The third-order neuronal cell body of the spinothalamic tract lies in the contralateral thalamus. The spinothalamic tract transmits sensory information such as pain, temperature, and crude touch. The pathway involves three neurons:

1. The first-order neuron, which carries sensory information from the peripheral receptors to the spinal cord.
2. The second-order neuron, which decussates (crosses to the opposite side) in the spinal cord and ascends to the thalamus.
3. The third-order neuron, which is located in the contralateral thalamus and sends axonal projections to the sensory cortex for further processing and perception.

Here’s why the other options are incorrect:

1. Pons: The pons is part of the brainstem, but it is not the location of the third-order neurons in the spinothalamic tract. The third-order neurons are found in the thalamus.
2. Medulla oblongata: The medulla oblongata is involved in some other sensory pathways, but not in the final relay of the spinothalamic tract, which occurs in the thalamus.
3. Ipsilateral thalamus: The third-order neurons are located in the contralateral thalamus because the second-order neurons cross to the opposite side of the body as they ascend.
4. Nucleus gracilis: The nucleus gracilis is part of the dorsal column-medial lemniscal pathway and is not involved in the spinothalamic tract, which processes different sensory information (pain and temperature).

Acetylcholinesterase is the enzyme responsible for degrading acetylcholine. It is found in the synaptic cleft, where it rapidly breaks down acetylcholine into acetate and choline after it has been released into the synapse. This breakdown is crucial for terminating the signal transmission at cholinergic synapses, ensuring that acetylcholine does not continue to stimulate receptors unnecessarily.

Here’s why the other options are incorrect:

1. Tyrosine hydroxylase: This enzyme is involved in the synthesis of catecholamines (dopamine, norepinephrine, and epinephrine), not the degradation of acetylcholine.
2. Thioesterase: Thioesterase enzymes are involved in the hydrolysis of thioesters, which are not related to acetylcholine metabolism.
3. Pectinesterase: This enzyme breaks down pectin, a component of plant cell walls, and is not involved in acetylcholine degradation.
4. Endoribonuclease: This enzyme is involved in RNA processing and degradation, and does not have a role in the breakdown of acetylcholine.

In the case of a hemisection of the spinal cord (also known as Brown-Séquard syndrome), there is typically a motor loss on the ipsilateral (same) side of the body due to damage to the corticospinal tract, which carries motor signals. However, the loss of temperature and pain sensation occurs on the contralateral (opposite) side of the body. This is because the fibers that transmit pain and temperature sensation cross to the opposite side of the spinal cord shortly after entering, specifically at or near the level of entry into the spinal cord.

Here’s why the other options are incorrect:

1. No sensory loss: There is always sensory loss associated with hemisection of the spinal cord. In this case, it affects the contralateral side due to the crossing of pain and temperature fibers.
2. Ipsilateral side: While motor loss occurs ipsilaterally due to damage to the corticospinal tract, temperature and pain sensation are lost contralaterally because the sensory fibers cross to the opposite side before ascending.
3. Ipsilateral upper limbs, contralateral lower limbs: This is not a typical pattern of sensory loss in Brown-Séquard syndrome. Sensory loss due to hemisection is usually contralateral, not divided by limbs in this way.
4. Sensory loss on both sides: Sensory loss would not occur on both sides unless there was a more severe lesion, such as complete spinal cord transection, which would involve damage to both sides of the spinal cord. Hemisection typically results in contralateral sensory loss only.

The reticular formation is a network of neurons located in the brainstem that plays a key role in regulating sleep, wakefulness, and arousal. It is involved in maintaining alertness, regulating the sleep-wake cycle, and controlling levels of consciousness. The reticular formation sends signals to the cortex to promote wakefulness and can also help induce sleep by modulating the activity of different brain regions.

Here’s why the other options are incorrect:

1. Substantia nigra: The substantia nigra is involved in the regulation of movement and is primarily associated with the basal ganglia. It plays a crucial role in motor control and is implicated in Parkinson’s disease, but it is not directly involved in sleep and awakening.
2. Medulla: The medulla is responsible for vital functions such as heart rate, breathing, and blood pressure regulation. While it is involved in autonomic functions, it is not directly involved in regulating sleep and wakefulness.
3. Pons: The pons is part of the brainstem and plays a role in sleep, especially REM sleep. It contains nuclei that help regulate sleep cycles, but the reticular formation is more broadly involved in the general regulation of wakefulness and sleep.
4. Nucleus ambiguus: The nucleus ambiguus is involved in motor control for speech and swallowing and is not directly associated with the regulation of sleep and awakening.

The floor of the inferior horn of the lateral ventricle is formed by the hippocampus, which is a key structure involved in memory formation and spatial navigation. The hippocampus is located in the medial temporal lobe and forms part of the limbic system. The inferior horn of the lateral ventricle, which extends into the temporal lobe, is closely related to the hippocampus.

Here’s why the other options are incorrect:

1. Amygdaloid nucleus: The amygdala is involved in emotions and memory, but it is not located in the floor of the inferior horn of the lateral ventricle. It is found in the temporal lobe, but more anterior and medial compared to the hippocampus.
2. Caudate nucleus: The caudate nucleus is part of the basal ganglia and is not involved in forming the floor of the inferior horn of the lateral ventricle. It is located more laterally in the brain.
3. Corpus callosum: The corpus callosum is a large bundle of nerve fibers that connects the two hemispheres of the brain, but it does not form the floor of the inferior horn of the lateral ventricle. It lies above the lateral ventricles.
4. Septum pellucidum: The septum pellucidum is a thin membrane separating the two lateral ventricles, but it does not form the floor of the inferior horn. It lies more medially and does not have the same structural role as the hippocampus in this region.

Monoamine oxidase (MAO) is the enzyme responsible for the breakdown of serotonin, as well as other neurotransmitters like dopamine, norepinephrine, and epinephrine. MAO is found in the mitochondria of nerve cells and breaks down serotonin into its inactive metabolites, primarily 5-hydroxyindoleacetic acid (5-HIAA).

Here’s why the other options are incorrect:

1. Catechol-O-methyl transferase (COMT): COMT is involved in the breakdown of catecholamines (like dopamine, norepinephrine, and epinephrine) by methylation, not serotonin.
2. Aromatic amino acid decarboxylase: This enzyme is involved in the conversion of aromatic amino acids (like tryptophan) to neurotransmitters (such as serotonin or dopamine), but it is not involved in serotonin breakdown.
3. Hydroxylase: Hydroxylases are enzymes that add hydroxyl groups to various molecules, but they are not responsible for breaking down serotonin. For example, tryptophan hydroxylase is involved in serotonin synthesis, not degradation.
4. Histidine decarboxylase: This enzyme is responsible for converting histidine to histamine, not serotonin breakdown.

The cell bodies of postganglionic parasympathetic neurons are located near the target organs. These neurons are part of the parasympathetic division of the autonomic nervous system, which works to conserve energy and promote “rest-and-digest” functions. The preganglionic neurons originate in the brainstem or sacral spinal cord, but their axons synapse in ganglia that are located very close to, or even within, the organs they innervate.

Here’s why the other options are incorrect:

1. Spinal cord: The cell bodies of preganglionic parasympathetic neurons originate in the spinal cord (specifically in the sacral region), but the postganglionic neurons are located near the target organs.
2. None of these: This option is incorrect because the correct answer is “near the target organs.”
3. Central nervous system: While the preganglionic parasympathetic neurons do have their cell bodies in the central nervous system (brainstem or sacral spinal cord), the postganglionic neurons do not. Postganglionic neurons’ cell bodies are found in ganglia located near the target organs.
4. Brainstem: The preganglionic parasympathetic neurons do originate from the brainstem, but the postganglionic cell bodies are not located in the brainstem.

