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Aphasic dementia and motor neuron disease.

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References
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1992;32:728-732
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meeting. Bull W H O 1992;70:27-33
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M and G antibodies in cerebrospinal fluid. J Clin Microbiol
1982;16:1034-1042
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J Clin Microbiol 1989;27:1983-1987
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with enterovirus in muscle of patients with inflammatory myopathies. Ann Neurol 1992;32:219-222
7. Henson .I,Rosenblum M, Armstrong D, Furneaux H . Amplification of JC virus DNA from brain and cerebrospinal fluid of
patients with progressive multifocal leukoencephalopathy. Neurology 1991;41:1967-197 1
8. Rowley AH, Whitley RJ, Lakeman FD, Wolinsky SM. Rapid
detection of herpes simplex virus DNA in cerebrospinal fluid
of patienrs with herpes simplex encephalitis. Lancet 1990;
335:440-44 1
9. Rotbart HA, Kinsella JP, Wasserman R L Persistent enterovirus
infection in culrure negative meningoencephaliris: demonstration by enzymatic RNA amplification. J Infect Dis 1990;
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Broca’s and Wernicke’s areas and other appropriate
regions
-- to support their clinical impression of aphasia. Our “takehome” message from this study of ALS dementia, which typically affects the frontotemporal region, is that the accompanying severe spastic dysarthria can obscure the diagnosis of
dementia and, by inference, asphasia. Moreover, the aphasia
tends to be submerged within the global cognitive deterioration complicating psychometric assessment.
W e were also concerned with the authors’ review of the
literature. They refer to motor neuron disease with dementia
as a nonhomogeneous “entity” and then confuse the picture.
Transmissible amyotrophic Creutzfeldt-Jakob (C-J) disease is
mentioned as an entity but in their reference to the seminal
work of Salazar and colleagues 121 they appear to have been
unaware of the conclusion of the latter authors that such
cases are, in fact, nontransmissible.Moreover, Salazar and colleagues [23 state that patients with dementia and “early amyotrophy are more closely related to classical amyotrophic lateral sclerosis than to transmissible Creutzfeldt-Jakob disease
and (therefore) do not deserve the label of amyotrophic
Creutzfeldt-Jakob disease.” The letter of Connolly and coworkers [3] to which they refer as evidence for a transmissible agent in amyotrophic form of C-J disease concerns an
earlier published case by the same authors and states that
brain tissue from their case was inoculated into a squirrel
monkey at the National Institutes o f Health, Bethesda, MD,
in 1971 [4). The result was reported as negative in 1983,
but in a subsequent personal communication with RodgersJohnston at the NIH, they were informed that histopathological changes in the monkey were consistent with C-J disease.
Connolly and co-workers [3] concluded from this that a
transmissible agent was present in their patient, a conclusion
that was unjustified considering that the monkey had survived for more than a dozen years. Earlier authors described
amyotrophic C-J disease based largely upon dementia accompanying ALS and, when available, autospy evidence of status
spongiosis in the outer three (not deeper) layers of the cerebral cortex which is incorrect [2, 51.
*DepartP1Zent of Clinical Nezirologtcal Sciences
Division of Neurology
f Depurtment of Psychological Sewices
University Hospital
London, Ontario NGA 5A5,Canadz
Aphasic Dementia and
Motor Neuron Disease
Arthur J. Hudson, MD,* and Jeff Martzke, PhDt
In the article by Caselli and associates [ 1) entitled, “Rapidly
Progressive Aphasic Dementia and Motor Neuron Disease,”
the authors present cases of frontotemporal dementia in classic amyotrophic lateral sclerosis (ALS) to demonstrate cortical aphasia [2]. However, the analysis of cortical speech disorder was, by their own account, almost impossible because
in all cases the patients were severely dysarthric, demented,
and paretic. It is surmised, because asphasia batteries were
not mentioned, that tests such as the Boston or Western
Aphasia Batteries, or Multilingual Aphasia Examination,
were not performed. Thus, while stating that an examination
of patients’ written responses demonstrated aphasia, no objective evidence of this was provided. Recognizing the difficulties of clinical assessment, it would have been helpful if
the authors had presented detailed pathological findings in
References
1. Caselli RJ, Windebank AJ, Petersen RC, et al. Rapidly progressive asphasic dementia and motor neuron disease. Ann Neurol
1993;33:200-207
2. Salazar AM, Masters CL, Gajdusek DC, Gibbs CJ Jr. Syndromes
of amyotrophic lateral sclerosis and dementia: relation to transmissible Creuafeldt-Jakob disease. Ann Neurol 1983;14: 17-26
3. Connolly JH, Allen IV, Dermott E. Transmissible agent in the
amyotrophic form of Creutzfeldt-Jakob disease. J Neurol Neurosurg Psychiatry 1988;51:1459-1460 (Letter)
4. Allen IV, Dermott E, Connolly JH, Hurwitz LJ. A study of a
patient with the amyotrophic form of Creutzfeldt-Jakob disease.
Brain 1971;94:715-724
5. Hudson AJ. Dementia and parkinsonism in amyotrophic lateral
sclerosis. In: Vinken PJ, Bruyn GW, Klawans HL, eds. Handbook of clinical neurology: diseases of the motor system, vol 59
(15). New York: Elsevier Science, 1991231-240
Annals of Neurology Vol 34
No 3’ September 1993 417
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motor, dementia, aphasia, disease, neurons
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