The proper sensory nucleus is derived from which of the following
A brain MRI scan taken from a 6-month-old baby revealed that while the overall size of the cerebral cortex was normal, the size of the pyramidal tracts was considerably smaller than normal. Which of the following is the most likely explanation for this defect
A.Reduction in the numbers of cortical neurons giving rise to pyramidal tract fibers
B.Reduction in the numbers of synaptic contacts made by pyramidal tract neurons
C.Reduction in the extent of myelin found on pyramidal tract neurons
D.Reduction in the amount of neurotransmitter released by pyramidal tract neurons
E.Reduction in the numbers of glial cells attached to pyramidal tract neurons
Which of the following is the most ubiquitous excitatory neurotransmitter in the brain?
Epileptiform activity is believed to include the activation of which of the following
Which of the following enzymes is directly responsible for the degradation of norepinephrine
Bladder functions are regulated by which of the following combinations of inputs
A.Vagal and sacral efferent fibers only
B.Vagal, sacral, and descending fibers from the cerebral cortex
C.Lumbar and sacral efferent fibers only
D.Lumbar, sacral, and descending fibers from the cerebral cortex
E.Lumbar, thoracic, and cervical fibers only
Synthesis and storage of norepinephrine can be prevented by which of the following substances
A 43-year-old male is recovering from an infectious disease and experiences a marked instability in his blood pressure with episodes of spiking of blood pressure. After a series of extensive examinations, it was concluded that this disorder was due to the effects of the infectious agent upon a component of the peripheral nervous system. Logical sites where an infectious agent could produce such an effect include which of the following
A.Superior ganglia of cranial nerves IX and X
B.Geniculate and trigeminal ganglia
C.Otic and superior salivatory ganglia
D.Carotid sinus and aortic arch
E.Carotid and aortic bodies
The lesion at B would most likely result in which of the following deficits?
A.Paralysis of the contralateral limbs
B.Loss of conscious proprioception of the contralateral side of the body
D.Lateral gaze paralysis
A patient with the lesion at A will generally show which of the following deficits?
B.Loss of ability to gaze medially
C.Loss of ability to show tracking movements
D.Loss of accommodation reflex
A person is told that he has astigmatism. To correct this defect, the optometrist prescribes which of the following lenses
A.Cylindrical lens because the cornea or lens is oblong
B.Concave lens because the eyeball is too long
C.Convex lens because the lens is too short
D.Neutral lens because the eyeball is normal but the cornea is too thin
E.Concave lens because the cornea is opaque
As a result of calcification of the internal carotid artery, which impinges upon the lateral half of the right optic nerve prior to its entrance to the brain of a 68-year-old woman, resulting in certain visual deficits. Which of the following is the most likely visual deficits
A.Total blindness of the right eye
B.Right nasal hemianopsia
C.Right homonymous hemianopsia
D.Right bitemporal hemianopsia
E.Right upper homonymous quadrantanopia
A 55-year-old woman complains of headaches and is subsequently diagnosed as having a tumor localized to the left parietal lobe. In addition to a variety of sensory deficits, further examination also reveals a reduction in her visual fields. Which of the following is the most likely visual deficit
A.Left homonymous hemianopsia
B.Right homonymous hemianopsia
C.Left upper quadrantanopia
D.Right upper quadrantanopia
E.Right lower quadrantanopia
The conscious perception of movement is mediated by which of the following receptors
B.Free nerve endings
An impairment in the ability to perform certain types of learned, complex movements (referred to as apraxia) usually results from a lesion of which of the following?
Which of the following is the primary transmitter released from terminals of both neostriatal and paleostriatal neurons?
The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has recently been applied experimentally with considerable success as a model for which of the following?
A man presents with a wide-based, ataxic gait during his attempts at walking. He also is unsteady and sways when standing and displays a tendency to fall backward or to either side in a drunken manner. A lesion is most likely located in which of the following?
A.Hemispheres of the posterior cerebellar lobe
B.Anterior limb of the internal capsule
D.Anterior lobe of the cerebellum
E.Flocculonodular lobe of the cerebellum
Which one of the following thalamic nuclei makes local connections with other thalamic nuclei and, additionally, projects to the basal ganglia
A.Centromedian thalamic nucleus
B.Medial geniculate thalamic nucleus
C.Lateral geniculate thalamic nucleus
D.Dorsomedial thalamic nucleus
E.Anterior thalamic nucleus
The supraoptic nucleus is most closely associated with which of the following?
D.Short-term memory functions
Lesions of the lateral hypothalamus will likely produce which of the following
A number of investigations have provided strong evidence that the suprachiasmatic nucleus plays an important role in which of the following
The CT scan below reveals that the patient has a glioma (T) on the right side of the brain. It is likely that the patient has sustained which of the following?
