Chapter: Neurophysiology; Topic: Synaptic Transmission; Subtopic: Excitatory Postsynaptic Potentials (EPSP)
KEYWORD DEFINITIONS
• EPSP – Depolarizing postsynaptic potential making neuron more likely to fire
• Na⁺ influx – Major ion movement causing EPSP
• Glutamate – Primary excitatory neurotransmitter
• Ligand-gated ion channels – Open when neurotransmitter binds
• Depolarization – Membrane potential becomes less negative
Lead Question – 2015
1. EPSP is due to?
A) K⁺ influx
B) Na⁺ efflux
C) Na⁺ influx
D) Ca²⁺ influx
Explanation:
An excitatory postsynaptic potential (EPSP) is generated when neurotransmitters like glutamate open ligand-gated channels, allowing Na⁺ ions to flow into the postsynaptic neuron. This inward Na⁺ current causes depolarization, bringing the membrane closer to the threshold for action potential firing. K⁺ influx and Na⁺ efflux would hyperpolarize the cell, while Ca²⁺ influx is typically associated with presynaptic neurotransmitter release rather than postsynaptic depolarization. Therefore, the correct answer is Na⁺ influx. EPSPs form the fundamental basis of excitatory synaptic integration in the CNS.
2. The main excitatory neurotransmitter in the CNS is:
A) GABA
B) Glycine
C) Glutamate
D) Serotonin
Explanation:
Glutamate is the principal excitatory neurotransmitter in the central nervous system, responsible for generating EPSPs by opening Na⁺ and Ca²⁺ permeable channels. GABA and glycine are inhibitory, while serotonin modulates mood and cognition. Therefore, the correct answer is Glutamate. Glutamatergic excitatory synapses are essential for learning, memory, and neural plasticity.
3. A patient develops seizures due to excessive excitatory activity. Which receptor is most likely overactivated?
A) NMDA receptor
B) GABA-A receptor
C) Glycine receptor
D) Serotonin receptor
Explanation:
Excessive activation of NMDA receptors permits prolonged Na⁺ and Ca²⁺ influx, greatly enhancing excitatory neurotransmission and potentially leading to seizures. GABA-A and glycine receptors mediate inhibition, and serotonin is modulatory. Thus, the correct answer is NMDA receptor. NMDA overactivation contributes to neuronal excitotoxicity seen in stroke and epilepsy.
4. IPSP is typically caused by which ion movement?
A) Na⁺ influx
B) K⁺ efflux
C) Ca²⁺ influx
D) Cl⁻ efflux
Explanation:
An inhibitory postsynaptic potential (IPSP) results from K⁺ efflux or Cl⁻ influx, both of which hyperpolarize the membrane, making action potential generation less likely. Na⁺ and Ca²⁺ influx are associated with depolarization. Therefore, the answer is K⁺ efflux. IPSPs counterbalance EPSPs, ensuring controlled neural activity.
5. Summation of multiple EPSPs occurring close in time at a single synapse refers to:
A) Spatial summation
B) Temporal summation
C) Inhibitory summation
D) After-hyperpolarization
Explanation:
Temporal summation occurs when successive EPSPs arrive rapidly at the same synapse, increasing the likelihood of reaching threshold. Spatial summation involves simultaneous EPSPs from different synapses. Therefore, the correct answer is Temporal summation. Summation allows neurons to integrate incoming signals and regulate firing patterns.
6. A patient with hypoxic injury shows decreased EPSP formation. Which mechanism is impaired?
A) Na⁺ channel opening
B) GABA release
C) Cl⁻ influx
D) K⁺ efflux
Explanation:
EPSPs depend on the opening of ligand-gated Na⁺ channels activated by glutamate. Hypoxia impairs ATP-dependent ion gradients and synaptic transmission, reducing Na⁺ influx and decreasing excitatory drive. GABA release, Cl⁻ influx, and K⁺ efflux are inhibitory mechanisms. Therefore, the correct answer is Na⁺ channel opening. Hypoxia often depresses CNS excitatory function first.
7. Which receptor subtype mediates fast EPSP?
A) AMPA receptor
B) NMDA receptor
C) GABA-B receptor
D) Glycine receptor
Explanation:
AMPA receptors mediate fast excitatory postsynaptic potentials by allowing rapid Na⁺ influx when glutamate binds. NMDA receptors are slower, voltage-dependent, and require depolarization to relieve Mg²⁺ block. GABA-B receptors are inhibitory metabotropic receptors. Thus, the correct answer is AMPA receptor. Fast EPSPs are crucial for rapid synaptic communication.
8. A 65-year-old with Alzheimer’s disease shows decreased cholinergic EPSPs. Which area degenerates first?
A) Substantia nigra
B) Basal forebrain nucleus (Nucleus basalis of Meynert)
C) Cerebellum
D) Red nucleus
Explanation:
Alzheimer’s disease features degenerative loss of cholinergic neurons in the nucleus basalis of Meynert, reducing acetylcholine-mediated EPSPs in the cortex and undermining cognition. Substantia nigra degeneration causes Parkinsonism. Cerebellum and red nucleus are unrelated to cortical cholinergic projections. Therefore, the correct answer is Basal forebrain nucleus. This deficit contributes to memory impairment in Alzheimer’s.
9. At the neuromuscular junction, the major excitatory ion responsible for depolarization is:
A) Cl⁻ influx
B) K⁺ efflux
C) Na⁺ influx
D) Ca²⁺ efflux
Explanation:
Acetylcholine binds nicotinic receptors at the neuromuscular junction, opening channels permeable mainly to Na⁺, which rapidly enters the muscle cell to produce an end-plate potential. Cl⁻ and K⁺ fluxes do not initiate NMJ depolarization. Thus, the correct answer is Na⁺ influx. End-plate potential triggers muscle action potential and contraction.
10. Which neurotransmitter is most closely associated with generating EPSPs in the hippocampus?
A) GABA
B) Glutamate
C) Dopamine
D) Glycine
Explanation:
Glutamate is the primary excitatory neurotransmitter in hippocampal circuits, essential for learning and memory. It activates AMPA and NMDA receptors to produce EPSPs. GABA and glycine are inhibitory, while dopamine modulates reward pathways. Therefore, the correct answer is Glutamate. Synaptic plasticity in the hippocampus relies heavily on glutamatergic EPSPs.
11. EPSPs bring membrane potential closer to threshold because they cause:
A) Hyperpolarization
B) Depolarization
C) Inhibition
D) After-potential
Explanation:
EPSPs are depolarizing events generated by inward Na⁺ currents, making the membrane potential less negative and more likely to trigger an action potential. Hyperpolarization and inhibition move the membrane away from threshold. After-potentials follow action potentials but are not part of EPSP formation. Therefore, the correct answer is Depolarization. EPSPs integrate until threshold is reached, initiating neuronal firing.
Chapter: Neurophysiology; Topic: Cerebellum; Subtopic: Cerebellar Cortex – Neuronal Types
KEYWORD DEFINITIONS
• Granule cells – Only excitatory neurons in cerebellar cortex (glutamatergic)
• Purkinje cells – Large inhibitory (GABAergic) projection neurons
• Basket & Stellate cells – Inhibitory interneurons
• Golgi cells – Inhibitory interneurons regulating granule cell activity
• Mossy & climbing fibers – Excitatory afferents to cerebellum
Lead Question – 2015
1. The only excitatory neurons in cerebellar cortex are?
A) Purkinje
B) Basket
C) Golgi
D) Granule cells
Explanation:
Granule cells are the only excitatory neurons in the cerebellar cortex and use glutamate as their neurotransmitter. All other cerebellar cortical neurons—including Purkinje, basket, stellate, and Golgi cells—are inhibitory and release GABA. Granule cells receive mossy fiber input and send their axons as parallel fibers to synapse on Purkinje cells. Therefore, the correct answer is Granule cells. Their excitatory output is essential for modulating cerebellar circuitry and coordinating fine motor control.
