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Frontal lobe disorder
Classification and external resources
ICD-10 F07
eMedicine article/1135866

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 and cerebrovascular disease. Impairment of frontal lobe functioning is also found in a range of psychiatric conditions including schizophrenia, attention deficit disorder and antisocial personality disorder. Frontal lobe impairment can be detected by recognition of typical clinical signs, use of simple screening tests, and specialist neuropsychiatric testing.

Anatomy and functions[edit | edit source]

File:Human brain lateral view description.JPG

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 concened with the planning, initiation and control of physical movement.[How to reference and link to summary or text] 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, in other words language production. The orbitofrontal cortex is concerned with response inhibition, impulse control , and social behaviour.[1]

Clinical assessment[edit | edit source]

History[edit | edit source]

Frontal lobe disorders may be recognised 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.[2]

Examination[edit | edit source]

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.[2] 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.[3]

Further investigation[edit | edit source]

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 sort 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.[4]

Individuals with frontotemporal dementia and Pick's disease will show frontal cortical atrophy on Computerised tomography or magnetic resonance imaging.[5] Frontal impairment due to head injuries, tumors or cerebrovascular disease will also be apparent on brain imaging.[6]

Dysexecutive syndrome[edit | edit source]

The Dysexecutive Syndrome consists of a number of symptoms [7] which tend to occur together (hence it being described as a syndrome). Broadly speaking, these symptoms fall into three main categories; Cognitive, Emotional & 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 the 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 [8] to suggest that the symptoms should not be labelled as a "syndrome" as such. Some of the latest imaging research [9] 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 Function 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 the 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 the Dysexecutive syndrome.

Cognitive Symptoms[edit | edit source]

Emotional Symptoms[edit | edit source]

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

Behavioural Symptoms[edit | edit source]

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 behavior, depression, aggression, inappropriate sexual behavior, 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 behavioral 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.[10].[11]

Causes of Frontal lobe dysfunction[edit | edit source]

Head trauma[edit | edit source]

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

Cerebrovascular disease[edit | edit source]

Cerebrovascular disease may cause a stroke in the frontal lobe.

Tumours[edit | edit source]

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

Degenerative diseases[edit | edit source]

Frontal lobe impairment is a feature of Alzheimer's disease, frontotemporal dementia and Pick's disease.[2]

Psychiatric disorders[edit | edit source]

There is evidence for frontal lobe impairment in schizophrenia, depression, attention deficit hyperactivity disorder (ADHD), and antisocial personality disorder or psychopathy

A large number of studies have documented abnormalities in working memory in schizophrenia, associated with disrupted functioning of the dorso-lateral prefrontal cortex. There is also evidence for disruption of neuronal connections between the temporal and frontal lobes in people with schizophrenia.[12] The characteristic dorso-lateral prefrontal cortex morphological abnormalities are said to be related to a general impaired ability to control and regulate behavior, which would correspond to deficits in several functional areas in schizophrenia.[13] A study of people with schizophrenia using MRI scanning and psychological assessment has also found that longer duration of illness was associated with lower gray matter volume in the left dorsomedial prefrontal cortex and the right middle frontal cortex, and these changes were associated with impaired working memory, attention and psychomotor speed.[14] Another MRI study of schizophrenia has found an association between orbitofrontal cortex volume reduction and a longer duration of illness, impaired executive functioning, and greater formal thought disorder.[15]

Research on children with ADHD has shown a general reduction of brain volume, but with a proportionally greater reduction in the volume of the left-sided prefrontal cortex. These findings are in keeping with the core ADHD features of inattention, hyperactivity, and impulsivity, but other brain regions have also been implicated in the causation of ADHD.[16] The prefrontal cortex is also implicated by functional magnetic resonance imaging (fMRI) studies which examine brain activation during tasks such as motor resonse inhibition; reduced prefrontal cortex activation is associated with higher ADHD behavioural scores.[17]

See also[edit | edit source]

Notes[edit | edit source]

  1. Frontal lobe syndromes. eMedicine Specialities. URL accessed on 2008-07-02.
  2. 2.0 2.1 2.2 Gelder et al. (2000) p 397-404
  3. Dubois, B, Slachevsky A, Litvan I, Pillon B (December 2000). The FAB: a Frontal Assessment Battery at bedside. Neurology 55 (11): 1621–6.
  4. Gelder et al. (2000) p 96
  5. Gelder et al. (2000) p 400
  6. Frontal lobe syndromes. eMedicine Specialities. URL accessed on 2008-07-02.
  7. Halligan P.W, Kischka U. & Marshall J.C. (2004) Handbook of Clinical Neuropsychology. Oxford University Press, 2004.
  8. 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.
  9. Gilbert, S.J. & Burgess, P.W. (2008). Executive Function. Current Biology, Vol.18, No. 3, 110 - 114.
  10. Macmillan, M. (2000). "The Damage to Gage's Psyche (Ch.6)" An Odd Kind of Fame: Stories of Phineas Gage, MIT Press.
  11. Macmillan, M. (2008). Phineas Gage – Unravelling the myth The Psychologist (British Psychological Society), 21(9): 828-831. (PDF)
  12. Ragland, JD, Yoon J, Minzenberg MJ, Carter CS (2007). Neuroimaging of cognitive disability in schizophrenia: search for a pathophysiological mechanism. International Review of Psychiatry 19 (4): 417–27.
  13. Crespo-Facorro, Benedicto, Barbadillo L; Pelayo-Teran JM; Rodriguez-Sanchez JM (2007). Neuropsychological functioning and brain structure in schizophrenia. International Review of Psychiatry 19 (4): 325–336.
  14. Premkumar P, P, Fannon D; Kuipers E; Cooke MA; Simmons A; Kumari V (2008). Association between a longer duration of illness, age and lower frontal lobe grey matter volume in schizophrenia. Behavioural Brain Research 193: 132.
  15. Nakamura, M, Nestor PG; Levitt JJ; Cohen AS; Kawashima T; Shenton ME; McCarley RW (2008). Orbitofrontal volume deficit in schizophrenia and thought disorder. Brain 131 (1): 180–95.
  16. Krain, Amy, Castellanos, Xavier (2006). Brain development and ADHD. Clinical Psychology Review 26 (4): 433–444.
  17. Rubia, Katya, Smith Anna, Brammer Michael, Toone Brian and taylor Eric (2005). Abnormal Brain Activation During Inhibition and Error Detection in Medication-Naive Adolescents With ADHD. American Journal of Psychiatry (6): 1067=-1075.

References[edit | edit source]

Gelder, M; López-Ibor J; Andreasen N (2000). New Oxford textbook of psychiatry, Oxford: Oxford University Press.

External links[edit | edit source]

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