Clinical Correlations in Neuroanatomy — MCQs
Not seen in case of hemorrhage in MCA territory is:
Superior temporal gyrus lesion leads to?
Wallenberg syndrome involves which artery?
Ptosis results from trauma to which nerve?
All of the following are true about Brown-Sequard syndrome, except which of the following?
Regarding brown sequard syndrome following are true statements except
A 62-year-old patient presents with left-sided arm and leg weakness, right-sided facial paralysis with lateral rectus gaze palsy, and nystagmus. Based on the clinical presentation, which of the following syndromes is most consistent with these symptoms?
A patient presents with a unilateral throbbing headache, photophobia, and excessive lacrimation. He also complains of hemifacial pain on the clenching of teeth. On examination, pupillary reaction, light reflex, and accommodation reflex are normal. Which of the following marked nerves is most likely involved in the above scenario?
What is the primary function of the superior cervical ganglion?
Which is correct about the image shown below?
Clinical Correlations in Neuroanatomy Indian Medical PG Practice Questions and MCQs
Question 1: Not seen in case of hemorrhage in MCA territory is:
- A. Contralateral hemiplegia
- B. Aphasia
- C. Urinary incontinence (Correct Answer)
- D. Dysarthria
Explanation: ***Urinary incontinence*** - Urinary incontinence is typically associated with **anterior cerebral artery (ACA)** territory lesions, which affect the **paracentral lobule** responsible for bladder control. - MCA territory hemorrhage primarily impacts motor, sensory, speech, and attentional functions, not direct bladder control. *Contralateral hemiplegia* - Hemorrhage in the MCA territory commonly affects the **motor cortex** and its descending tracts, leading to **weakness or paralysis** on the opposite side of the body [1]. - This is a very common and expected symptom in MCA strokes. *Aphasia* - If the dominant hemisphere (usually left) is affected,MCA territory hemorrhage often involves **Broca's and Wernicke's areas**, leading to various forms of **aphasia** (expressive or receptive speech difficulties) [1]. - This is a hallmark symptom of dominant MCA strokes. *Dysarthria* - Dysarthria, or difficulty with articulation of speech, can result from MCA territory hemorrhage affecting the motor pathways that control the **muscles of speech** [1]. - It often co-occurs with hemiplegia and other motor deficits.
Question 2: Superior temporal gyrus lesion leads to?
- A. Anomic aphasia
- B. Broca's aphasia
- C. Wernicke's aphasia (Correct Answer)
- D. Non-fluent aphasia
Explanation: ***Wernicke's aphasia*** - A lesion in the **superior temporal gyrus** (Wernicke's area) leads to Wernicke's aphasia, characterized by impaired **comprehension of language** [1]. - Patients with Wernicke's aphasia exhibit **fluent but meaningless speech** (word salad) and are often unaware of their deficits [1]. *Anomic aphasia* - Characterized by difficulty finding words, particularly nouns and verbs, and is often associated with lesions in the **angular gyrus** or **temporal lobe** [1]. - Speech remains fluent and grammatically correct, but it is marked by frequent pauses and circumlocutions as the individual struggles to retrieve specific words. *Broca's aphasia* - Results from damage to **Broca's area** in the posterior inferior frontal gyrus, causing **non-fluent speech** and difficulty with speech production [1]. - While comprehension is relatively preserved, patients struggle to form complete sentences and may exhibit agrammatism. *Non-fluent aphasia* - A broad category of aphasias, including Broca's aphasia, where speech production is notably impaired, and the output is effortful and characterized by **agrammatism** and **short, telegraphic sentences**. - **Wernicke's aphasia** is typically considered a **fluent aphasia**, as speech production itself is not interrupted, though its content is often incomprehensible [1].
Question 3: Wallenberg syndrome involves which artery?
