Keyword Definitions
• Two-point discrimination: Ability to distinguish two separate simultaneous tactile stimuli.
• Tactile acuity: Sharpness of touch perception depending on receptor density.
• Receptive field: Area of skin innervated by a single sensory neuron.
• Merkel cells: Slowly adapting mechanoreceptors specialized for shape and edges.
• Meissner corpuscles: Rapidly adapting mechanoreceptors detecting flutter and low-frequency vibration.
• Pacinian corpuscles: Rapidly adapting mechanoreceptors specialized for high-frequency vibration.
• Dorsal columns: Pathways carrying touch, vibration, and proprioception.
• Medial lemniscus: Brainstem tract formed by decussated dorsal column fibers.
• Somatosensory cortex: Postcentral gyrus area processing tactile information.
• Cortical magnification: Enlarged cortical representation of regions like lips and fingertips.
• Astereognosis: Inability to identify objects by touch.
Chapter: General Physiology
Topic: Sensory Physiology
Subtopic: Two-point Discrimination
Lead Question – 2012
The distance by which two touch stimuli must be separated to be perceived as two separate stimuli is greatest at?
a) The lips
b) The palm of the hand
c) The back of scapula
d) The dorsum of the hand
Explanation: Two-point discrimination threshold is largest where receptive fields are big and cortical representation is small. Proximal trunk regions have poorest tactile acuity. Therefore, the greatest minimum separable distance is on the back of the scapula. Answer: c) The back of scapula.
Question 2
Which receptor type contributes most to high-resolution two-point discrimination on fingertips?
a) Pacinian corpuscles
b) Merkel discs
c) Ruffini endings
d) Free nerve endings
Explanation: Edges and fine form are encoded by slowly adapting type I mechanoreceptors with small receptive fields. Merkel cell–neurite complexes provide the highest spatial resolution for static touch and contribute most to two-point discrimination on fingertips and lips. Answer: b) Merkel discs.
Question 3
A patient with a hemisection of the spinal cord loses two-point discrimination below the lesion. Which tract is involved?
a) Spinothalamic tract
b) Dorsal column pathway
c) Spinocerebellar tract
d) Corticospinal tract
Explanation: A hemisection damaging dorsal columns impairs ipsilateral discriminative touch, vibration sense, and conscious proprioception below the lesion. Two-point discrimination on the affected side is markedly reduced, while pain and temperature may remain spared. Answer: b) Dorsal column pathway.
Question 4
Where is the two-point discrimination threshold smallest in the body?
a) Fingertips
b) Palm
c) Back
d) Abdomen
Explanation: Two-point thresholds are smallest where receptor density is highest and receptive fields are tiniest. Fingertips have abundant Merkel and Meissner endings plus strong cortical magnification, enabling exquisite spatial acuity. Therefore, minimum separable distance is least at fingertips. Answer: a) Fingertips.
Question 5
Which pathway carries discriminative touch and vibration sense to the brain?
a) Spinothalamic tract
b) Corticospinal tract
c) Dorsal column–medial lemniscus pathway
d) Spinoreticular tract
Explanation: Discriminative touch, vibration, and conscious proprioception ascend ipsilaterally in the dorsal columns to nucleus gracilis and cuneatus, then decussate as internal arcuate fibers to form the medial lemniscus. They project to thalamic VPL and somatosensory cortex. Answer: c) Dorsal column–medial lemniscus pathway.
Question 6
In which cortical region is two-point discrimination primarily resolved?
a) Prefrontal cortex
b) Primary somatosensory cortex
c) Insular cortex
d) Cerebellum
Explanation: Two-point discrimination is ultimately resolved in the primary somatosensory cortex on the postcentral gyrus, especially area 3b, exhibiting cortical magnification for hands and lips. Lesions there cause astereognosis and impaired tactile acuity contralaterally. Answer: b) Primary somatosensory cortex.
Question 7
A patient has loss of two-point discrimination on the left hand. Lesion is most likely in?
a) Right primary somatosensory cortex
b) Left motor cortex
c) Right cerebellum
d) Left dorsal root ganglion
Explanation: Somatosensory pathways decussate before reaching the cortex. Loss of discriminative touch from the left hand arises with a lesion in the contralateral somatosensory cortex. Answer: a) Right primary somatosensory cortex.
Question 8
Which phenomenon sharpens spatial resolution in two-point discrimination by inhibiting neighboring neurons?
a) Rebound excitation
b) Temporal summation
c) Lateral inhibition
d) Referred sensation
Explanation: Lateral inhibition enhances sensory contrast by suppressing responses in adjacent receptive fields. This improves spatial acuity and is fundamental for resolving two-point discrimination. Answer: c) Lateral inhibition.
Question 9
Which clinical sign indicates impaired cortical processing of tactile stimuli despite intact primary sensory pathways?
a) Hyperalgesia
b) Allodynia
c) Astereognosis
d) Hyperreflexia
Explanation: Patients with cortical lesions affecting parietal sensory areas cannot identify objects by touch despite preserved basic tactile sensation. This condition is astereognosis. Answer: c) Astereognosis.
Question 10
A lesion in which thalamic nucleus impairs two-point discrimination from the contralateral body?
a) VPL nucleus
b) Medial geniculate nucleus
c) VPM nucleus
d) Lateral geniculate nucleus
Explanation: The ventral posterolateral (VPL) nucleus of the thalamus receives medial lemniscus inputs carrying discriminative touch, vibration, and proprioception from the contralateral body. Lesions here impair two-point discrimination. Answer: a) VPL nucleus.
Question 11
Two-point discrimination is impaired but pain sensation remains intact. Which tract remains unaffected?
a) Spinothalamic tract
b) Dorsal column–medial lemniscus pathway
c) Corticospinal tract
d) Reticulospinal tract
Explanation: Preservation of pain sensation indicates an intact spinothalamic tract. Impairment of two-point discrimination indicates dorsal column dysfunction. Answer: a) Spinothalamic tract.
Keyword Definitions
• Purkinje fibres: Large inhibitory neurons of cerebellar cortex using GABA as neurotransmitter.
• Deep cerebellar nuclei: Primary output centres of cerebellum receiving inhibitory Purkinje input.
• Climbing fibres: Excitatory inputs from inferior olivary nucleus synapsing on Purkinje cells.
• Mossy fibres: Excitatory afferents from spinal cord and brainstem projecting to granule cells.
• Basket cells: Inhibitory interneurons forming axo-somatic synapses on Purkinje cells.
• Stellate cells: Inhibitory interneurons acting on Purkinje dendrites in molecular layer.
• Spinocerebellar tracts: Convey unconscious proprioceptive information from muscles and joints.
• Granule cells: Excitatory interneurons giving rise to parallel fibres synapsing on Purkinje cells.
• GABA: Gamma-aminobutyric acid, main inhibitory neurotransmitter in CNS.
• Cerebellar cortex: Three-layered structure modulating motor coordination and balance.
• Motor learning: Cerebellar mechanism for adapting and fine-tuning skilled movements.
Chapter: Neurophysiology
Topic: Cerebellum
Subtopic: Purkinje Cell Function
Lead Question – 2012
Purkinje fibres are inhibitory for?
a) Deep cerebellar nuclei
b) Climbing fibre
c) Basket cells
d) Spinocerebellar tracts
Explanation: Purkinje cells are GABAergic neurons that project inhibitory signals to deep cerebellar nuclei, regulating motor output precision. They receive excitatory input from climbing and mossy fibres, while interneurons like basket and stellate cells refine their activity. Answer: a) Deep cerebellar nuclei. This inhibitory control ensures smooth coordination and balance.
Question 2
Which neurotransmitter is released by Purkinje cells?
a) Acetylcholine
b) Dopamine
c) GABA
d) Glutamate
Explanation: Purkinje cells are the sole output of the cerebellar cortex. They are inhibitory neurons releasing gamma-aminobutyric acid (GABA). This neurotransmitter suppresses activity of deep cerebellar nuclei, ensuring controlled modulation of motor output. Answer: c) GABA. Excitatory neurotransmitters like glutamate act via mossy and climbing fibre inputs.
