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spinal cord infarctions are rare , especially at the cervical level [ 1 , 2 ] .
posterior spinal infarctions are less common than those located in the anterior territory , due to a pial collateral network and the dual posterior spinal artery . in most cases ,
we report a rare case of posterior cervical cord infarction revealed by an unusual pure sensory clinical picture .
the patient was a 41-year - old male with a history of dyslipidaemia and arterial hypertension for which he had received treatment .
five days after a motorcycle accident , he suddenly developed acute paraesthesia in the left occipital and temporal area of the head and the left side of the nape of the neck .
a few hours later , the paraesthesia extended towards the left side of the face .
these symptoms persisted and , subsequently , sensory changes spread over the entire left side of the trunk and the left arm .
he was hospitalised 8 h after the onset of symptoms . at the time of admission , the sensory symptoms persisted and the physical examination was normal .
all sensory modalities , such as pinprick , touch , vibratory sense and position sense , were normal , and no motor abnormalities were found in the head , neck , trunk and limbs .
the patient did not have any pain , dysphagia , vertigo or dizziness , nausea or vomiting , horner 's syndrome , gait ataxia or urinary retention ( national institutes of health stroke scale = 0 ) .
nine hours after the onset of symptoms , an mri showed a small lesion affecting the left posterior area of the cervical spinal cord at the c1 level ( fig .
the lesion appeared as a punctiform hypersignal with a decreased apparent diffusion coefficient . in the flair sequence ,
mr angiography showed a hypoplastic left vertebral artery , terminating in the posterior inferior cerebellar artery ( pica ) with no connection to the basilar artery .
the cervical doppler and cervical axial t1-weighted sequences were normal , as were the heart and aortic arch on the transoesophageal echocardiogram .
a small upper cervical infarction in the left posterior spinal artery territory was diagnosed . during hospitalisation ,
aspirin , statin and anti - hypertension treatments were started in the acute phase and continued after discharge . during follow - up , sensory soft symptoms persisted , and an mri at 3 months showed no change in the evolution of the lesion or the appearance of the left vertebral artery .
indeed , even if sensory patterns appear as cardinal signs , our case emphasises that their distribution can be very variable .
unilateral spinal cord infarctions with hemisensory symptoms , as in our case , are rarely reported , and sensitive symptoms are more frequently associated with weakness of the limbs [ 2 , 4 , 5 ] . in most cases ,
spinal cord infarcts induce bilateral sensory disturbance because lesions are more frequently bilateral or because the spinothalamic tract and dorsal column are both affected by a unilateral lesion . in our case ,
the first symptoms consisted of acute paraesthesia located in the left occipital and temporal area of the head and the left side of the nape of the neck . to our knowledge , this kind of clinical onset has not yet been reported in cases of posterior spinal infarction .
furthermore , the isolated sensory symptoms extended , and the clinical picture was similar to that encountered in pure sensory stroke ( pss ) with faciobrachial distribution .
pss is a well - defined clinical syndrome in which hemisensory symptoms predominate without the appearance of other major neurological signs . in most cases ,
pss is a consequence of thalamic stroke , but the brain stem and cerebral cortex have been widely reported as other potential sites [ 8 , 9 ] .
nevertheless , in our patient , although the initial onset of symptoms was abrupt , secondary sensory symptoms developed gradually within a few hours .
this initial evolution , which is rare in cerebral infarction , seems to be more common in the case of medullary infarction [ 4 , 10 ] .
as shown on sagittal t2-weighted images , the lesion was strictly limited to the c1 level , whereas in most cases , the infarct affected several levels of the spinal cord or a combination of the medulla and upper cervical cord [ 1 , 3 , 11 , 12 ] .
there is a good correlation between the sensory symptoms , their systematisation and the anatomical location of the infarct . in terms of anatomical structures , the lesion affected the left posterior horn of the grey matter , a lateral part of the left posterior column , defined as the cuneate fasciculus , and a restricted posterior part of the left lateral column . at this level ,
as previously reported , these are the most frequently affected structures in cases of spinal posterior infarction [ 3 , 5 ] . the left anterior horn , spinothalamic tract and corticospinal tract were unaffected .
paraesthesia in the c2 dermatome , as observed in arnold 's neuralgia , was due to the posterior horn involvement , defined as the lesional syndrome of spinal involvement .
paraesthesia in the trunk and arm can be assimilated as the sublesional syndrome due to the damage to the lateral part of the dorsal column .
the systematisation of symptoms in our patient confirms the hypotheses that have already been reported on the somatotopy of the dorsal column , in which fibres from the rostral parts of the body are located laterally [ 13 , 14 ] .
our patient did not have any objective epicritic sensory disturbances , confirming that the dorsal column can not be the only ascending pathway required to transmit epicritic information .
the symptoms appearing on the left side of the face were due to the damage to the descending tract and nucleus of v , which are present at this level of the spinal cord .
most posterior spinal artery infarcts are the consequence of an aortic or vertebral artery disease .
intrinsic diseases of the intraspinal arteries or a cardioembolism are much less common [ 5 , 15 ] . after an extensive diagnostic workup , we did not find any evidence of artery dissection , a cardioembolic source or inflammatory arteritis , confirming that the cause of this type of infarct remains unknown .
nevertheless , because the left vertebral artery was smaller than the right one , a diagnosis of dissection was initially put forward . despite having had a motorcycle accident a few days earlier , the patient had no cervical pain or headaches , and no parietal haematoma was found on the mra or axial t1-weighted images of the neck . moreover , the appearance of the left vertebral artery was unchanged in an mra test 3 months later . the left vertebral artery terminated in the pica .
this particular arterial disposition raises questions as to the territory supplied by the vertebral artery and the origin of the posterior spinal artery . according to lasjaunias et al .
, some hypoplastic vertebral arteries supply only the cervical territories , such as the upper cervical cord . in these cases ,
these data could explain why , in our patient , the infarct did not extend to the medulla oblongata .
usually , posterior spinal arteries arise either from the vertebral artery or from the pica [ 16 , 17 ] . to our knowledge , no more specific anatomical information is available regarding the origin of posterior spinal arteries in cases of vertebral arteries terminating in the pica . in conclusion , our case illustrates an unusual clinical picture of posterior spinal artery infarction and confirms the difficulty of establishing this diagnosis .
this case highlights the complexity of the posterior spinal artery territory , especially at the level of the upper cervical cord .
spinal cord infarctions are rare , especially at the cervical level and in the posterior spinal artery territory . 
 moreover , this diagnosis is difficult to establish as the clinical picture varies . 
 even if sensory patterns appear as cardinal signs , their distribution can be very variable . 
 we report a rare case of posterior cervical cord infarction revealed by an unusual pure sensory clinical picture .