Dandy-Walker syndrome is a congenital malformation characterized by:

1. Cystic dilation of the fourth ventricle
2. Hypoplasia or agenesis of the cerebellar vermis
3. Enlargement of the posterior cranial fossa

• The posterior fossa is enlarged due to the cystic expansion of the fourth ventricle.
• This leads to hydrocephalus (due to obstruction of CSF flow).
• Symptoms may include developmental delay, ataxia, and increased head circumference due to hydrocephalus.

Why Are the Other Options Incorrect?

• Arnold-Chiari Type II: ❌
  • Chiari malformation type II is associated with herniation of the cerebellar tonsils and vermis through the foramen magnum.
  • It is seen in spina bifida (myelomeningocele).
  • Unlike Dandy-Walker syndrome, the posterior fossa is small rather than enlarged.
• Arnold-Chiari Type I: ❌
  • Chiari malformation type I involves herniation of the cerebellar tonsils, but the posterior fossa is normal-sized or small, not enlarged.
  • Symptoms include headaches, ataxia, and syringomyelia.
• Agenesis of the corpus callosum: ❌
  • This condition involves failure of the corpus callosum to form, leading to cognitive and motor impairments.
  • It does not affect the posterior cranial fossa.
• Holoprosencephaly: ❌
  • Defect in forebrain division (prosencephalon), leading to midline facial abnormalities (e.g., cyclopia, cleft lip/palate).
  • It affects the cerebrum, not the posterior fossa.

Two-point discrimination is a function of the dorsal column-medial lemniscus (DCML) pathway, which carries fine touch, vibration, and proprioception from the periphery to the brain.

Pathway of the DCML System:

1. First-order neurons: Sensory signals from the right hand travel via the dorsal column (fasciculus cuneatus) to the ipsilateral medulla.
2. Second-order neurons: These neurons decussate (cross over) in the medulla and continue in the contralateral medial lemniscus.
3. Third-order neurons: The signal reaches the thalamus (VPL nucleus) and then is relayed to the primary somatosensory cortex (postcentral gyrus of the parietal lobe).

Since the medial lemniscus carries contralateral sensory information, a left-sided lesion in the medial lemniscus at the medulla will cause loss of two-point discrimination in the right hand.

Why the Other Options Are Incorrect:

• Lateral lemniscus ❌
  • The lateral lemniscus is part of the auditory pathway, not involved in two-point discrimination.
• Lateral spinothalamic tract ❌
  • This tract carries pain and temperature sensation, not fine touch or two-point discrimination.
• Anterior spinothalamic tract ❌
  • This tract carries crude touch and pressure, but not fine touch or two-point discrimination.
• Right medial lemniscus at the medulla ❌
  • The medial lemniscus carries contralateral sensory information, so a lesion on the right side would affect the left hand, not the right hand.

The dorsal column-medial lemniscus (DCML) pathway is responsible for carrying fine touch, vibration, and proprioception to the brain. These sensations require high spatial and temporal resolution, meaning they can be precisely localized and discriminated.

The dorsal column is divided into two tracts:

1. Fasciculus gracilis (carries signals from the lower body).
2. Fasciculus cuneatus (carries signals from the upper body).

These fibers ascend ipsilaterally in the spinal cord and synapse in the medulla oblongata, where they decussate (cross over) and continue as the medial lemniscus to the thalamus (VPL nucleus) and then to the somatosensory cortex.

Why the Other Options Are Incorrect:

• Proprioception, fine touch, and crude touch ❌
  • The dorsal column carries proprioception and fine touch, but not crude touch. Crude touch is carried by the anterior spinothalamic tract.
• Pain and temperature ❌
  • These sensations are carried by the lateral spinothalamic tract, not the dorsal column.
• Proprioception and crude touch ❌
  • The dorsal column carries proprioception, but not crude touch. Crude touch is transmitted via the anterior spinothalamic tract.
• Proprioception only ❌
  • The dorsal column also transmits fine touch and vibration, not just proprioception.

Serotonin (5-hydroxytryptamine, 5-HT) is an indolamine neurotransmitter derived from the amino acid tryptophan. It plays an essential role in:

• Mood regulation (linked to depression and anxiety).
• Sleep-wake cycles (precursor of melatonin).
• Gastrointestinal function (present in enterochromaffin cells).
• Platelet aggregation and vasoconstriction.

Biosynthesis of Serotonin:

1. Tryptophan is converted to 5-hydroxytryptophan (5-HTP) by tryptophan hydroxylase.
2. 5-HTP is then converted to serotonin (5-HT) by aromatic L-amino acid decarboxylase.

Serotonin is also the precursor for melatonin, which regulates the circadian rhythm.

Why the Other Options Are Incorrect:

• Prostaglandin ❌
  • Prostaglandins are derived from arachidonic acid, not tryptophan. They play a role in inflammation and pain modulation.
• Chitin ❌
  • Chitin is a polysaccharide, found in fungal cell walls and insect exoskeletons, and is not related to neurotransmitters.
• Dopamine ❌
  • Dopamine is a catecholamine, derived from tyrosine, not tryptophan. It is involved in reward, motivation, and motor control.
• Leukotriene ❌
  • Leukotrienes are inflammatory mediators derived from arachidonic acid, not tryptophan.

Sensory ataxia is a type of ataxia caused by a loss of proprioceptive input to the central nervous system, leading to difficulty with coordination and balance, especially in the absence of visual input (e.g., worsening of balance in the dark).

The dorsal column-medial lemniscus (DCML) pathway is responsible for carrying:

• Fine touch
• Proprioception (position sense)
• Vibration sensation

Damage to this pathway results in loss of proprioception, leading to sensory ataxia. A classical test for sensory ataxia is the Romberg test, where a patient loses balance when their eyes are closed.

Why the Other Options Are Incorrect:

• Anterior spinothalamic tract ❌
  • This tract transmits crude touch and pressure, which do not significantly affect balance or coordination.
• Corticospinal tract ❌
  • The corticospinal tract controls voluntary motor function, not proprioception. Lesions cause motor weakness or paralysis, not sensory ataxia.
• Dorsal spinocerebellar tract ❌
  • This tract carries unconscious proprioception to the cerebellum, which is important for coordination. Lesions cause cerebellar ataxia, which is different from sensory ataxia (cerebellar ataxia does not worsen with eye closure).
• Ventral spinocerebellar tract ❌
  • This tract also carries unconscious proprioceptive signals but does not significantly contribute to sensory ataxia when damaged.

The superior sagittal sinus is a large venous sinus located within the falx cerebri, a dural fold that separates the two cerebral hemispheres.

Drainage Pathway of the Superior Sagittal Sinus:

1. Blood from the superior sagittal sinus flows posteriorly toward the confluence of sinuses, which is located at the internal occipital protuberance.
2. The confluence of sinuses receives blood from multiple sinuses, including the straight sinus and occipital sinus.
3. From the confluence, blood from the superior sagittal sinus primarily drains into the right transverse sinus, while the straight sinus typically drains into the left transverse sinus.
4. The transverse sinus continues as the sigmoid sinus, which then drains into the internal jugular vein.

Why the Other Options Are Incorrect:

• Ethmoidal sinus ❌
  • This is a paranasal sinus involved in draining mucus into the nasal cavity, not a venous sinus.
• Straight sinus ❌
  • The straight sinus drains blood from the inferior sagittal sinus and the great cerebral vein (vein of Galen), but not the superior sagittal sinus.
• Longitudinal sinus ❌
  • No anatomical structure called the “longitudinal sinus” exists in the brain’s venous drainage system.
• Sinusoidal sinus ❌
  • Sinusoids are specialized capillaries found in organs like the liver and spleen, not part of the brain’s venous drainage system.

GLUT-3 is the primary glucose transporter in the brain. It is a high-affinity transporter, meaning it efficiently transports glucose even when blood glucose levels are low. This ensures that neurons receive a constant supply of glucose, which is crucial for maintaining normal brain function.

Neurons have a high metabolic demand and rely almost exclusively on glucose for energy. Since GLUT-3 has a low Km (high affinity for glucose), it allows neurons to take up glucose efficiently, even in hypoglycemic conditions.

Why Are the Other Options Incorrect?

1. GLUT-2 (Incorrect)
   • GLUT-2 is found in the liver, pancreas (β-cells), kidneys, and intestines.
   • It has a high Km (low affinity for glucose), meaning it functions well when glucose levels are high, such as after a meal.
   • It does not play a major role in glucose transport in the brain.
2. GLUT-5 (Incorrect)
   • GLUT-5 is a fructose transporter, not a glucose transporter.
   • It is primarily found in the small intestine and spermatocytes, where it facilitates fructose absorption.
   • It is not involved in glucose uptake in the brain.
3. GLUT-4 (Incorrect)
   • GLUT-4 is the insulin-dependent glucose transporter found in skeletal muscle and adipose tissue.
   • The brain does not require insulin for glucose uptake, so GLUT-4 is not involved in neuronal glucose transport.
4. SGLT-1 (Incorrect)
   • SGLT-1 (Sodium-Glucose Linked Transporter 1) is a sodium-dependent transporter found in the small intestine and renal tubules.
   • It plays a role in active glucose absorption, but not in the brain, where glucose uptake occurs through facilitated diffusion (not active transport).

GLUT-3 is the primary glucose transporter in the brain. It is a high-affinity transporter, meaning it efficiently transports glucose even when blood glucose levels are low. This ensures that neurons receive a constant supply of glucose, which is crucial for maintaining normal brain function.

Neurons have a high metabolic demand and rely almost exclusively on glucose for energy. Since GLUT-3 has a low Km (high affinity for glucose), it allows neurons to take up glucose efficiently, even in hypoglycemic conditions.

Why Are the Other Options Incorrect?

1. GLUT-2 (Incorrect)
   • GLUT-2 is found in the liver, pancreas (β-cells), kidneys, and intestines.
   • It has a high Km (low affinity for glucose), meaning it functions well when glucose levels are high, such as after a meal.
   • It does not play a major role in glucose transport in the brain.
2. GLUT-5 (Incorrect)
   • GLUT-5 is a fructose transporter, not a glucose transporter.
   • It is primarily found in the small intestine and spermatocytes, where it facilitates fructose absorption.
   • It is not involved in glucose uptake in the brain.
3. GLUT-4 (Incorrect)
   • GLUT-4 is the insulin-dependent glucose transporter found in skeletal muscle and adipose tissue.
   • The brain does not require insulin for glucose uptake, so GLUT-4 is not involved in neuronal glucose transport.
4. SGLT-1 (Incorrect)
   • SGLT-1 (Sodium-Glucose Linked Transporter 1) is a sodium-dependent transporter found in the small intestine and renal tubules.
   • It plays a role in active glucose absorption, but not in the brain, where glucose uptake occurs through facilitated diffusion (not active transport).

Serotonin (5-hydroxytryptamine, 5-HT) is synthesized from the amino acid tryptophan through a two-step enzymatic process:

1. Tryptophan hydroxylase converts tryptophan into 5-hydroxytryptophan (5-HTP).
   • This step requires tetrahydrobiopterin (BH4) as a cofactor.
2. Aromatic L-amino acid decarboxylase (DOPA decarboxylase) then converts 5-HTP into serotonin (5-HT).
   • This step requires pyridoxal phosphate (Vitamin B6) as a cofactor.

Serotonin is involved in mood regulation, sleep, appetite, and vasoconstriction. It is primarily found in:

• CNS (raphe nuclei of the brainstem) → mood regulation and cognition
• Enterochromaffin cells of the GI tract → regulates gut motility
• Platelets → promotes vasoconstriction and clotting

Why Are the Other Options Incorrect?

1. Taurine (Incorrect)
   • Taurine is a sulfur-containing amino acid derived from cysteine.
   • It plays a role in bile salt formation, osmoregulation, and neural function but is not a precursor of serotonin.
2. Triacylglycerol (Incorrect)
   • Triacylglycerols (triglycerides) are lipids used for energy storage.
   • They are not involved in neurotransmitter synthesis.
3. Tyrosine (Incorrect)
   • Tyrosine is the precursor for dopamine, norepinephrine, and epinephrine (catecholamines), not serotonin.
   • It is also involved in thyroid hormone and melanin synthesis.
4. Tricarboxylic acid (Incorrect)
   • The tricarboxylic acid (TCA) cycle (Krebs cycle) is a metabolic pathway for energy production in mitochondria.
   • It does not directly synthesize neurotransmitters.

