encephalocele is a rare condition that consists of herniation of cerebral matter through openings of dura and skull the incidence of the congenital form is estimated to be 1 per 3,000 to 10,000 live births.1 
 2 many classification systems for encephalocele exist ; however , the most widely accepted is that from matson and ingraham,3 based on the location of the encephalocele : basal , sincipital , convexity , and atretic . convexity encephalocele , subdivided into frontal , parietal , occipital , and cervico - occipital , is the most common type.3 those lesions are usually located at midline , extending from the nasal region to the occiput , although off midline temporal regions have also been reported.4 
 5 a majority of the encephaloceles are congenital and manifest in childhood . here , we report a rare case of a traumatic intradiploic encephalocele ( ie ) presenting with contralateral hemiparesis several decades after an initial pediatric trauma . a 45-year - old caucasian , right - handed man presented to our emergency department ( ed ) with 3 to 4 weeks history of progressive gait disturbances and left lower extremity weakness . his pertinent medical history was negative for any recent history of head trauma , but was significant for a moderate traumatic brain injury ( tbi ) at the age of 9 years , where he fell off a tree and sustained a closed parietal skull fracture with no posttraumatic cognitive or neurologic deficits . he had no history of seizures , central nervous system infections , stroke , or brain tumor . his neurological exam at admission was significant for left hemiparesis ( strikingly more pronounced on lower than upper extremity ) and positive left pronator drift testing . he was initially seen in the ed where a magnetic resonance imaging ( mri ) showed ie of the right parasagittal parietal bone containing portions of the right precentral gyrus and surrounding brain parenchyma ( fig . a 3-mm ( a , b ) coronal and ( c ) axial reformats in both ( a ) brain and ( b ) bone windows on ( d ) ct and coronal mri showing herniated brain parenchyma . ct , computed tomography ; mri , magnetic resonance imaging . noncontrasted computed tomography ( ct ) demonstrated a well - circumscribed , 4.3  3.7 cm area of osteolysis in the right parasagittal parietal bone , with internal soft tissue attenuation ( fig . c ) , complete erosion of the inner table , and noncontiguous lytic changes of the outer table ( fig . 1b , c ) . mri with and without gadolinium contrast administration demonstrated a right parasagittal dural defect with intradiploic herniation of the right precentral gyrus ( fig . 1d ) . there was no restricted diffusion to suggest acute infarction ( fig . ( a ) axial 5 mm se ) t2 images , ( b ) axial 5 mm blood suppressed se t1 images , ( c ) axial 5 mm flair images , and ( d ) axial 5 mm postcontrast se t1 images ( 12 mm gadavist ) . ct , computed tomography ; mri , magnetic resonance imaging ; se , spin echo after initial neurosurgical evaluation in the ed , the patient was admitted to the neurosurgical ward and started on dexamethasone 4 mg intravenously every 6 hours . his left lower extremity weakness responded positively to the initial steroids therapy , with partial but transient improvement on his leg weakness to antigravity strength and ambulatory with a rolling walker . he was reluctant to proceed with surgical intervention initially , and elected to continue hospital observation for a few days . since no sustainable improvement on his strength was seen after 2 days of high - dose dexamethasone treatment , he decided to proceed with surgical intervention . under general anesthesia , and using ct - guided intraoperative frameless stereotactic navigation , the area correspondent to the encephalocele was identified and marked . the calvarium was exposed through a bicoronal incision . the bone overlying the encephalocele appeared to be mottled and thin . cortical brain matter was visualized directly underneath the most thinned portions of the right parietal bone . it appeared pale with no evidence of cortical vasculature , and the usual gyral anatomy had been lost . starting from the areas of bone dehiscence , the craniectomy was then extended centrifugally until identification of the normal inner table surrounding the whole encephalocele . once the margins of the encephalocele were completely identified and dissected , a large craniotomy incorporating the bone defect was completed using high - speed craniotome ( fig . the pial - arachnoid plane surrounding that area was very sclerotic and firmly adherent to the encephalocele pedicle . due to the risk of vascular injury to an already friable but apparently still eloquent brain , we decided not to proceed with arachnoidal opening or resection of the encephalocele sac . the bone flap was replaced with a titanium mesh used for coverage over the craniectomy site . ( a ) intraoperative picture showing large craniotomy incorporating the bone defect . the pial - arachnoid plane surrounding that area was very sclerotic and firmly adherent to the encephalocele pedicle . the defect was shown in ( b ) and ( c ) for dorsal and ventral side , respectively . he tolerated the procedure well and was kept in intensive care unit for 24 hours without complications . postoperative noncontrasted ct head revealed no ischemic changes on the surrounding parenchyma and adequate reduction of the encephalocele ( fig . ( c ) a 3-mm axial bone window and coronal reformats in