USMLE Step 1 Qs (9)

This is an example of the locked-in syndrome, or pseudocoma, caused by an infarction of the pontine tegmentum. Because the tracts mediating movement of the limbs and face run through this region, the patient is unable to move the face, as well as both arms and legs. Consciousness and eye movements are preserved. The pontine tegmentum is mainly supplied by the basilar artery. Complete occlusion of this artery causes deficits on both sides since this artery supplies both sides of the pons. Basilar artery occlusion causes damage to the basilar pons, where the corticospinal and corticobulbar tracts run. These tracts contain motor fibers mediating movement of the limb and face, respectively. This results in complete paralysis to both sides of the body and the face. None of the tracts in the other choices mediate conscious movement. Sensory loss, including loss of proprioception (feeling the movement of a limb), also occurs as a result of damage to the medial lemniscus bilaterally. This tract contains fibers from the dorsal columns and also runs through the pontine tegmentum. Patients with the locked-in syndrome are often mistaken for comatose patients due to their inability to move or speak. If the lesion spares the reticular formation, an area mediating consciousness in the pons, the patient will remain alert.

The CT scan of Louise's brain revealed a large, acute stroke of her upper pons and midbrain. Strokes of these areas often result from occlusion of the basilar artery and can produce coma, or a variant of hypersomnia called akinetic mutism or coma vigil. An EEG of a patient like this shows a pattern associated with slow-wave sleep, but eye movements are preserved. It is likely that the corticospinal tracts within the pons were damaged during this very large stroke, causing the increased tone from lack of inhibition, as well as the lack of movement in Louise's arms and legs. Infarctions of perforators of the basilar artery, supplying the reticular formation of the pons may cause coma. These perforators also supply the corticospinal tracts, causing the increased tone and weakness of Louise's legs, so a large stroke may involve both functions. Coma occurs because there is damage to the brainstem tegmentum, which is a major component of the ascending reticular activating system. Although it is not known exactly which area is precisely responsible for consciousness, lesions of this region, as well as projections from the medial regions of the midbrain reticular formation can produce coma. The two main monoaminergic systems of the reticular formation are the noradrenergic and serotonergic systems, originating in the locus ceruleus and raphe nuclei, respectively. The mesolimbic, mesostriatal, and mesocortical dopaminergic systems are located within the ventrorostral aspect of the brainstem, but not within the reticular formation.

Seizures similar to this one often begin with abnormal neuronal discharges in temporal lobe structures, which include the amygdala or hippocampus. These structures tend to have a lower threshold for this type of activity than other structures in the brain.

Excitatory postsynaptic potentials are considered to be an initiating cellular event for a seizure. To become a seizure, however, the cellular discharges require enhancement and synchronization.

Joe's forehead doesn't droop like the rest of his face because this region receives innervation from both sides of the cerebral cortex, giving this area a backup in case of damage. This can only occur when the lesion is above the level of nerve VII, where both sides no longer contribute to the innervation of the face. This type of weakness is called a central nerve VII lesion, because it occurs within the CNS. A peripheral nerve VII lesion is a lesion within the nerve VII nucleus, or distal. This type of lesion always involves the forehead in addition to the rest of the face. Nerve XII innervates the tongue, nerve V innervates sensation of the face, in addition to the muscles of mastication, but not the muscles of facial expression. The oculomotor nerve innervates four of the muscles that move the eyes.

This is an example of the locked-in syndrome, or pseudocoma, caused by an infarction of the pontine tegmentum. Because the tracts mediating movement of the limbs and face run through this region, the patient is unable to move the face, as well as both arms and legs. Consciousness and eye movements are preserved. The pontine tegmentum is mainly supplied by the basilar artery. Complete occlusion of this artery causes deficits on both sides since this artery supplies both sides of the pons. Basilar artery occlusion causes damage to the basilar pons, where the corticospinal and corticobulbar tracts run. These tracts contain motor fibers mediating movement of the limb and face, respectively. This results in complete paralysis to both sides of the body and the face. None of the tracts in the other choices mediate conscious movement. Sensory loss, including loss of proprioception (feeling the movement of a limb), also occurs as a result of damage to the medial lemniscus bilaterally. This tract contains fibers from the dorsal columns and also runs through the pontine tegmentum. Patients with the locked-in syndrome are often mistaken for comatose patients due to their inability to move or speak. If the lesion spares the reticular formation, an area mediating consciousness in the pons, the patient will remain alert.

Norma's head CT showed an old stroke in her left ventral thalamus and no new lesions. A stroke involving the ventral posterolateral nucleus of the thalamus, especially several months after the stroke can produce an entity called the Déjérine-Roussy syndrome, or thalamic pain syndrome. Although there is sensory loss on the contralateral side, there is pain or discomfort out of proportion to the stimulus on the affected side of the body. Emotional disturbance aggravates the response. Some patients describe the sensation as knifelike or hot. As the deficit (numbness) resolves, the pain may lessen. This syndrome may also occur in lesions of the parietal white matter, and is thought to occur as a result of an imbalance of afferent sensory impulses. Sensation of the limbs and trunk are projected through the ventral posterior lateral nucleus of the thalamus to the somatosensory cortex. Sensory information from the face is carried through the trigeminal system to the ventral posteromedial nucleus, from which it is projected to the somatosensory cortex. The spinothalamic tract is the only sensory pathway listed that mediates pain. The periaqueductal gray is one area of many that produces analgesia when stimulated in both animals and in humans. It is an area with a high density of opiate receptors and opioidergic neurons, and is thought to represent a key area in gating pain. Many neurotransmitters have been implicated as pain modulators, including the opiates and enkephalins, norepinephrine, serotonin, substance P, GABA, and acetylcholine. Most analgesic medications are designed to target a particular aspect of the pain pathway. In more recent years, the advent of a class of drugs called tricyclic antidepressants has added another dimension to medical pain treatment. The methylated forms of these medications are useful blockers of serotonin reuptake. Since serotonin is known to be a pain modulator, it is thought that blocking the reuptake of serotonin enhances its action and facilitates the action of intrinsic opiates to relieve pain. This is a common class of drugs used to treat chronic pain, since these medications are not addictive.

