The trigeminal nerve (CN V) has three divisions:

1. V1 – Ophthalmic: passes through superior orbital fissure, purely sensory (forehead, upper eyelid, cornea).

2. V2 – Maxillary: passes through foramen rotundum, purely sensory (midface: upper lip, lateral nose, cheek).

3. V3 – Mandibular: passes through foramen ovale, sensory + motor (lower face, jaw muscles).

The patient has sensory deficit in V2 distribution with no motor weakness, so the lesion involves foramen rotundum.

Foramen rotundum ✅

• Transmits maxillary nerve (V2).

• Purely sensory, explaining the facial numbness without mastication weakness.

• Lesion here → numbness over upper lip, lateral nose, and cheek, exactly as described.

Why the other options are WRONG ❌

• Foramen ovale ❌ → Transmits mandibular nerve (V3). Would cause jaw weakness + lower face numbness, not midface.

• Foramen spinosum ❌ → Transmits middle meningeal artery and meningeal branch of V3, not main trigeminal sensory fibers.

• Superior orbital fissure ❌ → Transmits ophthalmic nerve (V1) and eye muscles. Lesion → sensory loss in forehead/eye, not midface.

• Jugular foramen ❌ → Transmits cranial nerves IX, X, XI, unrelated to trigeminal sensation.

The foramen ovale in the middle cranial fossa transmits the mandibular nerve (V3).

• The mandibular nerve has both sensory and motor fibers.

  • Sensory: lower face, lower lip, chin, anterior 2/3 of tongue (general sensation)

  • Motor: muscles of mastication → weakness of jaw muscles when affected

The patient’s jaw weakness (motor) and numbness over lower lip and chin (sensory) point to mandibular nerve involvement.

Mandibular nerve (V3) ✅

• Only division of trigeminal nerve that carries motor fibers to muscles of mastication.

• Sensory fibers cover lower face, jaw, and anterior tongue.

• Lesion at foramen ovale → combination of sensory and motor deficits exactly as described.

Why the other options are WRONG ❌

Facial nerve ❌

• Controls facial expression muscles, not muscles of mastication.

• Does not pass through foramen ovale.

• Lesion would cause facial droop, not jaw weakness.

Maxillary nerve (V2) ❌

• Purely sensory division of trigeminal nerve.

• Supplies midface, upper lip, cheek.

• Lesion → no motor deficit of jaw.

Trochlear nerve ❌

• Motor nerve to superior oblique muscle of the eye.

• Lesion → vertical diplopia, not jaw weakness or facial numbness.

The circle of Willis is formed by:

• Anterior cerebral arteries (connected by anterior communicating artery)

• Internal carotid arteries

• Posterior cerebral arteries (connected via posterior communicating arteries)

Important: The anterior cerebral artery is a direct branch of the internal carotid artery, contributing to the circle.

Anterior cerebral artery ✅

• Direct branch of internal carotid.

• Supplies medial frontal and parietal lobes.

• Forms the anterior portion of the circle of Willis with the anterior communicating artery.

Why the others are WRONG ❌

• Basilar artery ❌ → Formed by union of vertebral arteries, not a branch of internal carotid.

• Anterior communicating artery ❌ → Connects both anterior cerebral arteries, not a branch of internal carotid itself.

• Posterior communicating artery ❌ → Connects internal carotid to posterior cerebral artery, not a major branch forming the circle itself.

• Posterior cerebral artery ❌ → Mainly from basilar artery, not internal carotid (in most adults).

The cerebral hemispheres control contralateral voluntary movement and sensory processing.

• The left hemisphere controls the right side of the body.

• Therefore, a lesion in the left cerebral hemisphere → right-sided weakness, sensory deficits, or other motor/sensory impairments.

Why the correct option is RIGHT ✔️

Impairment of the right side of the body ✅

• Due to decussation of corticospinal tracts in the medullary pyramids.

• Lesion in left motor cortex → contralateral (right) hemiparesis.

• Lesion in left sensory cortex → contralateral (right) loss of sensation.

Why the others are WRONG ❌

• Visual loss ❌ → Visual loss occurs depending on optic radiation or occipital cortex involvement, not general hemisphere injury.

• Intact speech ❌ → Left hemisphere contains Broca’s and Wernicke’s areas in most people, so speech may be affected.

• Numbness in the whole body ❌ → Only contralateral side is affected.

• Impairment of the left side of the body ❌ → Incorrect; the left hemisphere affects opposite side, not ipsilateral.

The sulcus limitans is a longitudinal groove in the neural tube that separates:

• Alar plate (sensory) – laterally

• Basal plate (motor) – medially

This separation is present only in regions where sensory and motor nuclei are both organized around the ventricular system.

The telencephalon does not develop true alar/basal plates in the same arrangement—hence no sulcus limitans.

Why the correct option is RIGHT ✔️

Telencephalon ✅

• Develops into cerebral hemispheres, which do not maintain the primitive alar–basal plate organization.

• Since this organization is absent, the sulcus limitans is also absent.

• Ventricular cavities of telencephalon (lateral ventricles) do not have the sensory–motor separation seen in the lower brainstem/spinal cord.

Why the other options are WRONG ❌

Metencephalon ❌

• Forms the pons and cerebellum.

• The pons retains alar/basal plates, and the sulcus limitans is present.

• Visibly separates motor (medial) and sensory (lateral) nuclei.

Mesencephalon (midbrain) ❌

• Sulcus limitans present around the cerebral aqueduct.

• Separates oculomotor/trochlear motor nuclei (medial) from sensory nuclei (lateral).

Myelencephalon ❌

• Forms the medulla.

