Case-based MCQ

A 74-year-old woman is brought to the emergency department due to worsening weakness and gait unsteadiness.  The patient has a history of ischemic stroke causing right-sided weakness and uses a cane to ambulate.  Over the past several days, she has been feeling weak and unsteady, and this morning she fell while getting out of bed.  She did not lose consciousness and has had no headache, vomiting, or vision loss.  The patient recently has had dysuria and urinary urgency, which have improved after taking trimethoprim-sulfamethoxazole.  Other medical conditions include hypertension, type 2 diabetes mellitus, and seizure disorder controlled with phenytoin.  Temperature is 37.1 C, blood pressure is 140/86 mm Hg, and pulse is 84/min.  Pupils are equal and briskly reactive, and extraocular movements are intact.  There is bilateral nystagmus on lateral gaze.  Muscle strength is diffusely decreased but more pronounced in the right extremities.  Deep tendon reflexes are increased throughout.  Dysmetria is present on finger-nose testing, and the gait is wide-based.  Which of the following is the most likely cause of this patient’s current condition? A. Epidural abscess B. Folate deficiency C. Medication toxicity D. Septic encephalopathy E. Subdural hematoma

Correct Answer Is E This patient’s presentation is most consistent with Tourette syndrome (TS).  TS, a neurological disorder with childhood onset, is characterized by a combination of vocal (eg, throat clearing) and motor (eg, blinking, shoulder shrugging) tics.  Tic severity typically peaks at age 10-12, and tics are exacerbated by anxiety, fatigue, and psychosocial stress.  When tics are severe and debilitating (eg, declining academic performance, psychosocial dysfunction), as in this patient, treatment options include behavioral suppressive therapy (eg, habit reversal training, substituting a voluntary movement incompatible with the tic) and pharmacological interventions. Pharmacotherapy of TS consists of: Antidopaminergic drugs:  Vesicular monoamine transporter type 2 (VMAT2) inhibitors (eg, tetrabenazine) function as dopamine depleters, whereas antipsychotic medications (eg, risperidone) block dopamine postsynaptic receptors and carry risks of parkinsonism, tardive dyskinesia, and metabolic effects.  VMAT2 inhibitors are therefore increasingly preferred as initial treatment over antipsychotics. Alpha-2 adrenergic receptor agonists (eg, guanfacine, clonidine) can be considered in patients with comorbid attention deficit hyperactivity disorder or behavioral symptoms. Antisense oligonucleotide therapy is an investigational treatment for Huntington disease (HD), a progressive neurodegenerative disorder characterized by choreiform movements and neuropsychiatric symptoms, including dementia.  However, it is an inherited condition (eg, family history of progressive motor and cognitive decline) that is most common in midlife, with diagnosis prior to the age of 20 being rare.  In addition, this patient’s partial response to behavioral suppressive therapy in middle school makes TS more likely than HD. Copper chelation therapy is used in the treatment of Wilson disease, an autosomal recessive disorder that presents with hepatic, neurologic, and psychiatric symptoms.  Neurological manifestations commonly include dysarthria, dystonia, ataxia, parkinsonism, and drooling, rather than the waxing and waning tics seen in this patient.  In addition, this patient has no hepatic impairment, making TS the more likely diagnosis. The GABA agonist medication clonazepam (a benzodiazepine) is a first-line treatment option for myoclonus; this patient’s motor and vocal tics are consistent with TS rather than myoclonus. Serotonergic drugs (eg, selective serotonin reuptake inhibitors) would not effectively target this patient’s tics.  These medications may help treat patients with TS who have comorbid anxiety or obsessive-compulsive disorder. Pharmacotherapy of Tourette syndrome consists of vesicular monoamine transporter type 2 (VMAT2) inhibitors, antipsychotic medications, and alpha-2 adrenergic receptor agonists.  VMAT2 inhibitors are increasingly preferred as initial treatment over antipsychotics due to a more favorable adverse effect profile

