USMLE Step 1 Qs (12)

1.

A 55-year-old female patient is admitted to the hospital for treatment of hypertension. Which of the following drugs is most appropriate to treat this disorder?

A.

Yohimbine
B.

Clonidine
C.

Sodium lactate
D.

Cholecystokinin
E.

Carbon dioxide

Correct Answer
B. Clonidine

Explanation
Clonidine has long been used effectively for the treatment of hypertension. The other choices listed are compounds that can induce panic attacks and are, therefore, inappropriate for the treatment for this patient. Clonidine is an adrenergic agonist whose functions are mediated by its actions upon 2 receptors. Administration of this drug results in an overall decrease in noradrenergic transmission. Although the precise mechanism by which the effects of clonidine become manifest is unknown, it may be that it reduces noradrenergic transmission by acting upon 2 presynaptic receptors, which typically produce autoinhibition of the noradrenergic pathways.

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2.

A 55-year-old female patient is admitted to the hospital for treatment of hypertension. The treatment of this combination of symptoms by the appropriate drug is mediated by its actions on which of the following receptors?

A.

Muscarinic ACh receptors
B.

Dopaminergic receptors
C.

alpha 2-adrenergic receptors
D.

Serotonergic receptors
E.

GABA receptors

Correct Answer
C. alpHa 2-adrenergic receptors

Explanation
Clonidine has long been used effectively for the treatment of hypertension. The other choices listed are compounds that can induce panic attacks and are, therefore, inappropriate for the treatment for this patient. Clonidine is an adrenergic agonist whose functions are mediated by its actions upon 2 receptors. Administration of this drug results in an overall decrease in noradrenergic transmission. Although the precise mechanism by which the effects of clonidine become manifest is unknown, it may be that it reduces noradrenergic transmission by acting upon 2 presynaptic receptors, which typically produce autoinhibition of the noradrenergic pathways.

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3.

As a result of a leg injury, a 30-year-old male developed chronic pain and was subsequently treated with morphine. Consequently, he developed an addiction to morphine. through which receptor it acts to develop an addiction ?

A.

Opioid nociceptin receptor
B.

Opioid mu receptor
C.

Opioid delta receptor
D.

Opioid kappa receptor
E.

Dopamine D2-receptor

Correct Answer
B. Opioid mu receptor

Explanation
Research conducted over the past 2 decades has shown that the actions of morphine are mediated through opioid mu receptors, while other opioid receptors appear not to play a significant role. Likewise, dopamine receptors are not involved in this process. The region of the brain where concentrations of opioid receptors are very heavily concentrated is the midbrain periaqueductal gray. This region plays an important role in the modulation of pain and is particularly responsive to opioid activation by morphine.

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4.

As a result of a leg injury, a 30-year-old male developed chronic pain and was subsequently treated with morphine. Consequently, he developed an addiction to morphine. In which a region of the brain has this receptor been shown through extensive research to be heavily concentrated?

A.

Mammillary bodies
B.

Precentral gyrus
C.

Midbrain periaqueductal gray
D.

Inferior olivary nucleus
E.

Deep pontine nuclei

Correct Answer
C. Midbrain periaqueductal gray

Explanation
Research conducted over the past 2 decades has shown that the actions of morphine are mediated through opioid receptors, while other opioid receptors appear not to play a significant role. Likewise, dopamine receptors are not involved in this process. The region of the brain where concentrations of opioid receptors are very heavily concentrated is the midbrain periaqueductal gray. This region plays an important role in the modulation of pain and is particularly responsive to opioid activation by morphine.

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5.

A 65-year-old male was admitted to the emergency room and was diagnosed with a stroke. Which of the following drugs might be given to the patient in order to reduce the deleterious effects of the stroke

A.

GABA antagonist
B.

Dopamine antagonist
C.

Norepinephrine antagonist
D.

NMDA antagonist
E.

Serotonin antagonist

Correct Answer
D. NMDA antagonist

Explanation
Glutamate has been implicated in ischemia-induced brain damage following brain trauma such as a stroke. It has also been shown that administration of NMDA-receptor antagonists following a stroke is effective in the treatment of stroke by reducing tissue infarction and neuronal cell death. The other choices listed in the question are not known to relate to the reversal of the deleterious effects of stroke. The NMDA-receptor antagonist is effective, in part, by decreasing disruption of the blood-brain barrier. It has been suggested that this becomes manifest by a blockade of the neuronal production of reactive oxygen species that occurs as a result of activation of NMDA receptors.

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6.

A 65-year-old male was admitted to the emergency room and was diagnosed with a stroke. Appropriate drug treatment could be effective by which of the following means?

A.

Raising the blood pressure
B.

Attempting to decrease disruption of the blood-brain barrier
C.

Reducing seizure activity in the cerebral cortex and limbic system
D.

Stabilizing body temperature
E.

Reducing brain serotonin levels in the brainstem and cerebral cortex

Correct Answer
B. Attempting to decrease disruption of the blood-brain barrier

Explanation
Glutamate has been implicated in ischemia-induced brain damage following brain trauma such as a stroke. It has also been shown that administration of NMDA-receptor antagonists following a stroke is effective in the treatment of stroke by reducing tissue infarction and neuronal cell death. The NMDA-receptor antagonist is effective, in part, by decreasing disruption of the blood-brain barrier. It has been suggested that this becomes manifest by a blockade of the neuronal production of reactive oxygen species that occurs as a result of activation of NMDA receptors. The other choices listed for the question have no known relationship to the process in question.

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7.

A patient is admitted to the hospital after experiencing increasing episodes of temporal lobe seizure activity. To treat this disorder, which of the following drugs should be administered?

A.

Physostigmine
B.

Bicuculline
C.

Pilocarpine
D.

Kainate
E.

Vigabatrin

Correct Answer
E. Vigabatrin

Explanation
One of the drugs that has been used effectively for the treatment of epilepsy, especially complex partial seizures involving the temporal lobe, has been vigabatrin. The other choices of drugs are ones that enhance convulsive activity either by facilitating excitatory transmitter function or by inhibiting inhibitory transmitter functions. Vigabatrin functions by enhancing GABA-mediated inhibition of neurons, perhaps by the inhibition of GABA-transaminase.

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8.

A patient is admitted to the hospital after experiencing increasing episodes of temporal lobe seizure activity. Appropriate drug treatment is effective because of which of the following?

A.

It blocks NMDA receptors
B.

It activates noradrenergic receptors
C.

It activates GABA receptors
D.

It activates cholinergic receptors
E.

It blocks dopamine receptors

Correct Answer
C. It activates GABA receptors

Explanation
One of the drugs that has been used effectively for the treatment of epilepsy, especially complex partial seizures involving the temporal lobe, has been vigabatrin. The other choices of drugs are ones that enhance convulsive activity either by facilitating excitatory transmitter function or by inhibiting inhibitory transmitter functions. Vigabatrin functions by enhancing GABA-mediated inhibition of neurons, perhaps by the inhibition of GABA-transaminase.

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9.

A 46-year-old man finds that, over a period of time, he has progressive bilateral weakness of both upper and lower limbs beginning with the muscles of the hands. However, testing reveals that sensory functions appear normal. Eventually, this individual is found to have wasting of muscles, fasciculations, and evidence of upper motor neuron (UMN) dysfunction together with an increase in tendon reflexes. After a few additional months, the patient develops facial weakness and an inability to swallow (dysphagia). Further analysis reveals abnormalities in the electromyegram (EMG) of the upper and lower extremities, denervation atrophy. However, the cerebrospinal fluid (CSF) remains normal. This patient is most likely suffering from which of the following?

A.

MS
B.

Poliomyelitis
C.

Amyotrophic lateral sclerosis (ALS)
D.

Myasthenia gravis
E.

A cerebral cortical stroke

Correct Answer
C. AmyotropHic lateral sclerosis (ALS)

Explanation
Amyotrophic lateral sclerosis is characterized by a progressive loss of motor functions, first seen as weakness in limb muscles, especially those of the fingers, and later of the other limbs. Sensory functions are not significantly affected. Over time, there is wasting, atrophy, and fasciculations of limb muscles followed by UMN signs. Electromyogram abnormalities can also be observed of the upper and lower extremities. In MS, there is also sensory loss, such as loss or blurring of vision, as well as bladder problems. Poliomyelitis and myasthenia gravis involve LMN symptoms, while a cerebral cortical stroke would result in a UMN disorder without LMN signs. In ALS, there is damage initially to ventral horn cells of the spinal cord, producing LMN signs. As the disease progresses, there is involvement of UMNs located in the lateral columns of the spinal cord (i.e., corticospinal dysfunction), thereby producing UMN signs such as an increase in tendon reflexes and the presence of an extensor plantar response. Sensory neurons are not involved in this disorder.

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10.

A 46-year-old man finds that, over a period of time, he has progressive bilateral weakness of both upper and lower limbs beginning with the muscles of the hands. However, testing reveals that sensory functions appear normal. Eventually, this individual is found to have wasting of muscles, fasciculations, and evidence of upper motor neuron (UMN) dysfunction together with an increase in tendon reflexes. After a few additional months, the patient develops facial weakness and an inability to swallow (dysphagia). Further analysis reveals abnormalities in the electromyegram (EMG) of the upper and lower extremities, denervation atrophy. However, the cerebrospinal fluid (CSF) remains normal. The neuronal regions affected include which of the following?

A.

Dorsal horns of the spinal cord
B.

Lateral columns of the spinal cord
C.

Ventral horns of the spinal cord
D.

Dorsal columns and ventral horns of the spinal cord
E.

Ventral horns and lateral columns of the spinal cord

Correct Answer
E. Ventral horns and lateral columns of the spinal cord

Explanation
Amyotrophic lateral sclerosis is characterized by a progressive loss of motor functions, first seen as weakness in limb muscles, especially those of the fingers, and later of the other limbs. Sensory functions are not significantly affected. Over time, there is wasting, atrophy, and fasciculations of limb muscles followed by UMN signs. Electromyogram abnormalities can also be observed of the upper and lower extremities. In MS, there is also sensory loss, such as loss or blurring of vision, as well as bladder problems. Poliomyelitis and myasthenia gravis involve LMN symptoms, while a cerebral cortical stroke would result in a UMN disorder without LMN signs. In ALS, there is damage initially to ventral horn cells of the spinal cord, producing LMN signs. As the disease progresses, there is involvement of UMNs located in the lateral columns of the spinal cord (i.e., corticospinal dysfunction), thereby producing UMN signs such as an increase in tendon reflexes and the presence of an extensor plantar response. Sensory neurons are not involved in this disorder.

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11.

A 55-year-old man, who has been suffering from hypertension for the past 8 years, experiences attacks of pain in the regions of the pharynx and ear, which are usually preceded by swallowing and coughing spells. Each attack, which lasted for an average of 1 minute, occurred a number of times; ultimately, this condition showed remission. Although the neurological examination was basically normal, a subsequent MRI was taken and revealed an abnormality at the base of the skull. Which of the following cranial nerves is most likely involved in this disorder?

A.

Nerve V
B.

Nerve VII
C.

Nerve IX
D.

Nerve XI
E.

Nerve XII

Correct Answer
C. Nerve IX

Explanation
Cranial nerve IX, the glossopharyngeal nerve, innervates the skeletal muscles of the pharynx. The motor component involved arises from the nucleus ambiguus of the medulla. This cranial nerve also contains afferents, a component of which arises from the superior ganglion. These sensory neurons convey somatosensory sensation, including pain afferents that ultimately synapse in the spinal trigeminal nucleus. The motor component of the glossopharyngeal nerve mediating swallowing and coughing constitutes a special visceral efferent (because it is derived from a visceral arch), and the sensory component conveying pain is referred to as a general somatic afferent fiber

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12.

A 55-year-old man, who has been suffering from hypertension for the past 8 years, experiences attacks of pain in the regions of the pharynx and ear, which are usually preceded by swallowing and coughing spells. Each attack, which lasted for an average of 1 minute, occurred a number of times; ultimately, this condition showed remission. Although the neurological examination was basically normal, a subsequent MRI was taken and revealed an abnormality at the base of the skull. The motor component of this cranial nerve arises from the which of the following substances?

A.

Otic ganglion
B.

Nodose ganglion
C.

Nucleus ambiguus
D.

Inferior salivatory nucleus
E.

Lateral reticular nucleus

Correct Answer
C. Nucleus ambiguus

Explanation
Cranial nerve IX, the glossopharyngeal nerve, innervates the skeletal muscles of the pharynx. The motor component involved arises from the nucleus ambiguus of the medulla. This cranial nerve also contains afferents, a component of which arises from the superior ganglion. These sensory neurons convey somatosensory sensation, including pain afferents that ultimately synapse in the spinal trigeminal nucleus. The motor component of the glossopharyngeal nerve mediating swallowing and coughing constitutes a special visceral efferent (because it is derived from a visceral arch), and the sensory component conveying pain is referred to as a general somatic afferent fiber

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13.

A 55-year-old man, who has been suffering from hypertension for the past 8 years, experiences attacks of pain in the regions of the pharynx and ear, which are usually preceded by swallowing and coughing spells. Each attack, which lasted for an average of 1 minute, occurred a number of times; ultimately, this condition showed remission. Although the neurological examination was basically normal, a subsequent MRI was taken and revealed an abnormality at the base of the skull. The cell bodies of the sensory component of the affected nerve are located in which of the following structures?

A.

Solitary nucleus
B.

Superior ganglion
C.

Geniculate ganglion
D.

Vestibular nuclei
E.

Trigeminal ganglion

Correct Answer
B. Superior ganglion

Explanation
Cranial nerve IX, the glossopharyngeal nerve, innervates the skeletal muscles of the pharynx. The motor component involved arises from the nucleus ambiguus of the medulla. This cranial nerve also contains afferents, a component of which arises from the superior ganglion. These sensory neurons convey somatosensory sensation, including pain afferents that ultimately synapse in the spinal trigeminal nucleus. The motor component of the glossopharyngeal nerve mediating swallowing and coughing constitutes a special visceral efferent (because it is derived from a visceral arch), and the sensory component conveying pain is referred to as a general somatic afferent fiber

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14.

A 55-year-old man, who has been suffering from hypertension for the past 8 years, experiences attacks of pain in the regions of the pharynx and ear, which are usually preceded by swallowing and coughing spells. Each attack, which lasted for an average of 1 minute, occurred a number of times; ultimately, this condition showed remission. Although the neurological examination was basically normal, a subsequent MRI was taken and revealed an abnormality at the base of the skull. The motor and sensory components of this nerve that were affected are respectively characterized as which of the following?

A.

General visceral efferent and general visceral afferent
B.

Special visceral efferent and general somatic afferent
C.

General somatic efferent and special visceral afferent
D.

Special visceral efferent and special visceral afferent
E.

