Upper motor neuron disease

A 67-year-old man was taken to the emergency room after collapsing in a movie theater. The patient regained consciousness and, several days later, displayed a right-side paralysis with pronounced spasticity. The neurologist concluded that the stroke might have involved:

a. Ventral horn cells

b. Cerebellum

c. Internal capsule

d. Postcentral gyrus

e. Pontine tegmentum

Answer: c

An upper motor neuron paralysis results in a paralysis or paresis of the contralateral limb(s), Babinski sign, spasticity, and hypertonicity. The most common sites where lesions produce this syndrome include the motor regions of the cerebral cortex, internal capsule, and other regions that contain the descending fi bers of the corticospinal and corticobulbar tracts, such as the basilar pons and lateral funiculus of the spinal cord. A lower motor neuron paralysis is characterized by a fl accid paralysis of the affected limbs and results from a lesion of the ventral horn cells that innervate the muscles in question directly. Regions such as the cerebellum, postcentral gyrus, and pontine tegmentum do not produce paralysis and spasticity when damaged. They do produce other defi cits, such as movement disorders with respect to the cerebellum, coma with respect to the pontine tegmentum, and somatosensory defi cits with respect to the postcentral gyrus, which are described in later chapters.

A patient presented with paralysis of the left side of the

limbs and left side of the lower face and deviation of the

tongue to the left with no atrophy and with no loss of taste

sensation. This constellation of defi cits most likely resulted

from a lesion of the:

a. Left internal capsule

b. Right internal capsule

c. Left pontine tegmentum

d. Ventromedial medulla on the right side

e. Ventromedial medulla on the left side

Answer: b

The right internal capsule contains corticospinal and corticobulbar fi bers that project to the contralateral spinal cord and to the brainstem. The corticobulbar fi bers that project predom-

inantly to the contralateral side include those fi bers that innervate motor nuclei of cranial nerves VII (lower facial muscles) and XII (hypoglossal). Therefore, a lesion of the right internal capsule will result in paralysis of the limbs on the left side, a deviation of the tongue to the left side (i.e., side opposite to the lesion), and paralysis of the right side of the lower face. A lesion of the right ventromedial medulla is too far caudal to affect corticobulbar fi bers that supply the facial nucleus. Because the defects are on the left side, all of the choices that involve a lesion on the same (i.e., left) side are incorrect because lesions of the corticospinal and corticobulbar fi bers result In motor defi cits that are manifested on the contralateral side.

A 35-year-old man suffered a stroke that did not cause paralysis. However, he discovered that he was unable to perform complex learned movements. The region of the cerebral cortex most likely affected by the stroke was the:

a. Precentral gyrus

b. Postcentral gyrus

c. Premotor cortex

d. Temporal neocortex

e. Prefrontal cortex

Answer: c

The premotor area is extremely important in providing sequencing or programming mechanism for learned movements. The most signifi cant inputs come from the posterior parietal cortex. The premotor cortex then signals the appropriate groups of neurons in the spinal cord (and/or brainstem) to respond in a particular set of sequences. Therefore, damage to this region would result in loss of the sequencing mechanism that is so necessary for the occurrence of complex learned movements. The resulting disorder is called apraxia . Damage to the postcentral gyrus will produce a somatosensory loss. Damage to the precentral gyrus will produce an upper motor neuron paralysis. Damage to the temporal cortex will produce an auditory loss, and damage to the prefrontal cortex will produce different kinds of intellectual defi cits, none of which include apraxia.

An investigator designed an experiment to characterize how neurons in the lower brainstem respond to administration of a specifi c neurotoxic substance. To effectively carry out this study, it was necessary to use a decerebrate preparation in which the region of the brain rostral to the pons was disconnected from the brainstem and spinal cord. Following this surgery, the investigator noted that the animal displayed marked rigidity of the limbs, which was most pronounced in the hind limbs. When the student of this investigator asked why there was such pronounced rigidity, the investigator should have provided which of the following reasons?

a. There is direct loss of inhibitory neurons from the motor

cortex to the spinal cord.

b. There is damage to the red nucleus with preservation of

the reticulospinal tracts and cerebellar cortex.

c. There is preservation of the lateral vestibulospinal tract

with loss of cortical inputs to reticular formation.

d. There is loss of hypothalamic inputs to the brainstem,

which normally have excitatory effects on inhibitory

pathways of the brainstem.

e. There is selective loss of input from the cerebral cortex

to the pontine reticular formation and medial reticulospi-

nal tract.