2. Purkinje cells release which neurotransmitter?
A) Glutamate
B) GABA
C) Glycine
D) Dopamine
Explanation:
Purkinje cells are the primary output neurons of the cerebellar cortex and are purely inhibitory, releasing GABA onto deep cerebellar nuclei. They integrate inputs from climbing and mossy fiber pathways. Glutamate is excitatory, dopamine modulates basal ganglia, and glycine mediates inhibition in the spinal cord. Thus, the correct answer is GABA. Their inhibitory output is crucial for coordinated movement.
3. A patient with cerebellar degeneration shows intention tremor. Which pathway is most affected?
A) Corticospinal tract
B) Mossy fiber pathway
C) Spinothalamic tract
D) Reticulospinal tract
Explanation:
The mossy fiber pathway provides major excitatory input to granule cells, modulating Purkinje cell activity. Damage disrupts cerebellar processing, resulting in intention tremor, dysmetria, and ataxia. Corticospinal and spinothalamic tracts serve motor output and sensory pathways respectively, while reticulospinal tracts mediate posture. Therefore, the correct answer is Mossy fiber pathway. These circuits fine-tune motor execution.
4. Climbing fibers originate from which nucleus?
A) Red nucleus
B) Inferior olivary nucleus
C) Dentate nucleus
D) Substantia nigra
Explanation:
Climbing fibers arise exclusively from the inferior olivary nucleus and form powerful excitatory synapses on Purkinje cells. These fibers produce complex spikes essential for motor learning. Red nucleus, dentate, and substantia nigra project to different motor pathways. Therefore, the correct answer is Inferior olivary nucleus. Climbing fiber dysfunction impairs cerebellar learning mechanisms.
5. Which cerebellar cell type receives parallel fiber input?
A) Purkinje cell
B) Basket cell
C) Golgi cell
D) All of the above
Explanation:
Parallel fibers, which are axons of granule cells, synapse extensively on Purkinje cells, basket cells, and stellate cells, influencing both inhibitory and excitatory circuitry. Golgi cells receive mossy fiber and granule cell collaterals. Therefore, the correct answer is All of the above. Parallel fibers play a central role in cerebellar cortical integration.
6. A 50-year-old alcoholic patient presents with truncal ataxia. Which cerebellar region is most likely affected?
A) Cerebrocerebellum
B) Vestibulocerebellum (flocculonodular lobe)
C) Spinocerebellum (vermis)
D) Dentate nucleus
Explanation:
Truncal ataxia results from vermis (spinocerebellum) damage, commonly seen in chronic alcoholism. This region regulates axial muscles and gait stability. Vestibulocerebellum controls eye and balance movements, cerebrocerebellum handles limb planning, and dentate nucleus coordinates fine limb movement. Therefore, the correct answer is Spinocerebellum. Clinical findings include a wide-based gait and midline instability.
7. Basket cells in cerebellar cortex are:
A) Excitatory
B) Inhibitory
C) Glycinergic
D) Dopaminergic
Explanation:
Basket cells are inhibitory interneurons using GABA as their neurotransmitter. They synapse on Purkinje cell bodies and modulate their activity. They are not excitatory, glycinergic, or dopaminergic. Therefore, the correct answer is Inhibitory. Their role is vital in shaping cerebellar output and timing of Purkinje cell firing.
8. Which cerebellar neurons form parallel fibers?
A) Golgi cells
B) Granule cells
C) Purkinje cells
D) Stellate cells
Explanation:
Granule cells send their axons upward to bifurcate into parallel fibers that synapse widely throughout the molecular layer. Purkinje cells have dendritic trees, Golgi cells are inhibitory, and stellate cells modulate Purkinje firing. Thus, the correct answer is Granule cells. Parallel fibers enable broad integration of sensory and motor information.
9. A patient with cerebellar lesion shows dysdiadochokinesia. This signifies impairment in:
A) Rapid alternating movements
B) Muscle tone
C) Pain sensation
D) Vision
Explanation:
Dysdiadochokinesia—difficulty performing rapid alternating movements—is a hallmark sign of cerebellar dysfunction. It arises due to impaired Purkinje cell modulation of motor timing. Muscle tone, pain, and vision are not directly responsible. Therefore, the correct answer is Rapid alternating movements. This clinical sign reflects the role of cerebellum in coordinating agonist–antagonist muscle switching.
10. Stellate cells in cerebellum act as:
A) Excitatory interneurons
B) Inhibitory interneurons
C) Motor neurons
D) Sensory relay neurons
Explanation:
Stellate cells, like basket cells, are inhibitory interneurons releasing GABA. They synapse on Purkinje dendrites, modulating cortical output. They are neither excitatory nor motor or sensory relays. Therefore, the answer is Inhibitory interneurons. These cells contribute to cerebellar timing and refinement of motor signals.
11. Which afferent fiber type excites granule cells?
A) Climbing fibers
B) Mossy fibers
C) Parallel fibers
D) Purkinje axons
Explanation:
Mossy fibers provide the primary excitatory input to granule cells, conveying sensory and cortical information. Climbing fibers excite Purkinje cells directly, parallel fibers arise from granule cells, and Purkinje axons are inhibitory outputs. Thus, the correct answer is Mossy fibers. This pathway forms the fundamental feed-forward circuit of the cerebellar cortex.
Chapter: Neurophysiology; Topic: Sleep Physiology; Subtopic: NREM Sleep Disorders – Parasomnias
KEYWORD DEFINITIONS
• NREM sleep – Non-rapid eye movement sleep with stages 1–4
• Slow-wave sleep – Deep sleep (Stages 3–4 NREM), associated with parasomnias
• Parasomnias – Abnormal behaviors during sleep (e.g., sleepwalking)
• REM sleep – Dreaming sleep with muscle atonia
• Arousal disorders – Occur during partial awakening from deep NREM sleep
Lead Question – 2015
1. Sleep walking is seen in which stage of sleep?
A) REM
B) Stage 1–2 NREM
C) Stage 2–3 NREM
D) Stage 3–4 NREM
Explanation:
Sleepwalking (somnambulism) is a classic NREM parasomnia occurring predominantly during deep slow-wave sleep, which corresponds to Stages 3–4 NREM. This stage is characterized by delta waves, reduced consciousness, and partial arousal phenomena. Because REM sleep involves muscle atonia, sleepwalking cannot occur during REM. Lighter NREM stages (1–2) do not typically generate complex motor behaviors. Therefore, the correct answer is Stage 3–4 NREM. It is most common in children and may be triggered by sleep deprivation, stress, or fever.
2. REM sleep is characterized by:
A) Muscle atonia
B) Increased muscle tone
C) Sleepwalking episodes
D) Violent movements
Explanation:
REM sleep features rapid eye movements, vivid dreaming, and generalized skeletal muscle atonia due to brainstem inhibition. This prevents acting out dreams. Increased muscle tone is typical of wakefulness, not REM. Sleepwalking and violent behaviors occur in NREM parasomnias, not REM. Thus, the correct answer is Muscle atonia. The atonia protects the sleeper from injury during dreams.
3. A 10-year-old child exhibits night terrors. These episodes occur most commonly in:
A) REM sleep
B) Stage 3–4 NREM sleep
C) Stage 1 sleep
D) Wakefulness
Explanation:
Night terrors occur during deep slow-wave sleep (Stages 3–4 NREM) and are classified as NREM parasomnias. They involve intense fear and autonomic activation but no dream recall. REM sleep produces nightmares with intact memory. Stage 1 sleep is light and not associated with parasomnias. Therefore, the correct answer is Stage 3–4 NREM sleep. These events typically resolve with age.
