Memory deficits in patients with schizophrenia: preliminary data from the Wechsler Memory Scale-Third Edition support earlier findings. (1/43)

OBJECTIVE: To determine whether memory data presented for a schizophrenia sample in the Technical Manual of the Wechsler Memory Scale-Third Edition support trends identified in a previously published review of studies employing an earlier version of the instrument, the Wechsler Memory Scale-Revised. DESIGN: Archival: reformulation of published data. PATIENTS: Patients with schizophrenia, Alzheimer's disease, Korsakoff's syndrome or traumatic brain injury (TBI) for whom intelligence and memory data were reported in the Technical Manual of the Wechsler Adult Intelligence Scale-Third Edition Wechsler Memory Scale-Third Edition (WAIS-III WMS-III). OUTCOME MEASURES: Mean Full Scale, Verbal, and Performance Intelligence Quotients of the WAIS-III and mean WMS-III Immediate and General Memory Indexes. Single-trial learning and learning slope data were also culled from the WAIS-III WMS-III Technical Manual. RESULTS: Memory indexes for patients with Alzheimer's disease or Korsakoff's syndrome were substantially lower than those for patients with schizophrenia or TBI. In tests of learning processes, patients with schizophrenia had an inferior ability to repeat material presented just once, in comparison with the standardization sample. However, they did relatively better with repeated presentations than patients with Alzheimer's disease or Korsakoff's syndrome. The learning slope for patients with schizophrenia demonstrated an ability to absorb and consolidate increasing amounts of material with repeated exposure that is inconsistent with pronounced memory impairment. CONCLUSIONS: Although patients with schizophrenia exhibit new learning deficiencies, their memory capabilities are not substantially weaker than their general intellectual abilities, and do not approach the memory impairment exhibited by patients with Alzheimer's disease or Korsakoff's syndrome.  (+info)

Brain correlates of memory dysfunction in alcoholic Korsakoff's syndrome. (2/43)

OBJECTIVES: To investigate the relation between anterograde amnesia and atrophy of brain structures involved in memory processing in alcoholic Korsakoff's syndrome. METHODS: The volume of brain structures involved in memory processing was measured with MRI from 13 subjects with Korsakoff's syndrome, 13 subjects with chronic alcoholism without Korsakoff's syndrome, and 13 control subjects. The brain structures analysed were the hippocampus, the parahippocampal gyrus, the mamillary bodies, the third ventricle, and the thalamus. Brain volumes were correlated with the delayed recall of a verbal learning test. RESULTS: Compared with subjects with chronic alcoholism and control subjects, subjects with Korsakoff's syndrome had a reduced volume of the hippocampus, the mamillary bodies, and the thalamus, and enlargement of the third ventricle. The impairment of delayed recall correlated with the volume of the third ventricle (r=-0.55, p=0.05) in the Korsakoff group. CONCLUSIONS: Anterograde amnesia in alcoholic Korsakoff's syndrome is associated with atrophy of the nuclei in the midline of the thalamus, but not with atrophy of the mamillary bodies, the hippocampus, or the parahippocampal gyrus.  (+info)

Degeneration of anterior thalamic nuclei differentiates alcoholics with amnesia. (3/43)

The specific neural substrate underlying the amnesia in alcoholic Korsakoff's psychosis is poorly defined because of the considerable brain damage found in many non-amnesic alcoholics, particularly those with Wernicke's encephalopathy. Using operational criteria to identify alcoholics with and without Korsakoff's psychosis, we have shown that many of the cortical and subcortical regions involved in the encoding and retrieval of episodic memory are either unaffected (hippocampus) or damaged to the same extent (prefrontal cortex and the cholinergic basal forebrain) in both amnesic and non-amnesic alcoholics. In the present study we analysed the diencephalic regions involved in episodic memory to determine the neural substrate for the amnesia observed in alcoholic Korsakoff's psychosis. The number of neurons in spaced serial sections containing the hypothalamic mamillary nuclei and the anterior and mediodorsal thalamic nuclei was estimated using unbiased stereological techniques. Neurodegeneration of the hypothalamic mamillary nuclei and the mediodorsal thalamic nuclei was substantial in both non-amnesic and amnesic alcoholics with Wernicke's encephalopathy. However, neuronal loss in the anterior thalamic nuclei was found consistently only in alcoholic Korsakoff's psychosis. This is the first demonstration of a differentiating lesion in alcoholic Korsakoff's psychosis and supports previous evidence that degeneration of thalamic relays are important in this memory disorder.  (+info)

A survey of the current clinical practice of psychiatrists and accident and emergency specialists in the United Kingdom concerning vitamin supplementation for chronic alcohol misusers. (4/43)

