-
- Andy OJ, M
Jurko Diencephalic Seizure Appl Neurophysiol
1983; 46; 62-67
- Flechter S, Cohen F,
Borenstein F, Regev I, Vardi J Yawning as a
paroxysmal sign of diencephalic seizures.
Archivio di Psicologia Neurologia e Pichiatria
1982;43:45-54
- Penfield
W, Jasper H Diencephalic autonomic seizures
Eplilepsy and the functionnal anatomy of the
human brain Little Brown et copany - Boston
1954
- Penfield
W The influence of
the diencephalon and hypophysis upon general
autonomic function
- Walusinski
O Yawning as a paroxysmal sign
of diencephalic seizures an original
observation
- Specchio
N, Carotenuto A et al. Ictal yawning in a
patient with drug-resistant focal epilepsy:
Video/EEG documentation and review of literature
reports. Epilepsy Behav. 2011;22(3):602-605
- Kuba
R, Musilová K, Brázdil M, Rektor
I. Peri-ictal yawning lateralizes the
seizure onset zone to the nondominant hemisphere
in patients with temporal lobe epilepsy Epilepsy
Behav 2010;19(3):311-314
- Nicotra
A, Khalil NM, Owbridge P, Hakda M, Beitverda
Y. Pathological yawning as an ictal seizure
manifestation in the elderly. BMJ case reports.
2012
-
- Les crises d'épilepsie
diencépahlique (épilepsie
partielle), rares, se manifestent par des
accès de bradychardie, variations
brutales de la pression artérielle, du
rythme respiratoire, du diamètre
pupillaire, d'élévation de la
température, de sueurs profuses, de
salivation extrême, de troubles des
postures, de troubles de la vigilance. Les
crises
gélastiques sont
caractérisées par des accès
de rire sans cause, (Pathological
laughter and crying) et témoignent le
plus souvent d'un hamartome de l'hypothalamus,
parfois d'autres tumeurs suprasellaires, de
séquelles de traumatismes craniens. Les
causes de ces épilepsies sont : tumorale
congénitale, des anomalies de la gyration
et/ou de la neurostructure d'un noyau, une
séquelle
dégénérative
localisée après virose herptique
ou à CMV, ou à une
neurosarcoïdose. L'EEG est souvent normal
et l'IRM fonctionnelle peut-être la seule
manière de visualiser la zone
pathologique. Les variations de la circulation
du LCR, des concentrations en
neuromédiateurs Hypocrétine, GABA
(déplétion post-ictale) commencent
seulement à être
étudiées.
-
- Voici un cas exceptionnel, évoquant
des crises épileptiques
générées par l'hypothalamus
et irradiant vers les noyaux thalamiques, sous
forme d'une baisse de la vigilance avec
salves irrépressibles de
bâillements, évoluant par crises de
20 à 30 minutes jusqu'à dix fois
par jour, se raréfiant sous
antiépileptiques, sans cause tumorale
retrouvée.
-
- « I am a thirty two year old female. In
my mid-twenties I began to develop an
'intolerance' to alcohol. Half a glass of wine
would make me extremely and uncontrollably
sleepy. It is only in retrospect that I realise
this problem started years ago - at the time it
just seemed normal to me.
-
- Two years ago, I started getting these
'sleepy attacks' during the day, without
alcohol. I got one every couple of days or so,
and seemed to be related to meals or food. I
still assumed it was some sort of allergic
reaction, although I couldn't pinpoint it at
all. Then these attacks became more frequent,
about one a day. This was the pattern for about
a month. Then suddenly, almost over night, I was
getting up to eight or ten attacks a day, not
related to meals specifically. They always
follow the same pattern - no warning, then
extreme drowsiness, accompanied by excessive
yawning and a feeling of being out of it, for up
to half an hour. Then I feel normal again.
It happens while driving, eating, talking,
walking, working etc. and is totally
uncontrollable. This has been the pattern for
the last two years. Some days are better than
others are, but generally I have about four to
six attacks a day. I do not actually fall
asleep, unless close to normal sleep time.
-
- Generally I sleep in excess of eight hours a
day, and fall asleep in a normal length of time.
My husband says that I am a fairly restful bed
partner.
-
- My father, who is a GP, watched my symptoms
getting worse and started reading up a little.
He sent me to Wentworth Hospital for tests. The
neurologist suspected seizures and tried to get
me to take some anti-seizure medication for a
month, which I refused to do Ð not wanting
to be a guinea pig. He also sent me for an MRI
and EEG and MSLT (without a polysomnogramme),
all of which where normal.
