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Epil=
eptic
myoclonus and progressive myoclonus
epilepsy
Jayant N. Acharya, M.D., D.M.
Department of Neurology
Wake Forest University Baptist Medical Center, Winston-Salem, NCIntroduction - Myoclonus
•Definition: Sudden, brief, shocklike, involuntary movements caused by muscular contractions or inhibitions (Fahn et al 1986)
=
• Origin: CNS, ? PNS
•Recent adv=
ances
in techniques have led to a better
understanding of physiology
•Bridges fields of epilepsy and movement disorders <=
/span>
History
Classification
&#=
8226;Clinical:
&=
#8211;Focal,
multifocal, segmental, generalized
&=
#8211;Stimulus
sensitive/insensitive
&=
#8211;Rest/action/intention
&=
#8211;Positive/negative
&#=
8211;Isolated,
rhythmic, periodic, irregular
Classification
•Etiologic (Fahn et al 1986):
–Ph=
ysiologic:
Hypnic jerks, anxiety, exercise, hiccups,
benign infantile myoclonus with feeding
–E=
ssential:
Hereditary, sporadic
–<=
b>Epileptic
–Sy=
mptomatic:
Storage diseases, spinocerebellar degeneration,
basal ganglia diseases, dementias, viral,
toxic, metabolic and physical encephalo-pathies, and focal CNS damage
Classification
•P=
hysiologic:
–Halliday (1967): Pyramidal, extrapyramidal, segmental
–Hallett (1985): Epileptic (cortical reflex, reticu=
lar reflex, prim. gen. epileptic), nonepileptic
–S=
hibasaki
(1996): Cortical, subcortical, spinal
–I=
LAE
(1997): Epileptic (cortical, thalamocortical, negative), nonepileptic (reticular reflex)<=
span
style=3D'mso-spacerun:yes'>
Investigations
&#=
8226;Electrophysiology:
&=
#8211;EEG
&=
#8211;Polygraphy:
EEG + EMG
&=
#8211;Jerk-locked
back averaging (JLBA)
&=
#8211;Somatosensory
evoked potentials (SSEP)
&=
#8211;Long
latency reflex (LLR): C reflex
&=
#8211;Silent
period
Investigations
&#=
8226;Others:
&=
#8211;Magnetoencephalography
(MEG)
&=
#8211;Magnetic
source imaging (MSI)
&=
#8211;Transcranial
magnetic stimulation (TMS)
&=
#8211;SPECT/PET
Cortical myoclonus
•Spontaneous/reflex, focal/generalized, rarely rhythmic (DD: tremor)
•Due to hyperexcitability of the sensorimotor cortex
•EMG: Abrupt onset, brief duration (20-60 ms), both agonist and antagonist, rostrocaudal lag
=
•JLBA: EEG spike precedes EMG discharge by 20 ms for hand (similar to MEP with TMS), =
localized to contralateral central area
Cortical myoclonus <=
span
style=3D'position:absolute;top:17.75%;left:8.42%;width:83.14%;height:9.25%=
'>(continued)
Thalamocortical myoclonus
•Similar to cortical but, from animal studies, reticular substance of thalamus generates <=
/span>rhythmicity of the hyperexcitable =
thalamocortical loop which produces =
generalized spikes mainly in the motor strip. Spikes follow same pathway as that of CM and produce a generalized jerk
• Etiology: Idiopathic generalized epilepsy
Reticular reflex myoclonus
•Proximal, often bila=
teral,
face involved but hands rare
•Due to hyperexcitabi=
lity
of caudal reticular formation
•EMG: 80-3=
30 ms,
polyphasic, single muscle or agonists + antagonist, bulbar to rostrocaudal l=
ag
Reticular reflex myoclonus =
(continued)
•JLBA: EEG spike n=
ot
time-locked to EMG, may follow EMG discharge
• No giant
SSEP
• LLR is
enhanced
•Etiology:
Post-anoxic, PME, uremic, startle, hyperekplexia, brainstem
infarct
Negative myoclonus
•History: Adams &=
Foley
(1949), Lance & Adams (1963), Shahani & Young
(1976)
•Inhibition
of muscular activity: Lapses interrupting continuous activity wh=
en maintaining
anti-gravity posture
•Gen/focal, isolated/combined with positive
myoclonus
• EMG: Sile=
nt
period
Negative myoclonus <=
span
style=3D'position:absolute;top:17.75%;left:8.42%;width:83.14%;height:9.25%=
'>(continued)
•EEG: related to slow=
wave
of spike-wave/positive component of polyspike
•TMS: cort=
ex -
response inhibited during myoclonus, cord - normal
excitability
•Origin: C=
ortical
(precentral vs. postcentral), subcortical
•Etiology:
Physiologic, asterixis, postural lapses (post hypoxic),
epileptic
Spinal myoclonus
=
226;Oligosegmental:
limited to muscles innervated by a few adjacent segments. Usually
rhythmic, slow.
R=
26;Plurisegmental
(propriospinal): muscles innervated by multiple segments. Rhythmic/
arrhythmic, spontaneous/stimulus-sensitive, axial +/-
limbs but no cranial muscles
Spinal myoclonus (continued)
=
211;EMG:
midthoracic generator-->up and down cord via slowly
conducting (3-11M/s) pathways
=
226;No
EEG correlate, giant SSEP or LLR enhancement
R=
26;Etiology:
Tumor, infection, trauma, ischemia, MS, unknown
Epileptic myoclonus
•Myoclonus in combina=
tion
with cortical epileptiform discharges which, in some <=
span
style=3D'position:absolute;top:44.25%;left:12.17%;width:86.89%;height:6.75=
%'>cases,
may be demonstrated only by back-averaging (IL=
AE
1997).
•Includes
cortical, thalamocortical and negative but not reticular
reflex/spinal.
•Cortical
and reticular reflex myoclonus may coexist in the same
patient
Epileptic myoclonus
&#=
8226;Differential
diagnosis:
&=
#8211;Nonmyoclonic
seizures: Spasms, tonic
–Nonepileptic
myoclonus: Opsoclonus-myoclonus, sleep, startle,
hyperekplexia
=
211;Nonepileptic,
nonmyoclonic: Tremor (cortical tremor, palatal), tics,
chorea, psychogenic
Epileptic myoclonus
&#=
8226;Etiology:
–Symptomatic:
Anoxia, head trauma, tumor, metabolic, degenerative, stroke, vira=
l infections
&=
#8211;Idiopathic
&=
#8211;Cryptogenic
Epileptic myoclonus
&#=
8226;Positive
myoclonus:
&=
#8211;Progressive
encephalopathies (cortical):
&=
#8226;Progressive
myoclonus epilepsy
&#=
8226;Rasmussen
disease (epilepsia partialis continua - EPC):
&#=
8211;Myoclonic
jerks arise from depths of Rolandic sulcus.
–Focal
seizures distinct from jerks arise from cortical surface.
