Chapter: Central Nervous System
Topic: Sensory Pathways
Subtopic: Dorsal Root Ganglion (DRG) Neurons
Keywords
- Dorsal root ganglion (DRG): Cluster of primary sensory neuron cell bodies in intervertebral foramina.
- Pseudounipolar neuron: Single process bifurcating into peripheral and central branches; soma is not in the conduction path.
- Satellite (capsular) cells: Glia enveloping DRG neuronal soma, providing metabolic support.
- Neural crest: Embryologic origin of DRG neurons and satellite cells/Schwann cells.
- Lipofuscin: Yellow-brown wear-and-tear pigment accumulating with age in long-lived neurons.
- Nissl substance: Rough endoplasmic reticulum in neuronal soma/dendrites; disperses during chromatolysis.
- T-junction: DRG axonal bifurcation reducing ectopic transmission; important in sensory signaling.
- Aδ and C fibers: Small-diameter nociceptive fibers with somata in DRG (sharp and dull pain).
- Herpes zoster: Varicella-zoster virus latency/reactivation in DRG causing dermatomal rash and pain.
- Autonomic ganglion: Multipolar neurons with synapses; contrasts with DRG which lacks intraganglionic synapses.
Lead Question – 2012
All the following features are seen in neurons from dorsal root ganglia, EXCEPT:
a) They are multipolar
b) They contain lipofuscin granules
c) They have centrally located nuclei
d) They are derived from neural crest cells
Explanation: DRG neurons are characteristically pseudounipolar (not multipolar), with large round soma, centrally located nuclei, prominent nucleoli, frequent lipofuscin, and neural crest origin. They lack synapses within the ganglion and are wrapped by satellite cells. Therefore, the false statement is a) They are multipolar.
Guessed Questions
1) The typical morphological type of a DRG neuron is:
a) Multipolar
b) Bipolar
c) Pseudounipolar
d) Pyramidal
Explanation: Primary sensory neurons in DRG are pseudounipolar with a single process that splits into peripheral and central branches at a T-junction. This design allows rapid transmission without synapsing on the soma. Correct answer: c) Pseudounipolar. Multipolar neurons are characteristic of autonomic ganglia and many CNS nuclei.
2) The glial cells that directly envelope DRG neuronal somata are:
a) Oligodendrocytes
b) Astrocytes
c) Satellite (capsular) cells
d) Microglia
Explanation: Satellite (capsular) cells form a continuous sheath around DRG neuronal soma, regulating the microenvironment and participating in pain modulation. Oligodendrocytes myelinate CNS axons, while Schwann cells (not listed) myelinate PNS axons. Correct answer: c) Satellite (capsular) cells.
3) A biopsy from a paraspinal ganglion shows large neurons with central nuclei, Nissl substance, lipofuscin, and no synapses between neurons. The structure is:
a) Sympathetic chain ganglion
b) Dorsal root ganglion
c) Ciliary ganglion
d) Enteric plexus
Explanation: Lack of intraganglionic synapses with centrally placed nuclei favors DRG. Autonomic ganglia (sympathetic/parasympathetic) contain multipolar neurons receiving synapses. DRG neurons are sensory and pseudounipolar. Correct answer: b) Dorsal root ganglion.
4) Embryologic origin of DRG neurons is:
a) Neural tube
b) Notochord
c) Neural crest
d) Mesoderm
Explanation: DRG neurons, Schwann cells, and satellite cells arise from neural crest, which migrates from the dorsal neural tube to form peripheral sensory ganglia. The neural tube forms CNS neurons and glia. Correct answer: c) Neural crest.
5) After transection of a peripheral branch of a DRG neuron, the soma shows chromatolysis. Which change is most typical?
a) Nuclear hyperchromasia and centralization
b) Nissl dispersal with eccentric nucleus and cell body swelling
c) Condensed Nissl with shrunken soma
d) Apoptotic bodies immediately
Explanation: Chromatolysis features dissolution of Nissl substance, cell body swelling, and eccentric displacement of the nucleus due to upregulated protein synthesis for axonal repair. Correct answer: b) Nissl dispersal with eccentric nucleus and cell body swelling.
6) Sharp, well-localized first pain from a pinprick is carried by fibers whose cell bodies lie in the DRG. These fibers are:
a) Aβ fibers
b) Aδ fibers
c) C fibers
d) Ia spindle afferents
Explanation: Aδ fibers are small, thinly myelinated afferents mediating fast, sharp pain and cold. Their somata reside in DRG. C fibers mediate slow, dull pain; Aβ carry touch/vibration; Ia are muscle spindle afferents. Correct answer: b) Aδ fibers.
7) A 65-year-old with dermatomal vesicular rash and burning pain over T6 likely has reactivation of varicella-zoster virus in the:
a) Ventral horn
b) Dorsal root ganglion
c) Sympathetic chain ganglion
d) Spinal cord dorsal column
Explanation: Herpes zoster lies dormant in DRG neurons and reactivates to cause dermatomal neuritis and rash. This localizes to the sensory ganglion at the affected level. Correct answer: b) Dorsal root ganglion.
8) Myelination of the peripheral process of a DRG neuron is performed by:
a) Oligodendrocytes
b) Schwann cells
c) Astrocytes
d) Microglia
Explanation: In the peripheral nervous system, Schwann cells myelinate individual axonal internodes, including the peripheral branch of DRG neurons. Oligodendrocytes myelinate CNS axons (multiple internodes). Correct answer: b) Schwann cells.
9) Functionally, the DRG neuron’s soma primarily:
a) Actively conducts action potentials
b) Serves trophic and metabolic roles while the impulse bypasses the soma
c) Generates synaptic potentials with neighboring DRG neurons
d) Integrates dendritic inputs from spinal interneurons
Explanation: In pseudounipolar neurons, the action potential travels from peripheral to central process across a T-junction, largely bypassing the soma. The soma provides metabolic support; DRG lacks interneuronal synapses. Correct answer: b) Serves trophic and metabolic roles….
10) Which feature best distinguishes a sympathetic ganglion from a DRG histologically?
a) Presence of satellite cells
b) Multipolar neurons receiving synapses within the ganglion
c) Central nuclei in neurons
d) Lipofuscin granules
Explanation: Autonomic (sympathetic) ganglia contain multipolar neurons receiving preganglionic synapses; DRG neurons are pseudounipolar with no intraganglionic synapses. Both have satellite cells and may show lipofuscin. Nuclei are often eccentric in autonomic ganglia. Correct answer: b) Multipolar neurons receiving synapses within the ganglion.
11) A patient with radicular pain from L5 nerve root compression has primary sensory neuron cell bodies located in the:
a) Dorsal horn lamina II
b) Dorsal root ganglion at L5
c) Ventral root
d) Sympathetic chain at L5
Explanation: Primary sensory neuron somata reside in the DRG at the corresponding spinal level (here, L5). Their central processes enter the dorsal root to synapse in dorsal horn or ascend in dorsal columns. Correct answer: b) Dorsal root ganglion at L5.
Chapter: Autonomic Nervous System | Topic: Peripheral Autonomic Ganglia | Subtopic: Sympathetic Ganglia
Keywords
Sympathetic ganglia — clusters of postganglionic neuronal cell bodies in the sympathetic chain and prevertebral plexuses.
Multipolar neuron — neuron with one axon and multiple dendrites; typical of autonomic ganglia.
Preganglionic fiber — myelinated B fiber from thoracolumbar spinal cord that synapses in ganglia.
