>>> Posting number 24646, 
                                          dated 29 Sep 1997 12:07:16

.....INTRODUCTION.....
Several subsequent posts shall delineate a remarkable parallel between three
traditional areas of research: Landau-Kleffner Syndrome (LKS) and a virus that is
known (i) to impair language in some persons, and (ii) to induce seizures or other
epileptiform atypicalities. We not that items i and ii are also seen in LKS.
      A post beginning "2 LKS" will provide a portrait of LKS, derived primarily
from citations.  Then, two posts will show that herpes simplex virus (HSV) can
induce language impairments as well as seizures and/or other atypical epileptiform
patterns.   A post beginning "3 LKS" will provide a portrait of HSV and language,
and a post beginning "4 LKS" will provide citations about HSV and seizure-like
activity. The overall gist of the following three posts is to provide documentation
for asking two questions:

I.    ARE SOME CASES OF LKS CAUSED BY HSV WITHIN THE CNS?
II.   OUGHT DIAGNOSTICS & INITIAL TREATMENTS BE CHANGED IN LKS?

Keeping in mind that HSV can be within the CNS and, while there, may be generating
*no* external signs or symptoms (1-3), the literature that shall be presented in the
following three posts suggests the *possibility* that at least some cases of LKS are
caused by subacute HSV within the CNS.    If that is a causal mechanism in some
cases of LKS, then altering the LKS diagnostic algorithm and modifying initial-
treament protocols might lead to significant improvements and reduction of further
deterioration. 
      Let us keep clear: This and the following three posts present a *hypothesis*
regarding HSV as the basis of some cases of LKS. Although anecdotal evidence (eg,
successful treatment with Acyclovir) is consistent with an HSV/LKS model, the
connection remains primarily hypothetical. However, as the citations indicate, the
hypothesis that some cases of LKS are caused by a subacute, intra-neuronal HSV
infection within the CNS is based upon numerous studies already in med literature.

Thus, the questions are re-iterated:

I.    ARE SOME CASES OF LKS CAUSED BY HSV WITHIN THE CNS?
II.   OUGHT DIAGNOSTICS & INITIAL TREATMENTS BE CHANGED IN LKS?


REFERENCES

1) Whitley RJ, Lakeman F. Herpes simplex virus infections of the central nervous
system: therapeutic and diagnostic considerations. Clinical
Infectious Diseases 20.414-20 1995.

2) Kimura H et al. Detection of viral DNA in neonatal herpes simplex virus
infections: frequent and prolonged presence of serum in cerebrospinal fluid. J
Infectious Diseases 164.289-93 1991.

3) Domingues RB et al. Evaluation of the range of clinical presentations of herpes
simplex encephalitis by using polymerase chain reaction of cerebrospinal fluid
samples. Clinical Infectious Diseases 25.86-91 1997.



      2 LKS & autism & virus
                                                >>> Posting number 24649, 
                                                dated 29 Sep 1997 12:23:52

This post provides a summary of LKS and delineates that language impairment is a
primary sign and often that impairment is accompanied by seizures or by other
atypical epileptiform activity. The following two posts will link HSV to language
impairment and to epileptiform activity or even to seizures. Together, these several
posts pose two questions for researchers, physicians, child development clinicians,
and parents:

I.    ARE SOME CASES OF LKS CAUSED BY HSV WITHIN THE CNS?
II.   OUGHT DIAGNOSTICS & INITIAL TREATMENTS BE CHANGED IN LKS?


<1>  Mouridsen SE.
The Landau-Kleffner Syndrome: a review.
     European Child & Adolescent Psychiatry.  4(4):223-8, 1995 Oct.
  The Landau-Kleffner syndrome or the syndrome of acquired epileptic aphasia was
first described in 1957. The disorder is characterised by gradual or rapid loss of
language in a previously normal child. All children have abnormal EEG compatible
with the diagnosis of epilepsy, however, only 70% have clinical seizures. The
present article presents a review of the current knowledge concerning this disorder.
Information is provided related to the clinical picture, etiology, pathogenesis,
treatment and outcome.