both ( b ) brain and ( a ) bone windows on postoperative ct . on 2-month follow - up , his preoperative left leg weakness has greatly improved with near resolution of preoperative hemiparesis . a 45-year - old caucasian , right - handed man presented to our emergency department ( ed ) with 3 to 4 weeks history of progressive gait disturbances and left lower extremity weakness . his pertinent medical history was negative for any recent history of head trauma , but was significant for a moderate traumatic brain injury ( tbi ) at the age of 9 years , where he fell off a tree and sustained a closed parietal skull fracture with no posttraumatic cognitive or neurologic deficits . he had no history of seizures , central nervous system infections , stroke , or brain tumor . his neurological exam at admission was significant for left hemiparesis ( strikingly more pronounced on lower than upper extremity ) and positive left pronator drift testing . he was initially seen in the ed where a magnetic resonance imaging ( mri ) showed ie of the right parasagittal parietal bone containing portions of the right precentral gyrus and surrounding brain parenchyma ( fig . a 3-mm ( a , b ) coronal and ( c ) axial reformats in both ( a ) brain and ( b ) bone windows on ( d ) ct and coronal mri showing herniated brain parenchyma . noncontrasted computed tomography ( ct ) demonstrated a well - circumscribed , 4.3  3.7 cm area of osteolysis in the right parasagittal parietal bone , with internal soft tissue attenuation ( fig . c ) , complete erosion of the inner table , and noncontiguous lytic changes of the outer table ( fig . mri with and without gadolinium contrast administration demonstrated a right parasagittal dural defect with intradiploic herniation of the right precentral gyrus ( fig . ( a ) axial 5 mm se ) t2 images , ( b ) axial 5 mm blood suppressed se t1 images , ( c ) axial 5 mm flair images , and ( d ) axial 5 mm postcontrast se t1 images ( 12 mm gadavist ) . ct , computed tomography ; mri , magnetic resonance imaging ; se , spin echo after initial neurosurgical evaluation in the ed , the patient was admitted to the neurosurgical ward and started on dexamethasone 4 mg intravenously every 6 hours . his left lower extremity weakness responded positively to the initial steroids therapy , with partial but transient improvement on his leg weakness to antigravity strength and ambulatory with a rolling walker . he was reluctant to proceed with surgical intervention initially , and elected to continue hospital observation for a few days . since no sustainable improvement on his strength was seen after 2 days of high - dose dexamethasone treatment , he decided to proceed with surgical intervention . after initial neurosurgical evaluation in the ed , the patient was admitted to the neurosurgical ward and started on dexamethasone 4 mg intravenously every 6 hours . his left lower extremity weakness responded positively to the initial steroids therapy , with partial but transient improvement on his leg weakness to antigravity strength and ambulatory with a rolling walker . he was reluctant to proceed with surgical intervention initially , and elected to continue hospital observation for a few days . since no sustainable improvement on his strength was seen after 2 days of high - dose dexamethasone treatment , he decided to proceed with surgical intervention . under general anesthesia , and using ct - guided intraoperative frameless stereotactic navigation , the area correspondent to the encephalocele was identified and marked . cortical brain matter was visualized directly underneath the most thinned portions of the right parietal bone . it appeared pale with no evidence of cortical vasculature , and the usual gyral anatomy had been lost . starting from the areas of bone dehiscence , the craniectomy was then extended centrifugally until identification of the normal inner table surrounding the whole encephalocele . once the margins of the encephalocele were completely identified and dissected , a large craniotomy incorporating the bone defect was completed using high - speed craniotome ( fig . the pial - arachnoid plane surrounding that area was very sclerotic and firmly adherent to the encephalocele pedicle . due to the risk of vascular injury to an already friable but apparently still eloquent brain , we decided not to proceed with arachnoidal opening or resection of the encephalocele sac . the bone flap was replaced with a titanium mesh used for coverage over the craniectomy site . ( a ) intraoperative picture showing large craniotomy incorporating the bone defect . the pial - arachnoid plane surrounding that area was very sclerotic and firmly adherent to the encephalocele pedicle . the defect was shown in ( b ) and ( c ) for dorsal and ventral side , respectively . he tolerated the procedure well and was kept in intensive care unit for 24 hours without complications . postoperative noncontrasted ct head revealed no ischemic changes on the surrounding parenchyma and adequate reduction of the encephalocele ( fig . ( c ) a 3-mm axial bone window and coronal reformats in both ( b ) brain and ( a ) bone windows on postoperative ct . on 2-month follow - up , his preoperative left leg weakness has greatly improved with near resolution of preoperative hemiparesis . a cephalocele is a protrusion of cerebral contents through a defect in the dura or skull . these lesions are classified according to their location and contents ( meninges , brain parenchyma , ventricles , and/or vasculature ) . the presence of brain parenchyma characterizes an encephalocele , whereas those without brain parenchyma are called meningocele . the location of these lesions varies as they may involve the posterior fossa , occipital , basal , frontoethmoidal , and/or parietal regions.6 
