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[Three cases of acute interhemispheric subdural hematoma].

Traumatic acute subdural hematomas over the convexity of the cerebral hemispheres are often encountered, but acute interhemispheric subdural hematomas are rare. Fourty-eight cases of acute subdural hematomas was admitted to our hospital between 1977 and 1986, and three cases of them (6%) were located in the interhemispheric subdural space. In this paper, these three cases are reported with 20 documented cases. Case 1: an 81-year-old female was admitted to our hospital because of headache, nausea and vomiting. She hit her occiput a week ago. CT scan demonstrated contusion in the right frontal lobe and a high density in the interhemispheric space of the right frontal region. Her complaints disappeared gradually by conservative therapy and she returned to her social life. Case 2: a 50-year-old male fell downstairs and hit his vertex. As he lost consciousness, he was admitted to our hospital. He was stuporous and had left-hemiparesis. Skull X-ray film showed fracture line extending from the right temporal bone to the left parietal bone across the midline. CT scan revealed intracerebral hematoma in both frontal lobe and right parietal lobe and subarachnoid hemorrhage in the basal cistern and Sylvian fissure of the right side. And interhemispheric subdural hematoma in the right parietal region was visualized. Angiography demonstrated a lateral displacement of the right callosomarginal artery and an avascular area between the falx and the callosomarginal artery. After admission his consciousness recovered and convulsion was controlled by drug. Left-hemiparesis was improved by conservative therapy and he was discharged on foot.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

[Individual differences in the venous formations of the parasagittal area of the neonatal cranial vault].

Diagnostics and treatment of intracranial hemorrhages in newborns, being one of the actual problems of pediatrics, are performed taking into account the parasagittal zone structure. To reveal borders of the parasagittal area in newborns in order to find optimal points for puncture of the superior sagittal sinus and subdural hematomas in this area, the investigation has been undertaken. One hundred mature and 50 premature newborns have been studied, their cerebral veins are injected with contrast mass, x-rayed and then the preparations fixed in 3%, 5% and 10% formalin are made ready. It has been stated that for puncture of the newborn subdural space two points should be used: a) on the coronal cross-line of the anterior fontanel, 20 mm away of its middle line at either side (in mature newborns) and 10 mm (in premature newborns), b) within the limits of the sutura lamboidea 30 mm the sagittal suture (in mature newborns) and 15 mm from the sagittal suture (in premature newborns).

Brain↗

Outcome of antenatally diagnosed intracranial hemorrhage: case series and review of the literature.

OBJECTIVES: Prenatal diagnosis of intracranial hemorrhage (ICH) has been widely reported. Hemorrhages may occur either within the cerebral ventricles, subdural space or infratentorial fossa. The aim of this study was to determine the sonographic criteria for the diagnosis of fetal ICH, the role of in utero magnetic resonance imaging (MRI) and the outcome of this condition. METHODS: The archives of our ultrasound laboratory and the literature were searched for all cases of antenatally diagnosed ICH. A grading system was used to classify the intraventricular lesions as suggested in postnatal sonographic studies. RESULTS: Adding our series of 16 fetuses to the 93 cases identified in the literature, a group of 109 fetal ICHs was obtained: 89 were intracerebral (79 intraventricular and 10 infratentorial) and 20 were subdural hemorrhages. Intraventricular lesions were mostly classified as severe (32 each for Grades III and IV). In 27 cases antenatal MRI was performed additionally to ultrasound and confirmed the sonographic findings. Of the entire group, 65 infants (59%) were reported to be alive 1 month after birth (51 intraventricular hemorrhages, three infratentorial hemorrhages, 11 subdural hematomas). At 12 months, of the 48 infants whose follow-up was available, 25 or 52% were judged neurologically normal (17/36 or 47% among the intraventricular hemorrhages, 6/9 or 66% among the hematomas, and 2/3 or 66% among the infratentorial hemorrhages). CONCLUSIONS: Fetal ICH may be accurately identified and categorized by antenatal sonography. The outcome is usually poor, especially for those fetuses affected by higher-grade intraventricular hemorrhages.

Cerebral Hemorrhage↗

Symptomatic subdural hygroma after petroclival meningioma surgery. Case report of a intractable complication.