• Has a well-developed sulcus limitans in the floor of the fourth ventricle.

• Sensory nuclei are lateral; motor are medial.

Spinal cord ❌

• Classic region where the sulcus limitans separates motor ventral horn from sensory dorsal horn in early development.

• Fully present during embryogenesis.

Cerebellar lesions cause coordination problems, not movement initiation problems.
So you see ataxia, intention tremor, hypotonia, nystagmus, dysdiadochokinesia, and gait ataxia.
A resting tremor, however, is a feature of Parkinson disease (basal ganglia lesion)—not the cerebellum.

Why the correct option is RIGHT ✔️

Resting tremors ✅

• Caused by dopamine deficiency from substantia nigra degeneration (Parkinson disease).

• Not generated by cerebellar circuits.

• Cerebellar tremors occur during movement (intention tremor), not at rest.

Why the other options are WRONG ❌

Dysdiadochokinesia ❌

• Inability to perform rapid alternating movements.

• Classical sign of cerebellar hemisphere lesion.

Ataxia ❌

• Lack of coordinated muscle movements.

• Seen in all cerebellar lesions (limb ataxia or truncal ataxia).

Gait issues ❌

• Cerebellar lesions cause wide-based, unsteady gait.

• Especially with vermis involvement.

Hypotonia ❌

• Cerebellum normally maintains muscle tone through descending pathways.

• Lesions cause reduced tone.

Parkinson disease is caused by degeneration of dopaminergic neurons in the substantia nigra pars compacta.
Motor pathways cross: the right basal ganglia control movements of the left side of the body.
Since the patient has left-sided resting tremor, the lesion must be in the right substantia nigra.

Why the correct option is RIGHT ✔️

 Right substantia nigra ✅

• The substantia nigra (pars compacta) produces dopamine, which modulates the contralateral basal ganglia circuitry.

• Degeneration here → reduced dopamine → left-sided tremor, rigidity, bradykinesia.

• Fits the classic presentation of unilateral early Parkinson disease.

Why the other options are WRONG ❌

 Bilateral substantia nigra ❌

• Would cause bilateral symptoms, not predominantly left-sided tremor.

• Parkinson typically starts asymmetrically, not bilaterally.

 Left globus pallidus ❌

• Globus pallidus lesions cause movement disorders, but Parkinson disease specifically arises from substantia nigra degeneration, not pallidal damage.

• Also: left pallidal lesion → right-sided symptoms, not left.

 Left substantia nigra ❌

• Left substantia nigra degeneration would cause right-sided motor symptoms.

• Opposite of what is seen here.

 Right globus pallidus ❌

• Pallidal lesions can cause rigidity/dystonia, but classical resting tremor and the pathology of Parkinson disease are due to nigral, not pallidal, degeneration.

The sella turcica is a depression located on the superior surface of the body of the sphenoid bone. It houses the pituitary gland, making the sphenoid the direct structural component.
Therefore, any fracture that disrupts the sella must involve the sphenoid bone, not surrounding bones.

Why the correct option is RIGHT ✔️

Sphenoid bone ✅

• The body of the sphenoid forms the sella turcica, consisting of:

  • Tuberculum sellae

  • Hypophyseal fossa (pituitary fossa)

  • Dorsum sellae

• A fracture in this bone directly compromises the pituitary gland, optic chiasm, and cavernous sinus structures that lie adjacent to it.

• It is the central bone of the skull base, making it the only logical answer.

Why the other options are WRONG ❌

Frontal bone ❌

• Forms the forehead, roof of the orbits, and contributes to the anterior cranial fossa.

• Located far anterior to the sella turcica; its fracture does not involve the pituitary fossa.

Ethmoid bone ❌

• Contributes to nasal cavity, cribriform plate, and portions of the medial orbital wall.

• Lies anterior and inferior to sphenoid but does not form the sella or its boundaries.

Temporal bone ❌

• Houses middle and inner ear structures (mastoid, petrous parts).

• Although it forms part of the lateral skull base, it has no structural contribution to the sella.

Basiocciput bone ❌

• The basilar part of occipital bone, located posterior to the sphenoid.

• Forms the clivus but does not contribute to the sella turcica; fractures here affect the brainstem area, not the pituitary fossa.

Horner’s syndrome is caused by interruption of sympathetic supply to the eye. The ptosis seen is due to paralysis of Müller’s (superior tarsal) muscle, a smooth muscle responsible for a small part of eyelid elevation.

Thus, Horner’s ptosis is mild/partial, not complete.

Complete ptosis occurs when the levator palpebrae superioris (LPS), supplied by CN III, is affected — not in Horner’s syndrome.

📚 Why Each Option is Right or Wrong

a. Partial drooping of eyelid — ✅ TRUE for Horner’s, so NOT the exception

• Sympathetic loss → Müller’s muscle paralysis → mild/partial ptosis.

 Complete drooping of eyelid — ❌ NOT TRUE → This is the exception (Correct answer)

• Complete ptosis requires paralysis of levator palpebrae superioris.

• Horner’s syndrome does not affect this muscle.

• Therefore, complete ptosis is NOT seen in Horner’s.

 Levator palpebrae superioris muscle involvement — ❌ Incorrect

• LPS is innervated by CN III (oculomotor) → not sympathetic.

• Horner’s only affects Müller’s muscle.

• So LPS is NOT involved, making this a true feature of Horner’s ptosis.

 Mydriatic pupil — ❌ Incorrect

• Horner’s causes miosis, not mydriasis.

• Lack of sympathetic supply → pupil constricts.

• Mydriasis would occur with parasympathetic loss (e.g., CN III palsy).