Epilepsia Partialis Continua
•R=
asmussen
disease
–O=
nset:
2-10 years (peak 6)
–P=
artial
motor seizures, myoclonus
–P=
rogressive
motor deficit
–M=
ental
retardation
–EEG: Abnormal background, asymmetric, focal slow, spikes
–A=
natomical
lesion diffuse and progressive
–E=
tiology:
May be viral
–H=
emispherectomy,
plasmapheresis, IVIG =
Epileptic myoclonus
&#=
8226;Positive
myoclonus
–Nonprogressive:
Idiopathic generalized epilepsy (thalamocortical)
&=
#8226;Only/mainly
myoclonic:
–Benign
myoclonic epilepsy of infancy: Associated with GTCS in adolescence
–Juvenile
myoclonic epilepsy (JME):
Associated with GTCS, absence.
=
211;Both:
Generalized myoclonus with generalized spikes/polyspikes on EEG.
<=
/div>
Benign Myoclonic
•Generalized myoclonu=
s in
first or second year
• Otherwise
normal
•Family hi=
story of
epilepsy may be present
•EEG: Generalized
spike-waves, early stages of sleep
• Easily co=
ntrolled
with valproate
Juvenile Myoclonic Epilepsy
Epileptic myoclonus
=
211;Nonprogressive:
Idiopathic generalized epilepsy (continued)
&=
#8226;Myoclonic
absence: Positive + negative
&=
#8226;Severe
myoclonic epilepsy of infancy (SMEI):
&#=
8211; Alternating convulsive seizures in=
1st
year
&#=
8211;Later,
massive myoclonus with EEG SWC
•Myoclonic astatic epilepsy - MAE (Doose, Dravet):
Gen myoclonus + other seizures
&=
#8211;Favorable:
Myo + GTCS + Abs (2/3) + tonic (1/3)
&=
#8211;Unfavorable:
Like LGS but earlier onset, more myo
Epileptic myoclonus
&#=
8226;Positive
myoclonus:
&=
#8211;Congenital
nonprogressive encephalopathy
&=
#8226;Nonspecific:
Malformations, chromosomal
&#=
8226;Angelman
syndrome: Continuous tremulous jerking of distal and fa=
cial
muscles with motor cortex spiking on JLBA
–Neonatal
myoclonic encephalopathy: Myoclonus with burst-suppression on E=
EG
Epileptic myoclonus
&#=
8226;Positive
myoclonus:
&=
#8211;Myoclonic
status:
&=
#8226;SMEI,
MAE, non-progressive encephalopathy
&#=
8226;Myoclonus
of face and extremities with obtundation
&=
#8226;EEG:
Diffuse slow/spikes
&=
#8226;SPECT:
Decreased cerebral blood flow
Epileptic myoclonus
&#=
8226;Negative
myoclonus
=
211;Definition:
Interruption of tonic muscular activity, time-locked to a
spike/sharp wave on EEG, without antecedent myoclonia (Tassinari
et al 1995)
&=
#8211;May
originate from various cortical areas&nbs=
p;
–Generalized:
cryptogenic (myoclonic absence), symptomatic (post-hypoxic)=
Epileptic myoclonus
&#=
8226;Negative
myoclonus
–Focal:
Lesion, partial benign epilepsy (continuous spikes during s=
low
sleep)
=
211;EEG:
Correlated with slow wave of SWC or positive transient of
polyspike
Genetics
=
226;Benign
myoclonic epilepsies with a defined chromosomal locus:
&=
#8211;AD
JME: 6p11
&=
#8211;HLA
associated JME: 6p21.3
&=
#8211;AD
CAE-->JME: 1p
&=
#8211;JME
within IGE susceptibility gene: 8
Genetics
=
226;Genetically
complex (multiple loci +/- environmental factors):
<=
/div>
&=
#8211;Onset
in 1st year: BMEI, SMEI
&=
#8211;Onset
early childhood: MAE &=
#13;
&=
#8211;Onset
late childhood: Myoclonic absence
&#=
8226;Progressive
myoclonus epilepsy:
–Rapid
progress: Most AR, fully penetrant, characteristic pathology
Therapy of myoclonus
&#=
8226;Helpful
drugs:
&=
#8211;Valproic
acid (1200-3000 mg): BMEI, JME
–Benzodiazepines:
Clonazepam, nitrazepam: IGE, reflex, focal dysplasia
&=
#8211;Ethosuximide:
MAE, ENM
=
211;Piracetam
(0.1-0.2 g/kg): Unknown mechanism, PME, post-anoxic,
Angelman
&=
#8211;5-HTP:
Post-anoxic, reticular reflex
&=
#8211;Acetazolamide
Therapy of myoclonus
&#=
8226;Helpful
drugs (continued):
&=
#8211;Zonisamide
(100-600 mg/kg): ULD
–Lamotrigine:
PME, JME, MAE; may worsen SMEI
&=
#8211;N-acetyl
cysteine: ULD
&=
#8211;TRH
&=
#8211;Stiripentol:
SMEI
&=
#8211;Primidone
(0.5-1g): Post-anoxic, PME
Therapy of myoclonus
&#=
8226;Helpful
drugs (continued):
&=
#8211;Lisuride
(IV): Cortical
&=
#8211;Sinemet,
fluoxetine, paroxetine: Reticular
&=
#8211;Baclofen,
tetrabenazine: Spinal
&#=
8226;Polytherapy
often needed
&#=
8226;Drugs
to be avoided:
&=
#8211;CBZ,
VGB, PHT
&#=
8226;Surgery
Treatment strategy for epileptic
myoclonus
=
226;Start
with VPA &/or BZ, avoid CBZ, PHT
&#=
8226;Obtain
a specific etiologic diagnosis:
=
211;Partial
nonprogressive lesion: BZ, VPA not helpful
&=
#8211;Rasmussen:
Steroids, PP, IVIG, surgery
&=
#8211;Partial-->sec
gen, CSWS: BZ, steroids
&=
#8211;IGE:
VPA
Treatment strategy for epileptic
myoclonus
&=
#8226;BMEI:
VPA+ESM
&=
#8226;JME:
BZ, LTG, PB
&=
#8226;MAE:
VPA+LTG
&#=
8211;SMEI:
VPA+BZ, stiripentol+clobazam
&=
#8211;Myoclonic
absence: VPA+ESM+LTG
–Nonprog
encephalopathies: VPA+BZ, Angelman: piracetam
=
211;Myoclonic
status: resistant; try VPA, BZ, steroids
Progressive myoclonus epilepsy
&#=
8226;Definition:
&=
#8211;Myoclonus
&=
#8211;Generalized
tonic-clonic seizures
&=
#8211;Progressive
neurologic dysfunction
&=
#8226;Dementia
&=
#8226;Ataxia
PME=
VERSUS PMA
=
;
PME
Myoclonus=
Ataxia &#=
13;
Dementia&=
#13;
Generaliz=
ed
tonic-clonic seizures•PMA
•
Myoclonus=
Ataxia=
3;
Little or=
no
dementia
seizures =
;
Progressive myoclonus epilepsy
&#=
8226;Main
causes:
&=
#8211;Lafora
disease (LD)
&=
#8211;Unverricht-Lundborg
disease (ULD)
&=
#8211;Neuronal
ceroid lipofuscinoses (NCL)
–Myoclonic
epilepsy with ragged-red fibres (MERRF)
&=
#8211;Sialidoses
Progressive myoclonus epilepsy
•Rare causes:
–DRPLA
–Noninfantile neuronopathic Gaucher’s
=
–Late onset Lafora disease
–Atypical inclusion body disease
–Action myoclonus-renal failure
–Neuroaxonal dystrophy
–Atypical GM2 gangliosidosis
RAMSAY HUNT SYNDROME
<=
span