Although subdural hygroma development after craniotomy or aneurysm surgery is a well-known complication and subdural peritoneal or V-P shunt are commonly successful procedures, there are situations that cannot be treated by available surgical options. We reported a case of a 28-year-old young man who developed a symptomatic subdural hygroma after removal of petroclival meningioma. This hygroma increased in size and became bilateral in spite of implantation of V-P with programmable valve at open pressure variable from 30 to 180 mmH2O, placement of subdural-peritoneal shunt with low-low valve or without valve and external diversion. The occurrence of this case showed that there other factors can play role in hygroma development as disturbance of normal CSF dynamic with shunt of CSF from basal arachnoidal to subdural spaces secondary to surgery and/or slow growth of petroclival meningioma as well as postoperative progressive cerebral atrophy. Actually there are not effective diagnostic tools to detect causes and therefore, there are restricted therapeutic possibilities. This potential and serious complication should be always considered when planning petroclival meningioma surgery because of the severe consequences on functional outcome.

Adult↗

A loss-of-resistance-to-negative-pressure test for subarachnoid puncture with narrow-gauge needles.

BACKGROUND AND OBJECTIVES: Approximately 5-10% of attempted myelograms are spoiled by partial subdural injection. Similar spillage of local anesthetics may underlie the wide variability of segmental spread reported for spinal anesthesia. A technique of applied negative pressure to avoid accidental subdural injection and to facilitate subarachnoid puncture with narrow gauge needles is described. METHODS: Hydraulic circuitry was designed to measure saline flow rates through spinal needles at hub-to-tip differential pressures of 55 mm Hg and 650 mm Hg. A model of dura and arachnoid membranes was constructed to demonstrate the effects of applied negative pressure on the subdural space during the passage of Quincke-tip and pencil-point needles. Cisternal puncture in 38 dogs and thoracic or lumbar subarachnoid puncture in 680 patients were performed using applied negative pressure to the needle hub. RESULTS: A sustained vacuum of -650 mm Hg at the hub of air-filled spinal needles was transmitted beyond the tip but fell to zero at the tip as the shaft filled with saline. Flow rates through the Quincke needles, ranging from 22-gauge to 29-gauge, rose 22- to 33-fold when a vacuum of -650 mm Hg was applied at the hub. Model dura and arachnoid membranes were separated by air-filled tips at atmospheric pressure but were juxtaposed by negative pressure applied to the hub. CONCLUSIONS: Negative pressure applied to the needle hub is transmitted to the tip without decrement in air-filled needles but not in fluid-filled needles. Clinical application of this principle by exertion of strong negative pressure at the hub during needle advancement facilitates rapid identification of cerebrospinal fluid, avoids unintentional subdural injection of local anesthetics or contrast media, and increases the safety of subarachnoid punctures above the termination of the spinal cord.

Animals↗

[Evaluation of subdural hemorrhage in infants after alleged minor trauma].

QUESTIONING: Recently the discussion concerning the causes of infantile subdural bleedings (SDB) has become quite controversial. The wide-spread interpretation that most of these cases are the result of abuse, especially by the shaken-baby-syndrome, was doubted, and the role of (even minor) accidental events was emphasized. METHODS: This situation should be analyzed basing on the official statistics of the causes of death in the city of Berlin (1978-1998) and the autopsy material of our institute (1978-1999). RESULTS: In this period, approximately 440.000 children lived their first year of life in our city. Only 80 violent deaths of infants (up to 1 year old) were recorded in the official statistics, including 27 deaths due to blunt forces, with 24 lethal head injuries as the main group. Only two cases were attributed to "falls under unclear conditions"; all other accidental cases were the results of traffic accidents or falls from a height. No death due to an undoubted minor fall was recorded, nor was any in our autopsy material. We investigated 10 cases of infantile SDB, all without skull fractures and gross brain injuries. Only 1 victim had a SDB of a significant volume; in all other cases only small amounts of blood were present in the subdural space. Bridging vein ruptures were directly demonstrated in 8 cases and were bilaterally in most instances; recently their detection has been simplified by postmortem x-ray using contrast material. All 10 cases were interpreted as typical acceleration-deceleration injuries (as in shaking), although only in 2 cases a confession of this procedure could be obtained. CONCLUSION: Comparing cases of accidental and non-accidental SDB in the literature, infantile SDB obviously cannot be looked at as a homogeneous entity: two quite different types should be kept separate: the patients suffering from an accidental SDB due to a minor fall mostly do not deteriorate immediately after the trauma, develop SDB of some volume, up to a space-occupying mass lesion, and have often a good prognosis. A lethal outcome is extremely uncommon; we have not observed a single case of an infantile lethal SDB resulting from such a minor injury for more than 20 years. The source of the SDB in those cases currently is unknown in most instances. The second group of infantile SDB includes the well-known group of shaken-baby-syndrome: no adequate history, infants dead or nearly dead on clinical presentation, often a poor outcome if the event is survived, typically no significant volume of SDB, and--according to our experiences--in all cases BV ruptures. This combination of several BV ruptures with no significant subdural bleeding is not compatible with a supposition of a minor fall causing this.