 7 
 8 depending on the etiology , cephaloceles are further classified as primary or secondary . in the case of primary cephaloceles , a congenital defect exists in the dura or skull , usually at the site of a cranial suture , representing a midline closure defect of the neural tube . in secondary cephaloceles , a preceding injury such as infection , tumor , trauma , or surgery is usually the underlying cause . in this case report , we present an extremely rare phenomenon of a symptomatic posttraumatic parietal ie manifesting 36 years following traumatic head injury . medline and pubmed database literature search revealed only 11 cases previously reported in the literature . five had no history of trauma , four cases9 
 10 
 11 ( including the present study ) were found to be posttraumatic and/or iatrogenic , and one did not comment on any supposed etiology for the encephalocele.12 therefore , traumatic injuries to the skull were the reported etiology of the cephalocele in approximately 40% of the literature cases . the initial insult typically occurs in childhood with a delayed diagnosis decades later after manifestation of signs and symptoms , if at all.13 
 14 
 15 
 16 
  abbreviation : nr , not reported ; lle , left lower extremity ; lue , left upper extremity ; rle , right lower extremity ; rue , right upper extremity . patil and etemadrezaie9 reported a 64-year - old man had head trauma 8 months prior to experiencing an enlarging palpable scalp mass . lenthall and penney10 reported a 15-month - old infant sustained a head injury and presented with growing fracture with pulsatile mass 9 months later . our patent presented with progressive hemiparesis 36 years following pediatric traumatic head injury . depending on where the lesion is , symptoms may vary widely , from seizures to aphasia , numbness , hemiparesis , or even asymptomatic . of the case reports , the most common symptoms are hemiparesis / weakness11 
 12 
 17 ( four patients including the present study ) , seizures5 
 17 ( two patients ) , palpable mass9 
 10 ( two patients ) ; one was incidentally found.18 
  surgical repair with or without excision of the herniated brain parenchyma is generally performed in symptomatic patients . clinical response is generally favorable with minor improvement in symptoms to completely asymptomatic on follow - up . in order for an encephalocele to occur d'almeida and king19 postulated that if only the inner table and dura mater are affected by the fracture from tbi , the diploic space is opened and enlarged over time by pulsation of cerebrospinal fluid ( csf ) . lenthall and penney10 stressed the importance of an outward driving force for enlargement of the diploic space secondary to normal brain growth , csf pulsatility , or increased intracranial pressure , as also seen in the coughing spell reported by loumiotis et al.12 patil and etemadrezaie9 proposed that low - velocity blunt injury may fracture only the inner table , which is thinner . the depression tears the dura and the recoil creates a negative pressure that forces the underlying arachnoid and brain into the diploic space . menk et al13 proposed that there could be congenital factors , although the article focused on intradiploic pseudomeningocele as opposed to ie . they proposed that intradiploic cyst develops through foveolae granulare which are anatomical and physiological defects that form a hollow space of the inner table . these granulations usually lie in the frontoparietal bone and near the superior sagittal sinus . in the setting of head trauma , dura and arachnoid membranes differential diagnosis includes epidermoid or dermoid cyst , cavernous hemangioma , eosinophilic granuloma , plasmacytoma , metastasis , and osteosarcoma.18 mri is necessary to establish a diagnosis . herniation of brain parenchyma through a dural defect into intradiploic space is what separates this lesion from the rest on the differential , as is seen in our case . however , definitive diagnosis still lies in surgical exploration and histopathological examination.13 
 20 
 21 
  surgical correction with craniotomy , reduction of herniated cortex , excision of herniated parenchyma , and cranioplasty have been reported as the optimal management strategy . if a patient remains asymptomatic , observation and regular follow - up may be adequate . surgical excision of the herniated brain parenchyma depends on the proximity to the location of the vital functional areas of the brain such as the motor cortex . in our case , because of the risk of vascular injury to an already friable but apparently still eloquent brain , we decided not to proceed with arachnoidal opening or resection of the encephalocele sac . functional mri , magnetic source imaging of evoked sensory potential , or intraoperative cortical mapping have been used to help with defining eloquent cortex.17 frameless neuronavigational systems as used in our case are recommended to enhance precision . regardless of the method , meticulous dissection must be exercised to maximize recovery and minimize complications . this case is unique in that the patient became symptomatic several decades after a pediatric head trauma .