style=3D'mso-special-format:bullet;position:absolute;left:-4.29%'>•<=
/span>Confusing
term, used inappropriately
<=
span
style=3D'mso-special-format:bullet;position:absolute;left:-4.39%'>•<=
/span>Does
not apply to a specific disease
•<=
/span>MERRF,
ULD, spinocerebellar degeneration
•<=
/span>Marseille
Consensus Group (1990): discard term, use PMA instead=
DISTRIBUTION
ELECTROPHYSIOLOGY GENERAL FINDINGS
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Epileptic myoclonus and progressive myoclonus epilepsy
•<=
/span>Vertex
positive spikes (sialidosis)
•Activation
in non-REM sleep (sialidosis, late infantile and juvenile
NCL)
•Photosensitivity to single flashes ( l=
ate infantile
and adult NCL)
•Absent ERG (late infantile and
juvenile NCL)
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Epileptic myoclonus and progressive myoclonus epilepsy
•<=
/span>Common:
Mediterranean, India
•<=
/span>Onset:
6-20 years
•<=
/span>Early
GTC, severe dementia
•<=
/span>“Occipital
seizures”: 50%
•<=
/span>Behavioral
changes frequent
•<=
/span>Death
2-10 years after onset
•<=
/span>Variations
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Epileptic myoclonus and progressive myoclonus epilepsy
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Epileptic myoclonus and progressive myoclonus epilepsy
• AR,
consanguinity
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Epileptic myoclonus and progressive myoclonus epilepsy
•<=
/span>Onset:
6-16 years
•<=
/span>Prominent
myoclonus, mild dementia
•<=
/span>Behavioral
changes
•<=
/span>No
visual symptoms or signs
•<=
/span>Variable
course, usually mild, many survive to old age
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Epileptic myoclonus and progressive myoclonus epilepsy
•EEG:
&=
#8211;Progressive
background slowing
&=
#8211;Generalized
spikes or polyspikes
&=
#8211;Photosensitivity
&=
#8211;Focal,
especially occipital discharges
=
211;Non-REM
sleep disorganized,discharges decreased
•Evoked potentials:
&=
#8211;Giant SSEPs, normal VEPs/BAEPs <=
/div>
ELECTROPHYSIOLOGY SPECIFIC
FINDINGS
LAFORA DISEASE: CLINICAL
<=
span
style=3D'mso-special-format:bullet;position:absolute;left:-4.42%'>•<=
/span>Visual
loss with normal optic fundus
LAFORA DISEASE: PATHOLOGY
Lafora
body:
&=
#8211;Sites
and types: brain, liver, skin, muscle
&=
#8211;Chemical
nature: polyglucosans
&=
#8211;LM:
PAS positive, diastase resistant
–EM:
granular and filamentous, no limiting membrane
&=
#8211;Atypical
inclusions
&=
#8211;Significance
and specificity
Lafora disease - Genetics
<=
span
class=3DBB style=3D'position:absolute;left:-4.5%'>•Gene (E=
PM2)
localized to chr 6q24
<=
span
class=3DBB style=3D'position:absolute;left:-3.93%'>•Encodes a=
protein
tyrosine phosphatase
•Mutations:
deleterious effects in putative protein product - laforin/
LAFPTPase
•?Imbalance
between glycogen synthase and branching enzyme activities
=
<=
span
class=3DBB style=3D'position:absolute;left:-4.09%'>•Genetic
heterogeneity (20%), ? clinical
Lafora disease - Genetics
&#=
8226;LD
in South India
<=
/div>
&=
#8211;Consanguinity
common in South India
&=
#8211;Karnataka:
33.1%
&=
#8211;Hindus>Muslims>Christians
–Hindus:
Uncle-niece, Muslims: First cousins
&=
#8211;Our
series (Acharya et al 1993):
&=
#8226;Consanguinity:
86.6%
&=
#8226;Majority
Hindus from Karnataka
Lafora disease - Genetics
=
226;Clinical
heterogeneity (Acharya et al 1995):
&=
#8211;3
families with multiple affected siblings
&#=
8226;Visual
and behavioral changes in all 3 members of 1 family but =
in
none of the other families
•Age of onset variable between but similar withi=
n 2
families
•Single seizure several years before onset of LD=
in
1 family
ULD: CLINICAL
<=
span
style=3D'mso-special-format:bullet;position:absolute;left:-3.96%'>•<=
/span>Worldwide,
esp. Finland, Mediterranean
ULD - Genetics
&#=
8226;AR
&#=
8226;Gene
(EPM1) localized to chr 21q22.3
&#=
8226;Encodes
cystatin B
&=
#8211;Member
of cysteine protease inhibitors
–Function:
inactivate proteases leaking from lysosomes,
Epileptic myoclonus and progressive myoclonus epilepsy
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Epileptic myoclonus and progressive myoclonus epilepsy
•<=
/span>Worldwide
•<=
/span>Onset:
3 - 65 years
•<=
/span>Other
features: deafness, myopathy, neuropathy, optic atrophy,
lipomas, stroke
•Marked intra and
interfamily variation in age of onset and severity
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Epileptic myoclonus and progressive myoclonus epilepsy
•<=
/span>Familial
or sporadic
•<=
/span>Mitochondrial
inheritance
•<=
/span>Single
base substitution at bp 8344 of mtDNA causing A ---> G
substitution in tRNA gene in most but not all familial <=
span
style=3D'position:absolute;top:68.25%;left:12.17%;width:79.4%;height:6.75%=
'>and
some sporadic cases
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Epileptic myoclonus and progressive myoclonus epilepsy
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{
if(g_supportsPPTHTML) return document.all(id);
else return document.getElementById(id);
}
function SldHasTrans() { return SlideObj.style.filter !=3D ""; }
function GetSldId() { return sId=3Dlocation.href.substring(location.href.la=
stIndexOf('/')+1) }
function HideMenu() { if( frames["PPTSld"] && PPTSld.document.all.item("ctx=
tmenu") && PPTSld.ctxtmenu.style.display!=3D"none" ) { PPTSld.ctxtmenu.styl=
e.display=3D'none'; return true } return false }
function IsWin( name ) { return window.name =3D=3D name }
function IsNts() { return IsWin("PPTNts") }
function IsSldOrNts() { return( IsWin("PPTSld")||IsWin("PPTNts") ) }
