Neurology Practice Questions

Q: A 60-year-old man has resting tremor, pill-rolling movements, rigidity, and bradykinesia. Which of the following is most likely to be decreased in this man?

Dopamine neurons in the substantia nigra. ***Dopamine neurons in the substantia nigra*** - The symptoms described—**resting tremor**, **pill-rolling movements**, **rigidity**, and **bradykinesia**—are classic signs of **Parkinson's disease** [5]. - Parkinson's disease is pathologically characterized by the degeneration of **dopamine-producing (dopaminergic) neurons** in the **substantia nigra pars compacta**, leading to decreased dopamine levels in the **striatum** [1]. *GABA neurons in the caudate nucleus and putamen* - **GABAergic neurons** in the **caudate nucleus and putamen** are primarily affected in conditions like **Huntington's disease**, where their degeneration leads to increased involuntary movements (chorea) [4]. - While there can be secondary changes in these neurons in Parkinson's, the primary deficit is not in GABA but in dopamine. *Serotonin neurons in the raphe nuclei* - **Serotonin neurons** in the **raphe nuclei** are involved in mood regulation, sleep, and appetite, and their dysfunction is primarily linked to conditions like **depression**, anxiety, and certain sleep disorders [3]. - While some serotonergic involvement can occur in Parkinson's, it is not the primary neurological deficit explaining the motor symptoms. *Acetylcholine neurons in the forebrain* - **Acetylcholine neurons** in the **nucleus basalis of Meynert** (part of the forebrain) are primarily implicated in **Alzheimer's disease**, where their degeneration contributes to cognitive decline [2]. - While some cholinergic deficits may be present in advanced Parkinson's, they are not the hallmark pathology or the initial cause of the characteristic motor symptoms.

Q: A 79-year-old woman is brought to the clinic for assessment of frequent falls. There is no loss of consciousness associated with the falls, and she reports no postural change or symptoms prior to the falls. She also describes difficulty in "getting going" when she starts walking and notices that her balance is "not right." Her gait is slow and shuffling on inspection. Which of the following is the most likely finding in a patient with Parkinson disease?

akinesia. ***Akinesia*** - The patient's symptoms of difficulty "getting going" and slow, shuffling gait are classic descriptions of **akinesia** or **bradykinesia**, a core motor symptom of Parkinson disease [1]. - **Akinesia** refers to the absence or loss of the power of voluntary movement, often manifesting as freezing of gait or difficulty initiating movements [1]. *Muscle atrophy* - This is not a typical feature of Parkinson disease; instead, patients may experience **rigidity** and **spasticity**, but not significant muscle wasting [1]. - Muscle atrophy is more characteristic of conditions like motor neuron disease or disuse. *Fine hand tremor with movement* - Parkinson disease typically presents with a **resting tremor** which improves with voluntary movement, rather than a tremor that occurs with movement (**action tremor**) [1]. - An action tremor is more typical of **essential tremor** [1]. *Pupillary constriction* - This is not a characteristic feature of Parkinson disease. - Pupillary changes are generally not a primary diagnostic criterion for Parkinson disease.

Q: Inability to abduct left eye with LMN fascial palsy on same side. The lesion is in

Left pons. ***Left pons*** - A lesion in the **left pons** can affect both the **left abducens nucleus** (leading to inability to abduct the left eye) and the **left facial nucleus or nerve fibers** (causing left lower motor neuron facial palsy). [2] - This specific combination of ipsilateral (same-sided) symptoms is characteristic of a brainstem lesion, particularly within the pons where these cranial nerve nuclei are in close proximity. [1] *Cerebellar lesions* - **Cerebellar lesions** primarily cause symptoms like **ataxia**, dysmetria, and nystagmia, but typically do not cause isolated cranial nerve palsies of the abducens and facial nerves. [1] - While coordinating movements, the cerebellum does not house the nuclei for direct eye abduction or facial muscle control. *CP angle tumor* - A **cerebellopontine (CP) angle tumor** can affect cranial nerves VI and VII, but it typically presents with other symptoms like **vestibulocochlear nerve (VIII) dysfunction (hearing loss, vertigo)** early on due to its anatomical location. - While it can eventually compress the abducens and facial nerves, the combination of **isolated abducens and facial palsy** without VIII nerve involvement points more directly to an intraparenchymal pontine lesion. *Right pons* - A lesion in the **right pons** would cause **right-sided inability to abduct the eye** and **right-sided LMN facial palsy**, not left-sided as described in the case. - Brainstem lesions typically produce ipsilateral cranial nerve deficits due to the close proximity of the nuclei and fascicles before decussation of some pathways.

