Evidence Of Mood Disorder Research Articles

1650 – Probable creutzfeld-jakob disease: a neuropsychiatric presentation

Creutzfeld-Jakob disease (CJD) is the commonest form of transmissible human subacute spongiform encephalopathy, with a worldwide distribution of 0.5 to 1.0 per million population. A retrospective review in 1998 from Singapore General Hospital revealed 5 possible cases over 2 years, in an island with a population of 4 million. We present a 76 year-old Chinese man, with a premorbid personality of an independent person who was neat and meticulous, admitted for a 3 month-history of progressive behavioural change, associated with memory impairment and unsteady gait. He had long-standing hypertension which was well-controlled. The abnormal behaviour included frequent complaints of people coming to his house to have meetings, frequent misplacing of his belongings, as well as decreased self-hygiene. This has affected his daily functioning. There were no other symptoms of dementia. Initial MMSE was 16/30, with impairment in 2-point orientation (place/person), the serial sevens, and delayed recall. There was marked inattention. There was no evidence of mood disorder. No perceptual disorder was elicited. The brain MRI revealed cortical hyperintensities (“cortical ribboning”) in right frontal, parietal, temporal, and caudate nucleus. Physical examination on the 5th day of admission revealed mild bradykinesia, mild hypertonia of all 4 limbs, mildly impaired proprioception, mildly unsteady gait, as well as occasional myoclonic jerks of the head. Electroencephalogram showed generalised fronto-central fairly rhythmical periodic complexes with triphasic morphology.Cerebrospinal fluid protein 14-3-3 were negative. Over the next 12 days, his Abbreviated Mental Test (AMT) decreased from 8/10 to 5/10. The clinical picture was highly suggestive of sporadic CJD.

SUCCESSFUL TREATMENT OF CHARLES BONNET SYNDROME WITH NOCTURNAL OXYGEN SUPPLEMENTATION

To the Editor: A 92-year-old woman with visual impairment due to dry macular degeneration was admitted to the hospital in January 2004 with an 8-week history of visual hallucinations. She saw flowers growing out of the walls, animals running around, and spiders crossing her meals. These hallucinations occurred intermittently during the day and lasted for minutes to hours. Although she was fully aware that the spiders were not real, she refused to eat and had lost 5 kg of body weight. She was taking the anticoagulant phenprocoumon for atrial fibrillation, bisoprolol for heart rate control, and ramipril for hypertension. She was fit and healthy for her age, lived alone, and had been able to care for herself with only a little daily support from her 70-year-old daughter. There was no personal or family history of psychiatric problems. Neurological examination was normal except for reduced visual acuity (20/400 on the Jaeger table). Her score on the short form of the Mini-Mental State Examination was normal at 20/21. There was no evidence of mood disorder, dementia, or mental illness on psychiatric assessment. An electrocardiogram confirmed atrial fibrillation, and echocardiography showed concentric left ventricular hypertrophy with normal systolic function. Chest X-ray and magnetic resonance imaging of the brain were normal. Intoxication, delirium, substance withdrawal, neurodegenerative disorders, and psychiatric disease were excluded as the cause of her symptoms. Her hallucinations persisted over the following 10 days in spite of treatment with haloperidol (10 mg twice a day) and risperidone (2 mg twice a day). Overnight pulse oximetry revealed severe intermittent hypoxemia with an oxygen desaturation index (ODI) of 56 per hour (normal <5/hour), a lowest nocturnal arterial oxygen saturation (SaO2) of 78% (normal >89%), and 184 minutes spent with SaO2 below 90% overnight (normal 0 minutes). Polysomnography established a diagnosis of severe obstructive sleep apnea. She did not tolerate nasal continuous positive pressure ventilation. Nocturnal oxygen supplementation through nasal cannulae at a flow rate of 3 L/min led to a significant reduction in nocturnal hypoxemia (ODI 3/hour, lowest nocturnal SaO2 89%, and 3 minutes spent below SaO2 of 90% overnight). After 2 nights of oxygen treatment, the hallucinations ceased. To establish causality, oxygen administration was halted. Hallucinations recurred after 2 days and ceased when oxygen was reinstated. She was discharged home with nocturnal oxygen supplementation. When she was readmitted 3 months later for upper gastrointestinal bleeding, oxygen therapy was not given during the first few days. Vivid visual hallucinations recurred and settled again after administration of oxygen (Figure 1). The relationship between hallucinations and oxygen treatment. Complex visual hallucinations in visually impaired, psychologically normal older people characterize Charles Bonnet syndrome (CBS). It can be associated with damage at any level of the visual tract, from cataracts and retinal disease to infarction of the occipital cortex. The most widely accepted diagnostic criteria for CBS are formed complex, persistent, or repetitive stereotyped visual hallucinations; full or partial insight into the unreal nature of the perceptions; absence of hallucinations in other sensory modalities; and absence of mental disorders.1 The most effective treatment is reversal of the visual impairment. Antipsychotic drugs are commonly prescribed but are largely ineffective.2 To the authors' knowledge, this is the first report of a causal relationship between intermittent hypoxemia and CBS. Hypoxia is associated with retinal dysfunction and poor night vision.3 A possible explanation for this patient's response to oxygen treatment would be that hypoxia affected the function of her already-compromised retina. Tissue hypoxia is a pathogenetic factor in macular degeneration, causing edema and longer-lasting but reversible changes in vision.4 This could have been sufficient to precipitate the hallucinations. Intermittent hypoxemia also has an immediate and delayed effect on cognitive function through induction of inflammation and modulation of neurotransmitters.5 This may have impaired cortical compensation and adjustment to a incomplete picture received from the damaged retina, and thus precipitated CBS. This case highlights the importance of a full clinical assessment in older patients presenting with visual problems.

Lord Clive Did Not Suffer a Mood Disorder

We aimed to clarify questions regarding Lord Clive's early suicidal behavior and mental health. We examined various historical texts. Clive suffered gallstones with episodes of cholecystitis. We could find no evidence that Clive engaged in suicidal behavior in his early life, nor evidence of a mood disorder (depression or bipolar disorder) throughout his life or at the time of his death. Although reports of famous people who have suffered mental disorders may help to decrease the stigma associated with these conditions, there is a need for caution before make such a diagnosis. In the case of Lord Clive, we could find no evidence of a major mood disorder.