Pathophysiology and Nonsurgical Treatment of Chronic Subdural Hematoma: From Past to Present to Future.

BACKGROUND: Chronic subdural hematoma (CSDH) is one of the more frequent pathologic entities in daily neurosurgical practice. Historically, CSDH was considered progressive recurrent bleeding with a traumatic cause. However, recent evidence has suggested a complex intertwined pathway of inflammation, angiogenesis, local coagulopathy, recurrent microbleeds, and exudates. The aim of the present review is to collect existing data on pathophysiology of CSDH to direct further research questions aiming to optimize treatment for the individual patient. METHODS: We performed a thorough literature search in PubMed, Ovid, EMBASE, CINAHL, and Google scholar, focusing on any aspect of the pathophysiology and nonsurgical treatment of CSDH. RESULTS: After a (minor) traumatic event, the dural border cell layer tears, which leads to the extravasation of cerebrospinal fluid and blood in the subdural space. A cascade of inflammation, impaired coagulation, fibrinolysis, and angiogenesis is set in motion. The most commonly used treatment is surgical drainage. However, because of the pathophysiologic mechanisms, the mortality and high morbidity associated with surgical drainage, drug therapy (dexamethasone, atorvastatin, tranexamic acid, or angiotensin-converting enzyme inhibitors) might be a beneficial alternative in many patients with CSDH. CONCLUSIONS: Based on pathophysiologic mechanisms, animal experiments, and small patient studies, medical treatment may play a role in the treatment of CSDH. There is a lack of level I evidence in the nonsurgical treatment of CSDH. Therefore, randomized controlled trials, currently lacking, are needed to assess which treatment is most effective in each individual patient.

Subdural Instillation of a Thrombolytic Agent for Treatment of Recurrent Subdural Hematoma.

OBJECTIVE: This study aims to report the case of a patient with recurrent subdural hemorrhage (SDH) who was administered tissue plasminogen activator through a subdural drain to enhance drainage and prevent recurrence. METHODS: An 85-year-old man was treated for subacute over chronic SDH that kept on reaccumulating despite serial twist drill drainage, burr hole drainage, and craniotomy. No coagulopathy was identified with adequate blood pressure control. RESULTS: Treatment with tissue plasminogen activator resulted in successful drainage of the SDH, and the patient had no further recurrence at 9-month follow-up.

Thoracolumbosacral spinal subdural abscess: magnetic resonance imaging appearance and limited surgical management.

STUDY DESIGN: Case report and review of relevant literature. OBJECTIVE: To report a rare case of a thoracolumbosacral spinal subdural abscess (SSA) and highlight the magnetic resonance imaging (MRI) appearance and surgical management. SUMMARY OF BACKGROUND DATA: SSA is rare, as most intraspinal abscesses are epidural in location. Extensive thoracolumbosacral SSA has only rarely been reported. The MRI features and options for limited surgical management are not well described. METHODS: A case report of SSA is presented and relevant literature is reviewed. RESULTS: An elderly female presented with worsening back pain and sepsis. MRI demonstrated an extensive intraspinal abscess, extending from the upper thoracic spine to the sacrum. Both axial and sagittal images demonstrated a subdural location of the collection, with preservation of the dorsal epidural fat and mass effect on the spinal cord. Cord compression was most marked at the T8 level. Limited midthoracic laminectomies were performed. The epidural space seemed normal intraoperatively. A limited longitudinal durotomy yielded purulent fluid. After intraoperative irrigation, primary dural repair was performed. At 2-year follow-up, the patient had no clinical, radiographical, or laboratory evidence of residual or recurrent spinal infection. CONCLUSION: Careful review of MRI can localize an intraspinal abscess to the subdural space. Even for extensive subdural collections, limited operative management can achieve excellent clinical outcome. LEVEL OF EVIDENCE: N/A.

Histological evidence for drug diffusion across the cerebral meninges into the underlying neocortex in rats.

Transmeningeal pharmacotherapy has been proposed to treat neurological disorders with localized pathology, such as intractable focal epilepsy. As a step toward understanding the diffusion and intracortical spread of transmeningeally delivered drugs, the present study used histological methods to determine the extent to which a marker compound, N-methyl-D-aspartate (NMDA), can diffuse into the neocortex through the meninges. Rats were implanted with bilateral parietal cortical epidural cups filled with 50 mM NMDA on the right side and artificial cerebrospinal fluid (ACSF) in the contralateral side. After 24 h, the histological effects of these treatments were evaluated using cresyl violet (Nissl) staining. The epidural NMDA exposure caused neuronal loss that in most animals extended from the pial surface through layer V. The area indicated by this neuronal loss was localized to the neocortical region underlying the epidural cup. These results suggest that NMDA-like, water soluble, small molecules can diffuse through the subdural/subarachnoid space into the underlying neocortex and spread in a limited fashion, close to the meningeal penetration site.

