Neurology Practice Questions

Q: A 60 y/o male suddenly experiences an intense headache, described as the worst headache of his life, followed by vomiting and photophobia. O/E he has neck stiffness and a dilated pupil on the right side. A CT scan reveals bleeding in the subarachnoid space. Which of the following is the most common cause of this condition?

Intracranial aneurysm. ***Intracranial aneurysm***- Rupture of an intracranial **saccular (berry) aneurysm** accounts for approximately 85% of all non-traumatic subarachnoid hemorrhage (SAH) cases, making it the most common cause [2].- The classic presentation of the **"worst headache of his life"** (thunderclap headache), meningismus (**neck stiffness**), and potential Third nerve palsy (dilated pupil due to compression) are highly suggestive of aneurysmal SAH [1].*Hypertension*- Uncontrolled **chronic hypertension** is the leading cause of non-traumatic **intraparenchymal hemorrhage (ICH)**, typically affecting deep brain structures like the basal ganglia.- While hypertension is a major risk factor for SAH, it is not the primary mechanism of bleeding; the rupture of an aneurysm is the direct immediate cause [1].*Arteriovenous malformation (AVM)*- AVMs are abnormal connections that can rupture, causing hemorrhagic stroke, but they are the second most common cause of SAH, accounting for less than 10% of cases.- AVM rupture often leads to a combination of **intraparenchymal hemorrhage** and SAH, and they are typically associated with younger patients.*Brain tumour*- Tumors rarely cause acute, massive SAH; when they bleed, it typically occurs within the tumor mass itself (**intratumoral hemorrhage**).- The clinical presentation usually involves subacute onset of symptoms and progressive focal neurological deficits, rather than the sudden, dramatic thunderclap headache characteristic of SAH [1].

Q: A patient reports difficulty switching between movements and experiences uncontrollable hand movements. What is the most likely diagnosis?

Dysdiadochokinesis. ***Dysdiadochokinesis***- This term refers to the impairment in the ability to perform **rapid alternating movements**, directly matching the complaint of "difficulty switching between movements" [2].- It is a classic sign of **cerebellar dysfunction**, which also accounts for the associated **uncontrollable movements** (often reflecting associated **ataxia** or **dysmetria**) [3].*Intentional Tremor*- This tremor is absent at rest, but its amplitude increases significantly as the patient attempts to reach a **visual target** (e.g., during the finger-to-nose test).- While it is a sign of **cerebellar disease**, the primary complaint in the stem is difficulty *switching* movements, which is characteristic of **dysdiadochokinesis**.*Metamorphosis*- This neurological term typically refers to **perceptual distortion** (specifically, *metamorphopsia* is the distortion of visual size or shape), which is unrelated to motor control or coordination.- It is not the term used to describe the inability to perform **rapid alternating movements** or uncontrolled movements due to cerebellar pathology.*Resting Tremor*- A resting tremor is maximal when the limb is completely relaxed and **supported against gravity**, classically seen in **Parkinson's disease** [1].- This tremor usually **improves significantly** or disappears entirely when the patient performs voluntary action, distinguishing it from intentional tremors and general lack of coordination.

Q: A 35-year-old woman presents with fluctuating muscle weakness, especially affecting her speech and swallowing. Repetitive nerve stimulation shows a decremental response. Her blood tests are negative for acetylcholine receptor (AChR) antibodies. Which of the following antibodies is most likely responsible for her symptoms?