The seizure described in this patient has progressed from a complex partial seizure to a generalized seizure. As indicated previously, this type of seizure involves all of the limbs. The patient falls to the ground and typically loses consciousness. The other choices involve seizures that are characterized differently than what was described in the progression of this case.

The corticospinal and corticobulbar tracts contain motor fibers originating in the precentral gyrus, mediating voluntary motor function of the face, arms, legs, and trunk. They pass through the internal capsule to the crus cerebri in the midbrain. The spinothalamic tract is a sensory tract, and could not cause the observed deficits. The rubrospinal tract only affects the spinal cord.

Norma's head CT showed an old stroke in her left ventral thalamus and no new lesions. A stroke involving the ventral posterolateral nucleus of the thalamus, especially several months after the stroke can produce an entity called the Déjérine-Roussy syndrome, or thalamic pain syndrome. Although there is sensory loss on the contralateral side, there is pain or discomfort out of proportion to the stimulus on the affected side of the body. Emotional disturbance aggravates the response. Some patients describe the sensation as knifelike or hot. As the deficit (numbness) resolves, the pain may lessen. This syndrome may also occur in lesions of the parietal white matter, and is thought to occur as a result of an imbalance of afferent sensory impulses. Sensation of the limbs and trunk are projected through the ventral posterior lateral nucleus of the thalamus to the somatosensory cortex. Sensory information from the face is carried through the trigeminal system to the ventral posteromedial nucleus, from which it is projected to the somatosensory cortex. The spinothalamic tract is the only sensory pathway listed that mediates pain. The periaqueductal gray is one area of many that produces analgesia when stimulated in both animals and in humans. It is an area with a high density of opiate receptors and opioidergic neurons, and is thought to represent a key area in gating pain. Many neurotransmitters have been implicated as pain modulators, including the opiates and enkephalins, norepinephrine, serotonin, substance P, GABA, and acetylcholine. Most analgesic medications are designed to target a particular aspect of the pain pathway. In more recent years, the advent of a class of drugs called tricyclic antidepressants has added another dimension to medical pain treatment. The methylated forms of these medications are useful blockers of serotonin reuptake. Since serotonin is known to be a pain modulator, it is thought that blocking the reuptake of serotonin enhances its action and facilitates the action of intrinsic opiates to relieve pain. This is a common class of drugs used to treat chronic pain, since these medications are not addictive.

The internal capsule is supplied primarily by the lenticulostriate branches of the middle cerebral artery. In addition, portions of the posterior limb of the internal capsule are supplied by the anterior choroidal artery, a branch of the internal carotid artery. Both the lateral striate branches and the anterior choroidal artery are small branches of larger arteries, and are more susceptible to damage (atherosclerosis) from high blood pressure and diabetes than the larger vessels.

This is an example of a complex partial seizure, most likely originating in the temporal lobe. A seizure is a paroxysmal derangment of the CNS due to rhythmic, synchronous discharges from cerebral neurons, causing changes in consciousness, sensation, and/or behavior. Complex partial seizures often start with a warning, or "aura." Since limbic structures are often involved, the seizure can include emotions, feelings of deja vu or jamais vu, or gastrointestinal sensations. Because olfactory pathways end in the temporal lobe, patients may experience smells as well. The seizure, itself, involves impairment of consciousness of some form, often manifested as staring, in addition to various stereotyped, automatic behaviors called automatisms. The latter may be manifested as chewing, repetitive swallowing, hand gestures, or vocalizations. These usually occur during the seizure, but may occur after it. After the seizure ends (the seizures usually last 1 to 2 minutes), the patient is often in a confused or postictal state for several minutes, or even up to several hours. Occasionally, a patient may manifest aggressive behavior while in the postictal state. Unless a structural lesion, such as a tumor, is present, the physical examination is usually normal. Verification of the diagnosis of epilepsy is done with the help of an EEG, which records potential differences of summed cortical action potentials over the scalp of a patient. Often, an epileptic spike, or sharp wave, is seen over the area from which the seizures arise. Epilepsy patients usually also have a CT scan or MRI to make certain that there is no structural lesion causing the seizures.

Since memory is a function that is mediated by the limbic system, a structure most likely involved in the generation of these seizures, it is possible that Lindsey will have memory problems in the future if she has frequent seizures. Early studies of patients who have undergone resection of portions of one or both temporal lobes have demonstrated the presence of memory deficits.

This case is an example of a lesion of the left (usually dominant) parietal lobe, most often in the angular gyrus, with some involvement of the precentral gyrus in the posterior frontal lobe. There is contralateral UMN weakness (with a positive Babinski sign), as well as several cortical sensory defects—specifically, right-left confusion, agraphia (inability to write, independent of motor weakness), acalculia (the inability to calculate), and finger agnosia (the inability to designate the fingers). The latter four elements are sometimes referred to as the Gerstmann syndrome by neurologists, and all represent spatial discriminatory functions of the parietal lobe (often the dominant parietal lobe, which is usually the left). The parietal lobe also subserves other visual-spatial functions such as construction of complex drawings. There are other locations within the CNS where UMN weakness can occur; however, the combination with parietal lobe signs can only occur in this location. If the damage was slightly more extensive, it may have involved Broca's area, causing aphasia.

Morris' leg weakness includes a positive Babinski sign, which is a UMN sign. Although this type of weakness may occur in several locations in the CNS, the combination with the cortical parietal signs can only occur in the left precentral gyrus if there is to be one lesion.