Answer: c

The lateral vestibular nucleus gives rise to the lateral vestibulospinal tract, which projects to all levels of the spinal cord. The tract passes in the ventral funiculus of the cord and innervates alpha and gamma motor neurons of extensors and provides powerful excitation of these neurons. A decerebrate preparation leaves this pathway intact, while other inhibitory inputs are lost, in particular, to the reticular formation and its descending motor pathways. Collectively, this allows for unopposed excitatory actions of the lateral vestibulospinal tract on extensor motor neurons. The other choices are incorrect. The infl uence of the motor cortex on the spinal cord is generally excitatory. The red nucleus excites fl exor motor neurons,and its loss would not account for decerebrate rigidity. In addition, reticulospinal pathways (in particular, the lateral reticulospinal tract) are dependent on inputs from the cerebral cortex,and, thus, their effects on spinal motor neurons would not be preserved. The medial reticulospinal tract facilitates extensor motor tone. Accordingly, the rigidity could not be accounted for by postulating a selective loss of cortical inputs to this pathway because it would imply that such loss would achieve just the opposite of rigidity. The hypothalamus has no known infl uences on extensor motor tone.

During what appeared to be routine surgery for a torn ligament, a middle-aged man suffered a stroke. After a few days, the patient showed some recovery because he was able to walk with some diffi culty, and, in addition, sensory functions seemed normal. However, a neurologic evaluation revealed a weakness in muscles that regulate breathing, speech, swallowing, and facial expression. A subsequent magnetic resonance imaging scan indicated that the stroke was limited but primarily affected the:

a. Premotor cortex

b. Medullary pyramids

c. Posterior limb of internal capsule

d. Genu of internal capsule

e. Anterior limb of internal capsule

Answer: d

The symptoms described in this case refl ect pseudobulbar palsy , which is characterized by weakness in the muscles of the head and face. It involves corticobulbar pathways that innervate, in part, cranial nerve motor nuclei. These fi bers are contained in the genu of the internal capsule. Damage to the premotor cortex would produce a form of apraxia. Damage to the medullary pyramids is too low to affect corticobulbar fi bers, which supply the facial nerve. The posterior limb of the internal capsule contains corticospinal fi bers, which have no infl uence on brainstem cranial nerve activity. The anterior limb of the internal capsule contains frontopontine fi bers, which synapse with pontine nuclei in the basilar pons and, thus, constitute part of a circuit linking the cerebral and cerebellar cortices. Accordingly, this pathway is not related to functions of cranial nerve motor nuclei.

Somatosensory system

A 47-year-old man complained to his physician that he had recently begun to experience some diffi culty in maintaining his balance while attempting to walk and loss of ability to recognize objects placed in his hand when his eyes were closed. His internist referred him to a local neurology clinic where a battery of tests revealed the presence of a growing tumor. The tumor was most likely affecting the:

a. Anterior spinocerebellar tract

b. Posterior spinocerebellar tract

c. Dorsolateral tract of Lissauer

d. Dorsal columns

e. Neospinothalamic tract

Answer: d

The dorsal columns of the spinal cord contain the fasciculus gracilis and fasciculus cuneatus. Patients with lesions in the dorsal columns have loss of kinesthetic sensation and, thus, are unable to identify the position of their limbs in space when their eyes are closed, and these patients also do not know if one of their joints is in fl exion or extension. In addition, they cannot identify the shape, size, or texture of objects in their hands by means of touch (astereognosis). These patients are unable to perceive vibration when it is applied to their bodies and, therefore, cannot maintain steady posture when their eyes are closed. The posterior and anterior spinocerebellar tracts are involved in nonconscious sensation of limb proprioception. The lateral neospinothalamic tract and dorsolateral tract of Lissauer are involved in mediating pain sensation.