Anti-MuSK antibodies. Detailed clinical evaluation of myasthenia gravis reveals that anti-MuSK antibodies target Muscle-Specific Kinase (MuSK), essential for clustering AChR at the NMJ [1]. Their presence confirms the diagnosis of Myasthenia Gravis (MG) in patients who are seronegative for AChR antibodies, often presenting with prominent bulbar and facial weakness [1]. Anti-dsDNA antibodies are specific for Systemic Lupus Erythematosus (SLE), an autoimmune disease that primarily causes arthritis, renal disease, and malar rash [2]. Although SLE can cause myositis or neuropathy, it does not typically present with the isolated, fluctuating postsynaptic weakness characteristic of Myasthenia Gravis and the decremental response. Anti-thyroid peroxidase (TPO) antibodies are primary markers for Hashimoto's thyroiditis, leading to hypothyroidism; screening for associated autoimmune thyroid disease is recommended in MG patients [1]. Anti-Ro antibodies, characteristic of Sjögren's Syndrome and SLE [2], primarily involve sicca symptoms and occasionally present with myositis, but not the hallmark features of ocular or bulbar MG.

Q: A patient presents with acute onset symmetric lower limb flaccid paralysis and absent deep tendon reflexes. Which condition is most likely?

Guillain-Barré syndrome. ***Guillain-Barré syndrome*** - This acute disorder is a **peripheral neuropathy** characterized by ascending, rapidly worsening, **symmetric weakness (flaccidity)** [1]. - The key distinguishing feature is the early and profound loss of deep tendon reflexes known as **areflexia**, corresponding to the damage of peripheral motor nerves/roots (a true lower motor neuron syndrome) [1]. *Multiple sclerosis* - MS is a **central nervous system** disorder causing demyelination in the brain and spinal cord, typically resulting in **upper motor neuron signs**. - Symptoms typically include spasticity, hyperreflexia, and sensory deficits, which directly contrast with the flaccidity and areflexia seen in this patient. *Amyotrophic lateral sclerosis* - ALS involves damage to both upper and lower motor neurons; while it causes LMN symptoms like flaccidity and atrophy, there is often concurrent **hyperreflexia or mixed reflexes** (UMN involvement) [2]. - It is a chronic, progressive neuronal disorder, not primarily defined by the acute, global **areflexia** consistent with GBS [2]. *Spinal cord injury* - Acute spinal cord injury leads to **spinal shock**, causing transient flaccid paralysis and areflexia below the level of the lesion, which eventually evolves into **spasticity and hyperreflexia**. - Unless the injury involves the **cauda equina** (LMN structure), persistent LMN signs with areflexia below the injury level are usually temporary or localized.

Q: A patient presents with the palsy of the face as shown. Which of the following is most likely involved?

7th nerve palsy. ***7th nerve palsy*** - The image shows features of a **lower motor neuron (LMN) lesion** of the **7th cranial (facial) nerve**, affecting both the upper and lower face. Note the inability to wrinkle the left forehead, incomplete eye closure, and drooping of the left corner of the mouth. - This condition, often idiopathic and termed **Bell's palsy**, results in paralysis of all ipsilateral muscles of facial expression, which are innervated by the facial nerve. *3rd nerve palsy* - A **3rd cranial nerve (oculomotor)** palsy would present with **ptosis** (drooping eyelid), a dilated pupil, and the eye positioned "down and out" due to unopposed action of the superior oblique and lateral rectus muscles. - It does not cause paralysis of the lower facial muscles, such as those involved in smiling. *Erb's palsy* - This is an injury to the **upper trunk (C5-C6)** of the **brachial plexus**, typically occurring at birth, which affects the muscles of the shoulder and arm. - It results in the characteristic "**waiter's tip**" posture of the arm and has no effect on the facial muscles. *Orbicularis oculi palsy* - This describes an isolated paralysis of the muscle that closes the eyelids. While this is a component of 7th nerve palsy, it is not the complete diagnosis. - The patient clearly has paralysis of other facial muscles, such as the **frontalis** (forehead) and **zygomaticus** (mouth), indicating a lesion of the main facial nerve trunk, not just a single branch.

Q: A young male presented with weakness in the lower half of the right side of his face, with drooping of the angle of his mouth. He is unable to raise his eyebrows and close his eyes on the right side. Which of the following is the most appropriate diagnosis?

