NEET-PG 2015

1414 Questions — Page 107 of 142

Internal Medicine

8 questions

Q1061

What does a motor score of 4 on the Glasgow Coma Scale indicate?

Q1062

Increased ICP is shown by

Q1063

Most common site of hypertensive intraparenchymal hemorrhage in the brain?

Q1064

Which of the following sites is responsible for the amnestic defect in Wernicke's Korsakoff syndrome:

Q1065

Which of the following is the most common initial presenting feature of multiple sclerosis:

Q1066

What are the expected neurological manifestations in a patient with complete absence of the corpus callosum?

Q1067

Which of the following is the MOST characteristic feature of Eaton-Lambert syndrome?

Q1068

What is the first symptom of Parkinson's disease?

NEET-PG 2015 - Internal Medicine NEET-PG Practice Questions and MCQs

Question 1061: What does a motor score of 4 on the Glasgow Coma Scale indicate?

A. Decorticate posturing
B. Withdrawal or flexion to pain (Correct Answer)
C. Decerebrate posturing
D. Localizes to pain

Explanation: A motor score of 4 on the **Glasgow Coma Scale (GCS)** signifies that the patient **withdraws or flexes their limb** away from a painful stimulus. - This response indicates a degree of purposeful movement but is not considered localization to the pain. *Decerebrate posturing* - This represents a GCS motor score of **2**, characterized by **extension and internal rotation of the arms** and extension of the legs in response to pain [1]. - It suggests severe damage to the **brainstem**, specifically below the red nucleus [1]. *Decorticate posturing* - This corresponds to a GCS motor score of **3**, where the patient exhibits **flexion and adduction of the arms** with extension of the legs to painful stimuli [1]. - It often indicates damage to the **corticospinal tracts** above the red nucleus [1]. *Localizes to pain* - This is a GCS motor score of **5**, where the patient **moves their hand beyond the chin** attempting to remove the painful stimulus. - It indicates a higher level of conscious response and purposeful movement compared to withdrawal.

Question 1062: Increased ICP is shown by

A. Reduction in GCS (Correct Answer)
B. Pupil constriction (Miosis)
C. Systemic hypotension
D. Tachycardia

Explanation: ***Reduction in GCS*** - A **decrease in Glasgow Coma Scale (GCS)** score is a primary indicator of increased intracranial pressure (ICP) due to compromised brain function [1], [2]. - Increased ICP can lead to **cerebral ischemia** and neuronal damage, manifesting as altered consciousness and lower GCS scores [1]. *Pupil constriction (Miosis)* - **Miosis**, or pupil constriction, is typically associated with **pontine lesions** or **opioid use**, and rarely directly with increased ICP unless it specifically involves brainstem compression at the pontine level. - Increased ICP more commonly causes **pupil dilation (mydriasis)**, especially unilateral, due to compression of the oculomotor nerve (CN III) [1]. *Systemic hypotension* - **Systemic hypotension** is generally *not* a direct sign of increased ICP; rather, increased ICP often results in **systemic hypertension** as part of Cushing's triad. - Hypotension in the context of brain injury might indicate **spinal shock** or other systemic issues, but generally not directly elevated ICP. *Tachycardia* - **Tachycardia** is also *not* typically associated with increased ICP; instead, **bradycardia** (slow heart rate) is a hallmark sign, forming part of Cushing's triad. - Tachycardia might suggest **hypovolemia**, **pain**, or other systemic stressors, but not directly increased ICP.

Question 1063: Most common site of hypertensive intraparenchymal hemorrhage in the brain?

