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Cushing was the first to offer a systematic descriptionof decompressive craniectomy for relief of intracranialpressure,2 and since that time, surgical decompression has

been advocated as a treatment for severe brain edemaassociated with high intracranial pressure.1,7,8,13,14,16,25,27

Some authors have reported that decompressive craniec-tomy reduces the risk of death in patients who sustainsevere cerebral edema after head injury. Recently we ob-served an increasing number of patients who underwent areplacement of the bone flap. The indications for repair of

large cranial bone defects are usually protective or cos-metic. To our knowledge, the first reported use of thecranioplasty technique to repair skull defects dates to

1670, when J. van Meekren successfully used a bone of adog to repair a cranial defect in man. Although the graftwas successful, it was removed because the church tookgreat offense to using an animal bone in man and viewedit as marring Gods image.24

Curative effects have been noted following cranioplas-ty.17,21,33 These procedures are usually performed monthsafter the initial injury or operation. A well-known indica-tion for cranioplasty is the STsevere headache, dizzi-ness, undue fatigability, poor memory, irritability, convul-sions, mental depression, and intolerance to vibration.9,11,36,37 In 1977 Yamaura and Makino37 coined the term syn-drome of the sinking skin flap and underlying tissue, andthey reasoned it was secondary to the action of atmos-

Neurosurg Focus 8 (1):Article 9, 2000

The influence of cranioplasty on postural blood flowregulation, cerebrovascular reserve capacity, and cerebralglucose metabolism

PETER A. WINKLER, M.D., WALTER STUMMER, M.D., RAINER LINKE, M.D.,KARTIK G. KRISHNAN, M.D., AND KLAUS TATSCH, M.D., PH.D.

Departments of Neurosurgery and Nuclear Medicine, Klinikum Grohadern,Ludwig Maximilians University of Munich, Munich, Germany

The indications for cranioplasty after decompressive craniectomy are cosmetic repair and, mainly, restoration ofcerebral protection. Although neurological improvement after cranioplasty is repeatedly noted, the reasons for this still

remain unclear. Few observations concerning the impact of CSF hydrodynamic and/or atmospheric pressure were pub-lished during the last decades. Relevant data concerning the cerebrovascular reserve capacity and cerebral glucosemetabolism before and after cranioplasty have been lacking until now. To gain further insight, the present study wasundertaken to investigate the impact of cranioplasty on indices of cerebral blood flow regulation and metabolism.

Thirteen patients in whom extensive craniectomies had been performed underwent a meticulous study of blood flowvelocities in the middle cerebral artery (MCA) and extracranial internal carotid artery (ICA), as assessed by transcra-nial Doppler (TCD) ultrasonography during postural maneuvers (supine and sitting positions) and during stimulationwith 1 g of acetazolamide for the interpretation of cerebrovascular reserve (CVR) capacity. Twelve patients underwent18-fluorodesoxyglucose positron emission tomography. These measurements were made before and 7 days after cran-ioplasty.

Cranioplasty improved preoperative differences in MCA blood flow velocities when comparing the injured with thenoninjured hemisphere. Similarly, cranioplasty resolved decreases in extracranial ICA blood flow in the injured hemi-sphere that were induced by postural changes, which was a constant finding prior to this procedure. More strikingly,however, the CVR capacity, which was severely impaired in both hemispheres, significantly increased after the pro-cedure. Metabolic deficits, which were observed in the injured as compared with the noninjured hemisphere, were

found to improve after reimplantation of the skull bone flap.Cranioplasty appears to affect postural blood flow regulation, CVR capacity, and cerebral glucose metabolismmarkedly. Thus, early cranioplasty is warranted to facilitate rehabilitation in patients after decompressive craniectomy.

KEY WORDS cranioplasty cerebrovascular reserve capacity

postural blood flow regulation cerebral glucose metabolism

syndrome of the trephined syndrome of the sinking bone flap

Neurosurg. Focus / Volume 8 / January, 2000 1

Abbreviations used in this paper: CBF = cerebral blood flow;CSF = cerebrospinal fluid; CVR = cerebrovascular reserve; ICA =internal carotid artery; MCA = middle cerebral artery; PET =positron emission tomography; ST = syndrome of the trephined;TCD = trancranial Doppler; 18-FDG = 18-fluorodesoxyglucose.