function SupportsPPTAnimation() { return( navigator.platform =3D=3D "Win32"=
&& navigator.appVersion.indexOf("Windows")>0 ) }
function SupportsPPTHTML()
{
var appVer=3Dnavigator.appVersion, msie=3DappVer.indexOf("MSIE "), ver=3D0
if( msie >=3D 0 )
ver=3DparseFloat( appVer.substring( msie+5, appVer.indexOf(";",msie) ) )
else
ver=3DparseInt(appVer)
return( ver >=3D 4 && msie >=3D 0 )
}
function _RSW()
{
if( !g_supportsPPTHTML || IsNts() ||
( !g_scaleInFrame && (!IsWin("PPTSld") || !parent.IsFullScrMode()) ) )
return
var padding=3D0;
if( IsWin("PPTSld") && parent.IsFramesMode() ) padding=3D6
cltWidth=3Ddocument.body.clientWidth-padding
cltHeight=3Ddocument.body.clientHeight-padding
factor=3D(1.0*cltWidth)/g_origW
if( cltHeight < g_origH*factor )
factor=3D(1.0*cltHeight)/g_origH
newSize =3D g_origSz * factor
if( newSize < 1 ) newSize=3D1
s=3DSlideObj.style
s.fontSize=3DnewSize+"px"
s.posWidth=3Dg_origW*factor
s.posHeight=3Dg_origH*factor
s.posLeft=3D(cltWidth-s.posWidth+padding)/2
s.posTop=3D(cltHeight-s.posHeight+padding)/2
if( g_scaleHyperlinks )
ScaleHyperlinks( factor )
}
function _InitAnimations()
{
animRuntimeInstalled =3D ''+document.body.localTime !=3D 'undefined';
isFullScreen =3D (window.name =3D=3D "PPTSld") && !parent.IsFramesMode();
g_animUseRuntime =3D g_showAnimation && animRuntimeInstalled && !(isFullSc=
reen && parent.IsSldVisited());
if( g_animUseRuntime ) {
collSeq =3D document.all.tags("seq");
if( collSeq !=3D null ) {
for(ii=3D0;ii numSlds )
gSldJumpIdx =3D numSlds;
if ( gSldJumpIdx >=3D 0 ) {
if ( gSldJumpIdx =3D=3D 0 )
gSldJumpIdx =3D 1;
var jumpTo =3D parseInt(gSldJumpIdx);
gSldJump =3D 0; gSldJumpIdx =3D "";
win.GoToSld( parent.GetSldList().mList[jumpTo-1].mSldHref )
}
}
}
function _KDH()
{
if( event.keyCode =3D=3D 8 ) {
event.returnValue =3D 0;
parent.GoToPrevSld();
}
}
function DocumentOnClick()
{
if( IsNts() || parent.HideMenu() ) return;
if( ( g_allowAdvOnClick && !parent.IsFramesMode() ) ||
(event && (event.keyCode=3D=3D32) ) )
parent.GoToNextSld();
}
var g_supportsPPTHTML =3D SupportsPPTHTML(), g_scaleInFrame =3D 1, gId=3D""=
, g_bgSound=3D"",
g_scaleHyperlinks =3D false, g_allowAdvOnClick =3D 1, g_showInBrowser =
=3D 0, gLoopCont =3D 0, gUseSldTimings =3D 1;
var g_showAnimation =3D g_supportsPPTHTML && SupportsPPTAnimation() && ( (w=
indow.name=3D=3D"PPTSld" && !parent.IsFramesMode()) || g_showInBrowser );va=
r g_animManager =3D null;
var g_animUseRuntime =3D false;
var g_animItemsToHide, g_animInteractiveItems, g_animSlideTime;
var g_animMainSequence =3D null;
var ENDSHOW_MESG=3D"End of slide show, click to exit.", SCREEN_MODE=3D"Fram=
es", gIsEndShow=3D0, NUM_VIS_SLDS=3D65, SCRIPT_HREF=3D"script.js", FULLSCR_=
HREF=3D"fullscreen.htm";
var gCurSld =3D gPrevSld =3D 1, g_offset =3D 0, gNtsOpen =3D gHasNts =3D gO=
tlTxtExp =3D 0, gHasNarration =3D 0, gOtlOpen =3D true
window.gPPTHTML=3DSupportsPPTHTML()
var gMainDoc=3Dnew Array(new hrefList("slide0001.htm",1,-1,1),new hrefList(=
"slide0002.htm",1,-1,1),new hrefList("slide0060.htm",1,-1,1),new hrefList("=
slide0004.htm",1,-1,1),new hrefList("slide0006.htm",1,-1,1),new hrefList("s=
lide0005.htm",1,-1,1),new hrefList("slide0007.htm",1,-1,1),new hrefList("sl=
ide0032.htm",1,-1,1),new hrefList("slide0008.htm",1,-1,1),new hrefList("sli=
de0013.htm",1,-1,1),new hrefList("slide0009.htm",1,-1,1),new hrefList("slid=
e0010.htm",1,-1,1),new hrefList("slide0033.htm",1,-1,1),new hrefList("slide=
0011.htm",1,-1,1),new hrefList("slide0025.htm",1,-1,1),new hrefList("slide0=
058.htm",1,-1,1),new hrefList("slide0059.htm",1,-1,1),new hrefList("slide00=
14.htm",1,-1,1),new hrefList("slide0015.htm",1,-1,1),new hrefList("slide004=
7.htm",1,-1,1),new hrefList("slide0016.htm",1,-1,1),new hrefList("slide0052=
.htm",1,-1,1),new hrefList("slide0017.htm",1,-1,1),new hrefList("slide0053.=
htm",1,-1,1),new hrefList("slide0054.htm",1,-1,1),new hrefList("slide0035.h=
tm",1,-1,1),new hrefList("slide0018.htm",1,-1,1),new hrefList("slide0038.ht=
m",1,-1,1),new hrefList("slide0019.htm",1,-1,1),new hrefList("slide0036.htm=
",1,-1,1),new hrefList("slide0084.htm",1,-1,1),new hrefList("slide0085.htm"=
,1,-1,1),new hrefList("slide0022.htm",1,-1,1),new hrefList("slide0023.htm",=
1,-1,1),new hrefList("slide0024.htm",1,-1,1),new hrefList("slide0027.htm",1=
,-1,1),new hrefList("slide0037.htm",1,-1,1),new hrefList("slide0051.htm",1,=
-1,1),new hrefList("slide0055.htm",1,-1,1),new hrefList("slide0056.htm",1,-=
1,1),new hrefList("slide0057.htm",1,-1,1),new hrefList("slide0061.htm",1,-1=
,1),new hrefList("slide0062.htm",1,-1,1),new hrefList("slide0063.htm",1,-1,=
1),new hrefList("slide0064.htm",1,-1,1),new hrefList("slide0065.htm",1,-1,1=
),new hrefList("slide0066.htm",1,-1,1),new hrefList("slide0067.htm",1,-1,1)=
,new hrefList("slide0068.htm",1,-1,1),new hrefList("slide0069.htm",1,-1,1),=
new hrefList("slide0070.htm",1,-1,1),new hrefList("slide0071.htm",1,-1,1),n=
ew hrefList("slide0072.htm",1,-1,1),new hrefList("slide0073.htm",1,-1,1),ne=
w hrefList("slide0074.htm",1,-1,1),new hrefList("slide0075.htm",1,-1,1),new=
hrefList("slide0076.htm",1,-1,1),new hrefList("slide0077.htm",1,-1,1),new =
hrefList("slide0078.htm",1,-1,1),new hrefList("slide0079.htm",1,-1,1),new h=
refList("slide0080.htm",1,-1,1),new hrefList("slide0081.htm",1,-1,1),new hr=
efList("slide0082.htm",1,-1,1),new hrefList("slide0083.htm",1,-1,1),new hre=
fList("slide0086.htm",1,-1,1));
/*********************************************
Frameset functions
These functions control slide navigation
and state of the frameset.
