PY10.1-20 | Central Nervous System Physiology — Gate Quiz

Correct! GABA is the principal inhibitory neurotransmitter in the CNS, acting on GABA-A (ionotropic, Cl⁻ channel) and GABA-B (metabotropic, K⁺/Ca²⁺ channels) receptors. GABA-A opens Cl⁻ channels → Cl⁻ influx → hyperpolarisation → reduced neuronal firing. Drugs enhancing GABA (benzodiazepines, barbiturates) have sedative, anticonvulsant, and anxiolytic effects.

Key concept: CNS neurotransmitters — Inhibitory: GABA (GABA-A: Cl⁻ channel; GABA-B: metabotropic), glycine (spinal cord/brainstem); Excitatory: Glutamate (AMPA, NMDA, kainate receptors); Modulatory: Dopamine (reward, motor), Serotonin (mood), Noradrenaline (attention), ACh (memory, cognition). Imbalance → neurological/psychiatric disorders.

Incorrect. GABA is the main inhibitory CNS neurotransmitter (acts via Cl⁻ channels). Glutamate is the main excitatory neurotransmitter.

Correct! The stretch reflex (knee jerk) is the ONLY monosynaptic reflex in the body. Ia primary afferent (from muscle spindle) → synapses DIRECTLY on the α-motor neuron → quadriceps contraction. Simultaneously, Ia collaterals inhibit the antagonist (hamstrings) via Ia inhibitory interneurons (reciprocal inhibition) — but the main arc is monosynaptic.

Key concept: Stretch reflex (knee jerk, biceps, ankle jerk) — monosynaptic (Ia afferent → α-motor neuron); tests spinal cord integrity at that level. Withdrawal (flexor) reflex — polysynaptic, crosses midline (crossed extension). Deep tendon reflexes graded 0–4+. Brisk reflexes in UMN lesions (disinhibition); absent in LMN or sensory nerve lesions. Reciprocal inhibition: Ia afferent inhibits antagonist via Ia inhibitory interneurons.

Incorrect. The patellar reflex is a MONOSYNAPTIC reflex — Ia afferent fibres synapse directly on the alpha-motor neuron without any intervening interneurons. It is the only truly monosynaptic reflex.

Correct! The cerebellum coordinates movement, posture, balance, and motor learning. It compares intended movement (from motor cortex) with actual movement (from proprioceptive feedback) and makes real-time corrections. Cerebellar lesions cause ipsilateral ataxia, dysmetria, intention tremor, dysdiadochokinesia, and nystagmus — but NOT weakness (the motor cortex initiates movement).

Key concept: Cerebellar functions — Coordination of voluntary movement (smooth, accurate); Maintenance of posture and balance (vestibulocerebellum); Motor learning (adaptation of motor programs); Cerebellar lesions cause IPSILATERAL deficits (unlike cortical lesions). DANISH mnemonic for cerebellar signs: Dysdiadochokinesia, Ataxia, Nystagmus, Intention tremor, Slurred speech (dysarthria), Hypotonia. Compare: Basal ganglia = motor planning; Cerebellum = motor execution/coordination.

Incorrect. The cerebellum coordinates movement smoothness, balance, posture, and motor learning. It does not initiate movement (motor cortex) or process pain (thalamus/sensory cortex).

Correct! Conscious sensory perception (somatosensory cortex, primary sensory cortex in parietal lobe) is NOT a hypothalamic function. The hypothalamus has no role in conscious perception — it regulates homeostatic and autonomic functions.

Key concept: Hypothalamus functions — EXHAUSTED mnemonic: Endocrine control (releasing hormones → pituitary), Xeroderma/temperature regulation (thermostat of the body), Hunger/satiety (lateral = hunger centre; ventromedial = satiety centre), ANS regulation, Urge/thirst (osmoreceptors → ADH), Sleep-wake (suprachiasmatic nucleus — biological clock), Traumatic/emotional responses (limbic integration), EtOH/sexual behaviour, Daily rhythms (circadian). Conscious sensory perception is in the thalamus/cortex.

Incorrect. The hypothalamus does NOT process conscious sensory perception — that is the somatosensory cortex. All other options are genuine hypothalamic functions.

Correct! REM sleep (paradoxical sleep) shows a desynchronised EEG (low-amplitude, high-frequency waves) similar to wakefulness — hence its historical name "paradoxical sleep." Features of REM: rapid eye movements, skeletal muscle atonia (via brainstem circuits), vivid dreaming, penile/clitoral tumescence, ↑autonomic activity, ↑heart rate variability.

Key concept: Sleep stages — NREM Stage 1: theta waves, light sleep; Stage 2: sleep spindles + K complexes; Stage 3: delta waves (>20% of epoch, slow-wave sleep); REM: desynchronised EEG, rapid eye movements, vivid dreams, atonia. Sleep cycle: ~90 min. More NREM early in night; more REM in morning. REM behaviour disorder: loss of atonia during REM → dream enactment → association with Parkinson's disease/synucleinopathies.

Incorrect. REM sleep shows a desynchronised (low-amplitude, high-frequency) EEG — similar to wakefulness, which is why it is called "paradoxical sleep." Delta waves are NREM Stage 3/4 (deep sleep).

Correct! Spasticity + brisk DTRs + positive Babinski (extensor plantar) = upper motor neuron (UMN) signs. Sudden onset + hypertension + face/arm/leg hemiplegia strongly suggests stroke involving the internal capsule (contralateral motor fibres compact here) or motor cortex. UMN lesion above the pyramidal decussation causes contralateral hemiplegia.

