Peripheral Nerve Disorders — MCQs

10 questions

Bilateral loss of ankle jerk and extensor plantar response is seen in:

All the following nerves are involved in entrapment neuropathy except -

Patient presenting with cutaneous vasculitis, glomerulonephritis, peripheral neuropathy, Which investigation is to be performed next that will help you diagnose the condition?

Brighton's criteria is used for:

Which of the following conditions is not associated with an increased risk of neuropathy caused by Isoniazid (INH)?

What is the characteristic feature of neuropraxia?

Arthritis mutilans is seen in?

Patient with ascending paralysis, areflexia and sphincter sparing is seen in?

A diabetic patient presents with sensory involvement, tingling, numbness, ankle swelling, and absence of pain. What is the most likely diagnosis?

Q10

What is the primary pathological mechanism in classical Guillain-Barré syndrome affecting the peripheral nervous system?

Peripheral Nerve Disorders Indian Medical PG Practice Questions and MCQs

Question 1: Bilateral loss of ankle jerk and extensor plantar response is seen in:

A. Amyotrophic lateral sclerosis
B. Lead poisoning
C. Freidrich's ataxia (Correct Answer)
D. Tabes dorsalis

Explanation: ***Freidrich's ataxia*** - **Friedreich's ataxia** is characterized by both **upper** (extensor plantar response) and **lower** (loss of ankle jerk) motor neuron signs due to degeneration of ascending and descending spinal tracts. - The combination of **ataxia**, **loss of ankle jerk reflexes**, and **extensor plantar responses** is highly suggestive of this condition. *Amyotrophic lateral sclerosis* - **ALS** typically presents with a combination of **upper** (extensor plantar response, spasticity) and **lower** (muscle atrophy, fasciculations, weakness) motor neuron signs [1]. - However, the loss of **ankle jerk reflexes** (a lower motor neuron sign) in addition to an **extensor plantar response** (an upper motor neuron sign) pointing specifically towards **Friedreich's ataxia** in this context. *Lead poisoning* - **Lead poisoning** primarily causes a **motor neuropathy**, leading to **weakness** and potentially **reduced or absent reflexes** [2]. - It does not typically cause **extensor plantar responses**, which are indicative of **upper motor neuron dysfunction**. *Tabes dorsalis* - **Tabes dorsalis**, a complication of **syphilis**, affects the **dorsal columns** and **dorsal roots**, leading to **sensory ataxia** and **loss of deep tendon reflexes**, including ankle jerks. - However, it does not typically cause an **extensor plantar response** as it involves **sensory** rather than **motor system degeneration**.

Question 2: All the following nerves are involved in entrapment neuropathy except -

A. Median nerve
B. Femoral nerve (Correct Answer)
C. Ulnar nerve
D. Lateral cutaneous nerve of thigh

Explanation: ***Femoral nerve*** - While the femoral nerve can be injured, it is **uncommonly involved** in entrapment neuropathy compared to other nerves. - Entrapment of the femoral nerve is rare and typically occurs in the **pelvis** or **inguinal region**, often due to trauma or mass effect. *Median nerve* - The median nerve is classically involved in **carpal tunnel syndrome**, where it is compressed at the wrist [1], [2]. - Symptoms include pain, numbness, and tingling in the thumb, index, middle, and radial half of the ring finger [1]. *Ulnar nerve* - The ulnar nerve is commonly entrapped at the **cubital tunnel** (elbow) or the **Guyon's canal** (wrist) [1]. - This leads to symptoms such as numbness and weakness in the small finger and ulnar half of the ring finger [1]. *Lateral cutaneous nerve of thigh* - This nerve is frequently entrapped as it passes under the **inguinal ligament**, causing **meralgia paresthetica**. - Symptoms include burning pain and numbness on the lateral aspect of the thigh.

Question 3: Patient presenting with cutaneous vasculitis, glomerulonephritis, peripheral neuropathy, Which investigation is to be performed next that will help you diagnose the condition?