Emma has had a stroke resulting from occlusion of medial branches of the left vertebral artery, presumably secondary to atherosclerosis (i.e., cholesterol deposits within the artery, which eventually occlude it). The resulting syndrome is called the medial medullary syndrome, because the affected structures are located in the medial portion of the medulla. These structures include: the pyramids, the medial lemniscus, the medial longitudinal fasciculus, and the nucleus of the hypoglossal nerve and its outflow tract. Emma's symptoms result from damage to the aforementioned structures, and may have been caused by the same process (atherosclerosis) that resulted in her heart disease. The weakness of her right side was caused by damage to the medullary pyramid on the left side. Her face was spared because fibers supplying the face exited above the level of infarct. However, a lesion in the corticospinal tract of the cervical spinal cord above C5 could cause arm and leg weakness, and spare the face, because facial fibers exit in the rostral medulla. A lesion in the inferior portion of the precentral gyrus of the left frontal lobe would cause right-sided weakness, but would include the face, because this area is represented more inferiorly than are the extremities. Her unsteady gait was a result of the weakness of her right side, but may also have been the result of the loss of position and vibration sense on that side from damage to the medial lemniscus (as demonstrated by the inability to identify the position of her toe with her eyes closed, and the inability to feel the vibrations of a tuning fork). Without position sense, walking becomes unsteady because it is necessary to feel the position of one's feet on the floor during normal gait. Damage to both the medial lemniscus and pyramids at this level causes problems on the contralateral side because this lesion is located rostral to the level where both of these fiber bundles cross to the opposite side of the brain. Damage to the descending component of the medial longitudinal fasciculus could only affect head and neck reflexes, but not gait. Gait is also unaffected by pain inputs. Deviation of the tongue occurs because fibers from the hypoglossal nucleus innervate the genioglossus muscle on the ipsilateral side of the tongue. This muscle normally protrudes the tongue toward the contralateral side. Therefore, if one side is weak, the tongue will deviate toward the side ipsilateral to the lesion when protruded. A lesion in the precentral gyrus causes protrusion of the tongue toward the side that is contralateral to the lesion, because it is rostral to the crossing of fibers into the hypoglossal nucleus. Emma's speech was dysarthric (slurred) because her tongue was weak on the left side. The physician saw this during the exam when her tongue deviated to the left when protruded. Since the weakness of the tongue is purely a motor problem, rather than an effect that is manifested by a lesion to higher centers in the cortex (which mediate the structure and function of speech), the grammar, content, and meaning of Emma's speech remained intact, as would be expected with an aphasia or agnosia.

Damage to the VA, VL, dorsomedial, and anterior thalamic nuclei would most likely result in motor impairment such as a hemiparesis (because of the connections of these nuclei with the motor and premotor cortices). Damage to the dorsomedial nucleus could also be linked with neuropsychological impairment, because of its connections with the prefrontal cortex and adjoining regions of the frontal lobe. The other processes mentioned in the question have not been shown to be related to these groups of nuclei. As noted earlier, the VA nucleus is associated with motor functions, not only in its projections to motor regions of the cerebral cortex—the premotor and prefrontal cortices—but also in the inputs that it receives from structures associated with motor functions such as the globus pallidus and substantia nigra.

The middle cerebral artery subserves the precentral gyrus, the area which has been damaged. The damage can be more widespread, depending upon which portion of the vessel becomes occluded. The anterior cerebral artery supplies the orbitofrontal cortex, deep limbic structures, as well as the cingulate gyrus. The posterior cerebral artery supplies the thalamus, portions of the temporal lobes, and portions of the midbrain. The anterior inferior cerebellar artery supplies the lateral inferior pons and portions of the cerebellum. Perforating branches of the basilar artery supply medial portions of the brainstem. The irregular heartbeat observed in this case is an example of aerial fibrillation, a heart rhythm that is often recognized by being "irregularly irregular". This rhythm can cause strokes by throwing small blood clots or emboli from the heart to the cerebral blood vessels and occluding them.

The CT scan of Louise's brain revealed a large, acute stroke of her upper pons and midbrain. Strokes of these areas often result from occlusion of the basilar artery and can produce coma, or a variant of hypersomnia called akinetic mutism or coma vigil. An EEG of a patient like this shows a pattern associated with slow-wave sleep, but eye movements are preserved. It is likely that the corticospinal tracts within the pons were damaged during this very large stroke, causing the increased tone from lack of inhibition, as well as the lack of movement in Louise's arms and legs. Infarctions of perforators of the basilar artery, supplying the reticular formation of the pons may cause coma. These perforators also supply the corticospinal tracts, causing the increased tone and weakness of Louise's legs, so a large stroke may involve both functions. Coma occurs because there is damage to the brainstem tegmentum, which is a major component of the ascending reticular activating system. Although it is not known exactly which area is precisely responsible for consciousness, lesions of this region, as well as projections from the medial regions of the midbrain reticular formation can produce coma. The two main monoaminergic systems of the reticular formation are the noradrenergic and serotonergic systems, originating in the locus ceruleus and raphe nuclei, respectively. The mesolimbic, mesostriatal, and mesocortical dopaminergic systems are located within the ventrorostral aspect of the brainstem, but not within the reticular formation.