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pheric pressure. In 1968 Langfitt18 experimentally showedthat the CSF pressure in the upright position is higher in amodel with a large bony defect than that in one with aclosed skull, whereas in 1976, Magnaes20 reported that the0 CSF pressure level and the hydrostatic indifferent pointwere cranially shifted in five patients with large flaccidskull defects, in whom the parameters returned to normal

levels after cranioplasty. Neurological improvement isrepeatedly noted, possibly caused by improvement inCBF after cranioplasty.

A controversial indication for cranioplasty is the pre-vention or amelioration of postoperative epilepsy.10 How-ever, in more recent studies the authors demonstrate thatcranioplasty does not alter the frequency or incidence ofpostoperative epilepsy.34 In only a few reports is a neuro-logical amelioration demonstrated in patients after thebone flap replacement.30,32 The personal case of one pa-tient, who recovered dramatically (his capacity for lan-guage was restored immediately after cranioplasty), stim-ulated us to conduct this prospective study to obtain moreinsight in the pathophysiological background of this con-dition (Werani, Radau, and Winkler, manuscript in prepa-ration).

Some information about the hydrodynamic studies ofCSF before and after cranioplasty is available, and previ-ous investigations were published by Fodstad, et al.5,6

Understandably, skull defects after decompressivecraniectomy might have greater impact on dynamic CBFregulation than on resting blood flow, thus contributing tothe impairment of normal brain function and metabolism.

Because this issue has not yet been previously ad-dressed, the present prospective study was designed toinvestigate the influence of cranioplasty on indices ofCBF as determined by TCD ultrasonography during pos-tural maneuvers. From the TCD findings the CVR reservecapacity (as a percentage value) was calculated. Further-more, the effect of cranioplasty on cerebral metabolismwas investigated using 18-FDG PET, which also served asan indicator of functional improvement.

All tests were performed by highly qualified profes-sionals. The first author (P.A.W.) was responsible for es-tablishing the TCD ultrasonography as a routine proce-dure at this institution in 1986. The PET studies weresupervised by the senior author (K.T.).

CLINICAL MATERIAL AND METHODS

This study was approved by the ethical committee of

the Ludwig Maximilian University.Surgical Protocol

Thirteen patients were included in this study. Data onthe clinical diagnoses and the time between explantationand reimplantation of bone flaps are presented in Table 1.In 10 (77%) of 13 cases the removed autologous bone flapwas reimplanted in an average of 11.1 weeks (range 620weeks),and in three cases (23%), a stereolithographicmethod was used to perform a three-dimensional recon-struction of the skull defect due to a long duration betweenexplantation of the bone flap and reconstruction of thedefect (the time lapse ranged from 3 years to an unknownperiod of time). Computerized tomography scanning was

performed in all patients both pre- and postoperatively ona routine basis (Fig. 1).

Measurement of Cerebrovascular Reserve Capacity

We used TCD ultrasonography to acquire informationon the CBF and thereby the CVR capacity. TranscranialDoppler ultrasonography (TC-2-64; EME, berlingen,Germany) to determine the blood flow velocities in theMCA and extracranial ICA was performed in all patientspre- and postoperatively. Measurements were obtainedprior to and 7 days after cranioplasty. Supine and sittingpositions were considered for postural changes in CBF byusing the same technique. The CVR capacity was calculat-ed after flow stimulation with 1 g of intravenously admi-nistered acetazolamide as: where V

stis the stimulated TCD

flow velocity and Vris the resting TCD flow velocity.

