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Overview of Cerebral Function

by Juebin Huang, MD, PhD

The cerebrum is divided by a longitudinal fissure into 2 hemispheres, each containing 5 discrete lobes. The frontal, temporal, parietal, and occipital lobes cover the brain’s surface; the insula is hidden under the Sylvian fissure (see see Figure: Areas of the brain.). Although specific functions are attributed to each lobe, most activities require coordination of multiple areas in both hemispheres. For example, although the occipital lobe is essential to visual processing, parts of the parietal, temporal, and frontal lobes on both sides also process complex visual stimuli.

Areas of the brain.

Function is extensively lateralized. Visual, tactile, and motor activities of the left side of the body are directed predominantly by the right hemisphere and vice versa. Certain complex functions involve both hemispheres but are directed predominantly by one (cerebral dominance). For example, the left hemisphere is typically dominant for language, and the right is dominant for spatial attention.

The cerebral cortex contains the primary sensory and motor areas as well as multiple association areas. The primary sensory areas receive somesthetic, auditory, visual, olfactory, and gustatory stimuli from specialized sensory organs and peripheral receptors. Sensory stimuli are further processed in association areas that relate to one or more senses. The primary motor cortex generates volitional body movements; motor association areas help plan and execute complex motor activity. Some cortical areas are heteromodal. They are not restricted to any single motor or sensory function but receive convergent information from multiple sensory and motor areas of the brain. Heteromodal association areas in the frontal, temporal, and parietal lobes integrate sensory data, motor feedback, and other information with instinctual and acquired memories. This integration facilitates learning and creates thought, expression, and behavior.

Frontal lobes

The frontal lobes are anterior to the central sulcus. They are essential for planning and executing learned and purposeful behaviors; they are also the site of many inhibitory functions. There are several functionally distinct areas in the frontal lobes:

  • The primary motor cortex is the most posterior part of the precentral gyrus. The primary motor cortex on one side controls all moving parts on the contralateral side of the body (shown on a spatial map called a homunculus—see Figure: Homunculus.); 90% of motor fibers from each hemisphere cross the midline in the brain stem. Thus, damage to the motor cortex of one hemisphere causes weakness or paralysis mainly on the contralateral side of the body.

  • The medial frontal cortex (sometimes called the medial prefrontal area) is important in arousal and motivation. If lesions in this area are large and extend to the most anterior part of the cortex (frontal pole), patients sometimes become abulic (apathetic, inattentive, and markedly slow to respond).

  • The orbital frontal cortex (sometimes called the orbital prefrontal area—see Figure: Areas of the brain.) helps modulate social behaviors. Patients with orbital frontal lesions can become emotionally labile, indifferent to the implications of their actions, or both. They may be alternately euphoric, facetious, vulgar, and indifferent to social nuances. Bilateral acute trauma to this area may make patients boisterously talkative, restless, and socially intrusive. With aging and in many types of dementia, disinhibition and abnormal behaviors can develop; these changes probably result from degeneration of the frontal lobe, particularly the orbital frontal cortex.

  • The left posteroinferior frontal cortex (sometimes called the Broca area or posteroinferior prefrontal area—see Figure: Areas of the brain.) controls expressive language function. Lesions in this area cause expressive aphasia (impaired expression of words—see Aphasia).

  • The dorsolateral frontal cortex (sometimes called the dorsolateral prefrontal area) manipulates very recently acquired information—a function called working memory. Lesions in this area can impair the ability to retain information and process it in real time (eg, to spell words backwards or to alternate between letters and numbers sequentially).

Homunculus.

Specific parts of the cortex control specific motor and sensory functions on the contralateral side of the body. The amount of cortical space given to a body part varies; eg, the area of the cortex that controls the hand is larger than the area that controls the shoulder. The map of these parts is called the homunculus (“little person”).

Parietal lobes

Several areas in the parietal lobes have specific functions.

  • The primary somatosensory cortex, located in the postrolandic area (postcentral gyrus) in the anterior parietal lobes, integrates somesthetic stimuli for recognition and recall of form, texture, and weight. The primary somatosensory cortex on one side receives all somatosensory input from the contralateral side of the body (see see Figure: Homunculus.). Lesions of the anterior parietal lobe can cause difficulty recognizing objects by touch (astereognosis).

