Abulia
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Symptoms and signs
The clinical condition denoted abulia was first described in 1838; however, since that time, a number of different, some contradictory, definitions have emerged.[6] Abulia has been described as a loss of drive, expression, behavior and speech output, with slowing and prolonged speech latency, and reduction of spontaneous thought content and initiative,[7] being considered more recently as 'a reduction in action emotion and cognition'.[6] The clinical features most commonly associated with abulia are:[6]
- Difficulty in initiating and sustaining purposeful movements
- Lack of spontaneous movement
- Reduced spontaneous speech
- Increased response-time to queries
- Passivity
- Reduced emotional responsiveness and spontaneity
- Reduced social interactions
- Reduced interest in usual pastimes
Especially in patients with progressive dementia, it may affect feeding.[8] Patients may continue to chew or hold food in their mouths for hours without swallowing it.[8] The behavior may be most evident after these patients have eaten part of their meals and no longer have strong appetites.[citation needed]
Differentiation from other disorders
Both
A 2002 survey of two movement disorder experts, two neuropsychiatrists, and two rehabilitation experts, did not seem to shed any light on the matter of differentiating abulia from other DDMs. The experts used the terms "
The study of motivation has been mostly about how stimuli come to acquire significance for animals. Only recently has the study of motivational processes been extended to integrate biological drives and emotional states in the explanation of purposeful behavior in human beings. Considering the number of disorders attributed to a lack of will and motivation, it is essential that abulia and apathy be defined more precisely to avoid confusion.[6]
Causes
Many different causes of abulia have been suggested. While there is some debate about the validity of abulia as a separate disease, experts mostly agree that abulia is the result of frontal lesions and not with cerebellar or brainstem lesions.[6] As a result of more and more evidence showing that the mesolimbic and the mesocortical dopamine system are key to motivation and responsiveness to reward, abulia may be a dopamine-related dysfunction.[7] Abulia may also result from a variety of brain injuries which cause personality change, such as dementing illnesses, trauma, or intracerebral hemorrhage (stroke), especially stroke causing diffuse injury to the right hemisphere.[9][10]
Damage to the basal ganglia
Injuries to the frontal lobe and/or the basal ganglia can interfere with an individual's ability to initiate speech, movement, and social interaction. Studies have shown that 5-67% of all patients with traumatic brain injuries and 13% of patients with lesions on their basal ganglia experience some form of diminished motivation.[2]
It may complicate rehabilitation when a stroke patient is uninterested in performing tasks like walking despite being capable of doing so. It should be differentiated from apraxia, when a brain injured patient has impairment in comprehending the movements necessary to perform a motor task despite not having any paralysis that prevents performing the task; that condition can also result in lack of initiation of activity.
Damage to the capsular genu
A case study involving two patients with
Damage to anterior cingulate circuit
The anterior cingulate circuit consists of the
Acute caudate vascular lesions
It s well documented that the caudate nucleus is involved in degenerative diseases of the central nervous system such as Huntington disease. In a case study of 32 acute caudate stroke patients, 48% were found to be experiencing abulia. Most of the cases where abulia was present were when the patients had a left caudate infarct that extended into the putamen as seen through a CT or MRI scan.[12]
Diagnosis
Diagnosis for abulia can be quite difficult because it falls between two other disorders of diminished motivation, and one could easily see an extreme case of abulia as akinetic mutism or a lesser case of abulia as apathy and therefore, not treat the patient appropriately. If it were to be confused with apathy, it might lead to attempts to involve the patient with physical rehabilitation or other interventions where a source of strong motivation would be necessary to succeed but would still be absent. The best way to diagnose abulia is through clinical observation of the patient as well as questioning of close relatives and loved ones to give the doctor a frame of reference with which they can compare the patient's new behavior to see if there is in fact a case of diminished motivation.[7] In recent years, imaging studies using a CT or MRI scan have been shown to be quite helpful in localizing brain lesions which have been shown to be one of the main causes of abulia.[6]
