- Email: [email protected]
SENILE DEMENTIA OF LEWY BODY TYPE AND SPECTRUM OF LEWY BODY DISEASE
1088 described. A sensitive in-vitro assay has been developed which enables protection to be measured over any chosen spectral interval. The details of this assay are to be published elsewhere; the results obtained for total sunblock cream 15 A + B show that a sun protection factor of 15 is indeed achieved, but that the mean protection factor for the LJVA (320-400 nm) spectral interval is only 4. It would seem reasonable to suggest that sunscreen manufacturers should publish, or describe in some detail within their promotional literature, the methods that have been used to measure the protection factors that are claimed. Department of Dermatology, Royal Victoria Infirmary, Newcastle upon Tyne, NE1 4LP
disease. The recognition of SDLT is clinically important since the proportion in the Newcastle series was at least 15%. Not only is it a common cause of dementia in the elderly but also, given the prevalence of dementia (13 % among those over 757), it may prove to be the most common form of Lewy body disease, exceeding Parkinson’s disease in the general population.
Newcastle General Hospital, Newcastle upon Tyne NE4 6BE 1 Yoshimura M. Cortical
P. M. FARR 2.
Medical Physics Department,
Dryburn Hospital, B. L. DIFFEY
Durham
SENILE DEMENTIA OF LEWY BODY TYPE AND SPECTRUM OF LEWY BODY DISEASE
3. 4. 5.
SIR,-Dr Lennox and colleagues (Feb 11,
R. H PERRY D. IRVING G. BLESSED E. K. PERRY A. F. FAIRBAIRN
p
323) suggest that
atypical dementia identified as senile dementia of Lewy body type (SDLT) (Jan 21, p 166) is diffuse Lewy body disease (DLBD). However, on the basis of published criteria for DLBD,1,2 its rarity,l3 and a comparison with cases in our series we maintain that SDLT is in a separate category. Japanese research workers have been prominent in classifying Lewy body disease1,2,4 (see review3), and three groups with brainstem lesions identical to those of Parkinson’s disease were distinguishedl,2 on the basis of the distribution and density of cortical Lewy bodies: Group A (diffuse Lewy body disease).-Numerous Lewy bodies widely distributed in cerebral cortex; Group B (transitional Lewy body disease).-Lewy bodies less frequent in cerebral cortex (subdivided into Parkinson’s disease with and without dementia); and Group C (brainstem Lewy body disease).-Few or no Lewy bodies in cerebral cortex (Parkinson’s disease without dementia). In the Newcastle series of 91 demented (and 5 non-demented Parkinson’s disease) patients, cases with Lewy body formation fell into five rather than three categories: (i) DLBD.-n 2, group A; (ii) Parkinson’s disease developing dementia.-n 7, group B; (iii) Parkinson’s disease without dementia.-n 5, groups Band C; (iv) SDLT or atypical5.-n = 14; and (v) Combined Alzheimer’s and Parkinson’s disease.-n = 1. Unlike Lennox et al we have not amalgamated groups A and B and restrict the diagnosis of DLBD to two cases (aged 73 and 74) matching the original descriptions of group A,1,2,4 in which neocortical Lewy body densities were at least ten times higher than they are in SDLT. Combined frontal, temporal, and parietal densities were 140 and 53/cmin the two patients compared with 4-4 (SD 4-2)/cm in SDLT. Densities were three or four times higher in limbic cortex (174 and 146 vs 44 [2S]/cm2), and within the range reported elsewhere’°3for DLBD of 2-3 per high-power field in deeper cortical layers. Substantia nigral neuron loss was also greater in DLBD than SDLT (158 and 162 vs 328 [152]). Lennox and colleagues’ broader use of the term DLBD would in practice include most cases of elderly Parkinson’s disease since most patients over 70 show cortical Lewy body formation (unpublished). In the spectrum of Lewy body disease,1,2 SDLT should be considered as a separate group (D, since they are distinguishable from Parkinson’s disease), or as a subdivision of group B. Ambiguity may arise when atypical cases are allocated to preexisting or incomplete classifications. Dickson et al6 suggested that most of their six cases of "DLBD" belonged to an intermediate group, and similar cases in previous reports may be retrospectively classifiable as SDLT. Since precise classification depends on neuropathological examination, clinical diagnosis may be facilitated by using the term Lewy body dementia to encompass these categories of demented patients with Lewy body disease (groups A, B, and D). This widens the defmition3 but would aid clinical recognition and allow assessment of common and distinguishing features in Lewy body =
=
=
6. 7.
