Complication of a large cranial defect Case report
KAMRAN TABADDOR, M . D . , AND JAMES LAMORCESE, M . D .
Department of Neurological Surgery, Albert Einstein College of Medicine, Bronx, New York
v' A patient with acute subdural hematoma was successfully treated with hemicraniectomy. He developed contralateral weakness 4 months after surgery which was reversed by cranioplasty. The presumptive mechanism is a gradient between atmospheric and intracranial pressure. Early cranioplasty is suggested to prevent this phenomenon. KEY WoRI)S 9 hemicraniectomy cranial defect 9 cranioplasty
INCE Ransohoff, et al., 7 advocated hemicraniectomy for the treatment of acute subdural hematomas, we have employed this technique with increasing frequency. We have recently encountered a remarkable complication resulting from the cranial defect of hemicraniectomy in which a patient developed a progressive hemiparesis readily reversed by cranioplasty.
s
Case Report
A 41-year-old man was admitted to the hospital following closed head trauma. General physical examination revealed changes compatible with mild alcoholic hepatitis. Neurologically he responded to painful stimuli appropriately on the left but he had a right-sided flaccid hemiplegia. The right pupil was 6 mm and only sluggishly reactive to light, while the left was 3 mm and briskly reactive. These findings were interpreted as evidence of a right hemispheric 506
9
subdural h e m a t o m a
9
mass with uncal herniation and contralateral brain-stem compression against the tentorial edge. Right cerebral angiography revealed the presence of a large subdural hematoma causing a marked shift of midline structures. A massive acute subdural hematoma was removed through a right hemicraniectomy. The underlying brain was contused and swollen. The postoperative course was complicated by pulmonary infections. The right hemiparesis present preoperatively cleared almost immediately after decompressive craniectomy. The bony decompression was full and tense for 10 days after surgery but gradually became soft and at the time of discharge from the hospital was slightly concave. He returned home 4 weeks after injury without neurological deficit. He was able to return to work 1 month later and was gainfully employed for 2 months before noticing a gradually developing weakness of the left hand. The scalp flap overlying the decompression was noticeably concave (Fig. 1 left). J. Neurosurg. / Volume 44 / April, 1976
C o m p l i c a t i o n of a large cranial d e f e c t
FIG. 1. Photographs of the patient, 4 months after hemicraniectomy (left), and 7 months after cranioplasty (right). Neurological examination at that time (4 months after surgery) revealed moderate weakness of the left arm, more pronounced in the distal muscle groups. Proprioceptive function was diminished to the same degree as the motor deficit. These symptoms progressed over the next month and resulted in complete paralysis of the left hand and marked weakness of the left arm. The left leg also became slightly weak and spastic. The patient also described an interesting phenomenon, namely the occurrence of involuntary movement of the left arm and hand with yawning. This phenomenon, however, was not reproducible in our clinic. A dynamic brain scan showed decreased flow to the right hemisphere and electromyography confirmed the lack of peripheral neuropathy. These findings were felt to be compatible with cortical compression; consequently the patient underwent cranioplasty with preformed acrylic mesh plate to restore the normal contour of the skull and reconstitute the rigid covering of the brain (Fig. 1 right). Postoperatively, his weakness and proprioceptive deficit improved dramatically. The sensory disturbances cleared almost completely prior to discharge from the hospital; however, there remained some disuse atrophy of the interosseous muscles and mild weakness of the hand. A repeat dynamic brain scan 1 month later demonstrated symmetrical flow to both hemispheres.