<2>  Kale U.  el-Naggar M.  Hawthorne M.
Verbal auditory agnosia with focal EEG abnormality: an unusual case of a
child presenting to an ENT surgeon with "deafness".
      Journal of Laryngology & Otology.  109(5):431-2, 1995 May.
Verbal auditory agnosia implies the failure to recognize sounds in a
patient who is nevertheless not deaf. We present a child referred to the
ENT outpatients for suspected hearing loss investigation. At one point she
had grommets inserted on the basis of a flat tympanogram but with no
effect. All hearing tests, including electrocochleography and distraction
tests, revealed normal hearing thresholds. At the age of three years and
three months, and on direct questioning of the parents, we discovered that
the child responded remarkably well to music. Paediatric neurologists made
the diagnosis of verbal auditory agnosia. The condition is very similar to
another acquired language disorder called Landau-Kleffner syndrome. It is
unusual for such a case to present primarily to an ENT surgeon.

<3>  Tuchman RF.  Rapin I.
Regression in pervasive developmental disorders: seizures and epileptiform
electroencephalogram correlates.
     Pediatrics.  99(4):560-6, 1997 Apr.
BACKGROUND: Approximately one third of the parents of children with
pervasive developmental disorders or autistic spectrum disorders reports
an early regression of unknown cause in their children's language,
sociability, and play. Seizures or an epileptiform electroencephalogram
(EEG) are associated with language regression in acquired epileptic
aphasia (Landau-Kleffner syndrome) and some other pediatric epileptic
syndromes. The importance of epilepsy or epileptic EEGs as contributors to
autistic regression is not known. METHOD: Subjects were 482 boys and 103
girls on the autistic spectrum seen consecutively in consultation by one
child neurologist. Data on autistic regression, seizures, sleep EEGs, and
cognitive function were entered prospectively into a data base. RESULTS:
Of the 585 children, 176 (30%) had a history of regression, and 66
children (11%) had a history of epilepsy, defined as two or more
unprovoked seizures. Among 392 children with available sleep EEGs, the EEG
was epileptiform in 59% of the 66 epileptic children and 8% of the 335
nonepileptic children. Regression had occurred equally among children
without seizures and in those with epilepsy. Regression was associated
with an epileptiform EEG in 14% of 155 nonepileptic children who had
undergone a regression, as opposed to 6% of 364 children with neither
regression nor epilepsy. Mean age at regression was 21 months. There was
no difference in the proportion of children with epilepsy or epileptiform
EEGs who had regressed before or after 2 years of age. Approximately half
of the epileptiform discharges were centrotemporal, whether or not the
child was epileptic or had regressed. Children with lower cognitive
function were more likely to have undergone regression than those with
better cognitive skills (34% vs 20%). CONCLUSION: Epilepsy or epileptiform
EEGs occur in a significant minority of autistic children with a history
of regression and in a smaller minority without regression. Prompt
recognition of regression and recording of prolonged sleep EEGs is
recommended, even though information on the potential efficacy of
antiepileptic treatment to improve language and behavior in autistic
children with epilepsy or an epileptiform EEG is still lacking.

        [I wonder how many of the Tuchman and Rapin patients
         have ever had PCR of CSF as a way to rule out or identify
         viral causes of each child's epilepsy? However, we must
         keep in mind that (i) PCR of CSF was not readily available in
         the years prior to 1990, and (ii) researchers and docs had
         not yet realized that certain viruses can have effects within
         the CNS even while producing no peripheral indications.]

<4>  Maquet P et al.
Regional cerebral glucose metabolism in children with deterioration of one or more
cognitive functions and continuous spike-and-wave discharges during sleep.
      Brain.  118 ( Pt 6):1497-520, 1995 Dec.
The Landau-Kleffner syndrome (LKS) and the syndrome of continuous spike-and-wave
discharges during slow sleep (CSWS) were originally described, and are still
considered, separately. The former combines an acquired aphasia with spike-and-wave
discharges that are activated by slow wave sleep, behavioural disturbances, and
sometimes epileptic seizures. The latter is characterized by continuous
spike-and-wave discharges during slow wave sleep, usually combined with global
intellectual deterioration and epileptic seizures. These two syndromes share many
common features: (i) onset during childhood; (ii) deterioration of cognitive
functions that were previously normally acquired; (iii) seizure type; (iv) EEG
pattern; (v) pharmacological reactivity; (vi) regression of the neuropsychological
symptoms, of the EEG abnormalities and of the seizures before the end of
adolescence; (vii) absence of obvious structural lesion detected by CT or MRI
scan...    The pathogenesis of this syndrome remains unknown...

