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Consciousness

We become conscious of only a fraction of the information reaching our brain. The conscious contents are stored in associative cortical areas that specialize in this task p. 346). Conscious awareness requires not only that the m specific afferents have been transmitted to the .2 cerebral cortex, but also nonspecific activation Sy by the ARAS through which neurons from the ry reticular formation activate wide areas of the so cerebral cortex via intralaminar neurons of £ the thalamus (^ A).

¡^ Damage to large areas of the cortex and/or jj breakdown of the ARAS brings about loss of consciousness. In addition, there may be pri-ul mary causes influencing neuronal excitability usc in the above-mentioned neuronal structures. E Ischemia (e.g., atherosclerotic vascular occlu-2 sion) or hypoxia (e.g., suffocation) (^ A1) im-<u pair excitability directly or by cell swelling. N Swelling of glial cells impairs, among other 2 functions, their capacity to take up K+ and thus to keep down the concentration of extracellular K+. This has an indirect effect on neuronal excitability. Part of the effect of tumors, abscesses, or bleeding is also exerted via ischemia or hypoxia (^ A1) in that they raise the cerebral pressure and thus impaircerebral perfusion by narrowing the blood vessels. Hypo-glycemia also modifies excitability, partly via cellular swelling (^A2). Hyponatremia and ammonia (NH4+) also act via this mechanism. The rise in NH4+ in hepatic encephalopathy (^p. 174) causes the formation of glutamine from a-ketoglutarate and glutamate in glial cells; the accumulation of glutamine causes them to swell. At first this swelling is counteracted by the removal of osmolytes, seen in magnetic resonance imaging as a decrease in the cerebral concentration of inositol. When this compensatory mechanism is exhausted, consciousness is lost.

The excitability of neurons is also affected by epilepsy (^ p. 338), hyperosmolarity (hy-pernatremia, hyperglycemia; ^A3) as well as by disorders of electrolyte (Ca2+, Mg2+, HPO42-) and acid-base metabolism (^ A4). Uremia (in renal failure) and diabetes mellitus act partly via changes in extracellular osmolarity and 342 electrolyte composition. Numerous substances can impair the excitability of the

ARAS A5), such as NMDA receptor antagonists, alcohol, narcotics, hypnotics, psychoactive drugs, anticonvulsives, Na+/K+-ATPase inhibitors (cardiac glycosides), heavy metals. Extreme excess or lack of hormones (e.g T3, T4, parathyroid hormone, adrenocorticoid hormones, pheochromocytoma) as well as massive neuronal excitation, for example, caused by pain or psychogenic disease (schizophrenia), can lead to loss of consciousness (^ A6). Lastly, neuronal excitability can also be so severely impaired by hyperthyroidism, hypothermia, inflammatory (e.g., meningitis) or mechanical damage, and neurodegenerative disease that it could lead to loss of consciousness (^ A7).

Loss of consciousness can be divided into several stages (^ A): in a state of drowsiness the patient can still be roused and will respond; in a stupor (profound sleep) patients can be awakened by vigorous stimuli; when in a coma this is no longer possible. In so-called "coma dépassé" vital functions will also have ceased (e.g., respiratory arrest).

The split brain represents a special abnormality of consciousness (^ B). Uniform consciousness presupposes communication between the two cerebral hemispheres. This takes place along large commissural fiber bundles through the corpus callosum and the anterior commissure. In treating uncontrollable epilepsy the commissural fibers have been transected in some patients, stopping this communication between the two hemispheres. The two hemispheres now produce two distinct kinds of consciousness: if an object (e.g., a saucepan) is placed into the right hand or placed in the right visual field, the patient can correctly name the object. But if the object is placed into the left hand or projected into the left visual field, the patient is able to recognize the object and, for example, find the appropriate saucepan cover with the left hand, but will not be able to name it.

A. Unconsciousness

A. Unconsciousness

'coma dépassé'

T3 C ra

Aphasias

Speech and language comprehension are tasks that engage a large part of the cerebral cortex. For this reason, lesions in various parts of the cortex may lead to an impairment of speech and of language comprehension.