Beta waves occur during states of increased mental activity, such as when a person is actively concentrating, problem-solving, or engaged in cognitive tasks. These waves are associated with a heightened state of alertness and focus, reflecting the brain’s engagement during tasks that require attention.

Here’s why the other options are incorrect:

1. Deep sleep: Deep sleep is associated with delta waves, not beta waves. Delta waves are slow and occur during the deepest stages of sleep.
2. Resting state: When a person is in a resting state but awake and relaxed, alpha waves are more prominent, not beta waves. Alpha waves are seen when a person is calm and not engaged in intense mental activity.
3. Brain disorders: While certain brain disorders (such as seizures) can cause abnormal beta wave activity, beta waves are not typically characteristic of all brain disorders. The presence of beta waves alone is not diagnostic of a brain disorder.
4. Emotional stress: Although emotional stress can cause an increase in beta waves, they are most directly associated with increased mental activity, such as intense focus and problem-solving. Emotional stress might lead to changes in brain wave patterns, but beta waves are primarily linked to cognitive effort.

Beta waves are one of the types of brain waves that are typically associated with an alert and focused mental state. They have a frequency range of 14 to 80 cycles per second (Hz). Beta waves are often seen during activities requiring concentration, active thinking, and problem-solving.

Here’s why the other options are incorrect:

1. 35-140 cycles per second: This frequency range is too high for beta waves and is not recognized as a typical range for any standard brain wave.
2. Less than 3.5 cycles per second: This range corresponds to delta waves, which are associated with deep sleep and unconscious states, not beta waves.
3. 8-13 cycles per second: This range corresponds to alpha waves, which are seen when the brain is in a relaxed, calm, and focused state, usually when you’re awake but relaxed.
4. 4-7 cycles per second: This frequency range is associated with theta waves, which are typically seen in light sleep or deep relaxation, not beta waves.

In the adult human body, the spinal cord typically ends at the level of the L1-L2 vertebrae. However, the subarachnoid space, where cerebrospinal fluid (CSF) is present, extends down to the level of the second sacral vertebra (S2). A needle inserted between the third and fourth lumbar vertebrae (L3-L4) typically reaches the subarachnoid space and is used to sample cerebrospinal fluid, as in procedures like a lumbar puncture (spinal tap).

Here’s why the other options are incorrect:

1. Coccygeal nerve: The coccygeal nerve is part of the terminal portion of the spinal cord, and it is located much lower, near the sacrum and coccyx. A needle at the L3-L4 level will not reach this nerve.
2. Spinal cord: The spinal cord ends at the L1-L2 level in adults, so a needle inserted between L3 and L4 would not reach the spinal cord itself. It would reach the cauda equina, a bundle of nerve roots.
3. Sacral nerve: The sacral nerves originate from the lower portion of the spinal cord, specifically from the sacral segments (S1-S5). They are located below the level where a needle would be inserted at L3-L4.
4. Stria terminalis: This is a structure related to the limbic system in the brain and is not part of the spinal cord or associated with the lumbar region. It has no relevance to a needle insertion at L3-L4.

The olfactory nerve (cranial nerve I) is most likely to be injured in an anterior cranial fossa fracture. The olfactory nerve fibers pass through the cribriform plate of the ethmoid bone, which is located in the anterior cranial fossa. A fracture in this region can damage these fibers, leading to anosmia (loss of smell). The other cranial nerves listed are located in different parts of the skull and are less likely to be affected by an anterior cranial fossa fracture.

The optic nerve (cranial nerve II) is the only one of the listed peripheral nerves that is myelinated by oligodendrocytes. Oligodendrocytes are responsible for the myelination of nerve fibers in the central nervous system (CNS), which includes the optic nerve, even though it is technically a cranial nerve. The other nerves listed (abducens, ophthalmic, hypoglossal, and accessory) are part of the peripheral nervous system and are myelinated by Schwann cells.

Acetylcholinesterase is an enzyme that breaks down acetylcholine, a neurotransmitter, into two components: acetic acid and choline. This breakdown occurs at the synaptic cleft after acetylcholine has been released to transmit nerve impulses. The choline can then be taken back up into the presynaptic neuron to be reused in the synthesis of new acetylcholine. Acetylcholinesterase plays a critical role in terminating the signal transmission to ensure that nerve impulses are not continuously active.

Monoamine oxidase (MAO) is the enzyme responsible for the conversion of serotonin to 5-hydroxy-3-indoleacetic acid (5-HIAA), which is the primary metabolite of serotonin. This process involves the oxidation of serotonin, leading to the production of 5-HIAA, which is then excreted in the urine. MAO plays a key role in the breakdown of neurotransmitters like serotonin, dopamine, and norepinephrine. The other enzymes listed are involved in different biochemical processes but not in the conversion of serotonin to 5-HIAA.

Difficulty with balance and slurred speech are symptoms typically associated with lesions in the cerebellum. The cerebellum plays a critical role in coordinating voluntary movements, balance, and speech. When there is damage to the cerebellum, it can lead to ataxia (lack of coordination), dysarthria (slurred speech), and other motor deficits. The other areas listed (cerebrum, pons, midbrain, and medulla) are involved in other functions, but these specific symptoms are most often linked to cerebellar lesions.

Dopamine has different effects depending on the type of receptor it binds to. At D1 receptors, dopamine typically exerts an excitatory effect, leading to an increase in neuronal activity. In contrast, at D2 receptors, dopamine generally exerts an inhibitory effect, reducing neuronal activity. This balance between excitation and inhibition is crucial for various brain functions, including motor control, mood regulation, and reward processing.

Tyrosine hydroxylase is the rate-limiting enzyme in dopamine synthesis. It catalyzes the conversion of the amino acid tyrosine to L-DOPA, which is a precursor for dopamine. This step is the slowest and most regulated in the process of dopamine production. The other enzymes listed are involved in the metabolism or further processing of dopamine but do not control the rate of its synthesis.

The cavernous sinus is a paired venous sinus located on either side of the sella turcica. It contains several important structures, including cranial nerves and the internal carotid artery. The lateral wall of the cavernous sinus houses the following nerves from superior to inferior:

1. Oculomotor nerve (CN III)
2. Trochlear nerve (CN IV)
3. Ophthalmic division of the trigeminal nerve (CN V1)
4. Maxillary division of the trigeminal nerve (CN V2)

The abducens nerve (CN VI) is unique in that it runs through the cavernous sinus (not on the lateral wall) alongside the internal carotid artery. The optic nerve (CN II), olfactory nerve (CN I), and mandibular nerve (CN V3) are not associated with the cavernous sinus.

The superior cerebral veins are responsible for draining blood from the superior aspect of the cerebral cortex. These veins ascend over the cerebral hemispheres and empty into the superior sagittal sinus, a major dural venous sinus located along the midline of the brain.

The superior sagittal sinus eventually drains into the confluence of sinuses, which then directs blood into the transverse sinuses and ultimately into the internal jugular vein.

Other options explained:

❌ Carotid sinus → A baroreceptor in the internal carotid artery, not a venous drainage structure.
❌ Diploic veins → Drain the bone marrow of the skull, not the cerebral cortex.
❌ Straight sinus → Receives blood from the inferior sagittal sinus and great cerebral vein (of Galen), not the superior cerebral veins.
❌ Inferior sagittal sinus → Runs along the inferior border of the falx cerebri and drains deep brain structures, not the superior cerebral veins.

The cerebellum plays a crucial role in coordinating complex motor activities, such as shooting a basketball. It ensures smooth, precise, and well-timed movements by integrating sensory input with motor output.

Functions of the cerebellum in motor control:
✅ Coordination of voluntary movements → Ensures smooth execution of shooting motion.
✅ Balance and posture → Helps maintain body stability while aiming and shooting.
✅ Motor learning → Adjusts and refines movements based on practice.
✅ Error correction → Detects and corrects deviations from intended motion.