Question 3
A patient has loss of coordination but preserved strength. Which structure is primarily affected?
a) Cerebellum
b) Basal ganglia
c) Motor cortex
d) Spinal cord anterior horn
Explanation: The cerebellum coordinates timing, precision, and smoothness of movement but does not initiate voluntary force generation. Lesions cause ataxia, dysmetria, and intention tremor without significant weakness. Answer: a) Cerebellum. Motor cortex lesions reduce strength, while basal ganglia dysfunction causes rigidity or tremor, not incoordination.
Question 4
Climbing fibres originate from which source?
a) Inferior olivary nucleus
b) Red nucleus
c) Vestibular nuclei
d) Pontine nuclei
Explanation: Climbing fibres arise exclusively from the inferior olivary nucleus and form powerful excitatory synapses directly on Purkinje cells. They regulate motor learning and coordination through long-term depression at parallel fibre synapses. Answer: a) Inferior olivary nucleus. Mossy fibres, instead, arise from pontine and spinal inputs.
Question 5
Damage to Purkinje cells would primarily result in?
a) Spastic paralysis
b) Ataxia
c) Rigidity
d) Hyporeflexia
Explanation: Purkinje cell loss disrupts cerebellar inhibitory control, impairing coordination of movement. This produces ataxia with unsteady gait, dysdiadochokinesia, and intention tremor. Answer: b) Ataxia. Spasticity results from corticospinal damage, rigidity from basal ganglia disease, and hyporeflexia from lower motor neuron lesions.
Question 6
Which interneuron inhibits Purkinje cells in cerebellar cortex?
a) Basket cells
b) Golgi cells
c) Pyramidal cells
d) Oligodendrocytes
Explanation: Basket cells provide inhibitory axo-somatic synapses directly on Purkinje neurons, limiting their firing. Stellate cells also inhibit dendrites. Golgi cells regulate granule cells. Answer: a) Basket cells. These interneurons fine-tune Purkinje output before it reaches deep cerebellar nuclei, optimizing cerebellar motor coordination and timing.
Question 7
Which cerebellar lesion leads to truncal ataxia and swaying while standing?
a) Vermis
b) Hemisphere
c) Flocculonodular lobe
d) Dentate nucleus
Explanation: Lesions in cerebellar vermis cause truncal ataxia with broad-based gait and inability to maintain upright posture. Answer: a) Vermis. Hemisphere lesions cause limb ataxia, flocculonodular lesions cause balance and nystagmus, while dentate involvement produces dysmetria and decomposition of movement. Clinical localization depends on specific cerebellar subdivisions.
Question 8
Mossy fibres synapse first on?
a) Purkinje cells
b) Basket cells
c) Granule cells
d) Stellate cells
Explanation: Mossy fibres relay information from spinal cord and brainstem. They terminate on granule cells in cerebellar cortex, which then give rise to parallel fibres. These parallel fibres excite Purkinje dendrites. Answer: c) Granule cells. Thus, mossy fibres indirectly influence Purkinje output by granule cell activation.
Question 9
Which symptom is most typical of cerebellar disease?
a) Rest tremor
b) Intention tremor
c) Hypokinesia
d) Spasticity
Explanation: Cerebellar lesions produce intention tremor, which appears during voluntary movement and worsens as target is approached. Answer: b) Intention tremor. Rest tremor suggests Parkinsonism, hypokinesia occurs in basal ganglia disease, and spasticity arises from pyramidal tract lesions. Cerebellum chiefly impairs timing and coordination of motor actions.
Question 10
Which cerebellar output nucleus is largest and projects to motor cortex via thalamus?
a) Fastigial nucleus
b) Globose nucleus
c) Dentate nucleus
d) Emboliform nucleus
Explanation: The dentate nucleus is the largest deep cerebellar nucleus, projecting to contralateral motor cortex via the ventrolateral thalamus. It coordinates planning, timing, and fine motor execution. Answer: c) Dentate nucleus. Fastigial controls posture, globose and emboliform modulate intermediate motor activities of limbs.
Question 11
Which tract conveys unconscious proprioception from muscles to cerebellum?
a) Corticospinal tract
b) Spinothalamic tract
c) Spinocerebellar tract
d) Rubrospinal tract
Explanation: Spinocerebellar tracts carry proprioceptive input from muscle spindles and Golgi tendon organs to cerebellum. This unconscious sensory feedback helps adjust movement in real time. Answer: c) Spinocerebellar tract. Corticospinal controls voluntary movement, spinothalamic transmits pain/temperature, rubrospinal influences flexor tone but not proprioception.
Keyword Definitions
• Dopamine: Catecholamine neurotransmitter crucial for motor control, motivation, and reward pathways.
• Nigrostriatal pathway: Dopaminergic pathway projecting from substantia nigra to striatum, vital for movement regulation.
• Serotonin: Neurotransmitter involved in mood, sleep, and appetite regulation.
• Cholinergic neurons: Use acetylcholine, important in learning, memory, and motor circuits.
• Adrenergic neurons: Release norepinephrine, essential for arousal, vigilance, and autonomic functions.
• Substantia nigra: Midbrain nucleus producing dopamine, degeneration causes Parkinsonism.
• Basal ganglia: Group of nuclei modulating movement initiation and suppression.
• Extrapyramidal system: Motor system controlling posture, tone, and coordination.
• Parkinson’s disease: Neurodegenerative disorder due to dopaminergic loss in nigrostriatal pathway.
• Dyskinesia: Involuntary abnormal movements due to neurotransmitter imbalance.
• Levodopa: Dopamine precursor used as therapy in Parkinson’s disease.
Chapter: Neurophysiology
Topic: Basal Ganglia
Subtopic: Nigrostriatal Pathway
Lead Question – 2012
Neurotransmitter involved in nigrostriatal pathway is?
a) Serotonin
b) Dopamine
c) Cholinergic
d) Adrenergic
Explanation: The nigrostriatal pathway is a dopaminergic tract connecting substantia nigra pars compacta with the striatum. It regulates voluntary movement by balancing excitatory and inhibitory signals in basal ganglia circuits. Loss of dopamine here causes Parkinsonism. Answer: b) Dopamine. Other neurotransmitters modulate but dopamine is the principal one involved.
Question 2
Which brain structure degenerates in Parkinson’s disease?
a) Substantia nigra pars compacta
b) Globus pallidus externa
c) Red nucleus
d) Subthalamic nucleus
Explanation: Parkinson’s disease arises from dopaminergic neuronal loss in substantia nigra pars compacta, leading to striatal dopamine deficiency. This impairs basal ganglia modulation, causing bradykinesia, rigidity, and tremor. Answer: a) Substantia nigra pars compacta. Subthalamic nucleus lesions cause hemiballismus, while pallidal and red nucleus lesions show different deficits.
Question 3
Which dopamine receptor subtype facilitates the direct pathway in basal ganglia?
a) D1 receptors
b) D2 receptors
c) D3 receptors
d) D4 receptors
Explanation: D1 receptors in striatum stimulate the direct pathway, enhancing movement by exciting striatal neurons projecting to internal globus pallidus. Dopamine binding here increases activity, disinhibiting thalamus and promoting cortical excitation. Answer: a) D1 receptors. D2 receptors inhibit indirect pathway, while D3 and D4 are extrastriatal predominantly.
Question 4
Which clinical feature is not typical of Parkinson’s disease?
a) Rest tremor
b) Bradykinesia
c) Rigidity
d) Spastic paralysis
Explanation: Parkinson’s disease is characterized by rest tremor, bradykinesia, rigidity, and postural instability. Spastic paralysis occurs in upper motor neuron lesions, not basal ganglia dysfunction. Answer: d) Spastic paralysis. Distinguishing Parkinsonism from pyramidal tract damage clinically relies on absence of spasticity and hyperreflexia, despite motor difficulties and tremors.
Question 5
Which neurotransmitter imbalance causes Huntington’s disease?
a) Loss of GABA and acetylcholine
b) Excess dopamine
c) Loss of dopamine
d) Increased serotonin
Explanation: Huntington’s disease features degeneration of striatal GABAergic and cholinergic neurons, combined with relative dopaminergic overactivity. This imbalance produces choreiform hyperkinetic movements. Answer: a) Loss of GABA and acetylcholine. Dopamine blockade may reduce symptoms, unlike Parkinson’s disease where dopamine replacement is therapeutic and symptomatically beneficial clinically.
