Neurology Practice Questions

Q: The most common cause of pontine hemorrhage is

Hypertension. Hypertension - **Chronic hypertension** leads to the weakening and rupture of small perforating arteries in the pons, making it the most common cause of **pontine hemorrhage** [1]. - The elevated pressure damages the **endothelium** and smooth muscle layers of these vessels, predisposing them to bleeding. *Diabetes* - While diabetes can cause microvascular complications, it is not considered the most common cause of **pontine hemorrhage**. - Its primary cerebral vascular complications include increased risk of **ischemic stroke** rather than hemorrhagic stroke in the pons. *Trauma* - **Traumatic brain injury** can cause various types of intracranial hemorrhage, but isolated **pontine hemorrhage** directly due to trauma is less common than that due to hypertension [1]. - Trauma typically results in contusions, subdural, or epidural hematomas, often in superficial brain regions. *Aneurysmal rupture* - **Aneurysmal rupture** is a common cause of subarachnoid hemorrhage, particularly from the Circle of Willis, but pontine hemorrhages are rarely caused by aneurysms within the pons itself [1]. - The vessels supplying the pons are typically small and perforating, not commonly forming dissecting or saccular aneurysms.

Q: Which of the following statements about decorticate posturing is false?

More dangerous than decerebrate lesion. ***More dangerous than decerebrate lesion*** - This statement is **false**. Decorticate posturing indicates damage **above the red nucleus**, which is a less severe brain injury compared to decerebrate posturing [1]. - **Decerebrate posturing** implies more caudal brainstem damage (below the red nucleus), often involving the pons or midbrain, indicating a more severe prognosis [1]. *Acute brain injuries* - **Decorticate posturing** is a common sign of **acute brain injuries**, especially those affecting the cerebral hemispheres or internal capsule [1]. - It arises from damage to pathways carrying motor information, leading to characteristic muscle responses [1]. *Subthalamic, corticothalamic, and frontal lobe lesions* - Lesions in these areas, particularly **above the red nucleus** and involving the **corticospinal tracts**, can lead to decorticate posturing [1]. - This type of posturing occurs due to the **disinhibition of the rubrospinal tract (which mediates upper limb flexion)** and the intact vestibulospinal and reticulospinal tracts (which mediate lower limb extension) [1]. *Flexion of arm & extension of lower limb* - Decorticate posturing is characterized by **flexion of the elbows and wrists** (arms adducted and internally rotated) and **extension, internal rotation, and plantar flexion of the legs** [1]. - This specific posture is often described as "mummy baby" or "bringing hands to the core."

Q: Migraine is due to

Cortical spreading depression. ***Cortical spreading depression*** - The current understanding is that **cortical spreading depression (CSD)** is the initiating event in migraine with aura, characterized by a wave of neuronal and glial depolarization that spreads across the cerebral cortex, leading to a temporary shutdown of neuronal activity [1]. - CSD is thought to activate the **trigeminal nerve**, subsequently causing the release of inflammatory neuropeptides and contributing to the pain phase [1]. *Dilatation of cranial blood vessels* - While **vasodilation of intracranial and extracranial blood vessels** does occur during the headache phase of migraine, it is now considered a *consequence* of the initial neurological events rather than the primary cause [1]. - This vasodilation contributes to the throbbing sensation of migraine pain but does not explain the aura or the initiation of the attack. *Constriction of cranial blood vessels* - **Vasoconstriction** was previously thought to be the cause of the migraine aura, but this theory has largely been disproven. - While some temporary constriction may precede CSD, it is not the primary mechanism behind the migraine attack. *Inflammation of the meninges* - While **neurogenic inflammation** of the meninges, involving the release of inflammatory mediators like **calcitonin gene-related peptide (CGRP)**, does play a role in sensitizing the trigeminal system and contributing to migraine pain, it is a downstream effect. - It is not the initial trigger for a migraine attack but rather part of the pain pathway activated by events like CSD.

Q: The most characteristic EEG finding in complex partial (psychomotor) seizures is:

Spikes over the temporal lobes. ***Spikes over the temporal lobes*** - **Complex partial seizures**, also known as **psychomotor seizures** or **temporal lobe seizures**, originate most commonly in the **temporal lobe**. - The characteristic EEG finding in these seizures is the presence of **sharp waves** or **spikes** specifically in the **temporal regions**, which can be unilateral or bilateral. *Diffuse Slowing* - **Diffuse slowing** on an EEG typically indicates **generalized brain dysfunction** or encephalopathy, which can be due to various causes like metabolic disturbances, drug effects, or widespread structural damage. - It is not a specific finding for focal seizures like complex partial seizures. *Generalized Spike and wave pattern* - A **generalized 3-Hz spike-and-wave pattern** is the hallmark EEG finding for **absence seizures** (a type of generalized seizure), not complex partial seizures. - This pattern is seen bilaterally and synchronously, reflecting a widespread cortical and thalamic network involvement. *Multifocal spikes* - **Multifocal spikes** indicate seizure activity originating from **multiple independent foci** in different brain regions. - While it points to epilepsy, it is not the most characteristic finding for a typical complex partial seizure, which usually arises from a single focus, most commonly in the temporal lobe.