**********************************************/
function FullScrInit()
{
g_allowAdvOnClick =3D GetCurSld().mAdvOnClk
document.body.style.backgroundColor=3D"black"
document.oncontextmenu=3Dparent._CM;
document.onkeydown =3D _KDH;
document.ondragstart=3DCancel
document.onselectstart=3DCancel
self.focus()
}
function Redirect( frmId )
{=09
var str=3Ddocument.location.hash,idx=3Dstr.indexOf('#'), sId=3DGetSldId()
if(idx>=3D0) str=3Dstr.substr(1);
if( window.name !=3D frmId && ( sId !=3D str) ) {
obj =3D GetObj("Main-File")
window.location.href=3Dobj.href+"#"+sId
return 1
}
return 0
}
var MHTMLPrefix =3D CalculateMHTMLPrefix();=20
function CalculateMHTMLPrefix()
{
if ( document.location.protocol =3D=3D 'mhtml:') {=20
href=3Dnew String(document.location.href)=20
Start=3Dhref.indexOf('!')+1=20
End=3Dhref.lastIndexOf('/')+1=20
if (End < Start)=20
return href.substring(0, Start)=20
else=20
return href.substring(0, End)=20
}
return '';
}
function GetTags(base,tag)
{
if(g_supportsPPTHTML) return base.all.tags(tag);
else return base.getElementsByTagName(tag);
}
function UpdNtsPane(){ if(frames["PPTNts"]) PPTNts.location.replace( MHTMLP=
refix+GetHrefObj( gCurSld ).mNtsHref ) }
function UpdNavPane( sldIndex ){ if(gNavLoaded) PPTNav.UpdNav() }
function UpdOtNavPane(){ if(gOtlNavLoaded) PPTOtlNav.UpdOtlNav() }
function UpdOtlPane(){ if(gOtlLoaded) PPTOtl.UpdOtl() }
function SetHasNts( fVal )
{
if( gHasNts !=3D fVal ) {
gHasNts=3DfVal
UpdNavPane()
}
}
function ToggleOtlText()
{
gOtlTxtExp=3D!gOtlTxtExp
UpdOtlPane()
}
function ClearMedia()
{
// Clear any sounds playing before launching another browser window. Other=
wise,
// in fullscreen mode, you'll continue to hear the sound in the frames mod=
e.
if (PPTSld.pptSound) PPTSld.pptSound.loop =3D 0;
}
function FullScreen()
{=20
if ( PPTSld.g_animUseRuntime )
PPTSld.document.body.pause();
ClearMedia();
var href =3D ( document.location.protocol =3D=3D 'mhtml:') ? FULLSCR_HREF =
: FULLSCR_HREF+"#"+GetHrefObj(gCurSld).mSldHref;
if(PPTNav.event.ctrlKey) {
var w =3D (window.screen.availWidth * 1.0) / 2.0
var h =3D w * (PPTSld.g_origH * 1.0) / PPTSld.g_origW
win =3D window.open( MHTMLPrefix+href,null,"toolbar=3D0,resizable=3D1,top=
=3D0,left=3D0," + "width=3D"+ w + ",height=3D" + h );
if( win.document.body && PPTSld.g_animUseRuntime )
win.document.body.PPTSldFrameset=3Dwindow;
}
else
{
win =3D window.open( MHTMLPrefix+href,null,"fullscreen=3Dyes" );
if( win.document.body && PPTSld.g_animUseRuntime )
win.document.body.PPTSldFrameset=3Dwindow;
}
}
function ToggleVNarration()
{
rObj=3DPPTSld.document.all("NSPlay")
if( rObj && !PPTSld.g_animUseRuntime ) {
if( (rObj.playState =3D=3D 1)||(rObj.playState =3D=3D 0) )
rObj.Play()
else if( rObj.playState =3D=3D 2 )
rObj.Pause()
else
return;
}
else if( PPTSld.g_animUseRuntime )
{
narObj =3D PPTSld.document.all("narrationID")
if( narObj )
narObj.togglePause()
}
}
function GetCurSldNum()
{ =20
obj=3DGetHrefObj(gCurSld)
if( obj.mOrigVis =3D=3D 1 )
return obj.mSldIdx
else =20
return gCurSld
}
function GetNumSlds()
{ =20
if( GetHrefObj(gCurSld).mOrigVis =3D=3D 1 )
return GetSldList().mNumVisSlds;
else
return GetSldList().mList.length
}
function GetSldNum( href )
{
for(ii=3D0; ii 1 )
PopSldList();
else if( !IsFramesMode() ) {
if( gLoopCont )
GoToFirst()
else
EndShow()
}
}
function GoToPrevSld()
{
ii=3DgCurSld-1
if( ii > 0 ) {
obj=3DGetHrefObj(ii)
while ( obj && ( obj.mVis =3D=3D 0 ) && ( ii>0 ) )
obj=3DGetHrefObj(--ii)
if( ii =3D=3D 0 ) ii=3D1
GoToSldNum(ii)
}
}
function GoToFirst(){ GoToSld( GetHrefObj(1).mSldHref ) }
function GoToLast()
{
ii=3DGetSldList().mList.length
if( ii !=3D gCurSld )
GoToSld( GetHrefObj(ii).mSldHref )
}
function GoToSldNum( num )
{
if( PPTSld.event ) PPTSld.event.cancelBubble=3Dtrue
obj =3D GetHrefObj( num )
obj.mVis=3D1
gPrevSld=3DgCurSld
gCurSld =3D num;
PPTSld.location.replace(MHTMLPrefix+obj.mSldHref)
if( IsFramesMode() ) {
UpdNavPane(); UpdOtlPane(); UpdNtsPane()
}
}
function GoToSld( href )
{
if( PPTSld.event ) PPTSld.event.cancelBubble=3Dtrue
GetHrefObj( GetSldNum(href) ).mVis=3D1
PPTSld.location.replace(MHTMLPrefix+href)
}
function SldUpdated( id )
{
if( id =3D=3D GetHrefObj(gCurSld).mSldHref ) return
gPrevSld=3DgCurSld
gCurSld=3DGetSldNum(id)
if( IsFramesMode() ) {
UpdNavPane(); UpdOtlPane(); UpdNtsPane()
}
}
function PrevSldViewed(){ GoToSld( GetHrefObj(gPrevSld).mSldHref ) }
function HasPrevSld() { return ( gIsEndShow || ( gCurSld !=3D 1 && GetHrefO=
bj( gCurSld-1 ).mVis =3D=3D 1 )||( GetCurSldNum() > 1 ) ) }
function HasNextSld() { return (GetCurSldNum() !=3D GetNumSlds()) }
function CloseWindow() {
if( HideMenu() ) return;
=09
var event =3D PPTSld.event;
if( !IsFramesMode() && event && (event.keyCode=3D=3D27 || event.keyCode=3D=
=3D32 || event.type=3D=3D"click" ) )
window.close( self );
CatchNumKeys( self, event );
}
function Unload() { gIsEndShow=3D0; }
function SetupEndShow() {
gIsEndShow=3D1;
PPTSld.document.body.scroll=3D"no";
PPTSld.document.onkeypress=3DCloseWindow;
PPTSld.document.onclick=3DCloseWindow;
PPTSld.document.oncontextmenu=3D_CM;
}
function EndShow()
{
if( IsFramesMode() ) return
if( PPTSld.event ) PPTSld.event.cancelBubble=3Dtrue
doc=3DPPTSld.document
var dir =3D doc.body.dir
if( dir !=3D "rtl" ) dir =3D "ltr";
doc.open()
doc.writeln(' 0) {
PushSldList(sldList,fEnd);
gCurSld =3D 1;
}
else
if( PPTSld.event ) PPTSld.event.cancelBubble=3Dtrue
}
function PushSldList(arr,fEnd) {
var ii =3D gSldStack.length;
gSldStack[ii] =3D new SldList(arr,gCurSld,fEnd);
GoToSld( gSldStack[ii].mList[0].mSldHref );
}
function PopSldList() {
if (gSldStack[gSldStack.length-1].fEndShow)
EndShow()
else {
gCurSld =3D gSldStack[gSldStack.length-1].mCurSld;
gSldStack[gSldStack.length-1] =3D null;
gSldStack.length--;
var sldList =3D gSldStack[gSldStack.length-1];
GoToSld( sldList.mList[gCurSld - 1].mSldHref );
}
}
var custShowList=3Dnew Array();
/*********************************************
Navigation button implementation
There are 2 types of buttons: ImgBtn, TxtBtn
implemented as function objects. They share
a similiar interface so the event handlers
can call SetActive, for example, on a button=20
object without needing to know exactly=20
what type of button it is.
