Galantamine-Memantine Combination for Cognitive Impairments Due to Electroconvulsive Therapy, Traumatic Brain Injury, and Neurologic and Psychiatric Disorders

Author(s):  
Maju Mathew Koola
2020 ◽  
Vol 35 (1) ◽  
pp. 1-13 ◽  
Author(s):  
Nancy Greer ◽  
Nina A. Sayer ◽  
Michele Spoont ◽  
Brent C. Taylor ◽  
Princess E. Ackland ◽  
...  

2008 ◽  
Vol 23 (3) ◽  
pp. 149-157 ◽  
Author(s):  
Sabrina Breed ◽  
Amanda Sacks ◽  
Teresa A. Ashman ◽  
Wayne A. Gordon ◽  
Karen Dahlman ◽  
...  

Author(s):  
Vani Rao

Traumatic brain injury (TBI) is a significant cause of disability in the United States, with an incidence of about 1.5 million cases per year (National Institutes of Health Consensus Development Panel, 1999). It is associated with both neurologic and psychiatric consequences. Although the neurologic problems usually stabilize with time, the psychiatric disorders often continue to remit and relapse. Factors associated with the development of psychiatric disorders include older age, arteriosclerosis, and chronic alcoholism, all of which interfere with the reparative process within the central nervous system. Other contributors to psychiatric disability include a pre-TBI history of psychiatric illness, illicit drug abuse, and lack of social support. Because post-TBI psychiatric disturbances interfere with rehabilitation and cause emotional and financial burden for patients and caregivers, early diagnosis and treatment are important. Post-TBI psychiatric disturbances are best classified according to their clinical presentation. These disturbances are discussed below and their pharmacologic and nonpharmacologic treatment strategies are recommended. The mood disturbances most commonly associated with TBI are major depression, mania, anxiety, and apathy. Major depression is seen in about 25% of people with TBI. Symptoms of major depression include persistent sadness; guilt; feelings of worthlessness; hopelessness; suicidal thoughts; anhedonia; and changes in patterns of sleep, appetite, and energy. Sometimes these symptoms may be associated with psychotic features such as delusions and hallucinations. It is important to remember that changes in sleep, appetite, or energy are not specific to the syndrome of major depression and may be due to the brain injury itself, or to the noise, stimulation, or deconditioning associated with hospitalization. If due to the latter conditions, gradual improvement occurs with time in most patients. Sadness in excess of the severity of injury and poor participation in rehabilitation are strong indicators of the presence of major depression. The presence of poor social functioning pre-TBI and left dorsolateral frontal and/or left basal ganglia lesion have been associated with an increased probability of developing major depression following brain injury ( Jorge et al., 1993a; Jorge et al., 2004). Major depression should be differentiated from demoralization, primary apathy syndrome, and pathologic crying.


2017 ◽  
Vol 88 (Suppl 1) ◽  
pp. A82.2-A82
Author(s):  
Peter Jenkins ◽  
Sara De Simoni ◽  
Niall Bourke ◽  
James Cole ◽  
David Sharp

Brain ◽  
2019 ◽  
Vol 142 (8) ◽  
pp. 2367-2379 ◽  
Author(s):  
Peter O Jenkins ◽  
Sara De Simoni ◽  
Niall J Bourke ◽  
Jessica Fleminger ◽  
Gregory Scott ◽  
...  

Abstract Cognitive impairment is common following traumatic brain injury. Dopaminergic drugs can enhance cognition after traumatic brain injury, but individual responses are highly variable. This may be due to variability in dopaminergic damage between patients. We investigate whether measuring dopamine transporter levels using 123I-ioflupane single-photon emission computed tomography (SPECT) predicts response to methylphenidate, a stimulant with dopaminergic effects. Forty patients with moderate-severe traumatic brain injury and cognitive impairments completed a randomized, double-blind, placebo-controlled, crossover study. 123I-ioflupane SPECT, MRI and neuropsychological testing were performed. Patients received 0.3 mg/kg of methylphenidate or placebo twice a day in 2-week blocks. Subjects received neuropsychological assessment after each block and completed daily home cognitive testing during the trial. The primary outcome measure was change in choice reaction time produced by methylphenidate and its relationship to stratification of patients into groups with normal and low dopamine transporter binding in the caudate. Overall, traumatic brain injury patients showed slow information processing speed. Patients with low caudate dopamine transporter binding showed improvement in response times with methylphenidate compared to placebo [median change = −16 ms; 95% confidence interval (CI): −28 to −3 ms; P = 0.02]. This represents a 27% improvement in the slowing produced by traumatic brain injury. Patients with normal dopamine transporter binding did not improve. Daily home-based choice reaction time results supported this: the low dopamine transporter group improved (median change −19 ms; 95% CI: −23 to −7 ms; P = 0.002) with no change in the normal dopamine transporter group (P = 0.50). The low dopamine transporter group also improved on self-reported and caregiver apathy assessments (P = 0.03 and P = 0.02, respectively). Both groups reported improvements in fatigue (P = 0.03 and P = 0.007). The cognitive effects of methylphenidate after traumatic brain injury were only seen in patients with low caudate dopamine transporter levels. This shows that identifying patients with a hypodopaminergic state after traumatic brain injury can help stratify the choice of cognitive enhancing therapy.


Sign in / Sign up

Export Citation Format

Share Document