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HYPERSOMNIA AND PLMS AFTER LACUNAR THALAMIC INFARCTION: A CASE
REPORT.
Michela Figorilli, Gioia Gioi, Patrizia Congiu, Francesco Marrosu e Monica Puligheddu.
Centro di medicina del Sonno, Dipartimento di Scienze Neurologiche e Cardiovascolari,
Università di Cagliari.
Introduction.
Sleep-wake disturbances are found in 20-50% of stroke patients. A decreased arousal due
to lesion involving the ascending arousal pathways is most commonly responsible for poststroke
hypersomnia. Secondary Hypersomnia could be a symptom of paramedian
thalamus ischemic infarction; also periodic leg movements during sleep (PLMs) and
restless leg syndrome (RLS) could be symptoms of disruption of thalamic sleep-generating
and arousal-maintaining mechanisms.
Case description.
A 48-year aged man whit a history of smoking, hypertension, Raynaud Syndrome,
essential polycytemia, prothrombin mutation and right Thalamic Stroke complained of
EDS. He describes mild snoring, sleep awakening, falling asleep at the wheel, apathy or
irritability, lapse in concentration, loss of short time memory. The patient had a normal
neurological and systemic examination; Epworth Sleepiness Scale scored 14, Berlin
Questionnaire with high risk of OSAS, normal neuropsychological assessment. The patient
underwent a VideoPolysomnography (VPSG) and a Multiple Sleep Latency Test (MSLT).
VPSG showed a 1 minute sleep latency, 18 arousals, N1 15,23%, N2 77,01%, N3 4,31%,
REM 0%, negative for OSAS and PLMS. MSLT showed a sleep latency of 5 minutes,
without SOREMP. MRI of brain showed a small lacunar stroke of the right thalamus,
hyperintense in T2 and hypointense in T1, without contrast enhancement. The patient was
treated with Modafinil 50 mg/die, programmed naps and good sleep hygiene. Modafinil
was interrupted after one month because of excessive irritability and insomnia, EDS was
improved by programmed naps and good sleep hygiene. After 4 years patient reports
worsening of EDS, discomfort in legs before sleep onset, movements of legs during sleep
time. A new VPSG showed altered sleep structure with 330 minutes of sleep, sleep
efficiency 72%, 1,5 minutes sleep latency, 29 arousals, N1 0,8%, N2 22,9%, N3 35,9%,
REM 12,7%, negative for OSAS but with PLM index 103,30 (episodes index 5,26) with
severe sleep fragmentation. MSLT showed a sleep latency of 7.4 minutes, without
SOREMP. In order to obtain a better sleep structure we introduced therapy with
Trazodone 50 mg/die. After 3 months patient reports EDS improvement and alleviation of
legs discomfort. A new VPSG shows 389,5 minutes of sleep, sleep efficiency 80%, 10,5
minute sleep latency, 8 arousals, N1 1%, N2 24,3%, N3 53%, REM 21,8%, negative for
OSAS, PLM index 19,16 and PLM episodes index 1,38.
Discussion and conclusion.
Abnormalities in sleep architecture (macro and micro) are suitable after strokes,
particularly in severe hypersomnias, following paramedian thalamic strokes where
persistent light sleep N1, reflect an inhability to regulate the sleep-wake transition and to
produce full wakfullness. In the present case, hypersomnia and PLMS-RLS are different
and temporally separate expression of a dysfunction in arousal systems due to a isolate
thalamic lacunar infarction. Trazodone improves sleep organization and stabilizes the
arousal pathways with a good framework and a reduction of the CAP rate, with a
consequent reduction of PLM and efficient sleep architecture.
Dott.ssa MICHELA FIGORILLI Dipartimento di Scienze Neurologiche e Cardiovascolari, Università
di Cagliari, Policlinico Universitario SS554, bivio per Sestu, 09042 Monserrato (CA) Italia.
michelafigorilli@libero.it
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