A 20-year-old college student comes to the office due to worsening abnormal movements.  The symptoms initially started in middle school when he would repeatedly blink and then shrug his shoulders.  The patient worked with a counselor who taught him techniques to suppress movements for periods of time, although these did not completely resolve them.  Over the past few years, the symptoms have gradually worsened.  Episodes now occur multiple times daily, particularly around highly stressful times at school.  His grades have declined, and he is embarrassed during class presentations.  The patient has no history of serious illness and takes no medications.  He occasionally smokes marijuana on weekends.  Family history is notable for the death of his father at age 50 from a stroke.  Vital signs are normal.  During the examination, the patient is visibly anxious.  He repeatedly blinks, clears his throat, and shrugs his shoulders.  The remainder of the physical examination shows no abnormalities.  Which of the following is the most appropriate treatment for this patient? A. Antisense oligonucleotide therapy B. Copper chelation therapy C. GABA agonist therapy D. Serotonin reuptake inhibition therapy E. VMAT2 inhibitor therapy

🧩 Medical Mnemonics Gerstmann's Syndrome AGRAFI 🔡

Agraphia ~ Agrafi 😉

'ph' makes the /f/ sound 🙄

• Angular Gyrus is damaged 🧠 • Right-left confusion ↔️ (confusion about directions) • Acalculia ➗ (difficulty with math) &  Agraphia ✍️ (difficulty writing) • FInger agnosia ✋ (inability to identify fingers) #neurology   〰〰〰〰〰〰〰〰〰〰〰 ©Medical Mnemonics

Correct Answer Is B This patient has a clinical diagnosis of Gerstmann’s Syndrome. The lesion is most commonly in the left parietal lobe, especially in right handed individuals. Clinical feature of Gerstmann’s syndrome include: -Acalculia (impairment of simple arithmetic). -Dysgraphia (impaired writing). -Finger anomia (an inability to name individual fingers such as the index and thumb). -Right-left confusion (an inability to tell whether a hand, foot, or arm of the patient or examiner is on the right or left side of the body). When Gerstmann’s syndrome is seen in isolation, it is commonly associated with damage to the inferior parietal lobule (especially the angular gyrus) in the left hemisphere.

A 62-year-old right-handed man, presented with new onset of difficulty in writing, inability to name individual fingers and inability to do simple calculations. Also, he is unable to tell whether you are standing on his right or left side during the assessment. Which of the following is the most likely site of lesion? A. Left temporal lobe B. Left parietal lobe C. Right parietal lobe D. Left frontal lobe E. Right frontal lobe

Correct Answer Is A The sixth cranial nerve palsy results to isolated weakness of abduction of the affected eye and horizontal binocular diplopia. On examination, there is an esotropia (inward deviation) that is worsened with gaze into the field of the affected lateral rectus muscle. Abduction is commonly limited on the side of the lesion. Poorly controlled diabetes is a predisposing factor. In the right cranial nerve palsy the right eye will be in an abnormal position (medially deviated), and the patient is diplopic on looking laterally to the right side. The third cranial nerve supplies the levator palpebrae muscle of the eyelid and 4 extraocular  muscles: the medial rectus, superior rectus, inferior rectus, and inferior oblique. These muscles adduct, depress,and elevate the eye. Patients with acute acquired third nerve palsy usually comp lain of the sudden onset of binocular horizontal, vertical, or oblique diplopia and a droopy eyelid. Pupil reflex remains intact in ischemic palsies (e.g. due to diabetes or midbrain infarcts). A person with fourth nerve palsy may complain of binocular (both eyes open) vertical diplopia and/or subjective tilting of objects (torsional diplopia). The affected eye is usually extorted because the superior oblique muscle is responsible for intorsion of the eye. Objects viewed in primary position, especially in down­ gaze may appear double when going down a flight of stairs so that the patient does not know which step to take first.