A. Putamen (Correct Answer)
B. Thalamus
C. Cerebellum
D. Pons

Explanation: ***Putamen*** - The **putamen** is the most frequent site for **hypertensive intraparenchymal hemorrhages** [1] due to the presence of numerous small, thin-walled arterioles (lenticulostriate arteries) that are highly susceptible to damage from chronic hypertension [1]. - Hemorrhages in this region often cause **contralateral hemiparesis**, **hemianesthesia**, and **gaze deviation** towards the side of the lesion due to involvement of nearby motor and sensory pathways [1]. *Thalamus* - While the **thalamus** is a common site for hypertensive hemorrhages, it is less common than the putamen [1], [2]. - Thalamic hemorrhages typically cause **contralateral sensory loss**, **oculomotor dysfunction**, and sometimes **aphasia** if the dominant hemisphere is affected. *Cerebellum* - **Cerebellar hemorrhages** are less frequent than those in the basal ganglia or thalamus [1]. - Symptoms usually include **ataxia**, **nystagmus**, vomiting, and potential brainstem compression if large. *Pons* - **Pontine hemorrhages** are among the most severe and are often rapidly fatal due to damage to vital brainstem structures [1], [2]. - They typically present with **coma**, **quadriparesis**, **pinpoint pupils**, and rapid progression to respiratory arrest.

Question 1064: Which of the following sites is responsible for the amnestic defect in Wernicke's Korsakoff syndrome:

A. Hippocampus
B. Mammillary body
C. Thalamus (Correct Answer)
D. Periventricular Grey matter

Explanation: ***Thalamus*** - Damage to the **medial dorsal nucleus of the thalamus** is a key pathological finding in Wernicke's Korsakoff syndrome, directly contributing to the severe **anterograde and retrograde amnesia** [1]. - The thalamus plays a crucial role in memory consolidation and retrieval, acting as a relay station for information processing between cortical and subcortical structures. *Mammillary body* - While **mammillary body damage** is characteristic of Wernicke-Korsakoff syndrome, it is primarily associated with the **acute Wernicke encephalopathy phase** and contributes to the overall amnesia through its connections with the thalamus and hippocampus, rather than being the sole site for the amnestic defect [1]. - The mammillary bodies are part of the **Papez circuit**, which is important for episodic memory, but their lesion alone doesn't fully explain the complete amnestic syndrome. *Hippocampus* - The **hippocampus** is critical for the formation of new memories, and its damage typically causes **anterograde amnesia**, as seen in conditions like temporal lobe epilepsy or anoxia. - While memory is affected, direct **hippocampal lesions are not the primary pathology** in Wernicke-Korsakoff syndrome; the memory impairment arises from damage to structures *connected* to the hippocampus, such as the thalamus and mammillary bodies. *Periventricular Grey matter* - The **periventricular grey matter** is involved in various autonomic functions and pain modulation, not directly in memory formation or retrieval. - While lesions in this area can occur in Wernicke-Korsakoff syndrome, they are not considered the primary cause of the **amnestic defect**.

Question 1065: Which of the following is the most common initial presenting feature of multiple sclerosis:

A. Optic Neuritis (Correct Answer)
B. Cerebellar Ataxia
C. Internuclear ophthalmoplegia
D. Diplopia

Explanation: ***Optic Neuritis*** - **Optic neuritis** is a very common initial symptom of multiple sclerosis, occurring in 20-25% of patients. - It presents with **unilateral vision loss** (often painful), blurred vision, and a central scotoma, reflecting inflammation and demyelination of the optic nerve [1]. *Cerebellar Ataxia* - While **cerebellar ataxia** (impaired coordination, balance, speech) can occur in MS, it is less common as an initial presenting symptom. - It often develops later in the disease course due to demyelination in the **cerebellum** or its connections [1]. *Internuclear ophthalmoplegia* - **Internuclear ophthalmoplegia (INO)** is a specific eye movement disorder common in MS but rarely the very first symptom [1]. - It results from a lesion in the **medial longitudinal fasciculus (MLF)**, causing impaired adduction of one eye during conjugate gaze with nystagmus in the abducting eye. *Diplopia* - **Diplopia** (double vision) can be an early symptom of MS, but it is less frequent as the very first presentation compared to optic neuritis [1]. - It typically arises from lesions affecting the **cranial nerves** controlling eye movements (III, IV, VI) or their brainstem nuclei.

Question 1066: What are the expected neurological manifestations in a patient with complete absence of the corpus callosum?