4. Which EEG pattern is characteristic of Stage 3–4 NREM sleep?
A) Alpha waves
B) Beta waves
C) Delta waves
D) Sleep spindles
Explanation:
Stages 3–4 NREM sleep, known as slow-wave sleep, are dominated by high-amplitude delta waves (0.5–2 Hz). Alpha waves occur in relaxed wakefulness, beta waves in active thinking, and sleep spindles in Stage 2 NREM. Thus, the correct answer is Delta waves. Delta activity reflects deep sleep with high arousal threshold.
5. A patient sleepwalks and has no memory of the event. The phenomenon is best classified as:
A) REM parasomnia
B) NREM parasomnia
C) Psychosis
D) Sleep apnea
Explanation:
Sleepwalking is a type of NREM parasomnia, occurring during deep slow-wave sleep, and is associated with amnesia for the episode. REM parasomnias involve dream enactment (e.g., REM behavior disorder). Psychosis is unrelated to sleep stages, and sleep apnea involves breathing disruption. The correct answer is NREM parasomnia. It is triggered by incomplete arousal from deep sleep.
6. REM Behavior Disorder (RBD) is caused by failure of:
A) REM sleep muscle atonia
B) Slow-wave sleep
C) Dream generation
D) GABAergic neurons
Explanation:
In RBD, loss of normal REM muscle atonia allows patients to act out dreams. Slow-wave sleep is intact, and dream generation remains functional. GABAergic neurons are involved but not uniquely responsible. Thus, the correct answer is REM sleep muscle atonia. This condition is associated with neurodegenerative disorders like Parkinson’s disease.
7. Sleep spindle appearance marks which sleep stage?
A) Stage 1
B) Stage 2
C) Stage 3
D) REM sleep
Explanation:
Stage 2 NREM sleep is characterized by sleep spindles (12–14 Hz) and K-complexes on EEG. These represent thalamocortical activity regulating sensory suppression. Stage 1 has theta waves, Stage 3–4 has delta waves, and REM has low-voltage mixed frequencies. Therefore, the correct answer is Stage 2. This stage comprises a large portion of total sleep time.
8. A patient with obstructive sleep apnea often experiences fragmentation of which sleep stage?
A) Stage 3–4 NREM
B) REM sleep
C) Wakefulness
D) Stage 1 sleep
Explanation:
Obstructive sleep apnea results in repeated nighttime arousals that disturb REM sleep substantially, reducing its duration and quality. Deep slow-wave sleep may also be fragmented but REM is most affected. Therefore, the correct answer is REM sleep. This contributes to daytime sleepiness and impaired memory consolidation.
9. Narcolepsy is associated with deficiency of:
A) GABA
B) Orexin (hypocretin)
C) Serotonin
D) Acetylcholine
Explanation:
Narcolepsy results from deficiency of orexin (hypocretin) produced in the lateral hypothalamus. This peptide stabilizes wakefulness. Loss of orexin leads to sleep attacks, cataplexy, and hallucinations. GABA promotes sleep but is not deficient. Serotonin and acetylcholine modulate sleep cycles but are not primary causes. Thus, the correct answer is Orexin. Narcolepsy is confirmed via CSF orexin levels and polysomnography.
10. Dreaming with vivid recall occurs mainly in:
A) Stage 3 NREM
B) REM sleep
C) Stage 1 NREM
D) Stage 2 NREM
Explanation:
Vivid, story-like dreaming occurs predominantly during REM sleep due to active cortical processing with muscle atonia. NREM dreams, when present, are brief and less structured. Therefore, the correct answer is REM sleep. This stage plays a key role in emotional regulation and memory consolidation.
11. Bruxism (teeth grinding) commonly occurs in:
A) REM sleep
B) Stage 1 NREM
C) Stage 2 NREM
D) Stage 4 NREM
Explanation:
Bruxism is most commonly observed during Stage 2 NREM sleep, which is characterized by sleep spindles and K-complexes. It is considered a parasomnia and may be triggered by stress or malocclusion. REM sleep prevents such movements due to muscle atonia. Therefore, the correct answer is Stage 2 NREM. Diagnosis may require polysomnography if severe.
Chapter: Gastrointestinal Physiology; Topic: Mineral Absorption; Subtopic: Factors Affecting Calcium Absorption
KEYWORD DEFINITIONS
• Calcium absorption – Uptake of calcium from intestine, mainly duodenum
• Phytates – Compounds in cereals that bind calcium and inhibit absorption
• Oxalates – Plant compounds forming insoluble calcium salts
• Vitamin D – Enhances calcium absorption
• Acidic pH – Improves calcium solubility and absorption
Lead Question – 2015
1. Calcium absorption is hampered by:
A) Protein
B) Lactose
C) Acid
D) Phytates
Explanation:
Phytates, found in cereals, legumes, and whole grains, bind calcium and form insoluble complexes that cannot be absorbed in the intestine. Protein and lactose actually enhance calcium absorption, while acidic pH increases calcium solubility. Therefore, the factor that hampers calcium absorption is Phytates. Individuals consuming diets high in unfermented cereals may develop calcium deficiency due to this inhibitory effect. Removing phytates through fermentation or soaking improves absorption significantly.
2. Which vitamin enhances intestinal calcium absorption?
A) Vitamin A
B) Vitamin D
C) Vitamin K
D) Vitamin E
Explanation:
Vitamin D increases the synthesis of calcium-binding proteins in the intestinal mucosa, significantly enhancing active calcium absorption. Vitamins A, K, and E do not play a primary role in calcium handling. Therefore, the correct answer is Vitamin D. Deficiency in vitamin D leads to reduced calcium uptake and conditions like rickets and osteomalacia.
3. A patient with celiac disease has low calcium levels. The cause is:
A) Excess protein intake
B) Increased phytate absorption
C) Damage to intestinal villi
D) Excess bile salts
Explanation:
Celiac disease causes villous atrophy, reducing surface area for nutrient absorption, including calcium. Protein does not impair calcium uptake, and bile salts are not directly involved. Phytate absorption is not increased in celiac disease. Therefore, the correct answer is Damage to intestinal villi. This malabsorption may manifest as low bone mineral density.
4. Calcium absorption occurs maximally in:
A) Stomach
B) Duodenum
C) Colon
D) Rectum
Explanation:
The duodenum has an acidic environment and abundant calcium transport proteins, making it the primary site for calcium absorption. The stomach has minimal absorption, while colon and rectum have little role. Thus, the correct answer is Duodenum. The duodenum’s short transit time and pH facilitate efficient uptake.
5. High dietary oxalates inhibit calcium absorption by:
A) Increasing vitamin D degradation
B) Binding calcium in intestine
C) Stimulating calcium efflux
D) Increasing renal calcium loss
Explanation:
Oxalates form insoluble calcium oxalate salts in the intestine, preventing calcium absorption. They do not affect vitamin D levels or calcium efflux. Renal calcium loss is unaffected. Thus, the correct answer is Binding calcium in intestine. Spinach and certain nuts have high oxalate content, reducing usable dietary calcium.
6. A patient with lactose intolerance may have decreased calcium absorption because:
A) Lactose enhances calcium absorption
B) Calcium is digested by lactase
C) Fat malabsorption causes calcium loss
D) Lactase stimulates vitamin D production
Explanation:
Lactose increases calcium solubility and aids its uptake. In lactose intolerance, individuals avoid dairy products, reducing calcium intake and losing lactose’s absorption-enhancing effect. Calcium is not digested by lactase, and lactase does not influence vitamin D. Therefore, the correct answer is Lactose enhances calcium absorption. This is important in dietary counseling.
7. Which hormone increases renal calcium reabsorption?
A) Calcitonin
B) Parathyroid hormone (PTH)
C) Insulin
D) Glucagon
Explanation:
PTH increases renal tubular calcium reabsorption, reduces phosphate reabsorption, and stimulates vitamin D activation. Calcitonin decreases serum calcium, while insulin and glucagon do not regulate calcium homeostasis. Therefore, the correct answer is PTH. PTH is essential for maintaining serum calcium during hypocalcemic states.