changes in the parkinsonian brain a contribution to the delineation of "diffuse Lewy body disease". J Neurol 1983; 229: 17-32. Kosaka K, Yoshimura M, Ikeda K, Budka H. Diffuse type of Lewy body disease progressive dementia with abundant cortical Lewy bodies and senile changes of varying degree: a new disease? Clin Neuropathol 1983; 3: 185-92. Gibb WRG, Esin MM, Lees AJ. Clinical and pathological features of diffuse cortical Lewy body disease (Lewy body dementia). Brain 1987; 110: 1131-53. Kosaka K, Matsushita M, Oyanagi S, Mehraein P. A cliniconeuropathological study of the "Lewy body disease". Psychiatr Neurol Jpn 1980; 5: 292-311 Irving D, Perry RH, Blessed G, Perry EK, Fairbairn A, Xuereb J. Neuropathological observations on an atypical dementing syndrome Neuropathol Appl Neurobiol 1988; 14: 511. Dickson DW, Davies P, Mayeux, et al. Diffuse lewy body disease: neuropathological and biochemical studies of six patients. Acta Neuropathol 1987; 75: 8-15. Kay DW, Bergmann K, Foster E, McKechnie AA, Roth M. Mental illness and hospital usage in the elderly: a random sample followed up. Compr Psychiatry 1970, 11: 26-35.
CONSERVATIVE MANAGEMENT OF ENTEROVIRUS INFECTIONS IN NEONATAL INTENSIVE CARE UNITS
SIR,-Dr Isaacs and his colleagues (March 11, p 543) suggest that reiteration of advice about handwashing may be an adequate response to infection with echovirus 11 in neonatal units. Their reasoning is that enterovirus infections in these units are common and often asymptomatic, that horizontally acquired infection is mild, and that closing a regional neonatal unit causes increased mortality in referring hospitals. In Cambridge we experienced the first outbreak of echovirus II to be associated with fatalities, in 1977:’ twins who died during this episode developed the infection 7 and 10 days after the index case and were attended at their delivery by a doctor who had symptoms. Their mother was never ill and had no evidence of enterovirus infection. There have been other reports of fatal enterovirus infection in neonatal units thought to have been acquired horizontally. The first case described by Speer and Yawnzmay have contracted fatal echovirus 11from a sibling. A death in Leicester in 1979 was thought to have resulted from horizontal transmission.3 We support the view of Carolane and colleagues4 that every enterovirus outbreak must be assessed individually and that access to the neonatal unit may need to be restricted. The Cambridge unit was not closed during the echovirus 7 episode in 1984.5 Admissions were restricted but nobody was denied intensive care and all babies were given normal human immunoglobulin intramuscularly. There is no evidence that intramuscular immunoglobulin is harmful. Although horizontal transmission is associated with a low mortality the risk is not negligible and should not be ignored. Clinical Microbiology and Public Health Laboratory, Addenbrooke’s Hospital, Cambridge CB2 2QW
T. G. WREGHITT
Rosie Maternity
J. M. RENNIE
Cambridge
Hospital,
G. M. GANDY
1. Nagington J, Wreghitt TG, Gandy G, Roberton NRC, Berry PJ. Fatal echovirus II m a special care baby unit. Lancet 1978; ii: 725-28. 2. Speer ME, Yawn DH. Fatal hepatoadrenal necrosis in the neonate associated with echovirus types 11 and 12 presenting as a surgical emergency J Pediatr Surg 1984, 19: 591-93. 3. Davies DP, Hughes CA, MacVicar J, Hawkes P, Mair HJ. Echovirus 11 infections in a special care baby unit. Lancet 1979; i: 96. 4. Carolane DJ, Long AM, McKeever PA, Hobs SJ, Roome AP. Prevention of spread of echovirus 6 in a special care baby unit. Arch Dis Child 1985; 60: 674-76. 5. Wreghitt TG, Gandy GM, King A, Sutehall G. Fatal neonatal echo 7 virus infection. Lancet 1984; ii: 465.
