with hearing loss, but episodes are accompanied by aural fullness or tinnitus, last 20 minutes to 24 hours, and often lack specific, identifiable triggers. Orthostatic hypotension causes lightheadedness, presyncope, or syncope when the patient assumes a standing position due to cerebral hypoperfusion.  It does not involve the vestibular system and therefore does not cause true vertigo or nystagmus. A perilymphatic fistula can occur after head trauma and result in episodic vertigo triggered by sudden pressure changes (eg, Valsalva maneuvers) or loud noises (Tullio phenomenon).