Postganglionic fiber — unmyelinated C fiber projecting to effector organs.
Neurotransmitters — acetylcholine (preganglionic); norepinephrine (postganglionic) for most sympathetic targets.
Paravertebral chain — bilateral sympathetic trunk alongside vertebral column.
Prevertebral ganglia — celiac, superior and inferior mesenteric ganglia supplying abdominal viscera.
Visceral reflexes — autonomic reflex arcs involving pre- and postganglionic neurons.
Chromaffin cells — adrenal medulla cells acting like sympathetic postganglionic neurons (release catecholamines into blood).
Autonomic dysreflexia — exaggerated sympathetic response seen with high spinal cord injury.
Lead Question - 2012
Neurons in sympathetic ganglia are ?
a) Unipolar
b) Bipolar
c) Pseudounipolar
d) Multipolar
Explanation: Sympathetic (autonomic) ganglia contain multipolar neurons with several dendrites and a single axon that receive preganglionic cholinergic input. These neurons form synapses within the ganglion and project postganglionic fibers to effectors. Therefore the correct answer is d) Multipolar.
Q1. Preganglionic sympathetic fibers originate from which spinal segments?
a) Cervical only
b) Thoracolumbar (T1–L2)
c) Sacral only
d) Craniosacral
Explanation: Preganglionic sympathetic neurons arise from the intermediolateral cell column of the spinal cord segments T1–L2 (thoracolumbar outflow). These fibers synapse in paravertebral or prevertebral ganglia. Correct answer: b) Thoracolumbar (T1–L2).
Q2. Postganglionic sympathetic fibers predominantly release which neurotransmitter at effector organs?
a) Acetylcholine
b) Norepinephrine
c) Dopamine
d) GABA
Explanation: Most sympathetic postganglionic neurons release norepinephrine acting on α and β receptors at target organs. Exceptions include sweat glands (sympathetic cholinergic) and adrenal medulla (releases epinephrine/norepinephrine into blood). Correct answer: b) Norepinephrine.
Q3. Which ganglia form the sympathetic chain alongside the vertebral column?
a) Paravertebral ganglia
b) Prevertebral ganglia
c) Dorsal root ganglia
d) Cranial parasympathetic ganglia
Explanation: Paravertebral (sympathetic chain) ganglia lie bilaterally along the vertebral column and connect segmentally. They mediate sympathetic distribution to body wall and limbs. Prevertebral ganglia are anterior near abdominal vessels. Correct answer: a) Paravertebral ganglia.
Q4. The adrenal medulla acts like a sympathetic ganglion because its chromaffin cells:
a) Are derived from neural crest and release catecholamines into blood
b) Contain multipolar neurons with axons
c) Release acetylcholine at distant organs
d) Form synapses with skeletal muscle
Explanation: Adrenal medullary chromaffin cells are neural-crest-derived and respond to preganglionic cholinergic input by secreting epinephrine and norepinephrine into the circulation, functioning as endocrine equivalents of postganglionic sympathetic neurons. Correct answer: a).
Q5. Which of the following is a feature of sympathetic ganglia histology?
a) Presence of synaptic boutons between ganglionic neurons
b) Pseudounipolar neuronal soma
c) No satellite cells
d) Myelinated postganglionic fibers only
Explanation: Sympathetic ganglia display multipolar neuronal somata receiving preganglionic synapses; satellite cells are present. Postganglionic fibers are typically unmyelinated. The distinguishing feature is intraganglionic synapses; correct answer: a) Presence of synaptic boutons between ganglionic neurons.
Q6. A lesion of the sympathetic chain at T1 (Horner’s syndrome) causes which features ipsilaterally?
a) Ptosis, miosis, anhidrosis
b) Mydriasis and hyperhidrosis
c) Flaccid paralysis
d) Loss of taste
Explanation: Interruption of sympathetic outflow to the face produces Horner’s syndrome: ipsilateral ptosis (levator palpebrae dysfunction), miosis (unopposed parasympathetic), and anhidrosis. Correct answer: a) Ptosis, miosis, anhidrosis.
Q7. Which embryologic origin is shared by sympathetic ganglion neurons?
a) Neural tube
b) Neural crest
c) Endoderm
d) Mesoderm
Explanation: Sympathetic ganglion neurons originate from migrating neural crest cells that differentiate into peripheral neurons and glia. Neural tube gives rise to CNS structures. Correct answer: b) Neural crest.
Q8. Which receptor type predominates on vascular smooth muscle mediating sympathetic vasoconstriction?
a) β1-adrenergic
b) α1-adrenergic
c) Muscarinic M2
d) Nicotinic
Explanation: Sympathetic vasoconstriction is mediated mainly by norepinephrine acting on α1-adrenergic receptors on vascular smooth muscle, causing increased intracellular calcium and contraction. Correct answer: b) α1-adrenergic.
Q9. Which pharmacologic agent blocks transmission at autonomic ganglia (both sympathetic and parasympathetic)?
a) Atropine
b) Hexamethonium
c) Propranolol
d) Phenylephrine
Explanation: Ganglionic blockers like hexamethonium antagonize nicotinic receptors at autonomic ganglia, interrupting both sympathetic and parasympathetic transmission. Atropine blocks muscarinic receptors at effector sites. Correct answer: b) Hexamethonium.
Q10. Which statement about sympathetic postganglionic fibers is correct?
a) They are myelinated and fast conducting
b) They are unmyelinated and form varicosities over targets
c) They synapse onto skeletal muscle endplates
d) They release GABA at target organs
Explanation: Postganglionic sympathetic fibers are typically thin, unmyelinated C fibers that form en passant varicosities along target tissues, releasing neurotransmitter diffusely. They do not innervate skeletal muscle motor endplates. Correct answer: b).
Q11. Which clinical condition results from excessive sympathetic activity causing sustained vasoconstriction?
a) Orthostatic hypotension
b) Raynaud’s phenomenon
c) Myasthenia gravis
d) Guillain–Barré syndrome
Explanation: Raynaud’s phenomenon involves exaggerated sympathetic-mediated vasoconstriction of digital arterioles in response to cold or stress, causing pallor and ischemia. Orthostatic hypotension is due to inadequate sympathetic compensation. Correct answer: b) Raynaud’s phenomenon.
Chapter: Central Nervous System | Topic: Visual Recognition | Subtopic: Face Perception & Agnosias
Keywords
Prosopagnosia — inability to recognize familiar faces despite intact vision.
Fusiform face area (FFA) — region in inferior temporal cortex specialized for face recognition.
Associative visual agnosia — failure to assign meaning to perceived objects despite intact perception.
Apperceptive agnosia — impaired object perception (shape/form) with intact elementary vision.
Right occipitotemporal cortex — often dominant for facial recognition tasks.
Visual associative cortex — links visual percepts to memory and meaning.
Alexia — loss of reading; can be visual-associative if cortex involved.
Topographic agnosia — inability to recognize familiar places/landmarks.
CFD (capgras) — delusional misidentification where face is recognized but person is believed to be impostor.
Face processing stream — ventral occipitotemporal pathway for object/face identification.
Lead Question - 2012
Pt. is able to recognise person by name but not by face. Lesion is in ?
a) Post parietal region
b) Occipital
c) Frontal lobe
d) Temporal lobe
Explanation: Inability to recognize faces (prosopagnosia) with preserved verbal identification indicates damage to the face-processing region — the fusiform face area in the inferior temporal (occipitotemporal) cortex, typically the right temporal lobe. Thus the correct answer is (d) Temporal lobe. This spares name retrieval via language networks.