Other options explained:

❌ Medulla → Controls autonomic functions (e.g., breathing, heart rate) but does not coordinate voluntary movement.
❌ Midbrain → Contains reflex centers for vision and hearing (tectum) and motor pathways (crus cerebri), but does not primarily coordinate complex movements.
❌ Globus pallidus → Part of the basal ganglia, involved in initiating and regulating voluntary movement, but does not directly fine-tune coordination like the cerebellum.
❌ Pons → Contains relay nuclei for communication between the cortex and cerebellum, but does not directly control motor coordination.

The substantia nigra is a pigmented, dopaminergic nucleus located in the midbrain that separates the crus cerebri (anterior part of the cerebral peduncle) from the tegmentum (middle part of the midbrain).

• The crus cerebri contains descending motor fibers (corticospinal, corticobulbar, corticopontine tracts).
• The substantia nigra plays a role in movement control (degeneration leads to Parkinson’s disease).
• The tegmentum contains ascending sensory pathways, cranial nerve nuclei, and the reticular formation.

Other options explained:

❌ Superior colliculus → Located in the midbrain tectum (roof), involved in visual reflexes, but does not separate the crus cerebri from the tegmentum.
❌ Trapezoid body → A structure in the pons involved in the auditory pathway, not related to the midbrain.
❌ Locus coeruleus → A noradrenergic nucleus in the pons involved in wakefulness and stress response, unrelated to the crus cerebri.
❌ Pontine nuclei → Located in the pons, responsible for relaying motor signals to the cerebellum, not involved in separating midbrain structures.

The foramen magnum is the largest opening in the base of the skull, allowing passage of key structures between the cranial cavity and spinal canal. The following structures pass through the foramen magnum:

✅ Medulla oblongata → Continues as the spinal cord.
✅ Anterior spinal arteries → Supply the anterior spinal cord.
✅ Vertebral veins → Drain blood from the vertebral venous plexus.
✅ Spinal root of the accessory nerve (CN XI) → Ascends through the foramen magnum before exiting via the jugular foramen.

However, the dura mater does not pass through the foramen magnum; rather, it attaches around its margins, helping form the cranial cavity’s protective covering.

Other options explained:

✔ Medulla oblongata → Exits through the foramen magnum, transitioning into the spinal cord.
✔ Anterior spinal arteries → Enter through the foramen magnum to supply the spinal cord.
✔ Vertebral veins → Pass through the foramen magnum along with the vertebral arteries.
✔ Spinal root of CN XI (Accessory nerve) → Enters the skull via the foramen magnum before exiting via the jugular foramen.

The reticular formation is a network of interconnected neurons located in the brainstem, specifically within the medulla, pons, and midbrain. It plays a crucial role in arousal, wakefulness, and maintaining consciousness through the reticular activating system (RAS).

• The reticular activating system (RAS) sends signals to the cerebral cortex via the thalamus to keep the brain alert and awake.
• Damage to the RAS can lead to coma or severe consciousness impairment.

Other options explained:

❌ Medulla → Controls autonomic functions (cardiac and respiratory centers) but is not primarily responsible for cortical wakefulness.
❌ Pons → Contains respiratory and motor relay centers but does not directly activate the cortex.
❌ Substantia nigra → Involved in dopaminergic pathways and movement control, not wakefulness.
❌ Nucleus ambiguus → Controls motor function of the pharynx and larynx (via cranial nerves IX & X), unrelated to wakefulness.

The reticular formation is a network of interconnected neurons located in the brainstem, specifically within the medulla, pons, and midbrain. It plays a crucial role in arousal, wakefulness, and maintaining consciousness through the reticular activating system (RAS).

• The reticular activating system (RAS) sends signals to the cerebral cortex via the thalamus to keep the brain alert and awake.
• Damage to the RAS can lead to coma or severe consciousness impairment.

Other options explained:

❌ Medulla → Controls autonomic functions (cardiac and respiratory centers) but is not primarily responsible for cortical wakefulness.
❌ Pons → Contains respiratory and motor relay centers but does not directly activate the cortex.
❌ Substantia nigra → Involved in dopaminergic pathways and movement control, not wakefulness.
❌ Nucleus ambiguus → Controls motor function of the pharynx and larynx (via cranial nerves IX & X), unrelated to wakefulness.

The cardiac and vasomotor centers are located in the medulla oblongata, which plays a vital role in regulating autonomic functions, including heart rate, blood pressure, and respiratory control.

• Cardiac center → Regulates heart rate and contractility through the autonomic nervous system (ANS).
• Vasomotor center → Controls blood vessel diameter by regulating sympathetic and parasympathetic tone, affecting blood pressure.

These centers are part of the reticular formation in the medulla and work in coordination with higher centers like the hypothalamus.

Other options explained:

❌ Hypothalamus → Regulates the autonomic nervous system (ANS) but does not directly control cardiac and vasomotor functions.
❌ Thalamus → A sensory relay center, not involved in cardiovascular regulation.
❌ Pons → Regulates respiration (apneustic & pneumotaxic centers) but not cardiac or vasomotor functions.
❌ Cerebellum → Coordinates movement and balance, not autonomic functions.

A lower motor neuron (LMN) lesion affects the anterior horn cells, spinal nerve roots, or peripheral nerves, leading to loss of motor function. The hallmark signs of LMN lesions include:

✅ Muscle wasting (atrophy) → Due to loss of trophic signals to muscles
✅ Hypotonia (flaccid paralysis) → Reduced muscle tone and weakness
✅ Hyporeflexia (decreased reflexes) → Loss of spinal reflexes
✅ Fasciculations → Visible, spontaneous muscle twitching due to denervation

Other options explained:

❌ Hyperreflexia → Seen in upper motor neuron (UMN) lesions, not LMN lesions.
❌ Positive Babinski’s sign → Present in UMN lesions, absent in LMN lesions.
❌ Hyperesthesia → Not a feature of LMN lesions; LMN lesions cause motor deficits, while sensory deficits depend on the affected nerve.
❌ Spasticity → A feature of UMN lesions, characterized by increased muscle tone and exaggerated reflexes.

In bacterial meningitis, cerebrospinal fluid (CSF) glucose is decreased because bacteria consume glucose and cause an inflammatory response that increases glucose uptake by white blood cells. Normally, CSF glucose is about 50-80 mg/dL (or ~2/3 of blood glucose levels), but in bacterial meningitis, it drops significantly.

Typical CSF findings in bacterial meningitis:

• ↓ Glucose (Low, <45 mg/dL) – due to bacterial consumption and increased WBC uptake.
• ↑ Neutrophils (Polymorphonuclear leukocytosis) – characteristic of bacterial infections.
• ↑ Proteins – due to increased permeability of the blood-brain barrier.
• Chloride – Generally normal; some sources mention mild reduction, but it is not a key diagnostic feature.
• Sodium – Usually normal, but may decrease in severe SIADH cases.

Other options explained:

• Neutrophils → Increased (CSF shows neutrophilic pleocytosis).
• Proteins → Increased (Due to blood-brain barrier disruption).
• Chloride → Generally normal; no significant decrease in bacterial meningitis.
• Sodium → Usually normal, but may decrease in severe SIADH cases.

Hyperalgesia and allodynia both refer to an increased sensitivity to pain, but they have distinct definitions:

• Hyperalgesia → An exaggerated pain response to a normally painful stimulus (e.g., touching an inflamed area hurts more than usual).
• Allodynia → Pain resulting from a normally non-painful stimulus (e.g., light touch causing pain in a sunburned area).