• So this is also NOT a feature of Horner’s, but the question asks the exception in ptosis features, and option (b) is more specific.

 Loss of function of short ciliary nerves — ❌ Incorrect

• Short ciliary nerves carry sympathetic fibers to the dilator pupillae.

• Damage → miosis, partial ptosis, and anhidrosis.

• This is indeed part of Horner’s pathophysiology.

The patient has a classic left MCA superior-division stroke pattern: contralateral weakness most pronounced in face and arm (lateral convexity of frontal lobe / motor cortex) plus Broca’s (expressive) aphasia — nonfluent speech with preserved comprehension — which localizes to the dominant (left) inferior frontal gyrus supplied by the superior branch of the MCA. The MCA supplies the lateral surfaces of frontal, parietal and temporal lobes that subserve language (dominant side) and face/arm motor/sensory function.

Why the correct option is right

• ✅ Middle cerebral artery: Supplies lateral cerebral cortex including primary motor & sensory areas for face/arm, and dominant hemisphere language areas (Broca’s and Wernicke’s regions via superior & inferior divisions). Occlusion (especially superior division) produces contralateral face/arm weakness and expressive aphasia when in dominant hemisphere.

Why the other options are incorrect (detailed)

• ❌ a. Anterior cerebral artery (ACA):

  • ACA supplies medial frontal & parietal lobes — leg > arm/face motor deficits, personality and executive dysfunction. Not consistent with face/arm-predominant weakness or Broca aphasia.

• ❌ c. Posterior cerebral artery (PCA):

  • PCA supplies occipital lobe and inferior temporal lobe — causes contralateral homonymous hemianopia, visual cortex deficits, or memory impairment. Language-dominant visual deficits only; not primary motor/expressive aphasia pattern.

• ❌ d. Basilar artery:

  • Supplies brainstem and cerebellar structures. Basilar occlusion causes brainstem signs (cranial nerve palsies, locked-in syndrome, ataxia) rather than isolated cortical face/arm weakness with aphasia.

• ❌ e. Anterior choroidal artery:

  • Small branch supplying internal capsule (posterior limb), optic tract, choroid plexus — lesions can cause contralateral hemiplegia, hemisensory loss and homonymous hemianopia. It may produce pure motor deficits but language (Broca) signs and lateral cortical face/arm predominance point more to an MCA cortical infarct.

• Sympathetic innervation to the head and face originates from preganglionic neurons in the intermediolateral cell column (IML) of T1–T2.

• These fibers ascend in the sympathetic chain to synapse in the superior cervical ganglion, then distribute to the eye and face.

• A lesion here interrupts preganglionic sympathetic fibers, producing classic Horner’s syndrome:

  • Ptosis (loss of superior tarsal muscle)

  • Miosis (loss of dilator pupillae)

  • Anhidrosis (loss of sympathetic sweat innervation)

This is the most classic and high-yield location tested for sympathetic pathway interruption.

❌ Why Other Options Are Incorrect (with detailed explanations):

• a. Nucleus ambiguus:
  Controls motor fibers of CN IX, X, XI (swallowing, speech).
  Not involved in sympathetic pathways to the head.

• c. Superior cervical ganglion:
  This is the final sympathetic relay for head/face.
  Damage can cause Horner’s syndrome, but the question asks about the origin of sympathetic outflow, which starts at T1–T2 IML, not the ganglion.

• d. Dorsal motor nucleus of vagus:
  Parasympathetic nucleus of CN X — controls thoracoabdominal organs, not head sympathetic function.

• e. Pelvic splanchnic nerves (S2–S4):
  These are parasympathetic, not sympathetic.
  They supply pelvic organs (bladder, colon, erectile tissue), not the eye or face.

• Brown-Séquard syndrome results from hemisection of the spinal cord.

• Classic features:

  • Ipsilateral motor weakness and loss of proprioception (corticospinal tract + dorsal column)

  • Contralateral loss of pain and temperature sensation (spinothalamic tract, which crosses 1–2 segments above entry)

• Typically caused by penetrating injuries (stab wounds) or tumors.

Why other options are incorrect (with detailed explanation):

• ❌ Central cord syndrome: Usually due to hyperextension injuries in elderly patients; causes greater weakness in upper limbs than lower limbs, with variable sensory loss.

• ❌ Anterior cord syndrome: Caused by anterior spinal artery infarct; results in bilateral motor loss and loss of pain and temperature, with preserved proprioception, unlike this case.

• ❌ Posterior cord syndrome: Rare; affects dorsal columns, causing loss of proprioception, vibration, and fine touch, but motor and pain/temperature are preserved.

• ❌ Conus medullaris syndrome: Affects the sacral cord and lumbar nerve roots, causing bilateral lower limb weakness, saddle anesthesia, and bladder/bowel dysfunction, not the hemisection pattern described.

• The non-dominant (usually right) parietal lobe is responsible for visuospatial skills and constructional abilities.

• Lesions here cause constructional apraxia, characterized by difficulty:

  • Copying geometric designs

  • Drawing objects

  • Assembling puzzles

• Patients may also have hemispatial neglect (ignoring one side of space).

Why other options are incorrect (with detailed explanation):

• ❌ Non-dominant temporal lobe: Mainly involved in visual memory and recognition of objects, not constructional skills.

• ❌ Dominant parietal lobe: Responsible for language-related functions (e.g., writing, calculation, praxis), not primarily visuospatial copying.

• ❌ Prefrontal cortex: Important for planning, decision-making, and executive function, but not geometric copying.

• ❌ Basal ganglia: Regulates motor control and movement, lesions cause movement disorders, not visuospatial deficits.

• ❌ Hippocampus: Critical for memory formation, not visuospatial construction.