Conditions where abulia may be present
- Normal pressure hydrocephalus
- Major depressive disorder
- Persistent depressive disorder
- Attention deficit hyperactivity disorder
- Schizophrenia
- Frontotemporal dementia
- Parkinson's disease
- Huntington's disease
- Pick's disease
- Progressive supranuclear palsy
- Traumatic brain injury
- Stroke
Alzheimer's disease
A lack of motivation has been reported in 25–50% of patients with Alzheimer's disease. While depression is also common in patients with this disease, abulia is not a mere symptom of depressions because more than half of the patients with Alzheimer's disease with abulia do not have depression. Several studies have shown that abulia is most prevalent in cases of severe dementia which may result from reduced metabolic activity in the prefrontal regions of the brain. Patients with Alzheimer's disease and abulia are significantly older than patients with Alzheimer's who do not lack motivation. Going along with that, the prevalence of abulia increased from 14% in patients with a mild case Alzheimer's disease to 61% in patients with a severe case of Alzheimer's disease, which most likely developed over time as the patient got older.[8]
Treatment
Most current treatments for abulia are pharmacological, including the use of antidepressants. However, antidepressant treatment is not always successful and this has opened the door to alternative methods of treatment. The first step to successful treatment of abulia, or any other DDM, is a preliminary evaluation of the patient's general medical condition and fixing the problems that can be fixed easily. This may mean controlling seizures or headaches, arranging physical or cognitive rehabilitation for cognitive and sensorimotor loss, or ensuring optimal hearing, vision, and speech. These elementary steps also increase motivation because improved physical status may enhance functional capacity, drive, and energy and thereby increase the patient's expectation that initiative and effort will be successful.[2]
There are 5 steps to pharmacological treatment:[2]
- Optimize medical status.
- Diagnose and treat other conditions more specifically associated with diminished motivation (e.g., apathetic hyperthyroidism, Parkinson's disease).
- Eliminate or reduce doses of SSRIs, dopamine antagonists).
- Treat depression efficaciously when both DDM and depression are present.
- Increase motivation through use of stimulants, dopamine agonists, or other agents such as cholinesterase inhibitors.
See also
References
- ^ Bailly, A. (2000). Dictionnaire Grec Français, Éditions Hachette.
- ^ a b c d Marin, R. S., & Wilkosz, P. A. (2005). Disorders of diminished motivation Archived 2012-11-22 at the Wayback Machine. Journal of Head Trauma Rehabilitation, 20(4), 377-388.
- ^ Berrios G.E. and Gili M. (1995) Will and its disorders. A conceptual history. History of Psychiatry 6: 87-104
- ^ Berrios G.E. and Gili M. (1995) Abulia and impulsiveness revisited. Acta Psychiatrica Scandinavica 92: 161-167
- ^ Sacks, Oliver (1973). Awakenings. United States: Vintage Books. p. 7.
- ^ a b c d e f g h i j k l Vijayaraghavan, L., Krishnamoorthy, E. S., Brown, R. G., & Trimble, M. R. (2002). Abulia: A Delphi survey of British neurologists and psychiatrists. [Article]. Movement Disorders, 17(5), 1052-1057.
- ^ a b c Jahanshahi, M., & Frith, C. D. (1998). Willed action and its impairments. [Review]. Cognitive Neuropsychology, 15(6-8), 483-533.
- ^ a b c Starkstein, S. E., & Leentjens, A. F. G. (2008). The nosological position of apathy in clinical practice. [Review]. Journal of Neurology, Neurosurgery, and Psychiatry, 79(10), 1088-1092.
- ^ a b Grunsfeld, A. A., & Login, I. S. (2006). Abulia following penetrating brain injury during endoscopic sinus surgery with disruption of the anterior cingulate circuit: Case report. [Article]. Bmc Neurology, 6, 4.
- ^ Kile, S. J., Camilleri, C. C., Latchaw, R. E., & Tharp, B. R. (2006). Bithalamic lesions of butane encephalopathy. [Article]. Pediatric Neurology, 35(6), 439-441.
- ^ Pantoni, L., Basile, A. M., Romanelli, M., Piccini, C., Sarti, C., Nencini, P., et al. (2001). Abulia and cognitive impairment in two patients with capsular genu infarct. [Article]. Acta Neurologica Scandinavica, 104(3), 185-190.
- ^ Kumral, E., Evyapan, D., & Balkir, K. (1999). Acute caudate vascular lesions. [Article]. Stroke, 30(1), 100-108.
External links
- The dictionary definition of abulia at Wiktionary