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Frontal lobe disorder

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Frontal lobe disorder
SpecialtyPsychiatry Edit this on Wikidata

Frontal lobe disorder is an impairment of the frontal lobe that occurs as a result of a number of diseases as well as 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 result from a range of causes including head trauma, tumours, degenerative diseases, neurosurgery and cerebrovascular disease. Impairment of frontal lobe functioning is also found in psychiatric patients due to prescribed medication, namely antipsychotics [1][2][3][4][5] . 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
Prefrontal Cortex
The top blue line denotes the central sulcus

The frontal lobe has three main areas, known as the precentral cortex, prefrontal cortex and the orbitofrontal cortex. These three areas are represented in both the left and the right cerebral hemispheres.

The precentral cortex or primary motor cortex is concerned with the planning, initiation and control of physical movement.[citation needed] 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.[6]

Clinical assessment

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.[7]

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.[7] 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.[8]

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.[9]

Individuals with frontotemporal dementia and Pick's disease will show frontal cortical atrophy on CT scans or MRIs.[10] Frontal impairment due to head injuries, tumours or cerebrovascular disease will also be apparent on brain imaging.[11]

Dysexecutive syndrome

Dysexecutive syndrome consists of a number of symptoms[12] which tend to occur together (hence it being described as a syndrome). Broadly speaking, these symptoms fall into three main categories; cognitive, emotional and 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[13] to suggest that the symptoms should not be labelled as a "syndrome" as such. Some of the latest imaging research[14] 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.

Cognitive symptoms

Emotional symptoms

  • 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 symptoms

Phineas Gage, who suffered a severe frontal lobe injury in 1848, has been called a case of dysexecutive syndrome. But 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".

In particular, the primary sources do not report utilization behaviour, depression, aggression, inappropriate sexual behaviour, or "inappropriate humour and telling of pointless and boring stories" (in fact, his audience was said to have found his stories entertaining). The oft-quoted statement by friends—that after the accident he was "no longer Gage"—admits interpretation as any number of behavioural or personality changes, not even necessarily of organic etiology. Although he was not able to return to his work for the railroad, after his physical recovery he was socially functional and self-supporting for the remainder of his life.[15][16]

Causes of frontal lobe dysfunction

Head trauma

Closed head injuries, for example from motor vehicle accidents, can cause damage to the orbitofrontal cortex. Pre-frontal lobotomies and antipsychotics, 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

Cerebrovascular disease may cause a stroke in the frontal lobe.

Tumours

Tumours such as meningiomas may present with a frontal lobe syndrome.

Degenerative diseases

Frontal lobe impairment is a feature of Alzheimer's disease, frontotemporal dementia and Pick's disease.[7]


Psychiatric medication

It has been proved that psychiatric drugs cause damage to pre frontal cortex.

Inumerable medical studies have shown, in the past 20 years, that use of neuroleptic psychiatric drugs (or antipsychotics) is linked with structural brain changes, especially when taking high dosages for a long time. These brain changes might include actual atrophy of the higher level parts of the brain. The atrophy can be seen in MRI scans and autopsy studies. In response to industry experts who claim that this shrinkage is from the "mental illness," studies demonstrate neuroleptics lead to analogous brain changes in monkeys [17].

See also

Notes

  1. ^ Petersen, KA (2005). "The Influence of Chronic Exposure to Antipsychotic Medications on Brain size before and after Tissue Fixation: A comparison of Haloperidol and Olanzapine in Macaque Monkeys". Neuropharmacology. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  2. ^ Ballesteros, J (2000). "Tardive dyxkinesia associated with higher mortality in paychiatric patients: results of a meta-analysis of seven independent studies". Clin Psychopharmacology. 20 (2): 188–194. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  3. ^ Christensen, E (1970). "Neuropathological investigations of 28 brains from patients with dyskinesia". Acta Psychiatrica Scandinavica. 46: 14–23.
  4. ^ Wade, James (1987). "Tardive Dyskinesia and Cognitive Impairment". Biological Psychiatry. 22: 393–395.
  5. ^ Whitaker, Robert. Mad in America.
  6. ^ "Frontal lobe syndromes". eMedicine Specialities. January 11, 2008. Retrieved 2008-07-02.
  7. ^ a b c Gelder et al. (2000) p. 397-404
  8. ^ Dubois, B (2000). "The FAB: a Frontal Assessment Battery at bedside". Neurology. 55 (11): 1621–6. PMID 11113214. {{cite journal}}: |access-date= requires |url= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  9. ^ Gelder et al. (2000) p. 96
  10. ^ Gelder et al. (2000) p. 400
  11. ^ "Frontal lobe syndromes". eMedicine Specialities. January 11, 2008. Retrieved 2008-07-02.
  12. ^ Halligan P.W, Kischka U. & Marshall J.C. (2004) Handbook of Clinical Neuropsychology. Oxford University Press, 2004.
  13. ^ 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.
  14. ^ Gilbert, S.J. & Burgess, P.W. (2008). Executive Function. Current Biology, Vol.18, No. 3, 110–114.
  15. ^ Macmillan, M. (2000). "The Damage to Gage's Psyche (Ch.6)". An Odd Kind of Fame: Stories of Phineas Gage. MIT Press. ISBN 0-262-13363-6.
  16. ^ Macmillan, M. (2008). "Phineas Gage – Unravelling the myth The Psychologist ([[British Psychological Society]]), 21(9): 828-831" (PDF). {{cite web}}: URL–wikilink conflict (help)CS1 maint: numeric names: authors list (link)
  17. ^ Dorph-Petersen, KA (9). "The influence of chronic exposure to Antipsychotic Medications on Brain Size before and after Tissue Fixation: A comparison of Haloperidol and Olanzapine in Macaque Monkeys". Neuropsychopharmacology. {{cite journal}}: Check date values in: |date= and |year= / |date= mismatch (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)

References

  • Gelder, M (2000). New Oxford textbook of psychiatry. Oxford: Oxford University Press. ISBN 0-19-852810-8. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  • Whitaker, Robert. Mad in America.
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