• The trigeminal nerve (CN V) is the largest cranial nerve and emerges from the anterolateral surface of the pons.

• It has three major branches:

  1. Ophthalmic (V1)

  2. Maxillary (V2)

  3. Mandibular (V3)

• CN V is responsible for sensory innervation of the face and motor innervation of the muscles of mastication.

Why other options are incorrect (with detailed explanation):

• ❌ Abducent (CN VI): Emerges at the pontomedullary junction; innervates lateral rectus muscle; much smaller in size.

• ❌ Facial (CN VII): Exits at the lateral aspect of the pons with CN VIII; smaller than CN V; controls facial expression muscles.

• ❌ Hypoglossal (CN XII): Exits anterior medulla; controls tongue muscles, not the largest nerve of the pons.

• ❌ Vagus (CN X): Exits posterolateral medulla; provides parasympathetic and motor innervation to thoracoabdominal organs; smaller than CN V.

• The vermis is the midline structure of the cerebellum connecting the two cerebellar hemispheres.

• It is involved in truncal coordination and posture, controlling proximal muscles.

• Lesions in the vermis often result in truncal ataxia, wide-based unsteady gait, and difficulty maintaining posture.

Why other options are incorrect (with detailed explanation):

• ❌ Cerebellar hemisphere: Refers to the lateral portions of the cerebellum; responsible for limb coordination rather than midline functions.

• ❌ Flocculonodular lobe: Located inferiorly, involved in balance and vestibular function; not the central connecting structure.

• ❌ Anterior lobe: Located superiorly; involved in coordination of limb movement, not the midline connecting structure.

• ❌ Posterior lobe: Largest lobe; primarily coordinates fine voluntary movements, lateral in position, not midline.

• The mastoid antrum is a pneumatic space in the temporal bone that communicates with the middle ear.

• Infections in the mastoid can lead to mastoiditis and may spread to adjacent venous sinuses.

• The sigmoid sinus lies adjacent to the mastoid air cells and directly receives venous drainage from the mastoid and middle ear.

• Infection can lead to sigmoid sinus thrombosis, which may result in septicemia or intracranial complications.

Why other options are incorrect (with detailed explanation):

• ❌ Transverse sinus: Runs posteriorly from the confluence of sinuses; not immediately adjacent to the mastoid air cells, so less commonly involved.

• ❌ Superior sagittal sinus: Located along the midline of the cranial vault; does not directly drain the mastoid region.

• ❌ Inferior sagittal sinus: Also midline, drains the falx cerebri; not related to mastoid venous drainage.

• ❌ Cavernous sinus: Located in the sphenoid region near the orbit; connected to facial and orbital veins but not directly linked to mastoid antrum infections.

• The patient demonstrates features of night terrors (sleep terrors), a parasomnia common in children, occurring during non-REM (NREM) sleep, specifically stage 3 (slow-wave sleep).

• Stage 3 NREM sleep is characterized by high-amplitude, low-frequency delta waves (0.5–4 Hz) on EEG.

• Night terrors occur early in the night when delta sleep predominates, and the child often does not remember the event, unlike nightmares which occur during REM sleep.

Why other options are incorrect (with detailed explanation):

• ❌ Alpha waves: Frequency 8–13 Hz; associated with relaxed wakefulness and eyes closed, not deep sleep.

• ❌ Beta waves: Frequency 13–30 Hz; associated with active thinking, alertness, and REM sleep, not slow-wave sleep.

• ❌ Gamma waves: Frequency >30 Hz; associated with higher cognitive functions like perception and memory, not sleep.

• ❌ Theta waves: Frequency 4–8 Hz; observed in stage 1 NREM sleep and drowsiness, not in deep sleep (stage 3) where night terrors occur.

• The suprachiasmatic nucleus (SCN) is located above the optic chiasm.

• It receives direct retinal input via the retinohypothalamic tract.

• Functions as the body’s master circadian clock, regulating:

  • Sleep-wake cycles

  • Hormonal rhythms (e.g., cortisol, melatonin)

  • Body temperature

• Lesions cause circadian rhythm disturbances (e.g., irregular sleep patterns).

Why other options are incorrect (with detailed explanation):

• ❌ Arcuate nucleus: Regulates feeding behavior and hormone release (e.g., GH, prolactin) but does not control circadian rhythms.

• ❌ Dorsomedial nucleus: Involved in emotional behavior, aggression, and satiety modulation, not circadian control.

• ❌ Paraventricular nucleus: Produces oxytocin, vasopressin, and CRH; regulates stress response and autonomic function, not biological clock.

• ❌ Ventromedial nucleus: Known as the satiety center, controlling feeding and body weight, not circadian rhythm.

• The lateral hypothalamic nucleus (LH) is the “feeding center”.

• Lesions cause:

  • Anorexia (loss of appetite)

  • Weight loss

• LH integrates hunger signals from peripheral hormones (like ghrelin) and stimulates feeding behavior.

Why other options are incorrect (with detailed explanation):

• ❌ Dorso-medial nucleus: Plays a role in emotional behaviors, aggression, and satiety modulation, but is not the primary feeding center. Lesions may cause behavioral changes rather than direct anorexia.

• ❌ Supra-chiasmatic nucleus: Acts as the body’s circadian clock, regulating sleep-wake cycles and hormone rhythms, but has no direct effect on appetite or weight.

• ❌ Supra-optic nucleus: Synthesizes ADH (vasopressin) and oxytocin, controlling water balance and lactation. Lesions may cause diabetes insipidus, but do not affect feeding.

• ❌ Ventromedial nucleus: Known as the “satiety center”. Lesions here cause hyperphagia and obesity, the opposite of anorexia and weight loss.