A.A UMN paralysis of the left side
D.Upper left quadrantanopia
E.Upper right quadrantanopia
Question 1 of 4
A lesion of which region in the diagram below will likely result in receptive aphasia?
Question 1 of 2
An individual who complains about disruption in limb muscle function is diagnosed with a disorder in which the transmitter released at the neuromuscular junction is not removed from the synaptic cleft.
Which of the following is the primary mechanism involved in removal of the transmitter at the neuromuscular junction
D.Actions of antibodies
E.Distribution of sodium and potassium ions along muscle membrane
Question 2 of 2
An individual who complains about disruption in limb muscle function is diagnosed with a disorder in which the transmitter released at the neuromuscular junction is not removed from the synaptic cleft.
Which of the following enzymes is required for the metabolism of the transmitter at the neuromuscular junction
Structures associated with sensory functions, such as the proper sensory nucleus and the spinal nucleus of cranial nerve V, are derived from the alar plate
Extensive myelination occurs in postnatal development. The failure of the pyramidal tracts to form myelin would account for the reduction in their size. In this particular situation, the size of the cerebral cortex was approximately normal, suggesting that there was no significant decrease in cortical cells. Variation in the numbers of synaptic contacts, transmitter formation, and glial cells would not account for a reduction in the size of the pyramidal tract
The largest numbers of excitatory synapses in the CNS are mediated by glutamate as it is believed that approximately half of the synapses in the brain release glutamate. For example, functions mediated by fibers that originate from the cerebral cortex and descend to such regions as the neostriatum, thalamus, brainstem, and spinal cord are generally believed to be mediated by glutamate. Many other neuronal systems throughout the brain and spinal cord utilize glutamate as well. Dopaminergic and noradrenergic neurons, while mostly excitatory, can also be inhibitory at some synapses and are less numerous than glutamate. Cholinergic and substance P synapses are also excitatory, but are likewise less numerous than glutamate.
Excitatory amino acids and, in particular, the glutamate family of compounds have long been thought to play an important role in epileptiform activity. Epileptiform activity typically includes AMPA-receptor activation. However, as the seizure becomes more intense, there is increased involvement of NMDA receptors. This is evidenced by the facts that NMDA antagonists can reduce the intensity and length of the seizure activity and that, following removal of human epileptic hippocampal tissue, there is an up-regulation of both AMPA and NMDA receptors. Metabotropic glutamate receptors have been shown to be present in the retina but have not yet been demonstrated to be present in regions of the brain that are typically epileptogenic. GABA and glycine are inhibitory transmitters; therefore, seizures would logically block such receptor activation. There has been no substantive evidence concerning the role of cortical nicotinic receptors in epilepsy.
Tryptophan hydroxylase, tyrosine hydroxylase, and choline acetyltransferase are enzymes that are critical for the biosynthesis of serotonin, catecholamines, and ACh, respectively. Dopamine -hydroxylase converts dopamine to norepinephrine. Catechol-O-methyltransferase and monoamine oxidase are critical for the metabolic degradation of catecholamines
The smooth muscle of the bladder is innervated by postganglionic fibers of the sympathetic nervous system that arise from the inferior mesenteric ganglion. This ganglion, in turn, receives its inputs from T12–L2 of the intermediolateral cell column of the spinal cord. The smooth muscle of the bladder also receives inputs from postganglionic parasympathetic fibers that are innervated by preganglionic fibers arising from S2–S4. The external sphincter of the bladder (striated muscle) is innervated by ventral horn cells from the spinal cord. These ventral horn cells, in turn, receive inputs from supraspinal neurons that arise, in part, from the cerebral cortex. It is these neurons that form a part of the substrate for voluntary control over bladder functions.
Noradrenergic activity can be blocked by a number of mechanisms. Reserpine, for example, prevents the synthesis and storage of norepinephrine in sympathetic nerve terminals. Guanethidine sulfate affects noradrenergic transmission by blocking the release of norepinephrine at the sympathetic endings. Competitive -receptor blockers include phenoxybenzamine hydrochloride and phentolamine, whereas metoprolol blocks 1 receptors. Since ACh is the transmitter at preganglionic synapses of both the parasympathetic and sympathetic nervous systems, hexamethonium chloride is an effective ganglionic blocker at these synapses.