Infranuclear facial palsy on right side. ***Infranuclear facial palsy on right side*** - **Infranuclear (peripheral) facial palsy** involves the facial nerve (CN VII) distal to the nucleus, causing complete paralysis of the entire ipsilateral side of the face including both upper and lower facial muscles. - The inability to raise eyebrows, close eyes, and drooping of the mouth on the **right side** indicates complete paralysis of the **right facial nerve**, characteristic of infranuclear lesions. *Supranuclear facial palsy on left side* - A **supranuclear (central) lesion** affects the face contralaterally, so a left-sided lesion would cause weakness on the **right face**, but the **upper face (forehead) would be spared**. - The patient's inability to raise eyebrows and close eyes contradicts supranuclear palsy, where **bilateral cortical input** to the upper facial nucleus preserves forehead function. *Infranuclear facial palsy on left side* - This diagnosis would cause complete paralysis of both upper and lower facial muscles on the **left side**. - The patient presents with weakness on the **right side** (drooping mouth, inability to raise eyebrow and close eye), making a left-sided lesion anatomically incorrect. *Supranuclear facial palsy on right side* - A **supranuclear lesion** on the right side would cause weakness of the **left lower face** due to contralateral presentation of central lesions. - Supranuclear lesions **never involve upper facial muscles** (forehead sparing) due to bilateral cortical innervation, contradicting this patient's inability to raise eyebrows and close eyes.

Q: Bell's palsy involves

Ipsilateral upper and lower halves of the face.. ***Ipsilateral upper and lower halves of the face.*** - **Bell's palsy** is the most common cause of **idiopathic peripheral (Lower Motor Neuron - LMN)** facial nerve paralysis [1]. - A peripheral (LMN) lesion affects the **entire distribution** of the facial nerve on the affected side, resulting in paralysis of all muscles, including those controlling the forehead and eye closure. - Facial nerve palsies affect the **ipsilateral** side of the face relative to the site of peripheral nerve injury or brainstem nuclear lesion. *Contralateral upper and lower halves of the face.* - This presentation would imply a **bilateral upper and lower facial paralysis**, which is highly unusual for a single lesion like Bell's palsy. - Facial nerve palsies affect the **ipsilateral** side of the face, not contralateral. *Ipsilateral lower half of the face.* - Paralysis limited to the **ipsilateral lower half of the face** while sparing the upper face (forehead) is characteristic of a **Central (Upper Motor Neuron - UMN)** lesion (like a stroke) located in the contralateral cortex [1]. - This does not define Bell's palsy, which is a **peripheral (LMN)** lesion affecting the entire face. *Contralateral lower half of the face.* - This pattern, involving **paralysis of the lower face contralateral** to the lesion while sparing the forehead, is the classic presentation of a **Central (Upper Motor Neuron - UMN)** lesion [1]. - UMN lesions spare the upper face because the **facial nerve nucleus** receives bilateral cortical input for the muscles of the forehead.

Q: A woman presents with a history of headaches for the past 9 months that worsen in a recumbent position and improves as the day progresses. She also gives a history of taking oral contraceptives. Fundal examination shows papilledema. There are no focal neurological deficits. What is the probable cause of her headaches?

Pseudotumor cerebri. ***Pseudotumor cerebri*** - The presentation of headache that worsens in the **recumbent position** (due to increased intracranial pressure, ICP) and improves when upright is highly characteristic of **Idiopathic Intracranial Hypertension (IIH)** [1]. - Confirmation of **papilledema** (swollen optic disc) in a young, likely obese female taking **oral contraceptives** (a risk factor) without other focal signs confirms the diagnosis of **pseudotumor cerebri** [1]. *Myasthenia gravis* - This disease is a neuromuscular disorder characterized by fluctuating **muscle weakness** (diplopia, ptosis, difficulty chewing) that worsens with activity and improves with rest. - It is not associated with primary headache or signs of increased intracranial pressure like **papilledema**. *Temporal arteritis* - This diagnosis is reserved for older patients (usually >50 years) presenting with severe localized headache, **jaw claudication**, tenderness over the temporal artery, and elevated inflammatory markers (ESR/CRP) [2]. - The positional nature of the headache and the patient's young age (implied by OCP use, a risk factor for IIH) make this diagnosis unlikely. *Chronic migraine* - Migraine is a diagnosis of exclusion that typically involves severe, often **pulsatile** headaches, sometimes with aura, photophobia, or nausea [3]. - While chronic migraine involves frequent headaches, it does not cause **papilledema** or have headaches classically exacerbated by the **recumbent position**, which points instead toward a structural or ICP-related etiology [2].