- A. Subclavian artery
- B. Posterior cerebral artery
- C. Posterior inferior cerebellar artery (Correct Answer)
- D. Anterior inferior cerebellar artery
Explanation: ***Posterior inferior cerebellar artery*** - **Wallenberg syndrome**, also known as **lateral medullary syndrome**, is most commonly caused by an infarction in the territory supplied by the **posterior inferior cerebellar artery (PICA)**. - The PICA supplies the **lateral medulla**, which contains several crucial nuclei and tracts, including the nucleus ambiguus, trigeminal nucleus, vestibular nuclei, and spinothalamic tract, leading to the characteristic clinical presentation of Wallenberg syndrome. *Subclavian artery* - The **subclavian artery** is a large artery in the upper thorax that supplies blood to the upper limbs, head, and neck. - While it can be involved in conditions like **subclavian steal syndrome**, it does not directly supply the lateral medulla responsible for Wallenberg syndrome. *Posterior cerebral artery* - The **posterior cerebral artery** primarily supplies the occipital lobe, temporal lobe, and parts of the thalamus and midbrain. - Infarction in the PCA territory typically leads to symptoms like **hemianopia**, visual field defects, and memory deficits, not the constellation of symptoms seen in Wallenberg syndrome. *Anterior inferior cerebellar artery* - The **anterior inferior cerebellar artery (AICA)** supplies the anterior and lateral parts of the cerebellum and the pontomedullary junction, leading to **lateral pontine syndrome** when infarcted. - Symptoms of AICA infarction include ipsilateral facial paralysis, hearing loss, and cerebellar ataxia, which are distinct from Wallenberg syndrome.
Question 4: Ptosis results from trauma to which nerve?
- A. VII
- B. VIII
- C. VI
- D. III (Correct Answer)
Explanation: III - **Ptosis**, or drooping of the eyelid, occurs due to paralysis of the **levator palpebrae superioris muscle**, which is innervated by the **oculomotor nerve (III)**. [1] - Damage to the oculomotor nerve can also lead to other symptoms like **diplopia**, **strabismus**, and a **dilated pupil**. *VII* - The **facial nerve (VII)** primarily controls muscles of facial expression, including the **orbicularis oculi**, which closes the eye. - Damage to the facial nerve results in difficulty closing the eye, not drooping of the upper eyelid. *VIII* - The **vestibulocochlear nerve (VIII)** is responsible for **hearing** and **balance**. - Trauma to this nerve would cause symptoms like **hearing loss**, **tinnitus**, or **vertigo**, with no direct impact on eyelid function. *VI* - The **abducens nerve (VI)** innervates the **lateral rectus muscle**, which abducts the eye. [2] - Injury to the abducens nerve causes the eye to turn inward (**esotropia**) and results in **diplopia**, but not ptosis.
Question 5: All of the following are true about Brown-Sequard syndrome, except which of the following?
- A. Ipsilateral Pyramidal Tract Features
- B. Contralateral Spinothalamic Tract Features
- C. Ipsilateral Plantar Extensor
- D. Contralateral Posterior Column Features (Correct Answer)
Explanation: ***Contralateral Posterior Column Features*** - This statement is incorrect because **posterior column** (dorsal column-medial lemniscus pathway) involvement in Brown-Séquard syndrome would manifest as **ipsilateral** loss of proprioception, vibration, and fine touch, as these fibers decussate in the medulla, not the spinal cord [1]. - Therefore, the hallmark of Brown-Séquard syndrome concerning posterior column deficits is **ipsilateral** to the lesion, not contralateral [1]. *Ipsilateral Pyramidal Tract Features* - The **pyramidal tract** (corticospinal tract) controls voluntary motor function, and its fibers decussate in the medulla [1]. - In Brown-Séquard syndrome, damage to this tract will result in **ipsilateral** motor weakness or paralysis below the level of the lesion [1]. *Contralateral Spinothalamic Tract Features* - The **spinothalamic tract** carries pain and temperature sensations, and its fibers decussate within one or two spinal cord segments of their entry [1]. - Therefore, a lesion on one side of the spinal cord will cause a loss of pain and temperature sensation on the **contralateral** side, typically one to two dermatomes below the lesion [1]. *Ipsilateral Plantar Extensor* - This refers to a **Babinski sign**, which is an abnormal reflex indicating upper motor neuron damage. - Given that the **pyramidal tract** is involved **ipsilaterally**, an ipsilateral plantar extensor response (upward movement of the big toe and fanning of the other toes) is expected below the level of the lesion.
Question 6: Regarding brown sequard syndrome following are true statements except
- A. Ipsilateral loss of pain and temperature below the level of lesion (Correct Answer)
- B. Ipsilateral spastic paralysis below the lesion
- C. Ipsilateral loss of conscious proprioception, vibration sensation at the level and below the level of lesion.
