Abstract
Although dementia is diagnosed by observing cognitive symptoms, noncognitive abnormalities are also highly prevalent. Although aggression is a common symptom, its presence is usually justifiable by a multitude of externally provoking factors. We present a case of Alzheimer’s disease with marked unwarranted violent behavior.
Introduction
Alzheimer’s dementia (AD) is one of the most compelling problems of social and public health. It usually leads to a marked decrease in the cognitive, mental, and also in the physical skills of the affected person who over time requires an increased amount of care, aid, and support. In course of time, the elderly patients with dementia manifest increasing difficulty in carrying out activities of daily living along with behavioral and psychological symptoms of dementia (BPSD) including signs of disturbed perception, thought content, mood, or behavior like hoarding, wandering, aggression, and disinhibition. 1 The BPSD tend to occur in clusters, which have been grouped into the categories of aggression, psychomotor agitation, psychosis, apathy, and depression. 2
Violent behavior is commonly seen in individuals with dementia, and although neuroleptics often alleviate these problems, 3 the mechanisms underlying aggressive behavior are still unknown in this disease. Literature suggests violent behavior to be usually in response to a psychopathology, interaction/communication difficulty, or impaired self-esteem among other causes via presumably a neurobiological dysregulation. 4 Here, we present a case with strikingly unwarranted violent behavior with no externally provoking factor or psychopathology in an individual with dementia.
Case Report
Mr A, a 78-year-old male, a case of AD was diagnosed 1 year previously and has since been managed on donepezil 10 mg/d for the same duration with slight improvement in memory. He presented with a history of exhibiting aggressive behavior for the last 1½ year, but the symptoms of undue aggression and violent behavior had become significantly worse in the past 2 months. Consequently, the patient became problematic to manage. He was highly aggressive and frequently resorted to hitting and head butting anyone at arm’s length of him regardless of whom it was without any externally provoking stimuli. He face was noticed to flush during the rage. His elder son, in an attempt to control his violent behavior replied with similar physical attacks which he regrets. The patient never reported of any delusional psychopathology or hallucinations, nor was there any hallucinatory behavior. He reported of remorse at times after the violent episode.
The general physical and systemic examination was normal. Although cooperative, Mr A displayed apathetic indifference and psychomotor retardation. He was unresponsive to verbal communication initially but later responded to questions. However, there were many inconsistencies in his story with vague content with slight latency of responses. Mood was irritable with restricted range and at times appeared dazed and childlike. No perceptual phenomena, delusions, obsessions, compulsions, or any anxiety symptom was elicited on serial mental state examinations. He was disoriented to the time and unable to do serial 7. He did not show aphasia or apraxia with intact cranial nerves. There was no weakness or muscle atrophy and gait was normal for age. Deep tendon reflexes were exaggerated; however, no Babinski sign was noted. Sensory examination was intact. His Mini-Mental State Examination score was 5, consistent with stage 3 of disease severity. 5
Laboratory workup, including hemogram, electrolytes, B12 assay, blood sugar, serum testosterone, Venereal Disease Research Laboratory (VDRL)/human immunodeficiency virus, liver/kidney function tests, chest X-ray, urine/stool examination, electrocardiography, electroencephalography, computed tomography scan head, and cerebrospinal fluid analysis yielded normal results. Examination of fundus did not show any sign of raised intracranial tension or abnormal deposits. Magnetic resonance imaging brain scan only reported generalized cortical atrophic age-related changes.
The assessment was made on the Agitated Behavior Scale, 6 and he was prescribed risperidone 1.5 mg/d. Family members were psychoeducated on various aspects of avoiding confrontation and dealing effectively with the patient during violent behavior. A week later, trihexyphenidyl 2 mg/d was added due to onset of extrapyramidal symptoms. Subsequently within 3 weeks, there was a significant improvement in his behavior with a reduction of 28 points compared with baseline on Agitated Behavior Scale.
Discussion
Violence is a common phenomenon in AD and about half of the sample of outpatients with AD is suggested to present with agitation, one third with violent behavior, and one fourth with verbal outbursts. 7 In a study of 262 patients of AD living in noninstitutional setting, 52% exhibited some aggressive behavior. 8 Of these, 91 (35%) patients were reported to be verbally aggressive and a further 46 (18%) assaulted their carers. Male gender and presence of dyspraxia were reported to increase the likelihood of violent behavior. 8
Higher behavioral dysfunction, agitation, and mood component scores have been associated with earlier age of AD onset and severity of cognitive impairment but not with age at assessment or number of apolipoprotein E epsilon4 alleles. 9 In a study of 75 patients with AD, 33% had verbal outbursts and 17% engaged in physical aggression. 10 Aggressive patients and nonaggressive patients did not differ regarding age, education, gender, level of depression, or severity of dementia. Physical aggression was associated with activity disturbance and hallucinations, and verbal aggression was associated with delusional ideation. No other clinical correlates of aggression were identified.
The exact cause of such behaviors in these patients remains unknown, although preservation of pigmented substantia nigra neurons has been suggested a risk factor for physical aggression in AD. 11 But the study did not compare violence in perspectives of provoked and unprovoked.
The dopaminergic system is involved in behavioral activation, motivated behavior, and reward processing. 12 It also plays an active role in the modulation of aggressive behaviors. In animal studies, hyperactivity in the dopamine system is associated with increases in impulsive aggression. 13
Muneoka et al reported a case of AD wherein the aggressiveness disappeared after an infarct in the anterior thalamic nucleus. 14 The authors suggested that the temporal lobe degeneration might have disturbed the frontal cortical function leading to aggression and the thalamic infarct may have reduced this disturbance, thus normalizing the frontal cortical function rather than causing impairment.
Several drugs have been implicated for treating aggression in patients with dementia including antipsychotics, cholinesterase inhibitors, anticonvulsants (eg, carbamazepine and valproate), antidepressants (eg, fluoxetine), and memantine, as well as the benzodiazepine lorazepam. 15 Neuroleptics are the first-line choice of psychotherapeutics for controlling severe aggression, especially the violent outbursts often seen in severely demented patients. But their efficacy for this problem is limited and their use is frequently complicated by side effects. 16 They are more effective for particular symptoms, such as anger, aggression, and paranoid ideas in patients with AD. However, they do not appear to improve cognition, functioning, care needs, or quality of life. 17
Aggressive behavior complicates management in a patient with AD and severely violent behavior among patients with AD has previously been described but having delusional psychopathology. 18 To our knowledge, a case as ours with an undue severe violent behavior in the absence of a delusional pathology or external provoking factor has never been reported before. Our case had no external provoking factor, strongly implicating an underlying neurobehavioral dysfunctioning leading to aggression which may be denoting an endophenotype in AD population. Hyperactivity in the dopamine system may have been responsible for these explosive impulsive behaviors as there was good response to the antipsychotic even though there was no prominent psychotic psychopathology.
Footnotes
The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
The authors received no financial support for the research, authorship, and/or publication of this article.