        [Again, 'twill be interesting to see how these researchers'
         findings progress as they consider stealth-like viruses
         within the CNS and use PVR of CSF as a diagnostic tool.]



      3 LKS & autism & virus
                                          >>> Posting number 24657, 
                                          dated 29 Sep 1997 12:50:00

This set of abstracts shows how the language impairments associated with
Landau-Kleffner syndrome are similar to what can occur during focal herpes
encephalitis. Among these cites, note the variation from person to person. Keep in
mind that most of these studies were done prior to PCR, so these studies may
represent a "tip of the iceberg", ie, language impairments induced by HSV may be
more common than has been realized.

<1>  Greer MK.  Lyons-Crews M.  Mauldin LB.  Brown FR 3d.
A case study of the cognitive and behavioral deficits of temporal lobe damage in
herpes simplex encephalitis.
      Journal of Autism & Developmental Disorders.  19(2):317-26, 1989
      Herpes simplex viral encephalitis is a fairly common nonepidemic encephalitis
which produces severe neurological sequelae in survivors. Most viral infections of
the central nervous system produce diffuse damage, but the herpes simplex virus
demonstrates a predilection for localization in the temporal and orbitofrontal
regions of the brain. This case study illustrates the highly significant language
difficulties, marked memory deficits, and propensity for physical aggression
following temporal lobe damage brought about by herpes encephalitis, and presents
the usefulness of a new diagnostic measure in delineating such a variable cognitive
pattern.

<2>  Sagawa S.  Kaga K.  Kaga M.  Tanaka Y.
[The acquisition of language through finger spelling in a child with auditory
agnosia (author's transl)]. [Japanese]
      No to Shinkei - Brain & Nerve.  34(5):485-91, 1982 May.
  A child with auditory agnosia for verbal and nonverbal sounds was reported. He was
born without difficulty and his early development was normal. At the age of 14
months, he suffered from herpes simplex encephalitis and fell in a trance. Soon
after he recovered from the illness, he found not to pay any attention to sounds and
not to speak any words. He was referred to Teikyo University hospital at 2.5 years
of age for the hearing measurement. The average threshold of conditioned orientation
reflex audiometry at 500, 1000 and 2000 Hz were 85 dB, while the threshold of
auditory brain stem response was 15 dB which is normal. CT scan demonstrated
bilateral lesions of superior temporal gyrus. Neurological examination revealed
nothing particular except the troubles with hearing and speech. He was made a
diagnosis of auditory agnosia. The speech therapy was started at two years old.
During the first three years, he was taught how to communicate with gestures and lip
reading. However, it was difficult for him to understand the meaning of gestures and
lip reading. During these years he could acquire lip reading of simple words. As to
environmental sounds, he could respond the telephone-bell and the organ at three
years and seven months old, but could not discriminate other sounds. At five years
old, finger spelling for his language education was introduced. He appeared to have
learned finger spelling more easily and could read and write several letters through
finger spelling within a month. One year after introduction of finger spelling, he
acquired about 60 words (54 nouns and 6 verbs) and could read words and two-words
sentences. However, the speed of his acquisition of language was very slow for his
age. Now, he can understand mother's simple instructions and communicate with his
mother and his speech therapist through finger spelling, but his responses toward
environmental sounds are not stable yet. The course of this patient suggests that
language acquisition of children with auditory agnosia might be different from that
of deaf children. The prognosis of auditory agnosia in children is controversial.
In this patient, the development of language is not good as well as in most previous
reports, perhaps because of extensive lesions of language area. The patients with
auditory agnosia is frequently mistaken for deaf or mentally retarded children. We
emphasize that the early diagnosis and early speech therapy with visual
communication are needed for these children.

<3>  Ku A.  Lachmann EA.  Nagler W.
Selective language aphasia from herpes simplex encephalitis.
     Pediatric Neurology.  15(2):169-71, 1996 Sep.