Positron Emission Tomography Studies

The clinical condition in 12 of the 13 patients permittedPET for assessment of cerebral metabolism prior to and 7days after cranioplasty. Patients fasted for at least 6 hoursprior to the examination (blood glucose levels 88137mg/dl precranioplasty and 78124 mg/dl postcranioplas-ty). Static PET studies were performed for 30 minutes,starting 30 minutes after the intravenous administration of18-FDG (range prior to cranioplasty 343405 MBa; rangeafter cranioplasty 325406 MBa) by using a tomograph(Siemens HR; Knoxville, TN) in two-dimensionalmode, permitting simultaneous acquisition of 63 contigu-

ous transverse sections of 2.46-mm thickness covering anaxial field of view of 15.5 cm. Tissue attenuation of 511-keV gamma radiation was measured for 15 minutes withthree 68-Ge rotating rod sources. The emission data werereconstructed by a filtered back projection reconstructionalgorithm in which a Hanning filter at a cut-off frequencyof 0.5 Nyquist was used. Positron emission tomographyexaminations were performed in the calm atmosphere of aroom with dimmed lighting, no conversation, and onlyambient noise from the scanner gantry fans.

Analysis of PET Data

Volumes of interest were defined for the quantitativeassessment of FDG uptake in the cortex of both hemi-spheres. To achieve comparability, the results of all PETstudies were coregistered to a standardized volume map,adjusting nine parameters, three each for rotation, transla-tion, and anisotropic scaling. The mean FDG uptakes inboth hemispheres were established before and after cran-ioplasty. Asymmetry between homologous regions wascalculated, and the influence of cranioplasty on cerebralglucose metabolism was estimated as:

P. A. Winkler, et al.

2 Neurosurg. Focus / Volume 8 / January, 2000

ipsilateral contralateral____________________ 200%ipsilateral + contralateral


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Statistical Analysis

All values here are presented as mean standard devi-

ation. The KolmogoroffSmirnow test was used to ana-lyze the normal distribution, and significance of data dif-ferences was tested using the two-tailed paired t-test orWilcoxons test. An error probability of p less than 0.05was considered significant. The PET results were corre-lated with the results of TCD investigations and neu-ropsychological tests or clinical findings.

RESULTS

Clinical Outcome

The diagnosis at the time of decompressive craniotomy,the patients clinical symptoms before cranioplasty, andthe condition there after are listed in Table 1.

An overall functional and cognitive improvement inpatients could be observed after they received theirimplants. However, functional and cognitive improve-

ment was not found in three patients in whom a significanttime lapse had occurred between craniectomy and cranio-plasty. In the patient in Case 4 with ArnoldChiari mal-formation, the reconstruction of the cranial defect effectedslight improvement: his cognitive function improvedslightly, and he became more cooperative, but ataxia re-mained unchanged, not considering the longest time lapsebetween decompressive craniectomy and reconstruction.In the patient in Case 3, although 18 years had lapsedbetween decompressive craniectomy and cranioplasty, aslight improvement was observed. However, in the patientin Case 7, one of the three long-term cases, ironically theclinical condition remained unchanged. In all other cases(except Case 2) either the clinical condition completely

Neurosurg. Focus / Volume 8 / January, 2000

Influence of cranioplasty on rehabilitation

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TABLE 1CLINICAL DATA OBTAINED IN 13 PATIENTS IN WHOM CRANIOPLASTY WAS PERFORMED AT DIFFERENT TIMES AFTER CRANIECTOMY*

Clinical OutcomeCase Age Reason for TimeNo. (yrs) Craniectomy Lapse Precranioplasty Postcranioplasty

1 34 SAH; SDH; rt ICH 12 wks rt hyperreflexia; anxiety; lack anxiety improved; restless-

of drive; reduced alertness, ness reduced; cooperativecooperation & learning ability

2 31 rt subtotal MCA infarction 20 wks lt hemineglect; lt hemiplegia; hemineglect improved;UMN facial paralysis paresis partially resolved;

spastic paresis of lt legimproved (could walk onher own); plegic arm

3 63 rt acute SDH 18 yrs lt severe paraparesis slight improvement in para-paresis

4 25 Arnold-Chiari malforma- unknown ataxia, lt hyperreflexia; func- cognititve function improved;tion; syringomyelia; in tional nystagmus; reduced cooperative; ataxia persistschildhood rt SDH; down- cognitionward displacement ofthalamic structures

