Damage to the opercular and triangular portions of the inferior frontal gyrus (also known as Brodmann area 44) causes a constellation of deficits in expressive language commonly referred to as Broca’s aphasia (41). Broca’s aphasia is also known as expressive, nonfluent, or motor aphasia, suggesting that most of the deficits are in expressive rather than receptive language processing. In fact, patients with Broca’s aphasia tend to have relatively good language comprehension skills. Patients who have a lesion of this area tend to produce very few words orally or in written form, exhibit extreme difficulty in word production, have impaired repetition and naming abilities, tend to leave out articles and qualifiers, and speak and write in a manner best described as “telegraphic.”

Patients with prefrontal lobe lesions tend to have difficulty with the initial acquisition of new information because of their poor attention and organizational skills. They also tend to make numerous errors of perseveration and commission (e.g., false-positive errors on cued memory recall tasks) because they have difficulty inhibiting inappropriate responses. Working memory, which refers to temporarily holding a limited amount of information in mind for a few seconds while manipulating it, also depends on intact frontal lobe functioning (40). Impairments in working memory can result in diminished declarative memory performance by limiting the amount of material that is acquired initially. Although the frontal cortex plays a role in various memory processes, deficits in retention of new information are more likely to be seen following a lesion of the temporal lobes (see below).

The prefrontal cortex is intrinsically involved in the capacity to focus or shift attention as required by changing task demands (73,74). Damage to the prefrontal cortex can result in numerous types of attentional deficits. For example, patients may be slow to react to stimuli and have attentional difficulties that are characterized by an inability to maintain or sustain focus, an inability to shift mental sets, and poor cognitive flexibility. Patients with prefrontal lesions can be described as having a “rigid” approach to problem solving in general and are often unable to benefit from contextual cues or even direct instructional sets that direct them to the correct solution. Once again, their cognitive style can be characterized by numerous
errors of perseveration, a deficit that may be seen across a variety of mental tasks and settings. An extreme example of this is when a patient is unable to stop making the same erroneous perseverative responses even though he or she can accurately state a correct answer.

Related to this “rigid” cognitive style is an inability to overcome literal associations. These patients tend to view events and interactions at face value and are unable to detect more subtle nuances and, therefore, the genuine meaning of events. This concrete approach also results in an inability to generate or appropriately use abstract notions, such as symbols, proverbs, and metaphors.

Finally, many patients with prefrontal lesions tend to have difficulties in both initiating and stopping behavior, a deficit that can dramatically affect cognitive functioning. Difficulties in initiation can be related to apathy, poor spontaneity, and productivity, whereas difficulties in stopping a behavior may be more closely related to poor impulse control or an inability to benefit from feedback suggesting the cessation of a behavior is warranted; difficulties in stopping behavior can also be caused by an inability to overcome perseverative responses. This type of disinhibition is often seen following lesions of the orbitofrontal circuitry, whereas symptoms such as spontaneity and apathy are more likely to follow injury to the anterior cingulate circuitry (25).

Lesions of the temporal cortex can cause deficits in visual discrimination, visual word recognition, pattern recognition, and even object recognition. These visual perceptual deficits can occur despite relatively normal performance on standard visual-spatial tasks. For example, patients with right temporal lobe lesions may have difficulty recognizing objects from incomplete or partially drawn figures, may fail to recognize salient aspects of pictures, and may have relatively poor spatial reasoning abilities (108).

Damage to the temporal cortex and medial temporal structures have long been known to result in material-specific memory deficits (32,83). Lesions of the left temporal lobe can result in impairment in the ability to encode and recall a list of aurally presented words, numbers, or letters; semantic memory; and verbal paired-associate learning (108). Patients with left temporal lobe lesions can have difficulty recalling words, which can also adversely affect fluent speech production. When severe, this inability is referred to as anomia. Patients with this disorder can have impaired comprehension of complex information and, therefore, find it difficult to learn new verbal material.

Patients with right temporal lobe lesions are more likely to have memory difficulties involving visual-spatial stimuli such as faces, nonverbalizable designs, and figures. They can also have difficulty with maze learning and any stimuli or task that does not readily lend itself to verbal tagging or labeling. Deficits in material-specific memory caused by unilateral temporal lobe lesions tend to produce relatively mild cognitive dysfunction that may only be noticeable with
neuropsychological testing. However, bilateral temporal lobe lesions can result in a global amnesia (i.e., a severe and pervasive deficit in forming new conscious memories for all types of material). Although amnesia has been noted after unilateral temporal lobe lesions (typically of the dominant hemisphere), the most likely cause of an amnestic stroke is bilateral infarction of the posterior cerebral arteries affecting inferomedial structures of the temporal lobe, including the hippocampus and amygdala. This type of bilateral infarction is not exceptional because both posterior cerebral arteries arise from a single basilar artery (108).