Specialized peripheral receptors, which specifically respond to changes in blood pressure, include the carotid sinus (associated with cranial nerve IX) and the aortic arch (associated with cranial nerve X). If these receptors (or the cell bodies associated with these receptors) are damaged, then one of the fundamental regulatory mechanisms for the control of blood pressure would be disrupted. The results of such a disruption would likely lead to increases and instability in blood pressure with evidence of spiking of blood pressure. Because these sensory receptors in these structures respond to increases in blood pressure, they are, in effect, stretch receptors and are consequently referred to as baroreceptors. The principal projection of the axons associated with these baroreceptors is the solitary nucleus of the medulla, which in turn, projects to autonomic nuclei such as the dorsal motor nucleus of the vagus nerve, ventrolateral medulla, and higher regions associated with autonomic functions, which include the PAG, hypothalamus, and limbic system.
Since the lesion is restricted to the medial aspect of the basilar part of the pons, the corticospinal tract would be affected, producing paralysis of the contralateral limbs. Although other structures would also be affected and could produce additional deficits, such deficits are not listed in this question. The other dysfunctions listed would not occur because they are associated with structures situated in the pontine tegmentum, which is not included in this lesion.
The lesion involves the superior colliculus. This structure receives inputs from the cerebral cortex and optic tract and its neurons respond to moving objects in the visual field. It is considered essential for the regulation of tracking movements. Lesions of the superior colliculus have not been shown to produce any of the other deficits listed in this question. Nystagmus is not likely to occur because the lesion does not involve the medial longitudinal fasciculus or the pontine gaze center.
In astigmatism, the shapes of the cornea and possibly the lens become oblong, resulting in differences in the curvature of the lens along the long and short axes. Thus, astigmatism is corrected with a cylindrical lens.
Calcification of the internal carotid artery could serve to disrupt nerve fibers proximal to it. One such group of fibers includes parts of the optic nerve. In this case, the component of the right optic nerve affected includes the lateral aspect, or those fibers that mediate vision associated with the nasal visual field of the right eye. If the damage were more extensive and if it involved the entire nerve, then total blindness of the right eye would have occurred.
Fibers from the left lateral geniculate destined for the upper bank of the calcarine fissure will mediate visual impulses associated with lower quadrants of the right visual fields for both eyes. This deficit is referred to as a right lower quadrantanopia.
Meissner's corpuscles, Merkel's receptors, and pacinian corpuscles respond to tactile, pressure, or possibly vibratory stimuli, while free nerve endings are associated with nociceptive stimuli. Joint capsules respond to movement of the limb, and the axons of these receptors contribute to the dorsal column–medial lemniscal system mediating the conscious perception of movement.
The premotor areas play an important role in the programming or sequencing of responses that compose complex learned movements. They receive significant inputs for this process from the posterior parietal lobule and, in turn, signal appropriate neurons in the brainstem and spinal cord (both flexors and extensors). Lesions of the postcentral gyrus produce a somatosensory loss. Lesions of the precentral gyrus produce paralysis. Neither lesions of the prefrontal cortex nor those of the cingulate gyrus have been reported to produce apraxia.
The major transmitter released at terminals of neostriatal and paleostriatal fibers is GABA. Thus, the output of the basal ganglia is mainly inhibitory. This suggests that thalamic influences upon the cortex are generated through the process of disinhibition, whereby neurons of the basal ganglia are inhibited. The presence of glycine in striatal neurons has yet to be demonstrated. Enkephalins are released from terminals of neostriatal-pallidal fibers but not from other efferent neurons of the striatum. Dopamine is released from the brainstem and some adjoining hypothalamic neurons but certainly not from striatal neurons. The neostriatum receives cortical inputs that utilize glutamate, but the release of GABA from terminals of striatal efferent fibers has not been demonstrated.
MPTP was discovered by accident when drug abusers who were using a synthetic heroin derivative developed signs of Parkinson's disease. It was discovered that their drug included the contaminant MPTP. As a consequence, MPTP has been applied systemically in a number of experimental animals, resulting in significant decreases in dopamine content of the brain due to the loss of dopaminergic neurons in the substantia nigra. These animals also developed symptoms similar to those seen in Parkinson's patients. For these reasons, this drug is currently being used for research purposes in order to develop a better understanding of this disease and to establish possible drug therapies for its treatment and eventual cure.
Since the flocculonodular lobe receives and integrates inputs from the vestibular system, it is understandable why lesions that disrupt this integrating mechanism for vestibular inputs would result in difficulties in maintaining balance. Indeed, this is a classic feature of lesions of the flocculonodular lobe but is not associated with lesions in the hemispheres of the posterior lobe, anterior limb of the internal capsule, or the dentate nucleus, which are functionally linked to the frontal lobe. Lesions of the anterior lobe also do not affect mechanisms of balance.