General somatic efferent and general somatic afferent

Correct Answer
B. Special visceral efferent and general somatic afferent

Explanation
Cranial nerve IX, the glossopharyngeal nerve, innervates the skeletal muscles of the pharynx. The motor component involved arises from the nucleus ambiguus of the medulla. This cranial nerve also contains afferents, a component of which arises from the superior ganglion. These sensory neurons convey somatosensory sensation, including pain afferents that ultimately synapse in the spinal trigeminal nucleus. The motor component of the glossopharyngeal nerve mediating swallowing and coughing constitutes a special visceral efferent (because it is derived from a visceral arch), and the sensory component conveying pain is referred to as a general somatic afferent fiber

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15.

In a classic experiment performed by Sherrington in the cat, marked rigidity was demonstrated in a decerebrate preparation. Similarly, an 80-year-old woman displayed rigidity, which resembled that shown in the cat after having a stroke. Which of the following is the likely location of the stroke?

A.

Thalamus
B.

Hypothalamus
C.

Upper midbrain
D.

Pons
E.

Spinal cord

Correct Answer
D. Pons

Explanation
Rigidity can occur by experimentally producing a decerebrate preparation (i.e., severing the brainstem at the level of the pons) and it appears clinically as well. In both situations, there has to be extensive destruction of brain tissue below the midbrain in the region of the pons, but which spares the medulla. In this way, the lateral vestibulospinal tract remains intact. This pathway powerfully facilitates extensor motor neurons and extensor reflexes, thus contributing significantly to the expression of decerebrate rigidity, in particular, when the descending inhibitory pathways, which arise from more rostral levels, are disrupted by the experimental procedure or stroke.

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16.

In a classic experiment performed by Sherrington in the cat, marked rigidity was demonstrated in a decerebrate preparation. Similarly, an 80-year-old woman displayed rigidity, which resembled that shown in the cat after having a stroke. The rigidity can be accounted in part by the unopposed action of which of the following?

A.

Rubrospinal tract
B.

Lateral vestibulospinal tract
C.

Corticospinal tract
D.

Medial vestibulospinal tract
E.

Lateral reticulospinal tract

Correct Answer
B. Lateral vestibulospinal tract

Explanation
Rigidity can occur by experimentally producing a decerebrate preparation (i.e., severing the brainstem at the level of the pons) and it appears clinically as well. In both situations, there has to be extensive destruction of brain tissue below the midbrain in the region of the pons, but which spares the medulla. In this way, the lateral vestibulospinal tract remains intact. This pathway powerfully facilitates extensor motor neurons and extensor reflexes, thus contributing significantly to the expression of decerebrate rigidity, in particular, when the descending inhibitory pathways, which arise from more rostral levels, are disrupted by the experimental procedure or stroke.

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17.

An individual experiences an ipsilateral paralysis of the soft palate and pharynx, producing hoarseness and dysphagia (inability to swallow) and, in addition, displays a loss of the carotid sinus reflex. Which of the following nerve groups if most likely affected?

A.

Cranial nerve XII
B.

Cranial nerve XI
C.

Cranial nerve X
D.

Cranial nerve VII
E.

Ventral horn cells of the cervical cord

Correct Answer
C. Cranial nerve X

Explanation
This individual who suffers a paralysis of the soft palate and pharynx, as well as loss of the carotid sinus reflex, sustains damage that includes cranial nerve X. It should be noted that several of these symptoms could have been incurred by damage to cranial nerve IX as well. However, in this question, cranial nerve IX was not listed as a choice. The axons of the nucleus ambiguus of cranial nerve X innervate the soft palate and pharynx. Damage to these neurons would frequently cause dysphagia, hoarseness, and paralysis of the soft palate. In addition, damage to the dorsal motor nucleus of the vagus constitutes an efferent limb for expression of the carotid sinus reflex. Thus, damage to these two nuclear groups would produce the constellation of deficits described for this case. The nucleus ambiguus is classified as a special visceral efferent fiber because it innervates skeletal muscle and it is derived from a visceral arch, while the dorsal motor nucleus innervates thoracic and abdominal viscera and is therefore classified as a general visceral efferent fiber.

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18.

An individual experiences an ipsilateral paralysis of the soft palate and pharynx, producing hoarseness and dysphagia (inability to swallow) and, in addition, displays a loss of the carotid sinus reflex. Which of the following nuclei is most likely damaged

A.

Solitary and lateral reticular nuclei
B.

Deep pontine and facial nuclei
C.

Dorsal motor nucleus and nucleus ambiguus
D.

Ventral horn of the cervical segment of the spinal cord
E.

Inferior salivatory and medial vestibular nuclei

Correct Answer
C. Dorsal motor nucleus and nucleus ambiguus

Explanation
This individual who suffers a paralysis of the soft palate and pharynx, as well as loss of the carotid sinus reflex, sustains damage that includes cranial nerve X. It should be noted that several of these symptoms could have been incurred by damage to cranial nerve IX as well. However, in this question, cranial nerve IX was not listed as a choice. The axons of the nucleus ambiguus of cranial nerve X innervate the soft palate and pharynx. Damage to these neurons would frequently cause dysphagia, hoarseness, and paralysis of the soft palate. In addition, damage to the dorsal motor nucleus of the vagus constitutes an efferent limb for expression of the carotid sinus reflex. Thus, damage to these two nuclear groups would produce the constellation of deficits described for this case. The nucleus ambiguus is classified as a special visceral efferent fiber because it innervates skeletal muscle and it is derived from a visceral arch, while the dorsal motor nucleus innervates thoracic and abdominal viscera and is therefore classified as a general visceral efferent fiber.

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19.

A 68-year-old woman had suffered from an infectious disorder for several weeks. Following recovery from this disorder, she experienced some loss of taste and an increase in salivation, together with pain spasms in the region of the pharynx, which extended into the ear. She also experienced some bradycardia and cardiac arrhythmia, as well as deviation of the uvula to the unaffected side. Which of the following cranial nerves is most directly involved in this deficit?

A.

Cranial nerve VII
B.

Cranial nerve IX
C.

Cranial nerve X
D.

Cranial nerve XI
E.

Cranial nerve XII

Correct Answer
B. Cranial nerve IX

Explanation
The cranial nerve that was directly affected was the glossopharyngeal nerve (cranial nerve IX). This is a mixed and complex nerve containing: (1) special visceral efferents from the nucleus ambiguus that supply the stylopharyngeus muscle (for elevation of pharynx in speech); (2) special visceral afferent fibers that transmit taste impulses from the posterior third of the tongue, general visceral afferent fibers associated with the inferior ganglion whose receptors lie in the carotid sinus that regulates cardiovascular functions; (3) general somatic afferents whose cell bodies lie in the superior ganglion of cranial nerve IX, and which mediate somatosensory information, including pain from the pharynx; and (4) general visceral efferent fibers that originate in the inferior salivatory nucleus, which are preganglionic and synapse in the otic ganglion. The postganglionic fiber from the otic ganglion innervates the parotid gland and mediates, in part, salivation. Thus, when this nerve is affected by an infectious agent, it results in the constellation of symptoms presented earlier in this case. Since the cell bodies of motor (or visceral motor) fibers (mediating motor and visceral effects) as well as the terminals of sensory afferents (mediating pain from the pharynx) lie in different regions of the medulla, it is very unlikely that such an effect could be the result of damage centrally. A much more likely occurrence is that the infectious agent produced disruption of the glossopharyngeal nerve peripherally, such as at the base of the skull or jugular foramen, where all the components run together and can be more easily affected.

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20.

A 68-year-old woman had suffered from an infectious disorder for several weeks. Following recovery from this disorder, she experienced some loss of taste and an increase in salivation, together with pain spasms in the region of the pharynx, which extended into the ear. She also experienced some bradycardia and cardiac arrhythmia, as well as deviation of the uvula to the unaffected side. Which of the following is the likely site of the lesion affecting this nerve

A.

Upper medulla
B.

Lower medulla
C.

Lower pons
D.

Upper pons
E.

Base of the skull

Correct Answer
E. Base of the skull

Explanation
The cranial nerve that was directly affected was the glossopharyngeal nerve (cranial nerve IX). This is a mixed and complex nerve containing: (1) special visceral efferents from the nucleus ambiguus that supply the stylopharyngeus muscle (for elevation of pharynx in speech); (2) special visceral afferent fibers that transmit taste impulses from the posterior third of the tongue, general visceral afferent fibers associated with the inferior ganglion whose receptors lie in the carotid sinus that regulates cardiovascular functions; (3) general somatic afferents whose cell bodies lie in the superior ganglion of cranial nerve IX, and which mediate somatosensory information, including pain from the pharynx; and (4) general visceral efferent fibers that originate in the inferior salivatory nucleus, which are preganglionic and synapse in the otic ganglion. The postganglionic fiber from the otic ganglion innervates the parotid gland and mediates, in part, salivation. Thus, when this nerve is affected by an infectious agent, it results in the constellation of symptoms presented earlier in this case. Since the cell bodies of motor (or visceral motor) fibers (mediating motor and visceral effects) as well as the terminals of sensory afferents (mediating pain from the pharynx) lie in different regions of the medulla, it is very unlikely that such an effect could be the result of damage centrally. A much more likely occurrence is that the infectious agent produced disruption of the glossopharyngeal nerve peripherally, such as at the base of the skull or jugular foramen, where all the components run together and can be more easily affected.

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21.

Julie is a 29-year-old office worker with diabetes, who awoke one morning with the inability to close her left eye and a left facial droop. Her left eye felt a bit dry, as well. She had run out of sick days and, hoping that the problem would go away, went to work. After several coworkers noticed that her face was drooping and that she was especially sensitive to loud noises on her left side, they convinced her to go to the nearest emergency room in order to make sure that she did not have a stroke. She was examined right away in the emergency room because of her age. The doctor noted right away that her mouth drooped on the left side. Her left eye was slightly closed. He tested her speech and mental status, which were normal, other than some slight slurring of her speech. Her vision and eye movements were also normal. Sensation and jaw movement were also normal, but when she was asked to wiggle her eyebrows, only the right side of her forehead moved. When asked to close her eyes tightly, and not allow him to open her eyes, her right eye would not open, but her left eye could not oppose the force. She was not able to hold air in her cheeks when asked to hold her breath, and when asked to smile, only the right side of her mouth elevated. She was very sensitive to noise on her left side. When asked to protrude her tongue, it did not deviate to either side, but if she closed her eyes and sugar water was placed on the left side of the anterior portion of her tongue, she could not identify it. The remainder of her examination was normal. A nurse asked if a head CT should be ordered in order to look for a stroke or tumor, but the doctor said that it wasn't necessary. He told Julie that he would draw some blood and give her a medication to take for a while. Assuming that the doctor was correct, and that this isn't a stroke, where in the nervous system has the damage occurred?

A.

Buccinator muscle
B.

Trigeminal nerve
C.

Facial nerve
D.

Glossopharyngeal nerve
E.

Hypoglossal nerve

Correct Answer
C. Facial nerve

Explanation
This is an example of Bell's palsy, or damage to the facial nerve distal to its nucleus in the pons. The motor weakness is LMN because of the involvement of the upper one-third of the face (this has bilateral innervation within the CNS). The loss of taste on the anterior two-thirds of the tongue and the hyperacusis (sensitivity to noise) point to damage that is distal to the brainstem because these are functions whose nerves join the facial nerve distal to its exit from the pons. This type of palsy may be caused by a virus and is more common among people with diabetes. This type of facial paralysis, involving the upper one-third of the facial muscles, is characteristic of an LMN facial nerve lesion. Since there is bilateral innervation within the CNS, from the prefrontal gyrus bilaterally until their synapse at the facial nerve nucleus, all UMN facial weakness spares the forehead. Since there is motor weakness of the face and since the chorda tympani nerve (which subserves taste) joins the facial nerve, it is likely that the lesion exists proximal to where the chorda tympani joins the facial nerve. A lesion in the lingual nerve (a branch of the trigeminal) would result in a loss of taste as well, but would also result in a loss of sensation to the face, not motor weakness. If the lesion occurred distal to the chorda tympani nerve, taste would have been spared. The facial nerve sends a branch to the stapedius muscle distal to the geniculate ganglion, but proximal to the chorda tympani nerve. Lesions proximal to this branch will cause weakness of the stapedius muscle. Contraction of this muscle normally serves as a mechanism for dampening the motion of the ossicles, thus lowering the amount of stimulation reaching the organ of Corti. If this muscle is paralyzed, hyperacusis, or increased acuity, as well as hypersensitivity to low tones will occur. Since the genu of the facial nerve is in close proximity to the nucleus of the abducens nerve, the pons is a likely location for this particular type of combination of findings. Since the damage to the facial nerve has occurred distal to the facial nerve nucleus, an LMN facial palsy is present. The lack of hyperacusis and the presence of normal taste imply that the lesion is proximal to the geniculate ganglion. Therefore, the lesion must be between the facial nerve nucleus and the geniculate ganglion, and the location in the pons is the most likely choice. If this clinical picture is present, then an infarct or tumor in the pons must be suspected, and, in this case, an imaging study would be more appropriate.

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22.

Julie is a 29-year-old office worker with diabetes, who awoke one morning with the inability to close her left eye and a left facial droop. Her left eye felt a bit dry, as well. She had run out of sick days and, hoping that the problem would go away, went to work. After several coworkers noticed that her face was drooping and that she was especially sensitive to loud noises on her left side, they convinced her to go to the nearest emergency room in order to make sure that she did not have a stroke. She was examined right away in the emergency room because of her age. The doctor noted right away that her mouth drooped on the left side. Her left eye was slightly closed. He tested her speech and mental status, which were normal, other than some slight slurring of her speech. Her vision and eye movements were also normal. Sensation and jaw movement were also normal, but when she was asked to wiggle her eyebrows, only the right side of her forehead moved. When asked to close her eyes tightly, and not allow him to open her eyes, her right eye would not open, but her left eye could not oppose the force. She was not able to hold air in her cheeks when asked to hold her breath, and when asked to smile, only the right side of her mouth elevated. She was very sensitive to noise on her left side. When asked to protrude her tongue, it did not deviate to either side, but if she closed her eyes and sugar water was placed on the left side of the anterior portion of her tongue, she could not identify it. The remainder of her examination was normal. A nurse asked if a head CT should be ordered in order to look for a stroke or tumor, but the doctor said that it wasn't necessary. He told Julie that he would draw some blood and give her a medication to take for a while. Julie's facial weakness is characteristic of which of the following?

A.

A muscle lesion
B.

A lesion of the internal capsule
C.

A superior brainstem lesion
D.

A UMN seventh-nerve lesion
E.