A. ANCA (Correct Answer)
B. RA factor
C. Hbsag
D. MIF

Explanation: ### ANCA - The combination of **cutaneous vasculitis**, **glomerulonephritis**, and **peripheral neuropathy** points towards a small-vessel vasculitis, for which **ANCA (anti-neutrophil cytoplasmic antibodies)** testing is crucial [1]. - ANCA is highly specific for conditions like **Granulomatosis with Polyangiitis (GPA)** and **Microscopic Polyangiitis (MPA)** [1]. ### RA factor - **Rheumatoid factor (RF)** is primarily associated with **rheumatoid arthritis**, which typically presents with symmetrical polyarthritis, not the constellation of symptoms described. - While RF can be positive in some vasculitides, it is not the most specific initial test for the given clinical presentation. ### Hbsag - **Hepatitis B surface antigen (HbsAg)** typically screens for **Hepatitis B infection**, which can cause **polyarteritis nodosa (PAN)**, a medium-vessel vasculitis. - However, the patient's symptoms (cutaneous vasculitis, glomerulonephritis) are more characteristic of **small-vessel vasculitis**, making ANCA a more direct investigation [1]. ### MIF - **MIF (Macrophage Migration Inhibitory Factor)** is a cytokine involved in inflammation, but it is not a routine diagnostic marker for vasculitis. - It is not used as a primary investigation to diagnose specific autoimmune or inflammatory conditions like vasculitis.

Question 4: Brighton's criteria is used for:

A. Myasthenia Gravis
B. Guillain Barre Syndrome (Correct Answer)
C. Muscular dystrophy
D. Polymyositis

Explanation: Guillain Barre Syndrome - The Brighton's criteria are a set of diagnostic criteria used to establish the certainty level of a diagnosis of Guillain-Barré Syndrome (GBS). - These criteria help in categorizing GBS cases into different levels of diagnostic certainty (Levels 1-4) based on clinical features and neurophysiological findings, aiding in research and clinical management. Myasthenia Gravis - Diagnosis of Myasthenia Gravis primarily relies on clinical presentation (fluctuating muscle weakness, fatigability), acetylcholine receptor antibody titers, and electromyography (EMG) with repetitive nerve stimulation [1]. - There are specific diagnostic tests and clinical scales for MG, but Brighton's criteria are not used for its diagnosis. Muscular dystrophy - Muscular dystrophy is diagnosed through a combination of clinical evaluation, muscle biopsy, genetic testing, and elevated creatine kinase (CK) levels. - These are a group of inherited disorders causing progressive muscle weakness and do not involve the use of Brighton's criteria. Polymyositis - Polymyositis is an inflammatory myopathy diagnosed by clinical features (proximal muscle weakness), elevated muscle enzymes (CK), EMG abnormalities, and characteristic findings on muscle biopsy. - Its diagnosis does not involve the use of the Brighton's criteria.

Question 5: Which of the following conditions is not associated with an increased risk of neuropathy caused by Isoniazid (INH)?

A. Uremia
B. Diabetes mellitus
C. Poor nutrition
D. Hyperthyroidism (Correct Answer)

Explanation: ***Hyperthyroidism*** - **Hyperthyroidism** is not typically associated with an increased risk of isoniazid-induced neuropathy. The neuropathy due to INH is primarily linked to **pyridoxine (vitamin B6) deficiency**. - While hyperthyroidism can cause its own set of neurological symptoms, it does not directly impair pyridoxine metabolism or exacerbate INH's neurotoxic effects. *Uremia* - **Uremia** (renal failure) can increase the risk of INH-induced neuropathy due to impaired drug excretion, leading to higher plasma concentrations of INH and its metabolites. - Patients with uremia often have compromised nutritional status and may experience vitamin deficiencies, further contributing to pyridoxine depletion. *Diabetes mellitus* - **Diabetes mellitus** is a significant risk factor for INH-induced neuropathy because it is an independent cause of **peripheral neuropathy** itself, making patients more susceptible to additional nerve damage. - Diabetic patients may also have altered pyridoxine metabolism or suboptimal nutritional intake, predisposing them to INH toxicity. *Poor nutrition* - **Poor nutrition**, particularly malabsorption or inadequate dietary intake, directly contributes to **pyridoxine (vitamin B6) deficiency**. - Isoniazid's mechanism of neurotoxicity involves interfering with pyridoxine metabolism, so pre-existing deficiency significantly increases the risk of neuropathy.