• The Romberg test assesses proprioception (joint position sense).

• The patient stands with feet together and eyes closed:

  • Normal proprioception → patient remains stable.

  • Dorsal column / proprioceptive deficits → patient sways or falls, producing a positive Romberg sign.

• This patient’s unsteady gait in the dark and impaired vibration/proprioception suggest dorsal column dysfunction, which the Romberg test confirms.

• Motor function is intact, differentiating this from cerebellar ataxia, which causes imbalance even with eyes open.

Why other options are incorrect (with detail):

• ❌ Exaggerated tendon reflexes: Indicates upper motor neuron lesion, not proprioceptive sensory loss.

• ❌ Loss of tendon reflexes: Suggests lower motor neuron or peripheral neuropathy, not isolated dorsal column deficit.

• ❌ Positive Babinski’s sign: Tests corticospinal tract / upper motor neuron function, unrelated to conscious proprioception.

• ❌ Impaired pain perception: Tests spinothalamic tract, which is intact in this patient.

• The ventral/anterior spinothalamic tract carries crude touch and pressure sensations.

• It crosses the spinal cord shortly after entering, so lesions typically cause contralateral deficits.

• Fine touch, vibration, and proprioception are carried by the dorsal column-medial lemniscus (DCML) pathway, which remains intact here.

• Pain and temperature are carried by the lateral spinothalamic tract, which is unaffected.

Why other options are incorrect (with detail):

• ❌ Dorsal column tract: Carries fine touch, vibration, and conscious proprioception. These sensations are intact, so the dorsal column is spared.

• ❌ Lateral spinothalamic tract: Transmits pain and temperature; these modalities are normal in this patient.

• ❌ Spinocerebellar tract: Conveys unconscious proprioception to the cerebellum. Damage causes ataxia, not loss of crude touch.

• ❌ Spino-reticular tract: Mediates pain modulation and arousal, not crude touch perception.

• The dorsal column-medial lemniscus (DCML) pathway carries:

  • Fine touch (discriminative touch)

  • Vibration sense

  • Conscious proprioception (joint position sense)

• Clinical features of dorsal column lesions:

  • Loss of vibration and proprioception

  • Positive Romberg sign (worsened balance with eyes closed)

  • Asterognosis (inability to recognize objects by touch)

• Pain and temperature are spared because they travel in the spinothalamic tracts.

Why other options are incorrect (with more detail):

• ❌ Anterior spinothalamic tract: Carries crude touch and pressure, not fine touch or vibration. Lesions may cause mild sensory loss but not the precise proprioceptive deficits seen here.

• ❌ Lateral spinothalamic tract: Responsible for pain and temperature sensation. Since these modalities are intact, this tract is not involved.

• ❌ Spinocerebellar tract: Conveys unconscious proprioception to the cerebellum. Lesions cause ataxia and coordination problems, but do not affect conscious vibration or position sense, which are impaired in this patient.

• ❌ Spino-reticular tract: Involved in pain modulation and alertness, not fine touch, vibration, or proprioception.

• The hypoglossal nerve (CN XII) controls intrinsic and extrinsic tongue muscles (except palatoglossus).

• Lesions of CN XII cause:

  • Ipsilateral tongue atrophy

  • Deviation of the tongue toward the side of the lesion on protrusion

  • Dysarthria (slurred speech) and dysphagia (difficulty swallowing)

• The hypoglossal canal in the posterior cranial fossa is the exit point for CN XII.

Why other options are incorrect:

• ❌ Jugular foramen: Transmits CN IX, X, XI. Lesions here cause palatal droop, hoarseness, and trapezius/SCM weakness, not isolated tongue deviation.

• ❌ Foramen rotundum: Transmits CN V2 (maxillary branch). Lesions cause facial sensory deficits, not tongue problems.

• ❌ Internal acoustic meatus: Transmits CN VII and VIII. Lesions cause facial weakness, hearing loss, or vertigo, not isolated tongue deviation.

• ❌ Foramen spinosum: Transmits middle meningeal artery, not cranial nerves.

• Bipolar neurons have two processes: one axon and one dendrite.

• They are specialized for sensory transmission.

• Typical locations include:

  • Olfactory epithelium → smell sensation.

  • Retina (photoreceptors) → vision.

  • Vestibulocochlear ganglia → hearing and balance.

• Other neurons:

  • Multipolar neurons are most common in the CNS (cortex, anterior horn, cerebellum).

  • Unipolar/pseudounipolar neurons are found in dorsal root ganglia.

Why other options are incorrect:

• ❌ Cerebral cortex: Mostly multipolar neurons, not bipolar.

• ❌ Cerebellar cortex: Contains Purkinje cells (multipolar) and granule cells, not bipolar neurons.

• ❌ Dorsal root ganglion: Contains pseudounipolar sensory neurons, not bipolar.

• ❌ Anterior horn cell of spinal cord: Multipolar motor neurons, not bipolar.

• Myelination is the process of forming a myelin sheath around axons to increase the speed of nerve impulse conduction.

• In the CNS, oligodendrocytes are the myelinating glial cells. Each oligodendrocyte can extend processes to myelinate multiple axons simultaneously.

• In the peripheral nervous system (PNS), Schwann cells perform myelination, but each Schwann cell myelinates only a single axonal segment.

Why other options are incorrect:

• ❌ Microglia: These are CNS immune cells responsible for phagocytosis, not myelination.

• ❌ Ependyma: Line the ventricular system and produce cerebrospinal fluid (CSF), do not myelinate.

• ❌ Astrocytes: Support neurons, maintain the blood-brain barrier, and regulate ions, but do not produce myelin.

