Internal Medicine
6 questionsWhich of the following sites is responsible for the amnestic defect in Wernicke's Korsakoff syndrome:
Which of the following is the most common initial presenting feature of multiple sclerosis:
What are the expected neurological manifestations in a patient with complete absence of the corpus callosum?
Which of the following is the MOST characteristic feature of Eaton-Lambert syndrome?
What is the first symptom of Parkinson's disease?
Isaac syndrome is characterized by -
NEET-PG 2015 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 971: 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 972: 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 973: 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 974: 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 975: 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].
Question 976: Isaac syndrome is characterized by -
- A. Peripheral nerve hyperexcitability (Correct Answer)
- B. Opsoclonus syndrome
- C. Encephalitis
- D. Limbic encephalitis syndrome
Explanation: Isaac syndrome is characterized by - ***Peripheral nerve hyperexcitability*** - Isaac syndrome, also known as **neuromyotonia** or **Isaacs' syndrome**, is fundamentally characterized by symptoms arising from **peripheral nerve hyperexcitability**. [1] - This hyperexcitability leads to continuous muscle fiber activity even at rest, manifesting as **muscle stiffness, cramps, myokymia, and fasciculations**. *Opsoclonus syndrome* - This syndrome is characterized by **rapid, irregular, chaotic eye movements** (**opsoclonus**) and often associated with **myoclonus (rapid muscle jerks)** and **ataxia (impaired coordination)**. - While it can be paraneoplastic, it involves the **central nervous system**, specifically the brainstem and cerebellum, not primarily peripheral nerve hyperexcitability. *Encephalitis* - **Encephalitis** is an inflammation of the **brain parenchyma**, typically caused by viral infections. - Its clinical presentation includes fever, headache, altered mental status, and seizures, which are distinct from the primary neuromuscular symptoms of Isaac syndrome. *Limbic encephalitis syndrome* - **Limbic encephalitis** is a form of encephalitis specifically affecting the **limbic system** of the brain, leading to symptoms like **memory loss, seizures, and psychiatric disturbances**. - This condition involves **central nervous system inflammation** and does not directly cause the peripheral nerve hyperexcitability seen in Isaac syndrome.
Pathology
1 questionsPlaques jaunes are seen in which condition?
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 971: Plaques jaunes are seen in which condition?
- A. Syphilis
- B. Head injury
- C. Endocarditis
- D. Atherosclerosis (Correct Answer)
Explanation: ***Head injury*** - **Plaques jaunes**, or yellow plaques, are primarily associated with brain injuries, particularly in areas of **contusion** or **hemorrhage** [1]. - These plaques may represent **lipid-laden macrophages** and indicate areas of *necrosis* and inflammation in the brain [1]. *Endocarditis* - Endocarditis is characterized by **vegetations** on heart valves rather than plaques in the brain. - Symptoms typically include **fever**, **murmurs**, and **embolization**, which do not involve yellow plaques. *Syphilis* - Syphilis may cause *gummatous lesions* but is not associated with yellow plaques in the brain. - Typical findings include **rash** and **ulcerative lesions**, particularly during the secondary stage. *Atherosclerosis* - Atherosclerosis involves **plaque formation** in blood vessels but these are not the same as **plaques jaunes** in neurological contexts. - It is characterized by **cholesterol** deposits and plaque rupture leading to cardiovascular events, not plaques seen in head injuries. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1262-1264.
Pharmacology
2 questionsWhich of the following metal ions is associated with secondary Parkinsonisms?
What is the drug of choice (DOC) for the treatment of subacute sclerosing panencephalitis (SSPE)?
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 971: Which of the following metal ions is associated with secondary Parkinsonisms?
