Topic: Nervous System; Subtopic: Motor Evoked Potentials and Neural Conduction
Keyword Definitions:
• Motor evoked potential (MEP): Electrical response recorded from muscles following stimulation of motor pathways, usually by transcranial magnetic or electrical stimulation.
• Central motor pathways: Pathways from motor cortex to spinal cord controlling voluntary movements.
• Peripheral motor pathways: Motor nerves transmitting impulses from spinal cord to skeletal muscles.
• Corticospinal tract: Major descending pathway responsible for fine motor control.
• Latency: Time interval between stimulus and response indicating conduction speed.
• Demyelination: Loss of myelin slowing nerve conduction and altering evoked potentials.
Lead Question - 2015
Motor evoked potential assess ?
a) Peripheral motor pathways
b) Central motor pathways
c) Both of the above
d) Regeneration in muscles
Explanation (Answer: b) Central motor pathways)
Motor Evoked Potentials (MEPs) are used to assess the integrity of central motor pathways, especially the corticospinal tract. They are elicited by transcranial magnetic stimulation over the motor cortex, and recorded from target muscles. Latency and amplitude reflect conduction through brain, spinal cord, and upper motor neuron pathways. Peripheral nerves contribute minimally, making MEPs useful in diagnosing multiple sclerosis, spinal cord lesions, and intraoperative monitoring of central motor integrity.
1. MEPs are most useful in detecting lesions of:
a) Lower motor neuron
b) Upper motor neuron
c) Neuromuscular junction
d) Muscle fibers
Explanation (Answer: b) Upper motor neuron)
MEPs primarily test upper motor neuron (UMN) pathways by stimulating the motor cortex and recording muscle responses. Damage in the corticospinal tract increases latency or abolishes MEPs. Lower motor neuron or muscle diseases affect compound muscle action potentials instead. Thus, MEPs are key for identifying central motor conduction defects in UMN disorders like stroke or multiple sclerosis.
2. During spinal surgery, MEPs help in:
a) Monitoring sensory integrity
b) Monitoring motor pathway integrity
c) Measuring muscle fatigue
d) Recording EEG activity
Explanation (Answer: b) Monitoring motor pathway integrity)
Intraoperative MEPs provide real-time monitoring of motor pathway function during spinal or neurosurgical procedures. Changes in amplitude or latency warn of potential corticospinal injury. Somatosensory evoked potentials (SSEPs) monitor sensory tracts, not motor. MEPs help prevent permanent paralysis during surgeries involving spinal cord or brainstem manipulation.
3. Latency of MEP is increased in:
a) Myasthenia gravis
b) Multiple sclerosis
c) Myopathy
d) Motor neuron disease
Explanation (Answer: b) Multiple sclerosis)
In multiple sclerosis, demyelination of central motor tracts delays conduction, increasing MEP latency. Amplitude may also decrease due to conduction block. Myasthenia gravis affects neuromuscular transmission, not central conduction. Myopathy affects muscle responses, not latency. Thus, prolonged latency in MEPs is diagnostic of demyelinating CNS disorders.
4. The stimulus used to elicit MEPs in clinical testing is usually:
a) Direct electrical stimulation
b) Transcranial magnetic stimulation
c) Infrared light pulses
d) Ultrasound stimulation
Explanation (Answer: b) Transcranial magnetic stimulation)
Transcranial magnetic stimulation (TMS) induces an electrical current in the motor cortex using magnetic fields. This activates descending corticospinal fibers and evokes motor responses in peripheral muscles. It is safe, noninvasive, and ideal for assessing central motor conduction. Electrical stimulation is used for peripheral nerve studies, not cortical activation.
5. Absence of MEPs in a patient with spinal cord injury indicates:
a) Peripheral neuropathy
b) Corticospinal tract disruption
c) Myasthenic crisis
d) Hypokalemia
Explanation (Answer: b) Corticospinal tract disruption)
Loss of MEP response indicates complete interruption of corticospinal pathways within the spinal cord. This helps localize the level of damage and predict prognosis. Peripheral nerves remain intact, ruling out peripheral neuropathy. Myasthenic crisis affects neuromuscular junction but not cortical conduction. MEP absence is an important prognostic marker in spinal injuries.
6. Clinical application of MEP in multiple sclerosis is:
a) Measuring muscle contraction
b) Detecting conduction block in central motor tracts
c) Estimating oxygen uptake
d) Evaluating sensory threshold
Explanation (Answer: b) Detecting conduction block in central motor tracts)
In multiple sclerosis, demyelination causes slowed conduction or complete block in corticospinal pathways. MEPs identify these changes by increased latency or absent motor responses. This helps in diagnosis and monitoring disease progression. It complements MRI in functional assessment, as it evaluates actual neural transmission integrity rather than structural changes alone.
7. In MEP testing, stimulation site for lower limb response is:
a) Parietal cortex
b) Occipital cortex
c) Vertex (Cz region)
d) Temporal lobe
Explanation (Answer: c) Vertex (Cz region)
For lower limb MEPs, stimulation is applied over the vertex region corresponding to leg representation in the motor cortex. Electrodes record responses from tibialis anterior or quadriceps muscles. This setup assesses corticospinal conduction from cortex to lumbosacral spinal segments. Parietal and occipital cortices are not involved in motor activation.
8. MEP amplitude primarily reflects:
a) Cortical excitability
b) Synaptic inhibition
c) Sensory input
d) Vascular perfusion
Explanation (Answer: a) Cortical excitability)
Amplitude of MEP correlates with excitability of motor cortex neurons and efficiency of corticospinal transmission. Decreased amplitude may indicate cortical suppression or conduction block. It can vary with anesthesia, fatigue, or disease. Sensory input and perfusion do not directly influence amplitude in MEP recordings.
9. Which anesthetic agent suppresses MEPs most markedly?
a) Ketamine
b) Propofol
c) Isoflurane
d) Nitrous oxide
Explanation (Answer: c) Isoflurane)
Isoflurane and other volatile anesthetics significantly depress cortical excitability, reducing MEP amplitude or abolishing responses. Intravenous agents like propofol and ketamine have less effect, making them preferable for intraoperative MEP monitoring. Nitrous oxide also suppresses but less intensely. Anesthesia choice is crucial for reliable MEP recording during surgery.
10. A patient with amyotrophic lateral sclerosis (ALS) shows MEP findings of:
a) Normal latency and amplitude
b) Prolonged latency and reduced amplitude
c) Increased amplitude
d) Absent sensory potentials
Explanation (Answer: b) Prolonged latency and reduced amplitude)
In ALS, both upper and lower motor neurons degenerate, causing prolonged MEP latency and decreased amplitude due to impaired central conduction. Sensory pathways remain intact. These changes help in distinguishing ALS from peripheral neuropathies. MEP testing assists in early detection of corticospinal tract dysfunction before overt clinical weakness.
11. MEPs are absent but sensory evoked potentials are normal in:
a) Spinal cord transection
b) Peripheral neuropathy
c) Myasthenia gravis
d) Cerebellar degeneration
Explanation (Answer: a) Spinal cord transection)
In spinal cord transection, motor pathways are completely interrupted, abolishing MEPs. Sensory pathways may remain intact initially, resulting in normal sensory evoked potentials (SEPs). This dissociation confirms motor pathway damage. Peripheral neuropathy or neuromuscular diseases affect both motor and sensory conduction, while cerebellar lesions spare MEPs.
Topic: Nerve and Muscle Physiology; Subtopic: Electromyography (EMG) and Muscle Activity
Keyword Definitions:
• Electromyography (EMG): Diagnostic test recording electrical activity produced by skeletal muscles using needle electrodes.
• Insertional activity: Brief burst of electrical activity seen when an electrode is inserted into a muscle, reflecting membrane stability.
• Resting potential: Electrical potential difference across the muscle membrane at rest.
• Fibrillation potentials: Spontaneous discharges from denervated muscle fibers indicating pathology.
• Motor unit potential (MUP): The sum of electrical signals from a motor neuron and its muscle fibers during voluntary contraction.
• Denervation: Loss of nerve supply leading to abnormal spontaneous muscle activity on EMG.
Lead Question - 2015
In electromyography (EMG) transient response at the time of insertion of electrode indicates ?
a) Spontaneous muscle activity
b) Voluntary muscle activity
c) Induced muscle activity
d) Cell membrane damage
Explanation (Answer: d) Cell membrane damage)
During EMG, the brief burst of electrical activity that appears at the moment of electrode insertion is called insertional activity. It occurs due to minor mechanical injury to the muscle fiber membrane by the needle, causing transient depolarization. Normally, it lasts less than 300 milliseconds. Prolonged or absent insertional activity indicates pathology such as denervation or fibrosis. Hence, the transient response signifies local cell membrane damage rather than voluntary or spontaneous activity.
