symptomatic trigeminal neuralgia ( tn ) is caused by a demonstrable structural lesion other than vascular compression , typically posterior fossa tumors or multiple sclerosis [ 1 , 2 ] .
this pain may be either persistent or intermittent , sometimes occurring in brief attacks that may reproduce tn features . here ,
we report the case of a patient with wallenberg s syndrome who started having shock - like painful paroxysms in the first division of the trigeminal nerve ( v1 ) .
a 41-year - old man visited our hospital reporting a 48-h lasting pain localized on the right side of his neck .
three hours before entering the emergency room , the patient felt sudden dizziness with gait instability and clumsiness of his right limbs .
his past medical history was remarkable for non - controlled hypertension as well as frequent alcohol and occasional cocaine intake .
the patient denied any drug intake in the past few days . on a general physical examination , the only relevant
the neurologic examination revealed moderate dysarthria , a right horner syndrome , vertical nystagmus in all extreme gaze positions , an absent right gag reflex , right facial and left two limb hypoalgesia and thermoanesthesia , mild paresis of the right limbs , and severe right limb ataxia .
an early brain computed tomography ( ct ) scan did not detect any significant abnormalities , but magnetic resonance imaging ( mri ) showed a recent infarction in the right lateral medulla ( fig . 
in addition , complete occlusion of the right vertebral artery was demonstrated on magnetic resonance angiography ( mra ; fig .  2 ) .
there was no evidence of a vascular contact at the root entry zone of the right trigeminal nerve.fig . 
a axial t2-weighted flair mri shows slight hyperintensities in the right lateral medulla and right cerebellum .
b diffusion - weighted mri demonstrates restricted water motion in the lesion shown in a , indicating recent infarctionfig . 
coronal maximum intensity projection from mra reveals occlusion of the right vertebral artery , which is likely due to artery dissection magnetic resonance imaging ( mri ) .
a axial t2-weighted flair mri shows slight hyperintensities in the right lateral medulla and right cerebellum .
b diffusion - weighted mri demonstrates restricted water motion in the lesion shown in a , indicating recent infarction magnetic resonance angiography ( mra ) .
coronal maximum intensity projection from mra reveals occlusion of the right vertebral artery , which is likely due to artery dissection forty - eight hours after admission , the patient suffered from aspiration pneumonia with breathing compromise and required intubation at the intensive care unit ( icu ) .
after several lung complications , he was eventually extubated and returned to our hospital ward 1  month after the stroke . at this moment
we found the same neurologic signs he presented at onset , though milder , including some sensory impairment on the right side of his face .
two days after leaving the icu , our patient started having brief electric shock - like pains in the whole distribution of the first division ( v1 ) of the right trigeminal nerve .
pain attacks fulfilled diagnostic criteria for symptomatic tn , according to the international classification of headache disorders , 2nd edition ( ichd - ii ) .
they lasted for 35  s , occurred at least 10 times per hour , and were given a score of 8 out of 10 on a visual analogue pain intensity scale .
treatment with gabapentin was initiated . while being on a dose of 300  mg t.i.d . , the patient experienced a decrease in both pain frequency and intensity plus a restriction of the pain to a more circumscribed periocular area .
when gabapentin was titrated up to 600  mg t.i.d , the pain was finally controlled . at discharge
he maintained this dose and had no recurrences of the pain through a 2-month follow - up .
it is widely accepted that the commonest cause of tn is compression of the trigeminal root entry zone by a blood vessel .
the term  classical tn  is applied to those cases with potential vascular compression or unknown etiology .
when a causative lesion other than vascular compression is demonstrated , a diagnosis of  symptomatic tn  is made .
overall , symptomatic tn accounts for 15% of cases of nt , and the majority of these are caused by cerebellopontine angle tumors or multiple sclerosis .
although a brainstem infarction had been previously suggested as a possible cause of tn , it was balestrino and leandri who reported the first well - documented case in 1997 .
these authors discovered a small ischemic lacune at the right lateral part of the pons in a patient with a 4-year history of ipsilateral second division ( v2 ) tn and slight sensory loss . in 1998
golby et al . described a patient who started having lancinating pain in v1 and v2 distributions on the left side .
he had experienced sudden hemifacial numbness 1  year before , and mri demonstrated an old ischemic lesion at the root entry zone of the trigeminal nerve . in 2004 peker et al . reported a female patient who suddenly developed a neuralgic pain in her left chin and cheek .