The lateral nucleus of the hypothalamus is involved in the activation of the sympathetic nervous system, leading to an increase in heart rate and blood pressure. It plays a crucial role in regulating autonomic functions, arousal, and feeding behavior.

• Sympathetic activation → Increases heart rate (tachycardia) and blood pressure (hypertension)
• Lesion of the lateral nucleus → Decreased sympathetic output, leading to bradycardia and hypotension

Why Are the Other Options Incorrect?

1. Anterior nucleus (Incorrect)
   • The anterior nucleus is responsible for cooling (heat dissipation) and parasympathetic activation.
   • It decreases heart rate and blood pressure, opposite to the function in the question.
   • “A/C = Anterior Cools” is a mnemonic to remember its role in temperature regulation.
2. Tuberomamillary nucleus (Incorrect)
   • The tuberomamillary nucleus is involved in wakefulness and arousal via histamine release.
   • It does not directly regulate heart rate or blood pressure.
   • Lesion here causes excessive sleepiness (hypersomnia).
3. Suprachiasmatic nucleus (Incorrect)
   • The suprachiasmatic nucleus (SCN) is the body’s master circadian clock, regulating sleep-wake cycles.
   • It does not control heart rate or blood pressure directly.
   • Mnemonic: “SCN = Sleep Control Nucleus”
4. Supraoptic nucleus (Incorrect)
   • The supraoptic nucleus is responsible for secreting antidiuretic hormone (ADH, vasopressin), which regulates water balance.
   • While ADH affects blood pressure indirectly via water retention, it is not primarily responsible for increasing heart rate and blood pressure.

Mental retardation is commonly associated with agenesis of the corpus callosum (ACC). Agenesis of the corpus callosum is a congenital condition where the corpus callosum, the structure that connects the two cerebral hemispheres, fails to develop. This can lead to a range of neurological and developmental issues, including:

• Cognitive impairments (mental retardation).
• Seizures.
• Delayed motor milestones.
• Social and behavioral difficulties.

Why the other options are less commonly associated:

1. Loss of sensory control:
   • While some individuals with ACC may experience sensory processing issues, a complete loss of sensory control is not a typical symptom.
2. Loss of coordination:
   • Mild coordination problems may occur, but severe loss of coordination is not a hallmark symptom of ACC.
3. Loss of speech:
   • Speech delays or difficulties may occur in some cases, but a complete loss of speech is rare and not a defining feature of ACC.
4. Loss of motor control:
   • While some individuals with ACC may experience mild motor delays, a complete loss of motor control is not typically associated with this condition.

A “bat-wing deformity” on brain MRI is a characteristic finding in agenesis of the corpus callosum (ACC). This deformity occurs due to the absence of the corpus callosum, leading to widening of the lateral ventricles and an abnormal appearance of the interhemispheric structures.

Key Features of Agenesis of Corpus Callosum (ACC):

✔️ Absent or underdeveloped corpus callosum (the major white matter tract connecting both hemispheres).
✔️ Bat-wing or racing car appearance on MRI due to:

• Widening of the lateral ventricles (colpocephaly).
• Elevation of the third ventricle into the interhemispheric fissure.
  ✔️ Associated with developmental delay, intellectual disability, and seizures (depending on severity).
  ✔️ May occur in isolation or as part of genetic syndromes (e.g., Aicardi syndrome, Andermann syndrome).

Since a bat-wing appearance is strongly associated with ACC, it is the most likely cause in this case.

Analysis of Each Option:

✅ Correct Option:
🔹 “Agenesis of corpus callosum”
✔️ True – The absence of the corpus callosum leads to ventricular widening, giving the brain an MRI appearance resembling a “bat-wing.”

🚫 Incorrect Options:

🔹 “Holoprosencephaly”
❌ Holoprosencephaly is a failure of forebrain (prosencephalon) division, leading to a single midline ventricle and abnormal facial development.
❌ MRI does not show a bat-wing deformity but instead shows fused cerebral hemispheres.

🔹 “Polymicrogyria”
❌ Polymicrogyria is characterized by abnormally small and excessive gyri, leading to a “pebble-like” cortex on MRI, not a bat-wing deformity.

🔹 “Lissencephaly”
❌ Lissencephaly (“smooth brain”) results from failed neuronal migration, leading to absent or underdeveloped gyri and sulci.
❌ The MRI shows a smooth brain surface, not a bat-wing deformity.

🔹 “Neuronal heterotopia”
❌ Neuronal heterotopia is a failure of neurons to migrate properly, leading to grey matter nodules in abnormal locations (e.g., periventricular nodular heterotopia).
❌ It does not produce a bat-wing deformity.

The extrapyramidal system is responsible for regulating involuntary movements, coordination, and muscle tone. It includes the basal ganglia, substantia nigra, and associated pathways.

Among the diseases listed, Parkinson’s disease is the most common extrapyramidal disorder. It primarily affects the dopaminergic neurons in the substantia nigra, leading to motor symptoms such as:

• Bradykinesia (slowness of movement)
• Resting tremor (“pill-rolling” tremor)
• Rigidity (“cogwheel rigidity”)
• Postural instability

Parkinson’s disease is caused by dopamine depletion in the nigrostriatal pathway, leading to disruption of basal ganglia function.

Why the Other Options Are Wrong?

❌ Fragile X Syndrome – Incorrect!

• Fragile X syndrome is a genetic disorder caused by CGG repeat expansion in the FMR1 gene on the X chromosome.
• It primarily affects cognition and behavior, not the extrapyramidal motor system.
• Symptoms include intellectual disability, hyperactivity, and autistic-like features, but not classic extrapyramidal symptoms.

❌ Huntington’s Disease – Incorrect!

• Huntington’s disease affects the basal ganglia, leading to chorea (involuntary jerky movements), dementia, and psychiatric symptoms.
• However, it is less common than Parkinson’s disease.

❌ Alzheimer’s Disease – Incorrect!

• Alzheimer’s disease is the most common cause of dementia, but it primarily affects cognition and memory, not extrapyramidal motor control.
• It is associated with beta-amyloid plaques and neurofibrillary tangles, rather than basal ganglia dysfunction.

❌ Wilson’s Disease – Incorrect!

• Wilson’s disease is a disorder of copper metabolism, leading to hepatic, psychiatric, and neurological symptoms.
• While it can cause extrapyramidal symptoms (dystonia, tremors, rigidity) due to copper accumulation in the basal ganglia, it is far less common than Parkinson’s disease.

A “cobweb” appearance of cerebrospinal fluid (CSF) is a classic finding in tuberculous (TB) meningitis. This appearance results from:

• High fibrin content in the CSF, which forms a gel-like or cobweb-like clot when the fluid is left standing.
• Increased protein concentration due to the inflammatory response.
• Moderate lymphocytic pleocytosis (increased white blood cells, predominantly lymphocytes).

This fibrin clot is not commonly seen in other types of meningitis, making it an important clue for tuberculous meningitis.

Why the Other Options Are Wrong?

❌ Viral Meningitis – Incorrect!

• Viral (aseptic) meningitis typically has clear CSF, with mildly increased protein, normal glucose, and lymphocytic pleocytosis.
• It does not produce a cobweb-like clot in CSF.

❌ Acute Pyogenic (Bacterial) Meningitis – Incorrect!

• Bacterial meningitis leads to turbid and purulent CSF with markedly elevated WBCs (mainly neutrophils), low glucose, and high protein.
• No cobweb clot is observed; instead, the CSF appears cloudy or thick with pus.

❌ Viral Encephalitis – Incorrect!

• Encephalitis primarily affects brain tissue rather than the meninges.
• CSF findings are similar to viral meningitis, and there is no cobweb appearance.

❌ Neurosyphilis – Incorrect!

• Neurosyphilis presents with mild pleocytosis, elevated protein, and normal or low glucose, but it does not form a cobweb-like fibrin clot.
• The Venereal Disease Research Laboratory (VDRL) test on CSF is positive in neurosyphilis.

The auditory pathway is responsible for transmitting sound signals from the cochlea to the auditory cortex. The major structures involved in the auditory pathway include:

1. Spiral Ganglion → First-order neurons in the cochlea.
2. Cochlear Nuclei → Receive input from the spiral ganglion.
3. Trapezoid Body → Crossed fibers contributing to the superior olivary nucleus.
4. Medial Geniculate Body (MGB) → Thalamic relay center for auditory information.

However, the Superior Colliculi are primarily involved in visual reflexes, eye movements, and coordination of head and neck movements in response to visual stimuli. They are not part of the auditory pathway, making them the correct answer.

Why the Other Options Are Wrong?

❌ Medial Geniculate Body – Incorrect!

• This thalamic nucleus relays auditory signals from the inferior colliculus to the auditory cortex in the temporal lobe.
• It is a key structure in the auditory pathway.

❌ Trapezoid Body – Incorrect!

• The trapezoid body is a collection of decussating (crossing) auditory fibers within the brainstem.
• It plays a role in binaural sound processing, which is crucial for localizing sounds.

❌ Spiral Ganglion – Incorrect!

• The spiral ganglion contains the first-order neurons of the auditory pathway.
• These neurons receive input from hair cells in the cochlea and send signals to the cochlear nuclei.

❌ Cochlear Nuclei – Incorrect!

• The cochlear nuclei in the brainstem receive auditory input from the spiral ganglion and send signals further along the pathway.
• They are an essential component of the auditory system.

The internal cerebral vein is an important deep vein of the brain that drains structures such as the thalamus, basal ganglia, and deep white matter.

• It is formed by the union of the thalamostriate vein and the choroidal vein near the interventricular foramen (foramen of Monro).
• The thalamostriate vein drains the thalamus and caudate nucleus.
• The choroidal vein drains the choroid plexus of the lateral ventricle.
• The internal cerebral veins (one on each side) then course posteriorly and join together at the great cerebral vein of Galen.

Why the Other Options Are Wrong?

❌ Superficial Cerebral Vein and the Basal Vein – Incorrect!

• The superficial cerebral veins primarily drain the cortex and empty into the superior sagittal sinus.
• The basal vein (of Rosenthal) drains deep structures and eventually joins the great cerebral vein (of Galen) but does not contribute directly to the formation of the internal cerebral vein.

❌ Superficial and Deep Middle Cerebral Vein – Incorrect!

• These veins are involved in draining the lateral aspects of the brain and empty into the cavernous sinus or basal vein but do not contribute to the internal cerebral vein.

❌ Anterior Cerebral Vein and Striate Vein – Incorrect!

• There is no significant anterior cerebral vein in the brain’s venous anatomy.
• The striate veins are small veins draining the basal ganglia, but they do not directly form the internal cerebral vein.

❌ Superior Cerebral Vein and the Great Cerebral Vein – Incorrect!

• Superior cerebral veins drain the superior cortex into the superior sagittal sinus.
• The great cerebral vein (of Galen) is formed by the union of the internal cerebral veins, not the other way around.

In bacterial meningitis, bacteria consume glucose and trigger an inflammatory response, leading to markedly decreased glucose levels in the cerebrospinal fluid (CSF). This is a key diagnostic marker for bacterial infections in the central nervous system (CNS).

• Normal CSF glucose: ~50–80 mg/dL (or ~⅔ of blood glucose)
• Bacterial meningitis: CSF glucose is markedly decreased (often <40 mg/dL or <50% of blood glucose)
• Viral (aseptic) meningitis: CSF glucose is usually normal or mildly decreased

Other CSF findings in bacterial meningitis:

• Increased neutrophils (neutrophilic pleocytosis)
• Increased protein
• Cloudy/turbid CSF
• Positive Gram stain and culture (if bacteria present)

Why the Other Options Are Wrong?

❌ Negative Gram Stain – Incorrect!

• A negative Gram stain does not rule out bacterial meningitis because some bacteria (e.g., Listeria, Mycobacterium tuberculosis, Neisseria meningitidis in early infection) may not always be visible on Gram stain.
• However, if positive, it strongly supports bacterial infection.

❌ Clear Appearance of CSF – Incorrect!

