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Disturbances of higher cerebral function 

Disturbances of higher cerebral function

Chapter:
Disturbances of higher cerebral function
Author(s):

Peter J. Nestor

and John R. Hodges

DOI:
10.1093/med/9780199204854.003.2441_update_001

Update:

Chapter reviewed; minor changes made and further reading added.

Updated on 28 Nov 2012. The previous version of this content can be found here.
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date: 25 March 2017

Clinico-pathological and imaging studies indicate strong associations between particular disorders of cognition and focal disease in the brain, but not all focal lesions induce specific loss of higher functions. Neuropsychological research has deepened our understanding by suggesting organizational frameworks for human cognitive faculties.

Neurological basis for cognition

The neocortex around the primary sensory and motor cortices is made up of unimodal association areas, which link to heteromodal association areas, with the linkage of topographical region to specific functional attribute becoming progressively less tightly defined. Other areas of the brain that interact with these association areas in a critical way for cognition include (1) limbic system—particularly in the domains of memory and emotion; (2) basal forebrain nuclei—important to the successful encoding of memory; (3) basal ganglia—relating to attention and speed of cognitive processing; (4) brainstem reticular formation—determining the level of arousal.

Clinical testing of cognition

Regardless of the suspected disorder, the clinician should always proceed in the following way: (1) ensure adequate attention to undergo further testing—if the patient has a profound attention deficit, then their cognition cannot be properly assessed; (2) assess language comprehension—almost all tests are going to be presented with verbal instruction; (3) leave tests of executive function and praxis to the end of the examination—they often require adequate levels of function in all other cognitive domains; and (4) always ask, ‘can this apparent disorder be explained in terms of a more elemental deficit?’

Particular tests of cognitive function can aid clinical diagnosis of cerebral disease and monitor treatment. It may also be possible to define the specific needs and deficiencies for which supportive aids may assist the patient.

Specific cognitive domains

Disorders of the higher functions of the brain can be described in terms of the following specific domains:

Attention—the ability to attend to a specific sensory stimulus and to maintain attention is an obligatory first step to any further cognitive processing. Breakdown in attentional processing is the central deficit in delirium or acute confusional states.

Language and related disorders—numerous terms are used to describe aphasic syndromes, but the best approach is to consider language fluency and paraphasias in spontaneous conversation, comprehension, naming, and repetition. Particular types of language and related disorders may be associated with particular anatomical lesions.

Visuospatial and perceptual disorders—a dorsal occipitoparietal pathway is concerned with spatial information and preparation for reaching (‘where?’ and ‘how?’); a ventral occipitotemporal pathway is concerned with identifying visual stimuli (‘what?’). Striking neuropsychological syndromes are seen following selective damage to one pathway.

Memory—(1) Implicit memory—unconscious memory systems, such as that responsible for conditioning as well as memory for motor tasks. (2) Explicit memory—the consciously appreciated memory, which is the category most relevant to clinical disease; divided into (a) episodic memory, referring to autobiographical recollection of personal events; typically impaired in Alzheimer’s disease and lesions of the limbic system; and (b) semantic memory, referring to factual knowledge and the store of objects and meanings; lesions of the temporal lobes cause loss of this memory, with a severe incapacity to name objects and recall the meaning of words.

Apraxia—a loss of ability to carry out skilled motor tasks that cannot be explained in terms of an elementary disorder of motor control (weakness or ataxia), primary sensory disturbance, or a global impairment of cognition. Usually the result of damage to the left (dominant) hemisphere, particularly the superior parietal lobule and the premotor area of the frontal lobe.

Personality and behavioural change—alterations in complex behaviour, personality and social comportment cannot be simply defined, but are broadly associated with frontal or anterior temporal lobe pathology.

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