Emma has had a stroke resulting from occlusion of medial branches of the left vertebral artery, presumably secondary to atherosclerosis (i.e., cholesterol deposits within the artery, which eventually occlude it). The resulting syndrome is called the medial medullary syndrome, because the affected structures are located in the medial portion of the medulla. These structures include: the pyramids, the medial lemniscus, the medial longitudinal fasciculus, and the nucleus of the hypoglossal nerve and its outflow tract. Emma's symptoms result from damage to the aforementioned structures, and may have been caused by the same process (atherosclerosis) that resulted in her heart disease. The weakness of her right side was caused by damage to the medullary pyramid on the left side. Her face was spared because fibers supplying the face exited above the level of infarct. However, a lesion in the corticospinal tract of the cervical spinal cord above C5 could cause arm and leg weakness, and spare the face, because facial fibers exit in the rostral medulla. A lesion in the inferior portion of the precentral gyrus of the left frontal lobe would cause right-sided weakness, but would include the face, because this area is represented more inferiorly than are the extremities. Her unsteady gait was a result of the weakness of her right side, but may also have been the result of the loss of position and vibration sense on that side from damage to the medial lemniscus (as demonstrated by the inability to identify the position of her toe with her eyes closed, and the inability to feel the vibrations of a tuning fork). Without position sense, walking becomes unsteady because it is necessary to feel the position of one's feet on the floor during normal gait. Damage to both the medial lemniscus and pyramids at this level causes problems on the contralateral side because this lesion is located rostral to the level where both of these fiber bundles cross to the opposite side of the brain. Damage to the descending component of the medial longitudinal fasciculus could only affect head and neck reflexes, but not gait. Gait is also unaffected by pain inputs. Deviation of the tongue occurs because fibers from the hypoglossal nucleus innervate the genioglossus muscle on the ipsilateral side of the tongue. This muscle normally protrudes the tongue toward the contralateral side. Therefore, if one side is weak, the tongue will deviate toward the side ipsilateral to the lesion when protruded. A lesion in the precentral gyrus causes protrusion of the tongue toward the side that is contralateral to the lesion, because it is rostral to the crossing of fibers into the hypoglossal nucleus. Emma's speech was dysarthric (slurred) because her tongue was weak on the left side. The physician saw this during the exam when her tongue deviated to the left when protruded. Since the weakness of the tongue is purely a motor problem, rather than an effect that is manifested by a lesion to higher centers in the cortex (which mediate the structure and function of speech), the grammar, content, and meaning of Emma's speech remained intact, as would be expected with an aphasia or agnosia

This is an example of the locked-in syndrome, or pseudocoma, caused by an infarction of the pontine tegmentum. Because the tracts mediating movement of the limbs and face run through this region, the patient is unable to move the face, as well as both arms and legs. Consciousness and eye movements are preserved. The pontine tegmentum is mainly supplied by the basilar artery. Complete occlusion of this artery causes deficits on both sides since this artery supplies both sides of the pons. Basilar artery occlusion causes damage to the basilar pons, where the corticospinal and corticobulbar tracts run. These tracts contain motor fibers mediating movement of the limb and face, respectively. This results in complete paralysis to both sides of the body and the face. None of the tracts in the other choices mediate conscious movement. Sensory loss, including loss of proprioception (feeling the movement of a limb), also occurs as a result of damage to the medial lemniscus bilaterally. This tract contains fibers from the dorsal columns and also runs through the pontine tegmentum. Patients with the locked-in syndrome are often mistaken for comatose patients due to their inability to move or speak. If the lesion spares the reticular formation, an area mediating consciousness in the pons, the patient will remain alert.

Norma's head CT showed an old stroke in her left ventral thalamus and no new lesions. A stroke involving the ventral posterolateral nucleus of the thalamus, especially several months after the stroke can produce an entity called the Déjérine-Roussy syndrome, or thalamic pain syndrome. Although there is sensory loss on the contralateral side, there is pain or discomfort out of proportion to the stimulus on the affected side of the body. Emotional disturbance aggravates the response. Some patients describe the sensation as knifelike or hot. As the deficit (numbness) resolves, the pain may lessen. This syndrome may also occur in lesions of the parietal white matter, and is thought to occur as a result of an imbalance of afferent sensory impulses. Sensation of the limbs and trunk are projected through the ventral posterior lateral nucleus of the thalamus to the somatosensory cortex. Sensory information from the face is carried through the trigeminal system to the ventral posteromedial nucleus, from which it is projected to the somatosensory cortex. The spinothalamic tract is the only sensory pathway listed that mediates pain. The periaqueductal gray is one area of many that produces analgesia when stimulated in both animals and in humans. It is an area with a high density of opiate receptors and opioidergic neurons, and is thought to represent a key area in gating pain. Many neurotransmitters have been implicated as pain modulators, including the opiates and enkephalins, norepinephrine, serotonin, substance P, GABA, and acetylcholine. Most analgesic medications are designed to target a particular aspect of the pain pathway. In more recent years, the advent of a class of drugs called tricyclic antidepressants has added another dimension to medical pain treatment. The methylated forms of these medications are useful blockers of serotonin reuptake. Since serotonin is known to be a pain modulator, it is thought that blocking the reuptake of serotonin enhances its action and facilitates the action of intrinsic opiates to relieve pain. This is a common class of drugs used to treat chronic pain, since these medications are not addictive.

The CT scan of Louise's brain revealed a large, acute stroke of her upper pons and midbrain. Strokes of these areas often result from occlusion of the basilar artery and can produce coma, or a variant of hypersomnia called akinetic mutism or coma vigil. An EEG of a patient like this shows a pattern associated with slow-wave sleep, but eye movements are preserved. It is likely that the corticospinal tracts within the pons were damaged during this very large stroke, causing the increased tone from lack of inhibition, as well as the lack of movement in Louise's arms and legs. Infarctions of perforators of the basilar artery, supplying the reticular formation of the pons may cause coma. These perforators also supply the corticospinal tracts, causing the increased tone and weakness of Louise's legs, so a large stroke may involve both functions. Coma occurs because there is damage to the brainstem tegmentum, which is a major component of the ascending reticular activating system. Although it is not known exactly which area is precisely responsible for consciousness, lesions of this region, as well as projections from the medial regions of the midbrain reticular formation can produce coma. The two main monoaminergic systems of the reticular formation are the noradrenergic and serotonergic systems, originating in the locus ceruleus and raphe nuclei, respectively. The mesolimbic, mesostriatal, and mesocortical dopaminergic systems are located within the ventrorostral aspect of the brainstem, but not within the reticular formation.