5 69 rt acute SDH (trauma) 12 wks gait disturbance; severe ataxia and gait disturbanceataxia significantly improved

6 56 lt frontal ICH 11 wks rt hemiparesis; severe complete improvement (diedmotoric aphasia of pulmonary embolism)

7 52 rt basal ganglia hema- 3 yrs lt spastic hemiparesis no change in clinical condi-toma tion

8 64 rt ICH 13 wks lt hemiplegia; disorien- greatly improved motortation; dysphagia activity; dysphagia im-

proved; no complications9 52 rt ICH 9 wks hemianopsia; hyperre- hemiparesis slightly im-

flexia; lt hemiparesis proved; no hyperreflexia;hemianopsia improved

10 45 EDH; rt frontoparietal 6 wks retrograde amnesia; gait improvement of alldisturbance; blurred vision symptoms

11 69 subtotal MCA infarction; 7 wks lt hemiparesis; lt facial improvement of allrt frontoparietotemporal; paralysis; lt hemineglect; symptomscoma dyspraxia lt hand

12 50 lt acute SDH 11 wks difficulty in finding words neurologically syptom free

13 49 frontoparietal meningio- 10 wks aphasia; hemiparesis rt slight normalization of all neuro-ma; bleeding during em- logical symptomsbolization procedure;midbrain compression& lt herniation

* EPH = epidural hematoma; ICH = intracerebral hematoma; SDH = subdural hematoma; SAH = subarachnoid hemor-rhage; UMN = upper motor neuron. At the time of cranioplasty. Stereolithographic three-dimensional reconstruction was used.


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improved or it reached normal levels in relation to dailysocial interaction. The patients became cooperative, with-out distress, and quite communicable after undergoingcranioplasty. Although her spastic paresis improved andshe could walk without support, the arm of one patient(Case 3) remained plegic at her 2 year follow up.

The CVR Capacity

No significant difference was observed in the restingblood flow velocities in extracranial ICA when compar-ing ipsilateral and contralateral hemipsheres and whenassessing the effects of cranioplasty (Fig. 2). However,although blood flow in the MCA was significantly im-paired in the ipsilateral as compared with the contralater-al hemisphere prior to the procedure, following cranio-plasty the impairment was only marginal, returning toalmost near-normal values.

By moving to the sitting position, the blood flow veloc-ity in the extracranial ICA significantly decreased on theside on which craniectomy had been performed as com-

pared with the intact contralateral hemisphere. Cranio-plasty resolved postural influences on extracranial ICAflow (Fig. 3).

Although the CVR capacity before cranioplasty wasseverely impaired in both hemispheres, after cranioplastya striking improvement was observed in this parameter inboth the ipsilateral as well as the contralateral extracranialICA (Fig. 4).

Results of the PET Studies

Cerebral metabolism as assessed by 18-FDG PET wasfound to be depressed in the injured compared with thecontralateral hemisphere (p 0.01). Cranioplasty result-

ed in a significantly increased uptake of 18-FDG in bothhemispheres (p 0.001), indicating globally enhancedmetabolism in the brain (Fig.5 upperand Table 2).



Fig. 1. Computerized tomography scans obtained before (uppertwo rows) and after (lower two rows) cranioplasty in a patient whohad undergone decompressive craniectomy for acute subduralhematoma 4 months previously.

Fig. 2. Bar graph depicting the influence of cranioplasty on resting TCD flow values obtained in 13 patients (averag-es SD). eICA = extracranial ICA; ipsi = ipsilateral hemiphere; contra = contralateral hemisphere. Vertical bars showthe TCD values in milliliters/second.


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However, the findings were more pronounced in theipsilateral hemisphere (ipsilateral and contralateral meanincreases ~ 12% and 4%, respectively). These results wereneither related to the injected FDG dose nor the blood glu-cose level. Metabolic asymmetry decreased from 35% to28% after cranioplasty. We found a significant correlation

between the FDG uptake in the injured hemisphere andthe extracranial ICA blood flow velocity assessed in su-pine and erect positions prior to (r = 0.870 and r = 0.860respectively, p 0.05) and after cranioplasty (r = 0.867, p 0.05), but not in the sitting position. There was no

dependent relationship between extracranial ICA flow andcortical FDG uptake contralaterally. Furthermore, no rela-tionship could be established between glucose metabolismand flow stimulation studies with acetazolamide or MCAblood flow measurements in either the ipsi- or contralat-eral hemispheres.