disease. The recognition of SDLT is clinically important since the proportion in the Newcastle series was at least 15%. Not only is it a common cause of dementia in the elderly but also, given the prevalence of dementia (13 % among those over 757), it may prove to be the most common form of Lewy body disease, exceeding Parkinson’s disease in the general population.
Newcastle General Hospital, Newcastle upon Tyne NE4 6BE 1 Yoshimura M. Cortical
P. M. FARR 2.
Medical Physics Department,
Dryburn Hospital, B. L. DIFFEY
Durham
SENILE DEMENTIA OF LEWY BODY TYPE AND SPECTRUM OF LEWY BODY DISEASE
3. 4. 5.
SIR,-Dr Lennox and colleagues (Feb 11,
R. H PERRY D. IRVING G. BLESSED E. K. PERRY A. F. FAIRBAIRN
p
323) suggest that
atypical dementia identified as senile dementia of Lewy body type (SDLT) (Jan 21, p 166) is diffuse Lewy body disease (DLBD). However, on the basis of published criteria for DLBD,1,2 its rarity,l3 and a comparison with cases in our series we maintain that SDLT is in a separate category. Japanese research workers have been prominent in classifying Lewy body disease1,2,4 (see review3), and three groups with brainstem lesions identical to those of Parkinson’s disease were distinguishedl,2 on the basis of the distribution and density of cortical Lewy bodies: Group A (diffuse Lewy body disease).-Numerous Lewy bodies widely distributed in cerebral cortex; Group B (transitional Lewy body disease).-Lewy bodies less frequent in cerebral cortex (subdivided into Parkinson’s disease with and without dementia); and Group C (brainstem Lewy body disease).-Few or no Lewy bodies in cerebral cortex (Parkinson’s disease without dementia). In the Newcastle series of 91 demented (and 5 non-demented Parkinson’s disease) patients, cases with Lewy body formation fell into five rather than three categories: (i) DLBD.-n 2, group A; (ii) Parkinson’s disease developing dementia.-n 7, group B; (iii) Parkinson’s disease without dementia.-n 5, groups Band C; (iv) SDLT or atypical5.-n = 14; and (v) Combined Alzheimer’s and Parkinson’s disease.-n = 1. Unlike Lennox et al we have not amalgamated groups A and B and restrict the diagnosis of DLBD to two cases (aged 73 and 74) matching the original descriptions of group A,1,2,4 in which neocortical Lewy body densities were at least ten times higher than they are in SDLT. Combined frontal, temporal, and parietal densities were 140 and 53/cmin the two patients compared with 4-4 (SD 4-2)/cm in SDLT. Densities were three or four times higher in limbic cortex (174 and 146 vs 44 [2S]/cm2), and within the range reported elsewhere’°3for DLBD of 2-3 per high-power field in deeper cortical layers. Substantia nigral neuron loss was also greater in DLBD than SDLT (158 and 162 vs 328 [152]). Lennox and colleagues’ broader use of the term DLBD would in practice include most cases of elderly Parkinson’s disease since most patients over 70 show cortical Lewy body formation (unpublished). In the spectrum of Lewy body disease,1,2 SDLT should be considered as a separate group (D, since they are distinguishable from Parkinson’s disease), or as a subdivision of group B. Ambiguity may arise when atypical cases are allocated to preexisting or incomplete classifications. Dickson et al6 suggested that most of their six cases of "DLBD" belonged to an intermediate group, and similar cases in previous reports may be retrospectively classifiable as SDLT. Since precise classification depends on neuropathological examination, clinical diagnosis may be facilitated by using the term Lewy body dementia to encompass these categories of demented patients with Lewy body disease (groups A, B, and D). This widens the defmition3 but would aid clinical recognition and allow assessment of common and distinguishing features in Lewy body =
=
=
6. 7.