a slight hypoesthesia was found in v2 and v3 territories , and mri showed a chronic infarction transecting the central trigeminal pathways within the pons . in 2006 ,
warren et al . described a female patient who presented with concurrent left trigeminal and glossopharyngeal neuralgia .
katsuno and teramoto have recently reported a patient with sudden onset of facial numbness and tn in the right v2 dermatome .
mri showed an acute pontine infarction , just at the root entry zone of the right trigeminal nerve .
the pathogenesis of tn secondary to a brainstem ischemic lesion is uncertain . the main hypothesis states that demyelination in the central trigeminal pathways would cause ephaptic transmission and thereby abnormal electric impulses , as it happens in multiple sclerosis .
other theories postulate that irritation of trigeminal structures in a bed made from the scar would be the base of excessive reactivity in an epileptic - like manner .
facial pain may be a feature of wallenberg s lateral medullary syndrome , along with a decrease of pain and temperature sensation of the face .
other clinical features include vertigo , eye movement disorders , an ipsilateral horner s syndrome , ipsilateral limb ataxia , and contralateral sensory deficit . in reviewing the literature , pain incidence rates following a lateral medullary infarction vary largely , with higher rates in follow - up observations .
the pain may start just at the stroke onset , but most patients have a latency between 2  weeks and 6  months .
some patients feel a constant , boring , pain , while others describe short pain attacks that occur either spontaneously or related to an innocuous stimulus .
therefore , wallenberg syndrome is a typical cause of central post - stroke pain , and this pain may occasionally take the attributes of a symptomatic tn . among 12 patients with wallenberg s syndrome , fitzek et al . found 6 patients with facial pain .
the latency between the stroke and pain onset ranged between 1  month and 2  years .
facial pain was always ipsilateral to the infarction , and was mostly localized in the periorbital region .
these patients reported short pain attacks lasting seconds to minutes , and three of them also had persistent pain .
although a diagnosis of tn was not made , the shortest pain attacks  i.e .
, those lasting just a few seconds  apparently had typical tn features . our patient also had neuralgiform pain attacks in association with a wallenberg s syndrome .
the painful paroxysms were brief and intense , fulfilling ichd - ii diagnostic criteria for symptomatic tn .
they started with a latency of 1  month after the stroke onset , which was in line with fitzek s series . while the hypoesthesia extended through the territory of the three trigeminal branches , the pain occurred in a v1 distribution .
this was also in accordance with fitzek s cases , whose pain was mostly centered in the periorbital region . in contrast , classical tn usually starts in v2 or v3 , and only very rarely affects v1 [ 1 , 11 ] .
the somatotopic arrangement of trigeminal fibers may possibly account for these topographical differences between tn due to nerve root compression and tn due to a lateral medullary infarction .
lesions of the dorso - lateral medulla involve both the trigeminal descending tract and the trigeminal spinal nucleus , and this may lead to sensory impairment and pain in the ipsilateral face . in fitzek
s clinical series of wallenberg s syndrome , patients with facial pain had lesions covering the trigeminal spinal tract and nucleus at the lower medulla , as demonstrated by mri .
in addition , the r2 blink reflex component was abnormal only in patients with facial pain .
likewise , sensory thresholds in the ipsilateral face were specifically elevated in those patients presenting with facial pain [ 3 , 10 ] .
the existing studies all deal with tn associated with multiple sclerosis and are small open - label trials .
three trials including a total of 19 patients with multiple sclerosis have reported an effect of gabapentin alone or associated with carbamazepine .
in fact , gabapentin , pregabalin or amitriptyline are currently recommended for first line treatment in central neuropathic pain .
indeed , he experienced significant improvement when the drug was initiated , and had complete relief with further titration . in conclusion
ischemic lesions covering the trigeminal spinal tract and nucleus at the lower levels of the medulla seem to be involved in the pathogenesis of the pain .
gabapentin might be an effective drug for symptomatic tn related to a lateral medullary infarction .
 symptomatic trigeminal neuralgia due to a brainstem infarction is said to be rare . 
 however , facial pain is not uncommon in wallenberg s syndrome . 
 facial pain related to a wallenberg s syndrome may be either persistent of intermittent , and occasionally occurs in brief attacks . here 
 , we report a patient with a right lateral medullary infarction who started having first division trigeminal neuralgia 1  month after the stroke . the pain paroxysms were suppressed with gabapentin . 
Introduction
Case report
Discussion