1. Increased insertional activity on EMG is seen in:
a) Myasthenia gravis
b) Myopathy
c) Denervated muscle
d) Fibrotic muscle
Explanation (Answer: c) Denervated muscle)
Denervation increases insertional activity because muscle fibers become hypersensitive and electrically unstable due to loss of neural input. Needle insertion excites these unstable membranes, producing prolonged discharges. Myasthenia affects neuromuscular transmission, not insertional activity. Fibrotic muscles show decreased activity. Denervation thus indicates nerve injury or neuropathy affecting motor control.
2. Decreased insertional activity is found in:
a) Acute neuropathy
b) Chronic myopathy
c) Muscle fibrosis
d) Neuromuscular junction disorder
Explanation (Answer: c) Muscle fibrosis)
Muscle fibrosis reduces insertional activity because the fibrotic tissue has fewer excitable fibers and poor membrane responsiveness. Normal muscles show short bursts; fibrotic ones remain electrically silent. This is seen in chronic myopathies or late-stage muscular dystrophy. Acute neuropathy increases, while NMJ disorders preserve normal insertional responses.
3. Fibrillation potentials in EMG indicate:
a) Myasthenia gravis
b) Denervation of muscle
c) Myotonia
d) Neuromuscular block
Explanation (Answer: b) Denervation of muscle)
Fibrillation potentials are spontaneous discharges from single muscle fibers due to denervation. They appear 1–3 weeks after nerve injury and indicate lower motor neuron damage. Myotonia shows repetitive discharges after activation. Myasthenia involves postsynaptic failure without fibrillations. Thus, fibrillations are a hallmark of denervated muscle activity on EMG.
4. Polyphasic motor unit potentials on EMG suggest:
a) Nerve regeneration
b) Muscle fatigue
c) Hypokalemia
d) Normal muscle contraction
Explanation (Answer: a) Nerve regeneration)
Polyphasic motor unit potentials result from asynchronous firing of muscle fibers during reinnervation. Regenerating nerve fibers reconnect with muscle fibers irregularly, producing complex waveforms. These indicate partial recovery after nerve injury. Normal MUPs are biphasic or triphasic, while polyphasic potentials suggest active reinnervation and healing.
5. A patient with acute lower motor neuron lesion will show which EMG finding?
a) Absence of insertional activity
b) Increased insertional and fibrillation activity
c) Normal MUPs
d) High-frequency myotonic discharges
Explanation (Answer: b) Increased insertional and fibrillation activity)
Acute LMN lesions cause increased insertional activity due to fiber irritability and denervation fibrillations. Over time, voluntary MUPs disappear. Myotonic discharges are seen in myotonia congenita. Thus, hyperactivity during insertion and spontaneous discharges without voluntary contraction confirm LMN pathology.
6. Insertional activity normally lasts for:
a) b) 50–300 ms
c) 500 ms
d) 1 second
Explanation (Answer: b) 50–300 ms)
Normal insertional activity is a brief burst of potentials lasting 50–300 milliseconds after needle insertion. This duration represents the muscle’s physiological response to minor membrane disruption. Prolonged activity indicates irritability or denervation, while absent activity occurs in fibrosis or severe muscle atrophy.
7. Complex repetitive discharges on EMG are typical of:
a) Myotonia congenita
b) Chronic denervation
c) Myasthenia gravis
d) Periodic paralysis
Explanation (Answer: b) Chronic denervation)
Complex repetitive discharges (CRDs) occur in chronic denervating disorders such as spinal muscular atrophy or longstanding neuropathies. They represent reinnervated muscle fibers firing repetitively in a self-sustained cycle. Myotonia causes waxing–waning discharges, not CRDs. Chronic denervation reflects adaptive but unstable neuromuscular activity.
8. Myotonic discharge pattern in EMG is described as:
a) Electrical silence
b) Dive bomber sound
c) Bursting polyphasic waves
d) Single fiber potential
Explanation (Answer: b) Dive bomber sound)
Myotonic discharges produce a characteristic “dive bomber” sound due to waxing and waning amplitude and frequency. They appear in myotonic disorders like myotonia congenita or dystrophic myotonia. The pattern reflects delayed muscle relaxation after contraction due to abnormal ion channel function. It is a diagnostic feature of myotonic syndromes.
9. EMG is primarily used to differentiate:
a) Central from peripheral lesions
b) Upper from lower motor neuron lesions
c) Sensory from motor conduction disorders
d) Cardiac from skeletal muscle activity
Explanation (Answer: b) Upper from lower motor neuron lesions)
Electromyography helps distinguish lower motor neuron or muscle disorders from central (UMN) lesions. UMN lesions show normal EMG but abnormal reflexes, while LMN lesions display fibrillations, positive sharp waves, or reduced recruitment. Thus, EMG confirms peripheral nerve or muscle pathology rather than central motor pathway dysfunction.
10. Absence of insertional activity with no voluntary response suggests:
a) Neuropathy
b) Myopathy
c) Muscle fibrosis or necrosis
d) Hyperkalemia
Explanation (Answer: c) Muscle fibrosis or necrosis)
When insertional activity is completely absent, it indicates loss of excitable muscle fibers due to fibrosis or necrosis. In such cases, needle insertion does not generate any electrical potential because muscle tissue is replaced by connective tissue. Neuropathy or myopathy usually retains insertional activity, while fibrosis signifies irreversible muscle damage.
11. During EMG, spontaneous fibrillation potentials at rest represent:
a) Voluntary contraction
b) Normal insertional activity
c) Denervation hypersensitivity
d) Fatigue potential
Explanation (Answer: c) Denervation hypersensitivity)
Fibrillation potentials arise from denervated muscle fibers developing hypersensitivity to acetylcholine. These spontaneous discharges occur at rest, appearing 1–3 weeks post denervation. They indicate ongoing nerve injury or chronic lower motor neuron lesion. Voluntary or fatigue potentials occur during muscle activity, not rest, distinguishing fibrillation as a pathological EMG sign.
Topic: Special Senses; Subtopic: Visual Cycle and Phototransduction
Keyword Definitions:
• Visual cycle: Biochemical pathway converting light into electrical signals in photoreceptor cells.
• Opsin: Protein component of visual pigment that binds retinal.
• Retinal: Light-sensitive derivative of vitamin A, existing in 11-cis and all-trans forms.
• Phototransduction: Conversion of light energy into a neural signal in rods and cones.
• Rhodopsin: Visual pigment in rod cells composed of opsin and 11-cis-retinal.
• Isomerization: Conversion of 11-cis-retinal to all-trans-retinal upon light absorption initiating vision.
Lead Question - 2015
True about visual cycle cascade ?
a) Associated with conformational change in opsin
b) Light causes isomerization of all-trans-retinol to 11 Cis-retinol
c) Retinol [alcohol] is involved
d) All are true
Explanation (Answer: a) Associated with conformational change in opsin)
The visual cycle begins when light strikes rhodopsin, converting 11-cis-retinal to all-trans-retinal, causing a conformational change in opsin that triggers a phototransduction cascade. Retinal, not retinol, is the active aldehyde form involved in vision. Light does not directly convert all-trans-retinol to 11-cis-retinol. Hence, the true statement is that the cascade is associated with opsin’s conformational change during photon absorption.
1. The visual pigment in rods is:
a) Iodopsin
b) Melanin
c) Rhodopsin
d) Photopsin
Explanation (Answer: c) Rhodopsin)
Rhodopsin is the visual pigment present in rod cells, responsible for scotopic (night) vision. It consists of the protein opsin bound to 11-cis-retinal. When light hits rhodopsin, 11-cis-retinal is converted to all-trans-retinal, initiating the phototransduction cascade. Iodopsin and photopsin are cone pigments for color vision, while melanin reduces light scatter.
2. Light absorption by rhodopsin leads to:
a) Hyperpolarization of photoreceptor
b) Depolarization of photoreceptor
c) Opening of sodium channels
d) Increased glutamate release
Explanation (Answer: a) Hyperpolarization of photoreceptor)
Upon light exposure, rhodopsin activation closes sodium channels via the cyclic GMP pathway, leading to hyperpolarization of the photoreceptor membrane. This reduces glutamate release at the synapse, signaling light perception. In darkness, sodium channels remain open, maintaining depolarization. Thus, light induces the opposite electrical state compared to dark conditions.
3. Which of the following converts all-trans-retinal back to 11-cis-retinal?
a) Retinal isomerase
b) Retinol dehydrogenase
c) Opsinase
d) Transducin
Explanation (Answer: a) Retinal isomerase)
Retinal isomerase in the retinal pigment epithelium catalyzes the conversion of all-trans-retinal back to 11-cis-retinal, regenerating the visual pigment. Retinol dehydrogenase interconverts retinal and retinol but not isomers. Transducin is a G-protein in the phototransduction cascade. This recycling ensures sustained visual function after exposure to light.