Both conditions occur due to sensitization of nociceptors (pain receptors) and changes in pain pathways in the nervous system, often due to:
✅ Inflammation (release of prostaglandins, bradykinin, histamine)
✅ Peripheral sensitization (nociceptors become more responsive)
✅ Central sensitization (spinal cord neurons become hyperexcitable)

Other options explained:

❌ Release of coagulation factors → Involved in blood clotting, not pain sensitivity.
❌ Tissue repair → Occurs after injury but does not directly cause hyperalgesia/allodynia.
❌ No release of chemicals → Pain sensitization involves chemical mediators like substance P, prostaglandins, and bradykinin.
❌ Decreased sensitivity of pain → This describes hypoalgesia, not hyperalgesia/allodynia.

The pneumotaxic center is located in the upper pons, specifically in the nucleus parabrachialis medialis of the pontine respiratory group. It plays a crucial role in regulating the breathing rate and rhythm by inhibiting the inspiratory center (dorsal respiratory group in the medulla), thus shortening inspiration and promoting expiration.

• A strong pneumotaxic signal → Short, rapid breaths (tachypnea).
• A weak pneumotaxic signal → Prolonged inspiration and deeper breaths (bradypnea).
• Works in coordination with the apneustic center (also in the pons) and medullary respiratory centers to maintain normal respiration.

Other options explained:

❌ Lower medulla → Houses the dorsal (inspiratory) and ventral (expiratory) respiratory groups, but not the pneumotaxic center.
❌ Midbrain → Not involved in respiratory control.
❌ Cerebellum → Coordinates movement, not respiration.
❌ Upper medulla → Contains respiratory centers but not the pneumotaxic center (which is in the pons).

Pontocerebellar fibers are fibers that originate from the pontine nuclei and travel to the cerebellum. These fibers cross the midline and continue as the middle cerebellar peduncle, forming the largest pathway connecting the pons and cerebellum.

• The middle cerebellar peduncle primarily carries afferent fibers to the cerebellar cortex, playing a crucial role in motor coordination and planning.

Other options explained:

❌ Crus Cerebri → Part of the cerebral peduncles in the midbrain, carrying descending motor fibers from the cortex to the brainstem.
❌ Superior cerebellar peduncle → Carries efferent fibers from the cerebellum to the midbrain and thalamus.
❌ Inferior cerebellar peduncle → Carries afferent fibers from the spinal cord and medulla to the cerebellum.
❌ Tegmentum → The core part of the brainstem containing nuclei, tracts, and the reticular formation, but not related to pontocerebellar fibers.

The midbrain (mesencephalon) receives its blood supply primarily from branches of the vertebrobasilar system, including:

✅ Posterior cerebral artery (PCA) and its peduncular branches → Supplies the cerebral peduncles and tectum.
✅ Posterior choroidal artery → Branch of PCA that contributes to the midbrain and thalamus.
✅ Interpeduncular branches of the basilar artery → Supply the interpeduncular fossa and nearby midbrain structures.
✅ Superior cerebellar artery (SCA) → Supplies the dorsal midbrain and superior cerebellum.

However, the middle cerebral artery (MCA) primarily supplies the lateral aspect of the cerebral hemispheres (including the frontal, parietal, and temporal lobes), but does not contribute to the midbrain’s blood supply.

Other options explained:

✔ Posterior cerebral artery (PCA) and its peduncular branch → Supplies midbrain structures, including the cerebral peduncles.
✔ Posterior choroidal artery → Supplies the thalamus and parts of the midbrain.
✔ Interpeduncular branches of the basilar artery → Directly supply the midbrain, especially near the interpeduncular fossa.
✔ Superior cerebellar artery (SCA) → Contributes to the dorsal midbrain.

Dopamine is synthesized from tyrosine through a series of enzymatic reactions:

1. Tyrosine hydroxylase converts tyrosine into L-DOPA (L-3,4-dihydroxyphenylalanine).
2. DOPA decarboxylase converts L-DOPA into dopamine.

Dopamine can then be further converted into norepinephrine and epinephrine in the catecholamine synthesis pathway.

Other options explained:

❌ Glycine → An inhibitory neurotransmitter in the spinal cord, not a dopamine precursor.
❌ Tryptophan → Precursor for serotonin (5-HT) and melatonin, not dopamine.
❌ Phenylalanine → A precursor for tyrosine, but dopamine is synthesized directly from tyrosine.
❌ Glutamate → An excitatory neurotransmitter, not related to dopamine synthesis.

The spinal cord is held in place and stabilized by:

1. Denticulate ligaments → These are extensions of the pia mater that anchor the spinal cord laterally to the dura mater, preventing excessive movement.
2. Filum terminale → A thin, fibrous extension of the pia mater that extends from the conus medullaris to attach the spinal cord inferiorly to the coccyx, preventing vertical movement.

Other options explained:

❌ Filum terminale and conus medullaris → The conus medullaris is the tapered end of the spinal cord, but it does not play a role in stabilization.
❌ Cauda equina and conus medullaris → The cauda equina consists of lumbar, sacral, and coccygeal nerve roots but does not stabilize the spinal cord.
❌ Denticulate ligaments and conus medullaris → The conus medullaris is an anatomical landmark but does not stabilize the spinal cord.
❌ Denticulate ligaments and cauda equina → The cauda equina is a bundle of nerves, not a stabilizing structure.

Tabes dorsalis is a late-stage manifestation of neurosyphilis, caused by Treponema pallidum (the bacterium responsible for syphilis). It primarily affects the dorsal columns and dorsal roots of the spinal cord, leading to:

• Loss of proprioception and vibration sense (due to dorsal column degeneration)
• Sensory ataxia (due to impaired proprioception)
• Positive Romberg sign (patient sways/falls when eyes are closed)
• Lightning pains (sudden, sharp pains due to dorsal root involvement)
• Argyll Robertson pupil (pupil accommodates but does not react to light)

Other options explained:

❌ Streptococcus pyogenes → Causes rheumatic fever, pharyngitis, impetigo, but not neurosyphilis.
❌ Chlamydia trachomatis → Causes chlamydia, lymphogranuloma venereum (LGV), and trachoma, but not tabes dorsalis.
❌ Bacillus cereus → Causes food poisoning, but has no neurological involvement.
❌ Neisseria gonorrhoeae → Causes gonorrhea, but does not lead to neurosyphilis.

Hemisection of the spinal cord is known as Brown-Séquard syndrome, which presents with a characteristic pattern of deficits:

1. Ipsilateral UMN signs below the lesion → Due to corticospinal tract damage (✅ True)
2. Ipsilateral loss of dorsal column sensations below the lesion → Due to dorsal column damage (✅ True)
3. Contralateral pain and temperature loss below the lesion → Due to spinothalamic tract damage, which crosses at the spinal cord level (✅ True)
4. Ipsilateral loss of all sensations at the level of the lesion → Due to local nerve root involvement (✅ True)

However, ipsilateral UMN signs do not appear at the level of the lesion. Instead, at the lesion level, there may be lower motor neuron (LMN) signs (flaccid paralysis, atrophy, and areflexia) due to damage to anterior horn cells or ventral roots.

Other options explained:

✔ Ipsilateral UMN signs below the lesion → Occurs due to corticospinal tract damage.
✔ Ipsilateral dorsal column sensory loss below the lesion → Due to dorsal column damage (loss of proprioception, vibration, and fine touch).
✔ Contralateral pain and temperature loss below the lesion → Due to spinothalamic tract damage, which crosses at the spinal level.
✔ Ipsilateral loss of all sensations at the level of the lesion → Due to local nerve root and dorsal horn damage.

