You will be presented with the full text of a biomedical research paper. Please write an abstract for this paper. Your response should include the abstract and no additional text.

Paper text:
particular presentations of migraine aura include hemiplegic migraine , in which aura consists of fully reversible motor weakness together with visual , sensory or speech disturbances , and basilar type migraine ( btm ) .
this is a rare form of migraine that could present with a dramatic clinical picture , mimicking other severe neurological disorders
btm presents symptoms referred to posterior cerebral circulation involvement : dysarthria , vertigo , tinnitus , hypoacusia , diplopia , ataxias , bilateral sensitive or visual deficits , and decreased level of consciousness . according to symptoms of typical aura ( ichd - ii ) , in both conditions aura lasts from 5 to 60  min , except for motor weakness ( in hemiplegic migraine ) that can last till 24  h .
patent foramen ovale ( pfo ) has been reported to have an elevated prevalence in patients suffering from migraine with aura ( ma ) .
the possibility that right - to - left shunt may be a  trigger  in the genesis of aura has also been suggested , even if it is yet debated whether the primary mechanisms of migraine are vascular or neurogenic .
recent reports concerning the relationship between ma and pfo included patients with motor weakness also [ 5 , 6 ] . in particular , in the report by anzola et  al .  
12% of patients with right - to - left shunt exhibited motor symptoms . here , we describe a peculiar case of a patient with features  suggestive  for hemiplegic migraine ( with prolonged hemiplegia and basilar symptoms ) associated with a basilar artery hypoplasia and in which a large pfo was found and surgically treated by percutaneous closure .
a 35-year - old male patient came to our attention 5-years ago because of acute motor weakness in the left side of his body , together with a slurred speech , dizziness , and mild headache .
the patient underwent the first episode 2-years before , when acutely he complained of same symptoms ( that lasted for 3  weeks ) .
he was a non smoker , and had a familial and medical history negative for nervous system disorders ( including migraine ) .
hematological screening for thrombophilic risk factors ( lac , thrombocythemia , etc . ) , brain ct , and mr imaging ( including dwi scan ) as in fig . 
.  1a rm scan with t2-flair ( fluid - attenuated - inversion - recovery ) technique , which shows a normal cerebral parenchyma .
rmi scan , performed using the adc ( apparent diffusion coefficient ) protocol , which shows no alteration of signal a rm scan with t2-flair ( fluid - attenuated - inversion - recovery ) technique , which shows a normal cerebral parenchyma .
rmi scan , performed using the adc ( apparent diffusion coefficient ) protocol , which shows no alteration of signal a mild hypertension ( 150/90  mm  hg ) was found , and a trans - esophageal - echocardiography ( tee ) showed a pfo with a large right - to - left shunt . on such basis a presumptive  cerebro - vascular  accident was diagnosed . antiplatelet inhibitor and anti - hypertensive drug ( ace - inhibitor )
were prescribed , and the patient was subsequently referred to an interventional center for trans - catheter pfo closure . a further diagnostic work - up with
magnetic resonance angiography showed a marked hypoplasia of vertebro - basilar system , ruling out other abnormalities of cerebral vessels and also deep venous thrombosis ( fig . 
2an angiographic rm scan ( using the time of flight technique , tof , with digital three - dimensional reconstruction and planar projection on a t1-weighted sequence ) , which shows the stenosis of the basilar artery an angiographic rm scan ( using the time of flight technique , tof , with digital three - dimensional reconstruction and planar projection on a t1-weighted sequence ) , which shows the stenosis of the basilar artery after the pfo closure , our patient experienced a full well - being until the summer 2007 , when he was referred to an emergency area for a new episode of acute weakness of the left side , prevalent in the arm and dysarthria , that completely recovered after 72  h. high blood pressure values were found and the ct scan of brain did not reveal ischemic or hemorrhagic acute lesion .
then a mr imaging and a mr angiography were obtained , confirming the basilar artery hypoplasia , previously observed .
the patient was hospitalized in a medical university center , and was evaluated for a new heart surgical treatment . after admission , he experienced a new episode with weakness of his left body , and again difficulty in the speech and dizziness
clinical picture gradually subsided within few days , and he was discharged with diagnosis of  possible hemiplegic migraine associated to basilar symptoms and stenosis of the basilar artery  .