Q2. Classic prosopagnosia most commonly results from lesion in which area?
a) Dorsal parietal cortex
b) Fusiform gyrus (inferior temporal)
c) Primary visual cortex (V1)
d) Broca’s area
Explanation: Acquired prosopagnosia typically follows lesions in the fusiform gyrus (inferior temporal/occipitotemporal region), especially on the right. The FFA processes holistic face information; damage disrupts face identity recognition while leaving basic vision and language intact. Correct answer: (b) Fusiform gyrus.
Q3. A patient sees an object but cannot name it though can describe its use. This suggests:
a) Apperceptive visual agnosia
b) Associative visual agnosia
c) Cortical blindness
d) Visual neglect
Explanation: Associative visual agnosia occurs when perceptual processing is adequate but the link to semantic knowledge is disrupted, so patients can describe object use but cannot name it. This localizes to higher-order ventral stream cortical areas. Correct answer: (b) Associative visual agnosia.
Q4. Which deficit indicates right occipitotemporal dysfunction rather than primary visual loss?
a) Hemianopia with macular sparing
b) Prosopagnosia with normal acuity
c) Complete blindness
d) Visual field neglect
Explanation: Prosopagnosia with preserved visual acuity and fields suggests cortical processing impairment in the right occipitotemporal region (FFA) rather than primary visual cortex damage. Hemianopia indicates V1 lesions; neglect implicates parietal cortex. Correct answer: (b).
Q5. Developmental (congenital) prosopagnosia is best characterized by:
a) Later-life stroke causing face blindness
b) Lifelong difficulty recognizing faces with normal IQ
c) Visual acuity loss from birth
d) Progressive dementia
Explanation: Developmental prosopagnosia presents from early life as a selective deficit in face recognition despite normal vision, intelligence, and no structural lesion. Patients rely on voice or context. Correct answer: (b). It reflects functional differences in face-processing networks.
Q6. Capgras syndrome differs from prosopagnosia because patients:
a) Cannot see faces
b) Recognize faces but believe they are impostors
c) Name faces accurately
d) Have primary visual loss
Explanation: In Capgras delusion, patients perceive faces and may name them but lack the normal affective familiarity, leading to belief that a known person is an impostor — a disconnection between recognition and emotional response. Correct answer: (b).
Q7. Which test best assesses prosopagnosia clinically?
a) Visual acuity chart
b) Benton Facial Recognition Test
c) Pupillary light reflex
d) Snellen chart
Explanation: The Benton Facial Recognition Test evaluates face perception and matching without requiring naming, useful to detect prosopagnosia. Visual acuity tests do not assess identity recognition. Correct answer: (b). Neuropsychological testing localizes processing deficits.
Q8. A lesion producing alexia without agraphia involves the visual word form area and typically spares:
a) Right inferior temporal lobe
b) Language output areas (e.g., Broca’s)
c) Primary visual cortex exclusively
d) Auditory comprehension
Explanation: Alexia without agraphia results from left occipitotemporal (visual word form area) lesions with intact language cortex, so patients can write but not read. It demonstrates modality-specific visual-associative deficits. Correct answer: (b).
Q9. Which hemisphere is more commonly dominant for face recognition in most right-handed people?
a) Left hemisphere
b) Right hemisphere
c) Both equally
d) Brainstem
Explanation: The right occipitotemporal region is typically dominant for holistic face processing in right-handed individuals; right-sided lesions more often produce prosopagnosia. Left-sided lesions can impair aspects of facial recognition but less commonly. Correct answer: (b) Right hemisphere.
Q10. Which rehabilitation strategy may help a patient with prosopagnosia?
a) Visual acuity correction only
b) Training to use non-face cues (voice, gait, context)
c) Surgical removal of fusiform gyrus
d) High-dose steroids
Explanation: Compensation training teaches reliance on non-facial cues (voice, clothing, context, unique features) to identify people, improving functioning despite persistent cortical deficit. There is no surgical or steroid cure for most acquired prosopagnosia. Correct answer: (b).
Q11. In a patient who recognizes names but not faces, which imaging finding is most likely?
a) Infarct in right inferior occipitotemporal cortex
b) Bilateral frontal lobe atrophy
c) Lesion of primary visual cortex
d) Left cerebellar infarct
Explanation: MRI showing a focal lesion or infarct in the right inferior occipitotemporal (fusiform) cortex fits classical acquired prosopagnosia with preserved language-based name recognition. Primary V1 lesions cause field defects, while frontal or cerebellar lesions produce different syndromes. Correct answer: (a).
Chapter: Central Nervous System Physiology
Topic: Cerebrospinal Fluid (CSF)
Subtopic: Biochemical Properties of CSF
Keyword Definitions:
• CSF: Clear fluid in brain and spinal cord providing cushioning and nutrient exchange.
• Plasma: Liquid component of blood carrying cells, proteins, and nutrients.
• CSF/Plasma Glucose Ratio: A diagnostic marker comparing CSF glucose levels to plasma glucose.
• Blood-Brain Barrier: Selective barrier regulating passage of substances into CSF.
• Meningitis: Inflammation of meninges often causing altered CSF glucose.
• Hypoglycorrhachia: Abnormally low CSF glucose, seen in infections and tumors.
• Hyperglycemia: High plasma glucose leading to proportionally higher CSF glucose.
• CSF Analysis: Laboratory test to evaluate neurological diseases.
Lead Question - 2012
CSF/plasma glucose ratio is ?
a) 0.2 - 0.4
b) 0.6 - 0.8
c) 1.2 - 1.6
d) 1.6 - 2.2
Explanation: The normal CSF/plasma glucose ratio is about 0.6 to 0.8. CSF glucose is typically two-thirds of plasma glucose. Reduced ratios occur in bacterial and TB meningitis, while viral meningitis usually maintains normal values. Answer: b) 0.6 - 0.8
--- Guessed Question 1
In bacterial meningitis, the CSF/plasma glucose ratio is usually:
a) Normal
b) Increased
c) Decreased
d) Unchanged
Explanation: Bacterial meningitis reduces CSF glucose due to bacterial metabolism. The CSF/plasma glucose ratio often falls below 0.4. This is a key diagnostic indicator. Answer: c) Decreased
--- Guessed Question 2
Which CSF finding is most suggestive of tuberculous meningitis?
a) Normal CSF glucose
b) CSF glucose ↓
c) CSF protein normal
d) No pleocytosis
Explanation: Tuberculous meningitis shows markedly reduced glucose, elevated proteins, and lymphocytic pleocytosis. This pattern helps distinguish it from viral meningitis. Answer: b) CSF glucose ↓
--- Guessed Question 3
A patient with viral meningitis is most likely to show which CSF/plasma glucose ratio?
a) 0.6 - 0.8
b) c) >1.0
d) 0.2
Explanation: Viral meningitis does not significantly affect CSF glucose, so the CSF/plasma ratio remains in the normal range of 0.6–0.8. Answer: a) 0.6 - 0.8
--- Guessed Question 4
Which condition most commonly causes low CSF glucose with elevated protein and lymphocytes?