**********************************************/
//----------------------------------
function ImgBtn( oId,bId,w,action )
//----------------------------------
{
var t=3Dthis
t.Perform =3D _IBP
t.SetActive =3D _IBSetA
t.SetInactive=3D _IBSetI
t.SetPressed =3D _IBSetP
t.SetDisabled=3D _IBSetD
t.Enabled =3D _IBSetE
t.ChangeIcon =3D null
t.UserAction =3D action
t.ChgState =3D _IBUI
t.mObjId =3D oId
t.mBorderId=3D bId
t.mWidth =3D w
t.mIsOn =3D t.mCurState =3D 0
}
function _IBSetA()
{
if( this.mIsOn ) {
obj=3Dthis.ChgState( gHiliteClr,gShadowClr,2 )
obj.style.posTop=3D0
}
}
function _IBSetI()
{
if( this.mIsOn ) {
obj=3Dthis.ChgState( gFaceClr,gFaceClr,1 )
obj.style.posTop=3D0=20
}
}
function _IBSetP()
{
if( this.mIsOn ) {
obj=3Dthis.ChgState( gShadowClr,gHiliteClr,2 )
obj.style.posLeft+=3D1; obj.style.posTop+=3D1
}
}
function _IBSetD()
{ =20
obj=3Dthis.ChgState( gFaceClr,gFaceClr,0 )
obj.style.posTop=3D0=20
}
function _IBSetE( state )
{
var t=3Dthis
GetObj( t.mBorderId ).style.visibility=3D"visible"
if( state !=3D t.mIsOn ) {
t.mIsOn=3Dstate
if( state )
t.SetInactive()
else
t.SetDisabled()
}
}
function _IBP()
{
var t=3Dthis
if( t.mIsOn ) {
if( t.UserAction !=3D null )
t.UserAction()
if( t.ChangeIcon ) {
obj=3DGetObj(t.mObjId)
if( t.ChangeIcon() )
obj.style.posLeft=3Dobj.style.posLeft+(t.mCurState-4)*t.mWidth
else
obj.style.posLeft=3Dobj.style.posLeft+(t.mCurState-0)*t.mWidth
}
t.SetActive()
} =20
}
function _IBUI( clr1,clr2,nextState )
{
var t=3Dthis
SetBorder( GetObj( t.mBorderId ),clr1,clr2 )
obj=3DGetObj( t.mObjId )
obj.style.posLeft=3Dobj.style.posLeft+(t.mCurState-nextState)*t.mWidth-obj=
.style.posTop
t.mCurState=3DnextState
return obj
}
//-----------------------------------------
function TxtBtn( oId,oeId,action,chkState )
//-----------------------------------------
{
var t=3Dthis
t.Perform =3D _TBP
t.SetActive =3D _TBSetA
t.SetInactive=3D _TBSetI
t.SetPressed =3D _TBSetP
t.SetDisabled=3D _TBSetD
t.SetEnabled =3D _TBSetE
t.GetState =3D chkState
t.UserAction =3D action
t.ChgState =3D _TBUI
t.mObjId =3D oId
t.m_elementsId=3D oeId
t.mIsOn =3D 1
}
function _TBSetA()
{
var t=3Dthis
if( t.mIsOn && !t.GetState() )
t.ChgState( gHiliteClr,gShadowClr,0,0 )
}
function _TBSetI()
{
var t=3Dthis
if( t.mIsOn && !t.GetState() )
t.ChgState( gFaceClr,gFaceClr,0,0 )
}
function _TBSetP()
{
if( this.mIsOn )
this.ChgState( gShadowClr,gHiliteClr,1,1 )
}
function _TBSetD()
{ =20
this.ChgState( gFaceClr,gFaceClr,0,0 )
this.mIsOn =3D 0
}
function _TBSetE()
{
var t=3Dthis
if( !t.GetState() )
t.ChgState( gFaceClr,gFaceClr,0,0 )
else
t.ChgState( gShadowClr,gHiliteClr,1,1 )
t.mIsOn =3D 1
}
function _TBP()
{
var t=3Dthis
if( t.mIsOn ) {=20
if( t.UserAction !=3D null )
t.UserAction()
if( !t.GetState )
return
if( t.GetState() )
t.SetPressed()
else
t.SetActive()
} =20
}
function _TBUI( clr1,clr2,lOffset,tOffset )
{
SetBorder( GetObj( this.mObjId ),clr1,clr2 )
Offset( GetObj( this.m_elementsId ),lOffset,tOffset )
}
function Offset( obj, top, left ){ obj.style.top=3Dtop; obj.style.left=3Dle=
ft }
function SetBorder( obj, upperLeft, lowerRight )
{
s=3Dobj.style;
s.borderStyle =3D "solid"
s.borderWidth =3D 1=20
s.borderLeftColor =3D s.borderTopColor =3D upperLeft
s.borderBottomColor=3D s.borderRightColor =3D lowerRight
}
function GetBtnObj(){ return gBtnArr[window.event.srcElement.id] }
function BtnOnOver(){ b=3DGetBtnObj(); if( b !=3D null ) b.SetActive() }