  • Areas posterolateral to the postcentral gyrus generate visual-spatial relationships and integrate these perceptions with other sensations to create awareness of trajectories of moving objects. These areas also mediate proprioception (awareness of the position of body parts in space).

  • Parts of the midparietal lobe of the dominant hemisphere are involved in abilities such as calculation, writing, left-right orientation, and finger recognition. Lesions in the angular gyrus can cause deficits in writing, calculating, left-right disorientation, and finger-naming (Gerstmann syndrome).

  • The nondominant parietal lobe integrates the contralateral side of the body with its environment, enabling people to be aware of this environmental space, and is important for abilities such as drawing. Acute injury to the nondominant parietal lobe may cause neglect of the contralateral side (usually the left), resulting in decreased awareness of that part of the body, its environment, and any associated injury to that side (anosognosia). For example, patients with large right parietal lesions may deny the existence of left-sided paralysis. Patients with smaller lesions may lose the ability to do learned motor tasks (eg, dressing, other well-learned activities)—a spatial-manual deficit called apraxia.

Temporal lobes

The temporal lobes are integral to auditory perception, receptive components of language, visual memory, declarative (factual) memory, and emotion. Patients with right temporal lobe lesions commonly lose the ability to interpret nonverbal auditory stimuli (eg, music). Left temporal lobe lesions interfere greatly with the recognition, memory, and formation of language.

Patients with epileptogenic foci in the medial limbic-emotional parts of the temporal lobe commonly have complex partial seizures, characterized by uncontrollable feelings and autonomic, cognitive, or emotional dysfunction. Occasionally, such patients have personality changes, characterized by humorlessness, philosophic religiosity, and obsessiveness.

Occipital lobes

The occipital lobes contain the primary visual cortex and visual association areas. Lesions in the primary visual cortex lead to a form of central blindness called Anton syndrome; patients become unable to recognize objects by sight and are generally unaware of their deficits, often confabulating descriptions of what they see. Seizures involving the occipital lobe can cause visual hallucinations, often consisting of lines or meshes of color superimposed on the contralateral visual field.

Insula

The insula integrates sensory and autonomic information from the viscera. It plays a role in certain language functions, as evidenced by aphasia in patients with some insular lesions. The insula processes aspects of pain and temperature sensation and possibly taste.

Pathophysiology

Cerebral dysfunction may be focal or global. Focal and global processes may also affect subcortical systems, altering arousal (eg, causing stupor or coma) or integration of thought (eg, causing delirium).

Focal dysfunction usually results from structural abnormalities (eg, tumors, stroke, trauma, malformations, gliosis, demyelination). Manifestations depend on the lesion’s location, size, and development rate. Lesions that are < 2 cm in diameter or that develop very slowly may be asymptomatic. Larger lesions, rapidly developing lesions (over weeks or months rather than years), and lesions that simultaneously affect both hemispheres are more likely to become symptomatic. Focal lesions in white matter can interrupt the connectivity between brain areas and cause the disconnection syndrome (inability to do a task that requires coordinated activity of 2 brain regions, despite retention of basic functions of each region).

Global dysfunction is caused by toxic-metabolic disorders or sometimes by diffuse inflammation, vasculopathy, major trauma, or disseminated cancer; these disorders affect multiple dimensions of cerebral function.

Recovery

Recovery from brain injury depends in part on the plasticity (ability of an area of the brain to alter its function) of the remaining cerebrum, a capacity that varies from person to person and is affected by age and general health. Plasticity is most prominent in the developing brain. For example, if the dominant hemisphere language areas are severely damaged before age 8 yr, the opposite hemisphere can often assume near-normal language function. Although capacity for recovery from brain injury is considerable after the first decade of life, severe damage more often results in permanent deficits. Gross reorganization of brain function after injury in adults is uncommon, although plasticity remains operative in certain specific areas of the brain throughout life.


Cerebral dysfunction syndromes

Specific syndromes include agnosia, amnesia, aphasia, and apraxia. Psychiatric conditions (eg, depression, psychosis, anxiety disorders) sometimes include similar elements.


Diagnosis

In general, diagnosis is clinical, often assisted by neuropsychologic testing. Diagnosis of the cause usually requires laboratory tests (blood and sometimes CSF analysis) and brain imaging, either structural (CT, MRI) or functional (PET, single-photon emission CT).

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