An LMN seventh-nerve lesion

Correct Answer
E. An LMN seventh-nerve lesion

Explanation
This is an example of Bell's palsy, or damage to the facial nerve distal to its nucleus in the pons. The motor weakness is LMN because of the involvement of the upper one-third of the face (this has bilateral innervation within the CNS). The loss of taste on the anterior two-thirds of the tongue and the hyperacusis (sensitivity to noise) point to damage that is distal to the brainstem because these are functions whose nerves join the facial nerve distal to its exit from the pons. This type of palsy may be caused by a virus and is more common among people with diabetes. This type of facial paralysis, involving the upper one-third of the facial muscles, is characteristic of an LMN facial nerve lesion. Since there is bilateral innervation within the CNS, from the prefrontal gyrus bilaterally until their synapse at the facial nerve nucleus, all UMN facial weakness spares the forehead. Since there is motor weakness of the face and since the chorda tympani nerve (which subserves taste) joins the facial nerve, it is likely that the lesion exists proximal to where the chorda tympani joins the facial nerve. A lesion in the lingual nerve (a branch of the trigeminal) would result in a loss of taste as well, but would also result in a loss of sensation to the face, not motor weakness. If the lesion occurred distal to the chorda tympani nerve, taste would have been spared. The facial nerve sends a branch to the stapedius muscle distal to the geniculate ganglion, but proximal to the chorda tympani nerve. Lesions proximal to this branch will cause weakness of the stapedius muscle. Contraction of this muscle normally serves as a mechanism for dampening the motion of the ossicles, thus lowering the amount of stimulation reaching the organ of Corti. If this muscle is paralyzed, hyperacusis, or increased acuity, as well as hypersensitivity to low tones will occur. Since the genu of the facial nerve is in close proximity to the nucleus of the abducens nerve, the pons is a likely location for this particular type of combination of findings. Since the damage to the facial nerve has occurred distal to the facial nerve nucleus, an LMN facial palsy is present. The lack of hyperacusis and the presence of normal taste imply that the lesion is proximal to the geniculate ganglion. Therefore, the lesion must be between the facial nerve nucleus and the geniculate ganglion, and the location in the pons is the most likely choice. If this clinical picture is present, then an infarct or tumor in the pons must be suspected, and, in this case, an imaging study would be more appropriate.

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23.

Julie is a 29-year-old office worker with diabetes, who awoke one morning with the inability to close her left eye and a left facial droop. Her left eye felt a bit dry, as well. She had run out of sick days and, hoping that the problem would go away, went to work. After several coworkers noticed that her face was drooping and that she was especially sensitive to loud noises on her left side, they convinced her to go to the nearest emergency room in order to make sure that she did not have a stroke. She was examined right away in the emergency room because of her age. The doctor noted right away that her mouth drooped on the left side. Her left eye was slightly closed. He tested her speech and mental status, which were normal, other than some slight slurring of her speech. Her vision and eye movements were also normal. Sensation and jaw movement were also normal, but when she was asked to wiggle her eyebrows, only the right side of her forehead moved. When asked to close her eyes tightly, and not allow him to open her eyes, her right eye would not open, but her left eye could not oppose the force. She was not able to hold air in her cheeks when asked to hold her breath, and when asked to smile, only the right side of her mouth elevated. She was very sensitive to noise on her left side. When asked to protrude her tongue, it did not deviate to either side, but if she closed her eyes and sugar water was placed on the left side of the anterior portion of her tongue, she could not identify it. The remainder of her examination was normal. A nurse asked if a head CT should be ordered in order to look for a stroke or tumor, but the doctor said that it wasn't necessary. He told Julie that he would draw some blood and give her a medication to take for a while. Damage to which area may have produced the defect in taste in the anterior two-thirds of her tongue?

A.

Intermediate nerve
B.

Glossopharyngeal nerve
C.

Lingual nerve
D.

Facial nerve, distal to the chorda tympani nerve
E.

Facial nerve, proximal to the chorda tympani nerve

Correct Answer
E. Facial nerve, proximal to the chorda tympani nerve

Explanation
This is an example of Bell's palsy, or damage to the facial nerve distal to its nucleus in the pons. The motor weakness is LMN because of the involvement of the upper one-third of the face (this has bilateral innervation within the CNS). The loss of taste on the anterior two-thirds of the tongue and the hyperacusis (sensitivity to noise) point to damage that is distal to the brainstem because these are functions whose nerves join the facial nerve distal to its exit from the pons. This type of palsy may be caused by a virus and is more common among people with diabetes. This type of facial paralysis, involving the upper one-third of the facial muscles, is characteristic of an LMN facial nerve lesion. Since there is bilateral innervation within the CNS, from the prefrontal gyrus bilaterally until their synapse at the facial nerve nucleus, all UMN facial weakness spares the forehead. Since there is motor weakness of the face and since the chorda tympani nerve (which subserves taste) joins the facial nerve, it is likely that the lesion exists proximal to where the chorda tympani joins the facial nerve. A lesion in the lingual nerve (a branch of the trigeminal) would result in a loss of taste as well, but would also result in a loss of sensation to the face, not motor weakness. If the lesion occurred distal to the chorda tympani nerve, taste would have been spared. The facial nerve sends a branch to the stapedius muscle distal to the geniculate ganglion, but proximal to the chorda tympani nerve. Lesions proximal to this branch will cause weakness of the stapedius muscle. Contraction of this muscle normally serves as a mechanism for dampening the motion of the ossicles, thus lowering the amount of stimulation reaching the organ of Corti. If this muscle is paralyzed, hyperacusis, or increased acuity, as well as hypersensitivity to low tones will occur. Since the genu of the facial nerve is in close proximity to the nucleus of the abducens nerve, the pons is a likely location for this particular type of combination of findings. Since the damage to the facial nerve has occurred distal to the facial nerve nucleus, an LMN facial palsy is present. The lack of hyperacusis and the presence of normal taste imply that the lesion is proximal to the geniculate ganglion. Therefore, the lesion must be between the facial nerve nucleus and the geniculate ganglion, and the location in the pons is the most likely choice. If this clinical picture is present, then an infarct or tumor in the pons must be suspected, and, in this case, an imaging study would be more appropriate.

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24.

Julie is a 29-year-old office worker with diabetes, who awoke one morning with the inability to close her left eye and a left facial droop. Her left eye felt a bit dry, as well. She had run out of sick days and, hoping that the problem would go away, went to work. After several coworkers noticed that her face was drooping and that she was especially sensitive to loud noises on her left side, they convinced her to go to the nearest emergency room in order to make sure that she did not have a stroke. She was examined right away in the emergency room because of her age. The doctor noted right away that her mouth drooped on the left side. Her left eye was slightly closed. He tested her speech and mental status, which were normal, other than some slight slurring of her speech. Her vision and eye movements were also normal. Sensation and jaw movement were also normal, but when she was asked to wiggle her eyebrows, only the right side of her forehead moved. When asked to close her eyes tightly, and not allow him to open her eyes, her right eye would not open, but her left eye could not oppose the force. She was not able to hold air in her cheeks when asked to hold her breath, and when asked to smile, only the right side of her mouth elevated. She was very sensitive to noise on her left side. When asked to protrude her tongue, it did not deviate to either side, but if she closed her eyes and sugar water was placed on the left side of the anterior portion of her tongue, she could not identify it. The remainder of her examination was normal. A nurse asked if a head CT should be ordered in order to look for a stroke or tumor, but the doctor said that it wasn't necessary. He told Julie that he would draw some blood and give her a medication to take for a while. Assuming that Julie had no prior problems with her ears or cochlear nerve, damage to the nerve supply of which muscle could cause the sensitivity to or distortion of noises?

A.

Digastric
B.

Platysma
C.

Buccinator
D.

Geniohyoid
E.

Stapedius

Correct Answer
E. Stapedius

Explanation
This is an example of Bell's palsy, or damage to the facial nerve distal to its nucleus in the pons. The motor weakness is LMN because of the involvement of the upper one-third of the face (this has bilateral innervation within the CNS). The loss of taste on the anterior two-thirds of the tongue and the hyperacusis (sensitivity to noise) point to damage that is distal to the brainstem because these are functions whose nerves join the facial nerve distal to its exit from the pons. This type of palsy may be caused by a virus and is more common among people with diabetes. This type of facial paralysis, involving the upper one-third of the facial muscles, is characteristic of an LMN facial nerve lesion. Since there is bilateral innervation within the CNS, from the prefrontal gyrus bilaterally until their synapse at the facial nerve nucleus, all UMN facial weakness spares the forehead. Since there is motor weakness of the face and since the chorda tympani nerve (which subserves taste) joins the facial nerve, it is likely that the lesion exists proximal to where the chorda tympani joins the facial nerve. A lesion in the lingual nerve (a branch of the trigeminal) would result in a loss of taste as well, but would also result in a loss of sensation to the face, not motor weakness. If the lesion occurred distal to the chorda tympani nerve, taste would have been spared. The facial nerve sends a branch to the stapedius muscle distal to the geniculate ganglion, but proximal to the chorda tympani nerve. Lesions proximal to this branch will cause weakness of the stapedius muscle. Contraction of this muscle normally serves as a mechanism for dampening the motion of the ossicles, thus lowering the amount of stimulation reaching the organ of Corti. If this muscle is paralyzed, hyperacusis, or increased acuity, as well as hypersensitivity to low tones will occur. Since the genu of the facial nerve is in close proximity to the nucleus of the abducens nerve, the pons is a likely location for this particular type of combination of findings. Since the damage to the facial nerve has occurred distal to the facial nerve nucleus, an LMN facial palsy is present. The lack of hyperacusis and the presence of normal taste imply that the lesion is proximal to the geniculate ganglion. Therefore, the lesion must be between the facial nerve nucleus and the geniculate ganglion, and the location in the pons is the most likely choice. If this clinical picture is present, then an infarct or tumor in the pons must be suspected, and, in this case, an imaging study would be more appropriate.

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25.

Julie is a 29-year-old office worker with diabetes, who awoke one morning with the inability to close her left eye and a left facial droop. Her left eye felt a bit dry, as well. She had run out of sick days and, hoping that the problem would go away, went to work. After several coworkers noticed that her face was drooping and that she was especially sensitive to loud noises on her left side, they convinced her to go to the nearest emergency room in order to make sure that she did not have a stroke. She was examined right away in the emergency room because of her age. The doctor noted right away that her mouth drooped on the left side. Her left eye was slightly closed. He tested her speech and mental status, which were normal, other than some slight slurring of her speech. Her vision and eye movements were also normal. Sensation and jaw movement were also normal, but when she was asked to wiggle her eyebrows, only the right side of her forehead moved. When asked to close her eyes tightly, and not allow him to open her eyes, her right eye would not open, but her left eye could not oppose the force. She was not able to hold air in her cheeks when asked to hold her breath, and when asked to smile, only the right side of her mouth elevated. She was very sensitive to noise on her left side. When asked to protrude her tongue, it did not deviate to either side, but if she closed her eyes and sugar water was placed on the left side of the anterior portion of her tongue, she could not identify it. The remainder of her examination was normal. A nurse asked if a head CT should be ordered in order to look for a stroke or tumor, but the doctor said that it wasn't necessary. He told Julie that he would draw some blood and give her a medication to take for a while. If Julie did not have the loss of taste and noise sensitivity, but did have the inability to move her left eye to the left, which area would now be damaged?

A.

The trigeminal and abducens nerves
B.

The facial and trigeminal nerves, distal to their exit from the brainstem
C.

The facial and abducens nerve nuclei within the pons
D.

The facial nerve, distal to the chorda tympani nerve
E.

The facial nerve, distal to the geniculate ganglion

Correct Answer
C. The facial and abducens nerve nuclei within the pons

Explanation
This is an example of Bell's palsy, or damage to the facial nerve distal to its nucleus in the pons. The motor weakness is LMN because of the involvement of the upper one-third of the face (this has bilateral innervation within the CNS). The loss of taste on the anterior two-thirds of the tongue and the hyperacusis (sensitivity to noise) point to damage that is distal to the brainstem because these are functions whose nerves join the facial nerve distal to its exit from the pons. This type of palsy may be caused by a virus and is more common among people with diabetes. This type of facial paralysis, involving the upper one-third of the facial muscles, is characteristic of an LMN facial nerve lesion. Since there is bilateral innervation within the CNS, from the prefrontal gyrus bilaterally until their synapse at the facial nerve nucleus, all UMN facial weakness spares the forehead. Since there is motor weakness of the face and since the chorda tympani nerve (which subserves taste) joins the facial nerve, it is likely that the lesion exists proximal to where the chorda tympani joins the facial nerve. A lesion in the lingual nerve (a branch of the trigeminal) would result in a loss of taste as well, but would also result in a loss of sensation to the face, not motor weakness. If the lesion occurred distal to the chorda tympani nerve, taste would have been spared. The facial nerve sends a branch to the stapedius muscle distal to the geniculate ganglion, but proximal to the chorda tympani nerve. Lesions proximal to this branch will cause weakness of the stapedius muscle. Contraction of this muscle normally serves as a mechanism for dampening the motion of the ossicles, thus lowering the amount of stimulation reaching the organ of Corti. If this muscle is paralyzed, hyperacusis, or increased acuity, as well as hypersensitivity to low tones will occur. Since the genu of the facial nerve is in close proximity to the nucleus of the abducens nerve, the pons is a likely location for this particular type of combination of findings. Since the damage to the facial nerve has occurred distal to the facial nerve nucleus, an LMN facial palsy is present. The lack of hyperacusis and the presence of normal taste imply that the lesion is proximal to the geniculate ganglion. Therefore, the lesion must be between the facial nerve nucleus and the geniculate ganglion, and the location in the pons is the most likely choice. If this clinical picture is present, then an infarct or tumor in the pons must be suspected, and, in this case, an imaging study would be more appropriate.

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26.

Herb, a 62-year-old man who has smoked two packs of cigarettes per day for 35 years, was suffering from a chronic cough that was attributed to smoking habit by his physician. One day, Herb noticed that his right eyelid drooped slightly and that his right pupil was smaller than the left. He also noticed that the inner side of his right hand was numb and that he had begun to drop things from his right hand. He had no other symptoms. Herb consulted his physician who directed him to a neurologist. The neurologist noted that although the right pupil was smaller than the left, it was still reactive to light. Although Herb's right eyelid drooped slightly, he could close his eyes tightly when asked to do so. The neurologist noted that Herb did not sweat on the right side of his face. He was unable to feel a pinprick on the inner surface of his right hand, and his right triceps and hand muscles were weak. Where in the nervous system has damage occurred?

A.

Left oculomotor nerve
B.

Right oculomotor nerve
C.

Edinger-Westphal nucleus
D.

Sympathetic fibers coursing from the hypothalamus to the intermediolateral cell column
E.