A 67-year-old woman was admitted to the emergency room complaining of brief, repetitive paroxysms of excruciating pain in the face region. Following a neurologic examination, it was concluded that the patient was suffering from trigeminal neuralgia. After pharmacological approaches failed to alleviate the pain, neurosurgery was recommended. The neurosurgeon’s goal was to surgically destroy a small region of the central nervous system. The most logical location of this lesion was the:

a. Dorsomedial pons

b. Ventromedial aspect of midbrain

c. Lateral aspect of lower medulla

d. Substantia gelatinosa

e. Basilar pons

Answer: c

Trigeminal neuralgia is characterized by episodes of excruciating pain that feel like stabbing. It is precipitated by activities like eating and brushing one’s teeth and is limited to the sensory distribution of the trigeminal nerve located in the face. Surgical intervention is sometimes necessary to relieve the pain. A rarely performed operation involves sectioning of the spinal trigeminal tract in the lower medulla caudal to the obex(caudal end of the rhomboid fossa, which forms the fl oor of the fourth ventricle). In this manner, afferent input to the caudal spinal trigeminal nucleus is interrupted, and pain is relieved. This procedure leaves the tactile sensibility intact. The nerve endings of peripheral processes of cells sensing pain in the face and the anterior two thirds of the head are located in the trigeminal (Gasserian) ganglion. The central processes of the sensory cells located in the trigeminal ganglion enter the brainstem at the level of the pons and descend laterally in the pons and medulla as the descending (or spinal) tract of the trigeminal nerve. These fi bers project to the caudal third of the spinal trigeminal nucleus. Thus, interruption of the pathway in the dorsomedial pons, ventromedial midbrain, and substantia gelatinosa of the spinal cord would not be helpful in relieving pain in this patient.

A neuroscientist wanted to design an experiment to investigate the brain mechanisms that regulate pain. This investigator discovered that, when electrical stimulation was applied to the midline of the medulla, pain sensation was attenuated. Which of the following possibilities could account for this observation?

a. Release of serotonin in the dorsal horn of spinal cord

b. Release of acetylcholine in the substantia gelatinosa

c. Release of norepinephrine from the central processes of

dorsal root ganglion cells

d. Increased release of substance P from the central

processes of dorsal root ganglion cells

e. Inhibition of enkephalinergic interneurons in the

substantia gelatinosa

Answer: a

Stimulation of raphe magnus neurons in the midline medulla is expected to result in the release of serotonin at their terminals in the dorsal horn and excite (not inhibit) enkephalin- containing interneurons located in the dorsal horn. Enkephalin is released in the dorsal horn, acts on opiate receptors on the terminals of central processes of nociceptive dorsal root ganglion cells, and decreases the release of transmitters involved in nociception (glutamate and substance P). Enkephalin also inhibits the second-order spinothalamic neurons located in the dorsal horn by activating their dendritic opiate receptors. Thus, nociception is attenuated by enkephalins by presynaptic and postsynaptic mechanisms. Acetylcholine is not involved in pain-sensing mechanisms in the spinal cord. Although norepinephrine can activate enkephalin-containing interneurons, it is released by the stimulation of pontine noradrenergic neurons (not central processes of dorsal ganglion cells).

Which of the following receptors signal changes in muscle activity?

a. Golgi tendon organs

b. Meissner’s corpuscle

c. Pacinian corpuscle

d. Merkel’s receptor

e. Ruffi ni’s corpuscle

Answer: a

Golgi tendon organs are activated by active contraction or stretching of the muscle and provide information regarding the activity of the muscle. Meissner’s corpuscles and Merkel’s receptors mediate the sensation of touch. Pacinian corpusclesare sensitive to vibration. Ruffi ni’s corpuscle senses the mag nitude and direction of stretch.

The terminals of nociceptive afferents release which one of the following transmitters?

a. Substance P

b. Gamma aminobutyric acid

c. Enkephalins

d. Serotonin

e. Acetycholine

Answer: a

The terminals of nociceptive afferents in the spinal cord release substance P and glutamate. Enkephalins and serotonin are not the transmitters released by the terminals of nociceptive afferents. These transmitters are released at different sites in the descending pain control circuits. Gamma aminobutyric acid and acetylcholine are inhibitory and excitatory neurotransmitters, respectively, in the central nervous system, and they are not involved in nociception.

