Frontal lobe disorder

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Frontal lobe disorder
Classification and external resources
Specialty Lua error in Module:Wikidata at line 446: attempt to index field 'wikibase' (a nil value).
ICD-10 F07
eMedicine article/1135866
Patient UK Frontal lobe disorder
[[[d:Lua error in Module:Wikidata at line 863: attempt to index field 'wikibase' (a nil value).|edit on Wikidata]]]

Frontal lobe disorder is an impairment of the frontal lobe that occurs due to disease or head trauma. The frontal lobe of the brain plays a key role in higher mental functions such as motivation, planning, social behaviour, and speech production. A frontal lobe syndrome can be caused by a range of conditions including head trauma, tumours, degenerative diseases, neurosurgery and cerebrovascular disease. Frontal lobe impairment can be detected by recognition of typical clinical signs, use of simple screening tests, and specialist neurological testing.

Anatomy and functions

Prefrontal Cortex
The top blue line denotes the central sulcus

The frontal lobe contains the precentral gyrus and prefrontal cortex and, by some conventions, the orbitofrontal cortex. These three areas are represented in both the left and the right cerebral hemispheres.

The precentral gyrus or primary motor cortex is concerned with the planning, initiation and control of fine motor movements dorsolateral to each hemisphere.[1] The dorsolateral part of the frontal lobe is concerned with planning, strategy formation, and other executive functions. The prefrontal cortex in the left hemisphere is involved with verbal memory while the prefrontal cortex in the right hemisphere is involved in spatial memory. The left frontal operculum region of the prefrontal cortex, or Broca's area, is responsible for expressive language, i.e. language production. The orbitofrontal cortex is concerned with response inhibition, impulse control, and social behaviour.[2]

Pathology

Various pathologies can occur affecting the frontal lobe. Some are as follows:

  • Foster Kennedy syndrome - It is caused due to tumor of frontal lobe and gives rise to ipsilateral optic atrophy and contralateral papilledema.
  • Frontal disinhibition syndrome, Rett syndrome and attention deficit hyperactivity disorder[3]
    • It is produced from frontal lobe damage often due to tumors.
    • Socially disinhibited and shows severe impairment of judgment, insight and foresight.
    • Antisocial behaviour is a characteristic feature of frontal disinhibition syndrome.
  • Frontal abulic syndrome[4][5]
    • Loss of initiative, creativity and curiosity
    • Pervasive emotional apathy and blandness
    • Akinetic mutism

Signs and symptoms

Dysexecutive syndrome[why?] consists of a number of symptoms[6] which tend to occur together (hence it being described as a syndrome). Broadly speaking, these symptoms fall into three main categories; cognitive, emotional or behavioural. Although many of these symptoms regularly co-occur, it is common to encounter patients who have several, but not all of these symptoms. This is one reason why some researchers are beginning to argue that dysexecutive syndrome is not the best term to describe these various symptoms (see criticisms below). The fact that many of the dysexecutive syndrome symptoms can occur alone has led some researchers[7] to suggest that the symptoms should not be labelled as a "syndrome" as such. Some of the latest imaging research[8] on frontal cortex areas suggests that executive functions may be more discrete than was previously thought. The argument is that rather than damage to the frontal cortex areas causing dysexecutive functions in general, that damage to multiple frontal cortex areas that are close together (but responsible for different cognitive functions) can cause the various symptoms of dysexecutive syndrome.

The counterargument is that there is a central executive corresponding to areas within the frontal lobes which is responsible for much of the executive system and executive function in general, and that damage to this area causes dysexecutive syndrome.

Urinary incontinence can occur in lesion of paracentral lobule area of frontal lobe.

Cognitive

Emotional

  • Difficulty in inhibiting emotions, anger, excitement, sadness etc.
  • Depression, possibly due to above.
  • Occasionally, difficulty in understanding others' points of view, leading to anger and frustration.

Behavioural

Frontal release signs

Causes

Head trauma

Closed head injuries, for example from motor vehicle accidents, can cause damage to the orbitofrontal cortex. Pre-frontal lobotomies and antipsychotics[citation needed], severing connections between the pre-frontal cortex and the rest of the brain, are effectively a form of iatrogenic trauma resulting in a frontal lobe syndrome.

Cerebrovascular disease may cause a stroke in the frontal lobe. Tumours such as meningiomas may present with a frontal lobe syndrome. Frontal lobe impairment is also a feature of Alzheimer's disease, frontotemporal dementia and Pick's disease.[9]

Diagnosis

Clinical history

Frontal lobe disorders may be recognized through a sudden and dramatic change in a person's personality, for example with loss of social awareness, disinhibition, emotional instability, aggression, irritability or impulsiveness (for example sexually inappropriate behaviour or spending money impulsively). Alternatively the disorder may become apparent because of mood changes such as depression, anxiety or apathy.[9]

Examination

On mental state examination a person with frontal lobe damage may show reduced speech, with reduced verbal fluency and impaired expressive language. The person might have flattened or blunted affect. Typically the person is lacking in insight and judgment, but does not have marked cognitive abnormalities or memory impairment (as measured for example by the mini-mental state examination). With more severe impairment there may be echolalia or mutism. Neurological examination may show primitive reflexes (also known as frontal release signs) such as the grasp reflex or the rooting reflex. These are reflexes normally found in babies, but normally suppressed and absent in adults. Akinesia (lack of spontaneous movement) and urinary incontinence will be present in more severe and advanced cases.[9] The frontal assessment battery (FAB), which includes simple tests of sequencing, behavioural inhibition, planning and frontal release signs, can be used as a screening test to elicit typical neurological and cognitive features.[10]

Further investigation

A range of neuropsychological tests are available for clarifying the nature and extent of frontal lobe dysfunction. For example, concept formation and ability to shift mental sets can be measured with the Wisconsin Card Sorting Test, planning can be assessed with the Mazes subtest of the WISC, switching between plans is assessed with the Trail-making test, and screening out distracting stimuli is assessed with the Stroop test.[11]

Individuals with frontotemporal dementia and Pick's disease will show frontal cortical atrophy on CT scans or MRIs.[12] Frontal impairment due to head injuries, tumours or cerebrovascular disease will also be apparent on brain imaging.[2]

History

Phineas Gage, who suffered a severe frontal lobe injury in 1848, has been called a case of dysexecutive syndrome. It must be noted however that Gage's psychological changes are typically grossly exaggerated: of the symptoms listed above, the only ones Gage can even arguably be said to have exhibited (based on primary sources) are "anger and frustration", slight memory impairment, and "difficulty in planning".[13][14]

See also

References

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  6. Halligan P.W, Kischka U. & Marshall J.C. (2004) Handbook of Clinical Neuropsychology. Oxford University Press, 2004.
  7. Stuss, D.T. & Alexander, M.P. (2007) Is there a Dysexecutive Syndrome? Philosophical transactions of the Royal Society of London. Series B, Biological Sciences, 362 (1481), 901-15.
  8. Gilbert, S.J. & Burgess, P.W. (2008). Executive Function. Current Biology, Vol.18, No. 3, 110–114.
  9. 9.0 9.1 9.2 Gelder et al. (2000) p. 397-404
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  11. Gelder et al. (2000) p. 96
  12. Gelder et al. (2000) p. 400
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References

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External links