Question 6
Which drug increases brain dopamine by crossing blood-brain barrier?
a) Levodopa
b) Dopamine
c) Carbidopa
d) Bromocriptine
Explanation: Dopamine itself cannot cross the blood-brain barrier. Levodopa, its precursor, is converted to dopamine in brain. Carbidopa prevents peripheral breakdown, enhancing central availability. Answer: a) Levodopa. Bromocriptine is a dopamine agonist, while dopamine injection only acts peripherally without improving Parkinson’s motor symptoms effectively within CNS.
Question 7
Which basal ganglia lesion produces hemiballismus?
a) Subthalamic nucleus
b) Putamen
c) Caudate nucleus
d) Globus pallidus interna
Explanation: Hemiballismus, a flinging hyperkinetic movement disorder, occurs due to contralateral subthalamic nucleus lesion. Subthalamus normally excites globus pallidus interna, inhibiting thalamus. Its damage reduces inhibition, causing excessive cortical motor output. Answer: a) Subthalamic nucleus. Other basal ganglia nuclei lesions cause Parkinsonism or chorea, not violent ballistic movements.
Question 8
Which dopaminergic pathway is associated with reward and addiction?
a) Nigrostriatal pathway
b) Mesolimbic pathway
c) Tuberoinfundibular pathway
d) Mesocortical pathway
Explanation: Mesolimbic pathway projects from ventral tegmental area to nucleus accumbens, mediating reward, reinforcement, and addiction. Answer: b) Mesolimbic pathway. Nigrostriatal controls movement, mesocortical regulates cognition and emotion, and tuberoinfundibular inhibits prolactin secretion. Dopamine thus has multiple distinct functional pathways in the central nervous system overall.
Question 9
Blockade of which dopamine pathway leads to drug-induced Parkinsonism?
a) Mesolimbic
b) Mesocortical
c) Nigrostriatal
d) Tuberoinfundibular
Explanation: Antipsychotic drugs blocking D2 receptors in the nigrostriatal pathway cause extrapyramidal symptoms resembling Parkinson’s disease. Answer: c) Nigrostriatal. Mesolimbic blockade improves psychosis, mesocortical blockade causes cognitive dulling, and tuberoinfundibular blockade elevates prolactin. Understanding pathway selectivity helps minimize antipsychotic side effects clinically during patient treatment overall effectively.
Question 10
Stimulation of which dopamine receptor subtype inhibits indirect pathway activity?
a) D1
b) D2
c) D3
d) D5
Explanation: D2 receptors inhibit striatal neurons of the indirect pathway, reducing thalamic suppression and promoting movement. Answer: b) D2. D1 receptors activate direct pathway, D3 and D5 have roles in limbic and cortical areas. Balanced D1/D2 signaling ensures smooth motor control within basal ganglia circuits clinically.
Question 11
Which hypothalamic hormone secretion is inhibited by tuberoinfundibular dopamine pathway?
a) Growth hormone
b) Cortisol
c) Prolactin
d) Thyroxine
Explanation: Dopaminergic neurons of tuberoinfundibular pathway inhibit prolactin release from anterior pituitary lactotrophs. Blockade or damage increases prolactin, causing galactorrhea and infertility. Answer: c) Prolactin. Dopamine agonists treat hyperprolactinemia, while antagonists may induce it. Other hypothalamic hormones are regulated differently by respective hypothalamic releasing factors clinically overall.
Keyword Definitions
• Proprioception: Sense of position and movement from muscles and joints.
• Vibration sense: Perception of oscillatory stimuli via large myelinated fibers.
• Dorsal columns: Ascending pathway for fine touch, vibration, and proprioception.
• Medial lemniscus: Brainstem tract formed by decussated dorsal column fibers.
• Fasciculus gracilis: Dorsal column for lower limb and trunk below T6.
• Fasciculus cuneatus: Dorsal column for upper limb and trunk above T6.
• VPL nucleus: Thalamic relay for body somatosensation to cortex.
• Romberg sign: Instability on eye closure indicating proprioceptive loss.
• Brown-Séquard syndrome: Hemisection causing ipsilateral dorsal column loss, contralateral pain loss.
• Tabes dorsalis: Neurosyphilis causing posterior column degeneration and sensory ataxia.
• Syringomyelia: Central canal cavity causing bilateral pain/temperature loss with spared dorsal columns.
• Asterognosis: Inability to recognize objects by touch despite intact basic sensation.
• Large-fiber neuropathy: Peripheral nerve disorder affecting vibration and position sense early.
Chapter: Neurophysiology
Topic: Somatosensory Pathways
Subtopic: Dorsal Column–Medial Lemniscus System
Lead Question – 2012
Loss of proprioception & fine touch ?
a) Anterior spinothalamic tract
b) Lateral spinothalamic tract
c) Dorsal column
d) Corticospinal tract
Explanation: Loss of proprioception, vibration, and fine discriminative touch indicates dorsal column–medial lemniscus pathway dysfunction. Large myelinated fibers ascend ipsilaterally to gracile and cuneate nuclei, then decussate to medial lemniscus and VPL. Answer: c) Dorsal column. Spinothalamic tracts carry pain and temperature; corticospinal mediates voluntary movement, not somatosensory modalities, primarily pathways.
Question 2
A 55-year-old with numb feet, gait unsteadiness, and positive Romberg has impaired vibration at toes. Which pathway is damaged?
a) Dorsal columns
b) Lateral corticospinal tract
c) Spinothalamic tract
d) Vestibulospinal tract
Explanation: Subacute combined degeneration from vitamin B12 deficiency damages large myelinated posterior column fibers, producing sensory ataxia, impaired vibration, and proprioceptive loss in legs. Answer: a) Dorsal columns. Lateral corticospinal damage causes weakness and spasticity; spinothalamic lesions impair pain and temperature; vestibulospinal tracts mediate balance reflexes without conveying discriminative touch signals.
Question 3
After a knife injury causing right T10 hemisection, which deficit occurs on the right below the lesion?
a) Loss of pain and temperature
b) Loss of vibration and proprioception
c) Flaccid paralysis below lesion
d) Bilateral pain loss
Explanation: Brown-Séquard hemisection causes ipsilateral loss of dorsal column modalities below the lesion from uncrossed ascent, and contralateral pain/temperature loss after spinothalamic decussation. Answer: b) Loss of vibration and proprioception. Flaccid paralysis occurs at the level from anterior horn involvement, not below. Bilateral pain loss suggests central cord lesions, not hemisection.
Question 4
Which thalamic nucleus relays body fine touch, vibration, and proprioception to cortex?
a) VPL nucleus
b) VPM nucleus
c) Lateral geniculate nucleus
d) Medial geniculate nucleus
Explanation: The ventral posterolateral thalamic nucleus relays somatosensory information from body—both medial lemniscus and spinothalamic—to the primary somatosensory cortex. Lesions impair discriminative touch, vibration, and proprioception contralaterally. Answer: a) VPL nucleus. VPM handles facial sensation; LGN vision; MGN audition. Precise localization of body sensation depends critically on intact VPL relay neurons.
Question 5
A patient with lightning pains, wide-based gait, and positive Romberg likely has damage to which structure?
a) Dorsal columns
b) Spinocerebellar tracts
c) Ventral horn cells
d) Substantia nigra
Explanation: Tabes dorsalis from neurosyphilis degenerates dorsal columns and roots, causing lightning pains, sensory ataxia, impaired vibration, and positive Romberg sign. Answer: a) Dorsal columns. Spinocerebellar tract disease produces limb ataxia without Romberg positivity; ventral horn disease causes lower motor neuron weakness; substantia nigra degeneration produces Parkinsonism, not sensory ataxia, classically.
Question 6
Fine touch from the right hand ascends initially in which tract?
a) Spinothalamic tract
b) Fasciculus gracilis
c) Fasciculus cuneatus
d) Dorsal spinocerebellar tract
Explanation: Fine touch and proprioceptive signals from the upper limb ascend in the ipsilateral fasciculus cuneatus to synapse in the cuneate nucleus before crossing as internal arcuate fibers. Answer: c) Fasciculus cuneatus. Fasciculus gracilis conveys lower limb input; spinothalamic carries pain and temperature; dorsal spinocerebellar conveys unconscious proprioception, not discriminative touch.