Visual System

Which one of the following statements is correct regarding photoreceptors?

a. Rods are specialized for day vision.

b. Rods contain more photosensitive pigment than cones.

c. Loss of cones in the retina causes night blindness.

d. Cones outnumber rods.

e. Rods are concentrated within the fovea.

The photopigment is more abundant in the rods, and these photoreceptors are specialized for night vision. Loss of rods causes only night blindness, while the loss of cones causes decreased visual acuity and defects in color vision. Rods are more numerous than cones. Rods are absent in the fovea, where the concentration of cones is very high

Which one of the following statements is correct regarding different retinal cell types?

a. Müller cells inhibit horizontal cells.

b. Both rods and cones fi re action potentials in response

to a light stimulus.

c. Loss of cones results in night blindness.

d. Ganglion cells represent the output of neurons in the retina.

e. Color is mediated by rod photoreceptors

Answer: d

The ganglion cells represent the output of neurons in the retina. Their axons form the optic nerve. Müller cells are glial cells unique to the retina. The rods and cones do not fi re action potentials; instead, they respond to the light stimulus by graded hyperpolarizing generator potentials. It is the loss of rods that causes night blindness. Color vision is mediated by cones, not by rods.

A 60-year-old man consulted a neurologist with a complaint of transient episodes consisting of light-headedness, vision disturbances, nausea, and unsteadiness. Angiographic examination revealed that the patient had a vascular occlusion of the right middle cerebral artery. A computed tomography scan revealed the presence of lesions in the inferior aspect of the right temporal lobe. The visual disorder most likely experienced by the patient is:

a. Total loss of vision in the left eye

b. Inability to see objects in the temporal visual fi elds of

both eyes

c. Inability to see objects in the left superior quadrants of

both eyes

d. Inability to see objects in the left inferior quadrants of

both eyes

e. Inability to see objects in the left visual fi eld of both eyes

Answer: c

A lesion in the inferior temporal lobe is likely to damage Meyer’s loop. This loop contains fi bers from the inferior halves of the retinae that carry information about the superior visual fi elds. Since the damage is in the right Meyer’s loop, the vision will be lost in both eyes: the superior quadrant of the nasal visual fi eld of the right eye and the superior quadrant of the temporal visual fi eld of the left eye. This disorder is referred to as a “superior left homonymous quadrantanopia,” “contralateral superior homonymous quadrantanopia,” or “pie-in-the-sky visual disorder.”

A 55-year-old woman with a long history of menstrual irregularity consulted with her ophthalmologist, indicating that she was experiencing visual disturbances that seemed to have worsened during the past couple of months. Her ophthallmologist referred her to a neurologist. A computed tomography scan of the patient’s head revealed the presence of a pituitary tumor impinging on the optic chiasm. Which one of the following visual defi cits is the patient likely to have?

a. Left (contralateral) homonymous hemianopia

b. Nyctalopia

c. Inferior left homonymous quadrantanopia with macular

sparing

d. Nonhomonymous bitemporal hemianopia

e. Strabismic amblyopia

Nonhomonymous bitemporal hemianopia involves a loss of vision in the temporal halves of both visual fi elds. It occurs when there is a lesion in the optic chiasm. A large pituitary tumor commonly causes nonhomonymous bitemporal hemianopia by compressing the optic chiasm. Because the nasal retinal fi bers cross in the optic chiasm, damage to the chiasm will produce a bitemporal hemianopia. Contralateral homonymous hemianopia occurs when there is damage to the optic tract on one side.

Inferior left homonymous quadrantanopia with macular sparing (contralateral inferior homonymous quadrantanopia with macular sparing or pie-in-the-fl oor visual disorder with macular sparing) occurs due to the lesion of the superior bank of the right calcarine fi ssure. Strabismic amblyopia occurs when the visual axes of the two eyes are not parallel. Nyctalopia (night blindness) is caused by vitamin A defi ciency that results in reduction of the amount of photosensitive pigment in rods and cones. In this situation, the level of light at night is insuffi cient to activate the depleted pigment; therefore, the person cannot see in the dark. Pituitary tumors are usually associated with defi ciencies in circulating follicle-stimulating and luteinizing hormones. These defi ciencies can result in menstrual irregularities.