Question 6: What is the characteristic feature of neuropraxia?

A. Damage to the endoneurium
B. Damage to the epineurium
C. No structural damage to the nerve (Correct Answer)
D. Damage to the axon

Explanation: ***No structural damage to the nerve*** - **Neuropraxia** is the mildest form of nerve injury, characterized by a **temporary block in nerve conduction** without structural damage to the axon or surrounding connective tissues. - This typically results in **temporary sensory and/or motor deficits** that fully resolve within weeks to months. *Damage to the endoneurium* - Damage to the **endoneurium** would indicate a more severe injury, such as **axonotmesis**, where the axon is damaged but the connective tissue sheaths are preserved. - This level of injury suggests that wallerian degeneration would occur distal to the lesion, leading to **slower and incomplete recovery**. *Damage to the epineurium* - Damage to the **epineurium**, along with the endoneurium and perineurium, signifies **neurotmesis**, the most severe nerve injury. - This involves a **complete transection of the nerve**, requiring surgical intervention for any chance of functional recovery. *Damage to the axon* - Damage to the **axon** itself, often alongside preserved connective tissues, is characteristic of **axonotmesis**. - While recovery is possible through axonal regeneration, it is **slower and less complete** than in neuropraxia.

Question 7: Arthritis mutilans is seen in?

A. Rheumatoid arthritis
B. Spondyloarthropathy
C. Reactive arthritis
D. Psoriatic arthropathy (Correct Answer)

Explanation: ***Psoriatic arthropathy*** - **Arthritis mutilans** is a severe, destructive form of psoriatic arthritis characterized by marked **osteolysis** and telescoping deformities of the digits [1]. - This condition is almost exclusively associated with **psoriatic arthritis**, representing its most aggressive subtype [1]. *Rheumatoid arthritis* - While rheumatoid arthritis can cause severe joint destruction, it typically manifests as **erosive arthritis** with joint deformities like **swan-neck** and **boutonnière deformities**, but not true arthritis mutilans [3]. - The pattern of bone destruction (osteolysis) seen in arthritis mutilans is distinct from the erosions in rheumatoid arthritis. *Spondyloarthropathy* - This is a broad category that includes diseases like ankylosing spondylitis and reactive arthritis, which primarily affect the **axial skeleton** and entheses. - While some spondyloarthropathies can cause peripheral joint involvement, they generally do not lead to the extreme osteolysis and telescoping digits characteristic of arthritis mutilans. *Reactive arthritis* - Reactive arthritis is an aseptic inflammatory arthritis that often follows infection, characterized by **oligoarthritis**, dactylitis, and enthesitis [2]. - This condition does not typically cause the severe, mutilating joint destruction seen in arthritis mutilans.

Question 8: Patient with ascending paralysis, areflexia and sphincter sparing is seen in?