J. Neurosurg. / Volume 44 / April, 1976
Discussion
The indications and results of hemicraniectomy in the treatment of acute subdural hematoma are beyond the scope of this communication. But since this procedure has been advocated in the past few years 6a the effect of the large cranial defect on the brain of the survivors has become apparent. To our knowledge, there has not been any report of progressive neurological deficit due merely to cranial defect, as was observed in the present case. The indications for repair of large cranial defects are usually protective, cosmetic, or, as some authors suggest, 1,~,' to prevent or decrease the incidence of posttraumatic epilepsy. Cortical brain damage as the result of direct pressure by the scalp, however, has never been mentioned. The exact pathogenesis in this case is not entirely clear. However, the development of progressive contralateral weakness with marked cortical sensory disturbance 2 months after craniectomy and its rapid reversal by cranioplasty suggest scalp pressure as the cause. The onset of the neurological deficit coincided with the appearance of a marked concavity of the cranial defect. The progression of the hemiparesis paralleled the progressive concavity of the scalp. It has been demonstrated 5 experimentally that the cerebrospinal fluid pressure in an upright position is higher in a model with a large 507
K. Tabaddor and J. LaMorgese cranial defect than in one with a closed calvaria. This is due to the fact that the atmospheric pressure is only transmitted to intracranial fossa by way of systemic circulation. Therefore, the gradient between the atmospheric pressure and intracranial pressure causes an inward displacement of the scalp over a cranial defect. If the defect is large enough to allow the transmission of this pressure gradient directly to the cerebral cortex, the occurrence of a neurological deficit is quite conceivable. But if the cranial defect is not sufficiently large, the scalp is stretched between the edges of the bony defect and absorbs atmospheric pressure, thus protecting the brain from continuous external pressure. It has been shown angiographically that after hemicraniectomy many patients demonstrate a contralateral shift of the midline structures while simultaneously demonstrating concavity of the scalp over the cranial defect? This again signifies the role of the atmospheric pressure in changing the dynamics and shifting the intracranial contents. Hence, an alternative explanation for the neurological deficit would be the downward shift of the brain stem resulting in the constellation of symptoms and signs shown in this patient. This case demonstrates the clinical occurrence of what could have been predicted from laboratory studies concerning the pathophysiological effect of a large cranial
508
defect. It also stresses the importance of early repair of such defects prior to the appearance of delayed neurological impairment. References
1. Erculei F, Walker AE: Posttraumatic epilepsy and early cranioplasty. J Neurosurg 20: 1085-1089, 1963 2. Gardner WJ: Closure of defects of the skull with tantalum. Surg Gynecol Obstet 80: 303-312, 1945 3. George AE, Morantz RA, Abad RM, et al: Neuroradiology of the posthemicraniectomy patient with special emphasis on the radiology of unilateral atrophy. Radiology 111:627-631, 1974 4. Grant FC, Norcross NC: Repair of cranial defects by cranioplasty. Ann Surg 110:488-512, 1939 5. Langfitt TW: Increased intracranial pressure. Clin Neurosurg 16:436-471, 1968 6. Morantz RA, Abad RM, George AE, et al: Hemicraniectomy for acute extracerebral hematoma: an analysis of clinical and radiographic findings. J Neurosurg 39:622-628, 1973 7. Ransohoff J, Benjamin MV, Gage EL Jr, et al: Hemicraniectomy in the management of acute subdural hematoma. J Neurosurg 34:70-76, 1971 Address reprint requests to: Kamran Tabaddor, M.D., Department of Neurological Surgery, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461.
J. Neurosurg. / Volume 44 / April, 1976
KAMRAN TABADDOR, M . D . , AND JAMES LAMORCESE, M . D .
Department of Neurological Surgery, Albert Einstein College of Medicine, Bronx, New York
v' A patient with acute subdural hematoma was successfully treated with hemicraniectomy. He developed contralateral weakness 4 months after surgery which was reversed by cranioplasty. The presumptive mechanism is a gradient between atmospheric and intracranial pressure. Early cranioplasty is suggested to prevent this phenomenon. KEY WoRI)S 9 hemicraniectomy cranial defect 9 cranioplasty
INCE Ransohoff, et al., 7 advocated hemicraniectomy for the treatment of acute subdural hematomas, we have employed this technique with increasing frequency. We have recently encountered a remarkable complication resulting from the cranial defect of hemicraniectomy in which a patient developed a progressive hemiparesis readily reversed by cranioplasty.
s
Case Report
A 41-year-old man was admitted to the hospital following closed head trauma. General physical examination revealed changes compatible with mild alcoholic hepatitis. Neurologically he responded to painful stimuli appropriately on the left but he had a right-sided flaccid hemiplegia. The right pupil was 6 mm and only sluggishly reactive to light, while the left was 3 mm and briskly reactive. These findings were interpreted as evidence of a right hemispheric 506
9
subdural h e m a t o m a
9
mass with uncal herniation and contralateral brain-stem compression against the tentorial edge. Right cerebral angiography revealed the presence of a large subdural hematoma causing a marked shift of midline structures. A massive acute subdural hematoma was removed through a right hemicraniectomy. The underlying brain was contused and swollen. The postoperative course was complicated by pulmonary infections. The right hemiparesis present preoperatively cleared almost immediately after decompressive craniectomy. The bony decompression was full and tense for 10 days after surgery but gradually became soft and at the time of discharge from the hospital was slightly concave. He returned home 4 weeks after injury without neurological deficit. He was able to return to work 1 month later and was gainfully employed for 2 months before noticing a gradually developing weakness of the left hand. The scalp flap overlying the decompression was noticeably concave (Fig. 1 left). J. Neurosurg. / Volume 44 / April, 1976
C o m p l i c a t i o n of a large cranial d e f e c t
FIG. 1. Photographs of the patient, 4 months after hemicraniectomy (left), and 7 months after cranioplasty (right). Neurological examination at that time (4 months after surgery) revealed moderate weakness of the left arm, more pronounced in the distal muscle groups. Proprioceptive function was diminished to the same degree as the motor deficit. These symptoms progressed over the next month and resulted in complete paralysis of the left hand and marked weakness of the left arm. The left leg also became slightly weak and spastic. The patient also described an interesting phenomenon, namely the occurrence of involuntary movement of the left arm and hand with yawning. This phenomenon, however, was not reproducible in our clinic. A dynamic brain scan showed decreased flow to the right hemisphere and electromyography confirmed the lack of peripheral neuropathy. These findings were felt to be compatible with cortical compression; consequently the patient underwent cranioplasty with preformed acrylic mesh plate to restore the normal contour of the skull and reconstitute the rigid covering of the brain (Fig. 1 right). Postoperatively, his weakness and proprioceptive deficit improved dramatically. The sensory disturbances cleared almost completely prior to discharge from the hospital; however, there remained some disuse atrophy of the interosseous muscles and mild weakness of the hand. A repeat dynamic brain scan 1 month later demonstrated symmetrical flow to both hemispheres.