Question 7
A patient cannot identify a key by touch in the left hand, yet basic touch is intact. Likely lesion?
a) Cerebellar hemisphere
b) Postcentral gyrus
c) Precentral gyrus
d) Dorsal horn
Explanation: Inability to recognize objects by touch with intact primary modalities indicates cortical sensory loss—astereognosis—from a contralateral parietal lesion, usually postcentral gyrus (primary somatosensory cortex). Answer: b) Postcentral gyrus. Precentral gyrus is motor; cerebellum coordinates movement but not stereognosis; dorsal columns carry signals, yet cortical interpretation is required for object recognition.
Question 8
Bilateral loss of pain and temperature over shoulders with preserved vibration suggests which tract is spared?
a) Spinothalamic tract
b) Lateral corticospinal tract
c) Anterior horn cells
d) Dorsal columns
Explanation: Syringomyelia damages decussating anterior commissural spinothalamic fibers in the cervical cord, causing bilateral cape-like pain and temperature loss while sparing dorsal column modalities. Answer: d) Dorsal columns are spared. Thus vibration and proprioception remain intact. Lateral corticospinal may be affected later causing weakness; dorsal spinocerebellar mediates unconscious proprioception effectively overall.
Question 9
A medial medullary infarct damaging the medial lemniscus causes which deficit?
a) Ipsilateral pain and temperature loss
b) Loss of contralateral discriminative touch
c) Ipsilateral loss of vibration
d) Bilateral pain loss
Explanation: A medial medullary lesion involving the medial lemniscus produces contralateral loss of fine touch, vibration, and proprioception from body due to disruption of dorsal column fibers. Answer: b) Loss of contralateral discriminative touch. Pain and temperature are carried by spinothalamic tract located laterally; hypoglossal involvement would cause ipsilateral tongue weakness.
Question 10
Which modality is typically earliest impaired in large-fiber diabetic neuropathy?
a) Impaired vibration sense
b) Spasticity
c) Hyperalgesia
d) Nystagmus
Explanation: Large-fiber peripheral neuropathy in diabetes affects vibration and position sense earliest, causing positive Romberg and sensory ataxia. Answer: a) Impaired vibration sense. Pain and temperature rely on small fibers; strength may be preserved; hyperreflexia suggests upper motor neuron disease, not peripheral neuropathy, which typically shows reduced or absent ankle reflexes.
Question 11
Which bedside test best assesses dorsal column proprioception?
a) Graphesthesia on palm
b) Vibration at medial malleolus
c) Great toe position sense
d) Hot/cold discrimination
Explanation: Testing joint position at the great toe assesses conscious proprioception via dorsal columns and medial lemniscus. Eyes are closed to remove visual cues. Answer: c) Great toe position sense. Tuning fork tests vibration, not position; pinprick examines spinothalamic pain; plantar response assesses corticospinal integrity, unrelated to dorsal column proprioceptive function.
Keyword Definitions
• Spinocerebellar tract: Pathways conveying unconscious proprioception to cerebellum for coordination.
• Dorsal spinocerebellar: Ipsilateral lower limb proprioceptive tract entering via inferior peduncle.
• Ventral spinocerebellar: Tract that double-crosses and conveys integrated movement signals to cerebellum.
• Cuneocerebellar: Upper limb equivalent of dorsal spinocerebellar, via accessory cuneate nucleus.
• Clarke’s column: Nucleus dorsalis (T1–L2) origin of dorsal spinocerebellar fibres.
• Inferior cerebellar peduncle: Major cerebellar input for dorsal spinocerebellar and cuneocerebellar tracts.
• Unconscious proprioception: Automatic sensory feedback used to adjust movement without awareness.
• Dysmetria: Overshoot or undershoot of target during voluntary movement, sign of cerebellar dysfunction.
• Intention tremor: Tremor appearing during voluntary movement, characteristic of cerebellar disease.
• Romberg sign: Sway or fall on eye closure from proprioceptive loss (dorsal column), not cerebellar typically.
• Heel-to-shin: Bedside test for lower limb cerebellar coordination and spinocerebellar function.
Chapter: Neurophysiology
Topic: Cerebellar Systems
Subtopic: Spinocerebellar Tracts and Function
Lead Question – 2012
True about spinocerebellar tract is?
a) Equilibrium
b) Smoothens and coordinates movement
c) Learning induced by change in vestibulo ocular reflex
d) Planning and programming
Explanation: Spinocerebellar tracts carry unconscious proprioceptive information from muscles and joints to the cerebellum, enabling real-time adjustment of ongoing movements and posture. They assist coordination and timing rather than motor planning or voluntary initiation. Therefore they smooth and coordinate movement. Answer: b) Smoothens and coordinates movement for precise limb control continuously.
Question 2
Dorsal spinocerebellar tract originates from which nucleus?
a) Clarke’s column
b) Accessory cuneate nucleus
c) Inferior olivary nucleus
d) Red nucleus
Explanation: The dorsal spinocerebellar tract arises from Clarke’s column (nucleus dorsalis) in spinal segments T1 to L2, conveying ipsilateral proprioceptive information from lower limbs to the cerebellum via the inferior cerebellar peduncle. It does not decussate. Answer: a) Clarke’s column. This tract is essential for unconscious proprioception and limb coordination clinically.
Question 3
A lesion of spinocerebellar tract produces which clinical sign?
a) Ipsilateral limb ataxia
b) Contralateral weakness
c) Loss of vibration sense only
d) Sensory level with aneasthesia
Explanation: Spinocerebellar tract lesions produce ipsilateral limb ataxia because most cerebellar afferents enter the cerebellum without crossing or double-cross, preserving same-side representation. Patients show dysmetria, decomposition of movement, and intention tremor on the affected side. Answer: a) Ipsilateral limb ataxia. Coordination deficits worsen with eyes closed and during rapid alternating movements.
Question 4
Which is true about ventral spinocerebellar tract?
a) It never crosses
b) It conveys conscious proprioception
c) It double-crosses
d) It terminates in thalamus
Explanation: The ventral spinocerebellar tract transmits integrated proprioceptive and interneuronal activity related to ongoing limb movement. It decussates twice: once in the spinal cord and again within the cerebellum, resulting in ipsilateral cerebellar representation ultimately. Answer: c) It double-crosses to reach the cerebellum. This anatomical feature explains localization of cerebellar signs.
Question 5
Primary modality carried by spinocerebellar tracts is?
a) Conscious proprioception
b) Unconscious proprioception
c) Pain and temperature
d) Fine tactile discrimination
Explanation: Spinocerebellar pathways convey unconscious proprioception from muscle spindles and Golgi tendon organs to cerebellar cortex, enabling automatic postural adjustments and gait coordination. They are distinct from dorsal columns that mediate conscious proprioception. Answer: b) Unconscious proprioception. Clinical lesions produce ataxia yet preserve conscious position sense; coordination testing reveals deficits often.
Question 6
Finger-to-nose test primarily assesses which system?
a) Cerebellar coordination including spinocerebellar input
b) Dorsal column conscious proprioception only
c) Spinothalamic tract function
d) Pyramidal tract strength
Explanation: Finger-to-nose test evaluates cerebellar coordination and proprioceptive integration including spinocerebellar inputs. Dysmetria, intention tremor, and decomposition of movement during this test indicate cerebellar dysfunction. It does not differentiate conscious from unconscious proprioception but assesses functional output of cerebellum. Answer: a) True. Clinically helps localize lesion to hemisphere or vermis region.
Question 7
Which hereditary disease affects spinocerebellar tracts prominently?
a) Multiple sclerosis
b) Amyotrophic lateral sclerosis
c) Friedreich ataxia
d) Myasthenia gravis
Explanation: Friedreich ataxia causes degeneration of spinocerebellar tracts, dorsal columns, and corticospinal tracts due to frataxin deficiency. Patients present with progressive gait ataxia, loss of vibration and proprioception, areflexia, and cardiomyopathy. Genetic testing confirms GAA repeat expansion. Answer: c) Friedreich ataxia. Onset usually adolescence; progression causes severe disability needing supportive care.