Accidents↗

Subdural empyema: CT findings.

CT scans in 49 patients with surgically proven subdural empyema were evaluated. The empyemas were crescentic or lentiform extra-axial hypodense collections (density approximating that of cerebrospinal fluid) with prominent, sharply etched medial rim enhancement. Enhancement of the adjacent cerebral cortex was identified in many cases. Mass effect was always present and in 10 cases so extensive that it overshadowed a small extra-axial collection. CT allowed for precise localization of the lesion, including contiguous or isolated involvement of the interhemispheric subdural space. Mortality was 12% (6/49 cases), a marked improvement when compared with mortality figures obtained prior to the advent of CT (40%). CT findings indicative of involvement of the adjacent parenchyma via retrograde thrombophlebitis with resultant infarction and/or abscess formation were associated with poor prognosis. Improvement in prognosis since the advent of CT is the direct result of early accurate diagnosis and timely intervention.

Adolescent↗

The neuroprotective effect of a new serotonin receptor agonist, BAY X3702, upon focal ischemic brain damage caused by acute subdural hematoma in the rat.

We tested the neuroprotective effect of a novel, high affinity serotonin (5-HT1A) agonist, BAY X3702, in a rat model of acute subdural hematoma (ASDH). Animals were treated with 0.01 mg/kg (n=8), 0.003 mg/kg (n=8) BAY X3702 or vehicle (n=4) 15 min before (i.v.) and after (continuous infusion) injection of 400 microl of autologous blood into the subdural space. The ischemic brain damage at 4 h after ASDH was 59.01+/-39 and 60.8+/-49 mm(3) for the low- and high-dose BAY X3702 group, respectively, which was significantly smaller compared to the vehicle-treated ASDH group (106.2+/-33 mm(3)). The result indicates that this novel, high affinity 5-HT(1A) agonist, BAY X3702, is neuroprotective in this model.

Animals↗

Posterior fossa hemorrhage in the term neonate.

Posterior fossa hemorrhage (PFH) in the newborn term infant has been infrequently reported, and before computed tomographic (CT) scanning most were identified at postmortem examination. The origin and causes of PFH in the term neonate differ from those in adults. The main possible causes are: (a) tentorial and falx disruption with avulsion of bridging veins due to mechanical compression and distortion of the head during the birth process, resulting in posterior fossa subdural collections and vermis hematoma, and (b) occipital osteodiastasis associated with cerebellar hemisphere laceration, with intracerebellar hematoma and subdural collections. Three full-term neonates with PFH were operated on with good outcome. Both of the possible causes contributed to the hemorrhage. Review of the literature to date has led to the following conclusions: (a) PFH in the term infant is frequently associated with breech delivery, forceps instrumentation, and prolonged labor with cranial molding. (b) Massive PFH is associated with dural sinus laceration, rupture of the vein of Galen, or rupture of hematoma into the subdural space. Symptoms may be delayed up to 96 hours in cases where there is a small continuing hemorrhage. (c) CT scanning with reconstructions is essential to provide precise localization of the hemorrhage and thus avoid errors in interpretation. (d) Prompt removal of PFH improves survival and decreases sequelae. (e) Shunting procedures are necessary in 36% of the cases.

Adolescent↗

The influence of regional spinal cord hypothermia on transcranial myogenic motor-evoked potential monitoring and the efficacy of spinal cord ischemia detection.