Reserpine inhibits the vesicular monoamine transporter (VMAT), which is responsible for transporting norepinephrine (NE), dopamine, and serotonin into presynaptic vesicles. By blocking VMAT, reserpine prevents NE storage, leading to:

• Depletion of norepinephrine from nerve terminals
• Reduced sympathetic activity (causing hypotension and bradycardia)
• Depression (due to serotonin and dopamine depletion)

Other options explained:

❌ Catechol-O-methyl transferase (COMT) → Breaks down catecholamines (NE, dopamine, epinephrine) but does not inhibit their storage.
❌ Imipramine → A tricyclic antidepressant (TCA) that blocks NE reuptake but does not prevent storage.
❌ Guanethidine → Inhibits NE release, but does not block its storage in vesicles.
❌ Monoamine oxidase (MAO) → Degrades NE in the cytoplasm, but does not prevent storage in vesicles.

Scopolamine is a competitive (reversible) antagonist of muscarinic acetylcholine receptors (mAChRs). It blocks parasympathetic nervous system effects by inhibiting acetylcholine (ACh) binding to muscarinic receptors, leading to:

• Decreased motion sickness (used as a transdermal patch)
• Pupil dilation (mydriasis)
• Reduced salivation and respiratory secretions (used in pre-anesthetic medication)
• CNS effects → Can cause sedation, confusion, and amnesia at high doses

Other options explained:

❌ Binds irreversibly to both muscarinic and nicotinic receptors → Scopolamine is reversible and does not affect nicotinic receptors.
❌ Binds irreversibly to muscarinic receptors → It is a competitive antagonist, meaning its effects are reversible.
❌ Binds irreversibly to nicotinic receptors → It does not affect nicotinic receptors (which are involved in neuromuscular transmission).
❌ Binds reversibly to nicotinic receptors → Scopolamine has no effect on nicotinic receptors (found in ganglia and NMJ).

A saccular aneurysm (berry aneurysm) is a small, sac-like bulging of a cerebral artery, typically at bifurcation points of the circle of Willis. It is the most common cause of subarachnoid hemorrhage (SAH) when it ruptures.

Predisposing factors include:
✅ Cigarette smoking → Weakens blood vessels and promotes hypertension, increasing aneurysm risk.
✅ Hypertension → Causes stress on arterial walls.
✅ Connective tissue disorders (e.g., Ehlers-Danlos, Marfan syndrome).
✅ Polycystic kidney disease (ADPKD) → Strong association with berry aneurysms.
✅ Family history of aneurysms.

Other options explained:

❌ Tumors → May compress vessels but do not directly cause saccular aneurysms.
❌ Bacterial infections → Can cause mycotic aneurysms, not saccular aneurysms.
❌ Viral infections & Infections → Some infections may affect vessel integrity, but they are not primary risk factors for saccular aneurysms.

The refractory period after an action potential occurs due to the inactivation of voltage-gated sodium (Na⁺) channels, which prevents immediate re-firing of the neuron.

The refractory period is divided into:

1. Absolute Refractory Period → No new action potential can be generated, regardless of stimulus strength.
   • Cause: Inactivated Na⁺ channels that cannot reopen until the membrane repolarizes.
2. Relative Refractory Period → A stronger-than-normal stimulus can generate a new action potential.
   • Cause: Activated K⁺ channels that keep the membrane hyperpolarized, making it harder to reach threshold.

Other options explained:

❌ Inactivated potassium channels → Potassium channels do not inactivate; they return to their resting state.
❌ Activated sodium channels → Sodium channels activate during depolarization, but the refractory period occurs due to their inactivation.
❌ Activated calcium channels → Calcium channels play a role in neurotransmitter release but do not cause the refractory period.
❌ Activated potassium channels → Contribute to the relative refractory period, but the absolute refractory period is due to inactivated Na⁺ channels.

The difference in ionic concentration across a membrane is called a concentration gradient. This gradient drives the passive movement of ions from an area of high concentration to low concentration through diffusion.

• The concentration gradient is essential for membrane potential, nerve impulse transmission, and muscle contraction.
• For example, in neurons:
  • Sodium (Na⁺) is higher outside the cell than inside.
  • Potassium (K⁺) is higher inside the cell than outside.

Other options explained:

❌ Ionizing potential → Refers to the energy required to remove an electron from an atom, unrelated to membrane gradients.
❌ Osmolarity → Measures the total solute concentration in a solution, not specific to ion gradients across membranes.
❌ Diffusion potential → The electrical potential created by the movement of ions down their concentration gradient.
❌ Action potential → A rapid electrical impulse generated by ion movements, but it depends on the pre-existing concentration gradient.

A single axon terminal at a neuromuscular junction (NMJ) contains approximately 300,000 vesicles of acetylcholine (ACh). Each vesicle holds about 1,000 to 10,000 molecules of ACh.

When an action potential reaches the terminal, about 100–200 vesicles fuse with the presynaptic membrane and release their contents into the synaptic cleft, initiating muscle contraction.

Other options explained:

❌ 500, 70, 2,000, 10,000 → These numbers are far too low for the total vesicle count in an axon terminal. The actual amount is much higher, though only a small fraction is released per impulse.

In developing countries, older adults are the most likely age group to experience a stroke. This is primarily due to:

• Increased prevalence of hypertension, diabetes, and smoking
• Limited access to preventive healthcare
• Higher rates of untreated cardiovascular disease
• Aging population with cumulative vascular risk factors

While strokes can occur in younger individuals due to conditions like cardioembolic events, sickle cell disease, or vasculitis, the vast majority of strokes still occur in older adults due to atherosclerosis and hypertension.

Other options explained:

❌ Adolescents, young adults, teenagers, and children → While strokes can occur in younger populations due to genetic, hematologic, or congenital factors, they are far less common than in older adults.

Uncal herniation occurs when the medial part of the temporal lobe (uncus) is displaced downward and medially through the tentorial notch, compressing nearby structures. One of the most critical effects is compression of the oculomotor nerve (CN III), leading to:

• Oculomotor paralysis → Dilated, fixed pupil (due to parasympathetic fiber compression)
• Ptosis (drooping eyelid) and “down and out” eye position (due to loss of CN III function)
• Contralateral hemiparesis (compression of cerebral peduncle affecting corticospinal tract)
• Duret hemorrhages in the midbrain and pons due to brainstem compression

Other options explained:

❌ Chewing difficulties → More likely due to trigeminal nerve (CN V) dysfunction, not uncal herniation.
❌ Kidney disease → Unrelated to brain herniation.
❌ Breathing cessation → Occurs in tonsillar herniation, where the medulla is compressed.
❌ Crescent-shaped lesion → Characteristic of subdural hematoma, not uncal herniation.

• An encephalocele is a neural tube defect characterized by the protrusion of brain tissue and meninges through a defect in the skull.

• It results from incomplete closure of the cranial part of the neural tube during embryonic development.

Encephaloceles can occur in different locations, but the anterior cranial fossa is the most commonly involved area, especially in clinical practice.

Understanding the Cranial Fossae:

• Anterior cranial fossa: Houses the frontal lobes. Forms the roof of the orbits and nasal cavity.

• Middle cranial fossa: Contains the temporal lobes.

• Posterior cranial fossa: Contains the cerebellum, pons, and medulla.

Why anterior cranial fossa?

• It is closely related to the nasal cavity and orbital roof — both relatively weak spots.

• Defects here can lead to frontoethmoidal encephaloceles (brain tissue herniating through the foramen cecum or cribriform plate into the nasal area).

Clinically:

• Frontoethmoidal encephaloceles → Swelling over the nose, forehead, or between the eyes.

• Occipital encephaloceles (posterior fossa defects) are less common but can be serious.

Evaluate Each Option:

. Medial cranial fossa
🔴 Incorrect —
There is no standard anatomical structure called the “medial cranial fossa.” Possibly a confusion with middle cranial fossa. Medial structures aren’t a major site for encephaloceles.

. Posterior cranial fossa
🔴 Incorrect —
Posterior fossa defects do occur (especially occipital encephaloceles), but overall incidence is less than anterior fossa defects.