8. Phosphate binds calcium and reduces its absorption. This is most pronounced in intake of:
A) Meat
B) Whole grains
C) Fruits
D) Fats
Explanation:
Whole grains contain high levels of phytates and phosphates, which bind calcium and reduce absorption. Meat does not contain significant phytates. Fruits and fats have minimal effect on calcium binding. Thus, the correct answer is Whole grains. Dietary modification helps improve calcium bioavailability.
9. Which condition increases calcium absorption?
A) Achlorhydria
B) Low vitamin D
C) Acidic gastric pH
D) High fiber intake
Explanation:
Acidic pH increases calcium solubility, enhancing absorption. Achlorhydria reduces acid and decreases uptake. Low vitamin D also reduces absorption, and high fiber (with phytates) may bind calcium. Therefore, the correct answer is Acidic gastric pH. Elderly individuals with reduced acid secretion often have poorer calcium absorption.
10. A 55-year-old woman with osteoporosis is advised calcium supplements with meals. Reason?
A) Calcium binds fat
B) Gastric acid improves calcium solubility
C) Calcium is digested better with proteins
D) Calcium requires bile for absorption
Explanation:
Calcium dissolves better in an acidic environment created during meals, improving its absorption. Fat-binding, protein digestion, and bile are unrelated. Therefore, the correct answer is Gastric acid improves calcium solubility. Co-administration with meals maximizes uptake.
11. A patient has chronic antacid use. This reduces calcium absorption because:
A) Antacids convert calcium to free ionized form
B) Antacids decrease gastric acidity
C) Antacids degrade vitamin D
D) Antacids increase phytate levels
Explanation:
Antacids neutralize gastric acid, reducing calcium solubility and intestinal absorption. They do not degrade vitamin D or influence phytates. Thus, the correct answer is Antacids decrease gastric acidity. Long-term use can contribute to hypocalcemia and bone loss.
Chapter: Neurophysiology; Topic: Motor System; Subtopic: Cortical Motor Areas – Suppressor Strip
KEYWORD DEFINITIONS
• Suppressor strip – Area anterior to precentral gyrus that inhibits stretch reflex
• Stretch reflex – Monosynaptic reflex causing muscle contraction when stretched
• Motor cortex – Region responsible for voluntary movement
• Upper motor neurons – Neurons controlling spinal motor circuits
• Muscle tone – Resistance to passive stretch regulated by reflex pathways
Lead Question – 2015
1. Suppressor Strip on anterior edge of pre-central gyrus has following function?
A) Increase extensor tone
B) Pain perception
C) Inhibition of stretch reflex
D) Voluntary movement
Explanation:
The suppressor strip lies just anterior to the primary motor cortex in the frontal lobe. Its major role is inhibition of the stretch reflex and modulation of muscle tone. By reducing excessive reflex activity, it prevents hyperreflexia and spasticity. Pain perception is mediated by somatosensory cortex, extensor tone by vestibulospinal pathways, and voluntary movement by the primary motor cortex itself. Therefore, the correct answer is Inhibition of stretch reflex. Lesions in this region cause exaggerated reflexes due to loss of inhibitory control.
2. The primary motor cortex corresponds to which Brodmann area?
A) Area 4
B) Area 6
C) Area 3
D) Area 22
Explanation:
The primary motor cortex, responsible for initiating voluntary movements, corresponds to Brodmann area 4. Area 6 represents the premotor/supplementary motor regions, area 3 belongs to the somatosensory cortex, and area 22 is Wernicke’s area. Therefore, the correct answer is Area 4. Damage to area 4 produces contralateral weakness and loss of fine motor control.
3. A patient with a lesion in the supplementary motor area will likely have difficulty with:
A) Planning complex movements
B) Visual processing
C) Hearing
D) Pain localization
Explanation:
The supplementary motor area (SMA) coordinates complex and bimanual movements and internally driven motor sequences. Damage produces difficulty initiating planned movements (motor apraxia). Visual processing occurs in occipital cortex, hearing in temporal cortex, and pain localization in somatosensory cortex. Thus, the correct answer is Planning complex movements. SMA lesions often cause difficulty with coordinated motor tasks.
4. Hyperreflexia following stroke is due to loss of:
A) Spinal cord reflex arcs
B) Cortical inhibition
C) Muscle fibers
D) Peripheral nerve conduction
Explanation:
Upper motor neurons, including suppressor areas, provide inhibitory control over spinal reflexes. When cortical inhibition is lost after stroke, reflexes become exaggerated. Spinal reflex arcs remain intact, muscle fibers are unaffected initially, and peripheral conduction is normal. Therefore, the correct answer is Cortical inhibition. This mechanism explains spasticity in UMN lesions.
5. The corticospinal tract decussates at the:
A) Pons
B) Midbrain
C) Medullary pyramids
D) Spinal cord dorsal horn
Explanation:
Nearly 80–90% of corticospinal fibers cross at the pyramidal decussation in the medulla to form the lateral corticospinal tract. The pons and midbrain transmit but do not primarily decussate these fibers. Dorsal horn contains sensory, not motor, pathways. Therefore, the correct answer is Medullary pyramids. This crossing explains contralateral motor deficits.
6. A patient presents with spasticity and exaggerated reflexes. Which lesion is most likely?
A) Lower motor neuron lesion
B) Upper motor neuron lesion
C) Neuromuscular junction defect
D) Myopathy
Explanation:
Spasticity and hyperreflexia occur due to upper motor neuron (UMN) lesions, which remove inhibitory influence on spinal reflexes, including suppressor strip control. LMN lesions cause flaccidity, neuromuscular junction defects cause fatigability, and myopathies cause proximal weakness. The correct answer is Upper motor neuron lesion. This presentation is typical of stroke or spinal cord injury.
7. Premotor cortex is responsible for:
A) Simple reflex movements
B) Planning movements based on external cues
C) Vision
D) Touch perception
Explanation:
The premotor cortex (Brodmann area 6) organizes movement patterns triggered by external stimuli such as visual or auditory cues. Simple reflexes occur in the spinal cord, vision in the occipital lobe, and touch in the somatosensory cortex. Therefore, the correct answer is Planning movements based on external cues. It works closely with SMA to coordinate motor output.
8. Which neurotransmitter is primarily used by corticospinal neurons?
A) GABA
B) Dopamine
C) Glutamate
D) Glycine
Explanation:
Corticospinal neurons are excitatory and use glutamate as their primary neurotransmitter. GABA and glycine are inhibitory, while dopamine is modulatory in basal ganglia circuits. Thus, the correct answer is Glutamate. Excitatory drive from motor cortex facilitates precise motor control.
9. A tumor compressing the precentral gyrus would cause:
A) Sensory loss
B) Motor weakness
C) Memory impairment
D) Visual field defect
Explanation:
The precentral gyrus contains the primary motor cortex; its compression causes contralateral weakness or paralysis. Sensory loss occurs with postcentral gyrus lesions, memory impairment involves hippocampus, and visual defects arise from occipital lobe lesions. Therefore, the correct answer is Motor weakness. Motor maps in this region allow localization of deficits.
10. The stretch reflex involves which afferent fiber type?
A) Type Ia fibers
B) C fibers
C) A-delta fibers
D) Type II taste fibers
Explanation:
Type Ia fibers from muscle spindles detect rapid stretch and initiate the monosynaptic stretch reflex. C fibers carry pain, A-delta fibers carry fast pain and temperature, and taste fibers have no role. Thus, the correct answer is Type Ia fibers. These inputs are modulated by cortical suppressor systems to maintain tone.