A 73-year-old type II diabetic man presents with sudden onset of horizontal diplopia, better when he looks at a near object and worse looking at distance. On examination, the left eye is deviated towards medial side. Which one of the following is the most likely diagnosis?   A. Left sixth cranial nerve palsy B. Right Sixth cranial nerve palsy C. Right third cranial nerve palsy D. Left third cranial nerve palsy E. Left fourth cranial nerve palsy

Correct Answer Is C This patient has developed clinical features of an ischemic stroke and requires urgent treatment. The treatment of acute ischemic stroke includes: – Airway, Breathing, Circulation Managment. – Thrombolysis. – Antiplatelet medications (aspirin, clopidogrel) The thrombolytics therapy involves administration of clot buster medication such as alteplase, tenecteplase, etc. wth 4 hours of the onset of the stroke. Following is the list of absolute contraindications to thrombolytics therapy: 1- Uncertainty about the time of stroke onset (e.g. patients awakening from sleep). 2- Neurologic surgery, serious head trauma, or previous stroke in past 3 months. 3- Hypertension: systolic blood pressure above 180mmHg; or diastolic blood pressure above 110mmHg on repeated measures. 4. Clinical presentation suggestive of subarachnoid haemorrhage even i the CT scan is normal. 5- History of intracranial haemorrhage. 6- Seizure at stroke onset. 7- Suspected/confirmed endocarditis. Peptic ulcer disease with a history of gastrointestinal bleeding two weeks ago is a relative contraindication to using aspirin as well as alteplase. So this patient should be given clopidogrel only for the treatment of acute stroke. Anticoagulation with warfarin or full therapeutic doses of unfractionated heparin, low molecular weight heparin or danaparoid should be avoided in acute ischemic stroke. Studies show that the reduction in recurrent stroke is offset by an increased rate of haemorrhage.

A 56-year old lady is brought to the emergency department by an ambulance. She developed right leg weakness and left sided facial droop an hour ago. She has past medical history of hypertension, hyperlipidemia and peptic ulcer disease (GI bleeding two weeks ago). On examination, her blood pressure is 130/85mmHg, respiratory rate is 18 breaths per minute, heart rate is 110 beats per minutes and oxygen saturation is 100% at room air. On the neurological examination, she is found to have hypertonia and reduced power in the right leg, and right-sided facial palsy. The Babinski sign is positive. CT scan of the brain does not show any evidence of an intracranial bleed.ECG shows sinus rhythm. Which of the following is the most appropriate therapy for this patient? A. Heparin B. Warfarin C. Clopidogrel D. Aspirin E. Thrombolysis

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Correct Answer Is C This patient has the classic presentation of a third palsy. The third cranial nerve supplies the levator muscles of the eyelid and four extraoccular muscles: the medial rectus (eye adduction), superior rectus (eye depression), inferior rectus (eye elevation), and inferior oblique(eye elevation). Additionally, the third cranial nerve constricts the pupil through its parasympathetic fibers that supply the smooth muscles of the ciliary body and the sphincter of the iris. The third nerve begins as a nucleus in the midbrain that consists of several subnuclei that innervate the individual extraoccular muscles, the eyelids, and the pupils. The etiology of the third cranial nerve palsy is vast and includes conditions such as: lschemia (e. diabetes and midbrain infarcts) Compressive effects of aneurysms such as those of the posterior communciating artery, internal carotid artery and basilar Trauma Infections Infiltrative diseases (e.g. neoplasms) Demyelination Space occupying tumors Meningitis Herniation Inflammatory diseases   Of the given options, only a posterior communicating aneurysm can cause a third nerve palsy as a cause of such presentation. Compression of the third nerve by an enlarging intracranial aneurysm is the most dreaded etiology. The most common site of an aneurysm causing a third nerve palsy is the posterior communicating artery.In the setting of an acute third nerve palsy, the aneurysm is believed to be progressively and acutely enlarging and is at imminent risk of rupture with catastrophic outcomes. Midbrain infarcts can cause third cranial nerve palsy. However, since the etiology is ischemic (such as in diabetes) the pupillary light reflex is expected to be unaffected most of the time. Furthermore, with a midbrain infarct, an isolated third nerve palsy as the sole presenting symptom is very unlikely and other signs and symptoms related to a midbrain infarct are expected. Right 6th nerve palsy presents with horizontal binocular diplopia upon looking laterally to the affected side. Furthermore, lesions of the sixth cranial nerve do not cause ptosis. The fourth cranial nerve palsy presents with binocular vertical diplopia. Ptosis is not a feature. Lesions of occipital cortex are associated with impaired vision and visual fields deficits, none of which are present here. Furthermore, ptosis is not a feature.  