A 50-year-old woman reported to her ophthalmologist that she was experiencing visual disturbances in her right eye. A computed tomography scan of her head revealed a lesion in her right optic nerve, and she was diagnosed as having a Marcus-Gunn pupil. Which one of the following responses was observed when the ophthalmologist performed a swinging fl ashlight test in this patient?

a. When light was shone on her right eye, both pupils

constricted.

b. When light was shone on her right eye, both pupils dilated.

c. When light was shone on her left eye, the left pupil

constricted.

d. When light was shone on her left eye, both pupils dilated.

e. When light was shone on her left eye, the left pupil dilated.

Patients with Marcus-Gunn pupil have a lesion of one of the optic nerves. A swinging fl ashlight test to evaluate pupillary light refl ex involves quick movement of the light source back and forth from one eye to another. When light is shone on the normal eye, both pupils constrict. When the light is shone on

the eye with the optic nerve lesion, lesser signals reach the Edinger-Westphal nucleus. This nucleus senses the lesser intensity of light and consequently shuts off the parasympathetic response to the light, causing the paradoxical dilatation of both pupils. In Adie’s pupil, there is a prolonged and sluggish constriction of the pupil to light. Subsequent to the pupillary constriction, the dilation of the pupil is delayed. In these patients, there are pathological changes in the ciliary ganglion.

A 47-year-old woman was admitted to a local hospital after complaining of a gradual loss of hearing in one ear over time. In addition, the patient also reported some unsteadiness in balance that developed after the initial hearing loss. A magnetic resonance imaging (MRI) scan and a thorough neurological examination further revealed a facial palsy and a loss of corneal refl ex on the side of the face ipsilateral to the hearing loss. The most likely cause of this disorder as revealed by the MRI and clinical evaluations was:

a. A tumor in the region extending from the external to the

middle ear

b. An acoustic neuroma of the cerebellopontine angle

affecting cranial nerve VIII

c. A vascular occlusion affecting the medial two thirds of

the basilar pons

d. A tumor affecting the midline region of the cerebellar cortex

e. A vascular lesion involving the medial longitudinal

fasciculus and adjoining regions of the dorsal pons

Ipsilateral hearing loss coupled with some loss of balance and with facial palsy and loss of corneal refl ex on the same side as the hearing loss could only occur as a result of damage to cranial nerve (CN) VII and CN VIII. The most common place where this is likely to occur is the cerebellopontine angle, where an acoustic neuroma would affect not only CN VIII but also CN VII because of its proximity to CN VIII. The other choices are not logically possible. A tumor of the external or middle ear could not account for the defi cits due to damage to CN VII. A vascular occlusion of the medial two thirds of the basilar pons would not affect CN VIII. Damage to the cerebellum or medial longitudinal fasciculus would not affect auditory functions.

A 41-year-old man was diagnosed as having multiple sclerosis. During the course of this disorder, this patient exhibited signs of vertigo and nystagmus. The most likely explanation of these symptoms is a reduction of conduction velocity in neurons affecting the:

a. Inner ear

b. Cranial nerve IV

c. Cerebellum

d. Cerebral peduncle

e. Red nucleus

A 27-year-old man who had been in good health reported to his primary physician that he had episodes of dizziness. Over time, the dizziness tended to decrease, but the patient began to experience tinnitus and hearing loss, and both of these symptoms became progressively worse. A neurological examination revealed no other signs of neurological dysfunctions. The patient was treated with anticholinergics with some degree of success. The most likely basis of the disorder in this patient is:

a. A lesion of the medial longitudinal fasciculus

b. A tumor of the cerebellum

c. A tumor impinging on cranial nerve (CN) VIII and CN VII

at the cerebellopontine angle

d. An abnormal volume of endolymph of the inner ear

e. A lesion of the dorsolateral pons affecting the lateral

lemniscus

Answer: d

Because the patient experienced both auditory and vestibular symptoms but showed no other clinical signs, the site of dysfunction had to be limited to cranial nerve (CN) VIII. Such effects are typically of peripheral origin. In this case, the patient was suffering from Ménière’s disease, which involves the inner ear, where the effects are likely manifested through alterations of endolymphatic homeostasis. The lesions to the other structures provided as choices do not involve the constellation of defi cits indicated in this case. Cerebellar or medial longitudinal fasciculus lesions would produce vestibular but not auditory defi cits, damage to the dorsolateral pons involving the lateral lemniscus would affect only hearing (and, perhaps, somesthetic pathways), and a tumor of the cerebellopontine angle would affect both CN VIII and CN VII (see explanation to Question 1). In this case, there were no symptoms suggesting damage to CN VII.