Although it is well known that B-vitamin deficiencies directly affecting the brain are common in alcohol misuse, no concise guidelines on the use of vitamin supplements in alcohol misusers currently exist in the UK. The purpose of this study was to assess current practice and opinion among UK physicians. Questionnaires were completed by a total of 427 physicians comprising Accident and Emergency (A&E) specialists and psychiatrists, with a response rate of 25%. The main findings were that vitamin deficiency was perceived as being uncommon amongst alcohol misusers (<25%) and there was no consensus as to which B vitamins are beneficial in treatment or the best method of administration of B-vitamin supplementation. The majority of psychiatrists favoured oral administration for prophylaxis against the Wernicke-Korsakoff syndrome in chronic alcohol misusers and parenteral therapy in patients with signs of Wernicke-Korsakoff syndrome. Whilst only just over half the A&E specialists expressed a preference, most favoured parenteral therapy in both cases. Most respondents did not currently have a unit policy/protocol on the management of vitamin supplementation in chronic alcohol misusers. Overall, the findings suggest that there is wide variation in current practice and highlight the need for guidelines in this area.  (+info)

Status-like recurrent pilomotor seizures: case report and review of the literature. (5/43)

A diabetic 66 year old man who presented with pilomotor seizures in his right hemibody is described. The seizures recurred with an increasing frequency, leading to a status-like condition associated with Korsakoff's syndrome. An EEG was performed and several electroclinical seizures were recorded. Brain MRI was negative. The patient, who was treated with carbamazepine, became seizure free after 1 week. Memory and behaviour gradually returned to normal within 3 weeks. There was no further neurological episode during an 8 year follow up. Hyperosmolar, non-ketotic hyperglycaemia was considered to be the cause of the seizures. The pathophysiology of pilomotor seizures is discussed and the literature on the subject reviewed.  (+info)

Structural MRI volumetric analysis in patients with organic amnesia, 1: methods and comparative findings across diagnostic groups. (6/43)

BACKGROUND: If they are to be replicable, MRI volume measurements require explicit definitions of structures and of criteria for delineating these structures on MRI. Previously published volumes in healthy subjects show considerable differences in measurements across different studies, including a fourfold variation in estimates of hippocampal volume. Previous neuroimaging reports in patients with Korsakoff syndrome have generally found widespread or non-specific change, whereas in patients with herpes encephalitis the extent of pathological involvement reported beyond the temporal lobes has varied. METHOD: In the present study, a clear set of anatomical criteria and detailed MRI segmentation procedures were applied to measure whole brain, frontal and temporal lobe, and anterolateral and medial temporal volumes, as well as thalamic areas in patients with organic amnesia (from Korsakoff's syndrome, herpes encephalitis, and focal frontal lesions) as well as healthy controls. RESULTS: Patients with Korsakoff's syndrome showed decreased thalamic measurements but no significant changes in the medial temporal lobes, whereas patients with herpes encephalitis showed severe medial temporal but not thalamic atrophy. In the patients with known frontal lobe lesions, quantitative analysis on MRI showed reduced frontal lobe volume but no significant temporal lobe or thalamic atrophy. CONCLUSION: Quantified MRI can be a useful technique with which to examine brain-cognitive relations, provided that detailed techniques are explicitly described. In particular, specific patterns of volume change can be found in vivo in patients with Korsakoff's syndrome and those with herpes encephalitis.  (+info)

A case of Korsakoff's syndrome improved by high doses of donepezil. (7/43)

We present a case of Korsakoff's syndrome that was successfully treated with high doses of donepezil, an inhibitor of acetylcholine esterase, known to retard the progress of symptoms in Alzheimer's disease. The patient was a 46-year-old married Japanese woman who began to drink alcohol after she married. After several years of drinking she developed typical symptoms of the Korsakoff syndrome. Donepezil was started after treatment with thiamine or thiamine plus fluvoxamine had failed. Her amnestic symptoms as well as her quality of life improved markedly during donepezil treatment. Inhibition of acetylcholine esterase may be an effective treatment for Korsakoff's syndrome.  (+info)

Reversible acute axonal polyneuropathy associated with Wernicke-Korsakoff syndrome: impaired physiological nerve conduction due to thiamine deficiency? (8/43)

Acute axonal polyneuropathy and Wernicke-Korsakoff encephalopathy developed simultaneously in three patients. Nerve conduction studies (NCS) detected markedly decreased compound muscle action potentials (CMAPs) and sensory nerve action potentials (SNAPs) with minimal conduction slowing; sympathetic skin responses (SSRs) were also notably decreased. Sural nerve biopsies showed only mild axonal degeneration with scattered myelin ovoid formation. The symptoms of neuropathy lessened within two weeks after an intravenous thiamine infusion. CMAPs, SNAPs, and SSRs also increased considerably. We suggest that this is a new type of peripheral nerve impairment: physiological conduction failure with minimal conduction delay due to thiamine deficiency.  (+info)