Question 8
Dorsal spinocerebellar fibres enter cerebellum via which peduncle?
a) Inferior cerebellar peduncle
b) Middle cerebellar peduncle
c) Superior cerebellar peduncle
d) None of the above
Explanation: Dorsal spinocerebellar fibers ascend ipsilaterally and enter cerebellum through the inferior cerebellar peduncle, carrying lower limb proprioceptive information. Ventral spinocerebellar fibers primarily enter via superior peduncle after double crossing. Knowledge of peduncle entry assists lesion localization. Answer: a) Inferior cerebellar peduncle. Distinguishing peduncle entry aids accurate lesion localization clinically rapidly.
Question 9
Romberg sign in spinocerebellar or cerebellar lesions is usually?
a) Positive only with eyes open
b) Negative (does not depend on vision)
c) Positive only with vibration loss
d) Always bilateral sensory level
Explanation: Romberg sign becomes positive when proprioceptive input via dorsal columns is lost, causing increased sway with eye closure. Cerebellar or spinocerebellar lesions produce ataxia independent of visual input, so patients remain unstable with eyes open and closed; Romberg is typically negative. Answer: b) Negative. Clinical testing distinguishes lesion location effectively.
Question 10
Best bedside test for lower limb spinocerebellar function is?
a) Romberg test alone
b) Vibration at toe only
c) Rapid alternating foot movements only
d) Heel-to-shin test
Explanation: Heel-to-shin maneuver tests lower limb coordination and cerebellar integration of proprioceptive input including spinocerebellar feedback. Patients with spinocerebellar tract or cerebellar hemisphere lesions exhibit dysmetria and inability to maintain a smooth, straight movement along the shin. Answer: d) Heel-to-shin test. It detects ipsilateral coordination deficits and helps lateralize lesions accurately.
Question 11
Unconscious proprioception from the upper limb is conveyed by?
a) Dorsal spinocerebellar tract
b) Cuneocerebellar tract
c) Ventral spinothalamic tract
d) Lateral corticospinal tract
Explanation: Cuneocerebellar tract carries unconscious proprioceptive input from upper limbs via accessory cuneate nucleus to the cerebellum through inferior peduncle, analogous to dorsal spinocerebellar tract for lower limbs. Lesions impair ipsilateral upper limb coordination and contribute to ataxia. Answer: b) Cuneocerebellar tract. Clinically causes dysmetria and intention tremor during voluntary tasks.
Keyword Definitions
• Vomiting centre: Brainstem nuclei coordinating emesis reflex integrating multisource inputs.
• Area postrema: Chemoreceptor trigger zone at floor of fourth ventricle, outside BBB.
• Nucleus tractus solitarius (NTS): Primary visceral sensory nucleus relaying vagal afferents.
• Chemoreceptor trigger zone (CTZ): Detects blood-borne emetic agents and drugs.
• Vestibular nuclei: Brainstem centers mediating motion and balance inputs causing motion sickness.
• Reticular formation: Medullary network housing central pattern generator for vomiting.
• Ondansetron: 5-HT3 receptor antagonist used for chemotherapy and postoperative nausea.
• Scopolamine: Antimuscarinic antiemetic effective for motion sickness via vestibular blockade.
• Apomorphine: Dopamine agonist that stimulates CTZ and induces vomiting pharmacologically.
• Projectile vomiting: Forceful vomiting often from raised intracranial pressure or posterior fossa lesions.
• NK1 antagonist (Aprepitant): Blocks substance P to prevent chemotherapy-induced nausea and vomiting.
Chapter: Neurophysiology
Topic: Brainstem Reflexes
Subtopic: Vomiting Mechanisms and Clinical Correlates
Lead Question – 2012
Vomiting centre is situated in the: (September 2008)
a) Hypothalamus
b) Midbrain
c) Pons
d) Medulla
Explanation: Vomiting is coordinated by a reflex center located in the medulla oblongata, integrating signals from chemoreceptor trigger zone, vestibular system, GI tract, and higher centers. Lesions or irritants trigger emesis via medullary nuclei. Answer: d) Medulla. This clinically explains why brainstem lesions often produce persistent vomiting and autonomic disturbances.
Question 2
Which structure functions as the chemoreceptor trigger zone for emesis?
a) Nucleus ambiguus
b) Nucleus tractus solitarius
c) Area postrema
d) Dorsal motor nucleus of vagus
Explanation: The chemoreceptor trigger zone lies in the area postrema of the dorsal medulla at the floor of the fourth ventricle, outside the blood-brain barrier, detecting blood-borne emetic agents and drugs. It relays to the vomiting center to initiate emesis. Answer: c) Area postrema. This localization explains sensitivity to chemotherapeutic agents.
Question 3
Visceral afferents from the gastrointestinal tract synapse primarily in which nucleus relevant to vomiting?
a) Hypoglossal nucleus
b) Nucleus tractus solitarius
c) Inferior olivary nucleus
d) Dorsal motor nucleus of vagus
Explanation: Visceral afferents from gastrointestinal tract travel via vagus and glossopharyngeal nerves to the nucleus tractus solitarius in the medulla, which integrates sensory input and projects to the vomiting center and reticular formation. This pathway mediates reflex emesis from gastric irritation or inflammation. Answer: b) Nucleus tractus solitarius clinically important centrally.
Question 4
Which antiemetic class blocks serotonin-mediated vagal and CTZ signals effectively?
a) Dopamine antagonists
b) Anticholinergics
c) 5-HT3 receptor antagonists
d) NK1 receptor antagonists
Explanation: 5-HT3 receptor antagonists such as ondansetron block serotonin-mediated stimulation of vagal afferents and the chemoreceptor trigger zone, effectively preventing chemotherapy-induced and postoperative nausea. They act centrally and peripherally with good efficacy and tolerability and are first-line antiemetics in many protocols. Answer: a) Ondansetron. Widely used clinically for nausea control effectively.
Question 5
Motion sickness and vestibular-induced vomiting primarily involve which structures?
a) Area postrema only
b) Vestibular nuclei
c) Cerebellar vermis only
d) Hypothalamus exclusively
Explanation: Vestibular apparatus and vestibular nuclei in brainstem detect motion and send signals to vomiting center and cerebellum; conflicts between visual and vestibular input provoke motion sickness and emesis via connections to nucleus tractus solitarius and area postrema. Antihistamines reduce vestibular input. Answer: b) Vestibular nuclei. Used antiemetics target this pathway.
Question 6
Which drug class is known to directly stimulate the CTZ and produce emesis historically?
a) Anticholinergics
b) Serotonin antagonists
c) Dopamine agonists (e.g., apomorphine)
d) NK1 antagonists
Explanation: Apomorphine, a dopamine agonist, stimulates D2 receptors in the chemoreceptor trigger zone (area postrema), provoking profound emesis. Historically used as an emetic, it demonstrates pharmacologic activation of vomiting circuits. Dopamine antagonists block this reflex therapeutically. Answer: c) Apomorphine. Now replaced by safer antiemetics in teaching.
Question 7
Strong risk factors for postoperative nausea and vomiting include which of the following?
a) Male sex and smoking
b) Female sex and opioid use
c) Elderly age exclusively
d) Short duration surgeries only
Explanation: Risk factors for postoperative nausea and vomiting include female sex, history of motion sickness or prior PONV, nonsmoking status, use of volatile anesthetics or opioids, lengthy surgery, and younger age. Multimodal prophylaxis reduces incidence by targeting multiple pathways. Answer: b) Female sex and opioid exposure are significant risk contributors clinically.
Question 8
Best prophylactic agent for motion sickness is?
a) Ondansetron
b) Metoclopramide
c) Domperidone
d) Scopolamine
Explanation: Anticholinergic scopolamine applied transdermally blocks muscarinic receptors in vestibular nuclei and central vomiting pathways, preventing motion-induced nausea and vomiting. Histamine H1 antagonists like promethazine also help. Side effects include dry mouth, blurred vision, and sedation. Answer: d) Scopolamine. It is recommended prophylactically for susceptible patients before travel or procedures commonly.
Question 9
The central pattern generator coordinating emesis resides in which region?
a) Medullary reticular formation
b) Hypothalamus
c) Midbrain periaqueductal gray
d) Pontine tegmentum exclusively
Explanation: Emesis results from activation of a central pattern generator located in the medullary reticular formation and adjacent reticular nuclei, coordinating respiratory, upper GI, and pharyngeal muscles to produce vomiting. This network receives multisensory inputs including chemoreceptor trigger zone and vestibular signals. Answer: a) Medullary reticular formation critical for protective reflexes.
