You should know where primary visual, auditory, somatosensory and motor cortices are located:See figure 15.
The two cerebral hemispheres are not functionally equivalent. The following functional asymmetries have been well-documented:
Limbus means rim. Structures of the limbic cortex form a ring around the brainstem and diencephalon. Limbic structures include (going in a circle) the amygdala, hippocampus and parahippocampal gyrus, cingulate cortex, orbitofrontal, and insular cortex. Limbic regions tend to have a more primitive structure than neocortex, and are highly interconnected with basal forebrain and hypothalamus.
Only a few will be mentioned.
Aphasia is most often associated with damage to left hemisphere cortex. The following distinctions are useful:
| Syndrome | Spont. Speech | Comprehension | Repetition | Naming |
|---|---|---|---|---|
| Perisylvian aphasias | ||||
| Broca's | Non-fluent ("Telegraphic") | Good | Poor | Poor |
| Wernicke's | Fluent (phonemic paraphasias) | Poor | Poor | Poor |
| Conduction | Fluent (phonemic paraphasias) | Good | Poor | Poor |
| Global | Non-fluent | Poor | Poor | Poor |
| Trans-cortical aphasias | ||||
| Transcortical motor | Non-fluent | Good | Good | Var. |
| Transcortical sensory | Fluent (semantic paraphasias) | Poor | Good | Poor |
| Mixed Transcortical | Non-fluent | Poor | Good | Poor |
| Anomic | Fluent (circumlocution..) | Good | Good | Poor |
Structures around the sylvian fissure mediate auditory language repetition. Auditory signals are processed by Heschl's gyrus (primary auditory cortex), and phonemic analysis probably takes place in the adjacent auditory association cortex (Wernicke's area). Speech is encoded by more anterior regions (among them, Broca's area, in front of the motor cortex), and these regions direct the adjacent motor cortex to produce the appropriate movements. Damage to any of these regions impairs language repetition, the hallmark of the perisylvian aphasias. Language comprehension requires that the phonetically analyzed information be communicated to regions outside the perisylvian region (among them, the angular gyrus).
These are characterized by intact repetition. Lesions are more varied than with perisylvian aphasias. In addition to the cortical localizations noted, transcortical aphasias may result from subcortical damage.
Neurological deficits may result not only from destruction of cortical regions that subserve specific functions, but also from disconnections between these areas. An example is the syndrome of alexia without agraphia (pure word blindness, Djerine's syndrome). Most commonly caused by left posterior cerebral artery territory infarction, the lesion disconnects the right visual cortex from the left hemisphere language centers. The left visual cortex is destroyed. The patient cannot read in the intact left visual field, but other language functions are normal. See figure 18.
Patients fail to respond, or respond more slowly, to stimuli presented in the field opposite the lesion. They may initially appear hemianopic, or hemianesthetic, but eventually it can be shown that sensory function is normal, if their attention can be maintained. Patients may also have anosognosia: failure to recognize their deficits. They may explicitly deny a hemiplegia, or fail to recognize that they have had a stroke. Neglect is more frequent and more severe with right than with left hemisphere lesions.
The core features of the amnesic syndrome are: (1) Anterograde amnesia, an inability to learn new information after the onset of amnesia. (2) Retrograde amnesia, an inability to retrieve information that was learned prior to the onset of amnesia. (3) Normal attention and intellectual function: Many amnesics have normal language, praxis, visuospatial, and even frontal lobe function. Unless you specifically test memory, they may appear to be normal. Furthermore, certain kinds of memory are spared in the amnesic syndrome: patients can learn routines such as motor skills, and mirror reading; their behavior may be influenced by information that they cannot consciously recall. These spared functions are thus mediated by different brain structures. It is thought, for example, that motor memories and habits may be mediated through the basal ganglia, but this remains to be clarified. Diseases associated with the amnesic syndrome include stroke or tumor, if any of the critical areas is affected, head injury, Wernicke-Korsakoff disorder from thiamine deficiency, and Alzheimer's disease (which affects the hippocampus and basal forebrain). In Alzheimer's disease, cognitive deficits (aphasia, apraxia, visuospatial disorders) soon combine with amnesia to produce a more complex clinical picture.
The frontal lobes have a high-order executive role in behavior. Without their guidance, we are left at the mercy of immediate stimuli. Frontal patients may therefore demonstrate stimulus-bound behavior: they may use available objects even when there is no reason to do so (utilization behavior), they perseverate (re-use the most recent responses), and they do not seek understanding beyond what is most obvious. They may demonstrate pseudopsychopathic behavior, failing to consider the consequences of their actions, making irresponsible decisions in business, and at times making inappropriate sexual advances (despite often overall reduced libido). Patients with frontal dementias also fail to organize their experience, and do not plan for the future. They often forget things, not because they cannot encode new memories, but because they fail to initiate memory searches when appropriate. For example, the patient may be told to go to the store to buy five items, but when he gets to the store he is attracted to a magazine, reads it, and then comes home with nothing. When asked why he was sent to the store, he can recall the items he was supposed to have purchased; he just forgot to remember them when it was appropriate. [The patient with the classical amnesic syndrome would not recall the list after distraction.] Patients with orbitofrontal lesions appear to have most difficulty inhibiting inappropriate behavior. Patients with medial lesions tend to be akinetic, and fail to initiate behavior.