- A. Magnesium (Mg)
- B. Selenium (Se)
- C. Manganese (Mn) (Correct Answer)
- D. Molybdenum (Mo)
Explanation: ***Manganese (Mn)*** - Chronic exposure to high levels of **manganese** can lead to **manganism**, a neurological disorder characterized by **Parkinsonian-like symptoms**, including bradykinesia, rigidity, and gait disturbances [1]. - This is due to manganese accumulation in the **basal ganglia**, particularly the **globus pallidus**, affecting dopaminergic pathways. *Magnesium (Mg)* - **Magnesium** is an essential mineral vital for numerous bodily functions, including nerve and muscle function. - While imbalances can cause neurological issues (e.g., tremors with hypomagnesemia), it is not directly associated with **secondary parkinsonism**. *Selenium (Se)* - **Selenium** is a trace element with antioxidant properties, important for thyroid hormone metabolism and immune function. - Both deficiency and toxicity can cause various health problems, but it is not known to cause **secondary parkinsonism**. *Molybdenum (Mo)* - **Molybdenum** is an essential trace element that functions as a cofactor for several enzymes. - No known association exists between molybdenum exposure, deficiency, or toxicity and the development of **secondary parkinsonism**.
Question 972: What is the drug of choice (DOC) for the treatment of subacute sclerosing panencephalitis (SSPE)?
- A. Abacavir
- B. Inosine pranobex (Correct Answer)
- C. Glatiramer
- D. Interferon
Explanation: ***Inosine pranobex*** - **Inosine pranobex (Isoprinosine)** is considered the **oral drug of choice** for treating **subacute sclerosing panencephalitis (SSPE)**, particularly in the early stages, as it has shown success in delaying disease progression. - This drug works by **modulating the immune system** and enhancing T-cell function, which helps control the persistent measles virus infection in the CNS. - **Note:** Best outcomes are achieved when inosine pranobex is combined with **intrathecal/intraventricular interferon-alpha**, but as a single oral agent, inosine pranobex is the primary choice. *Abacavir* - **Abacavir** is an **antiretroviral drug (NRTI)** used in the treatment of **HIV infection**. - It inhibits reverse transcriptase and has **no role** in treating measles virus-induced SSPE. *Glatiramer* - **Glatiramer acetate** is an **immunomodulatory drug** used in **multiple sclerosis (MS)**. - It works by mimicking **myelin basic protein** to reduce immune attacks on myelin, but is **not effective** against viral infections like SSPE. *Interferon* - **Interferon-alpha** (particularly **intrathecal/intraventricular** administration) has been used in **SSPE** as **combination therapy** with inosine pranobex, showing improved outcomes. - However, when given systemically alone, it has **significant side effects** and **variable efficacy**. - As a single answer option without specifying the route, **inosine pranobex** is preferred as the primary oral DOC.
Psychiatry
1 questionsIn Alzheimer's disease (AD), which of the following is NOT commonly seen in early stages?
NEET-PG 2015 - Psychiatry NEET-PG Practice Questions and MCQs
Question 971: In Alzheimer's disease (AD), which of the following is NOT commonly seen in early stages?
- A. Apraxia
- B. Aphasia
- C. Agnosia
- D. Acalculia (Correct Answer)
Explanation: ***Acalculia*** - **Acalculia**, the inability to perform mathematical calculations, is generally **not an early feature** of Alzheimer's disease. - It typically emerges in **middle-to-late stages** as parietal lobe involvement progresses. - Early AD primarily affects **episodic memory, orientation, and mild language difficulties** before significantly impairing complex cognitive tasks like calculation. *Aphasia* - **Mild anomia** (word-finding difficulty) and naming problems are **common early symptoms** of Alzheimer's disease. - Patients often struggle with spontaneous speech and may use circumlocutions to compensate. - This reflects early involvement of temporal-parietal language areas. *Agnosia* - **Agnosia** (inability to recognize objects, faces, or sounds despite intact sensory function) typically appears in **middle-to-late stages**, not early AD. - Early AD is characterized by memory loss and mild language problems, with agnosia developing later as cortical atrophy progresses. - However, among the later features listed, aphasia is clearly the earliest. *Apraxia* - **Apraxia** (inability to perform learned motor tasks despite intact motor function) is a **middle-stage feature**, not an early manifestation. - Early AD patients retain the ability to perform routine motor tasks; apraxia develops as the disease progresses and involves premotor and parietal cortices. - Like agnosia, this is not an early feature.