based on the entity of the shunt , surgical pfo closure was not considered , and anticoagulant therapy ( warfarin ) was prescribed .
one month later , the patient came back to our observation because of a severe and abrupt dizziness with unsteady gait , suddenly followed by difficulty of speech articulation , diplopia , paresthesia , progressive weakness of the left side , nausea , and vomiting . in the next hours
this condition lasted for almost 5  h ; then the patient partially recovered , complaining of a mild throbbing occipital headache .
complete recovery of speech occurred after 1  week persisting with only slight hyposthenia of the left arm .
in our case some of the clinical features of the aura ( dysarthria , diplopia , dizziness etc . ) during attacks were expression of brainstem dysfunction , so fulfilling the criteria for diagnosis of basilar - type migraine ( ichd - ii ) .
however , the presence of the motor weakness ( consistent across attacks ) and the length of the aura ( more than 1  week ) , made the inclusion in this nosographic category inadequate . indeed , according to the last international classification of headache disorders 2nd edition revision ( ichd - ii ) ,
basilar - type migraine should be diagnosed only when no motor weakness occurs ; therefore the diagnosis of sporadic hemiplegic migraine ( no familial history of migraine in our patient ) could appear more appropriated , even if the lack of visual or sensory symptoms makes diagnosis very puzzling .
moreover the slow resolution of the motor aura that went beyond 24  h could be interpreted as  persistent aura without infarction  and the attacks classifiable as  probable migraine with aura  .
familial hemiplegic migraine has basilar - type symptoms in 60% of cases and recently a novel mutation in the atp1a2 gene ( r548h ) in members of a family with btm has been detected , suggesting that btm and familial hemiplegic migraine ( fhm ) may be allelic disorders [ 7 , 8 ] .
several data in literature indicate an increased incidence of pfo in ma patients compared with general population [ 9 , 10 ] .
a closure of pfo in patients with transient cerebral ischemia suffering from ma induced an improvement of ma episodes .
however , the role of pfo in migraine pathogenesis remains to be established and , based on the recently published mist trial data , there is no sufficient evidence that recurrence of migraine is improved by pfo closure . on such basis , in the present case the 4-year persisting remission of migraine can not be convincingly attributed to the pfo closure .
similarly , taking the natural history of hemiplegic migraine also into account , notoriously difficult to predict , it is not obvious to establish a causal link between pfo re - opening and attack relapsing .
nevertheless , it can not be excluded that , in our patient , pfo plays a role , at least as cofactor , in the complex pathogenetic mechanisms of migraine .
finally , it is interesting to note that our patient also had a marked hypoplasia of the basilar artery . there is a causal relationship between these conditions or is the association just coincidental ?
it is worth noting that in our patient , symptoms of brain - stem dysfunction were consistent across all attacks . since the original description of birkerstaff   that attributed the brainstem dysfunction in btm to the  constriction  of the basilar artery ,
 reversible vertebro - basilar ischemia  has been described in patients with btm and fhm [ 14 , 15 ] .
recently , it has been reported in a case of basilar artery fenestration and hypoplasia of the right posterior cerebral artery in a woman with basilar - type migraine . about the possible role of basilar artery stenosis
, it is to be noted that a higher frequency of hypoplastic vertebral artery ( va ) was found in ma .
the authors suggested that hypoplasia of va may be an additional factor leading to hypoperfusion in the posterior circulation during the aura phase .
more recently chuang et  al . hypothesized that va hypoplasia contributes to migraine trough complex neurovascular pathways rather than trough its low - flow volume .
although vascular mechanisms are recently considered less relevant in migraine pathogenesis , vascular factors could play a role in some phases of the cascade underlying the migraine attack .
we describe the case of a patient with atypical hemiplegic migraine and associated basilar symptoms , where a large patent foramen ovale ( pfo ) and hypoplasia of basilar artery were found . the longer period of 4-year remission of the headache attacks was coincident with the percutaneous pfo closure . 
 when 5  years after , hemiplegic migraine attacks relapsed , with more relevant basilar symptoms , a mild re - opening of pfo was found . 
 the atypical presentation of attacks with basilar symptoms and prolonged hemiplegia does not strictly fit the diagnostic criteria of ichd - ii .