<4>  Van Hout A.  Lyon G.
Wernicke's aphasia in a 10-year-old boy.
      Brain & Language.  29(2):268-85, 1986 Nov.
  We report the case of a ten-year-old boy, who, after herpes simplex encephalitis,
presented a sensory aphasia having much in common with Wernicke's aphasia in adults.
The genesis of neologisms appeared very similar to the mechanisms described by
Buckingham and Kertesz (1974, Brain and Language, 1, 43-61)...

<5>  Barbarotto R.  Capitani E.  Laiacona M.
Naming deficit in herpes simplex encephalitis.
     Acta Neurologica Scandinavica.  93(4):272-80, 1996 Apr.
OBJECTIVES--The preferential involvement of living categories in naming impairment
is well recognised in Herpes Simplex Encephalitis (HSE)... anatomo-functional
aspects of category dissociation...
CONCLUSION--Language impairment, disproportionately severe for the naming of living
exemplars, is frequently observed in HSE, is clinically relevant and should be
specifically investigated.

<6>  Ingles JL.  Mate-Kole CC.  Connolly JF.
Evidence for multiple routes of speech production in a case of fluent aphasia.
     Cortex.  32(2):199-219, 1996 Jun.
A case study is reported of a 24-year old woman who developed fluent aphasia with
superior reading relative to auditory comprehension following herpes simplex
encephalitis. Her language disturbance showed exceptional features: oral reading,
repetition and naming to confrontation were severely impaired and yet her
spontaneous speech recovered to be relatively intact. These features are not
consistent with Wernicke's aphasia, pure word deafness or any classic aphasic
syndromes. These findings indicate the presence of several routes for phonological
output that may be differentially impaired.

<7>  Erdem S.  Kansu T.
Alexia without either agraphia or hemianopia in temporal lobe lesion due to herpes
simplex encephalitis.
     Journal of Neuro-Ophthalmology.  15(2):102-4, 1995 Jun.

<8>  Luzzatti C.  Davidoff J.
Impaired retrieval of object-colour knowledge with preserved colour naming.
     Neuropsychologia.  32(8):933-50, 1994 Aug.
  Two cases (G.G. and A.V.) are described of cognitive impairment resulting from
herpes simplex infection. Both cases demonstrated anomic disorders and impairments
in drawing but only in G.G.'s drawings was there a reliable selective impairment for
items from natural categories. Both cases, however, showed an impairment for the
retrieval of knowledge concerning the colours of objects...

<9>  Massengill R Jr.  Weir W.  Lamb C.  Rosenfeld JA.
Anomia as a symptom of herpes simplex encephalitis.
     American Family Physician.  48(3):408, 413, 1993 Sep 1.

<10>  Sartori G.  Job R.  Miozzo M.  Zago S.  Marchiori G.
Category-specific form-knowledge deficit in a patient with herpes simplex virus
encephalitis.
     J of Clinical & Experimental Neuropsychology.  15(2):280-99, 1993
  In-depth case study of a herpes simplex virus encephalitis patient who presents
with a relatively clear knowledge disorder and anterograde amnesia in the absence
of any other major cognitive deficit. The main neuropsychological feature is a
category-specific impairment restricted to living things. The patient misnamed
pictures of animals and vegetables, could not accurately draw animals from memory
or verbally describe their visual appearance, and was not accurate in sorting
pictures of real animals from pictures of unreal animals... From this case study and
a review of other reported cases we claim that such deficit of form-knowledge is a
consequence of the extensive lesions that affect bilaterally the inferior parts of
the temporal lobes. The patient here described thus offers further empirical
evidence for the crucial role of the inferotemporal cortex in processing visual
knowledge about concepts.