J. Neurosurg. / Volume 44 / April, 1976
Discussion
The indications and results of hemicraniectomy in the treatment of acute subdural hematoma are beyond the scope of this communication. But since this procedure has been advocated in the past few years 6a the effect of the large cranial defect on the brain of the survivors has become apparent. To our knowledge, there has not been any report of progressive neurological deficit due merely to cranial defect, as was observed in the present case. The indications for repair of large cranial defects are usually protective, cosmetic, or, as some authors suggest, 1,~,' to prevent or decrease the incidence of posttraumatic epilepsy. Cortical brain damage as the result of direct pressure by the scalp, however, has never been mentioned. The exact pathogenesis in this case is not entirely clear. However, the development of progressive contralateral weakness with marked cortical sensory disturbance 2 months after craniectomy and its rapid reversal by cranioplasty suggest scalp pressure as the cause. The onset of the neurological deficit coincided with the appearance of a marked concavity of the cranial defect. The progression of the hemiparesis paralleled the progressive concavity of the scalp. It has been demonstrated 5 experimentally that the cerebrospinal fluid pressure in an upright position is higher in a model with a large 507
K. Tabaddor and J. LaMorgese cranial defect than in one with a closed calvaria. This is due to the fact that the atmospheric pressure is only transmitted to intracranial fossa by way of systemic circulation. Therefore, the gradient between the atmospheric pressure and intracranial pressure causes an inward displacement of the scalp over a cranial defect. If the defect is large enough to allow the transmission of this pressure gradient directly to the cerebral cortex, the occurrence of a neurological deficit is quite conceivable. But if the cranial defect is not sufficiently large, the scalp is stretched between the edges of the bony defect and absorbs atmospheric pressure, thus protecting the brain from continuous external pressure. It has been shown angiographically that after hemicraniectomy many patients demonstrate a contralateral shift of the midline structures while simultaneously demonstrating concavity of the scalp over the cranial defect? This again signifies the role of the atmospheric pressure in changing the dynamics and shifting the intracranial contents. Hence, an alternative explanation for the neurological deficit would be the downward shift of the brain stem resulting in the constellation of symptoms and signs shown in this patient. This case demonstrates the clinical occurrence of what could have been predicted from laboratory studies concerning the pathophysiological effect of a large cranial
508
defect. It also stresses the importance of early repair of such defects prior to the appearance of delayed neurological impairment. References
1. Erculei F, Walker AE: Posttraumatic epilepsy and early cranioplasty. J Neurosurg 20: 1085-1089, 1963 2. Gardner WJ: Closure of defects of the skull with tantalum. Surg Gynecol Obstet 80: 303-312, 1945 3. George AE, Morantz RA, Abad RM, et al: Neuroradiology of the posthemicraniectomy patient with special emphasis on the radiology of unilateral atrophy. Radiology 111:627-631, 1974 4. Grant FC, Norcross NC: Repair of cranial defects by cranioplasty. Ann Surg 110:488-512, 1939 5. Langfitt TW: Increased intracranial pressure. Clin Neurosurg 16:436-471, 1968 6. Morantz RA, Abad RM, George AE, et al: Hemicraniectomy for acute extracerebral hematoma: an analysis of clinical and radiographic findings. J Neurosurg 39:622-628, 1973 7. Ransohoff J, Benjamin MV, Gage EL Jr, et al: Hemicraniectomy in the management of acute subdural hematoma. J Neurosurg 34:70-76, 1971 Address reprint requests to: Kamran Tabaddor, M.D., Department of Neurological Surgery, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461.
J. Neurosurg. / Volume 44 / April, 1976