Parasympathetic fibers coursing from the Edinger-Westphal nucleus

Correct Answer
D. Sympathetic fibers coursing from the hypothalamus to the intermediolateral cell column

Explanation
Herb's drooping eyelid, small pupil, and lack of sweating on the right side are examples of Horner's syndrome. This is caused by the interruption of sympathetic fibers anywhere along their course from the hypothalamus and brainstem, to the intermediolateral cell column in the upper thoracic levels of the spinal cord where neurons, supplying sympathetic innervation to the pupil, the levator palpebrae superioris muscle of the eyelid and sweat glands of the face, are located. Interruption of this sympathetic innervation will result in the drooping of the upper eyelid (ptosis), pupillary constriction (miosis; due to unopposed action of the parasympathetic innervation of the circular muscles of the iris), and lack of sweating on the face. Parasympathetic or oculomotor damage causes pupillary dilation, rather than constriction. Herb could close his eyes tightly because this function is mediated by the seventh nerve, which is not damaged by this lesion. Preganglionic sympathetic neurons are predominantly cholinergic, and postganglionic sympathetic neurons are predominantly noradrenergic. Horner's syndrome may be caused by either a preganglionic or postganglionic lesion. The location may be determined by the use of eyedrops specifically targeted at a particular neurotransmitter. One cause of interruption of the sympathetic fibers is a tumor of the apex (top portion) of the lung, called a Pancoast tumor. Because the apex of the lung is in close proximity to the spine, a Pancoast tumor may compress the upper thoracic spinal cord where the sympathetic fibers exit from it. Compression of the adjacent spinal nerves between C8 and T2, entering the brachial plexus, also interrupts the nerve supply to the hand and triceps muscle, causing numbness and weakness in these areas. Pancoast tumors do not often cause respiratory symptoms early on in their course because they are located far from the mainstem bronchi. Because these tumors have this unique location, the neurological abnormalities often predate the respiratory problems. The neurologist suspected that Herb may have a Pancoast tumor in the lung because of his long history of smoking.

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27.

Herb, a 62-year-old man who has smoked two packs of cigarettes per day for 35 years, was suffering from a chronic cough that was attributed to smoking habit by his physician. One day, Herb noticed that his right eyelid drooped slightly and that his right pupil was smaller than the left. He also noticed that the inner side of his right hand was numb and that he had begun to drop things from his right hand. He had no other symptoms. Herb consulted his physician who directed him to a neurologist. The neurologist noted that although the right pupil was smaller than the left, it was still reactive to light. Although Herb's right eyelid drooped slightly, he could close his eyes tightly when asked to do so. The neurologist noted that Herb did not sweat on the right side of his face. He was unable to feel a pinprick on the inner surface of his right hand, and his right triceps and hand muscles were weak. Herb's small pupil is due to which of the following?

A.

Unopposed action of the muscles with parasympathetic innervation
B.

Unopposed action of the muscles with sympathetic innervation
C.

Both sympathetic and parasympathetic damage
D.

A lesion in the nucleus of the third nerve
E.

A lesion distal branches of the trochlear nerve

Correct Answer
A. Unopposed action of the muscles with parasympathetic innervation

Explanation
Herb's drooping eyelid, small pupil, and lack of sweating on the right side are examples of Horner's syndrome. This is caused by the interruption of sympathetic fibers anywhere along their course from the hypothalamus and brainstem, to the intermediolateral cell column in the upper thoracic levels of the spinal cord where neurons, supplying sympathetic innervation to the pupil, the levator palpebrae superioris muscle of the eyelid and sweat glands of the face, are located. Interruption of this sympathetic innervation will result in the drooping of the upper eyelid (ptosis), pupillary constriction (miosis; due to unopposed action of the parasympathetic innervation of the circular muscles of the iris), and lack of sweating on the face. Parasympathetic or oculomotor damage causes pupillary dilation, rather than constriction. Herb could close his eyes tightly because this function is mediated by the seventh nerve, which is not damaged by this lesion. Preganglionic sympathetic neurons are predominantly cholinergic, and postganglionic sympathetic neurons are predominantly noradrenergic. Horner's syndrome may be caused by either a preganglionic or postganglionic lesion. The location may be determined by the use of eyedrops specifically targeted at a particular neurotransmitter. One cause of interruption of the sympathetic fibers is a tumor of the apex (top portion) of the lung, called a Pancoast tumor. Because the apex of the lung is in close proximity to the spine, a Pancoast tumor may compress the upper thoracic spinal cord where the sympathetic fibers exit from it. Compression of the adjacent spinal nerves between C8 and T2, entering the brachial plexus, also interrupts the nerve supply to the hand and triceps muscle, causing numbness and weakness in these areas. Pancoast tumors do not often cause respiratory symptoms early on in their course because they are located far from the mainstem bronchi. Because these tumors have this unique location, the neurological abnormalities often predate the respiratory problems. The neurologist suspected that Herb may have a Pancoast tumor in the lung because of his long history of smoking.

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28.

Herb, a 62-year-old man who has smoked two packs of cigarettes per day for 35 years, was suffering from a chronic cough that was attributed to smoking habit by his physician. One day, Herb noticed that his right eyelid drooped slightly and that his right pupil was smaller than the left. He also noticed that the inner side of his right hand was numb and that he had begun to drop things from his right hand. He had no other symptoms. Herb consulted his physician who directed him to a neurologist. The neurologist noted that although the right pupil was smaller than the left, it was still reactive to light. Although Herb's right eyelid drooped slightly, he could close his eyes tightly when asked to do so. The neurologist noted that Herb did not sweat on the right side of his face. He was unable to feel a pinprick on the inner surface of his right hand, and his right triceps and hand muscles were weak. Which pair of neurotransmitters is involved in the pathway that has been damaged?

A.

Substance P and acetylcholine (ACh)
B.

Norepinephrine and epinephrine
C.

5-HT and GABA
D.

GABA and ACh
E.

ACh and norepinephrine

Correct Answer
E. ACh and norepinepHrine

Explanation
Herb's drooping eyelid, small pupil, and lack of sweating on the right side are examples of Horner's syndrome. This is caused by the interruption of sympathetic fibers anywhere along their course from the hypothalamus and brainstem, to the intermediolateral cell column in the upper thoracic levels of the spinal cord where neurons, supplying sympathetic innervation to the pupil, the levator palpebrae superioris muscle of the eyelid and sweat glands of the face, are located. Interruption of this sympathetic innervation will result in the drooping of the upper eyelid (ptosis), pupillary constriction (miosis; due to unopposed action of the parasympathetic innervation of the circular muscles of the iris), and lack of sweating on the face. Parasympathetic or oculomotor damage causes pupillary dilation, rather than constriction. Herb could close his eyes tightly because this function is mediated by the seventh nerve, which is not damaged by this lesion. Preganglionic sympathetic neurons are predominantly cholinergic, and postganglionic sympathetic neurons are predominantly noradrenergic. Horner's syndrome may be caused by either a preganglionic or postganglionic lesion. The location may be determined by the use of eyedrops specifically targeted at a particular neurotransmitter. One cause of interruption of the sympathetic fibers is a tumor of the apex (top portion) of the lung, called a Pancoast tumor. Because the apex of the lung is in close proximity to the spine, a Pancoast tumor may compress the upper thoracic spinal cord where the sympathetic fibers exit from it. Compression of the adjacent spinal nerves between C8 and T2, entering the brachial plexus, also interrupts the nerve supply to the hand and triceps muscle, causing numbness and weakness in these areas. Pancoast tumors do not often cause respiratory symptoms early on in their course because they are located far from the mainstem bronchi. Because these tumors have this unique location, the neurological abnormalities often predate the respiratory problems. The neurologist suspected that Herb may have a Pancoast tumor in the lung because of his long history of smoking.

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29.

Herb, a 62-year-old man who has smoked two packs of cigarettes per day for 35 years, was suffering from a chronic cough that was attributed to smoking habit by his physician. One day, Herb noticed that his right eyelid drooped slightly and that his right pupil was smaller than the left. He also noticed that the inner side of his right hand was numb and that he had begun to drop things from his right hand. He had no other symptoms. Herb consulted his physician who directed him to a neurologist. The neurologist noted that although the right pupil was smaller than the left, it was still reactive to light. Although Herb's right eyelid drooped slightly, he could close his eyes tightly when asked to do so. The neurologist noted that Herb did not sweat on the right side of his face. He was unable to feel a pinprick on the inner surface of his right hand, and his right triceps and hand muscles were weak. Damage to which of the following fibers caused the numbness and weakness of his hand?

A.

Damage to the ipsilateral cerebral peduncle
B.

Damage to the corticospinal tract
C.

Damage to the cervical spinal roots entering the brachial plexus
D.

Infarction of the basilar artery
E.

Damage to the median nerve

Correct Answer
C. Damage to the cervical spinal roots entering the brachial plexus

Explanation
Herb's drooping eyelid, small pupil, and lack of sweating on the right side are examples of Horner's syndrome. This is caused by the interruption of sympathetic fibers anywhere along their course from the hypothalamus and brainstem, to the intermediolateral cell column in the upper thoracic levels of the spinal cord where neurons, supplying sympathetic innervation to the pupil, the levator palpebrae superioris muscle of the eyelid and sweat glands of the face, are located. Interruption of this sympathetic innervation will result in the drooping of the upper eyelid (ptosis), pupillary constriction (miosis; due to unopposed action of the parasympathetic innervation of the circular muscles of the iris), and lack of sweating on the face. Parasympathetic or oculomotor damage causes pupillary dilation, rather than constriction. Herb could close his eyes tightly because this function is mediated by the seventh nerve, which is not damaged by this lesion. Preganglionic sympathetic neurons are predominantly cholinergic, and postganglionic sympathetic neurons are predominantly noradrenergic. Horner's syndrome may be caused by either a preganglionic or postganglionic lesion. The location may be determined by the use of eyedrops specifically targeted at a particular neurotransmitter. One cause of interruption of the sympathetic fibers is a tumor of the apex (top portion) of the lung, called a Pancoast tumor. Because the apex of the lung is in close proximity to the spine, a Pancoast tumor may compress the upper thoracic spinal cord where the sympathetic fibers exit from it. Compression of the adjacent spinal nerves between C8 and T2, entering the brachial plexus, also interrupts the nerve supply to the hand and triceps muscle, causing numbness and weakness in these areas. Pancoast tumors do not often cause respiratory symptoms early on in their course because they are located far from the mainstem bronchi. Because these tumors have this unique location, the neurological abnormalities often predate the respiratory problems. The neurologist suspected that Herb may have a Pancoast tumor in the lung because of his long history of smoking.

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30.

Mike is a 35-year-old man who had optic neuritis (an inflammation of the optic nerve causing blurred vision) several years before. He was told that he had a 50% chance of eventually developing multiple sclerosis (MS), a degenerative disease of the CNS white matter. One day, he noticed that he had double vision and felt weak on his right side. Although he noted that the symptoms were becoming steadily worse throughout the day, he attributed this to stress from his job as a stockbroker, and in order to relax, he decided to take a drive in his car. While he was driving, his vision became steadily worse. As he was about to pull over to the side of the road, he saw two trees on the right side of the road. Uncertain which was the actual image, he attempted to place his right foot on the break pedal. Mike suddenly realized that he was unable to lift his right leg, and his car collided with the tree. A pedestrian on the side of the road called the EMS, and Mike was brought to a nearby emergency room. A neurologist was called to see Mike because the emergency room physicians thought he may have had a stroke, despite his young age. The neurologist spoke to Mike, then examined him. He found that his left eye was deviated to the left and down. When he attempted to look to his right, his right eye moved normally, but his left eye was unable to move further to the right than the midline. His left pupil was dilated and did not contract to light from a penlight. His left eyelid drooped, and he had difficulty raising it. In addition, the right side of his mouth remained motionless when he attempted to smile, but his forehead was symmetric when he raised his eyebrows. Mike's right arm and leg were markedly weak. The neurologist told Mike that he wasn't certain that this was necessarily a stroke, but admitted him to the hospital for observation and tests. A lesion in which of the following nerves caused Mike's double vision?

A.

Optic nerve
B.

Oculomotor nerve
C.

Cervical sympathetic fibers
D.

Trochlear nerve
E.

Abducens nerve

Correct Answer
B. Oculomotor nerve

Explanation
The third cranial nerve (oculomotor) controls four of the six extraocular muscles that move the eye. When this nerve fails to function, the eye remains deviated laterally due to the unopposed action of the other two extraocular muscles. When the eyes no longer move together, patients have double vision because the visual cortex now receives two different images. In addition, fibers originating in the third nerve nucleus innervate the levator palpebrae superioris, a muscle that helps to lift the eyelid. Damage to the optic nerve causes loss of vision, blurred vision, and a central scotoma (blind spot in the center of the visual field). Damage to the cervical sympathetic fibers causes Horner's syndrome, consisting of ptosis (drooping of the eyelid), miosis (constriction of the pupil), and anhydrosis (loss of sweating), not eye movement abnormalities. The actions of the superior oblique, the muscle innervated by the trochlear nerve, include intorsion, depression, and abduction. The abducens nerve mediates the lateral rectus muscle, which abducts the eye. The eye is depressed and abducted due to the unopposed actions of the superior oblique and lateral rectus muscles, which together move the eye downward and abduct it (see earlier discussion for the actions of these muscles). The other four muscles are innervated by the oculomotor nerve, which presumably has been damaged. This is an example of Weber's syndrome, or a lesion involving the third cranial nerve outflow tract, and the corticospinal and corticobulbar tracts in the cerebral peduncles of the midbrain. Weber's syndrome may occur as a result of an occlusion of the interpeduncular branches of the posterior cerebral artery (which supply this portion of the midbrain), a tumor pressing on this area, an aneurysm (circumscribed dilation of an artery) of the posterior communicating artery, or a plaque (lesion) related to multiple sclerosis. Fibers from the Edinger-Westphal nucleus are affected by lesions of the midbrain as well, and because they are instrumental in constricting the pupil, this lesion causes the patient to have a dilated pupil. If there is a mass that is external to the midbrain, but pressing on the oculomotor nerve, then the preganglionic parasympathetic fibers traveling to the ciliary ganglion, which, in turn, innervate the pupillary constrictor muscles, can be damaged, also causing a dilated pupil. Cervical sympathetic fibers cause pupillary dilatation, so damage to these fibers causes pupillary constriction (see Horner's syndrome, earlier). Involvement of the cerebral peduncle causes damage to the corticospinal and corticobulbar tracts, resulting in weakness of the contralateral face, arm, and leg. The motor deficit is contralateral because the corticospinal tracts cross in the medullary pyramids, below the level of the lesion. The upper portion of Mike's face was spared in this case (as well as in any other UMN lesion) because the face is innervated bilaterally until the level of the caudal pons, so a unilateral lesion results in sparing of this portion of the face. The combination of a third-nerve palsy and contralateral hemiparesis can only occur in the midbrain. The observed effects relating to cranial nerve III could not be accounted for by cortical damage. Likewise, damage to the cervical cord would not affect the third nerve.

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31.