. Anterior cranial fossa
🔵 Correct —
This is the most common site of encephaloceles, especially frontoethmoidal encephaloceles involving the nasal bridge and frontal bone.

. Lateral cranial fossa
🔴 Incorrect —
No specific “lateral cranial fossa” exists anatomically. The lateral aspects are part of the middle cranial fossa, but not typically involved.

. Middle cranial fossa
🔴 Incorrect —
Middle cranial fossa defects might cause herniations of temporal lobe structures, but encephaloceles here are rare compared to anterior ones.

Spina bifida meningomyelocele is a severe form of spina bifida, a neural tube defect in which both the meninges and the spinal cord herniate through a defect in the vertebral arch.

• The spinal cord and meninges protrude, forming a fluid-filled sac covered by a thin layer of skin or exposed tissue.
• This condition can cause neurological deficits, including motor and sensory impairment below the level of the lesion.
• Commonly occurs in the lumbar and sacral regions.
• It is associated with Arnold-Chiari malformation Type II and hydrocephalus.

Other options explained:

❌ Protrusion of spinal cord → Only spinal cord involvement describes myelocele.
❌ Depression of meninges and vertebral arch → Incorrect; there is herniation, not depression.
❌ Depression of meninges and spinal cord → Incorrect; there is protrusion, not depression.
❌ Protrusion of meninges → This describes spina bifida meningocele, a milder form where only the meninges protrude without spinal cord involvement.

Gliosis is a process in which astrocytes undergo hyperplasia and hypertrophy in response to CNS injury, ischemia, inflammation, or neurodegeneration. It serves as a repair mechanism in the brain and spinal cord.

• Astrocyte proliferation and hypertrophy → Leads to the formation of a glial scar, which helps contain damage but can inhibit neuronal regeneration.
• Increased expression of glial fibrillary acidic protein (GFAP) → A hallmark of gliosis.

Other options explained:

❌ Myelin sheath → Involves oligodendrocytes (not related to gliosis).
❌ Fibers → Axonal fibers may be affected, but gliosis is an astrocytic response.
❌ Fibroblasts → Present in peripheral tissue repair, but gliosis is a CNS-specific process.
❌ Macrophages → Microglia act as CNS macrophages, but gliosis is distinct from their function.

In tuberculous (TB) meningitis, cerebrospinal fluid (CSF) glucose levels decrease due to active bacterial metabolism and the inflammatory response. Mycobacterium tuberculosis consumes glucose and causes increased blood-brain barrier permeability, leading to low CSF glucose relative to blood glucose.

CSF Findings in TB Meningitis:

• ↓ Glucose (<45 mg/dL or <50% of blood glucose)
• ↑ Protein (often >100 mg/dL)
• ↑ Lymphocytes (lymphocytic pleocytosis)
• ↑ Opening pressure
• Cobweb-like fibrin clot when CSF is left standing

Other options explained:

❌ Lymphocytes → Increase (predominantly lymphocytic response)
❌ Proteins → Increase due to blood-brain barrier disruption
❌ Neutrophils → May be present early but later shift to a lymphocyte-dominant response
❌ Cerebrospinal fluid (CSF) → The amount of CSF does not decrease, but its composition changes

The internal cerebral vein is a major deep venous structure in the brain. It is formed by the union of the thalamostriate vein and the choroidal vein near the interventricular foramen (of Monro).

Once formed, the internal cerebral veins run posteriorly and join with the basal veins of Rosenthal, eventually contributing to the formation of the great cerebral vein (of Galen), which drains into the straight sinus.

Other options explained:

❌ Anterior cerebral vein and striate vein → These do not directly contribute to the formation of the internal cerebral vein.
❌ Superior cerebral vein and the great cerebral vein → The superior cerebral veins drain into the superior sagittal sinus, not forming the internal cerebral vein.
❌ Superficial cerebral vein and the basal vein → Superficial cerebral veins drain the cortex, while the basal vein (of Rosenthal) is separate and later joins the internal cerebral vein.
❌ Superficial and deep middle cerebral vein → These veins drain into different sinuses and do not contribute to the internal cerebral vein.

The auditory pathway is responsible for transmitting sound signals from the cochlea to the auditory cortex. The major relay centers in this pathway include:

✅ Spiral ganglion → First-order neurons located in the cochlea.
✅ Cochlear nuclei → Receive input from the spiral ganglion and send projections bilaterally.
✅ Trapezoid body → A key decussation site for auditory fibers in the brainstem.
✅ Medial geniculate body (MGB) → A relay center in the thalamus for auditory signals.

The superior colliculi, however, are NOT part of the auditory pathway. Instead, they play a role in the visual system, particularly in coordinating eye movements and reflexes.

Other options explained:

❌ Medial geniculate body (MGB) → An essential relay in the thalamus for auditory signals.
❌ Trapezoid body → Important for bilateral hearing processing in the brainstem.
❌ Cochlear nuclei → The first central relay station for auditory input in the brainstem.
❌ Spiral ganglion → The first-order neurons of the auditory pathway located in the cochlea.

A “cobweb appearance” of cerebrospinal fluid (CSF) is a characteristic finding in tuberculous (TB) meningitis. This occurs due to high protein content and fibrin mesh formation when the CSF is left standing.

• In TB meningitis, the CSF appears slightly cloudy, and when left in a test tube, a fine fibrin web or cobweb-like clot forms due to increased fibrinogen.
• CSF findings in TB meningitis:
  • High protein (>100 mg/dL)
  • Low glucose (<45 mg/dL or <50% of blood glucose)
  • Lymphocytic pleocytosis (↑ lymphocytes)
  • Acid-fast bacilli (AFB) on Ziehl-Neelsen stain

Other options explained:

❌ Viral encephalitis → CSF is usually clear, with normal or slightly elevated protein and normal glucose.
❌ Acute pyogenic (bacterial) meningitis → CSF is cloudy/purulent, with very high neutrophils, low glucose, and high protein, but no cobweb appearance.
❌ Neurosyphilis → CSF shows lymphocytic pleocytosis, increased protein, and positive VDRL, but no cobweb-like fibrin clot.
❌ Viral meningitis → CSF is usually clear, with high lymphocytes, normal glucose, and slightly increased protein (no cobweb appearance).

The lateral spinothalamic tract carries pain and temperature sensations from the body to the brain. This pathway decussates (crosses over) at the level of entry in the spinal cord, meaning:

• A lesion in the right lateral spinothalamic tract → causes loss of pain and temperature on the left side of the body (contralateral).
• A lesion in the left lateral spinothalamic tract → causes loss of pain and temperature on the right side of the body (contralateral).

Other options explained:

❌ Contralateral loss of crude touch → Crude touch is carried by the anterior spinothalamic tract, not the lateral spinothalamic tract.
❌ Ipsilateral loss of crude touch → Also incorrect, as crude touch is not in the lateral spinothalamic tract.
❌ Ipsilateral loss of pain and temperature → Incorrect, because pain and temperature pathways cross over in the spinal cord.
❌ Ipsilateral loss of fine touch and two-point discrimination → Fine touch and two-point discrimination are carried by the dorsal column-medial lemniscus pathway, not the spinothalamic tract.

The lateral spinothalamic tract carries pain and temperature sensations from the body to the brain. This pathway decussates (crosses over) at the level of entry in the spinal cord, meaning:

• A lesion in the right lateral spinothalamic tract → causes loss of pain and temperature on the left side of the body (contralateral).
• A lesion in the left lateral spinothalamic tract → causes loss of pain and temperature on the right side of the body (contralateral).