The CT scan of Louise's brain revealed a large, acute stroke of her upper pons and midbrain. Strokes of these areas often result from occlusion of the basilar artery and can produce coma, or a variant of hypersomnia called akinetic mutism or coma vigil. An EEG of a patient like this shows a pattern associated with slow-wave sleep, but eye movements are preserved. It is likely that the corticospinal tracts within the pons were damaged during this very large stroke, causing the increased tone from lack of inhibition, as well as the lack of movement in Louise's arms and legs. Infarctions of perforators of the basilar artery, supplying the reticular formation of the pons may cause coma. These perforators also supply the corticospinal tracts, causing the increased tone and weakness of Louise's legs, so a large stroke may involve both functions. Coma occurs because there is damage to the brainstem tegmentum, which is a major component of the ascending reticular activating system. Although it is not known exactly which area is precisely responsible for consciousness, lesions of this region, as well as projections from the medial regions of the midbrain reticular formation can produce coma. The two main monoaminergic systems of the reticular formation are the noradrenergic and serotonergic systems, originating in the locus ceruleus and raphe nuclei, respectively. The mesolimbic, mesostriatal, and mesocortical dopaminergic systems are located within the ventrorostral aspect of the brainstem, but not within the reticular formation.

The pyramidal cell is a cell in the cortex that uses glutamate, an excitatory neurotransmitter, whereas most other types of cortical neurons use GABA, an inhibitory neurotransmitter. The spike, one identifying feature of an epileptic seizure seen on an EEG recorded on the scalp, is initiated by a depolarization shift, which is thought to be generated by EPSPs.

Damage to the VA, VL, dorsomedial, and anterior thalamic nuclei would most likely result in motor impairment such as a hemiparesis (because of the connections of these nuclei with the motor and premotor cortices). Damage to the dorsomedial nucleus could also be linked with neuropsychological impairment, because of its connections with the prefrontal cortex and adjoining regions of the frontal lobe. The other processes mentioned in the question have not been shown to be related to these groups of nuclei. As noted earlier, the VA nucleus is associated with motor functions, not only in its projections to motor regions of the cerebral cortex—the premotor and prefrontal cortices—but also in the inputs that it receives from structures associated with motor functions such as the globus pallidus and substantia nigra.

June had a seizure, which began focally on the left motor strip (the left precentral gyrus), moved up the motor strip, then secondarily generalized, or spread throughout the cortex. The phenomenon whereby there is twitching of an extremity that spreads to other areas on that extremity or other areas of the body is called a Jacksonian march. This phenomenon is named for Hughlings Jackson, a neurosurgeon who was instrumental in mapping out the cerebral cortex and describing the somatotopic organization of the cortex of the prefrontal gyrus called a homunculus (meaning little man). Observing patients with a Jacksonian march helped him to identify areas represented at each location of the motor strip.

Emma has had a stroke resulting from occlusion of medial branches of the left vertebral artery, presumably secondary to atherosclerosis (i.e., cholesterol deposits within the artery, which eventually occlude it). The resulting syndrome is called the medial medullary syndrome, because the affected structures are located in the medial portion of the medulla. These structures include: the pyramids, the medial lemniscus, the medial longitudinal fasciculus, and the nucleus of the hypoglossal nerve and its outflow tract. Emma's symptoms result from damage to the aforementioned structures, and may have been caused by the same process (atherosclerosis) that resulted in her heart disease. The weakness of her right side was caused by damage to the medullary pyramid on the left side. Her face was spared because fibers supplying the face exited above the level of infarct. However, a lesion in the corticospinal tract of the cervical spinal cord above C5 could cause arm and leg weakness, and spare the face, because facial fibers exit in the rostral medulla. A lesion in the inferior portion of the precentral gyrus of the left frontal lobe would cause right-sided weakness, but would include the face, because this area is represented more inferiorly than are the extremities. Her unsteady gait was a result of the weakness of her right side, but may also have been the result of the loss of position and vibration sense on that side from damage to the medial lemniscus (as demonstrated by the inability to identify the position of her toe with her eyes closed, and the inability to feel the vibrations of a tuning fork). Without position sense, walking becomes unsteady because it is necessary to feel the position of one's feet on the floor during normal gait. Damage to both the medial lemniscus and pyramids at this level causes problems on the contralateral side because this lesion is located rostral to the level where both of these fiber bundles cross to the opposite side of the brain. Damage to the descending component of the medial longitudinal fasciculus could only affect head and neck reflexes, but not gait. Gait is also unaffected by pain inputs. Deviation of the tongue occurs because fibers from the hypoglossal nucleus innervate the genioglossus muscle on the ipsilateral side of the tongue. This muscle normally protrudes the tongue toward the contralateral side. Therefore, if one side is weak, the tongue will deviate toward the side ipsilateral to the lesion when protruded. A lesion in the precentral gyrus causes protrusion of the tongue toward the side that is contralateral to the lesion, because it is rostral to the crossing of fibers into the hypoglossal nucleus. Emma's speech was dysarthric (slurred) because her tongue was weak on the left side. The physician saw this during the exam when her tongue deviated to the left when protruded. Since the weakness of the tongue is purely a motor problem, rather than an effect that is manifested by a lesion to higher centers in the cortex (which mediate the structure and function of speech), the grammar, content, and meaning of Emma's speech remained intact, as would be expected with an aphasia or agnosia.