11. Damage to suppressor strip leads to:
A) Loss of pain sensation
B) Flaccid paralysis
C) Increased stretch reflex activity
D) Loss of vision
Explanation:
Suppressor strip damage removes inhibitory control over spinal reflexes, resulting in hyperreflexia and increased muscle tone. Pain sensation involves somatosensory cortex, flaccid paralysis reflects LMN lesions, and vision relates to occipital cortex. Therefore, the correct answer is Increased stretch reflex activity. This is a defining feature of upper motor neuron dysfunction.
Chapter: Neurophysiology; Topic: Brainstem Reflexes; Subtopic: Oculocephalic Reflex (Doll’s Eye Reflex)
KEYWORD DEFINITIONS
• Doll’s eye reflex – Brainstem reflex where eyes move opposite to head movement
• Oculocephalic reflex – Assesses integrity of midbrain and pons
• Brainstem function – Essential for basic reflexes and consciousness
• Comatose patient testing – Used when voluntary eye movement cannot be assessed
• Vestibulo-ocular reflex (VOR) – Stabilizes gaze during head movement
Lead Question – 2015
1. Doll's eye reflex is used in?
A) Hemiplegic
B) Paraplegic
C) Unconscious patient
D) Cerebral palsy
Explanation:
The Doll’s eye reflex (oculocephalic reflex) is used to assess brainstem integrity in comatose or unconscious patients. When the head is rapidly rotated, intact brainstem function causes the eyes to move in the opposite direction, indicating preserved vestibulo-ocular pathways. It is not used for hemiplegia, paraplegia, or cerebral palsy assessment. Absence of this reflex suggests severe brainstem dysfunction. Therefore, the correct answer is Unconscious patient. This reflex must not be tested in suspected cervical spine injury.
2. Doll’s eye reflex helps assess which structure?
A) Cerebellum
B) Brainstem
C) Basal ganglia
D) Spinal cord
Explanation:
The oculocephalic (Doll’s eye) reflex evaluates brainstem integrity, specifically the vestibular nuclei, pons, and midbrain centers that coordinate eye movements. Cerebellum regulates coordination, basal ganglia regulate movement initiation, and spinal cord reflexes are unrelated. Thus, the correct answer is Brainstem. The presence or absence of this reflex assists in coma evaluation.
3. A comatose patient shows absent Doll’s eye reflex. This suggests damage to:
A) Cortical motor areas
B) Brainstem gaze centers
C) Cerebellar hemispheres
D) Spinal interneurons
Explanation:
Absent Doll’s eye reflex indicates injury to the brainstem gaze centers including pontine and midbrain nuclei. Cortical damage does not abolish this reflex, nor do cerebellar or spinal injuries. Therefore, the correct answer is Brainstem gaze centers. This finding may suggest poor neurological prognosis if persistent.
4. The physiological basis of Doll's eye reflex is:
A) Spinocerebellar pathway activation
B) Vestibulo-ocular reflex
C) Corticospinal tract activity
D) Reticular formation inhibition
Explanation:
The Doll’s eye reflex is generated by the vestibulo-ocular reflex (VOR), where vestibular input causes the eyes to move opposite to head movement to maintain visual fixation. Corticospinal and reticular pathways are not directly involved. Thus, the correct answer is Vestibulo-ocular reflex. It is fundamental for gaze stabilization even without vision.
5. In a cervical spine injury patient, Doll’s eye reflex should:
A) Always be tested
B) Never be tested
C) Be tested after 24 hours
D) Be tested only during intubation
Explanation:
This reflex requires rapid passive head movement. In suspected cervical spine injury, such movement may worsen spinal damage; therefore, it must not be tested. The correct answer is Never be tested. Safer alternatives include caloric testing for assessing brainstem function.
6. Cold caloric testing stimulates which canal to mimic Doll’s eye reflex?
A) Posterior semicircular canal
B) Horizontal semicircular canal
C) Anterior semicircular canal
D) Otolith organs
Explanation:
Cold caloric testing primarily activates the horizontal semicircular canal to generate vestibulo-ocular responses similar to those seen in Doll’s eye reflex. Posterior and anterior canals are not targeted by standard caloric testing. Thus, the answer is Horizontal semicircular canal. It is used when passive head rotation is unsafe.
7. In a conscious patient, lack of Doll’s eye reflex means:
A) Normal finding
B) Brainstem failure
C) Spinal cord lesion
D) Cerebellar injury
Explanation:
In conscious individuals, Doll’s eye reflex is normally absent because voluntary eye fixation suppresses VOR. Therefore, absence is normal in awake patients. Brainstem failure is only implied when absent in comatose patients. Thus, correct answer is Normal finding. Conscious fixation overrides reflexive eye movements.
8. Active eye movement in the same direction as head movement in a comatose patient indicates:
A) Intact reflex
B) Absent brainstem reflex
C) Spinal cord injury
D) Upper motor neuron lesion
Explanation:
If a comatose patient’s eyes move with the head rather than opposite, the Doll’s eye reflex is absent, indicating impaired brainstem function. Spinal lesions or UMN lesions do not affect this reflex. Therefore, the correct answer is Absent brainstem reflex. This finding may indicate severe neurological compromise.
9. Doll’s eye reflex is mediated by which cranial nerves?
A) II and III
B) III, IV, and VI
C) V and VII
D) IX and X
Explanation:
The reflex involves extraocular movements coordinated by cranial nerves III (oculomotor), IV (trochlear), and VI (abducens). Vestibular input arises from cranial nerve VIII. Thus, the correct answer is III, IV, and VI. The coordinated response signifies intact pontine and midbrain centers.
10. A patient with metabolic coma and intact Doll's eye reflex indicates:
A) Preserved brainstem function
B) Brain death
C) Spinal shock
D) Cortical blindness
Explanation:
Presence of Doll’s eye reflex in coma signifies an intact brainstem. Brain death criteria require its absence. Spinal shock and cortical blindness do not affect this reflex. Therefore, the correct answer is Preserved brainstem function. It helps differentiate metabolic coma from structural brainstem lesions.
11. Doll’s eye reflex becomes absent in brain death because of failure of:
A) Cortical integration
B) Pontine and midbrain nuclei
C) Spinal interneurons
D) Cerebellar pathways
Explanation:
Brain death involves complete and irreversible loss of brainstem reflexes, including those mediated by pontine and midbrain nuclei responsible for the oculocephalic reflex. Therefore, the correct answer is Pontine and midbrain nuclei. Absence of this reflex is a core part of brain death testing.
Chapter: Autonomic Nervous System; Topic: Sympathetic Division; Subtopic: Neurotransmitter Secretion – Adrenal Medulla
KEYWORD DEFINITIONS
• Sympathetic system – Part of ANS mediating fight-or-flight responses
• Adrenal medulla – Modified sympathetic ganglion secreting epinephrine & norepinephrine
• Chromaffin cells – Cells in adrenal medulla that act like postganglionic neurons
• Catecholamines – Stress hormones (epinephrine, norepinephrine)
• Preganglionic fibers – Cholinergic fibers stimulating adrenal medulla
Lead Question – 2015
1. Part of sympathetic system which secrete chemical transmitter?
A) Cardiac ganglion
B) Cervical sympathetic chain
C) Adrenal medulla
D) Thoracic sympathetic chain
Explanation:
The adrenal medulla acts as a modified sympathetic ganglion derived from neural crest cells. Unlike other sympathetic ganglia, its chromaffin cells directly secrete catecholamines (mainly epinephrine and norepinephrine) into the bloodstream when stimulated by preganglionic sympathetic fibers. Cardiac, cervical, and thoracic sympathetic chains do not release hormones; they release neurotransmitters only at synapses. Therefore, the correct answer is Adrenal medulla. This endocrine function allows rapid systemic sympathetic activation during stress.