4. In vitamin A deficiency, which symptom appears first?
a) Night blindness
b) Photophobia
c) Conjunctival xerosis
d) Keratomalacia
Explanation (Answer: a) Night blindness)
Night blindness (nyctalopia) is the earliest sign of vitamin A deficiency because rods cannot regenerate rhodopsin without adequate 11-cis-retinal. Persistent deficiency leads to xerophthalmia, Bitot’s spots, and keratomalacia. Vitamin A is vital for the visual cycle and epithelial maintenance. Early treatment reverses night blindness completely.
5. The G-protein involved in phototransduction is:
a) Transducin
b) Rhodopsin
c) Retinal-binding protein
d) Guanylate cyclase
Explanation (Answer: a) Transducin)
Transducin is the G-protein activated by photoexcited rhodopsin (metarhodopsin II). It activates phosphodiesterase, which reduces cGMP levels, leading to closure of sodium channels and hyperpolarization. Rhodopsin is the receptor, not the G-protein. Guanylate cyclase restores cGMP in darkness, helping reset the cycle.
6. The vitamin required for regeneration of visual pigment is:
a) Vitamin D
b) Vitamin E
c) Vitamin A
d) Vitamin K
Explanation (Answer: c) Vitamin A)
Vitamin A (retinol) is the precursor for retinal, the light-sensitive molecule in the visual cycle. Its deficiency prevents regeneration of rhodopsin, impairing dark adaptation. Vitamin D regulates calcium, E is antioxidant, and K assists in coagulation. Thus, adequate vitamin A is essential for normal vision and photoreceptor function.
7. Retinol is converted to retinal by:
a) Alcohol dehydrogenase
b) Retinol dehydrogenase
c) Retinal isomerase
d) Transducin
Explanation (Answer: b) Retinol dehydrogenase)
Retinol dehydrogenase oxidizes retinol (vitamin A alcohol) into retinal (vitamin A aldehyde). This reaction is reversible and part of the visual cycle. Retinal combines with opsin to form rhodopsin. Alcohol dehydrogenase acts mainly on ethanol, while retinal isomerase converts isomers of retinal, not retinol itself.
8. Which event occurs first in the visual cycle after photon absorption?
a) Activation of transducin
b) Isomerization of 11-cis-retinal to all-trans-retinal
c) Breakdown of cGMP
d) Closure of Na⁺ channels
Explanation (Answer: b) Isomerization of 11-cis-retinal to all-trans-retinal)
The first event after light absorption is isomerization of 11-cis-retinal to all-trans-retinal, altering opsin’s structure and initiating the phototransduction cascade. This leads to activation of transducin, cGMP hydrolysis, and Na⁺ channel closure. Hence, this photochemical reaction is the key trigger converting light to an electrical signal.
9. During dark adaptation, rhodopsin levels:
a) Increase
b) Decrease
c) Remain constant
d) Fluctuate randomly
Explanation (Answer: a) Increase)
In darkness, rhodopsin synthesis increases as 11-cis-retinal is regenerated, enhancing rod sensitivity. This adaptation restores scotopic vision, enabling detection of dim light. In bright light, rhodopsin breaks down rapidly. Vitamin A deficiency prevents proper regeneration, delaying dark adaptation and causing night blindness.
10. Visual cycle defect causing congenital stationary night blindness involves:
a) Mutation in transducin gene
b) Rhodopsin kinase defect
c) Retinal isomerase deficiency
d) Opsin overproduction
Explanation (Answer: c) Retinal isomerase deficiency)
Congenital stationary night blindness occurs when retinal isomerase is deficient, preventing regeneration of 11-cis-retinal. This disrupts rhodopsin formation, impairing rod photoreceptor response. Mutations in transducin or rhodopsin kinase affect signaling but not regeneration. The result is lifelong poor night vision without progression.
11. Bleaching of rhodopsin refers to:
a) Conversion of 11-cis-retinal to all-trans-retinal
b) Destruction of opsin
c) Breakdown of retinal to retinol
d) Inactivation of transducin
Explanation (Answer: a) Conversion of 11-cis-retinal to all-trans-retinal)
Bleaching is the process where light converts 11-cis-retinal to all-trans-retinal, leading to loss of pigment color in rhodopsin. This initiates the visual cascade, producing metarhodopsin II and activating transducin. Bleaching reverses when all-trans-retinal is converted back to 11-cis-retinal in the retinal pigment epithelium, restoring visual sensitivity.
Topic: Muscle Physiology; Subtopic: Smooth Muscle Contraction Mechanism
Keyword Definitions:
• Smooth muscle: Non-striated involuntary muscle found in walls of hollow organs.
• Calmodulin: Calcium-binding protein that activates myosin light chain kinase (MLCK).
• Myosin light chain kinase (MLCK): Enzyme that phosphorylates myosin to initiate contraction.
• Troponin: Regulatory protein in skeletal and cardiac muscles absent in smooth muscle.
• Phosphorylation: Addition of phosphate group essential for myosin–actin interaction in smooth muscle.
• Latch mechanism: Sustained contraction of smooth muscle with minimal ATP consumption.
Lead Question - 2015
True about smooth muscle contraction ?
a) Troponin plays an important role
b) Calmodulin has no role
c) Phosphorylation of myosin
d) All of the above
Explanation (Answer: c) Phosphorylation of myosin)
Phosphorylation of myosin is the key step in smooth muscle contraction. Calcium binds to calmodulin, activating MLCK, which phosphorylates the myosin light chain, allowing cross-bridge formation with actin. Unlike skeletal muscle, smooth muscle lacks troponin. Calmodulin replaces troponin’s role. Dephosphorylation by myosin phosphatase relaxes the muscle. This mechanism supports sustained contraction at low energy cost (latch state).
1. The regulatory protein in smooth muscle contraction is:
a) Troponin
b) Tropomyosin
c) Calmodulin
d) Myosin phosphatase
Explanation (Answer: c) Calmodulin)
Calmodulin serves as the calcium-binding regulatory protein in smooth muscle, analogous to troponin in skeletal muscle. When calcium binds calmodulin, it activates MLCK, which phosphorylates myosin light chains to initiate contraction. Tropomyosin is present but does not block binding sites as in skeletal muscle. Myosin phosphatase reverses phosphorylation during relaxation.
2. Smooth muscle contraction is initiated by increase in:
a) cAMP
b) Intracellular calcium concentration
c) Sodium influx
d) Chloride efflux
Explanation (Answer: b) Intracellular calcium concentration)
Calcium influx or release from the sarcoplasmic reticulum increases intracellular Ca²⁺, binding to calmodulin and activating MLCK. This phosphorylation of myosin initiates contraction. In contrast, increased cAMP leads to relaxation by inhibiting MLCK. Sodium and chloride ions are not directly involved in the contraction process of smooth muscle.
3. Latch state in smooth muscle helps in:
a) Rapid contraction
b) Sustained contraction with low energy
c) Muscle fatigue
d) Myosin degradation
Explanation (Answer: b) Sustained contraction with low energy)
The latch state allows smooth muscle to maintain tension for prolonged periods with minimal ATP consumption. After myosin dephosphorylation, cross-bridges remain attached, maintaining force without active cycling. This mechanism is crucial in organs like the bladder, uterus, and blood vessels that require continuous tone with low metabolic demand.
4. Drug that causes smooth muscle relaxation by increasing cAMP:
a) Norepinephrine
b) Epinephrine (via β₂ receptors)
c) Acetylcholine
d) Histamine
Explanation (Answer: b) Epinephrine (via β₂ receptors))
Epinephrine acts on β₂-adrenergic receptors to increase cAMP levels, inhibiting MLCK and promoting smooth muscle relaxation. This mechanism underlies bronchodilation and vasodilation. Norepinephrine via α-receptors causes contraction, while acetylcholine and histamine usually increase contraction in visceral smooth muscle through Ca²⁺ release mechanisms.
5. Which enzyme mediates smooth muscle relaxation?
a) Myosin light chain kinase
b) Myosin phosphatase
c) Adenylate cyclase
d) Guanylate cyclase
Explanation (Answer: b) Myosin phosphatase)
Myosin phosphatase dephosphorylates myosin light chains, leading to relaxation of smooth muscle. This process is enhanced by increased cyclic nucleotides such as cGMP (via nitric oxide). Myosin light chain kinase promotes contraction, while adenylate and guanylate cyclases regulate second messengers but not direct dephosphorylation.