Simply put, spoken language is first perceived in the primary auditory cortex A; marked in violet) and then in the sensory speech center (Wernicke's area, marked in light blue). Written words are transmitted via the primary (gray-blue) and secondary (dark blue) visual cortex to area 39, where acoustic, optical, and sensory perceptions are integrated. When writing, the premotor cortex is activated via the arcuate fasciculus of the pre-motor cortex that, in turn, activates the motor cortex via the basal ganglia and the thalamus. In right-handed people the structures involved are predominantly localized in the left hemisphere, and speech disorders (aphasia) are almost always the result of lesions in the left hemisphere.

Each of the above-mentioned structures can cease functioning, for example, due to traumatic or ischemic damage. Depending on which cerebral area is affected, abnormalities characteristic for each will develop.

Broca's aphasia is caused by a lesion of the motor speech center in area 44 and the neighboring areas 9,46, and 47. Spontaneous speech (verbal output) is grammatically incorrect and the patient typically communicates by using single words and is incapable of repeating someone else's words (impaired repitition ability). Language comphrehension is not, or less markedly, impaired. As a rule patients cannot write normally. However, if the lesion is limited to area 44, the ability to write is preserved (a rare disorder, called aphemia).

Wernicke's aphasia results from a lesion in the sensory speech region, i.e., in the posterior portion of the temporal gyrus of the auditory association cortex (area 22) and/or the supra-marginal gyrus (area 40). Language comprehension is impaired in these patients. At the same time they also lose the ability to repeat words spoken by somebody else. Spontaneous speech is fluent; sometimes patients speak all the time (logorrhea). However, in doing so they may make occasional phonetic ("spill" instead of "spin") or semantic errors ("mother" instead of "woman" [paraphasia]) or create new words (neologisms).

In conductive aphasia the connection between sensory and motor speech center (arcuate fasciculus) is interrupted. Speech is fluent (although sometimes paraphasic) and comprehension is good. However, their repetition ability is greatly impaired. They are also unable to read aloud, even though they understand the text they read.

In global aphasia (damage to both the sensory and the motor centers, e.g., by occlusion of the medial cerebral artery) both spontaneous speech and comprehension are impaired.

Anomic aphasia is the result of a lesion in the temporal lobe in the region of the medial and inferior gyri. Patients' speech is largely normal but it is difficult for them to find the right word for certain objects. In achromatic aphasia (lesion at the left inferior temporal lobe close to temporal-occipital border) the person cannot name a color (even though it is correctly recognized and objects can normally be sorted by color).

Transcortical motor aphasia is caused by a lesion in the anterior inferior frontal lobe near the Broca speech center. Spontaneous speech is markedly impaired, while repetition and comprehension are normal.

Transcortical sensory aphasia occurs after a lesion in the parietal-temporal association cortex near the Wernicke speech center or area 39. The patient can speak fluently and repetition is normal. However, there is a problem understanding words and finding the right word; reading and writing are impossible.

Subcortical aphasia is due to lesions in the region ofthe basal ganglia (especially the caudate nucleus) and the thalamus. There are transient disorders of comprehension and finding of words.

Word which is heard

Word which is read

Primary auditory cortex Secondary auditory cortex (Wernicke's area)

Primary visual cortex

Secondary visual cortex

Area 39

Anterior superior frontal lobe

Premotor cortex (Broca's area)

Basal ganglia, cerebellum

Thalamus

Motor cortex

Area 39

Anterior superior frontal lobe

Premotor cortex (Broca's area)

Thalamus

Motor cortex

Type

Spontaneous speech

Repetition of words

Language comprehension

Finding words

Broca's aphasia

abnormal

abnormal

normal

impaired

Wernicke's aphasia

fluent (at times logorrhea, paraphasia, neologisms)

abnormal

impaired

impaired

Conduction aphasia

fluent, but paraphasic

markedly impaired

normal

abnormal, paraphasic

Global aphasia

abnormal

abnormal

abnormal

abnormal

Anomic aphasia

fluent

normal, but anomic

normal

impaired

Achromatic aphasia

fluent

normal, but anomic

normal

impaired

Motor transcortical aphasia

abnormal

normal

normal

abnormal

Sensory transcortical aphasia

fluent

fluent

abnormal

abnormal

Subcortical aphasia

fluent

normal

abnormal (transient)

abnormal (transient)

T3 C ra

Disorders of Memory

Two forms of memory are distinguished: Declarative, explicit memory (semantic or episodic) stores memory that can only be recalled consciously (^ A). It is needed, for example, in order to be able to recognize certain things (apples, animals, faces). Procedural, implicit memory (^ A3) does not require conscious activation for storage and recall. It is required, e.g. for learning to play the piano.