Q: A 32-year-old woman presents to you for evaluation of headache. The headaches began at age 18, were initially unilateral and worse around the time of her menses. Initially the use of triptans two or three times a month would provide complete relief. Over the past several years, however, the headaches have become more frequent and severe. Triptans provide only partial relief; the patient requires a combination of acetaminophen, caffeine, and butalbital to achieve some improvement. Prophylactic medications including beta-blockers, tricyclics, and topiramate have been unsuccessful in preventing the headaches, and she has been to the emergency room three times over the past 2 weeks for a "pain shot." The general physical examination is unremarkable. Her funduscopic examination shows no evidence of papilledema, and a careful neurological examination is likewise normal. What is the most likely explanation for her headache syndrome?

Medication overuse headache. The patient's history of increasing headache frequency and severity, decreased response to triptans, and frequent use of combination analgesics (acetaminophen, caffeine, butalbital) strongly suggests **medication overuse headache (MOH)**. This condition is characterized by daily or near-daily headaches in a patient with a primary headache disorder, caused or exacerbated by **chronic excessive use of acute headache medications** [1]. **CNS vasculitis** is less likely given the long history of headaches starting in menses (suggesting a primary headache disorder) [2]. While it can cause headaches, CNS vasculitis typically presents with acute or subacute onset of various neurological deficits. **Space-occupying intracerebral lesion** is unlikely given the normal neurological examination and absence of papilledema [2]. Headaches due to brain tumors often worsen over time, but are typically associated with other neurological signs or symptoms, such as focal deficits, which are not present here.

Q: Two or more oligoclonal bands in cerebrospinal fluid are most often positive in-

Multiple sclerosis. Multiple sclerosis - The presence of two or more oligoclonal bands (OCBs) in the cerebrospinal fluid (CSF) is a hallmark finding in multiple sclerosis (MS), indicating intrathecal immunoglobulin synthesis [1]. - OCBs are found in over 90% of MS patients, reflecting a chronic inflammatory process within the central nervous system [1]. Acute bacterial meningitis - CSF analysis in acute bacterial meningitis typically shows elevated white blood cell count (neutrophils), decreased glucose, and elevated protein, but not characteristic OCBs [2]. - While there may be a generalized immune response, it does not typically produce the specific, persistent OCB pattern seen in MS. Subarachnoid hemorrhage - CSF findings in subarachnoid hemorrhage are characterized by xanthochromia (yellow discoloration due to bilirubin), red blood cells, and elevated protein, but OCBs are not a diagnostic feature [2]. - OCBs are related to intrathecal immunoglobulin production, not the breakdown products of blood. Polyneuropathy - Polyneuropathies, such as Guillain-Barré syndrome, are characterized by albuminocytological dissociation (elevated protein with normal cell count) in CSF, or other findings depending on the specific cause. - While some inflammatory neuropathies can have CSF abnormalities, they do not typically present with the same diagnostic pattern of OCBs as observed in MS.

Q: A 26-year-old woman complains of early fatigue and weakness in doing strenuous activity. Her symptoms are worse near the end of the day. She appears well, muscle bulk, tone, and reflexes are normal. Handgrip strength decreases with repetitive testing.For the above patient with muscle weakness, select the most likely anatomic site for the disorder

neuromuscular junction. ***neuromuscular junction*** - The **fatigability** and **end-of-day worsening** of weakness, along with the **decreased handgrip strength with repetitive testing**, are classic signs of **myasthenia gravis**, a disorder of the neuromuscular junction [1], [2]. - In myasthenia gravis, **acetylcholine receptor antibodies** block or destroy receptors at the neuromuscular junction, impairing nerve-to-muscle signal transmission [3]. *muscle* - Primary muscle disorders (myopathies) typically present with **proximal muscle weakness** but do not usually show the characteristic **fatigability with repetitive use** or end-of-day worsening. - Muscle bulk, tone, and reflexes would often be affected in significant primary muscle disease. *peripheral nerve* - Peripheral nerve disorders (neuropathies) usually cause **sensory changes** (tingling, numbness) along with motor weakness, and often present with **diminished reflexes**. - The distinguishing feature of **fatigability with repetitive testing** is not typical of peripheral neuropathies. *anterior horn cell* - Anterior horn cell disorders, such as **amyotrophic lateral sclerosis (ALS)**, cause progressive weakness, muscle atrophy, and fasciculations. - While they cause weakness, they typically do not exhibit the significant **day-to-day fluctuation** or **fatigability with repetitive use** described.