Q: Which of the following drugs is approved for treatment of both relapsing-remitting AND primary progressive multiple sclerosis?

Ocrelizumab. ***Ocrelizumab*** - This **anti-CD20 monoclonal antibody** is uniquely approved for both **relapsing-remitting MS (RRMS)** and **primary progressive MS (PPMS)**. - It targets **CD20-expressing B cells**, providing comprehensive disease modification across different MS phenotypes. *Fingolimod* - This **sphingosine 1-phosphate receptor modulator** is approved only for **relapsing-remitting MS**, not primary progressive MS. - While effective for RRMS, it lacks the **dual indication** that makes Ocrelizumab the most comprehensive treatment option. *Omalizumab* - This **anti-IgE monoclonal antibody** is used for **severe allergic asthma** and **chronic idiopathic urticaria**. - It has **no role in multiple sclerosis treatment** and works through IgE-mediated allergic pathways unrelated to MS pathophysiology. *Natalizumab* - This **integrin receptor antagonist** is used for MS but is typically reserved as **second-line therapy** due to **PML risk**. - Unlike Ocrelizumab, it is **not approved for primary progressive MS** and requires careful monitoring for serious complications.

Q: Which of the following speech patterns is most indicative of Wernicke's aphasia?

Fluent but nonsensical speech. ***Fluent but nonsensical speech*** - Wernicke's aphasia is characterized by **fluent**, often grammatically correct, speech that is **devoid of meaning** and often includes **paraphasias** (word substitutions) and **neologisms** (made-up words). - Patients have significant **comprehension deficits**, making meaningful conversation difficult despite preserved speech fluency. - This is also known as **receptive aphasia** or **sensory aphasia**, caused by damage to Wernicke's area in the superior temporal gyrus. *Normal speech with comprehension* - This describes **healthy speech patterns**, where both production and understanding of language are intact. - It directly contradicts the definition of **aphasia**, which involves impairment in language abilities. *Non-fluent speech with intact comprehension* - This describes **Broca's aphasia** (expressive aphasia), where speech production is effortful and halting. - Unlike Wernicke's aphasia, patients with Broca's aphasia have **preserved comprehension** but struggle with speech output. - The key differentiator is that Wernicke's has **fluent speech with poor comprehension**, while Broca's has **non-fluent speech with good comprehension**. *Speech with meaningful content* - This indicates that the speaker can convey understandable and relevant information, which is precisely what is lacking in **Wernicke's aphasia**. - In Wernicke's aphasia, the content is typically **empty** or **circumlocutory**, making it difficult to extract any coherent meaning.

Q: In the context of seizure disorders, gustatory hallucinations are most commonly associated with which of the following?

Temporal lobe epilepsy. ***Temporal lobe epilepsy*** - Gustatory hallucinations, often described as **metallic or bitter tastes**, are a characteristic type of **sensory aura** in temporal lobe seizures - Seizures originating in the **temporal lobe**, particularly involving the **insula and opercular regions**, can affect areas involved in taste perception - These hallucinations are highly localizing signs suggesting **temporal lobe origin** of seizures - Note: In psychiatric contexts, gustatory hallucinations are more commonly associated with **schizophrenia and psychotic disorders** *Generalized tonic-clonic seizures* - These seizures involve **widespread bilateral electrical activity** in the brain - Typically present with loss of consciousness, body stiffening (tonic phase), and rhythmic jerking (clonic phase) - While an aura may precede them if they evolve from a focal seizure, **isolated gustatory hallucinations are not characteristic** of primary generalized seizures *Panic disorder* - Panic disorder involves sudden episodes of intense fear with physical symptoms like **palpitations, dyspnea, chest pain, and dizziness** - Does not primarily involve **sensory hallucinations** as a core diagnostic feature - Patients may report altered perceptions during panic attacks but not true gustatory hallucinations *Substance use disorder* - Certain substances can induce hallucinations, but these are more commonly **visual or auditory** - Hallucinogens may cause complex sensory distortions, but **gustatory hallucinations are not the predominant feature** - Withdrawal states typically produce visual hallucinations (e.g., alcohol withdrawal) rather than gustatory ones

Q: Paraneoplastic cerebellar ataxia in Hodgkin's disease is associated with an autoantibody.

