A case of posterior cerebral artery territory infarction with micropsia as the chief complaint

A 63-year-old man was admitted to the hospital complaining that all objects in his vision suddenly appeared small. Examination on admission revealed amnesia of recent events, recognition memory deficits, emotional disturbance, right upper quadrantanopsia and micropsia. The patient was diagnosed as posterior cerebral artery territory infarction based on brain CT scan and MRI findings which showed an ischemic lesion involving the left occipital lobe and hippocampus. We regarded the quadrantanopsia to have originated in the occipital lobe lesion and memory and emotional disturbances to have originated in the hippocampal lesion. After admission, micropsia and disturbances of memory and emotion improved within a month, but the quadrantanopsia did not recover. A comparison of the 25th and 2nd day brain CT scans indicated that the low density of the ischemic lesion near the hippocampus had become less clear and smaller. These findings suggest that the pathogenesis of micropsia in this case was a visual perceptional abnormality due to edematous change in the structures near the hippocampus. Cases of occipital artery territory infarction with micropsia, disturbances of memory and emotion, and quadrantanopsia appear to be rare, but micropsia may be overlooked since it is often masked by disturbance of memory or emotion.     

Parkinson's disease with syncope as a chief complaint induced by prominent postprandial hypotension]

A 77-year-old man developed syncope after meals at the age of 75. He had been treated with anti-Parkinson's drugs such as levodopa for 18 years as a patient with idiopathic Parkinson's disease (PD). The medications had been very effective to his parkinsonism. Ambulatory blood pressure was recorded every 20 minutes throughout one day by indirect measurement using a Colin medical instrument monitor (ABPM-630). The subsequent data disclosed that postprandial hypotension (PPH) was associated with the frequent after-meal syncope. It was also found that oral ingestion of a solution containing 50 grams of glucose caused a marked and prolonged hypotension during the resting supine position. Plasma norepinephrine failed to show any increment. Plasma vasopressin slightly increased while pulse rate, plasma renin activity, osmolality, and hematocrit did not change despite the production of severe hypotension of a relative acute onset. Signs of glucose intolerance and hyperinsulinemic response were observed. Indications of systemic autonomic nervous dysfunctions were revealed in various autonomic nervous function tests. Physical treatment combined with medication such as droxidopa, midodrine and especially caffeine and fludrocortisone proved to be effective on PPH. The authors confirmed the existence of PD with symptomatic PPH. In addition, we considered this present case as an example of "progressive autonomic failure with PD" (Bannister, 1988).     

综合医院和精神专科医院心理咨询门诊的焦虑主诉患者症状学调查

目的:比较综合医院和精神专科医院心理咨询门诊以焦虑为主诉的患者症状学特点及相关因素。方法:采用自编调查表对以焦虑为主诉就诊于综合医院及精神专科医院心理门诊的患者进行人口学及症状学调查和分析。结果:综合医院组(449例)与精神专科医院组(972例)间性别、年龄、文化程度、婚姻、工作、经济状况比较差异有统计学意义(χ2=5.743~54.181,P0.05或P0.001)。患者例数50%的症状两组相同,依次为睡眠症状、疲劳、担忧、情绪低落、紧张、犹豫不决、急躁和心慌;紧张、犹豫不决、急躁的频数综合医院组明显高于专科医院组(χ2=6.078,χ2=4.954,χ2=4.034;P均0.05)。多元回归分析显示,初中文化、已婚、经济状况差是情绪症状影响因素(t=-1.983,t=-2.335,t=3.805;P0.05或P0.001);出生地、工作或学习、经济状况差是躯体症状影响因素(t=-3.205,t=2.469,t=4.051;P0.05或P0.001)。结论:综合医院和精神专科医院以焦虑为主诉的患者主要症状相同;综合医院患者情绪症状更突出;经济状况差是情绪及躯体症状的共同影响因素。     

754例头晕患者经颅多普勒与颈部血管超声检查结果对比分析

目的探讨经颅多普勒(TCD)与颈部血管超声(CVUS)在门诊头晕患者中的诊断价值。方法回顾性对比分析神经内科门诊754例主诉头晕患者的TCD及CVUS检查结果。结果 CVUS的异常检出率显著高于TCD(c~2=165. 517,P0. 001);与单一检查方法相比,CVUS联合TCD检查的异常检出率更高(72. 02%)。两种方法对血管狭窄或闭塞的检出率无差异(P=0. 211),联合两种检查方法可以显著提高血管狭窄的检出率。年龄对头晕患者出现血流参数异常具有一定的预测价值(P 0. 001)。CVUS能更早的识别头晕患者血管异常状态。结论联合CVUS和TCD检查有助于发现门诊头晕患者脑血管异常;头晕患者年龄越大,更易出现脑血流动力学异常,但由血管狭窄引起的脑供血不足并不是门诊头晕患者主要的致病原因。     

Approach to the patient with a sleep complaint

There have always been sleep disorders, many of which have been recognized for centuries, and some of our treatments have even been dated from the past. However, there has been a dramatic increase in knowledge about sleep disorders and their treatments in the past 20 years. It is now possible to objectively diagnose most sleep disorders and new, specific treatments can be instituted. The recent recognition of chronobiology has resulted in an understanding of the alterations in the sleep-wake pattern of humans. Genetic causes of sleep disorders, such as advanced sleep phase syndrome, have shed new light on disorders that were previously believed to be largely behaviorally produced. Neurochemical changes have led to a better understanding of the pathophysiology of some disorders such as narcolepsy. However, despite advances in our understanding of sleep disorders, accurate diagnosis and treatment always requires a detailed understanding of the patient's sleep-wake cycle and medical history. The art of good sleep medicine still lies in the ability of the clinician to take a thorough history, develop a differential diagnosis, and formulate a treatment plan. This article details the important elements of the clinical evaluation.     

Fatigue: a non-specific complaint?

Community surveys and primary care studies confirm that fatigue is a common symptom experienced by the majority, and may be accepted as part of everyday life when a cause is readily identifiable by the subject. Although associated with many physical and psychiatric conditions, it is infrequent in primary care as a main or presenting complaint. Recent interest has focused on prolonged and severe fatigue states, now termed ‘chronic fatigue syndrome’, but to date few community or primary care studies have been conducted. Comparison between studies is hindered by variation in syndrome definition and non-standardized measures of fatigue. Such studies suggest a multifactorial aetiology; however, psychiatric disorders, in particular depression and anxiety, affect the majority of sufferers.     

Neuropsychological evidence of a factitious memory complaint

The authors describe a patient who complained of a severe memory loss. Information gathered from the history, interview, and testing suggested malingering. The patient was then assessed by a strategy called Symptom Validity Testing. Her score was statistically worse than chance, which provided compelling evidence that she was faking bad.