-
- Since I have had a consultation and EEG with
Dr M G, Meulmed, Pretoria. She came recommended
by a sleep disorders support group. She
diagnosed me with pathological sleepiness and
recommended ritalin (cf méthylphenidate =
amphetamine). I was dissapointed with the
consultation, because as she herself admitted,
the term 'pathological sleepiness' is a dumping
ground or term for unexplained sleepiness. I
have used reactivan for a month or two, and it
initially helped, but I got to the point where I
would have to up the dose to get the same
effect. So I stopped using it rather. I did not
try Ritalin.
-
- When I experience an attack, it feels
something like this:
- I will be normally alert and engrossed in my
work, social activity and will become aware of
an impending attack sometimes by a feeling of
wanting to yawn Ð sometimes just a sense
like a weight has been attached to my mind and
is slowing me down. I also get irritable,
sensitive to noise and light and other stimuli.
The attack, with constitutes a feeling of
diminshed awareness and extreme drowisiness,
lasts about 20 minutes. I yawn uncontrollably
and cannot surpress a yawn. The yawns are
frequent and huge, with a sense of urgency which
is relieved temporarily by the yawn. I can
tell immediately almost to the second when it is
over. The 'fog' seeems to lift in my mind.
During the attack my body temperature seems to
drop and it is often accompanied by goose bumps
and cold. My eyes tear and nose runs a bit. I
seldom fall asleep during an attack. I have
never been a sleepy person during the day, and I
fight the attacks like crazy. Its like being
switched off against your will. I feel unwell
during an attack, and they can be quite severe,
although I never lose consciousness or
awareness. Sometimes my whole day can be a
write-off Ð since the between periods are
also foggy, with an impending sense of an attack
all the time. I get short stabbing pains in the
head sometimes during the attack and sometimes
in isolation. I get sensations on my scalp, like
a ticklish feeling on my forehead, which comes
and goes intermittently.
-
- I cannot control the attacks,
although I can sometimes with extreme effort
postpone it for half an hour or so. Chewing some
gum can postpone an attack a while.
-
- Driving has become a real problem, since I
will almost certainly have an attack, even on
short trips. I will be driving in an alert
state, will experience an attack, and will
resume driving in alert fashion once over. My
work as an architect is severly affected,
especially on a bad day.
-
- I have had a 24 hour EEG at Entabeni
Hospital under Dr H S, my current neurologist.
He has been wonderful. His best attempts at
diagnosis have been possibly epilepsy or a form
of migraine aura. He had me on Epilim,(cf
valproate sodique = dépakine) which had
very good results. I am trying to conceive now,
and am off the Epilim, which means that my
symptoms have got worse again. They never go
away entirely, with my best day having one
attack, and my worst as many as fifteen, almost
head to head, and lasting up to forty
minutes.
-
- I have had HLA typing for narcolepsy, which
was negative.
- I am average weight, physically active,
insulin resistant, asthmatic and otherwise
healthy. There is a family history of strokes.
(My mothers father) A concern for me is that the
Epilim, which controlled my symptoms so well,
has recently been linked to a worsening in PCOS
and insulin resistance, although this does not
seem to be an accepted fact. »
-
- Référence
:
- Benarroch, E. E. (1993). "The central
autonomic network: functional organization,
dysfunction, and perspective." Mayo Clin Proc
68(10): 988-1001. The central autonomic
network (CAN) is an integral component of an
internal regulation system through which the
brain controls visceromotor, neuroendocrine,
pain, and behavioral responses essential for
survival. It includes the insular cortex,
amygdala, hypothalamus, periaqueductal gray
matter, parabrachial complex, nucleus of the
tractus solitarius, and ventrolateral medulla.
Inputs to the CAN are multiple, including
viscerosensory inputs relayed on the nucleus of
the tractus solitarius and humoral inputs
relayed through the circumventricular organs.
The CAN controls preganglionic sympathetic and
parasympathetic, neuroendocrine, respiratory,
and sphincter motoneurons. The CAN is
characterized by reciprocal interconnections,
parallel organization, state-dependent activity,
and neurochemical complexity. The insular cortex
and amygdala mediate high-order autonomic
control, and their involvement in seizures or
stroke may produce severe cardiac arrhythmias
and other autonomic manifestations. The
paraventricular and other hypothalamic nuclei
contain mixed neuronal populations that control
specific subsets of preganglionic sympathetic
and parasympathetic neurons. Hypothalamic
autonomic disorders commonly produce hypothermia
or hyperthermia. Hyperthermia and autonomic
hyperactivity occur in patients with head
trauma, hydrocephalus, neuroleptic malignant
syndrome, and fatal familial insomnia. In the
medulla, the nucleus of the tractus solitarius
and ventrolateral medulla contain a network of
respiratory, cardiovagal, and vasomotor neurons.