Question 10
Projectile vomiting without nausea often indicates which pathology?
a) Gastroenteritis
b) Metabolic alkalosis only
c) Posterior fossa lesion compressing medulla
d) Peripheral vestibular neuritis
Explanation: Projectile vomiting without preceding nausea suggests increased intracranial pressure or posterior fossa lesion compressing medullary centers. Vomiting may be forceful and predominantly nocturnal. Early recognition mandates neuroimaging to identify obstructive hydrocephalus or tumor. Answer: c) Posterior fossa lesion causing medullary compression requiring urgent neurosurgical decompression to prevent herniation and death.
Question 11
Which agent is recommended to prevent both acute and delayed chemotherapy-induced emesis when combined with others?
a) Ondansetron alone
b) Aprepitant (NK1 antagonist)
c) Metoclopramide alone
d) Scopolamine patch
Explanation: Aprepitant, an NK1 receptor antagonist, blocks substance P signaling in vomiting pathways, reducing acute and delayed chemotherapy-induced nausea and vomiting when combined with 5-HT3 antagonists and corticosteroids. It improves control of emesis after highly emetogenic chemotherapy. Answer: b) Aprepitant. Recommended in guidelines for high emetic risk regimens to reduce vomiting.
Keyword Definitions
• Central chemoreceptors: Medullary sensors responding to CSF pH/CO₂ changes and driving ventilation.
• Peripheral chemoreceptors: Carotid and aortic body receptors sensing arterial O₂, CO₂ and pH.
• Carotid body: Small chemo-sensitive organ at carotid bifurcation.
• Aortic body: Chemoreceptor tissue near aortic arch.
• Area postrema: Brainstem chemoreceptive region outside blood-brain barrier.
• Nucleus tractus solitarius (NTS): Medullary visceral sensory nucleus receiving vagal and glossopharyngeal afferents.
• Hypercapnia: Elevated arterial CO₂ stimulating central chemoreceptors.
• Hypoxia: Low arterial O₂ primarily stimulating peripheral chemoreceptors.
• Ventilatory drive: Neural control that adjusts rate and depth of breathing.
• Respiratory reflexes: Integrated responses coordinating breathing with cardiovascular state.
• Respiratory failure: Clinical condition from inadequate ventilation or gas exchange.
Chapter: Respiratory Physiology
Topic: Chemoreceptors and Respiratory Control
Subtopic: Central and Peripheral Chemoreceptors
Lead Question – 2012 (177)
Chemoreceptors are located in which area?
a) Medulla
b) Arch of aorta
c) Bifurcation of carotid artery
d) All of the above
Explanation: Chemoreceptors that regulate ventilation are both central and peripheral: central receptors in the medulla sense CSF pH changes from CO₂; peripheral chemoreceptors reside in the carotid bifurcation and aortic arch sensing arterial O₂, CO₂ and pH. They act together to regulate breathing. Answer: d) All of the above.
Question 2
Central chemoreceptors primarily respond to which stimulus?
a) Arterial O₂ fall
b) CSF pH change due to CO₂ diffusion
c) Blood glucose levels
d) Systemic blood pressure changes
Explanation: Central chemoreceptors in the ventrolateral medulla detect changes in CSF pH produced by CO₂ diffusion across the blood-brain barrier. This mechanism drives ventilation in response to hypercapnia and maintains acid-base homeostasis. Peripheral O₂ sensing is separate. Answer: b) CSF pH change due to CO₂ diffusion.
Question 3
Peripheral chemoreceptors that sense hypoxia at the carotid bifurcation transmit via which nerve?
a) Vagus nerve (X)
b) Glossopharyngeal nerve (IX)
c) Hypoglossal nerve (XII)
d) Facial nerve (VII)
Explanation: Carotid body afferents travel in the glossopharyngeal nerve (cranial nerve IX) to the nucleus tractus solitarius, which relays to respiratory centers, producing rapid ventilatory responses to hypoxia. Answer: b) Glossopharyngeal nerve (IX).
Question 4
Aortic body chemoreceptors convey information primarily via which pathway?
a) Glossopharyngeal nerve (IX) only
b) Vagus nerve (X) afferents
c) Trigeminal nerve (V) afferents
d) Direct spinal tract only
Explanation: Aortic arch chemoreceptors send afferent signals largely through vagal (X) fibers to the nucleus tractus solitarius in the medulla, complementing carotid body input to adjust ventilation and autonomic reflexes. Answer: b) Vagus nerve (X) afferents.
Question 5
Which chemoreceptor set predominates in response to acute hypoxemia?
a) Central medullary chemoreceptors
b) Peripheral carotid chemoreceptors
c) Renal chemoreceptors
d) Cortical chemoreceptors
Explanation: Peripheral carotid chemoreceptors are the primary detectors of arterial hypoxemia, responding rapidly to low PaO₂ and increasing ventilation quickly; central chemoreceptors mainly respond to CO₂/pH changes. Answer: b) Peripheral carotid chemoreceptors.
Question 6
Which condition blunts the ventilatory response to hypoxia due to carotid body removal or dysfunction?
a) Enhanced hypoxic drive
b) Diminished hypoxic ventilatory response
c) Increased cough reflex
d) Hyperventilation at rest
Explanation: Loss or dysfunction of carotid bodies reduces the rapid ventilatory response to hypoxia, causing a blunted hypoxic ventilatory drive clinically; patients rely more on central CO₂ sensitivity, risking inadequate ventilation during low oxygen states. Answer: b) Diminished hypoxic ventilatory response.
Question 7
Drugs that depress central chemoreceptor sensitivity commonly cause which effect?
a) Tachypnea
b) Hypoventilation and hypercapnia
c) Increased oxygen saturation
d) Enhanced hypoxic drive
Explanation: Sedatives and opioids depress central chemoreceptor responsiveness, reducing ventilatory drive to CO₂ and causing hypoventilation with rising arterial CO₂ and respiratory acidosis; careful monitoring and dose adjustment are clinically required. Answer: b) Hypoventilation and hypercapnia.
Question 8
Which bedside test best evaluates peripheral chemoreceptor function?
a) Hypercapnic ventilatory challenge
b) Hypoxic ventilatory response testing
c) Valsalva maneuver only
d) Pupillary reflex testing
Explanation: Hypoxic ventilatory response testing assesses peripheral chemoreceptor sensitivity by measuring ventilation changes when inspired oxygen is lowered; it helps distinguish peripheral dysfunction from central CO₂ responsiveness. Answer: b) Hypoxic ventilatory response testing.
Question 9
Which pathology explains reduced central chemosensitivity causing sleep hypoventilation?
a) Medullary lesion or congenital central hypoventilation syndrome
b) Peripheral nerve entrapment
c) Middle ear infection
d) Muscle strain
Explanation: Central hypoventilation may arise from medullary damage or congenital central hypoventilation syndrome, impairing CO₂ detection and ventilation particularly during sleep, often necessitating ventilatory support. Answer: a) Medullary lesion or congenital central hypoventilation syndrome.
Question 10
Which combination best describes chemoreceptor roles?
a) Carotid bodies sense CO₂ only; medulla senses O₂ only
b) Peripheral receptors detect hypoxia quickly; central receptors monitor CO₂/pH continuously
c) Aortic arch controls consciousness; carotid bodies control heart rate only
d) None of the above
Explanation: Peripheral receptors (carotid and aortic bodies) detect hypoxia rapidly and signal ventilatory increase; central medullary chemoreceptors continuously monitor CO₂/pH to regulate baseline ventilation. Together they coordinate appropriate respiratory responses. Answer: b) Peripheral receptors detect hypoxia quickly; central receptors monitor CO₂/pH continuously.
Question 11
Which clinical statement is correct regarding chemoreceptor physiology?
a) Only central receptors respond to severe hypoxia
b) Peripheral receptors play no role in ventilatory adaptation at altitude
c) Both central and peripheral chemoreceptors integrate to control ventilation
d) Chemoreceptors exclusively control heart rate, not breathing
Explanation: Ventilatory control reflects integrated input from central and peripheral chemoreceptors, with each contributing specific sensitivity to CO₂/pH and O₂ changes; combined signaling ensures respiratory adaptation to metabolic demands, altitude, and disease states. Answer: c) Both central and peripheral chemoreceptors integrate to control ventilation.