<11>  Arlazoroff A.  Carpel CL.  Zonis H.  Goldenberg E.  Zekler E.
Incomplete Kluver-Bucy syndrome and fluent aphasia.
      Brain & Language.  23(2):300-6, 1984 Nov.
  A case of probable herpetic viral encephalitis is presented. The clinical picture
following the acute phase of disease was dominated by severe fluent aphasia,
prominent oral tendencies, visual agnosia, and a decrease in fear reactions. Most
of these symptoms, with the obvious exception of aphasia, are similar to those
observed by Kluver and Bucy in rhesus monkeys that underwent bitemporal lobectomy.
These manifestations may be explained by the tendency of the herpes simplex virus
to invade the temporal lobes. "Agnosia" in the auditory field and changes in vocal
behavior were observed by H. Kluver and P. C. Bucy (1939, Archives of Neurology and
Psychiatry, 42, 949-1000) in some of their bitemporal monkeys. The association of
sensory aphasia, as observed in this case, with the auditory "agnosia" observed in
some bitemporal monkeys, is discussed.                                            



      4 LKS & autism & virus
                                          >>> Posting number 24661, 
                                          dated 29 Sep 1997 13:05:49

These citations, abstracts, and comments delineate that HSV within the CNS can
induce seizures and other epileptiform patterns. Landau-Kleffner syndrome (LKS)
includes late-onset loss of language, often accompanied by seizures or other
epileptiform patterns. Now that increasing evidence implicates HSV in the etiologies
of many cases of seizures and in many cases of language impairment, questions for
researchers, doctors, and parents is: Are *some* cases of LKS actually a reflection
of an underlying HSV infection within the CNS? Would some (but *not all*) cases of
LKS respond to treatment with acyclovir or similar pharmaceuticals? Of particular
importance is that HSV can be active within the CNS, even while producing no
exterior, peripheral signs (10-12).

<1>  Cornford ME.  McCormick GF. Adult-onset temporal lobe epilepsy
associated with smoldering herpes simplex 2 infection. Neurology
48(2):425-30, 1997.
  A 40-year-old man with chronic genital herpes simplex infection developed partial
complex temporal lobe seizures of insidious onset, with EEG and MRI evidence of a
unilateral temporal lobe destructive, atrophic process. Extensive workup did not
reveal an infectious etiology. Three years of escalating number and severity of
daily seizures with memory loss led to temporal lobectomy. Histologic study revealed
active, low-level viral infection in the resected hippocampus and temporal lobe
cortex, with immunohistochemical evidence for infection by herpes simplex 2,
principally in neurons. In situ hybridization confirmed the presence of herpes
simplex virus in neurons. Anticonvulsant-resistant seizure episodes began to recur
several times daily soon after surgery, but the addition of acyclovir to the
treatment regimen resulted in a substantial reduction in seizure occurrence,
maintained for the subsequent 2.5 years.
        [I can't help but note how long this person waited until
         the HSV diagnosis was confirmed. The recent Archives of
         Neurology article (9) ought make this connection occur sooner
         in some patients.]

<2>  Jay V et al. Pathology of chronic herpes infection associated with
seizure disorder: a report of two cases with tissue detection of herpes
simplex virus 1 by the polymerase chain reaction. Pediatric Pathology &
Laboratory Medicine.  15(1):131-46, 1995.
  Although uncommon, the association of chronic encephalitis with epilepsy is well
recognized. While a viral etiology has been suspected based on the morphology, to
date no virus has been successfully cultured from the brain in patients with
Rasmussen's encephalitis...Thus our cases represent two examples of chronic
encephalitis associated with a seizure disorder, where a definitive viral etiology
was documented by PCR.
        [This study used tissue-samples, not CSF. Also, the kids were
         of the worst-case type, and thus a bit different from milder
         variations of HSV effects upon epileptiform activity and
         language.]

<3>  Weber T et al. Clinical implications of nucleic acid amplification
methods for the diagnosis of viral infections of the nervous system.
Journal of Neurovirology.  2(3):175-90, 1996 Jun.
  Amplification of viral nucleic acids from the cerebrospinal fluid (CSF) has
considerably improved the diagnosis of several acute, subacute and chronic viral
infections of the nervous system. In herpes simplex virus (HSV) encephalitis (HSE)
the polymerase chain reaction (PCR) has become the method of choice for the rapid,
non invasive diagnosis. Other herpes virus associated diseases which can now be
reliably diagnosed are encephalitis, ventriculoencephalitis, polymyeloradiculitis,
myelitis and an inflammatory polyradiculoneuropathy caused by cytomegalovirus (CMV),
HSV, varicella-zoster virus (VZV) or Epstein-Barr virus (EBV), EBV associated
primary B-cell-lymphoma of the brain, acute aseptic meningitis in young adults
allied with VZV, and meningoencephalitis with recurrent seizures due to human herpes
virus type 6 (HHV-6)...