Unintended subdural injection: a complication of epidural anesthesia--a case report.

Epidural anesthesia is practiced in virtually every clinical setting. Its safety and versatility have supported increasing use for more and varied therapies. In a healthy patient in whom near-complete left hemiparesis developed following a routine continuous epidural anesthetic for labor, subdural deposit of the local anesthetic was suspected. The following case and discussion may help illustrate the mechanism behind this complication and how it can be detected, treated, and, possibly, avoided.

Extensive sensory block caused by accidental subdural catheterization during epidural labor analgesia.

A 32-year-old parturient requested epidural analgesia for labor. A lumbar epidural block was performed at the L1-2 interspace. Thirty minutes after the loading dose of the local anesthetic mixture, she suffered numbness in both arms and high sensory block up to the C6 dermatome without significant motor blockade. The retained epidural catheter was later confirmed radiologically to be in the subdural space. Accidental subdural catheterization is a rare complication of epidural block. Due to the smaller potential space, a subdural injection usually produces a high level block disproportional to the volume injected. Thus, patients receiving epidural block should be closely monitored following injection of local anesthetics regardless of the concentration or volume administered.

Inadvertent subdural spread complicating cervical epidural steroid injection with local anaesthetic agent.

Although cervical epidural steroid injection with local anaesthetic is considered a safe technique and widely practiced, complications may occur. We report a patient experiencing unexpected delayed high block, moderate hypotension and unconsciousness eight to ten minutes after an apparently normal cervical epidural steroid injection. The most probable diagnosis was a subdural block. Anatomical peculiarities of the epidural and subdural space in the cervical region increase the risk of subdural spread during cervical epidural injection. Fluoroscopic guidance is important during cervical epidural injection to increase certainty of correct needle placement, thus minimizing the risk of complications.

Accidental subdural catheterization due to complication of epidural anesthesia--a case report.

Although accidental subdural injection is a well-recognized complication of epidural block, only a mere handful cases have been substantially proven by radiological evidence. Here we report a case of subdural catheterization during the attempt of epidural anesthesia for a gynecological procedure. Its clinical course and radiological findings are compared with those of the cases previously reported in literature. Whenever there is the occurrence of widespread of sensory block together with respiratory distress and hemodynamic unstability following epidural injection of local anesthetic, a subdural injection should be considered in spite of a negative confirmation. Repeated subdural injection of a local anesthetic at the same site may predispose patients to serious morbidity. Therefore, we recommend that when a subdural injection is evident or suspected, reinsertion of the catheter in the epidural space via another entry or contemplation of a switch to another anesthetic technique is mandatory.

Subdural block--from a spinal? A case report.

INTRODUCTION: Multicompartmental blocks are commonly described in epidurals but not spinals. We describe a case of subarachnoid block performed in an obese patient which resulted in a clinical presentation resembling that of a subdural block. CLINICAL PICTURE: A 29-year-old woman, scheduled for saucerisation of thigh carbuncle, was administered 2.1 mL of hyperbaric bupivacaine. The spinal resulted in a late onset of sensory block that extended to the neck and upper limbs. There was no sympathetic or motor blockade. TREATMENT/OUTCOME: The block receded spontaneously without causing any cardiovascular or respiratory compromise. CONCLUSIONS: The diagnosis of subdural block must be considered in patients with unusual presentations after a spinal anaesthetic. Factors affecting spread of hyperbaric bupivacaine are also highlighted.

[Subdural, extra-arachnoid block as a complication of stellate ganglion block: documentation with ultrasound]. / Subdurale, extraarachnoidale Blockade als Komplikation des Ganglion-Stellatum-Blocks: Dokumentation mittels Sonographie.

