Chapters 4 and 6 mapped the primary motor cortex (precentral gyrus of the frontal lobe), primary somatosensory cortex (postcentral gyrus of the parietal lobe), and the primary visual cortex (calcarine cortex of the posterior occipital lobe) onto the cerebral hemispheres. The primary auditory cortex is housed in the superior temporal gyrus of the temporal lobe. Knowing the locations of the motor cortex and these three primary sensory cortices allows for a logical deduction of the functions of the rest of the cortical surface as is discussed below.
The hemisphere contralateral to the side of handedness is considered the dominant hemisphere (e.g., the left hemisphere in a right-handed patient), and the hemisphere ipsilateral to the side of handedness is considered the nondominant hemisphere (e.g., the right hemisphere in a right-handed patient). Most patients are right-handed, so their left hemisphere is the dominant hemisphere. Language dysfunction is most commonly due to lesions in the dominant (usually left) hemisphere, whereas neglect (see “Attention” below) is most commonly due to lesions in the nondominant (usually right) hemisphere (causing left-sided neglect).
The parietal lobe regions bounded by the somatosensory cortex anteriorly and the visual cortex posteriorly are ideally situated to combine visual and spatial information, playing roles in awareness of the body in space, spatial reasoning, and mathematical processing (Fig. 7–1). The projection from the occipital lobe superiorly to the parietal lobe (the dorsal stream) is referred to as the “where” pathway: Visual information is processed here to determine where things are in space with respect to the body. Lesions here can cause neglect: The patient is unaware of one half of the world. Neglect is more common with lesions in the nondominant parietal lobe, which is most commonly the right parietal lobe causing left-sided neglect. Examination findings in patients with neglect may include extinction to double simultaneous stimulation (see Ch. 4), lack of awareness of deficits (anosognosia; e.g., not acknowledging that a paretic limb is weak despite inability to move it), and in severe cases, inability to recognize the neglected body parts as one’s own.
Lesions in the angular gyrus of the dominant (usually left) parietal lobe can cause Gerstmann’s syndrome: left-right confusion, inability to count (acalculia), inability to name the fingers (finger agnosia), and inability to write (agraphia).
Parietal lesions can also cause difficulty performing a complex learned action (apraxia). This can be demonstrated by asking a patient to mime an action (e.g., “pretend you are taking out a pack of matches and lighting one,” or “pretend you are brushing your teeth”). There are several types of apraxia:
Limb-kinetic apraxia refers to a loss of dexterity in performing actions.
Ideational apraxia refers to inability to conceive of the idea of how to accurately perform an action, leading to errors in how the action is performed.
Ideomotor apraxia refers to inability to convert an idea about how to do something into a motor plan. Affected patients may be able to explain the intended action but are unable to perform it normally, making errors in sequencing and/or timing of the component movements of complex learned actions.
Although these terms are commonly confused, their names provide clues to what they signify: kinetic is difficulty with movements themselves, ideational is loss of the idea of how to perform an action, and ideomotor is difficulty translating an idea into a motor plan. The latter two types of apraxia are generally caused by lesions of the parietal lobe in the dominant (usually left) hemisphere.
The temporal lobes are ideally located to combine sensory input from olfactory, auditory, visual, and somatosensory cortices. The temporal lobes are thus ideally suited to play a role in recognition memory, since memories are internal representations of sensory experiences. Lesions of the medial temporal lobes (including the hippocampus) can cause amnesia. The flow of visual information inferiorly to the temporal lobe (the ventral stream) is referred to as the “what pathway:” visual information is processed here to determine what things are (recognition memory). The dominant (usually left) inferior temporal lobe houses the visual word form area necessary for reading, and the nondominant (usually right) inferior temporal lobe houses the face recognition area. Inability to read is called alexia and inability to recognize faces is referred to as prosopagnosia.
The inferior frontal gyrus lies in proximity to the auditory and motor cortices and is adjacent to the premotor cortex for the face. It is therefore ideally positioned to combine auditory and motor functions for speech production. The inferior frontal gyrus houses Broca’s area for speech production. Wernicke’s area for speech recognition lies at the junction of the auditory cortex (superior temporal gyrus) and the parietal cortex, where auditory regions are adjacent to parietal regions involved in awareness of one’s surroundings. In most right-handed patients, language is localized to the left hemisphere, and this is true in many left-handed patients as well. However, in some patients (more commonly left-handed patients), language may localize to the right hemisphere. Lesions in and around Broca’s and Wernicke’s areas lead to speech disturbances (aphasia).