To form declarative memory (^ A1) the information first of all reaches the corresponding association cortex (e.g., the secondary visual cortex) via the particular primary sensory cortical area (e.g., the primary visual cortex). From here, via the entorhinal cortex (area 28), the information reaches the hippocampus, which is essential for long-term storage of declarative memory. With mediation from structures in the diencephalon, basal forebrain, and prefrontal cortex the item is again stored in the asssociation cortex. In this way the information is first taken up, via the sensory memory, by the short-term memory, which can hold on to the content for only a few seconds to minutes. The information can be transferred to the long-term memory, for example, through being rehearsed (^ A2). Such rehearsal is not an essential precondition for the formation of long-term memory, however.

It is particularly the transfer into long-term memory that is impaired in lesions of the above-named structures in neurodegenerative diseases (e.g., Alzheimer's disease; ^ p. 348), trauma, ischemia, alcohol, carbon monoxide, and inflammation. In addition, memory formation can be temporarily stopped by electric shock. The most important transmitter in the hippocampus is glutamate (NMDA receptors). Memory formation is promoted by norepinephrine and acetylcholine (nicotinergic receptors).

Lesions in the hippocampus or its connections result in anterograde amnesia (^A2). The affected patients will from that moment on no longer be able to form any new declarative memory. They will remember events prior to the lesion but none subsequent to it.

Retrograde amnesia (^ A2), i.e., the loss of already stored information, occurs in disorders in the relevant associative cortical fields. De pending on the extent and localization of the disorder, the loss can be reversible or irreversible. In the former case the patient will lose items of memory, but they can be retrieved. In irreversible loss the particular items are permanently lost.

Transitory bilateral functional disturbance of the hippocampus can cause anterograde and retrograde (days to years) amnesia (transient global amnesia). In Korsakoff's syndrome (frequent in chronic alcoholics) both antero-grade and retrograde amnesia can occur. Patients thus affected often try to cover up gaps in memory by means ofconfabulations.

The procedural (implicit) memory (^ A3) is not impaired in lesions of the hippocampus. It allows imprinting, learning of skills, sensitization, habituation, and conditioning. Depending on the task, cerebellum, basal ganglia, amygdala and cortical areas are involved. Both the cerebellum and basal ganglia play an important role when learning skills. Relevant afferent impulses reach the cerebellum via olivary and pontine nuclei. The storage capacity of the cerebellum can be lost by, for example, toxic damage, degenerative diseases, and trauma. Dopaminergic projections of the substantia nigra also play a part in the formation of procedural memory.

The amygdala is important in conditioning anxiety reactions. It receives its information from the cortex and thalamus and influences motor and autonomic functions (e.g., muscle tone, palpitations [awareness of tachycardias], goose-pimples) via the reticular formation and hypothalamus. Removal of the amygdala (e.g., by trauma or opiates) cancels conditioned anxiety reactions. Bilateral removal of the amygdala with portions of the hippocampus and temporal lobe results in amnesia and dis-inhibited behavior (Kluver-Bucy syndrome).

Prefrontal cortex

Basal í Diencephalon i Ascocte prosencephalon--—'

Prefrontal cortex

Glutamate (NMDA), acetylcholine, nicotine, norepinephrine

Basal í Diencephalon i Ascocte prosencephalon--—'

Trauma,

Degeneration,

tumors,

alcohol, CO,

inflammation,

electric shock,

ischemia

epilepsy

Glutamate (NMDA), acetylcholine, nicotine, norepinephrine

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