Agraphia, an inability to write, has been associated with lesions in the angular gyrus itself or connections to this region within the left parietal lobe. Less commonly, these deficits can be seen following right hemisphere lesions as well. There are several types of agraphia, but the particular type of agraphia seen following posterior dominant hemisphere lesions tends to be characterized by well-formed letters joined together but with incorrect spellings, abnormal word order, and frequent omissions (11). This is in contrast to the more anterior type of agraphia characterized by large, crude, scrawling output that is poorly constructed and agrammatic. Isolated agraphia (not in the context of aphasia), which can also be seen following lesions of the angular gyrus, can co-occur with acalculia.

Acalculia refers to the inability to perform certain mathematical operations. It can be seen following damage of the left parietal lobe and often co-occurs with agraphia. Several types of agraphia and acalculia reflect a disruption of more complicated higher order cognitive processes. One form of acalculia, in which patients cannot comprehend or write numbers correctly or even substitute one number for another, can be seen after damage to the dominant hemisphere language areas. Damage to the nondominant parietaloccipital junction can result in a visual-spatial discrimination problem that causes an acalculia that is characterized by poor placement of numbers in space such that the numbers are not aligned properly to allow for complex calculations. In this case, patients can understand numbers, symbols, and computation signs and may even be able to successfully complete most mathematical operations.

Disorders of spatial orientation, including contralateral neglect, are seen after right parietal lesions. Contralateral neglect involves the neglect of visual, tactile, and auditory stimulation from the side of the body or hemifield that is contralateral to the site of the lesion. Allegri (3) reported that left-sided neglect after right hemisphere lesions is more common (31% to 46%) than right-sided neglect following lesions in the left hemisphere (2% to 12%). Thus, although unilateral neglect can be seen following left parietal infarcts, this is relatively rare compared with most patients who present with a left neglect corresponding to right parietal damage. Unilateral neglect has also been observed following frontal and subcortical vascular damage as well. Patients with parietal lesions can also experience route-finding problems and an inability to recognize objects that might ordinarily serve as landmarks (i.e., topographic agnosia). Additionally, patients with left parietal lesions can also present with significant right-left spatial disorientation problems.

A more holistic knowledge about landmarks and direction information is a function referred to as “wayfinding.” Wayfinding probably involves multiple neural mechanisms, and the exact neural circuitry involved in disorders of wayfinding is controversial. However, a recent study by van Asselen et al. (105) examined the neuroanatomic correlates of wayfinding in 31 patients with known unilateral stroke locations via magnetic resonance imaging (MRI). These patients were tested in a series of tasks including landmark recognition, landmark ordering, route reversal, and even route drawing. The findings suggested that landmark recognition was impaired by right hippocampal formation damage with a relatively weaker association being seen between landmark ordering and dorsolateral prefrontal cortical damage. Route drawing appeared to be related to right temporal damage, whereas route reversal (or tracing a route from end to
beginning) was impacted by several cerebral regions including the right hippocampal formation, the right posterior parietal cortex, the right dorsolateral prefrontal cortex, and the right temporal lobe.

Apraxia can be simply defined as an inability to carry out purposeful movement in the absence of some type of motor disturbance such as a paralysis. Many different types of apraxia occur, with one of the most notable forms being constructional apraxia, or the inability to perform familiar sequences of movements when making or preparing something (108). Interestingly, this deficit is seen when patients can still perform all of the individual actions or steps involved in a particular sequence. For example, a patient may be able to perform all of the individual steps needed to mail a letter (e.g., licking the stamp and sealing the envelope) but is unable to make the proper sequence of movements to actually complete the task of mailing the letter. Constructional disorders characterized by an inability to draw or construct objects or shapes have also been observed following lesions to either hemisphere, with qualitative differences in the process and product of the construction providing valuable clues as to lesion laterality. For example, the drawings of patients with right hemisphere lesions are frequently seen as fragmented and characterized by poor spatial relations. These drawings can also be characterized by poor or faulty orientation. Conversely, patients with left hemisphere lesions may produce better spatial orientation and relations, but their drawing can be overly simple, lack detail, and be especially labored to produce. More recently, it has been suggested that there are actually two different but complementary systems for encoding spatial relations (categorical and coordinate). Therefore, there may actually be two qualitatively different forms of constructional apraxia caused by unilateral lesions (64). This may suggest why some authors, such as Sunderland et al. (102), suggest that disorders of constructional apraxia are very resistant to recovery, whereas other authors, such as Nys et al. (80), have posited that they have the best prognosis.

