Sciences de la Santé
inhibiting the ion current. When a depolarization of
the post-synaptic membrane occurs by the opening
of AMPA channels for instance, Mg2+ molecules are
removed from their inhibitory sites, and allow Ca2+
and Na+ ions to enter. When let it in normal amounts,
Ca2+ ionsgenerate signalling pathways that reinforce
synaptic transmission. A process which is fundamental
for special types of memories.
What also grabs our attention concerning these
receptors, is the presence of a site in the pore of the
channel that could inhibit the NMDA receptor if bound
to a hallucinogenic drug phencylidinePCP (also known
as angel dust). It owns its name to the hallucinations
induced by blocking the NMDA receptors.
We acknowledge therefore, that any kind of disturbance
of the natural mechanism of NMDA receptors would
highly influence the synaptic plasticity which plays a
considerable role in the storage of information and
other higher brain functions.
When the antibodies addressed against NMDAR bind
to them, they leadto their internalization from the
cell surface and to a state of relative NMDA receptor
hypofunction. Resulting in the symptoms of the disease
which were proved to be reversible with the removal of
the antibodies (4,5).
Phases of theillness in anti-NMDA receptor en-
cephalitis:
Viral prodromal phase:
Most patients present in the first 5 days (no
more than 2 weeks) non-specific cold or viral-like
symptoms: fever, drowsiness, asthenia, headaches,
myalgias, upper respiratory symptoms, nausea and
even diarrhea. Preceding the beginning of psycho-
behavioural changes.
Initial psychiatric symptoms:
Considering the common absence of neurologic
manifestations in this period, patients usually see a
psychiatrist first. For this reason, the diagnosis of anti
NMDA encephalitis could be confused at this stage
with other mental illnesses such as schizophrenia. They
often experience various mental symptoms over which
schizophrenia-like symptoms govern; chiefly psychosis,
which is characterized as a defective or lost contact with
reality, resulting in delusional ideas, suspiciousness,
hallucinations, disorganized speech, such as switching
topics erratically and loss of self-awareness. Moreover,
patients usually show emotional disturbances (anxiety,
fear, loneliness, apathy…), strange behaviours (such as
smiling oddly at their own reflection in a mirror) and
agitation in addition to paranoia, mood changes and
personality transitions. They can easily and suddenly
become cantankerous and aggressiveleading to their
withdrawalfrom society.
Furthermore, short-term amnesia, confusion and
cognitive impairment can be difficult to detect at the
onset of the phase, because of the prominence of the
psychiatric signs and could even be sub-syndromal.
Interestingly, children show different symptoms:
sleep dysfunction, irritability, behavioural flare-ups,
hyperactivity and hyper-sexuality seem to take the
place of psychotic symptoms.
This phase usually lasts from 1 to 3 weeks but could be
protracted in some cases in a less severe manner.
Seizures can occur at this phase and the patients fall
into unresponsiveness driving them to the hospital.
Unresponsive phase:
Patients at this stage go through a debilitated
state. Akinetic, they undergo progressive decay in
speech and language such as a reduced fluency of
speech (alogia), mimicking the examiner’s movements
or words (echolalia) and uttering; along with a
catatonic behaviour by being unresponsive to verbal
commands and mutism despite their eyes being open.
Paradoxically, they can occasionally be passive to some
‘’suggestive’’orders of the examiner.
This phase is also accompanied by Catalepsy-like
symptoms (presenting muscle rigidity and fixity of
posture despite external stimuli) and athetoid dystonic
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AUTOMNE 2018 /HIVER 2019