a) Viral meningitis
b) Tuberculous meningitis
c) Subarachnoid hemorrhage
d) Normal pressure hydrocephalus
Explanation: Tuberculous meningitis typically presents with low glucose, high protein, and lymphocytic predominance. Answer: b) Tuberculous meningitis
--- Guessed Question 5
Increased CSF glucose compared to plasma is seen in:
a) Hyperglycemia
b) Hypoglycemia
c) Meningitis
d) None
Explanation: CSF glucose reflects plasma levels. In hyperglycemia, CSF glucose increases but more slowly, keeping the ratio near normal. Answer: a) Hyperglycemia
--- Guessed Question 6
CSF/plasma glucose ratio helps primarily in diagnosis of:
a) Epilepsy
b) Stroke
c) Meningitis
d) Brain tumor
Explanation: The ratio is mainly valuable in meningitis. Bacterial and TB meningitis reduce the ratio, while viral meningitis keeps it normal. Answer: c) Meningitis
--- Guessed Question 7
A lumbar puncture shows CSF glucose 20 mg/dl, plasma glucose 100 mg/dl. What is the CSF/plasma ratio?
a) 0.2
b) 0.5
c) 0.8
d) 1.2
Explanation: Ratio = 20/100 = 0.2, which is abnormally low. This strongly suggests bacterial or TB meningitis. Answer: a) 0.2
--- Guessed Question 8
In which condition is CSF glucose usually normal?
a) Viral meningitis
b) Bacterial meningitis
c) TB meningitis
d) Fungal meningitis
Explanation: Viral meningitis maintains normal CSF glucose, unlike bacterial, TB, or fungal meningitis which lower glucose levels. Answer: a) Viral meningitis
--- Guessed Question 9
Which barrier controls glucose entry into CSF?
a) Meninges
b) Blood-brain barrier
c) Pia mater
d) Dural venous sinuses
Explanation: The blood-brain barrier regulates glucose entry into CSF by selective transport, ensuring stable CSF composition. Answer: b) Blood-brain barrier
--- Guessed Question 10
A patient with suspected bacterial meningitis has a CSF/plasma ratio of 0.3. What additional CSF finding is expected?
a) Low protein
b) Neutrophilic pleocytosis
c) Eosinophilia
d) Normal cell count
Explanation: Bacterial meningitis typically shows low glucose, high protein, and neutrophilic pleocytosis. This triad is highly diagnostic. Answer: b) Neutrophilic pleocytosis
Chapter: Peripheral Nerve Physiology | Topic: Nociception & Pain Fibres | Subtopic: Sensory Fiber Types
Keywords
Peripheral nociceptors — sensory receptors that signal tissue-damaging stimuli.
Aδ fibres — thin myelinated fibres conducting fast sharp pain.
C fibres — small unmyelinated fibres conducting slow burning/dull pain.
Aβ fibres — large myelinated fibres for touch and vibration, not primary nociception.
Conduction velocity — speed of action potential propagation determined by diameter and myelination.
Spinothalamic tract — ascending pathway transmitting pain and temperature to thalamus.
Substance P / CGRP — neuropeptides released by nociceptors mediating pain and neurogenic inflammation.
Gate control theory — modulation of pain by non-nociceptive afferents at spinal level.
Central sensitization — heightened dorsal horn responsiveness after persistent nociceptive input.
Local anaesthetics — block sodium channels, preferentially affecting small diameter fibres first.
Lead Question - 2012
Burning pain is carried by which type of fibres ?
a) A alpha
b) A delta
c) A beta
d) C
Explanation: Burning, slow, poorly localized pain is typically transmitted by small unmyelinated C fibres that conduct at low velocity and carry polymodal nociceptive input. Aδ fibres convey fast sharp pain. Therefore the correct answer is d) C. C-fibre activity also mediates neurogenic inflammation via Substance P and CGRP.
Q1. Fast, well-localized sharp pain (first pain) is carried mainly by:
a) A alpha
b) A delta
c) C fibres
d) A beta
Explanation: First, sharp pain is mediated by thinly myelinated Aδ fibres that have higher conduction velocity than C fibres and project through the spinothalamic tract to somatosensory cortex, producing rapid, localized pain sensations. Hence the correct answer is b) A delta.
Q2. Which fibres primarily transmit touch and vibration?
a) A beta
b) C fibres
c) A delta
d) A gamma
Explanation: Large myelinated Aβ fibres carry discriminative touch, pressure, and vibration information via the dorsal column–medial lemniscal pathway. They are not primary nociceptors. Correct answer: a) A beta. Activation of Aβ fibres can modulate pain via gate control mechanisms in the dorsal horn.
Q3. Which ascending pathway carries pain and temperature to the brain?
a) Dorsal columns
b) Spinothalamic tract
c) Corticospinal tract
d) Spinocerebellar tract
Explanation: The anterolateral system, chiefly the spinothalamic tract, transmits nociceptive and thermoreceptive signals from spinal cord to thalamus and cortex. Dorsal columns carry vibration and proprioception. Correct answer: b) Spinothalamic tract.
Q4. Which neuropeptide released from nociceptors contributes to neurogenic inflammation?
a) GABA
b) Substance P
c) Dopamine
d) Serotonin
Explanation: Substance P and CGRP released from peripheral terminals of C fibres promote vasodilation, plasma extravasation, and immune cell recruitment, producing neurogenic inflammation and sensitization. This augments pain. Correct answer: b) Substance P.
Q5. Local anaesthetics block which channels to prevent nociception?
a) Calcium channels
b) Sodium channels
c) Potassium channels
d) Chloride channels
Explanation: Local anaesthetics inhibit voltage-gated sodium channels, preventing action potential initiation and propagation in sensory fibres. Small-diameter unmyelinated C and thin myelinated Aδ fibres are blocked preferentially, producing analgesia. Correct answer: b) Sodium channels.
Q6. Which clinical sign suggests small fibre (C/Aδ) neuropathy?
a) Loss of vibration sense
b) Burning distal pain with preserved reflexes
c) Pure motor weakness
d) Loss of proprioception
Explanation: Small-fibre neuropathy causes burning, shooting pain and dysesthesias in a distal stocking distribution with relatively preserved muscle strength and large-fibre modalities like vibration. Reflexes may be normal early. Correct answer: b) Burning distal pain with preserved reflexes.
Q7. Gate control theory proposes that activation of which fibres inhibits pain transmission?
a) C fibres
b) A beta fibres
c) A delta fibres
d) Sympathetic efferents
Explanation: Large-diameter Aβ fibres carrying touch input activate inhibitory interneurons in dorsal horn, reducing transmission from nociceptive Aδ/C fibres to projection neurons. This underlies analgesic effects of rubbing or TENS. Correct answer: b) A beta fibres.
Q8. Central sensitization results in which clinical phenomenon?
a) Hypoalgesia
b) Allodynia (pain to non-painful stimuli)
c) Loss of reflexes
d) Improved proprioception
Explanation: Persistent nociceptive input induces dorsal horn hyperexcitability and synaptic plasticity, producing allodynia and hyperalgesia where innocuous stimuli become painful. This is central sensitization seen in chronic pain syndromes. Correct answer: b) Allodynia.
Q9. Which fibre type has the slowest conduction velocity?
a) A alpha
b) A beta
c) A delta
d) C fibres
Explanation: Unmyelinated C fibres have the smallest diameter and slowest conduction velocity (~0.5–2 m/s), mediating slow burning pain and autonomic reflexes. Aα/Aβ are fastest. Correct answer: d) C fibres.