Medullary autonomic disorders may cause
orthostatic hypotension, paroxysmal
hypertension, and sleep apnea. Neurologic
catastrophes, such as subarachnoid hemorrhage,
may produce cardiac arrhythmias, myocardial
injury, hypertension, and pulmonary edema.
Multiple system atrophy affects preganglionic
autonomic, respiratory, and neuroendocrine
outputs. The CAN may be critically involved in
panic disorders, essential hypertension,
obesity, and other medical conditions.
- John S. Imaging and epilepsy Duncan Brain
(1997), 120, 339Ð377
- J. Parvizi,
Pathological laughter and crying: a link to the
cerebellum Brain 2001,
124 (Pt 9): 1708-19
- Khadilkar, S., K. Menezes, et al. (2001).
"Gelastic epilepsy--a case report with SPECT
studies." J Assoc Physicians India 49: 581-3.
A 24 years male presented with daily
episodes of uncontrollable laughter followed by
urinary incontinence since the age of nine
years. Some of these attacks progressed to
generalized tonic-clonic seizures. General and
neurological examination did not reveal any
abnormality. Ictal and interictal video EEGs
were normal. MRI showed a hypothalamic
hamartoma. Interictal SPECT scan showed normal
perfusion in the hamartoma. SPECT scan obtained
four minutes after beginning of seizure showed
that the perfusion increased in right cingulate
gyrus but not in the hamartoma, suggesting the
involvement of the cingulate gyrus in the
seizure origin or pathway.
- Akman, C. I., R. Schubert, et al. (2002).
"Gelastic seizure with tectal tumor, lobar
holoprosencephaly, and subependymal nodules:
clinical report." J Child Neurol 17(2): 152-4.
Gelastic seizures are characterized by
inappropriate, stereotyped laughter and are
often first recognized when other epileptic
manifestations occur. They are frequently
associated with hypothalamic hamartomas. Central
nervous system developmental abnormalities are
rarely reported with gelastic seizures. There is
only one case report of gelastic seizure caused
by holoprosencephaly. We report a 2-year-old
girl with multiple brain structural
abnormalities including tectal tumor (possibly
hamartoma), multiple subependymal nodules, and
holoprosencephaly. She developed seizures during
the newborn period and presented with gelastic
seizure and simple partial seizure at 3 months
of age.
- Sturm, J. W., F. Andermann, et al.
(2000). ""Pressure to laugh": an unusual
epileptic symptom associated with small
hypothalamic hamartomas." Neurology 54(4):
971-3. Gelastic seizures are the hallmark of
the epilepsy syndrome associated with
hypothalamic hamartomas. Patients typically
develop cognitive deterioration and refractory
seizures. The authors describe three patients
with small hypothalamic hamartomas without these
features and thus identify a mild end to the
clinical spectrum. All had the unusual symptom
of "pressure to laugh," often without actual
laughter. This symptom could be dismissed as
psychogenic but should be recognized as a clue
to the presence of this unusual lesion.
- Boeve, B. F., E. F. Wijdicks, et al.
(1998). "Paroxysmal sympathetic storms
("diencephalic seizures") after severe diffuse
axonal head injury." Mayo Clin Proc 73(2):
148-52. We describe a patient with a severe
traumatic head injury who exhibited paroxysmal
sympathetic storms, similar to those described
in "diencephalic seizures." No epileptiform
activity was evident on electroencephalography,
and therapeutic levels of anticonvulsants failed
to alter the spells; however, use of morphine
sulfate abolished them. The features of this and
several previously reported cases refute the
primary roles of the diencephalon and seizures
in this syndrome. Rather, in the setting of
already compromised autonomic neuronal
integrity, subtle fluctuations in
intraventricular pressure or activation of
reflexes triggered from muscle mechanoreceptors
or chemoreceptors during episodes of hypertonia
are more likely. "Paroxysmal sympathetic
storms," a more appropriate descriptive term for
these phenomena, should be recognized; thus,
unnecessary diagnostic evaluations can be
minimized, and appropriate therapy can be
initiated.
- Morris, H. H., 3rd (1988). "Sudden
diencephalic events." Ann Neurol 23(2):
208.
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