Damage to the VA, VL, dorsomedial, and anterior thalamic nuclei would most likely result in motor impairment such as a hemiparesis (because of the connections of these nuclei with the motor and premotor cortices). Damage to the dorsomedial nucleus could also be linked with neuropsychological impairment, because of its connections with the prefrontal cortex and adjoining regions of the frontal lobe. The other processes mentioned in the question have not been shown to be related to these groups of nuclei. As noted earlier, the VA nucleus is associated with motor functions, not only in its projections to motor regions of the cerebral cortex—the premotor and prefrontal cortices—but also in the inputs that it receives from structures associated with motor functions such as the globus pallidus and substantia nigra.

The major descending pathways from the amygdala are the stria terminalis and the ventral amygdalofugal pathway. The medial forebrain bundle is a major pathway of the lateral hypothalamus. The mamillothalamic and corticospinal tracts do not involve the amygdala.

The language problem is an example of Broca's aphasia, a deficit seen with lesions of Broca's area and manifested by defects in the motor aspect of speech, leaving the patient's speech halting and nonfluent. People with Broca's aphasia tend to repeat certain phrases, as well as leave out pronouns. Since the language centers are usually located on the dominant side of the brain (the left side for a right-handed person), this lesion must be on the left side of Joe's brain. Wernicke's aphasia is a problem with the sensory aspect of speech, where the patient can speak fluently, but the speech sounds like gibberish. The area of disruption in this type of aphasia is usually in Wernicke's area, a region of the posterior superior temporal lobe. Dysarthria is slurred speech, but makes grammatical sense. Alexia is the inability to read. Pure-word deafness is a type of sensory aphasia where language, reading, and writing are only mildly disturbed, but auditory comprehension of words is very abnormal. This arises from lesions of the posterior temporal lobe.

This is an example of the locked-in syndrome, or pseudocoma, caused by an infarction of the pontine tegmentum. Because the tracts mediating movement of the limbs and face run through this region, the patient is unable to move the face, as well as both arms and legs. Consciousness and eye movements are preserved. The pontine tegmentum is mainly supplied by the basilar artery. Complete occlusion of this artery causes deficits on both sides since this artery supplies both sides of the pons. Basilar artery occlusion causes damage to the basilar pons, where the corticospinal and corticobulbar tracts run. These tracts contain motor fibers mediating movement of the limb and face, respectively. This results in complete paralysis to both sides of the body and the face. None of the tracts in the other choices mediate conscious movement. Sensory loss, including loss of proprioception (feeling the movement of a limb), also occurs as a result of damage to the medial lemniscus bilaterally. This tract contains fibers from the dorsal columns and also runs through the pontine tegmentum. Patients with the locked-in syndrome are often mistaken for comatose patients due to their inability to move or speak. If the lesion spares the reticular formation, an area mediating consciousness in the pons, the patient will remain alert.

Dysarthria is slurred speech, occurring from lesions affecting innervation of the tongue, lips, and palate. We are given evidence that her tongue is weak in that her tongue points to the right. The interruption of fibers traveling to the hypoglossal nerve from the left side eventually innervates the right genioglossus muscle, which pulls the tongue to the left. Dysarthria is a motor phenomenon, unlike aphasia, which is a disruption of language. Language is primarily generated in the cerebral cortex; therefore, because the lesion spares the cortex, there were no signs of aphasia.

Emma has had a stroke resulting from occlusion of medial branches of the left vertebral artery, presumably secondary to atherosclerosis (i.e., cholesterol deposits within the artery, which eventually occlude it). The resulting syndrome is called the medial medullary syndrome, because the affected structures are located in the medial portion of the medulla. These structures include: the pyramids, the medial lemniscus, the medial longitudinal fasciculus, and the nucleus of the hypoglossal nerve and its outflow tract. Emma's symptoms result from damage to the aforementioned structures, and may have been caused by the same process (atherosclerosis) that resulted in her heart disease. The weakness of her right side was caused by damage to the medullary pyramid on the left side. Her face was spared because fibers supplying the face exited above the level of infarct. However, a lesion in the corticospinal tract of the cervical spinal cord above C5 could cause arm and leg weakness, and spare the face, because facial fibers exit in the rostral medulla. A lesion in the inferior portion of the precentral gyrus of the left frontal lobe would cause right-sided weakness, but would include the face, because this area is represented more inferiorly than are the extremities. Her unsteady gait was a result of the weakness of her right side, but may also have been the result of the loss of position and vibration sense on that side from damage to the medial lemniscus (as demonstrated by the inability to identify the position of her toe with her eyes closed, and the inability to feel the vibrations of a tuning fork). Without position sense, walking becomes unsteady because it is necessary to feel the position of one's feet on the floor during normal gait. Damage to both the medial lemniscus and pyramids at this level causes problems on the contralateral side because this lesion is located rostral to the level where both of these fiber bundles cross to the opposite side of the brain. Damage to the descending component of the medial longitudinal fasciculus could only affect head and neck reflexes, but not gait. Gait is also unaffected by pain inputs. Deviation of the tongue occurs because fibers from the hypoglossal nucleus innervate the genioglossus muscle on the ipsilateral side of the tongue. This muscle normally protrudes the tongue toward the contralateral side. Therefore, if one side is weak, the tongue will deviate toward the side ipsilateral to the lesion when protruded. A lesion in the precentral gyrus causes protrusion of the tongue toward the side that is contralateral to the lesion, because it is rostral to the crossing of fibers into the hypoglossal nucleus. Emma's speech was dysarthric (slurred) because her tongue was weak on the left side. The physician saw this during the exam when her tongue deviated to the left when protruded. Since the weakness of the tongue is purely a motor problem, rather than an effect that is manifested by a lesion to higher centers in the cortex (which mediate the structure and function of speech), the grammar, content, and meaning of Emma's speech remained intact, as would be expected with an aphasia or agnosia.