Q10. Which analgesic mechanism involves opioid receptors in the dorsal horn?
a) NSAID inhibition of COX
b) Activation of μ-opioid receptors reducing neurotransmitter release
c) Local anaesthetic sodium channel block
d) TRPV1 activation
Explanation: Opioids bind μ receptors on presynaptic nociceptive terminals and postsynaptic dorsal horn neurons, inhibiting substance P release and hyperpolarizing neurons, reducing pain transmission centrally. This is a principal mechanism for strong analgesics. Correct answer: b) Activation of μ-opioid receptors.
Chapter: Central Nervous System Physiology
Topic: Nerve Fibers and Conduction
Subtopic: Sensitivity to Pressure and Hypoxia
Keyword Definitions:
• Nerve Fibers: Axons classified based on diameter, conduction velocity, and function (A, B, C fibers).
• A Fibers: Large, myelinated fibers with rapid conduction, subdivided into alpha, beta, gamma, delta.
• B Fibers: Small, myelinated preganglionic autonomic fibers.
• C Fibers: Small, unmyelinated fibers, slow conduction, pain and temperature transmission.
• Hypoxia Sensitivity: Vulnerability of fibers to oxygen deprivation.
• Pressure Sensitivity: Susceptibility of fibers to mechanical compression.
• Neuropraxia: Temporary conduction block often due to compression.
• Paresthesia: Abnormal tingling or numb sensation due to nerve dysfunction.
Lead Question - 2012
A man slept with head over forearm, next morning he complains of tingling, numbness over forearm. It is caused by?
a) Sensitivity to hypoxia is A > B > C
b) Sensitivity to pressure is A > B > C
c) Sensitivity to hypoxia is C > B > A
d) Sensitivity to pressure is B > A > C
Explanation: Large myelinated A fibers are more susceptible to compression due to their size and myelin sheath. This explains temporary numbness or tingling after sleeping on a limb. Small unmyelinated C fibers are more resistant. Hence, sensitivity to pressure is A > B > C. Answer: b) Sensitivity to pressure is A > B > C
--- Guessed Question 1
Which nerve fibers are most sensitive to hypoxia?
a) A fibers
b) B fibers
c) C fibers
d) All equally
Explanation: Unmyelinated C fibers require continuous metabolic support and are highly sensitive to hypoxia. In oxygen deprivation, C fibers lose function first, causing early loss of pain and temperature sensation. Answer: c) C fibers
--- Guessed Question 2
Temporary conduction block without axonal damage due to compression is termed:
a) Axonotmesis
b) Neurotmesis
c) Neuropraxia
d) Wallerian degeneration
Explanation: Neuropraxia is a transient conduction block due to mechanical compression, as in the case of sleeping on an arm. Recovery is complete within days to weeks as no axonal damage occurs. Answer: c) Neuropraxia
--- Guessed Question 3
Which type of fibers mediate burning pain?
a) A alpha
b) A beta
c) A delta
d) C fibers
Explanation: Burning, dull, poorly localized pain is transmitted by unmyelinated C fibers. A delta fibers carry sharp, pricking pain. Thus, chronic tingling or burning after compression is mediated by C fibers. Answer: d) C fibers
--- Guessed Question 4
Which fibers are blocked earliest by local anesthetics?
a) A alpha
b) A delta
c) B fibers
d) C fibers
Explanation: Small, myelinated B fibers (preganglionic autonomic) are most sensitive to local anesthetics, followed by C fibers, then A delta, and lastly large motor A alpha fibers. Answer: c) B fibers
--- Guessed Question 5
Patient develops numbness after tight bandage. Most likely affected fibers are:
a) A fibers
b) B fibers
c) C fibers
d) None
Explanation: Mechanical compression preferentially affects large myelinated A fibers, leading to numbness and weakness. Unmyelinated C fibers remain relatively preserved. Answer: a) A fibers
--- Guessed Question 6
Which sensation is first affected during hypoxia?
a) Pain
b) Touch
c) Autonomic functions
d) Vibration
Explanation: Pain is mediated by C fibers, which are highly hypoxia-sensitive. Thus, pain sensation is often first impaired in hypoxic conditions. Answer: a) Pain
--- Guessed Question 7
Compression of radial nerve during deep sleep leads to:
a) Wrist drop
b) Foot drop
c) Claw hand
d) Facial palsy
Explanation: Radial nerve palsy due to compression in sleep ("Saturday night palsy") leads to weakness of wrist extensors, manifesting as wrist drop. Answer: a) Wrist drop
--- Guessed Question 8
Which nerve fiber type has the slowest conduction velocity?
a) A alpha
b) A beta
c) B fibers
d) C fibers
Explanation: Unmyelinated C fibers have the slowest conduction velocity (~0.5–2 m/s) compared to fast-conducting A alpha fibers (~100 m/s). Answer: d) C fibers
--- Guessed Question 9
Which fibers are most pressure-sensitive clinically leading to tingling?
a) A fibers
b) B fibers
c) C fibers
d) All equally
Explanation: Large, heavily myelinated A fibers are most pressure-sensitive, hence tingling and numbness are due to their dysfunction. Answer: a) A fibers
--- Guessed Question 10
Loss of touch and vibration but preserved pain after compression indicates damage to:
a) A alpha and beta fibers
b) A delta fibers
c) C fibers
d) B fibers
Explanation: Touch and vibration are carried by large A alpha and A beta fibers, which are most pressure-sensitive. C fibers carrying pain remain intact initially, explaining preserved pain sensation. Answer: a) A alpha and beta fibers
Chapter: Sensory Physiology | Topic: Visual Transduction | Subtopic: Photoreceptor Proteins
Keywords
Transducin — a heterotrimeric G-protein in photoreceptor cells involved in phototransduction.
Rhodopsin — light-sensitive pigment in rod outer segments that activates transducin.
Phototransduction — process converting photon absorption into electrical signals in retina.
cGMP phosphodiesterase — enzyme activated by transducin to lower cGMP and hyperpolarize photoreceptors.
Rods and cones — retinal photoreceptors for scotopic and photopic vision respectively.
Retinal — chromophore (11-cis-retinal) that changes conformation on photon absorption.
Hyperpolarization — photoreceptor response to light due to decreased cGMP-gated current.
Dark current — inward Na⁺/Ca²⁺ current in photoreceptors maintained by cGMP.
Visual cycle — enzymatic regeneration of 11-cis-retinal in retinal pigment epithelium.
G-protein coupled receptor (GPCR) — rhodopsin is a GPCR that activates transducin.
Lead Question - 2012
Transducin is a protein found in:
a) Glomerulus
b) Retina
c) Skeletal muscle
d) Adrenal medulla
Explanation: Transducin is a G-protein located in photoreceptor outer segments of the retina; it couples activated rhodopsin to cGMP phosphodiesterase. Upon photon capture transducin activates PDE, lowers cGMP, closes cGMP-gated channels and hyperpolarizes the photoreceptor. Correct answer: b) Retina.
Q1. Which pigment initiates phototransduction by activating transducin?
a) Hemoglobin
b) Melanin
c) Rhodopsin
d) Opsin in kidney
Explanation: Rhodopsin in rod outer segments absorbs photons, isomerizes 11-cis-retinal to all-trans-retinal, and activates the GPCR rhodopsin which then activates transducin, initiating the phototransduction cascade. Correct answer: c) Rhodopsin.
Q2. Activation of transducin leads directly to activation of which enzyme?
a) Adenylate cyclase
b) cGMP phosphodiesterase
c) Na⁺/K⁺ ATPase
d) Phospholipase C
Explanation: Activated transducin (Gαt) stimulates cGMP phosphodiesterase, decreasing cytoplasmic cGMP, closing cGMP-gated cation channels and hyperpolarizing photoreceptors. This is central to light signal transduction. Correct answer: b) cGMP phosphodiesterase.