2. The adrenal medulla primarily releases:
A) Acetylcholine
B) Epinephrine
C) Dopamine
D) Serotonin
Explanation:
The adrenal medulla secretes mainly epinephrine (≈80%) and a smaller amount of norepinephrine (≈20%) in response to sympathetic stimulation. These catecholamines amplify fight-or-flight responses. Acetylcholine is the neurotransmitter of preganglionic sympathetic fibers, dopamine is a precursor, and serotonin is unrelated. Thus, the correct answer is Epinephrine. This hormonal release supports rapid cardiovascular and metabolic adjustments.
3. Chromaffin cells of adrenal medulla are analogous to:
A) Preganglionic neurons
B) Postganglionic sympathetic neurons
C) Sensory neurons
D) Interneurons
Explanation:
Chromaffin cells function as modified postganglionic sympathetic neurons but release catecholamines into the bloodstream instead of synapses. They are stimulated by acetylcholine from preganglionic fibers. Sensory neurons and interneurons have no such endocrine role. Therefore, the correct answer is Postganglionic sympathetic neurons. Their hormonal output provides widespread sympathetic activation.
4. A patient with pheochromocytoma has elevated blood catecholamines due to a tumor in the:
A) Adrenal cortex
B) Adrenal medulla
C) Pancreas
D) Thyroid
Explanation:
Pheochromocytoma originates from chromaffin cells of the adrenal medulla, causing excess secretion of epinephrine and norepinephrine. The adrenal cortex secretes steroid hormones, pancreas secretes insulin/glucagon, and thyroid produces T3/T4. Thus, the correct answer is Adrenal medulla. Symptoms include episodic hypertension, sweating, and tachycardia.
5. Which receptor mediates epinephrine-induced vasodilation in skeletal muscle?
A) α1 receptor
B) β2 receptor
C) β1 receptor
D) M3 receptor
Explanation:
Epinephrine activates β2 receptors in skeletal muscle vessels, causing vasodilation and enhancing blood flow during stress. α1 receptors cause vasoconstriction, β1 receptors act on the heart, and M3 receptors mediate parasympathetic effects. Therefore, the correct answer is β2 receptor. This selective dilation supports increased muscular activity.
6. Preganglionic sympathetic fibers release:
A) Norepinephrine
B) Acetylcholine
C) Dopamine
D) Epinephrine
Explanation:
All preganglionic sympathetic fibers are cholinergic, releasing acetylcholine at nicotinic receptors. Norepinephrine is mostly released by postganglionic fibers except in sweat glands. Dopamine and epinephrine are not synaptic transmitters here. Thus, the correct answer is Acetylcholine. This cholinergic activation includes stimulation of adrenal medulla.
7. A patient with sympathetic overactivity shows tachycardia and sweating. Sweating is mediated by:
A) Adrenergic fibers
B) Cholinergic sympathetic fibers
C) Parasympathetic fibers
D) Hormonal epinephrine only
Explanation:
Sweat glands are an exception in sympathetic system—they are innervated by cholinergic sympathetic postganglionic fibers acting on muscarinic receptors. Most other sympathetic targets are adrenergic. Parasympathetic pathways do not innervate sweat glands. Therefore, the correct answer is Cholinergic sympathetic fibers. This arrangement helps thermoregulation during stress.
8. Which enzyme is necessary for conversion of norepinephrine to epinephrine in adrenal medulla?
A) MAO
B) COMT
C) PNMT
D) Tyrosine hydroxylase
Explanation:
Phenylethanolamine N-methyltransferase (PNMT) converts norepinephrine to epinephrine and is highly expressed in adrenal medulla under cortisol influence. MAO and COMT degrade catecholamines; tyrosine hydroxylase is required earlier in synthesis. Thus, the correct answer is PNMT. This enzyme drives high epinephrine output.
9. Sympathetic stimulation increases blood glucose by:
A) Decreasing glucagon
B) Increasing glycogenolysis
C) Blocking lipolysis
D) Increasing insulin secretion
Explanation:
Catecholamines from adrenal medulla stimulate β receptors to increase glycogenolysis and lipolysis, raising blood glucose during stress. Insulin secretion decreases via α2 receptors. Thus, the correct answer is Increasing glycogenolysis. This ensures fuel availability for fight-or-flight activity.
10. Loss of adrenal medulla function leads to impaired response to:
A) Standing from sitting
B) Acute stress
C) Digestion
D) Vision adaptation
Explanation:
Without adrenal medullary catecholamines, the body cannot mount a full fight-or-flight response, reducing ability to handle acute stress. Standing reflex involves noradrenergic neurons, digestion is parasympathetic, and vision adaptation is unrelated. Therefore, the correct answer is Acute stress. Patients may show poor tolerance to sudden emergencies.
11. Adrenal medulla is embryologically derived from:
A) Endoderm
B) Mesoderm
C) Neural crest cells
D) Neural tube
Explanation:
Chromaffin cells of adrenal medulla originate from neural crest cells, similar to sympathetic postganglionic neurons. Cortex comes from mesoderm. Neural tube forms CNS neurons. Therefore, the correct answer is Neural crest cells. This explains its similarity to sympathetic ganglia.
Chapter: Autonomic Nervous System; Topic: Sympathetic vs Parasympathetic Distribution; Subtopic: Organs with Only Sympathetic Innervation
KEYWORD DEFINITIONS
• Sympathetic system – Mediates fight-or-flight responses
• Parasympathetic system – Mediates rest-and-digest functions
• Skin – Receives sympathetic supply only (sweat glands, piloerector muscles, blood vessels)
• Sweat glands – Activated by cholinergic sympathetic fibers
• Vasoconstriction – Sympathetic control of cutaneous vessels
Lead Question – 2015
1. Which of the following has direct innervation from sympathetic system but no parasympathetic supply?
A) Heart
B) Intestine
C) Skin
D) None
Explanation:
The skin receives only sympathetic innervation, which controls sweat glands, vasoconstriction, and piloerection. Parasympathetic fibers do not supply the skin. In contrast, the heart and intestines have both sympathetic and parasympathetic innervation. Thus, structures like cutaneous blood vessels, sweat glands, and hair follicles are under exclusive sympathetic control. Therefore, the correct answer is Skin. This unique distribution enables rapid thermoregulatory and stress-related responses via sympathetic activation.
2. Sweat glands are innervated by:
A) Adrenergic sympathetic fibers
B) Cholinergic sympathetic fibers
C) Parasympathetic fibers
D) Sensory fibers
Explanation:
Sweat glands are supplied by an exceptional type of sympathetic postganglionic fiber that is cholinergic and acts on muscarinic receptors. Parasympathetic fibers do not innervate sweat glands. Sensory fibers do not control sweating. Therefore, the correct answer is Cholinergic sympathetic fibers. This mechanism supports thermoregulation during heat stress.
3. Which structure lacks parasympathetic innervation?
A) Lacrimal gland
B) Bronchi
C) Skin blood vessels
D) Salivary glands
Explanation:
Blood vessels of the skin do not receive parasympathetic supply and are controlled only by sympathetic vasoconstrictor fibers. Lacrimal, bronchial, and salivary glands are all supplied by parasympathetic fibers. Therefore, the correct answer is Skin blood vessels. This exclusive sympathetic control helps regulate body temperature and peripheral resistance.
4. A patient with sympathetic overactivity presents with excessive sweating. The hyperactivity is due to stimulation of:
A) Adrenergic α receptors
B) Muscarinic receptors
C) GABA receptors
D) Dopamine receptors
Explanation:
Sweating is mediated by cholinergic sympathetic fibers that act on muscarinic receptors. Adrenergic fibers regulate vasomotor tone but not sweating. GABA and dopamine receptors have no role in sweat gland activation. Hence, the correct answer is Muscarinic receptors. This makes sweating an unusual sympathetic cholinergic response.