Key concept: UMN vs LMN — UMN lesion: spasticity, ↑DTRs, Babinski +, clonus, no wasting; LMN lesion: flaccidity, ↓DTRs, fasciculations, muscle wasting, NO Babinski. Babinski sign (extensor plantar): toe dorsiflexion on plantar stimulation — normally PRESENT in infants (corticospinal tract not fully myelinated) and UMN lesions. Absent in normal adults. Internal capsule stroke (posterior limb): contralateral hemiplegia (face, arm, leg). Lateral medullary syndrome (PICA): ipsilateral face + contralateral body sensory loss (crossed syndrome).

Incorrect. Spasticity, brisk reflexes, and Babinski sign are UMN signs. Flaccidity, wasting, fasciculations, and absent reflexes are LMN signs. The combination with sudden onset and hypertension localises this to a UMN stroke.

Correct! The BBB is formed by tight junctions (claudin-5, occludin) between adjacent cerebral capillary endothelial cells — significantly tighter than peripheral capillaries. Astrocyte end-feet (foot processes) surround the capillaries and induce/maintain the BBB properties. Pericytes also contribute to BBB integrity.

Key concept: BBB structure: endothelial tight junctions + astrocyte foot processes + pericytes. Functions: prevents entry of pathogens, polar molecules, large proteins; allows O₂, CO₂, glucose (GLUT-1), fat-soluble drugs, ethanol. Breaks down in: meningitis, brain tumours, stroke, trauma → vasogenic oedema. Circumventricular organs (area postrema, subfornical organ) LACK BBB — allows drug sensing (nausea via vomiting centre). Lipophilic drugs (anaesthetics, opioids) cross easily; hydrophilic drugs do not.

Incorrect. The BBB is formed by tight junctions between cerebral capillary endothelial cells (supported by astrocyte foot processes). These tight junctions prevent paracellular transport of hydrophilic molecules.

Correct! Postganglionic sympathetic fibres release noradrenaline (norepinephrine) at their effector organs. Exceptions: (1) sweat glands (eccrine) → acetylcholine (sympathetic cholinergic); (2) adrenal medulla → releases adrenaline + noradrenaline directly into blood. All preganglionic fibres (sympathetic and parasympathetic) release acetylcholine.

Key concept: ANS neurotransmitters — All preganglionic (both systems): ACh (nicotinic N receptors at ganglia). Parasympathetic postganglionic: ACh (muscarinic M receptors). Sympathetic postganglionic: Noradrenaline (α₁, α₂, β₁, β₂ adrenoceptors) — EXCEPT sweat glands (ACh, muscarinic) and some vasodilator vessels. Adrenal medulla = modified sympathetic ganglion → releases Adrenaline (80%) + NA (20%) into blood.

Incorrect. Postganglionic SYMPATHETIC fibres release noradrenaline (adrenergic). EXCEPTIONS: sweat glands (sympathetic but cholinergic, release ACh); adrenal medulla (releases adrenaline + NA into blood = modified sympathetic postganglionic neurons).

Correct! Parkinson's disease is caused by degeneration of dopaminergic neurons in the substantia nigra pars compacta → reduced dopamine input to the striatum (caudate + putamen). This disrupts the balance between the direct pathway (facilitates movement) and indirect pathway (inhibits movement), resulting in reduced thalamic activation → reduced cortical motor output → bradykinesia, rigidity, resting tremor.

Key concept: Parkinson's — Loss of SNc dopaminergic neurons (Lewy bodies = α-synuclein aggregates). Dopamine normally facilitates movement via direct pathway (D1 receptors) and inhibits braking via indirect pathway (D2 receptors). Treatment: L-DOPA + carbidopa (prevents peripheral conversion); dopamine agonists; MAO-B inhibitors. Cardinal features: tremor (resting, 4–6 Hz, pill-rolling), rigidity (cogwheel), akinesia/bradykinesia, postural instability (TRAP mnemonic).

Incorrect. Parkinson's disease = loss of dopaminergic neurons in substantia nigra pars compacta → ↓striatal dopamine → imbalanced basal ganglia circuits → motor symptoms (bradykinesia, rigidity, resting tremor, postural instability).

Correct! Normal CSF: protein 0.15–0.45 g/L (very low, vs ~70 g/L plasma), glucose ~2.5–4.4 mmol/L (~60–70% of blood glucose), <5 lymphocytes/mm³, clear, colourless. Low protein (because BBB restricts protein entry) and no RBCs distinguish normal CSF from haemorrhage or meningitis.

Key concept: CSF — Produced: choroid plexus (500 mL/day); Volume: ~150 mL; Turnover: 3–4 times/day. Normal values: protein 0.15–0.45 g/L, glucose 2.5–4.4 mmol/L, cells <5/mm³ (lymphocytes). Circulation: lateral ventricles → foramen of Monro → 3rd ventricle → aqueduct of Sylvius → 4th ventricle → subarachnoid space → absorbed by arachnoid granulations into sagittal sinus. LP findings: meningitis (↑protein, ↓glucose, ↑cells), SAH (xanthochromia), GBS (↑protein, normal cells — albuminocytological dissociation).

Incorrect. Normal CSF has very low protein (0.15–0.45 g/L) compared to plasma (70 g/L), glucose ~60% of plasma, and <5 cells/mm³ (lymphocytes only). High protein, low glucose, or many cells = infection/disease.