Mike is a 35-year-old man who had optic neuritis (an inflammation of the optic nerve causing blurred vision) several years before. He was told that he had a 50% chance of eventually developing multiple sclerosis (MS), a degenerative disease of the CNS white matter. One day, he noticed that he had double vision and felt weak on his right side. Although he noted that the symptoms were becoming steadily worse throughout the day, he attributed this to stress from his job as a stockbroker, and in order to relax, he decided to take a drive in his car. While he was driving, his vision became steadily worse. As he was about to pull over to the side of the road, he saw two trees on the right side of the road. Uncertain which was the actual image, he attempted to place his right foot on the break pedal. Mike suddenly realized that he was unable to lift his right leg, and his car collided with the tree. A pedestrian on the side of the road called the EMS, and Mike was brought to a nearby emergency room. A neurologist was called to see Mike because the emergency room physicians thought he may have had a stroke, despite his young age. The neurologist spoke to Mike, then examined him. He found that his left eye was deviated to the left and down. When he attempted to look to his right, his right eye moved normally, but his left eye was unable to move further to the right than the midline. His left pupil was dilated and did not contract to light from a penlight. His left eyelid drooped, and he had difficulty raising it. In addition, the right side of his mouth remained motionless when he attempted to smile, but his forehead was symmetric when he raised his eyebrows. Mike's right arm and leg were markedly weak. The neurologist told Mike that he wasn't certain that this was necessarily a stroke, but admitted him to the hospital for observation and tests. Where in the nervous system did the damage occur?

A.

Left frontal lobe
B.

Right frontal lobe
C.

Left eye
D.

Cervical spinal cord
E.

Midbrain

Correct Answer
E. Midbrain

Explanation
The third cranial nerve (oculomotor) controls four of the six extraocular muscles that move the eye. When this nerve fails to function, the eye remains deviated laterally due to the unopposed action of the other two extraocular muscles. When the eyes no longer move together, patients have double vision because the visual cortex now receives two different images. In addition, fibers originating in the third nerve nucleus innervate the levator palpebrae superioris, a muscle that helps to lift the eyelid. Damage to the optic nerve causes loss of vision, blurred vision, and a central scotoma (blind spot in the center of the visual field). Damage to the cervical sympathetic fibers causes Horner's syndrome, consisting of ptosis (drooping of the eyelid), miosis (constriction of the pupil), and anhydrosis (loss of sweating), not eye movement abnormalities. The actions of the superior oblique, the muscle innervated by the trochlear nerve, include intorsion, depression, and abduction. The abducens nerve mediates the lateral rectus muscle, which abducts the eye. The eye is depressed and abducted due to the unopposed actions of the superior oblique and lateral rectus muscles, which together move the eye downward and abduct it (see earlier discussion for the actions of these muscles). The other four muscles are innervated by the oculomotor nerve, which presumably has been damaged. This is an example of Weber's syndrome, or a lesion involving the third cranial nerve outflow tract, and the corticospinal and corticobulbar tracts in the cerebral peduncles of the midbrain. Weber's syndrome may occur as a result of an occlusion of the interpeduncular branches of the posterior cerebral artery (which supply this portion of the midbrain), a tumor pressing on this area, an aneurysm (circumscribed dilation of an artery) of the posterior communicating artery, or a plaque (lesion) related to multiple sclerosis. Fibers from the Edinger-Westphal nucleus are affected by lesions of the midbrain as well, and because they are instrumental in constricting the pupil, this lesion causes the patient to have a dilated pupil. If there is a mass that is external to the midbrain, but pressing on the oculomotor nerve, then the preganglionic parasympathetic fibers traveling to the ciliary ganglion, which, in turn, innervate the pupillary constrictor muscles, can be damaged, also causing a dilated pupil. Cervical sympathetic fibers cause pupillary dilatation, so damage to these fibers causes pupillary constriction (see Horner's syndrome, earlier). Involvement of the cerebral peduncle causes damage to the corticospinal and corticobulbar tracts, resulting in weakness of the contralateral face, arm, and leg. The motor deficit is contralateral because the corticospinal tracts cross in the medullary pyramids, below the level of the lesion. The upper portion of Mike's face was spared in this case (as well as in any other UMN lesion) because the face is innervated bilaterally until the level of the caudal pons, so a unilateral lesion results in sparing of this portion of the face. The combination of a third-nerve palsy and contralateral hemiparesis can only occur in the midbrain. The observed effects relating to cranial nerve III could not be accounted for by cortical damage. Likewise, damage to the cervical cord would not affect the third nerve.

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32.

Mike is a 35-year-old man who had optic neuritis (an inflammation of the optic nerve causing blurred vision) several years before. He was told that he had a 50% chance of eventually developing multiple sclerosis (MS), a degenerative disease of the CNS white matter. One day, he noticed that he had double vision and felt weak on his right side. Although he noted that the symptoms were becoming steadily worse throughout the day, he attributed this to stress from his job as a stockbroker, and in order to relax, he decided to take a drive in his car. While he was driving, his vision became steadily worse. As he was about to pull over to the side of the road, he saw two trees on the right side of the road. Uncertain which was the actual image, he attempted to place his right foot on the break pedal. Mike suddenly realized that he was unable to lift his right leg, and his car collided with the tree. A pedestrian on the side of the road called the EMS, and Mike was brought to a nearby emergency room. A neurologist was called to see Mike because the emergency room physicians thought he may have had a stroke, despite his young age. The neurologist spoke to Mike, then examined him. He found that his left eye was deviated to the left and down. When he attempted to look to his right, his right eye moved normally, but his left eye was unable to move further to the right than the midline. His left pupil was dilated and did not contract to light from a penlight. His left eyelid drooped, and he had difficulty raising it. In addition, the right side of his mouth remained motionless when he attempted to smile, but his forehead was symmetric when he raised his eyebrows. Mike's right arm and leg were markedly weak. The neurologist told Mike that he wasn't certain that this was necessarily a stroke, but admitted him to the hospital for observation and tests. Damage to which of the following fibers caused the enlarged, unreactive pupil on the left?

A.

Medial longitudinal fasciculus
B.

Frontal or pontine eye fields
C.

Edinger-Westphal nucleus or preganglionic parasympathetic fibers
D.

Trochlear nerve
E.

Cervical sympathetic fibers

Correct Answer
C. Edinger-WestpHal nucleus or preganglionic parasympathetic fibers

Explanation
The third cranial nerve (oculomotor) controls four of the six extraocular muscles that move the eye. When this nerve fails to function, the eye remains deviated laterally due to the unopposed action of the other two extraocular muscles. When the eyes no longer move together, patients have double vision because the visual cortex now receives two different images. In addition, fibers originating in the third nerve nucleus innervate the levator palpebrae superioris, a muscle that helps to lift the eyelid. Damage to the optic nerve causes loss of vision, blurred vision, and a central scotoma (blind spot in the center of the visual field). Damage to the cervical sympathetic fibers causes Horner's syndrome, consisting of ptosis (drooping of the eyelid), miosis (constriction of the pupil), and anhydrosis (loss of sweating), not eye movement abnormalities. The actions of the superior oblique, the muscle innervated by the trochlear nerve, include intorsion, depression, and abduction. The abducens nerve mediates the lateral rectus muscle, which abducts the eye. The eye is depressed and abducted due to the unopposed actions of the superior oblique and lateral rectus muscles, which together move the eye downward and abduct it (see earlier discussion for the actions of these muscles). The other four muscles are innervated by the oculomotor nerve, which presumably has been damaged. This is an example of Weber's syndrome, or a lesion involving the third cranial nerve outflow tract, and the corticospinal and corticobulbar tracts in the cerebral peduncles of the midbrain. Weber's syndrome may occur as a result of an occlusion of the interpeduncular branches of the posterior cerebral artery (which supply this portion of the midbrain), a tumor pressing on this area, an aneurysm (circumscribed dilation of an artery) of the posterior communicating artery, or a plaque (lesion) related to multiple sclerosis. Fibers from the Edinger-Westphal nucleus are affected by lesions of the midbrain as well, and because they are instrumental in constricting the pupil, this lesion causes the patient to have a dilated pupil. If there is a mass that is external to the midbrain, but pressing on the oculomotor nerve, then the preganglionic parasympathetic fibers traveling to the ciliary ganglion, which, in turn, innervate the pupillary constrictor muscles, can be damaged, also causing a dilated pupil. Cervical sympathetic fibers cause pupillary dilatation, so damage to these fibers causes pupillary constriction (see Horner's syndrome, earlier). Involvement of the cerebral peduncle causes damage to the corticospinal and corticobulbar tracts, resulting in weakness of the contralateral face, arm, and leg. The motor deficit is contralateral because the corticospinal tracts cross in the medullary pyramids, below the level of the lesion. The upper portion of Mike's face was spared in this case (as well as in any other UMN lesion) because the face is innervated bilaterally until the level of the caudal pons, so a unilateral lesion results in sparing of this portion of the face. The combination of a third-nerve palsy and contralateral hemiparesis can only occur in the midbrain. The observed effects relating to cranial nerve III could not be accounted for by cortical damage. Likewise, damage to the cervical cord would not affect the third nerve.

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33.

Mike is a 35-year-old man who had optic neuritis (an inflammation of the optic nerve causing blurred vision) several years before. He was told that he had a 50% chance of eventually developing multiple sclerosis (MS), a degenerative disease of the CNS white matter. One day, he noticed that he had double vision and felt weak on his right side. Although he noted that the symptoms were becoming steadily worse throughout the day, he attributed this to stress from his job as a stockbroker, and in order to relax, he decided to take a drive in his car. While he was driving, his vision became steadily worse. As he was about to pull over to the side of the road, he saw two trees on the right side of the road. Uncertain which was the actual image, he attempted to place his right foot on the break pedal. Mike suddenly realized that he was unable to lift his right leg, and his car collided with the tree. A pedestrian on the side of the road called the EMS, and Mike was brought to a nearby emergency room. A neurologist was called to see Mike because the emergency room physicians thought he may have had a stroke, despite his young age. The neurologist spoke to Mike, then examined him. He found that his left eye was deviated to the left and down. When he attempted to look to his right, his right eye moved normally, but his left eye was unable to move further to the right than the midline. His left pupil was dilated and did not contract to light from a penlight. His left eyelid drooped, and he had difficulty raising it. In addition, the right side of his mouth remained motionless when he attempted to smile, but his forehead was symmetric when he raised his eyebrows. Mike's right arm and leg were markedly weak. The neurologist told Mike that he wasn't certain that this was necessarily a stroke, but admitted him to the hospital for observation and tests. Damage to which of the following area caused Mike's weakness?

A.

Left precentral gyrus
B.

Right precentral gyrus
C.

Left cervical spinal cord
D.

Right cervical spinal cord
E.

Left cerebral peduncle

Correct Answer
E. Left cerebral peduncle

Explanation
The third cranial nerve (oculomotor) controls four of the six extraocular muscles that move the eye. When this nerve fails to function, the eye remains deviated laterally due to the unopposed action of the other two extraocular muscles. When the eyes no longer move together, patients have double vision because the visual cortex now receives two different images. In addition, fibers originating in the third nerve nucleus innervate the levator palpebrae superioris, a muscle that helps to lift the eyelid. Damage to the optic nerve causes loss of vision, blurred vision, and a central scotoma (blind spot in the center of the visual field). Damage to the cervical sympathetic fibers causes Horner's syndrome, consisting of ptosis (drooping of the eyelid), miosis (constriction of the pupil), and anhydrosis (loss of sweating), not eye movement abnormalities. The actions of the superior oblique, the muscle innervated by the trochlear nerve, include intorsion, depression, and abduction. The abducens nerve mediates the lateral rectus muscle, which abducts the eye. The eye is depressed and abducted due to the unopposed actions of the superior oblique and lateral rectus muscles, which together move the eye downward and abduct it (see earlier discussion for the actions of these muscles). The other four muscles are innervated by the oculomotor nerve, which presumably has been damaged. This is an example of Weber's syndrome, or a lesion involving the third cranial nerve outflow tract, and the corticospinal and corticobulbar tracts in the cerebral peduncles of the midbrain. Weber's syndrome may occur as a result of an occlusion of the interpeduncular branches of the posterior cerebral artery (which supply this portion of the midbrain), a tumor pressing on this area, an aneurysm (circumscribed dilation of an artery) of the posterior communicating artery, or a plaque (lesion) related to multiple sclerosis. Fibers from the Edinger-Westphal nucleus are affected by lesions of the midbrain as well, and because they are instrumental in constricting the pupil, this lesion causes the patient to have a dilated pupil. If there is a mass that is external to the midbrain, but pressing on the oculomotor nerve, then the preganglionic parasympathetic fibers traveling to the ciliary ganglion, which, in turn, innervate the pupillary constrictor muscles, can be damaged, also causing a dilated pupil. Cervical sympathetic fibers cause pupillary dilatation, so damage to these fibers causes pupillary constriction (see Horner's syndrome, earlier). Involvement of the cerebral peduncle causes damage to the corticospinal and corticobulbar tracts, resulting in weakness of the contralateral face, arm, and leg. The motor deficit is contralateral because the corticospinal tracts cross in the medullary pyramids, below the level of the lesion. The upper portion of Mike's face was spared in this case (as well as in any other UMN lesion) because the face is innervated bilaterally until the level of the caudal pons, so a unilateral lesion results in sparing of this portion of the face. The combination of a third-nerve palsy and contralateral hemiparesis can only occur in the midbrain. The observed effects relating to cranial nerve III could not be accounted for by cortical damage. Likewise, damage to the cervical cord would not affect the third nerve.

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34.

A 17-year-old high school football player presented to a neurology clinic because his mother thought that he may have acquired neck problems during a game. A month before, he had sustained a concussion from a blow to his head from another player. Shortly after, she noted that he intermittently tilted his head to the side. When asked what was the matter, he simply said that sometimes he had double vision, and that the images were situated on top of each other vertically, making it difficult to go down stairs. When examined, there was no neck pain or limitation of motion. He tended to keep his head tilted to the right side. When asked to follow the doctor's finger with his head in a straight position, his left eye would not move downward when his eyes were turned to the right, and tended to remain slightly deviated toward the left. At this point, he stated that he had double vision, and felt better if his head was tilted to the right. The remainder of his eye movements, as well as the remainder of his exam, was normal. In which of the following nerves has the damage occurred?

A.

The oculomotor nerve
B.

The abducens nerve
C.

The trochlear nerve
D.

The trigeminal nerve
E.

The facial nerve

Correct Answer
C. The trochlear nerve

Explanation
Damage to the trochlear nerve causes weakness of the superior oblique muscle, resulting in the inability of the orbit to deviate downward when the eye is intorted. To compensate for the classically vertical double vision, the patient tends to tilt his head to the contralateral side, causing the contralateral eye to intort. The trochlear nerve supplies the superior oblique muscle. The trochlear nerve is the only nerve to decussate peripherally, and also to emerge from the dorsal aspect of the brainstem. In this case, the damaged nerve emerged from the right (contralateral) dorsal midbrain. The action of the superior oblique muscle is to rotate the orbit medially and downward. Because the trochlear nerve is not only the smallest cranial nerve but also has the longest course of any cranial nerve, it is especially vulnerable to trauma. One of the most common causes of trochlear nerve palsy is trauma.

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35.