Keyword Definitions
• Taste transduction: Mechanisms by which chemical stimuli are converted to neural signals.
• ENaC: Epithelial sodium channels mediating salty taste via Na+ influx.
• Gustducin: Taste G-protein involved in sweet, umami, and bitter signalling cascades.
• PKD2L1: Proton-sensitive channel implicated in sour taste transduction.
• Chorda tympani: Facial nerve branch (VII) carrying anterior two-thirds taste.
• Nucleus tractus solitarius (NTS): Medullary gustatory relay receiving cranial nerve afferents.
• VPM nucleus: Thalamic relay for facial/gustatory sensory information to cortex.
• Dysgeusia: Distorted taste perception commonly seen in disease or after drugs.
• Ageusia: Loss of taste sensation.
• Taste cell turnover: Continuous replacement of taste receptor cells from basal progenitors.
Chapter: Neurophysiology
Topic: Gustation (Taste Physiology)
Subtopic: Taste Transduction Mechanisms and Clinical Correlates
Lead Question – 2012
Salty taste is due to?
a) Ca+2 channels
b) Na+ channels
c) G-protein
d) H+ channels
Explanation: Salt taste transduction primarily occurs via epithelial sodium channels on taste receptor cells which allow Na+ influx, depolarizing the cell and triggering neurotransmitter release to gustatory nerves. This receptor mechanism explains perception of salty stimuli. Answer: b) Na+ channels. Clinically, sodium channel blockers reduce salty perception in experimental settings commonly.
Question 2
Sour taste transduction is primarily mediated by?
a) G-protein coupled receptors
b) Voltage-gated Ca2+ channels
c) ENaC channels
d) H+ (proton) channels
Explanation: Sour taste arises from H+ ions entering taste receptor cells through proton-sensitive channels (e.g., PKD2L1 or HCN modulation), causing depolarization and neurotransmitter release to gustatory afferents. This transduction distinguishes acidity in foods and guides ingestion or rejection. Answer: d) H+ channels. Clinically, sour detection may be reduced in zinc deficiency.
Question 3
Bitter taste receptors transduce signals via which mechanism?
a) ENaC-mediated depolarization
b) Ionotropic glutamate receptors
c) G-protein coupled T2R receptors
d) Direct H+ gating
Explanation: Bitter taste perception relies on G-protein–coupled T2R receptors activating gustducin and PLCβ2, increasing intracellular calcium and neurotransmitter release, signaling potential toxins and causing aversive responses. Genetic variability affects sensitivity to bitter compounds clinically. Answer: c) G-protein. Pharmacologic blockade of these pathways blunts bitter detection during drug therapy in some patients.
Question 4
Sweet taste transduction occurs through?
a) ENaC channels
b) Ionotropic receptors only
c) G-protein coupled T1R receptors
d) H+ channels
Explanation: Sweet taste is mediated by heterodimeric T1R2/T1R3 G-protein–coupled receptors activating gustducin and second messenger cascades, increasing intracellular calcium to depolarize taste cells and signal pleasant carbohydrate-rich nutrition. Artificial sweeteners selectively activate these receptors. Answer: c) G-protein. Clinical disorders like diabetes may alter sweet perception via receptor and central processing changes.
Question 5
Umami (savory) taste primarily uses which receptors?
a) ENaC only
b) Ionotropic serotonin receptors
c) T1R1/T1R3 G-protein receptors or mGluRs
d) Voltage-gated Na+ channels
Explanation: Umami taste responds to L-glutamate via T1R1/T1R3 G-protein–coupled receptors or mGluR receptors, enhancing savory flavor perception and signaling protein-rich foods. Monosodium glutamate exemplifies this transduction. Answer: c) G-protein. Clinical taste disturbances in chemotherapy can reduce umami sensitivity, contributing to anorexia and weight loss requiring dietary counseling often for patient recovery.
Question 6
Taste from anterior two-thirds of tongue is carried by?
a) Chorda tympani (facial nerve VII)
b) Glossopharyngeal nerve (IX)
c) Vagus nerve (X)
d) Hypoglossal nerve (XII)
Explanation: Taste from anterior two-thirds of tongue is transmitted by the chorda tympani branch of facial nerve (VII), carrying modality-specific signals to nucleus of solitary tract. Lesions produce ipsilateral ageusia and dysgeusia impacting appetite and nutrition. Answer: a) Chorda tympani (facial nerve). Testing assesses gustatory function clinically and guides management decisions.
Question 7
First central relay for taste afferents is?
a) Ventral posterolateral nucleus (VPL)
b) Nucleus tractus solitarius (NTS) in medulla
c) Insular cortex directly
d) Hypothalamus
Explanation: Primary central relay for gustatory afferents is the nucleus of the solitary tract in the medulla, receiving inputs from facial, glossopharyngeal, and vagus nerves and projecting to thalamus and cortex for taste perception and reflexes like salivation. Answer: b) Nucleus tractus solitarius (NTS). Lesions impair gustatory reflexes and taste perception.
Question 8
Which pharmacologic agent reduces salty taste by blocking ENaC experimentally?
a) Lidocaine
b) Amiloride
c) Ondansetron
d) Scopolamine
Explanation: Epithelial sodium channel (ENaC) blockers such as amiloride reduce perception of salty taste by inhibiting Na+ entry into taste cells, demonstrating pharmacologic modulation of taste transduction. This informs pathophysiology and potential therapies for dysgeusia. Answer: b) Na+ channels. Clinical trials assess amiloride's effect on taste alteration in various disorders today.
Question 9
Which condition commonly causes ipsilateral anterior two-thirds taste loss?
a) Bell's palsy
b) Stroke of occipital lobe
c) Otitis externa only
d) Myasthenia gravis
Explanation: Bell's palsy commonly causes ipsilateral anterior two-thirds taste loss due to chorda tympani fiber involvement within the facial nerve; patients report dysgeusia and ageusia with associated facial weakness. Distinguishing peripheral facial palsy from central lesions guides prognosis and therapy, often including corticosteroids. Answer: a) Bell's palsy improving recovery in many.
Question 10
Approximate turnover time of taste receptor cells is?
a) Several years
b) Ten to fourteen days
c) Months
d) Hours
Explanation: Taste receptor cells have a high turnover, regenerating from basal progenitors approximately every ten to fourteen days, maintaining gustatory sensitivity and repair after injury; disrupted regeneration from chemotherapy or aging contributes to chronic dysgeusia and nutritional problems. Answer: b) ~10 days. Monitoring taste during chemotherapy aids patient counseling and management.
Question 11
Thalamic relay for taste to cortex is which nucleus?
a) VPL nucleus
b) VPM nucleus
c) Lateral geniculate nucleus
d) Medial geniculate nucleus
Explanation: Gustatory signals ascend to the ventral posteromedial nucleus of the thalamus, which relays taste information to the insular and frontal opercular cortex for conscious perception, discrimination, and hedonic valuation, integrating with olfactory input for flavor. Lesions produce contralateral taste deficits. Answer: b) VPM nucleus. Taste testing aids localization of lesions.
Keyword Definitions:
Resting Membrane Potential: Electrical potential difference across a cell membrane at rest.
Potassium Equilibrium: Balance between inward and outward K+ movement.
Surface Electrodes: External electrodes that measure global, not intracellular potentials.
Action Potential: Rapid depolarization and repolarization event in excitable tissue.
Sodium-Potassium Pump: Active transport maintaining high intracellular K+ and low Na+.
Lead Question - 2012
Resting membrane potential in nerve fibre
a) Is equal to the potential of ventricular muscle fibre
b) Can be measured by surface electrodes
c) Increases as extracellular K+ increases
d) Depends upon K+ equilibrium
Explanation: Resting membrane potential in nerve fibres is around –70 mV, determined mainly by K+ equilibrium across the membrane. It cannot be measured by surface electrodes, only by microelectrodes. Increased extracellular K+ reduces negativity, not increases it. Correct answer: d) Depends upon K+ equilibrium.