A 56-year-old man presents to the emergency department with complaint of diplopia. On examination, he has a right-sided ptosis. His visual acuity and visual fields are otherwise not impaired. His right eye is depressed inferiorly and laterally and he is not able to look at to the left side. The pupillary light reflex of the right eye is sluggish. The neurological examination is otherwise unremarkable. Which one of the following can be the most likely cause to this presentation? A. Midbrain infarct B. Right 6th nerve palsy C. Posterior communicating artery aneurysm D. Right 4th nerve palsy E. A lesion in the occipital cortex

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Correct Answer Is E This patient with cervical spine spondylosis (ie, nonspecific, degenerative cervical spine joint changes) was involved in a rear-end collision and developed subsequent upper extremity weakness, reflex loss, and sensation changes, raising strong suspicion for central cord syndrome, an incomplete acute spinal cord injury.  Most cases arise when an older individual with a stenotic cervical spinal canal (eg, due to cervical spondylosis) experiences a hyperextension injury to the neck (eg, whiplash due to rear-end collision); this compresses the spinal cord between a hypertrophied ligamentum flavum posteriorly and a bulging disc/osteophyte complex anteriorly, leading to damage to the central spinal cord (grey matter). Patients primarily develop upper extremity manifestations, including: -Weakness due to damage to the alpha motor neuron cell bodies in the anterior horn of the spinal cord -Pain, temperature, and sensory loss in dermatomes at and surrounding the level of injury due to damage to the posterior grey column -Reflex loss (eg, tricep reflex) at the level of injury due to damage to fibers as they cross from the dorsal to ventral horn Due to the more central location of the lesion, the lateral spinal tracts running to the sacrum (eg, bowel, bladder) and lower limbs are generally spared. Workup begins with spinal imaging; x-ray is often normal but may show cervical spondylosis.  Cervical myelogram is generally diagnostic and often demonstrates persistent cord compression; treatment with glucocorticoids and/or surgery is usually required. Acute stress disorder is common after severe motor vehicle collisions and is generally characterized by agitation, anxiety, and fear.  Numbness, weakness, and loss of reflexes in the upper extremities would be atypical. Brachial plexus injury (nerve roots C5-T1) is generally characterized by shoulder or arm pain, upper extremity muscle weakness, atrophy (after weeks), and sensory loss; however, most cases are unilateral.  In addition, traumatic injury to the brachial plexus usually occurs when there is downward traction on the shoulder and the neck is forced to the contralateral side (not during hyperextension injury). Malingering is when a patient simulates an illness to obtain obvious external benefit (eg, money, medications, work benefits).  This patient’s reflex, motor, and sensory abnormalities on physical examination make malingering less likely. Postconcussion syndrome is generally marked by headache, dizziness, cognitive impairment (eg, loss of concentration/memory), irritability, anxiety, and noise sensitivity.  Although it can occur following whiplash injury, upper extremity weakness, sensory loss, and reflex abnormalities would be atypical. Central cord syndrome is common after whiplash-type injuries in older adults with underlying cervical spondylosis.  Damage to the central cervical spinal cord causes upper extremity motor, sensory, and reflex abnormalities; sacral (eg, bowel/bladder) and lower extremity function is generally preserved.

A 62-year-old woman comes to the office due to upper extremity weakness and numbness.  Three days ago, the patient was involved in a motor vehicle collision in which a truck rear-ended her vehicle.  The patient did not hit her head or lose consciousness but experienced a tingling and burning sensation in all extremities, which she attributed to the stress of the accident.  Since then, she has had numbness in her upper extremities and clumsiness of her hands.  She reports difficulty picking up objects but has had no leg weakness or bowel or bladder disturbance.  The patient is upset that the other driver refused to accept fault but reports no other ongoing stressors.  She has a history of hypertension and osteoarthritis.  Vital signs are within normal limits.  Neck and back examination show no deformity or tenderness.  There is weakness of hand grip bilaterally, and the triceps reflex is decreased on both sides.  Decreased pinprick sensation is present on the fingers.  The remainder of the neurologic examination is normal.  Cervical spine x-ray reveals no vertebral dislocation or fracture, but diffuse spondylotic changes are present.  Which of the following is the most likely cause of this patient’s symptoms? A. Acute stress disorder B. Brachial plexus injury C. Malingering D. Postconcussion syndrome E. Spinal cord injury