anti-Tr. ***anti-Tr*** - The **anti-Tr (DNER)** antibody is specifically associated with **paraneoplastic cerebellar degeneration** in the context of **Hodgkin's lymphoma** [1]. - It targets the **delta/notch-like epidermal growth factor-related receptor (DNER)**, which is expressed in cerebellar Purkinje cells [1]. *anti-Yo antibodies* - **Anti-Yo (PCA-1)** antibodies are strongly associated with **paraneoplastic cerebellar degeneration** but are typically found in **gynecological cancers** (ovarian, breast) and small-cell lung cancer, not Hodgkin's. - They target the **Purkinje cell cytoplasm** and cause widespread neuronal loss. *anti-PQ antibodies* - **Anti-PQ (P/Q-type voltage-gated calcium channel)** antibodies are primarily associated with the Lambert-Eaton Myasthenic Syndrome (LEMS), a paraneoplastic syndrome causing **muscle weakness** [2]. - While LEMS can be paraneoplastic, it does not typically manifest as **cerebellar ataxia** [2]. *voltage-gated calcium channel antibodies* - While generically referring to antibodies against **voltage-gated calcium channels**, this term is most commonly linked to **Lambert-Eaton Myasthenic Syndrome (LEMS)** [2]. - LEMS typically causes **proximal muscle weakness** and autonomic dysfunction, not cerebellar ataxia [2].

Q: Which of the following is not a contraindication for the use of rtPA in stroke management?

Presence of coma. ***Presence of coma*** - While a severe neurological deficit, **coma itself is not an absolute contraindication** for rtPA if the stroke is acute ischemic and within the treatment window, and other contraindications are absent. - The decision to administer rtPA in comatose patients is complex and based on careful assessment of neurological impairment due to **ischemia**, not just a state of reduced consciousness. *BP >185/110 mm Hg* - **Elevated blood pressure** above 185/110 mmHg is a **major contraindication** for rtPA because it significantly increases the risk of **intracranial hemorrhage**. - Blood pressure must be **controlled below this threshold** before rtPA can be safely administered. *Heparin in the past 24 hrs* - Recent use of **anticoagulants**, especially heparin, within 24 hours, indicates a higher **risk of bleeding** if rtPA is given. - This significantly raises the potential for **hemorrhagic transformation** of the ischemic stroke. *Lesion occupying >1/3 of middle cerebral artery territory* - A **large ischemic lesion** (e.g., >1/3 of MCA territory) on initial imaging is a **contraindication** due to increased risk of **hemorrhagic conversion** and **edema** after reperfusion [1]. - Giving rtPA to such large lesions is associated with poorer outcomes and higher mortality [1].

Question 1

The most common cause of pontine hemorrhage is

Accepted Answer

Hypertension

Answer

Diabetes

Answer

Trauma

Answer

Aneurysmal rupture

Question 2

Which of the following statements about decorticate posturing is false?

Accepted Answer

More dangerous than decerebrate lesion

Answer

Flexion of arm & extension of lower limb

Answer

Acute brain injuries

Answer

Subthalamic, corticothalamic, and frontal lobe lesions

Question 3

Migraine is due to

Accepted Answer

Cortical spreading depression

Answer

Dilatation of cranial blood vessels

Answer

Constriction of cranial blood vessels

Answer

Inflammation of the meninges

Question 4

The most characteristic EEG finding in complex partial (psychomotor) seizures is:

Accepted Answer

Spikes over the temporal lobes

Answer

Diffuse Slowing

Answer

Generalized Spike and wave pattern

Answer

Multifocal spikes

Question 5

Which of the following drugs is approved for treatment of both relapsing-remitting AND primary progressive multiple sclerosis?

Accepted Answer

Ocrelizumab

Answer

Fingolimod

Answer

Omalizumab

Answer

Natalizumab

Question 6

Which of the following speech patterns is most indicative of Wernicke's aphasia?

Accepted Answer

Fluent but nonsensical speech

Answer

Normal speech with comprehension

Answer

Non-fluent speech with intact comprehension

Answer

Speech with meaningful content

Question 7

Which test is most useful in diagnosing a clinically occult lesion in multiple sclerosis?

Accepted Answer

MRI for detecting white matter lesions in multiple sclerosis

Answer

Evoked potentials for diagnosing clinically occult lesions in multiple sclerosis

Answer

CT scan for large hemispheral strokes

Answer

Evoked potentials for brainstem involvement in stroke

Question 8

In the context of seizure disorders, gustatory hallucinations are most commonly associated with which of the following?

Accepted Answer

Temporal lobe epilepsy

Answer

Generalized tonic-clonic seizures

Answer

Panic disorder

Answer

Substance use disorder

Question 9

Paraneoplastic cerebellar ataxia in Hodgkin's disease is associated with an autoantibody.

Accepted Answer

anti-Tr

Answer

anti-Yo antibodies

Answer

anti-PQ antibodies

Answer

voltage-gated calcium channel antibodies

Question 10

Which of the following is not a contraindication for the use of rtPA in stroke management?

Accepted Answer

Presence of coma

Answer

BP >185/110 mm Hg

Answer

Heparin in the past 24 hrs

Answer

Lesion occupying >1/3 of middle cerebral artery territory

Neurology — MCQs

Neurology — MCQs

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