Anosognosia can be defined generally as the failure to perceive illness. Numerous types of anosognosias exist. Asomatognosia, or loss of knowledge about the body or about a bodily condition, is a disorder that can be seen following damage to the parietal cortex of either hemisphere, of which many varieties exist. Anosodiaphoria refers to a general indifference to a disorder. An inability to name and localize body parts is known as autotopagnosia. These agnosias all stem from lesions to the left parietal cortex. Patients with right parietal or frontal infarcts have been shown to have significantly fewer introspective capacities and less concern over their illness than patients with infarcts in other regions, despite similar degrees of cognitive impairment (52).

Occlusion of the posterior cerebral artery resulting in bilateral visual cortex damage can lead to a condition known as cerebral or cortical blindness, a condition characterized by an inability to distinguish forms or patterns despite intact responsiveness to light changes (68). Cerebral blindness may be accompanied by a period of confusion, amnesia, or even unconsciousness. Astonishingly, patients who are cerebrally blind (or more commonly referred to as “cortically blind”) can exhibit visually responsive behaviors and be able to detect visual stimuli in the blind field without the experience of vision (85), a phenomenon called “blindsight.” Hartmann et al. (48) described a patient with cerebral blindness resulting from bioccipital and left parietal lesions who, although denying visual perception, correctly named objects, colors, and famous faces; recognized facial emotions; and read various types of single words with greater than 50% accuracy when they were presented in the upper right visual field. When questioned about his apparent visual abilities, the patient continued to deny visual perceptual awareness, typically stating, “I feel it.” The authors suggest that this type of denial of visual perception is best explained as a disconnection of the parietal lobe attention system from regions controlling visual perception. In direct opposition to “blindsight,” patients with Anton syndrome fail to appreciate the fact that they are blind and make elaborate confabulations and rationalizations as to their impaired performance. Anton syndrome typically stems from lesions of the bilateral occipital lobe and most likely is caused by the disruption of corticothalamic connections (27).

Visual agnosias are characterized by defective visual perception or distortion of visual stimuli, despite normal visual input, and can be seen following infarction of the visual association areas (10). For example, visual object agnosia is characterized by intact visual perception of
the visual stimulus but an inability to recognize the object. Patients with this neurobehavioral disorder can often draw the object or copy a picture of it, confirming intact visual perceptual abilities. This type of agnosia can be seen after lesions of the dominant occipital lobe (108). Simultagnosia (Balint syndrome) is characterized by an inability to perceive more than one aspect of a stimulus at one time, despite the ability to identify and remember single aspects of features of an object. This neurobehavioral deficit may be partially caused by an inability to shift attentional focus and direct gaze (10). Another more rare type of visual agnosia is characterized by an inability to recognize familiar faces. This disorder is referred to as prosopagnosia, and in severe cases, some patients do not even recognize their own reflection in the mirror. The neuroanatomic underpinnings of this disorder are still in question; however, prosopagnosia has been associated with bilateral, left, and right hemisphere lesions of both the parietal and occipital lobe (67). Some suggestion exists for a relatively greater frequency of bilateral and nondominant lesions to a greater degree (33), as well as for a relatively greater degree of dysfunction seen following right versus left hemisphere lesions (66). Finally, another type of visual agnosia for colors has also been known to follow occipital lobe lesions. This type of neurobehavioral disorder can take on various manifestations, including an inability to distinguish color hues (i.e., achromatopsia), an inability to name colors (i.e., color anomia), and an inability to associate particular colors with objects and vice versa (i.e., color agnosia) (60). Table 18-1 summarizes some of the more common neurobehavioral disorders following cortical stroke and hemorrhage that have been described in more detail earlier. The anatomic localization of some of these disorders is somewhat equivocal, and deficits assigned solely to left hemisphere lesions assume left hemisphere language dominance.