Case-based MCQ

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Correct Answer Is C Phenytoin is a commonly used, long-acting antiepileptic medication that inhibits voltage-gated sodium channels.  Acute toxicity initially manifests with signs of cerebellar dysfunction: horizontal nystagmus (ie, nystagmus on lateral gaze), ataxia (eg, wide-based gait), dysmetria (eg, on finger-nose testing), slurred speech, and nausea/vomiting are common, and hyperreflexia may occur.  Severe toxicity results in altered mental status (eg, lethargy, confusion), coma, paradoxical seizures, and death.  Rapid intravenous infusions of phenytoin or its prodrug fosphenytoin can also result in hypotension and bradyarrhythmia. Toxicity typically occurs after dosing adjustments or initiation of medications that interfere with the pharmacodynamics of phenytoin.  Because phenytoin is highly protein-bound and is hepatically metabolized by the cytochrome p450 system, medications that inhibit the cytochrome p450 system (eg, trimethoprim-sulfamethoxazole [as in this patient], fluconazole) or that displace phenytoin from plasma proteins (eg, valproic acid) increase the risk of drug toxicity.  Patients with renal or hepatic dysfunction are also at increased risk.  Management involves supportive care with gastric decontamination and possibly hemodialysis. Epidural abscesses (which may result from hematogenous spread of infection) may cause weakness and hyperreflexia; however, patients typically have fever, malaise, and back pain.  Lower extremity hyperreflexia is possible, but diffuse hyperreflexia would be unlikely.  In addition, epidural abscess is unlikely to cause cerebellar dysfunction and nystagmus. Folate deficiency (which is associated with phenytoin use) typically causes macrocytic anemia and mood disturbances or psychosis but may rarely cause paresthesias and weakness.  However, nystagmus and cerebellar dysfunction would be unexpected. Septic encephalopathy is characterized by delirium (waxing and waning altered mentation) and confusion.  Focal neurologic deficits, as seen in this patient, would be unexpected.  In addition, although the patient likely had a urinary tract infection, symptoms have improved and she does not have fever, tachycardia, tachypnea, or hypotension to suggest sepsis. Acute subdural hematoma usually occurs after trauma (eg, fall) and often causes coma at the time of injury (or shortly thereafter).  Chronic subdural hematoma has an indolent course with gradually worsening headache, cognitive impairment, and somnolence that occurs over a period of weeks.  This patient’s symptoms preceded the fall, and nystagmus would be unexpected. Phenytoin is highly protein-bound and metabolized hepatically by the cytochrome p450 system; medications that inhibit cytochrome p450 (eg, trimethoprim-sulfamethoxazole, fluconazole) or that displace phenytoin from plasma proteins (eg, valproic acid) increase the risk of drug toxicity.  Common symptoms of acute phenytoin toxicity include horizontal nystagmus, ataxia, and nausea/vomiting, and significant toxicity can result in altered mental status, coma, and death.  

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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