A 17-year-old high school football player presented to a neurology clinic because his mother thought that he may have acquired neck problems during a game. A month before, he had sustained a concussion from a blow to his head from another player. Shortly after, she noted that he intermittently tilted his head to the side. When asked what was the matter, he simply said that sometimes he had double vision, and that the images were situated on top of each other vertically, making it difficult to go down stairs. When examined, there was no neck pain or limitation of motion. He tended to keep his head tilted to the right side. When asked to follow the doctor's finger with his head in a straight position, his left eye would not move downward when his eyes were turned to the right, and tended to remain slightly deviated toward the left. At this point, he stated that he had double vision, and felt better if his head was tilted to the right. The remainder of his eye movements, as well as the remainder of his exam, was normal. Which of the following muscles is weakened?

A.

Superior rectus
B.

Inferior rectus
C.

Lateral rectus
D.

Superior oblique
E.

Inferior oblique

Correct Answer
D. Superior oblique

Explanation
Damage to the trochlear nerve causes weakness of the superior oblique muscle, resulting in the inability of the orbit to deviate downward when the eye is intorted. To compensate for the classically vertical double vision, the patient tends to tilt his head to the contralateral side, causing the contralateral eye to intort. The trochlear nerve supplies the superior oblique muscle. The trochlear nerve is the only nerve to decussate peripherally, and also to emerge from the dorsal aspect of the brainstem. In this case, the damaged nerve emerged from the right (contralateral) dorsal midbrain. The action of the superior oblique muscle is to rotate the orbit medially and downward. Because the trochlear nerve is not only the smallest cranial nerve but also has the longest course of any cranial nerve, it is especially vulnerable to trauma. One of the most common causes of trochlear nerve palsy is trauma.

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36.

A 17-year-old high school football player presented to a neurology clinic because his mother thought that he may have acquired neck problems during a game. A month before, he had sustained a concussion from a blow to his head from another player. Shortly after, she noted that he intermittently tilted his head to the side. When asked what was the matter, he simply said that sometimes he had double vision, and that the images were situated on top of each other vertically, making it difficult to go down stairs. When examined, there was no neck pain or limitation of motion. He tended to keep his head tilted to the right side. When asked to follow the doctor's finger with his head in a straight position, his left eye would not move downward when his eyes were turned to the right, and tended to remain slightly deviated toward the left. At this point, he stated that he had double vision, and felt better if his head was tilted to the right. The remainder of his eye movements, as well as the remainder of his exam, was normal. From which portion of the brainstem has the damaged nerve emerged?

A.

Right ventral midbrain
B.

Right dorsal midbrain
C.

Left ventral midbrain
D.

Left dorsal midbrain
E.

Left ventral pons

Correct Answer
B. Right dorsal midbrain

Explanation
Damage to the trochlear nerve causes weakness of the superior oblique muscle, resulting in the inability of the orbit to deviate downward when the eye is intorted. To compensate for the classically vertical double vision, the patient tends to tilt his head to the contralateral side, causing the contralateral eye to intort. The trochlear nerve supplies the superior oblique muscle. The trochlear nerve is the only nerve to decussate peripherally, and also to emerge from the dorsal aspect of the brainstem. In this case, the damaged nerve emerged from the right (contralateral) dorsal midbrain. The action of the superior oblique muscle is to rotate the orbit medially and downward. Because the trochlear nerve is not only the smallest cranial nerve but also has the longest course of any cranial nerve, it is especially vulnerable to trauma. One of the most common causes of trochlear nerve palsy is trauma.

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37.

A 17-year-old high school football player presented to a neurology clinic because his mother thought that he may have acquired neck problems during a game. A month before, he had sustained a concussion from a blow to his head from another player. Shortly after, she noted that he intermittently tilted his head to the side. When asked what was the matter, he simply said that sometimes he had double vision, and that the images were situated on top of each other vertically, making it difficult to go down stairs. When examined, there was no neck pain or limitation of motion. He tended to keep his head tilted to the right side. When asked to follow the doctor's finger with his head in a straight position, his left eye would not move downward when his eyes were turned to the right, and tended to remain slightly deviated toward the left. At this point, he stated that he had double vision, and felt better if his head was tilted to the right. The remainder of his eye movements, as well as the remainder of his exam, was normal. Which of the following is the action of the weak muscle?

A.

Outward and upward rotation of the orbit
B.

Outward and downward rotation of the orbit
C.

Inward and upward rotation of the orbit
D.

Inward and downward rotation of the orbit
E.

Deviation of the orbit laterally

Correct Answer
D. Inward and downward rotation of the orbit

Explanation
Damage to the trochlear nerve causes weakness of the superior oblique muscle, resulting in the inability of the orbit to deviate downward when the eye is intorted. To compensate for the classically vertical double vision, the patient tends to tilt his head to the contralateral side, causing the contralateral eye to intort. The trochlear nerve supplies the superior oblique muscle. The trochlear nerve is the only nerve to decussate peripherally, and also to emerge from the dorsal aspect of the brainstem. In this case, the damaged nerve emerged from the right (contralateral) dorsal midbrain. The action of the superior oblique muscle is to rotate the orbit medially and downward. Because the trochlear nerve is not only the smallest cranial nerve but also has the longest course of any cranial nerve, it is especially vulnerable to trauma. One of the most common causes of trochlear nerve palsy is trauma.

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38.

A 17-year-old high school football player presented to a neurology clinic because his mother thought that he may have acquired neck problems during a game. A month before, he had sustained a concussion from a blow to his head from another player. Shortly after, she noted that he intermittently tilted his head to the side. When asked what was the matter, he simply said that sometimes he had double vision, and that the images were situated on top of each other vertically, making it difficult to go down stairs. When examined, there was no neck pain or limitation of motion. He tended to keep his head tilted to the right side. When asked to follow the doctor's finger with his head in a straight position, his left eye would not move downward when his eyes were turned to the right, and tended to remain slightly deviated toward the left. At this point, he stated that he had double vision, and felt better if his head was tilted to the right. The remainder of his eye movements, as well as the remainder of his exam, was normal. How could the head trauma have caused the double vision?

A.

Direct damage to the eye
B.

Damage to the occipital lobes
C.

Damage to the midbrain
D.

Damage to the pons
E.

Damage to the cranial nerve peripherally

Correct Answer
E. Damage to the cranial nerve peripHerally

Explanation
Damage to the trochlear nerve causes weakness of the superior oblique muscle, resulting in the inability of the orbit to deviate downward when the eye is intorted. To compensate for the classically vertical double vision, the patient tends to tilt his head to the contralateral side, causing the contralateral eye to intort. The trochlear nerve supplies the superior oblique muscle. The trochlear nerve is the only nerve to decussate peripherally, and also to emerge from the dorsal aspect of the brainstem. In this case, the damaged nerve emerged from the right (contralateral) dorsal midbrain. The action of the superior oblique muscle is to rotate the orbit medially and downward. Because the trochlear nerve is not only the smallest cranial nerve but also has the longest course of any cranial nerve, it is especially vulnerable to trauma. One of the most common causes of trochlear nerve palsy is trauma.

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39.

Susan is a 32-year-old woman, who recently stopped taking her birth control pills in order to become pregnant. However, after several months, her menstrual period failed to resume. Prior to beginning the birth control pills several years before, she had been having normal cycles. She also noticed headaches, which had been increasing in severity over the past several months. Recently, she became aware of difficulty with her peripheral vision. Thinking that she might be pregnant, she sought the attention of her gynecologist. Her doctor ran a pregnancy test, which was negative. She told her that there may be another cause of the absence of her menstrual cycle, and she sent Susan's blood for levels of various hormones. When Susan returned to find out the results of the tests, her gynecologist told her that the level of the hormone prolactin was high. Susan remembered her headaches and visual symptoms, and informed her doctor, who promptly referred her to a neurologist. The neurologist listened to Susan's story, and examined her. She found only that Susan was unable to see fingers in the temporal fields (lateral half of each visual field) of both of her eyes. The remainder of her neurologic exam was normal. The neurologist told Susan that she would like to order a magnetic resonance imaging (MRI) test of her head, in order to find out why she had the headaches, visual problem, and high prolactin levels. A tumor in which of the following areas could cause a high prolactin level?

A.

Adenohypophysis
B.

Neurohypophysis
C.

Amygdala
D.

Hippocampus
E.

Adrenal gland

Correct Answer
A. AdenohypopHysis

Explanation
The MRI of Susan's head revealed a pituitary microadenoma, a benign tumor arising from the anterior pituitary or adenohypophysis. This particular tumor consisted of cells that secrete the hormone prolactin, which is not only the stimulating factor for lactation, but inhibits menstruation when levels are high. It is common for this tumor's symptoms to be manifested during the child-bearing years. The visual problem is called bitemporal hemianopsia. Since the pituitary gland is in very close proximity to the optic chiasm, pituitary tumors often invade this structure. Since only the medial fibers (which perceive the temporal field of each eye) in each optic nerve cross, these are the fibers damaged by these tumors, and the patient will be unable to see either temporal visual field. Both the central scotoma (an island of visual loss surrounded by normal vision in one eye), which is usually seen with lesions of the retina or optic nerve, and the papilledema (blurring of the optic disc margin when viewed by fundoscopic examination due to increased intracranial pressure) would not be caused by damage to the optic chiasm. The optic chiasm can be compressed by pituitary tumors, causing bitemporal hemianopsia. The prolactin-releasing factor is found in the arcuate nucleus of the hypothalamus and activates the lactotropic cells of the anterior pituitary gland. Several different peptides, including dopamine, have the capacity to raise the level of prolactin in the blood. Specifically, the tuberoinfundibular dopaminergic system regulates prolactin secretion through direct projection to the pituitary. For this reason, a newer treatment for prolactin-secreting microadenomas is the drug bromocriptine, a dopamine agonist commonly used in the treatment of Parkinson's disease. By giving a dopamine agonist, serum prolactin increases, inhibiting production by the tumor cells, and eventually the tumor size shrinks. This has become either an alternative or first-line treatment prior to trying radiation or surgery.

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40.

Susan is a 32-year-old woman, who recently stopped taking her birth control pills in order to become pregnant. However, after several months, her menstrual period failed to resume. Prior to beginning the birth control pills several years before, she had been having normal cycles. She also noticed headaches, which had been increasing in severity over the past several months. Recently, she became aware of difficulty with her peripheral vision. Thinking that she might be pregnant, she sought the attention of her gynecologist. Her doctor ran a pregnancy test, which was negative. She told her that there may be another cause of the absence of her menstrual cycle, and she sent Susan's blood for levels of various hormones. When Susan returned to find out the results of the tests, her gynecologist told her that the level of the hormone prolactin was high. Susan remembered her headaches and visual symptoms, and informed her doctor, who promptly referred her to a neurologist. The neurologist listened to Susan's story, and examined her. She found only that Susan was unable to see fingers in the temporal fields (lateral half of each visual field) of both of her eyes. The remainder of her neurologic exam was normal. The neurologist told Susan that she would like to order a magnetic resonance imaging (MRI) test of her head, in order to find out why she had the headaches, visual problem, and high prolactin levels. Which of the following types of neurologic visual loss can cause a loss of peripheral vision?

A.

Central scotoma
B.

Superior quadrantanopsia
C.

Bitemporal hemianopsia
D.

Homonymous hemianopsia
E.

Papilledema

Correct Answer
C. Bitemporal hemianopsia

Explanation
The MRI of Susan's head revealed a pituitary microadenoma, a benign tumor arising from the anterior pituitary or adenohypophysis. This particular tumor consisted of cells that secrete the hormone prolactin, which is not only the stimulating factor for lactation, but inhibits menstruation when levels are high. It is common for this tumor's symptoms to be manifested during the child-bearing years. The visual problem is called bitemporal hemianopsia. Since the pituitary gland is in very close proximity to the optic chiasm, pituitary tumors often invade this structure. Since only the medial fibers (which perceive the temporal field of each eye) in each optic nerve cross, these are the fibers damaged by these tumors, and the patient will be unable to see either temporal visual field. Both the central scotoma (an island of visual loss surrounded by normal vision in one eye), which is usually seen with lesions of the retina or optic nerve, and the papilledema (blurring of the optic disc margin when viewed by fundoscopic examination due to increased intracranial pressure) would not be caused by damage to the optic chiasm. The optic chiasm can be compressed by pituitary tumors, causing bitemporal hemianopsia. The prolactin-releasing factor is found in the arcuate nucleus of the hypothalamus and activates the lactotropic cells of the anterior pituitary gland. Several different peptides, including dopamine, have the capacity to raise the level of prolactin in the blood. Specifically, the tuberoinfundibular dopaminergic system regulates prolactin secretion through direct projection to the pituitary. For this reason, a newer treatment for prolactin-secreting microadenomas is the drug bromocriptine, a dopamine agonist commonly used in the treatment of Parkinson's disease. By giving a dopamine agonist, serum prolactin increases, inhibiting production by the tumor cells, and eventually the tumor size shrinks. This has become either an alternative or first-line treatment prior to trying radiation or surgery.

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41.

Susan is a 32-year-old woman, who recently stopped taking her birth control pills in order to become pregnant. However, after several months, her menstrual period failed to resume. Prior to beginning the birth control pills several years before, she had been having normal cycles. She also noticed headaches, which had been increasing in severity over the past several months. Recently, she became aware of difficulty with her peripheral vision. Thinking that she might be pregnant, she sought the attention of her gynecologist. Her doctor ran a pregnancy test, which was negative. She told her that there may be another cause of the absence of her menstrual cycle, and she sent Susan's blood for levels of various hormones. When Susan returned to find out the results of the tests, her gynecologist told her that the level of the hormone prolactin was high. Susan remembered her headaches and visual symptoms, and informed her doctor, who promptly referred her to a neurologist. The neurologist listened to Susan's story, and examined her. She found only that Susan was unable to see fingers in the temporal fields (lateral half of each visual field) of both of her eyes. The remainder of her neurologic exam was normal. The neurologist told Susan that she would like to order a magnetic resonance imaging (MRI) test of her head, in order to find out why she had the headaches, visual problem, and high prolactin levels. A lesion adjacent to which of the following structures caused Susan's visual problem

A.

Optic nerve
B.

Optic radiations
C.

Retina
D.

Optic chiasm
E.