Which one of the following events is elicited by the mechanical displacement of the cochlear hair cell stereocilia toward the kinocilium?

a. There is an infl ux of K ? (potassium) through the mem-

branes of the cilia, which is followed by an infl ux of Ca 2?

(calcium) through the voltage-gated Ca 2? channels.

b. The hair cells on which the cilia are located are

hyperpolarized.

c. Effl ux of Ca 2? (calcium) through the voltage-gated

channels located in the hair cell membrane occurs.

d. An inhibitory transmitter (probably gamma aminobutyric

acid) is released by the hair cell.

e. There is an infl ux of Na ? (sodium) through the membranes

of the cilia, the hair cell is depolarized, and an action

potential is elicited in the afferent nerve terminal.

Answer: a

The air pressure waves cause the tympanic membrane to vibrate which, in turn, results in oscillatory movements of the foot of the stapes against the oval window (not round window). These pressure waves in the perilymph displace only specifi c portions of the basilar membrane depending on the frequency of the sound stimulus. The movement of the basilar membrane with respect to the tectorial membrane results in the displacement of stereocilia. Mechanical displacement of the stereocilia (e.g., in lateral direction) causes an infl uxof K ? (potassium) through their membranes, the hair cell is depolarized, and there is an infl ux of Ca 2? (calcium) through the voltage- sensitive Ca 2? channels in their membranes. The infl ux of Ca 2? triggers the release of the transmitter (probably glutamate) that, in turn, elicits an action potential in the afferent nerve terminal at the base of the hair cell.

A caloric test was performed on a 50-year-old man complaining of dizziness and vertigo to exclude impairment of the vestibulo-ocular pathways. Which one of the following observations would indicate normal function of vestibuloocular pathways in this person?

a. Irrigation of the left external auditory canal with cold

water resulted in nystagmus beating toward the right.

b. Irrigation of the left external auditory canal with cold

water resulted in nystagmus beating toward the left.

c. Irrigation of the left external auditory canal with warm

water resulted in nystagmus beating toward the right.

d. Irrigation of the right external auditory canal with warm

water resulted in nystagmus beating toward the left.

e. Nystagmus was attenuated when the left external

auditory canal was irrigated with warm water.

Answer: a

In a normal individual, cold water produces nystagmus beating opposite to the side in which the water was introduced(remember the mnemonic “COWS”), while warm water produces nystagmus beating to the same side in which the water was introduced. Recall that the terms “leftward-beating” and “rightward-beating” indicate the direction of the nystagmus. Attenuation of nystagmus indicates a lesion in the vestibulo-ocular pathway.

Olfactory information can reach the cerebral cortex by which one of the following routes?

a. Olfactory bulb → hippocampus → anterior thalamic

nucleus → prefrontal cortex

b. Olfactory bulb → piriform cortex → amygdala →

prefrontal cortex

c. Olfactory bulb → septal area → cingulate gyrus →

prefrontal cortex

d. Olfactory bulb → bed nucleus of stria terminalis → ventro-

posterolateral nucleus of the thalamus → prefrontal cortex

e. Olfactory bulb → hypothalamus → thalamus → prefrontal

cortex

Answer: b

The signals generated by olfactory stimuli reach the olfactory bulb and are transmitted directly to the prefrontal cortex. It should be noted that there is another pathway for transmission of olfactory stimulation that involves relay of signals to the mediodorsal thalamus and then prefrontal cortex. However, the signals generated by visual, taste, and auditory stimuli must be fi rst relayed to the thalamus.

The efferent fi bers from the olfactory bulb arise from which one of the following neurons?

a. Periglomerular cells

b. Granule cells

c. Mitral cells

d. Golgi cells

e. Olfactory receptor cells

Answer: c

The efferent fi bers exiting the olfactory bulb are the axons of mitral and tufted cells. The periglomerular cells and granule cells are gamma aminobutyric acid (GABA)-ergic interneurons; they have short axons that do not enter the olfactory tract. There are no Golgi cells and olfactory receptor cells in the olfactory bulb.