Q: Myasthenia gravis may be associated with:

Thymoma. ***Thymoma*** - Approximately 10-15% of patients with **myasthenia gravis** (MG) have an associated **thymoma**, a tumor of the thymus gland [1]. - The thymus gland plays a crucial role in the development of T-cells and can be involved in the production of **autoantibodies** that target acetylcholine receptors in MG. *B lymphocyte dysfunction* - While MG is an **autoimmune disease** characterized by autoantibodies produced by **B cells**, "B lymphocyte dysfunction" is a general statement and not the most specific or common association as an underlying cause or specific comorbidity. - The dysfunction is the result of the autoimmune process, not typically the initiating association. *Viral infection* - While certain **viral infections** can trigger or exacerbate autoimmune conditions, there isn't a direct or consistently strong association between a specific viral infection and the development of myasthenia gravis as a primary cause. - MG typically involves a more systemic autoimmune response targeting the **neuromuscular junction**. *Drug intake* - Some medications can *exacerbate* myasthenia gravis, or induce a myasthenia-like syndrome (e.g., **aminoglycosides**, **beta-blockers**, **magnesium**). - However, drug intake is generally not considered a primary *cause* or a common associated comorbidity that develops *with* myasthenia gravis in the same way a thymoma is.

Q: Most common symptom of Wernicke's encephalopathy

Confusion. ***Confusion*** - **Confusion** is the most common symptom of **Wernicke's encephalopathy**, occurring in over 80% of cases. - It presents as a state of altered mental status, ranging from mild disorientation to profound encephalopathy [1]. *Ocular changes* - **Ocular changes**, such as **nystagmus** and **ophthalmoplegia**, are common but present in less than 30% of patients. - While being a classic triad component, they are not the most frequently observed symptom [1]. *Ataxia* - **Ataxia**, characterized by difficulty with coordination and gait, is also part of the classic triad but occurs in less than 25% of cases [1]. - It often manifests as a wide-based, unsteady gait. *Hypothermia* - **Hypothermia** can occur in severe cases of Wernicke's encephalopathy due to **hypothalamic dysfunction**, but it is not a common presenting symptom. - It is often seen in more advanced or neglected instances of the disease.

Q: Fasciculation is seen in -

LMN type of lesion. ***LMN type of lesion*** - **Fasciculations** are spontaneous, visible twitchings of muscle bundles, indicative of **lower motor neuron (LMN) pathology** [1]. - They result from the **denervation hypersensitivity** of muscle fibers that have lost their normal nerve supply, leading to spontaneous firing [1]. *Peripheral neuropathy* - While some severe peripheral neuropathies can involve LMN damage, **fasciculations** are not a primary and consistent feature across all types. - Peripheral neuropathies often present with sensory symptoms, weakness, and **diminished reflexes** without prominent fasciculations unless there is significant axonal loss. *UMN type of lesion* - **Upper motor neuron (UMN)** lesions are characterized by spasticity, **hyperreflexia**, positive Babinski sign, and **no fasciculations** [1], [2]. - UMN lesions affect motor pathways in the brain and spinal cord *above* the anterior horn cells, so the direct innervation of muscle fibers remains intact [2]. *Myoneural junction* - Disorders of the **myoneural junction** (neuromuscular junction), such as myasthenia gravis, cause muscle weakness that fatigues with sustained effort. - These conditions do not typically cause **fasciculations**; instead, they might feature **fatigability** and **ptosis**, but not spontaneous muscle twitches.