- D. Ipsilateral flaccid paralysis at the level of lesion
Explanation: ***Ipsilateral loss of pain and temperature below the level of lesion*** - In Brown-Séquard syndrome, the **spinothalamic tract** decussates at the spinal cord level. Therefore, a lesion on one side of the spinal cord will cause **contralateral loss of pain and temperature** below the level of the lesion [1], [2]. - An ipsilateral loss of pain and temperature below the lesion would imply an unusual or additional injury mechanism, making this statement incorrect in the context of a classic Brown-Séquard presentation. *Ipsilateral spastic paralysis below the lesion* - The **corticospinal tract**, responsible for voluntary motor control, descends ipsilaterally before decussating in the medulla. - A lesion in the spinal cord thus causes **ipsilateral motor weakness or paralysis** below the level of the lesion, often spastic due to upper motor neuron involvement [1]. *Ipsilateral loss of conscious proprioception, vibration sensation at the level and below the level of lesion.* - The **dorsal columns**, which carry conscious proprioception and vibration sensation, ascend ipsilaterally in the spinal cord [2]. - Therefore, a hemi-section of the cord will result in **ipsilateral loss** of these sensations at and below the lesion [1]. *Ipsilateral flaccid paralysis at the level of lesion* - At the level of the lesion, the **lower motor neurons (LMNs)** in the anterior horn are directly affected [3]. - This leads to **flaccid paralysis** and hyporeflexia in the muscles innervated by the damaged segment [3].
Question 7: A 62-year-old patient presents with left-sided arm and leg weakness, right-sided facial paralysis with lateral rectus gaze palsy, and nystagmus. Based on the clinical presentation, which of the following syndromes is most consistent with these symptoms?
- A. Foville syndrome (Correct Answer)
- B. Benedict's syndrome
- C. Millard-Gubler syndrome
- D. Wallenberg syndrome
Explanation: ***Foville syndrome*** - This syndrome is characterized by a **pontine lesion** affecting the **abducens nucleus (cranial nerve VI)**, leading to ipsilateral gaze palsy, and the **facial nucleus (cranial nerve VII)**, causing ipsilateral facial weakness. [1] - The **crossed hemiparesis (left-sided arm and leg weakness)** results from involvement of the corticospinal tracts, and **nystagmus** can occur due to vestibular nucleus involvement, consistent with the patient's presentation. [1] *Benedict's syndrome* - This is a midbrain syndrome involving the **red nucleus** and **oculomotor nerve (cranial nerve III)**, causing ipsilateral oculomotor palsy and contralateral cerebellar ataxia. - It does not explain the patient's **facial weakness** or **abducens palsy**. *Millard-Gubler syndrome* - This pontine syndrome involves the **abducens nerve (cranial nerve VI)** and **facial nerve (cranial nerve VII)** in the pontine base, leading to ipsilateral gaze palsy and ipsilateral facial paralysis. - However, the hemiparesis in Millard-Gubler syndrome is typically **contralateral** to the lesion, but the facial paralysis and gaze palsy are usually due to direct nerve involvement rather than nuclear involvement, and **nystagmus** is not a characteristic feature. *Wallenberg syndrome* - This syndrome, also known as **lateral medullary syndrome**, is caused by a lesion in the **dorsolateral medulla** and presents with a constellation of symptoms including **ipsilateral ataxia**, **Horner's syndrome**, **high-pitched dysphagia**, and **contralateral loss of pain and temperature sensation**. [1] - It does not typically involve **facial weakness**, **abducens palsy**, or **hemiparesis** in the manner described.
Question 8: A patient presents with a unilateral throbbing headache, photophobia, and excessive lacrimation. He also complains of hemifacial pain on the clenching of teeth. On examination, pupillary reaction, light reflex, and accommodation reflex are normal. Which of the following marked nerves is most likely involved in the above scenario?