6. Nitric oxide causes smooth muscle relaxation through:
a) Decreasing calcium levels
b) Activation of guanylate cyclase
c) Increasing cGMP
d) All of the above
Explanation (Answer: d) All of the above)
Nitric oxide (NO) diffuses into smooth muscle cells and activates guanylate cyclase, increasing cGMP. cGMP lowers intracellular calcium and enhances myosin phosphatase activity, causing relaxation. This mechanism mediates vasodilation in blood vessels and penile erection via the NO–cGMP pathway, targeted by drugs like sildenafil.
7. Smooth muscle does not show:
a) Gap junctions
b) Troponin
c) Actin and myosin filaments
d) Calmodulin
Explanation (Answer: b) Troponin)
Troponin is absent in smooth muscle. Instead, contraction is regulated by calmodulin-mediated activation of MLCK. Smooth muscle cells are interconnected by gap junctions allowing coordinated contraction. They contain actin and myosin filaments, though not organized into sarcomeres, giving the muscle a smooth appearance under microscopy.
8. Source of calcium for smooth muscle contraction is:
a) Only extracellular fluid
b) Only sarcoplasmic reticulum
c) Both extracellular and sarcoplasmic stores
d) Endoplasmic reticulum of neurons
Explanation (Answer: c) Both extracellular and sarcoplasmic stores)
Calcium required for smooth muscle contraction comes from both extracellular influx through voltage-gated channels and intracellular release from the sarcoplasmic reticulum. The relative contribution depends on muscle type. Drugs that block calcium entry (e.g., nifedipine) cause relaxation by reducing cytosolic calcium levels essential for contraction.
9. A patient receiving a β₂ agonist for asthma experiences muscle relaxation because:
a) Decreased cAMP
b) Increased cAMP inhibits MLCK
c) Increased calcium activates calmodulin
d) Increased potassium depolarizes cells
Explanation (Answer: b) Increased cAMP inhibits MLCK)
β₂-adrenergic stimulation increases cAMP, which inhibits MLCK activity even in the presence of calcium. This prevents phosphorylation of myosin light chains, promoting relaxation of bronchial smooth muscle. Hence, β₂ agonists like salbutamol act as bronchodilators by blocking calcium-dependent contractile mechanisms.
10. Smooth muscle contraction differs from skeletal muscle contraction because:
a) It requires troponin
b) It depends on actin phosphorylation
c) It involves myosin phosphorylation
d) It requires ATP-independent action
Explanation (Answer: c) It involves myosin phosphorylation)
Smooth muscle contraction uniquely depends on phosphorylation of myosin light chains by MLCK following Ca²⁺–calmodulin activation. Skeletal muscle contraction instead depends on troponin–tropomyosin regulation of actin binding. Both require ATP, but smooth muscle sustains tone longer through the latch mechanism and slower cross-bridge cycling.
11. Clinically, calcium channel blockers relieve hypertension by:
a) Decreasing vascular smooth muscle contraction
b) Increasing cardiac output
c) Activating calmodulin
d) Stimulating MLCK
Explanation (Answer: a) Decreasing vascular smooth muscle contraction)
Calcium channel blockers like amlodipine inhibit voltage-gated calcium entry into vascular smooth muscle cells, reducing intracellular calcium. This prevents calmodulin activation and MLCK stimulation, causing vasodilation and lower blood pressure. They act selectively on arterial smooth muscle, improving cardiac workload and oxygen delivery.
Topic: Respiratory Physiology; Subtopic: Pulmonary Reflexes Controlling Respiration
Keyword Definitions:
• Hering–Breuer reflex: A lung inflation reflex that prevents overinflation by prolonging expiration and inhibiting inspiration.
• J-reflex (Juxtacapillary reflex): Triggered by pulmonary C-fiber activation, causing apnea and rapid shallow breathing.
• Head’s paradoxical reflex: Opposite of Hering–Breuer reflex; promotes inspiration during lung inflation.
• Proprioceptors: Receptors in muscles and joints that modulate breathing during movement.
• Stretch receptors: Pulmonary receptors sensitive to lung expansion.
• Expiration: Phase of respiration involving passive or active outflow of air from lungs to atmosphere.
Lead Question - 2015
Increase in duration of expiration is due to?
a) J-reflex
b) Head's paradoxical reflex
c) Hering-Breuer reflex
d) Proprioceptors
Explanation (Answer: c) Hering-Breuer reflex)
The Hering–Breuer inflation reflex is mediated by stretch receptors in the bronchi and bronchioles. During lung inflation, these receptors send inhibitory signals via the vagus nerve to the inspiratory center, stopping inspiration and prolonging expiration. This reflex prevents overinflation, particularly in neonates and during deep breathing. It is a protective mechanism controlling breathing rhythm.
1. Hering–Breuer reflex is mediated by which nerve?
a) Glossopharyngeal
b) Vagus
c) Trigeminal
d) Phrenic
Explanation (Answer: b) Vagus)
The vagus nerve carries afferent impulses from pulmonary stretch receptors to the medullary respiratory center during the Hering–Breuer reflex. Cutting the vagus nerve abolishes this reflex, leading to deeper and slower respiration. It is thus a vagal-mediated protective mechanism against excessive lung expansion.
2. Head’s paradoxical reflex results in:
a) Inhibition of inspiration
b) Stimulation of inspiration
c) Prolonged expiration
d) Apnea
Explanation (Answer: b) Stimulation of inspiration)
Head’s paradoxical reflex is an inspiratory-promoting reflex triggered by lung inflation. It opposes the Hering–Breuer reflex and helps maintain inspiration during exercise or sighs. It ensures periodic deep breaths to maintain alveolar ventilation. This reflex is also important for sustaining rhythmic breathing under physiological conditions.
3. J-receptors are located in:
a) Bronchial smooth muscle
b) Pulmonary capillaries
c) Alveolar macrophages
d) Carotid bodies
Explanation (Answer: b) Pulmonary capillaries)
Juxtacapillary (J) receptors lie in the alveolar walls near pulmonary capillaries. They are stimulated by pulmonary congestion or edema, triggering rapid, shallow breathing, bronchoconstriction, and sometimes apnea. These reflexes are important in left heart failure and interstitial lung diseases, causing dyspnea.
4. Which reflex prevents overinflation of lungs?
a) J-reflex
b) Hering–Breuer reflex
c) Head’s paradoxical reflex
d) Chemoreceptor reflex
Explanation (Answer: b) Hering–Breuer reflex)
The Hering–Breuer reflex prevents overdistension of lungs by terminating inspiration through vagal inhibition of the inspiratory center. It plays a vital role in neonates, maintaining rhythmic respiration and protecting delicate lung tissue from injury during excessive inflation.
5. The afferent pathway of J-receptor reflex is:
a) Sympathetic nerve
b) Glossopharyngeal nerve
c) Vagus nerve
d) Phrenic nerve
Explanation (Answer: c) Vagus nerve)
J-receptor reflex impulses are carried via unmyelinated vagal C fibers to the medullary respiratory centers. This causes apnea followed by rapid shallow breathing. These receptors detect pulmonary congestion, edema, and capillary distension, forming part of the body’s defense to prevent alveolar overfilling.
6. In an athlete, which reflex aids in increased ventilation during exercise?
a) Proprioceptor reflex
b) J-reflex
c) Hering–Breuer reflex
d) Head’s paradoxical reflex
Explanation (Answer: a) Proprioceptor reflex)
Proprioceptors in joints and muscles sense movement and send excitatory signals to respiratory centers to enhance breathing during physical activity. This reflex ensures rapid adjustment of ventilation to meet increased oxygen demand even before significant changes in blood gases occur.
7. Clinical significance of J-receptors is seen in:
a) Emphysema
b) Pulmonary edema
c) Bronchial asthma
d) Pneumothorax
Explanation (Answer: b) Pulmonary edema)
In pulmonary edema, fluid accumulation stimulates J-receptors, leading to rapid, shallow breathing and a sensation of dyspnea. This reflex is protective, helping to limit further fluid exchange and maintain oxygenation, though it contributes to the feeling of breathlessness in patients with left-sided heart failure.
8. In premature infants, which reflex helps maintain rhythmic breathing?
a) Head’s paradoxical reflex
b) Hering–Breuer reflex
c) J-reflex
d) Proprioceptor reflex
Explanation (Answer: b) Hering–Breuer reflex)
In neonates, the Hering–Breuer reflex prevents apnea and maintains breathing rhythm by alternating inspiration and expiration based on lung stretch receptor feedback. This ensures appropriate tidal volume and prevents alveolar collapse or overdistension during early life when respiratory control is immature.
9. Which reflex is abolished after bilateral vagotomy?
a) J-reflex
b) Hering–Breuer reflex
c) Chemoreceptor reflex
d) Baroreceptor reflex
Explanation (Answer: b) Hering–Breuer reflex)
The Hering–Breuer reflex depends on intact vagal afferents. Bilateral vagotomy removes stretch receptor input, causing deeper and slower breathing patterns. The chemoreceptor and baroreceptor reflexes remain intact because they use glossopharyngeal and other pathways.