Q3. Photoreceptor response to light is a:
a) Depolarization
b) Hyperpolarization
c) Action potential firing
d) No change
Explanation: Light activation leads to reduced cGMP, closure of cGMP-gated Na⁺ channels, decreased inward dark current and membrane hyperpolarization of photoreceptors. This graded hyperpolarization reduces glutamate release. Correct answer: b) Hyperpolarization.
Q4. Which retinal cells regenerate 11-cis-retinal as part of the visual cycle?
a) Müller glia
b) Retinal pigment epithelium (RPE)
c) Ganglion cells
d) Bipolar cells
Explanation: The retinal pigment epithelium (RPE) performs enzymatic steps to convert all-trans-retinal back to 11-cis-retinal, replenishing the chromophore for photopigments. This visual cycle is essential for sustained phototransduction. Correct answer: b) Retinal pigment epithelium (RPE).
Q5. Which photoreceptors primarily use transducin in their signal cascade?
a) Rods
b) Cones
c) Ganglion photoreceptors only
d) Both rods and cones
Explanation: Both rods and cones possess phototransduction cascades that employ G-proteins homologous to transducin (rod transducin Gαt1, cone transducins Gαt2), so both use transducin-like proteins to activate PDE. Correct answer: d) Both rods and cones.
Q6. A defect in transducin function would most likely cause:
a) Color blindness only
b) Night blindness and impaired phototransduction
c) Loss of accommodation
d) Elevated intraocular pressure
Explanation: Impaired transducin prevents effective activation of PDE, blunting photoreceptor hyperpolarization and reducing sensitivity, particularly affecting scotopic (rod-mediated) vision, causing night blindness and phototransduction defects. Correct answer: b) Night blindness and impaired phototransduction.
Q7. Which event follows activation of cGMP phosphodiesterase in photoreceptors?
a) Increased intracellular cGMP
b) Closure of cGMP-gated cation channels
c) Increased glutamate release
d) Depolarization
Explanation: PDE lowers cGMP levels, resulting in closure of cGMP-gated Na⁺/Ca²⁺ channels, decreased inward current and reduced glutamate release due to photoreceptor hyperpolarization. Correct answer: b) Closure of cGMP-gated cation channels.
Q8. Which molecule directly undergoes photoisomerization to start phototransduction?
a) 11-cis-retinal
b) Opsin protein backbone
c) cGMP
d) Transducin
Explanation: The chromophore 11-cis-retinal within rhodopsin photoisomerizes to all-trans-retinal upon photon absorption, changing rhodopsin conformation and activating transducin, initiating the cascade. Correct answer: a) 11-cis-retinal.
Q9. Which test assesses rod (scotopic) function most directly?
a) Photopic visual acuity
b) Dark adaptation test
c) Color vision test
d) Pupillary light reflex
Explanation: Dark adaptation measures recovery of visual sensitivity in low light, reflecting rod photoreceptor and transducin-PDE cascade function. Delayed or impaired dark adaptation suggests rod/transducin pathway dysfunction. Correct answer: b) Dark adaptation test.
Q10. Which class of receptors does rhodopsin belong to?
a) Ligand-gated ion channel
b) Tyrosine kinase receptor
c) G-protein coupled receptor (GPCR)
d) Nuclear receptor
Explanation: Rhodopsin is a GPCR embedded in photoreceptor membranes; upon photon-induced conformational change it activates transducin (a G-protein), classifying rhodopsin as a light-activated GPCR. Correct answer: c) G-protein coupled receptor (GPCR).
Chapter: Central Nervous System Physiology | Topic: Hypothalamic Functions | Subtopic: Preoptic Area & Homeostasis
Keyword Definitions
Preoptic nucleus — hypothalamic region with warm-sensitive neurons controlling heat-loss responses.
Thermoregulation — physiological processes maintaining core temperature via autonomic and behavioral responses.
Hyperthermia — abnormally high body temperature due to failed heat dissipation or excessive heat production.
Hyperphagia — excessive eating driven by hypothalamic or metabolic disturbances.
Hyperdipsia — excessive thirst and fluid intake, often osmotic or hypothalamic in origin.
Homeostasis — coordinated regulation of internal milieu (temperature, thirst, hunger, endocrine balance).
Autonomic output — hypothalamic control of sympathetic and parasympathetic tone influencing temperature and metabolism.
POA lesions — can disrupt fever responses, thermoregulatory set points, and heat-loss mechanisms.
Fever vs hyperthermia — fever raises set point via pyrogens; hyperthermia is failure of dissipation.
Clinical relevance — hypothalamic injury, stroke, tumors can produce dysautonomia and temperature dysregulation.
Lead Question - 2012
Lesion of preoptic nucleus of hypothalamus causes?
a) Hyperphagia
b) Hyperdypsia
c) Hyperthermia
d) Hyperglycemia
Explanation: The preoptic area contains warm-sensitive neurons that initiate heat-loss responses (vasodilation, sweating). Lesioning these neurons abolishes heat-loss mechanisms, producing uncontrolled rise in body temperature (hyperthermia). This is not primarily a feeding or thirst center. Correct answer: c) Hyperthermia.
Q1. Damage to the lateral hypothalamic area typically causes:
a) Anorexia
b) Hyperphagia
c) Polydipsia
d) Hypothermia
Explanation: The lateral hypothalamus is the feeding (hunger) center; lesions produce anorexia and weight loss, while stimulation causes hyperphagia. Thus damage causes lack of eating rather than increased appetite. Correct answer: a) Anorexia (lesion → anorexia; stimulation → hyperphagia).
Q2. A lesion of the supraoptic nucleus would most likely produce:
a) Diabetes insipidus (polyuria, polydipsia)
b) Cushing’s syndrome
c) Hyperthermia
d) Adipsia
Explanation: The supraoptic nucleus produces vasopressin (ADH); damage causes central diabetes insipidus with polyuria and compensatory polydipsia. This is a classic hypothalamic endocrine deficit. Correct answer: a) Diabetes insipidus (polyuria, polydipsia).
Q3. Which hypothalamic lesion produces hyperphagia and obesity in animals?
a) Ventromedial nucleus lesion
b) Lateral hypothalamic lesion
c) Preoptic lesion
d) Suprachiasmatic lesion
Explanation: The ventromedial hypothalamus is a satiety center; lesions remove restraining signals leading to hyperphagia and obesity. Lateral lesions cause anorexia. Correct answer: a) Ventromedial nucleus lesion.
Q4. Destruction of the suprachiasmatic nucleus (SCN) leads to:
a) Loss of circadian rhythms
b) Hyperthermia
c) Polyphagia
d) Diabetes insipidus
Explanation: The SCN is the master circadian pacemaker; lesions disrupt sleep-wake, hormonal, and temperature rhythms. This abolishes regular circadian patterns but does not directly cause fever or thirst disorders. Correct answer: a) Loss of circadian rhythms.
Q5. Fever (pyrogen-mediated) differs from hyperthermia because fever involves:
a) Raised hypothalamic set point
b) Failure of heat dissipation
c) Ambient heat overload
d) Direct injury to preoptic neurons
Explanation: Fever results from pyrogens raising the hypothalamic thermostat (set point), inducing chills and thermoregulatory defenses to reach the new set point. Hyperthermia is failure of heat loss without set-point change. Correct answer: a) Raised hypothalamic set point.