Which one of the following statements regarding the transduction of the taste stimulus is correct when a chemical molecule interacts with a specifi c membrane site on the microvilli of a taste receptor cell?

a. The exposure of microvilli to an acid results in the depo-

larization of the receptor cell by opening of an amiloride-

sensitive Na ? (sodium) channel.

b. The exposure of microvilli to an acid results in the de-

polarization of the receptor cell by closure of K ? (potas-

sium) channels.

c. The exposure of microvilli to a bitter substance results in

the activation of adenylate cyclase in the receptor cell.

d. The exposure of microvilli to a sweet substance results

in the activation of phospholipase C in the receptor cell.

e. The exposure of microvilli to a salty substance results in

the activation of G protein in the receptor cell.

Answer: b

Sour taste, elicited by acids, is mediated by depolarization of the receptor cell due to closure of voltage-dependent K ? (potassium) channels. The following statements show that the other choices are incorrect. Bitter substances activate a G protein, phospholipase C is activated, inositol triphosphate is generated, and the taste receptor cell is depolarized by release of Ca 2? (calcium) from intracellular stores. Sweet substances activate a G protein, adenylate cyclase is activated, cyclic adenosine

monophosphate is generated, a phosphokinase is activated, K ? channels are closed, and the taste receptor cell is depolarized. A salty substance depolarizes a taste receptor cell by infl ux of Na ?( sodium) through amiloride-sensitive Na ? channels.

Which one of the following statements regarding the central pathways that mediate the taste sensation is correct?

a. The central processes of sensory neurons in the genicu-

late ganglion terminate in the rostral solitary nucleus.

b. The secondary neurons located in the solitary nucleus

project directly to the cortical taste area.

c. The sensory fi bers innervating the epiglottis travel in the

facial nerve.

d. The taste buds located in the anterior third of the tongue

are innervated by the peripheral processes of the unipolar

neurons located in the petrosal ganglion of cranial nerve IX.

e. The secondary neurons mediating taste sensation are

located in the nucleus ambiguous

Answer: a

The taste buds on the anterior two thirds of the tongue are innervated by the facial nerve (cranial nerve [CN] VII); the sensory neurons mediating the sensation of taste from this region of the tongue are located in the geniculate ganglion of the facial nerve. The taste buds on the posterior one third of the tongue are innervated by the glossopharyngeal nerve (CN IX); the sensory neurons involved in the taste sensation from this portion of the tongue are located in the inferior (petrosal) ganglion of the glossopharyngeal nerve. The taste buds on the epiglottis are innervated by the vagus nerve (CN X); the sensory neurons involved in the taste sensation from the epiglottis and the pharyngeal wall are located in the inferior (nodose) ganglion of the vagus nerve. The central processes of these sensory neurons (i.e., sensory neurons located in the geniculate, petrosal, and nodose ganglia) enter the solitary tract and terminate in the rostral portion (gustatory region) of the solitary nucleus. The axons of secondary neurons located in the rostral portion of the solitary nucleus ascend in the solitario-thalamic tract (near the medial lemniscus) and terminate in the ventral posteromedial nucleus (VPM) of the thalamus. The neurons in the VPM send their projections to the cortical taste area of the postcentral gyrus.

Emotion

Oxytocin is:

a. Synthesized in the medial hypothalamus and released in

the posterior pituitary

b. Synthesized in the medial hypothalamus and released in

the anterior pituitary

c. Synthesized in the paraventricular nucleus and released

in the anterior pituitary

d. Synthesized in the paraventricular nucleus and released

in the posterior pituitary

e. Synthesized in the lateral hypothalamus and released in

the median eminence

Answer: d

Oxytocin is synthesized in the paraventricular nucleus and is transported down the axons to their terminals in the posterior pituitary. Oxytocin is then distributed through the blood stream to its target organ in and around the epithelial cells of the mammary gland, where it helps to trigger the milk ejection refl ex upon sensory stimulation.

