Mood disorders memory impairments

Tablet combination therapy Adverse reactions occurring in at least 3% of patients include the following Abdominal pain alopecia anemia anorexia anxiety arthralgia back pain bacterial infection blurred vision concentration impairment cough depression dermatitis diarrhea dizziness dry mouth/skin dyspepsia dyspnea eczema fatigue/asthenia headache hypothyroidism increased sweating injection site reaction insomnia irhtability/anxiety/nervousness lymphopenia memory impairment mood alteration myalgia nausea neutropenia pain pruritus pyrexia rash resistance mechanism disorders rigors thrombocytopenia vomiting weight decrease.

Neuropsychological impairments in mood disorders, particularly those of working memory and executive function, are the most convincing and objective demonstrations of an impairment of consciousness. Since these impairments do not correlate with the severity of the mood disturbance and persist upon recovery they are not simply epiphenomena of the mood disturbance but rather may index trait pathology in susceptible individuals. It has previously been argued that mood disturbance and neuropsychological impairment may result from disturbances in two different neurochemical systems, the serotonin (5-HT) system and the hypothalamic-pituitary-adrenal (HPA) axis, between which there is a close interaction (McAllister-Williams et al., 1998). 

Tryptophan depletion in healthy volunteers impairs the retrieval of learnt material (Park et al., 1994), an effect probably mediated through a selective impairment of episodic memory consolidation (Riedel et al., 1999 Schmitt et al., 2000). However, tryptophan depletion appears to have no effect on working memory (Riedel et al., 1999) and either no effect or an enhancement of tests of executive function (Park et al., 1994 Schmitt et al., 2000). Thus the abnormality in episodic memory in mood disorders could conceivably be related to an impairment in the 5-HT system, but such an impairment is unlikely to account for the abnormalities in working memory and executive function. Clearly then, changes in consciousness occurring in affective disorders are unlikely to be explainable on the basis of an abnormality in a single neurochemical system. 

The effectiveness of gabapentin has been studied in 22 patients with bipolar disorder who had an incomplete response to other mood stabilizers (5). Somnolence was common (six patients) adverse events that occurred in two patients each included irritability, memory impairment, headache, and tremor. One patient dropped out because of a mild rash. 

B. Survivors of serious poisoning may suffer numerous overt neurologic sequelae consistent with a hypoxic-ischemic insult, ranging from gross deficits such as parkinsonism and a persistent vegetative state to subtler personality and memory disorders. Various studies suggest that the incidence of subtle neuropsychiatric sequelae such as impaired memory and concentration and mood disorders may be as high as 47%. 

Huntington s disease, an autosomal dominant disorder, has a mean age-of-onset of 43-48 years. Symptoms appear gradually and worsen over a period of about 15 years until death occurs. Mood disturbance, impaired memory, and hyperrefiexia are often the first signs, followed by abnormal gait, chorea (loss of motor control), dystonia, dementia, and dysphagia. Cases of juvenile onset (<10 years old) are more severe and most frequently occur when the defective allele is inherited paternaily. About 25% of cases have late onset, slower progression, and milder symptoms. 

Rapid and sometimes serious mood swings to mania or depression, and other adverse effects, including enuresis, aggression, impaired memory, sedation, and ataxia, can occur in patients with panic disorder treated with alprazolam (SEDA-19, 34 SEDA-20, 31). 

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