• ❌ Schwann cells: Myelinate axons in the PNS, not the CNS.

• During spinal cord development, the neural tube differentiates into three layers:

  1. Ventricular layer – lining the central canal; contains proliferating neuroblasts.

  2. Mantle layer – forms the gray matter of the spinal cord.

  3. Marginal layer – forms the white matter (axonal projections).

• The lateral walls of the spinal cord form a groove called sulcus limitans, which divides:

  • Dorsal (posterior) alar plate → primarily sensory neurons; forms posterior horn.

  • Ventral (anterior) basal plate → primarily motor neurons; forms anterior horn.

Why other options are incorrect:

• ❌ Basal plate: Gives rise to anterior (ventral) horn, not posterior horn; mainly motor neurons.

• ❌ Ependymal layer: Lines the central canal; it is the proliferative zone, not directly forming horns.

• ❌ Mantle layer: Becomes the gray matter overall, but the specific differentiation of posterior horn comes from alar plate within the mantle layer.

• ❌ Marginal zone: Forms the white matter (axons), not the gray matter of posterior horn.

• AFP (alpha-fetoprotein) is a glycoprotein produced by the fetal liver, yolk sac, and gastrointestinal tract.

• It crosses into the amniotic fluid and maternal serum.

• High maternal serum AFP is mainly associated with open fetal defects where AFP leaks into the amniotic fluid, such as spina bifida or anencephaly.

• Low AFP is often seen in chromosomal disorders like Down syndrome.

Why the correct option is right:

• ✅ Neural tube defect: Open defects in the fetal spine or skull allow AFP to leak into maternal serum. Screening for elevated AFP is a standard prenatal test for conditions like spina bifida (myelomeningocele) and anencephaly.

Why other options are incorrect:

• ❌ Down syndrome: AFP is usually low, not high. Screening uses AFP along with other markers like hCG and inhibin-A (quadruple test).

• ❌ Congenital heart defect: AFP levels are not affected, because the heart defect does not expose fetal proteins to maternal blood. Detection relies mainly on ultrasound.

• ❌ Renal agenesis: While bilateral renal agenesis can cause oligohydramnios, AFP is not a reliable marker for kidney defects. Diagnosis is ultrasound-based.

• ❌ Microcephaly: Head size abnormalities do not cause AFP leakage, so maternal AFP levels remain normal. Detection is via ultrasound.

Oligodendrocytes are the myelinating cells of the central nervous system (CNS), responsible for forming the myelin sheath around CNS axons.

• They originate from neuroectoderm-derived neuroblast cells, specifically from ventricular zone progenitors during development.

• In Multiple Sclerosis (MS), autoimmune-mediated damage targets these oligodendrocytes, leading to CNS demyelination and the classic neurological symptoms.

Why the Correct Answer Is Right 👍

• Derived from neuroblasts of the neural tube (CNS progenitor cells).

• Different from Schwann cells, which myelinate PNS axons and arise from neural crest cells.

• Responsible for CNS myelination, essential for rapid conduction of action potentials.

Why the Other Options Are Wrong (with detail) ❌

Ependymal cells ❌

• Line the ventricles and produce CSF, but do not myelinate neurons.

Mesenchymal cells ❌

• Give rise to connective tissue, bone, cartilage, not CNS neurons or glia.

Neural crest cells ❌

• Give rise to Schwann cells (PNS myelination), peripheral neurons, and some craniofacial structures.

• Not a source of CNS oligodendrocytes.

Ventricular cells ❌

• General progenitor term, but the specific CNS myelinating lineage comes from neuroblasts, not generic ventricular cells.

The cerebellar cortex is organized into three layers: molecular, Purkinje, and granular layers.

Purkinje cells are large inhibitory neurons that form the sole output of the cerebellar cortex.

• They release GABA, which inhibits deep cerebellar nuclei, regulating motor coordination and timing.

• They integrate excitatory input from parallel fibers (granule cells) and climbing fibers to fine-tune motor activity.

Why the Correct Answer Is Right 👍

• Purkinje cells are the primary inhibitory neurons of the cerebellar cortex.

• They modulate and inhibit the activity of deep cerebellar nuclei, preventing excessive motor output.

• Their GABAergic activity is essential for smooth, coordinated movement.

Why the Other Options Are Wrong (with detail) ❌

Basket cells ❌

• Inhibitory interneurons in the molecular layer, but their effect is local, not the main cortical output.

Granule cells ❌

• Excitatory neurons using glutamate, forming parallel fibers that excite Purkinje cells.

• Not inhibitory.

Stellate cells ❌

• Inhibitory interneurons in the molecular layer.

• Provide local inhibition to Purkinje dendrites but are not the primary output.

Pyramidal cells ❌

• Found in the cerebral cortex, not cerebellum.

• Excitatory, not inhibitory.

The cerebral cortex has six layers, each with distinct cell types:

• Pyramidal cells are the primary excitatory neurons of the cortex, responsible for sending output signals.

• Large pyramidal cells, including Betz cells in the primary motor cortex, are located in Layer V — the internal pyramidal layer.

• These neurons project to subcortical structures such as the spinal cord, brainstem, and other cortical areas, forming corticospinal, corticobulbar, and corticopontine tracts.

Why the Correct Answer Is Right 👍

• Layer V (Internal pyramidal layer) contains large pyramidal neurons for long-range projection.

• Prominent in the precentral gyrus as Betz cells, key for voluntary motor control.

• Functions as the main cortical output layer.

Why the Other Options Are Wrong (with detail) ❌

Molecular layer (Layer I) ❌

• Mostly axons and dendrites, very few neurons.