The centromedian nucleus is a classical nonspecific thalamic nucleus. It can modulate cortical activity by making local connections with specific thalamic nuclei, and therefore modify the specific thalamic inputs to different regions of the cerebral cortex. In addition, the centromedian nucleus also projects to the putamen. This projection is sometimes referred to as the thalamostriatal projection. Since the centromedian nucleus receives considerable inputs from the cerebral cortex, this connection to the putamen provides a basis by which the cerebral cortex can influence the basal ganglia in addition to its direct projections to the neostriatum.
The supraoptic nucleus, like the paraventricular nucleus, contains magnocellular neurons that synthesize vasopressin and oxytocin and transport these hormones down their axons to the posterior pituitary. For this reason, the supraoptic nucleus plays a significant role in the regulation of water balance. There is no evidence to support the notion that the supraoptic nucleus has a role in feeding behavior, temperature regulation, sexual behavior, or short-term memory functions.
Lesions of the lateral hypothalamus are likely to produce aphagia. Feeding behavior is elicited by stimulation of the lateral hypothalamus. Neurons in this region respond to the sight or taste of food. Since drinking is also associated with lateral hypothalamic functions, a lesion of this structure would also disrupt this behavior. Lesions of the lateral hypothalamus do not produce either hypertension or sexual behaviors. The neurons regulating these functions are elsewhere within the hypothalamus.
Recent studies have demonstrated that the suprachiasmatic nucleus controls the biologic clock of internal circadian rhythms. During the light phase of the light-dark cycle, metabolic activity (measured by 14C-2-deoxyglucose autoradiography) within the suprachiasmatic nucleus is significantly increased. In contrast, during the dark phase, there is very little metabolic activity.
The tumor is situated in the lentiform nucleus and internal capsule. Therefore, corticospinal fibers will be affected, causing a UMN paralysis of the left side. Dyskinesia would not be seen because any effects normally seen in association with damage to the basal ganglia would be masked by the effects of the damage to the internal capsule. Since the cerebellum was not involved, there would be no intention tremor. Neither would there be any visual deficits from this glioma since optic nerve fibers are not involved. The following schematic diagram indicates the approximate extent of the tumor. Labeled are the caudate nucleus (C), the globus pallidus (GP), the internal capsule (IC), the putamen (P), and the tumor (T).
This figure is a lateral view of the cerebral cortex. Cells in the "arm" area of the primary motor cortex (H) project their axons to the cervical level of the spinal cord. This area receives major input from the ventrolateral nucleus of the thalamus. The leg region of the primary somatosensory cortex (A) lies immediately caudal to the central sulcus, is almost devoid of pyramidal cells, and is referred to as a granulous cortex. Damage to the cells situated in the region of the dorsal border of the superior temporal gyrus and the adjoining area of the inferior parietal lobule (Wernicke's area) (C) causes impairment in the appreciation of the meanings of written or spoken words.
The primary, secondary, and tertiary auditory receiving areas in the cortex are located mainly in the superior temporal gyrus (D). It is the final receiving area for inputs from the medial geniculate nucleus, which represents an important relay in the transmission of auditory signals to the cortex. An additional area of the cortex governing speech (F) is called the motor speech area, or Broca's area. It is situated in the inferior aspect of the frontal lobe immediately rostral and slightly ventral to the precentral gyrus. Lesions of this region produce impairment of the ability to express words in a meaningful way or to use words correctly. The orbital frontal cortex (E) lies in a position inferior and rostral to Broca's motor speech area. This region governs higher-order intellectual functions and some aspects of emotional behavior.
The caudal aspect of the middle frontal gyrus (G) contains cells that, when activated, produce conjugate deviation of the eyes. This action is believed to be accomplished, in part, by virtue of descending projections to the superior colliculus, pretectal region, and horizontal gaze center of the pons. Lesions of the posterior parietal lobe (B) of the nondominant hemisphere will produce a disorder of body image, referred to as sensory neglect. The patient will frequently fail to recognize or neglect to shave or wash those body parts. The patient may even fail to recognize the presence of a hemiparesis involving that part of the body as well. The precentral gyrus (H) constitutes the primary motor cortex. Lesions of this region produce a UMN paralysis involving a contralateral limb.
There are three basic mechanisms by which the transmitter is removed from the synaptic cleft: (1) enzymatic degradation, (2) reuptake, and (3) diffusion. In the case of the neuromuscular junction, ACh (and not glutamate) is the neurotransmitter and the primary mechanism involves enzymatic degradation. The enzyme involved is acetylcholinesterase, which helps break down ACh into acetate and choline. Choline is then taken up by the presynaptic terminal. Concerning the other choices, choline acetyltransferase is the enzyme involved in the synthesis of ACh, glutaminase, and glutamine synthetase are involved in the formation of glutamate from glutamine and glutamine from glutamate, respectively. Serine hydroxymethyltransferase is the enzyme that converts serine into glycine.
(see above explanation).