OBJECTIVE: Myogenic motor-evoked responses to transcranial electrical stimulation (transcranial myogenic motor-evoked potentials) can rapidly detect spinal cord ischemia during thoracoabdominal aortic aneurysm repair. Recent evidence suggests that regional spinal cord hypothermia increases spinal cord ischemia tolerance. We investigated the influence of subdural infusion cooling on transcranial myogenic motor-evoked potential characteristics and the time to detect spinal cord ischemia in 6 pigs. METHODS: Regional hypothermia was produced by subdural perfusion cooling. A laminectomy and incision of the dura were performed at L2 to advance 2 inflow catheters at L4 and L6, to cool the lumbar subdural space with saline solution. Two temperature probes were advanced at L3 and L5, and 1 cerebrospinal fluid pressure line was advanced at L4. Spontaneous cerebrospinal fluid outflow was allowed. Spinal cord ischemia was produced by clamping a set of critical lumbar arteries, previously identified by transcranial myogenic motor-evoked potentials and lumbar artery clamping. The time between the onset of ischemia and detection with transcranial myogenic motor-evoked potentials (amplitude < 25%) was determined at cerebrospinal fluid temperatures of 37 degrees C and 28 degrees C. Thereafter, the influence of progressive cerebrospinal fluid cooling on transcranial myogenic motor-evoked potential amplitude and latency was determined. RESULTS: The time necessary to produce ischemic transcranial myogenic motor-evoked potentials, after the clamping of critical lumbar arteries, was not affected at moderate subdural hypothermia (3.8 +/- 0.9 min) compared with subdural normothermia (3.2 +/- 0.5 min; P =.6). Thereafter, progressive cooling resulted in a transcranial myogenic motor-evoked potential amplitude increase at 28 degrees C to 30 degrees C and was followed by a progressive decrease. Response amplitudes decreased below 25% at 14.0 degrees C +/- 1.1 degrees C. The influence of cerebrospinal fluid temperature on transcranial myogenic motor-evoked potential amplitude was best represented by a quadratic regression curve with a maximum at 29.6 degrees C. In contrast, transcranial myogenic motor-evoked potential latencies increased linearly with decreasing subdural temperatures. CONCLUSIONS: Detection of spinal cord ischemia with transcranial myogenic motor-evoked potentials is not delayed at moderate subdural hypothermia in pigs. At a cerebrospinal fluid temperature of 28 degrees C, transcranial myogenic motor-evoked potential amplitudes are increased. Further cerebrospinal fluid temperature decreases result in progressive amplitude decreases and latency increases.

Animals↗

[A case of subdural empyema with transient cerebral white matter lesions].

We reported a fourteen years old male with subdural empyema followed by consecutive magnetic resonance imaging (MRI) examination. He was admitted to our hospital, complaining incomplete paresis of the left upper extremities, headache and high fever. The first MRI T2-weighted image at admission revealed an abnormal high intensity in the right frontal subdural space, indicating an abscess. Antibiotics therapy and a burr hole operation were effective and he made a remarkable recovery. One month later, the third MRI T2-weighted image showed an abnormal high intensity in the deep white matter of the right frontal lobe, which had not been detected in the subsequent MRI after the operation. On the other hand, the meningeal enhancement on the second Gd-DTPA enhanced MRI was more thickened than the previous meningeal enhancement. This abnormal high intensity on MRI had disappeared two month later, when the meningeal enhancement had grown thin. These data suggested the meningeal enhancement was relative to the transient high intensity which was considered to represent brain edema. We concluded that careful observation and serial MRI examination might be necessary in patient with subdural empyema even after disappearance of all symptoms.

Acute Disease↗

Motor cortex stimulation for deafferentation pain.

OBJECT: The authors tested a modified motor cortex stimulation (MCS) protocol for the treatment of deafferentation pain in 15 patients: eight patients with poststroke pain, four with brachial plexus injury, two with phantom limb pain, and one with spinal cord injury. METHODS: Preoperative pharmacological tests were performed with phentolamine, lidocaine, ketamine, thiopental, morphine, and a placebo. In 12 patients we placed a 20- or 40-grid electrode in the subdural space to determine the best stimulation point for pain relief over a few weeks and therefore the optimum position for a permanent internal device. In four patients, the MCS devices were implanted in the interhemispheric fissure to reduce lower-extremity pain. In one patient, the MCS device was placed within the central sulcus, and a 20-grid electrode was placed on the brain surface. In two patients with pain extending from the upper extremity to the hyperbody, dual-electrode devices were implanted to drive two electrodes. In 10 of the 15 patients MCS-induced pain reduction was achieved (four with excellent, two with good, and four with fair alleviation of pain). The result of pharmacological testing indicated that patients with ketamine sensitivity seem to be good candidates for MCS. CONCLUSIONS: Test stimulation with a subdural multigrid electrode was helpful in locating the best stimulation point for pain relief.

