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Decompressive craniotomy has a place in acute hemispheric infarctions. Patient selection should be guided by CT to exclude those with huge dominant hemispheric lesions that make reasonable neurologic recovery unattainable. Intracranial pressure monitoring should reduce the severity of neurologic sequelae by providing earlier, more timely operative intervention.
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Delayed traumatic intracerebral hematomas found after an initially unrevealing computerized tomographic scan have been reported occasionally. Such hemorrhage may occur in an area of brain contusion with cerebral vessel injury. Four cases of intracerebral hematoma appearing after evacuation of a different traumatic intracranial mass lesion are reported. This suggests that an intracranial mass lesion may tamponade cerebral venous oozing in an area of brain contusion and delay the accumulation of intracerebral blood, accounting for the late discovery of a parenchymal hematoma. (Neurosurgery, 5: 653--655, 1979).
Forty-five infants with myelomeningocele in whom hydrocephalus was absent or adequately controlled developed signs and symptoms of the Arnold-Chiari malformation before the age of 3 months. All of them underwent laminectomy and opening of the dura mater for hindbrain decompression. The clinical presentation included swallowing difficulty, apneic episodes, stridor, bronchial aspiration, arm weakness, and opisthotonos. Within 2 weeks of the initial clinical presentation, the neurological status of 14 patients (31%) deteriorated dramatically and culminated in irreversible neurological deficits. In all patients, compression of the brain stem occurred in the spinal canal. A transverse dural band constricting the dural sac at the C-1 level was noted in 41% of the patients, and a mild degree of arachnoidal adhesion was noted in 23%. The lowermost level of the cerebellar tongue or medullary kink was located at C-1 to C-4 in 28 cases and at C-5 to T-1 in 17 cases. Twenty-eight (62%) of the patients were alive and 17 (38%) had died at the last follow-up assessment. All survivors showed improvement of their overall neurological function. Twenty-four made a complete recovery. The majority of deaths were attributed to respiratory failure. Early recognition of symptoms and prompt decompressive laminectomy are essential for successful management of the Arnold-Chiari malformation in infants.
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Ten patients with prior spinal cord trauma were examined preoperatively by metrizamide computed tomography (CT) and were studied subsequently by intraoperative spinal sonography. On comparing intraoperative sonography with metrizamide CT, it was found that metrizamide CT tends to overestimate the size and number of posttraumatic cysts, that areas of myelomalacia on metrizamide CT correspond to areas of abnormal echogenicity on intraoperative sonography, and that intracyst septations are seen only on intraoperative sonography. By monitoring the position of the shunting catheter during surgery, intraoperative sonography can assure its proper intramedullary placement and demonstrate the successful decompression of the cyst. If no cyst is found with intraoperative sonography, further surgery is obviated. Intraoperative sonography is recommended for all cases where decompression of cord cysts is planned.
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Between January, 1981, and July, 1991, 17 infants under 1 month of age were admitted to The Hospital for Sick Children with the signs and symptoms of a Chiari II malformation. These patients' presentation included swallowing difficulty (71%), stridor (59%), apneic spells (29%), aspiration (12%), weakness of cry (18%), and arm weakness (53%). Decompression of the Chiari II malformation was performed in all patients, with a time interval between onset of symptoms and surgery ranging from 1 to 121 days. Fifteen patients (88%) remain alive, all of whom have shown a complete recovery. The mean follow-up period in this group of patients was 65 months. Two patients died, one due to respiratory arrest 8 months after decompression and the other because of shunt infection and peritonitis 7 years after decompression. These results support the concept that compressive forces, rather than a primary intrinsic disorder of the brain-stem nuclei, play a crucial etiological role in the development of a symptomatic Chiari II malformation. Early recognition of the symptoms of Chiari II malformation should be followed by immediate decompressive laminectomy in order to promote a prompt and full neurological recovery.
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In leprosy, involvement of the posterior tibial nerve leads to sensory loss in the plantar aspect of the foot. As a result plantar ulcers are common and lead to deformity and disability. Restoration of plantar sensation can prevent ulcer formation. Posterior tibial decompression was done for the recovery of sensation in the plantar aspect of the foot. Seventy-two patients under went decompression on 84 feet, 25 received steroids pre- and post-operatively. The recovery of sensation was better if surgery was done before 6 months of onset of anaesthesia. Decompression along with steroids gave better results than decompression alone in patients with active neuritis especially in BT cases whereas in BB, BL and LL cases there was no significant improvement of sensation. The results are discussed.
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This article reports two cases of vascular decompression for tinnitus, both of which were successful. The pathophysiology of vascular compression syndromes in general and specifically eighth nerve vascular compression syndromes is reviewed. The anatomy of the anterior inferior cerebellar artery and its relationship to the eighth nerve complex is discussed in detail and the literature of vascular compression syndrome reviewed. Although no unequivocal definitive test procedure is available for preoperative diagnosis of vascular compression syndrome, the presence of the following features makes the diagnosis more likely: I-III interpeak latency abnormalities on auditory brain stem response (ABR), abnormalities of stapedius reflex, unilateral sensorineural hearing loss, ipsilateral electronystagmography (ENG) abnormalities, especially spontaneous nystagmus, and radiographic visualization of a vessel contacting the eighth nerve complex.
A case presenting with signs of spinal cord compression due to double contiguous thoracic disc herniation (TDH) is reported. A 66-year-old woman presented with a 4-month history of intermittent episodes of weakness and numbness in the lower extremities, and urinary dysfunction. Six weeks prior to admission complete paraplegia developed. The diagnosis was established by MRI. Treatment consisted of complete excision of the herniated discs (T8-T9 and T9-T10) and decompression of the spinal cord with a right transpedicular approach combined with standard posterior approach. The postoperative course was uneventful, and the improvement was dramatic. We also include a review of other 39 case reports from the literature. This article highlights the importance of consideration of TDH when one deals with a case with an anterior mass causing spinal cord compression.
BACKGROUND: Thoracic outlet compression syndrome is characterised by a variety of symptoms relating to compression of the neurovascular bundle. Though no one test is specific for the syndrome, relief of symptoms may be obtained following surgery in up to 99% of cases. PATIENTS AND METHODS: The notes of 118 patients operated on in 126 operations by a single surgeon using a supraclavicular approach were reviewed. Symptoms, pre-operative investigations, and complications were all documented. Outcome at 6 weeks, 6, 12 and 24 months follow-up was also recorded. In addition, 61 patients were contacted by telephone, in order to assess current level of symptoms. RESULTS: Symptoms were predominantly motor, sensory or vasomotor, and were present for a mean of 19.6 months prior to surgery. Complications were rare, but included a pneumothorax requiring a chest drain (n = 1) and infraclavicular anaesthesia (n = 13). The mean duration of hospital stay was 2.1 days. At 6 weeks follow up, 86.5% of patients reported either an improvement, or complete resolution of their symptoms. Sixty-one patients were contactable, a mean of 55 months following decompression. Of these, 44 (72.1%) were either improved or asymptomatic. CONCLUSION: Decompression for thoracic outlet compression syndrome through a supraclavicular approach encompassing first rib resection leads to good long-term results with few complications.