Lateral geniculate nucleus

Correct Answer
D. Optic chiasm

Explanation
The MRI of Susan's head revealed a pituitary microadenoma, a benign tumor arising from the anterior pituitary or adenohypophysis. This particular tumor consisted of cells that secrete the hormone prolactin, which is not only the stimulating factor for lactation, but inhibits menstruation when levels are high. It is common for this tumor's symptoms to be manifested during the child-bearing years. The visual problem is called bitemporal hemianopsia. Since the pituitary gland is in very close proximity to the optic chiasm, pituitary tumors often invade this structure. Since only the medial fibers (which perceive the temporal field of each eye) in each optic nerve cross, these are the fibers damaged by these tumors, and the patient will be unable to see either temporal visual field. Both the central scotoma (an island of visual loss surrounded by normal vision in one eye), which is usually seen with lesions of the retina or optic nerve, and the papilledema (blurring of the optic disc margin when viewed by fundoscopic examination due to increased intracranial pressure) would not be caused by damage to the optic chiasm. The optic chiasm can be compressed by pituitary tumors, causing bitemporal hemianopsia. The prolactin-releasing factor is found in the arcuate nucleus of the hypothalamus and activates the lactotropic cells of the anterior pituitary gland. Several different peptides, including dopamine, have the capacity to raise the level of prolactin in the blood. Specifically, the tuberoinfundibular dopaminergic system regulates prolactin secretion through direct projection to the pituitary. For this reason, a newer treatment for prolactin-secreting microadenomas is the drug bromocriptine, a dopamine agonist commonly used in the treatment of Parkinson's disease. By giving a dopamine agonist, serum prolactin increases, inhibiting production by the tumor cells, and eventually the tumor size shrinks. This has become either an alternative or first-line treatment prior to trying radiation or surgery.

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42.

Susan is a 32-year-old woman, who recently stopped taking her birth control pills in order to become pregnant. However, after several months, her menstrual period failed to resume. Prior to beginning the birth control pills several years before, she had been having normal cycles. She also noticed headaches, which had been increasing in severity over the past several months. Recently, she became aware of difficulty with her peripheral vision. Thinking that she might be pregnant, she sought the attention of her gynecologist. Her doctor ran a pregnancy test, which was negative. She told her that there may be another cause of the absence of her menstrual cycle, and she sent Susan's blood for levels of various hormones. When Susan returned to find out the results of the tests, her gynecologist told her that the level of the hormone prolactin was high. Susan remembered her headaches and visual symptoms, and informed her doctor, who promptly referred her to a neurologist. The neurologist listened to Susan's story, and examined her. She found only that Susan was unable to see fingers in the temporal fields (lateral half of each visual field) of both of her eyes. The remainder of her neurologic exam was normal. The neurologist told Susan that she would like to order a magnetic resonance imaging (MRI) test of her head, in order to find out why she had the headaches, visual problem, and high prolactin levels. Which hypothalamic nucleus regulates prolactin secretion?

A.

Suprachiasmatic nucleus
B.

Preoptic nucleus
C.

Paraventricular nucleus
D.

Supraoptic nucleus
E.

Arcuate nucleus

Correct Answer
E. Arcuate nucleus

Explanation
The MRI of Susan's head revealed a pituitary microadenoma, a benign tumor arising from the anterior pituitary or adenohypophysis. This particular tumor consisted of cells that secrete the hormone prolactin, which is not only the stimulating factor for lactation, but inhibits menstruation when levels are high. It is common for this tumor's symptoms to be manifested during the child-bearing years. The visual problem is called bitemporal hemianopsia. Since the pituitary gland is in very close proximity to the optic chiasm, pituitary tumors often invade this structure. Since only the medial fibers (which perceive the temporal field of each eye) in each optic nerve cross, these are the fibers damaged by these tumors, and the patient will be unable to see either temporal visual field. Both the central scotoma (an island of visual loss surrounded by normal vision in one eye), which is usually seen with lesions of the retina or optic nerve, and the papilledema (blurring of the optic disc margin when viewed by fundoscopic examination due to increased intracranial pressure) would not be caused by damage to the optic chiasm. The optic chiasm can be compressed by pituitary tumors, causing bitemporal hemianopsia. The prolactin-releasing factor is found in the arcuate nucleus of the hypothalamus and activates the lactotropic cells of the anterior pituitary gland. Several different peptides, including dopamine, have the capacity to raise the level of prolactin in the blood. Specifically, the tuberoinfundibular dopaminergic system regulates prolactin secretion through direct projection to the pituitary. For this reason, a newer treatment for prolactin-secreting microadenomas is the drug bromocriptine, a dopamine agonist commonly used in the treatment of Parkinson's disease. By giving a dopamine agonist, serum prolactin increases, inhibiting production by the tumor cells, and eventually the tumor size shrinks. This has become either an alternative or first-line treatment prior to trying radiation or surgery.

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43.

Susan is a 32-year-old woman, who recently stopped taking her birth control pills in order to become pregnant. However, after several months, her menstrual period failed to resume. Prior to beginning the birth control pills several years before, she had been having normal cycles. She also noticed headaches, which had been increasing in severity over the past several months. Recently, she became aware of difficulty with her peripheral vision. Thinking that she might be pregnant, she sought the attention of her gynecologist. Her doctor ran a pregnancy test, which was negative. She told her that there may be another cause of the absence of her menstrual cycle, and she sent Susan's blood for levels of various hormones. When Susan returned to find out the results of the tests, her gynecologist told her that the level of the hormone prolactin was high. Susan remembered her headaches and visual symptoms, and informed her doctor, who promptly referred her to a neurologist. The neurologist listened to Susan's story, and examined her. She found only that Susan was unable to see fingers in the temporal fields (lateral half of each visual field) of both of her eyes. The remainder of her neurologic exam was normal. The neurologist told Susan that she would like to order a magnetic resonance imaging (MRI) test of her head, in order to find out why she had the headaches, visual problem, and high prolactin levels. Which neurotransmitter system regulates prolactin secretion

A.

Tuberoinfundibular dopaminergic system
B.

Nigrostriatal dopaminergic system
C.

Mesolimbic dopaminergic system
D.

Mesocortical dopaminergic system
E.

Mesostriatal dopaminergic system

Correct Answer
A. Tuberoinfundibular dopaminergic system

Explanation
The MRI of Susan's head revealed a pituitary microadenoma, a benign tumor arising from the anterior pituitary or adenohypophysis. This particular tumor consisted of cells that secrete the hormone prolactin, which is not only the stimulating factor for lactation, but inhibits menstruation when levels are high. It is common for this tumor's symptoms to be manifested during the child-bearing years. The visual problem is called bitemporal hemianopsia. Since the pituitary gland is in very close proximity to the optic chiasm, pituitary tumors often invade this structure. Since only the medial fibers (which perceive the temporal field of each eye) in each optic nerve cross, these are the fibers damaged by these tumors, and the patient will be unable to see either temporal visual field. Both the central scotoma (an island of visual loss surrounded by normal vision in one eye), which is usually seen with lesions of the retina or optic nerve, and the papilledema (blurring of the optic disc margin when viewed by fundoscopic examination due to increased intracranial pressure) would not be caused by damage to the optic chiasm. The optic chiasm can be compressed by pituitary tumors, causing bitemporal hemianopsia. The prolactin-releasing factor is found in the arcuate nucleus of the hypothalamus and activates the lactotropic cells of the anterior pituitary gland. Several different peptides, including dopamine, have the capacity to raise the level of prolactin in the blood. Specifically, the tuberoinfundibular dopaminergic system regulates prolactin secretion through direct projection to the pituitary. For this reason, a newer treatment for prolactin-secreting microadenomas is the drug bromocriptine, a dopamine agonist commonly used in the treatment of Parkinson's disease. By giving a dopamine agonist, serum prolactin increases, inhibiting production by the tumor cells, and eventually the tumor size shrinks. This has become either an alternative or first-line treatment prior to trying radiation or surgery.

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44.

Sam is a 62-year-old man, previously healthy, who was brought to a neurologist by his daughter because of increasing difficulty walking. His daughter noticed that for the past year, he had difficulty getting out of a chair and took a lot of time to begin to walk. When he did walk, he walked with a slow, shuffling gait. In addition, she had noticed some changes in his face, and that he had been drooling excessively. His signature on checks became progressively smaller from the beginning of his name to the end, and he had developed a new tremor. She brought him in to make sure this wasn't just "aging." The neurologist examined Sam and noticed immediately that Sam's facial expression was masklike, with few eyeblinks. When asked to write a sentence, the letters became progressively smaller toward the end of the sentence. His speech was soft and monotonous, and he had a slow, resting pill-rolling tremor in both of his hands. He had very little spontaneous movement, and his arms, legs, and trunk were stiff. When the neurologist tried to flex his arm, he felt many catches, similar to a cogwheel. There was no weakness, sensory problems, or abnormalities in his reflexes. When asked to walk, Sam took many tries to rise from his chair. When he finally stood up, his posture was stooped and flexed. His gait was slow, his feet shuffled when he walked, and his arms didn't swing with his steps. The neurologist told Sam's daughter that she was correct that this wasn't aging, and explained to her all of the details about a new medication that Sam needed to take. Damage to which of the following structures in particular causes Sam's problem with movement

A.

Substantia gelatinosa
B.

Substantia nigra, pars reticularis
C.

Substantia nigra, pars compacta
D.

Caudate nucleus
E.

Thalamus

Correct Answer
C. Substantia nigra, pars compacta

Explanation
Sam has Parkinson's disease, a degenerative condition caused by progressive loss of dopaminergic cells in the substantia nigra, pars compacta. This is an area that controls the speed and spontaneity of movement, so damage to this area can produce deficits that include: a slow shuffling gait with a tendency to move progressively faster (festinating gait); problems with maintaining size in handwriting, with a tendency to write with small letters (micrographia); masklike facial expression with a paucity of eyeblinks; and difficulty getting out of a chair. Other problems include a soft, monotonous voice; muscle rigidity (lead-pipe rigidity); a tremor at rest that is "pill-rolling"; and a combination of a tremor and rigidity, especially in the arms, which, when flexion is attempted, elicits a "cogwheeling" property. Failure to swallow with a normal frequency makes drooling a problem. Dementia (senility) is also a problem with Parkinson's patients, especially later in the course of the disease. The blood supply to the substantia nigra arises from the posterior circulation, specifically the posteromedial branches of the posterior cerebral artery and branches of the posterior communicating artery. The lenticulostriate branches of the middle cerebral artery supply other portions of the basal ganglia, such as the striatum and the globus pallidus. The anterior choroidal artery also supplies some of the telencephalic nuclei of the basal ganglia. The majority of cells that are lost in this disease are dopaminergic cells in the substantia nigra, pars compacta. Only the pars compacta region of the substantia nigra contains dopaminergic neurons. Medications are currently available to lessen the symptoms of Parkinson's disease. Some of these medications contain various concentrations of L-dopa, an immediate precursor to dopamine. Dopamine itself doesn't cross the blood-brain barrier, so it cannot be directly replaced. Medications that antagonize the breakdown of catecholamines by monoamine oxidase can increase the amount of dopamine available for the remaining cells in the substantia nigra.

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45.

Sam is a 62-year-old man, previously healthy, who was brought to a neurologist by his daughter because of increasing difficulty walking. His daughter noticed that for the past year, he had difficulty getting out of a chair and took a lot of time to begin to walk. When he did walk, he walked with a slow, shuffling gait. In addition, she had noticed some changes in his face, and that he had been drooling excessively. His signature on checks became progressively smaller from the beginning of his name to the end, and he had developed a new tremor. She brought him in to make sure this wasn't just "aging." The neurologist examined Sam and noticed immediately that Sam's facial expression was masklike, with few eyeblinks. When asked to write a sentence, the letters became progressively smaller toward the end of the sentence. His speech was soft and monotonous, and he had a slow, resting pill-rolling tremor in both of his hands. He had very little spontaneous movement, and his arms, legs, and trunk were stiff. When the neurologist tried to flex his arm, he felt many catches, similar to a cogwheel. There was no weakness, sensory problems, or abnormalities in his reflexes. When asked to walk, Sam took many tries to rise from his chair. When he finally stood up, his posture was stooped and flexed. His gait was slow, his feet shuffled when he walked, and his arms didn't swing with his steps. The neurologist told Sam's daughter that she was correct that this wasn't aging, and explained to her all of the details about a new medication that Sam needed to take. Which of the following neurotransmitters is deficient?

A.

Norepinephrine
B.

Glutamate
C.

Dopamine
D.

ACh
E.

GABA

Correct Answer
C. Dopamine

Explanation
Sam has Parkinson's disease, a degenerative condition caused by progressive loss of dopaminergic cells in the substantia nigra, pars compacta. This is an area that controls the speed and spontaneity of movement, so damage to this area can produce deficits that include: a slow shuffling gait with a tendency to move progressively faster (festinating gait); problems with maintaining size in handwriting, with a tendency to write with small letters (micrographia); masklike facial expression with a paucity of eyeblinks; and difficulty getting out of a chair. Other problems include a soft, monotonous voice; muscle rigidity (lead-pipe rigidity); a tremor at rest that is "pill-rolling"; and a combination of a tremor and rigidity, especially in the arms, which, when flexion is attempted, elicits a "cogwheeling" property. Failure to swallow with a normal frequency makes drooling a problem. Dementia (senility) is also a problem with Parkinson's patients, especially later in the course of the disease. The blood supply to the substantia nigra arises from the posterior circulation, specifically the posteromedial branches of the posterior cerebral artery and branches of the posterior communicating artery. The lenticulostriate branches of the middle cerebral artery supply other portions of the basal ganglia, such as the striatum and the globus pallidus. The anterior choroidal artery also supplies some of the telencephalic nuclei of the basal ganglia. The majority of cells that are lost in this disease are dopaminergic cells in the substantia nigra, pars compacta. Only the pars compacta region of the substantia nigra contains dopaminergic neurons. Medications are currently available to lessen the symptoms of Parkinson's disease. Some of these medications contain various concentrations of L-dopa, an immediate precursor to dopamine. Dopamine itself doesn't cross the blood-brain barrier, so it cannot be directly replaced. Medications that antagonize the breakdown of catecholamines by monoamine oxidase can increase the amount of dopamine available for the remaining cells in the substantia nigra.

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46.

Sam is a 62-year-old man, previously healthy, who was brought to a neurologist by his daughter because of increasing difficulty walking. His daughter noticed that for the past year, he had difficulty getting out of a chair and took a lot of time to begin to walk. When he did walk, he walked with a slow, shuffling gait. In addition, she had noticed some changes in his face, and that he had been drooling excessively. His signature on checks became progressively smaller from the beginning of his name to the end, and he had developed a new tremor. She brought him in to make sure this wasn't just "aging." The neurologist examined Sam and noticed immediately that Sam's facial expression was masklike, with few eyeblinks. When asked to write a sentence, the letters became progressively smaller toward the end of the sentence. His speech was soft and monotonous, and he had a slow, resting pill-rolling tremor in both of his hands. He had very little spontaneous movement, and his arms, legs, and trunk were stiff. When the neurologist tried to flex his arm, he felt many catches, similar to a cogwheel. There was no weakness, sensory problems, or abnormalities in his reflexes. When asked to walk, Sam took many tries to rise from his chair. When he finally stood up, his posture was stooped and flexed. His gait was slow, his feet shuffled when he walked, and his arms didn't swing with his steps. The neurologist told Sam's daughter that she was correct that this wasn't aging, and explained to her all of the details about a new medication that Sam needed to take. Which of the following is a precursor to the deficient neurotransmitter, and can be given as a medication to improve Sam's movement?

A.

Tyrosine
B.

Choline
C.

Acetyl-CoA
D.

Tryptamine
E.