Aged↗

Motor cortex stimulation for central and peripheral deafferentation pain. Report of eight cases.

The authors tested a modified motor cortex stimulation protocol for treatment of central and peripheral types of deafferentation pain. Four patients with thalamic pain and four with peripheral deafferentation pain were studied. Preoperative pharmacological tests of pain relief were performed using phentolamine, lidocaine, ketamine, thiopental, and placebo. In five patients we placed a 20- or 40-electrode grid in the subdural space to determine the best stimulation point for pain relief for a few weeks before definitive placement of a four-electrode array. In three patients, the four-electrode array was implanted in the interhemispheric fissure as a one-stage procedure to treat lower-extremity pain. In two patients with pain extending from the extremity to the trunk or hip, dual devices were implanted to drive two electrodes. Six of eight patients experienced pain reduction (two each with excellent, good, and fair relief) from motor cortex stimulation. No correlation was apparent between pharmacological test results and the effectiveness of motor cortex stimulation. Patients with peripheral deafferentation pain, including two with phantom-limb pain and two with brachial plexus injury, attained pain relief from motor cortex stimulation, with excellent results in two cases. Testing performed with a subdural multiple-electrode grid was helpful in locating the best stimulation point for pain relief. Motor cortex stimulation may be effective for treating peripheral as well as central deafferentation pain.

Aged↗

Chronic subdural haematoma treatment with a rigid endoscope.

Surgical treatment is the method of choice in cases of chronic subdural haematoma--as a rule: trephination, drainage with lavage, or repeated drainage (drain reinsertion where the haematoma has been evacuated insufficiently). A poorly manageable but non-negligible group is made up of patients (about 5-12 % of all cases) where the less invasive methods of choice keep failing. The equally mini-invasive endoscopic technique appears to be one of the suitable therapeutical approaches before resorting to open-surgery revision. The adapted technique of rigid endoscope insertion permitting sufficient revision and treatment of the subdural space concerned is presented. The method is demonstrated on three case reports where routine trephination with lavage, drainage and repeated drain insertion failed. A very good improvement in clinical condition and graphic findings was achieved in two patients. In the remaining one, the neurological lesion improved ad integrum despite a tiny residual haematoma as visualized by CT. Two weeks later, a clinical relapse had developed and the patient was treated with new trephination and drain reinsertion. The technical aspects of the modification of the endoscopic technique are discussed: stressing the advantages or low-degree invasiveness, scope for keeping intact the inner membrane of the haematoma and avoiding direct invasion of the cerebral tissue. The limits of the method are discussed as well. The authors regard this method as a useful addition to the surgical armamentarium, especially in cases of chronic subdural haematomas resisting conventional approaches.

Aged↗

Spontaneous arterial subdural hematoma.

the occurrence of spontaneous arterial subdural hematomas is very rare. We report five patients who presented with sudden severe headache and who developed progressive neurological deficits, two becoming comatose. None had a history of trauma. A diagnosis of subarachnoid hemorrhage was suspected in all patients, but all proved to have subdural hematomas caused by "spontaneous" rupture of a cortical artery. Nineteen similar cases have been reported in the English literature. The source of bleeding was identified as a cortical artery located near the sylvian region in four of our five patients and in most of the reported cases. There are several possible anatomical situations that may predispose a cortical artery to "spontaneous" rupture: (a) spontaneous rupture of a cortical artery at the point of origin of a fragile arterial twig, especially a right-angled branch, a point of potential weakness; (b) rupture of a small artery traversing the subdural space and connecting a cortical artery to the dura mater (a "bridging" artery); (c) adhesions between a cortical artery and arachnoid or dura mater; (d) a knuckle of cortical artery protruding through the arachnoid and adherent to the dura mater. In each situation, the artery is probably torn by a sudden movement of the brain during a vigorous head movement, not severe enough to be considered trauma.

Adult↗

[A case of idiopathic spinal cord herniation].