<4>  O'Meara M.  Ouvrier R. Viral encephalitis in children. Current
Opinion in Pediatrics.  8(1):11-5, 1996.
  Knowledge about the role of viruses in encephalitis and other diseases of the
central nervous system has been greatly expanded since the advent of polymerase
chain reaction testing. It is known that the spectrum of disease caused by herpes
simplex virus, for example, is much wider than was previously recognized. Evidence
is mounting that infectious agents may have a causative role in diseases such as
recurrent febrile seizures and Rasmussen encephalitis. This review examines the
recent advances in treating viral encephalitis and puts these developments into
perspective.

<5>  Barthez-Carpentier MA et al. Relapse of herpes simplex encephalitis.
Journal of Child Neurology.  10(5):363-8, 1995 Sep.
  We report five children who had recurrent central nervous system signs after
conventional acyclovir therapy for herpes simplex encephalitis. Secondary
exacerbation was characterized clinically by severe ballismic movement disorder in
all five children, associated with fever, impairment of consciousness, and seizures.
Biologic analysis in all children and magnetic resonance imaging and neuropathology
studies of the brain in three cases were compatible with inflammatory reaction. In
contrast, all viral cultures remained negative, herpes simplex virus antigen in one
child and DNA tested by polymerase chain reaction in four children were undetectable
in the first samples of cerebrospinal fluid during the relapse, suggesting a
postinfectious, immune-mediated mechanism of relapse in these patients.
        [This is a most important study as we contemplate and research
         the role of viruses in autism and LKS, etc. In a conversation
         today, 9.28.97, Myron Levin, MD, a top-notch herpes researcher
         with extensive clinical-diagnostic experience, mentioned that
         PCR of CSF might show negative results if, in the person, the
         virus was totally latent within neurons at the time immediately
         preceeding the CSF sampling. Thus, another relapse possibility
         is viral activation.]

<6>  Jay V et al. Chronic encephalitis and epilepsy (Rasmussen's
encephalitis): detection of cytomegalovirus and herpes simplex virus 1 by
the polymerase chain reaction and in situ hybridization.
     Neurology.  45(1):108-17, 1995 Jan.
  We made a pathologic diagnosis of chronic encephalitis on surgical resections or
autopsy material in 10 patients with intractable seizures and studied the specimens
by immunohistochemistry for herpes simplex virus (HSV) 1 and 2 and cytomegalovirus
(CMV) as well as by the polymerase chain reaction (PCR) for viral DNA sequences
(HSV1, HSV2, and CMV). We also assessed eight patients (nonepileptic) with
pathologically documented or clinically suspected encephalitis and five resections
from epileptics without encephalitis. Immunohistochemistry for viral antigens was
negative in all cases. Using PCR assay, CMV was present in six and HSV1 in two of
10 epilepsy patients with chronic encephalitis. We demonstrated CMV by in situ
hybridization in two of the six patients positive for CMV by PCR. We found no viral
sequences by PCR in five epileptics without encephalitis. Of the eight patients
(nonepileptic) with clinically suspected or pathologically confirmed encephalitis,
two cases showed CMV sequences by PCR. These observations suggest that PCR allows
detection of viral sequences in some cases of chronic encephalitis associated with
epilepsy that may be missed by in situ hybridization.       
      [Again we note that the researchers were using tissue samples,
         which was justified due to the severity of the cases.]

<7>  Jones CM et al. Acute encephalopathy and status epilepticus
associated with human herpes virus 6 infection.
     Developmental Medicine & Child Neurology.  36(7):646-50, 1994 Jul.
  A previously healthy 22-month-old boy presented in status epilepticus with high
fever. He was comatose, with upper respiratory-tract infection. The seizures
responded to anticonvulsant therapy. The boy's temperature returned to normal within
24 hours and he recovered slowly from his encephalopathy. On the third hospital day,
he exhibited the characteristic rash of reseola infantum. Acute infection with human
herpes virus 6 (HHV-6) was established serologically by enzyme immunoassay. HHV-6
DNA was not detected by polymerase chain reaction in CSF or serum at the onset of
illness, but was found three months later in the child's saliva. The pathogenesis
of the patient's encephalopathy is discussed. It is concluded that HHV-6 infection
should be considered in infants and young children with febrile status epilepticus.