A. G.B.S (Correct Answer)
B. Botulinism
C. Snake bite
D. Polio

Explanation: **G.B.S** - **Guillain-Barré Syndrome (GBS)** is characterized by **ascending paralysis** and **areflexia**, meaning loss of deep tendon reflexes [1]. - **Sphincter sparing** is also typical in GBS, differentiating it from other causes of paralysis where autonomic involvement can lead to bladder and bowel dysfunction [1]. *Botulism* - Botulism typically presents with **descending paralysis**, weakness starting in the cranial nerves and progressing downwards. - While it causes significant muscle weakness and can lead to **areflexia**, the pattern of paralysis (descending vs. ascending) and the presence of prominent cranial nerve involvement help distinguish it. *Snake bite* - Neurotoxic snake bites can cause **flaccid paralysis** and **areflexia**, but the paralysis often starts at the site of the bite or affects cranial nerves preferentially before generalized ascending paralysis. - The history of a **snake bite** and presence of **local envenomation signs** (swelling, pain) would also be prominent. *Polio* - Polio primarily causes **asymmetric flaccid paralysis** and **areflexia**, due to the destruction of anterior horn cells in the spinal cord. - Unlike GBS, polio does not typically present with an ascending pattern affecting both sides symmetrically and often involves sensory sparing.

Question 9: A diabetic patient presents with sensory involvement, tingling, numbness, ankle swelling, and absence of pain. What is the most likely diagnosis?

A. Charcot's joint (Correct Answer)
B. Gout
C. Rheumatoid arthritis
D. Ankylosing spondylitis

Explanation: ***Charcot's joint*** - This condition is characterized by **neuropathic arthropathy**, resulting from nerve damage (often due to **diabetes**), leading to sensory involvement, **numbness**, and **absence of pain** [1]. - The loss of protective sensation and repeated microtrauma contribute to joint destruction, often manifesting as **swelling** and deformity, particularly in the feet and ankles [1]. *Gout* - Gout typically presents with sudden, severe episodes of **pain**, redness, and swelling in a single joint, most commonly the **big toe**. - It is caused by **uric acid crystal deposition** and is not primarily associated with sensory deficits or chronic painless swelling. *Rheumatoid arthritis* - This is a **chronic autoimmune** inflammatory disease primarily affecting the **small joints** of the hands and feet symmetrically, causing pain, stiffness, and swelling. - It does not typically present with sensory neuropathy or painless joint destruction in the way described. *Ankylosing spondylitis* - This is a **chronic inflammatory disease** primarily affecting the **spine and sacroiliac joints**, causing progressive stiffness and pain that improves with activity. - It is not associated with peripheral joint neuropathy, numbness, or painless ankle swelling [1].

Question 10: What is the primary pathological mechanism in classical Guillain-Barré syndrome affecting the peripheral nervous system?

A. It blocks neurotransmitter release.
B. It causes demyelination of peripheral nerves. (Correct Answer)
C. It inhibits muscle contraction.
D. It leads to axonal degeneration.

Explanation: ***It causes demyelination of peripheral nerves.*** - Classical Guillain-Barré syndrome (AIDP - Acute Inflammatory Demyelinating Polyneuropathy) is an autoimmune disorder where the immune system attacks the **myelin sheath** surrounding peripheral nerves. - This **demyelination** impairs nerve signal conduction, leading to weakness and paralysis. - AIDP represents the most common form of GBS in Western countries (~85-90% of cases). *It blocks neurotransmitter release.* - Conditions like **Lambert-Eaton myasthenic syndrome** primarily involve antibodies targeting presynaptic voltage-gated calcium channels, thereby reducing neurotransmitter release. - While GBS affects nerve conduction, its primary mechanism is not the blockage of neurotransmitter release at the synapse. *It inhibits muscle contraction.* - Inhibition of muscle contraction is a downstream effect of impaired nerve innervation, but the fundamental problem in GBS is with the **nerve itself**, not the muscle's ability to contract directly. - Conditions like **myasthenia gravis** directly affect neuromuscular transmission by blocking acetylcholine receptors on muscle fibers. *It leads to axonal degeneration.* - While **axonal variants** of GBS exist (AMAN - Acute Motor Axonal Neuropathy; AMSAN - Acute Motor-Sensory Axonal Neuropathy), particularly common in Asia, the **classical and most common form** is characterized by **primary demyelination** (AIDP). - Pure axonal degeneration as a primary pathology is seen in specific GBS variants, not the classical presentation. - Secondary axonal damage can occur in severe or prolonged cases.

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