• In bacterial meningitis, CSF is typically cloudy or turbid due to high WBCs and protein.
• Clear CSF is more characteristic of viral (aseptic) meningitis or normal CSF.

❌ Presence of Lymphocytes – Incorrect!

• Lymphocytic predominance is a hallmark of viral (aseptic) meningitis, tuberculous meningitis, or fungal meningitis.
• Bacterial meningitis shows predominantly neutrophils (polymorphonuclear leukocytes, PMNs).

❌ Decreased Protein Level – Incorrect!

• Bacterial infections increase CSF protein, not decrease it, due to the breakdown of the blood-brain barrier and inflammation.
• Elevated protein is seen in bacterial, tuberculous, and fungal meningitis.

The anterior spinal artery (ASA) supplies the anterior two-thirds of the spinal cord, making the spinal cord the most affected region in case of ASA thrombosis.

Structures Affected by Anterior Spinal Artery Thrombosis:

• Corticospinal tract → Causes bilateral motor weakness (paralysis) below the lesion.
• Spinothalamic tract → Causes bilateral loss of pain and temperature sensation below the lesion.
• Autonomic fibers → May cause urinary and bowel dysfunction.

This results in anterior spinal artery syndrome, characterized by:

• Bilateral motor paralysis (due to corticospinal tract involvement).
• Loss of pain and temperature sensation (spinothalamic tract affected).
• Preserved proprioception and vibratory sensation (since the posterior columns are spared, as they are supplied by the posterior spinal arteries).

Why the Other Options Are Wrong?

❌ Cerebellum – Incorrect!

• The cerebellum is mainly supplied by the posterior inferior cerebellar artery (PICA), anterior inferior cerebellar artery (AICA), and superior cerebellar artery (SCA).
• The anterior spinal artery does not supply the cerebellum, so it remains unaffected.

❌ Pons – Incorrect!

• The pons is mainly supplied by the basilar artery and its branches (pontine arteries).
• The anterior spinal artery does not supply the pons, so it is not significantly affected.

❌ Medulla – Incorrect!

• While the anterior spinal artery does supply part of the medulla, the primary effect of ASA thrombosis is on the spinal cord, making the spinal cord the most affected region.
• The medullary infarct caused by ASA thrombosis would result in medial medullary syndrome, but the spinal cord is more severely impacted overall.

❌ Midbrain – Incorrect!

• The midbrain is primarily supplied by the posterior cerebral artery (PCA) and basilar artery branches.
• The anterior spinal artery does not supply the midbrain, so it is unaffected.

Explanation:

In tuberculous meningitis (TBM), the characteristic cerebrospinal fluid (CSF) findings include:

• ↓ Glucose (hypoglycorrhachia) due to bacterial metabolism and impaired glucose transport.
• ↑ Proteins due to increased permeability of the blood-brain barrier and breakdown of the mycobacterial cell wall.
• ↑ Lymphocytes as it is a chronic granulomatous infection.
• ↑ CSF pressure due to inflammation and obstruction of CSF flow.
• Neutrophils may be present initially but later replaced by lymphocytes.

Thus, glucose decreases in TBM, making it the correct answer.

Why the Other Options Are Wrong:

1. Lymphocytes (↑ Increased)
   • TBM is a chronic infection, so lymphocytes predominate in the CSF.
   • Unlike pyogenic (bacterial) meningitis, where neutrophils dominate, TBM is primarily a lymphocytic response.
2. Neutrophils (↔ May increase initially, but later ↓)
   • Neutrophils may be seen in early TBM, but as the infection progresses, lymphocytes take over.
   • This makes neutrophils an incorrect answer because their count does not stay decreased throughout.
3. Cerebrospinal Fluid (CSF) (↔ No decrease, rather ↑ pressure)
   • The CSF volume does not decrease in TBM.
   • Instead, there is an increase in CSF pressure due to inflammatory exudate blocking CSF circulation.
4. Proteins (↑ Increased)
   • TBM causes a marked elevation of CSF protein levels due to increased blood-brain barrier permeability.
   • Since proteins increase and not decrease, this is an incorrect choice.

The third and lateral ventricles communicate with the fourth ventricle via the cerebral aqueduct (Aqueduct of Sylvius), which is located in the midbrain. If this aqueduct is blocked (a condition known as aqueductal stenosis), cerebrospinal fluid (CSF) cannot flow from the third ventricle into the fourth ventricle, leading to enlargement of the third and lateral ventricles due to CSF accumulation (non-communicating hydrocephalus).

This condition is often seen in congenital hydrocephalus in children and can be visualized on radiographic imaging (such as CT or MRI) as dilation of the third and lateral ventricles, while the fourth ventricle remains normal.

Why the Other Options Are Wrong:

1. Cerebellum (✗)
   • The cerebellum is located posteriorly and primarily affects the fourth ventricle when there is obstruction (e.g., Chiari malformations, posterior fossa tumors).
   • It does not cause isolated third and lateral ventricular dilation.
2. Medulla (✗)
   • The medulla is located below the fourth ventricle and does not contribute to CSF obstruction at the third and lateral ventricles.
   • If the foramen of Magendie or Luschka were blocked (which are located near the medulla), it would cause enlargement of the fourth ventricle, not the third and lateral.
3. Pons (✗)
   • The pons is located anterior to the fourth ventricle and does not directly affect the cerebral aqueduct.
   • It is more associated with pontine gliomas, which may compress the fourth ventricle but would not selectively enlarge the third and lateral ventricles.
4. Cerebrum (✗)
   • The cerebrum consists of the cerebral hemispheres and does not house the cerebral aqueduct.
   • A lesion in the cerebrum may cause cortical atrophy or localized pressure effects, but it would not specifically block CSF flow at the aqueduct.

In viral (aseptic) meningitis, cerebrospinal fluid (CSF) analysis typically shows:

• ↑ Increased protein (moderate elevation due to the immune response).
• ↑ Increased lymphocytes (predominantly mononuclear cells, unlike bacterial infections where neutrophils predominate).
• Normal glucose (unlike bacterial or tuberculous meningitis, which lower CSF glucose).
• Clear CSF (unlike bacterial meningitis, which often appears cloudy).

Thus, increased protein is a hallmark of viral infections, making it the correct answer.

Why the Other Options Are Wrong:

1. Cloudy Appearance (✗)
   • Viral meningitis typically has clear CSF, while bacterial meningitis causes a cloudy or turbid appearance due to pus and a high white blood cell count.
2. Neutrophils (✗)
   • Neutrophils are characteristic of bacterial meningitis, not viral.
   • In viral infections, lymphocytes predominate rather than neutrophils.
3. Decreased Glucose (✗)
   • Bacterial and tuberculous meningitis cause decreased glucose because bacteria metabolize glucose.
   • Viral infections do not consume glucose, so levels remain normal.
4. Increased Glucose (✗)
   • Glucose levels in viral meningitis remain normal, not increased.
   • Increased glucose in CSF is rare and not a diagnostic feature of infections.

The limbic system is a complex set of brain structures that play a key role in emotion, behavior, memory, and motivation. The major components of the limbic system include:

1. Cingulate gyrus – Involved in emotional processing and behavior regulation.
2. Parahippocampal gyrus – Important for memory encoding and retrieval.
3. Hippocampal formation – Crucial for learning and memory.
4. Amygdaloid nucleus (Amygdala) – Processes emotions, especially fear and aggression.
5. Mammillary bodies – Play a role in recollective memory.
6. Anterior thalamic nuclei – Involved in alertness and learning.
7. Subcallosal gyrus – Associated with limbic functions, including emotional processing.

This makes the correct answer the most comprehensive list of limbic system components.

Why the Other Options Are Wrong:

1. Cingulate gyrus and the uncus (✗)
   • While the cingulate gyrus is part of the limbic system, the uncus is a part of the parahippocampal gyrus but is not a primary constituent of the limbic system on its own.
2. Amygdaloid nucleus, red nucleus, and vestibular nucleus (✗)
   • The amygdaloid nucleus (amygdala) is part of the limbic system.
   • The red nucleus is part of the midbrain, involved in motor coordination, not limbic functions.
   • The vestibular nucleus is involved in balance and coordination, unrelated to limbic functions.
3. Pulvinar of the thalamus and substantia nigra (✗)
   • The pulvinar is involved in visual processing and attention, not limbic functions.
   • The substantia nigra is a dopaminergic nucleus of the basal ganglia, involved in motor control (e.g., Parkinson’s disease) and not a part of the limbic system.
4. Hippocampal formation (✗) [Partially Correct but Incomplete]
   • While the hippocampal formation is a key limbic structure, this option excludes other critical limbic system components such as the amygdala, mammillary bodies, and anterior thalamic nuclei.

Gliosis is a reactive process in which astrocytes undergo hypertrophy (enlargement) and hyperplasia (increase in number) in response to CNS injury, inflammation, ischemia, or neurodegenerative diseases. This process leads to the formation of a glial scar, which helps to contain damage but can also inhibit neuronal regeneration.

Gliosis is a hallmark of CNS pathology, seen in conditions such as:

• Stroke
• Multiple sclerosis
• Traumatic brain injury
• Neurodegenerative diseases (e.g., Alzheimer’s, Parkinson’s)

During gliosis, astrocytes express more glial fibrillary acidic protein (GFAP), a marker of astrocyte activation.

Why the Other Options Are Wrong:

1. Fibers (✗)
   • Gliosis is not related to an increase in fibers but rather to the proliferation of astrocytes.
2. Fibroblasts (✗)
   • Fibroblasts are involved in scar formation in connective tissue, not the CNS.
   • In the CNS, glial cells (astrocytes), not fibroblasts, form the response to injury.
3. Macrophages (✗)
   • CNS macrophages (microglia) are involved in phagocytosis and inflammation, but they do not undergo hyperplasia/hypertrophy in gliosis.
   • Microglial activation (not gliosis) occurs in neuroinflammatory diseases.
4. Myelin Sheath (✗)
   • The myelin sheath is produced by oligodendrocytes (CNS) and Schwann cells (PNS).
   • Gliosis is not a process of myelin production or damage; instead, it is the proliferation of astrocytes in response to CNS injury.

Explanation:

Meningitis is an infectious disease caused by bacterial, viral, fungal, or parasitic infections, not by hypertension. It involves inflammation of the meninges (protective layers around the brain and spinal cord) and is typically associated with fever, neck stiffness, altered mental status, and headache.

On the other hand, all the other options are cerebrovascular diseases that result from hypertension-related damage to blood vessels in the brain.

Why the Other Options Are Wrong (They Are Related to Hypertension):

1. Slit Hemorrhage (✗)
   • Small hemorrhages caused by rupture of tiny penetrating arterioles weakened by hypertension.
   • These hemorrhages heal as slit-like cavities in the brain.
2. Hyaline Arteriolar Sclerosis (✗)
   • Chronic hypertension causes hyaline arteriolosclerosis, leading to thickening of small arteries and arterioles.
   • This contributes to ischemia and infarcts in organs, including the brain.
3. Lacunar Infarcts (✗)
   • Small, deep infarcts caused by occlusion of penetrating arteries, often due to hypertension-induced arteriolosclerosis.
   • Commonly found in the basal ganglia, pons, and deep white matter.
4. Acute Hypertensive Encephalopathy (✗)
   • Hypertensive crisis leads to cerebral edema, increased intracranial pressure (ICP), and neurological symptoms.
   • It is a life-threatening condition that requires immediate blood pressure control.

Spina bifida meningomyelocele is a neural tube defect where both the meninges and spinal cord protrude through a defect in the vertebral column due to failure of neural tube closure during embryonic development. It is the most severe form of spina bifida cystica and can lead to:

• Neurological deficits (e.g., paralysis, loss of sensation below the lesion).
• Hydrocephalus (often due to associated Arnold-Chiari malformation).
• Bladder and bowel dysfunction due to sacral nerve involvement.

This condition is linked to folic acid deficiency during pregnancy, making periconceptional folate supplementation an essential preventive measure.

Why the Other Options Are Wrong:

1. Protrusion of meninges (✗)
   • This describes spina bifida meningocele, where only the meninges protrude, but the spinal cord remains inside.
2. Depression of meninges and vertebral arch (✗)
   • Spina bifida does not cause depression of structures; instead, it leads to protrusion due to incomplete vertebral closure.
3. Depression of meninges and spinal cord (✗)
   • There is no depression, but rather an outpouching of these structures.
4. Protrusion of spinal cord (✗)
   • While the spinal cord does protrude, meningomyelocele specifically involves both the spinal cord and meninges, making this answer incomplete.