function BtnOnDown(){ b=3DGetBtnObj(); if( b !=3D null ) b.SetPressed() }
function BtnOnOut(){ b=3DGetBtnObj(); if( b !=3D null ) b.SetInactive() }
function BtnOnUp()
{
b=3DGetBtnObj()
if( b !=3D null )
b.Perform()
else
Upd()
}
function GetNtsState(){ return parent.gNtsOpen }
function GetOtlState(){ return parent.gOtlOpen }
function GetOtlTxtState(){ return parent.gOtlTxtExp }
function NtsBtnSetFlag( fVal )
{
s=3Ddocument.all.item( this.m_flagId ).style
s.display=3D"none"
if( fVal )
s.display=3D""
else
s.display=3D"none"
}
function _BSetA_Border(){ b =3D gBtnArr[this.mObjId]; if( b !=3D null ) b.S=
etActive() }
function _BSetI_Border(){ b =3D gBtnArr[this.mObjId]; if( b !=3D null ) b.S=
etInactive() }
function _BSetP_Border(){ b =3D gBtnArr[this.mObjId]; if( b !=3D null ) b.S=
etPressed() }
function _BSetA_BorderImg()
{=20
b =3D gBtnArr[this.mBorderId]=20
if( b !=3D null && this.mIsOn && !b.GetState() ) {
obj=3Dthis.ChgState( gHiliteClr,gShadowClr,2 )
obj.style.posTop=3D0
}
}
function _BSetI_BorderImg()
{=20
b =3D gBtnArr[this.mBorderId]
if( b !=3D null && this.mIsOn && !b.GetState() ) {
obj=3Dthis.ChgState( gFaceClr,gFaceClr,1 )
obj.style.posTop=3D0
}
}
var gHiliteClr=3D"THREEDHIGHLIGHT",gShadowClr=3D"THREEDSHADOW",gFaceClr=3D"=
THREEDFACE"
var gBtnArr =3D new Array()
gBtnArr["nb_otl"] =3D new TxtBtn( "nb_otl","nb_otlElem",parent.ToggleOtlPan=
e,GetOtlState )
gBtnArr["nb_otlElem"] =3D new TxtBtn( "nb_otl","nb_otlElem",parent.ToggleOt=
lPane,GetOtlState )
gBtnArr["nb_nts"] =3D new ImgBtn( "nb_nts","nb_ntsBorder",10,parent.ToggleN=
tsPane )
gBtnArr["nb_nts"].SetActive =3D _BSetA_BorderImg;
gBtnArr["nb_nts"].SetInactive =3D _BSetI_BorderImg;
gBtnArr["nb_ntsBorder"] =3D new TxtBtn( "nb_ntsBorder","nb_ntsElem",parent.=
ToggleNtsPane,GetNtsState )
gBtnArr["nb_ntsElem"] =3D new TxtBtn( "nb_ntsBorder","nb_ntsElem",parent.To=
ggleNtsPane,GetNtsState )
gBtnArr["nb_prevBorder"] =3D gBtnArr["nb_prev"]=3D new ImgBtn( "nb_prev","n=
b_prevBorder",30,parent.GoToPrevSld )
gBtnArr["nb_nextBorder"] =3D gBtnArr["nb_next"]=3D new ImgBtn( "nb_next","n=
b_nextBorder",30,parent.GoToNextSld )
gBtnArr["nb_sldshw"]=3D new ImgBtn( "nb_sldshw","nb_sldshwBorder",18,parent=
.FullScreen )
gBtnArr["nb_sldshwBorder"] =3D new TxtBtn( "nb_sldshw","nb_sldshwBorder",pa=
rent.FullScreen,null )
gBtnArr["nb_sldshwBorder"].SetActive =3D _BSetA_Border;
gBtnArr["nb_sldshwBorder"].SetInactive =3D _BSetI_Border;
gBtnArr["nb_sldshwText"] =3D new TxtBtn( "nb_sldshw","nb_sldshwText",parent=
.FullScreen,null )
gBtnArr["nb_sldshwText"].SetActive =3D _BSetA_Border;
gBtnArr["nb_sldshwText"].SetInactive =3D _BSetI_Border;
gBtnArr["nb_voice"] =3D gBtnArr["nb_voiceBorder"] =3D new ImgBtn( "nb_voice=
","nb_voiceBorder",18,parent.ToggleVNarration )
gBtnArr["nb_otlTxtBorder"] =3D gBtnArr["nb_otlTxt"]=3D new ImgBtn( "nb_otlT=
xt","nb_otlTxtBorder",23,parent.ToggleOtlText )
gBtnArr["nb_ntsBorder"].m_flagId=3D "nb_nts"
gBtnArr["nb_ntsBorder"].SetFlag =3D NtsBtnSetFlag
gBtnArr["nb_otlTxt"].ChangeIcon=3D GetOtlTxtState
/*********************************************
Context menu implementation
_CM() is the function that's hooked up to
the oncontextmenu event. Once we're asked to
show the menu, we first build it by creating
DIVs on-the-fly. Then we position it=20
within the screen area so it doesn't get
clipped.
Creating the DIVs using createElement() means
we don't have to write out any extra HTML
into the slide HTML files.
