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 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

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 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 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 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 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.

🧩 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

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

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 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 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 26-year-old man comes to the office for follow-up related to painless progressive visual loss in the right eye. Recent ophthalmological evaluation revealed macular edema due to 2 retinal lesions consistent with capillary hemangioblastoma. He underwent laser photocoagulation treatment, and the vision in his right eye has improved. The patient has no other medical conditions. His father died from a cerebral hemorrhage at age 52. MRI of the brain with gadolinium reveals 2 small, cystic, enhancing nodules in the cerebellum. Renal ultrasonography reveals multiple cysts in both kidneys. Which of the following is the most likely diagnosis?

A. Autosomal dominant polycystic kidney disease
B. Autosomal recessive polycystic kidney disease
C. Li-Fraumeni syndrome
D. Neurofibromatosis type 2
E. Von Hippel-Lindau disease

Correct Answer Is E

This patient has evidence of von Hippel-Lindau (VHL) disease, an autosomal dominant disorder that results in benign and malignant multiorgan tumors.  The most common tumors associated with VHL are hemangioblastomas of the central nervous system (CNS) (particularly in the cerebellum, with a classic cystic nodular radiographic appearance) and retina.  Although the tumors are noninvasive, symptoms occur due to hemorrhage or compression of surrounding tissues.  Bleeding from retinal tumors can lead to retinal exudates and impaired vision or, if untreated, retinal detachment with vision loss.  Acute hemorrhage in a brain tumor can result in herniation and death (as likely occurred in this patient’s father).

Malignant manifestations include renal cell carcinoma (RCC), which occurs in upward of 70% of patients by age 60.  RCCs are of the clear cell subtype and typically bilateral.  They are often preceded by the formation of multiple renal cysts, which are considered a premalignant condition.  Pheochromocytomas also occur with increased frequency and are characterized by paroxysms of hypertension, tachycardia, and diaphoresis.  Less common manifestations include vascular tumors of the endolymphatic sac in the ear and pancreatic disease (eg, cysts, neuroendocrine tumors).  Genetic testing for germline VHL mutations is key to diagnosis.  Management requires frequent tumor surveillance beginning in infancy or early childhood.

Autosomal dominant polycystic kidney disease also manifests as CNS and renal disease.  However, the CNS disease is largely due to aneurysms (which would not appear as cystic nodules on imaging) rather than tumors; the renal disease is characterized by progressive parenchymal obliteration by cysts, which commonly leads to flank pain and hematuria; and the condition is not associated with retinal capillary hemangioblastomas.

Patients with autosomal recessive polycystic kidney disease are typically diagnosed in infancy or childhood.  Although the disease is associated with multiple renal cysts, patients characteristically develop end-stage renal disease in early childhood, and hepatobiliary involvement is common (eg, hepatic fibrosis, liver cysts).  It is not associated with hemangioblastomas.

Li-Fraumeni syndrome is an autosomal dominant disorder associated with alterations of the tumor protein p53 gene.  It usually results in early onset of malignancies such as sarcomas, breast cancer, and adrenal carcinomas.  CNS disease is characterized by gliomas and medulloblastomas, not hemangiomas.

Neurofibromatosis type 2 is another autosomal dominant disorder with marked CNS and ophthalmologic features.  However, it is more commonly characterized by schwannomas, particularly of the vestibular nerve, and meningiomas.  Cataracts and retinal hamartomas are common ophthalmic manifestations.

Von Hippel-Lindau disease is an autosomal dominant disorder resulting in benign and malignant multiorgan tumors.  The most common tumors are hemangioblastomas of the central nervous system and retina.  Other common manifestations include renal cell carcinoma (often preceded by the formation of premalignant renal cysts) and pheochromocytoma.

A 32-year-old male presents to your clinic concerning about the two occasions over the past week during which he has noticed blood in his semen. He has never noticed this before. There is no pain with urination or ejaculation and no urinary frequency. He reports no anorexia, bone pain or weight loss. He has had several casual sexual relationships with women over the past 12 months. He has no significant past medical history and takes no regular medications. There is no family history or other risk factors for prostate cancer.

On examination, his temperature is 36.8C and blood pressure is 135/85 mmHg and genital examination and digital rectal examination are unremarkable. Systems review shows no clinical signs of chronic liver disease, leukaemia or lymphoma.

Which initial investigations would be most appropriate for him at this stage?

A. Urine microscopy, culture & sensitivities; urine cytology; full blood count; coagulation studies; chlamydia & gonorrhoea PCR
B. Urine microscopy, culture & sensitivities; full blood count; prostate specific antigen; chlamydia & gonorrhoea PCR; coagulation studies
C. Urine microscopy, culture & sensitivities; urine cytology; prostate specific antigen; pelvic computed tomography; chlamydia & gonorrhoea PCR
D. Urine microscopy, culture & sensitivities; full blood count; urine cytology; scrotal ultrasound; cystoscopy
E. Urine microscopy, culture & sensitivities; chlamydia & gonorrhoea PCR; full blood count; pelvic computed tomography; cystoscopy

A 57-year-old man arrives at the hospital with nausea, dark urine, and decreased urine output for 2 days.  For the past week, the patient has had generalized fatigue, muscle pain, and weakness.  He reports no recent fever, chills, sore throat, skin infection, or abdominal pain.  Medical history is significant for coronary artery disease with stenting to the right coronary artery, hypertension, gout, and obstructive sleep apnea.  Current medications include aspirin, ticagrelor, simvastatin, metoprolol, lisinopril, and colchicine.  The patient does not use alcohol, tobacco, or illicit drugs.  Temperature is 37 C (98.6 F), blood pressure is 140/90 mm Hg, pulse is 88/min, and respirations are 18/min.  There is no orthostasis.  Skin turgor is normal.  Oropharynx is clear.  Cardiopulmonary examination shows no abnormalities.  The abdomen is soft, nontender, and without bruit; there are no masses felt.  There is no peripheral edema.  The right great toe is slightly inflamed.  Laboratory studies reveal the following:

Complete blood count
    Hemoglobin 13.8 g/dL
    Platelets 260,000/mm3
    Leukocytes 11,000/mm3
Serum chemistry
    Sodium 136 mEq/L
    Potassium 5.6 mEq/L
    Chloride 94 mEq/L
    Bicarbonate 18 mEq/L
    Blood urea nitrogen 50 mg/dL
    Creatinine 4.2 mg/dL
    Glucose 100 mg/dL
Urinalysis
    Protein none
    Blood 3+
    White blood cells 1-2/hpf
    Red blood cells 1-2/hpf
Baseline laboratory studies conducted a month ago were normal.  Which of the following is most helpful to establish a diagnosis?

A. 24 hour urine protein measurement
B. Renal ultrasonogram
C. Renal vascular imaging
D. Serum complement levels
E. Serum creatine phosphokinase

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