Saccular (berry) aneurysms are outpouchings of cerebral arteries, commonly occurring at branch points in the Circle of Willis due to weakened vessel walls. These aneurysms are at risk of rupture, leading to subarachnoid hemorrhage (SAH).

A key risk factor is genetic connective tissue disorders that weaken blood vessel walls, such as:

• Ehlers-Danlos Syndrome (EDS) – A defect in collagen synthesis leading to vascular fragility.
• Marfan Syndrome – A defect in fibrillin-1 affecting vessel integrity.
• Autosomal dominant polycystic kidney disease (ADPKD) – Associated with intracranial aneurysms.

Other risk factors include hypertension, smoking, and atherosclerosis.

Why the Other Options Are Wrong:

1. Parkinson’s (✗)
   • Parkinson’s disease is a neurodegenerative disorder affecting the dopaminergic system, not the blood vessels.
2. Alzheimer’s (✗)
   • Alzheimer’s disease is associated with amyloid plaques and neurodegeneration, but not vascular wall weakness leading to aneurysms.
3. Diabetes (✗)
   • Diabetes is associated with atherosclerosis and small vessel disease, but it is not a primary cause of saccular aneurysms.
4. Poliomyelitis (✗)
   • Poliomyelitis is a viral infection affecting the anterior horn cells of the spinal cord, leading to motor neuron damage, but it has no connection to aneurysm formation.

In neonates (newborns), the most common causes of acute pyogenic (bacterial) meningitis are:

1. Escherichia coli – Gram-negative bacillus, commonly transmitted from the maternal genital tract during birth.
2. Group B Streptococcus (GBS) – Another leading cause of neonatal meningitis, often acquired from the birth canal.
3. Listeria monocytogenes – Can cross the placenta or be transmitted during delivery.

Neonatal immune systems are immature, making them more susceptible to bacterial infections. E. coli (K1 strain) has a capsular antigen that enhances its ability to invade the meninges.

Why the Other Options Are Wrong:

1. Necator americanus (✗)
   • A hookworm causing iron-deficiency anemia, but it does not cause meningitis.
2. Neisseria meningitidis (✗)
   • A major cause of meningitis in older children, adolescents, and adults, but not the primary cause in neonates.
3. Toxoplasma gondii (✗)
   • A protozoan causing congenital toxoplasmosis, leading to intracranial calcifications, hydrocephalus, and chorioretinitis, but not acute bacterial meningitis.
4. Listeria monocytogenes (✗) [Partially Correct but Less Common]
   • Listeria can cause neonatal meningitis, but E. coli is more common.
   • Listeria is typically acquired transplacentally or from contaminated food during pregnancy.

Chronic bacterial meningoencephalitis refers to a long-standing, progressive infection of the meninges and brain parenchyma caused by slow-growing bacteria.

Mycobacterium tuberculosis (TB meningitis) is a leading cause of chronic bacterial meningoencephalitis.

• It typically results from hematogenous spread of TB from the lungs.
• It presents with gradual onset of fever, headaches, night sweats, weight loss, and neurological deficits.
• CSF findings include:
  • ↑ Lymphocytes
  • ↑ Protein
  • ↓ Glucose (hypoglycorrhachia)
  • Acid-fast bacilli (AFB) on CSF analysis

If untreated, TB meningitis can lead to hydrocephalus, infarcts, and brainstem involvement, causing severe neurological damage.

Why the Other Options Are Wrong:

1. Streptococcus pneumoniae (✗)
   • A major cause of acute bacterial meningitis, but it does not cause chronic meningoencephalitis.
2. Herpes simplex (✗)
   • Herpes simplex virus (HSV-1) causes viral encephalitis, not bacterial meningoencephalitis.
   • It leads to necrotizing encephalitis, especially in the temporal lobes.
3. Plasmodium falciparum (✗)
   • Causes cerebral malaria, which affects the brain but is not a bacterial infection.
4. Neisseria meningitidis (✗)
   • Causes acute bacterial meningitis, primarily in adolescents and young adults, but does not cause chronic meningoencephalitis.

A stroke is a medical condition in which there is sudden loss of blood supply to a part of the brain, leading to neurological deficits. It is classified under cerebrovascular diseases and results from:

1. Ischemic Stroke (85%) – Due to thrombotic or embolic occlusion of cerebral arteries.
   • Causes: Atherosclerosis, embolism (from heart or carotid arteries), or small-vessel disease.
   • Leads to infarction and neuronal death.
2. Hemorrhagic Stroke (15%) – Due to rupture of cerebral blood vessels, causing intracerebral or subarachnoid hemorrhage.
   • Causes: Hypertension, aneurysm rupture, arteriovenous malformations (AVMs), or anticoagulant use.

Both types lead to neurological deficits like hemiparesis, aphasia, or vision disturbances, depending on the affected area of the brain.

Why the Other Options Are Wrong:

1. Accumulation of excess CSF (✗)
   • Describes hydrocephalus, not stroke.
   • Stroke involves vascular damage, not CSF accumulation.
2. Increased number of glial cells (✗)
   • Refers to gliosis, which is a reaction to CNS injury, not the cause of stroke.
3. Genetic malformations of the brain (✗)
   • Congenital brain malformations (e.g., Chiari malformation, Dandy-Walker syndrome) do not cause stroke.
   • Stroke is an acquired cerebrovascular event.
4. Infection of the brain (✗)
   • Refers to encephalitis or meningitis, which are infections, not vascular events.

iral (aseptic) meningitis is caused by viruses such as enteroviruses (Coxsackievirus, Echovirus), HSV-2, and arboviruses. Unlike bacterial meningitis, viral meningitis typically presents with:

• Increased lymphocytes (lymphocytic pleocytosis) in cerebrospinal fluid (CSF), as the immune response is driven by viral infections.
• Mildly elevated protein levels.
• Normal or slightly decreased glucose (but not significantly low like in bacterial or TB meningitis).
• Clear CSF appearance (not cloudy, as seen in bacterial meningitis).

Since viral meningitis is self-limiting, it usually has a better prognosis compared to bacterial meningitis.

Why the Other Options Are Wrong:

1. Neutrophils decrease (✗) [Partially True but Not the Best Answer]
   • Neutrophils may be present early in viral meningitis, but lymphocytes predominate later.
   • However, the defining feature is the increase in lymphocytes, making that the best answer.
2. Glucose increases (✗)
   • Glucose levels remain normal in viral meningitis.
   • Bacterial and TB meningitis decrease CSF glucose.
3. Proteins decrease (✗)
   • Protein levels are slightly increased or normal, not decreased.
   • Bacterial and TB meningitis have more elevated protein levels compared to viral meningitis.
4. Bacteria infection (✗)
   • Viral meningitis is caused by viruses, not bacteria.
   • Bacterial meningitis has neutrophilic predominance, low glucose, and high protein.

Encephalocele is a neural tube defect in which brain tissue and meninges herniate through a skull defect.

The location of the encephalocele depends on the site of the skull defect, and the most common site is the anterior cranial fossa, especially in frontal or ethmoidal bones.

These defects often present as:

• Nasoethmoidal encephaloceles (most common)

• Frontoethmoidal encephaloceles

• These herniations may even protrude externally through the nose or forehead.

❌ Why the Other Options Are Incorrect:

1. Middle cranial fossa

   • Less commonly involved.

   • Usually houses the temporal lobes, but skull defects here are rarer.

2. Posterior cranial fossa

   • Can be involved in occipital encephaloceles, which are less common overall but more common in Western populations than Asia.

   • Still, anterior cranial fossa defects dominate globally.

3. Medial cranial fossa

   • No such specific anatomical term; likely confused with “middle cranial fossa”.

4. Lateral cranial fossa

   • Not a standard anatomical term used in describing skull fossae.

Lacunar infarcts are small, deep infarcts (<15 mm in size) that occur due to the occlusion of small penetrating arteries supplying the deep structures of the brain, such as the basal ganglia, thalamus, internal capsule, pons, and deep white matter.

They are most commonly caused by:

• Hypertension – Leads to hyaline arteriolosclerosis, causing vessel narrowing.
• Diabetes mellitus – Contributes to microangiopathy.
• Lipohyalinosis – Small vessel damage due to chronic hypertension.

Since these infarcts affect deep brain structures, they can cause specific stroke syndromes, including pure motor stroke, pure sensory stroke, ataxic hemiparesis, or dysarthria-clumsy hand syndrome.

Why the Other Options Are Wrong:

1. Venules (✗)
   • Lacunar infarcts are due to arterial occlusion, not venous occlusion.
2. Jugular Vein (✗)
   • The jugular vein drains blood from the brain but does not supply blood to deep brain structures, so it is not involved in lacunar infarcts.
3. Aorta (✗)
   • The aorta gives rise to major arteries supplying the brain, but lacunar infarcts occur in small penetrating arteries, not large vessels.
4. Basilar Artery (✗)
   • The basilar artery supplies the brainstem and cerebellum. While a basilar artery occlusion can cause brainstem strokes, it does not cause lacunar infarcts, which occur in small penetrating arteries.

In acute bacterial meningitis, the cerebrospinal fluid (CSF) typically shows:

• ↓ Decreased glucose (hypoglycorrhachia) – Bacteria consume glucose, leading to a lower concentration.
• ↑ Increased protein – Due to inflammation and bacterial breakdown.
• ↑ Markedly increased neutrophils (neutrophilic pleocytosis) – Indicative of a bacterial infection.
• Cloudy CSF appearance due to increased white blood cells and proteins.

Since bacterial meningitis reduces CSF glucose, an increase in CSF glucose is not a feature of the disease.

Why the Other Options Are Wrong (They Are Features of Bacterial Meningitis):

1. Headache (✓ Feature of bacterial meningitis)
   • Caused by meningeal inflammation and increased intracranial pressure (ICP).
2. Neck Stiffness (✓ Feature of bacterial meningitis)
   • A hallmark of meningismus, due to meningeal irritation.
   • Present in Kernig’s sign and Brudzinski’s sign.
3. Clouding of Consciousness (✓ Feature of bacterial meningitis)
   • Due to cerebral edema, increased ICP, or bacterial toxins affecting brain function.
4. Photophobia (✓ Feature of bacterial meningitis)
   • Light sensitivity due to meningeal irritation.

Parkinson’s disease (PD) is a neurodegenerative disorder caused by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta, which leads to dopamine deficiency in the basal ganglia. This results in motor symptoms characterized by:

• Resting tremor (“pill-rolling” tremor)
• Bradykinesia (slowness of movement)
• Rigidity (cogwheel or lead-pipe rigidity)
• Postural instability (frequent falls)

The loss of dopamine-producing neurons leads to impaired modulation of the direct and indirect pathways of the basal ganglia, causing movement abnormalities. Histologically, Lewy bodies (eosinophilic inclusions of α-synuclein) are seen in affected neurons.

Why the Other Options Are Wrong:

1. Lack of sleep (✗)
   • Sleep disturbances are common in Parkinson’s disease, but they do not cause it.
2. Trinucleotide repeats (✗)
   • Trinucleotide repeat expansions cause Huntington’s disease (CAG repeats in HTT gene), not Parkinson’s.
3. Deficiency in iron (✗)
   • Iron deficiency can cause anemia and cognitive issues, but it does not lead to Parkinson’s disease.
4. Damage to spinal cord (✗)
   • Parkinson’s disease affects the basal ganglia, not the spinal cord.

Parkinson’s disease (PD) is a neurodegenerative disorder that primarily affects the basal ganglia, specifically due to the loss of dopaminergic neurons in the substantia nigra pars compacta. The hallmark symptoms of Parkinson’s disease are:

1. Rigidity – Increased muscle tone (cogwheel or lead-pipe rigidity).
2. Tremors – Resting tremor (“pill-rolling tremor”), which decreases with voluntary movement.
3. Postural Instability – Difficulty maintaining balance, leading to falls.
4. Bradykinesia – Slowness of movement, difficulty initiating voluntary movements.