<8>  Holmes GL.  Lombroso CT. Prognostic value of background patterns in
the neonatal EEG. J of Clinical Neurophysiology.  10(3):323-52, 1993.
  The prognostic value of background activity in the neonatal EEG has been well
established. Whereas in older children the neonatal EEG is useful in the diagnosis
of seizures, in neonates the test also provides a particularly valuable assessment
of cerebral functioning following a variety of insults... Although abnormalities on
the neonatal EEG are not specific for diagnosis, certain EEG patterns may be highly
suggestive for the diagnosis of pyridoxine dependency and neonatal herpes
encephalitis. In both term and preterm infants, the prognostic value of the neonatal
EEG is increased by performing serial studies.

<9>   Sanders VJ et al. Presence of herpes simplex DNA in surgical tissue
from human epileptic seizure foci detected by polymerase chain reaction:
preliminary study. Archives of Neurology 54.8.954-60 1997 (August).
<10>  Whitley RJ, Lakeman F. Herpes simplex virus infections of the
central nervous system: therapeutic and diagnostic considerations.
Clinical Infectious Diseases 20.414-20 1995.
<11>  Kimura H et al. Detection of viral DNA in neonatal herpes simplex
virus infections: frequent and prolonged presence of serum in
cerebrospinal fluid. J Infectious Diseases 164.289-93 1991.
<12>  Domingues RB et al. Evaluation of the range of clinical presentations of
herpes simplex encephalitis by using polymerase chain reaction of cerebrospinal
fluid samples. Clinical Infectious Diseases 25.86-91 1997.



.....CONCLUSION.....

These series of posts, their comments, and citations addressed two issues:    
1. ARE SOME CASES OF LKS CAUSED BY HSV WITHIN THE CNS?
2. OUGHT DIAGNOSTICS & INITIAL TREATMENTS BE CHANGED IN LKS?

In my opinion, the answer to each question is Yes. In other words, some cases of LKS
are likely to be caused by subacute, intra-neuronal HSV within the CNS; and
diagnostics and initial treatments ought be modified so as to include the HSV/CNS
possibility. 
      The anecdotes about Acyclovir (an anti-HSV pharmaceutical) are significant;
acyclovir helps some kids with language loss and helps in some cases of seizures.
Furthermore, treatments with steroids (an immuno-suppressant) would not only help
suppress HSV-caused inflammation but, in the long run, would allow HSV to achieve
maximum destruction. As a result, while steroids are helpful in the early stages,
that helpfulness may be masking and even contributing to subsequent deterioration. 
      A better diagnostic protocol would include either an initial (pre-steroid)
trial with Acylcovir. If rapid improvement was noted, then steroids become contra-
indicated for that child; if no rapid improvement is noted, then HSV is not likely
to be the underlying cause and other treatment options can be initiated. 

                                *       *       *

Tc: Most but not all strains of HSV respond to Acyclovir. However, PCR of CSF or of
brain-tissue is highly unlikely circa 1999 and the next several years.POSTING HISTORY

>>> Posting number 24646, dated 29 Sep 1997 12:07:16
Sender:       SJU Autism and Developmental Disablities List
              
From:         Teresa Binstock
Subject:      1 LKS & autism & virus

>>> Posting number 24649, dated 29 Sep 1997 12:23:52
Sender:       SJU Autism and Developmental Disablities List
              
From:         Teresa Binstock 
Subject:      Re: 2 LKS & autism & virus

>>> Posting number 24657, dated 29 Sep 1997 12:50:00
Sender:       SJU Autism and Developmental Disablities List
              
From:         Teresa Binstock
Subject:      Re: 3 LKS & autism & virus

>>> Posting number 24661, dated 29 Sep 1997 13:05:49
Sender:       SJU Autism and Developmental Disablities List
              
From:         Teresa Binstock 
Subject:      4 LKS & autism & virus