10. A patient with pulmonary fibrosis shows prolonged expiration. The mechanism involves:
a) Stimulation of stretch receptors
b) Activation of J-receptors
c) Inhibition of medullary centers
d) Increased vagal tone
Explanation (Answer: a) Stimulation of stretch receptors)
In pulmonary fibrosis, reduced lung compliance leads to exaggerated activation of stretch receptors even at lower volumes. This triggers the Hering–Breuer reflex, increasing expiration duration to prevent overdistension of stiff lungs. The vagus nerve mediates this feedback, maintaining stable ventilation under restrictive lung conditions.
11. A diver experiences prolonged expiration after surfacing; which reflex explains it?
a) J-reflex
b) Hering–Breuer reflex
c) Head’s paradoxical reflex
d) Baroreceptor reflex
Explanation (Answer: b) Hering–Breuer reflex)
Upon resurfacing, the diver’s lungs rapidly expand, stimulating pulmonary stretch receptors that activate the Hering–Breuer reflex. This reflex halts inspiration and prolongs expiration to prevent lung overinflation due to rapid decompression and gas expansion, ensuring safe ventilation control under variable pressure environments.
Topic: Nervous System Physiology; Subtopic: Wallerian Degeneration and Nerve Regeneration
Keyword Definitions:
• Wallerian degeneration: Process of degeneration of the distal segment of a nerve fiber after axonal injury.
• Axon: Long nerve fiber that transmits impulses away from the neuronal cell body.
• Neurolemma: Schwann cell sheath aiding in regeneration of peripheral nerves.
• Chromatolysis: Reversible cellular change in the neuron after axonal injury.
• Regeneration: Repair of injured nerve fibers, mainly in the peripheral nervous system.
• Myelin sheath: Lipid-rich covering that insulates nerve fibers and enhances conduction speed.
Lead Question - 2015
Wallerian degeneration is for ?
a) Nerve degeneration
b) Muscle degeneration
c) Nerve regeneration
d) Muscle regeneration
Explanation (Answer: a) Nerve degeneration)
Wallerian degeneration refers to the process of degeneration of the distal portion of a nerve fiber after it is severed from the cell body. It involves breakdown of the axon and myelin sheath distal to the injury site, while Schwann cells and macrophages clear debris. This degeneration facilitates subsequent nerve regeneration in the peripheral nervous system but not in the central nervous system due to absence of neurilemma and inhibitory factors.
1. Wallerian degeneration occurs in:
a) Axon distal to site of injury
b) Axon proximal to site of injury
c) Cell body of neuron
d) Dendrites only
Explanation (Answer: a) Axon distal to site of injury)
Wallerian degeneration affects the segment of the axon distal to the site of injury. The distal axon and its myelin sheath disintegrate due to lack of nutrient support from the neuronal cell body. This process begins within 24–36 hours after injury and is essential for clearance before regeneration in peripheral nerves.
2. Which cells are responsible for myelin removal during Wallerian degeneration?
a) Microglia
b) Schwann cells and macrophages
c) Astrocytes
d) Oligodendrocytes
Explanation (Answer: b) Schwann cells and macrophages)
In the peripheral nervous system, Schwann cells and recruited macrophages clear the myelin debris during Wallerian degeneration. Schwann cells also secrete neurotrophic factors that promote axonal regrowth. In contrast, the central nervous system lacks efficient macrophage activity, hindering regeneration due to myelin-associated inhibitors and absence of neurolemma.
3. Regeneration of axons in the CNS is limited due to:
a) Lack of Schwann cells
b) Presence of myelin inhibitory proteins
c) Glial scar formation
d) All of the above
Explanation (Answer: d) All of the above)
Axonal regeneration in CNS fails due to absence of Schwann cells, presence of inhibitory proteins such as Nogo-A, and formation of glial scars by astrocytes. These factors block axonal sprouting and remyelination. In contrast, peripheral nerves regenerate efficiently due to supportive Schwann cells and permissive extracellular environment.
4. Which of the following occurs first in Wallerian degeneration?
a) Myelin fragmentation
b) Axonal swelling and disintegration
c) Macrophage infiltration
d) Schwann cell proliferation
Explanation (Answer: b) Axonal swelling and disintegration)
The first morphological change in Wallerian degeneration is axonal swelling and breakdown distal to injury, usually within 24 hours. This is followed by myelin fragmentation, macrophage infiltration, and Schwann cell proliferation to clear debris and prepare the nerve for potential regeneration.
5. Chromatolysis refers to:
a) Breakdown of axon
b) Degeneration of distal nerve segment
c) Dissolution of Nissl bodies in neuron cell body
d) Myelin sheath regeneration
Explanation (Answer: c) Dissolution of Nissl bodies in neuron cell body)
Chromatolysis occurs in the cell body proximal to axonal injury. Nissl bodies disperse and the nucleus moves to the periphery, reflecting increased protein synthesis for regeneration. It is a reversible adaptive response aiding recovery unless the injury is severe or the neuron is in the CNS.
6. In peripheral nerve injury, regeneration begins:
a) Immediately after injury
b) Within 24 hours
c) After clearance of myelin debris
d) Only if CNS neurons are involved
Explanation (Answer: c) After clearance of myelin debris)
Regeneration begins only after myelin debris is cleared by Schwann cells and macrophages. Clean endoneurial tubes guide new axonal sprouts from the proximal stump toward target organs. Delay in debris clearance impairs regeneration, highlighting the crucial role of immune and glial cell cooperation in the process.
7. The first sign of Wallerian degeneration in light microscopy is:
a) Myelin beading
b) Axonal swelling
c) Nuclear pyknosis
d) Endoneurial edema
Explanation (Answer: a) Myelin beading)
Myelin beading appears as irregular varicosities in the myelin sheath soon after axonal transection. It signifies disintegration of the axolemma and onset of degeneration. This precedes fragmentation and phagocytosis. These changes are identifiable within 24–48 hours in the distal segment of the injured nerve.
8. A 35-year-old patient with crush injury of radial nerve recovers slowly because:
a) Myelin debris clearance is delayed
b) Schwann cells are destroyed
c) Axon regeneration is blocked by fibrosis
d) All of the above
Explanation (Answer: d) All of the above)
In crush injuries, extensive damage delays debris clearance, may destroy Schwann cells, and cause fibrosis, all slowing axonal regrowth. Regeneration rate averages 1–3 mm/day. Proper alignment and intact neurolemma enhance recovery, but severe damage results in incomplete functional restoration.
9. Successful nerve regeneration in PNS requires:
a) Intact endoneurial tube
b) Presence of Schwann cells
c) Healthy neuron cell body
d) All of the above
Explanation (Answer: d) All of the above)
Peripheral nerve regeneration depends on an intact endoneurial tube guiding axonal sprouts, viable Schwann cells producing neurotrophic factors, and a healthy neuronal cell body for new axon synthesis. Disruption of any element limits recovery, emphasizing the coordinated role of structural and biochemical support in regeneration.
10. Wallerian degeneration does not occur in:
a) Peripheral nerve
b) Central nervous system
c) Spinal root injury
d) Cranial nerve distal to ganglion
Explanation (Answer: b) Central nervous system)
True Wallerian degeneration with functional regeneration occurs only in the peripheral nervous system due to Schwann cell activity. In the CNS, degeneration is incomplete and non-reparative due to oligodendrocyte inhibition and glial scarring. Thus, CNS neurons rarely regenerate after injury.
11. A patient with transected sciatic nerve shows regeneration over months. Which process preceded regeneration?
a) Chromatolysis
b) Wallerian degeneration
c) Gliosis
d) Synaptic inhibition
Explanation (Answer: b) Wallerian degeneration)
In peripheral nerve injury, regeneration follows Wallerian degeneration, which removes distal axonal and myelin debris. This cleanup allows Schwann cells to proliferate, align, and guide new axonal sprouts from the proximal stump toward the target organ. Without prior degeneration, regeneration cannot proceed effectively.
Topic: Nervous System; Subtopic: Spinal Reflexes and Motor Control
Keyword Definitions:
• Reflex: An involuntary, automatic, and stereotyped response to a specific stimulus.
• Withdrawal reflex (Flexor reflex): A polysynaptic spinal reflex that causes withdrawal of a limb from a painful stimulus.
• Reciprocal inhibition: Mechanism that relaxes antagonist muscles during a reflex action.
• Crossed extensor reflex: A reflex causing extension of the opposite limb to maintain balance during withdrawal.
• Golgi tendon reflex: Protective reflex preventing muscle damage due to excessive tension.
• Stretch reflex: Monosynaptic reflex maintaining muscle tone and posture (e.g., knee jerk reflex).