An experiment was conducted in cats to determine the effects of stimulation of the medial amygdala on the activity of medial hypothalamic neurons. After determining that stimulation of the medial amygdala powerfully excited medial amygdaloid neurons, the investigator sought to further test the relationship between these regions by destroying the major pathway that links these two regions and then testing to see whether stimulation of the medial amygdala no longer affected medial hypothalamic neuronal activity. The most likely pathway that was destroyed by the investigator was the:

a. Mammillothalamic tract

b. Medial forebrain bundle

c. Stria terminalis

d. Stria medullaris

e. Ventral amygdalofugal fi bers

Answer: c

The investigator experimentally cut the stria terminalis because it arises from the medial amygdala and projects directly to the rostrocaudal extent of the medial hypothalamus. It serves as a

very important source of excitatory input to this region of the hypothalamus. The mammillothalamic tract projects from the mammillary bodies to the anterior thalamic nucleus. The medial forebrain bundle contains ascending and descending fi bers that pass through the lateral hypothalamus and do not directly link the amygdala with the medial hypothalamus. The stria medullaris contains fi bers that pass mainly from the habenular nuclei to the ventral aspect of the rostral forebrain and has no direct relationship with either the medial hypothalamus or medial amygdala.

Ventral amygdalofugal fi bers connect mainly the lateral aspects of the amygdala with the lateral hypothalamus and parts of the brainstem. Again, this pathway does not mediate direct inputs from the medial amygdala to the medial hypothalamus.

Lesions of the medial hypothalamus will result in:

a. Aphagia

b. Diabetes insipidus

c. Hyperphagia

d. Increased sexual behavior

e. Failure to regulate body temperature

Answer: c

Lesions of the medial hypothalamus result in a disorder called “hypothalamic hyperphagia,” which is characterized by marked increases in food intake and obesity. Aphagia is produced by lesions of the lateral hypothalamus. Diabetes insipidus is associated with lesions of the supraoptic region. Destruction of the medial hypothalamus blocks sexual behavior. Thermal regulation is governed by the anterior (for heat loss) and posterior (for heat conservation) regions of the hypothalamus.

A lesion of the lateral hypothalamus is discovered after an examination in which a magnetic resonance imaging scan was done. Which of the following disorders would likely be present, and which pathway would most likely be damaged?

a. Hyperphagia—stria terminalis

b. Aphagia—medial forebrain bundle

c. Dysphagia—stria medullaris

d. Hypertension—mammillotegmental fi bers

e. Fever—corticohypothalamic fi bers

Answer: b

Lesions of the lateral hypothalamus have been associated with aphagia. The major pathway passing through the lateral hypothalamus is the medial forebrain bundle. It contains descending

fi bers, which arise from different groups of neurons in the lateral hypothalamus and septal area, and ascending fi bers that pass to different regions of the forebrain, which also arise from the lateral hypothalamus as well as from the brainstem, including monoaminergic cell groups. The medial hypothalamus is the region that most directly is associated with hyperphagia. Dysphagia is associated with lesions of the lower brainstem and, in particular, neurons associated with cranial nerves IX and X. Hypertension is most closely associated with the posterior hypothalamus and the region of the medial hypothalamus. Lesions of the lateral hypothalamus are not known to result in hypertension. Fever is associated with excitation of the preoptic region and septal area. Lesions of the lateral hypothalamus would most likely not cause major increases in body temperature.

Surgical lesions designed to reduce blood pressure and

manifestations of violent and related emotional responses

in schizophrenic patients have been made in the:

a. Medial preoptic region

b. Lateral preoptic region

c. Posterior lateral hypothalamus

d. Posterior medial hypothalamus

e. Supraoptic nucleus

Answer: d

The posterior medial hypothalamus is referred to as the ergotropic triangle of the hypothalamus and is the region where surgical lesions have been placed to cause reductions in blood pressure.

Lesions of this region also reduce aggressive and related forms of emotional responses. Presumably, the sites of the lesions serve to disrupt many of the descending fi bers from the medial hypothalamus to the midbrain periaqueductal gray matter and lower regions of the brainstem that integrate forebrain control of sympathetic activity as well as rage and violent forms of behavior. The preoptic region, lateral hypothalamus, and supraoptic nucleus have not been known to cause increases in blood pressure and are not associated specifi cally with the control of rage behavior. The preoptic region is closely associated with temperature regulation, the lateral hypothalamus is associated with

feeding and predatory behavior, and the supraoptic nucleus is

associated with control of functions of the posterior pituitary.

Limbic system