5. Piloerection (goosebumps) occurs due to activation of:
A) Parasympathetic fibers
B) Sympathetic fibers
C) Somatic motor fibers
D) Enteric nervous system
Explanation:
Piloerection is produced by contraction of arrector pili muscles, which are innervated exclusively by sympathetic fibers. Parasympathetic fibers do not innervate skin structures. Somatic motor fibers do not reach these muscles. Therefore, the correct answer is Sympathetic fibers. This reaction is associated with emotional stress and cold exposure.
6. Which organ receives both sympathetic and parasympathetic supply?
A) Sweat glands
B) Blood vessels of skin
C) Heart
D) Hair follicles
Explanation:
The heart receives both sympathetic and parasympathetic innervation, allowing dual modulation of rate and contractility. Sweat glands, cutaneous vessels, and hair follicles receive only sympathetic supply. Therefore, the correct answer is Heart. This dual innervation provides balance between fight-or-flight and rest-and-digest states.
7. A comatose patient has warm, flushed skin due to loss of sympathetic tone. Which vessel type is affected?
A) Coronary arteries
B) Cutaneous blood vessels
C) Renal blood vessels
D) Pulmonary veins
Explanation:
Cutaneous blood vessels are exclusively sympathetically innervated. Loss of sympathetic tone results in vasodilation, causing warm and flushed skin. Coronary, renal, and pulmonary vessels are regulated differently and not under exclusive sympathetic control. Thus, the correct answer is Cutaneous blood vessels. This illustrates the importance of sympathetic activity in thermoregulation.
8. Which neurotransmitter is released by sympathetic fibers supplying sweat glands?
A) Norepinephrine
B) Acetylcholine
C) Epinephrine
D) Dopamine
Explanation:
Sweat glands receive cholinergic sympathetic fibers that release acetylcholine at muscarinic receptors. This is a major exception in sympathetic physiology. Norepinephrine and epinephrine are involved in other sympathetic functions but not sweating. Therefore, the correct answer is Acetylcholine. This explains paradoxical sweating even when adrenergic function is impaired.
9. Which of the following tissues has purely sympathetic vasoconstrictor control?
A) Brain
B) Heart
C) Skin
D) Liver
Explanation:
Skin blood vessels receive only sympathetic vasoconstrictor innervation with no parasympathetic influence. Brain and heart have tightly regulated local mechanisms, and liver vasculature is influenced by multiple autonomic inputs. Therefore, the correct answer is Skin. This allows rapid redistribution of blood during shock and stress.
10. During fear, skin becomes pale due to:
A) Parasympathetic activation
B) Sympathetic vasoconstriction
C) Muscarinic inhibition
D) Sweat gland paralysis
Explanation:
Sympathetic stimulation causes vasoconstriction of cutaneous vessels, reducing blood flow and producing pallor. Parasympathetic activation produces no effect on skin. Muscarinic inhibition and sweat paralysis do not explain the color change. Therefore, the correct answer is Sympathetic vasoconstriction. This physiological response prioritizes blood flow to essential organs.
11. The sympathetic nervous system increases heat loss through which mechanism?
A) Parasympathetic vasodilation
B) Sympathetic vasodilation in skin
C) Sympathetic sweating
D) Enteric reflexes
Explanation:
Sympathetic stimulation of sweat glands enhances evaporative heat loss. Vasodilation in skin is primarily a passive loss of sympathetic tone, not parasympathetic action. Enteric reflexes are unrelated. Thus, the correct answer is Sympathetic sweating. Sweat evaporation is the most effective cooling mechanism in humans.
Chapter: Neurophysiology; Topic: Peripheral Nerve Injury; Subtopic: Seddon Classification – Neuropraxia
KEYWORD DEFINITIONS
• Neuropraxia – Temporary conduction block without structural nerve damage
• Axonotmesis – Axonal damage with intact connective tissue
• Neurotmesis – Complete nerve disruption including connective tissue
• Endoneurium – Innermost protective nerve layer around individual axons
• Epineurium – Outermost connective tissue sheath of a peripheral nerve
Lead Question – 2015
1. Neuropraxia is?
A) Damage to axon
B) Damage to endoneurium
C) Damage to epineurium
D) No structural damage
Explanation:
Neuropraxia is the mildest form of nerve injury in Seddon’s classification. It involves a temporary block in nerve conduction without any structural damage to the axon or the surrounding connective tissue layers. Recovery is complete and usually rapid once the compressive or ischemic cause is removed. There is no Wallerian degeneration, distinguishing it from axonotmesis and neurotmesis. Therefore, the correct answer is No structural damage. Common causes include mild compression, pressure palsies, and transient ischemia.
2. Axonotmesis is characterized by:
A) No structural damage
B) Axonal damage with intact connective tissue
C) Complete nerve transection
D) Epineurial rupture
Explanation:
Axonotmesis involves disruption of the axon with intact endoneurial and epineurial sheaths, allowing guided regeneration. Wallerian degeneration occurs distal to injury. Neuropraxia has no structural injury, while neurotmesis involves complete nerve rupture. Thus, the correct answer is Axonal damage with intact connective tissue. Recovery may take months depending on regeneration speed.
3. Neurotmesis leads to:
A) Full recovery without intervention
B) Complete nerve disruption
C) Temporary conduction block
D) No Wallerian degeneration
Explanation:
Neurotmesis is the most severe nerve injury with complete disruption of axon and supporting structures. Wallerian degeneration occurs distally, and spontaneous recovery is unlikely without surgical repair. Neuropraxia causes conduction block only, and axonotmesis retains connective tissue scaffolding. Therefore, the correct answer is Complete nerve disruption. Prognosis is poor without repair.
4. A patient with wrist drop after sleeping on arm overnight likely has:
A) Neurotmesis
B) Axonotmesis
C) Neuropraxia
D) Endoneurial tear
Explanation:
Prolonged external compression of the radial nerve, such as “Saturday night palsy,” causes transient conduction block consistent with neuropraxia. Recovery occurs in days to weeks as no structural damage exists. Neurotmesis or axonotmesis would produce prolonged deficits. Thus, the correct answer is Neuropraxia. This highlights the reversible nature of mild compressive injuries.
5. Wallerian degeneration occurs in which type of nerve injury?
A) Neuropraxia
B) Axonotmesis
C) None
D) Neuropraxia and neurotmesis both
Explanation:
Wallerian degeneration occurs when axons are damaged, as in axonotmesis and neurotmesis. It does not occur in neuropraxia because the axon remains intact. Therefore, the correct answer is Axonotmesis. This process clears distal debris and allows regeneration guided by connective tissue sheaths.
6. Which protective layer surrounds individual nerve fibers?
A) Epineurium
B) Perineurium
C) Endoneurium
D) Sarcolemma
Explanation:
The endoneurium surrounds individual axons within a nerve. The perineurium encloses fascicles, and the epineurium wraps the entire nerve. Sarcolemma surrounds muscle fibers, not nerves. Thus, the correct answer is Endoneurium. These layers are crucial for structural integrity and regeneration pathways.
7. A mild ulnar nerve injury with full recovery in 2 weeks indicates:
A) Neurotmesis
B) Partial transection
C) Neuropraxia
D) Axonotmesis
Explanation:
Rapid and complete recovery within a short period indicates neuropraxia, meaning conduction block without structural injury. Axonotmesis requires axonal regeneration and takes months, while neurotmesis involves severe disruption. Therefore, the correct answer is Neuropraxia. Compression injuries at the elbow often present this way.
8. In neuropraxia, motor and sensory loss occurs because:
A) Axon is destroyed
B) Myelin compression blocks conduction
C) Endoneurium ruptures
D) Nerve is transected
Explanation:
Neuropraxia is caused by localized myelin compression or ischemia that temporarily blocks nerve conduction without damaging axons. Thus, motor and sensory deficits occur but recover fully. Endoneurium rupture and nerve transection correspond to more severe injuries. The correct answer is Myelin compression blocks conduction. This explains the reversible nature of neuropraxia.