Q: A 26-year-old male with a history of respiratory tract infection 4 weeks ago is unable to stand or walk for the past 2 weeks and the weakness is progressive, ascending, and symmetrical in nature. The lower limbs were involved before and gradually the upper limbs were also affected. On examination you note areflexia. Pain and proprioception are preserved. What is the probable diagnosis?

Guillain Barre syndrome. ***Guillain Barre syndrome*** - **Acute inflammatory demyelinating polyradiculoneuropathy (AIDP)** - most common GBS variant [1] - Classic presentation: **progressive, ascending, symmetrical weakness** starting in lower limbs [1] - **Areflexia** is a hallmark feature due to peripheral nerve involvement [1] - **Preceding infection** (respiratory or gastrointestinal) occurs in 60-70% of cases, typically 1-4 weeks prior [1] - **Preserved sensory examination** for pain and proprioception (though may have paresthesias) [1] - **Motor weakness predominates** over sensory symptoms [1] - Diagnosis confirmed by: CSF showing albuminocytologic dissociation, nerve conduction studies showing demyelination - Treatment: **IV immunoglobulin (IVIG)** or **plasmapheresis** *Myasthenia gravis* - Presents with **fatigable weakness**, worsens with activity - **Ocular and bulbar muscles** typically affected first (ptosis, diplopia, dysphagia) - **Reflexes are preserved** (not areflexia) - No ascending pattern of weakness - Positive acetylcholine receptor antibodies, abnormal repetitive nerve stimulation *Polymyositis* - **Proximal muscle weakness** (shoulder and hip girdle), not ascending pattern - **Subacute onset** over weeks to months (not acute 2 weeks) - **Elevated creatine kinase (CK)** levels - Reflexes typically preserved initially - Muscle biopsy shows inflammatory infiltrates *Multiple sclerosis* - **Relapsing-remitting pattern** with episodes separated in time and space - **Sensory symptoms prominent** (numbness, tingling, vision changes) - **Hyperreflexia** with upper motor neuron signs (not areflexia) - Does not present with acute ascending paralysis - MRI shows demyelinating plaques in CNS

Q: A young male patient presents with ptosis and muscle weakness, which reportedly worsens in the evening and improves in the morning. This is relieved by neostigmine. What is the likely diagnosis?

Myasthenia gravis. ***Myasthenia gravis***- The presentation of muscle weakness, specifically **ptosis**, that worsens with fatigue (evening) or activity and improves with rest (morning), is the classic hallmark of the autoimmune condition **Myasthenia Gravis (MG)**.- The dramatic improvement upon administration of **neostigmine** (an acetylcholinesterase inhibitor) is diagnostic, confirming impaired transmission at the **neuromuscular junction** due to autoantibodies against **acetylcholine receptors (AChR)** [1].*Huntington chorea*- This is a progressive, inherited neurodegenerative disorder primarily characterized by involuntary, jerky movements (**chorea**) and cognitive decline. - It is related to excessive CAG trinucleotide repeats on chromosome 4, leading to neuronal loss in the **caudate nucleus**, and does not respond to neostigmine.*Amyotrophic lateral sclerosis*- ALS is a motor neuron disease characterized by progressive and unrelenting weakness due to the loss of both **upper and lower motor neurons**.- The weakness in ALS is permanent, not fluctuating diurnally, and does not improve with acetylcholinesterase inhibitors like neostigmine.*External ophthalmoplegia*- This is a descriptive term referring to weakness or paralysis of the external eye muscles; while it is often seen in MG (where it is often called ocular MG), it is a symptom, not the overall diagnosis.- This term does not explain the generalized muscle weakness, the pattern of **fatigability**, or the characteristic response to **neostigmine**.