This person displays a complex partial seizure, which is characterized by a confusional state with brief losses of consciousness. It is called a partial seizure because the seizure involves a localized region, reflected by jerks of the muscles of a specific part of the body. The focus of this seizure is typically in the temporal lobe, such as the amygdala, hippocampal formation, or adjoining cortical regions. A simple partial seizure does not involve loss of consciousness. Absence seizures are nonconvulsive seizures and are also called petit mal seizures. Generalized seizures typically involve all of the limbs. The patient falls to the ground and loses consciousness.

Since seizure generation requires excitation, or a loss of inhibition, the only correct choice is the inhibition of GABA, an inhibitory neurotransmitter. All the other choices cause inhibition only. Many new anticonvulsant medications are currently being designed to either enhance GABA activity, or inhibit the excitatory neurotransmitter, glutamate.

Joe's condition is an example of a left inferior frontal lobe cortical stroke, including the region of Broca's area and the left precentral gyrus. The weakness on his right side confirms this, since the left side of the brain controls the right side of the body. The right leg is most likely less involved than the arm because the leg area of the precentral gyrus extends onto the medial aspect of the frontal lobe, an area served by a different artery than that serving the arm and face areas. The internal capsule contains motor fibers traveling to the cortex, but usually does not involve language. The thalamus contains many sensory, motor, and association areas, but only rarely causes language problems. Functions of the pontine reticular formation do not include language. The corpus callosum is a white matter structure that connects the hemispheres. Lesions of the posterior aspect may cause language problems, such as alexia without agraphia (the ability to write, but not to read), but would not cause both an aphasia as well as weakness.

The infarct caused damage to posterior thalamic nuclei. When these structures are damaged, a disorder referred to as thalamic pain can ensue. In this condition, light cutaneous stimulation is sufficient to produce severe pain. The projections from nuclei situated in this region project principally to the parietal and occipital lobes and play a role in the regulation of pain (although the precise mechanisms remain unknown). The other processes offered as alternate choices have not been shown to be related to functions of the posterior thalamus

Norma's head CT showed an old stroke in her left ventral thalamus and no new lesions. A stroke involving the ventral posterolateral nucleus of the thalamus, especially several months after the stroke can produce an entity called the Déjérine-Roussy syndrome, or thalamic pain syndrome. Although there is sensory loss on the contralateral side, there is pain or discomfort out of proportion to the stimulus on the affected side of the body. Emotional disturbance aggravates the response. Some patients describe the sensation as knifelike or hot. As the deficit (numbness) resolves, the pain may lessen. This syndrome may also occur in lesions of the parietal white matter, and is thought to occur as a result of an imbalance of afferent sensory impulses. Sensation of the limbs and trunk are projected through the ventral posterior lateral nucleus of the thalamus to the somatosensory cortex. Sensory information from the face is carried through the trigeminal system to the ventral posteromedial nucleus, from which it is projected to the somatosensory cortex. The spinothalamic tract is the only sensory pathway listed that mediates pain. The periaqueductal gray is one area of many that produces analgesia when stimulated in both animals and in humans. It is an area with a high density of opiate receptors and opioidergic neurons, and is thought to represent a key area in gating pain. Many neurotransmitters have been implicated as pain modulators, including the opiates and enkephalins, norepinephrine, serotonin, substance P, GABA, and acetylcholine. Most analgesic medications are designed to target a particular aspect of the pain pathway. In more recent years, the advent of a class of drugs called tricyclic antidepressants has added another dimension to medical pain treatment. The methylated forms of these medications are useful blockers of serotonin reuptake. Since serotonin is known to be a pain modulator, it is thought that blocking the reuptake of serotonin enhances its action and facilitates the action of intrinsic opiates to relieve pain. This is a common class of drugs used to treat chronic pain, since these medications are not addictive.

A CT scan of Helen's head was done in the emergency room, which showed a new infarct or stroke in the genu and anterior portion of the posterior limb of the left internal capsule. This is the region of the internal capsule through which most of the fibers of the corticospinal and corticobulbar tracts pass in a somatotopically organized fashion before entering the brainstem. Because most of these fibers pass through a very small region, a small infarct can cause deficits in a wide distribution of areas. In this case, Helen has weakness in her face and tongue, causing her slurred speech, in addition to weakness of her arm and leg. In addition, since somatosensory fibers destined for the postcentral gyrus occupy a position in the internal capsule caudal to the corticospinal tract fibers, these fibers are spared and Helen has no sensory deficits. The only other area in the CNS that can cause a pure motor hemiparesis is the basilar pons, an area through which corticospinal and corticobulbar fibers also run. The vascular supply of this region consists of perforators from the basilar artery, which are small and subject to atherosclerotic disease.

This is an example of the locked-in syndrome, or pseudocoma, caused by an infarction of the pontine tegmentum. Because the tracts mediating movement of the limbs and face run through this region, the patient is unable to move the face, as well as both arms and legs. Consciousness and eye movements are preserved. The pontine tegmentum is mainly supplied by the basilar artery. Complete occlusion of this artery causes deficits on both sides since this artery supplies both sides of the pons. Basilar artery occlusion causes damage to the basilar pons, where the corticospinal and corticobulbar tracts run. These tracts contain motor fibers mediating movement of the limb and face, respectively. This results in complete paralysis to both sides of the body and the face. None of the tracts in the other choices mediate conscious movement. Sensory loss, including loss of proprioception (feeling the movement of a limb), also occurs as a result of damage to the medial lemniscus bilaterally. This tract contains fibers from the dorsal columns and also runs through the pontine tegmentum. Patients with the locked-in syndrome are often mistaken for comatose patients due to their inability to move or speak. If the lesion spares the reticular formation, an area mediating consciousness in the pons, the patient will remain alert.