Other options explained:

❌ Contralateral loss of crude touch → Crude touch is carried by the anterior spinothalamic tract, not the lateral spinothalamic tract.
❌ Ipsilateral loss of crude touch → Also incorrect, as crude touch is not in the lateral spinothalamic tract.
❌ Ipsilateral loss of pain and temperature → Incorrect, because pain and temperature pathways cross over in the spinal cord.
❌ Ipsilateral loss of fine touch and two-point discrimination → Fine touch and two-point discrimination are carried by the dorsal column-medial lemniscus pathway, not the spinothalamic tract.

The sympathetic nervous system (SNS) is responsible for the “fight or flight” response, which prepares the body for emergencies by increasing heart rate, redirecting blood flow, and enhancing alertness.

One key function of sympathetic stimulation is vasoconstriction of blood vessels in the skin. This occurs via α1-adrenergic receptors, which reduce blood flow to non-essential areas (skin, GI tract) and increase blood supply to skeletal muscles, heart, and brain.

Other options explained:

❌ Increased peristalsis → Parasympathetic effect (sympathetic stimulation decreases peristalsis to conserve energy).
❌ Pupillary constriction → Mediated by the parasympathetic nervous system (sympathetic stimulation causes pupil dilation/mydriasis via α1-receptors).
❌ Defecation → Controlled by the parasympathetic nervous system (sympathetic stimulation inhibits bowel movement).
❌ Decreased force of heart contraction → Sympathetic stimulation increases heart rate and contractility via β1-adrenergic receptors.

The corpus callosum is the largest white matter structure in the brain, connecting the left and right cerebral hemispheres. It allows communication between the two sides of the brain, coordinating sensory, motor, and cognitive information.

• Agenesis means failure to develop — meaning the corpus callosum is partially or completely absent from birth.

• It can occur isolated or as part of syndromic conditions (e.g., Aicardi syndrome, trisomies, fetal alcohol syndrome).

Effects depend on severity but commonly involve intellectual, developmental, and coordination difficulties.

Evaluate Each Option:

A. Loss of speech
🔴 Incorrect —
Speech is mainly localized in specific cortical regions (e.g., Broca’s area, Wernicke’s area).
Although agenesis can cause developmental delays, isolated speech loss is not the hallmark symptom.
Primary speech centers can still develop normally even without the corpus callosum.

B. Loss of motor control
🔴 Incorrect —
Gross motor function is controlled by motor cortices and descending corticospinal tracts.
In agenesis of the corpus callosum, basic motor pathways remain intact; however, fine coordination between hemispheres may suffer — but complete motor control loss is not characteristic.

C. Loss of coordination
🔴 Incorrect —
Although bimanual coordination (using both hands together) may be impaired because of poor interhemispheric communication, generalized “loss of coordination” points more to cerebellar dysfunction, not specifically corpus callosum issues.

D. Mental retardation
🔵 Correct —
Agenesis of the corpus callosum is classically associated with cognitive deficits, often presenting as intellectual disability (formerly termed “mental retardation”).

• Many affected individuals show delays in milestones, learning difficulties, and abstract thinking challenges.

• The severity can range widely: Some individuals have only subtle learning disabilities, while others have profound developmental delays.

E. Loss of sensory control
🔴 Incorrect —
Sensory inputs are processed mainly in the somatosensory cortex and are not dependent on the corpus callosum to reach the brain.
Corpus callosum agenesis would not prevent sensory input reception or primary sensory control.

🔥 Final Answer:

✅ D. Mental retardation

Anterior cord syndrome results from damage to the anterior two-thirds of the spinal cord, often due to infarction of the anterior spinal artery. This affects:

✅ Corticospinal tract → Leading to bilateral motor paralysis (below the lesion)
✅ Spinothalamic tract → Causing loss of pain & temperature sensation

The dorsal column-medial lemniscus (DCML) pathway, which carries proprioception, vibration, and two-point discrimination, is spared because it is located in the posterior third of the spinal cord, which is not affected in anterior cord syndrome.

Other options explained:

❌ Crude touch and two-point discrimination → Crude touch is carried by the anterior spinothalamic tract (affected in anterior cord syndrome), while two-point discrimination is part of the dorsal column (which is spared).
❌ Fine touch and pressure → Fine touch is carried by the dorsal column (spared), but pressure sensation is part of the anterior spinothalamic tract, which is affected.
❌ Pain and temperature → Carried by the lateral spinothalamic tract, which is damaged.
❌ Vibration, crude touch, and pressure → Crude touch and pressure are affected, but vibration is spared.

Serotonin (5-hydroxytryptamine or 5-HT) is synthesized from the amino acid tryptophan through the following biochemical pathway:

1. Tryptophan hydroxylase converts tryptophan into 5-hydroxytryptophan (5-HTP).
2. Aromatic L-amino acid decarboxylase converts 5-HTP into serotonin (5-HT).

Serotonin plays an important role in mood regulation, sleep, appetite, and cognition. It is also a precursor for melatonin, which regulates the sleep-wake cycle.

Other options explained:

❌ Tri-acyl glycerol → A form of fat storage, not involved in serotonin synthesis.
❌ Tri-carboxylic acid → Refers to the TCA (Krebs) cycle, which is involved in energy metabolism, not neurotransmitter synthesis.
❌ Tyrosine → Precursor for dopamine, norepinephrine, and epinephrine, not serotonin.
❌ Taurine → A sulfur-containing amino acid involved in bile salt formation and neuronal development, but not in serotonin production.

A positive Babinski sign (upward movement of the big toe with fanning of the other toes when the sole of the foot is stroked) is a hallmark of an upper motor neuron (UMN) lesion. Normally, this reflex is suppressed in adults due to descending inhibition from the corticospinal tract.

Features of UMN Lesions:

✅ Hyperreflexia → Exaggerated reflexes due to loss of inhibitory control
✅ Hypertonia → Increased muscle tone (spasticity)
✅ Spastic paralysis → Stiff, weak muscles with increased reflexes
✅ Positive Babinski sign → Indicative of corticospinal tract dysfunction

Other options explained:

❌ Muscle atrophy → Seen in lower motor neuron (LMN) lesions due to denervation
❌ Decreased muscle tone → LMN lesions cause hypotonia or flaccidity
❌ Flaccid paralysis → Characteristic of LMN lesions, where there’s complete loss of muscle tone
❌ Fasciculations → Involuntary muscle twitching seen in LMN lesions due to denervation

Hyperalgesia refers to an exaggerated pain response to a stimulus that normally causes pain. This occurs due to sensitization of nociceptors (pain receptors) in conditions like inflammation, nerve damage, or chronic pain syndromes.

There are two types:

• Primary hyperalgesia → Increased pain sensitivity at the site of injury (due to peripheral sensitization).
• Secondary hyperalgesia → Increased pain sensitivity in surrounding uninjured areas (due to central sensitization).

Other options explained:

• Loss of taste sensation → Known as ageusia.
• Increased sensitivity to heat → More related to thermal hyperesthesia rather than hyperalgesia.
• Decreased sensitivity to pain → Known as hypoalgesia.
• Decreased sensation in limbs → Known as hypoesthesia.

A positive Romberg test occurs when a patient loses balance upon closing their eyes while standing with feet together. This test assesses proprioception, which is carried by the dorsal column–medial lemniscus (DCML) pathway.

• With eyes open → Vision helps compensate for impaired proprioception.
• With eyes closed → If proprioception is damaged, the patient will sway or fall, indicating a positive Romberg sign.

The dorsal column carries fine touch, vibration, and proprioception, so a lesion here leads to sensory ataxia, which worsens when visual input is removed.

Other options explained:

• Lateral corticospinal tract → Motor control, not proprioception. Lesion causes spastic paralysis.
• Anterior spinothalamic tract → Carries crude touch & pressure, not proprioception.
• Dorsal spinocerebellar tract → Involved in unconscious proprioception, but does not cause a positive Romberg test.
• Lateral spinothalamic tract → Carries pain & temperature, not proprioception.