**********************************************/
var sNext=3D"Next",sPrev=3D"Previous",sEnd=3D"End Show",sFont=3D"Arial",sAr=
row=3D"Arrow",sFreeform=3D"Freeform",sRect=3D"Rectangle",sOval=3D"Oval"
function ShowMenu()
{
BuildMenu();
var doc=3DPPTSld.document.body,x=3DPPTSld.event.clientX+doc.scrollLeft,y=
=3DPPTSld.event.clientY+doc.scrollTop
m =3D PPTSld.document.all.item("ctxtmenu")
m.style.pixelLeft=3Dx
if( (x+m.scrollWidth > doc.clientWidth)&&(x-m.scrollWidth > 0) )
m.style.pixelLeft=3Dx-m.scrollWidth
m.style.pixelTop=3Dy
if( (y+m.scrollHeight > doc.clientHeight)&&(y-m.scrollHeight > 0) )
m.style.pixelTop=3Dy-m.scrollHeight
m.style.display=3D""
}
function _CM()
{
if( !parent.IsFullScrMode() ) return;
if(!PPTSld.event.ctrlKey) {
ShowMenu()
return false
} else
HideMenu()
}
function BuildMenu()
{
if( PPTSld.document.all.item("ctxtmenu") ) return
var mObj=3DCreateItem( PPTSld.document.body )
mObj.id=3D"ctxtmenu"
mObj.style.visibility=3D"hidden"
var s=3DmObj.style
s.position=3D"absolute"
s.cursor=3D"default"
s.width=3D"120px"
SetCMBorder(mObj,"menu","black")
var iObj=3DCreateItem( mObj )
SetCMBorder( iObj, "threedhighlight","threedshadow" )
iObj.style.padding=3D2
CreateMenuItem( iObj,sNext,M_GoNextSld,M_True )
CreateMenuItem( iObj,sPrev,M_GoPrevSld,M_HasPrevSld )
=09
CreateSeparator( iObj )
CreateMenuItem( iObj,sEnd,M_End,M_True )
mObj.style.visibility=3D"visible"
}
function Cancel() { window.event.cancelBubble=3Dtrue; window.event.returnVa=
lue=3Dfalse }
function Highlight() { ChangeClr("activecaption","threedhighlight") }
function Deselect() { ChangeClr("threedface","menutext") }
function Perform()
{
e=3DPPTSld.event.srcElement
if( e.type=3D=3D"menuitem" && e.IsActive() )
e.Action()
else
PPTSld.event.cancelBubble=3Dtrue
}
function ChangeClr( bg,clr )
{
e=3DPPTSld.event.srcElement
if( e.type=3D=3D"menuitem" && e.IsActive() ) {
e.style.backgroundColor=3Dbg
e.style.color=3Dclr
}
}
function M_HasPrevSld() { return( parent.HasPrevSld() ) }
function M_GoNextSld() { if( gIsEndShow ) M_End(); else GoToNextSld() }
function M_GoPrevSld() { if( gIsEndShow ) { gIsEndShow=3D0; history.back();=
PPTSld.event.cancelBubble=3Dtrue; } else GoToPrevSld() }
function M_True() { return true }
function M_End() { window.close( self ) }
function CreateMenuItem( node,text,action,eval )
{
var e=3DCreateItem( node )
e.type=3D"menuitem"
e.Action=3Daction
e.IsActive=3Deval
e.innerHTML=3Dtext
if( !e.IsActive() )
e.style.color=3D"threedshadow"
e.onclick=3DPerform
e.onmouseover=3DHighlight
e.onmouseout=3DDeselect
s=3De.style;
s.fontFamily=3DsFont
s.fontSize=3D"9pt"
s.paddingLeft=3D2
}
function CreateSeparator( node )
{
var sObj=3DCreateItem( node )
SetCMBorder(sObj,"menu","menu")
var s=3DsObj.style
s.borderTopColor=3D"threedshadow"
s.borderBottomColor=3D"threedhighlight"
s.height=3D1
s.fontSize=3D"0px"
}
function CreateItem( node )
{
var elem=3DPPTSld.document.createElement("DIV")
node.insertBefore( elem )
return elem
}
function SetCMBorder( o,ltClr,rbClr )
{
var s=3Do.style
s.backgroundColor=3D"menu"
s.borderStyle=3D"solid"
s.borderWidth=3D1
s.borderColor=3DltClr+" "+rbClr+" "+rbClr+" "+ltClr
}
------=_NextPart_01C4074D.C10E69C0
Content-Location: file:///C:/C5596224/myoclonus_grand_round_files/fullscreen.htm
Content-Transfer-Encoding: quoted-printable
Content-Type: text/html; charset="us-ascii"
Epileptic myoclonus and progressive myoclonus epilepsy
&=
#8211;Relation
to symptoms unclear
<=
/div>
------=_NextPart_01C4074D.C10E69C0
Content-Location: file:///C:/C5596224/myoclonus_grand_round_files/slide0072.htm
Content-Transfer-Encoding: quoted-printable
Content-Type: text/html; charset="us-ascii"
<=
/div>
NCL: CLINICAL
•Worldwide, esp. Finland, Newfoundland
•Late infantile:
&=
#8211;Onset:
2 1/2 - 4 years
&=
#8211;Severe
dementia, late visual failure
–Optic
fundi: pallor, macular degeneration, attenuation of retinal
vessels
&=
#8211;Death
5 years after onset
NCL: CLINICAL
•Juvenile
&=
#8211;Onset:
4 - 10 years
&=
#8211;Visual
failure first symptom
&=
#8211;Death:
8 years after onset
•Adult:
&=
#8211;Onset:
30 years
&=
#8211;No
visual failure, normal fundi
&=
#8211;Death:
12 years after onset
•Intermediate
NCL: PATHOLOGY
•LM: LFB, PAS and Sudan IV positive, autofluorescent lipofuscin in cytoplasm
•EM: inclusions
&=
#8211;Late
infantile: curvilinear
&=
#8211;Juvenile
and adult: fingerprint
&=
#8211;Variations
•Storage material: lipid + protein (subunit c of
mitochondrial ATP synthase) &n=
bsp;
NCL: GENETICS AND BIOCHEMISTRY
•Genetics:
&=
#8211;Juvenile:
linked to chromosome 16
&=
#8211;Late
infantile and adult: unknown
•Biochemistry:
–Elevated
urinary and brain dolichols and dolichol phosphates
&=
#8211;Not
very sensitive or specific
MERRF: CLINICAL
MERRF: GENETICS
MERRF: PATHOLOGY
•Dysfunction in the respiratory chain
•LM: RRF in muscle (MGT stain)
•EM: abnormal forms
•Biochemistry:
&=
#8211;increased
serum lactate
–abnormal
assays of mitochondrial respiratory enzymes
SIALIDOSIS: CLINICAL
•Least common, type II mainly in Japan
•Type I (“cherry-red
spot-myoclonus”)
&=
#8211;Onset:
adolescence
&=
#8211;Severe
myoclonus, no dementia
&=
#8211;Visual
failure, cherry-red spot in fundus
•Type II:
–Like
I, but with dysmorphic features, low intellect since early life=
SIALIDOSIS:BIOCHEMISTRY AND
GENETICS
•Biochemistry:
&=
#8211;Severe
neuraminidase deficiency in I and II
&=
#8211;Partial
galactosidase deficiency in II
•Genetics:
&=
#8211;Type
I: localization unknown
&=
#8211;Type
II: ? chromosome 20
PME - TREATMENT
·Traditional AEDs:
&=
#8211;VPA
+ BZD
&=
#8211;Phenytoin
may be contraindicated
·Newer AEDs:
&=
#8211;Zonisamide,
? lamotrigine
·Other:
&=
#8211;5-HTP,
piracetam, N-acetyl cysteine, CoQ
&=
#8211;Alcohol
PMA
PME
CLINICAL CLUES
Onset: 6-20
Early, severe
dementia
Occipital
seizures
Visual failure,
norm=
al
fundi
LD
Onset: 2-50
<=
/b>Severe
dementia
Visual failure,
with=
OA,
MD
N=
CL
Onset: 6-16
Prominent
myoclonus
Ataxia
Minimal or
no
dementia
ULD
Onset: 3-65
Deafness
Optic atrophy
Short
stat=
ure
Neuropathy
MERRF
Onset: 8-30&nb=
sp;
<=
/div>
Cherry-red
spot=
Prominent
myoclonus
Dysmorphic
features
SIALIDOSIS
ELECTR=
OPHYSIOLOGY
Confirm PME
Relatively
specific
findings
Presymptomatic
diagnosis
FINAL
DIAGNOSIS
P=
athological
Skin: LD, NCL
Liver: LD
Muscle: MERRF,
=
;
NCL, LD
Brain: LD, NCL
Biochemical
Sialidosis -
N-acetyl neuraminidase deficiency
Clinical
ULD
Genetic
ULD
MERRF
?LD, NCL,
Sial=
idosis
' + ENDSHOW_MESG + '
![](3D"notes_flag.gif")
No=
tes![](3D"buttons.gif")