Norma's head CT showed an old stroke in her left ventral thalamus and no new lesions. A stroke involving the ventral posterolateral nucleus of the thalamus, especially several months after the stroke can produce an entity called the Déjérine-Roussy syndrome, or thalamic pain syndrome. Although there is sensory loss on the contralateral side, there is pain or discomfort out of proportion to the stimulus on the affected side of the body. Emotional disturbance aggravates the response. Some patients describe the sensation as knifelike or hot. As the deficit (numbness) resolves, the pain may lessen. This syndrome may also occur in lesions of the parietal white matter, and is thought to occur as a result of an imbalance of afferent sensory impulses. Sensation of the limbs and trunk are projected through the ventral posterior lateral nucleus of the thalamus to the somatosensory cortex. Sensory information from the face is carried through the trigeminal system to the ventral posteromedial nucleus, from which it is projected to the somatosensory cortex. The spinothalamic tract is the only sensory pathway listed that mediates pain. The periaqueductal gray is one area of many that produces analgesia when stimulated in both animals and in humans. It is an area with a high density of opiate receptors and opioidergic neurons, and is thought to represent a key area in gating pain. Many neurotransmitters have been implicated as pain modulators, including the opiates and enkephalins, norepinephrine, serotonin, substance P, GABA, and acetylcholine. Most analgesic medications are designed to target a particular aspect of the pain pathway. In more recent years, the advent of a class of drugs called tricyclic antidepressants has added another dimension to medical pain treatment. The methylated forms of these medications are useful blockers of serotonin reuptake. Since serotonin is known to be a pain modulator, it is thought that blocking the reuptake of serotonin enhances its action and facilitates the action of intrinsic opiates to relieve pain. This is a common class of drugs used to treat chronic pain, since these medications are not addictive.

There is somatotopic organization of the motor strip, and cortical neurons are included among the most likely to generate seizures, making this area the most likely to cause such a pattern

The CT scan of Louise's brain revealed a large, acute stroke of her upper pons and midbrain. Strokes of these areas often result from occlusion of the basilar artery and can produce coma, or a variant of hypersomnia called akinetic mutism or coma vigil. An EEG of a patient like this shows a pattern associated with slow-wave sleep, but eye movements are preserved. It is likely that the corticospinal tracts within the pons were damaged during this very large stroke, causing the increased tone from lack of inhibition, as well as the lack of movement in Louise's arms and legs. Infarctions of perforators of the basilar artery, supplying the reticular formation of the pons may cause coma. These perforators also supply the corticospinal tracts, causing the increased tone and weakness of Louise's legs, so a large stroke may involve both functions. Coma occurs because there is damage to the brainstem tegmentum, which is a major component of the ascending reticular activating system. Although it is not known exactly which area is precisely responsible for consciousness, lesions of this region, as well as projections from the medial regions of the midbrain reticular formation can produce coma. The two main monoaminergic systems of the reticular formation are the noradrenergic and serotonergic systems, originating in the locus ceruleus and raphe nuclei, respectively. The mesolimbic, mesostriatal, and mesocortical dopaminergic systems are located within the ventrorostral aspect of the brainstem, but not within the reticular formation.

The infarct caused damage to posterior thalamic nuclei. When these structures are damaged, a disorder referred to as thalamic pain can ensue. In this condition, light cutaneous stimulation is sufficient to produce severe pain. The projections from nuclei situated in this region project principally to the parietal and occipital lobes and play a role in the regulation of pain (although the precise mechanisms remain unknown). The other processes offered as alternate choices have not been shown to be related to functions of the posterior thalamus.

These deficits are visual-spatial in nature, and are characteristic of damage to the dominant parietal lobe.

The visual defect that Morris experiences is a homonymous hemianopsia, resulting from damage to the optic radiations traveling from the lateral geniculate nucleus to the visual cortex in the occipital lobe. These split so that inferior images are carried through the parietal lobe and superior images through the temporal lobes, but in large infarcts, the defect is more likely to involve more fibers of this tract. Since the optic radiations carry representations of the ipsilateral temporal field and the contralateral nasal field (only the nasal field fibers cross), this defect is noted clinically as the inability to detect objects in the regions described. Often, the patient will only notice bumping into objects on the side ipsilateral to the stroke, since turning of the eyes can compensate for the nasal field defect.

Very often, there is inhibition following a seizure, which accounts for drowsiness or a postictal state after the seizure has finished. Sometimes, epileptic discharges spread to other areas of the cortex, recruiting contiguous areas of the cortex through callosal, commissural, and sometimes thalamic circuits to eventually involve a large area of the cortex, causing the movements of the entire body. This occurs with a generalized seizure. If the cortices of both hemispheres become involved, there may be impairment or loss of consciousness. The cells (often pyramidal cells) in the cortex can generate a seizure through high-frequency, synchronous discharges in large groups. If the seizure begins focally, as this one did, there may be a Todd's paralysis, as June had, where there is transient paralysis of the involved motor area during the postictal period.

The hippocampal formation includes the hippocampus, the dentate gyrus, and the subiculum. All of the other structures listed are within the limbic system, but do not lie within the hippocampal formation

The artery serving this region (both posterior frontal and parietal lobes) is the right middle cerebral artery, which originates at Willis's circle. Because it continues in a nearly straight line from the internal carotid artery, it is a common route for small emboli formed from blood clots in the internal carotid artery. The bruit noted over the right common carotid artery in this patient is most likely a result of a thrombus (clot) that occludes part of the lumen of the artery. These emboli can occlude the middle cerebral artery because it is considerably smaller than the internal carotid artery. Since the middle cerebral artery has many branches through which an embolus may travel, but the territory of this stroke is large, it is likely that the embolus lodged in a more proximal location in this case.