Correct Answer Is A The left middle cerebral artery supplies the cortex around the sylvian fissure, as well as some of the frontal lobe structures involved in speech. The optic radiation loops through the temporal lobe on its way to the occipital cortex and is usually damaged with occlusion of the middle cerebral artery. The likely speech disorder with an injury of the left frontal lobe is a Broca aphasia. Comprehension would be expected to be largely intact, but if the patient has damage to enough of the temporal lobe cortex, a Wernicke aphasia might develop. Choroidal artery occlusions might produce focal weakness, but speech problems would be less likely. Occlusion of the PICA can produce a variety of brainstem and cerebellar signs, but this combination of deficits would be unlikely with a lesion outside the cerebral cortex. Anterior cerebral artery stroke would be expected to cause lower extremity weakness and would not affect vision, although it could result in decreased speech production. Vertebral or basilar artery occlusion would primarily affect brainstem or cerebellar structures. If either posterior cerebral artery had its blood supply compromised, there could be visual loss and a posterior (fluent) aphasia

A 72-year-old woman has the abrupt onset of right face and hand weakness, disturbed speech production, and a right homonymous hemianopsia. This is most likely attributable to occlusion of which of the following arteries? A. Left middle cerebral artery B. Left anterior cerebral artery C. Left vertebrobasilar artery D. Right anterior choroidal artery E. Left posterior inferior cerebellar artery (PICA)

Correct Answer Is A This patient has a history consistent with temporal arteritis (ie, giant cell arteritis), which is treated with high-dose oral glucocorticoids tapered slowly over a prolonged period.  Many patients develop complications of therapy due to the long duration of treatment with supra-physiological doses of glucocorticoids.  In addition to hyperglycemia and bone loss, treatment may be associated with glucocorticoid-induced myopathy (GIM).  GIM is one of the most common types of drug-induced myopathy and typically occurs weeks to months after starting glucocorticoid therapy.  Acute myopathy following very high-dose pulse glucocorticoid therapy can occur in critically ill patients but is not as common as chronic myopathy complicating long-term glucocorticoid use.  The mechanism is thought to be due to increased muscle catabolism and decreased anabolism as a direct effect of glucocorticoids. This risk of GIM rises with higher doses of glucocorticoids (generally >40 mg hydrocortisone daily or its equivalent).  Patients typically develop painless proximal muscle weakness (lower extremity before upper extremity) that manifests as difficulty in daily activities such as getting up from a chair, climbing stairs, or brushing hair.  There is no muscle inflammation or tenderness, and creatine kinase and erythrocyte sedimentation rate (ESR) are normal.  Muscle power improves after discontinuation of glucocorticoids, but recovery can take weeks to months. Inflammatory myositis can present with symmetric proximal muscle weakness.  However, the muscles are generally tender on palpation and creatine kinase and ESR levels are usually elevated. Mononeuritis multiplex is usually seen in vasculitis and is caused by nerve damage in 2 or more nerves in separate parts of the body.  Patients typically develop asymmetric peripheral nerve findings such as wrist or foot drop. Multiple sclerosis typically presents with 2 or more episodes of various neurologic symptoms with interval resolution rather than chronic/progressive symptoms. Neuromuscular junction diseases such as myasthenia gravis may cause proximal muscle weakness.  However, they usually cause more upper- than lower-extremity disease and usually have associated ocular symptoms.  Muscle weakness is typically fluctuating; more muscle weakness is observed later in the day and following exercise. Glucocorticoid-induced myopathy is a complication of chronic corticosteroid use.  It is characterized by painless proximal muscle weakness, which is more prominent in the lower extremities.  There is no muscle inflammation or tenderness, and creatine kinase level and erythrocyte sedimentation rate are normal.  Glucocorticoid-induced myopathy slowly improves once the offending medication is discontinued