The improvement of the glucose metabolism demon-strated in the injured hemisphere after cranioplasty was agood predictive value for a patients clinical outcome. Wefound an increase of FDG uptake in 10 of 12 patients.During follow up, all these patients presented with an



5

Fig. 3. Bar graph showing the influence of cranioplasty on postural changes in TCD values as assessed in extracra-nial ICA (means SD).

Fig. 4. Bar graph depicting the influence of cranioplasty on CVR capacity (means SD).


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overall improvement and a reduction of the symptoms.The PET results and clinical condition remained un-

changed only in the patient in Case 7. Normalization of allneurological symptoms was observed in the patient inCase 13, whereas the mean cortical FDG uptake remainedstable.

Nevertheless, in the latter case we found obviouschanges in the regional glucose metabolism, particularlyin the margins of the defect.

DISCUSSION

Several authors4,911,21,26,31,34,35 have described the ST theappearance of symptoms weeks and months after craniec-tomy, with aggravation of symptoms when the patientchanges body position and relief or reduction of symp-

toms after cranioplasty. In the literature there are very fewcase reports in which the ST is described. Large concave

cranial defects were present in all reported cases. A vari-ety of theories have been developed regarding the role ofthe bony defect of the cranium in the development of theneurological symptoms. The size and location of the cra-nial defect may be important.31,33

Derangement of CSF hydrodynamics6,12,18,19 as well asregionally impaired CBF9,28 are well documented.

In 1979 Fodstad and colleagues5 reported their study ofCSF hydrodynamics in 18 patients (13 men and 5 womenaged 2359 years [average age 40.5 years]. In 15 cases thelarge cranial defect was caused by decompressive craniec-tomy that had been performed to treat various conditions(eight trauma, five subarachnoid hemorrhage, two tumors,and one encephalitis) and in two cases because of postop-



Fig. 5. Upper: Positron emission tomography scans demonstrating the influence of cranioplasty on cerebral metabo-lism. Upper Row: Scans obtained prior to cranioplasty. Lower Row: Scans obtained after cranioplasty. Lower: Bargraph showing quantitative evaluation of effects of crainioplasty on cerebral metabolism in 12 patients (means SD).


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erative flap infection. In patients in whom large defectswere present before and after cranioplasty the constant-pressure infusion method was used to study CSF hydro-dynamics.3 The results of the CSF hydrodynamic studiesbefore and after cranioplasty were somewhat varied andnot easy to interpret. In eight of the patients normal CSF

hydrodynamic values were observed before and after cra-nioplasty; all of these patients had flat and rigid skull de-fects. In seven other patients with low and one with highresting pressure and sinus pressure preoperatively, normalvalues were demonstrated after cranioplasty. These pa-tients had large defects with flaccid concavity of the skinflap. In 11 patients the investigators measured the CSFpressure both in the supine and the sitting position. Theyfound that the CSF pressure tended to change in the sittingposition after cranioplasty. At the same time the pulseamplitude became larger. There was also a striking changein elastance and pulse-related CSF pressure variations insome patients after cranioplasty. In five patients the elec-troencephalograph findings were improved after cranio-

plasty, and many of the patients with changed CSF hydro-dynamics preoperatively claimed that they experiencedfewer episodes of headache and vertigo after the opera-tion. The authors concluded that despite the fact that theirseries was small and their findings somewhat confusing,some conclusions could be inferred from their data. Thechange in CSF hydrodynamics with an improved clinicalpicture in patients with skull defects could be explained bythe stretching or a distortion of the dura and the underly-ing cerebral cortex due to the atmospheric pressure withpossible shifting of the intracranial contents. This is sup-ported by the fact that the patients who benefited mostfrom cranioplasty were those in whom there were largedefects near the dural sinuses with concave deformity of

the skin flap that allowed transmission of the atmosphericpressure directly to the cerebral cortex. Such cranial de-fects should therefore be repaired as early as possible.