The authors experienced a case of idiopathic spinal cord herniation with duplicated dura mater. A 63-year-old woman presented right dominant slowly progressive spastic paraplegia and dissociated sensory disturbance. Magnetic resonance imaging (MRI) demonstrated an enlarged dorsal arachnoid space associated with an apparently focally narrowed thoracic cord. The cord was kinked towards the anterior and closely applied to vertebral body at the level of Th3-4. Computed tomographic myelography (CTM) revealed homogeneous filling at dorsal arachnoid space immediately after injection and no defects. At operation multilocular arachnoid cyst and duplicated dura mater was respectively observed dorsally, and ventrally. From defected area of the inner layer, a ventral part of the spinal cord was incarcerated between the two dural layers. After rejection of arachnoid cyst and inner layer was performed, the patient recovered neurologically. Idiopathic spinal cord herniation is a rare disease that shows slowly progressive myelopathy at middle age. The herniations were observed at ventral thoracic cord in all reported cases. The mechanism of this disease is still uncertain. But at least three successive factors seem to be necessary for formation of herniation, 1) abnormal structure of the dura mater such as defect, diverticulum and duplication; 2) adhesion between the cord and the destructive dura mater, and 3) continuous cerebrospinal fluid (CSF) pressure pushing the cord outward from subdural space. In the thoracic spine, mobility is limited compared with the cervical and lumbar spine, and because of physiological curvature the cord situates rather ventrally. For these reasons the incidence of adhesion might be higher at ventral thoracic spine. Although neuroradiological imagings especially MRI and CTM were useful, operative findings were necessary for definitive diagnosis in many reported cases. Considering the effectiveness of surgical treatment, study of the ventral side of the cord should be important to avoid misdiagnosis.

Female↗

The effect of the glycine site-specific N-methyl-D-aspartate antagonist ACEA1021 on ischemic brain damage caused by acute subdural hematoma in the rat.

Acute subdural hematoma (SDH) complicates about 20% of severely head-injured patients, and death and severe disability frequently result, yet over half of these patients may have been conscious, at some time after injury, implying secondary mechanisms of brain damage. Drugs that block the "excitotoxic" effects of glutamate at the N-methyl-D-aspartate (NMDA) receptor have generally been effective in reducing ischemic brain damage associated with SDH in animal models, yet these agents all appear to be associated with major behavioral side effects, in conscious patients, at neuroprotective doses. We therefore evaluated the effects of treatment with a novel antagonist for the glycine binding site of the NMDA receptor (ACEA1021) upon ischemic brain damage, in the rat SDH model. ACEA1021 may be free of psychomotor effects, and may thus permit high dose therapy in conscious trauma and stroke patients. SDH was produced by the slow injection of 0.4 mL autologous blood into the subdural space overlying the parietal cortex. brain damage was assessed histologically at 8 coronal planes, in animals sacrificed 4 h after induction of hematoma. Both pre- and posttreatment with ACEA1021 significantly reduced hemispheric ischemic damage produced by SDH. The magnitude of neuroprotection with this compound (26 to 39% reduction in infarct size) is similar to other NMDA antagonists, and the robust posttreatment effect implies that human studies with this compound should be performed in head injured patients, subject to completion of toxicology testing.

Animals↗

ICP monitoring in the rat: comparison of monitoring in the ventricle, brain parenchyma, and cisterna magna.

Various methods of continuous intracranial pressure (ICP) monitoring during experimental procedures in the rat have been described. However, no systematic comparison of ICP monitoring in the ventricle, brain parenchyma, and cisterna magna has been reported. Since accurate and reliable ICP measurements are important in experimental models of traumatic brain injury, the present study was conducted to compare simultaneous ICP measurements from ventricular, cisterna magna, and intraparenchymal monitors during ICP changes. Subdural hematoma was produced by infusion of 0.3 ml of autologous blood into the subdural space over 6 min. The ventricular and the intraparenchymal fiberoptic catheter produced reliable and comparable pressure recordings, that did not statistically differ (p = 0.4), throughout the one hour monitoring time. In contrast, the cisterna magna catheter was less reliable and produced significantly lower readings throughout the monitoring time (p<0.001). The intraparenchymal device produced greater cortical damage than the ventricular catheter. In conclusion, ventricular ICP monitoring is the preferred method under these circumstances, since it is accurate and induces least brain damage.

Animals↗