We present a patient who developed a high central neural block after stellate-ganglion-blockade. The underlying pathophysiology was assessed via sonographic imaging. Stellate ganglion block was performed in a 19-year old patient according to the standard technique. Multiple aspiration tests were negative and a test dose of 3 ml bupivacaine 0.25% was injected. After a 3 min interval another 5 ml were injected. Two minutes after the local anaesthetic administration the patient reported nausea and sensations in the upper extremity. Spontaneous respiration efforts stopped, and the patient became unconscious. Tracheal intubation was performed, and the patient was ventilated in a controlled mode for two hours. Heart rate as well as blood pressure remained within the normal range. Neurologic recovery occurred rapidly and extubation was performed about two and a half hours after the event. Our sonographic studies demonstrated a local anaesthetic depot directly at the root of C 6, with a mean diameter of 10 mm and a length of 5 to 6 cm (about a third smaller than expected). Sonographic studies and clinical symptoms of our patient are most likely to occur with a subdural extra-arachnoidal block. Ultrasonographic guided puncture enhances the patient's safety by the opportunity to directly visualise transverse process, nerval root as well as local anaesthetic depot. In case of depot formation directly at the nerval root, injection may be stopped and the needle repositioned. Furthermore, direct visualisation of the great vessels (A. vertebralis) prevents intravascular injection and haematoma formation.

Neuroprotection by dextromethorphan in acute experimental subdural hematoma in the rat.

Experimental acute subdural hematoma in the rat has been shown to produce a zone of apparent infarction under the clot, and excitatory amino acid toxicity appears to play a role in the damage observed. We report the effect of dextromethorphan, a commonly used antitussive and a noncompetitive NMDA-type glutamate receptor antagonist, on the volume of histologic damage seen at 72 h after acute subdural hematoma in the rat. Sixty-five Long-Evans rats underwent placement of acute subdural hematoma using the "cranial window" model. Fourteen animals received oral dextromethorphan, 10 mg/kg/dose, twice daily for 3 days, and an additional 20 animals also received a single 20 mg/kg intraperitoneal dose 15 min after clot placement in addition to the oral regimen. Control animals received equal volumes of sterile water. Brain lesions in all animals were characterized by well-circumscribed infarctions underlying the subdural hematoma. Lesion volume in control animals was 88.3 +/- 9.3 mm3 (mean +/- standard error of the mean), while animals receiving dextromethorphan had significantly smaller lesions, which was independent of dosing schedule (59.9 +/- 9.2 mm3)(p = 0.0403). Animal weight was also found to be a significant covariate (p = 0.038). Because of its safety in humans and efficacy as a neuroprotectant in a variety of models, dextromethorphan may be a promising agent for clinical use, particularly in children.

Effect of lidocaine on the meninges in an experimental animal model.

Arachnoiditis has been reported in patients who had received previous epidural injections of anesthetic agents. The purpose of this study was to determine if epidural injections of lidocaine are sufficient to cause arachnoiditis. Four monkeys that received a single epidural injection of lidocaine hydrochloride 1% were compared to four controls that had epidural injections of 0.9% saline. Four dogs that had multiple epidural injections of lidocaine hydrochloride 1% were compared to four controls that had multiple injections of saline. All animals were killed on the eighty-fourth day of the experiment. The dural sac, containing nerve roots and spinal cord, was removed intact from the lumbar spinal canal, fixed, sectioned, stained, and examined microscopically for evidence of arachnoid inflammation and fibrosis. No significant changes were found in the treated animals. Lidocaine hydrochloride 1% injected singly or repeatedly in the epidural space does not appear to be a cause of significant chronic meningeal reaction.

Dynamic response of the intracranial system in the conscious dog to papaverine hydrochloride.

The influence of papaverine on the intracranial system of the dog was studied by measuring the pressure-depth-time response for the intact intracranial system, i.e., for the subarachnoid and subpial compartments. This was accomplished by a measurement system which provided an accurate pressure-depth determination and a uniform rate of transducer insertion. Distinct regions of the intracranial system (subarachnoid, transitional, and subpial) were identified from inflections in the pressure response curve. The test parameter, brain relative stiffness (BRS), was obtained by determining the slope of the pressure response values within the subpial region. This parameter is a measure of the "stiffness" or elasticity of bring tissue within the test configuration. A bolus injection of papaverine (1 mg per kilogram, i.v.) caused an increase in the transitional region, a compensatory reduction in the subarachnoid space, and an increase in BRS. It is postulated that at normotensive arterial blood pressure, cerebrovascular expansion caused by papaverine resulted in increased brain tissue elasticity, i.e., an increase in the pressure-depth response for the subpial region. Possible implications for this increase are discussed. Experiments should be conducted in which local blood flow studies are coupled with measurements of brain elastic response.