changes in the parkinsonian brain a contribution to the delineation of "diffuse Lewy body disease". J Neurol 1983; 229: 17-32. Kosaka K, Yoshimura M, Ikeda K, Budka H. Diffuse type of Lewy body disease progressive dementia with abundant cortical Lewy bodies and senile changes of varying degree: a new disease? Clin Neuropathol 1983; 3: 185-92. Gibb WRG, Esin MM, Lees AJ. Clinical and pathological features of diffuse cortical Lewy body disease (Lewy body dementia). Brain 1987; 110: 1131-53. Kosaka K, Matsushita M, Oyanagi S, Mehraein P. A cliniconeuropathological study of the "Lewy body disease". Psychiatr Neurol Jpn 1980; 5: 292-311 Irving D, Perry RH, Blessed G, Perry EK, Fairbairn A, Xuereb J. Neuropathological observations on an atypical dementing syndrome Neuropathol Appl Neurobiol 1988; 14: 511. Dickson DW, Davies P, Mayeux, et al. Diffuse lewy body disease: neuropathological and biochemical studies of six patients. Acta Neuropathol 1987; 75: 8-15. Kay DW, Bergmann K, Foster E, McKechnie AA, Roth M. Mental illness and hospital usage in the elderly: a random sample followed up. Compr Psychiatry 1970, 11: 26-35.
CONSERVATIVE MANAGEMENT OF ENTEROVIRUS INFECTIONS IN NEONATAL INTENSIVE CARE UNITS
SIR,-Dr Isaacs and his colleagues (March 11, p 543) suggest that reiteration of advice about handwashing may be an adequate response to infection with echovirus 11 in neonatal units. Their reasoning is that enterovirus infections in these units are common and often asymptomatic, that horizontally acquired infection is mild, and that closing a regional neonatal unit causes increased mortality in referring hospitals. In Cambridge we experienced the first outbreak of echovirus II to be associated with fatalities, in 1977:’ twins who died during this episode developed the infection 7 and 10 days after the index case and were attended at their delivery by a doctor who had symptoms. Their mother was never ill and had no evidence of enterovirus infection. There have been other reports of fatal enterovirus infection in neonatal units thought to have been acquired horizontally. The first case described by Speer and Yawnzmay have contracted fatal echovirus 11from a sibling. A death in Leicester in 1979 was thought to have resulted from horizontal transmission.3 We support the view of Carolane and colleagues4 that every enterovirus outbreak must be assessed individually and that access to the neonatal unit may need to be restricted. The Cambridge unit was not closed during the echovirus 7 episode in 1984.5 Admissions were restricted but nobody was denied intensive care and all babies were given normal human immunoglobulin intramuscularly. There is no evidence that intramuscular immunoglobulin is harmful. Although horizontal transmission is associated with a low mortality the risk is not negligible and should not be ignored. Clinical Microbiology and Public Health Laboratory, Addenbrooke’s Hospital, Cambridge CB2 2QW
T. G. WREGHITT
Rosie Maternity
J. M. RENNIE
Cambridge
Hospital,
G. M. GANDY
1. Nagington J, Wreghitt TG, Gandy G, Roberton NRC, Berry PJ. Fatal echovirus II m a special care baby unit. Lancet 1978; ii: 725-28. 2. Speer ME, Yawn DH. Fatal hepatoadrenal necrosis in the neonate associated with echovirus types 11 and 12 presenting as a surgical emergency J Pediatr Surg 1984, 19: 591-93. 3. Davies DP, Hughes CA, MacVicar J, Hawkes P, Mair HJ. Echovirus 11 infections in a special care baby unit. Lancet 1979; i: 96. 4. Carolane DJ, Long AM, McKeever PA, Hobs SJ, Roome AP. Prevention of spread of echovirus 6 in a special care baby unit. Arch Dis Child 1985; 60: 674-76. 5. Wreghitt TG, Gandy GM, King A, Sutehall G. Fatal neonatal echo 7 virus infection. Lancet 1984; ii: 465.