Lead Question - 2015
Withdrawal reflex is also known as ?
a) Extension reflex
b) Stretch reflex
c) Golgitendon reflex
d) Flexor reflex
Explanation (Answer: d) Flexor reflex)
The withdrawal reflex, also called the flexor reflex, is a protective spinal reflex that withdraws a body part from a painful or noxious stimulus. It involves activation of flexor muscles and inhibition of extensors through polysynaptic pathways in the spinal cord. This reflex is ipsilateral and rapid, essential for minimizing tissue injury. The reflex is often accompanied by a contralateral crossed extensor reflex to maintain posture and balance.
1. The receptor involved in the withdrawal reflex is:
a) Muscle spindle
b) Golgi tendon organ
c) Nociceptor
d) Pacinian corpuscle
Explanation (Answer: c) Nociceptor)
Nociceptors are pain receptors that detect damaging stimuli like heat, pressure, or injury. They initiate the withdrawal reflex by sending afferent impulses to the spinal cord, activating interneurons that stimulate flexor muscles and inhibit extensors. This automatic response protects the body from potential harm by removing the affected limb from danger.
2. Which of the following is an example of a monosynaptic reflex?
a) Flexor reflex
b) Crossed extensor reflex
c) Stretch reflex
d) Withdrawal reflex
Explanation (Answer: c) Stretch reflex)
The stretch reflex is the only monosynaptic spinal reflex. It involves direct synaptic transmission between a sensory neuron and a motor neuron without interneurons. Examples include the knee jerk (patellar) reflex. It maintains muscle tone and posture, contrasting with the polysynaptic nature of the withdrawal reflex.
3. The efferent pathway of withdrawal reflex involves:
a) Alpha motor neurons
b) Gamma motor neurons
c) Interneurons only
d) Sympathetic fibers
Explanation (Answer: a) Alpha motor neurons)
In the withdrawal reflex, afferent pain signals activate spinal interneurons that synapse with alpha motor neurons. These motor neurons cause contraction of flexor muscles and inhibition of antagonistic extensors through reciprocal inhibition. This rapid response ensures immediate withdrawal from harmful stimuli like heat or sharp objects.
4. Crossed extensor reflex occurs:
a) On the same side of stimulation
b) On the opposite side of stimulation
c) In both sides simultaneously
d) Only in upper limbs
Explanation (Answer: b) On the opposite side of stimulation)
The crossed extensor reflex occurs contralaterally. When one limb withdraws due to pain, the opposite limb extends to maintain balance. For example, stepping on a sharp object causes withdrawal of one leg and extension of the other. This is mediated by interneurons crossing the spinal cord midline.
5. Which statement is true about the flexor reflex?
a) Monosynaptic
b) Always accompanied by reciprocal inhibition
c) Mediated by muscle spindle
d) Controlled by cerebellum only
Explanation (Answer: b) Always accompanied by reciprocal inhibition)
The flexor reflex involves reciprocal inhibition—activation of flexor muscles and simultaneous inhibition of extensors. This coordination ensures effective limb withdrawal. It is a polysynaptic reflex involving interneurons and does not require supraspinal control, although descending pathways can modulate it.
6. A patient with spinal cord injury above the lumbar level shows exaggerated withdrawal reflexes. The reason is:
a) Hyperpolarization of neurons
b) Loss of inhibitory descending control
c) Absence of pain receptors
d) Muscle fatigue
Explanation (Answer: b) Loss of inhibitory descending control)
After spinal cord injury, descending inhibitory influences from higher centers are lost. This leads to hyperexcitability of spinal reflex circuits, producing exaggerated or hyperactive withdrawal reflexes. Clinically, this manifests as spasticity or exaggerated flexion in response to minimal stimuli.
7. The main neurotransmitter in the withdrawal reflex arc is:
a) Dopamine
b) Acetylcholine
c) Glutamate
d) Serotonin
Explanation (Answer: c) Glutamate)
Glutamate is the principal excitatory neurotransmitter mediating synaptic transmission in the withdrawal reflex. It activates spinal interneurons and alpha motor neurons. Glycine and GABA act as inhibitory neurotransmitters for antagonist muscles, ensuring coordinated movement during reflex withdrawal.
8. Golgi tendon reflex causes:
a) Muscle contraction
b) Muscle relaxation
c) Flexor withdrawal
d) Joint extension
Explanation (Answer: b) Muscle relaxation)
The Golgi tendon reflex protects muscles and tendons from excessive tension by causing muscle relaxation. Golgi tendon organs sense force and send inhibitory signals to alpha motor neurons, reducing contraction strength. This reflex ensures prevention of muscle or tendon damage during heavy load bearing.
9. Which type of reflex is lost first in peripheral nerve injury?
a) Flexor withdrawal reflex
b) Crossed extensor reflex
c) Deep tendon reflex
d) Pain reflex
Explanation (Answer: c) Deep tendon reflex)
In peripheral neuropathies, loss of deep tendon (stretch) reflexes occurs first due to involvement of large myelinated fibers. The flexor withdrawal reflex, being polysynaptic and slower, may persist longer. Reflex testing helps localize the level and type of neural damage in clinical practice.
10. In a burn injury, a rapid withdrawal of hand occurs due to activation of:
a) Proprioceptors
b) Nociceptors
c) Chemoreceptors
d) Thermoreceptors
Explanation (Answer: b) Nociceptors)
Nociceptors are specialized pain receptors that trigger the withdrawal reflex in response to harmful stimuli like burns. Their afferent signals activate spinal interneurons that initiate immediate muscle contraction for limb withdrawal. This rapid response prevents deeper tissue damage and is purely protective.
11. The contralateral component of the withdrawal reflex helps in:
a) Reducing pain sensation
b) Maintaining posture and balance
c) Inhibiting ipsilateral flexors
d) Decreasing muscle tone
Explanation (Answer: b) Maintaining posture and balance)
The crossed extensor reflex complements the withdrawal reflex by extending the opposite limb, thereby maintaining posture and equilibrium during withdrawal. This coordinated motor response allows the body to shift weight and prevent falls when one limb withdraws rapidly from a painful stimulus.
Topic: Muscle Physiology; Subtopic: Excitation-Contraction Coupling and Ionic Imbalance
Keyword Definitions:
• Tetany: Sustained, involuntary muscle contraction caused by increased neuronal excitability.
• Calcium (Ca²⁺): Essential for muscle contraction and neuromuscular stability.
• Magnesium (Mg²⁺): Cofactor that stabilizes nerve and muscle membranes; its deficiency enhances excitability.
• Sodium (Na⁺): Major extracellular ion responsible for depolarization during action potential.
• Potassium (K⁺): Maintains resting membrane potential; imbalance alters muscle excitability.
• Neuromuscular junction: Synapse between motor neuron and muscle fiber responsible for initiating contraction.
Lead Question - 2015
Tetany in muscle occurs in spite of normal serum Ca²⁺ level. Which ion is responsible?
a) Mg²⁺
b) Ca²⁺
c) K⁺
d) Na⁺
Explanation (Answer: a) Mg²⁺)
Magnesium deficiency causes increased neuronal excitability leading to tetany even when serum calcium is normal. Mg²⁺ acts as a natural calcium channel blocker, stabilizing nerve membranes. Low Mg²⁺ enhances acetylcholine release at the neuromuscular junction, producing hyperexcitability and muscle spasms. Clinically, this is seen in malnutrition, chronic diarrhea, or diuretic use. Correction of magnesium restores neuromuscular stability.
1. Hypomagnesemia causes tetany due to:
a) Reduced acetylcholine release
b) Enhanced neuromuscular excitability
c) Increased threshold potential
d) Blocked sodium channels
Explanation (Answer: b) Enhanced neuromuscular excitability)
Hypomagnesemia lowers the threshold for neuronal firing, leading to hyperexcitability and spontaneous muscle contractions. Mg²⁺ normally stabilizes neuronal membranes and regulates calcium influx. Its deficiency causes repetitive firing and clinical tetany despite normal calcium levels, a classic example of ionic imbalance affecting neuromuscular control.
2. Carpopedal spasm in a patient with normal calcium suggests deficiency of:
a) Sodium
b) Magnesium
c) Potassium
d) Phosphate
Explanation (Answer: b) Magnesium)
Carpopedal spasm is a typical sign of tetany due to magnesium deficiency. Low Mg²⁺ increases acetylcholine release, causing sustained muscle contraction. Even if calcium is normal, Mg²⁺ deficiency disrupts neuromuscular stability. Intravenous magnesium rapidly reverses the symptoms, confirming its essential role in membrane stabilization.