• Does not contain pyramidal cells.

External pyramidal layer (Layer III) ❌

• Contains smaller pyramidal cells projecting to other cortical areas, not spinal cord.

External granular layer (Layer II) ❌

• Contains small granular neurons involved in intracortical communication.

• Lacks large pyramidal output neurons.

Multiform layer (Layer VI) ❌

• Contains various types of neurons, mainly projecting to thalamus.

• Not the primary site of large pyramidal output cells.

Betz cells are large pyramidal neurons located in the primary motor cortex (precentral gyrus).
They are the largest neurons in the CNS and play a critical role in voluntary motor control, as they give rise to the corticospinal (pyramidal) tract.

Histologically, Betz cells are found in Layer V (internal pyramidal layer) of the cerebral cortex.

Why the Correct Answer Is Right 👍

• Layer V contains large pyramidal neurons that project to spinal motor neurons.

• Betz cells are prominent in motor areas, particularly precentral gyrus.

• Responsible for fine motor control, especially of the distal limbs.

Why the Other Options Are Wrong (with detail) ❌

Layer I (Molecular layer) ❌

• Mostly contains axons and dendrites, few neurons.

• Does not contain Betz cells.

Layer II (External granular layer) ❌

• Contains small pyramidal and granular neurons.

• Functions in intracortical communication, not corticospinal output.

Layer III (External pyramidal layer) ❌

• Contains pyramidal neurons projecting to other cortical areas.

• Not the origin of corticospinal tracts.

Layer VI (Multiform / fusiform layer) ❌

• Contains neurons projecting primarily to thalamus.

• Not involved in direct motor output to spinal cord.

Bacterial meningitis is characterized by acute inflammation of the meninges, especially the subarachnoid space.
The key pathological hallmark is a massive influx of neutrophils, which attempt to contain the infection but also contribute to inflammation, increased intracranial pressure, and impaired CSF flow.

The response is rapid and intense because bacteria trigger strong cytokine release, activating neutrophils as the first-line defenders.

Why the Correct Answer Is Right 👍

• Neutrophils dominate the CSF in bacterial meningitis.

• They accumulate in the subarachnoid space, causing purulent exudate.

• This mechanism explains fever, neck stiffness, and high CSF WBC count.

Why the Other Options Are Wrong (with detail) ❌

Demyelination of CNS neurons ❌

• Seen in multiple sclerosis, not acute bacterial meningitis.

• Bacterial infection primarily affects meninges, not myelin.

Formation of Lewy bodies in brain tissue ❌

• Characteristic of Parkinson’s disease and Lewy body dementia.

• Not associated with meningitis or infection.

Degeneration of myelin sheaths ❌

• Associated with demyelinating diseases like MS, Guillain-Barré, or metabolic disorders.

• Bacterial meningitis does not directly damage myelin.

Herpes simplex virus encephalitis (most commonly HSV-1) is a medical emergency that requires rapid and accurate diagnosis.
The most accurate and definitive test is PCR testing of the CSF, which detects HSV DNA with very high sensitivity and specificity.

It is non-invasive, fast, and has largely replaced brain biopsy.

Why the Correct Answer Is Right 👍

• CSF PCR is the gold standard for diagnosing HSV encephalitis.

• Can detect very small amounts of viral DNA.

• Highly accurate even early in the disease.

• Rapid results guide immediate acyclovir therapy.

Why the Other Options Are Wrong (with detail) ❌

Brain Biopsy ❌

• Historically diagnostic, but highly invasive.

• Now only considered when PCR is negative but suspicion remains extremely high.

CT Scan ❌

• May show temporal lobe abnormalities, but not specific and not diagnostic.

• Mainly used to rule out contraindications before LP.

Herpes Serology (blood tests) ❌

• Shows antibodies, not active CNS infection.

• Many people are seropositive without encephalitis → low diagnostic value.

Viral Culture ❌

• HSV is difficult and slow to culture.

• Not practical for acute diagnosis.

In any patient with suspected CNS infection (fever, nausea, vomiting, headache) PLUS focal neurological deficit, the first priority is to exclude raised intracranial pressure or a mass lesion before performing a lumbar puncture.

A CT scan of the head is the safest and best initial test because it quickly identifies:

• Mass effect

• Midline shift

• Space-occupying lesions

• Risk of brain herniation

Performing a lumbar puncture before imaging in such patients can be fatal.

Why the Correct Answer Is Right 👍

• Focal neurological deficits indicate possible increased ICP or mass lesion.

• CT is rapid, widely available, and safe.

• Prevents catastrophic herniation prior to lumbar puncture.

Why the Other Options Are Wrong (with detail) ❌

CSF Examination ❌

• LP is contraindicated until imaging rules out mass effect.

• Cannot be performed first in a patient with focal deficits.

Gram Staining of CSF ❌

• Requires CSF obtained via LP, which is unsafe initially.

Brain Biopsy ❌

• Highly invasive, never the initial test.

• Reserved for unclear cases after imaging and CSF studies.

CSF PCR ❌

• Also requires CSF from LP.

• Not the first step when there is risk of herniation.

Pain modulation in the CNS involves descending inhibitory pathways that originate from the periaqueductal gray (PAG), nucleus raphe magnus, and other brainstem nuclei.
These pathways project down the spinal cord to suppress pain transmission at the dorsal horn.

Serotonin (5-HT) is one of the key inhibitory neurotransmitters released by these descending fibers.
It acts on interneurons that then release enkephalins, which block pain signals by inhibiting substance P release from primary afferents.

Why the Correct Answer is Right 👍

• Serotonin is released by the raphe nuclei, a major component of the descending analgesic system.