9. Best investigation to assess peripheral nerve injury severity:
A) EEG
B) Nerve conduction study
C) PET scan
D) X-ray
Explanation:
Nerve conduction studies differentiate between neuropraxia (conduction block), axonotmesis (reduced amplitude), and neurotmesis (absent conduction). EEG, PET, and X-ray are unsuitable for peripheral nerve assessment. Therefore, the correct answer is Nerve conduction study. It provides functional insight into nerve integrity.
10. Recovery in axonotmesis occurs due to:
A) Axonal regeneration along intact sheaths
B) Immediate reconnection
C) CNS plasticity
D) Increased myelination only
Explanation:
In axonotmesis, axonal regrowth occurs along preserved endoneurial tubes at ~1–3 mm/day. Immediate reconnection does not occur, and CNS plasticity is limited to central pathways. Myelination alone cannot restore lost axons. Therefore, correct answer is Axonal regeneration along intact sheaths. This anatomical preservation allows partial to full recovery.
11. A clean laceration of the median nerve with complete loss of function suggests:
A) Neuropraxia
B) Axonotmesis
C) Neurotmesis
D) Branch block only
Explanation:
A complete nerve laceration disrupts axons and connective layers, representing neurotmesis. Spontaneous recovery is unlikely without surgical repair. Neuropraxia shows no structural damage, and axonotmesis preserves connective sheaths. Therefore, the correct answer is Neurotmesis. Early repair improves outcomes.
Chapter: Cell Physiology; Topic: Membrane Potentials; Subtopic: Resting Membrane Potential in Smooth Muscle
KEYWORD DEFINITIONS
• Resting membrane potential (RMP) – Electrical potential difference across cell membrane at rest
• Smooth muscle – Involuntary muscle with unstable RMP
• Ion permeability – Determines RMP based on K⁺, Na⁺, and Cl⁻ conductance
• Slow waves – Rhythmic oscillations in smooth muscle membrane potential
• Depolarization – Shift of membrane potential toward positivity
Lead Question – 2015
1. RMP in smooth muscles?
A) -90 mV
B) -70 mV
C) -150 mV
D) -40 mV
Explanation:
Smooth muscle cells have a less negative resting membrane potential compared to skeletal muscle and neurons. Their RMP typically ranges from –40 mV to –60 mV, depending on tissue type and ionic conductance. This relatively depolarized baseline allows spontaneous rhythmic activity and slow wave generation. Skeletal muscle has an RMP near –90 mV, cardiac muscle around –85 mV, and neurons approximately –70 mV. Therefore, the correct answer is –40 mV. This makes smooth muscle highly responsive to neural and hormonal inputs.
2. Typical RMP of skeletal muscle is:
A) –40 mV
B) –55 mV
C) –90 mV
D) –30 mV
Explanation:
Skeletal muscle fibers maintain a highly negative RMP of about –90 mV due to high potassium permeability and large inwardly rectifying K⁺ currents. This stabilizes the membrane and prevents spontaneous contractions. Values like –40 mV or –55 mV represent smooth muscle or neurons, not skeletal muscle. Therefore, the correct answer is –90 mV. This helps maintain excitability and proper neuromuscular function.
3. A patient with hypokalemia shows hyperpolarized smooth muscle cells. Reason?
A) Increased Na⁺ influx
B) Decreased K⁺ efflux
C) Increased K⁺ gradient across membrane
D) Reduced Cl⁻ permeability
Explanation:
Hypokalemia increases the electrochemical gradient for K⁺, leading to increased efflux and a more negative RMP (hyperpolarization). Smooth muscle becomes less excitable. Na⁺ influx and Cl⁻ permeability changes are not primary determinants here. Therefore, the correct answer is Increased K⁺ gradient across membrane. This may reduce gut motility and vascular tone.
4. RMP of neurons is closest to:
A) –70 mV
B) –30 mV
C) –10 mV
D) +10 mV
Explanation:
Neuronal RMP is typically around –70 mV, determined mainly by high K⁺ permeability and fewer Na⁺ leak channels. Depolarized values like –30 mV or –10 mV are abnormal, while positive membrane potentials occur only during action potentials. Thus, the correct answer is –70 mV. This baseline is essential for rapid signal conduction.
5. Depolarization of smooth muscle is primarily caused by influx of:
A) Na⁺ only
B) Ca²⁺
C) Cl⁻
D) HCO₃⁻
Explanation:
Smooth muscle action potentials rely heavily on Ca²⁺ influx through voltage-gated channels rather than Na⁺ influx, as in neurons. Ca²⁺ entry triggers contraction and depolarization. Cl⁻ and bicarbonate do not initiate depolarization. Thus, the correct answer is Ca²⁺. This mechanism links electrical and mechanical activity.
6. A 55-year-old patient with GI hypomotility likely has smooth muscle that is:
A) Depolarized excessively
B) Hyperpolarized
C) Firing continuous action potentials
D) In refractory period
Explanation:
Hyperpolarization makes smooth muscle less excitable, reducing contractile activity and contributing to hypomotility. Excessive depolarization or continuous firing would cause hypermotility, not hypomotility. Refractory periods are brief and cannot explain persistent reduction. Therefore, the correct answer is Hyperpolarized. This state decreases GI peristalsis.
7. Which ion is mainly responsible for maintaining RMP in all excitable tissues?
A) Na⁺
B) Ca²⁺
C) K⁺
D) Mg²⁺
Explanation:
Potassium (K⁺) is the major determinant of RMP due to high membrane permeability and its equilibrium potential. Na⁺ and Ca²⁺ contribute minimally at rest, while Mg²⁺ has little direct role. Therefore, the correct answer is K⁺. Alterations in K⁺ levels strongly influence excitability across tissues.
8. Smooth muscle shows slow waves because of:
A) Pacemaker interstitial cells of Cajal
B) Skeletal motor neurons
C) High frequency Na⁺ channels
D) Increased myelin thickness
Explanation:
Slow wave rhythms originate from interstitial cells of Cajal (ICC), which act as pacemakers in the GI tract. They generate rhythmic oscillations that modulate smooth muscle excitability. Skeletal neurons, Na⁺ channels, and myelin do not mediate slow waves. Thus, the correct answer is Pacemaker interstitial cells of Cajal. This mechanism coordinates peristalsis.
9. Smooth muscle contraction is primarily triggered by Ca²⁺ binding to:
A) Troponin C
B) Calmodulin
C) Tropomyosin
D) Myosin light chain phosphatase
Explanation:
Smooth muscle contraction begins when Ca²⁺ binds to calmodulin, forming a complex that activates myosin light chain kinase (MLCK). Unlike skeletal muscle, smooth muscle lacks troponin. Tropomyosin has a structural role but not regulatory. Therefore, the correct answer is Calmodulin. This pathway enables sustained contractions with low energy use.
10. A hypertensive patient’s arterioles show increased smooth muscle tone due to:
A) Depolarization of RMP
B) Hyperpolarization of RMP
C) Reduced Ca²⁺ entry
D) Increased K⁺ efflux
Explanation:
Depolarization brings the membrane closer to threshold and increases Ca²⁺ entry, leading to elevated smooth muscle tone and vasoconstriction. Hyperpolarization, reduced calcium entry, or increased K⁺ efflux would decrease tone. Thus, the correct answer is Depolarization of RMP. This contributes significantly to increased peripheral resistance.
11. Which of the following smooth muscles has the most unstable RMP?
A) Vascular smooth muscle
B) GI smooth muscle
C) Iris sphincter muscle
D) Bronchiolar smooth muscle
Explanation:
GI smooth muscle exhibits highly unstable RMP due to pacemaker activity from ICC, producing rhythmic slow waves. Vascular, iris, and bronchiolar muscles have more stable potentials. Therefore, the correct answer is GI smooth muscle. This instability is essential for coordinated motility patterns.