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Letters   |    
Transience of Dysexecutive Syndrome But Permanence of Motor Deficits in the Course of Recurrent Subfrontal Meningioma
Esat Fahri Aydin, M.D.; Erol Ozan, M.D.
The Journal of Neuropsychiatry and Clinical Neurosciences 2013;25:E19-E19. doi:10.1176/appi.neuropsych.12060141
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Dept. of Psychiatry Atatürk University School of Medicine Turkey

Correspondence: Türkiye e2628@yahoo.com; Türkiye erolozan@gmail.com

Copyright © 2013 American Psychiatric Association

To the Editor: The frontal-subcortical circuits: dorsolateral prefrontal, anterior cingulate, and orbitofrontal circuits constitute the framework that mediates the executive control of cognition, emotion, and behavior by connecting non-motor areas of frontal cortex to basal ganglia and thalamus. The dorsolateral prefrontal circuit mediates the organization of information to facilitate a response (i.e., the executive functions), and the anterior cingulate circuit is required for motivated behavior. The orbitofrontal circuit has lateral and medial divisions. The medial portion integrates visceral–amygdalar functions with the internal state of the organism, whereas the lateral portion is involved with integration of limbic and emotional information into contextually-appropriate behaviors. Impaired executive functions, apathy and disinhibition/impulsivity, are hallmarks of non-motor circuit dysfunction.1,2 The case below inspired us to highlight recoverability of non-motor circuit functions thanks to fascinating brain plasticity.

A 66-year-old woman with urinary and fecal incontinence, headache, and worsening of pre-existing left hemiparesis consulted preoperatively for progressive behavioral changes ongoing for 10 months. While she was a person displaying contextually appropriate behaviors and participating in daily activities; she gradually became detached, devoid of self-generated behavior, also was irritable and behaved inappropriately. She was even indifferent to her urinary and fecal incontinence. On occasion, she exhibited disinhibition and impulsivity,3 characterized by uncontrollable swearing and throwing of objects. Furthermore, seemingly unable to suppress the urge, she consumed food whenever presented, despite the fact that she had just eaten a full meal (namely, utilization behavior).3 Motor examination revealed left-sided weakness, more prominent in the arm (MRC: 2/5). Brain imaging demonstrated a midline subfrontal meningioma of 30×10×25-mm size, compressing predominantly the right lobe. The day after consultation, the mass was excised totally, and pathology demonstrated a transitional meningioma. Three months after surgery, the dysexecutive syndrome3 fully recovered; however, left hemiparesis persisted. Interestingly, at age 38, she had undergone a decompression surgery for a subfrontal meningioma, as well. Reportedly, she displayed ongoing antisocial behavior3 characterized by emotional disengagement, reduced goal-directed behavior, and unpredictable aggressive outbursts for 1 year. Aforementioned dysexecutive symptoms3 preceded a left hemiparesis, which occurred 2 months before total excision. In the follow-up, although dysexecutive syndrome3 had recovered entirely, left hemiparesis persisted, with incomplete recovery, until further deterioration due to recurrence.

Several aspects of this case are worth mentioning: Her suffering from a combination of orbitofrontal and anterior cingulate symptoms confirm the suggestion that circuits originating from these cortical areas are not segregated, but interconnected.3 Another point is plastic peri-lesional compensatory reorganization, providing optimal functioning, which is more efficient in slow-growing tumors.4 However, brain plasticity involves more sophisticated functions, such as cognitive, emotional, and behavioral processes, since executive control of these skills is mediated by parallel networks.4 On the other hand, sensorimotor areas are less prone to plasticity, probably due to their older time of maturation, as well as mainly unimodal and serial organization.4 The lack of parallel alternative pathways explains the difficulty or even impossibility of functional restoration after any damage.4 Needed operational criteria and quantitative scales will help in early detection of seemingly recoverable dysexecutive behaviors.

Tekin  S;  Cummings  JL:  Frontal-subcortical neuronal circuits and clinical neuropsychiatry: an update.  J Psychosom Res 2002; 53:647–654
[CrossRef] | [PubMed]
 
Bonelli  RM;  Cummings  JL:  Frontal-subcortical circuitry and behavior.  Dialogues Clin Neurosci 2007; 9:141–151
[PubMed]
 
Krause  M;  Mahant  N;  Kotschet  K  et al:  Dysexecutive behaviour following deep brain lesions: a different type of disconnection syndrome? Cortex 2012; 48:97–119
[CrossRef] | [PubMed]
 
Duffau  H:  The “frontal syndrome” revisited: lessons from electrostimulation mapping studies.  Cortex 2012; 48:120–131
[CrossRef] | [PubMed]
 
References Container
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References

Tekin  S;  Cummings  JL:  Frontal-subcortical neuronal circuits and clinical neuropsychiatry: an update.  J Psychosom Res 2002; 53:647–654
[CrossRef] | [PubMed]
 
Bonelli  RM;  Cummings  JL:  Frontal-subcortical circuitry and behavior.  Dialogues Clin Neurosci 2007; 9:141–151
[PubMed]
 
Krause  M;  Mahant  N;  Kotschet  K  et al:  Dysexecutive behaviour following deep brain lesions: a different type of disconnection syndrome? Cortex 2012; 48:97–119
[CrossRef] | [PubMed]
 
Duffau  H:  The “frontal syndrome” revisited: lessons from electrostimulation mapping studies.  Cortex 2012; 48:120–131
[CrossRef] | [PubMed]
 
References Container
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