Chorea, however, is not a feature of Parkinson’s disease. Instead, it is seen in Huntington’s disease, where excessive, involuntary, jerky, dance-like movements occur due to damage to the striatum (caudate and putamen).

Why the Other Options Are Correct Features of Parkinson’s Disease:

1. Rigidity (✓ Feature of PD)
   • Muscle stiffness due to increased muscle tone.
2. Tremors (✓ Feature of PD)
   • Classic resting tremor that disappears with movement.
3. Postural Instability (✓ Feature of PD)
   • Impaired balance and frequent falls.
4. Bradykinesia (✓ Feature of PD)
   • Slowed movement and difficulty initiating actions.

Huntington’s disease (HD) is a neurodegenerative disorder caused by a trinucleotide (CAG) repeat expansion in the HTT gene on chromosome 4, leading to progressive degeneration of the striatum (caudate nucleus and putamen).

The hallmark symptom of Huntington’s disease is chorea, which refers to:

• Involuntary, rapid, jerky, dance-like movements
• Affecting the face, limbs, and trunk
• Worsens over time and progresses to dystonia, rigidity, and cognitive decline

HD is associated with:

• Behavioral changes (aggression, depression, psychosis)
• Dementia (cognitive decline)
• Hyperkinesia (excessive movement, including chorea)

Why the Other Options Are Wrong:

1. Cogwheel Rigidity (✗)
   • Seen in Parkinson’s disease, not Huntington’s.
   • HD is characterized by hyperkinesia (excess movement), whereas Parkinson’s has rigidity and bradykinesia (slowed movement).
2. Enlarged Posterior Fossa (✗)
   • Seen in Joubert syndrome (cerebellar malformation), not Huntington’s.
   • HD is characterized by atrophy of the caudate nucleus, which can be seen on brain imaging.
3. Hallucinations (✗)
   • Hallucinations are more characteristic of schizophrenia or Lewy body dementia, not Huntington’s disease.
4. Resting Tremors (✗)
   • Seen in Parkinson’s disease, not Huntington’s.
   • HD has chorea (excessive, involuntary movements), not tremors.

Uncal herniation occurs when the medial temporal lobe (uncus) is displaced downward through the tentorial notch, compressing nearby structures. This is a life-threatening condition commonly caused by increased intracranial pressure (ICP) due to trauma, stroke, or mass effect (tumor, hemorrhage).

One of the hallmark signs of uncal herniation is oculomotor nerve (CN III) compression, leading to:

• Ipsilateral oculomotor nerve palsy → Dilated, non-reactive (“blown”) pupil
• Ptosis (drooping eyelid) due to paralysis of levator palpebrae superioris
• “Down and out” eye deviation (due to unopposed CN IV and VI action)

Additional features include:

• Contralateral hemiparesis (compression of the cerebral peduncle)
• Duret hemorrhages in the brainstem due to stretching of perforating arteries

If untreated, uncal herniation progresses to coma and death due to brainstem compression.

Why the Other Options Are Wrong:

1. Breathing cessation (✗) [More Common in Tonsillar Herniation]
   • Occurs in tonsillar herniation, where the cerebellar tonsils compress the medulla, affecting respiratory centers.
   • Uncal herniation affects CN III before reaching the medulla.
2. Crescent-shaped lesion (✗) [Feature of Subdural Hematoma]
   • Subdural hematomas appear as crescent-shaped lesions on CT scans.
   • Uncal herniation involves brain shift and CN III compression, not hematoma shape.
3. Kidney disease (✗)
   • Uncal herniation is a neurological emergency, unrelated to kidney disease.
4. Chewing difficulties (✗) [More Related to CN V Dysfunction]
   • The trigeminal nerve (CN V) controls mastication (chewing), but it is not affected in uncal herniation.

Stroke is most commonly seen in older adults, particularly those above 60 years of age, due to an increased prevalence of hypertension, diabetes, atherosclerosis, and other cerebrovascular risk factors.

In developing countries, stroke risk is further elevated due to:

• Poor control of hypertension and diabetes
• Limited access to healthcare and preventive measures
• Higher rates of smoking and unhealthy diets

While strokes can occur in younger individuals due to conditions like cardioembolism, hypercoagulable states, or sickle cell disease, the vast majority of strokes occur in older adults due to chronic vascular diseases.

Why the Other Options Are Wrong:

1. Children (✗) [Rare, Usually Due to Congenital Causes]
   • Strokes in children are rare and typically due to congenital heart disease, sickle cell disease, or infections (e.g., meningitis, vasculitis).
2. Adolescents (✗) [Rare, Usually Due to Genetic or Autoimmune Causes]
   • Strokes in adolescents are very uncommon and usually linked to genetic disorders, vasculitis, or trauma.
3. Teenagers (✗) [Extremely Rare, Usually Trauma-Related]
   • Teenage strokes are highly unusual and often caused by trauma (e.g., carotid dissection), clotting disorders, or drug use (e.g., stimulants).
4. Young adults (✗) [Can Happen, But Less Common Than in Older Adults]
   • Young adults can suffer from strokes due to cardioembolic sources (e.g., atrial fibrillation, patent foramen ovale) or hypercoagulable states, but strokes are far more common in older adults

Magnetic Resonance Imaging (MRI) is the preferred imaging modality for detecting spinal cord lesions because it provides high-resolution images of soft tissues, including:

• Spinal cord
• Nerve roots
• Intervertebral discs
• Ligaments and surrounding soft tissues

MRI is highly sensitive for identifying:

• Spinal cord tumors (ependymomas, astrocytomas, metastases)
• Multiple sclerosis (MS) plaques
• Spinal cord infarction or ischemia
• Syringomyelia (fluid-filled cavity in the spinal cord)
• Compression from herniated discs or trauma

T2-weighted MRI is especially useful for detecting edema, inflammation, and demyelination in the spinal cord.

Why the Other Options Are Wrong:

1. X-ray (✗) [Limited to Bone, Not Soft Tissue]
   • X-rays are useful for bony structures (fractures, vertebral misalignment), but they do not provide details of spinal cord pathology.
   • Cannot detect tumors, demyelination, or spinal cord compression.
2. PET/CT (✗) [Used for Metabolic Imaging, Not Structural]
   • Positron Emission Tomography (PET) is used for metabolic activity, mainly in cancer detection.
   • CT provides good bone detail but is not as effective as MRI for soft tissues.
3. Myelography (✗) [Invasive and Outdated for Most Cases]
   • Myelography (X-ray with contrast in CSF) was historically used for spinal cord imaging but has been largely replaced by MRI.
   • Still used when MRI is contraindicated (e.g., pacemaker patients).
4. CT Scan (✗) [Better for Bone, Inferior for Soft Tissue]
   • CT scans are best for fractures and bony abnormalities but provide poor resolution for spinal cord and soft tissue compared to MRI.
   • Contrast-enhanced CT can help in trauma cases but is not preferred over MRI for cord lesions.

Stenosis of the cerebral aqueduct (Aqueduct of Sylvius) causes obstruction of cerebrospinal fluid (CSF) flow between the third and fourth ventricles, leading to enlargement of the third and lateral ventricles while the fourth ventricle remains normal.

Since the obstruction prevents CSF from flowing freely, it is classified as non-communicating hydrocephalus (also called obstructive hydrocephalus).

Key Features of Non-Communicating Hydrocephalus:

• Cause: Blockage of CSF flow within the ventricular system.
• Common Sites of Blockage:
  • Cerebral aqueduct (Aqueduct of Sylvius) → Causes aqueductal stenosis.
  • Foramen of Monro (between lateral and third ventricles).
  • Foramen of Magendie & Luschka (outflow of fourth ventricle).
• Ventricular Enlargement:
  • Lateral & third ventricles enlarged, fourth ventricle normal or small.
• Symptoms:
  • Increased intracranial pressure (ICP) → Headache, vomiting, papilledema.
  • In infants → Enlarged head (before sutures close), bulging fontanelle.

Why the Other Options Are Wrong:

1. Non-Obstructive Hydrocephalus (✗) [Incorrect Terminology]
   • The term “non-obstructive hydrocephalus” is not commonly used in classification.
   • Hydrocephalus is either communicating (no blockage) or non-communicating (blockage).
2. Communicating Hydrocephalus (✗) [CSF Flow is Blocked Within Ventricular System]
   • In communicating hydrocephalus, CSF flow is not blocked within the ventricles but instead fails to be absorbed properly at the arachnoid granulations.
   • Causes include post-meningitis scarring, subarachnoid hemorrhage, and choroid plexus overproduction.
   • In aqueductal stenosis, the blockage is within the ventricles, making it non-communicating hydrocephalus.
3. Hydrocephalus Ex Vacuo (✗) [Brain Atrophy, Not CSF Obstruction]
   • Occurs when brain tissue shrinks due to atrophy (e.g., Alzheimer’s disease, stroke), making the ventricles appear enlarged.
   • No actual CSF flow obstruction in hydrocephalus ex vacuo.
4. Normal Pressure Hydrocephalus (✗) [Seen in Elderly with Normal ICP]
   • A type of communicating hydrocephalus seen in elderly patients.
   • CSF absorption is impaired, but ICP remains normal.
   • Classic triad: “Wet, Wobbly, Wacky”
     • Urinary incontinence (“wet”)
     • Gait instability (“wobbly”)
     • Dementia (“wacky”)
   • Not caused by aqueductal stenosis.

Guillain-Barré syndrome (GBS) is an acute immune-mediated demyelinating disorder affecting the peripheral nervous system (PNS). It is characterized by:

• Autoimmune destruction of myelin in peripheral nerves.
• Ascending muscle weakness starting in the lower limbs and progressing upward.
• Areflexia (loss of deep tendon reflexes).
• History of recent infection (commonly Campylobacter jejuni, CMV, or EBV).
• Respiratory involvement in severe cases (requiring ventilatory support).

GBS is a polyradiculoneuropathy, meaning it affects multiple nerve roots and peripheral nerves in an acute setting.

Why the Other Options Are Wrong:

1. It is a non-inflammatory disorder (✗) [False, GBS is an Inflammatory Disorder]
   • GBS is a severe inflammatory neuropathy, with T-cell and macrophage-mediated demyelination of peripheral nerves.
   • CSF shows increased protein with normal WBC count (“albuminocytologic dissociation”), a sign of inflammation.
2. It is an infective polyneuropathy (✗) [False, It is Immune-Mediated]
   • GBS is not a direct infection of nerves but rather an immune-mediated attack following an infection.
   • Unlike leprosy (Mycobacterium leprae), which directly infects nerves, GBS occurs post-infection due to molecular mimicry.
3. Miller Fisher is a common variant (✗) [False, It is a Rare Variant]
   • Miller Fisher syndrome (MFS) is a rare variant of GBS.
   • MFS Triad: Ophthalmoplegia, Ataxia, Areflexia.
   • Associated with anti-GQ1b antibodies.
   • While it is a known variant, the classic form of GBS (acute inflammatory demyelinating polyneuropathy, AIDP) is much more common.
4. It is a chronic demyelinating mononeuropathy multiplex (✗) [False, GBS is Acute and Polyneuropathic]
   • GBS is acute, while chronic inflammatory demyelinating polyneuropathy (CIDP) is the chronic counterpart.
   • Mononeuropathy multiplex affects multiple individual nerves asymmetrically (seen in vasculitis, diabetes, leprosy), whereas GBS is a symmetrical polyneuropathy.

The splenium is the posterior part of the corpus callosum and is primarily involved in the interhemispheric transfer of visual information between the occipital lobes, which are responsible for vision and visual association.

• It connects the visual cortices of both hemispheres, particularly linking the visual association areas in the occipital lobes.
• Damage to the splenium can lead to visual disconnection syndromes, such as alexia without agraphia (pure word blindness).

Why the Other Options Are Wrong:

1. Rostrum (✗) [Connects Orbitofrontal Cortex, Not Visual Areas]
   • The rostrum is the anterior-most part of the corpus callosum.
   • It is involved in frontal lobe connections, not visual processing.
2. Body (✗) [Connects Sensorimotor and Higher-Order Cortical Areas]
   • The body of the corpus callosum connects parietal and sensorimotor areas, not the occipital visual areas.
3. Isthmus (✗) [Transition Zone Between Body and Splenium]
   • The isthmus is a narrow region between the body and splenium and does not primarily connect visual areas.
4. Genu (✗) [Connects Prefrontal Cortex, Not Visual Cortex]
   • The genu is the anterior part of the corpus callosum and is associated with prefrontal connections (higher cognitive functions, decision-making).
   • It has no role in visual processing.

