USMLE Step 1 Qs (13)

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

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

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

Explanation
An infarct that affects the medial thalamus, which includes the dorsomedial nucleus, and midline thalamic and intralaminar nuclei, can result in abnormalities in memory, attention, and drowsiness. The other choices offered for the question have not been shown to be related to functions associated with medial thalamic structures. A key input into the medial thalamus is the reticular formation. In this manner, the medial and intralaminar thalamus represent a relay from reticular formation to the cerebral cortex. Since a major function of the reticular function is to regulate states of sleep and wakefulness, these thalamic nuclei thus contribute to these states. When these nuclei are damaged, this mechanism is affected, resulting in drowsiness. Because of the connections of the medial thalamus with much of the frontal lobe, including the prefrontal cortex, damage to the medial thalamus would also affect the functions of these cortical regions, which involve memory and other cognitive processes.

Explanation
An infarct that affects the medial thalamus, which includes the dorsomedial nucleus, and midline thalamic and intralaminar nuclei, can result in abnormalities in memory, attention, and drowsiness. The other choices offered for the question have not been shown to be related to functions associated with medial thalamic structures. A key input into the medial thalamus is the reticular formation. In this manner, the medial and intralaminar thalamus represent a relay from reticular formation to the cerebral cortex. Since a major function of the reticular function is to regulate states of sleep and wakefulness, these thalamic nuclei thus contribute to these states. When these nuclei are damaged, this mechanism is affected, resulting in drowsiness. Because of the connections of the medial thalamus with much of the frontal lobe, including the prefrontal cortex, damage to the medial thalamus would also affect the functions of these cortical regions, which involve memory and other cognitive processes.

Explanation
The cerebrovascular accident produced damage of the right primary visual cortex. Therefore, this would result in a homonymous hemianopsia of the left visual fields. Since the damage was confined to the occipital lobe, there would be little effect upon other processes such as speech, motor functions, or intellectual activities.

Explanation
The occipital lobe is supplied by the posterior cerebral artery. The calcarine cortex (primary visual cortex) is supplied by a branch of this artery, the calcarine artery. The anterior cerebral artery supplies the medial aspect of the frontal lobe and the anterior-medial aspect of the parietal lobe. The middle cerebral artery supplies the lateral aspect of the frontal and parietal lobes. The superior cerebellar artery supplies the dorsolateral aspect of a portion of the pons and the cerebellum. The striate arteries arise from the anterior and middle cerebral arteries and supply portions of the internal capsule and neostriatum.

Explanation
The arterial occlusion involves both the temporal and occipital regions of cortex. Therefore, it would affect Wernicke's area as well as primary visual areas of the occipital lobe. The patient would most likely present with receptive aphasia as well as a right homonymous hemianopsia. The lesion would not likely produce marked intellectual deficits since the prefrontal cortex was spared; nor would it produce hemiballism since there was no damage to the subthalamic nucleus.

Explanation
Although the tissue affected involves parietal, temporal, and occipital lobes, the primary artery affected is the middle cerebral artery. The unusual feature of this occlusion is that it appears that the middle cerebral artery extends more caudally than usual. Nevertheless, the middle cerebral artery is the only one of the choices presented that could account for the damage to the temporal and parietal cortices. The anterior cerebral artery supplies the medial aspects of the frontal and parietal lobes; the posterior cerebral artery supplies the occipital cortex (visual areas); the posterior choroidal artery mainly supplies part of the tectum, the medial and superior aspects of the thalamus, and the choroid plexus of the third ventricle. The superior cerebellar artery supplies the dorsolateral aspect of a portion of the pons and the cerebellum.

Explanation
Jane is not only unable to move her left side (hemiparesis), but ignores its existence (anosagnosia or the syndrome of hemineglect, see below). Even though she neglects her left side, the blink reflex should still be intact if she only neglects the side. Therefore, a visual field deficit, called a homonymous hemianopsia, is present on the left side, in which the left temporal and right nasal fields are damaged. There may also be some degree of primary sensory loss, which can be difficult to evaluate when a patient neglects the same side.

Explanation
Jane's deficits result from lesions of the posterior frontal cortex, as well as from some contribution of corticospinal tract fibers to the parietal lobe and deeper motor cortical structures. In addition, the neglect and hemisensory loss result from damage to the parietal cortex. The homonymous hemianopsia results from damage to the deep portion of the parietal lobe where the optic radiations pass to the superior and inferior banks of the visual cortex, causing the visual field defect.