3. Magnesium acts physiologically as:
a) Calcium channel activator
b) Natural calcium antagonist
c) Potassium transporter
d) Sodium pump inhibitor
Explanation (Answer: b) Natural calcium antagonist)
Magnesium functions as a natural calcium antagonist by blocking calcium influx into presynaptic terminals, preventing excessive neurotransmitter release. Deficiency leads to uncontrolled calcium entry, enhancing excitability and causing tetany. It also regulates cardiac excitability and smooth muscle tone, maintaining electrical stability throughout the body.
4. In severe magnesium deficiency, serum calcium decreases because:
a) Parathyroid hormone release decreases
b) Calcitonin increases
c) Renal calcium excretion decreases
d) Vitamin D level rises
Explanation (Answer: a) Parathyroid hormone release decreases)
Severe hypomagnesemia inhibits parathyroid hormone (PTH) secretion and reduces its peripheral action, resulting in hypocalcemia. This secondary effect can cause severe muscle spasms and seizures. Correction of magnesium deficiency restores PTH secretion and normal calcium homeostasis, preventing persistent neuromuscular irritability.
5. Latent tetany can be elicited clinically by:
a) Babinski sign
b) Trousseau’s sign
c) Romberg’s test
d) Rinne’s test
Explanation (Answer: b) Trousseau’s sign)
Trousseau’s sign is positive when carpal spasm occurs upon inflating a blood pressure cuff above systolic pressure for 3 minutes. It indicates latent tetany due to neuromuscular hyperexcitability, often caused by hypocalcemia or hypomagnesemia. It is a valuable bedside test for assessing ionic imbalances affecting muscle excitability.
6. Chvostek’s sign is due to:
a) Hypokalemia
b) Hypocalcemia or hypomagnesemia
c) Hypercalcemia
d) Hypermagnesemia
Explanation (Answer: b) Hypocalcemia or hypomagnesemia)
Chvostek’s sign is elicited by tapping the facial nerve anterior to the ear, producing twitching of facial muscles. It reflects increased neuromuscular excitability due to hypocalcemia or hypomagnesemia. Both ions stabilize membranes; their deficiency lowers the threshold for depolarization, causing hyperresponsive muscle activity.
7. Excessive magnesium in the body causes:
a) Muscle tetany
b) Depressed reflexes
c) Increased excitability
d) Spastic paralysis
Explanation (Answer: b) Depressed reflexes)
Hypermagnesemia depresses neuromuscular transmission and decreases reflexes due to reduced acetylcholine release and calcium entry. It causes muscle weakness, hypotension, and bradycardia. High magnesium levels inhibit nerve conduction and cardiac contractility, contrasting the excitatory effects seen in magnesium deficiency.
8. In tetany due to alkalosis, excitability increases because:
a) Ionized calcium decreases
b) Sodium permeability decreases
c) Magnesium concentration rises
d) pH decreases
Explanation (Answer: a) Ionized calcium decreases)
Alkalosis increases calcium binding to albumin, reducing the free ionized calcium fraction without changing total calcium levels. This decreases threshold potential, enhancing neuronal excitability and causing tetany. Clinically, respiratory alkalosis during hyperventilation can precipitate hand or foot spasms due to transient hypocalcemia.
9. A 50-year-old alcoholic patient presents with tetany and normal calcium. Likely cause:
a) Vitamin D deficiency
b) Magnesium deficiency
c) Hyperkalemia
d) Sodium excess
Explanation (Answer: b) Magnesium deficiency)
Chronic alcoholism causes magnesium loss via urine and poor dietary intake. Hypomagnesemia induces tetany despite normal calcium due to neuromuscular hyperexcitability. Intravenous magnesium replacement alleviates symptoms. This is a classic example of alcohol-related electrolyte imbalance leading to secondary neurological manifestations.
10. Which of the following is NOT a feature of hypomagnesemia?
a) Tetany
b) Muscle weakness
c) Cardiac arrhythmias
d) Respiratory depression
Explanation (Answer: d) Respiratory depression)
Hypomagnesemia causes tetany, muscle cramps, and cardiac arrhythmias due to increased excitability. Respiratory depression occurs in hypermagnesemia from excessive neuromuscular blockade, not deficiency. Correcting magnesium imbalance is crucial to prevent complications, especially in critically ill or malnourished patients.
11. Which electrolyte abnormality produces tetany even with normal serum calcium?
a) Hyperkalemia
b) Hypomagnesemia
c) Hypernatremia
d) Hypercalcemia
Explanation (Answer: b) Hypomagnesemia)
Hypomagnesemia mimics hypocalcemia by increasing neuromuscular excitability and producing tetany even with normal calcium levels. Mg²⁺ deficiency alters calcium channel function and acetylcholine release. It is often seen in malabsorption, alcoholism, or prolonged diuretic therapy. Restoring magnesium quickly corrects symptoms and stabilizes neuromuscular activity.
Topic: Nervous System; Subtopic: Pain Pathways and Transmission
Keyword Definitions:
• Pain: An unpleasant sensory and emotional experience due to actual or potential tissue damage.
• Unspecified pain pathway: A slower, polysynaptic pain pathway responsible for deep, diffuse pain sensations.
• Visceral pain: Pain originating from internal organs, poorly localized and often referred.
• Spinoreticular tract: Ascending tract carrying diffuse pain sensations to the brainstem.
• Neuropathic pain: Pain resulting from nerve injury, burning or shooting in nature.
• Somatic pain: Pain arising from skin, muscles, and joints, usually sharp and well localized.
Lead Question - 2015
Unspecified pain pathway is for?
a) Neuropathic pain
b) Trauma
c) Visceral pain
d) Psychogenic pain
Explanation (Answer: c) Visceral pain)
The unspecified pain pathway, also known as the paleospinothalamic or spinoreticular pathway, transmits deep, dull, and poorly localized pain such as visceral pain. These fibers are slow-conducting C fibers that relay signals through multiple synapses in the brainstem before reaching the thalamus. This type of pain is often associated with emotional and autonomic responses such as nausea or sweating and is difficult to pinpoint anatomically due to widespread convergence of visceral afferents.
1. Which tract carries the impulses of fast, well-localized pain?
a) Spinothalamic tract
b) Spinoreticular tract
c) Spinomesencephalic tract
d) Spinocerebellar tract
Explanation (Answer: a) Spinothalamic tract)
The neospinothalamic tract carries fast, sharp, and well-localized pain through Aδ fibers to the thalamus. It allows precise localization of pain stimuli, such as a pinprick. This contrasts with the paleospinothalamic (unspecified) tract, which transmits dull, aching, and poorly localized pain sensations.
2. The neurotransmitter mainly involved in transmission of slow pain is:
a) Acetylcholine
b) Substance P
c) GABA
d) Dopamine
Explanation (Answer: b) Substance P)
Substance P is the primary neurotransmitter released by C fibers in the dorsal horn of the spinal cord during slow (unspecified) pain transmission. It activates second-order neurons in the spinoreticular and paleospinothalamic tracts, conveying dull, throbbing pain often linked with tissue injury and inflammation.
3. Which fibers transmit slow, burning pain sensation?
a) Aα
b) Aβ
c) Aδ
d) C fibers
Explanation (Answer: d) C fibers)
C fibers are unmyelinated, small-diameter fibers responsible for transmitting slow, burning, and poorly localized pain. They conduct at a velocity of about 0.5–2 m/s and are responsible for the second wave of pain sensation following acute injury, mediated via the unspecified pain pathway.
4. A 45-year-old patient presents with dull abdominal pain and nausea. Which pathway transmits this type of pain?
a) Spinothalamic
b) Spinoreticular
c) Spinocerebellar
d) Corticospinal
Explanation (Answer: b) Spinoreticular)
Visceral pain, which is dull, diffuse, and accompanied by autonomic symptoms, is transmitted through the spinoreticular (unspecified) tract. The pain fibers synapse in the reticular formation before ascending to the thalamus and limbic system, contributing to the emotional and autonomic components of pain perception.
5. Which of the following is true regarding the unspecified pain pathway?
a) Mediates fast pain
b) Uses Aδ fibers
c) Polysynaptic with multiple relays
d) Allows precise localization of pain
Explanation (Answer: c) Polysynaptic with multiple relays)
The unspecified (paleospinothalamic) pathway is polysynaptic, involving multiple relays in the spinal cord, reticular formation, and thalamus. It conveys dull, aching, and poorly localized pain. This pathway also interacts with the limbic system, explaining the emotional distress associated with chronic visceral pain.
6. Which structure modulates the perception of slow pain in the brain?
a) Cerebellum
b) Limbic system
c) Hypothalamus
d) Amygdala only
Explanation (Answer: b) Limbic system)
The limbic system modulates emotional and behavioral responses to slow or visceral pain transmitted by the unspecified pathway. It associates pain with anxiety, fear, or distress. This is why visceral pain often evokes strong emotional reactions compared to localized somatic pain.