The decussation of the pyramids occurs at the lower medulla, where corticospinal tract fibers cross over to the opposite side before descending into the spinal cord.

At this level, the medial lemniscus is not yet formed, because:

• The gracile and cuneate nuclei, which process proprioceptive and fine touch sensations, are located here.
• The internal arcuate fibers cross the midline just above this level to form the medial lemniscus in the upper medulla.

Thus, the medial lemniscus is not present at the level of the pyramidal decussation.

Why the Other Options Are Wrong (These Structures Are Present at This Level):

1. Posterior Spinocerebellar Tract (✓ Present)
   • Carries unconscious proprioception from the lower limbs to the cerebellum.
   • It remains ipsilateral and is seen in the lateral part of the medulla and spinal cord.
2. Lateral Spinothalamic Tract (✓ Present)
   • Carries pain and temperature sensations from the opposite side of the body.
   • It is located in the anterolateral medulla and spinal cord.
3. Spinal Tract of Trigeminal Nerve (✓ Present)
   • Carries pain and temperature sensation from the face to the spinal nucleus of the trigeminal nerve.
   • It descends in the lateral medulla and cervical spinal cord.
4. Accessory Nucleus (✓ Present)
   • Located in the cervical spinal cord (C1-C5) and gives rise to the spinal accessory nerve (CN XI), which controls the sternocleidomastoid and trapezius muscles.
   • Found at the lower medulla and upper cervical spinal cord.

The Papez circuit is a neural pathway involved in the control of emotions, memory, and learning, and it is a key component of the limbic system.

The circuit consists of the following structures:

1. Hippocampus → Sends output via the fornix
2. Mammillary bodies (hypothalamus) → Relay signals to the anterior thalamic nucleus
3. Anterior nucleus of the thalamus → Projects to the cingulate gyrus
4. Cingulate gyrus → Sends fibers back to the hippocampus via the entorhinal cortex

This closed-loop system is crucial for:

• Memory consolidation (hippocampus)
• Emotional processing (limbic system)
• Behavioral responses

Damage to the Papez circuit, such as in Korsakoff’s syndrome (thiamine deficiency), leads to anterograde amnesia and confabulation.

Why the Other Options Are Wrong:

1. Cerebral Cortex (✗) [Higher Cognitive Functions, Not the Primary Site of the Papez Circuit]
   • The cerebral cortex is involved in higher cognitive functions like reasoning and decision-making.
   • However, the Papez circuit specifically belongs to the limbic system, which interacts with the cortex but is not a part of it.
2. Brainstem (✗) [Involved in Reflexes and Autonomic Control, Not Emotion and Memory]
   • The brainstem (midbrain, pons, medulla) controls basic life functions like breathing, heart rate, and reflexes.
   • It does not play a primary role in memory or emotional processing.
3. Posterior Fossa (✗) [Contains the Cerebellum and Brainstem, Not the Papez Circuit]
   • The posterior fossa houses the cerebellum and parts of the brainstem, which regulate balance and coordination.
   • It is not involved in memory or emotions.
4. Reticular Formation (✗) [Controls Arousal and Wakefulness, Not Memory Processing]
   • The reticular formation is a network in the brainstem that regulates alertness, consciousness, and autonomic functions.
   • It is not part of the Papez circuit.

Monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT) are enzymes responsible for the degradation (inactivation) of catecholamines, such as:

• Dopamine (DA)
• Epinephrine (E)
• Norepinephrine (NE)

These enzymes terminate the action of catecholamines by metabolizing them into inactive metabolites.

How MAO and COMT Work:

1. Monoamine Oxidase (MAO)
   • Located in presynaptic nerve terminals, liver, and brain.
   • Deaminates catecholamines into inactive metabolites.
   • Two types:
     • MAO-A: Metabolizes serotonin (5-HT), norepinephrine, dopamine.
     • MAO-B: Preferentially metabolizes dopamine.
   • Clinical relevance:
     • MAO inhibitors (MAOIs) increase monoamine levels (used in depression & Parkinson’s).
2. Catechol-O-Methyltransferase (COMT)
   • Found in liver, synapses, and peripheral tissues.
   • Methylates catecholamines into inactive forms.
   • Clinical relevance:
     • COMT inhibitors (e.g., entacapone, tolcapone) prolong dopamine activity (used in Parkinson’s disease).

Together, MAO and COMT regulate catecholamine levels in the CNS and peripheral nervous system, preventing excessive neurotransmitter activity.

Why the Other Options Are Wrong:

1. Activation of Acetylcholine (✗) [Not Related to MAO or COMT]
   • Acetylcholine (ACh) is broken down by acetylcholinesterase (AChE), not MAO or COMT.
2. Inactivation of Aldosterone (✗) [Not a Monoamine or Catecholamine]
   • Aldosterone is a steroid hormone, not a catecholamine.
   • It is degraded by hepatic metabolism, not MAO or COMT.
3. Activation of Catecholamines (✗) [MAO & COMT Do the Opposite]
   • MAO and COMT break down catecholamines, not activate them.
   • Catecholamines are synthesized from tyrosine via the catecholamine biosynthetic pathway.
4. Activation of Non-Catecholamines (✗) [MAO & COMT Target Catecholamines Only]
   • Non-catecholamines (e.g., serotonin, histamine) have different metabolic pathways.
   • MAO does break down serotonin, but COMT does not.

The visual reflex pathway (specifically the pupillary light reflex) involves afferent (sensory) and efferent (motor) pathways to control pupil constriction in response to light.

Pathway of the Pupillary Light Reflex:

1. Light enters the eye → Stimulates retinal photoreceptors.
2. Optic nerve (CN II) carries afferent signals to the pretectal nucleus in the midbrain.
3. The pretectal nucleus sends bilateral projections to the Edinger-Westphal nucleus (parasympathetic nucleus of CN III).
4. The Edinger-Westphal nucleus sends efferent parasympathetic fibers via the oculomotor nerve (CN III).
5. These fibers synapse at the ciliary ganglion and travel via the short ciliary nerves to the sphincter pupillae muscle, causing pupillary constriction (miosis).

Why the Other Options Are Correct Parts of the Visual Reflex Pathway:

1. Optic nerve (✓) [Afferent limb]
   • Carries light signals from the retina to the pretectal nucleus.
2. Pretectal nucleus (✓) [Relays signals to both Edinger-Westphal nuclei]
   • Located in the midbrain, responsible for bilateral activation of the pupillary reflex.
3. Edinger-Westphal nucleus of CN III (✓) [Parasympathetic control]
   • Sends efferent parasympathetic fibers to the ciliary ganglion.
4. Short ciliary nerve (✓) [Final output to sphincter pupillae muscle]
   • Carries postganglionic parasympathetic fibers from the ciliary ganglion to the sphincter pupillae muscle, causing pupil constriction.

Why the “Main Motor Nucleus of the 3rd Cranial Nerve” is Incorrect (Not Involved in the Visual Reflex Pathway):

• The main motor nucleus of the oculomotor nerve (CN III) controls extraocular muscles (superior rectus, inferior rectus, medial rectus, inferior oblique, and levator palpebrae superioris), NOT the pupillary reflex.
• The pupillary light reflex is mediated by the Edinger-Westphal nucleus (parasympathetic), NOT the main motor nucleus of CN III.

A lumbar puncture (spinal tap) is typically performed by inserting a needle between the L3 and L4 vertebrae (or sometimes L4 and L5) to collect cerebrospinal fluid (CSF) from the subarachnoid space.

At this level, the spinal cord has already terminated at the conus medullaris (L1-L2 in adults), so the needle enters the cauda equina, a bundle of spinal nerve roots floating in CSF.

The cauda equina (“horse’s tail”) consists of:

• Lumbar nerve roots (L2-L5)
• Sacral nerve roots (S1-S5)
• Coccygeal nerve root

These nerves are mobile, so they move away from the needle, minimizing the risk of damage.

Why the Other Options Are Wrong:

1. Filum Terminale (✗) [Thin Extension Below Cauda Equina]
   • The filum terminale is a thin, fibrous extension of the pia mater that anchors the spinal cord to the coccyx.
   • It is much smaller than the cauda equina and unlikely to be hit during a lumbar puncture.
2. Sacral Enlargement (✗) [Located Lower in the Spinal Cord]
   • The sacral enlargement supplies nerves for the lower limbs and pelvic organs, but it is located at the sacral level, not at L3-L4.
3. Femoral Nerve (✗) [Located Anteriorly, Not in the Spinal Canal]
   • The femoral nerve (L2-L4) is located in the anterior thigh, not in the spinal canal.
   • A lumbar puncture is performed posteriorly, so it does not contact the femoral nerve.
4. Conus Medullaris (✗) [Ends Above L3-L4]
   • The conus medullaris (the tapered end of the spinal cord) is usually at L1-L2 in adults.
   • Since a lumbar puncture is done at L3-L4, the needle would not hit the conus medullaris.

Nocturnal enuresis (bedwetting) refers to involuntary urination during sleep, not voluntary urination. It is most commonly seen in children but can also occur in adults with underlying medical or neurological conditions.

Since nighttime enuresis is involuntary, the statement “voluntary urination during sleep” is incorrect, making it the best choice.

Analysis of Each Option:

🚫 Incorrect Statement (Correct Answer):
🔹 “Nighttime enuresis – voluntary urination during sleep”
❌ Incorrect – Nocturnal enuresis is involuntary, meaning the person has no control over urination while sleeping.

✅ Correct Statements (Incorrect Choices):

🔹 “Nocturia – waking up multiple times in the night to urinate”
✔️ True – Nocturia is a condition where a person wakes up multiple times at night to urinate. It can be caused by excessive fluid intake, diabetes, bladder dysfunction, or prostate enlargement.

🔹 “Sleep apnea – interrupted breathing while sleeping”
✔️ True – Sleep apnea involves repeated pauses in breathing during sleep, often due to airway obstruction (obstructive sleep apnea) or neurological causes (central sleep apnea).

🔹 “Insomnia – difficulty falling asleep”
✔️ True – Insomnia is a common sleep disorder where a person has trouble falling asleep, staying asleep, or waking up too early.

🔹 “Bed wetting – involuntary urination during sleep”
✔️ True – Bedwetting (nocturnal enuresis) is involuntary urination during sleep, most commonly seen in children but also in some adults with medical conditions.

A tract is a bundle of axons that transmits nerve impulses within the central nervous system (CNS). Tracts are found in the spinal cord and brain and generally run in a superior-inferior direction, meaning they connect different levels of the CNS (e.g., brain to spinal cord, or different spinal levels).

Types of Tracts:

1. Ascending (Sensory) Tracts → Carry sensory information from the spinal cord to the brain
   • Examples:
     • Spinothalamic tract (pain, temperature, crude touch)
     • Dorsal columns (gracile & cuneate fasciculi) (fine touch, proprioception)
2. Descending (Motor) Tracts → Carry motor commands from the brain to the spinal cord
   • Examples:
     • Corticospinal tract (voluntary motor control)
     • Reticulospinal tract (postural control)

Since tracts generally run superior-inferior (brain ↔ spinal cord), the correct answer is “a bundle of axons that transmit nerve impulses between the superior and inferior parts of the body.”

Why the Other Options Are Wrong:

1. “A bundle of neurons that transmit nerve impulses between the ventral and dorsal parts of the body” (✗)
   • Tracts are made of axons, not entire neurons.
   • The dorsal-ventral organization is used for reflex pathways and spinal cord organization, not tracts.
2. “A bundle of axons that transmit nerve impulses between the left and right sides of the body” (✗)
   • This describes commissural fibers, such as the corpus callosum, not spinal tracts.
3. “A bundle of neurons that transmit nerve impulses between the superior and inferior parts of the body” (✗)
   • Again, tracts consist of axons, not neurons.
   • Neurons include cell bodies, dendrites, and axons, but tracts only contain axons.
4. “A bundle of axons that transmit nerve impulses between the anterior and posterior parts of the body” (✗)
   • Tracts primarily run longitudinally (superior-inferior) rather than in an anterior-posterior direction.
   • Anterior-posterior communication is mainly through local circuits within the spinal cord.