L-dopa

Correct Answer
E. L-dopa

Explanation
Sam has Parkinson's disease, a degenerative condition caused by progressive loss of dopaminergic cells in the substantia nigra, pars compacta. This is an area that controls the speed and spontaneity of movement, so damage to this area can produce deficits that include: a slow shuffling gait with a tendency to move progressively faster (festinating gait); problems with maintaining size in handwriting, with a tendency to write with small letters (micrographia); masklike facial expression with a paucity of eyeblinks; and difficulty getting out of a chair. Other problems include a soft, monotonous voice; muscle rigidity (lead-pipe rigidity); a tremor at rest that is "pill-rolling"; and a combination of a tremor and rigidity, especially in the arms, which, when flexion is attempted, elicits a "cogwheeling" property. Failure to swallow with a normal frequency makes drooling a problem. Dementia (senility) is also a problem with Parkinson's patients, especially later in the course of the disease. The blood supply to the substantia nigra arises from the posterior circulation, specifically the posteromedial branches of the posterior cerebral artery and branches of the posterior communicating artery. The lenticulostriate branches of the middle cerebral artery supply other portions of the basal ganglia, such as the striatum and the globus pallidus. The anterior choroidal artery also supplies some of the telencephalic nuclei of the basal ganglia. The majority of cells that are lost in this disease are dopaminergic cells in the substantia nigra, pars compacta. Only the pars compacta region of the substantia nigra contains dopaminergic neurons. Medications are currently available to lessen the symptoms of Parkinson's disease. Some of these medications contain various concentrations of L-dopa, an immediate precursor to dopamine. Dopamine itself doesn't cross the blood-brain barrier, so it cannot be directly replaced. Medications that antagonize the breakdown of catecholamines by monoamine oxidase can increase the amount of dopamine available for the remaining cells in the substantia nigra.

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47.

Sam is a 62-year-old man, previously healthy, who was brought to a neurologist by his daughter because of increasing difficulty walking. His daughter noticed that for the past year, he had difficulty getting out of a chair and took a lot of time to begin to walk. When he did walk, he walked with a slow, shuffling gait. In addition, she had noticed some changes in his face, and that he had been drooling excessively. His signature on checks became progressively smaller from the beginning of his name to the end, and he had developed a new tremor. She brought him in to make sure this wasn't just "aging." The neurologist examined Sam and noticed immediately that Sam's facial expression was masklike, with few eyeblinks. When asked to write a sentence, the letters became progressively smaller toward the end of the sentence. His speech was soft and monotonous, and he had a slow, resting pill-rolling tremor in both of his hands. He had very little spontaneous movement, and his arms, legs, and trunk were stiff. When the neurologist tried to flex his arm, he felt many catches, similar to a cogwheel. There was no weakness, sensory problems, or abnormalities in his reflexes. When asked to walk, Sam took many tries to rise from his chair. When he finally stood up, his posture was stooped and flexed. His gait was slow, his feet shuffled when he walked, and his arms didn't swing with his steps. The neurologist told Sam's daughter that she was correct that this wasn't aging, and explained to her all of the details about a new medication that Sam needed to take. The antagonism of which of the following enzymes by drugs will increase the amount of the deficient neurotransmitter?

A.

Choline acetyltranferase
B.

Monoamine oxidase
C.

GABA transaminase
D.

Acetylcholinesterase
E.

Tyrosine hydroxylase

Correct Answer
B. Monoamine oxidase

Explanation
Sam has Parkinson's disease, a degenerative condition caused by progressive loss of dopaminergic cells in the substantia nigra, pars compacta. This is an area that controls the speed and spontaneity of movement, so damage to this area can produce deficits that include: a slow shuffling gait with a tendency to move progressively faster (festinating gait); problems with maintaining size in handwriting, with a tendency to write with small letters (micrographia); masklike facial expression with a paucity of eyeblinks; and difficulty getting out of a chair. Other problems include a soft, monotonous voice; muscle rigidity (lead-pipe rigidity); a tremor at rest that is "pill-rolling"; and a combination of a tremor and rigidity, especially in the arms, which, when flexion is attempted, elicits a "cogwheeling" property. Failure to swallow with a normal frequency makes drooling a problem. Dementia (senility) is also a problem with Parkinson's patients, especially later in the course of the disease. The blood supply to the substantia nigra arises from the posterior circulation, specifically the posteromedial branches of the posterior cerebral artery and branches of the posterior communicating artery. The lenticulostriate branches of the middle cerebral artery supply other portions of the basal ganglia, such as the striatum and the globus pallidus. The anterior choroidal artery also supplies some of the telencephalic nuclei of the basal ganglia. The majority of cells that are lost in this disease are dopaminergic cells in the substantia nigra, pars compacta. Only the pars compacta region of the substantia nigra contains dopaminergic neurons. Medications are currently available to lessen the symptoms of Parkinson's disease. Some of these medications contain various concentrations of L-dopa, an immediate precursor to dopamine. Dopamine itself doesn't cross the blood-brain barrier, so it cannot be directly replaced. Medications that antagonize the breakdown of catecholamines by monoamine oxidase can increase the amount of dopamine available for the remaining cells in the substantia nigra.

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48.

John is a 57-year-old man who has always been a very heavy drinker, often consuming 2 pints of whiskey per day, for many years. Upon the urging of his wife, he decided to seek medical attention for help with problems with his gait, which has steadily worsened over the past several months. He noticed that he now needed to stand with his feet far apart in order to maintain his balance and that he waddled when he walked. The doctor who evaluated him tested his memory and speech carefully, as well as his cranial nerves, and was unable to find any deficits. There was no weakness, sensory loss, or abnormalities in his reflexes. When asked to touch the doctor's finger, then his nose, John missed his nose slightly, but rapidly corrected the movement on both sides. When asked to slide his right heel down his left shin, his heel slid sideways and clumsily across the bone until it reached his ankle. The response with the left heel was similar. When asked to walk, John walked with his feet very far apart. If he attempted to walk in a tandem fashion, with one heel in front of the other toe, he began to fall, and the doctor needed to catch him. The doctor ordered an magnetic resonance imaging (MRI) of John's head. What term could one use for John's gait?

A.

Stiff
B.

Festinating
C.

Ataxic
D.

Spastic
E.

Shuffling

Correct Answer
C. Ataxic

Explanation
An ataxic gait is an unsteady gait. Gaits due to motor weakness or spasticity tend to involve circling of the weak leg (circumduction); festinating or shuffling gaits, which are often due to parkinsonism or disease of the basal ganglia, involve a stooped posture with shuffling of the feet and very small steps. An ataxic gait may result from motor incoordination due to cerebellar disease, or from lack of proprioception in the lower extremities due to disease in the posterior column system (gait becomes unsteady when a patient is unable to detect the location of his or her feet). Degeneration of both systems may occur due to alcoholism, although in this case, we are told that John does not have any sensory deficits when this modality is tested in isolation. This is an example of alcoholic cerebellar degeneration. It is caused by degeneration (probably through nutritional deficiency) of neurons in the cerebellar cortex, particularly of the Purkinje cells, and is usually restricted to anterior and superior parts of the vermis, as well as anterior portions of the anterior lobes. For this reason, most of the deficits in this syndrome involve midline structures such as the trunk, which are represented most in the vermis. Trunk instability usually causes problems with gait. In addition, because the cerebellar homunculus represents the legs in the anterior portion of the anterior lobe, the legs are affected more than the arms. Loss of volume within the vermis of the cerebellum is readily visualized, especially on an MRI of the brain, because this technique allows good visualization of the posterior fossa. If these changes are visualized, then the condition is most likely chronic (as also indicated by the history) and most likely irreversible. However, it is important to make sure that the patient is well nourished, takes vitamins, and stops drinking in order to prevent other neurologic problems from occurring. Damage to other brain regions listed do not cause such damage. The spinocerebellum receives sensory inputs from the spinal cord and is instrumental in controlling posture and movement. It includes the vermis and the intermediate hemisphere. The cerebrocerebellum consists of the lateral hemispheres and is instrumental in the planning of movement. The dentate nucleus comprises the cell bodies that form the superior cerebellar peduncle. The brachium pontis corresponds to the middle cerebellar peduncle. The spinocerebellar cortical (Purkinje) cells project to the fastigial and interposed nuclei. Purkinje cells are found in the cerebellar cortex. None of the other choices are cells that are found in the cerebellum.

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49.

John is a 57-year-old man who has always been a very heavy drinker, often consuming 2 pints of whiskey per day, for many years. Upon the urging of his wife, he decided to seek medical attention for help with problems with his gait, which has steadily worsened over the past several months. He noticed that he now needed to stand with his feet far apart in order to maintain his balance and that he waddled when he walked. The doctor who evaluated him tested his memory and speech carefully, as well as his cranial nerves, and was unable to find any deficits. There was no weakness, sensory loss, or abnormalities in his reflexes. When asked to touch the doctor's finger, then his nose, John missed his nose slightly, but rapidly corrected the movement on both sides. When asked to slide his right heel down his left shin, his heel slid sideways and clumsily across the bone until it reached his ankle. The response with the left heel was similar. When asked to walk, John walked with his feet very far apart. If he attempted to walk in a tandem fashion, with one heel in front of the other toe, he began to fall, and the doctor needed to catch him. The doctor ordered an magnetic resonance imaging (MRI) of John's head. A gait problem of this type could be caused by lesions in which of the following system(s)?

A.

Cerebellar tracts only
B.

Posterior columns only
C.

Corticospinal tracts
D.

Both the cerebellar and posterior column systems
E.

Spinothalamic system

Correct Answer
D. Both the cerebellar and posterior column systems

Explanation
An ataxic gait is an unsteady gait. Gaits due to motor weakness or spasticity tend to involve circling of the weak leg (circumduction); festinating or shuffling gaits, which are often due to parkinsonism or disease of the basal ganglia, involve a stooped posture with shuffling of the feet and very small steps. An ataxic gait may result from motor incoordination due to cerebellar disease, or from lack of proprioception in the lower extremities due to disease in the posterior column system (gait becomes unsteady when a patient is unable to detect the location of his or her feet). Degeneration of both systems may occur due to alcoholism, although in this case, we are told that John does not have any sensory deficits when this modality is tested in isolation. This is an example of alcoholic cerebellar degeneration. It is caused by degeneration (probably through nutritional deficiency) of neurons in the cerebellar cortex, particularly of the Purkinje cells, and is usually restricted to anterior and superior parts of the vermis, as well as anterior portions of the anterior lobes. For this reason, most of the deficits in this syndrome involve midline structures such as the trunk, which are represented most in the vermis. Trunk instability usually causes problems with gait. In addition, because the cerebellar homunculus represents the legs in the anterior portion of the anterior lobe, the legs are affected more than the arms. Loss of volume within the vermis of the cerebellum is readily visualized, especially on an MRI of the brain, because this technique allows good visualization of the posterior fossa. If these changes are visualized, then the condition is most likely chronic (as also indicated by the history) and most likely irreversible. However, it is important to make sure that the patient is well nourished, takes vitamins, and stops drinking in order to prevent other neurologic problems from occurring. Damage to other brain regions listed do not cause such damage. The spinocerebellum receives sensory inputs from the spinal cord and is instrumental in controlling posture and movement. It includes the vermis and the intermediate hemisphere. The cerebrocerebellum consists of the lateral hemispheres and is instrumental in the planning of movement. The dentate nucleus comprises the cell bodies that form the superior cerebellar peduncle. The brachium pontis corresponds to the middle cerebellar peduncle. The spinocerebellar cortical (Purkinje) cells project to the fastigial and interposed nuclei. Purkinje cells are found in the cerebellar cortex. None of the other choices are cells that are found in the cerebellum.

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50.

John is a 57-year-old man who has always been a very heavy drinker, often consuming 2 pints of whiskey per day, for many years. Upon the urging of his wife, he decided to seek medical attention for help with problems with his gait, which has steadily worsened over the past several months. He noticed that he now needed to stand with his feet far apart in order to maintain his balance and that he waddled when he walked. The doctor who evaluated him tested his memory and speech carefully, as well as his cranial nerves, and was unable to find any deficits. There was no weakness, sensory loss, or abnormalities in his reflexes. When asked to touch the doctor's finger, then his nose, John missed his nose slightly, but rapidly corrected the movement on both sides. When asked to slide his right heel down his left shin, his heel slid sideways and clumsily across the bone until it reached his ankle. The response with the left heel was similar. When asked to walk, John walked with his feet very far apart. If he attempted to walk in a tandem fashion, with one heel in front of the other toe, he began to fall, and the doctor needed to catch him. The doctor ordered an magnetic resonance imaging (MRI) of John's head. Where in the brain would a neurologist expect to visualize a lesion on an MRI scan?

A.

Red nucleus
B.

Cerebellar vermis
C.

Substantia nigra
D.

Internal capsule
E.

Basilar pons

Correct Answer
B. Cerebellar vermis

Explanation
An ataxic gait is an unsteady gait. Gaits due to motor weakness or spasticity tend to involve circling of the weak leg (circumduction); festinating or shuffling gaits, which are often due to parkinsonism or disease of the basal ganglia, involve a stooped posture with shuffling of the feet and very small steps. An ataxic gait may result from motor incoordination due to cerebellar disease, or from lack of proprioception in the lower extremities due to disease in the posterior column system (gait becomes unsteady when a patient is unable to detect the location of his or her feet). Degeneration of both systems may occur due to alcoholism, although in this case, we are told that John does not have any sensory deficits when this modality is tested in isolation. This is an example of alcoholic cerebellar degeneration. It is caused by degeneration (probably through nutritional deficiency) of neurons in the cerebellar cortex, particularly of the Purkinje cells, and is usually restricted to anterior and superior parts of the vermis, as well as anterior portions of the anterior lobes. For this reason, most of the deficits in this syndrome involve midline structures such as the trunk, which are represented most in the vermis. Trunk instability usually causes problems with gait. In addition, because the cerebellar homunculus represents the legs in the anterior portion of the anterior lobe, the legs are affected more than the arms. Loss of volume within the vermis of the cerebellum is readily visualized, especially on an MRI of the brain, because this technique allows good visualization of the posterior fossa. If these changes are visualized, then the condition is most likely chronic (as also indicated by the history) and most likely irreversible. However, it is important to make sure that the patient is well nourished, takes vitamins, and stops drinking in order to prevent other neurologic problems from occurring. Damage to other brain regions listed do not cause such damage. The spinocerebellum receives sensory inputs from the spinal cord and is instrumental in controlling posture and movement. It includes the vermis and the intermediate hemisphere. The cerebrocerebellum consists of the lateral hemispheres and is instrumental in the planning of movement. The dentate nucleus comprises the cell bodies that form the superior cerebellar peduncle. The brachium pontis corresponds to the middle cerebellar peduncle. The spinocerebellar cortical (Purkinje) cells project to the fastigial and interposed nuclei. Purkinje cells are found in the cerebellar cortex. None of the other choices are cells that are found in the cerebellum.

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