The aphasias can be categorized based on the patient’s ability to produce speech, comprehend speech, and repeat words and phrases (Table 7–1). In a pure Broca’s aphasia, the primary deficit is in production of speech (nonfluent or expressive aphasia), but the patient can generally still comprehend. However, patients with Broca’s aphasia may have difficulty with comprehension of grammatically complex phrases (e.g., “The tiger was eaten by the lion. Who survived?”). In the most severe Broca’s aphasias, the patient is mute. When less severe, the patient may have effortful speech with frequent errors. Since comprehension is generally largely preserved in Broca’s aphasia, the patient is aware of and frustrated by the inability to speak. In a pure Broca’s aphasia, the patient cannot repeat phrases stated by the examiner but can comprehend (i.e., can follow commands). If a patient has an expressive aphasia with preserved repetition, this is called a transcortical motor aphasia.
| Speech Production | Speech Comprehension | Repetition | Lesion Location (Most Commonly in Left Hemipshere) | |
|---|---|---|---|---|
| Broca’s aphasia | Impaired | Preserved | Impaired | Inferior frontal gyrus (Broca’s area) |
| Transcortical motor aphasia | Impaired | Preserved | Preserved | Anterior/superior to Broca’s area |
| Wernicke’s aphasia | Preserved | Impaired | Impaired | Posterior superior temporal gyrus (Wernicke’s area) |
| Transcortical sensory aphasia | Preserved | Impaired | Preserved | Parietal, posterior to Wernicke’s area |
| Global aphasia | Impaired | Impaired | Impaired | Broca’s and Wernicke’s areas |
| Mixed transcortical aphasia | Impaired | Impaired | Preserved | Extensive lesions often involving middle cerebral artery–anterior cerebral artey (MCA-ACA) watershed region |
| Conduction aphasia | Preserved | Preserved | Impaired | Arcuate fasciculus |
In pure Wernicke’s aphasia, comprehension is impaired (receptive aphasia), and although the prosody (melody and rhythm) of speech is preserved (fluent aphasia), the content is nonsensical. The patient cannot understand his or her own nonsensical speech, and so may not appear concerned by the deficit. In pure Wernicke’s aphasia, a patient cannot repeat phrases. If repetition is preserved in a receptive aphasia, this is called a transcortical sensory aphasia.
If both production and comprehension are impaired, this is called a global aphasia. Rarely, patients with both productive and receptive aphasia are still able to repeat what they hear, a scenario called mixed transcortical aphasia.
Note that all of the transcortical aphasias are characterized by preserved repetition, and named for the primary language deficit: transcortical motor aphasia is characterized by a deficit in speech production (motor output), transcortical sensory aphasia is characterized by a deficit in speech comprehension (“sensation” of speech), and mixed transcortical aphasia is characterized by a mix of both expressive and receptive aphasia.
If a patient’s only language deficit is repetition with preserved comprehension and production, this is called a conduction aphasia, since conduction between Wernicke’s area and Broca’s area (via the arcuate fasciculus) is disrupted.
Sudden-onset aphasia is most commonly due to stroke in the left middle cerebral artery territory, but can also be due to a seizure or postictal state if the seizure activity originates in or spreads to language regions. More subacute development of aphasia can be seen with a left-sided chronic subdural hematoma or a tumor affecting language regions. Aphasia can also develop even more insidiously due to neurodegenerative diseases such as primary progressive aphasia (see Ch. 22).
In addition to regions involved in language and motor control, the frontal lobes support executive functions including working memory, decision making, abstract reasoning, and emotional processing. Frontal lobe lesions can cause abulia (decreased initiative, motivation, speech, and emotional response), behavioral disinhibition, and/or impairments in any of the above executive functions.
The higher order functions of the occipital lobes are discussed in Chapter 6.
The thalamus and basal ganglia are “islands” of gray matter in the subcortical white matter (Fig. 7–2). Both are nodes in a variety of circuits that begin and/or end in the cortex, brainstem, and/or cerebellum.
The left and right thalamus are positioned on either side of the third ventricle, just superior to the midbrain. The thalamus is a collection of nuclei, most of which project to one or more cortical regions (only the reticular nuclei do not project to the cortex, but rather to other thalamic nuclei) (Table 7–2). Four basic types of circuitry pass through thalamic nuclei en route to the cortex:
Sensory pathways. All sensory pathways synapse in the thalamus, which transmits sensory information to the respective sensory cortices. Smell is the only sensory modality that reaches the cortex before the thalamus (transmitted directly to the olfactory cortex, which then transmits smell information to the thalamus (dorsomedial nucleus)).
Motor control pathways. The ventral anterior (VA) and ventral lateral (VL) nuclei of the thalamus participate in cortical–basal ganglia–cortical loops and cerebellar–cortical pathways.
Consciousness/arousal pathways. These pathways begin in the brainstem reticular activating system and project to both thalami, which in turn project diffusely throughout the cortex.
Cognition/emotion pathways. Corticocortical loops pass through the thalamus, playing roles in diverse cognitive functions. One such loop is the circuit of Papez which participates in memory and emotion: hippocampus→fornix→mamillary bodies→anterior nucleus of the thalamus→anterior cingulate→entorhinal cortex→hippocampus.
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