A saccular (berry) aneurysm is a balloon-like outpouching of a cerebral artery, typically occurring at branch points of the Circle of Willis due to weakness in the arterial wall.

Cigarette smoking is a major predisposing factor for saccular aneurysms because it:

• Damages vascular endothelial cells, increasing the risk of aneurysm formation.
• Induces chronic inflammation, weakening the arterial wall.
• Increases blood pressure, which exacerbates aneurysm formation and rupture risk.

Other important risk factors include:

• Hypertension
• Genetic disorders (e.g., Ehlers-Danlos syndrome, Marfan syndrome, Autosomal Dominant Polycystic Kidney Disease (ADPKD))
• Advanced age
• Excessive alcohol consumption

Aneurysms can rupture, leading to subarachnoid hemorrhage (SAH), presenting with a sudden, severe “thunderclap” headache and potentially fatal consequences.

Why the Other Options Are Wrong:

1. Infections (✗) [Associated with Mycotic Aneurysms, Not Saccular Aneurysms]
   • Infections can cause mycotic aneurysms, which are different from saccular aneurysms.
   • Mycotic aneurysms result from infected emboli weakening arterial walls (e.g., in infective endocarditis).
2. Viral Infections (✗) [Not a Direct Cause]
   • Viral infections, like HIV or CMV, can affect vascular health but are not major causes of saccular aneurysms.
3. Bacterial Infections (✗) [Cause Mycotic, Not Saccular Aneurysms]
   • Bacterial endocarditis can cause mycotic aneurysms by infecting arterial walls, but this is not the mechanism of saccular aneurysms.
4. Tumors (✗) [Not a Primary Risk Factor]
   • Tumors can compress blood vessels, but they do not cause the arterial wall weakness that leads to saccular aneurysms.

Scopolamine is a competitive, reversible antagonist of muscarinic acetylcholine receptors (mAChRs). It blocks parasympathetic activity by inhibiting the effects of acetylcholine (ACh) at muscarinic receptors in the central and peripheral nervous system.

Mechanism of Action:

• Scopolamine selectively binds to muscarinic receptors (M1-M5) and prevents acetylcholine from exerting its effects.
• It is reversible, meaning its effects can be overcome by increasing ACh levels (e.g., with cholinesterase inhibitors).
• It does not bind irreversibly, nor does it affect nicotinic receptors.

Clinical Uses:

• Motion sickness prevention (M1 blockade in the vestibular system).
• Preoperative sedation (crosses the blood-brain barrier and has CNS depressant effects).
• Treating nausea and vomiting (antiemetic action via the brainstem).
• Cycloplegia and mydriasis (used in ophthalmology to dilate pupils).

Why the Other Options Are Wrong:

1. Binds irreversibly to both muscarinic and nicotinic receptors (✗) [Incorrect Binding & Receptor Type]
   • Scopolamine binds reversibly, not irreversibly.
   • It selectively blocks muscarinic receptors but does not affect nicotinic receptors.
2. Binds irreversibly to muscarinic receptors (✗) [Incorrect Binding Type]
   • Scopolamine is a reversible, competitive antagonist at muscarinic receptors.
   • Irreversible muscarinic blockers are rare and usually involve chemical modifications.
3. Binds irreversibly to nicotinic receptors (✗) [Incorrect Binding & Receptor Type]
   • Nicotinic receptors are found in autonomic ganglia and neuromuscular junctions.
   • Scopolamine does not bind to nicotinic receptors at all.
4. Binds reversibly to nicotinic receptors (✗) [Incorrect Receptor Type]
   • Scopolamine is not a nicotinic receptor antagonist.
   • It is highly selective for muscarinic receptors.

Reserpine is an adrenergic neuron-blocking drug that inhibits the storage of norepinephrine (NE) into synaptic vesicles by blocking the vesicular monoamine transporter (VMAT-2) in presynaptic neurons.

Mechanism of Action:

• Reserpine blocks VMAT-2, preventing the transport of norepinephrine, dopamine, and serotonin into synaptic vesicles.
• As a result, these neurotransmitters remain in the cytoplasm, where they are rapidly degraded by monoamine oxidase (MAO).
• This leads to depletion of norepinephrine from nerve terminals, resulting in reduced sympathetic activity (sympatholytic effect).

Clinical Uses:

• Hypertension (historically used, now rarely due to side effects).
• Treatment of psychotic disorders (in the past, due to its effects on dopamine depletion).

Side Effects:

• Depression (due to serotonin and dopamine depletion).
• Hypotension and bradycardia (due to reduced norepinephrine).

Why the Other Options Are Wrong:

1. Monoamine Oxidase (MAO) (✗) [Breaks Down NE, Does Not Block Storage]
   • MAO breaks down norepinephrine in the cytoplasm, but it does not prevent storage in vesicles.
   • MAO inhibitors (e.g., phenelzine, selegiline) increase norepinephrine levels, the opposite of reserpine’s effect.
2. Catechol-O-Methyl Transferase (COMT) (✗) [Degrades NE in the Synapse, Not Storage]
   • COMT is an enzyme that metabolizes norepinephrine in the synaptic cleft, not in storage vesicles.
   • COMT inhibitors (e.g., entacapone, tolcapone) are used in Parkinson’s disease.
3. Guanethidine (✗) [Inhibits NE Release, Does Not Block Storage]
   • Guanethidine prevents the release of norepinephrine from synaptic vesicles but does not block storage.
   • Works by displacing NE from vesicles and preventing vesicular fusion.
4. Imipramine (✗) [Inhibits NE Reuptake, Not Storage]
   • Imipramine is a tricyclic antidepressant (TCA) that inhibits norepinephrine reuptake at the synapse, increasing NE levels.
   • It does not prevent storage in vesicles.

First, when we talk about hemisection of the spinal cord (also called Brown-Séquard syndrome), we are referring to damage to one-half of the spinal cord — the right or the left side.

Because different sensory and motor tracts cross (decussate) at different levels, the pattern of deficits is very predictable.

Let’s quickly review what happens:

Now based on this:

Evaluate Each Option:

A. Ipsilateral loss of all sensations at the level of the lesion
🔵 True finding — Damage to the spinal cord at a particular segment can damage the dorsal roots and gray matter entering at that level, leading to loss of all modalities (pain, temperature, touch, proprioception) at the level of the lesion on the same side.

B. Ipsilateral loss of dorsal column sensations below the level of the lesion
🔵 True finding — Since dorsal column fibers ascend uncrossed in the spinal cord and cross over only at the medulla, injury to the hemicord will cause ipsilateral loss of fine touch, vibration, and proprioception below the lesion.

C. Contralateral pain and temperature loss below the level of the lesion
🔵 True finding — The spinothalamic tract carrying pain and temperature crosses early in the spinal cord (1–2 segments above entry). Therefore, hemisection leads to contralateral loss of pain and temperature below the lesion.

D. Ipsilateral upper motor neuron (UMN) signs at the level of the lesion
🔴 False finding —
At the level of the lesion, you generally get lower motor neuron (LMN) signs, not UMN signs.
Why? Because the anterior horn cells (which are the lower motor neurons) are destroyed directly at the lesion site, causing flaccid paralysis, atrophy, fasciculations — all signs of LMN damage.
UMN signs (like hyperreflexia, spasticity, Babinski sign) happen below the lesion where the corticospinal tracts are interrupted but the anterior horn cells are intact.

E. Ipsilateral upper motor neuron (UMN) signs below the level of the lesion
🔵 True finding —
Damage to the corticospinal tract on one side causes UMN signs below the lesion — spasticity, hyperreflexia, clonus, etc.

🔥 Final Answer:

✅ D. Ipsilateral upper motor neuron (UMN) signs at the level of the lesion

Explanation:

Hemisection of the spinal cord, known as Brown-Séquard syndrome, results in a characteristic pattern of sensory and motor deficits based on the location of the lesion and the pathways involved.

Pathway Involvement in Brown-Séquard Syndrome:

1. Corticospinal Tract (Motor, Descending) → Ipsilateral Paralysis Below the Lesion
   • Decussates (crosses) at the medullary pyramids, so damage above decussation causes contralateral loss, but spinal cord hemisection causes ipsilateral motor loss below the lesion.
2. Dorsal Column-Medial Lemniscus (Fine Touch, Vibration, Two-Point Discrimination, Proprioception) → Ipsilateral Loss Below the Lesion
   • Decussates in the medulla, so spinal cord hemisection affects the ipsilateral side below the lesion.
3. Spinothalamic Tract (Pain & Temperature) → Contralateral Loss Below the Lesion
   • Decussates at the spinal cord level (1-2 levels above entry), so damage results in contralateral loss below the lesion.

Summary of Sensory and Motor Loss in Brown-Séquard Syndrome:

Why the Other Options Are Wrong:

1. No sensory loss occurs (✗) [Incorrect]
   • Sensory loss does occur, affecting fine touch/proprioception ipsilaterally and pain/temperature contralaterally.
2. Upper limbs only (✗) [Incorrect]
   • The location of sensory loss depends on the level of spinal cord injury, not just the upper limbs.
3. Ipsilateral side of the face, contralateral side of the trunk (✗) [Incorrect]
   • Facial sensation is controlled by cranial nerve V (trigeminal nerve), not the spinal cord.
4. Contralateral side at the level of the lesion (✗) [Incorrect]
   • Contralateral pain and temperature loss occurs below the lesion, not at the level of the lesion.
   • Two-point discrimination (dorsal column function) is lost ipsilaterally below the lesion.

Tabes dorsalis is a late-stage complication of neurosyphilis, caused by Treponema pallidum, the bacterium responsible for syphilis. It specifically affects the dorsal columns and dorsal roots of the spinal cord, leading to progressive sensory ataxia and impaired proprioception.

Key Features of Tabes Dorsalis:

• Loss of proprioception and vibration sense (due to dorsal column degeneration).
• Sensory ataxia (wide-based, unsteady gait).
• Positive Romberg sign (patient loses balance when eyes are closed).
• Severe, lightning-like pain in the legs (due to dorsal root involvement).
• Argyll Robertson pupil (accommodates but does not react to light).

Pathogenesis:

1. T. pallidum invades the central nervous system (CNS) during tertiary syphilis.
2. The dorsal columns and dorsal root ganglia degenerate, leading to loss of fine touch, proprioception, and vibratory sense.

Why the Other Options Are Wrong:

1. Bacillus cereus (✗) [Food Poisoning, Not Neurosyphilis]
   • Causes food poisoning (vomiting or diarrhea) due to toxin production.
   • Does not affect the spinal cord or cause tabes dorsalis.
2. Streptococcus pyogenes (✗) [Causes Rheumatic Fever, Not Syphilis]
   • Causes pharyngitis, rheumatic fever, scarlet fever, and necrotizing fasciitis.
   • Does not cause neurosyphilis or tabes dorsalis.
3. Chlamydia trachomatis (✗) [Causes Genital Infections, Not Neurosyphilis]
   • Causes sexually transmitted infections (STIs) such as urethritis, pelvic inflammatory disease (PID), and trachoma.
   • Does not affect the dorsal columns of the spinal cord.
4. Neisseria gonorrhoeae (✗) [Causes Gonorrhea, Not Syphilis]
   • Causes gonorrhea, which can lead to urethritis, cervicitis, and disseminated gonococcal infection (DGI).
   • Does not cause chronic spinal cord degeneration.

Alpha is not an opioid receptor. The known opioid receptors are:

1. μ (mu)
2. δ (delta)
3. κ (kappa)
4. Nociceptin receptor (NOP, previously called zeta).

The term “alpha” does not refer to any recognized opioid receptor.

Why the other options are opioid receptors:

1. μ (mu):
   • The μ receptor is the primary target of morphine and other opioid analgesics. It mediates pain relief, euphoria, and respiratory depression.
2. δ (delta):
   • The δ receptor is involved in modulating pain, mood, and addiction. It has a lower affinity for most opioid drugs compared to the μ receptor.
3. κ (kappa):
   • The κ receptor is involved in pain modulation, dysphoria, and diuresis. It is activated by drugs like pentazocine.
4. Zeta:
   • The zeta receptor is an outdated term for the nociceptin receptor (NOP), which is a non-classical opioid receptor involved in pain regulation and other functions.