MCQ 2
A patient with hyperkalemia develops reduced resting membrane potential. What mechanism explains this?
a) Increased Na+ conductance
b) Decreased K+ gradient
c) Increased chloride influx
d) Enhanced Na+-K+ ATPase activity
Explanation: Hyperkalemia reduces the concentration gradient for potassium, lowering efflux and reducing negativity of resting potential. Correct answer: b) Decreased K+ gradient.
MCQ 3
Which ion movement contributes most to resting membrane potential?
a) Active calcium transport
b) Sodium influx
c) Potassium efflux
d) Chloride trapping
Explanation: Resting potential is mostly due to passive potassium efflux through leak channels. Na+ and Cl– have smaller roles. Correct answer: c) Potassium efflux.
MCQ 4
What is the approximate value of neuronal resting membrane potential?
a) +30 mV
b) 0 mV
c) –70 mV
d) –120 mV
Explanation: Resting membrane potential in neurons averages –70 mV, reflecting high K+ permeability and Na+/K+ pump activity. Correct answer: c) –70 mV.
MCQ 5
Resting membrane potential is measured using?
a) Surface electrodes
b) Patch clamp or microelectrodes
c) ECG leads
d) EMG surface electrodes
Explanation: Intracellular recording with glass microelectrodes or patch clamp measures true resting potential, not surface electrodes. Correct answer: b) Patch clamp or microelectrodes.
MCQ 6
A patient has hypokalemia. What happens to resting membrane potential?
a) Becomes less negative
b) Becomes more negative
c) No change
d) Oscillates
Explanation: In hypokalemia, extracellular K+ falls, increasing the gradient, making resting potential more negative (hyperpolarized). Correct answer: b) Becomes more negative.
MCQ 7
The Na+/K+ ATPase contributes to resting potential by?
a) Pumping 3 Na+ out and 2 K+ in
b) Pumping 2 Na+ in and 3 K+ out
c) Pumping equal Na+ and K+
d) Passive diffusion of ions
Explanation: The pump actively moves 3 Na+ out for every 2 K+ in, contributing directly to negativity of resting potential. Correct answer: a) Pumping 3 Na+ out and 2 K+ in.
MCQ 8
In ischemia, resting membrane potential decreases. Why?
a) Excess chloride influx
b) Pump failure due to ATP depletion
c) Enhanced potassium efflux
d) Excessive sodium extrusion
Explanation: ATP depletion in ischemia stops Na+/K+ ATPase, causing Na+ retention, K+ loss, and reduced resting potential. Correct answer: b) Pump failure due to ATP depletion.
MCQ 9
A nerve cell with –70 mV resting potential is depolarized to –50 mV. This means?
a) Membrane becomes more negative
b) Membrane becomes less negative
c) No change in excitability
d) Cell is in refractory period
Explanation: Depolarization reduces negativity, moving closer to threshold and increasing excitability. Correct answer: b) Membrane becomes less negative.
MCQ 10
Which disease involves abnormal resting potential due to ion channel defect?
a) Myasthenia gravis
b) Hyperkalemic periodic paralysis
c) Parkinson’s disease
d) Huntington’s disease
Explanation: In hyperkalemic periodic paralysis, Na+ channel mutations alter resting potential stability, causing episodic weakness. Correct answer: b) Hyperkalemic periodic paralysis.
MCQ 11
Resting membrane potential is closest to equilibrium potential of which ion?
a) Sodium
b) Potassium
c) Chloride
d) Calcium
Explanation: Because of high membrane permeability to K+, resting potential is closest to potassium equilibrium potential. Correct answer: b) Potassium.
Keyword Definitions:
Epinephrine: A catecholamine hormone that regulates glucose metabolism and stress response.
Insulin: Hormone from pancreatic beta cells that lowers blood glucose.
Alpha Receptors: Adrenergic receptors responsible for vasoconstriction and reduced insulin secretion.
Beta Receptors: Adrenergic receptors that mediate increased heart rate and glycogenolysis.
Muscarinic Receptors: Cholinergic receptors not significantly involved in insulin regulation by epinephrine.
Lead Question - 2012
Epinephrine reduces insulin by?
a) Alpha action predominantly
b) Beta action predominantly
c) Alpha and beta
d) Muscarinic receptors
Explanation: Epinephrine reduces insulin secretion mainly via alpha-adrenergic receptor action on pancreatic beta cells. Beta receptors are less involved. Muscarinic receptors are unrelated. Thus, suppression of insulin release occurs predominantly through alpha effects. Correct answer: a) Alpha action predominantly.
MCQ 2
A diabetic patient under stress has high blood glucose due to?
a) Increased insulin secretion
b) Reduced glucagon
c) Epinephrine-mediated inhibition of insulin
d) Muscarinic stimulation of beta cells
Explanation: Stress elevates catecholamines, particularly epinephrine, which inhibits insulin via alpha receptors and raises glucose levels. Correct answer: c) Epinephrine-mediated inhibition of insulin.
MCQ 3
Epinephrine increases blood glucose levels by?
a) Stimulating glycogenolysis and gluconeogenesis
b) Increasing insulin release
c) Blocking glucagon
d) Enhancing glucose uptake in muscles
Explanation: Epinephrine promotes glycogenolysis and gluconeogenesis in liver and muscle while decreasing insulin. This raises blood glucose. Correct answer: a) Stimulating glycogenolysis and gluconeogenesis.
MCQ 4
Which receptor subtype primarily inhibits insulin secretion?
a) Beta-1
b) Beta-2
c) Alpha-2
d) Muscarinic M3
Explanation: Alpha-2 adrenergic receptors are present on pancreatic beta cells and mediate inhibition of insulin release by epinephrine. Correct answer: c) Alpha-2.
MCQ 5
A patient with pheochromocytoma has hyperglycemia due to?
a) Increased insulin
b) Catecholamine-induced insulin suppression
c) Enhanced insulin sensitivity
d) Reduced cortisol secretion
Explanation: Catecholamine excess from pheochromocytoma suppresses insulin through alpha-adrenergic action and increases glycogen breakdown, producing hyperglycemia. Correct answer: b) Catecholamine-induced insulin suppression.
MCQ 6
During hypoglycemia, epinephrine helps by?
a) Increasing insulin
b) Reducing glucagon
c) Inhibiting insulin and stimulating glycogenolysis
d) Blocking cortisol
Explanation: Epinephrine corrects hypoglycemia by inhibiting insulin secretion, stimulating glucagon, and enhancing glycogen breakdown. Correct answer: c) Inhibiting insulin and stimulating glycogenolysis.
MCQ 7
Which of the following is not a direct effect of epinephrine?
a) Inhibition of insulin
b) Lipolysis in adipose tissue
c) Direct increase in insulin secretion
d) Glycogenolysis in muscle
Explanation: Epinephrine does not directly increase insulin secretion; instead, it suppresses it. Correct answer: c) Direct increase in insulin secretion.
MCQ 8
In exercise, blood glucose is maintained partly because?
a) Epinephrine reduces insulin secretion
b) Epinephrine promotes glucose uptake
c) Insulin levels rise rapidly
d) Muscarinic stimulation dominates
Explanation: During exercise, epinephrine reduces insulin secretion and promotes hepatic glucose output, ensuring adequate energy supply. Correct answer: a) Epinephrine reduces insulin secretion.
MCQ 9
Why does epinephrine suppress insulin during stress?
a) To conserve glucose for brain and muscles
b) To store more glucose
c) To enhance fat deposition
d) To increase protein synthesis
Explanation: Epinephrine limits insulin to spare glucose for essential tissues like brain and muscle during stress. Correct answer: a) To conserve glucose for brain and muscles.
MCQ 10
Which adrenergic receptor action increases glycogenolysis but also inhibits insulin?
a) Alpha-1
b) Alpha-2
c) Beta-2
d) Both alpha-2 and beta-2
Explanation: Beta-2 promotes glycogenolysis, while alpha-2 suppresses insulin. Epinephrine acts through both pathways simultaneously. Correct answer: d) Both alpha-2 and beta-2.
MCQ 11
Epinephrine’s effect on insulin can be clinically significant in?
a) Hypoglycemia management
b) Anaphylaxis treatment with epinephrine injection
c) Obesity therapy
d) Cortisol deficiency
Explanation: Epinephrine used in anaphylaxis also lowers insulin, which can transiently increase glucose levels in patients. Correct answer: b) Anaphylaxis treatment with epinephrine injection.