White matter consists mainly of myelinated nerve fibers, which give it its characteristic white appearance due to the myelin sheath surrounding axons. Myelin, produced by oligodendrocytes in the CNS, enhances the conduction velocity of nerve impulses.

White matter:
✔ Contains mainly myelinated nerve fibers → TRUE
✔ Does not contain nerve cell bodies → TRUE (Cell bodies are in gray matter)
✔ Contains fibrous astrocytes → TRUE (These are a type of glial cell found in white matter)
✔ Contains oligodendrocytes and microglial cells → TRUE (Oligodendrocytes produce myelin; microglia act as immune cells of the CNS)
✘ Contains mainly unmyelinated nerve fibers → FALSE, as white matter primarily consists of myelinated axons

The dorsal column-medial lemniscus (DCML) pathway is responsible for fine touch, vibration, and proprioception. A lesion in this pathway leads to sensory ataxia, which is a loss of coordination due to impaired proprioceptive input, rather than motor dysfunction.

• Patients with sensory ataxia often have difficulty walking in the dark or on uneven surfaces because they rely more on vision to compensate for their lack of proprioception.
• Positive Romberg’s sign → If a patient sways or falls when closing their eyes while standing with feet together, it suggests dorsal column dysfunction.

Other options:

• Loss of pain sensation → Due to lateral spinothalamic tract lesion
• Loss of temperature sensation → Also due to lateral spinothalamic tract lesion
• Apraxia → A motor planning disorder due to a cortical lesion
• Motor ataxia → Due to cerebellar dysfunction, not dorsal column damage

The dorsal horn of the spinal cord is responsible for receiving and processing sensory inputs, including pain, temperature, and touch. It is present at all levels of the spinal cord, not just in the cervical region.

Key facts about the dorsal horn:

• It is smaller than the ventral horn.
• It receives sensory information from the body via afferent neurons.
• It contains substantia gelatinosa, which plays a role in modulating pain and is homologous to the spinal trigeminal nucleus in the brainstem.

Since the dorsal horn is present throughout the entire length of the spinal cord, the statement that it is found “only in the cervical region” is incorrect.

The dorsal column-medial lemniscus (DCML) pathway carries fine touch (discriminative touch), vibration, and proprioception. It allows for highly localized tactile discrimination, meaning it helps in recognizing textures, shapes, and precise locations of stimuli.

• Fine touch (discriminative touch) → Recognizing textures, shapes, and precise locations
• Vibration sense → Detected by Pacinian corpuscles
• Proprioception → Awareness of body position, detected by muscle spindles and Golgi tendon organs

Crude touch is instead carried by the anterior spinothalamic tract, and pain & temperature are carried by the lateral spinothalamic tract.

Two-point discrimination is a function of the dorsal column-medial lemniscus (DCML) pathway, which is responsible for fine touch, vibration, and proprioception. The sensory fibers from the right hand travel up the right dorsal column, cross over (decussate) at the medulla, and then continue through the left medial lemniscus before reaching the contralateral sensory cortex.

Since the person has lost two-point discrimination in the right hand, the lesion must be on the contralateral (left) side of the medial lemniscus at the level of the medulla.

Renshaw cells are specialized inhibitory interneurons found in the ventral horn of the spinal cord. Their primary function is to modulate motor neuron activity through a negative feedback mechanism known as recurrent inhibition.

• Mechanism: When alpha motor neurons fire, they send collateral signals to Renshaw cells. In response, Renshaw cells release glycine, an inhibitory neurotransmitter, which then suppresses excessive motor neuron firing.
• This feedback loop prevents overexcitation of muscles, helping in smooth and controlled movements.
• Dysfunction of Renshaw cells has been implicated in disorders such as tetanus, where the toxin inhibits glycine release, leading to uncontrolled muscle contractions and spastic paralysis.

The other options relate to different neural functions:

• Blood-brain barrier: Formed by astrocytes.
• CSF formation: By choroid plexus cells.
• Phagocytosis: Function of microglia.
• Excitatory interneurons: Not the role of Renshaw cells, which are inhibitory.

Hemisection of the spinal cord refers to damage affecting one half of the spinal cord, typically due to trauma, tumors, or ischemia. This condition is known as Brown-Séquard syndrome and presents with characteristic neurological deficits:

• Ipsilateral (same side) motor loss due to damage to the corticospinal tract.
• Ipsilateral loss of proprioception, vibration, and fine touch due to dorsal column involvement.
• Contralateral (opposite side) loss of pain and temperature sensation due to damage to the spinothalamic tract, which decussates (crosses) at the spinal level.

The other options describe different neurological syndromes affecting the brainstem or spinal cord but are not related to hemisection of the spinal cord.

Deep tendon reflexes (DTRs) are monosynaptic reflexes that involve the muscle spindles, sensory neurons, and motor neurons, leading to a quick contraction of the corresponding muscle. These reflexes include the biceps reflex, brachioradialis reflex, patellar reflex, and ankle reflex, all of which test the integrity of specific spinal cord segments.

The conjunctival reflex, on the other hand, is not a deep tendon reflex. It is a superficial reflex involving the trigeminal nerve (afferent limb, CN V) and the facial nerve (efferent limb, CN VII), leading to a blink response when the conjunctiva is touched. Since it does not involve the classic stretch reflex mechanism seen in DTRs, it is the correct answer.

Dandy-Walker syndrome is a congenital malformation characterized by enlargement of the posterior cranial fossa due to abnormal development of the cerebellum and fourth ventricle. It results from:

• Hypoplasia or agenesis of the cerebellar vermis.
• Cystic dilation of the fourth ventricle.
• Enlarged posterior cranial fossa, often with hydrocephalus.

This leads to symptoms such as developmental delay, poor muscle coordination, and increased intracranial pressure due to ventricular enlargement.

Why not the other options?

• Agenesis of the corpus callosum → Affects cortical connectivity, not the posterior fossa.
• Arnold-Chiari type I → Causes herniation of cerebellar tonsils through the foramen magnum but does not enlarge the posterior fossa.
• Arnold-Chiari type II → Causes hindbrain malformation with downward displacement of the cerebellum and medulla, often associated with myelomeningocele, but does not enlarge the posterior fossa.
• Holoprosencephaly → A defect in forebrain division, leading to midline facial abnormalities, unrelated to the posterior fossa.

Thus, Dandy-Walker syndrome is the correct answer, as it is the only condition associated with posterior cranial fossa enlargement.

Superficial reflexes are polysynaptic reflexes that are elicited by stimulating the skin or mucous membranes, leading to a response from skeletal muscles. These reflexes involve both sensory and motor pathways and require intact upper motor neurons (UMNs) and lower motor neurons (LMNs).

Examples of Superficial Reflexes:

✅ Conjunctival reflex → Blinking in response to conjunctival stimulation (CN V1 afferent, CN VII efferent).
✅ Abdominal reflex → Contraction of abdominal muscles when the skin of the abdomen is stroked (T7–T12 spinal segments).
✅ Corneal reflex → Blinking in response to corneal stimulation (CN V1 afferent, CN VII efferent).
✅ Plantar reflex → Toe flexion upon plantar stimulation (Babinski sign is an abnormal response).

Why is the Patellar Reflex NOT a Superficial Reflex?

The patellar reflex (knee jerk reflex) is a deep tendon (monosynaptic stretch) reflex, not a superficial reflex. It is:

• Monosynaptic → Involves a direct synapse between sensory and motor neurons in the spinal cord (L2–L4 spinal segments).
• Elicited by stretching the quadriceps muscle via the patellar tendon tap, leading to quadriceps contraction and knee extension.
• Does not require cortical processing, unlike superficial reflexes, which involve the brain.

Thus, the patellar reflex is not a superficial reflex, making it the correct answer.