7. Referred pain occurs because:
a) Shared spinal segments between somatic and visceral afferents
b) Crossed corticospinal fibers
c) Unmyelinated fibers’ slow conduction
d) Pain receptor desensitization
Explanation (Answer: a) Shared spinal segments between somatic and visceral afferents)
Referred pain occurs due to convergence of visceral and somatic afferents on the same spinal neurons. The brain misinterprets visceral pain as originating from a somatic region. For example, cardiac pain is referred to the left arm or jaw due to overlapping thoracic segments (T1–T5).
8. Which of the following is not true regarding visceral pain?
a) Poorly localized
b) Often referred to body surface
c) Transmitted by Aδ fibers
d) Associated with autonomic symptoms
Explanation (Answer: c) Transmitted by Aδ fibers)
Visceral pain is transmitted mainly by unmyelinated C fibers via the unspecified pain pathway. It is dull, poorly localized, and often accompanied by autonomic symptoms like nausea or sweating. The pain may be referred due to shared spinal cord pathways with somatic afferents.
9. A patient with chronic pancreatitis experiences deep, aching abdominal pain. The tract involved is:
a) Spinothalamic
b) Spinoreticular
c) Spinomesencephalic
d) Dorsal column
Explanation (Answer: b) Spinoreticular)
In chronic visceral conditions such as pancreatitis, pain is transmitted via the spinoreticular tract (unspecified pathway). This pathway’s diffuse, polysynaptic nature leads to poorly localized, persistent pain often associated with emotional distress, characteristic of visceral pathology.
10. The main difference between neospinothalamic and paleospinothalamic tracts is:
a) Fiber type and speed
b) Number of synapses
c) Localization accuracy
d) All of the above
Explanation (Answer: d) All of the above)
The neospinothalamic tract uses myelinated Aδ fibers, conducts rapidly, and provides precise localization of pain, while the paleospinothalamic (unspecified) tract uses unmyelinated C fibers, has multiple synapses, conducts slowly, and produces diffuse, emotional pain perception — typically visceral in origin.
11. Which of the following best describes the unspecified pain pathway?
a) Monosynaptic, localized
b) Polysynaptic, diffuse, emotional
c) Olfactory in origin
d) Linked to proprioception
Explanation (Answer: b) Polysynaptic, diffuse, emotional)
The unspecified pain pathway is polysynaptic and transmits dull, poorly localized pain often associated with emotion and autonomic responses. It involves the reticular formation and limbic system, contributing to the diffuse and affective nature of visceral pain sensations.
Topic: Nervous System; Subtopic: Pain Pathways and Nerve Fiber Classification
Keyword Definitions:
• Pain: An unpleasant sensory and emotional experience associated with tissue injury.
• Aδ fibers: Thinly myelinated nerve fibers responsible for fast, sharp, localized pain.
• C fibers: Unmyelinated fibers transmitting slow, dull, burning pain.
• Spinothalamic tract: Ascending pathway transmitting pain and temperature sensations.
• Polymodal nociceptors: Sensory receptors responding to mechanical, thermal, and chemical stimuli.
• Referred pain: Pain perceived at a site distant from its origin due to shared neural pathways.
Lead Question - 2015
Pain is carried by which nerve fibers?
a) Aα, Aβ
b) Aα, Aγ
c) Aδ, C
d) Aγ, C
Explanation (Answer: c) Aδ, C)
Pain sensation is transmitted by two types of nerve fibers — Aδ and C fibers. Aδ fibers are thinly myelinated and convey fast, sharp, well-localized pain, while C fibers are unmyelinated and carry slow, burning, and poorly localized pain. These fibers synapse in the dorsal horn of the spinal cord, primarily in laminae I and II (substantia gelatinosa). Aδ fibers activate the neospinothalamic tract, whereas C fibers activate the paleospinothalamic tract. Together, they ensure both immediate withdrawal and prolonged awareness of pain.
1. Which tract carries fast pain sensations to the brain?
a) Neospinothalamic tract
b) Spinocerebellar tract
c) Dorsal column
d) Spinoreticular tract
Explanation (Answer: a) Neospinothalamic tract)
The neospinothalamic tract transmits fast pain impulses from Aδ fibers. These signals ascend directly to the thalamus, providing sharp, well-localized pain sensations. This pathway allows quick withdrawal from harmful stimuli and contributes to the conscious perception of acute pain.
2. Which of the following fibers are unmyelinated?
a) Aα
b) Aβ
c) C fibers
d) Aδ fibers
Explanation (Answer: c) C fibers)
C fibers are unmyelinated and conduct impulses at 0.4–2 m/s. They are responsible for transmitting dull, aching, and burning pain. Due to lack of myelin, these fibers conduct more slowly than Aδ fibers. Their prolonged activation contributes to the persistence of chronic pain sensations.
3. Aδ fibers carry which type of pain?
a) Burning pain
b) Sharp, pricking pain
c) Diffuse pain
d) Chronic pain
Explanation (Answer: b) Sharp, pricking pain)
Aδ fibers transmit fast, pricking, and well-localized pain sensations through rapid conduction. They are thinly myelinated fibers that allow the brain to perceive pain quickly and accurately, helping initiate protective withdrawal reflexes against harmful stimuli like pinpricks or burns.
4. The neurotransmitter released by Aδ fibers in the dorsal horn is:
a) Serotonin
b) Glutamate
c) Substance P
d) GABA
Explanation (Answer: b) Glutamate)
Glutamate is the primary excitatory neurotransmitter released by Aδ fibers in the dorsal horn. It produces fast excitatory postsynaptic potentials (EPSPs), mediating acute, localized pain. In contrast, Substance P released by C fibers causes prolonged depolarization and sustains slow pain responses.
5. Which of the following tracts carries slow, burning pain?
a) Neospinothalamic
b) Paleospinothalamic
c) Spinocerebellar
d) Dorsal column
Explanation (Answer: b) Paleospinothalamic)
The paleospinothalamic tract conveys slow, burning, and aching pain through unmyelinated C fibers. This pathway involves multiple synapses, projecting to the brainstem, reticular formation, and limbic system, contributing to the emotional and autonomic responses to pain stimuli.
6. A 30-year-old man experiences dull, diffuse abdominal pain due to appendicitis. The fiber type involved is:
a) Aα
b) Aβ
c) Aδ
d) C fibers
Explanation (Answer: d) C fibers)
Visceral pain, like the dull, aching pain of appendicitis, is transmitted by unmyelinated C fibers. These fibers carry slow pain signals to the brain via the spinoreticular pathway, resulting in diffuse, poorly localized sensations associated with autonomic responses like nausea.
7. The lamina of the spinal cord that receives pain fibers is:
a) Lamina I and II
b) Lamina III
c) Lamina V only
d) Lamina VII
Explanation (Answer: a) Lamina I and II)
Pain fibers synapse in Lamina I (marginal zone) and Lamina II (substantia gelatinosa) of the dorsal horn. These regions process nociceptive information before it ascends via the spinothalamic tracts. Neurotransmitters such as glutamate and substance P play vital roles here.
8. Loss of pain and temperature sensation on the contralateral side of the body is due to lesion in:
a) Spinocerebellar tract
b) Dorsal column
c) Lateral spinothalamic tract
d) Corticospinal tract
Explanation (Answer: c) Lateral spinothalamic tract)
A lesion in the lateral spinothalamic tract results in contralateral loss of pain and temperature below the level of injury because the tract crosses within one or two segments of the spinal cord. This tract carries impulses transmitted by Aδ and C fibers to the thalamus.
9. Which ion influx is responsible for depolarization in pain fibers?
a) Calcium
b) Sodium
c) Chloride
d) Potassium
Explanation (Answer: b) Sodium)
Depolarization in pain fibers occurs due to the influx of sodium ions through voltage-gated sodium channels. This initiates the action potential that transmits pain impulses to the spinal cord. Many analgesic drugs (like local anesthetics) work by blocking these sodium channels.
10. A patient with diabetic neuropathy has burning foot pain. The affected fibers are:
a) Aδ fibers
b) C fibers
c) Aβ fibers
d) Aα fibers
Explanation (Answer: b) C fibers)
Burning neuropathic pain in diabetic neuropathy results from injury to unmyelinated C fibers. These fibers are sensitive to metabolic damage from chronic hyperglycemia, leading to hyperalgesia, allodynia, and spontaneous burning sensations characteristic of neuropathic pain syndromes.
11. Which of the following neurotransmitters mediates prolonged, slow pain?
a) Dopamine
b) GABA
c) Substance P
d) Serotonin
Explanation (Answer: c) Substance P)
Substance P is released by C fibers in response to noxious stimuli and mediates slow, burning pain. It acts on neurokinin-1 (NK1) receptors, causing sustained depolarization and enhanced pain perception. Chronic pain conditions often involve increased Substance P activity in the dorsal horn.