• Enhances endogenous opioid activity in the spinal cord.

• Reduces transmission of nociceptive signals to higher centers.

Why the Other Options Are Wrong (with detail) ❌

Glutamate ❌

• This is the main excitatory neurotransmitter for pain transmission in the dorsal horn.

• It enhances pain, not inhibits it.

Substance P ❌

• A classic pain-promoting neuropeptide.

• Released by nociceptive C-fibers to carry slow, burning pain signals.

Neurokinin ❌

• Neurokinins (like NK-1) are pain facilitators, not inhibitors.

• Involved in inflammatory pain pathways.

Calcitonin Gene-Related Peptide (CGRP) ❌

• A potent vasodilator and pain mediator.

• Heavily involved in migraine pathophysiology; it does not inhibit pain.

Carbidopa is given together with L-DOPA in Parkinson’s disease to inhibit peripheral DOPA decarboxylase, the enzyme that converts L-DOPA into dopamine outside the brain.

Since dopamine cannot cross the blood–brain barrier, premature conversion in the periphery would:

• Reduce the amount of L-DOPA reaching the brain

• Increase peripheral side effects (nausea, vomiting, arrhythmias)

Carbidopa cannot cross the BBB, so it only blocks L-DOPA breakdown outside the brain, allowing more L-DOPA to reach the CNS, where it can be converted into dopamine and improve motor symptoms.

Why the Correct Answer is Right 👍

• Carbidopa inhibits peripheral DOPA decarboxylase.

• This increases CNS availability of L-DOPA.

• Reduces peripheral dopamine-related side effects.

• Does not interfere with dopamine synthesis in the brain.

Why the Other Options Are Wrong (with detail) ❌

It is nonpolar than dopamine ❌

• Polarity differences are not the therapeutic reason.

• Dopamine itself is too polar to cross the BBB; this option is irrelevant.

L-DOPA is polar than carbidopa ❌

• Their polarity comparison does not explain the benefit of combined therapy.

• The key effect is enzyme inhibition, not polarity.

It cannot pass BBB ❌ (Partially true, but not the reason)

• Carbidopa indeed does not cross the BBB.

• BUT the therapeutic purpose is enzyme inhibition, not simply the inability to cross.

It inhibits tyrosine hydroxylase ❌

• Tyrosine hydroxylase converts tyrosine → L-DOPA.

• Carbidopa has no effect on this enzyme.

• Inhibiting it would block dopamine synthesis entirely.

Thiamine (Vitamin B₁) is essential for carbohydrate metabolism and neuronal function.
It serves as a cofactor for key enzymes such as pyruvate dehydrogenase, α-ketoglutarate dehydrogenase, transketolase, and branched-chain ketoacid dehydrogenase.

Deficiency impairs ATP production, especially affecting nervous tissue and the myocardium, which have high metabolic demands.
This results in the two classic forms of Beri Beri:

• Dry Beri Beri: Peripheral neuropathy, muscle wasting, loss of reflexes.

• Wet Beri Beri: Cardiomyopathy, high-output heart failure, edema.

Why the Correct Answer is Right 👍

• Thiamine deficiency directly causes both wet and dry Beri Beri.

• Nerve and heart tissue become energy-deprived → neuropathy + heart failure.

• Seen in malnutrition, alcoholism, chronic illness, and post-bariatric surgery.

Why the Other Options Are Wrong (with detail) ❌

Riboflavin ❌

• Deficiency causes cheilosis, glossitis, corneal vascularization, and dermatitis.

• Does not cause neuropathy or cardiomyopathy.

Cyanocobalamin (Vitamin B₁₂) ❌

• Deficiency leads to megaloblastic anemia, peripheral neuropathy, and subacute combined degeneration of the spinal cord.

• No wet or dry Beri Beri association.

Niacin (Vitamin B₃) ❌

• Deficiency causes pellagra (the 3 D’s: dermatitis, diarrhea, dementia).

• Not linked to cardiomyopathy or neuropathy of Beri Beri.

Pyridoxamine (Vitamin B₆) ❌

• Deficiency causes peripheral neuropathy, anemia, seizures, and dermatitis.

• Does not produce the cardiac findings characteristic of Wet Beri Beri.

Myasthenia Gravis (MG) is an autoimmune disease where antibodies attack postsynaptic acetylcholine receptors at the neuromuscular junction.
This leads to:

• Fatigable muscle weakness (worse with use, better with rest)

• Ocular symptoms like ptosis and diplopia

• Bulbar weakness (difficulty swallowing)

The Tensilon (edrophonium) test, a short-acting AChE inhibitor, temporarily increases ACh at the neuromuscular junction, improving strength — a hallmark of MG.

Why the Correct Option is Right 👍

 Myasthenia Gravis — ✅

• Fluctuating weakness

• Ptosis, diplopia

• Worsens with use

• Improves with edrophonium
  All classic MG features.

Why the Other Options Are Wrong ❌

 Lambert-Eaton Myasthenic Syndrome (LEMS) — ❌

• Strength improves with repeated use (opposite of MG)

• Involves presynaptic Ca²⁺ channels, not ACh receptors

• Poor response to edrophonium

 Botulism — ❌

• Caused by botulinum toxin preventing ACh release

• Symptoms include fixed dilated pupils and severe paralysis

• Does NOT improve with edrophonium

 Guillain-Barré Syndrome — ❌

• Ascending paralysis, not fatigability

• Autoimmune demyelination

• No ocular involvement early on

• Tensilon test has no role

 Muscular Dystrophy — ❌

• Progressive muscle wasting

• Onset typically in childhood

• Not associated with fatigability or edrophonium response