A. Mild cognitive impairment
B. Seizures
C. No significant neurological deficits
D. Severe developmental delays (Correct Answer)

Explanation: ***Severe developmental delays*** - Complete agenesis of the corpus callosum often results in **significant neurological impairments** due to the disruption of interhemispheric communication essential for coordinated brain function. - This typically manifests as **intellectual disability**, **developmental delays** in motor and speech skills, and difficulties with complex cognitive tasks. *Mild cognitive impairment* - While some individuals with partial agenesis or isolated cases might present with mild cognitive issues, **complete absence** usually leads to more profound deficits. - Mild impairment would not fully capture the extensive neurological challenges associated with a total lack of such a critical brain structure. *Seizures* - Seizures can occur in patients with corpus callosum agenesis, but they are not the **most encompassing** or universally expected neurological manifestation. - Seizures are often part of a broader syndrome of developmental abnormalities rather than the primary expected outcome of the agenesis itself. *No significant neurological deficits* - The corpus callosum is vital for **integrating information** between the cerebral hemispheres, affecting a wide range of sensory, motor, and cognitive functions. - Therefore, its complete absence almost invariably leads to notable neurological deficits, making a lack of significant issues highly unlikely.

Question 1067: Which of the following is the MOST characteristic feature of Eaton-Lambert syndrome?

A. Repeated electrical stimulation enhances muscle power in it. (Correct Answer)
B. Neostigmine is not effective for this syndrome.
C. It is commonly associated with small cell lung cancer.
D. It can affect the ocular muscles.

Explanation: ***Repeated electrical stimulation enhances muscle power in it.*** - A hallmark feature of **Lambert-Eaton Myasthenic Syndrome (LEMS)** is the **potentiation of muscle strength** with repeated or high-frequency nerve stimulation [2]. - This is due to the disease pathophysiology where repeated stimulation allows the accumulation of **intracellular calcium**, leading to increased acetylcholine release at the neuromuscular junction. *Neostigmine is not effective for this syndrome.* - While it's largely true that **acetylcholinesterase inhibitors** like neostigmine are less effective in LEMS compared to myasthenia gravis, they can still provide some minor symptomatic relief [1]. - Therefore, stating it's *not effective* might be an oversimplification, and it's not the *most characteristic* feature. *It is commonly associated with small cell lung cancer.* - Although LEMS is frequently a **paraneoplastic syndrome** linked to **small cell lung cancer (SCLC)**, this association is a cause/etiology, not a direct characteristic feature of the neuromuscular dysfunction itself [1], [2]. - Approximately 50-60% of LEMS cases are paraneoplastic, with SCLC being the most common underlying malignancy [2]. *It can affect the ocular muscles.* - **Ocular muscle involvement** (e.g., ptosis, diplopia) is a prominent and often initial symptom in **myasthenia gravis** [2]. - In LEMS, ocular muscle weakness is **much less common** and typically mild, if present, distinguishing it from myasthenia gravis.

Question 1068: What is the first symptom of Parkinson's disease?

A. Rigidity
B. Tremors (Correct Answer)
C. Postural instability
D. Bradykinesia

Explanation: ***Tremors*** - A resting **tremor**, often starting unilaterally in a hand or foot, is frequently the **initial motor symptom** of Parkinson's disease [1]. - This tremor is typically **slow**, rhythmic, and may involve a "pill-rolling" motion of the fingers [1]. *Postural instability* - **Postural instability** tends to be a later symptom, emerging as the disease progresses and affecting balance and gait [2]. - It is not usually the **presenting complaint** in the early stages of Parkinson's disease [2]. *Rigidity* - **Rigidity**, characterized by increased muscle tone and resistance to passive movement, often develops after tremors or bradykinesia [1]. - It can manifest as **cogwheel** or **lead-pipe rigidity** and contributes to the stooped posture and reduced arm swing observed in Parkinson's patients [1]. *Bradykinesia* - **Bradykinesia** (slowness of movement) is a core motor symptom, often described as difficulty initiating or continuing movements [1]. - While present early, **tremors** are often the first symptom noticed by the patient or their family, making bradykinesia a close second in sequence [1].

Pathology

1 questions

Q1061

Plaques jaunes are seen in which condition?

Pharmacology

1 questions

Q1061

Which of the following metal ions is associated with secondary Parkinsonisms?