In a second published series, Fodstad, et al.,6 describedcranial bone defects in 40 patients after craniectomy inwhom extensive CSF hydrodynamic investigations were

performed using CSF infusion test before and after cran-ioplasty. The results of these investigations were shown tobe related to the clinical signs of the patients before andafter cranioplasty and to the size and location of the skullbone defect. After cranioplasty the patients were classifiedinto the following four groups.

Group I consisited of true ST patients; 14 patientswith symptoms of ST, which was aggravated during theVasalva maneuver or by changes in body position. Theirsymptoms were not present before craniectomy and werereduced or relieved after repair of the cranial bone defect.Group II was comprised of partial ST patients; eightpatients with symptoms of ST not present before craniec-tomy. The symptoms were more or less relieved after

cranioplasty but were unaffected by the Vasalva maneuveror positional changes. Group III consisited of other pa-tients; 12 patients with neurological deficits that could berelated to their primary disease or the surgical procedure.Group IV was made up of symptom-free patients; sixpatients without ST or neurological deficits.6

The CSF hydrodynamic variables that were changedbefore and normalized after cranioplasty included the fol-lowing: resting pressure; sagittal sinus pressure; buffervolume, elastance at resting pressure; and pulse variationsat resting pressure.6 In Group I, 79% of the patients expe-rienced relief of symptoms and 21% were improved aftercranioplasty. All these patients had flaccid skin flaps thatbecame concave while in the upright position. In 10 of



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TABLE 2INDIVIDUAL AND MEAN IMPROVEMENTS IN PET-DOCUMENTED VALUES ON THE

SIDE OF RECONSTRUCTION AND THE CONTRALATERAL SIDE, AS WELL AS OVERALLCLINICAL OUTCOME*

PET ImprovementAfter Cranioplasty (% value)

Case Ipsilateral Contralateral Overall ClinicalNo. Side Side Improvement

1 8.8 4.0 yes2 27.9 4.6 yes3 18.7 6.0 yes (slight)4 13.6 8.4 yes (slight)5 10.3 2.4 yes (partial)6 17.1 4.9 yes7 0.2 8.8 no8 13.6 5.4 yes9 13.0 0.4 yes

10 6.7 4.7 yes11 15.8 9.3 yes

12 yes13 0.1 3.7 yes

mean improve-ment SD 12.1 2.3% 4.5 1.1% yes

* = results could not be interpreted.


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the Bayerische Motorenwerke GmbH (BMW), Munich, Germany.The help of Mrs. Stein, formerly of the Department of Nuclear Me-dicine, Klinikum Grosshadern, in conducting the PET studies ishighly appreciated. We thank Prof. Dr. Norbert Mai and Dr. JochenQuintern from the Department of Neurology, Ludwig MaximiliansUniversity, Munich for their valuable advice for standardizing theevaluation of clinical outcome of the patients presented in thisseries.

References

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20. Magnaes B: Body position and cerebrospinal fluid pressure.Part 2: Clinical studies on orthostatic pressure and the hydro-static indifferent point. J Neurosurg 44:698705, 1976

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29. Reynaud JP, Benezech J, Gary-Bobo A, et al: Chirurgie rparat-ice de la voute craninne aprs hmicraniectomie. Ann ChirPlast 26:314318, 1981

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31. Shuttleworth CB: The repair of bony defects of the cranium.

Can Med Assoc J 11:562565, 192132. Suzuki N, Suzuki S, Iwabuchi T: Neurological improvementafter cranioplasty. Analysis by dynamic CT scan. Acta Neuro-chir 122:4953, 1993

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Manuscript received October 19, 1999.Accepted in final form January 10, 2000.Address reprint requests to: Peter A. Winkler, M.D., Department

of Neurosurgery, Klinikum Grohadern, Ludwig Maximilians Uni-versity of Munich Marchioninistrae 15, D-81377 Munich, Ger-many. email: [email protected].



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