Question 1

A 60 y/o male suddenly experiences an intense headache, described as the worst headache of his life, followed by vomiting and photophobia. O/E he has neck stiffness and a dilated pupil on the right side. A CT scan reveals bleeding in the subarachnoid space. Which of the following is the most common cause of this condition?

Accepted Answer

Intracranial aneurysm

Answer

Hypertension

Answer

Brain tumour

Answer

Arteriovenous malformation (AVM)

Question 2

A patient reports difficulty switching between movements and experiences uncontrollable hand movements. What is the most likely diagnosis?

Accepted Answer

Dysdiadochokinesis

Answer

Metamorphosis

Answer

Resting Tremor

Answer

Intentional Tremor

Question 3

A 35-year-old woman presents with fluctuating muscle weakness, especially affecting her speech and swallowing. Repetitive nerve stimulation shows a decremental response. Her blood tests are negative for acetylcholine receptor (AChR) antibodies. Which of the following antibodies is most likely responsible for her symptoms?

Accepted Answer

Anti-MuSK antibodies

Answer

Anti-TPO antibodies

Answer

Anti-dsDNA antibodies

Answer

Anti-Ro antibodies

Question 4

A patient presents with acute onset symmetric lower limb flaccid paralysis and absent deep tendon reflexes. Which condition is most likely?

Accepted Answer

Guillain-Barré syndrome

Answer

Multiple sclerosis

Answer

Spinal cord injury

Answer

Amyotrophic lateral sclerosis

Question 5

A patient presents with the palsy of the face as shown. Which of the following is most likely involved?

Accepted Answer

7th nerve palsy

Answer

Erb's palsy

Answer

3rd nerve palsy

Answer

Orbicularis oculi palsy

Question 6

A young male presented with weakness in the lower half of the right side of his face, with drooping of the angle of his mouth. He is unable to raise his eyebrows and close his eyes on the right side. Which of the following is the most appropriate diagnosis?

Accepted Answer

Infranuclear facial palsy on right side

Answer

Supranuclear facial palsy on left side

Answer

Infranuclear facial palsy on left side

Answer

Supranuclear facial palsy on right side

Question 7

Bell's palsy involves

Accepted Answer

Ipsilateral upper and lower halves of the face.

Answer

Contralateral upper and lower halves of the face.

Answer

Ipsilateral lower half of the face.

Answer

Contralateral lower half of the face.

Question 8

A woman presents with a history of headaches for the past 9 months that worsen in a recumbent position and improves as the day progresses. She also gives a history of taking oral contraceptives. Fundal examination shows papilledema. There are no focal neurological deficits. What is the probable cause of her headaches?

Accepted Answer

Pseudotumor cerebri

Answer

Myasthenia gravis

Answer

Temporal arteritis

Answer

Chronic migraine

Question 9

A 26-year-old male with a history of respiratory tract infection 4 weeks ago is unable to stand or walk for the past 2 weeks and the weakness is progressive, ascending, and symmetrical in nature. The lower limbs were involved before and gradually the upper limbs were also affected. On examination you note areflexia. Pain and proprioception are preserved. What is the probable diagnosis?

Accepted Answer

Guillain Barre syndrome

Answer

Myasthenia gravis

Answer

Polymyositis

Answer

Multiple sclerosis

Question 10

A young male patient presents with ptosis and muscle weakness, which reportedly worsens in the evening and improves in the morning. This is relieved by neostigmine. What is the likely diagnosis?

Accepted Answer

Myasthenia gravis

Answer

Huntington chorea

Answer

Amyotrophic lateral sclerosis

Answer

External ophthalmoplegia

Neurology — MCQs

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