- A. Hypoglossal nerve
- B. Oculomotor nerve
- C. Trigeminal nerve (Correct Answer)
- D. Facial nerve
Explanation: ***Trigeminal nerve*** - The patient's symptoms of **unilateral throbbing headache**, **photophobia**, **excessive lacrimation**, and **hemifacial pain exacerbated by clenching teeth** are characteristic of trigeminal autonomic cephalalgias, such as **cluster headache** or **paroxysmal hemicrania**. These conditions involve the trigeminal nerve and its parasympathetic connections. - The image indicates **cranial nerve V** (trigeminal nerve) as structure 2, which has sensory innervation to the face and motor innervation to the muscles of mastication. **Hemifacial pain on clenching teeth** directly implicates the trigeminal nerve. *Oculomotor nerve* - The oculomotor nerve (cranial nerve III) primarily controls most **eye movements** and **pupil constriction**. - While headaches can sometimes affect pupil size (e.g., Horner's syndrome in cluster headache may involve sympathetic fibers that travel with cranial nerves), the core symptoms of facial pain on teeth clenching are not directly related to oculomotor nerve function. The normal pupillary and light reflexes also indicate its intact function. *Hypoglossal nerve* - The hypoglossal nerve (cranial nerve XII) is responsible for **tongue movement**. - Symptoms like headache, facial pain, photophobia, or lacrimation are not associated with hypoglossal nerve dysfunction. *Facial nerve* - The facial nerve (cranial nerve VII) controls **facial expressions**, **taste from the anterior two-thirds of the tongue**, and **lacrimation/salivation**. - While it contributes to lacrimation, the primary symptoms of unilateral throbbing headache and hemifacial pain, particularly exacerbated by teeth clenching, are not characteristic of facial nerve involvement.
Question 9: What is the primary function of the superior cervical ganglion?
- A. Is the largest cervical ganglion
- B. Supplies sympathetic fibers to the dilator pupillae muscle (Correct Answer)
- C. Deep petrosal nerve of pterygopalatine ganglion is derived from plexus around internal carotid artery
- D. Left superior cervical cardiac branch goes to deep cardiac plexus
Explanation: Supplies sympathetic fibers to the dilator pupillae muscle - The superior cervical ganglion is the primary source of postganglionic sympathetic fibers to the head and neck. - One of its key functions is providing sympathetic innervation to the dilator pupillae muscle [1] via the long ciliary nerves, causing mydriasis (pupil dilation) [2]. - This represents a clear physiological function of the ganglion in autonomic control of the eye. Is the largest cervical ganglion - While the superior cervical ganglion is indeed the largest of the three cervical sympathetic ganglia, this is an anatomical characteristic, not a function. - Size is a structural feature, not a physiological role. Left superior cervical cardiac branch goes to deep cardiac plexus - The superior cervical ganglion does contribute cardiac branches to the cardiac plexus for sympathetic innervation of the heart. - However, this describes an anatomical pathway rather than the primary function itself, and specifying "left" and "deep cardiac plexus" makes it overly specific rather than addressing overall function. Deep petrosal nerve of pterygopalatine ganglion is derived from plexus around internal carotid artery - The superior cervical ganglion does send postganglionic fibers forming a plexus around the internal carotid artery, which contributes to the deep petrosal nerve. - However, this is an anatomical derivation/pathway, not a functional description of what the ganglion does physiologically.
Question 10: Which is correct about the image shown below?
- A. A = Choroidal fissure, B= Body of fornix
- B. A = Internal capsule, B= Body of fornix
- C. A = Insula, B= Body of fornix
- D. A = Septum pellucidum, B= Body of fornix (Correct Answer)
Explanation: ***A = Septum pellucidum, B= Body of fornix*** - The image displays a coronal section of the brain. **A** points to the **septum pellucidum**, which is a thin, triangular membrane that separates the anterior horns of the lateral ventricles and extends from the corpus callosum to the fornix. - **B** points to the **body of the fornix**, a C-shaped bundle of nerve fibers in the brain that acts as the major output tract of the hippocampus. *A = Choroidal fissure, B= Body of fornix* - The **choroidal fissure** is the gap between the fornix and the thalamus, where the choroid plexus is located; it is not indicated by A. - While B is correctly identified as the body of the fornix, A is clearly a septal structure. *A = Internal capsule, B= Body of fornix* - The **internal capsule** is a white matter structure located deep within the brain, medial to the lentiform nucleus and lateral to the caudate nucleus and thalamus; it is not A. - The structure indicated by A is a thin membrane separating the lateral ventricles, not the dense white matter of the internal capsule. *A = Insula, B= Body of fornix* - The **insula** is a portion of the cerebral cortex folded deep within the lateral sulcus, which separates the frontal and parietal lobes from the temporal lobe; it is not indicated by A. - A is a midline structure, whereas the insula is a lateral structure deep in the cerebrum.
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