Q6. A patient with hypothalamic lesion presents with persistent hyperphagia and rage; which nucleus is likely affected?
a) Ventromedial nucleus
b) Preoptic nucleus
c) Paraventricular nucleus
d) Lateral hypothalamic area
Explanation: Ventromedial nucleus lesions remove satiety signals causing hyperphagia and aggression (sham rage). The lateral hypothalamus promotes feeding when stimulated. Paraventricular lesions affect autonomic and endocrine outputs. Correct answer: a) Ventromedial nucleus.
Q7. Lesion of preoptic area interferes with which autonomic thermoregulatory response?
a) Sweating and cutaneous vasodilation
b) Salivation
c) Pupillary constriction
d) Gastrointestinal motility
Explanation: The preoptic area triggers heat-loss responses such as sweating and vasodilation. Lesions abolish these mechanisms, leading to impaired heat dissipation and hyperthermia. Other autonomic functions are mediated by different hypothalamic regions. Correct answer: a) Sweating and cutaneous vasodilation.
Q8. Paraventricular nucleus (PVN) lesions primarily affect:
a) Oxytocin and CRH release influencing endocrine and autonomic functions
b) Visual processing
c) Primary motor control
d) Vestibular reflexes
Explanation: PVN neurons produce CRH and oxytocin and modulate sympathetic outflow; lesions disrupt HPA axis regulation and autonomic balance. This leads to endocrine and autonomic dysfunction rather than direct motor or visual deficits. Correct answer: a).
Q9. Central fever after hypothalamic hemorrhage is due to:
a) Disruption of preoptic heat-loss neurons
b) Bacterial infection
c) Peripheral inflammation only
d) Increased sweating
Explanation: Hypothalamic injury can cause central fever by damaging preoptic/POA neurons that mediate heat loss and set-point regulation; this produces sustained hyperthermia without infection. Correct answer: a) Disruption of preoptic heat-loss neurons.
Q10. A lesion of arcuate nucleus would most likely cause:
a) Disordered appetite regulation and altered GnRH/release control
b) Loss of temperature sensation
c) Loss of visual fields
d) Cerebellar ataxia
Explanation: The arcuate nucleus integrates peripheral metabolic signals (leptin, ghrelin) and influences appetite, prolactin and GnRH modulation. Lesions disrupt feeding and reproductive hormone regulation. It is not primarily involved in temperature sensation or motor coordination. Correct answer: a).
Chapter: Central Nervous System Physiology | Topic: Hypothalamic Control | Subtopic: Thermoregulation and Shivering
Keywords
Thermoregulation — physiological processes that maintain core body temperature.
Preoptic area (POA) — hypothalamic region sensing temperature and coordinating heat-loss responses.
Posterior hypothalamus — activates heat-production mechanisms including shivering and sympathetic vasoconstriction.
Shivering — involuntary rhythmic skeletal muscle contractions generating heat under hypothalamic drive.
Warm-sensitive neurons — in POA; stimulate heat-loss (sweating, vasodilation).
Cold-sensitive pathways — activate posterior hypothalamus to produce heat via shivering and autonomic output.
Pyrogens — raise hypothalamic set point producing fever (distinct from hyperthermia).
Thermal effector organs — skeletal muscle (shivering), skin vessels (vasomotor), sweat glands.
Behavioral responses — seeking shelter/clothing under hypothalamic and cortical influence.
Clinical relevance — hypothalamic lesions can produce hypothermia or hyperthermia and loss of shivering.
Lead Question - 2012
Shivering is controlled by: (also in September 2012, March 2013)
a) Dorsomedial nucleus
b) Posterior hypothalamus
c) Perifornical nucleus
d) Lateral hypothalamic area
Explanation: Shivering—involuntary rhythmic skeletal muscle contractions that generate heat—is driven by cold-sensitive pathways activating the posterior hypothalamus. The posterior hypothalamic area orchestrates motor and sympathetic outputs for heat production. Therefore the correct answer is b) Posterior hypothalamus, responsible for shivering and thermogenic responses.
Q1. Lesion of the preoptic area typically causes:
a) Hypothermia
b) Hyperthermia
c) Diabetes insipidus
d) Hyperphagia
Explanation: The preoptic area contains warm-sensitive neurons initiating heat-loss responses. Lesioning it abolishes heat-dissipation, producing uncontrolled rise in body temperature (hyperthermia). Thus the correct answer is b) Hyperthermia. This differs from DI or appetite disturbances tied to other hypothalamic nuclei.
Q2. Fever differs from hyperthermia because fever results from:
a) Ambient heat overload
b) Raised hypothalamic set point due to pyrogens
c) Failure of sweating
d) Posterior hypothalamic lesion
Explanation: Fever arises when pyrogens raise the hypothalamic thermoregulatory set point, causing the body to conserve and generate heat until the new set point is reached. This distinguishes fever from hyperthermia, which is failure of heat loss. Correct answer: b).
Q3. Which hypothalamic area promotes heat production when activated by cold?
a) Anterior hypothalamus
b) Posterior hypothalamus
c) Suprachiasmatic nucleus
d) Arcuate nucleus
Explanation: Cold signals activate cold-sensitive afferents that stimulate the posterior hypothalamus to increase thermogenesis by shivering and sympathetic activation. The anterior (preoptic) area mediates heat loss. Correct answer: b) Posterior hypothalamus, which triggers heat-generating mechanisms.
Q4. Which effector mediates most rapid heat production in humans?
a) Brown adipose tissue
b) Shivering (skeletal muscle activity)
c) Increased thyroid secretion
d) Skin vasodilation
Explanation: Shivering produces immediate heat via rhythmic skeletal muscle contractions under posterior hypothalamic control, providing rapid thermogenesis. Brown adipose tissue contributes in infants, while thyroid changes and vasomotor adjustments are slower. Correct answer: b) Shivering.
Q5. Which sign indicates activation of heat-loss mechanisms?
a) Vasoconstriction
b) Shivering
c) Sweating and cutaneous vasodilation
d) Piloerection
Explanation: Heat-loss responses include sweating and cutaneous vasodilation mediated by preoptic area signals. These lower core temperature by evaporative cooling and increased skin blood flow. Correct answer: c) Sweating and cutaneous vasodilation, opposite to shivering which produces heat.
Q6. A patient with impaired shivering after hypothalamic surgery most likely had damage to:
a) Ventromedial nucleus
b) Posterior hypothalamus
c) Suprachiasmatic nucleus
d) Lateral hypothalamus
Explanation: Surgical damage to the posterior hypothalamus abolishes cold-induced shivering and some sympathetic thermogenic responses. Therefore impaired shivering after hypothalamic surgery suggests posterior hypothalamic injury. Correct answer: b) Posterior hypothalamus.
Q7. Which autonomic response accompanies shivering to preserve core temperature?
a) Cutaneous vasodilation
b) Cutaneous vasoconstriction
c) Diaphoresis
d) Increased salivation
Explanation: To conserve heat during shivering, sympathetic-mediated cutaneous vasoconstriction reduces blood flow to the skin, minimizing heat loss. This complements muscular heat production. Correct answer: b) Cutaneous vasoconstriction.
Q8. Which hypothalamic nucleus is the master clock for circadian temperature rhythm?
a) Suprachiasmatic nucleus (SCN)
b) Paraventricular nucleus
c) Dorsomedial nucleus
d) Lateral hypothalamus
Explanation: The suprachiasmatic nucleus (SCN) entrains circadian rhythms including daily fluctuations in body temperature by signaling other hypothalamic areas. Lesions disrupt rhythmic temperature variations. Correct answer: a) Suprachiasmatic nucleus (SCN).
