Cortical response to exogenous visual stimulation during visual hallucinations

Cortical response to exogenous visual stimulation during visual hallucinations

rehydration solution were donated to the hospitals in the affected area in Kenya by Japan International Cooperation Agency. Total cost for this supply...

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rehydration solution were donated to the hospitals in the affected area in Kenya by Japan International Cooperation Agency. Total cost for this supply was about US$8000 and supplies were enough to treat 1500 people. Hygiene practices, including heat treatment of drinking water, were improved by health education. The outbreak of cholera and shigellosis subsided by August, 1994. Urgent supply of the appropriate drugs and improvement of hygienic practices through health education are important and effective in the control of outbreaks of diarrhoeal countries. We believe that ours controlling similar outbreaks of diarrhoeal diseases in the developing

diseases in developing is a model case for cholera and/or other countries.

*Yoshio lijima. Joseph O Oundo, Kenichiro Taga, Suleiman M Saidi, Takeshi Honda *Centre for Microbiology Research, Kenya Medical Research Institute, PO Box 54840 Nairobi, Kenya: and Research Institute for Microbial Diseases, Osaka University, Japan

1

Crumley B,

Michaels M, Purvis A.

Cry

the forsaken country. Time

1994; 144: 10-19.

Cortical response to exogenous visual stimulation during visual hallucinations SIR-Functional magnetic resonance (MR) imaging offers visualisation of cortical activation in real time. Temporal resolution is limited only by the delay in vascular transit from capillaries to capacitance veins, unlimited repeat examinations are possible, and substantial activation can be detected in single subjects. Periodic visual stimulation in normal volunteers induces a periodic response in the MR signal recorded from primary visual cortex (Vl) and extrastriate areas.’ Activation within VI accompanies visual imagery and recall,2,3 but the distribution of cortical activation during visual hallucinosis is unknown. A 74-year-old man with cortical Lewy body dementia presented with continuous complex visual hallucinations. These disappeared after 15 days of treatment with risperidone 1 mg twice daily. 4 weeks later, risperidone was discontinued and after a further 4 days continuous hallucinations returned. Two sets of multislice echoplanar images were collected from this patient by use of a GE Signa 1-5 T machine with an advanced nuclear MR operating console on the day of risperidone discontinuation (not hallucinating) and 7 days later (hallucinating). The experimental set-up and scanning parameters were identical for both times. Over5 min, he was exposed to a cycle of 30 s of darkness, followed by 30 s of 8 Hz pattern-flash photic stimulation via light-proof stimulating goggles (model S10VS; Grass Instruments). At

Figure: 70

MR

images

on

(left)

and off

(right) risperidone

each of 3 contiguous 5 mm thick transverse slices through the brain, 100 T2*-weighted MR images (TE 40 ms, TR 3000 ms) depicting bold contrast’ were acquired. Images were analysed by time-series regression modelling. At each pixel in each slice, we estimated power in the MR signal at the on-off frequency of exogenous visual stimulation. A given pixel was said to be activated by visual stimulation if the t statistic for power exceeded a critical value ascertained by randomisation testing. In the figure, pixels activated with a probability of type 1 error less than 0-001 are coloured red. When the patient was not hallucinating, he showed the normal pattern of response. 7

days later, during hallucinations, the

area of cortical activation is less extensive and the difference in the proportion of total pixels activated is significant (p<00001). When visual stimuli from both endogenous and exogenous sources are presented they compete, resulting in diminution of the cortical response to exogenous periodic stimulation. Visual hallucinations could therefore result from reduced responsiveness of the visual cortex to peripheral sensory input, perhaps disinhibiting endogenous visual memories in inferior temporal cortex. Alternatively, such endogenouslydriven activity may itself inhibit the visual cortex. Either mechanism could explain the involuntary nature of visual hallucinations which distinguishes them from imagery. We thank Dr Tim Cox, Mark Allin, and Chris Andrew.

*Robert Howard, Steve Williams, Edward Bullmore, Michael Brammer, John Mellers, Peter Woodruff, Anthony David Institute of

Psychiatry,

De

Crespigny Park,

Denmark Hill, London SE5 8AF, UK

Kwong KK, Belliveau JW, Chesler DA, et al. Dynamic magnetic resonance imaging of human brain activity during primary sensory activity. Proc Natl Acad Sci USA 1992; 89: 5675-79. 2 Le Bihan D, Turner R, Zeffiro TA, et al. Activation of human primary visual cortex during visual recall: a magnetic resonance imaging study. Proc Natl Acad Sci USA 1993; 90: 11802-05. 3 Kosslyn SM, Alpert NM, Thompson WL, et al. Visual mental imagery activates topographically organised visual cortex: PET investigations. J Cog Neurosci 1993; 5: 263-87. 4 Ogawa S, Lee T-M, Nayak AS, et al. Brain magnetic resonance imaging with contrast dependent blood oxygenation. Proc Natl Acad Sci USA 1990; 87: 9868-72. 1

Immunity to pneumococcal infections SIR-As Reid

points out in his Oct 8 commentary, that splenectomy predisposes to infection from encapsulated bacteria is well recognised. However, splenectomy is one extreme of the spectrum of hyposplenia, a condition associated with various systemic disorders such as sickle cell anaemia, thalassaemia, chronic liver disease, lupus, coeliac disease, HIV, and bone marrow transplantation. Therefore, in addition to patients who do not have a spleen, the group with functional asplenia should also be addressed. The spleen has a key role in antibody production, especially in response to carbohydrate antigens and in the elimination of opsonised and the unopsonised particulate matter from circulation. In the absence of a functioning spleen, higher antibody levels are required for macrophages at other sites such as the liver, to effectively take over its phagocytic function.2 The benefit of immunisation with different types of polyvalent pneumococcal vaccine has been conclusively demonstrated only in healthy subjects, whereas similar benefit in various at-risk groups is at best contentious.3 Quantitative measurements of pneumococcal specificantibody might not be a satisfactory method of assessing immunity in these patients who lack a splenic phagocytic mass, since we still do not have a defined protective level of antibody either in the presence or absence of a spleen.