Q: Chorea is NOT seen in

Tourette syndrome. ***Tourette syndrome*** - **Tourette syndrome** is primarily characterized by **motor and vocal tics**, which are sudden, repetitive, nonrhythmic movements or vocalizations. - While it involves involuntary movements, these are distinct from the continuous, flowing, dance-like movements of **chorea**. *Rheumatic fever* - **Sydenham's chorea** (St. Vitus' dance) is a major manifestation of **acute rheumatic fever**, particularly in children. - It is characterized by **involuntary, purposeless, jerky movements** affecting the face, trunk, and extremities. *Creutzfeldt-Jakob disease* - This rapidly progressive, fatal neurodegenerative disease often presents with various neurological symptoms including **chorea**, **myoclonus**, and ataxia. - The abnormal movements are due to widespread neuronal loss, particularly in the **basal ganglia**. *Huntington's disease* - **Huntington's disease** is a classic cause of **chorea**, characterized by progressive degeneration of neurons in the **caudate and putamen** [1]. - The chorea is typically generalized and worsens over time, accompanied by cognitive decline and psychiatric symptoms.

Question 1

A 60-year-old man has resting tremor, pill-rolling movements, rigidity, and bradykinesia. Which of the following is most likely to be decreased in this man?

Accepted Answer

Dopamine neurons in the substantia nigra

Answer

GABA neurons in the caudate nucleus and putamen

Answer

Serotonin neurons in the raphe nuclei

Answer

Acetylcholine neurons in the forebrain

Question 2

A 79-year-old woman is brought to the clinic for assessment of frequent falls. There is no loss of consciousness associated with the falls, and she reports no postural change or symptoms prior to the falls. She also describes difficulty in "getting going" when she starts walking and notices that her balance is "not right." Her gait is slow and shuffling on inspection. Which of the following is the most likely finding in a patient with Parkinson disease?

Accepted Answer

akinesia

Answer

muscle atrophy

Answer

fine hand tremor with movement

Answer

pupillary constriction

Question 3

Inability to abduct left eye with LMN fascial palsy on same side. The lesion is in

Accepted Answer

Left pons

Answer

Cerebellar lesions

Answer

CP angle tumor

Answer

Right pons

Question 4

A 32-year-old woman presents to you for evaluation of headache. The headaches began at age 18, were initially unilateral and worse around the time of her menses. Initially the use of triptans two or three times a month would provide complete relief. Over the past several years, however, the headaches have become more frequent and severe. Triptans provide only partial relief; the patient requires a combination of acetaminophen, caffeine, and butalbital to achieve some improvement. Prophylactic medications including beta-blockers, tricyclics, and topiramate have been unsuccessful in preventing the headaches, and she has been to the emergency room three times over the past 2 weeks for a "pain shot." The general physical examination is unremarkable. Her funduscopic examination shows no evidence of papilledema, and a careful neurological examination is likewise normal. What is the most likely explanation for her headache syndrome?

Accepted Answer

Medication overuse headache

Answer

CNS vasculitis

Answer

Status migrainosus

Answer

Space-occupying intracerebral lesion

Question 5

Two or more oligoclonal bands in cerebrospinal fluid are most often positive in-

Accepted Answer

Multiple sclerosis

Answer

Acute bacterial meningitis

Answer

Subarachnoid hemorrhage

Answer

Polyneuropathy

Question 6

A 26-year-old woman complains of early fatigue and weakness in doing strenuous activity. Her symptoms are worse near the end of the day. She appears well, muscle bulk, tone, and reflexes are normal. Handgrip strength decreases with repetitive testing.For the above patient with muscle weakness, select the most likely anatomic site for the disorder

Accepted Answer

neuromuscular junction

Answer

muscle

Answer

peripheral nerve

Answer

anterior horn cell

Question 7

Myasthenia gravis may be associated with:

Accepted Answer

Thymoma

Answer

B lymphocyte dysfunction

Answer

Viral infection

Answer

Drug intake

Question 8

Most common symptom of Wernicke's encephalopathy

Accepted Answer

Confusion

Answer

Ocular changes

Answer

Ataxia

Answer

Hypothermia

Question 9

Fasciculation is seen in -

Accepted Answer

LMN type of lesion

Answer

Peripheral neuropathy

Answer

UMN type of lesion

Answer

Myoneural junction

Question 10

Chorea is NOT seen in

Accepted Answer

Tourette syndrome

Answer

Rheumatic fever

Answer

Creutzfeldt-Jakob disease

Answer

Huntington's disease

Neurology — MCQs

Neurology — MCQs

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