In the parasympathetic nervous system (PNS), the cell bodies of postganglionic neurons are located in ganglia within or near the walls of the target organs (also known as intramural ganglia).

Pathway of Parasympathetic Fibers:

1. Preganglionic neurons – Located in the brainstem (cranial nerves) or sacral spinal cord (S2-S4).
2. Postganglionic neurons – Located in intramural ganglia (within organ walls) or terminal ganglia (near the organ).
3. Neurotransmission:
   • Preganglionic fibers release acetylcholine (ACh) at nicotinic receptors in ganglia.
   • Postganglionic fibers release acetylcholine (ACh) at muscarinic receptors in target organs.

Examples of Intramural Ganglia in the Parasympathetic System:

• Ciliary ganglion (eye) → Controls pupil constriction.
• Pterygopalatine ganglion (lacrimal & nasal glands) → Stimulates tear and mucus production.
• Otic ganglion (parotid gland) → Stimulates salivation.
• Submandibular ganglion (submandibular & sublingual glands) → Stimulates salivation.
• Enteric ganglia (gut) → Regulates digestion.

Why the Other Options Are Wrong:

1. Cell bodies in central nervous system (✗) [Preganglionic Neurons Are Here, Not Postganglionic]
   • The cell bodies of preganglionic neurons are in the brainstem (cranial nerves) or sacral spinal cord.
   • Postganglionic neurons are located in peripheral ganglia near or within the organs.
2. Autonomic ganglia in abdomen (✗) [More Common in the Sympathetic System]
   • While some autonomic ganglia exist in the abdomen (e.g., celiac ganglion, superior mesenteric ganglion), they belong to the sympathetic nervous system, not the parasympathetic.
3. Autonomic ganglia in pelvis (✗) [Misleading, As They Are Still Intramural]
   • Pelvic parasympathetic ganglia exist within pelvic organs (e.g., bladder, reproductive organs, rectum), but they are considered intramural ganglia, making “ganglion in the visceral walls” the more precise answer.
4. Sympathetic trunk (✗) [Only for Sympathetic Nervous System]
   • The sympathetic trunk (paravertebral ganglia) contains postganglionic sympathetic neurons, not parasympathetic neurons.
   • The parasympathetic system does not use the sympathetic trunk.

The spinal cord is held in place by two key structures:

1. Denticulate Ligaments → Lateral Stability
   • Extensions of the pia mater that attach the spinal cord laterally to the dura mater.
   • Prevent excessive side-to-side movement.
2. Filum Terminale → Vertical Stability
   • A fibrous extension of the pia mater that anchors the conus medullaris to the coccyx.
   • Prevents upward displacement of the spinal cord.

Together, these structures stabilize the spinal cord within the vertebral column.

Why the Other Options Are Wrong:

1. Filum terminale and conus medullaris (✗) [Only One Anchoring Structure]
   • Filum terminale provides inferior stabilization.
   • Conus medullaris is simply the end of the spinal cord, not a stabilizing structure.
2. Cauda equina and conus medullaris (✗) [No Direct Anchoring Role]
   • Cauda equina consists of nerve roots, which exit the spinal cord but do not anchor it.
   • Conus medullaris is the termination of the spinal cord, but it does not hold it in place.
3. Denticulate ligaments and cauda equina (✗) [Cauda Equina Does Not Stabilize]
   • Denticulate ligaments stabilize laterally.
   • Cauda equina consists of spinal nerves, which do not hold the spinal cord in place.
4. Denticulate ligaments and conus medullaris (✗) [Conus Medullaris Is Not an Anchoring Structure]
   • Denticulate ligaments provide lateral stability.
   • Conus medullaris is simply the tapered end of the spinal cord, not an anchoring structure.

Morphine is primarily used for relief from chest pain, particularly in the context of myocardial infarction (heart attack). Morphine is a potent opioid analgesic that is highly effective in managing severe pain, including the intense pain associated with cardiac ischemia. It also helps reduce anxiety and cardiac workload, making it a key drug in the management of acute coronary syndromes.

Why the other options are less appropriate:

1. Pain in limbs:
   • While morphine can be used for severe pain in the limbs (e.g., due to trauma or cancer), it is not the most specific or common indication for its use.
2. Migraine:
   • Morphine is not typically used for migraines. Migraines are usually treated with medications like triptans, NSAIDs, or antiemetics.
3. Pain in kidney:
   • Kidney pain (e.g., due to renal colic from kidney stones) is often managed with NSAIDs or other analgesics. Morphine may be used in severe cases, but it is not the first-line treatment.
4. Referred pain:
   • Referred pain is pain perceived at a location other than the site of the painful stimulus. Morphine may be used for referred pain in some cases, but it is not a specific indication

Microglial cells are the primary phagocytic and immune cells of the central nervous system (CNS). They function as the CNS-resident macrophages, removing dead cells, pathogens, and debris to maintain homeostasis.

Key Functions of Microglia:

• Phagocytosis of pathogens, cellular debris, and dead neurons.
• Release of inflammatory mediators (cytokines, chemokines).
• Respond to CNS injury, ischemia, and neurodegenerative diseases (e.g., Alzheimer’s, Parkinson’s).
• Antigen presentation to activate other immune responses.

Microglia originate from the yolk sac during embryonic development, unlike other CNS glial cells, which arise from the neural tube.

Why the Other Options Are Wrong:

1. Oligodendrocytes (✗) [Myelination, Not Phagocytosis]
   • Oligodendrocytes produce myelin in the CNS, insulating axons for faster conduction.
   • They do not have phagocytic functions.
2. Astrocytes (✗) [Support & Blood-Brain Barrier, Not Phagocytosis]
   • Astrocytes provide structural and metabolic support for neurons.
   • They help maintain the blood-brain barrier and regulate neurotransmitters.
   • While they can assist in clearing neurotransmitters and toxins, they do not act as professional phagocytes.
3. Ependymal Cells (✗) [CSF Production, Not Phagocytosis]
   • Ependymal cells line the ventricles and produce cerebrospinal fluid (CSF).
   • They have cilia to circulate CSF but do not have phagocytic properties.
4. Satellite Cells (✗) [PNS Support, Not Phagocytosis]
   • Satellite cells are supportive glial cells in the peripheral nervous system (PNS).
   • They surround neuronal cell bodies in ganglia, providing nutritional and structural support but do not perform phagocytosis.

The lateral spinothalamic tract is responsible for transmitting pain and temperature sensations from the body to the brain. Damage to this tract results in loss of pain and temperature sensation on the contralateral side of the body below the level of the lesion because the fibers decussate (cross) in the spinal cord.

Pathway of the Lateral Spinothalamic Tract:

1. Peripheral receptors (nociceptors) detect pain & temperature.
2. Sensory neurons (first-order neurons) enter the spinal cord via the dorsal root ganglion (DRG).
3. Second-order neurons decussate (cross) in the anterior white commissure within 1-2 spinal segments.
4. Fibers ascend in the lateral spinothalamic tract to the thalamus (VPL nucleus).
5. Third-order neurons project from the thalamus to the somatosensory cortex (postcentral gyrus, parietal lobe).

Clinical Significance:

• Lesion in the lateral spinothalamic tract (e.g., spinal cord injury, syringomyelia, Brown-Séquard syndrome) leads to:
  • Contralateral loss of pain and temperature below the lesion (because of early decussation).

Why the Other Options Are Wrong:

1. Corticospinal tract (✗) [Motor Control, Not Pain Sensation]
   • Controls voluntary motor function, not sensory perception.
   • Damage causes paralysis or weakness (not sensory loss).
2. Dorsal column-medial lemniscal pathway (✗) [Fine Touch & Proprioception, Not Pain]
   • Carries fine touch, vibration, and proprioception from the body to the brain.
   • Damage results in loss of proprioception and fine touch, but not pain sensation.
3. Anterior spinothalamic tract (✗) [Crude Touch, Not Pain]
   • Carries crude touch and pressure, not pain and temperature.
   • Damage leads to loss of crude touch sensation but not pain loss.
4. Cuneocerebellar tract (✗) [Proprioception from Upper Limb, Not Pain]
   • Transmits unconscious proprioception from the upper limbs to the cerebellum.
   • Damage affects coordination, not pain sensation.

The anterior spinothalamic tract is responsible for carrying crude touch and pressure sensations from the periphery to the brain. Damage to this tract results in loss of crude (light) touch sensation, often on the contralateral side below the level of the lesion because it decussates (crosses) in the spinal cord.

Pathway of the Anterior Spinothalamic Tract:

1. First-order neurons (sensory receptors) detect crude touch and pressure.
2. Sensory fibers enter the spinal cord via the dorsal root ganglion (DRG).
3. Second-order neurons decussate (cross) within 1-2 spinal levels in the anterior white commissure.
4. Fibers ascend in the anterior spinothalamic tract to the thalamus (VPL nucleus).
5. Third-order neurons project to the somatosensory cortex (postcentral gyrus of the parietal lobe).

Clinical Significance:

• Lesions in the anterior spinothalamic tract cause contralateral loss of crude touch and pressure below the level of the lesion.
• Unlike the dorsal column-medial lemniscus pathway, which transmits fine touch, the anterior spinothalamic tract transmits less precise, poorly localized touch sensations.

Why the Other Options Are Wrong:

1. Dorsal Column-Medial Lemniscus Pathway (✗) [Fine Touch & Proprioception, Not Crude Touch]
   • Carries fine touch, vibration, and proprioception, but not crude touch or pressure.
   • Damage leads to loss of fine touch and proprioception, not crude touch.
2. Rubrospinal Tract (✗) [Motor Control, Not Sensory]
   • Involved in motor control, particularly flexor muscle tone.
   • Has no role in touch sensation.
3. Lateral Spinothalamic Tract (✗) [Pain & Temperature, Not Touch]
   • Carries pain and temperature sensations, not light/crude touch.
   • Damage leads to loss of pain and temperature sensation contralaterally, but not touch.
4. Cuneocerebellar Tract (✗) [Proprioception from Upper Limbs, Not Touch]
   • Transmits unconscious proprioception from the upper limbs to the cerebellum.
   • Has no role in light touch sensation.

The pyramids of the medulla are formed by the corticospinal tract, which carries motor signals from the cerebral cortex to the spinal cord. These fibers are responsible for voluntary motor control, particularly for movements of the limbs and trunk.

Pathway of the Corticospinal Tract (Pyramidal Tract):

1. Origin: Begins in the primary motor cortex (precentral gyrus, Brodmann area 4).
2. Descent: Travels through the internal capsule → midbrain (cerebral peduncles) → pons → medulla (forms the pyramids).
3. Decussation (Crossing):
   • 85–90% of fibers cross at the pyramidal decussation (in the caudal medulla) and form the lateral corticospinal tract (LCST), which controls limb muscles.
   • 10–15% do not cross and form the anterior corticospinal tract (ACST), which controls axial (trunk) muscles.
4. Termination: The tract synapses on lower motor neurons in the anterior horn of the spinal cord, leading to muscle contraction.

Thus, the pyramids of the medulla consist of corticospinal fibers before they decussate.

Why the Other Options Are Wrong:

1. Corticopontine fibers (✗) [Project to the Pons, Not Medullary Pyramids]
   • These fibers connect the cortex to the pons, playing a role in cerebellar coordination via the pontocerebellar tract.
   • They do not contribute to the pyramidal structure in the medulla.
2. Corticobulbar fibers (✗) [Terminate in Brainstem, Not Spinal Cord]
   • These fibers control cranial nerve motor nuclei (e.g., for facial movement, swallowing, speech).
   • They terminate in the brainstem and do not contribute to the pyramidal tract.
3. Rubrospinal fibers (✗) [Originate from Red Nucleus, Not Cortex]
   • Rubrospinal fibers originate from the red nucleus in the midbrain, controlling flexor muscle tone in the upper limbs.
   • They do not form the pyramids.
4. Vestibulospinal fibers (✗) [Originate from Vestibular Nuclei, Not Cortex]
   • Vestibulospinal tracts control balance and posture, originating from the vestibular nuclei in the brainstem, not the cortex.
   • They do not pass through the pyramids.