Q9. Which pharmacologic agent can reduce shivering by central action?
a) Acetaminophen (paracetamol)
b) Meperidine (pethidine)
c) Epinephrine
d) Dobutamine
Explanation: Meperidine centrally suppresses shivering via opioid and α2-adrenergic effects in the hypothalamus and brainstem. It is used to treat postoperative shivering. Correct answer: b) Meperidine (pethidine).
Q10. In hypothermia, which behavioral response is initiated by cortical and hypothalamic centers?
a) Removing clothing
b) Seeking warmth and adding clothing
c) Inducing sweat
d) Increasing water intake
Explanation: Behavioral thermoregulation includes seeking warmth and adding clothing to reduce heat loss; these actions are driven by hypothalamic signals integrated with cortical decision-making. Correct answer: b) Seeking warmth and adding clothing.
Chapter: Central Nervous System Physiology | Topic: Neuronal Membrane & Action Potential | Subtopic: Voltage-Gated Sodium Channels
Keywords
Voltage-gated sodium channels — proteins that open on depolarization allowing Na⁺ influx to initiate action potentials.
Axon initial segment (AIS) / Axon hillock — region where action potentials are usually initiated due to high Na⁺ channel density.
Nodes of Ranvier — gaps in myelin with concentrated Na⁺ channels enabling saltatory conduction.
Soma — neuronal cell body; integrates synaptic inputs but has lower Na⁺ channel density than AIS.
Dendrites — receive inputs and may have Na⁺ channels for back-propagation, but fewer than AIS.
Action potential threshold — lowest depolarization required to open sufficient Na⁺ channels to trigger spike.
Saltatory conduction — rapid impulse propagation between nodes of Ranvier in myelinated axons.
Ankyrin-G — scaffold protein essential for clustering Na⁺ channels at the axon initial segment.
Local anaesthetics — block voltage-gated Na⁺ channels to prevent action-potential propagation.
Channelopathies — disorders caused by mutations in sodium channel genes affecting excitability and causing seizures or paralysis.
Lead Question - 2012
Sodium channels are maximum in which part of neuron ?
a) Soma
b) Axon hillock
c) Dendrites
d) Axon
Explanation: The axon hillock (axon initial segment) has the highest density of voltage-gated sodium channels and is the usual trigger zone for action potentials. This high channel concentration, organized by ankyrin-G and associated scaffolds, lowers the threshold for spike initiation. Correct answer: b) Axon hillock.
Q1. Where along myelinated axons are sodium channels highly concentrated to enable saltatory conduction?
a) Internodal myelin
b) Nodes of Ranvier
c) Soma membrane
d) Dendritic spines
Explanation: Nodes of Ranvier are unmyelinated gaps densely populated with voltage-gated sodium channels. Action potentials are regenerated at these nodes, allowing rapid saltatory conduction down the axon. This arrangement increases conduction velocity and metabolic efficiency. Correct answer: b) Nodes of Ranvier.
Q2. Which scaffolding protein is essential for clustering sodium channels at the axon initial segment?
a) Ankyrin-G
b) Tubulin
c) Actin
d) Spectrin
Explanation: Ankyrin-G anchors voltage-gated sodium channels and other membrane proteins to the axon initial segment cytoskeleton, maintaining high local channel density necessary for action-potential initiation. Disruption of ankyrin-G disperses channels and reduces neuronal excitability. Correct answer: a) Ankyrin-G.
Q3. Local anaesthetics such as lidocaine produce analgesia primarily by blocking which channels?
a) Voltage-gated potassium channels
b) Voltage-gated sodium channels
c) Voltage-gated calcium channels
d) Ligand-gated chloride channels
Explanation: Local anaesthetics bind to and block voltage-gated sodium channels, preventing initiation and propagation of action potentials in sensory fibers. Small nociceptive fibers are preferentially blocked, producing loss of pain and temperature sensation. Correct answer: b) Voltage-gated sodium channels.
Q4. A mutation that reduces sodium-channel availability in the axon hillock would most likely cause:
a) Increased neuronal firing
b) Decreased excitability and possible weakness
c) Faster action potentials
d) Enhanced synaptic transmission
Explanation: Reduced sodium-channel availability at the axon initial segment raises the threshold for spike initiation, decreasing neuronal excitability and impairing signal transmission. Clinically this may cause muscle weakness, conduction block, or epileptic phenotypes depending on neuronal population affected. Correct answer: b) Decreased excitability and possible weakness.
Q5. Dendritic sodium channels support which physiological process relevant to synaptic plasticity?
a) Action-potential back-propagation
b) Neurotransmitter synthesis
c) Axonal myelination
d) Vesicle recycling
Explanation: Voltage-gated sodium channels in dendrites allow action potentials to back-propagate into the dendritic tree, modulating calcium entry and synaptic strength. This back-propagation contributes to spike-timing-dependent plasticity and learning. Correct answer: a) Action-potential back-propagation.
Q6. During the relative refractory period, why is a larger stimulus required to elicit an action potential?
a) All Na⁺ channels are permanently removed
b) Many Na⁺ channels are inactivated and K⁺ conductance is increased
c) Membrane potential is more positive than threshold
d) Synaptic inputs are inhibited
Explanation: After an action potential, a subset of Na⁺ channels remains inactivated and K⁺ channels remain open, hyperpolarizing the membrane; a stronger depolarizing input is thus required to reach threshold. This defines the relative refractory period. Correct answer: b) Many Na⁺ channels are inactivated and K⁺ conductance is increased.
Q7. Which feature increases axonal conduction velocity most effectively?
a) Decreasing axon diameter
b) Increasing myelination and axon diameter
c) Reducing Na⁺ channel density at nodes
d) Increasing internodal capacitance
Explanation: Larger axon diameter and increased myelination raise conduction velocity by reducing internal resistance and membrane capacitance. Adequate sodium-channel density at nodes is also required. Correct answer: b) Increasing myelination and axon diameter.
Q8. Which antiepileptic medication exerts effects by stabilizing the inactivated state of sodium channels?
a) Phenytoin
b) Levodopa
c) Fluoxetine
d) Propranolol
Explanation: Phenytoin binds voltage-gated sodium channels, prolonging their inactivated state and limiting repetitive firing of neurons. This mechanism reduces seizure propagation in many epilepsy syndromes. Correct answer: a) Phenytoin.
Q9. Which region is the most common site for initiation of spontaneous epileptic discharges due to high excitability?
a) Axon hillock / initial segment
b) Distal axon terminals
c) Soma nucleus
d) Myelin sheath
Explanation: The axon initial segment’s high density of sodium channels and low threshold make it a frequent locus for abnormal spontaneous discharges in epilepsy. Pathologic increases in excitability here can produce paroxysmal firing. Correct answer: a) Axon hillock / initial segment.
Q10. Which pathological process directly reduces sodium-channel clustering at the AIS leading to reduced excitability?
a) Mutation or loss of ankyrin-G
b) Increased myelination
c) Enhanced Na⁺ channel synthesis
d) Elevated extracellular potassium only
Explanation: Loss or dysfunction of ankyrin-G disrupts anchoring of sodium channels at the AIS, dispersing them and impairing action-potential initiation. This reduces neuronal excitability and can contribute to neurological disease. Correct answer: a) Mutation or loss of ankyrin-G.