Explanation
The posterior frontal lobe, as well as the parietal lobe, are supplied by the middle cerebral artery. Areas supplied by this artery, such as primary and supplementary motor areas, and the primary and secondary somatosensory cortices may be affected. As a result, the patient may have left-sided weakness and UMN facial weakness that spares the forehead, and hemisensory loss.

Explanation
If the lesion is deep enough, the patient may have a visual field cut, called a homonymous hemianopsia, where fibers traveling from the optic chiasm to the occipital cortex within the optic radiations are interrupted, and the patient doesn't see the left temporal and the right nasal visual field. It is common for patients with neglect not to notice the areas of blindness because they ignore the left side. Patients with this problem are usually advised not to drive a car.

Explanation
Jane's problem is an example of the syndrome of hemineglect, which arises from a lesion of the posterior parietal lobe. This area is essential for spatial organization. If this area, usually on the nondominant (right) side, is no longer functioning, the patient will live in a world that consists solely of a right side. Patients with the syndrome of hemineglect will look only to the right side (if the lesion is on the right), and when asked to look to the left, often will not cross the midline with their eyes. Especially when the lesion is acute, these patients will not acknowledge any person or objects on their left side, and it is not unusual for a patient to complain of losing her glasses when they are on a table on the left side. Since these patients see only the right side of everything, they will put all of the numbers of a clock on the right side of the clock, and will bisect a line on its right side. In addition, they will only comb the right side of their hair, dress the right side of their bodies, and shave the right side of their faces. When confronted with a left-sided entity, such as a left arm, they will often ignore the question, or may even go as far as claiming it belongs to someone else. In resolving lesions where the patient now has sensation and acknowledgment on the left side, she may still display extinction to double simultaneous stimuli where, if both sides are touched simultaneously, the patient feels the touch only on the right side and "extinguishes" the stimulus on the left. However, it is important to remember that neglect can resemble weakness because the patient won't move the left side.

Explanation
This case is an example of a condition called normal-pressure hydrocephalus. This may be caused by various nonprogressive meningeal and ependymal diseases, such as chronic meningitis and subarachnoid hemorrhages, which can initially block CSF absorption. Initially, the CSF pressure is high, which results in the enlargement of the ventricles. The CSF pressure becomes normal because the CSF absorption begins again. However, the enlarged ventricles, despite normal CSF pressure, cause hydrostatic impairment to the central white matter surrounding the ventricles. Maximal ventricular expansion is usually located in the frontal lobes with preservation of the cortical gray matter and other subcortical structures. As a result, patients with this condition have diminished frontal lobe functions, namely, gait problems without any weakness, as well as urinary incontinence and dementia. Frontal lobe dysfunction can also cause the reappearance of primitive reflexes, which disappear shortly after birth, such as the grasp reflex. Late in the course of normal-pressure hydrocephalus, the patient may develop frontal lobe incontinence, where he or she becomes indifferent to the incontinence, much like a very small child. Headaches are rare in this particular type of hydrocephalus. Normal-pressure hydrocephalus is usually diagnosed with a thorough neurological examination, in addition to a head CT, which shows enlarged ventricles and, occasionally, interstitial fluid within the white matter adjacent to the lateral ventricles. [Measurement of CSF pressures with a lumbar puncture and radionuclide cisternography (a procedure where a radionuclide is injected intrathecally, and its distribution is observed over a period of 24 hours) is also helpful.] Occasionally, shunting procedures, which allow the CSF to drain into the peritoneal cavity or the blood, are helpful if performed early in the course of this condition.

Explanation
The major mechanism underlying hydrocephalus is decreased absorption of CSF. (In the case of normal-pressure hydrocephalus) Another cause of decreased absorption is obstruction of CSF flow by a tumor. Low blood pressure does not cause enlarged ventricles. High blood pressure only causes hydrocephalus as a result of hypertensive crisis, but not chronically. Decreased blood flow in the brain can actually be used as a temporizing measure to acutely decrease intracranial pressure in emergencies, in order to make room for expanding tissue through the mechanism of decreasing PCo2 in the brain with a ventilator.

Explanation
The major location for reabsorption of CSF are the arachnoid villi within the ventricular system. In the case of this particular patient, there is a history of a subarachnoid hemorrhage, which may have caused obstruction within this area

Explanation
The frontal horns of the lateral ventricles are the area of greatest expansion; thus, the expansion would affect the adjoining white matter of the frontal lobe. The other areas listed are subcortical and gray matter areas, which are located further from the expanding frontal horns, and are less affected. The pituitary gland is quite distant from the frontal horns, as well.